Prep For Clinical Practice

Question 1

-Absorbed dose

Answer 1

total amount of radiation absorbed by an object (International System of unit or SI unit: Gray (Gy)).

Question 2

Equivalent dose

Answer 2

absorbed dose x radiation weighing factor, to account for how harmful a type of radiation is to biological tissues (SI unit: Sievert (Sv)).

Question 3

Effective dose:

Answer 3

equivalent dose x tissue weighing factor, to account for the radiosensitivity of different organs and the increased risk of the patient developing stochastic (see below) effects (SI unit: Sievert (Sv)).

Question 4

Direct damage:

Answer 4

results in break of molecular bonds within cells (eg DNA).

Question 5

Indirect damage

Answer 5

esults in interaction with water leading to creation of free radicals, which in turn can break molecular bonds within cells.

Question 6

Deterministic effects

Answer 6

they occur at a specific dose threshold and represent tissue reactions; the severity of these effects is dose-dependent. Rapidly dividing cells are most sensitive and radiation sickness reflects body systems affected (eg dermatitis, burns, cataract, gastrointestinal disturbance or changes in blood). The latter are known as somatic effects.

Question 7

Stochastic effects

Answer 7

represent effects that have no threshold and occur randomly. The severity of the effects is not dose-dependent, but the probability for the effects to occur is dose-dependent.

Carcinogenic effect: tumors may be induced decades after the radiation exposure
Genetic effects: mutations may occur in the chromosomes of germ cells in the ovaries or testes, with potential effects in the offspring.

Question 8

ALARP

Answer 8

he main goal is to keep the radiation dose As Low As Reasonably Practicable (Achievable) at all times

Doses are kept lower than the threshold for deterministic effects.
As there is no threshold for stochastic effects, doses should always be kept as low as possible.

Question 9

Too high kVp will lead to

Answer 9

increased scatter production by the patient, increased scatter in the radiography room and reduced image contrast

Question 10

oo low kVp may lead to

Answer 10

increased exposure time, with a likelihood of motion artifacts and a need for repeat examination.

Question 11

Use a grid for subjects greater than

Answer 11

10 cm thick.

Question 12

Methods of protection against scatter radiation

Answer 12

time, distance, shielding

Question 13

Dosimetry

Answer 13

Measurement of radiation exposure

Question 14

Compton absorption

Answer 14

photon of electromagnetic energy interacts with a loosely bound electron in the outer shell of an atom.
The photon displaces the loosely bound electron which can ionize other atoms.
The photon is diverted and continues in a different direction with a lower energy ’Scattered radiation.

Increases with increasing energy.
As energy increases more of scattered radiation is directed in a forward direction, ie more likely to reach x-ray film.
Independent of atomic number of tissue.

Question 15

Production of scatter

Answer 15

catter is produced when x-rays interact with matter.
Lower energy than primary beam.
Travel in any direction.
Very important inlarge animal radiography.
At high kV less of the primary beam is converted to scatter but more scattered radiation is moving forward towards the film.
Increases with increasing volume of tissue irradiated.

ncreases radiation exposure to personnel.
Increases radiation dose to patient.
Reduces film contrast (increases overall film density in a non-specific way).

Question 16

how is scatter reduced?

Answer 16

collumation

Compress patient

Reduces volume of tissue irradiated.
Can be achieved using Bucky band - a webbing strap which can be tightened around the body (particularly abdomen).

Reduce kVReduce scatter affecting filmGrids

Placed between film and patient to absorb scatter.
Most scatter is travelling in an oblique direction and therefore is unable to pass through grid.
Results in increased exposure factors required.
Grid lines can appear on film.

Alternative filtration devices

Air gap between patient and film:
    Radiation travelling obliquely misses film.
    Important in large animal radiography where film is often some distance from object.
    Air gap increases magnification and reduces image sharpness.
Filter between patient and film: 

Lead backing to film cassettes

Reduce effects of scatter on film

Intensifying screens (particularly rare earth) intensify primary photons more than scatter.
Screens also increase gamma so that film contrast is enhanced and effect of scatter is reduced.

Question 17

When compiling an exposure chart as many variables as possible should be kept constant: what variables are these

Answer 17

Film focal distance.
Object film distance.
Processing
Film type
Intensifying screen type Radiography
Use of grid use.
Line mains compensation.

Question 18

Variable kV

Answer 18

This is used if:

Machine allows variation in kVp of 1-2.
Due to the variation in dog size and shape selecting an exposure based on dogs weight may be inaccurate.
Breed variability in conformation can be overcome by basing exposure on tissue thickness. Keep mAs constant and as high as possible and alter kV based on tissue thickness. A grid should be used if tissue depth is >10 cm and may be useful in smaller obese animals.

Question 19

Grids

Answer 19

If using a grid the exposure will need to be increased.
Multiply grid factor by mAs to obtain new mAs.

Question 20

X-rays

Answer 20

electromagnetic radiation.
Their usefulness stems from a number of properties:

Travel in straight lines.
Can pass through a vacuum.
Travel at constant speed.
Variably absorbed by body tissue.
Affect photographic film to produce a latent image ause certain substances to fluoresce (emit visible light)

X-rays are produced when electrons are rapidly deccelerated

Question 21

Kilovoltage (kV) control

Answer 21

Alters the potential difference applied across the tube head during exposure.
Alters the speed and energy with which electrons hit the target and hence the pentrating power of the subsequent x-ray beam.
In some machines it is linked to mA so that if high mA is selected, kV must be reduced.

Question 22

Milliamperage (mA) control

Answer 22

Controls the heating of the filament and hence the number of electrons released by the cathode.
This directly affects the quantity of x-rays produced.

Question 23

Timer (x rays)

Answer 23

The time for which the exposure is applied affects the number of x-rays produced.
The quantity is usually measured as a combination of amperage and time, ie mAs.
The longer the exposure the more chance there is of a patient moving so it is preferable to use the highest mA permissible with a given kV and reduce the exposure time accordingly.
Older machines had clockwork timers but new machines have electronic timers which are quieter and more accurate.

Question 24

Portable x ray machines

Answer 24

Stationary anode (heat lost by convection and conduction).
Self or half wave rectified.
Often fixed mA
Occasionally fixed kV.
Run from domestic supply (13 amp).
Cheaper than mobile/3-phase machines to buy and maintain.
Can be dismantled and used for domicillary examinations.

Question 25

mobile x ray machines

Answer 25

Rotating anode (heat lost by radiation) Usually full wave rectified - 2-pulse. May be capacitor discharged. High and variable mA facilitating shorter exposure times. Higher output allows grid and grid use to be used more readily. More expensive to buy and maintain than portable machines. Limited to use within the practice unless van or trailer used!

Question 26

3-phase x ray machines

Answer 26

Rotating anode. Full wave rectified - 6 pulse. High and variable mA and kV. Very high exposures and short exposure times possible. Expensive to buy and service. Fixed installation ’ dedicated room needed.

Question 27

Medium frequency (high frequency) x-ray machines

Answer 27

An invertor increases the frequency of the electrical supply so that with vastly increased number of pulses the ripple factor is negligible and the generator is equivalent to a constant potential unit. Used in some mobile machines which may use a battery supply and some fixed machines which run off a 13 amp supply.

Question 28

Pharmacokinetics

Answer 28

what the body does to the drugp

Question 29

Pharmacodynamics (PD)

Answer 29

What the drug does to the body

Question 30

ADME

Answer 30

Absorption (administration), distribution, metabolism and elimination; ADME Given the heterogonous structure of bodies, on top of its target a drug will inevitably interact with more than one element (side effects possible). Understanding the ADME (absorption/distribution/metabolism/excretion) of a compound is central to any therapy.

Question 31

A - Routes of Administration

Answer 31

Enteral routes: Directly into the gastrointestinal tract Sublingual Swallowing Rectal Parenteral routes: Topical admin. Intradermal admin. Subcutaneous admin. Intramuscular admin. Intravascular admin. Inhalation

Question 32

Intravascular administration

Answer 32

Mostly used when there is a need to control accurately the body concentration of drugs. Typically used when compounds have narrow margins of safety between therapeutic and toxic index (e.g. induction agents/anticancer drugs). Drawback: Drug injected cannot be recalled . A slow infusion administration is needed to avoid side effects.

Question 33

Inhalation administration

Answer 33

Gas and aerosols: Rapid systemic effect but dependent on: 1- the tidal volume 2- the size of the aerosol particle (not true for gas). The smaller the more likely to reach alveolar ducts and sacs. Otherwise get stacked in bronchi.

Question 34

D - Distribution

Answer 34

Distribution around the body occurs after drug reaches circulation It must then penetrate tissues to act consider Movement of drugs across membranes- passive, active, ionic Active transport / Carrier mediated transport In general, compounds that rapidly cross membranes have: a. Low degree of ionization b. High lipid/water partition in the non ionized form c. Relatively low MW < 1000 d. A biological affinity with transporters/facilitated diffusion (e.g. cephalporins are absorbed by a transporter for dipeptides)

Question 35

Effect of ionization on drugs crossing membranes

Answer 35

Must be neutral to cross the membrane (if too charged they would associate with many other molecules which would impair their ability to diffuse). Many drugs are weak acids or weak bases Recall that weak acids (HA) donate (H+) to form anions: HA↔H++A- Recall that weak bases (B) accept a proton (H+) to form cations: BH+ ↔B+ H+ Recall Henderson-Hasselbalch equation: pH=pKa+log[nonprotonated/protonated] pH=pKa: protonated form equal to nonprotonated concentration pHpKa: vice versa (dont need to know this just understad concept) An example! Effects of ionization on the macrolide antibiotic erythromycin Erythromycin pka = 8.8 Plasma pH = 7.4. Milk pH = 6.5 Given pH = pka + log non-ionized/ionized In milk, 199.5 ionized to every non-ionized, in plasma 25 parts ionized to every nonionized = ION TRAPPING

Question 36

Chemical Properties of Drugs- isomers

Answer 36

constitutional isomers setrioisomers- diastereomers (cis/trans)- conformers, rotamers enantomers

Question 37

M - Drug metabolism

Answer 37

Lipophilic drugs must follow a very special treatment to become hydrophilic (polar), often inactive, and then be excreted. The drug transformation may be a two phase reaction (but the phase I may be sufficient to inactive and excrete the drug) In the liver the major drug metabolising enzymes act in the Smooth Endoplasmic Reticulum of Liver Cells (hepatocytes)

Question 38

aneamia can effect

Answer 38

drug metabolism

Question 39

Metabolism and CYPs

Answer 39

The majority of CYPs are found in the liver, but certain CYPs are also present in the cell wall of the intestine. The mammalian CYPs are bound to the endoplasmic reticulum, and are therefore membrane bound CYP 3A4, CYP 2D6, and CYP 2C9 are especially involved in the metabolism of xenobiotics and drugs in humans (and probably veterinary species)

Question 40

Metabolism & Glucuronidation

Answer 40

The major phase II drug metabolising family of enzymes are the Uridine Diphosphate Glucuronyl Transferases (UGTs) Cats are deficient in UGTs – Limited ability to perform glucuronidation – Paracetamol toxicity Metabolites known as glucuronide conjugates – Excreted in bile and urine – Limited stability and can hydrolyse in the gut – Undergo enterohepatic recirculation

Question 41

major routs of Drug excretion

Answer 41

renal billary- faeces pulminoary

Question 42

minor routs of excretion

Answer 42

mammary salivary

Question 43

Biliary excretion

Answer 43

Parent drug or metabolites may either be excreted in bile and eliminated via the GI tract or recycle several times before entering the systemic circulation (the drug follows bile salts) Specific liver transporters are involved in the biliary excretion of metabolized drugs Drugs can be very long lasting (e.g. Antibiotics)

Question 44

renal excretion

Answer 44

passive filtration, secretion and reabsorbtion

Question 45

Pharmacokinetic Drug-DrugInteractions

Answer 45

Tissue/plasma levels of one drug altered by another one – Absorption • Change in gastric pH • Alteration in bacterial flora • Decreased gastric emptying – metaclopramide – Excretion • Sodium bicarbonate makes urine more alkaline – increases excretion of weak acids (why?) • Probenecid reduces renal excretion of penicillins – Some drugs reduce circulation and may therefore reduce • Clearance • Elimination – Eg alpha-2 agonists – Metabolism • Enzyme inhibition/induction

Question 46

Quantitative Pharmacokinetics (PK)

Answer 46

Changes in plasma/tissue drug concentration with time

Question 47

Quantitative Pharmacodynamics (PD)

Answer 47

– Changes in biological response with time

Question 48

Absorption kinetics

Answer 48

IV infusion = zero order kinetics (straight line on grph) IM/SC/oral = tend to follow first order kinetics. (increasing line on graph) Absorption rate from oral administration tends to be proportional to amount of drug (first order) Amount of drug at administration site decreases with time therefore, rate of absorption decreases

Question 49

Drug Elimination Rate

Answer 49

The amount of parent drug eliminated from the body per unit time – occurs after distribution Volume of water in glass tank is analogous to the volume of blood plus interstitial fluid (body water) also described as the initial volume of distribution (Vi) Concentration of contaminant in water = 100 mg / 10 L = 10 mg / L This is analogous to drug concentration in blood immediately after IV bolus dosing Contaminant stuck on glass is in equilibrium with contaminant in solution Concentration of contaminant in solution = 30 mg / 10 L = 3 mg / L This is analogous to the concentration of a drug in blood after distribution to tissue

Question 50

Volume of distribution

Answer 50

Vd usually given in litres/kg TBW approx. 0.6LKg ECF approx. 0.1-0.3L/Kg Vd of 0.1-0.3L/Kg drug most likely water soluble and mainly in ECF. E.g., midazolam or NSAIDs Vd high (2L/Kg +) drug accumulates in another site – e.g., fentanyl in fat

Question 51

Properties of X-rays and Gamma Rays:

Answer 51

No charge and no mass Invisible and cannot be felt Travel at speed of light Travel in straight line Penetrate all matter to some degree Cause some substances to fluoresce Expose photographic emulsion Ionise atoms X-rays are produced by the interaction of electrons with an atom 2 types: Characteristic Bremsstrahlung (braking)

Question 52

Cathode

Answer 52

coiled tungsten wire The cathode in an X-ray tube generates a stream of electrons via thermionic emission Potential difference applied across the X-ray tube accelerates the electrons towards the positively charged anode These hit and interact with the atoms within the target area of the anode resulting in the release of X-rays

Question 53

Radiodensity (or radiopacity)

Answer 53

is opacity to the radio wave and X-ray portion of the electromagnetic spectrum: that is, the relative inability of those kinds of electromagnetic radiation to pass through a particular material.

Question 54

Scatter

Answer 54

The effect of the X-ray beam striking another atom Lower energy radiation produced in the patient’s body tissues - Compton Effect Amount depends on: Density/atomic no. of the patient/tissue Increases in kV- higher penetration higher dose- may stay in tissues- domino effect of ionisation Larger area (collimation) As the size of the field increases, the amount of scatter will increase Properties May travel in any direction Image degradation Ionisation in tissues Radiation dose – patient, YOU!

Question 55

Harmful effects of X-rays

Answer 55

Genetic effects Increased risk of DNA mutation and inherited abnormalities with ionising radiation Somatic effects Skin erythema, BM hypoplasia, abortion.. Carcinogenic effects- Rapidly dividing cells most susceptible Persons under 18 Pregnant women (foetus) Bone marrow Gonadal tissue/repro organs Germinal layers of skin (and gut)

Question 56

legilation on radiation saftey

Answer 56

Ionising Radiations Regulations 2017 (IRR17) BVA Guidance Notes for the Safe use of Ionising Radiations in Veterinary Practice Must appoint a Radiation Protection Advisor and a Radiation Protection Supervisor Must define and identify a controlled area Must draw up and follow Local Rules

Question 57

Radiation Protection Advisor

Answer 57

External to practice Advanced knowledge of radiation (e.g. Radiation Physicist or Veterinary Diploma holder) Must hold a RPA Certificate of Competence Initially helps design and setup radiography facilities (or when any significant changes) Establishes Local Rules Annual visits to advise on: Room design Layout and shielding Siting and use of equipment Local Rules Dosimetry

Question 58

Radiation Protection Supervisor

Answer 58

Member of staff within practice Responsible for day-to-day supervision and enforcement of rules Makes sure local rules are followed Keeps local rules and other paperwork up to date Understand legal requirements Ensures radiation doses are kept to a minimum Manage radiation emergencies Consults with RPA where necessary

Question 59

Local Rules (for x-ray

Answer 59

Code of conduct for performing radiography Should be in an easily visible place Should be read and understood by every member of staff involved in radiography Detail equipment, procedures and access restrictions List RPA, RPS and any staff involved in radiography Define controlled areas (in practice and for mobile work) Includes written arrangements for making radiographs, including restraint, record keeping and protective clothing

Question 60

Controlled Area (for x-ray)

Answer 60

Area where there is risk of significant radiographic exposure Determined by Radiation Protection Advisor Should be clearly defined with warning signs Primary beam stopped by 4½ inches of brick (double thickness) or 1mm of lead Scattered radiation stopped by single brick thickness Radiation not stopped by wood or glass (lead glass and lead lining may be used in protective doors)

Question 61

Creating controlled area (for x-rays) in the field

Answer 61

Don’t take radiographs in the stable Too confined Cant visualise behind stable wall Stay in open area/yard with good line of sight in the direction of the primary beam Work on 20 metre control zone Based on Inverse Square Law, at that distance, the dose from a single diagnostic radiograph will be negligible Double the distance reduces the exposure risk 4-fold

Question 62

Dose Monitoring

Answer 62

Film badges or TLDs (thermoluminescent dosimeters) most commonly used Must be worn by all staff involved in radiography on a regular basis Must be regularly checked (usually every 1-3 months, depending on practice) The badge must be OVER the lead, not underneath it Worn on the chest/neck area

Question 63

Film-focal Distance

Answer 63

The closer the x-ray tube to the film or plate, the more “concentrated” the x-ray beam and vice versa The exposure varies according to the inverse square law Particularly in-field radiography Maintain source-image distance (SID) for the radiograph itself

Question 64

Controlling Scatter

Answer 64

1. To reduce scatter produced: Adequate collimation Use lowest kV compatible with a diagnostic image 2. To reduce amount of scatter reaching the plate: Use of a grid Functions: Absorb secondary scattered radiation Allows primary beam to pass through to form the useful image on the film Used when x-raying patient/part >10cm thick Grid factor – when a grid is used, the amount of exposure required increases. The exposure factors increased is the mAs 3. Reduce effect of scatter on personnel

Question 65

Milliampere-seconds (mAs)

Answer 65

The number of electrons generated at the cathode is determined by the mA (milliamperes) and exposure time mA relates to the tube current Milliampere-seconds (mAs) is the product of mA and time in seconds The mA governs the current applied to the filament and this is applied for a specific time (= sec.) Increased mA = Increased tube current -> Increased number of electrons -> Greater number of x-rays are produced HOWEVER The energy of the x-rays is unchanged mA x sec = mAs mAs is a measure of the number of X-rays produced

Question 66

the kV (kilovolts)

Answer 66

Potential difference applied across the X-ray tube Aka The energy of the electrons striking the anode is determined by the kV (kilovolts) applied (sometimes called kVp = kilovolt peak) Increase kV.. Increased energy of electrons Increasing kV = Increased electron acceleration  Increased energy of electrons = Greater number of x-rays are produced AND X-rays have increased energy = increased penetrating power

Question 67

Quality (x ray)

Answer 67

penetrating power of the beam

Question 68

Intensity (xray)

Answer 68

amount of radiation in the beam mA affects intensity only

Question 69

3 basic things for Xray production:

Answer 69

Source of electrons (through thermionic emission) A means of accelerating those electrons (kV) A means of decelerating the electrons (slamming into the anode)

Question 70

Attenuation

Answer 70

Reduction in intensity of the X-ray beam as it passes through the matter Due to absorption or scatter or both!

Question 71

Absorption

Answer 71

The energy from X-ray photon transferred to atoms of absorber. As more energy is absorbed, the number of X-rays reaching the film reduces – and therefore affects the appearance of the radiograph! So tissues are seen on a radiograph in various shades of grey according to how much they absorb.

Question 72

Interaction of X-rays with tissues

Answer 72

The five basic densities: Metal – White (all x-rays absorbed) Bone – nearly white Soft tissue/Fluid – mid grey Fat – dark grey Gas – very dark/black (few x-rays absorbed)

Question 73

The optimal radiograph

Answer 73

Well positioned Good collimation, centring Good definition, no film faults A wide range of well differentiated shades of grey This means a balance of kV and mAs to ensure there is enough penetration of the patient with sufficient X-rays passing through Exposure charts help obtain consistent results!

Question 74

Pink Camels Collect Extra Large Apples

Answer 74

positioning centering collumation expousure labling artifacts

Question 75

Positioning

Answer 75

Position the area of interest as close as possible to the cassette Anatomical distortion Rotation Standard radiographic positions Use a reference text for standard views Described in detail in later lectures and in CS booklets

Question 76

Centring

Answer 76

Centre the primary beam over the area of interest Can lead to distortion on the image Centre in middle of area of interest AND middle of the cassette

Question 77

Collimation

Answer 77

Scatter contributes to image opacity And increases radiation hazard Collimate beam to minimum size necessary But include enough! The primary beam should ALWAYS be contained within the area of the cassette Is it collimated sufficiently? Safety Describe the number of unexposed borders seen within the boundary of the film/cassette. 0% 25% 50% 100% for 1,2,3,4 sides seen

Question 78

Exposure

Answer 78

underexposed- too white overexposed- too dark

Question 79

Contrast

Answer 79

Difference between radiographic densities Seen as shades of grey Ideal is with extremes of black and white To improve contrast, must adjust the penetration of the X-ray beam.. How? … This will change the amount of the x-ray beam absorbed by the tissues and therefore the shades of grey

Question 80

Labelling

Answer 80

abelling: Patient details and date Exposed onto film, digital (embedded) Side markers – should always be exposed onto the image Side of body/recumbency (L/R)

Question 81

Artefacts:

Answer 81

Things that shouldn’t be there! Sandbags, troughs, driplines, collars!

Question 82

radiographic quality

Answer 82

Blurring Magnification Distortion Scatter Good definition? Any film faults? Pink Camels..

Question 83

Blurring (xray)

Answer 83

Movement Involuntary e.g. breathing Voluntary e.g. conscious How do we overcome this? Chemical restraint, positioning aids

Question 84

Magnification/Distortion (xray)

Answer 84

Primary beam diverges with distance from the tube Can also lead to geometric distortion if object is positioned obliquely to the beam

Question 85

Beam intensity

Answer 85

Amount of radiation (number of X-ray photons) in beam affected by mAs and KV

Question 86

Beam quality

Answer 86

Beam quality Penetrating power of beam affected by KV

Question 87

Density of the image

Answer 87

Amount of blackening of the image Affected by mAs and KV (film)

Question 88

Contrast of the image

Answer 88

The range of shades of grey in the image Affected by KV (film)

Question 89

The Ultrasound Machine

Answer 89

(Ultra) Sound Waves Medium required (liquid, solid, gas) for propagation Piezoelectric crystals oscillate = sound waves Reflected differently by different tissue types Picked up by transducer = image Piezoelectric crystals – an electric voltage is applied to the crystals which causes them to oscillate which is then transmitted as an ultrasound wave into the body. The wave hits something, bouncing back as an echo. The crystals converts the receiving echo into electricity which is then converted into a real-time image on the screen The transmitted sound waves pass through the thin layer of skin, but bounce off fluids, tissues and internal organs. These reflected waves are received by the probe, which converts them into electric signals which is the converted into an image

Question 90

Gain- ultrasound

Answer 90

overall brightness

Question 91

TGC (Time Gain Compensation)

Answer 91

selectively adjusting the gain at different depths Near field vs far field accounts for diffrent layers

Question 92

Focus zones and position

Answer 92

The pulse of ultrasound can be manipulated to be at its narrowest at a particular depth, the focal position. Maximise image quality The focal zone is typically positioned at or just below the object you are evaluating. like a zoom on a tissue

Question 93

Depth

Answer 93

“zooms in” in 1cm graduations. Higher the depth, lower the image quality. Depth = the time it takes for the echo to return from the organ

Question 94

Frequency

Answer 94

- image resolution at the level of the object being evaluated.  highest frequency for a superficial object (in the near field).  lowest frequency for a deeper object 

Question 95

Higher frequency (ultrasound)

Answer 95

decreased penetration but with increased resolution

Question 96

lower frequency (ultrasound)

Answer 96

Lower frequency = better penetration with decreased resolution

Question 97

Echogenicity

Answer 97

Echogenicity is a measure of acoustic reflectance, i.e. the ability of a tissue to reflect an ultrasound wave. Or “how many echoes are bounced back” The source of echogenicity is impedance mismatching between tissues

Question 98

Hyperechoic

Answer 98

= tissues that produce strong echoes Fat, bone, stones, air Bright/white as ultrasound is reflected

Question 99

Hypoechoic

Answer 99

tissues that produce few echoes Soft tissue, muscle Grey as some ultrasound passes through the tissue, some is reflected

Question 100

Anechoic

Answer 100

structures that produce no echoes Fluid Dark as no ultrasound waves are reflected

Question 101

Reverberation echo:

Answer 101

Produced by a pulse bouncing back and forth between two interfaces Transducer:Tissue or tissue:tissue More likely to occur from highly reflective surfaces like gas and bone

Question 102

Homogenous

Answer 102

uniform

Question 103

Heterogenous

Answer 103

non-uniform

Question 104

Shadowing

Answer 104

Complete reflection of the sound beam Zone deep to structure will be anechoic Bone, gas, calculi

Question 105

Mirror Image

Answer 105

A strongly reflective, obliquely orientated surface may reflect the sound beam distally instead of returning it to the transducer Takes longer for the sound waves to return, the image will appear deeper to the structure it is reflecting

Question 106

drug volume=

Answer 106

(weight x dosage)/ drug concentration

Question 107

drug dosage=

Answer 107

(mg/kg) /weight

Question 108

Flow rate =

Answer 108

Volume (ml) / Time (hours) Drop Rate

Question 109

Total Body (Blood) Clearance

Answer 109

the volume of blood plasma cleared of parent drug per time unit or a constant relating to the rate of elimination to the blood/plasma concentration

Question 110

Bioavailability

Answer 110

how much of the drug taken orally that actually gets to the blood plasma

Question 111

one compartment model

Answer 111

body is seen as one single compartment

Question 112

two compartment model

Answer 112

bosy is seen as teo compartments vessel rich group and then to other tissues in the brain heart and kidneys

Question 113

vessel rich group

Answer 113

Lung, brain, heart, and major organs (liver, kidney) have a relatively high blood flow (vessel-rich group [VRG]) compared with muscle and fat and are more susceptible to anesthetic drug-related effects

Question 114

theraputic window

Answer 114

the plasma concentration at which the drug is effective

Question 115

Tmax

Answer 115

the point on the curve where the drug is most active in the body

Question 116

Constant rate infusions

Answer 116

a loading dose is given and then a low, constant rate of the drug i given to keep within theraputic window

Question 117

multiple dosing

Answer 117

giving multiple dosing to keep drug level in theraputic range can lead to overdose

Question 118

loading dose

Answer 118

A loading dose is an initial higher dose of a drug that may be given at the beginning of a course of treatment before dropping down to a lower maintenance dose A loading dose is most useful for drugs that are eliminated from the body relatively slowly, i.e. have a long systemic half-life Without an initial higher dose, it would take a long time for the concentration of these drugs to reach therapeutic levels Examples include ketamine and fentanyl

Question 119

what type of biological molecules can drugs interact with

Answer 119

most often proteins e.g Enzymes (e.g. ACE inhibitors, aspirin, neostigmine) Carrier Molecules (e.g. flavonoid – Pgp antagonist, digoxin) Ion channels (e.g. verapamil - L-type calcium channel antagonist) Receptors (e.g. benzodiazepine – GABA receptor agonist, adrenoceptor agonists and antagonists ) Structural proteins (e.g. Taxol – Tubulin “agonist”) DNA (e.g. anti cancer agents like Doxorubicin) (dont need to memorise)

Question 120

Lipophilicity (Hydrophobicity)

Answer 120

drugs that are hydrophobic may stay in cell membrane and dissrupt cell membrane this is how inhaled anathetic drugs have a CNS effect vey lipid soluble molecules take only low doses to produce an anethetic effect

Question 121

receptors

Answer 121

Protein molecules whose function is to recognise and respond to endogenous chemical signals. – Chemicals which mimic the endogenous signals (i.e. drugs) will also elicit an effect. Drugs need to bind to receptors with high affinity and high specificity However…drugs generally lack complete specificity

Question 122

Dose response curves

Answer 122

how do we know a drug is doing what we want shaped graphs x axis= concentration y axix= effect of drug shows at a low does there is little effect rapid increase in the theraputic window platues at high does- this could be where you see side effects

Question 123

Potency

Answer 123

amount of drug required to produce 50% of its maximal effects. Used to compare drugs within a chemical class (usually expressed in milligrams/kg). Example: if 5 mg/kg of drug A relieves pain as effectively as 10 mg/kg of drug B, drug A is twice as potent as drug B.

Question 124

Efficacy

Answer 124

the maximum therapeutic response that a drug can produce (example: morphine vs buprenorphine) the tendency of a drug to activate the receptor once bound

Question 125

Agonism

Answer 125

an agonist produces a responce in a receptor a full agonist If the activation is 100%, namely each time a drug interacts with its target there is a response then the agonist is said to be a “full agonist” If the activation is <100%, the agonist is said “partial agonist”. Partial agonists have lower efficacy than full agonists – even with maximal occupancy of receptors. An agonist has affinity and efficacy – therefore elicits a biological response

Question 126

Affinity

Answer 126

the tendency of a drug to bind to the receptor

Question 127

Antagonism

Answer 127

Antagonist: molecule/drug that binds a receptor without activation Antagonist have affinity but zero efficacy (as they block the target activity) Main types of antagonism: • Competitive • Non-competitive • Irreversible

Question 128

competative antagonists

Answer 128

Competitive agonists compete with agonists for the receptor binding site. The chemical structure of the agonist and competitive antagonist are often similar (lock and key hypothesis). Antagonist binds to receptor in such a way as to prevent agonist binding Competitive antagonism is surmountable – additional agonist can overcome the receptor blockade. Addition of a competitive antagonist shifts the dose response curve of the agonist to the right (e.g. methadone/naloxone)- more drug will have to be given to overcome the block decrece potency but not efficacy

Question 129

Non-competitive Antagonism

Answer 129

Non-competitive antagonists either bind to a different receptor site, blocking the desired receptor OR Block the chain of events “post” binding - acting “downstream” of the receptor. ketamine is an example of this decrese potency and efficacy

Question 130

Irreversible Antagonism

Answer 130

Antagonist dissociates from the receptor only very slowly or not at all. The antagonist forms covalent bonds with the receptor. Irreversible antagonism is insurmountable – additional agonist cannot overcome the receptor blockade. Often used in drug discovery, rarely in practice – risky asprin and omeprozol, anticancer drugs

Question 131

Inverse agonism

Answer 131

drug that reduces the activation of a receptor with constitutive activity (example: GABAA receptor)- these receptors fire without stimulation Can be regarded as drugs with negative efficacy.

Question 132

Therapeutic index =

Answer 132

toxic dose (or LD50) ÷ effective dose (or ED50) EC50: Effective concentration. The dose required for an individual to experience 50% of the maximal effect. ED50: Effective dose. The dose for 50% of the population to obtain the therapeutic effect

Question 133

EC50:

Answer 133

Effective concentration. The dose required for an individual to experience 50% of the maximal effect.

Question 134

ED50:

Answer 134

Effective dose. The dose for 50% of the population to obtain the therapeutic effect.

Question 135

Would an ideal drug have a small or large therapeutic index?

Answer 135

large! ideally you want a large toxic dose and small effective dose

Question 136

Drug receptor types

Answer 136

Ion channel cell surface transmembrane receptor- things tha topen up to let ions in and out of cells to change polarity and make them less or more likley to fire- drugs can open and close these channels Ligand regulated enzyme- brings molecules toghther to form active catalitic domain G-protein coupled receptors Protein synthesis regulating receptor- can upregulate or decrease. acth stimulation test

Question 137

Tachyphylaxis (“rapid protection”).

Answer 137

Reduction in drug tolerance which develops after a short period of repeated dosing. Not common. Often due to a lack of a co-factor. the bosy runs out of the effect the drug asks it to produce happens in mainly IV drugs- addrenaline not self antagonism

Question 138

Self-Antagonism

Answer 138

When a drug becomes antagonistic to its own effects

Question 139

Loss of target sensitivity

Answer 139

Change in receptors- become resistant to drug stimulation/conformational changes Loss of receptors - endocytosis Exhaustion of mediators- degradation/low re-expression level Increased metabolic degradation- higher concentration of drugs are needed Physiological adaptation- crosstalk between body systems, one takes over Drug transporters- drug removed from receptor sites

Question 140

Drug-drug interactions

Answer 140

Potential outcomes of drug-drug interactions: • Action of one or more drugs is ENHANCED • Development of totally NEW EFFECTS • INHIBITORY effects on one drug on the other • NO CHANGE

Question 141

ligand regulated enzyme

Answer 141

the binding of an extracellular ligand causes enzymatic activity on the intracellular side

Question 142

G-protein coupled receptors

Answer 142

integral membrane proteins that are used by cells to convert extracellular signals into intracellular responses activated by agonists When a ligand binds to the GPCR it causes a conformational change in the GPCR, which allows it to act as a guanine nucleotide exchange factor (GEF). The GPCR can then activate an associated G protein by exchanging the GDP bound to the G protein for a GTP. The G protein's α subunit, together with the bound GTP, can then dissociate from the β and γ subunits to further affect intracellular signaling proteins or target functional proteins directly depending on the α subunit type GPCRs are an important drug target

Question 143

CRI

Answer 143

constant rate infusion the use of low levels of agents to maintain theraputic dose

Question 144

CD

Answer 144

controlled drug

Question 145

TIVA

Answer 145

total intravenous anaesthesia

Question 146

PO/SC/IM/IV are all ...

Answer 146

dosing routes

Question 147

describe the diffrent sites analgesia may act on

Answer 147

They may act at the site of injury and decrease the pain associated with an inflammatory reaction (e.g. NSAIDs) They may alter nerve conduction (e.g. local anaesthetics) They may modify transmission in the dorsal horn (e.g. opioids & some antidepressants) They may affect the central component and the emotional aspects of pain (e.g. opioids & antidepressants)

Question 148

Opioids

Answer 148

Natural (opiate) and synthetic (opioid) drugs Endogenous opiates Opioid receptors identified; mu(most important), delta, kappa (important in birds), nociceptin Effect depends on dose, route, species, stimulus etc CVS effects, pruritis, urinary retention, ileus, pancreatic duct, temperature, miosis, mydraisis, vomiting & nausea, mania & respiratory depression?- MOSTLY IN PEOPLE, side effects limited in vet species decrease the likly hood that pain signals will be firesd at primary and secondary neurons- work a t a numebr of sites

Question 149

Morphine

Answer 149

The most efficacious opioid at relieving pain It is a full agonist at mu, delta and kappa receptors Not licensed. (CD II) Nevertheless still used widely CRIs and epidurals plus horses

Question 150

Methadone

Answer 150

opiate A synthetic mu agonist (full) & affinity for NMDA receptor Has effects as a norepinephrine and serotonin reuptake inhibitor Following IV - duration of action is approximately 4 hours (can be longer with sc) Vomiting – not usually Use as premed, for sedation, intra op (v slow IV), on recovery, and as CRI Poor oral availability Licensed for dogs and cats. CD II

Question 151

Pethidine (Meperidine)

Answer 151

Synthetic agonist at the mu receptor Also shown to block sodium channels Agonist at alpha 2 B subtypes Negative inotropic effects but tends to increase heart rate NOT IV- Can induce histamine release, im only Pethidine should not be administered to dogs receiving selegiline Monoamine oxidase inhibitor + pethidine ≡ serotonin syndrome CD II (licensed for dogs, cats, horses) Spasmodic colic DOA (duration of action) ≈ 90 minutes- short acting

Question 152

Fentanyl

Answer 152

Fentanyl is a highly lipid soluble short acting mu opioid agonist. CD II Uses: Intraoperatively as bolus, with peak analgesic effects occurring in 3-5 minutes At induction with a benzodiazepine For compromised patients, fentanyl + benzodiazepine may be sufficient for intubation CRIs are very effective Transdermal fentanyl patches Respiration slows or may cease following a bolus Bradycardia can be significant Fentanyl ‘spot on’ licensed for dogs (Recuvyra)

Question 153

Codeine

Answer 153

has been used in dogs (often with paracetamol) for mild to moderate pain (post op) but…..

Question 154

Oxycodone

Answer 154

has also been advocated for use in dogs (post op), but little information is currently available

Question 155

Naloxone

Answer 155

for antagonism of pure mu opioids

Question 156

Tramadol

Answer 156

Tramadol is popular! But there is a lack of data in dogs, better in cats It is commonly prescribed to humans – now licensed in dogs It is a synthetic analogue of codeine; it is a low potency mu selective partial agonist PRODRUG with LIMITED metabolism in dogs It has an alpha 2 adrenergic effect and inhibits 5HT reuptake CDIII Very limited value in dogs but useful in cats

Question 157

Buprenorphine

Answer 157

a partial agonist with a strong affinity for mu receptors (mild kappa antagonist) Highly potent but not as efficacious as pure opioids Peak effect IV admin 45-60mins- long wait time Mild to moderate pain, good sedation, long duration of action, preservative in multi dose vials Licensed for dogs and cats and horses OTM route works v well (cats>dogs) - Better than butorphanol for analgesia but as it is a partial agonist you cannot increase the effect by giving more- occupies and blocks the receptors for about 6 hours Allows patients a night sleep and is good for mild to moderate pain

Question 158

OTM route

Answer 158

oral trans mucosal

Question 159

Butorphanol

Answer 159

Only mixed one! is a kappa opioid agonist and mu antagonist (short-medium duration) Its actions differ to that of the other opioids Available as oral form (Torbutrol) Useful in combination with acepromazine for sedation e.g. cardiac patients Licensed for dogs, cats & horses Antitussive- suppresses cough LIMITED ANALGESIA- Blocks mu receptors for up to 6 hours! But only 10 mins of analgesia and prevents use of other opiod analgesis

Question 160

Alfentanil, sufentanil and remifentanil

Answer 160

can be used during anaesthesia to blunt sympathetic stimulation All have context sensitive half lives shorter than fentanyl Remifentanil is metabolized by plasma esterases Remifentanil always given by CRI Given as low dose (for analgesia) or higher doses as part of TIVA MAC reduction of these opioids has been shown in dogs and cats None licensed for dogs and cats

Question 161

Local Anaesthetic (LA) Agents

Answer 161

block the sodium channels in nerve fibers, blocking transmission the unionised local anethetic enters cell, becomes ionised and is then able to block the sodium channel it can also affect eh membrane directly LAs are weak bases and largely ionised at physiological pH. - Problem in inflamed tissue Their speed of onset is inversely related to their degree of ionization. -Longer to start working in inflamed tissue Their duration of effect is directly related to their degree of protein-binding. Their potency is related to their lipid solubility. Lidocaine Prilocaine (+lidocaine) Bupivicaine Mepivicaine Ropivicaine Etidocaine Amethocaine Proparacaine Cocaine

Question 162

Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

Answer 162

Inhibit prostaglandin production by interfering with cyclo-oxygenase (COX)- COX 1, 2 Now thought also to have a spinal action Synergistic with other drugs iv, im, sc, po non sterodials vlock the production of cyclooxygenase and therfore the production of PGG2- steriods also act earlier of this pathway so they should not be used toghter- gastric ulcration Some licensed for pre-operative use Carprofen and meloxicam have revolutionized perioperative pain management in UK in last 3 decades Traditional NSAIDs are contraindicated in patients with: Renal or hepatic insufficiency Hypovolaemia Congestive heart failure & pulmonary disease Coagulopathies, active haemorrhage Spinal injuries Gastric ulceration Concurrent use of steroids Shock, trauma (esp head trauma) Pregnancy

Question 163

COX 1

Answer 163

NSAI block the production of this enzyme Prostaglandin (PG) synthesis attributable to COX 1 along length of GIT PGs play a role in regulating renal blood flow, reducing vascular resistance & enhance organ perfusion COX 1 is found in neurones and in the foetus, amniotic & uterine tissue Blood platelets contain COX 1 Cox 1 = ‘housekeeping’? BUT Earlier NSAIDS also inhibit COX1

Question 164

COX 2

Answer 164

NSAIDs with a more favourable GIT profile were being sought before COX 2 was discovered When COX 2 was discovered in 1991 it was shown that 3 drugs (carprofen, etodolac & meloxicam) with an enhanced GIT protective profile inhibited COX 2 Then assumed that COX 2 selective NSAIDs were the answer... This has not been shown to hold true Deracoxib & firocoxib – problems in humans, not all coxibs have problems! COX 2 induction in heliobacter pylori gastritis, IBD & bacterial infections Therefore COX 2 inhibition may exacerbate the situation... Supported by transgenic studies COX 2 may have a role in GI defence In summary do not equate COX 2/COX 1 inhibition ratios to overall in vivo safety!

Question 165

Licensed NSAIDs for horses

Answer 165

Phenylbutazone Suxibuzone Firocoxib Meloxicam Flunixin meglumine Vedaprofen Carprofen

Question 166

Grapiprant (Galliprant)

Answer 166

New class of piprant NSAIDs- Non-cyclooxygenase inhibiting non-steroidal anti-inflammatory drug- blocks EP4 further down in pathway instead Licenced for treatment of mild to moderate osteoarthritis pain and inflammation in dogs Has been called ‘next step’ when ‘traditional’ NSAIDs are not tolerated Approved for use in dogs from 9 months of age and favourable safety profile Once daily administration (chewable tablet) – 2mg/kg Adverse events include vomiting, diarrhoea, decreased appetite and tiredness. Often dogs will adjust but washout between NSAIDs essential Not for use in cats

Question 167

What is paracetamol?

Answer 167

Paracetamol: 10 - 15 mg/kg PO two to three times daily. Is it a NSAID? Analgesic & antipyretic Mechanism of action unknown! Thought to inhibit COX-3(??) but recent data suggest there may be another site

Question 168

Alpha-2 Adrenoceptor Agonists

Answer 168

good sedatives between opiates and nonsteriodals Bind to alpha 2 receptors Receptors widespread Drugs have other actions (sedation, ↓HR etc) Systemic, epidural, peripherally Synergism with LA’s Dogs/cats Medetomidine (45 minutes) Dexmedetomidine (45 minutes) Horses Xylazine (30 minutes) Detomidine (45 minutes) Romifidine (60-70 minutes) Cattle Xylazine Detomidine Very useful drugs Sedative action Analgesic (& reduce MAC) Compatible with other drugs & potential to antagonise (atipamezole), IV, IM, epidurally, buccally (detomidine) Small volume Alpha 2 receptors: 3 subtypes (4) A,B,C Diverse sites: CNS & PNS Side effects- Hyper (B) then normo/hypotension (A) Decreased CO & HR, increased SVR Respiratory depression Increased urine production Decreased GI motility Decreased surgical stress response Hyperglycaemia, GH enhanced Thermoregulation affected Sweating

Question 169

NMDA Antagonists

Answer 169

Ketamine As induction agents As analgesics peri op Ketamine for fractious cats (sprayed in mouth) Very versatile Will improve the patient’s post op comfort

Question 170

Ketamine

Answer 170

It has been shown that at low doses ketamine can prevent the ’wind up’ and sensitisation of dorsal horn cells 0.5mg/kg after induction Can be used in the pre-med CRI e.g. Add 60mg ketamine to 1L LRS and administer at 10ml/kg/hr to dogs intra op (10mcg/kg/min) NMDA Antagonists As induction agents As analgesics peri op Ketamine for fractious cats (sprayed in mouth) Very versatile Will improve the patient’s post op comfort

Question 171

Premed combinations

Answer 171

Acepromazine + opioid Alpha 2 agonist + opioid or BZD or ketamine BZD + Ket Opioid + BZD Alpha 2 + BZD + opioid

Question 172

Post operative period in regards to anelgesic drugs

Answer 172

How long should we provide analgesia for? 24-72 hours for routine ops Involve the owner Rescue analgesia (what is yours?) What options do we have available? NSAIDs (daily, oed, monthly) Opioids (patch, long acting formulations, oral forms (tramadol, morphine, OTM buprenorphine) LA blocks Adjuncts for chronic pain (amantadine, gabapentin etc)

Question 173

side effects of antibiotics

Answer 173

Direct toxicity – aminoglycosides Drug interactions – sulphonamides and alpha-2 agonists May reduce normal protection – gut flora May cause tissue site necrosis (tetracyclines) Chloramphenicol has been shown to cause a reduced immune response Some can cause reduced metabolism Potential residues in food producing animals RESISTANCE Hypersensitivity Anaphylactoid reactions

Question 174

What Influences Success of antibiotics

Answer 174

Bacterial susceptibility Pharmacokinetics and tissue penetration Most tissues – concentration is perfusion limited Free drug concentration in plasma is related to, or equal to that in tissue In some tissues – concentration is permeability limited where non inflamed CNS Eye Lung Prostate Mammary gland Local factors Abscess - pus - necrosis – inactivates aminoglycosides and sulphonamides Foreign material – bacterial glycocalix Slowed bacterial growth – less susceptible to cephalosporins and penicillins Low pH/low oxygen – erythromycin, fluoroquinolones Haemoglobin - penicillins Wound cleansing and drainage Compliance

Question 175

Factors Affecting Choice of antibiotic

Answer 175

Presence of infection (Gram stain culture and sensitivity) Spectrum Habitual reliance on broad spectrum indicates low standard of diagnosis Bacteriocidal versus bacteriostatic Cost Toxicity Concurrent disease Pregnancy Habit…..! Dosage and frequency Route Duration and re-evaluation Acute versus chronic infection Immunocompromise Septic arthritis Osteomyelitis Combination therapy Not bacteriostat + bacteriocide

Question 176

Peptidoglycan is unique to bacteria, making it ....

Answer 176

good antibiotic target

Question 177

Amoxicillin-clavulanate

Answer 177

Penicillin based – -lactamase inhibitor Staphs, streps Gram negatives Escherichia and Klebsiella spp variable Pseudomonas enterobacter resistant

Question 178

Lincosamides

Answer 178

Penicillin based – -lactamase inhibitor Usually bacteriostatic GI irritation –do not use in horse except foals, never in rabbits Basic drugs – ion trapping in milk

Question 179

Fluoroquinolones

Answer 179

Penicillin based – -lactamase inhibitor Reserve for serious gram-negative systemic infections Do not use routinely and non-selectively If used, use the correct dose!

Question 180

Potentiated sulphonamides

Answer 180

Penicillin based – -lactamase inhibitor Old but useful – resistance growing

Question 181

Aminoglycosides

Answer 181

Penicillin based – -lactamase inhibitor Gentamicin – gram-negative aerobes

Question 182

Adjuncts

Answer 182

Probiotics? Anti-tetanus toxin Foaming agents –foot rot

Question 183

prophylactic use of antibiotics

Answer 183

Not indicated for routine, clean surgery where no inflammation is present, GI system not invaded and aseptic technique has not been broken But do use for: Dental procedures Leukopenia Contaminated surgery Where infection would be disastrous – orthopaedic Administer before procedure and within 3-5 hours of contamination Slow IV Appropriate to contaminating pathogen

Question 184

licensed antifungals

Answer 184

Ketoconazole Fungiconazol 200 mg tablets for dogs – dermatphytosis. Used off licence for systemic infections. Itraconazole oral solution for cats and birds, e.g. Itrafungol 10 mg/ml Oral Solution (treats M. Canis). Used off licence for systemic infections. Miconazole. In various shampoos and ear drop preparations. Nystatin ear drops - Canaural Terbinafine – in various ear drops for dogs Clotrimazole- in various ear drops for dogs Enilconazole. Imaverole Concentrate for Cutaneous Emulsion – cattle, horses and dogs vs dermatophytosis Bovilis® Ringvac MSD Animal Health UK Limited vaccination for cattle

Question 185

unlicnened antifunglas

Answer 185

Amphotericin b Climbazole Fluconazole Silver sulfadiazine Tiabendazole

Question 186

treatment of ringworm

Answer 186

Clipping of the hair coat, especially small animals, removes infected hairs, stimulates new hair growth and hastens recovery Systemic ketoconazole (dogs), itraconazole (cats) plus a topical treatment (e.g. miconazole) Treatment with ketoconazole suppresses testosterone concentrations and increases progesterone concentrations and may affect breeding effectiveness in male dogs during and for some weeks after treatment Treatment of dermatophytosis should not be limited to treatment of the infected animal(s) Measures to prevent introduction of M.canis into groups of cats may include isolation of new cats, isolation of cats returning from shows or breeding, exclusion of visitors and periodic monitoring by Wood's lamp or by culturing for M.canis Bovilis® Ringvac reduces clinical signs of ringworm caused by Trichophyton verrucosum (prophylactic dose) and shortens the recovery time of infected cattle showing clinical signs of ringworm (therapeutic dose) Initially the whole herd should be vaccinated (two vaccinations 10-14 days apart). Subsequently, (closed herds) only young calves require revaccination at around 2 weeks of age, followed by a second injection 10-14 days later. New animals should receive a full vaccination course. No subsequent doses are required. Can be used during pregnancy (?lactation). Administration is by intramuscular injection.

Question 187

Aspergillosis treatment

Answer 187

First line treatment = topical clotrimazole formulated in a polyethylene glycol base Indwelling tubes trephined into the frontal sinuses or via the nares as a single infusion. The infused solution is left in place for 1 hr, during which the dog’s position is changed periodically ~80% success rate Also reports of enilconazole (bid for 7–14 days), via tubes implanted surgically into the frontal sinuses Systemic treatments of ketoconazole, itraconazole, fluconazole, voriconazole, and Posaconazole reported In horses, surgical exposure and curettage have been used for guttural pouch mycosis. Topical natamycin and oral potassium iodide have been reported effective Itraconazole (3 mg/kg, bid for 84–120 days) has been reported effective in Aspergillus rhinitis in horses

Question 188

aspergiliosis diagnosis

Answer 188

Imaging (radiographs/CT) of the nasal cavity can show turbinate tissue destruction Visualization of fungal plaques by rhinoscopy together with serologic and either mycologic or radiographic evidence of disease is gold standard . Culture result alone is not appropriate (ubiquitous and can be isolated from the nasal cavities of healthy patients) Systemic disease is usually diagnosed by culture of the organism, often from urine

Question 189

Two pharmacological approaches to viral control

Answer 189

effective vaccines or antiviral therapy

Question 190

licensed Antiviral agents

Answer 190

One licensed agent Virbagen Omega Contains recombinant omega interferon of feline origin For cats (sc) and dogs (iv) Licenced for treatment of canine parvovirus, feline leukaemia virus (FeLV), and feline immunodeficiency virus (FIV) Interferons increase the cell's resistance to a virus

Question 191

unlicenced antiviral agents

Answer 191

Aciclovir Famciclovir Ganciclovir Lamivudine Zidovudine Oseltamivir for treatment of viral diseases in dogs (parvovirus and parainfluenza) has also been reported

Question 192

Biochemistry/haematology/serology of FIP

Answer 192

Hypergammaglobulinaemia; raised bilirubin without liver enzymes being raised, lymphopenia; non-regenerative anaemia, high antibody titre to FCoV

Question 193

FIP treatment

Answer 193

Feline interferon omega (Virbagen Omega) or human interferon alfa-2b have been used – limited success Stimulate body’s response Immunosuppressive and anti-inflammatory drugs reduce inflammation. Commonest immunosuppressive drug used in FIP is prednisolone (corticosteroid) but no placebo-controlled trials showing prednisolone to be better than other anti-inflammatories GS-441524 is a nucleoside analogue Two published studies from UC Davis in 2018 and 2019. Results were 100% (10/10) recovery rate reported in experimentally infected cats and 84% (25/31) recovery rate in naturally infected cats. Of the recovered cats, owners reported that they returned to “near normal” within two weeks of treatment The 2019 study proposed the optimized treatment protocol for GS-441624 use as 4.0 mg/kg given as a subcutaneous injection once daily for at least 12 weeks can only buy it for research currently

Question 194

Equine vaccines

Answer 194

Routinely equine flu, tetanus, equine herpes virus, equine rotavirus and now strangles Following 2019 equine flu outbreak in the UK some governing bodies moved from annual to six-monthly requirements All vaccination records should be kept up to date in the horse’s passport document Up-to-date vaccination record is a requirement of many sporting governing bodies for horses competing under their rules

Question 195

Cattle vaccines – what’s available?

Answer 195

Bovine viral diarrhoea Very common disease in the UK. About 60% of cattle in the EU test positive for exposure to the BVD virus. Timings for all BVD vaccines are to aim for full protection to occur at least two to three weeks prior to service. Infectious bovine rhinotracheitis Live and inactivated vaccines are available. Live vaccines have rapid onset of immunity and are of use in the face of an outbreak to reduce clinical signs and improve the immunity quickly but inactivated vaccines appear to be better at producing longer-term immunity Leptospirosis Two vaccines are available in the UK for leptospirosis control. In both cases a primary course of two doses four to six weeks apart, followed up with annual boosters, is preferably given in the spring before the period of highest risk. Calf enteric disease – rotavirus, coronavirus and Escherichia coli A number of vaccines are available for immunising pregnant cows and heifers to raise antibodies to rotavirus, coronavirus and Escherichia coli. After birth, the calves gain protection in their gut from drinking the colostrum and milk that is fortified with these antibodies. Some minor differences exist in the timing of the various vaccines. Pneumonia vaccines Calf pneumonia vaccines are available for infectious bovine rhinotracheitis, parainfluenza type three, bovine respiratory syncitial virus, Pasteurella, Mannheimia haemolytica and Histophillus somni, and many combinations are available depending on what protection is needed. It is important to identify the common diseases present and the age calves become infected Lungworm The only lungworm vaccine available uses irradiated live lungworm larvae that create an immune response from the animal, but the larvae do not continue to reproduce, so do not cause clinical disease. The vaccine is a two-dose programme given approximately four weeks apart to youngstock at the beginning of their first grazing season. The second dose should be given at least two weeks before turnout, and vaccinated and unvaccinated stock should not be mixed for at least two weeks after the second dose has been given. It is preferable for calves to be exposed to low levels of lungworm larvae throughout the grazing season to stimulate and maintain this immunity. If the worming protocol on the farm is too effective, there may be small exposure of the calves to lungworm, allowing very little natural immunity to build up, and this leads to insufficient long-term immunity in adult cattle, which can develop the disease in subsequent grazing years. Clostridial diseases Vaccinations against clostridial diseases are routinely given to sheep, but the uptake is much less in the cattle sector. A number of products exist on the market. Ringworm Mastitis STARTVac, covers the main mastitis causing pathogens, E coli, Coliforms, Staph aureus and Coagulase-Negative Staphylococci (CNS), but does not protect against Strep uberis. It involves a complicated programme and is quite expensive Salmonella In the face of a Salmonella outbreak on farm, a fluid vaccine can be used to improve immunity to S. enterica serovar Dublin and S enterica serovar Typhimurium Bluetongue Not routinely used in UK but two vaccinations are available

Question 196

Pig vaccines – what’s available?

Answer 196

Porcine parvovirus Porcine reproductive and respiratory syndrome E.coli Clostridia Erysipelas Mycoplasma hyopneumoniae Lawsonia intracellularis Atrophic rhinitis Glasser’s Disease Aujeszky’s Disease Salmonella typhimurium Also relatively new intramuscular vaccine to control ileitis in pigs The bacterial disease is present on most pig farms in the UK and causes widespread digestive health problems There are often no visible signs of ill health, but an infection with the bacterium Lawsonia intracellularis can lead to poor feed conversion ratios (FCR) and reduced growth rates More serious infection levels also cause diarrhoea and result in increased herd mortality rates.

Question 197

Sheep vaccines – what’s available?

Answer 197

Vaccines available in the UK for sheep Clostridial diseases, e.g. lamb dysentery, pulpy kidney, tetanus, braxy, blackleg Pasteurellosis Ovine abortion, e.g. toxoplasmosis and enzootic abortion Louping ill Contagious pustular dermatitis (Orf) Footrot

Question 198

Dog Core vaccines in the UK

Answer 198

Canine Distemper Virus (D) Canine Adenovirus/Infectious Canine Hepatitis (H) Canine Parvovirus (P) Leptospirosis (L). Please be advised that vaccines are multivalent; preparations are available containing different Leptospira strains.

Question 199

Core vaccines

Answer 199

protect animals from severe, life-threatening diseases that have global distribution and which ALL dogs and cats, regardless of circumstances or geographical location, should receive. Non-core vaccinations protect from disease where the animal’s geographical location, lifestyle or environment puts them at risk, e.g. rabies vaccination before overseas travel. (

Question 200

Dog non-core vaccines in the UK

Answer 200

Bordetella bronchiseptica +/- Canine parainfluenza virus (“Kennel Cough” vaccine): vaccination should be considered for dogs before kennelling or other situations in which they mix with other dogs (e.g. dog shows, training classes) Rabies: legal requirement for dogs travelling abroad / returning to the UK Canine Herpes Virus: for breeding bitches Leishmaniasis: before travelling to endemic areas Borrelia burgdorferi (Lyme disease): for dogs at high risk of exposure

Question 201

Cat core vaccines in the UK

Answer 201

Feline enteritis (feline parvovirus) (P) Cat flu (feline calicivirus (C) and herpes virus (H)

Question 202

Cat non–core vaccines in the UK

Answer 202

Feline leukaemia vaccine (FeLV) (this may be considered a core vaccine for all cats that go outdoors or are in contact with cats which go outdoors). Chlamydophila felis (Chlamydia) Rabies: legal requirement for cats travelling abroad / returning to the UK Bordetella bronchiseptica

Question 203

Rabbit vaccines

Answer 203

Myxomatosis Two forms of Rabbit Viral Haemorrhagic Disease (RHD) caused by RHDV-1 and RHDV-2 strains where local risks and individual veterinary advice indicate the need

Question 204

ferret vaccines

Answer 204

Rabies: legal requirement for ferrets travelling abroad / returning to the UK Distemper: No vaccine currently licensed for use in ferrets in the UK, some owners ask for canine distemper vaccines in discussion with their vet

Question 205

what is the mode of action and target of penicillin

Answer 205

inhibits cells wall synthesis gram postitive bacteria

Question 206

what is the mode of action and target of ampicillin

Answer 206

inhyibits cell wall syntheisis broad spectrum

Question 207

what is the mode of action and target of Bacitracin

Answer 207

inhibits cell wall syntheisis gram positive bacteria (applied as skin ointment)

Question 208

what is the mode of action and target of cephalosporin

Answer 208

inhibits cell wall syntheisis gram positive bacteria

Question 209

what is the mode of action and target of tetracycline

Answer 209

inhibits protien synthesis broad spectrum has wide spread, plasmid mediated imunity

Question 210

what is the mode of action and target of streptomycin

Answer 210

inhibits protien synthesis gram neg tuberculosis

Question 211

what is the mode of action and target of sulfa drug

Answer 211

inhibits cell motabolism bacterial meningitis urinary tract infections

Question 212

what is the mode of action and target of rifampicin

Answer 212

inhibits RNA synthesis gram positive bacteria gram negative bacteria

Question 213

what is the mode of action and target of quinolones

Answer 213

inhibits DNA synthesis urinary tract infections

Question 214

what is the mode of action of polyenes

Answer 214

(amphotericin, B Nystatin) interacts with sterols in cell membrane to cause cellular leak

Question 215

what is the mode of action of antibiotics (against antifungals)

Answer 215

griseofulvin inhibits mitosis (via the microtubules)

Question 216

what is the mode of action of azoles

Answer 216

fluconazole itraconazole ketoconazole ect inhibits ergosterol synthesis (inhibits cell membrane)

Question 217

what is the mode of action of allylamines

Answer 217

terbinafine inhibits ergosterol (cell membrane)

Question 218

what is the mode of action of thicocarbamate

Answer 218

tolnaftate inhibits ergostero (cell membrane)

Question 219

what is the mode of action and target of antimetabolite

Answer 219

flucytosine inhibits dna and rna synthesis

Question 220

what is the mode of action and target of profens

Answer 220

flurbiprofen ibuprophen directly damages the fungal cytoplasmic membrane

Question 221

what are the components of a surgical theatre

Answer 221

Surgical environment should have several distinct areas: Changing area Surgical prep/induction Scrub area Operating theatre Recovery Utility

Question 222

Skin disinfectants

Answer 222

Chlorhexidine 2% with or without 70% isopropyl alcohol Not suitable for broken skin, wounds, mucous membranes Povidone iodine 7.5% Suitable for contact with mucous membranes Non-povidone iodine (alcohol free) For use with ocular surgery Equally effective at reducing bacterial counts Chlorhexidine has greatest residual action

Question 223

what class of antibiotis inhibit cell wall synthesis

Answer 223

penicillin ampicillin bacitracin cephalosporin

Question 224

what class of antibiotis inhibit protein synthesis

Answer 224

tetracyclin streptomycin

Question 225

what class of antibiotis inhibit cell metabolism

Answer 225

sulfa drug

Question 226

what class of antibiotis inhibit RNA synthesis

Answer 226

rifampicin

Question 227

what class of antibiotis inhibit DNA synthesis

Answer 227

Quinolones

Question 227

comon bacterial agents of Bite wounds, trauma and contaminated wounds

Answer 227

Staphylococcus spp, Streptococcus spp, Pasteurella spp, anaerobes

Question 228

comon bacterial agents of Osteomyelitis

Answer 228

Staphylococcus spp, Streptococcus spp, Proteus, Pseudomonas (cat/dog), anaerobes

Question 229

Septic arthritis

Answer 229

Staphylococcus spp, Streptococcus spp, coliforms

Question 230

What is General Anaesthesia?

Answer 230

Controlled, reversible depression of the CNS so as to produce lack of awareness of painful inputs (nociception) Minimal depression of hind brain functions – cardiovascular centres

Question 231

What is Local Anaesthesia/analgesia?

Answer 231

Local anaesthesia (local analgesia) – not aiming for CNS depression

Question 232

what are the components of the anethetic triad

Answer 232

unconciousness muscle relaxation analgesia one drug does not do all of these therefore we need a cocktail

Question 233

The less anaesthetic you give…

Answer 233

…the better for the patient’s physiology Less cell and organ damage Quicker recoveries Quicker return to normal appetite Better functioning immune systems

Question 234

Balanced Anaesthesia

Answer 234

Using multiple drugs to minimise the dose and the side-effects of any one of them Results in lower doses of potent anaestheticsless CNS depression Better achievement of the goal of anaesthesia

Question 235

Hypnosis

Answer 235

artificially induced sleep

Question 236

analgesia

Answer 236

Anti-nociception

Question 237

Muscle relaxation

Answer 237

From the same agent producing hypnosis or From a centrally acting muscle relaxant - diazepam or From a specific neuromuscular junction blocking agent - curare

Question 238

modern stages of anesthesia

Answer 238

Conscious Anaesthetised Dead Unconsciousness is an all or nothing thing Level of CNS depression Specific signs related to muscle relaxation

Question 239

Signs related to brain stem depression

Answer 239

Respiratory rate Heart rate Blood pressure

Question 240

Minimising anesthesia risk

Answer 240

Support Oxygen Fluids Warmth Monitoring During anaesthesia Recovery Anaesthesia record sheet Legal record The trained anaesthetist

Question 241

Tranquilisation

Answer 241

relief of anxiety

Question 242

Sedation –

Answer 242

central depression, drowsiness

Question 243

Narcosis

Answer 243

drug induced sleep produced by narcotics - opium like drugs

Question 244

Dissociative anaesthesia

Answer 244

induced by drugs such as ketamine that dissociate the thalamo-cortical and limbic systems

Question 245

The Anaesthetic Process

Answer 245

IDENTICAL for all species History and examination The anaesthetic plan Place iv cannula Premedicate, allow to settle Induce anaesthesia – injectable agent Once intubated do ABC AIRWAY, BREATHING, CIRCULATION Connect to anaesthetic machine and supply volatile anaesthetic in oxygen (or us total injectable with top ups) Alter inspired concentration in response to physical signs Supply analgesia separately Recover following anaesthesia Continue to monitor until patient comfortable/discharged

Question 246

Why are combinations of agents used for anesthesia?

Answer 246

One agent could be used to induce and produce all 3 desired effects of the triad (unable to perceive painful stimuli, relaxed muscles, unconsciousness) but with massive physiological depression Eg isoflurane, sevoflurane But usually injectable agents are used in combination “Balanced anaesthesia” E.g. ketamine: if used alone, poor muscle relaxation Add medetomidine: improved analgesia and muscle relaxation

Question 247

Why is Airway Management Important?

Answer 247

Allows delivery of oxygen and inhaled anaesthetic gas Most anaesthetics cause respiratory depression Loss of airway reflexes = prone to airway obstruction Brachycephalics obstruct All the above cause hypoxia- high mortality Allows scavenging and environmental protection Allows intermittent positive pressure ventilation (IPPV) Allows ventilator support in ICU setting ‘Protects the airway’ Under normal anaesthesia Reflux 40-60% in anaesthetised dogs Most of this is silent – may not be witnessed When carrying out oral/pharyngeal procedures E.g. Dental work and associated debris Allows airway management during bronchoscopy Allows one lung ventilation

Question 248

Pre-Anaesthetic Fasting?

Answer 248

Recommended in adult dogs/cats 3-6 hours, water until premed <3 = food present. >6 = stomach pH drops so reflux is damaging Neonates = from 0.5 to 3 hours – monitor glucose Horses withdraw concentrate overnight (to reduce gas distension) – controversial Ruminants withdraw 6 hours and reduce concentrates ( to reduce gas distention) 12-24 hours Small exotics/furries – shorter times depending on species

Question 249

intubation methods

Answer 249

Endotracheal tubes Supraglottic airway devices V-gels (rabbits)/I-gels (cats) Laryngeal mask airways Face masks Others (Tracheostomy tubes) (Arndt endobronchial blockers)

Question 250

Endotracheal Tubes (ETT)

Answer 250

Various types available Most are cuffed with a visible pilot balloon Inflate to ~25mmHg – use manometer if possible Murphy, Magill or Cole Use of laryngoscope advisable Flow = ∆𝑃𝜋𝑟4/8∩𝐿 Go as large as possible What size shall I place? Selection based on nasal septal width = 21% accurate Selection based on tracheal palpation = 46% accurate Best technique = visualise larynx using laryngoscope Spray lidocaine (only cats as the have larygneal spazm) and WAIT Try largest but have a range available Cut to length – minimise dead space Not possible with armoured tubes

Question 251

Red Rubber ETT

Answer 251

Red rubber in common use Crack over time + non-repairable Prone to kinking Irritant Not possible to visualise blockages Low volume high pressure cuff Can lead to tracheal trauma but good seal Difficult to recommend

Question 252

PVC and Silicone ETT

Answer 252

More popular than rubber Disposable but reused, silicone tubes repairable Less prone to kinking compared to rubber Non-irritant Allows visualisation of blockages Usually high volume low pressure cuff Less risk of tracheal trauma but relatively good seal Recommended

Question 253

Armoured Endotracheal Tubes

Answer 253

Wire coil embedded in wall Resist kinking but more difficult to place without stylet If bitten may permanently obstruct Useful in ophthalmic cases Impossible to reduce dead space Contraindicated in MRI

Question 254

Cole Pattern Tubes

Answer 254

Designed for emergency use in paediatric anaesthesia The shoulder of the tube should impact in the larynx to provide a gas-tight seal However movement or IPPV tends to dislodge the tube Still quite useful for exotic animal anaesthesia- snake ect

Question 255

Supraglottic Airway Devices (SADs)

Answer 255

Developed originally for human anaesthesia Major cardiovascular and laryngospasm problems in humans ETT remain ‘gold standard’ veterinary specific LMAs achieving popularity for short uncomplicated procedures Increasing evidence of their effectiveness in veterinary patients

Question 256

Veterinary Specific SADs

Answer 256

V-gels are veterinary specific (rabbits and cats) 2 species where ETT placement can be challenging Designed to anatomical standards Can be used to protect the airway the same as an ETT IPPV is possible Channels to divert regurgitation can be incorporated Very useful for short procedures and for bronchoscopy Always use capnography

Question 257

Face Masks for anesthesia

Answer 257

Should cover nose and mouth Not whole head Avoid eyes Beware of dead space – choose the shape Transparent masks preferable Ensure a good seal using rubber diaphragms Have been used for anaesthetic induction – NOT recommended Stage 2 excitement and no airway protection Very useful for provision of supplemental oxygen

Question 258

Complications of Airway Management

Answer 258

High pressure/low volume (red rubber and some silicone ETT) exert pressure on a small part of the tracheal mucosa. May see tracheitis or pressure necrosis This can lead to tracheal strictures Extreme cases may see tracheal rupture Post-op subcutaneous emphysema in cats – but still recommended to use a cuff ALWAYS disconnect from breathing system when changing position whenever a change in recumbency is needed Especially with dental cases where head and neck movement is common Always inflate carefully preferably with manometer Or listen for leaks ETT over insertion – carefully measure Should be at level of thoracic inlet Too long potential one lung ventilation Cleaning and storage of ETT and LMAs Usually stored on wall brackets ideally keep covered to avoid contamination Common cause of tracheitis is insufficient rinsing of ETT tubes LMAs need to be thoroughly dried after cleaning or tend to degrade

Question 259

What Type Of Intravenous Cannula?

Answer 259

‘Over the needle’ 24-10 gauge, 1.9-13.3 cm long Relatively stiff material ‘Through the needle’ Large bore insertion needle Cannula passed through the needle Central veins Not used commonly Peel away – place through an over the needle cannula Seldinger/over the wire cannula

Question 260

placment of cannula

Answer 260

Cephalic Most used site as animals easiest to restrain Start distally (can then use the higher site) Saphenous Veins Requires more assistance Medial or lateral saphenous Use vein on caudal aspect of leg as it ascends Medial easier in cat – straighter Good choice in brachycephalics Jugular- horse Useful for long term therapy & regular sampling Well tolerated Multilumen cannulae available right (straighter in the dog) The Auricular Veins Useful in animals with large or floppy ears, rabbits, ruminants too EMLA cream can help to reduce discomfort

Question 261

What size of cannula should u use?

Answer 261

22g (blue) for v small patients 20g (pink) or greater for most patients including cats >20kg dogs use 18g Very large dogs use 16g or 14g

Question 262

maintinance of a placed intravenous cannula

Answer 262

Check cannula regularly and flush q 6 hours with heparinised saline (1IU/ml); does this help ???? Normal cannulae can be maintained for up to 3 days after which they should be replaced (exceptions do occur) Swab ports prior to injection Replace giving sets, bungs and T ports after 3 days

Question 263

complications a cannula

Answer 263

Extravasation Thrombosis (where do the thrombi occur) Thrombophlebitis Infection Emboli (air, catheter) Exsanguination What would you do in these situations?

Question 264

what are the functions of an anesthetic machine?

Answer 264

Delivery of oxygen / nitrous oxide at known rate. Delivery of known concentration of IAA. Removal of exhaled gases from patient. Recirculation or removal of exhaled gases. Facilitate IPPV/ CPR.Delivery of oxygen / nitrous oxide at known rate. Delivery of known concentration of IAA. Removal of exhaled gases from patient. Recirculation or removal of exhaled gases. Facilitate IPPV/ CPR.

Question 265

Gas Source of an enesthetic machine function?

Answer 265

Molybdenum steel cylinders Specific yokes and Bodok seal Colour coded (e.g. oxygen = black/white top). Also piped gas from large cylinders. Usual sizes = E,G,F Oxygen ; pressure = contents Nitrous oxide ; liquid with vapour above. Therefore volume of gas in cylinder = (Wt. Cylinder – Empty Wt. Cylinder) x 534

Question 266

Needle valve and flowmeter.

Answer 266

Regulate flow into low pressure side of machine. Flowmeter = graduated glass tube with floating bobbin/ball. Can stick. Read at TOP of bobbin/middle of ball. Rotate.

Question 267

Back bar

Answer 267

Horizontal part of the anaesthetic machine circuit between the rotameter block and the common gas outlet Vaporisers are mounted on the back bar, enabling volatile agents to be added to the fresh gases. The pressure in the back bar is approximately 1 kPa at the outlet end, and may be 7–10 kPa at the rotameter end Contains a ‘blow off’ or pressure relief valve at the outlet end plus safety features to only allow one vaporiser in use

Question 268

Intermittent positive pressure ventilation (IPPV)

Answer 268

Intermittent manual – ‘sighing’. A good habit! Close valve + short inspiration up to 20cm water. Chest supra-maximal. OPEN VALVE AGAIN. Continuous manual. Repeated sighing. Can be tiring. Will allow breathing control but turn down vaporiser. Mechanical. Ventilator. TV – 10-20ml/kg. Use large TV with slow rates. Various types. Frees anaesthetist and regular rhythm.

Question 269

Soda Lime

Answer 269

USA – baralime. 90% = calcium hydroxide; Ca(OH)2 +CO2 -> CaCO3 + H2O + Heat. Therefore gas warmed and humidified. Colour change – usually to purple but NOT permanent so change if needed at end of anaesthetic. Dust. Tracking of gas. Dead space. Resistance. Hyperthermia. Exhaustion – colour change, no heat, increased heart/resp rate and bp, wound ooze, red mms.

Question 270

Gas storage safety aspects

Answer 270

Oxygen/nitrous support combustion – naked flames/heat/electrical sparks. Puncture cylinders – rocket effect; chain/ secure well. Move with carts. Store upright in dedicated area. Keep tops dust free – plastic and blow dust off briefly before attachment. Clearly label full/in use/empty.

Question 271

Inhaled anaesthetic agent storage safety

Answer 271

Ether – highly flammable. Halothane/Isoflurane/Sevoflurane. Store upright in cool cupboard and avoid breakages. Fill vaporisers at end of each day. Recap bottles when empty. If spill – open windows, wear gloves/mask and use absorbent into airtight container.

Question 272

Scavenging

Answer 272

Prolonged exposure to anaesthetic gases potentially detrimental Some anaesthetic are ozone gases Legal requirement to control pollution Control of substances hazardous to health (COSHH) Need to vent waste anaesthetic gases Recommended max concentrations (UK) * 100 ppm Nitrous oxide * 50 ppm isoflurane * 10 ppm halothane Excess gas vented via pressure relief (pop-off valve/APL valve) Disc held by weak spring Connected to wide –bore scavenge tubing

Question 273

Types of scavenging

Answer 273

Charcoal cannister e.g. Cardiff aldasorber Passive - window - hole in wall - vent to outside Active - pumped outside

Question 274

Charcoal canister

Answer 274

Cardiff aldasorber Charcoal absorbs halogenated anaesthetics Does not absorb nitrous oxide Increasing weight indicates exhaustion Heating causes release of gases

Question 275

Active scavenging

Answer 275

Collecting & transfer system Receiving system - valveless open-ended reservoir - bacterial filter Pump to generate vacuum

Question 276

Scavenging systems and safety

Answer 276

IMPORTANT – long term exposure to IAAs/nitrous possibly associated with; Abortion/congenital problems. Halothane hepatotoxicity. Neurological problems – memory. Bone marrow suppression/anaemia (nitrous). ?renal toxicity with methoxyflurane. Therefore; Cuffed tubes Closed breathing systems Wear gloves and fill vaporisers at end of day in fume hood Key filling system Turn on gas flows only if animal connected Avoid mask induction and ventilate room – 20 air changes an hour Monitor and inspect equipment Oxygen failure alarm Nitrous cut-off or oxygen failure protection device: if oxygen pressure is lost then the other gases can not flow past their regulator Hypoxic-mixture alarms (hypoxy guards or ratio controllers) to prevent gas mixtures which contain less than 21-25% oxygen being delivered to the patient Often chain linked (link 25 system). Located on the rotameter assembly, unless electronically controlled. Ventilator alarms, which warn of low or high airway pressures. Interlocks between the vaporizers preventing inadvertent administration of more than one volatile agent concurrently Pin Index Safety System on gas cylinders Pipeline gas hoses have non-interchangeable Schrader valve connectors, which prevents hoses being accidentally plugged into the wrong wall socket

Question 277

Ambulatory infusion:

Answer 277

An animal is freely moving without need for a tether to connect with the catheter. This is normally only possible with larger animals that can be fitted with jackets to carry an infusion pump and compound reservoir. Totally implanted pumps can sometimes be used in rodents but have size limitations.

Question 278

Atraumatic:

Answer 278

Minimal tissue injury is caused during the procedure

Question 279

Biocompatibility:

Answer 279

Good toleration of implants by animal tissues after implantation.

Question 280

Biofilm

Answer 280

A coating which develops on implanted materials derived from the animal's own tissue fluids and cells

Question 281

Catheter/cannula:

Answer 281

Flexible tube inserted into body cavities or organs for medical or experimental procedures

Question 282

Dehiscence:

Answer 282

Bursting open or splitting along natural or sutured lines.

Question 283

Haematogenous spread

Answer 283

Spread of microbial infection through the blood stream

Question 284

Thrombogenic:

Answer 284

Property of causing or promoting blood clotting (thrombosis).

Question 285

Breathing system requirements

Answer 285

Supply fresh gas & anaesthetic to patient Allow removal of carbon dioxide Allow scavenging Enable positive pressure ventilation Easy to use & clean Inexpensive to buy and use

Question 286

Re-breathing systems

Answer 286

Expired gas is ‘scrubbed’ of CO2 Chemical CO2 absorber Low fresh gas flow Economical Expensive to buy Large and cumbersome Conserves heat and moisture Increases resistance to breathing Only suitable for larger animals e.g. > 10 kg Large animal systems available

Question 287

formula Working out gas flow requirements for rebreathing systems

Answer 287

Minimum requirement is metabolic oxygen demand i.e. 10 ml/ kg/ minute However, must supply minimum vaporizer flow e.g.Penlon sigma (sevoflurane) 0.25 Lmin-1

Question 288

Denitrogenation

Answer 288

With any rebreathing system where carrier gas is oxygen Use higher flows for ~10 minutes- 2l or 3 l per minute Risk of alveolar hypoxia N.B also after short disconnections – movement between theatres etc can also increase to deliver more anethesia

Question 289

Non-rebreathing systems

Answer 289

High gas flow requirements Loss of heat and moisture Cheap to purchase, expensive to run Low resistance to respiration Suitable for very small patients

Question 290

formula for Working out gas flow requirements for non rebreathing systems

Answer 290

Based on multiples of minute volume, where minute volume is; Respiratory rate x Tidal volume OR 200 ml per kg

Question 291

Magill non rebreathing system

Answer 291

Reservoir bag at fresh gas inlet Awkward to use 1 x Vm (Vm = Vt x RR) or (Vm =200ml/kg) no ippv

Question 292

Lack non rebreathing syste

Answer 292

Co-axial Magill 1 x minute volume Damage to inner limb results in rebreathing no ippv

Question 293

Mini Lack non rebreathing system

Answer 293

Alternative to T-piece for patients under 10 kg Bodyweight range 1-10kg 1 x minute volume No bag twist hazard Very low resistance Easy to clean smooth bore tubing no ippv

Question 294

T-piece

Answer 294

Suitable for very small patients, < 8 kg 2-3 x Vm- half as efficent at lck or magill Suitable for IPPV

Question 295

Bain non rebreathign system

Answer 295

Co-axial T-piece Suitable for 7 – 10 kg 2- 3 X Vm Beware – damage to inner tub

Question 296

Humphrey ADE

Answer 296

3 different modes - lever upright (lack) - lever down (T-piece) - circle Versatile, suitable for 4 kg - >20 kg Pros Compact Well designed Scavenge at machine end Straightforward conversion to IPPV (Nb increase flow) Applies PEEP Increases FRC Prevents microatalectasis Lowers work of breathing in human infants Cons Cost Very heavy – strain on common gas outlet Flows of 50ml/kg/min in lever up (lack) not substantiated in animals Relies on 3 human references Unquantified resistance from inspiratory/expiratory valves Hoses pinch at valve end and start to crack Colour codes misleading (S. African) Excessive (unquantified) mechanical dead space Surprising lack of veterinary controlled trials Soda lime canister capacity 690ml Filled with soda lime capacity 345ml This intergranular volume falls as anaesthesia progresses as soda lime is used up Expired volume must not exceed this or expired breath will not be completely scrubbed of carbon dioxide This leads to maximum limit of 29kg dog with tidal volume of 12ml/kg

Question 297

Morphology of necrosis

Answer 297

Continued swelling and hypereosinophilia Nuclear changes: Pyknosis = shrinkage Karyorrhexis = fragmentation Karyolysis = dissolution Inflammation

Question 298

Pyknosis

Answer 298

shrinkage or condensation of a cell with increased nuclear compactness or density

Question 299

Karyorrhexis

Answer 299

the destructive fragmentation of the nucleus of a dying cell whereby its chromatin is distributed irregularly throughout the cytoplasm.

Question 300

Karyolysis

Answer 300

he complete dissolution of the chromatin of a dying cell due to the enzymatic degradation by endonucleases.

Question 301

Causes of necrosis - anoxia

Answer 301

Reduction or cessation of ATP production due to hypoxia or anoxia respectively will result in loss of function on energy-dependent cell pumps: -Na+/K+ pumps Results in cell swelling due to osmotic pressure ONCOTIC NECROSIS- Cell swelling is the typical feature and distinguishes it from apoptosis -Calcium efflux pumps are also affected resulting in accumulation of intracellular calcium

Question 302

describe membrane damage as a Cause of necrosis –

Answer 302

Membranes can be directly damaged by: Pore-forming infectious agents/toxins- One of the best examples of membrane damage by pore-forming toxins are those produced by Clostridium perfringens Reactive oxygen species (ROS) Phospholipase activation Protease activation- cytoseletal damage Viruses can damage cell membranes as they leave the host cell. Enveloped viruses require incorporation of host cell membrane to form part of their envelope Viruses that bud off from the outer cell membrane (retroviruses) do so quietly, leaving an intact host cell Those that bud from the golgi or RER (flavi, corona, arteri, bunya), and those that bud from nuclear membrane (herpes) lyse the cell as they go Non-enveloped viruses can also only leave the host cell upon lysis Additionally, viruses may causes cell lysis due to disruption of the cytocavitary network and other homeostatic mechanisms when they “hijack” intracellular processes for replication Viruses will also induce apoptosis

Question 303

how do viruses cause cell membrae damage

Answer 303

Viruses can damage cell membranes as they leave the host cell. Enveloped viruses require incorporation of host cell membrane to form part of their envelope Viruses that bud off from the outer cell membrane (retroviruses) do so quietly, leaving an intact host cell Those that bud from the golgi or RER (flavi, corona, arteri, bunya), and those that bud from nuclear membrane (herpes) lyse the cell as they go Non-enveloped viruses can also only leave the host cell upon lysis Additionally, viruses may causes cell lysis due to disruption of the cytocavitary network and other homeostatic mechanisms when they “hijack” intracellular processes for replication Viruses will also induce apoptosis

Question 304

describe free radicals as a Cause of necrosis –

Answer 304

Free radicals are any molecule with a free electron Reactive oxygen species (ROS) and reactive nitrogen species (NO) Produced by oxidative metabolism, therefore most frequently made by mitochondria, but will also damage the mitochondria if cannot be removed. Vitamin E and selenium are important co-factors in the neutralisation of free radicals

Question 305

Programmed cell death - apoptosis

Answer 305

Apoptosis is normal- Embryological, Physiological May be due to a pathological process: Organ not receiving stimulus- portosystemic shunt Cell contains infectious agent Cell is irreparably damaged DNA is irreparably damaged Cell is cancerous Two main mechanisms of apoptosis Intrinsic- due to something within the cells. meachanism within the cell tell cellt to die Extrinsic- more complex. binding of death ligand with cell receptor

Question 306

morphology of apoptosis compared to necrosis

Answer 306

Morphology differs to necrosis: Cell is shrunken No/minimal inflammation- only a few inflamatory cells coming to clean up dead cell Chromatin condensation around nuclear periphery (most characteristic)- Formation of cytoplasmic blebs = apoptotic bodies as oposed to bursting out as in Karyorrhexis, Karyolysis There are different types of programmed cell death

Question 307

Fresh Gas Flow Calculations

Answer 307

• To calculate fresh gas flow calculations we first need to calculate the animals minute volume (MV). • All our non-rebreathing systems require 1-1.5 or 2-3 times the minute volume to run effectively and efficiently. This is know as the circuit or system factor. • To calculate the minute volume (MV) we need to know the volume of air inspired or expired in one breath (tidal volume) and over a minute (minute volume) • Minute Volume (MV) = Tidal Volume (TV) x Respiration Rate (RR) • Tidal Volume (TV) = 10-15ml/kg • We then multiply this amount with the system/circuit factor. • Alternatively, the MV can be estimated using 200ml/kg/min. fgf= MV x CF

Question 308

A 4 year old Male Entire Staffordshire Bull Terrier presents at your practice for a dental descale and polish (routine). His Pre-op bloods and physical exam are normal. He weighs 19.8kg. 1. Which of the following would be a suitable choice of breathing system for this patient? If not, why not? a. Bain b. Parallel Lack c. Circle d. T-piece

Answer 308

b

Question 309

Aims of premedication

Answer 309

Sedation and anxiolysis (The reduction of anxiety by means of sedation or hypnosis) facilitating handling of the animal Reduction of the stress for the animal- reduce adrenaline, prevent cardiac problems Reduction the amount of other anaesthetic agents Provision of a balanced anaesthesia technique Provision of analgesia Counter the effects of other anaesthetic agents to be administered during the anaesthesia procedure e.g. atropine to prevent an opioid mediated bradycardia Contribute to a smooth, quiet recovery after anaesthesia

Question 310

ideal Properties of drugs of pre med drugs

Answer 310

Reliable sedation and anxiolysis Have minimal effects on the cardiovascular system Cause minimal respiratory depression –animals will not be intubated following premedication until induction of anaesthesia, therefore they should breathe spontaneously after premedication Provide analgesia, e.g. Opioid component Be antagonisable: The ability to antagonise the effects of premedication may be desirable to hasten recovery from anaesthesia

Question 311

Alpha2 Adrenoceptor Agonists (Alpha-2s) as premeds

Answer 311

Potent sedative and analgesic drugs- keeps patient really sedated. very good for very sick patients post op as anelgesia Xylazine was the first a2 agonist to be used in veterinary practice Superseded by medetomidine & dexmedetomidine (cats & dogs), both lasting about 45 minutesas xylazine is assosiated with death Xylazine (30minutes), detomidine (45 minutes)and romifidine (60 minutes, less ataxia) used in horses- only real difference is leanth of action Xylazine and detomidine used in cattle- licenced for food animals The superior selectivity of dexmedetomidine makes it the theoretical a2 agonist of choice for use in small animals work on alpha 2 receptiors on presynaptic neurons- widly distributed on cns- alpha 2s activate alpha 2 receptors and provides negative feedback and reduces release of neurotransmitor Sedation is profound & dose related Alpha 2 agonists provide good analgesia through an agonist effect at spinal cord A2 receptors The duration of analgesia provided by a 10 µg/kg dose of dexmedetomidine is approximately 1 hour Intra-op analgesia improved The dose of induction and maintenance agents required after alpha 2 agonists are dramatically reduced in small animals- be careful of this Intravenous induction agents must be given slowly and to effect (vein to brain circulation time is slowed) Alpha 2 agonists produces a biphasic effect on blood pressure (initial increase followed by a return to normal or slightly below normal values) Heart rate is decreased throughout the period of a2 agonist administration HR 45-60bpm dogs and 100-120 bpm cats Alpha2agonists cause a reduction in cardiac output & in healthy animals. Urine production is increased due to a reduction in vasopressin and renin secretion avoid these drugs in patients with heart issues Endogenous insulin secretion is reduced leading to a transient hyperglycaemia- do not test for diabetes after administration of these drugs Both liver blood flow and the rate of metabolism of other drugs by the liver are reduced Peripheral vasoconstriction tends to reduce peripheral heat loss As a consequence it can be easier to maintain normothermia during the peri-operative period compared to animals given acepromazine Small ruminants are quite sensitive to alpha 2 agonists Alpha 2 sedation and analgesia is rapidly antagonised by the administration of atipamezole, a specific alpha2 adrenergic receptor antagonist- wont always antagonise cardiovascular effects Reversal is advantageous because the recovery period is noted to be a high risk time for anaesthetic complications IM atipamezole produces smooth and good quality recoveries IV atipamezole produces a very rapid, excitable recovery from anaesthesia and this route of administration is not recommended It is important to ensure that analgesia is supplemented with different classes of drugs Atipamazole rarely used in horses and cattle

Question 312

Phenothiazines

Answer 312

Acepromazine commonest/only licensed one Sedation and anxiolysis that is initially dose dependent- less flat out sedation can last 46 hours- lasts through recovery With larger doses the duration of action is more prolonged The quality and reliability of sedation can be improved by combination with an opioid (neuroleptanalgesia) Addition of an opioid also provides analgesia, advantageous since acepromazine itself is not analgesic To maximise sedation the animal should be left undisturbed for 30-40 minutes after administration  Less reliable sedation cf dexmedetomidine Acepromazine (ACP) is an antagonist of a1 adrenoreceptors and can cause peripheral vasodilation and a fall in arterial blood pressure- will bleed more Avoid in animals with marked cvs disease or animals in shock Acepromazine is long lasting & non-reversible(!) so avoid in hypotensive animals Acepromazine has anti-arrhythmic properties which may be advantageous during anaesthesia- decreses central arythmia, very potent at this Reduction in body temperature occurs due to a resetting of thermoregulatory mechanisms combined with increased heat loss due to peripheral vasodilation No evidence to suggest that acepromazine alters seizure threshold despite what some say Giant breeds of dog may be “more sensitive” to the effects of acepromazine Some boxer dogs are sensitive to even small doses of acepromazine, which has been attributed to acepromazine induced orthostatic hypotension or vasovagal syncope in this breed Although acepromazine is not contraindicated in boxers, it is not the premedicant of choice in this breed - a very low dose (≤0.01 mg/kg) is recommended and animals should be monitored carefully after administration Acepromazine is a dopamine antagonist- Anti-emetic Contraindicated in breeding stallions- causes repro problems comes in gell for horses and tablet ofr dogs and cats as well as injectable

Question 313

neuroleptanalgesia

Answer 313

combination of opiod and Phenothiazines (ACP)

Question 314

Benzodiazepines

Answer 314

Midazolam or diazepam (MA coming for midazolam, diazepam has MA in France) Benzodiazepines alone produce minimal or no sedation in healthy cats and dogs May even cause excitation due to loss of learned “inhibitory” behaviour Benzodiazepines are therefore given in combination with other sedatives In dogs benzodiazepines often combined with opioids because both classes of drugs are cardiovascularly stable and the combination can provide reliable sedation In cats benzodiazepine and opioid is not very sedative, so benzodiazepine is most commonly combined with ketamine These drugs have minor effects on cardiorespiratory systems Therefore these drugs tend to be used as premedicants in animals with cardiovascular compromise. Benzodiazepines are commonly used to manage convulsions, particularly as a first line intervention for animals presenting in status epilepticus

Question 315

Premedication drug combinations (dogs and cats)

Answer 315

Acepromazine + opioid Alpha 2 agonist + opioid Alpha 2 agonist + BZD Alpha 2 agonist + Ketamine BZD + Ketamine Opioid + BZD Alpha 2 agonist + BZD + opioid

Question 316

how to choose premeds for anethesia

Answer 316

Reason for anaesthesia or sedation Duration of sedation required Procedure to be carried out Degree of pain expected from the procedure Species and breed of the patient Age of the patient ASA classification of the patient

Question 317

Injectable Induction,Why choose it?

Answer 317

Can be injected: direct from needle/syringe (IM, SC, IV) via IV cannula/syringe (IV only) Renders patient unconscious by drug reaching brain directly via blood - rapid and smooth

Question 318

Injectable Induction Agents in Common Use – Small Animals

Answer 318

Propofol Alphaxalone Dissociative agent & benzodiazepine

Question 319

Inhalant Induction

Answer 319

Simple Choice of agent critical Speed Pungency Not generally recommended – VERY POOR for the patient and associated with higher mortality distressing for animal

Question 320

propofol

Answer 320

pros- Quick recovery with no hangover cons-Apnoea if given too quickly Propofol (‘milk of amnesia’) Most commonly used anaesthetic in UK (dogs and cats) Alkyl phenol, white emulsion 10mg/ml Soyabean oil, glycerol, egg lecithin, no preservative, NaOH (changes pH) Supports bacteria and endotoxin Use within 24 hours A multi-dose vial with preservative was available (‘Propoflo Plus’ – Zoetis) 28d shelf life Rapid onset of action -rapid uptake by CNS Short period of unconsciousness (5-10 mins) Large volume of distribution (lipophilic) Rapid smooth emergence due to redistribution & efficient metabolism (hepatic and extra hepatic) metabolites inactive good for patietn swith hepatic problems as it is alos metabolised in the lungs Respiratory depression (apnoea) - IPPV - Speed of injection should be slow, less needed if given over longer period Cardiovascular depression Rapid and smooth recovery Suitable for top ups or TIVA Muscle relaxation usually ok- can cause extention and rigisity of legs, wait it out or give muscle relaxant Anticonvulsant Not irritant, pain reported not Analgesic ↓ ICP (patients with raised and normal ICP) problems- Rigidity, twitching Apnoea Profound bradycardia Care in hypoproteinaemia Heinz body anaemia in cats ??? Use for patients with pancreatitis / hyperlipoproteinaemia or diabetic hyperlipidaemia Pain on injection ? Local reaction (clear formulation, discontinued)

Question 321

Alfaxalone

Answer 321

Is suitable for cats and dogs (& other spp) Alfaxalone is a clear colourless neuroactive steroid Causes anaesthesia by activating the GABA (inhibitory) receptor has a short plasma elimination half life and is cleared from the body relatively quickly Alfaxalone can be give as repeated boluses or as TIVA to maintain anaesthesia Premedication is preferable Anaesthesia induction is smooth, and the injection is given slowly over 60 seconds. Occasional apnoea is seen and IPPV may be necessary (more than propofol) The drug has good cardiovascular stability, causes no histamine release and produces good muscle relaxation Animals should not be disturbed during recovery as excitement can occur

Question 322

Dissociative Agents

Answer 322

Ketamine (also Tiletamine in Europe/USA) Weak organic base pH 3.5 Racemic 10% solution (100mg/ml) IV, IM, SC, IP, PO, epidural Dissociative state Used in many species for induction and analgesia

Question 323

What is ‘dissociative anaesthesia’?

Answer 323

Dissociative anaesthesia = detached from surroundings- Patient may have their eyes open and make reflex movements during surgery In recovery the patient may be agitated- Hallucinations are associated with human ketamine anaesthesia, Can be reduced by premedication with benzodiazepines Ketamine increases the intracranial pressure- causes rigitity, give other meds along side this

Question 324

Ketamine

Answer 324

Can be combined with BZD, alpha 2 agonists, acepromazine, opioids Versatile induction agent and wide safety margin Invariably needs to be combined with something Rapid induction Respiratory effects are mixed – bronchodilation and RR usually preserved but my stop! GOOD ANALGESIA CVS effects depend on dose Muscle tone ↑ and jerky movements Salivation and lacrimation ↑ Ketamine can be diluted with sterile water or physiological saline Stormy recovery if disturbed or not adequately premedicated Depth assessment is different (eyes open) Corneal drying - use ‘Lacrilube’ or similar tears Vomiting common with alpha 2 combinations avoid in patients with GI obstruction Avoid in patients with ↑ Intra ocular pressure, ocular surgery, fever, hyperthyroidism schedual 2 control drugs- records important

Question 325

MAC

Answer 325

Minimal Alveolar Concentration (MAC) The alveolar concentration (at 1 atm) producing immobility in 50% of patients in response to a noxious stimulus i.e. Potency MAC is for healthy, un-premedicated patients MAC affected by Age, N2O, hypotension, hypoxia, anaemia, opioids, sedatives , LAs, pregnancy premeds reduce mac- not nsaids though MAC not affected by Stimulation, duration, species, sex, CO2, NSAIDs

Question 326

Concentration of agent rises in plasma at a rate that depends upon

Answer 326

Ventilation Concentration of agent in carrier gas Cardiac output (inversely) Solubility of agent in the body (inversely)- the more soluble the slower the effect

Question 327

Blood:gas partition coefficient =

Answer 327

Solubility This is the ratio of the amount of anaesthetic in blood and gas when the two phases are of equal pressure and volume The LESS soluble agents (low coefficient) are washed away less quickly therefore the alveolar concentration rises FASTER

Question 328

Blood: gas partition coefficient

Answer 328

The LESS soluble agents (low coefficient) are washed away less quickly therefore the alveolar concentration rises FASTER

Question 329

a fat animal will recover from anethesia slower than a thin one. why?

Answer 329

Recovery is the reverse of induction, so dependant on blood solubility, redistribution will have occurred into the fat, which then acts as a depot of anaesthetic so (depending on fat solubility) a fat animal will recover slower than a thin one….

Question 330

ideal anasthetic agent

Answer 330

Stable No preservatives Non-inflammable Cheap Ozone friendly Non metabolised Non-toxic No CVS effects Analgesic

Question 331

What are negative effects of inhaled agents?

Answer 331

To the animal- Cardiorespiratory depression Formation of carbon monoxide with soda lime (Formation of other toxic gases) To the anaesthetist- Little or no evidence apart from nitrous oxide Bone marrow suppression Teratogenesis

Question 332

Nitrous oxide – becoming obsolete (why?)

Answer 332

H and S issues Expensive Analgesic Min CVS & resp effects V high MAC > 100%

Question 333

Isoflurane

Answer 333

Lower solubility Different CV depression ‘SAFER’ in dog CEPSAF

Question 334

summerise the considerations made with anethetic agents

Answer 334

Most anaesthetics induced by injection and maintained by an inhalational agent. Recovery faster with a less soluble agent such as sevoflurane but MAC is higher MAC is altered in states such as pregnancy and with other drugs Scavenging is important although little evidence for problems All inhalants are CV depressants Evidence supports use of isoflurane over halothane No data supporting further reduction of risk with sevoflurane

Question 335

methods other than vapors to maintain anaesthesia

Answer 335

TIVA = total intravenous anaesthesia PIVA = partial intravenous anaesthesia Often used in horses but increasingly in small animals Offer environmental advantages

Question 336

TIVA

Answer 336

total intravenous anaesthesia Can be used for short procedures in small animals/aggressive patients E.g. ‘quad’ anaesthesia for cat neuters The Cat Group Routinely used for field procedures in horses E.g. ‘GGE, ketamine, alpha-2 agonist – so called triple drip Various ‘recipes’ GGE (Guaifenesin, a centrally acting skeletal muscle relaxant with little or no analgesic properties) Supplied as 5% guaifenesin in 5% dextrose and infused to effect until signs of ataxia are seen, at which time IV bolus of ketamine is given Maintained with infusion given to effect However, always remember Protect the airway – regurgitation risk (which species?) Supply oxygen Have a means to ventilate

Question 337

PIVA

Answer 337

partial intravenous anaesthesia Goals of PIVA Reduce MAC Reduce cardiopulmonary depression Provide additional analgesia Improve environmental impact (Improve plane of anaesthesia) Reduced cardiopulmonary depression, and less inhalant can be used Analgesia provision Less pollution & organ toxicity Improved intra operative conditions Improved outcome? We don’t know yet Evidence based medicine Cardiopulmonary depression will still occur Most IV drugs accumulate over time Additional equipment required the ideal drug- MAC reduction Analgesic Minimal toxicity Minimal effects on the body Short context sensitive half life Compatible with other drugs NO single drug meets these requirements Hence the need for combinations

Question 338

combinations for PIVA

Answer 338

Inhalant+ Lidocaine- Analgesic MAC reduction (25%)- not for cats !!! Ketamine- Often given as boluses during anaesthesia Ketamine CRI (30% MAC reduction) Alpha 2 agonists (not licensed as CRIs)- Xylazine, detomidine, medetomidine and dexmedetomidine can be given as small (tiny) boluses Bradycardia ! Can also be given as CRIs Opioids – various commonly used Combinations may be the key Remember most drugs accumulate over time Lidocaine + ketamine have been shown to improve cardiovascular stability during isoflurane anaesthesia Many combinations are possible and again we must used evidence based medicine to recommend the recipes

Question 339

what can be measured on a monitor during anesthesia

Answer 339

Capnograph- The term capnography refers to the noninvasive measurement of the partial pressure of carbon dioxide (CO2) in exhaled breath expressed as the CO2 concentration over time. Blood pressure ECG Pulse oximeter Cardiac output

Question 340

What Should We Monitor in a patient under anesthesia?

Answer 340

CNS depression- Eye position, jaw tone, EEG, BIS, etAA Physiology and homeostasis- Respiratory: Oesophageal stethoscope, capnograph, pulse oximeter Cardiovascular : Blood pressure (MAP), pulse, ECG Delivery of oxygen = how much oxygen is being carried to the tissues by how much blood pressure

Question 341

Temperature under anesthesia

Answer 341

Anaesthetised, sedated and critical patients unable to regulate temperature Measure temperature using rectal thermometer (may under read) or oesophageal thermoprobe (gold standard) Core-periphery differences Use bubble wrap, socks, hot water beds, lamps, low flow anaesthesia, warm theatre, heated pads, blankets, themovents/HMEs Temperature affects many aspects of anaesthesia Increased pain Increased wound infections Delayed recovery Core temperature support?- Consider warm saline irrigation Circle systems (rebreathing system) Consider warm water enemas

Question 342

Hypothermia during anaesthesia

Answer 342

Temperature falls due to Reduced shivering Vasodilation Reset thermoneutral point- opiods Open body cavity Cold gases Dry gases Wetting and prep

Question 343

monitoring pule during anethesia

Answer 343

Use peripheral pulses Get used to palpating pulses at different sites Femoral artery Dorsal metatarsal artery Lingual artery Auricular artery Compare dorsal metatarsal artery and femoral artery With hypotension dorsal metatarsal artery disappears use fingertips to locate artery

Question 344

Pulse Oximetry

Answer 344

Displays percentage oxygen saturation of haemoglobin Accuracy is affected by poor circulation (common in critical patients) ambient light movement of the probe chow-chows Limitations- High/low heart rates Probe design Useful post-op saturating on room air? Early warning? Cyanosis – crude estimation But ‘On a cliff edge How is the haemoglobin saturation SPO2% (reading from pulse oximeter) related to PaO2 (partial pressure of oxygen in the blood)? Oxygen content is dependent on both SaO2 and PaO2 Oxygen content = (1.39 x Hb x SPO2%) + (0.003 x PaO2)

Question 345

SPO2%

Answer 345

the haemoglobin saturation

Question 346

PaO2

Answer 346

amount of oxygen disolved in the plasma drives SPO2%

Question 347

Cyanosis

Answer 347

not enough oxygen in the blood Hb of 15g/dL (PCV 45%) Cyanosis may start to manifest at SpO285% - no other signs Haemoglobin of 9 g/dL (PCV 27%) The threshold SaO2 level for cyanosis is lowered to about 73% (PaO2 38 mm Hg), the patient would certainly have other signs

Question 348

Oxygen Content

Answer 348

Blood gas analysis- pH HCO3 PCO2 PO2 Arterial blood gases- the most accurate Capnography – a good alternative for (PACO2)

Question 349

Electrocardiogram (ECG)

Answer 349

ECG analysis does not give information about the mechanical activity of the heart Important for arrhythmia diagnosis and monitoring response to treatment Various arrhythmias may be seen Tachycardia (sinus) may be the result of Nociception- pulling on ovaries Hypercapnia Hypovolaemia Hypokalaemia And many more… ECG may show characteristic changes depending on the underlying cause Bradycardia (less common) Drugs (e.g. alpha-2 agonists, opioids) Hypothermia Electrolyte disturbances e.g. severe hyperkalaemia Knowledge of the patient is vital to determine treatment; Alpha-2 agonist-induced bradycardia with second degree AV blocks treatment is antagonism of the original dose Opioid-induced bradycardia treatment is the administration of an anticholinergic (contraindicated following alpha-2 agonist administration)

Question 350

Capnography

Answer 350

Capnography (carbon dioxide measurement) conveys information relating to both respiratory and cardiac function The end tidal carbon dioxide concentration is measured from the alveolar plateau and should remain constant with unchanged ventilation and cardiac output Main-stream (measured directly in the box) and side-stream machines (measured via a water trap are available need to be scavenged from! Normal ET CO2 = 35–45 mm Hg Hyperventilation – Decreased ETCO2 Hypoventilation - Increased ETCO2 obstructive pattern- sharks fin pattern: asthma kinked endotrachial tube not reaching baseline- rebreathing: sodalime has run out non rebreathing apperatus has inadiquate flow Other indicators Oesophageal intubation Leak at cuff/Patient disconnection Adequacy of resuscitation Normal variation – cardiac oscillations

Question 351

Arterial Blood Pressure Monitoring methods

Answer 351

Non-invasive blood pressure (NIBP) monitoring, sphygmomanometry, oscillometric ( & HDO) Doppler Invasive blood pressure monitoring Finger on pulse? NO (Systolic 90-150 feels the same)

Question 352

Monitoring Blood Pressure- Doppler

Answer 352

Set up takes a few minutes Piezoelectric crystal placed over artery (clip fur, use gel) Locate artery with distinct noise of arterial pulse Cuff placed proximal to probe Cuff size must be accurate Audible signal v useful Systolic pressure only (cats?)

Question 353

Non-invasive blood pressure (NIBP) monitoring- oscillometric

Answer 353

Cuff size must be accurate- must go 1/3 of the way around small cuff size makes reading high- large cuf size makes reading low Unreliable in cats & small dogs Quite expensive More accurate methods available High definition oscillometric devices– the future?, fast can cope with high HR & poor perfusion but clinically poor

Question 354

Invasive blood pressure monitoring- Artery cannulation

Answer 354

Direct arterial pressure via an arterial cannula “gold standard” Usually placed in the dorsal pedal artery Auricular and facial arteries also used Cannula is attached via saline-filled non-distensible tubing to an electrical transducer which gives continuous ‘beat to beat’ diastolic, mean and systolic arterial pressures Must label cannula, line & flush regularly (hep saline) Never inject any other drugs Tubing must be narrow bore and non-compliant to amplify signal

Question 355

Causes of decreased blood pressure include

Answer 355

Intravascular fluid loss (haemorrhage, third space losses) Failing myocardial function Sepsis Relative hypovolaemia (vasodilation – drugs/sepsis)

Question 356

determining renal perfusion

Answer 356

Although blood pressure monitoring is important it does not tell us directly about organ perfusion Assessing urine output may be of equal value in determining renal perfusion Aim for 1-2ml/kg/hr intraoperatively

Question 357

treatment of Hypothermic patient with bradycardia and low blood pressure

Answer 357

Anticholinergic treatment and warming to raise heart rate and subsequently blood pressure

Question 358

treatment of Septic patient with tachycardia but poor blood pressure

Answer 358

Intravenous fluid therapy to improve status Patients with advanced sepsis require pressor support Noradrenaline Dopamine Phenylephrine

Question 359

Central Venous Pressure (CVP)

Answer 359

Used as an approximation of right atrial filling pressure (late guide) but of limited clinical value in anaesthesia ?Acts as a guide to correct fluid therapy (late guide) May aid in detection of tricuspid valve problems

Question 360

Central Nervous System Monitoring

Answer 360

Aims -Adequate ‘depth’ for procedure undertaken Electroencephalogram (EEG) Experimentally – Bispectral index (BIS)

Question 361

Electroencephalogram (EEG)

Answer 361

Raw signal data Spectral edge frequency Auditory evoked potentials Very limited clinical value

Question 362

Anaesthesia Recovery

Answer 362

The process of allowing a patient to regain consciousness after anaesthesia Recovery is the most common time for an anaesthetic-related death Recovery Involves- inhalant- Turn off inhalant. Remain on oxygen. Allow inhalant to be breathed off. injectable-Turn off infusion/stop top-ups. Drugs are metabolised/re-distributed. Goal of recovery is to ensure patients return to the physiological norm as quickly as possible Key points: Heat loss leading to hypothermia Extubation Only perform when patient can swallow and has control of airway Care with brachycephalic breeds IV access Leave cannular in for 1 hour after patient appears stable for patients not on longer term IV fluids

Question 363

causes and solutions to prolonged recovery

Answer 363

Hypothermia Excessive pre-med use Patient too deep during maintenance Hypoglycaemia Choice of inhalant Choice of induction agent solutions- Heat supplementation Reconsider premed use Closer monitoring to give as little anaesthetic as possible IV fluids Use faster acting inhalant Use shorter acting induction agent

Question 364

causes and solutions of airway instructions

Answer 364

Debris or gauze left after dental procedures Body fluids eg vomit, blood solutions- Clear oral cavity then extubate after patient gains control of swallow reflex

Question 365

causes and solutions of agitated recovery

Answer 365

Inadequate use of premeds or analgesics solutions- Reconsider premed and analgesic protocol and dose rates

Question 366

Recovery in BOAS Patients

Answer 366

Sedation (acepromazine followed by alpha-2 agonist or vice versa) Don’t forget analgesia (NSAIDS* +/- opioids) *caution if steroids Oxygen supplementation Monitoring plan Leave IV cannula in situ Check for regurgitation prior to extubation EXTUBATE LATE - after the head is raised Very well tolerated! Be prepared to re-intubate Have a full dose of induction agent ready Tracheostomy

Question 367

When to re-intubate?

Answer 367

SPO2 consistently low on room air If reading 80 something then consider oxygen / re-intubation Pulling tongue out assists readings Obvious effort/distress Cyanosis Paradoxical breathing

Question 368

Post operative analgesia

Answer 368

Untreated pain leads to; Chronic pain states Wound infection Wound breakdown and interference Occasional reports of diabetes mellitus Catabolic states (insulin resistance) Welfare concerns Unhappy owners Will anything given pre or intraoperatively last into recovery period? What is the predicted degree of pain post operatively? Is it a requirement that the animal is fully conscious rapidly post operatively ? Is a slower recovery required? What is the preferred route of administration? Enteral – oral , rectal, transmucosal Parentral – intravenous, intramuscular, subcutaneous, transdermal How long is the predicted length of analgesic requirement? Intermittent bolus Continuous rate infusion

Question 369

How Can We Apply Local Anaesthetic Techniques in addition to general anethesia?

Answer 369

Somatic infiltration generally reliable & safe Multiple intradermal (or s/c) injections Usually administered in sedated/anaesthetised animals Lidocaine spray – ‘Intubeaze’ (2%) Lidocaine jelly (2%) for catheterising the urethra Lidocaine & prilocaine cream (EMLA) useful for IV cannula placement Proparacaine 0.5% and butacaine 2% topical on cornea (10-20 minutes) can improve recovery

Question 370

How Do We Use Local Anaesthetic?

Answer 370

Intravenous route- Only use lidocaine IV More benefit in soft tissue pain?? Can be used in both dogs and horses Decreases MAC and reduces opioid requirements Can also be useful post-op AVOID in cats- very sensitive Somatic infiltration generally reliable & safe Multiple intradermal (or s/c) injections Usually administered in sedated/anaesthetised animals Lidocaine spray – ‘Intubeaze’ (2%) Lidocaine jelly (2%) for catheterising the urethra Lidocaine & prilocaine cream (EMLA) useful for IV cannula placement Proparacaine 0.5% and butacaine 2% topical on cornea (10-20 minutes) Small animals Splash blocks Epidurals Dental blocks Limb nerve blocks Intraoperative articular blocks Farm animals Cornual block Caudal epidural Inverted L-block IVRA Paravertebral Horses Diagnostic nerve blocks Epidural Eye and dental blocks Intraoperative + intraarticular

Question 371

small animal anesthetic techniques

Answer 371

Splash blocks Epidurals Dental blocks Limb nerve blocks Intraoperative articular blocks

Question 372

Farm animals anesthetic techeniques

Answer 372

Cornual block Caudal epidural Inverted L-block IVRA Paravertebral

Question 373

Horse anesthetic techniques

Answer 373

Diagnostic nerve blocks Epidural- caudal Eye and dental blocks Intraoperative + intraarticular

Question 374

Local Blocks

Answer 374

Revise anatomy! Place local anaesthetic in region of the nerve Nerve Location Techniques- Nerve stimulator, Ultrasound of femoral triangle

Question 375

Head/Dental Blocks

Answer 375

infraorbital n.- upper lip, nose, roof of nose, skin rosral to canal maxillary n. - maxilla, upper teeth, nose upper lip rigeminal n.- akinesia of globe, desensitises eye and orbit mental n,- lower lip, incisors mandibular n.- mandible, teeth, akin, mucosa

Question 376

Infraorbital Block

Answer 376

upper lip, nose, roof of nose, skin rosral to canal Transbuccal Transdermal Place needle into canal

Question 377

Maxillary Block

Answer 377

Tmaxilla, upper teeth, nose upper lip ransorbital approach Transdermal approach Ventral to notch in zygomatic arch Transmucosal – cannula into infra-orbital canal

Question 378

Mental Block

Answer 378

lower lip, incisors Mandibular nn Mental foramen

Question 379

Mandibular Block

Answer 379

Medial mandible Just rostral to angular process Or transmucosal – medial aspect mandible mandible, teeth, akin, mucosa

Question 380

Ophthalmic Blocks

Answer 380

Auriculopalpebral Supraorbital 3 point Petersen block Retrobulbar

Question 381

Forelimb Blocks

Answer 381

Brachial plexus Median Radial and ulnar (RUMM block) Digital

Question 382

Hindlimb Nerve Blocks

Answer 382

Sciatic Femoral Tibial Fibular Digital Motor- ok in small animals but bad in large animals- flighty horse will be stressed by loss of use of limbs Sensory

Question 383

Forelimb Blocks

Answer 383

Brachial plexus Median Radial and ulnar (RUMM block) Digital

Question 384

Intercostal Blocks

Answer 384

Useful for: Rib fractures & flail chests Chest drains Thoracic surgery

Question 385

‘Soaker’ Cathetersv

Answer 385

Useful for analgesia for total ear canal ablations (TECA), limb amputations & extensive reconstructive surgery Relatively large bore (6 - 12 French) catheters with very tiny holes Allow distribution of local anesthetic into the surgical site Placed just before closing incision and secured to the skin at the end of the surgery

Question 386

Intravenous Regional Anaesthesia (IVRA)

Answer 386

Esmarch bandage applied and tourniquet proximal After removal of the bandage 0.25-0.5% lidocaine (2.5mg-5mg/kg) injected using a vein distal to tourniquet Tourniquet can be left in place for up to 90 minutes Used in conjunction with GA or heavy sedation Common in cattle -digit amputation

Question 387

Paravertebral Anaesthesia

Answer 387

Predominantly used in farm animals – traditionally! Inject L.A around spinal nerves emerging from vertebral canal Advantages Desensitizes large area Good muscle relaxation - motor Reduced I/abdominal pr ?simple/quick Less L.A required than infiltration

Question 388

Epidural Analgesia

Answer 388

Indications Abdominal and hind quarter surgery in small animals under light GA Post operative analgesia Standing surgery in farm animals and horses Post operative analgesia for above surgeries or injuries

Question 389

Caudal Epidural Analgesia

Answer 389

Commonest technique in large animals Inject slowly over 5-10sec Iml/100kg 2% lidocaine Max effect in 10 min - lasts c. 60 min Useful in small animals – tail amputations, perineal surgery

Question 390

Epidural Analgesia Complications

Answer 390

Accidental vascular injection Haematoma formation Subarachnoid injection Infection Hypotension Respiratory depression due to cephalad spread Nerve damage Pruritis Urinary retention Motor dysfunction Hypothermia

Question 391

Supporting Anaesthetised Patients

Answer 391

Influence on outcome – evidence base Ethical considerations Common sense…. Supporting oxygenation: Indications During all anaesthetics Pre-induction Recovery Increased FIO2- Methods Flow by Intranasal Intratracheal Tracheostomy Incubator Mask

Question 392

Hypothermia during anaesthesia:

Answer 392

Hypothermia causes Increased pain Wound infection Delayed recovery Temperature falls due to Reduced shivering Vasodilation Reset thermoneutral point Behavioural modification Open body cavity Cold gases Dry gases Wetting and prep

Question 393

Core temperature support

Answer 393

Active warming Minimise heat loss Circle systems (rebreathing system) Pre-clip Warm environment Minimise wetting Aim for short anaesthesia time Drug choices?

Question 394

Support of renal function during anesthesia

Answer 394

Fluids during anaesthesia 5 x maintenance.. Why? 10ml/kg/hr dogs (less for cats) Estimated output 1-2ml/kg/hr Measurement Volume - use of collection systems specific gravity

Question 395

Minimal Support for anesthesia

Answer 395

Baseline monitoring Oesophageal stethoscope Finger on pulse Ventilation rate Monitoring record (BP, capnography, temperature) Fluids and intravenous access Oxygen Analgesia

Question 396

what breathing system would you use on a 5 kilo patient

Answer 396

a tpiece if you neet to ippv a lack if not

Question 397

what breathing system would you use on a 10 kilo or above patient

Answer 397

a rebreathing system effiecine with lower flows cant be used for patients lees than ten kilos due to valve and sodalime- resistance

Question 398

minute volume (MV)

Answer 398

the volume breathed per miniute on average this is 200ml per kg

Question 399

risks of equine GA

Answer 399

duration of anesthesia corellates with increased risk difficult to manage after and hour and a half factors that effect duration: -caseload -skill of surgeon and staff - current condition of surgeon and staff- time of day or week, have they had a break why increased risk- big flighty cardiopulmanory depression- nit designed to lie down - experience with anesthesia- horse thats experienced it before is more acoustomed to it specific risks- cardiac arrest, fracture (esspecially of a long bone- mares who have recetly had foals most at risk)

Question 400

feild equine anesthesia

Answer 400

minor procedures castration, sacrcoid removals ect Total Intreveneous Anesthesia- TIVA extra boluses of ketamine to maintain anesthesia check the feild- stones, watercourses, batteries, holes, slopes, type of fence (barbed wire)- anything that could injusre horse as it goes down draw up all drugs and palce iv cannula- get all equipment ready fit horse with padded head collar have help and a plan administer drugs and induce anesthesia position horse- if horse in lateratl, bottom forelimb forward, hind limbs parallel

Question 401

hospital equine anesthesia

Answer 401

more majour surgery horse is intubated-same as small animals but cannot visulise the larynx- use gag endoscope up the nares could be used dorsal recumbancy is maintianed when using oxygen in isofurane monitor as usual pre-oxygen rarly tolerated but used in very sick cases theater equipmetn must be checked- hoist, inflatable beds

Question 402

equine premed

Answer 402

aim is to produce a horse sedate enough for ketamine could use propofol but requires large amount healthy horses ofter recive acp intramuscularly- only drug assosiated with improved outcome- not good for colic due to vasodilation iv jugular canula- want to place on uppermost side depending on surgery alpha 2 agonists also used- xylazine- quick acting, can top up, good for colics romifodine- takes 5 to 10 mins, longest acting, less ataxia, could take too long. lasts 45 mins, detomidine- interediate, lasts 45 mins, small volumes can tell sedation by knocking on sinuses or indeifference to lip being touched GGe- used in horses not healthy enough for an Alpha 2 (specifically for cardiovascular problems)- muscle relaxant infuse IV until horse is "knuckling then give etamine and microdose of APHA 2

Question 403

equine induction agents

Answer 403

ketamine- dissociative good anesthesia must not be used alone- causes sezures eyes remain open and central can be used as top ups (dont exceed induction dose)- every 10-20 mins takes 2 mins to go down use head to guide which side horse goes down in Used in combination with acepromazine, alpha 2 agonists, BZDs or guaifenesin (GGE)

Question 404

give an example of the "recipe" for a GA eqine feild induction

Answer 404

ACP- wait 30-45 mins detomidien IV- wait 5 mins, check heart rate (> 20 BPM), chek for adiquate sedation diazepam/ katamine iv for induction ketamine iv top ups every 8-15 mins or triple drip (GGE, Ketamine, Alpha 20 add 1/4 doese detomidine after 4/5 doses i using katamine alone with ketamine continue to give top ups of alpha 2

Question 405

problems suring equine anesthesia

Answer 405

arterial blood pressure low PO2 high CO2- vetilate patient bradycardia- common tachycardia- rare aponea pain movment poor recovary

Question 406

methods of equine hospital recovery

Answer 406

free recovery rope recovery

Question 407

anaesthesia of ruminents

Answer 407

licenced drugs for food animals must be considered many orocedures done standing usually achived via iv (calves cna be masked) diffucult cows may drink chloral hydrate iv cannula placment??

Question 408

intubation of ruminents

Answer 408

small ruminents -direct visulisation larger ruminents- intubated by palpation, developed skill cuffed tubes- regurgitation risk! rumenants have a rumen!!!

Question 409

induction of anesthesia in pigs

Answer 409

deep im (just behind ear- dont go into back or hindlimb), iv or mask with inhalant ketamine, alfaxalone, propofol ketamine combinations malignant hyperthermia- rare condition of pigs. after exposure to inhalant, rapidly fatal- can be treated with drug intubation is challenging- larynx is complex

Question 410

anasthetic risk for rabbits

Answer 410

difficult to intubate- lidocane needed, big fleshy tounge difficult to handle lack of familiarity sublinical disease small lungs prone to hypothermia

Question 411

rabbit premed

Answer 411

if in doubt go low with dose buprenorphine- 30 40 mins to peak if given Im

Question 412

maintanence and monitoring or rabbits

Answer 412

difficult to monitor depth

Question 413

gi support of rabbuts for anestheisa

Answer 413

gut stasis big killer

Question 414

Why do we Encounter Dysrhythmias?

Answer 414

Older/sick patients Multiple underlying conditions Cardiovascular depression Vasoactive drugs (which?), inhaled anaesthetic agents (effects?) Hypothermia Fluid loss Overstimulation Nociception

Question 415

ECG triangle

Answer 415

lead 2 (left leg)- standard lead, most diryhtmias recorded in lead 1(right arm) lead 3(left leg)

Question 416

ecg wave

Answer 416

p wave- atrial depolarisation qrs complex- ventricular depolarisation t wave- repolarisation of ventricals qrs complex is bigger as it is a cordinated movmemt involving punjinke fibres. t wave is doen by individual myocytes st segment should be at same level as baselinw but is often below- indicates myocardial hypoxia a big q wave could mean a thickened intraventricular septum ecg does not tell you anything about the pulse- Pulseless electrical activity can occur- electrical activity without actual beat of the heart

Question 417

st segment depression indicates...

Answer 417

myocardial hypoxia

Question 418

Dysrhythmia Interpretation

Answer 418

What is the rate What is the overall rhythm Is there a P for every QRS Is there a QRS for every P Are there aberrant (usually ventricular) complexes What do the monitors tell you about the patient?

Question 419

Sinus arrhythmia

Answer 419

Perfectly normal rhythm Often seen in fit anaesthetised patients Sign of high vagal tone? Be careful of procedures that stimulate vagus such as ocular surgery

Question 420

(1st degree) and 2nd Degree A-V Block

Answer 420

Occasional p waves with no QRS Common to see Can be caused by vagal stimulation or very ‘deep’ anaesthesia Can be idiopathic Commonly as a result of alpha-2 agonists Very rarely HIGH dose opioids Will be heard as missed heartbeats Treatment?- do you need to?- Is treatment necessary? How would you decide? If necessary, antagonise the alpha-2 agonist (or administer naloxone?) Problem with this? Decrease anaesthetic depth If still no response and reduced cardiac output? Consider atropine/glycopyrrolate

Question 421

3rd degree AV block

Answer 421

P waves and qrs doing own thing Artial pacemaker cells and avn are not working in sync Impulse not originating in avn REAL PROBLEM Treatment while under anesthesia– Stop further deterioration, ensure all other parameters are normal- depth of anesthesia ect pacemaker can be places

Question 422

Atrail Fibrilation and ventricular ectopic

Answer 422

Gap of complexes different Height of complexes different No pause after ventricles contract worring!!! ventricular ectopic-electric signals in the heart starting in a different place and travelling a different way through the heart. Treatment? Stop further deterioration, ensure all other parameters are normal Recover asap, ?amiodarone Then cardiology Rate control if there is underlying heart disease – medical mx Electrical DC cardioversion may be an option

Question 423

Ventricular premature complexes (VPCs) plus compensatory pause

Answer 423

Fairly regular but with a few ventricular ectopic beats- strange and occasional variation in size of qrs complex Is the pause good or bad? Treatment? Check physiology – often due to hypoxia or hypercapnia. Sometimes low blood pressure Add analgesia – may be due to nociception Possible lidocaine if becoming frequent

Question 424

Ventricular tachycardia (V tach)

Answer 424

Some normal beats Others wide, abnormal ventricular beats Ventricular tachycardia (V tach) Often a deterioration of SVT – treat underlying cause Often as a result of sepsis or a major underlying condition May deteriorate into ventricular fibrillation (often fatal) Treatment = underlying cause, lidocaine, amiodarone, magnesium Ensure all other parameters normal

Question 425

Ventricular escape

Answer 425

Triphasic qrs Actually quite normal Ventriclas are firing to restart normal rhythm Would you treat this? Possible due to alpha-2 agonists or high dose opioids? What would you do? Treat cause otherwise ensure all other physiology is normal- probebly no nead to treat

Question 426

Whatever the Cause of abnomal ECGs, you should always

Answer 426

Apply First Principles.. Check physiological parameters and correct if possible Oxygen, carbon dioxide, temperature, heart rate External factors and correct if possible Blood loss, surgery, nociception, drug reaction (contrast for example) Antagonise drugs (or add more – nociception) Finish surgery as soon as possible – into ICU

Question 427

Imaging Modalities for imaging the thorax:

Answer 427

Radiography Widely available Non-invasive Time and cost-efficient Ultrasonography (echocardiography- imaging the heart) Complementary First choice for cardiac disease no good if lungs are full of air Computed Tomography (CT) Where radiography and US fail Higher sensitivity

Question 428

Assess technical quality

Answer 428

Positioning Centring/Collimation Exposure factors (Inspiratory) Labelling No Artefacts

Question 429

Restraint methods for imaging the thorax

Answer 429

Chemical General Anaesthesia- Avoids voluntary patient movement Allows control of respiratory movement Facilitates good oxygenation Increased atelectasis of the dependent lung Sedation- Safer if suspect CVS or pleural disease e.g. butorphanol Can lead to respiratory depression (so monitor and flow by O2) No control of respiration Physical restraint alone – does not mean manual restraint Difficult to get good quality images Rabbit burrito/cats in resp distress in a box can work well.

Question 430

how do you decide which views to take on a radiograph

Answer 430

A minimum of 2 orthogonal views Beyond that – case dependent! Routine (inc cardiac) cases – RL and DV Screening for metastases RL + LL + VD/DV Specific lung pathology – RL + LL + VD Appearance unclear on one lateral and DV/VD – take the other lateral

Question 431

taking a right lateral view

Answer 431

Right lateral preferred Cardiac silhouette position more consistent Diaphragm obstructs less lung field More lung between cardiac silhouette and thoracic wall Position: Right lateral recumbency legs secured cranially, neck extended foam wedge to prevent rotation Centering/Collimation Centre beam slightly caudal to caudal border of scapula Collimate to thoracic inlet, thoracic spine, sternum and diaphragm (cranial abdomen)

Question 432

taking a ventral dorsa/ dorsal ventral view

Answer 432

DV/VD centring/collimation Ensure symmetrical positioning with spine and sternum superimposed (to avoid axial rotation) Centre beam in midline, at level of caudal border of scapula Collimate to thoracic inlet, diaphragm and body wall (skin edges) – unless investigation requires otherwise. vd Heart rotates to one side and distorts shadow May produce better pulmonary detail Can see more of the lung fields dv Safer in dyspnoeic patient Heart lies in anatomically correct position – easier to interpret cardiac silhouette

Question 433

Timing of exposure when imaging the thorax

Answer 433

Aim for peak inspiration: Diaphragmatic line straight dorsally – T12/13 Expiration: Diaphragmatic line domed, increased contact with CS – T10/11

Question 434

Avoiding movement blur when imaging the thorax

Answer 434

Good restraint Good radiographic technique Exposure time - High kV / low mAs technique Relevant to film radiography Low mAs minimises exposure time High kV reduces the high contrast appearance of the thorax Less relevant with digital radiography Use a grid if thickness > 10cm Controls scattered radiation Timing of the exposure At peak inspiration May need to use the expiratory pause in a conscious panting animal

Question 435

Radiopacities

Answer 435

The five basic densities: Metal – White (all x-rays absorbed – most opaque)radiopaque Bone – nearly white Soft tissue/Fluid – mid grey Fat – dark grey Gas – very dark/black (few x-rays absorbed – most lucent)- radiolucent

Question 436

Border obliteration​

Answer 436

How visible is the border of the structure being evaluated?​ Structures of the same opacity which are in contact will appear as one shadow​ Border obliteration​ (silhouette sign or border effacement​)

Question 437

Mass effect

Answer 437

Displacement of structures due to adjacent space-occupying lesions e.g. fluid or mass

Question 438

Interpretation of thoratic Radiology

Answer 438

1.Assess technical quality (Pink Camels..) 2. Assess the respiratory system 3. Assess the cardiac silhouette 4. Assess everything except the heart and lungs General Principles: Be consistent! Ensure you evaluate: Thoracic boundaries Pleural space Lower airways and lung fields Mediastinum Heart and blood vessels Always ask: Is the radiographic diagnosis consistent with clinical findings? Is the quality of the radiograph adequate to permit a confident radiographic diagnosis?

Question 439

Roentgen Signs

Answer 439

Number Location Size Shape Margination Radiopacity

Question 440

Pulmonary Vasculature on imaging

Answer 440

Normal vasculature Normal pulmonary vessels are clearly visible in central and middle zones Vessels taper towards the periphery In lateral view Artery is dorsal to bronchus and vein Veins are ventral to bronchus and artery In DV view Veins are medial to arteries so.. veins are ventral and central

Question 441

Lung Patterns on imaging

Answer 441

Lung disease different characteristic radiological appearances depending on which component of the lung is affected. Known as lung patterns: Bronchial Alveolar Vascular Interstitial Diffuse Nodular

Question 442

lung varitation Dogs vs Cats

Answer 442

In dogs, caudodorsal lungs very close to spine, right up to the tip In cats, diverge slightly from the spine around caudal T11/cr T12 due to the larger sublumbar muscles

Question 443

Cardiac Silhouette

Answer 443

Assess the cardiac silhouette Generalised enlargement Individual chamber enlargement: left atrium right atrium Left ventricle Right ventricle Change in great vessels VD​ Diaphragm often appears as 3 ‘humps’​ Distance between diaphragm & heart is greater than for DV​ Better visualisation of accessory lobe​ Gas should be in the pylorus​ Right and ventral​ DV​ Diaphragm appears as a single dome​ Gas should be in the fundus​ Left and dorsal​

Question 444

Normal Heart Size - Cat

Answer 444

Cat - Normal width (DV) < 2/3 width of thorax Normal short axis (lateral) = cranial 5th rib to caudal 7th rib Normal long axis (lateral) 2/3 height of thorax

Question 445

Vertebral Heart Scores

Answer 445

Leanghth + Width = VHS Normal values: Dog = 8.5 – 10.5 Cats = 7.5

Question 446

Pericardial Effusion on imaging

Answer 446

Cardiac silhouette grossly enlarged Globoid appearance Ultrasound = sensitive indicator!

Question 447

Pneumothorax on imaging

Answer 447

Lung retraction from thoracic wall Space between heart and sternum

Question 448

Example recipe for GA Hospital

Answer 448

Acepromazine im, wait approx 30-45 minutes Detomidine iv, wait 5 minutes, HR>20 bpm, adequate sedation must be apparent Diazepam/ketamine iv for induction (can use ketamine alone) Intubate, maintain on isoflurane in oxygen Monitor depth, keep ABP > 70mmHg, and PCO2 <60mmHg IPPV if necessary. Sedate for recovery

Question 449

Achieving a secure airway in a rabbit

Answer 449

Obligate nasal breather need to disengage the soft palate from the epiglottis to visualise larynx Big fleshy tongue Narrow gape cheeks VERY sensitive larynx I always use lidocaine spray prior to an ETT Depth Test - jaw tone??, tongue withdrawal (care), cough when local applied to larynx. Breath holding vs apnoea. Raise the head and extend the neck to disengage the soft palate Ideally visualise the larynx to intubate the patient apply local to larynx otoscope/laryngoscope slightly curved ET tube, no cuff ~1 mm diameter for every kg bw

Question 450

Right parasternal long-axis view

Answer 450

obtained with the transducer in the parasternal window with the transducer index mark pointed toward the patient's right shoulder (10 o'clock) in the third or fourth intercostal space.

Question 451

Depth of an ultrasound

Answer 451

this adjusts the field of view (the real-time image should fill the field)

Question 452

Gain of an ultrasound

Answer 452

power (high gain = white image)

Question 453

Sector Width of an ultrasound

Answer 453

(the smaller the sector angle, the faster the frame rate and the higher the resolution of the real-time image) Sector width affects frame rate. The narrower the width, the higher the frame rate.

Question 454

Focus of an ultrasound

Answer 454

make sure you place the focal point at the depth level of interest on the image

Question 455

Right-sided ultrasound views – why do we want them?

Answer 455

Subjective assessment of chamber size and systolic function Evaluate the mitral and tricuspid valves Measure chamber size (particularly the left ventricle and left atrium)* Evaluate some measurements of systolic function

Question 456

How to perform a basic echo exam

Answer 456

PREPARATION clip fur dont sedate when posible ECG trace – don’t worry about where your ECG clips are. You just want the timing intervals. Remember your cardiac cycles. Beginning of the QRS is end-diastole. End of the T wave is end-systole. Choose the correct transducer according to patient size. Palpate the apex beat prior to scanning. POSTURE – avoid twisting to look at the screen. Use an arm rest. Try to relax and DON’T PRESS TOO HARD! Use more gel….takes a few minutes to soak in. Try to ultrasound as many patients as possible to get a good technique and develop consistency. PRACTISE! Understand cardiac pathophysiology well. make sure image fills screen obtain Right Parasternal Long-axis Four Chamber View- asses systolic function: Interventricular septum, Interatrial septum, Mitral valve Watch the left ventricle contract turn thumb and tip probe till left ventrical is curcular- Right Parasternal Short-axis View (papillary muscle level) tip transducer upwards ot visulise mitral valve- fish mouth view tilt it further to visulise the aortic valve

Question 457

Measurements – How to Make Them on an echocardiogram

Answer 457

As a general rule, measurements should be taken from 3 cardiac cycles then averaged. Most importantly, ensure that the view is correct and well aligned before taking any measurements. It is best not to make measurements if your image is substandard.

Question 458

Fractional Shortening

Answer 458

FS (%) = (LVDd – LVDs)/ LVDd LVDd=Left ventricular internal diameter during diastole LVDs=Left ventricular internal diameter during systole FS% is affected by many external factors therefore has its limitations standard reference ranges can be obained measure of contractillity and function can be effected by preload, afterload and contractility

Question 459

Cornell measurement

Answer 459

When assessing LV diameter, use published breed specific reference ranges when possible, however, these are not always available OR the dog may be a cross breed. What then? LVDd=Left ventricular internal diameter during diastole For those dogs which are cross breeds are pure bred dogs with no published reference ranges available, then the “Cornell method” scales the LVDd (cm) to bodyweight (kg). Cornell formula; LVDd cm/BWˆ0.294 For the “EPIC Study”*, dogs were classified as having enlarged left ventricles when the LVDdALLO was >1.7

Question 460

E-Point to Septal Separation (EPSS)

Answer 460

an easy measurement to obtain that is accurate in estimating the LVEF. EPSS is measured in the parasternal long axis view (PLAX) of the heart, which gives a view of the left ventricle and is often used to assess its function. sensitive and specific for ventricular function

Question 461

Indications for Echocardiography

Answer 461

Investigation of a heart murmur*. Investigation of breathlessness, cough and/or collapse. Investigation of an arrhythmia. Investigation of a gallop rhythm. Investigation of the presence, significance and cause of pericardial disease. Investigation of ascites or pleural effusions whereby noncardiac disease has been excluded. Investigation of unexplained pyrexia. Breed screening (in particular for preclinical dilated cardiomyopathy). Assessment pre-chemo.

Question 462

Eupnoea

Answer 462

Normal respiration

Question 463

Tachypnoea

Answer 463

Increased respiratory rate (not necessarily depth)

Question 464

Apnoea

Answer 464

Absence of respiration

Question 465

Hypoventilation Hyperventilation are both examples of

Answer 465

Alterations in ventilation at the alveolar level

Question 466

Hypercarbia

Answer 466

Increased CO2 in blood•Hypoventilation•Incprodnof CO2Primary drive for respiration

Question 467

Hypoxaemia

Answer 467

Decreased O2 in blood•Poor O2 intake•Hypoventilation•Increased O2 consumption•Decreased O2 carrying capacity

Question 468

Differentials for tachypnoea

Answer 468

Primary cardiac disease Neurological disease- Damage to respiratory control centre Metabolic disease- Acidosis/alkalosis, Increased PaCO2 Hyperthermia- Cooling mechanism Stress Pain Abdominal discomfort- Restricted movement of diaphragm Primary respiratory disease

Question 469

OBSTRUCTIVE RESPIRATORY PATTERNs

Answer 469

LRT Obstruction- Thickening, inflammation and mucus Causes increased expiratory effort Small airways held open during inspiration Early collapse during expiration e.g asthma positive pressure of inspiration created allows easire passage of air. experation needs more effort dont get stertor or sridor with this pattern URT Obstruction- Causes marked inspiratory effort Dynamic collapse of soft tissues due negative pressure associated with inspiration Inspiratory STRIDOR or STERTOR as animal breathes in, negative pressure is created meaning there will be more effort needed to inspire than expire with this pattern

Question 470

Restrictive Respiratory Pattern

Answer 470

Expansion of the thorax restricted> Decreased tidal volumeTachypnoea / short-shallow breaths> Hypoventilation restriction can be in lungs, in pleural space or withing ribs or diaphram.

Question 471

Paradoxical Respiratory Pattern

Answer 471

results form significant trauma to the ribcage road traffic accidents Paradoxical movement of the chest wall: -Trauma –“Flail” chest -Terminal respiratory failure –fatigue of muscles

Question 472

SEROUS

Answer 472

Nasal Discharge Inc. nasal secretionsAllergic rhinitisAcute InflammationViral infection

Question 473

MUCOID nasal discharge

Answer 473

Nasal Discharge

Question 474

PURULENT Nasal Discharge

Answer 474

Bacterial infection1o or opportunisticpathogen

Question 475

HAEMORRHAGIC Nasal Discharge

Answer 475

TraumaClotting disorderVascular diseas

Question 476

Nasal Discharge

Answer 476

Can be difficult to identify •Intermittent nature •Cleaning / Licking of nasal planum Character of the discharge + Unilateral or Bilateral Presentation + Knowledge of common diseases URT Origins (usually unilateral)- •Nasal cavity •Paranasal sinuses •Guttural Pouch (horses)- could be bilateral •Nasopharyngeal - could be bilateral •Trachea- could be bilateral LRT Origins ( will be consistantly and evenly bilateral)- •Bronchoalveolarspace •Oedema, Pneumonia •Pulmonary vasculature •Haemorrhage

Question 477

Coughing

Answer 477

Upper respiratory tract- •Harsh, dry, hacking cough •Tracheitis or tracheobronchitis •Often productive Lower Respiratory Tract- •Soft, chesty cough •Pneumonia •Lower airway inflammation •Cardiogenic

Question 478

Respiratory Sounds

Answer 478

Normal: Tracheal / Bronchovesicular- •Normal air movement through airways •Increase airflow > Harsh intensity Abnormal: Wheezes- Air passing through narrow airways Bronchoconstriction Crackles/Rales- Air passing through fluid Oedema, harmorrhage, pneumonia Dull/Absent- No air movement though lung Pleural rubs Friction between pleural surfaces Systematic auscultation- larynx, trachea, multiple points thorax: craniodorsa, caudodorsa, Hilus, cranioventra

Question 479

Accentuating Respiratory Sounds

Answer 479

Adventitious noises can difficult to detect during normal: respiration- •Subclinical inflammatory airway disease / asthma •Interstitial disease Re-breathing exam (plastic bag over horses nose) -Increase tidal> volumeIncrease air flow> Accentuate adventitious noise

Question 480

PERCUSSION- assessing resonance of air-filled structures

Answer 480

Thoracic percussion–Lung Parenchyma•Pulmonary consolidation•Pleural fluid accumulationGenerally used as adjunct to auscultation Sinus percussion- •Altered resonance in paranasalsinuses •Fluid / pus •Cysts / Masses Very useful assessment in horses

Question 481

what is visualised in an endoscopy

Answer 481

Nasal meati Nasopharynx Ethmoid turbinates Nasomaxillary opening Guttural Pouches Trachea can be done without sedation in horses, and possibly while ridden (dynamic endoscopy)- can diagnose Laryngeal Hemiplagia (recurrent laryngeal neuropathy)

Question 482

Laryngeal Hemiplagia

Answer 482

(recurrent laryngeal neuropathy) Common cause of poor performance in race horses •Also occurs in dogs, in association with hypothyroidism paralysis of larangel cartilages, usually of the recurrent laryngeal nerve

Question 483

RHINOSCOPY

Answer 483

used to investigating URT disorders Restricted access in small animals- •Rigid rhinoscope •Narrow-bore flexible endoscope •Otoscope Indications- •Nasal foreign body •Nasal mass –biopsy

Question 484

RADIOGRAPHY to Investigate URT disorders

Answer 484

Commonly used to assess paranasal sinuses- Lateral, dorsoventral and oblique projections Cheap•Quick•Readily available•Doesn’t usually require GA•Excellent for assessing lung parenchyma Identification of; •Fluid accumulation in sinus (sinusitis) (fluid line) •Soft tissue masses •Distortion/destruction of normal bony architecture

Question 485

Nasal / Nasopharyngeal Swab

Answer 485

Not appropriate as a screening tool- •Wide array of commensal bacterial flora •Contamination of sample is impossible to avoid Only use for identification/isolation of specific pathogen(s)- •Virus identification •Bacterial isolation -Streptococcus equi equi, Influenza, herpes, IBR

Question 486

nvestigating LRT disorders using radiography

Answer 486

Cheap •Quick •Readily available •Doesn’t usually require GA•Excellent for assessing lung parenchyma 1.Ensure good (and safe) positioning 2.Obtain 3 standard views if possible- RL, LL. DV 3.Expose on inspiration

Question 487

Radiographic Patterns- Interstitial

Answer 487

•Interstitiumis the space between the alveoli and capillaries •Interstitiumbecomes more prominent •Air still present in alveoli and normal vessels seen Diffuse(unstructured) -e.g. oedema/ diffuse lymphoma. the tissue around the broncheoles is more radiodense Nodular –e.g. soft tissue mass ie. neoplasia/abscess- tissue around bronchi is more radiodense but in a more "smattered" pattern Underexposure, expiration or obesity can look similar –often misdiagnosed

Question 488

Bronchial Radiographic Patterns

Answer 488

Thickened bronchi •Infiltration/mineralisation of bronchial walls or due to peribronchialchanges •Classical ‘donuts’ or ‘tramlines’ •Bronchi may be more obvious in the periphery of the lungs where normally wouldn’t be seen

Question 489

Alveolar Radiographic Pattern

Answer 489

Consolidation or collapse of alveoli Air in alveoli is replaced by fluid (oedema/haemorrhage) or cells Air bronchogram is commonly seenCan be focal or diffuse Examples; bronchopneumonia, aspiration pneumonia, oedema, haemorrhage, neoplasia, lung lobe collapse or torsion

Question 490

Vascular Radiographic Pattern

Answer 490

Any changes to the size, course or opacity of the pulmonary vessels •Vessels may be larger or smaller than normal or may be tortuous •Commonly seen associated with cardiac disease •Tortuous vessels seen with heartworm •Differentials depend on vessels affected

Question 491

Pleural Disease

Answer 491

Pleural effusion: •Fluid in the pleural space •Transudate, exudate, haemorrhage, chyle Pneumothorax: Air in the pleural space Both cause lung edges to move away from the thoracic wall

Question 492

investigating LRT disorders- ULTRASONGRAPHY

Answer 492

Cheap •Very Quick •Readily available •Ideal where sedation/GA is contraindicated Excellent for assessing; •Pleural space •Pleural effusion •Diseased lung tissue

Question 493

RESPIRATORY SECRETION SAMPLING

Answer 493

investigating LRT disorders TRACHEAL WASH- Sampling of tracheal mucus Trans-endoscopic Trans-tracheal Representative of tracheal secretions and ascending lower airway secretions- wont tell if left lung/ right lung Cytology + Culture BRONCHALVEOLAR LAVAGE- Sampling of bronchoalveolarspace Trans-endoscopic Blind Cytology only

Question 494

Syncope

Answer 494

another word for fainting or passing out

Question 495

Cardiogenic syncope

Answer 495

Intermittent, profound hypotension resulting in marked reduction in blood flow to brain Estimated blood pressure fall ≤50% Arrhythmia: Asystole – sinus arrest or ventricular standstill Marked reduction in cardiac output – rapid V Tach Duration 10-30 seconds: Activity level and presence/ absence structural heart disease Pulmonary hypertension Most common cause bradyarrhythmias Might be intermittent

Question 496

Pre-syncope/ episodic weakness

Answer 496

Intermittent, profound hypotension resulting in reduction in blood flow to brain BUT lesser degree of hypotension cf. syncope Arrhythmia: Less rapid v tach SVT Less profound bradyarrhythmias Structural heart disease and pulmonary hypertension may exacerbate- Excitement/ exertion

Question 497

Bradycardias

Answer 497

Disorder of impulse formation and conduction systems of the heart Dogs <60bpm and cats <100bpm Bradycardias to consider: Advanced AV block (High grade 2nd degree and 3rd degree) Sinus arrest Atrial standstill due to hyperkalaemia Persistent atrial standstill Can be drug induced: ACP Opioids Alpha2-agonists B-blockers, calcium channel antagonists and potassium channel blockers are all c/i in sinus bradycardia, SSS and AVB greater than 1st degree Sinus bradycardia usually high vagal tone and does not result in syncope

Question 498

Tachycardias

Answer 498

Supraventricular and ventricular tachycardias Dogs >160bpm and cats >200bpm Supraventricular tachycardia Most common is atrial fibrillation (AF)- New onset – weakness, collapse or syncope. no consistent p waves loss of atrial contraction and also variable diastolic filling time reduce CO SVT is an umbrella term-AF, accessory pathways, atrial flutter… Regular SVT less common cause of syncope- less syncope because regular rhythm and activation of the heart is normal sequence. Ventricular tachycardia- Boxers and Dobermanns Can drop CO dramatically Sudden death – more so when abnormal function of LV drop of CO due to short diastolic filling time, lack of atrial connection, aberrant sequence of ventricular activation

Question 499

Neurocardiogenic syncope

Answer 499

Also called vasovagal syncope Profound hypotension due to combination of bradyarrhythmia AND vasodilation Sudden autonomic nervous system failure Withdrawal of sympathetic tone Abrupt increase in vagal tone Triggering events are variable Coughing (tussive) Excitement e.g. excited boxer Situational e.g. micturition, defecation, vomiting, sneezing… Exacerbated by structural heart disease (SAS) or concurrent GIT disease Neurally mediated syncope represents an exaggeration of the CV reflexes that normally control the circulation. Syncope occurs when these reflees intermittently become inappropriate in response to a trigger. It is likely that dogs that suffer this type of syncope have some sort of disorder of autonomic control. Remember that bradycardia can occur on its own as can vasodilation or they can occur together. The degree to which one predominates over the other will vary and persist to differing degrees. The medulla is the control centre of the reflex. Neurocardiogenic syncope is an adrenergically stimulated vagal reflex bradycardia/ Vagal mechanoreceptors (C-fibres) initiate the reflex when stretched- they are found in the in the ventricle, LA and LA-PV junction and Pas Triggered by fight or flight scenarios Apparently healthy individuals or predisposed individuals: Genetics DCM High preload Diagnosis often presumptive Common situation is exertion/ excitement in small breed dog with advanced MMVD- Hyperdynamic ventricle – increased by sympathetic surge Vagal afferents when suddenly stretched trigger reflex In this cohort it is often a sign of v high preload and impending/ overt CHF Can also occur on diuretics if preload reduced too much Diuertics is usually treatment of MMVd and syncope associated with high preload. Although if over diurese can cause syncope due to empty ventricle Boxers- Bimodal age at 6-24 months 0r 7-10 years Triggered by exertion with excitement Older Boxers also ARVC! Both can occur in same dog Situational syncope- Easily identified trigger e.g. cough Common in small, middle-aged or elderly dogs Often associated with tracheal/ bronchial compression or big LA Tussive syncope – transient bradycardia +/- reduced cardiac output Cats with HCM- On exertion Pulmonary hypertension, outflow tract obstruction (pulmonic/ sub-aortic): Severe - exertional syncope due to inability to increase RV output Impaired right-sided inflow: Compression, pericardial effusion with tamponade Hypoxia and hypoglycaemia (insulinoma) Severe anaemia with exertion Exercise induced – Labradors, Border collies

Question 500

Non-syncopal collapse

Answer 500

Wide range of diseases Difficult to differentiate from cardiogenic/ neurocardiogenic Neurological conditions Profound hypoxaemia- Can also have tussive syncope Metabolic disorders- Hypoadrenocorticism Hypoglycaemia

Question 501

Diagnostics for syncopy

Answer 501

Blood tests- Complete blood count Biochemistry & electrolytes Cardiac troponin I NT-proBNP? Basal cortisol? Fasted glucose level? Ammonia/ BAST? Thyroid panel? Blood pressure -Especially if present collapsed ECG- Bradyarrhythmia Tachyarrhythmia Thoracic and abdominal imaging- POCUS Radiography Abdominal ultrasound Echocardiography- Structure and function

Question 502

Viral causes of livestock respiritory diseae

Answer 502

In cattle the most common viral causes of pneumonia are Parainfluenza 3 (PI3) and Respiratory Synctial Virus (RSV). IBR can affect any age of stock but is rarely found in young calves. In the endemic setting it is insidious, causing low grade respirator disease in stock. The real problems are seen when it enters a naive population as it causes severe disease and transmits rapidly. Following infection it becomes latent in the cows cells, recrudescing at times of stress. Bovine viral diarrhoea virus (BVD) as the name suggests doesn’t cause respiratory disease directly but it significantly affects the immune system opening the door for other pathogens. It is therefore commonly considered as part of the respiratory disease complex.

Question 503

bacterial causes of livestock respiritory diseae

Answer 503

Mannheimia haemolytica Pasturella multocida Histophilus somnus Mycoplasma spp. Others A variety of bacterial pathogens can act as opportunistic pathogens but we commonly recognise four bacterial species as causing respiratory disease in cattle. M.haemolytica is probably the most significant and most severe. It can act as a primary disease agent, particularly at times of stress (shipping fever), but frequently is the sequel of viral infections. This is also true of P.multocida and H.somnus. Mycoplasma is increasingly recognised as a cause of respiratory disease in all ages of stock, both primary and secondary. As already discussed, these pathogens rarely act in isolation and diagnostic samples (eg post mortem) yielding these pathogens does not necessarily make them the instigating agent. Possibly the greatest significance of the bacterial species involvement is to explain why we use antimicrobials in the treatment of respiratory disease and why we see different response rates to different antimicrobials on different farms.

Question 504

fog fever

Answer 504

respiritory disease Trypthophan toxicity Fog fever is seen rarely in cattle grazing lush pasture. It is due to an excess of tryptophan in the diet which the animal can’t process quickly enough resulting in toxic damage to the lungs

Question 505

Farmers lung

Answer 505

respiritory disease Allergic reaction to moulds

Question 506

Two Main Causes of Coughing

Answer 506

CARDIAC DISEASE Cardiomegaly causing left mainstem bronchus compression Congestive heart failure (fulminant pulmonary oedema) RESPIRATORY DISEASE Upper airway dz(laryngeal paralysis, BUAS, tracheal collapse) Lower airway dz(infectious/ inflammatory/ neoplastic) CLINICAL EXAM IS SO IMPORTANT

Question 507

HEART FAILURE (HF)

Answer 507

HF = a clinical syndrome where cardiac output and tissue perfusion are maintained at the expense of increased cardiac filling pressures. -Forward and backward failure -Right-and left-sided heart failure -Systolic and diastolic failure -Acute and chronic heart failure will cause drop in blood pressure and therefor trigger THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM (RAAS)- causes vasoconstriction and odema

Question 508

AETIOLOGIES of heart failur

Answer 508

-Chronic Myxomatous Mitral Valve Dz/CMVD -Dilated Cardiomyopathy/DCM-Hypertrophic Cardiomyopathy/HCM-Pericardial Effusion/PE-Restrictive Cardiomyopathy/RCM AETIOLOGIES•Patent DuctusArteriosus•Mitral Valve Dysplasia•Tricuspid Valve Dysplasia•Pulmonic Stenosis

Question 509

aCUTE HF: TREATMENT

Answer 509

OXYGEN IV FUROSEMIDE- im if too stressed MINIMAL STRESS PIMOBENDAN- vasodilator, increases contractillity

Question 510

waht to look for in a radiograph to diagnose heart failure

Answer 510

1.Is there cardiomegaly? vhs greater than 8-10 in dogs 2.Is there left atrial enlargement? 3.Is there tracheal elevation? 4.Is there an abnormal lung pattern? 5.Are the pulmonary vessels normal?

Question 511

Signs of heart failure

Answer 511

Cough (do not trust this as a sign of HF) Dyspnoea (not always detected by the owner) Increased sleeping respiratory rate (SRR) Exercise intolerance

Question 512

Non-cardiac causes of NT-proBNP

Answer 512

Systemic hypertension Hyperthyroidism Renal failure

Question 513

Calculating the drip rate

Answer 513

The steps to calculate the drip rate are the following.. Calculate the hourly rate according to the total volume requirement (more on this later) This is all you need to input if you are using an infusion pump Calculate the minute rate: divide the hourly rate by 60 minutes Calculate the drops per minute: multiple the minute rate by the giving set drip factor Calculate the drops per second (drip rate): divide the drop per min by 60 seconds

Question 514

Creating a fluid therapy plan

Answer 514

Step 1 – Resuscitation If shock is present step 1 must be followed first. When the patient no longer shows signs of shock, or if no shock is present, move to step 2. Step 2 – Rehydration Is the patient is showing signs of dehydration? Step 3 – Maintenance Is the patient is not eating/drinking normally? Step 4 – Ongoing losses Does the patient have continuous fluid losses (e.g. vomiting) To create a fluid therapy plan: 1. Deal with Step 1 first if required. Stop when the patient no longer shows signs of shock. 2. Work out if Steps 2, 3 and 4 apply to your patient. If they do, calculate the volume of fluids needed in each of the Steps 2, 3 and 4 and then add them together. This total must be administered in 24-48 hours. Monitor the patient to guide continuity of fluids, identify complications and resolution of clinical signs.

Question 515

Fluid deficit in dehydration is determined by:

Answer 515

Fluid deficit (litres) = Body weight (kg) x % dehydration (as a decimal)

Question 516

fluid defecit of a patient with No clinical signs, but patient has history of fluid loss

Answer 516

<5%

Question 517

fluid defecit of a patient with Tacky mucous membranes, ? Thirst,

Answer 517

5-6%

Question 518

fluid defecit of a patient with Skin tenting (moderate), dry mm’s, sunken eyes, slightly prolonged CRT

Answer 518

6-8%

Question 519

fluid defecit of a patient with Skin tenting (moderate), dry mm’s, sunken eyes, slightly prolonged CRT plus Increased pulse rate, cold peripheries

Answer 519

8-10%

Question 520

fluid defecit of a patient with Skin tenting (moderate), dry mm’s, sunken eyes, slightly prolonged CRT, Increased pulse rate, cold peripheries plus prolonged CRT, Tented skin stands in place, Pulses weak

Answer 520

10-12%

Question 521

fluid defecit of a patient with Collapse, signs of hypovolaemic shock

Answer 521

12-15%

Question 522

Which route/s might you use to administer fluids to your patient if Dehydration is severe

Answer 522

Intravenous

Question 523

Which route/s might you use to administer fluids to your patient if it is a Mild case of dehydration

Answer 523

Oral. Subcutaneous.

Question 524

The aim of the maintenance step in the fluid therapy plan is to

Answer 524

provide the daily requirements of water and electrolytes lost by sensible and insensible losses for patients that are not eating or drinking normally.

Question 525

Normal losses of fluid

Answer 525

Insensible e.g. Sweating, panting Sensible e.g. Urine, faeces

Question 526

Abnormal fluid losses

Answer 526

Usually secondary to illness E.g. vomiting, diarrhoea, blood loss, inappetence

Question 527

Maintenance volume can be calculated in two ways:

Answer 527

Estimate of sensible + insensible losses= 40-60ml/kg/day (2-2.5ml/kg/hour) (tend to use the higher end for small dogs and lower end for large dogs – this method can under/over estimate requirements) Accurate method (used in patients <2kg or >40kg)= Daily fluid requirement in ml = Body weight (kg) x 30 + 70 The volume is administered over a 24-48 hour period The patient must be constantly re-evaluated to assess for signs of over hydration

Question 528

Ongoing losses can also be estimated as:

Answer 528

0.5ml-2ml/kg/hour

Question 529

Ongoing losses

Answer 529

This step is to try and replace any abnormal loss of fluids to continue in the next few hours-days. E.g. diarrhoea doesn’t generally stop as soon as they start treatment, it can take a while! Ongoing losses can be estimated visually or measured directly (e.g. Urine production via urinary catheter or by patient weight loss after an additional fluid loss) Ongoing losses can also be estimated as: Patients must be reassessed in 4-6 hrs to check if volumes need to be adjusted

Question 530

Aims of fluid therapy

Answer 530

Maintenance of normal physiology – e.g. during anaesthesia. many patients will not drink at vets so will be fluid deficient Improvement of organ function e.g. kidney, heart, liver The correction of electrolyte disturbances The correction of hypovolaemia- blood loss The correction of acid base disturbances (Total parenteral nutrition (TPN) - usually partial parenteral nutrition (PPN) used in animals)- not commonly done in adult animals Is there a requirement for therapy? (ie assess patient, consider losses) What type of fluid? Which route? What volume? How fast? When to stop? End points? replace like with like- heatstoke= water loss so replace water

Question 531

parameters to asses Perfusion status and hydration status

Answer 531

Pulse quality CRT Heart rate Demeanour- collapse ofter due to hypovolemia Skin tent Blood pressure Mucous membranes Eye position- eyes will sink and third eye often prolapses with dehydration

Question 532

What is the daily maintenance rate for an animal?

Answer 532

2.5ml/kg/hour ≈60ml/kg/day {Or (30 x Kg) + 70 ???} Factor it into your plan

Question 533

Types of fluid

Answer 533

Crystalloids (hypotonic, isotonic, hypertonic)- electrolites in water that mimic plasma without protien and cells Colloids- protien in water. mimics plasma without electrolytes and cells Blood products- HBOCS (hemoglobin-based oxygen carrying solutions) –££ & problems…. heartmans if first line fluid

Question 534

Isotonic Crystalloid fluids

Answer 534

Isotonic-Lactated Ringer’s solution (LRS) aka Hartmann’s Na+ 130 mEq/l , Cl– 109mEq/l Buffered, contains lactate as a bicarbonate precursor- treats and controls acidosis Inadequate potassium for long term therapy- pk for hypokolemic patients as potassium lever lower than plasma so dilutes plasma levels Good for shock, diuresis, during anesthesia & can use for maintenance (can add other things to it) Only 25% remains in vascular space after 12 minutes- need to give more tan you think If in doubt, choose Hartmann’s!

Question 535

Hypotonic crystalloid fluids

Answer 535

0.18% NaCl 0.18% NaCl + 5% glucose Do you really want to use this ???

Question 536

Hypertonic saline- crystalloid fluids

Answer 536

!!! can easily be mistaken form heartmans and will cause issues!!! Draws water from interstitial space Transient effect (10-15 mins) Rapid restoration of MAP, increased myocardial contractility, CO & oxygen delivery 2ml/kg over 10 min, can repeat once but must follow with isotonic fluids More commonly used in large animals (e.g. prior to colic surgery) but can be used in dogs and cats (carefully) Also used in severe life-threatening raised Intra Cranial Pressure Used in GDVS and colic surgeries Treatment of raised intercranial pressure follow up with normal crystaline to restore fluid

Question 537

Fluid type - colloids

Answer 537

Support circulating blood volume better than crystaliods e.g. severe hypovolaemia, haemorrhage, hypoproteinaemia Exert a colloid osmotic pressure More rapid initial re-expansion of volume Only 1/4 of crystalloid administered remains in circulation in 40 mins Support circulation longer than crystalloids Types artificial -gelatins, dextrans, starches, HBOCs natural colloids e.g. albumin, plasma However, no evidence of clinical superiority over crystalloids

Question 538

colloids good for volume expansion

Answer 538

Oxypolygelatin Dextran 40 Pentastarch Hetastarch Albumin Whole blood Plasma

Question 539

colloids good for half life

Answer 539

Hetastarch Dextran 70 Pentastarch Dextran 40 Oxypolygelatin

Question 540

Colloids – Gelatins (ntk)

Answer 540

Oxypolygelatins Plasma half life 2-4 hours (manufacturer data) Weight average 30,000 D -pulls an equivalent volume of water from interstitial space No need for concurrent crystalloid but often do give both Produces osmotic diuresis No direct coagulation effects 15 ml/kg total

Question 541

Colloids – starches (ntk

Answer 541

Plasma half life 25 hours (hetastarch) - due to molar substitution Initial elimination by tissue uptake Excretion by metabolism - serum amylase rises Volume expanded by volume given Reversal of microvascular permeability ?anti inflammatory effect ? Direct coagulation effects Increased APT in dogs (factor VIII precipitation) Anaphylaxis in 0.0005-0.085% human patients Nausea and vomiting in cats - slow administration Up to 40 ml/kg/day

Question 542

Fluid type – blood products

Answer 542

‘Natural’ colloids Chosen according to clinical requirement- Whole blood pRBCs Ffp Cryoprecipitate Match the fluid to the loss Replace like for like- Blood issue?- blood Liver issue?- plasma Breaking down red cells? – give packed red cells

Question 543

Oxyglobin Solution

Answer 543

purified bovine haemoglobin given to patients without enough red cells to increase oxygen capacity of the blood very expensive supply scarse cause patients to pee hemoglobin very potent colloid

Question 544

Intravenous access for fluid therapy

Answer 544

Commonest route used Relatively simple to master Consider the different veins that can be used e.g. cephalic, saphenous, jugular, auricular, lateral thoracic Select large bore cannula (flow α r 4) more concentrated the solution the less it likes proliferal vein- dextrose Complications can & do occur Extravasation Thrombosis Thrombophlebitis Infection Emboli Exsanguination

Question 545

routes for fluid therapy

Answer 545

Oral- best Rectal Subcutaneous- good for small furries but not great option Intraosseous- puppies and kittens particularly. can be treated by vein. lots of LA Intraperitoneal- experemental situations- rats ect intravenous- most common

Question 546

Volume and rate of replacement of fluid

Answer 546

Calculate total deficit (% fluid deficit + losses – see earlier charts) Add on maintenance fluids Acute (replace ½ total deficit over first 1-2 hours) then consider rate thereafter (over 24 or 48 hours) – keep monitoring ins and outs In cases of shock can give 60-90ml/kg/hr (<1hr though, and MUCH less in cats) Chronic losses – replace over 3-4 days OR BASE RESPONSE ON CLINICAL SIGNS!! Monitor regularly and respond to changes

Question 547

Anaesthesia - Why Give Fluids?

Answer 547

Intravenous fluid therapy is generally recommended for any anaesthetised patient The aim is to maintain circulating volume to ensure adequate perfusion and oxygen delivery to organs Allows an ‘open vein’ Ancillary drugs/PIVA Emergency situations helps negate bad effects of anesthesia- Fluid deficits caused by peri-operative fasting Vasodilatory effects of anaesthetic drugs leading to a relative hypovolaemia Acepromazine, isoflurane Losses from the respiratory tract (worsened by endotracheal intubation) Use HME’s, low flow anaesthesia if appropriate IPPV (with PEEP/CPAP)- Reduces urine output via alterations in renal vein pressure and altered ADH However, alpha-2 agonists increase urine output Extra(epi)durals with local anaesthesia- Hypovolaemia due to vasodilation Surgical site losses- Evaporative Third space Haemorrhage

Question 548

Contra-Indications of fluids

Answer 548

Risk of volume overload in, for example, cardiac patients Risk of anaphylactoid reactions and interference with clotting tests (colloids) ?Cost

Question 549

Common differential diagnoses for respiratory disease in exotics

Answer 549

Infectious- Bacterial Viral Fungal Non-infectious- Environmental Heat stress Diaphragmatic hernia Pregnancy toxaemia Gastric dilatation Cardiac disease Pulmonary neoplasia

Question 550

clinical signs in exotic respiritory disease

Answer 550

Oculonasal discharge Facial asymmetry Oral exam Auscultation Over trachea Whole thorax  crackles, wheezing, referred sounds & vocalisation Heart rate & rhythm

Question 551

diagnosics for exotic upper respiritory infection

Answer 551

Culture and sensitivity from a deep nasal swab Nasolacrimal duct flush- Cytology, Culture Rhinoscopy Skull radiography Advanced imaging- CT

Question 552

diagnosics for exotic lower respiritory infection

Answer 552

Thoracic radiography – R & L lateral and DV views Caudal lung lobes large and are well aerated Assessment of cranial lung lobes difficult  small in some species = normal Assess lung patterns Bacterial pneumonia- Alveolar pattern Air bronchograms Diffuse, localised, lobar Changes may not be present in early stages Solitary mass- Neoplasia Abscessation Consolidation

Question 553

exotic respiritory diseases tested for by pcr

Answer 553

Chlamydia PCR – Chlamydia caviae (guinea pigs) Conjunctival scrapings  intracytoplasmic, coccoid, basophilic organisms (elementary and reticulate bodies) Myxomatosis PCR Rabbit haemorrhagic disease PCR Distemper virus Bordetella bronchiseptica, Mycoplasma pulmonis, Pasteurella multocida

Question 554

exotic respiritory diseases tested for by post mortem

Answer 554

good for large groups of animals Lung congestion Fibrin adhesions Fibrosis Suppurative lesions Pulmonary abscesses Granulomas Lung consolidation Myocarditis Tracheitis Bronchitis Otitis media/interna Septicaemia

Question 555

ferret respiritory diseases

Answer 555

Pneumonia uncommon- Clinical signs are similar to other species Viral- Canine distemper virus Influenza virus Bacterial – often secondary to another disease process Streptococcus zooepidemicus S. pneumoniae Streptococci groups C and G Other bacteria- Escherichia coli, Klebsiella pneumoniae, Bordetella bronchiseptica, Listeria monocytogenes, Pseudomonas aeruginosa

Question 556

respiritory disease in rats

Answer 556

Very common health problem Major pathogens- Mycoplasma pulmonis Streptococcus pneumoniae Corynebacterium kutscheri Minor pathogens- Cilia-associated respiratory (CAR) bacillus Haemophilus spp. Sendai virus Pneumonia virus of mice Rat respiratory virus Sialodacryoadenitis (SDA) Interact synergistically- Chronic respiratory disease Bacterial pneumonia

Question 557

respiritory disease guinea pigs

Answer 557

Pneumonia is a significant disease Subclinical infection - clinical signs when stressed Opportunistic bacteria- Bordetella bronchiseptica, Streptococcus pneumoniae, Klebsiella pneumoniae, Streptobacillus moniliformis, Staphylococcus aureus, E. coli, Pasteurella pneumotropica, Pasteurella multocida, Streptococcus zooepidemicus, Streptococcus pyogenes, Citrobacter freundii, Yersinia pseudotuberculosis, Pseudomonas aeruginosa, Chlamydia caviae. Viral aetiologies Adenovirus, Parainfluenza virus

Question 558

respiritory disease in chinchillas

Answer 558

Pneumonia is relatively uncommon Potential pathogens- Streptococcus, Klebsiella, Pasteurella, Bordetella, Pseudomonas Viral causes not reported

Question 559

respiritory disease in rabbits

Answer 559

Viral aetiologies- Myxomatosis Rabbit haemorrhagic disease Other causes- Neoplasia Irritants Nasal foreign bodies Cardiac disease Gastric dilatation Bacterial aetiologies- Pasteurella multocida, Bordetella bronchiseptica Pasteurella multocida- Chronic and acute infections A commensal Bordetella bronchiseptica- Common flora within rabbit respiratory tract Predisposes to the development of pasteurellosis

Question 560

clinical signs of respiritory disease in reptiles

Answer 560

open-mouth breathing, exaggerated respiratory effort, increased gulping motions in the throat, repeated yawning in snakes, tracheal discharges, respiratory noise, ocular and nasal discharges (care not to confuse with secretions from salt gland in some species (e.g., green iguana), facial swellings, altered buoyancy in aquatic species.

Question 561

reptile diagnostics for respiritory disease

Answer 561

History & clinical exam Radiography Advanced imaging (CT) Endoscopy Haematology & biochemistry Nasal flush & tracheal wash Cytology Culture and sensitivity PCR

Question 562

Snakes – differential diagnosis

Answer 562

Viral- Arenavirus (inclusion body disease) Ophidian paramyxovirus Sunshine virus Nidovirus Bacterial disease- Often secondary Chlamydia pneumoniae- Zoonotic potential Mycobacterium- Zoonotic potential

Question 563

Birds – clinical signs in respiritory disease

Answer 563

Dyspnoea Mouth breathing Tail bobbing Discharge from nares Respiratory noise Loss or change of voice Exam (if safe to do so)- Eyes/nares Rhinoliths Choanal slit Auscultate heart, lungs and air sacs

Question 564

Birds – respiritory disease diagnostic techniques

Answer 564

Haematology and biochemistry Diagnostic imaging Sinus flush and aspirates- Cytology Culture and sensitivity Endoscopy PCR/serology

Question 565

Birds – respiritory disease Differentials

Answer 565

Bacterial -E.coli, Haemophilus spp., Pseudomonas spp., Streptococcus, Staphylococcus, Mycobacterium spp., Chlamydia psittaci Fungal - Aspergillus spp., Candidia spp. Viral - pox Parasites - trichomoniasis Nutrition - hypovitaminosis A Lower respiratory tract disease- Bacterial air sacculitis Fungal air sacculitis Chlamydia psittaci Transmitted through aerosols of respiratory secretions, faecal material or feather dust Grey parrots susceptible Clinical signs- Respiratory secretions Diarrhoea Weight loss Poor feathering Conjunctivitis

Question 566

Component Therapy Versus Whole Blood

Answer 566

Component Therapy: Benefits- Maximising resource utilisation Flexible dosing and administration Reduced transfusion volume Minimising immune sensitisation Immediately available on site Extended shelf life Limitations- Need knowledge of what activity each product has Multiple storage areas are required due to different product temperature ranges Whole Blood: Benefits- No processing requirement Storage easier as single storage temperature Limitations- Shorter shelf life Need a suitable in-house donor to be available Inexperienced staff collecting the blood

Question 567

Fresh Versus Stored Whole Blood

Answer 567

Collected whole blood is called Fresh Whole Blood (FWB) and it is classed as FWB for 6 hours. During this time it should be kept at room temperature After 6 hours it is reclassed as Stored Whole Blood (SWB) and must be refrigerated In SWB the activity of Factor I (Fibrinogen), Factor VIII and von Willebrand’s Factor will likely have declined to below therapeutically useful levels and platelets have been shown to be less responsive and have a poor lifespan once transfused (24 hours max) There is however new compelling evidence that chilled platelets in SWB retain their ability to contribute to clot formation

Question 568

Use of Red Cells

Answer 568

Fresh Whole Blood- Source of all erythrocytes, haemostatic proteins, plasma proteins, immunoglobulins, antiproteases and platelets Blood loss/ Haemostatic resuscitation Haemostatic protein deficiency with blood loss ? Arrest active haemorrhage in patient with thrombocytopenia or thrombopathia Packed Red Blood Cells- Source of erythrocytes Anaemia Blood loss /haemostatic resuscitation +/- Fresh Frozen Plasma

Question 569

Use of Plasma

Answer 569

Fresh Frozen Plasma (FFP)- Source of all haemostatic proteins (labile and non labile), antiproteases, immunoglobulins and plasma proteins- DIC Adder Bites Consumptive coagulopathy Haemophilia A and B von Willebrand’s Factor Deficiency Bleeding due to Angiostrongylus Acute haemorrhagic shock 1 year as Fresh Frozen Plasma + 4 year Fresh Plasma Shelf Life Frozen Plasma (FP) and Cryosupernatant (Cryo-S): Source of plasma proteins, immunoglobulins, antiproteases and non labile factors: II, V, VII, IX, X, XI and XII HGE Anticoagulant Rodenticide Toxicity Hepatic coagulopathy Haemophilia B Hypoproteinaemia Resuscitative IVFT Immunoglobulin transfer + Cryo-S can be used to treat hypoalbuminaemia FP 5 year Shelf Life Cryo-S 1 year Shelf Life Cryoprecipitate (Cryo-P): Source of labile factors: I, VIII, XIII and vWF and fibronectin Von Willebrand’s Disease- resuces chances of bleeding during surgery Haemophilia A Hypofibrinogenaemia 1 year Shelf Life

Question 570

Use of Platelets

Answer 570

Platelet Concentrate (PC): Source of platelets- Uncontrolled or life-threatening haemorrhage due to thrombocytopenia/thrombopathia Prophylactic treatment in patients with hereditary thrombopathia prior to surgery Contains some red blood cells – typing recommended Shelf Life of 3 days

Question 571

Erythrocyte Antigens

Answer 571

Antigens are surface molecules capable of stimulating an immune response found on lots of things such as drugs, infectious organisms, pollens, plasma proteins and blood cells Erythrocyte antigens are the antigens found on red blood cells and the presence of an erythrocyte antigen determines the blood type of the individual Antigens are genetically determined characteristics and each erythrocyte antigen is inherited independently of other erythrocyte antigens meaning a single antigen can be present or multiple different antigens in any combination Expression of an erythrocyte antigen = Positive for that blood type No expression of an erythrocyte antigen = Negative for that blood type 10 canine erythrocyte antigens have been identified Their antigenicity varies as will the degree of the immune response; some antigens will not provoke a response whilst for others the response will be strong- DAE-1, DEA-8 Antigenicity is influenced in part by the antigen’s: Size Complexity Biological activity The first exposure to a non-self antigen may include the production of antigen-specific alloantibodies which are retained for life This individual is now sensitised to that antigen A subsequent encounter will cause an antigen-antibody mediated immune response

Question 572

: What makes an antigen more clinically significant when performing a blood transfusion?

Answer 572

More antigenic antigens produce a more profound immune response and the greater the strength of an adverse reaction The greater the likelihood antigen exposure will occur the more it is a concern High prevalence of Positive dogs = less likely to encounter a Negative dog Low prevalence of Positive = less likely to encounter a Positive dog 50:50 prevalence of Positive and Negative = high chance of a Positive and Negative encounter

Question 573

Blood Typing in Dogs

Answer 573

Most antigenic blood type is DEA 1. Expression of this antigen on the red cell surface in Positive dogs is variable from strong through to weak. Distribution of DEA 1 antigen in the canine population is around 50:50 Administering DEA 1 Positive red cells to a DEA 1 Negative recipient will result in DEA 1 sensitisation on first exposure Subsequent exposure in a sensitised dog can cause an Acute Haemolytic Transfusion Reaction (AHTR) as a result of the extravascular +/- the intravascular destruction of the transfused cells Preferably type and type match recipient and product/donor with regards to DEA 1 status in all dogs prior to red cell and platelet transfusion

Question 574

Blood Typing Methodologies

Answer 574

In house typing kits available to determine DEA 1 status in the UK Immunochromatographic, card and gel technologies are used in in-house typing kits Immunochromatographic kits (QuickTest from Alvedia) consists of porous paper strip along which the sample migrates. The strip is impregnated with a line of monoclonal DEA 1 antibody that attaches to DEA 1 antigen (if present) and a control line impregnated with anti-glycophorin antibody that attaches to red cells regardless of blood type.

Question 575

Cross Matching in Dogs

Answer 575

In dogs clinically significant alloantibodies will not be present in transfusion naïve individuals but all previously transfused dogs should be cross matched if they were given red cells 4 or more days ago to detect any clinically significant alloantibodies that have been generated that will react with a donor red cell antigen in the pending transfusion Major cross match evaluates the recipient’s plasma for the presence of alloantibodies against donor erythrocytes to determine the likelihood of a haemolytic transfusion reaction Minor cross match evaluates the donor’s plasma for the presence of alloantibodies against recipient erythrocytes to determine the likelihood of a haemolytic transfusion reaction

Question 576

The Major Cross Match

Answer 576

Two reactions indicate incompatibility and the presence of existing recipient alloantibodies when recipient plasma is mixed with donor red cells: Haemagglutination - a reversible red cell phenomenon caused by antigen-antibody binding and the cross-linking of antibodies causing red cells to clump together Haemolysis – activation of complement results in lysis of the red cells and release of haemoglobin causing pink or red tinged plasma Gel based tests: porous gel matrix block in the tube allows single red cells to pass through but not agglutinated clusters of cells A crude version of the cross match can also be performed in house without the use of a commercial kit Positive control – the red cells have agglutinated and are too large to pass through the sieve-like gel Negative control – the red cells Have passed through the gel Patient test tube indicating compatibility when to do this? Any recipient that has had a previous transfusion reaction Any recipient with an unknown transfusion history Any recipient that has received red cell product 4 or more days ago PBB provides a crossmatch service via IDEXX cross matching the recipient against 6 stored packed red blood cell units.

Question 577

Minor cross match may be considered if transfusing very large volumes of plasma to ....

Answer 577

detect any clinically significant alloantibodies in the donor plasma to recipient’s red cells

Question 578

Feline Blood Types

Answer 578

Blood types: A, B, AB and Mik negative or positive Naturally occurring antibodies to non-self red cell antigens in type A and B and some Mik negative cats Strength and titre of antibodies varies: Type B cats have a high titre of anti-A antibodies Type A cats have a lower titre of weaker anti-B antibodies Type AB cats have no antibodies to either the A or B antigen In house kits are available for determining A/B status. Cats must be blood typed and the recipient and product/donor must be type matched

Question 579

Feline Cross Matching

Answer 579

Transfusion naïve cats can have clinically significant alloantibodies to other blood types so cross matching even the first transfusion is recommended Red Cell Transfusions = Major Cross Match Plasma Transfusions = Minor Cross Match (donor plasma for alloantibodies to recipient red cells) Whole Blood = Major and Minor Cross Match (Alvedia/EmMa Test)

Question 580

What tests can you use to evaluate the Urinary Tract?

Answer 580

Imaging (Radiography, Ultrasound, CT) Clinical pathology (Haematology and Biochemistry tests) - path Urinalysis Surgical – biopsy, visualisation

Question 581

Stranguria

Answer 581

difficulty urinating Generally disorders of: The lower urinary tract (bladder or urethra) The genital tract (prostate, vagina) Both Two processes have potential to cause stranguria: Non-obstructive stranguria- Mucosal irritation/inflammation of lower urinary/genital tract in fection Obstructive stranguria - Obstruction or narrowing of the urethra/bladder neck. spasms, stones A thorough history - ask the right questions Signalment Dogs – bacterial cystitis/urethritis, urinary calculi Cats – idiopathic cystitis, urolithiasis Palpate the bladder size Stranguria + large bladder may be obstructed = emergency! Physical Exam: Assessment of urethral patency Bladder Palpation – be very carefull!!! bladders blocked for long period of time are painful and fragile. can also cause backflow of urin into kidneys and cause kidney faliur Digital rectal palpation- In all stranguric dogs. Especially males! External genitalia and perineum

Question 582

Haematuria

Answer 582

haem/blood in the urine can be macoscopic or microscopic Haematuria causes: Iatrogenic haematuria- trauma caused by method used to obtain sample- e.g irritation by catheter Pathological haematuria Genital sources (if voided)- trauma to penis Determine if systemic (coagulopathies) or localised to the urinary tract Do they have clinical signs associated with LUTD? Has bleeding been noticed from other sites? Trauma? Rodenticides? Blood in faeces? Pattern to urine pigmentation? Clinical exam: Look for haemorrhage at other sites- look for coagulopathy Abdomen, thorax, mucosae (especially mouth, axillae, groin) Palpate and assess kidneys for size, symmetry, discomfort- more reliable in smaller animals Examine the external genitalia can be found by 1.Gross “pigmenturia” red, brown or black urine 2. Urinalysis: positive haem possible causes: Haematuria Haemoglobinuria Myoglobinuria Gross haematuria: >150 RBCs/hpf Occult haematuria: Positive Hb on dipstick >5 RBCs/hpf but not visibly pink Care re: interpretation if catheterised/cysto Both can be accompanied by clinical signs (stranguria, dysuria, pollakiuria) Is it consistent throughout urination? Initial haematuria: At beginning of voiding - lower urogenital tract (bladder neck, urethra, vagina/vulva, penis, prepuce) Terminal haematuria: At end of voiding -Upper urinary tract (bladder, ureters, kidneys or intermittent bleeding) Total haematuria: throughout voiding - upper UT, diffuse bladder dz, prostatic or proximal urethra, coagulopathies So how do I know if it’s Haematuria? Clinical signs, gross inspection Haematology/biochemistry- Anaemia? CK? Positive dipstick Centrifuge sample to examine for intact RBCs: Supernatant clear with pellet of RBCs present = haematuria Supernatant pigmented with absence of RBCs in pellet = haemoglobinuria or myoglobinuria 5. Sediment evaluation for RBCs if haematuria - always take into account collection method 6. not always able to tell

Question 583

Dysuria

Answer 583

pain or discomfort upon urination

Question 584

Pollakiuria

Answer 584

abnormal frequent passage of small amounts of urine

Question 585

Periuria

Answer 585

urination at inappropriate sites

Question 586

Anuria

Answer 586

failure of urine production by the kidneys

Question 587

Oliguria

Answer 587

reduction in urine production

Question 588

Polyuria

Answer 588

Increase urine production

Question 589

Haemoglobinuria

Answer 589

spill over of exess haeomoglobin form plasma pink-red urine Intravascular lysis of RBCs- haemolytic anemia Lysis of RBCs within the urinary excretory- USG <1.008, pH>7

Question 590

Myoglobinuria

Answer 590

rare in dogs and cats (seen more in horses) Extensive skeletal muscle damage/myopathies- might see in racing greyhounds and horse Creatinine Kinase will show on biochem test

Question 591

Full Urinalysis

Answer 591

Macroscopic examination (colour, transparency/turbidity) Microscopic examination Chemical examination (dipstick tests and urine specific gravity) Microbiological examination by culture Part of the database for animals with signs of: Renal disease Lower urinary tract disease Many medical problems (particularly those with multi-systemic signs) Part of a geriatric or pre-anaesthetic screen Hand-in-hand with biochemistry for any sick patient. Tubular function USG – Loop of Henle, Distal Tubules Proximal Tubules Dipstick - PT Glomerular function- Biochemistry Dipstick Haemorrhage, infection, inflammation…

Question 592

Urine Collection Methods

Answer 592

Micturition Cystocentesis Catheterisation Note: always record in your notes which collection method was used, as results can be significantly affected.

Question 593

micturition as a urine collection method

Answer 593

“free catch”- can be got form- Mid-flow- allows intitial flow to wash out contaminants Naturally voided or Manual expression Table-top- make sure to make this cea rin notes Advantages: Easy (generally) and may be left to owner (naturally voided - dog) Non-traumatic, non-invasive Use of modified litter can be used for initial screening of cats (KatKor) Disdvantages: Risk of non-compliance, resentment (dog) Risk of haematuria and bladder rupture with manual expression Variable volume Likely to be contaminated - sample unsuitable for culture Collection vessel may affect results- glucose from food containers, cleaning fluids can contaminate sample

Question 594

Cystocentesis

Answer 594

Advantages: Quick with no need to wait for spontaneous urination Easier than voided sample from cats Aseptic collection with no urethral contamination (so ideal for culture) Easy to perform when bladder moderately distended and patient (dog or cat) adequately restrained Better tolerated (cf. catheterisation) Lower risk of iatrogenic haematuria and iatrogenic infection (cf. catheterisation) Disadvantages: Requires some experience Needs adequate volume of urine in bladder Iatrogenic micro-/(macro-)scopic haemorrhage possible Contraindicated if: bladder severely diseased – risk of rupture, clotting problems

Question 595

Catheterisation as a method for urine collection

Answer 595

Advantages: No need to wait for spontaneous micturition Relatively, rather than absolutely, free of risk of bacterial contamination- use quantitative urine culture Usually an ample sample volume Advantages: No need to wait for spontaneous micturition Relatively, rather than absolutely, free of risk of bacterial contamination use quantitative urine culture Usually an ample sample volume Catheterisation in the Queen Blind insertion Get body as straight as possible Advance catheter along ventral vaginal wall along midline Should enter urethra!

Question 596

waht makes a good urin sample

Answer 596

Aim is to obtain a urine sample with in vitro characteristics similar to the original urine (in vivo) If sample is not processed immediately, consideration should be given to sample storage and preservation Collect and analyse with 60 mins Or refrigerate (upto 12 hours)- after this cells lyse and crystals form. Artefacts= Calcium oxolate, Struvite should be analysed at room temp- affects usg and crystals Refrigeration artefacts: In vitro crystal formation (especially calcium oxolate dihydrate) Falsely decreased results due to inhibition of enzymatic reactions SG falsely increased Room temperature artefacts: Bacterial overgrowth Alter pH Decrease chemicals metabolised by bacteria (e.g. glucose) Alter urine culture results Timing of Collection: Early morning or after fasting- Advantages: Most concentrated sample (relative water deprivation overnight) – evaluates concentrating capacity Gives the highest yield of cells, casts and bacteria Disadvantages: Glucosuria may be less obvious than in a post-prandial sample Cytology – cells may be altered due to prolonged exposures to variations in pH and osmolality

Question 597

Gross Inspection of urin

Answer 597

Colour- Light yellow or amber Odour- Should not be offensive Transparency/turbidity- Concentrated and end flow samples more likely to be turbid Normal = clear/slightly cloudy Volume- 5ml

Question 598

Routine Urine Chemistry

Answer 598

Specific gravity (SG) refractometer pH Dipstick- Remember – do not dip the stick!

Question 599

Urine Specific Gravity

Answer 599

Assessment of concentrating ability Measured with a Refractometer NOT dipstick Best practice: Read urine supernatant Ranges in hydrated patients: Dogs - 1.015 to 1.045 Cats - 1.035 to 1.060 Interpret in light of animals hydration status, comorbidities, BUN/Creat/Glucose/Protein conc First morning sample Isosthenuria - 1.008-1.012 - Specific gravity (SG) of glomerular filtrate Hyposthenuria – <1.008 = active dilution Well concentrated - >1.030 (dog) or >1.035 (cat) Interpret in light of animals hydration status, comorbidities, BUN/Creat/Glucose/Protein conc

Question 600

Dipstick

Answer 600

Leucocytes- not valid Nitrite- not valid Urobilinogen- not valid Protein pH Blood/Haem USG- not valid Ketone Bilirubin Glucose

Question 601

pH measurement on a urine dipstick

Answer 601

Rough estimate of systemic acid-base status pH values stable for 24 hrs (if fridged!) Meters more precise and accurate than dipstick analysis Important in management of urolithiasis and UTIs Direct effect upon crystal type (struvite) Direct effect on sediment findings: RBCs, WBCs, casts Causes/examples: High pH >7.5 UTI by urease-producing bacteria Metabolic alkalosis Herbivores Low pH <7- UTI caused by acid-producing bacteria Normal in carnivores (5.5-7.5) Metabolic acidosis

Question 602

Bilirubin on urine dipsticks

Answer 602

Normal metabolism of Hb from erythroctyes results in hepatic formation of conjugated bilirubin- Primary excretion via GIT, and to a lesser extent, in urine via kidneys Urine testing – screen for: Intravascular haemolytic dz Cholestatic hepatobiliary dz Cannot be used to rule-out dz. Interpret in light of USG Normal in concentrated urine of dogs (USG >1.030)-Male>Female, Also ferrets Always abnormal in cats

Question 603

Haem on urine dipsticks

Answer 603

Screen for presence of haemoglobin Free haemoglobin from lysis RBCs Lysis of RBC’s when contact pad = + result Intravascular (abnormal) Dilute or extremely alkaline urine can also lyse RBCs – false +! Free myoglobin from damaged myocytes (abnormal) Sediment evaluation <5 RBCs/hpf is normal finding (won’t cause a + on dipstick!) Always take into account collection method

Question 604

Glucose on urine dipsticks

Answer 604

Small molecule, freely passes through glomerulus into filtrate- Normally removed from urine by renal tubules Presence in urine (abnormal >trace): Exceed renal threshold e.g. hyperglycaemia- Diabetes mellitus, Stress-induced hyperglycaemia in cats Proximal renal tubular dysfunction Serum biochemistry +/- fructosamine Remember: effect on USG Renal thresholds: Cats - 14-15mmol/L Dogs – 10-12mmol/L

Question 605

Ketones on urine dipsticks

Answer 605

Ketones: Acetone Acetoacetic acid Beta-hydroxybutyrate- ost abundant Produced as alternative energy source to meet demands (negative energy balance)- E.g. aberrant carbohydrate metabolism (as in diabetes mellitus) Ketonuria precedes ketonaemia Urine screening for DM! Diuretic effect Predisposition to hypoNa and HypoK

Question 606

Ketones on urine dipsticks

Answer 606

Ketones: Acetone Acetoacetic acid Beta-hydroxybutyrate- ost abundant Produced as alternative energy source to meet demands (negative energy balance)- E.g. aberrant carbohydrate metabolism (as in diabetes mellitus) Ketonuria precedes ketonaemia- Urine screening for DM! Diuretic effect Predisposition to hypoNa and HypoK

Question 607

Protein on urine dipsticks

Answer 607

Screen for diseases that cause: protein loss by the kidneys (e.g. renal proteinuria)- Tubular disease, Glomerular barrier alterations Excess production of protein (less likely)- Overload proteinuria Dipstick most sensitive to albumin- Other proteins at high levels (e.g. Ig, Hb) Urine electrophoresis Always interpret in context of: USG pH >7.5 may cause false positive Sediment Normal Urine: -/trace >1.025 <2+ > 1.030 (dogs) <1.015 should be none. Protein:Creatinine ratio (UP:UC)- Quantitative Creatinine not reabsorbed/secreted so conc is static Standardises protein concentration Evidence for glomerular or tubular proteinuria UPC should be <0.5 for Dogs and <0.4 for cats (IRIS guidelines) Interpretation confounded by other causes of protein in urine E.g. pre-renal overload or post-renal proteinuria e.g. bacteriuria, pyuria, haematuria

Question 608

Microscopic Examination of urine

Answer 608

Sediment Examination- Crystalluria Renal tubular casts Epithelial cells Blood cells Bacteria

Question 609

Renal Tubular Casts

Answer 609

Proteinaceous plugs of dense, mesh-like mucoprotein +/- cells accumulate in distal portion of nephron Low number (<2/HPF) can be normal Increased number relates to tubular disease Try to identify associated cells, e.g. epithelial, WBC, RBC

Question 610

Epithelial Cells in microsopic urinary analysis

Answer 610

Routinely see a small number (<= 2-5/HPF) Type of cell may be difficult to identify, but may help to identify location of disease if increased number: Renal tubular cells Transitional cells- renal pelvis, ureter, bladder, proximal 2/3 urethra Squamous cells- Distal 1/3 urethra

Question 611

Blood Cells in microsopic urinary analysis

Answer 611

Erythrocytes Haematuria – prev discussed Leucocytes: Cystocentesis sample - <3/HPF. - <8/HPF catheter/voided High counts = pyuria +/- bacteria

Question 612

Bacteria in microsopic urinary analysis

Answer 612

May be present for reasons other than UTI, e.g. contamination overgrowth in stored sample Pyuria + bacteriuria = active UTI- Urine Culture & Sensitivity Silent Urinary tract infections can also occur!

Question 613

urine samle for Culture & Sensitivity

Answer 613

Obtain urine by cystocentesis Usually boric acid container- bacteriostatic Submit to external laboratory Is patient receiving parenteral antibiotics?

Question 614

Crystalluria

Answer 614

Precipitate out when urine saturated with dissolved minerals Do not indicate presence of, or predisposition to form urinary calculi May get in vivo without disease Cold temperature/prolonged storage increases formation in vitro – so use fresh, non-refrigerated sample within 1 hour Useful for: provisional identification of existing calculi before analysis When pathological types are identified

Question 615

Magnesium ammonium phosphate

Answer 615

urinary crystal struvite Most commonly seen in dogs and cats Neutral-alkaline urine- UTI’s Diet

Question 616

Cystine

Answer 616

urinary crystal Hexagonal Acidic Urine Abnormal finding Inherited defect in proximal renal tubular transport of AA’s Concentrated, acidic urine Radiolucent

Question 617

Calcium oxalate dihydrate

Answer 617

urinary crystal radiopeic calcium crystal can be an artifact of stirage in fridge Cross-striations, “envelope” Acidic urine Can be seen in clinically normal animals or storage artefact Or urolithiasis, hypercalcuria, hyperoxaluria..

Question 618

Calcium oxalate monohydrate

Answer 618

urinary crystal radiopeic calcium crystal Picket fence Abnormal in cats/dogs Ethylene glycol (anti freeze) ingestion- Not 100% sensitive Can be seen in normal horse

Question 619

Calcium Carbonate

Answer 619

urinary crystal Alkaline Urine Yellow-brown or colourless Common in equine Not seen in dogs and cats

Question 620

Bilirubin in urine

Answer 620

can be see Orange-reddish brown Low number routinely observed in dogs

Question 621

Ammonium biurate Crystals

Answer 621

urinary crystal Acidic urine Abnormal finding in most breeds Routine finding in Dalmations

Question 622

Amorphous Crystals

Answer 622

urinary crystal Aggregates/no defining shape Urates - acidic Phosphates – alkaline Xanthene

Question 623

Urolithiasis

Answer 623

A calculus (stone) in the urinary tract- Single or multiple Cystolith, ureterolith, nephrolith… Remember – Crystals do NOT = Urolith Recognised in all species Common urolith types vary with species Calcium carbonate – horses, rabbits Magnesium ammonium sulphate, calcium oxolate – dogs, cats One mineral normally predominates Increased precipitation of excretory metabolites Multi-factoral! Genetic/breed factors e.g. cystine stones in SBT Metabolic disease e.g. urate stones with PSS Inappropriate diet e.g. ram lambs fed concentrate UTI e.g. struvite stones in dogs Clinical Signs- Nephroliths Asymptomatic Incidental finding on x-rays Associated with pyelonephritis Pain, pyuria, pyrexia Ureteroliths As above Renomegaly – uni/bilateral +/- pain Renal failure if bilateral “big kidney-little kidney” cats Cystoliths True LUT signs Dysuria, pollakiuria, haematuria Occasionally palpable on physical exam Depending on size/number Urethroliths True LUT signs Abdominal discomfort Licking at penis/vulva, trying to urinate but can’t Urethral obstruction - post-renal azotaemia - AKI - renal azotaemia Does the clinical history/physical exam suggest stones? Plain radiographs: Radiopaque stones: Struvite Calcium oxolate Calcium phosphate Radiolucent stones: Ammonium urate Cystine Abdominal Ultrasound Easy to miss Rectal examination to palpate urethra

Question 624

treating an acute urinary sytem obstruction

Answer 624

Nephroliths, Ureteroliths, Cystoliths and non obstructive urethroliths.. Later. Urethral Obstruction Treat as an emergency unless partial obstruction Stabilise the patient but do not delay Manage hyperK, IVFT Decompress the bladder? Retrograde urohydropulsion using catheter Urethrostomy- More appropriate for recurrent problems, not emergency treatment

Question 625

What are the receptors called that detect plasma osmolality and where are they ?

Answer 625

What are the receptors called that detect plasma osmolality and where are they

Question 626

Where is ADH released from?

Answer 626

ADH is a substance produced naturally in an area of the brain called the hypothalamus. It is then released by the pituitary gland at the base of the brain

Question 627

Where does ADH act in the kidney?

Answer 627

The main action of ADH in the kidney is to regulate the volume and osmolarity of the urine. Specifically, it acts in the distal convoluted tubule (DCT) and collecting ducts (CD

Question 628

Name two stimuli that may cause ADH release

Answer 628

elevated plasma osmolality and decreased effective circulating volume. Increased plasma osmolality causes shrinkage of a specialized group of cells in the hypothalamus called osmoreceptors

Question 629

How does ADH cause urine to be concentrated in the kidney?

Answer 629

ADH increases the permeability to water of the distal convoluted tubule and collecting duct, which are normally impermeable to water

Question 630

What clinical condition arises in patients which fail to produce ADH?

Answer 630

Diabetes insipidus

Question 631

What are the clinical consequences of a lack of ADH?

Answer 631

dehydration, hyperosmolality, hypovolemia, and eventual death in severe cases

Question 632

What conditions might lead to high ECF Sodium

Answer 632

Dehydration A disorder of the adrenal glands. A kidney disease. Diabetes insipidus

Question 633

Is Sodium maintained within a relatively narrow range?

Answer 633

yes

Question 634

Which hormone is released as a consequence of a rise in plasma K+?

Answer 634

When K+ plasma levels increase enough, hyperkalemia induces aldosterone secretion. Aldosterone, in turn, promotes renal K+ secretion

Question 635

What clinical condition arises in patients which fail to produce aldosterone

Answer 635

Addison's disease

Question 636

What is the fate of glucose that enters the glomerulus?

Answer 636

Glucose that enters the nephron along with the filtrate after passing through the glomerulus, passes from the tubule of nephron where it is selectively reabsorbed and sent back into the blood.

Question 637

Why is there glucose in the urine of animals with Diabetes mellitus?

Answer 637

Once blood glucose reaches a certain level, the excess is removed by the kidneys and enters the urine. This is why dogs and people with diabetes mellitus have sugar in their urine (glucosuria) when their insulin levels are low.

Question 638

What is the consequence of Diabetes Mellitus on the urine volume?

Answer 638

In diabetes, the level of sugar in the blood is abnormally high. Not all of the sugar can be reabsorbed and some of this excess glucose from the blood ends up in the urine where it draws more water. This results in unusually large volumes of urine

Question 639

How will the presence of glucose in urine affect USG

Answer 639

the addition of glucose caused the USG to increase

Question 640

How will the presence of glucose in urine affect Osmolality

Answer 640

glucose can also add significantly to the osmolality when it is abundant in urine

Question 641

Why is there usually no protein detected in the urine?

Answer 641

most protein molecules are too large for the filters (glomeruli)

Question 642

In what circumstances might you find haemoglobin in the urine?

Answer 642

If the level of hemoglobin in the blood rises too high

Question 643

In what circumstances might you find myoglobin in the urine?

Answer 643

extensive damage to your skeletal muscles, resulting in the rapid breakdown of muscle

Question 644

What are the potential outcomes of losing lots of albumin in urine?

Answer 644

kidney disease

Question 645

Thirst and urination determined by interplay of:

Answer 645

Plasma osmolality - Determines blood pressure – baroreceptors (pressure) and osmoreceptors (water) Osmolality integrated into thirst centre in the brain Hypothalamic – Posterior pituitary gland – ADH axis Regulates water reabsorption in collecting duct Renal function- Needed to produce concentrated urine

Question 646

Urine Concentration

Answer 646

Adequate secretion of ADH and kidneys must be able to respond normally Enough functioning nephrons A concentration gradient in renal medulla when 2/3 of kidney lost this process is impares

Question 647

Mechanisms of PUPD

Answer 647

polyurea polydypsia 2 basic reasons: Primary polyuria (insesant urination) with secondary compensatory polydipsia- Most common, Several mechanisms Primary polydipsia (insesant need to drink) with consequent PU

Question 648

Primary Polydipsia

Answer 648

Uncommon in small animals- In dogs behaviour resulting in increased drinking referred to as psychogenic polydipsia Horses>others Cerebrocortical dysfunction- Central lesion affecting hypothalamus/thirst centre and ADH Endocrine disorders

Question 649

Pathophysiology of Primary PU

Answer 649

1. Lack of ADH produced by hypothalamus Cannot concentrate urine Compensatory PD Primary central diabetes insipidus- ongenital/idiopathic, rare. (Acquired neoplastic/trama also v.rare) 2. Inability of DT/CD cells to respond to ADH ADH has no action in DCT Nephrogenic diabetes insipidus Primary - ↓receptors/inability to bind due to mutation VERY rare Secondary- Reduced sensitivity to ADH- E.coli toxins in pyelonephritis and pyometra/prostatic abscess or any pyogenic infection in the body Hyperadrenocorticism - cortisol interacts with ADH at the receptor level Interference with action of ADH at tubule: Hypercalcaemia Hypokalemia ADH receptor downregulation: Obstuction of ureters/ bladder - post-renal azotaemia conditions Hypokalemia 3. Osmotic Diuresis A minimum volume of water must be excreted with waste solutes by the kidney. Concentration of solutes within the glomerular filtrate > proximal tubular capacity for reabsorption = increased water excreted = primary polyuria 5. Reduced medullary concentration gradient Unable to concentrate urine in Loop of Henle Controlled by Na+ and urea in medulla

Question 650

Chronic Kidney Disease

Answer 650

Nephrons are lost and replaced with inflammatory and fibrous tissue: -Reduced water reabsorption within distal tubules and collecting ducts -Inability to maintain counter-current mechanism Signalment: Older animals (any age!) Clinical Signs Weight loss, ↓BCS Inappetence PUPD Oral ulcers Diagnostics: Biochem/haematology signs- Renal azotaemia, Non-regenerative anaemia (kidneys produce erythropoietin) , Hypokalaemia +/- hyperphosphatemia Inappropriate USG Proteinuria (UP:UC, dipstick)

Question 651

Pyelonephritis

Answer 651

Inflammation of the renal pelvis- Acute or chronic +/- Bacterial infection Dogs>cats Clinical signs: PUPD: Endotoxins interfere with ADH Inflammation interferes with medullary osmotic gradient Chronic ->loss of nephrons - >CKD LUTD signs- haematuria, pollakiuria, dysuria, stranguria Renal/lumbar spinal pain Unilateral/bilateral renomegaly Acute – pyrexia, lethargy Diagnostics: US Haematology – left shift inflammatory leucogram Urine culture & sensitivity (cystocentesis, pyelocentesis)

Question 652

pyometra

Answer 652

Infection in the progesterone-primed uterus Usually E.coli Signalment: Older, entire bitches Clinical Signs: Open  mucoid to purulent discharge at vulva Closed  lethargy, pyrexia, inappetance, V+D, PUPD Diagnostics: Left shift leucogram Azotaemia Imaging -> US +/- radiography

Question 653

Hyperthyroidism

Answer 653

Signalment: Cats >7yo Clinical signs: Polyphagia with weight loss Intermittent V+D Hyperactivity and behavioural changes PUPD Clinical exam: ↓ BCS Tachycardia, heart murmur, gallop rhythm +/- thyroid goitre Diagnostics: Biochem -> ↑ ALT, ↑tT4- +/- free T4, TSH CKD

Question 654

Hyperadrenocorticism

Answer 654

Signalment: Middle aged-older Dog >6-9yo Clinical signs: PUPD Polyphagia Pot-bellied Skin thinning, haircoat changes Diagnostics: Biochem -> ↑ALP USG -> <1.020 ACTH stimulation test Low dose dexamethasone suppression test (LDDS) Urine Cortisol:Creatinine ratio

Question 655

Hypoadrenocorticism

Answer 655

Loss of adrenocortical cells = glucocorticoid and mineralocorticoid deficiency Signalment: Younger dogs – 2-5yo Clinical signs: Vague “waxing and waning” GI signs Collapse, shock Diagnostics: Biochem -> Na:K ratio<23 ACTH stimulation test the great pretender- sometimes ccan cuase PUPD due to electrolyte imabalence bu this is not a common presentation

Question 656

Diabetes Mellitus

Answer 656

Persistent Hyperglycaemia and glucosuria Signalment: Dogs & cats, any age Clinical signs: Weight loss Polyphagia Lethargy PUPD Diagnostics: Biochem -> hyperglycemia Urine -> Glucose + Fructosamine

Question 657

Hypercalcaemia

Answer 657

Hypercalcemia due to number of conditions: Signalment: Dogs>Cats Clinical signs: PUPD Variable, depending on cause Diagnostics: Biochem ->↑ total Ca (influenced by albumin)- Ionised Ca Work up depending on cause Causes: HOGSINYARD • Hyperparathyroidism • Osteolysis • Granulomatous disease • Spurious (false or fake) sample • Idiopathic (cats) • Neoplasia • Young animals • Addisons (Hypoadrenocorticism) • Renal disease • D Hypervitaminosis D

Question 658

Hepatic Disease

Answer 658

Variable causes of hepatic disease Signalment: Dogs, any age Cats Clinical signs: PUPD Non specific, depending on cause Diagnostics: Biochem -> ↑ liver enzymes (ALT, ALP, GGT) Function: ↓ urea, cholesterol, albumin, glucose- Bile Acid Stimulation Test Imaging

Question 659

Central Diabetes insipidus:

Answer 659

rare Lack of ADH by the hypothalamus/posterior pituitary Causes: Idiopathic Neoplastic Head trauma Clinical signs: Extreme PUPD Diagnostics: Only performed after exclusion of other causes of PUPD USG <1.008 Water Deprivation Test – DANGEROUS, can caus ekidney faluire Desmopressin trial

Question 660

Congenital Nephrogenic Diabetes insipidus:

Answer 660

rare Lack of response to ADH by the kidney Clinical signs: Extreme PUPD Diagnostics: Only performed after exclusion of other causes of PUPD USG <1.008 Water Deprivation Test – DANGEROUS Desmopressin trial

Question 661

Primary Psychogenic Polydipsia

Answer 661

Rare Behavioural, young dogs Clinical signs: Extreme PUPD Diagnostics: Only performed after exclusion of other causes of PUPD Water Deprivation Test – Dangerous

Question 662

water deprivation test

Answer 662

depriving an animal of water then testing the urine specific gravity if normal then test respones to synthetic ADH if positive : Central Diabetes insipidus if negative: Congenital Nephrogenic Diabetes Insipidus if USG is high: Primary Psychogenic Polydipsia

Question 663

In PUPD cases, what is more comon? primary polyurea or primary polydypsia

Answer 663

Primary Polyuria

Question 664

clinical examlple of PUPD- History 10yo FE Staffordshire Bull Terrier Drinking more for last 2 weeks Off colour and vomiting, normal faeces Possible weight loss? Not sure whether spayed No medications No diet/environmental change Clinical examination Mucus membranes slightly tacky Thoracic auscultation normal Abdomen tense, difficult to palpate No visible vaginal discharge Temperature 39.2C

Answer 664

can rule out that its not drug related Primary Problems Polydipsia Vomiting Mild pyrexia Probable secondary problems Weight loss- due to vomiting Inappetance - due to naeusea 5% dehydration- due to polydipsia and vominting Differential diagnoses - PUPD • Renal • Hepatic • Endocrine – diabetes mellitus, diabetes insipidus, hyperadrenocorticism, hypoadrenocorticism • Infectious – pyelonephritis, pyometra • Electrolytes – hypokalemia, hypercalcaemia • Iatrogenic – diuretics, steroids etc Differential diagnoses - Vomiting Primary GI tract problem Inflammatory, infectious, obstructive, motility disorder, toxic Intra-abdominal, extra GI problem Pancreatitis, diabetes mellitus, hepatitis, renal disease, pyometra, splenitis, hypoadrenocorticism, obstruction from large mass Extra-abdominal Fear, pain, vestibular disease, toxic diagnostics- Urinalysis- USG determine whther animal is truly PUPD, can show no protien, whether there is infection bloods- CBC, can show dehydration (concentrated pcv), neutrophils can show infection, liver enzymes normal (rules out liver disease), electrolystes ok (rules out hyperthyroidism), calcium is fine (rules out hypoclacemia)

Question 665

azotaemia

Answer 665

azotemia is a biochemical abnormality, defined as elevation, or buildup of, nitrogenous products (BUN-usually ranging 7 to 21 mg/dL), creatinine in the blood, and other secondary waste products within the body can be normal varitaion an be pre renal, renal or post real will not be detected in blood until about 70% of renal function is lost

Question 666

pre-renal azotaemia

Answer 666

any process that reduces RBF- Dehydration/hypovolaemia hypotension/shock clinical signs- other indicators of hypovolaemia or shock blood indictaiors of dehydration: PCV/ total protien/ lactate

Question 667

renal azotaemia

Answer 667

primary rena disease that results in reduced GFR glomerular disease tubular disease interstitial disease clinical signs- other indicators of hypovolaemia or shock blood indictaiors of dehydration: PCV/ total protien/ lactate

Question 668

post renal azotaemia

Answer 668

defective excretion distal to the nephron obstruction (increased intratubular pressure rupture of urinary tract generally distinctive in presentation- dysuria reversable but may have renal component if nephron becomes damaged

Question 669

hyposthenuric

Answer 669

the secretion of urine of low specific gravity due to inability of the kidney to concentrate the urine normally. can activly dilute urine so some function of idney

Question 670

hypersthenuric

Answer 670

A condition where the osmolality of the urine is elevated activly concentrating urine, good nephorn function

Question 671

isosthenuric

Answer 671

Isosthenuria refers to the excretion of urine whose specific gravity (concentration) is neither greater (more concentrated) nor less (more diluted) than that of protein-free plasma, typically 1.008-1.012. Isosthenuria reflects damage to the kidney's tubules or the renal medulla. potential loss of nephron function

Question 672

RENAL FAILURE

Answer 672

Reduced renal function Loss of renal reserve Acute Kidney Injury (AKI)? Chronic Kidney Disease (CKD)? Acute-on-chronic? What is causing the damage? How much damage has been done? Is it reversible? What is the prognosis? clinical signs- URAEMIA Polyuria/Polydypsia Dehydration Anorexia/inappetance Weight loss Vomiting Halitosis Oral ulceration Gastrointestinal bleeding Weakness / lethargy Palor of mucous membranes Neurological signs

Question 673

AKI

Answer 673

Acute kidney disease Sudden onset of signs Polyuria may progress to oliguria/anuria as renal function lost Advanced signs of uraemia may not have had time to develop

Question 674

CKD

Answer 674

chronic kidney disease Most common sign is weight loss Advanced CKD is most common cause of uraemia Usually have a long term history of PU & PD URAEMIA Polyuria/Polydypsia Dehydration Anorexia/inappetance Weight loss Vomiting Halitosis Oral ulceration Gastrointestinal bleeding Weakness / lethargy Palor of mucous membranes Neurological signs

Question 675

URAEMIA

Answer 675

a buildup of toxins in your blood. It occurs when the kidneys stop filtering toxins out through your urine. Polyuria/Polydypsia Dehydration Anorexia/inappetance Weight loss Vomiting Halitosis Oral ulceration Gastrointestinal bleeding Weakness / lethargy Palor of mucous membranes Neurological signs

Question 676

Excretory failure

Answer 676

Due to diminished GFR Retention of non-protein nitrogenous waste BUN, Creatinine

Question 677

(renal) Metabolism Failure

Answer 677

Failure to catabolise some polypeptide hormones Insulin, Glucagon, GH

Question 678

(renal) Failure to Synthesise

Answer 678

Failure to make calcitriol (vit D3) - 2o hyperparathyroidism Failure to synthesis erythropoietin -anaemia

Question 679

effects of acccumulation of ‘uraemic toxins/substances

Answer 679

UREA- Weakness, anorexia, vomiting, glucose intolerance, haemostatic disorders Creatinine (Creatine, Guanidine etc)- Weight loss, platelet dysfunction Peptides and polypeptide hormones: Parathyoid hormone- Osteodsyrtophy Insulin- Hyperinsulinamia Growth Hormone- Insulin resistance Aromatic amino acid derivatives: Tryptophan, Tyrosine etc-Anorexia Alphatic amines- Uraemic breath, encephalopathy Ribonuclease- Impaired erythropoiesis cAMP-Abnormal platelet function

Question 680

renal dysfunction

Answer 680

Inability to produce urine Inability to concentrate or dilute urine in response to bodies requirements

Question 681

renal Electrolyte abnormalities

Answer 681

Hyponatraemia - Renal sodium wastage Hypo- or hyper- calcaemia Hypo- or hyper- kalaemia - alteration to secretory function Hyperphosphataemia - Renal retention of phosphate

Question 682

renal Acid-base homeostasis

Answer 682

Kidneys is vital for normal acid-base homeostasis, and to do so normally it must: Reabsorb all the bicarbonate from the renal filtrate- 70-80% done in the proximal tubule 20-30% done in the distal convoluted tubule (DCT) Excrete the daily metabolic acid load (H+ ions) generated - Active excretion takes place at DCT Tubular dysfunction will result in; Loss of bicarbonate in urine Reduce acid secretion from DCT -> METABOLIC ACIDOSIS- RENAL TUBULAR ACIDOSIS

Question 683

renal dysfunctions role in systemic hypertension

Answer 683

Alteration in function or control of the renin-angiotensin-aldosterone-system (RAAS) can have a profound effect on systemic blood pressure Common complication of chronic renal failure in cats

Question 684

Clinical Features of Renal Failure

Answer 684

URAEMIA Polyuria/Polydypsia Dehydration Anorexia/inappetance Weight loss Vomiting Halitosis Oral ulceration Gastrointestinal bleeding Weakness / lethargy Palor of mucous membranes Neurological signs POSSIBLE DIAGNOSTIC FINDINGS Azotaemia Hyperphosphataemia Metabolic acidosis Systemic hypertension Hyperkalaemia or hypokalaemia Hypercalcaemia or hypocalcaemia Anaemia (normocytic, normochromic) Haemostatic disorder Secondary hyperparathyroidism Osteodystrophy Hormone imbalances

Question 685

clinical sign of renal faliure

Answer 685

Acute: Animal presents with sudden onset dullness, weak, off-food PU/PD or anuric/oliguric OR, with signs of urinary obstruction/abdominal trauma OR, with history of access / ingestion of known toxin, or nephrotoxic drug administration WITH or WITHOUT signs of uraemia Chronic: Animal presents with long term weight loss only Or, with weight loss and recent history of PU/PD for a few weeks With possible history of vomiting (more likely in dogs) Progressive weakness and evidence of pale mucous membranes

Question 686

diagnostic methods of renal faliur

Answer 686

Blood Biochemistry & Haematology Identify Azotaemia Investigate presence of; Electrolyte abnormalities Acid-base imbalance Anaemia Platelet disorders OBTAIN A URINE SAMPLE Establish the USG Dogs = isosthenuric. Cats may have higher SG in CKD Full urinalysis - look for signs of intrinsic renal failure

Question 687

Rabbit unique calcium metabolism

Answer 687

Blood calcium levels reflect dietary intake Readily absorbed from intestines Does not depend on activated vitamin D Ionised and total calcium serum concentrations are higher than those in other species Rabbit absolutely dependent on the kidney for calcium osmoregulation Renal fractional excretion of calcium = 45-60% compared with <2% in mammals that regulate calcium uptake from the GI tract and eliminate excess in faeces.

Question 688

acute renal failure signs in exotics

Answer 688

Non specific (anorexia, lethargy) Pain (bruxism – pain scoring recommended) Other signs, e.g., GI ileus/stasis

Question 689

chronic renal failure signs in exotics

Answer 689

Weight loss PUPD Poor body condition Occasionally haematuria Reduced appetite GI stasis

Question 690

Cystitis/urolithiasis signs in exotics

Answer 690

Urine scald Vocalisation when passing urine Haematuria Urinary incontinence Urine dribbling Dysuria = Pain or burning sensation while passing urine. Stranguria = Slow, painful discharge of small volumes of urine expelled only by straining despite a feeling of urgency Pollakiuria = frequent, abnormal urination during the day.

Question 691

Common differential diagnoses for urinary disease in exotics

Answer 691

Infectious- Bacterial Viral Parasitic- e.caniculli Non-infectious- Environmental Urine sludge Calculi – obstruction Neoplasia Toxic Other diseases not related to urinary system Prostatic cysts (endocrine) Normal – porphyrin, food pigments

Question 692

causes of urinary disease in exotics

Answer 692

Diet water Bottle vs bowl Design of enclosure Exercise – sedentary rabbits more prone to sludge Conspecifics Recent changes to husbandry or routine- extreme changes in temp Vaccination status (rabbits & ferrets)- canine distemper , rhd Neutering status (e.g., neutered male ferret may develop prostatic cysts or prostate enlargement ) Observation Evaluate demeanour and stance

Question 693

diagnostics for uriary porblems in exotics

Answer 693

Blood work Rabbits – Lateral saphenous vein, cephalic vein or marginal ear vein Ferrets – Jugular vein or cranial vena cava (under GA) Assess: Blood urea nitrogen (BUN), creatinine (low normall levels in ferrets comparitivly), inorganic phosphate, total calcium, ionised calcium, potassium, PCV Limitations- Circadian rhythms Diet can affect values Muscle loss Symmetrical dimethylarginine (SDMA) recommended Serology for some disease processes: E. cuniculi serology Radiography- Abdominal radiography: Plain and contrast Ultrasonography- Bladder wall, neck or urethral abnormalities Identification of cystoliths or urethroliths Advanced imaging- CT Endoscopy For species where challenging to distinguish between haematuria and vaginal/uterine bleeding  e.g., rabbits – urethra opens into the ventral aspect of the vaginal body

Question 694

Rabbit urinalysis

Answer 694

Rabbits excrete alkaline urine Average volume produced = 130ml/kg/day (range 20-350ml/kg/day) Urine pigments gives rabbit urine a yellow, brown or red colour. Some pigments are a result of the breakdown of endogenous compounds  bile pigments, porphyrins, flavins Food ingested can lead to urine colouration Distinguish between haematuria and porphyrin pigments- Positive reaction for blood on dipstick Identifying >5 RBCs per high-power field on urine sediment examination. Porphyrins may fluoresce under a Wood’s lamp Excreted calcium precipitates in the alkaline urine to form calcium complex crystals  gives the urine a creamy and thick appearance. Urine sediment can be seen normally in samples

Question 695

exotics urine sampling methods

Answer 695

Sampling techniques Free catch from litter trained rabbits using non-absorbable products designed for cats as a replacement litter Sedation and cystocentesis - recommended for obtaining a sample for culture GA urethral catheterisation -diagnostic and therapeutic Challenges – urinary catheterisation ferrets Penis J-shaped penis, making catheterisation tricky. Os-penis Palpated easily, caudal to preputial opening Groove on the bone, supports urethra

Question 696

urinalysis in exotics

Answer 696

Urinalysis, sediment and bacterial C+S C+S Only useful BEFORE antibiotic treatment started Normal values (rabbit – Reusch et al, 2009; Varga Smith, 2022) pH 7.6-8.3 Specific gravity 1.003-1.036 Leucocytes and erythrocytes occasionally seen <5RBCs hpf Protein trace Glucose trace Ketones and occult blood absent Casts, epithelial cells and bacteria absent Crystals = large amounts of calcium carbonate monohydrate, anhydrous calcium carbonate and calcium oxalate and ammonium magnesium phosphate (struvite) may be seen Urinary protein and creatinine ratio (UPC) 0.11-0.40 Species specific considerations - small rodents- Urinary obstruction possible in male mice  infection of preputial and bulbourethral glands Urine volume 0.5ml-2.5ml/day (mouse) 13-23ml/day (rat) 5.1-8.4ml/day (hamster) 2-4 drops/day (gerbil) Most differences seen related to animal’s native environment and water conservation. Gerbils- Loop of Henle is comparatively longer ->concentrate urine more effectively. Urinary calculi common Cystitis Often older sows Ascending infection E. coli Streptococcus spp.

Question 697

blood pressure in exotics

Answer 697

Systemic hypertension is a common feature of renal failure due to the renin-angiotensin-aldosterone system Rabbits Mean arterial blood pressure = 80-91mmHg Systolic BP = 92.7-135mmHg Diastolic BP = 64-75mmHg Ferrets Systolic BP = 80-120mmHg

Question 698

common causes of renal disease in rabbits

Answer 698

Common causes of renal disease Encephalitozoon cuniculi Chronic renal failure in older rabbits Renoliths Other urinary conditions - Hypercalciuria/urine sludge Bacterial nephritis Hydronephrosis Papillary necrosis with renal mineralisation.

Question 699

what is Most common causes of renal disease in pet rabbits

Answer 699

E.cuniculi Infection with Encephalitozoon cuniculi – a microsporidian parasite Diagnostics- IgG & IgM E cuniculi serology C-reactive protein PCR

Question 700

Osmoregulation in birds

Answer 700

Kidneys Large intestine Salt glands (some species) Renal system- Kidneys Ureters Urodeum (structure in the cloaca) Birds are uricotelic

Question 701

Avian kidney

Answer 701

Fixed, ventral depressions, synsacrum Extend from the lungs to the caudal synsacrum Renal fossa: symmetrical and retroperitoneal Three distinct renal divisions Do not have lobes but have lobules Cortical (reptilian) nephrons – approx 70% Mammalian (medullary) nephrons – approx. 30% this means dosing is different consider portla system Relevance of the anatomy Swelling of kidney -> neuropraxia: birds will present as lame

Question 702

Renal portal system

Answer 702

present in birds and reptiles Makes a venous ring Portal blood receives blood though: External iliac veins Internal iliac veins The ischiatic veins Caudal mesenteric vein Renal portal valve shunts blood to kidney OR back to heart depending on adrenergic or cholinergic innervation RELEVANCE = DRUGS AND INFECTION

Question 703

clinical signs of renal disease in birds

Answer 703

Observations- Droppings in cage: White urates = normal Green = biliverdinuria (severe hepatic disease) Golden yellow or brownish yellow = hepatic disease or vitamin administration Red/brown = toxicity (lead), nephritis, haemolysis, polyomavirus, warfarin-type poisons Clinical signs Polyuria, anuria or oliguria Polydipsia Non-specific signs Lameness

Question 704

diagnostics for renal disease in birds

Answer 704

Blood work- Persistently high uric acid Filtration decreased by 70-80% before plasma uric acid is elevated UA may rise with severe dehydration Will rise postprandially in carnivorous birds Urinalysis- Problems with sampling -need ureteral urine Urinary GGT (some labs) - over 20 U/L suspicious of some renal insult. NAG (N-acetyl-β-D-glucosaminidase  renal tubular enzyme (not available in many labs)  studied in chickens Diagnostic imaging- Radiography: Kidney lies in a fossae on ventral surface of the synsacrum Contrast may be beneficial Ultrasound: May be challenging due to air sacs but useful if kidney surrounded by fluid or tissue CT: IV in basilic (wing vein)- remember portal system, can cause nephrotoxicity Endoscopy- Renal biopsy to achieve a definitive diagnosis Histopathology Culture and sensitivity PCR Cytology – e.g., look for uric acid crystals

Question 705

differentials for renal disease in birds

Answer 705

Bacterial -> acquired from haematogenous route Fungal -> Aspergillus spp. Viral -> herpesvirus, adenovirus, paramyxovirus and avipoxvirus can affect the kidney as part of a generalised infectious process. Parasites -> protozoal infections. Microsporidia have been found in association with nephritis Nutrition ->Fatty liver/kidney syndrome Neoplasia Gout Toxicities -> heavy metals, poisonous plants, potential nephrotoxic drugs Obstructions ->cloacoliths, tumours, pressure from egg binding

Question 706

differentials for renal disease in reptiles

Answer 706

Environmental Bacterial Viral Fungal Parasitic (Hexamita or Entamoeba) Calculi in species with a bladder Gout Neoplasia Post hibernation complications

Question 707

risk factors and clinical designs of renal disease in reptiles

Answer 707

Risk factors- Provision of purine rich high-protein diets Low humidity Lack or unsuitable water source Nephrotoxic medications Clinical signs- Depression Weakness Dehydration Pharyngeal oedema Palpation of enlarged kidney (iguanas – via digital cloacal palpation)

Question 708

assesing dehydration in reptiles

Answer 708

PCV BLOOD PROTEINS URINE SG SKIN TENTING TACKY MMS ALL UNRELIABLE hibernating tortouses will recycle bladdder contents- can be cause of renal disease if the animal doesnt drink after waking

Question 709

roentgen signs

Answer 709

The radiologic (roentgen) signs are abnormal: Number. Position. Size. Shape. Opacity. Margination. Decreased. Congenital absence (rare)

Question 710

Left Atrial to Aortic root ratio

Answer 710

In veterinary clinical practice, the left atrial-to-aortic root ratio (LA/Ao) in right parasternal short axis view is the most commonly used method to evaluate left atrial (LA) size in dogs [6, 8, 12, 13, 26]. This ratio provides an index of LA size that is independent of body size. dogs; <1.6 cats ; < 1.5 is normal. Typically cats with heart failure have significantly increased LA:Ao of >1.8.

Question 711

what are the steps to check the breathing system is safe and ready for use:

Answer 711

1. Connect breathing system to anaesthetic machine and scavenging system 2.Cover patient end of breathing system with your thumb and close APL valve 3. Fill breathing system with oxygen using flush button or turning oxygen flow meter on 4. Squeeze inflated reservoir bag, check whether it keeps its shape/size and listen for sounds of leaking gas in any part of the system 5. Open the APL valve with your thumb still in place 6. Squeeze reservoir bag and check exit through scavenging tubing is patent

Question 712

radiography abdominal VD positioning

Answer 712

Positioning: Use radiolucent cradle to ensure no axial rotation Centring: At level of caudal edge of last rib (slightly more caudal in cats) In midline Collimation To greater trochanter caudally To lateral body wall Aim to include whole of abdomen in survey films

Question 713

radiograph anbdominal lateral positioning

Answer 713

Positioning: Pad sternum +/- between hindlimbs to prevent axial rotation Pull hindlimbs caudally (and forelimbs cranially) Centring: At level of caudal edge of last rib (slightly more caudally in cats) Half to third way up from ventral body wall Collimation To greater trochanter caudally To ventral body wall and collimate off some dorsal tissues if possible Aim to include whole of abdomen in survey films

Question 714

advantages and disadvantages of using radiography to view the kidneys

Answer 714

Advantages: Number, location, size, shape, symmetry Presence of mineralised opacities Addition of contrast agents useful Disadvantages: Beware of superimposition Limited if fluid or lack of fat No information on internal architecture

Question 715

Contrast Agents

Answer 715

Used when plain radiography gives insufficient organ detail Positive Contrast Agents High atomic number, e.g. compounds containing barium or iodine Appear more radiopaque than surrounding body tissues Negative Contrast Agents Gases, e.g. room air or carbon dioxide Appear radiolucent

Question 716

Intravenous Urography (IVU)

Answer 716

Positive contrast media Anatomical and functional information- IVU provides only very crude assessment of renal function (excretion) Sequential radiographs taken Information obtained at each stage of the IVU: Immediate VD (kidneys) 5 mins – VD (whole abdomen) 10 mins – lateral (whole abdomen) 15 mins – lateral (bladder neck) Others as needed

Question 717

advantages and disadvantages of using ultrasound to view the kidneys

Answer 717

can see images on different planes- saggital, transverse, dorsal dorsal plane gives best view of pelvis better view of internal archatechture Advantages: Safe, cheap, avoids ionising radiation Assessment of internal architecture Focus and diffuse lesions Disadvantages: Requires operator experience

Question 718

kidney ultrasound anatomy

Answer 718

Renal Cortex- Evenly granular Hypoechoic (occasionally isoechoic) to the liver in dogs Often more echogenic in cats Medulla- Hypoechoic to cortex Look for a good ‘cortico-medullary’ definition Pelvis- Recognised in the normal kidney by echogenic peripelvic fat

Question 719

advantages and disadvantages of using radiograph to view the blader

Answer 719

Plain Radiographs: Advantages: Detection of radiopaque cystoliths Size and location Addition of contrast agents can provide more information Disdvantages: Limited value for evaluating for disease without contrast

Question 720

Retrograde Contrast Cystography

Answer 720

Fast, simple, inexpensive Sedated/GA required Negative, positive or double contrast Uses: Bladder wall assessment Location or integrity Radiolucent cystouroliths Which contrast media? Air (pneumocystogram) Cheap, readily available Useful to identify bladder and show position and wall thickness Poor mucosal detail and may miss small tears. can very rarley casue air embolysm so some peopple use co2 Positive contrast cystogram Expensive Main indication is suspected bladder rupture Double contrast cystogram- similarly to a conventional cystogram, but gas is also introduced through the Foley catheter Excellent mucosal detail and contrast puddle provides useful contrast (e.g. radiolucent calculi)

Question 721

advantages and disadvantages of using ultrasound to view the blader

Answer 721

Advantages: Detect radiolucent cystourolith Cystocentesis Surrounding structure assessment Disadvantages- Degree of distension affects shape, size and wall thickness Ultrasonographic appearance 3-layers Inner mucosal interface (hyperechoic) Muscle layer (hypoechoic) Outer serosal layer (hyperechoic) polyps will have no shadowing cystolyths will have shadowing

Question 722

advantages and disadvantages of using radiography to view the uethra

Answer 722

Plain radiographs yield minimal diagnostic information Always include entire pelvis and male urethra 2 lateral views: hindlimbs caudally and cranially

Question 723

Feline Lower Urinary Tract Disease

Answer 723

A collection of conditions that can affect the bladder and/or urethra in cats: Urolithiasis Bacterial infections- RELlTIVLY UNCOMMON IN CATS, SEEN MORE IN OLDER CATS Urethral plugs Anatomical defects Neoplasia Feline Idiopathic cystitis- common, espessialy in younger cats

Question 724

Clinical Signs of FLUTD

Answer 724

Lower Urinary Tract signs: Dysuria (77%)- +/- vocalisation &/or pain Pollakiuria (78%) Haematuria (71%) Stranguria (70%) Periuria (70%) Signs of urethral obstruction? Behavioural changes: - associated with PAIN Loss of litter training Aggression Excessive grooming- Not just around rear but around caudoventral abdomen “Constipation” Stilted gait as are uncomfortable Abdominal pain

Question 725

iFLUTD

Answer 725

The typical Feline Idiopathic cystitis cat: young or middle aged (<10years) neutered overweight inactive mainly indoor dry diet multi cat house New Theories: Interstitial cystitis in people- neurogenic inflammation mucosal defects- Increased bladder wall permeability, Altered GAG layer Neuroendocrine imbalance triggered by stress neurogenic inflamation- Characterised by submucosal histopathological changes in the urothelium Damaged urothelium vasodilation haemorrhage Lymphocytic infiltrate Muscularis fibrosis increased mast cells (20% of patients) diagnosis- Signalment Are there any clues to the possible underlying cause? Age of cat - infection or idiopathic cystitis? Clinical history Is this the first episode or a recurrent episode? Are they a multi cat household? Stressful events recently? Pattern of behaviour Are there features that increase the likelihood of: UTI Neoplasia Urolith rule these out managment- iFLUTD… pain relief – 5-7 days how do we treat a disease if we don’t understand the cause? Control the discomfort Buprenorphine Glucocorticoids have no benefit in clinical trials and may cause pupd NSAIDs placebo controlled trial with meloxicam showed no benefit (Dorsch 2009 ECVIM) Flush the bladder with saline --> urohydrodistension Lidocaine Self-limiting! Increase water intake Produce a dilute urine and increasing flushing out of bladder wet diet free access to water water fountains tuna water reduce stress- consider social factors, resources

Question 726

physical examination of obstructed cat

Answer 726

Bladder palpation- distended? firm painful Penis discoloured +/or swollen Dehydrated Often systemically ill if obstructed Bradycardia Non obstructed cat- Bladder palpation- small thickened? painful? Systemic signs are uncommon but could indicate concurrent disease

Question 727

flud diagnostics

Answer 727

Urinalysis Haematology and Biochemistry- Unremarkable unless systemic disease Essential in obstructed cats Radiography +/- contrast Ultrasound- Not for urethra! Cystoscopy Exclusion of other causes - iFLUTD

Question 728

Urethral Obstruction Causes

Answer 728

Uroliths- Struvite (magnesium ammonium phosphate) Calcium oxalate Urethral plugs- Protein-colloid matrix Mucoproteins, albumin, globulin Cells – RBCs, WBCs, epithelial cells +/- crystalline material ‘Idiopathic’ obstruction- Functional not physical obstruction urethral spasm mucosal oedema Complicating issue in male cats… a design fault!

Question 729

Unblocking the blocked cat

Answer 729

Stabilise the patient- haematology, biochemistry, electrolytes- Correct the electrolyte disturbances; HyperK+- Calcium gluconate if bradycardic, Dextrose Fluid therapy in all cases- Hartmann’s or 0.9% sodium chloride Cystocentesis? – Care.- Advance the needle through the bladder wall at a 45-degree angle directed toward the trigone General anaesthesia Aseptic technique and a gentle hand are fundamental to urethral catheter placement.- Extrude the penis and retract it caudally to straighten the urethra. Advance a urinary catheter into the urethra to the site of obstruction – never force past obstruction! Saline flushing as catheter advanced Rectal palpation by assistant Once the urethra is patent, advance catheter flush and drain the bladder multiple times with sterile saline to remove debris and help prevent rapid recurrent UO.

Question 730

Halsted’s Principles

Answer 730

Strict Asepsis Gentle Tissue Handling Haemostasis Preservation of the blood supply No tension on tissues Good approximation of tissues Obliteration of dead space

Question 731

maintaining haemostasis during surgery

Answer 731

applying Digital pressure- 60 seconds for minor, 5 mins for majour Haemostats- crushes tissues Packing with surgical swabs- good for deeper or more delecate tiussues, can disloge blood clots when removed Lavage with saline- allows visulisation Ligatures- good for thigs that likly wont clot Topical haemostatic agents Tourniquets- limb amputations Diathermy- electrocautory

Question 732

Sutures

Answer 732

Placement of sutures in tissue Sutures are used to: Close tissue planes Re-appose vital structures close dead space Retract tissues with minimal handling Stabilize and exteriorize tissue and organs.

Question 733

Monofilament

Answer 733

Advantages: Smooth surface Low friction less drag less tissue trauma No bacterial harbouring as nowhere to stick No capillarity Disadvantages Poor handling Poor knotting ‘Memory’ Stretch

Question 734

Multifilament

Answer 734

Advantages: Strength Soft & pliable Good handling Disadvantages Harbour bacteria Capillary action ‘wicking’ in the suture material gaps Tissue trauma Drag/chatter/cutting

Question 735

Absorbable sutures

Answer 735

Absorbable, or soluble, sutures undergo degradation and a rapid loss of tensile strength within 60 days Intended primary for short term use Good in feral cats/vicious animal Absorption routes: Proteolysis e.g. catgut Hydrolysis e.g. vicryl Advantages Broken down by body No foreign material left Disadvantages Shorter wound support Examples: Multifilament: Catgut- bad for inflamation Polyglactin 910 (vicryl)- well tolerated, long absorbtion Monofilament Polydioxanone (PDS) Poliglecaprone 25 (monocryl)

Question 736

Catgut

Answer 736

multifilament Removed (rapidly) by proteolysis & phagocytosis Plain catgut approx. 7-10 days tensile strength Chromic catgut 10-14 days Any situation that needs short term support Derived from ruminant intestine Doesn’t have a predictable absorption rate so don’t know how long its going to last known to produce intense tissue reactions.

Question 737

Polyglactin 910 (Vicryl)

Answer 737

multifilament Braided synthetic absorbable Good handling Good knotting Coating ensures smooth passage through tissue Also Vicryl Rapide

Question 738

Lactomer 9-1 (Polysorb)

Answer 738

Strong braided absorbable multifilament Similar to vicryl Finer, more compliant superior handling, less memory Tensile strength >21 days

Question 739

Polydioxanone (e.g. PDS, PDS II)

Answer 739

Synthetic absorbable monofilament High initial strength Predictable absorption Long term wound support e.g. linea alba or other tissues that take a while to heal Smooth passage through tissue as is monofilament Poor handling and poor knotting Minimal tissue reaction

Question 740

Poliglecaprone 25 (e.g. Monocryl)

Answer 740

Monofilament synthetic absorbable Excellent strength Good handling 7 days 50% tensile strength remains

Question 741

Non-Absorbable sutures

Answer 741

Retained permanently or retain tensile strength >60 days These elicit a tissue reaction that results in encapsulation of the material by fibrous tissue Advantages Permanent wound support (e.g. hernia) Disadvantages Suture sinus Material becomes encapsulated and eventually becomes an abscess Foreign body Suture extrusion

Question 742

Silk

Answer 742

Twisted/Braided biological suture material Made from silk worm cocoon Non-absorbable- doeas technically but takes long time Excellent handling Suture standard Good knot security Nice and soft e.g. good to use for entropian Disadvantages Tissue reactions common Rapid loss of strength Ultimately fragments - eventually breaks off Long term foreign body reactions Never to be used in presence of infection

Question 743

Polyamide (Nylon e.g. monosof, ethilon)

Answer 743

non-absorbable Monofilament or multifilament Usually used for skin closure High memory Hydrolysed slowly

Question 744

principles of chosing suture material

Answer 744

tensile steanght should match streanghth of tissue rate of loss of streangth should match wound gain of streangth will sutre alter healing- reaction ect mechanical prprties should match wound tissue Suture characteristics Suture/tissue interaction Tissue characteristics Wound characteristics Patient factors Surgeon factors

Question 745

Why spay?

Answer 745

Elective -prevention of breeding potential Treatment of disease-Neoplasia, pyometra Stabilise systemic disease e.g. diabetes Population control Increased lifespan Commonly reported advantages for performing sterilisation are: reduced risk of mammary neoplasia reduced sexual behavioural problems Reduced stress of pseudopregnancy

Question 746

When to spay?

Answer 746

Age: Younger Reduced risk mammary tumours https://bestbetsforvets.org/bet/579 Incidence of other neoplasia? bitches >3 months post-season

Question 747

Ligaments of he uterus

Answer 747

Broad ligaments: Mesometrium- uterus, cervix, vagina Mesovarium- ovary Mesosalpinx- surrounds oviduct bursa formed by the mesovarium and mesosalphinx Proper ligament of the ovary (O to H) Suspensory ligament of the ovary (O to wall)- break to expose ovary Round ligament of the uterus

Question 748

Open OVH/OVE method

Answer 748

Landmarks: Caudal to umbilicus Steps: Stab incision for linea alba- insision extended via sissors hook ovary Stretch/break suspensory ligament make window in mesometrium Clamp & ligate pedicle Transect the pedicle distal to ligatures Check for haemorrhage Repeat on other side for ovh- ligate and cut at tip of uterine horn

Question 749

Laparoscopic OVE

Answer 749

Advantages: Quicker return to activity Less post operative pain Weak evidence Disadvantages: Operator training and experience Kit Cost Complications -> convert to open anyway

Question 750

Ovarian Remnant Syndrome

Answer 750

Oestral activity (2w-9years later) More common after routine procedures Hormonal investigations ? R > L ovary may be easier to find residual tissue in oestrus. may see enlarged ovarian vessels on functional side. Submit tissue for histopath Always open ovarian bursa after surgery to check whole ovary removed.

Question 751

Urinary Sphincter Mechanism Incompetence (USMI)

Answer 751

Most common non-neurogenic cause of canine incontinence Typical case = older, spayed bitch Several factors may be involved: Ageing or lack of oestrogen cause changes in urethral support structures (collagen) Abnormal position of bladder or urethra (“intra-pelvic bladder”) Reduced amount of smooth muscle in the urethra Obesity - increases intra-abdominal pressure and makes things worse Breed predispositions (genetic factors?) Recent systematic review stated evidence not strong enough to determine link between neutering or age of neutering and urinary incontinence in bitches

Question 752

OVH in the queen

Answer 752

Left flank: Landmarks: iliac crest, greater trochanter and the caudal ribs Advantages: Reduced infection Easier to monitor – ferals Disadvantages: Difficulty exposing repro tract? Midline: Umbilicus -> pubic brim <12 weeks; go 2/3 of way back from umbilicus to pubic brim halfway for > 12 weeks Advantages: Better exposure/visualisation Larger wound e.g. pregnancy Disadvantages: Difficult to monitor e.g. feral Increased contamination risk

Question 753

Why castrate?

Answer 753

Advantages Prevention of some neoplasia Prevention of testosterone-stimulated disease Reduced male behaviour Disadvantages Increase risk of some neoplasia Reduced male behaviour (important for guarding / performance dogs) Delayed growth plate closure (if pre-pubertal neuter) Can increase risk of fractures Low testosterone (concern if castrated late)

Question 754

when to castrate

Answer 754

Early vs. conventional neutering Fixed age? Prepubertal? Cats <4-6 months Dogs – more variable Early: Delayed physeal closure (not shown to be associated with growth plate fracture) ? Increased risk of osteosarcoma in Rottweilers/ joint disease and neoplasia in Golden Retrievers

Question 755

relevent anatomy of testes

Answer 755

located in an evagination of the peritoneum (vaginal tunic) covered by Tunica albuginea Visceral layer of vaginal tunic Eight layers: Skin (scrotum) Dartos External spermatic fascia Cremaster muscle (only in one part) Internal spermatic fascia Parietal vaginal tunic (Vaginal cavity) Visceral vaginal tunic Tunica abuginea (Testis) q

Question 756

surgical method of neutering the dog

Answer 756

Pre-operative evaluation: Physical examination Palpation of scrotum and inguinal canal Check there are two descended testicles! Pre-operative analgesia General anaesthetic Dorsal recumbency Aseptic skin prep Note: do not clip the scrotal hair!! Single mid-line incision Commonly performed as: Modified (open then subsequently closed) Closed Open Which approach? Pre-scrotal: Between scrotum and prepuce- most popular in dogs Scrotal

Question 757

Open Castration

Answer 757

Internal spermatic fascia is incised Provides direct visualisation of the spermatic cord and BV’s

Question 758

Closed Castration

Answer 758

Parietal vaginal tunic not incised

Question 759

What is the definition of a fertile ram?

Answer 759

“…capable of getting 85% of 60 normal healthy naturally cycling ewes in lamb in the first cycle in a commercial situation” “…a mature ram lamb is expected to achieve pregnancies from 85% of 40 normal, healthy, naturally cycling ewes in the first cycle"

Question 760

stages of fertilaization involving the sperm

Answer 760

Sperm Capacitation- Freshly ejaculated sperm are unable or poorly able to fertilize. Rather, they must first undergo a series of changes known collectively as capacitation. Sperm-Zona Pellucida Binding- Binding of sperm to the zona pellucida is a receptor-ligand interaction with a high degree of species specificity. The carbohydrate groups on the zona pellucida glycoproteins function as sperm receptors. The Acrosome Reaction- acrosome - a huge modified lysosome that is packed with zona-digesting enzymes and located around the anterior part of the sperm's head.The acrosome reaction provides the sperm with an enzymatic drill to get throught the zona pellucida Penetration of the Zona Pellucida- The constant propulsive force from the sperm's flagellating tail, in combination with acrosomal enzymes, allow the sperm to create a tract through the zona pellucida. These two factors - motility and zona-digesting enzymes- allow the sperm to traverse the zona pellucida. Sperm-Oocyte Binding- Once a sperm penetrates the zona pellucida, it binds to and fuses with the plasma membrane of the oocyte. Binding occurs at the posterior (post-acrosomal) region of the sperm head.

Question 761

Testosterone

Answer 761

Produced by the Leydig cells of the testes Initiates Pubertal development of the testis then optimises spermatogenesis in adulthood Targets the Sertoli cells

Question 762

Follicle Stimulating Hormone

Answer 762

Targets the Sertoli cells Produced by the anterior pituitary gland Initiates pubertal development and maintains spermatogenesis during adulthood

Question 763

Luteinizing Hormone

Answer 763

Produced by the anterior pituitary gland Targets the Leydig cells

Question 764

Ram Fertility exam

Answer 764

3 stage process 1 – Full clinical exam and reproductive tract examination (RAM MOT) 2 - Pre-breeding exam (PBE) 3 – PBE certification

Question 765

How long does spermatogenesis take in the ram?

Answer 765

47–48days

Question 766

By what age do 90% of rams have a mature sized scrotal circumference?

Answer 766

> 14 months

Question 767

Methods of Semen Collection in ram

Answer 767

Artificial Vagina (AV Collection)- Defined as ‘Gold Standard’ Attempt first if appropriate Rams require training Ewe Teaser – Be aware of Welfare Implications Not practically Feasible in many commercial situations Vaginal Aspiration (VA)- Teaser Ewe required Welfare Disease Risk Contamination – blood, pus, inflammatory exudate white cells Difficult to Interpret Ensure rams remain separated from ewes, ideally >14 days prior to examination Electro Ejaculation (EEJ)- Commonly Used in field conditions A small population of Rams fail to ejaculate – caution with failing rams Often highly successful following teasing

Question 768

asssesing Gross Motility of sperm

Answer 768

A function of both motility and concentration Low Power x 40 Scored on a Scale 1-5: 1 – No Swirl, generalised oscillation of individual cells only 2 – Very Slow distinct swirl 3 – Slow Distinct Swirl 4 – Moderately Fast Distinct Swirl 5 – Fast distinct swirl with continuous dark waves

Question 769

assesing Progressive Motility of sperm

Answer 769

Perform at 100x and 400x Magnifications Critical to perform Previously 30% minimum acceptable Now 60 % minimum acceptable No circling, zig-zagging or floating “… ability of individual cells to achieve progressive, unidirectional, linear motility at a rate of at least 1x times cell length per second”

Question 770

Morphological examination of semen sample

Answer 770

Relationship to ‘fertility’ Reflects Physiological and/or pathological status of the testes Reflects maturation and transport processes occurring within the epididymides. Useful diagnostic tool when dysfunction has been identified. A MUST DO for PBE Nigrosin Eosin Stained Smear High Power magnification X1000 (X100 Lens) Oil Immersion Perform Morphology Count Assess minimum 100 cells ≥70% to achieve Pass Handling Issues Identified!

Question 771

Common Sperm abnormalities

Answer 771

Defects of the sperm head- Pyriform Heads Micro/Macrocephalic Sperm Nuclear Vacuoles Knobbed Acrosome Defect Detached Heads Defects of the sperm tail- Proximal Cytoplasmic Droplets Distal Cytoplasmic Droplets Distal Midpiece Reflex Severely coiled tails/Dag Defect Coiled Principal Piece Bent Tails - Hypotonic Shock Abaxial Tails Accessory Tails

Question 772

List 5 common disease of sheep which may affect ram fertility

Answer 772

Epididymitis (Brucella Ovis)- Epididymitis is a venereal disease of rams caused by the bacteria Brucella ovis. Epididymitis means inflammation of the epididymitis, the tubular portion of the testicle that collects the sperm produced by the testes and stores it until it is ready to transport. Severely affected rams will often have at least one enlarged epididymis and may show pain when the testicle is manipulated. can also be caused by Corynebac- terium ovis (the "cheesy gland" germ Brucellosis- also known as ‘bruce-o’ is a bacterial disease that permanently infects the testes and epididymis of rams, rendering them infertile. It also temporarily infects the reproductive tracts of ewes, meaning that ewes can potentially spread the infection to uninfected rams. Rams also pick up infection from each other in the ram paddock. Sheep brucellosis is practically incurable, so control of the disease relies on sound biosecurity and testing to eliminate infected animals. large worm burdens “pizzle-rot” or enzootic posthitis. Pizzle-rot is an infection of the sheath of the penis and is caused by the bacteria Corynebacterium renale. Pizzle-rot can also be caused by high protein diets that include a crude protein value higher than 16%.

Question 773

stages of labour in cattle

Answer 773

Stage one labour (start of contractions) : 8-12 hours Stage two labour (from amniotic sac rupture to calf out): >2 hours Stage three labour (passing of fetal membranes): 4-6 hours Suggested intervention points during stage 2 (Oklahoma state research): 30 mins no progress cow 60 mins no progress heifer

Question 774

what is assessed in the initial examilation of a calving cow

Answer 774

Local conditions (Mal)presentation FM disproportion Obstruction Twins Malformation (Metabolic – hypocalcaemia- calcium drives muscle contraction)

Question 775

Feto-maternal disproportion

Answer 775

calf too big/ dam too small Dam factors- Age, weight, parity, BCS, nutrition Calf factors- Gestation length, breed, sire, exess nutriom Bones or soft tissue?- bcs Herd level significance?- cow selection? bull selection? often causes crossed legs presentation due to stuck shoulders

Question 776

Obstruction in calving

Answer 776

Normal’- Undilated cervix Abnormal- Undilated cervix- abnormal presentation causes abnoral factors and cervix doestn dilate Uterine torsion- often have milk fever when corrected Pelvic abnormalities

Question 777

Obstruction in calving

Answer 777

Normal’- Undilated cervix Abnormal- Undilated cervix- abnormal presentation causes abnoral factors and cervix doestn dilate Uterine torsion- often have milk fever when corrected Pelvic abnormalities

Question 778

Immediate post-calving management

Answer 778

‘Tears and Spares’ check Rehydration Nutrition Management of stress Client management Lessons to be learned Herd-level implications Retained fetal membranes Nerve damage Tears or bleeding Uterine prolapse Hypocalcaemia Trauma (Other concurrent disease)

Question 779

Management of the neonate

Answer 779

Start breathing Shock, rubbing, positioning Assisted ventilation Correct acidosis Iodine navel Colostrum ID

Question 780

Management of the neonate

Answer 780

Start breathing Shock, rubbing, positioning Assisted ventilation Correct acidosis Iodine navel Colostrum ID

Question 781

if the dominant bull is infertile...

Answer 781

he will stop fertile bulls servicing cows while not servicing cows himself

Question 782

Fully fertile mature bull running with 50 cycling healthy cows should deliver:

Answer 782

60% in calf in 3 weeks <10% empty after 9 weeks- this can be skewed by issues with the cows TAKE CARE!- Herd circumstances- weather, grass quality , diet, heat stressect Changing status

Question 783

name a few causes of infertility in bulls

Answer 783

Poor libido Injury Overwork Nutrition Corpus cavernosum rupture Persistent frenulum Corkscrew deviation IPBP Penile trauma Fibropapilloma Testicular hypoplasia Orchitis Epidydimitis Seminal vesiculitis Testicular degeneration Systemic illness BVD Genetic malformation Iatrogenic these can be catagorised as: Failure to mount Failure to achieve intromission/ejaculate Failure to achieve fertilization Reaching the ovum Producing a viable zygote

Question 784

Bull Breeding Soundness Evaluation

Answer 784

Physical exam- bull must Sustain himself Locate females in oestrus Mount those females BCS- too thin= underlyign health issue. to fat= testicles retain too much heat Heart &lungs Eyes Jaw Locomotion- Lameness Conformation- strain when working, genetics Abnormalities External genitalia Palpation of testes External genitalia Scrotal circumference External genitalia Penis Internal genitalia Accessory sex glands Semen analysis- bull bust Inseminate Fertilize Libido/service assessment- bull must NOT KILL ANYONE IN THE PROCESS Infectious disease?- bull from small closed heard would be niave to infectous disease

Question 785

semen collection in bull

Answer 785

Mated female- Internal AV inseted into cow in heat Artificial vagina Ampullae massage Electroejaculation (EEJ)

Question 786

Fresh cow check

Answer 786

Health check Temp, smell (infection), rumen fill, hydration Appetite +/- Ketones +/- Vaginal exam

Question 787

Metritis

Answer 787

Uterine infection post calving (~3 – 21dim, mainly 4-7d)- Voluminous purulent discharge Smelly, red-brown usually Involves the myometrium and the endometrium Usually results in systemic illness Fever Inappetence Depression Treatment: Systemic antibiotics NSAID Fluid therapy Energy – prop glycol Herd situation? prevelance- 3%- 25% of cows ~$500/case (J. Perez-Baez 2021)

Question 788

Post Natal Check

Answer 788

Often around 30 days in milk Two assessments: Resumption of normal cyclicity Uterus involuted and free of infection- Endometritis, Abscesses Herd level assessment useful- Proportion of cows cycling Proportion of cows ‘dirty’

Question 789

Endometritis

Answer 789

Uterine infection limited to the endometrium >21days in milk Often called ‘whites’ – white, purulent discharge No systemic effects on cow health ~£160/case (AHDB) Diagnosis – vaginal exam, metricheck, US Treatment – if CL; PGF2a, or ‘washout’. cow to be taken out of progeserone heavy staye and put into estrus as its protective against infection discharge can be graed 0-3- metri checker

Question 790

Post calving uterine infections

Answer 790

thickened wall see puss on ultrasound dystocia risk factor- malpresentation, twins age metabolic stasis poor imune function stress concurrent disease hygean retained fetal membranes

Question 791

Not Seen Bulling cow check

Answer 791

After voluntary wait period (~50dim) Assess whether cow not been or not seen in oestrus Various hormonal interventions available Interventions escalate in severity as DIM increases (Heat delay/service delay) Beware of pregnancy! Actions depend on DIM, ovarian status, co-morbidities; PGF2alpha GnRH P4 (Oestrogens – not in UK/EU) Synchronisation protocols ~100% submission rate Double prost Ovsynch 56 CIDR/PRID synch Cosynch… Pregnant! Cystic ovaries- Follicular cyst – thin walled, fluid filled structure >30mm diameter persisting on the ovary for >10 days in the absence of a CL Luteal cyst/part luteinised cyst – wall thickness greater than 3mm True anoestrus Uterine disease- Chronic endometritis, pyometra, mucometra Difficult to truly diagnose ovarian dysfunction at one visit!

Question 792

cow Pregnancy Diagnosis

Answer 792

Transrectal ultrasonography: >28 days Manual palpation: >~35 days Later gestation – fremitus, cotyledon bouncing PAG testing ( pregnancy assosiated glycoprotien)– milk recording Progesterone monitoring – eg De Laval VMS systems Knocking Non-return (animal does not appear to come back into heat) Benefits of transrectal ultrasonography vs manual: More accurate assessment of uterus (and ovarian structures) Can detect twins Can detect fetal heartbeat and assess viability Less likely to cause iatrogenic abortion Can sex embryos (55-60d) Benefits of manual palpation Cheap, no kit required Possibly easier in later gestation than US?

Question 793

Aging Pregnancies

Answer 793

Farm records! Practice Ultrasonography Manual palpation

Question 794

diagnosisng twins in cows

Answer 794

multiple corpora lutea- most commonly double ovulation rather than split embryo twin line two fetus visible often one fetus may dies

Question 795

Submission Rate

Answer 795

Proportion of eligible animals served within a given time period (usually 21 days) AYR target: >60% All about heat detection Provided cows are cycling factors effecting it: enviromental factors- confidence in floor, light, fpace managment factors- fertility interventions, what other cows they are housed with cow factors- health, genetics

Question 796

Conception Rate

Answer 796

Proportion of served animals Pregnant at PD Not a true measure of fertilisation rate- effected by when you PD (Early Eembrionic Death /Late ED) AYR target >40% factors: enviroment- cow comfort, flooring, temp, food and water managment factors- bull choice, breed choice, teqnique cow factors- health, uterine enviroment

Question 797

Pregnancy Rate

Answer 797

Proportion of eligible animals pregnant in a given time period (usually 21 days) PR = Submission Rate x Conception Rate For example: (SR 60%) x (CR 40%) = PR 24% AYR target: >20%

Question 798

Block Calving Systems

Answer 798

Spring vs Autumn Resource planning and requirements Cow choice Seasonal management strategy Seasonal output spring block- smaller cow, lower grazing. peak yeailds= peak grass growth autumn block= larger cow

Question 799

Block calving fertility management

Answer 799

Fertility visit structure: Clean checks PSM -21d PSM -7d PSM +7d PSM +21d PDs Different strategies 12 block calving- 12 block breeding- fertility managment for year over

Question 800

Block Calving KPIs

Answer 800

Submission Rate: >90% Conception Rate: >60% 3 week I/C rate: >50% 6 week I/C rate: >75% 12 week empty rate: <8% Often AI and bulls

Question 801

KPIs

Answer 801

key performance indicators for cow fertility

Question 802

Heifer management

Answer 802

Aim to calve in well-grown heifers by 24 months Which means they need to be In Calf at 15 months- Heat detection Synchronisation start inseminating at 12 months Age at first calving KPIs… Av vs %? Better measures? % 2nd lact?

Question 803

follicular stasis

Answer 803

reproductive condition ofchelonians Pre-ovulatory egg binding Often seen in the older, female tortoise kept alone If follicles are not resorbed  inflammation of the follicles  coelomitis CS  anorexia, HL paresis, generalised weakness Due to an inability to produce progesterone  failure of regression of follicles. Recent exposure to a male after a period of prior isolation? Inappropriate diet? Inappropriate husbandry? Stress? Lack of hibernation, light and temperature change? Still in need of further research disgnosis- Blood work – raised calcium, raised proteins Ultrasonography Advanced imaging treatment- Fluids Nutritional support Correct husbandry Often surgical  hormonal implants ineffective for these cases

Question 804

COELIOTOMY

Answer 804

entering the coelomic cavity Ligation – haemoclips or absorbable monofilament suture material Closure - absorbable monofilament suture material Skin closure Everting suture pattern Suture choice often non-absorbable and strong. Skin suture removal not to be removed for at least 6-10 weeks

Question 805

PLASTRONOTOMY

Answer 805

Heart > in the midline intersection of the pectoral and abdominal scutes. Plastron hinge -: often between the abdominal and femoral scutes. Abdominal veins - parallel, running in a craniocaudal direction below the plastron

Question 806

Ovariectomy in chelonians

Answer 806

The prefemoral approach- Preferred method if possible – less traumatic and faster recovery time Useful in species with a larger prefemoral fossa Craniocaudal incision is made in the skin Blunt dissect underlying abdominal muscles Dissect coelomic membrane Closure – simple interrupted or continuous pattern for coelomic membrane, muscle and fat. Closure – everting pattern for the skin

Question 807

Dystocia – egg retention

Answer 807

Non-obstructive factors Lack of suitable nesting site Stress Hypocalcaemia Infection of oviduct Poor muscle tone Obstructive factors Oversized eggs Malformed eggs Oviductal stricture Space occupying lesions Clinical signs- No presenting signs are pathognomonic for dystocia No signs Abnormal posture Hind limb paresis Anorexia Malodorous cloacal discharge Faecal or urinary retention Cloacal organ prolapse treatment- chelonians Fluids Nutritional Support Provision of nesting site Calcium gluconate Oxytocin- Induces parturition/egg laying when uterine inertia is present (as long as there is no evidence of obstruction) trteatment- lizards and snakes More commonly seen in oviparous (egg-laying snakes) >pythons, rat snakes, king snakes milk snake Less commonly seen in ovoviviparous (live-bearing) snakes > boas, garter snakes

Question 808

cloacla prolapse

Answer 808

Prolapse – advice to client moist substrate (no woodchip or sand), lubricate tissue Cover with cling film/glove Identify tissue Gastrointestinal impactions Dystocia Parasitism Hypocalcaemia Space occupying lesion Faecal/foreign body impaction Dystocia Ultrasonography – follicles Blood work – hypocal Faecal analysis - parasites treatment- Address underlying causes Analgesia General anaesthetic to replace prolapse- Manually Surgically Care – must check for intussusception Amputation >necrotic phallus

Question 809

dystocia of birds

Answer 809

Dystocia- Caudal uterus Vagina Uterovaginal sphincter EMERGENCY if compresses blood vessels and/or nerves Radiography (conscious) treatment- Stabilisation Warmth Fluid therapy Calcium PGE2 gel GA  manual delivery

Question 810

Chronic egg laying in birds

Answer 810

Small psittacines >cockatiels Produce repeated clutches or a larger than normal clutch Depletion of calcium and protein stores Poor bone density Weight loss Pathological fractures Dystocia prevetion- Environmental modification- Reduce photoperiod Remove nesting material Behavioural modification- Training Leaving in eggs Nutritional modification- Encourage foraging Hormonal manipulation- Deslorelin (Suprelorin)- Desensitises GnRH receptors, thereby decreasing release of LH & FSH Cabergoline (Galastop)- Potent selective inhibition of prolactin May have beneficial effect in birds with chronic egg laying. In birds it also conjectured that its action could be mediated via its effect as a dopamine agonist. Leuprolide acetate (Lupron)- Leuprolide acetate is a synthetic nonapeptide that is a potent gonadotropin-releasing hormone receptor (GnRHR) agonist

Question 811

What is mastitis and how do cows get it?

Answer 811

Pathogen gets into the udder cistern → inflammation of the mammary gland All mastitis risk factors fit into at least one of 3 categories: The udders natural defences are compromised Bacteria numbers are increased at the teat end The udders natural defences are by-passed Mastitis is a game of risk and numbers! Teat skin should be smooth, thick firmly adhered, no glands. Defenses: The Teat (Streak) Canal: Keratinocytes Lipid secretions Sphincter muscle Phagocytes (somatic cells) Frequent milking Antibodies Lactoferrin Classifications: Peracute/ acute / chronic Clinical / sub-clinical Environmental / contagious From a therapeutic perspective may be graded as Mild - abnormal milk Moderate - abnormal milk and abnormal gland Severe - abnormal milk, abnormal gland, and sick cow

Question 812

clinical signs of mastitis in the individual cow

Answer 812

Abnormal milk and/or udder- Secretion Size Texture Agalactia-n absence or faulty secretion of milk Blind or non-functional glands Hungry neonate- esspecially in beef hers, a hungry calf might be a problem with the cow Pain – altered gait Enlargement of the supramammary lymph nodes Teat and skin lesions Visual examination (Gland and teats)- hard? hot? Palpation of the gland Palpation of the supra mammary lymph nodes- inflamed? Inspect mammary gland secretions (stripping)- thick clots? Perform a California Mastitis Test (Rapid Mastitis Test) Check the skin adjacent to the udder Inspect and palpate the mammary veins

Question 813

California milk test (CMT)

Answer 813

The test uses a reagent that is added to a sample of milk. If the test is positive and a quarter is infected, the CMT mixture will appear thickened and gel-like. good for subclinical disease

Question 814

Septic mastitis

Answer 814

Most commonly caused by coliforms Systemic signs of endotoxemia in severe cases- weakness, depression, inappetence fever, scleral injection tachycardia, tachypnea rumen stasis, diarrhea Endotoxaemia induces hypocalcaemia Bacteraemia Mortality common with endotoxic shock, MODS

Question 815

Summer mastitis

Answer 815

“Dry cow" or “Summer" mastitis, caused by Trueperella pyogenes Most infections occur during the dry period The incidence of infection is increased by filthy, wet, or muddy environments for dry cows Purulent infection often leads to abscessation of the gland The organism may be spread by flies

Question 816

Pathogen diagnosis-mastitic cow

Answer 816

(+/- clinical signs, SCC, response to treatment) Individual milk culture or PCR some may be on far- to detect gram neg strainsdue to that being able tobe treated without antibiotics

Question 817

signs of mastitis in the herd

Answer 817

Bulk Milk Cell Count is too high (over 200) – I’m not being paid the quality bonus There are too many clinical cases – I’m spending too much time treating cows after milking Bulk Milk Cell Count is too high (over 400) – the milk company is going to penalise me I have too many chronic high SCC cows that won’t cure – I am culling too many cows I’ve lost another cow to E.coli, that’s the 3 one this month- too many cows are dying and they are expesive to replace common causes from most common to least:

Question 818

signs of mastitis in the herd

Answer 818

Bulk Milk Cell Count is too high (over 200) – I’m not being paid the quality bonus There are too many clinical cases – I’m spending too much time treating cows after milking Bulk Milk Cell Count is too high (over 400) – the milk company is going to penalise me I have too many chronic high SCC cows that won’t cure – I am culling too many cows I’ve lost another cow to E.coli, that’s the 3 one this month- too many cows are dying and they are expesive to replace common causes from most common to least: Incorrect teat spray volume or application Teat end damage Excessive vacuum Over milking Under milking Unsuitable teat cup liners Cup slip poor cluster removal

Question 819

what shoud be investigated whnn investigating a herd wide problem with mastitis

Answer 819

Staff and Farm profile Bulk and Individual cow SCC Clinical case data Milk cultures & PCR Milking machine static test Milking machine dynamic test Milking routine Cow:parlour interaction teat cup slips Teat condition Cow behaviour milking time per cow Completeness of milking cluster alignment Teat disinfection The environment Drying off Calving

Question 820

clinical signs of mastitits within a herd

Answer 820

Genetics report- to inform rate of mastitis resistance improvement? Age demographic and replacement rate of the herd Purchases from other herds? Were any herd checks done beforehand? Any culls for clinical mastitis? High BMSCC High Bactoscan High number of clinical cases High number of repeat cases High number of chronic SCC numbers High number of deaths from mastitis

Question 821

Milk quality & herd mastitis surveillance

Answer 821

Herd mastitis surveillance: Tests performed by the milk factory on Bulk Tank Milk include: Bulk Milk Cell Count (BMCC) Protein, Fat, Urea Total plate count or Bactoscan Coliform count Thermoduric count Freeze Point (extraneous water) On farm data Clinical case rates Culling/death rate for mastitis Antibiotic IMM tube use Herd recording (Individual Cow Somatic Cell Counts – ICSCC)/ (Conductivity-robots) Lab tests: Individual cow milk cultures (or PCR) Bulk Milk PCR (for Strep agalactiae or Mycoplasma) Milking machine test report (eg Vardia/ Advanced Milking Solutions

Question 822

WHY PERFORM A REPRODUCTIVE EXAM n a mare

Answer 822

Pre-breeding •Breeding management (detection of follicular growth/optimum time to breed/post breeding problems) •Infertility workup •Pre-purchase examination •Pregnancy diagnosis •Import/Export- some regulations require it

Question 823

Poor conformation of the vulva in the mare can lead to

Answer 823

Pneumo-Urovagina ■Vaginitis, cervicitis, endometritis ■Infertility can be negated with caslick

Question 824

Windsucker Test

Answer 824

Part the vulvar lips and listen for an in-rush of air•Tests the integrity of the vaginal vestibular sphincter

Question 825

tr a n s r e c t a l U l t r a s o u n d in the mare

Answer 825

Uterus:Cycle staging- •Estrus:endometrial folds•Diestrus: homogenus echotexture Endometrial cysts•Intrauterine fluid•Pregnancy (twins, sexing, viability)•Abnormalities

Question 826

vaginal exam of the mare

Answer 826

Visual exam: ■Speculum exam ■Vaginoscopy- Allows to evaluate: A. Changes in cervix during estrus cycle- ESTRUS: ■Secretions ↑ (moist) ■Vascularity ↑ (pink) ■Relaxation ↑ (open) DIESTRUS: ■Secretions↓ (dry Vascularity↓ (pale) ■Relaxation↓ (closed) B. Abnormalities■Anatomical■Accumulation material (urine, pus, blood)■Inflammation (vaginitis, cervicitis)■Varicosities■Tears/Lacerations (cervix, vagina)■Adhesions 2. Manual Exam (digital evaluation): ■Cervix integrity:■Patency■Tone■Adhesions■Other abnormalities (Better evaluated in diestrus) ■Vagina integrity

Question 827

how is daily sperm output of the stallion is linearly related to testis mass:

Answer 827

■Mass can be estimated by measuring testis volume: ■TV=0.52*height*width*length ■DSO=(0.024*TV)-0.76 (billions)

Question 828

semen collection methods from the stallion

Answer 828

First consider: ■Restraint ■Tr a i n e d p e r s o n n e l ■Proper facilities ■Estrous female, phantom Methods: ■Artificial vagina ■Electroejaculation ■Manual collection

Question 829

Semen Evaluation in the stallion

Answer 829

Odour ■Volume ■Color ■Sperm concentration (100-400 million/ml) ■To t a l n u m b e r of sperm ■Sperm motility ■Semen pH (optional) ■Sperm morphology ■Cytology - other cell types ■Bacteriology / virology ■Flow cytometry/fluorescence(advanced)

Question 830

Hemospermia

Answer 830

still fertile indicates problems within stallion hard to preserve

Question 831

Oligospermia/azoospermia

Answer 831

no/ reduced sprem production Obstructive disease- ■Alkaline phosphatase ■Testicular degeneration (Idiopatic or after insult) ■Te s t i c u l a r h y p o p l a s i a ■Overuse

Question 832

bitch oestrus cycle

Answer 832

Pro-oestrous (10 days)- peak in oestrogen Oestrous (10 days)- behavioural definition, bitch is receptive Luteal phase- metoestrus/ dioestrus (2 month)- progesterone and lh spike Pregnant or non-pregnant Anoestrous (4.5 months) P4 from CL only LH and prolactin luteotrophic- help maintain cl and therefore progesterone

Question 833

bitch gestation

Answer 833

Average gestation in the bitch is 63-64 days (range 56-72 days) calculated either from preovulatory surge of luteinizing hormone (LH) (65 ± 1 days) day of ovulation (63 ± 1 days) time of fertilization (60 ± 1 days)

Question 834

General principles of small animal pregnancy diagnosis

Answer 834

Detection of protein / endocrinological changes associated with pregnancy 2. Detection of the fetus or fetal membranes either directly or indirectly: Abdominal palpation Ultrasound examination Radiographic examination 3. Detection of physical changes in the dam which are associated with her accommodating a fetus (increased size of the uterus) 4. Detection of maternal changes that are secondary to endocrinological changes History When was she mated? Have you noticed any changes in size of abdomen/teats? Have you noticed any changes in behaviour? Have you noticed any vulval discharge? When was her last season?- if shes in luteal phase it could be pyo

Question 835

clinical signs of small animal pregnacy

Answer 835

Secondary Changes- Teat and mammary gland-more obvious in first timer- Reddening Enlargement Secretions- small amount o vaginal secretion at beginning Increase HR Physical Changes- Increased appetite Weight gain Abdominal enlargement in later pregnancy Relaxation of the perineal tissue/vulva

Question 836

Plasma Progesterone Concentration for pregnancy diagnosis in bithc

Answer 836

No rapid return to oestrus Not sufficiently different between pregnant and non-pregnant bitches this is why psuedo pregancy occurs can use plasma relaxin conc instead

Question 837

Plasma Relaxin Concentration for pregnacy diagnosis in the bitch

Answer 837

Values elevated in pregnancy from day 25 onwards and are diagnostic whilst a viable placenta is present better than progesterone

Question 838

when can abdominal palpation diagnose pregnancy in the bitch

Answer 838

From 21 days Before this, the pregnant and non-pregnant uterus is not reliably palpated Day 21 – 32 Aprox 1.5-3.5cm, round, firm and well separated “Chain of walnuts” After day 32 Gestational sacs become more confluent and lose their distinction - “sausages” After day 50 the puppies may be balloted directly

Question 839

radiography for pregancy diagnossi in the bitch

Answer 839

Limited use in early pregnancy as Fetal calcification after day 41-44 (av – 42d)- uterus may be seen to be enlarged but this may also be pyo So radiographic diagnosis from day 45 Can determine number, position and relative size of fetuses from d50 Valuable in dystocia cases gold standard for determining number

Question 840

ultrasonography for pregnancy diagnosis

Answer 840

Fetal structures from day 17 Fetal heartbeats detected from approx. 24-28 days of pregnancy Cannot assess number of fetuses Has limitations, particularly in early gestation Cannot be accurately used to count foetuses Fetal heart movements 28-30 days after ovulation IF known False negatives False positives

Question 841

using ultrasonography for gestational age

Answer 841

Appearance of certain organs E.g. kidneys last 20 days of gestation (see table for reference) Measurement of foetal dimensions – less useful in later gestation- Gestational sac (or chorionic cavity) diameter in early pregnancy Crown-rump length Head diameter Trunk diameter Nb. These measurements are breed-specific

Question 842

Pseudopregnancy

Answer 842

All entire non-pregnant bitches go through pseudopregnancy Long luteal phase (~66d) Clinical signs  Prolactin Covert/physiological Overt/Clinical Queen- Sterile matings Behaviours less commonly seen Hyperaemia of nipples as in pregnancy - red teats What do you do?- Nothing Prolactin inhibitors- Cabergoline (galastop, finilac) Bromocriptine Do not spay

Question 843

Pyometra

Answer 843

Occurs during the luteal phase Due to bacterial colonisation at oestrus Can be open or closed Most common in middle aged and elderly bitches Pyometra may also be induced by: therapeutic administration of oestrogens for treatment of unwanted pregnancy therapeutic administration of progestogens for prevention of oestrus

Question 844

Pregnancy Diagnosis (Queen)

Answer 844

Polyoestrous Return to oestrous confirms non-pregnancy BUT lack of return is not specific for pregnancy Behavioural changes not useful Physical changes.. Can be subtle Reddening of mammary glands d21 Enlargement of mammary glands d50 Manual palpation – d21-25 optimal Relaxin – d25 Ultrasonography – 3 weeks post mating Radiography – mineralisation of fetal skeleton at d40.

Question 845

Accidental Pregnancies

Answer 845

Indications: Unwanted mating (misalliance) Size mismatch Age High risk of dystocia Medical indications Get a good history +/- vaginal cytology Options: Surgical Approach- overyhystorectamy in late pregnacy ovaryectomy in early pregnacy- ONLY IN EARLY PREGNANCY 2. Pharmacological Approach Drugs that act on the uterus: Oestrogens e.g. oestradiol benzoate Alters transit time of zygote Within first 5 days of mating not common due to side effects Anti-progestogens Synthetic steroids that compete with progesterone Aglepristone (Alizin) Day 1 - 45 Drugs that act on the ovaries: Prostaglandins – luteolytic Bitch and Queen corpora lutea are ‘autonomous’ for first 15 days of luteal phase PG’s of little use before day 20 Repeated treatments are necessary dogs very sensitive to it so not first line Drugs that act on the pituitary gland: Dopamine agonists (prolactin inhibitors) e.g. bromocriptine and cabergoline No activity before 30d, moderate activity 30-40d Suspected/Early pregnancy – Aglepristone Mid-pregnancy 22-40 days – Aglepristone Confirm by USS before and after (10d), repeat if necessary Signs of parturition Late pregnancy >40d after mating PGF2a Dopamine agonists Combination

Question 846

Predicting parturition

Answer 846

Bitch A number of clinical indicators of impending parturition may be used, including: Measurement of progesterone and LH during oestrous Behavioural changes close to parturition- Restless Seek seclusion/excessively attentive Inappetant Nesting behaviour Shivering Clinical signs close to parturition- Relaxation of pelvic, perineal and abdominal musculature Increased HR Decline in body temperature Measurement of progesterone in late pregnancy- rappid drop indicates partuition Around ovulation assists in prediction of whelping dates: the date on which progesterone first exceeds 1.8 ng/mL (~2 ng/mL) predicted the day of parturition within: ±1 day – 67% precision ±2 days – 90% ±3 days - 100% Around due date: <2.8ng/ml = 99% chance of whelping within 48 hours <1.0ng/ml = 100% >5ng/ml = <2% chance of spontaneous parturition within 12 hrs Diagnostic imaging Queen Induced ovulator – ovulation follows mating by 24-36 hours Gestation = 52 to 74 days when recorded from the last mating or first mating to parturition, mean pregnancy length is 65– 66 days. No significant reduction in temperature

Question 847

stages of partuition- bitch

Answer 847

Stages: Stage of preparation Production of relaxin (placenta) Causes relaxation of the pubic symphysis, vulval and perineal tissues First stage parturition Onset of contractions Restlessness, nesting, temperature drop Second stage parturition Expulsion of the foetus Third stage parturition Expulsion of the placenta and foetal membranes Puerperium

Question 848

Dystocia

Answer 848

Normal birth = expulsive forces are sufficient to propel a fetus of normal size and disposition through a birth canal of adequate size Dystocia occurs if any of these are abnormal or insufficient. Inadequate expulsive forces Inadequacy of birth canal Presentation or disproportion (relative to the dam) of the fetus Defects of expulsive forces: Intrinsic defects of uterine contractility Nervous voluntary inhibition of labour Failure of contraction due to mineral/hormonal imbalances (primary inertia) Exhaustion of uterine muscle or depletion of pituitary oxytocin stores (secondary inertia) Defects in adequacy of birth canal: Functional disturbances of genitalia e.g. incomplete cervical dilation Obstructions e.g. neoplasia Pelvic malconformations e.g. brachycephalics or past #’ Management of primary inertia (49% of bitches, 37% queens): Exercise to stimulate contractions Digital stimulation (feathering) to stimulate endogenous oxytocin Calcium borogluconate IV No response to Ca oxytocin Perform a vaginal exam If not successful C-section Management of secondary inertia (23% of both): Correction of the cause of dystocia Nothing OR Ca2+, oxytocin C-sec as before. Is the birth premature or overdue? Has the dam given birth before – if so where there complications and what where these? What is known about the sire (and his size)? What has recently been observed in this bitch? Has there been recent vulval discharge? Have uterine / abdominal contractions been noted and if so when? Have any fetal membranes / fluid been expulsed? Have any fetuses been delivered?

Question 849

when to get involved in partuition of the bitch

Answer 849

Second stage parturition Expulsion of the foetus Weak, irregular straining for more than 2– 4 hours Strong, regular straining for more than 20– 30 minutes Fetal fluid was passed more than 2– 3 hours previously, but nothing more has happened Greenish discharge is seen but no puppy is born within 2– 4 hours (red-brown in the queen) More than 2– 4 hours have passed since the birth of the last puppy and more remain The bitch has been in the second stage of parturition for more than 12 hours.

Question 850

Foetal distress

Answer 850

Normal fetal HR = 180-240 bpm <180bmp = Foetal distress Foetal HR <150bpm at full term = immediate intervention required

Question 851

Emergency Cesarean Section indications:

Answer 851

Primary or secondary uterine inertia nonresponsive to medical therapy Uterine rupture or torsion Fetal malposition without success of correction by manipulation vaginally. Fetal death with remaining viable but distressed fetuses. Fetal distress with decreased heart rate. 150-180 bpm consider CS <150 bpm – immediate CS

Question 852

Reproduction management of the exotic female.

Answer 852

Approaches Traditional ventral abdominal midline (rabbits) Flank (guinea pigs and rats) Bilateral Unilateral Combination of the two Laparoscopic approach (zoo animals)

Question 852

Reproduction management of the exotic female.

Answer 852

Approaches Traditional ventral abdominal midline (rabbits) Flank (guinea pigs and rats) Bilateral Unilateral Combination of the two Laparoscopic approach (zoo animals)

Question 853

Reproduction management of the exotic femaleexotic male

Answer 853

Terminology ‘Castrate’ – removal of the testicles Scrotal Open Closed Prescrotal Open Closed Abdominal approach Vasectomy Vas deferens ligated and incised Medical management Implants Hormonal injections Options vary depending on the species Separation of the two sexes Isolation of social species  welfare implications Housing animals of same sex may lead to fighting implant-In response to testosterone ferrets produce sebaceous secretions and a musky odour Can place deslorelin implant, SC between scapulae every 18-24 months GnRH implan> Plasma FSH and testosterone concentrations, testis size and spermatogenesis were all suppressed after Deslorelin implant Owners to monitor >once testes increase in size again > time to place another implant

Question 854

Ferrets – Teaser/vasectomised males

Answer 854

Natural mating (vasectomised male/’teaser’ male) Good option for owners/working ferreters with many jills. Mating appears violent  biting and dragging the jill by neck Pseudopregnancy lasts approximately 42 days Increased aggression towards owners and cage mates Abdominal enlargement Mammary gland development Risk of disease transmission if vasectomised hobs shared. Will not change smell or hormonal behaviour Leaves options for future breeding of the female

Question 855

Vasectomy- ferrets

Answer 855

Vasectomised males are used to take jills out of oestrus without the risk of pregnancy Vasectomised ferrets will retain their musky odour, as this is dependent on testosterone levels. The spermatic cord is palpated cranial to the testis, and a 10 mm skin incision made directly over it, approximately 20 mm cranial to one scrotal sac The vaginal process is identified. The parietal tunica of the vaginal process is incised and spermatic cord is exposed The white vas deferens is identified and a short portion is separated from the spermatic cord. Double ligate at a distance of approximately 0.5cm and excise between the ligatures. Submission of excised tissue for histological examination is recommended, to confirm proper excision. Mild scrotal swelling may be observed postoperatively >usually resolves over 2–3 days The vasectomised hob should not be used for 7 weeks after surgery

Question 856

Ferrets – management of oestrus

Answer 856

Proligestone (Delvosteron, MSD Animal Health) Suppresses/postpones the breeding season – maintains jill in anoestrus Give 50mg per ferret in the Spring = 0.5ml per jill, administered via SC route Signs of season often reduced within 10 -11 days One injection often covers whole breeding season – but not always! Pyometra risk May be discontinued in 2023 Hormonal implant (Deslorelin acetate) GnRH agonist Licensed in males (9.4mg), off license in females 4.7mg used in both sexes but off license Reversible control of ovarian activity Ovarian suppression for approximately 18-24 months Easy to place as an outpatient Brief GA Placed SC between scapulae Surgical neutering Ovariectomy or ovariohysterectomy depending on concurrent disease Castration Permanent method Likelihood of developing adrenal disease.

Question 857

Spaying rabbits

Answer 857

prevents Unwanted pregnancies Uterine disease Cystic endometrial hyperplasia Pseudopregnancy Aneurysm Neoplasia Rabbits are sexually mature at 4-6 months Neoplasia – adenocarcinoma  50-80% in certain breeds >4 years old Free living European hares (feral) in Australia  21% of does had reproductive disease Post mortem examination in pet rabbits Mean year for neoplasia = 6 years Youngest with neoplasia confirmed = 12 months. Can we just perform ovariectomy? Does depend on how early uterine disease can occur. Anecdotally, reported in a 6 month old rabbit! Unique anatomy Two uterine horns Two cervices No uterine body Long and flaccid vagina Often large amount of uterine fat in mature rabbits Vagina fills with urine during micturition Techniques Ventral midline abdominal approach Ovariovaginectomy often described 2 cervices, empty directly into the large vagina Ligate ovarian pedicles and ligate at cranial vagina Ligature placed around vaginal side of cervices Risk of urine leakage through the vaginal stump Must use a transfixing ligature Oversew Risk of including ureters and blood vessels supplying the bladder if ligature placed too low. Other points to consider Prone to fat necrosis Adhesions ‘internal scar tissue’ form around devitalised or traumatised tissue. To minimise the risk of adhesions Minimise tissue handling, always use instruments Gentle surgical technique Care with haemostasis Never use dry swabs Irrigate tissues with warmed sterile saline Choose suture material wisely! Use the finest suture material that is practical Do not use biological sutures (cat gut)

Question 858

reproductive managment of rodents

Answer 858

Reproductive management of rodents often requires surgery Approach for the female Traditional ventral midline Flank

Question 859

flank approch to spaying in rodents

Answer 859

Find your landmarks. Identify The spine The last rib The pelvis Gentle simultaneous pressure on these three points will produce a bulge of soft tissue in the centre > incision site. Incise through skin (can be thick) Blunt dissect through muscles The external oblique Internal laminar muscles Once you have incised the muscle there will be internal fat Fat will be associated with The reproductive tract The kidneys The spleen The GI tract Retract the fat until you can see the distal uterine horn and ovary Ligate the ovarian pedicle In the guinea pig can perform whole procedure from the one incision In the rat often a bilateral flank approach is required. Ventral midline approach Large incision needed Challenging – deep body cavity, ovaries located cranially and dorsally Longer surgery time Longer recovery time If large ovarian cysts can still perform flank approach Remove fluid from cysts with a sterile needle and syringe.

Question 860

advantages and disadvantages of radiography

Answer 860

Advantages: Gives a global overview/screening Assessment of adjacent thorax and skeleton Good for detecting gas or mineralisation Very useful for acute conditions (particularly vomiting) Cheap and widely available Disadvantages: Superimposition of structures Lack of inherent radiographic contrast (cf. thorax) Soft tissue and fluid appear the same (water radiopacity) Magnification Less useful for chronic conditions (particularly diarrhoea)

Question 861

Minimising scattered radiation

Answer 861

Low kV, collimation, use of a grid

Question 862

Minimising scattered radiation

Answer 862

Low kV, collimation, use of a grid

Question 863

Avoiding movement blur in a radiograph

Answer 863

Appropriate physical +/- chemical restraint

Question 864

how would you deal with Low inherent contrast (soft tissue/fluid and fat) in a radiograph

Answer 864

Low kV (film)

Question 865

patient preparation for a radiograph

Answer 865

Fasted, empty bladder and bowels, clean coat

Question 866

important landmarks in an abdominal radiograph

Answer 866

Liver Stomach Spleen Kidneys Small intestines Colon Urinary bladder

Question 867

border obliteration

Answer 867

Mesenteric fat highlights the serosal surface of the abdominal organs Structures of the same opacity in contact with each other = border obliteration (border effacement/silhouette sign) e.g in acites- fluid has same contrast

Question 868

Abdominal Contrast Studies

Answer 868

Contrast media: Either more radiopaque or radiolucent than surrounding tissue Document function by taking sequential still images (e.g. barium series) or using real time radiography (e.g. fluoroscopy)

Question 869

describe a normal liver on a lateral radiograph

Answer 869

Roughly triangular in shape with smooth distinct margins- when enlarged edges will be rounded instead. Soft tissue opacity Demarcated by the diaphragm cranially and the stomach caudally- Gastric axis should between parallel to the ribs and perpendicular to the spine (lateral) and perpendicular to the spine (VD) entral lobe- Fairly sharp angle Extends to slightly beyond the level of the costal arch May see gall bladder ventrally in cat when it is small (hypoplasic)- Cranial displacement of stomach Absence of caudoventral angle Significance dependent on clinical signs, etc. seen inDeep-chested dogs

Question 870

hepatomegaly on a radiograph

Answer 870

Projection of caudoventral margin well beyond the costal arch Rounding of caudoventral angle Caudal displacement of stomach axis

Question 871

describe the normal spleen on a radiograph

Answer 871

Location and size variable- Smaller in the cat (usually not visible on lateral views) Flattened triangle on lateral view (tail of spleen) Triangular mass next to left abdominal wall on VD (head of spleen)

Question 872

Splenomegaly on a radiograph

Answer 872

Generalised splenomegaly is common Subjective assessment Wide normal range Overlap maximum physiological/ minimum pathological size Spleen enlarges following ACP / barbiturates Localised splenomegaly- Look for changes in shape as well as size

Question 873

describe the stomach on radiograph

Answer 873

Rugal folds are often seen as parallel linear soft tissue opacities If the stomach is completely collapsed and empty it may not be seen at all Recap: Fundus and body lie to left of midline Pylorus to the right and ventrally radiographs of the stomach can show- Changes in location, size, shape and margination

Question 874

describe the small intestine on radiograph

Answer 874

Pylorus and duodenum are identifiable by location Rest of small intestine fills “the space where there is nothing else!” Cats tend to have less intestinal gas than dogs Roughly even diameter throughout Diameter in(dogs): <1.4 x L5 unlikely obstructed >2.4 x L5 likely obstructed Look at the shape and distribution of the intestinal loops Symmetrical peristaltic constrictions Beware of “pseudo-thickening” SI (or stomach) wall may appear thickened in plain images with partial filling with gas

Question 875

viral causes of bovine Diarrhoea

Answer 875

-Rotavirus -Coronavirus -Bovine Viral Diarrhoea- young stock

Question 876

bacterial causes of bovine Diarrhoea

Answer 876

•E.coli •Salmonella species- agressive mortality rate •Clostridia species •Mycobacterium paratuberculosis (Johne’s)- slow incubation- vertical infection as calves, presents at 3-5 ears

Question 877

Parasitic causes of bovine Diarrhoea

Answer 877

Protozoal: •Cryptosporidium- disease of hygene •Cocci Worms: •Strongyles •Fluke

Question 878

Nutritional causes of bovine Diarrhoea

Answer 878

•Milk scours •Peri-weaning Scours •SARA •Grain overload •Dietary changes

Question 879

Environmental & Husbandry causes of bovine Diarrhoea

Answer 879

Exposure to pathogens usually as a result of failed husbandry -Failure passive transfer of antibodies -Poor hygiene of equipment -Poor hygiene of housing -Mixing of age groups -Stress

Question 880

Scour Check Kits

Answer 880

•Used to detect common pathogens in young calves •Rotavirus, Coronavirus, Cryptosporidum& E. coli •Can be used on farm, results in 10 minutes from small faecal sample •Easy to interpret -two lines positive, one line negative

Question 881

Faecal Worm Egg Counts for scours

Answer 881

•Preparation of faeces in a salt solution to look for worm eggs or cocci oosysts •Quick test to indirectly assess parasite burden •Test performed off farm either in-house or sent off to external lab •Used to look for gut worms and cocci oocysts in youngstock & adults •Can also be used in series to test wormer efficacy

Question 882

Faecal Culture for scours

Answer 882

•Microbiology for bacterial causes of GI disease. •Can be used for Salmonella, Johnes, Clostridial toxin detection and Rota/Coronavirus •Can be done in-house or sent to external lab •Can be slow to yield results

Question 883

Serology for scours

Answer 883

•Blood sampling for specific diseases •Can be used if clinical suspicion of Johnes or BVD at an individual animal level •Tested in an external lab

Question 884

bulk Milk Surveillance for scours

Answer 884

•Used to monitor disease in adult cows •Can be used to monitor Fluke, BVD, IBR, Johnes, Salmonella •Useful comparing results year on year •Take into account vaccination status for some diseases when interpreting results

Question 885

disease of the caecum in the horse

Answer 885

One of the most common diseases of the caecum in horses is impaction: Type 1 = accumulation of dry ingesta Poor dentition? Sand Type 2 = abnormal caecal motility resulting in a more fluid consistency Much more likely to rupture than the colon much more prone to rupture than any other part of horse gastro tract Caecocolic intussusception- colon intercepts into caecum, possibly assosiated with tape worms Unclear pathogenesis Motility issue Ileocaecal intussusception more common Inflammation of the caecum is referred to as typhlitis Cyathostomins- mass emergances, may not cause clinical signs Anoplocephala perfoliata Small strongyles also known as cyathostomins, are extremely prevalent amongst the equine population worldwide. Horses can carry large worm burdens without displaying clinically significant symptoms and with a negative faecal worm egg count The clinical syndrome of larva. cyathostominosis (cyathostomiasis), occurs as a result of mass emergence of hypobiotic intestinal stages. High fatality rates due to diffuse severe and acute damage to the caecal mucosa.

Question 886

Caecal infections in birds

Answer 886

Protozoa predominate as the cause of infectious typhlitis in poultry; Eimeria tenella- Variably severe clinical signs Major disease of production Exudative to erosive DIFFERENT STRAINS INFECT DIFFERENT PORTIONS OF THE TRACT Histomonas meleagridis- Spread by a worm Turkeys and peafowl Caecal cores Necrotizing typhlitis Hepatitis Caecal cores can also be seen in Salmonella enterica Pullorum Other systemic signs- SEPTICEMIA

Question 887

Right dorsal colitis

Answer 887

NSAID use in horses, as well as being associated with gastric ulcers and renal papillary necrosis, can result in right dorsal colitis Due to decreased production of prostaglandin via NSAID inhibition of (COX-2) resulting in vasoconstriction.

Question 888

Infectious colitis

Answer 888

Oedema disease of pigs Enterotoxaemic colibacillosis E. coli F18 Pathogenesis: Associated with dietary changes at weaning Bacterial overgrowth in small intestine Produce verotoxin (Shiga-like) Necrosis of enterocytes and endothelial cells Leakage from vessels results in oedema, which in the brain results in swelling and neurological signs Classical gross post mortem presentation is marked oedema of the spiral colone E.coli Swine dysentery- Necrohaemorrhagic enterocolitis Brachyspira hyodysenteriae Salmonellosis Histiocytic ulcerative colitis Boxer dogs and their kin E. coli Histiocytes - granulomatous

Question 889

E. Coli

Answer 889

Escherichia coli is one of the first bacteria to colonize the GIT of infants and establishes as a life-long resident of the normal intestinal microbiota in humans (Eggesbø et al., 2011). Non-pathogenic E. coli strains provide benefit to the host in many ways, including aiding absorption of vitamin K and B12 (Blount, 2015) Some E. coli strains can cause disease: Enterotoxigenic (ETEC)- covers villi, produces enterotoxins IT and ST resulting in endocytosis Enteropathogenic (EPEC)- structural injury to enterocites resulting in loss of microvilli and osmotic dirhoea and secretory dihroa Enterohaemorrhagic (EHEC)- easirer to see post mortem- lysis, damage to cells, haemoragic E.coli can be typed according to their various pathogenicity factors and surface markers Adhesins (fimbriae or pillia)- Fimbriae commonly found in pigs: F4 (K88), F5 (K99), F6 (987P), F18, F41 Toxins Serotype (O, H, K)

Question 890

Salmonellosis

Answer 890

All salmonella species are enteroinvasive Zoonotic and reportable enterica species serovar Typhimurium - Second most important cause of food poisoning in humans Pathogenicity factors include ability to neutralise NO in phagocyte-Are phagocytosed but able to survive within phagolysosome Pathophysiology: Septicaemia- Fibrinoid necrosis of vessels and DIC Hepatitis and pneumonia S. choleraesuis Acute enteric - Necrotising ileotyphlocolitis S. typhimurium Chronic enteric- Button ulcers – ddx classical swine fever S. typhimurium Rectal strictures

Question 891

Trichuris

Answer 891

Trichuris spp. Whipworm Carnivores, ruminants, pigs people Direct life cycle Clinical signs- Transient, recurring large bowel diarrhoea with or without blood Rarely, severe infestations result in pseudo-Addison’s

Question 892

Histiocytic ulcerative colitis

Answer 892

Boxer dogs and their kin genetic issue with response to E. coli Histiocytes - granulomatous

Question 893

Rectal prolapse

Answer 893

Often secondary to inflammation But can be due to other reasons Dystocia Urinary disease Perineal hernia

Question 894

Anal furunculosis

Answer 894

breed issue- GSDs Immune-mediated Peri-anal fistulation- A fistula is an opening between areas of the body that are not usually connected. In this case between the anus and skin Furunculosis is generally a term used to imply a deep infection of the dermis, typically with ruptured hair follicles and free hair shafts which themselves add to the immune reaction

Question 895

Epithelial tumours of the canine intestine

Answer 895

tend to be upper GIT In the cat, more commonly lower GIT Papilloma and polyp- dachhound Adenoma Carcinoma

Question 896

causes of colic

Answer 896

Smooth muscle spasm Inflammation- Colitis / Ulceration Distension Impaction- Gas accumulation Obstruction Impaction- Tension on the mesentery Displacement Tissue congestion/infarction/necrosis- Torsion/volvulus Strangulation (both could cause endotoxaemia- gut wall is compromised and horse absobs endotoxins from gut bacteria, causing systematic reaction)

Question 897

Clinical Signs of Colic

Answer 897

Inappetence Reduced faecal output Vocalising/grunting Agitation Pawing at the ground Lip curling Flank Watching Lying down- For long periods, Repeatedly Stretching to urinate Rolling / Thrashing Sweating excessively Straining Mild signs – Restless, Pawing, Flank watching Gas build up / inflammation of GIT / Smooth muscle spasms Moderate signs - Lying down flat out, groaning Impaction or other simple obstruction Very fractious, violent rolling Acute, severe strangulation Dull, unresponsive End-stage – Severe illness due to colic

Question 898

“False” colic

Answer 898

Any non-gastrointestinal source of abdominal pain Liver disease / hepatomegaly Urinary disease- Renal pain Bladder Dz (urolithiasis) Peritonitis Intra-abdominal abscess Intra-abdominal neoplasia Reproductive disorders- displacments post foaling Other Non-abdominal, pain mistaken for colic Oesophageal obstruction Rhabdomyolosis (tying-up) Laminitis Pleuroneumonia

Question 899

clinical exam for colicing horse

Answer 899

Aim of clinical examination is to; Assess the severity of the horse’s condition Establish appropriate ‘level’ of treatment Conservative ‘in-field’ treatment Referral for more intensive medical therapy Referral for surgical intervention Examination should be targeted, quick but thorough – be systematic doese not need to be full clinical examination- aim is to establish prognosis Observe from a distance Current status of colic- Pain or signs of depression Respiratory rate & depth Abdominal distension Presence of faeces Evidence of duration / severity- Traumatic injuries Disrupted bedding Shavings/soil on back Rapid assessment of cardiovascular status- Heart Rate Pulse quality Jugular refill MM Colour CRT this can show the difference between normal and endotoxaemia Moisture content of oral MM is an assessment of hydration status; if bad horse should be reffered for fluid therapy Assessment of hydration status & hypovolaemia- dehydration mm moistrure heart rate- heart rate of 80= tahcycardia and horse is cardiovascularyly compromised CRT PCV lactate- indicates anarobic respiration- necrosis ect Assessment of Gastrointestinal Tract Auscultation - GIT borborygmi of the ascending colon (caecum & LC) Auscultation of GIT has some degree of specificity but low degree of sensitivity. Hypermotility- Increased smooth muscle activity - ‘spasm’ colic Local hypomotility- Localised stasis of GIT General absence- GIT ileus – common finding in most colics Very useful for monitoring cases – e.g. progressive loss of motility - =Absent + =Hypomotile ++ =Normomotile +++ = Hypermotile Other assessment: Rectal Temperature- Most uncomplicated colics will have normal rectal temperature- Low core temp – usually associated with severe/end stage shock- Pyrexia – Can indicate alternate diagnosis, e.g. peritonitis Digital pulses – not appropriate to assess circulation – only useful to assess for presence of laminitis Respiration: Tachypnoea – usually due to pain, but could be associated with endotoxaemia (metabolic acidosis) Detailed auscultation of lungs rarely necessary Pain and colic assessment- Pain will only cause a mild-moderate increase in HR (40-60bpm) Marked-severe tachycardia (>60bpm) is a sign of hypovolaemia Pain will cause tachypnoea Pain can make it very difficult to examine the horse Administer quick-acting, potent analgesic alpha 2-agonist Xylazine (Rompun, Virbaxyl), Detomidine (Domosedan), Romifidine (Sedivet) +/- opioid- Butorphanol (Torbugesic ) Try to assess CV status before giving alpha 2-agonist

Question 900

diagnostics for colic

Answer 900

Nasogastric Intubation: Nasogastric reflux Fluid/ingesta reflux from the stomach >2 Litres of fluid is abnormal Usually indicative of small intestinal obstruction (physical or functional) Can occur due to LC displacement (pressure on duodenum) Presence of gastric reflux has significant diagnostic value Majority of cases with reflux need referring to hospital Relieving reflux is also very therapeutic >8L will stretch stomach and be a significant source of pain Trans-Rectal Examination (TRE): Abnormalities: - Impaction - Distension (Gas accumulation) - Displacement - Masses Abdominocentesis- Assess for presence of changes in peritoneal fluid- good prognostic indicator Serosanguineous colour change and or Increased protein concentration- Serosal compromise – leakage of blood components Increased Lactate concentration- Anaerobic tissue metabolism Presence of ingesta- Rupture of GIT tract High WBC count- Peritonitis Abdominal Ultrasonography: Adjunctive to all other examinations Can assess structures not palpable on rectal Excellent for assessing; Thickness of intestinal wall Distension of small intestine Motility of intestine Presence of displacements Peritoneal fluid Foals – can visualise entire abdomen

Question 901

treatment for colic

Answer 901

Analgesia Imperative to provide some form of analgesia to a colic case NSAID- The most common form of analgesics used to treat colic Slow onset and long duration of activity Flunixin meglumine (Finadyne Solution)- 1.1 mg/kg iv Potent visceral analgesic Can masks deterioration in CVS status Ketaprofen (Ketofen) 1.1 - 2.2mg/kg iv Phenylbutazone (Equipalazone Injection) 4.4mg/kg iv Alpha-2 agonists Potent analgesics with rapid onset and short duration of action Allow rapid re-assessment of case progression Xylazine (Rompun, Virbaxyl) Dose rate: 0.2-1.1mg/ml Analgesia for 15-20min Detomidine (Domosedan) Dose rate: 0.01-0.02mg/kg Analgesia for 1-2 hours Romifidine (Sedivet) Dose rate: 0.04-0.08mg/kg Analgesia for 1-3 hours Opiods Not first line analgesic Usually reserved for higher degree of pain Butorphanol (Torbugesic) 0.05-0.075mg/kg iv Potent analgesic; 1 hour duration Spasmolytics (Anticholinergics)- N-Butylscopolamine (Buscopan Injectable ) Smooth muscle relaxant Rapid onset and short duration of activity Good for; Treating hypermotile/spasm type colic ‘Gas’ colic Relaxing rectum prior to rectal examination General Rules For first-line treatment, or where diagnosis is uncertain, use short acting analgesic agents Assessing progression, rapid recurrence of pain or deteriorating CV status is vital in the decision to refer Beware the potent anti-inflammatory effects of flunixin, which can significantly ‘mask’ the early signs of endotoxaemia. Only administer NSAIDs after the diagnosis or CV status have been established Fluid Therapy: Enteric fluids Indicated in the vast majority of colic cases- Most cases will have a degree of dehydration Contraindicated if NG reflux is present, or suspect small intestinal lesion Excellent way to rehydrate the colonic content (impactions) Bolus(es) of isotonic fluids (tap water + NaCl + KCl) 5-8L can be given q2hrs Purgatives Liquid Paraffin; Magnesium Sulphate (Epsom Salts) Decision to refer- Essentially, any indicators that the case won’t resolve with simple conservative therapy (analgesics & enteric fluids) Non-response to analgesia Significant CV compromise Rapid deterioration despite therapy Complex abnormalities on rectal exam Presence of NG reflux Recurrent/chronic cases with unclear Dx 82.9% survival rate for 1st opinion cases

Question 902

Approach to Weight loss in the Horse

Answer 902

Reduced Intake?- Not wanting to eat Disease or chronic pain Not able to eat Dental disease or Dysphagia Not being allowed to eat Social hierarchy Not being fed enough Poor or Inadequate diet Poor Absorption?- Inadequate presentation of nutrients Dental Disease Gastrointestinal Disease Parasitism Diarrhoea Ulcerative GI disease Inflammatory disease - Small Intestine, Colon, both Neoplasia - Lymphoma Decreased Utilisation?- Disorder of nutrient metabolism Liver Disease Excessive Loss?- Protein losing enteropathy Increased Requirement ?- Increased demand/Consumption Bacterial infections Chronic Viral infection Neoplasia

Question 903

HYPOALBUMINAEMIA

Answer 903

Loss of albumin Protein losing enteropathy Protein-losing nephropathy Chronic blood loss Reduced production Hepatopathy Malnutrition Chronic inflammation Negative acute phase protein Anaemia Low grade, normocytic normochromic (non-regenerative) anaemia is also common finding in weight loss “Anaemia of chronic disease” Decreased RBC production Reduced RBC lifespan

Question 904

gasteroscopy for weight loss in the horse

Answer 904

Weight loss generally only present in more advanced cases of gastric ulceration Altered or reduced appetite Delayed gastric emptying Other forms of GIT ulceration could cause weight loss through causing malabsorption Right dorsal colitis associated with NSAID toxicity Gastroscopic examination used to obtain trans-endoscopic duodenal mucosal biopsies Indicated where there is evidence of small intestinal malabsorption

Question 905

Abdominal Ultrasonography for weight loss in the horse

Answer 905

In context of weight loss, can give information on; Thickness of Small intestine and Colon Assess characteristic of thickening Are mural layers visible? Peritoneal fluid volume Presence of intra-abdominal masses Liver evaluation (or u/s guided biopsy)

Question 906

Abdominocentesis for weight loss in the horse

Answer 906

Assess for presence of changes in peritoneal fluid Low sensitivity, but good specificity for: Peritoneal inflammation / Bacterial involvement WBC > 5 x109/l Protein concentration > 20g/l Increased Lactate concentration Serosanguineous colour change Neoplasia Rare to diagnose intra-abdominal neoplasia on PF alone <50% solid tumours exfoliate cells Usually presents as low grade peritoneal inflammation

Question 907

Oral Glucose Absorption Test (OGAT)

Answer 907

Simple and inexpensive test to assess absorptive capacity of small intestine Normal Approximate doubling of baseline serum glucose 2 hours after dosing (70-100% increase) Partial Malabsorption 15-65% increase in serum glucose at 2 hours, or slower to peak Total Malabsorption Serum glucose not increasing above 15% of baseline

Question 908

Faecal Blood Test

Answer 908

Evidence of frank blood in faeces indicates colonic/rectal bleeding (Upper GIT bleeding is digested in the colon so not represented in faeces) Faecal Occult blood test Detects albumin and haemoglobin separately Proposed to differentiate between different sources of pathology Varying evidence for diagnostic value

Question 909

Osmotic Diarrhoea

Answer 909

results from the presence of osmotically active, poorly absorbed solutes in the bowel lumen that inhibit normal water and electrolyte absorption. Certain laxatives such as lactulose and citrate of magnesia or maldigestion of certain food substances such as milk are common causes of osmotic diarrhea.

Question 910

Secretory Diarrhoea

Answer 910

occurs when your body secretes electrolytes into your intestine. This causes water to build up. It can be caused a number of factors, including: bacterial infection such as salmonella and E. coli.

Question 911

diarrhoea caused by Increased gut mucosal permeability

Answer 911

ncreased intestinal permeability or hyperpermeability. That means their guts let more than water and nutrients through — they “leak”.

Question 912

diarrhoea cause by Abnormal gut motility

Answer 912

hypermotility can casue this

Question 913

SI Diarrhoea

Answer 913

normal to large volume watery Melaena- Black colored stools that occur as a result of gastrointestinal bleeding. This bleeding usually comes from the upper gastrointestinal (GI) tract, which includes the mouth, esophagus, stomach, and the first part of the small intestine. borborygmi- the sound that the stomach and intestines make as food, fluids, and gas move through them. weight loss +/- vomiting inappetance *SI can still be urgent

Question 914

LI Diarrhoea

Answer 914

Urgency/increased frequency straining/tenesmus haematochezia- Rectal bleeding (or haematochezia) is the passage of fresh blood per rectum small volume passed more often mucus fresh blood “incontinence”

Question 915

Adsorbants

Answer 915

May reduce diarrhoea Efficacy not proven Kaolin Pectin Chalk Bismuth subsalicylate Magnesium aluminium silicate Activated charcoal Alter intestinal flora/bind flora Coat or protect mucosa Absorb toxins Bind water and possibly antiscretory

Question 916

Faecal analysis

Answer 916

Is it infectious?  History Systemically unwell D+ is acute & haemorrhagic D+ is very severe Multiple animals in crowded environment Owner or pet is immunocompromised Faecal – parasites – SNAP Giardia/ELISA Faecal – virology– SNAP Parvo Faecal for microbiology? Bacteria – Salmonella, Campylobacter, Clostridia (Viruses) Faecal for parasites – OR JUST TREAT? Nematodes Cestodes Giardia – multiple pooled samples?

Question 917

Trypsin-like immunoreactivity

Answer 917

Exocrine Pancreatic Insufficiency Clinical signs: Steatorrhea - fatty loose faeces Dramatic polyphagia Weight loss

Question 918

Stages of vomiting

Answer 918

Prodromal phase: Nausea- Hypersalivation Loss of appetite Lip licking Excessive swallowing Retching Retrograde duodenal contractions Rhythmic inspiratory movements against a closed glottis Dilation of the cardia and low oesophageal sphincter Expulsion Reduced oesophageal and pharyngeal tone Contraction of abdominal muscles to actively expulse gastric/duodenal contents Programmed, overlapping and coordinated events help minimise risk of adverse events such as aspiration

Question 919

The vomiting reflex

Answer 919

Two separate centres CRTZ Humoral pathway chemical stimuli BBB is permeable in the area of the CRTZ Vomiting centre in brainstem Several brain stem nuclei Receives nerve impulses via 2 (neural) pathways: Central Peripheral coordinates and integrates vomiting Also Vestibular apparatus input for motion sickness Substance P neurotransmitter binds to NK-1 receptors NK-1 receptors location: cell membrane vomiting centre CRTZ

Question 920

Dysphagia

Answer 920

can be mistaken for vomiting Gagging Dropping food Retching Difficulty eating Exaggerated swallowing Ptyalism Fear of eating swallowing difficulties

Question 921

Maropitant

Answer 921

Anti-emetic selective NK1 receptor antagonist effective against peripheral pathways central pathways Visceral analgesia in cats

Question 922

Metoclopramide

Answer 922

Anti-emetic dopamine, 5-HT3 & H1 receptor antagonist central>peripheral pathway effects variable prokinetic effect cats & dogs

Question 923

indications to investigate vomiting

Answer 923

History: several days duration or fast deterioration persistent vomiting “not keeping anything down” haematemesis blood? coffee grounds? SI diarrhoea weight loss Concurrent signs (anorexia, fever etc) Physical examination: weak, collapsed mm: dry/tacky, pale or congested tachycardia, bradycardia, arrhythmia weak & thready or hyperdynamic pulses hypothermia or pyrexia abdominal pain or distension melaena, haemorrhagic diarrhoea

Question 924

vomiting resulting from Primary GI problem

Answer 924

Primary disease should be suspected if: An abnormality is palpable in the gut e.g. foreign body The vomiting is associated with significant and concurrent diarrhoea The patient is clinically and historically normal in all other respects The onset of vomiting significantly preceded any development of signs of malaise – depression and/or anorexia. The vomiting is consistently related in time to eating (although this can also occur with pancreatitis)

Question 925

vomiting results from a Metabolic problem secondarily causing GI signs (secondary GI disease)

Answer 925

Often have evidence from the history and/or clinical exam of abnormalities affecting other organ systems e.g. jaundice/PUPD Vomiting is usually intermittent, unrelated to eating and may often occur subsequent to the onset of other signs of malaise. Generally not usually bright, alert and happy. Usually ill (depressed/inappetant) before vomiting was observed. Exception to the rules: Pancreatitis. Secondary GI disease diagnostics: Biochemistry, haematology Urinalysis +/- imaging

Question 926

Patients that are unable to digest carbohydrates effectively may require

Answer 926

an increase in protein provisions in place of carbohydrates. However, high protein diets may be contraindicated in patients with co morbidities such as hepatic disease, pancreatitis and renal disease

Question 927

calorie dense diets

Answer 927

Fat is calorie dense so is indicated to critically ill patients where nutritional volume is difficult to consume. Therefore, calorie dense diets allow for a reduced portion of food to be given. High fat content diets ,however, are contraindicated in cases of pancreatitis.

Question 928

Resting energy requirement (RER)

Answer 928

the energy (number of calories) required for normal function in fasted patients under thermo-neutral conditions. RER = 70 x (bodyweight BW in kg)0.75 OR For animals weighing 3kg-25kg RER = (30 x BW in kg) +70 The calculated RER should always be viewed as a starting point and feeding volumes can be adjusted as required, depending on the status and progression of the patient. Water volumes should also be taken into consideration, especially when using a diet which requires blending as fluid overload may occur. Diluting food with water will dilute the calories and reduce calorific density. Tube flush volumes should be recorded and included in the total volume per feed guidelines. Enteral feeding of anorexic patients should commence with one third of the patient’s total RER for the first 12 to 24 hours.  If well tolerated, this amount can be increased every 12 hours until full RER is reached. If the patient vomits, feeding should be discontinued until vomiting has resolved. Thereafter reduce the volume when feeding is resumed and increase the volume more slowly.  Excessive nutrition during times of illness may increase the risk for hyperglycemia and other metabolic complications so should be avoided. Feeding frequency is determined by hospital hours, staff availability, and patient tolerance of volume fed. Ideally, feeding frequency can be every 4 to 6 hours initially and later decreased to every 6 to 8 hours after it is clear that the patient can tolerate the feedings. 

Question 929

calculating energy requirements

Answer 929

Weigh the patient (regularly) Calculate the RER. This will give you the number of calories required per day (kcal/day) Select the appropriate diet for the patient and the type of feeding tube Divide the energy requirement of the patient (kcal/day) by the energy content of the diet (kcal/ml or gram) to provide the daily amount of food required Divide the total amount of food per day by the number of feeds per day Do not exceed 5-10ml/kg per feed when reintroducing food Write up the feeding plan and keep a detailed record.

Question 930

Entereal vs Parenteral nutrition

Answer 930

Enteral = giving nutrients into the GI system i.e. assisted feeding  Parenteral = giving nutrients IV, sometimes via central line IF THE GUT WORKS… USE IT! – Enteral feeding best option if possible Parenteral is more complicated and expensive than enteral feeding. There is also a risk of villous atrophy and risk of bacterial growth at the line site if not kept clean. 

Question 931

Feeding Tubes 

Answer 931

There are 4 main types of feeding tubes which can be placed for assisted feeding in dogs and cats: 1.  Naso-oesophogeal (NO) or nasogastric (NG) tube- most commonly used as they are easiest to place and manage 2.  Oesophagostomy (O) tube  3.  Gastrostomy (PEG) tube  4.  Enterostomy or jejunostomy tube- usually placed during abdominal surgery and are reserved for patients with gastric or pancreatic disease. They require a near constant infusion of commercially prepared diet.  Tubes are named for where they enter the GI tract.  Tube selection will depend on multiple factors… Patient condition Illness/injury Food required Availability of resources including staff Financial factors Duration of assisted feeding required

Question 932

Naso-oesophageal Tube

Answer 932

Small bore tube passed through the nostril of the patient  Indicated in any patient with malnutrition that will not undergo oral, pharyngeal, esophageal, gastric, or biliary tract surgery Can be placed conscious so no need to GA potentially high-risk patient  In place for 3-5 days (up to 10 days) Small bore tube so requires commercially prepared liquid diet  Advantages – easy to place – no GA required, cheap, can be used immediately and removed at any time, patient can eat and drink around the tube   Disadvantages – short term use only, sometimes patient removes them as irritate the face, placed at the head end – can be difficult to manage in patients that bite, can only give liquid oral medications, not crushed tablets, can increase risk of reflux 

Question 933

Oesophagostomy tube 

Answer 933

Surgically placed into the oesophagus  (GA required) Oesophagostomy tube feeding is indicated in anorexic patients with disorders of the oral cavity or pharynx, or anorexic patients with a functional gastrointestinal tract distal to the oesophagus. E.g jaw fracture Contraindicated in patients with a primary or secondary oesophageal disorder (e.g., oesophageal stricture, after oesophageal foreign body removal or oesophageal surgery, esophagitis, megaesophagus). Wider bore tube than NG  Can prepare own diets ( blended in ‘gruel’ form) or use commercially prepared  Can be left in place for weeks/months Advantages – easy to place and manage, can feed own blended diet, the patient can eat and drink around the tube, can be removed at any time, can give crushed oral medications Disadvantages – requires short GA to place, at the head end so can be difficult in patients who bite, requires some wound management and risk of local infection at placement site, rarely stricture can form where tube enters oesophagus  

Question 934

Gastrostomy tube  

Answer 934

Placed directly into stomach through body wall, bypasses oral cavity and oesophagus  Gastrostomy tube placement is contraindicated in patients with primary gastric disease (e.g., gastritis, gastric ulceration, gastric neoplasia) or disorders causing persistent vomiting. Must stay in place for 10-14 days (minimum 7 days) after placement to allow 'seal' to form between stomach and abdominal wall, preventing leaks into abdominal cavity which may lead to pancreatitis  Can be left in place for months-years (tube may need to be replaced but this can be performed through the same stoma)  Advantages – long term use, further from head so can be easier to manage in patients who bite, large bore tube so can feed variety of diets in larger volumes, can give crushed medications Disadvantages – unable to use immediately after placement (24 hours), requires GA to place, risk of local infection at placement site, risk of pancreatitis/peritonitis if incorrectly placed and ‘leaks’

Question 935

Jejunostomy Feeding Tube or “J-tube”

Answer 935

Invasive, challenging to place Mid-long term support Bypasses upper GIT Patient if able to eat via the oral route still whilst tube is in place if required Jejunum does not have storage capacity Required trickle feeding NOT bolus feeding Tend to be referral cases

Question 936

Total Parenteral Nutrition (TPN)

Answer 936

The practice of feeding the patient via the intravenous route (usually by a central venous catheter) Used on short term basis (3-5 days) Reserved only for use when: The patient is unable to be fed enterally e.g. failure of the GIT The patient is at an increased risk of aspiration Other methods of assisted feeding have failed to ensure adequate intake of nutrition TPN aims to meet all of the patients energy and protein requirements Partial parental nutrition (PPN) aims to meet some of the requirements, alongside other methods of nutritional support e.g. tube feeding Intensive nursing required

Question 937

Postural Feeding

Answer 937

Typically used for patients presenting with Megaoesophagus Daily food intake should be split into 3 – 4 smaller meals a day Food should be soft wet food – never hard kibble Ideal the patient should be in a sitting position During each meal, the wet food should be rolled into small balls and fed from a height

Question 938

HYPERNATRAEMIA 

Answer 938

s a deficit of water relative to sodium and can result from a number of causes, including free water losses, inadequate free water intake, and, more rarely, sodium overload

Question 939

MALOCCLUSION 

Answer 939

the teeth are not aligned properly

Question 940

•VOLVULUS SYNDROME

Answer 940

occurs when a loop of intestine twists around itself and the mesentery that supports it, causing bowel obstruction

Question 941

Scald/Ovine Interdigital Dermatitis

Answer 941

Seen in sheep continuously exposed to wet pasture – often lambs but can be seen in housed ewes when straw becomes wet and warm Fusebacterium Necrophorum – can be zoonotic – human wounds have been swabbed and F. Necrophorum found – wear gloves when examining lame sheep! Mild and transient lameness, rapidly resolves with treatment Dermatitis involving some or all of the skin between the claws of the feet – skin between claws appears red and inflamed with white discharge V common, less important than footrot/CODD, but associated with pathogenesis of foot abscesses and foot rot

Question 942

Footrot

Answer 942

Footrot – 90% of lameness in the national flock Dichelobacter Nodusus (Bacteroides) BUT needs F. necorphorum to facilitate epidermal invasion D.nodosus – obligate parasite, can’t survive in the environment for more than 1 week Also requires devitalised skin – chronic exposure to wet conditions and faecal contamination Fly strike can occur in affected feetVery effective vaccine against footrot. Acts as treatment and prevention. Timing is important A second injection can be needed 4-6 weeks One injection will last 6 months. Diagnosis is essential genetic element to susceptibility to scald and footrot.

Question 943

CODD

Answer 943

Contagious Ovine Digital Dermatitis Relatively ‘new’ disease – ongoing research Bacteria – treponeme species. Some association with cattle with Bovine Digital Dermatitis Link between CODD and footrot Usually SEVERE lameness with one claw of one foot affected Initially ulcers develop on the coronary band which then under-run the hoof, can lead to whole hoof avulsion Graded 1-5 Can lead to permanent hoof growth problems Often needs systemic treatment with antibiotic and NSAIDs

Question 944

White line separation

Answer 944

Often individual rather than ‘whole flock’ issue Unknown aetiology – walking on stony ground, nutritional imbalance? ‘Shelley Hoof’ Separation of the hoof wall from the underlying tissues Lameness caused by dirt packing into space created Can lead to abscess formation

Question 945

Toe Granuloma

Answer 945

Painful red swellings caused by: Over-trimming Chronic untreated lesions Chemical irritation

Question 946

Joint Ill

Answer 946

Most common – Septic arthritis ‘Joint-ill; Strep. Dysgalactiae, (e.coli, erisypelas sometimes isolated in older lambs) Transmission still unknown – cord/tagging/tailing/castrating/oral/vaginal canal? Vaginal canal transmission thought to be most significant Septic arthritis = swollen joints, ill thrift, death 1-2% of flocks, can be up to 50% of lambs in severe outbreaks Lamb outdoors if possible! Reduces bacterial load for newborn lambs Research evidence suggests that wearing long disposable gloves for lambing will be the most effective method to reduce the prevalence within a flock

Question 947

Hyaline Cartilage

Answer 947

The principal component of hyaline cartilage is type II collagen. Collagen: The most abundant protein in mammals (up to 35% of the proteome). At least 28 different types of collagen. Made of amino acids, wound to form a triple-helix, which are aligned in elongated fibrils (there are also non-fibrillar collagens). Hyaline cartilage components… Collagens Aggrecan Hyaluronan Link protein COMP Decorin Fibromodulin Fibronectin Chondroadherin

Question 948

Equine Osteoarthritis (OA)

Answer 948

Age-related degenerative musculoskeletal disease. Loss of articular cartilage, abnormal bone proliferation, synovial membrane dysfunction and subchondral sclerosis. Commonly affects hock, pastern, coffin, fetlock, carpal (knee) and stifle joints. Estimated that up to 60% of equine lameness is related to OA. Leading welfare issue in horses - resulting in substantial morbidity and mortality. Abnormal loading (physiological strain) of normal cartilage or Normal loading (physiological strain) of abnormal cartilage or Both: Abnormal loading (physiological strain) of abnormal cartilage Initially, OA was been considered to be a disease of articular cartilage. However, recent research has indicated that the condition involves the entire joint. Loss of articular cartilage - thought to be the primary change, but a combination of cellular changes and biomechanical stresses causes several secondary changes. Secondary Changes: Subchondral bone remodelling Osteophytes Bone marrow lesions Changes in the synovium Changes in the joint capsule Changes in the ligaments Changes in the peri-articular muscles Meniscal tears and extrusion Evidence supports the hypothesis that OA is a bone disease instead of, or in addition to, a cartilage disease. Spontaneous OA animal models show a change in the density and metabolism of subchondral bone prior to any signs of cartilage damage

Question 949

Cartilage Homeostasis

Answer 949

In normal cartilage there is homeostasis between cartilage synthesis and cartilage degradation Synthesis Growth factors Hyaluronic acid / GAGs Tissue inhibitors of MMPs (TIMPs) Degradation Cytokines (TNFα, Il-1β) ADAMTSs (aggrecanases) MMPs (collagenases)

Question 950

OA Pathogenesis

Answer 950

During the early stages of OA, the cartilage surface is still intact. The molecular composition and organisation of the Extra cellular matrix (ECM) is altered first. Articular chondrocytes, which possess little regenerative capacity and have a low metabolic activity in normal joints, exhibit a transient proliferative response and increased matrix synthesis (Col2, aggrecan etc.) attempting to initiate repair causing by pathological stimulation. This response is characterized by chondrocyte cloning to form clusters and hypertrophic differentiation, including expression of hypertrophic markers such as Runx2, ColX, and Mmp13. Changes in the composition and structure of the articular cartilage further stimulate chondrocytes to produce more catabolic factors involved in cartilage degradation. As proteoglycans and then the collagen network breakdown, cartilage integrity is disrupted. Articular chondrocytes then undergo apoptosis and the articular cartilage will eventually be completely lost. The reduced joint space, resulting from total loss of cartilage, causes friction between bones, leading to pain and limited joint mobility. Other signs of OA, including subchondral sclerosis, bone eburnation, osteophyte formation, as well as loosening and weakness of muscles and tendons will also appear.

Question 951

Osteo Arthritis - Altered Metabolism

Answer 951

Metabolism has a key role in the physiological turnover of synovial joint tissues, including articular cartilage. In OA, chondrocytes and cells in joint tissues other than cartilage undergo metabolic alterations and shift from a resting regulatory state to a highly metabolically active state. Inflammatory mediators, metabolic intermediates and immune cells influence cellular responses in the pathophysiology of OA. Key metabolic pathways and mediators might be targets of future therapies for OA.

Question 952

grading criteria for equine osteoarthritis

Answer 952

wear lines- graded 0-3 erosions- graded 0-3 palmar athrosis (osteochondral lesions distal palmar aspect of metacarpus)- graded- 0-3

Question 953

Histopathology of equine osteoarthritis

Answer 953

Chondrocyte Necrosis Chondrone Formation Fissuring Focal Cell Loss less Stain Uptake (Safranin O)

Question 954

Gelsolin

Answer 954

Multifunctional protein involved cell shape determination, secretion and chemotaxis. Gelsolin knockout mouse model - arthritis exacerbation (Aidinis et al., 2005). Exogenous gelsolin administration - chondroprotective properties, protecting murine cartilage decreases in horses with OA

Question 955

Alanine

Answer 955

Alanine is one of the main amino acid residues which constitutes collagen. It may be that the reduction in alanine abundance identified with OA cartilage is resultant of degradation of the cartilage collagen framework, which are subsequently released into the SF resulting in the elevated synovial abundance

Question 956

Creatine

Answer 956

Nonessential amino acid involved in cellular energy metabolism, maintaining cellular adenosine triphosphate (ATP) levels (muscle and brain) Previous human and equine studies also identified elevated SF creatine in OA SF Approximately 95% of stored creatine is located within skeletal muscle (Snow and Murphy, 2001). Thus, given the association of muscle atrophy with OA, this elevation in synovial creatine may be reflective of an associated muscle mass loss

Question 957

Stranguria

Answer 957

painful, frequent urination of small volumes that are expelled slowly only by straining Generally disorders of: The lower urinary tract (bladder or urethra) The genital tract (prostate, vagina) Both Two processes have potential to cause stranguria: Non-obstructive stranguria Mucosal irritation/inflammation of lower urinary/genital tract Obstructive stranguria Obstruction or narrowing of the urethra/bladder neck Palpate the bladder size Stranguria + large bladder may be obstructed = emergency!

Question 958

Haematuria

Answer 958

blood in the urine Haematuria causes: Iatrogenic haematuria Pathological haematuria Genital sources (if voided) Do they have clinical signs associated with LUTD? Has bleeding been noticed from other sites? Trauma? Rodenticides? Blood in faeces? Pattern to urine pigmentation? Look for haemorrhage at other sites Abdomen, thorax, mucosae (especially mouth, axillae, groin) Palpate and assess kidneys for size, symmetry, discomfort Examine the external genitalia Gross “pigmenturia” red, brown or black urine 2. Urinalysis: positive haem 3 possible causes: Haematuria Haemoglobinuria Myoglobinuria Gross haematuria: >150 RBCs/hpf Occult haematuria: Positive Hb on dipstick >5 RBCs/hpf but not visibly pink Care re: interpretation if catheterised/cysto Both can be accompanied by clinical signs (stranguria, dysuria, pollakiuria)

Question 959

Dysuria

Answer 959

discomfort or burning with urination

Question 960

Pollakiuria

Answer 960

increased frequency of urination

Question 961

Periuria

Answer 961

urination at inappropriate sites

Question 962

Anuria

Answer 962

failure of urine production by the kidneys

Question 963

Oliguria

Answer 963

reduction in urine production

Question 964

Polyuria

Answer 964

Increase urine production

Question 965

signs of a lame cow

Answer 965

head bobbing stride leanght joint rigitity toe tipping cadence/timing of strides lordosis

Question 966

The 90% rule for cattle lamness

Answer 966

90% of the time it’s in the claw 90% of the time it’s on the back feet 90% of the time it’s the lateral claw on the back feet

Question 967

Foot trimming – Dutch 5 Step

Answer 967

1. Toe length 2. Match 3. Model- correct weight distribution on wall of horn 4. Create height 5. Investigate/trim loose horn

Question 968

Non-infectious cow foot lesions

Answer 968

White Line Disease Sole Ulcers Trauma Iatrogenic Trimming Experimental Nutritional? Presentation of pain elsewhere?

Question 969

Infectious cow foot lesions

Answer 969

Digital derematitis Foul in the foot Foot and Mouth Disease MCF Polyarthritis – mycoplasma, joint ill

Question 970

White Line Disease

Answer 970

a range of presentations, all at the white line. can travel up to coronary band- if this happens the entire wall of horm must be removed risk factors- Horn integrity- more common in aging cattle with weakened horn Surfaces- deep tracks Stockmanship- stressed, fearful, pushed around cows, most important risk factor Treatment: Block other claw Remove all loose horn NSAID Prevention Good cow surfaces Good stockmanship Appropriate nutrition

Question 971

Sole Ulcers

Answer 971

one of the commonest causes of lameness in dairy cattle. It is an area of damaged sole horn which has completely lost the horn tissue except for the corium Disruption to horn growth due to pressure on the corium underneath P3 Risk Factors: metabolic- pregnancy, relaxation of the ddft, drops p3 and rotates it Standing time- biggest, lying time 14 hours is optimum Surfaces- softer surfaces (pasture) mean cows weigh distribution is more optimal Foot trimming Fat mobilisation- fat pad reduction during pregnacy and lac due to neg energy Inflammation large long term effects- bone spur formation in P3 treatment: Remove pressure Block Trim loose horn NSAID Prevention: Cow comfort – minimise standing times Maximise transition health Ensure cows aren’t lame in dry yards Prompt ID and treatment Foot trimming technique and strategy predominantly a result of poor transition (pregnancy and lactation)

Question 972

Digital Dermatitis in cows

Answer 972

Multifactorial Strong bacterial component Treponeme spp Genetic susceptibility Hoof hygiene chronic condition- prior infection huge risk M1- new infection, not painful M2- acute active lesions, inflamed M3- healing, black plauqes M4- chronic but dormant M4.1- chronic and reactivated M2- treat topically M4- footbath prevention- clenliness vigilnce with heifers foot bathing for M4

Question 973

Foul in the foot

Answer 973

Bacterial infection of interdigital tissue F. Necrophorum et al Painful, swollen ID space Characteristic fragrance foul smell can result in deep infections Treatment Systemic antimicrobials NSAID Local treatments Prevention Similar to DD Minimise risk of interdigital trauma

Question 974

Heel horn erosion

Answer 974

a change in the appearance of the surface of the bulb of the heel in cows Prevention: Hygiene and trimming of loose heel horn

Question 975

Interdigital hyperplasia

Answer 975

fibrous mass that protrudes from the interdigital space of the feet of cattle related to laws spreading adn streaching interdigital skin may be caused by poor trimming

Question 976

Fissures in cattle

Answer 976

Horizontal- thimble foot horizontal fissues indicate stopped horn growth- metabloic vertical needs trimming all the way back axial- iatrogenic- bad hoof triming

Question 977

Toe lesions

Answer 977

white line, absesses, Thin soles Thin soles most common- Abrasion, Over-trimming not much can be done- thn blocks for those with no pain

Question 978

Corkscrew Claws

Answer 978

Don’t tend to occur on well managed farms… Medial corkscrew claws are a different phenomenon

Question 979

Deep Digital Sepsis

Answer 979

Terminal presentation. deep nfection

Question 980

Footbathing cattle

Answer 980

3-4x/week Not too strong/acidic (below pH3) No more than 200 cows Effective design required Commonest ingredients – formalin, CuSO4

Question 981

common signs of lamness in horses

Answer 981

Heat Effusion (swelling) Discharge Muscle atrophy Lameness!

Question 982

Initial examination for lameness

Answer 982

Complete clinical history: - signalment - duration - previous issues - speed of onset - exercise induced - known trauma - any treatment started - any pattern? Observation stationary - size/shape - hoof pastern angle - hoof capsule - coronary band conformation - shoe type, wear pattern, position Palpation coronary band/ coffin joint (DIPJ)/lateral cartilages/ heel bulbs Remove dirt/false horn Symmetry/heels? Hoof testers

Question 983

Gait assessment

Answer 983

Hard straight line Flexion tests Soft and hard lunge Ridden sometimes required hard level non slip surface is important

Question 984

Flexion tests

Answer 984

Apply stress or pressure on an anatomical region of the limb for set period of time Horse then trotted off and observed for the effects of the test on gait Controversial amongst the equine population Can induce lameness that may be unrelated to the baseline lameness Responses must be interpreted carefully

Question 985

how can you tell if a horse has forelimb lamness

Answer 985

head is highest during the phase when horse is taking eight on the lambe limb

Question 986

how can you tell if a horse has hindlimb lamness

Answer 986

increased verticle displacment of the tuber coxae in the lame limb copared to sound limb

Question 987

what tools are available to diagnose lameness in horses

Answer 987

3 grading systems: 1-5: american 1-8: sue dison 1-10: one to use 10/10- non weight baring 8-9/ 10 - toe touching 3/10 seen every stride 1/10- not lame

Question 988

Nerve blocks

Answer 988

Time consuming and hazardous! Valuable tool for localisation Mepivicaine administered perineurally lasts 90-120min – can be up to 3hours. less tissue reaction than other options Intra-articularly lasts approximately 1hr lidocane cheaper but more reaction in the foot- Palmar digital Abaxial sesamoid Coffin joint Navicular bursa DFTS? False positive Will the horse warm out of the lameness? Proximal diffusion? Clinician bias False negative Misdirection of needle outside of the fascia that surrounds the neurovascular bundle or into synovial structure. Local anaesthetic inadvertently injected into a blood vessel Clinician bias Other limitations Mechanical lameness that doesn't respond to anaesthesia- dont do if horse warms out of lameness Desensitisation of skin but not deeper structures.

Question 989

Palmar digital nerve block

Answer 989

What does it block? Sole Navicular apparatus Soft tissues of the heel Coffin joint Distal portion of the DDFT Distal sesamoidean ligament inserted distally two points on palmar aspect of foot abouve heel bulbs How? 25g 2/3in needle (25g if cobby!) Needle separate from syringe- makes sure you are not in blood vessel, makes it easier to keep needle in if trouble with horse 1.5ml mepivicaine- larger volumes give larger spread and so less diagnostic Proximal edge of the cartilage of the foot- can palpate neurovascular bundle Evaluate before 10mins

Question 990

Abaxial sesamoid nerve block

Answer 990

What does it block? Foot Middle phalanx PIPJ Distopalmar aspects of the proximal phalanx Distal portion of the SDFT and DDFT Distal sesamoidean ligaments Distal annular ligament Fetlock How? 25g 2/3in needle (25g if cobby!) Needle separate from syringe- makes sure you are not in blood vessel, makes it easier to keep needle in if trouble with horse 2.5ml mepivicaine Base of the proximal sesamoids- can feel neurovascular bundle Direct needle distally.

Question 991

Coffin joint block

Answer 991

What does it block? Coffin joint! Navicular apparatus Branches of the palmar digital nerves Toe region of the sole (larger volumes – heel region of the sole) Minimal benefit over PDNB quick block horse finds it uncomfortable How? 20g 1.5in needle Needle separate from syringe 5-6ml mepivicaine Lateral approach with the limb off the ground May be better tolerated May enter navicular bursa or DFTS

Question 992

Navicular bursa block

Answer 992

What does it block? Navicular bursa Navicular bone and associated ligament's Solar toe pain Distal DDFT Does not block the coffin joint How? Hickman block 20g spinal needle Desensitise skin Ideally with radiographic guidance- needle will be inserted, radiograph will be takein, if it sits on the palmar aspect of navicular bone, the la will be injected Omnipaque? 3-4ml

Question 993

Digital flexor tendon sheath block

Answer 993

What does it block? Lesions within the DFTS The portion of DDFT in the foot distal to the DFTS How? Palmar aspect of the pastern (out of choice)- sheeth is superficial Tourniquet applied- encorages la to move distally 20g 1-1.5inc needle Needle must remain superficial to the DDFT

Question 994

Foot balance radiographs

Answer 994

Gross imbalance can induce lameness Correct early on in a lameness investigation Leave the shoes on longterm poor foot balence leads to pathology Lateromedial- Foot positioned flat Weight bearing on 2-5cm block Horizontal beam centred on coronary band halfway between toe and heel Dorso-palmar imbalance - Long toe/ low heel common finding What to assess: Solar surface angle in front feet Long toe/low heel Osteophyte/entheseophyte associated with coffin joint and naviucular bone Margin and cortico-medullary definition navicular bone Dorsopalmar (weightbearing)- How? Leave shoes on Foot positioned flat Weight bearing on 2-5cm block Horizontal beam centred on coronary band Often foot not aligned with pastern/fetlock. What to assess? Medial –lateral imbalance – abnormal stress though the joints. Coffin joint space should be even. Ossification of the lateral cartilages Dorso proximal palmaro distal oblique- (Dorsal 65 degree proximal-palmarodistal oblique weight bearing – pedal/ navicular bone) Shoes off – pack well with putty Could use DPr-PaDiO Standing on cassette tunnel Some elongation of radiographic anatomy Much easier to perform when limited people. What to assess: Navicular bone- Cyst like lesions Distal border fragments and lucent zones Medullary sclerosis Pedal bone- Fractures Keratomas Osteitis Palmaroproximal – palmarodistal oblique of the navicular bone (skyline)- How? Cassette tunnel Caudal to the contralateral limb with heel on ground 45o angle X-ray beam centred between the bulbs of the heel and collimated to the navicular bone What to assess: Palmar cortex of the navicular bone Corticomedullary definition Lucencies within the spongiosa Cyst like lesions? Limited to bony changes Limited assessment of soft tissues. By the time radiographic changes are seen its likely disease is well developed. Advancement in diagnostic imaging has lead to improvement in treatment success rates. Able to provide a more reliable prognosis with a definitive diagnosis.

Question 995

MRI

Answer 995

Utilises radiowaves, strong magnetic fields and computer technology MRI uses the hydrogen nuclei (protons) found in body water due to their magnetic properties Once a magnetic field is applied the spinning protons rotate to align with the magnetic field. A radiofrequency pulse is then applied forcing the protons out of alignment The radiofrequency pulse is then removed and the electromagnetic energy released is converted into black and white images. Different sequences are set up to look at different aspects In the equine veterinary world its being used to improve the accurary and efficacy of diagnostics for lameness investigations. horses must have GA Radiographs show only bone Ultrasound provides soft tissue detail Ultrasound very limited in the foot. Image bilateral limbs Pre-fracture pathology and subtle soft tissue damage Foot penetrations Able to image within the hoof capsule! Indications? Where radiographs are negative or unclear and US access is difficult in a localised area. Penetrating injuries When GA is unadvisable Acute onset lameness during exercise Cases that do not respond to treatment as expected. Monitor progress/ readiness for competition.

Question 996

Computed Tomography

Answer 996

Series of x-rays emitted from various angles and the detectors measure attenuation Provide a 3D image via advanced mathematical algorithms reconstructing the image Benefits over radiographs- No super imposition or complex overlap of anatomy Can orientate images to view key structures 3D image capture in 60 second scan time.

Question 997

Gamma Scintigraphy

Answer 997

 Radioactive technetium  Bone tracing agent  Identifying fractures  Poor performance cases  Difficult areas to examine/radiograph

Question 998

SUB–SOLAR ABSCESS

Answer 998

The most common cause of acute lameness in horses Ascending bacterial infection into the chorium (solar dermis) Lesions in the white line “Nail bind” Penetration injuries Risk Factors Poor foot conformation Seedy Toe Wet, muddy conditions Seen both in shod & unshod horses Chronic Laminitis / PPID- white line streaches and splays Diagnosis Acute & severe unilateral lameness Grade 3 or 4 (AAEP lameness scale) Increased digital pulsation to affected hoof – “Bounding pulses” Heat in the hoof +/- distal limb swelling Repeatable and marked pain response on application of hoof testers Differential Diagnosis- Solar Bruising, Pedal bone fracture, Laminitis (rare to be unilateral) TREATMENT AIM TO ENCOURAGE DRAINAGE- drainage will be black/grey Remove Shoe Pare and clean the sole ‘Explore’ any discoloured tracts or defects in the white line (Sedation infrequently required) ​ NB: Nerve block contraindicated in NWB lameness POULTICE To soften hoof prior to curetting To maintain drainage after abscess open Poultice should be changed 2-3 times daily Provide pain relief 24-48 hours NSAID therapy Phenylbutazone 4.4 mg/kg IV or PO BID Antibiotics are not indicated for un-complicated abscess Tetanus Prophylaxis Check tetanus vaccination status If in doubt  Administer tetanus antitoxin

Question 999

Chronic Abscess

Answer 999

Will rupture at coronary band or heel bulb Still aim to encourage drainage distally May require repeat flushing

Question 1000

Purulent Abscess

Answer 1000

Deeper/sensitive structure involved Will require further diagnostics – Radiography Likely to need more extensive surgery Antimicrobial therapy indicated

Question 1001

Solar Penetrations

Answer 1001

If nail/wire is still in place Leave it in situ - support leg with bandage/splint Obtained radiographs if possible If nail/wire already removed by owner Try to identify tract and carefully pare sole to expose chorium (solar dermis) Clean, lavage and dress the lesion BEWARE delay in onset of lameness Further investigations ASAP if any suspicion of complications; Contrast Radiography/MRI Potential Sequelae- Damage to Pedal bone- Pedal osteitis  Sequestrum formation Damage to Soft tissue structures- Insertion of Deep digital flexor tendon Impar Ligament Synovial Infection- 56% survival from hospital 36% return to normal athletic function Navicular bursa Distal interphalangeal joint Digital tendon sheath Simple, uncomplicated penetration; As per solar abscess – pare and poultice Antibiotics only if clear evidence of infection Judicious use of analgesia / NSAIDs Penetrations with synovial penetration; Broad-spectrum antimicrobial therapy Procaine Penicillin, 22mg/kg IM BID (or IV QID) Gentamicin, 6.6mg/kg IV SID SURGICAL INTERVENTION Arthroscopic lavage of synovial cavity TETANUS PROPHYLAXIS

Question 1002

Hoof Trauma

Answer 1002

FOOT CAST Support Sterility Protection Pain Relief fracture managment PRIORITIES Establish diagnosis to INFORM PROGNOSIS Stabilise the limb Provide analgesia Situational awareness (finances, logistics, future athletic aims) Allow owner to make informed decision on treatment Prioritise welfare and recognize role of euthanasia

Question 1003

parameters for assesing lamness

Answer 1003

head nod- down on sound for front lameness hip drop, hip hike- hindlimb lamenessy limb movement- joint angle changes, stride leanght, stance duration, adduction/abduction, limb protration sound of hoof hitting carrage tail carrige track quality of movment- "stifff" ect

Question 1004

what is the best movment paraemter to detect and quantify lameness

Answer 1004

alterations in weightbrearing forces on the ground

Question 1005

describe an exam for lamness in small animals

Answer 1005

step 1- history Step 2. Hands off: Observe Observe sitting and standing Uneven weight distribution on a particular limb Muscle asymmetry Join angulations/conformation Loading position of feet and toes Asymmetries in ways limbs are positioned Swellings Observe sitting -> standing Particularly useful if stifle issues Positive sit test Weight shifting Observe - Moving Analyse gait and lameness Contraindicated in severe lameness or major traumatic injury Observe prior to treatments Walk and trot Repeat on different surfaces – concrete, gravel, grass Lameness score 5 or 10 point scale – subjective Kinematic/kinetic gait analysis - objective Head nod- down on sound Stride length and duration Limb tracking- limb should be stight Gait abnormalities are not always painful Some are conformational Muscle contractures Limb shortening Joint arthrodesis Some are neurological Ataxia knuckling 3.Hands-on examination General Clinical Exam 2. Orthopaedic Examination Be methodical Minimal restraint Palpate painful areas last 3. Neurological Examination Proprioceptive testing Reflex testing Symmetry Manipulation: May be painful – be gentle Some manipulations better performed under sedation or general anaesthesia instability: laxity (looseness), sub-luxation or luxation (dislocated) pain range of motion: flex, extend, abduct, adduct, rotate reduced or increased? Crepitus

Question 1006

Lameness Grading in small animals

Answer 1006

0- no lamness 1- subtle and only observed in trot 2- mild lameness in walk, worse in trot 3- obvious in both gautes 4- observeavle in both gautes with periods on non weight baring 5- non wiegh bearing most/all of the time

Question 1007

signs of Forelimb lameness in small animals

Answer 1007

Placement on lame limb – head raises Placement of sound limb – head dips

Question 1008

signs of hindlimb lameness in small animals

Answer 1008

Placement of lame limb – pelvis rises Placement of sound limb – pelvis dips Weight shift to forelimbs Bilateral lameness Abnormal tracking – affected limbs wider Forelimbs – short choppy strides and circumduction Hindlimbs Hips – waddling/oscillating gait at walk Stifles – short stilted strides and circumduction Bunny-hopping

Question 1009

lameness effecting the elbow of small animals

Answer 1009

Complex hinge joint Common site of lameness in large breed dogs: Elbow dysplasia- hard to see sue to it being bilateral Effusion -> lateral epicondyle and olecranon

Question 1010

lameness effecting the shoulder of small animals

Answer 1010

Biceps Tendon test Abduction test to assess medial instability under GA/sedation examine after elbow to distinguish between elbow and shoulder pain

Question 1011

lameness effecting the Pelvic Limb of small animals

Answer 1011

Tarsus Tibiotarsal joint only appreciable motion Assess for laxity and luxations Palpated and stressed Hyperflexion SDFT Calcaneal tendon Tibia & Fibula Deep palpation to elicit osseus source of pain Detect focal area of swelling Abnormal conformation

Question 1012

Stifle Examination

Answer 1012

Synovial effusion -> palpate either side of the patellar ligament. Chronic cranial cruciate ligament instability results in medial fibrosis and thickening -> medial buttress Patella position ->patellar luxation Partial CCL rupture Craniomedial band rupture Cranial drawer only in flexion Intact caudolateral band taut in extension – prevents cranial drawer Caudolateral band rupture No cranial drawer Craniomedial band taut in flexion and extension – prevents cranial drawer. CCL Positive Sit Test Cranial Draw Tibial Compression Test/Tibial thrust

Question 1013

Patella Luxation

Answer 1013

Medial>Lateral patella luxation More common in smaller dogs Insidious in onset Skipping intermittent lameness Graded in severity from I to IV: Grade 1: subclinical. Patella can be manipulated out of place but will return to its normal position Grade 2: the patella luxates when the stifle is placed through a normal range of movement, spontaneously. Grade 3: permanent luxation but the patella can be manually returned (reduced) to the femoral trochlear sulcus by the examiner, but the patella luxates again. Grade 4: permanent luxation and the patella cannot be returned to the femoral trochlear sulcus.

Question 1014

lamness resulting from te hips in small animals

Answer 1014

Hip examination: Decreased ROM especially in extension Crepitus Pain Laxity Note ->Hip extension also results in extension of the lumbosacral joint and passive extension of the stifle – beware false-positives. Extension and abduction of the hip = hip pain

Question 1015

Ortolani test

Answer 1015

More objective assessment of hip laxity Must be done under sedation/GA Angle of subluxation  the point at which the hip subluxates Angle of reduction  the point at which the femoral head returns to the acetabulum

Question 1016

Abnormalities can be classified according to distribution within the skeleton:

Answer 1016

Monostotic – involving a single bone (e.g. an osteosarcoma) Polyostotic – multiple bones are involved (as seen with multiple myeloma or haematogenous osteomyelitis Focal – may involve a specific bone region (e.g. the metaphysis) Generalized – involving all bones (as may be seen with metabolic conditions) Symmetrical or Asymmetrical

Question 1017

Bone reacts to pathological processes in a limited number of ways:

Answer 1017

change in alignment change in contour increased or decreased bone mass.

Question 1018

Aggressive vs non-aggressive changes in radiographs of bones

Answer 1018

Aggressive lesion  rapid bony change where there is minimal time for the bone to respond and remodel Non-aggressive lesion  benign, slow-growing, more chronic process with time for bone to remodel. Wide spectrum in between! This can be assessed by looking at the nature of any: Bone destruction (lysis) Periosteal reaction Lytic edge character Cortical disruption Transition from normal to abnormal bone Rate of change (10-14 days)

Question 1019

Periosteal Reactions:

Answer 1019

New bone production: Artifact (superimposition) New bone production secondary to injury continiuos (solid, lammelar, lamellated) vs interupted (thin brush like, sunburst, amorphus)

Question 1020

bone loss in radiographs

Answer 1020

Aggressive vs non-aggressive changes Patterns of bone lysis: Artifact (superimposition) Real due to generalised or focal bone loss geofraphic lysis- least agressive moth eaten lysis permiative bone lysis- most agressive

Question 1021

Stages of wound healing

Answer 1021

1. Haemorrhage/Coagulation - Immediate haemorrhage Vasoconstriction Vasodilation Blood clot forms ‘Scab’ 2. Inflammation/Debridement - 6 hours after injury Neutrophils -> Monocytes -> Macrophages Macrophages – ESSENTIAL TO WOUND HEALING Wound exudate – serosanguinous to purulent – NORMAL finding Inflammatory phase can be minimal in apposed wound e.g. surgical incision 3. Reparative .- Granulation tissue – Identified between day 3 and 5 of wound healing Fibroblasts Angiogenesis – capillaries advance 0.4-1mm/ day Collagen Develops from wound margins Contraction - 5-9 days after injury Epithelialisation - Visible 4-5 days after injury Pink smooth margin to wound Monolayer of cells 4. Maturation Re-organisation of collagen Can take Months – Years 80% Strength of normal tissue

Question 1022

stage one of wound healing

Answer 1022

Haemorrhage/Coagulation - Immediate haemorrhage Vasoconstriction Vasodilation Blood clot forms ‘Scab’

Question 1023

stage two of wound healing

Answer 1023

nflammation/Debridement - 6 hours after injury Neutrophils Monocytes Macrophages Macrophages – ESSENTIAL TO WOUND HEALING Wound exudate – serosanguinous to purulent – NORMAL finding Inflammatory phase can be minimal in apposed wound e.g. surgical incision

Question 1024

stage three of wound healing

Answer 1024

Reparative- Granulation tissue – Identified between day 3 and 5 of wound healing Fibroblasts Angiogenesis – capillaries advance 0.4-1mm/ day Collagen Develops from wound margins Contraction 5-9 days after injury Epithelialisation Visible 4-5 days after injury Pink smooth margin to wound Monolayer of cells

Question 1025

stage four of wound healing

Answer 1025

maturation- Re-organisation of collagen Can take Months – Years 80% Strength of normal tissue

Question 1026

First Intention wound healing

Answer 1026

Healing of a wound where skin edges are closely re-approximated

Question 1027

Second Intention wound healing

Answer 1027

Gap left between wound edges and natural healing allowed to occur nsuitable for surgical closure, extensive contamination or devitalisation Allow to heal by granulation, contraction and epithelialisation

Question 1028

Immediate Primary wound healing

Answer 1028

Incision/Clean e.g. surgical incision closes imediatly

Question 1029

Delayed Primary wound closure

Answer 1029

Clean contaminated – contaminated closes Up to 2-3 days after wounding. Inflammatory phase over

Question 1030

Secondary wound closure

Answer 1030

Contaminated or Dirty closes Up to 5-7 days after wounding. Granulation tissue present

Question 1031

Approach to wound management in abrasions

Answer 1031

partial skin thickness wound Rapidly re-epithelialise Can be more severe – shearing injuries e.g. RTA heals by Second Intention

Question 1032

Approach to wound management in avulsions

Answer 1032

valuation – Avulsion = skin torn from underlying attachments e.g. de-gloving injury of distal heals by Delayed Primary Closure Secondary Closure Second Intention

Question 1033

Approach to wound management in Incisions

Answer 1033

smooth wound edges with minimal trauma e.g. surgical wound heals by Immediate Primary Closure

Question 1034

Approach to wound management in laceration

Answer 1034

= ragged incision with variable damage to surrounding tissues Immediate Primary Closure? Delayed Primary Closure Secondary Closure

Question 1035

Approach to wound management in burns

Answer 1035

Classified by depth - First degree: superficial Second degree: partial thickness Third degree: full thickness Secondary Closure Second Intention

Question 1036

Approach to wound management in Punctures

Answer 1036

e.g. bite wounds or ballistic missile Minimal external skin damage Extensive underlying tissue damage Foreign material e.g. dirt/debris/hair in wound Surgical exploration indicated Consider underlying structures! - penetration of body cavities??? Delayed Primary Closure Secondary Closure

Question 1037

Poor local blood supply to a wound =

Answer 1037

slow granulation tissue formation and increased risk of wound infection Can be difficult to assess in the early stages

Question 1038

pproach to wound management - debriding

Answer 1038

emove devitalised tissue, foreign material, bacteria from wound Sedation/GA/local Clip hair from around wound SHARP excision with scalpel Conservative with skin Radical with fat/muscle Preserve bone/tendons/blood vessels/nerves where possible Bleeding good indicator of tissue viability NO point leaving in obviously necrotic tissue

Question 1039

Approach to wound management -Lavage

Answer 1039

DILUTION IS THE SOLUTION TO POLLUTION TYPE OF FLUID TAP WATER – CHEAP and readily available. Useful for grossly contaminated large wounds HARTMANNS/STERILE SALINE (0.9%) – fluid of choice. Still relatively cheap, minimally toxic to cells 20 or 50ml syringe with 18G needle DO NOT USE UNDILUTED ANTISEPTICS E.G. CHLORHEXIDINE FOR WOUND LAVAGE

Question 1040

Barriers to wound healing

Answer 1040

Infection Movement Foreign Material Necrotic tissue Local factors – pH, Shape of wound Poor blood supply Health Status Iatrogenic Factors Cell transformation Patient Temperament Client Temperament

Question 1041

Principles of Open Wound Management

Answer 1041

Assess at every stage: Degree of inflammation Degree of exudate Presence and quality of granulation tissue Skin edges Degree of epithelialisation

Question 1042

Primary contact layer for Bandaging Inflammatory/Debridement wounds

Answer 1042

Wet to dry Moisture retentive Honey Negative pressure MagPrimary contact layer for Bandaging Inflammatory/Debridement wounds gots q24 hours for 1st 3 days then q48 hours

Question 1043

Primary contact layer for Bandaging Reparative – early stages wounds

Answer 1043

Wet to dry? Moisture retentive Honey Negative pressure

Question 1044

Primary contact layer for Bandaging Reparative – later stage/good granulation bed wounds

Answer 1044

Moisture retentive Foam/absorptive Hydrogel if drying out

Question 1045

Nutrition associated diseases in exotics

Answer 1045

Commonly referred to as MBD Results from inadequate dietary calcium and/or vitamin D3, imbalance in the calcium-to-phosphorus ratio and/or lack of UV light provision. Persistent hypocalcaemia will lead to hyperparathyroidism. This causes an increase in production of parathyroid hormone (PTH)  promotes calcium resorption from the bones . Uncommon in snakes Eat warm-blooded whole prey items Exceptions ->Green snakes Insectivorous Most commonly seen in herbivorous, insectivorous and omnivorous reptiles. Increased incidence in herbivorous and insectivorous species  challenging with diets Diurnal species may be more susceptible More in juvenile animals due to an increase in demand for growth. Parents may play an essential role Vitamin D3 Calcium Genetic status Skeletal development during embryonic development  influences bone quality in later life Less common in adult reptiles (with the exception of reproductively active females) as long bones and/or shell are no longer growing, reducing the calcium demand. Similar clinical signs may be seen in adults and usually are due to other metabolic diseases such as renal secondary hyperparathyroidism (RSHP). Differentials for bone and joint changes RSHP Traumatic fractures Osteomyelitis Gout/pseudogout Abscesses Cellulitis Neoplasia lizards- Brachycephalic appearance to the head Deformity of mandibular and maxillary bones Soft and pliable Deformed jaw  characteristic smile appearance Kyphosis and scoliosis of the spine May see decreased neurological function to the rear limbs Hypocalcaemic tetany Partial depolarisation of nerves and muscles  tremors, twitching and seizures Tremors and fasciculations may be seen, especially during handling Seizure, tetany and/or flaccid paresis of limbs/tail. chelonians- Beak may be overgrown and can develop a parrot beak-like appearance. Prolapse of the cloaca, colon, rectum or phallus due to a lack of calcium on smooth muscle. Carapace and plastron may be soft, the shape of the shell may be distorted and there may be difficulty in ambulating due to the inability to lift the plastron from the ground.

Question 1046

hypocalcaemia birds

Answer 1046

Hypocalcaemia Inadequate dietary calcium and/or vitamin D3 Lack of UV light provision. Commonly seen in Grey Parrots Commonly seen in birds fed seed diet. Lethargy Fluffed-up Shaking/tremoring Seizures Pathological fractures Limb deformities Dystocia Clinical examination Full blood profile Ionised calcium low Radiography Serum 25-hydroxycholecalciferol

Question 1047

Exotic mammals – NSHP

Answer 1047

Less commonly diagnosed with NSHP Reported in Nonhuman primates Sugar gliders Skunks Exotic cats Guinea pigs Rabbits NSHP not uncommon in sugar gliders Causes Suboptimal husbandry Suboptimal nutrition Low calcium Low vitamin D3 High phosphorus Clinical signs Acute collapse CNS abnormalities Seizures Hind limb weakness Osteoporosis

Question 1048

Hypovitaminosis E

Answer 1048

Birds Associated with muscle weakness Localised wing paralysis Poor digestion Embryonic and hatchling mortalities Rabbits Cause of muscular dystrophy Degeneration and necrosis of skeletal muscle fibres Long-term storage of feed can decrease vitamin E content

Question 1049

Vitamin B deficiency

Answer 1049

Chondrodystrophy Short, widened leg bones Distortion of the hock Slipped tendon/gastrocnemius tendon movement from trochlear groove – also called perosis Associated with nutritional deficiencies Vitamin B deficiencies Pyridoxine (vitamin B6) Biotin (vitamin B7) Folic acid (vitamin B9) Niacin (vitamin B3) Manganese deficiency Choline deficiency Zinc deficiency

Question 1050

Myopathies in exotics

Answer 1050

Myopathy = muscle disease Capture myopathy = exertional rhabdomyolysis Occurs as a result of stress & physical exertion Important in capture and restraint of wild or zoo animals Ungulates susceptible Some bird species  long legged wading birds and ratites Myopathy in poultry Associated with heavy, large birds Can be associated with different infectious organisms Fungi Bacteria Viruses Protozoa Trematodes Mycobacterial infections Zoonotic implications Weight loss, severe muscle wasting, atrophy of pectoral muscles (birds) Granulomatous lesions in bones and joints Identification of acid-fast microorganisms

Question 1051

neoplasia in exotic

Answer 1051

Tumours of the musculoskeletal system Squamous cell carcinomas of the mandible Leiomyosarcomas Osteoma/Osteosarcomas Chondrosarcomas Rhabdomyomas/rhabdomyosarcomas Sarcomas Chordomas Chordoma -ferrets Commonly occur at tip of the tail

Question 1052

Osteomyelitis in exotics

Answer 1052

Osteomyelitis  infection of bone or medullary canal Bacterial osteomyelitis Staphylococcus spp. Streptococcus spp. Gram-negative aerobic bacteria Sometimes anaerobic infections Sometimes fungi Diagnosis Radiographs Culture of samples Culture of implants  implants used for internal fixation can act as a nidus of infection, or a sequestrum may be present

Question 1053

Gout

Answer 1053

Gout  painful! Visceral gout - crystals within internal organs Articular gout – crystals in joints Periarticular gout – crystals in the tissues around the joint Clinical exam Poor body condition Subcutaneous nodules near joints Pain on palpation Diagnosis History Clinical exam Bloods  Uric acid high FNA and cytology  birefringent needle-shaped urate crystals Radiography  Osteolysis and proliferative densities around joints

Question 1054

Structure of the skin

Answer 1054

Epidermis Superficial Derived from ectoderm Dermis Deeper Derived from mesoderm Subcutis/Hypodermis

Question 1055

structure of Epidermis

Answer 1055

Most superficial layer 4 cell types : Keratinocytes ∼ 85% Langerhans cells ∼ 3– 8% Melanocytes ∼ 5% Merkel cells ∼ 2%

Question 1056

Keratinocytes

Answer 1056

form the bulk of the epidermis. Produced from the stratum basale Constantly reproduced and then shed as dead horny cells. Anchored to each other by desmosomes Structural and immune functions: produce structural keratins phagocytic and capable of processing antigens produce cytokines (IL-1, IL-3, prostaglandins, leukotrienes, interferon) Pemphigus foliaceus- a rare autoimmune condition that causes painful and itchy blisters and sores to form on your skin.

Question 1057

Langerhans cells

Answer 1057

mononuclear dendritic cells immune surveillance of the skin found basally or suprabasilar Functions: antigen processing and presentation to helper T lymphocytes induction of cytotoxic T lymphocytes directed to modified alloantigens production of cytokines including IL-1 phagocytic activity.

Question 1058

Melanocytes

Answer 1058

Dendritic cells found within epidermis, hair follicle and ducts of sebaceous and sweat glands. In epidermis, each melanocyte communicate with 10– 20 keratinocytes to form the ‘epidermal melanin unit’. Each melanocyte produces eumelanin or pheomelanin within melanosomes  melanosomes migrate to the end of dendrites and transfer melanin to adjacent epidermal cells. functions: production of protective colouration and for sexual attraction barrier against ionising radiation scavengers for cytotoxic radicals contribution to inflammatory response via production of cytokines

Question 1059

Merkel Cells

Answer 1059

Dendritic epidermal cells in basal cell layer of the epidermis or just below. Functions: specialised slow-adapting mechanoreceptors influencing cutaneous blood flow and sweat production coordinating keratinocytes proliferation controlling of hair cycle by maintaining and stimulating hair follicle stem cell population.

Question 1060

layers of the epidermis

Answer 1060

Stratum Basale Stratum Spinosum Stratum Granulosum Stratum Lucidum Stratum Corneum

Question 1061

Stratum Basale

Answer 1061

Single layer columnar cells Mostly keratinocytes Anchoring: To Basement Membrane Zone (BMZ)/dermis hemidesmosomes KC to KC desmosome Initial site of keratin production Stem cell function Proliferating- very mitotically active, skin produced here

Question 1062

Stratum Spinosum

Answer 1062

Generally 1-2 cells thick Footpads, nasal planum and MCJ’s upto 20 cell layers Desmosomes mediate adhesion between keratinocytes Important in barrier function

Question 1063

Stratum Granulosum

Answer 1063

Not always present in haired skin (1-2 cell thick if is) Cornified envelope and degeneration of cells starts in this level various lipids and enzymes-secreted extracellularly (watertight seal)

Question 1064

Stratum Lucidum

Answer 1064

Compact layer of dead keratinocytes only found in footpads and nasal planum.

Question 1065

Stratum Corneum

Answer 1065

Outermost layer of skin Flattened cornified anucleate cells Constantly shed

Question 1066

Basement Membrane Zone (BMZ)

Answer 1066

Separates epidermis from the dermis Acts as a physical barrier- maintians arcatechtue AND STRUCTURE Regulates nutrition Aids in wound healing

Question 1067

The Dermis

Answer 1067

The dermis forms the middle of the three layers and is comprised of dense connective tissue that is vascular. - Thickness of dermis determines the thickness of the skin It is this layer that contains the nerve fibres, nerve endings and elastic fibres in addition to the hair follicles, and the sweat and sebaceous glands that grow down from the epidermis. Tensile strength and elasticity of skin Made up of: Insoluble fibres ->collagen and elastin ->resist tensile forces Soluble polymers -> proteoglycans and hyaluronan -> dissipate compressive forces

Question 1068

Hypodermis

Answer 1068

The hypodermis or subcutaneous layer lies beneath the dermis and consists of loose connective tissue. Predominant cell type – lipocyte (90%) Energy reserve Thermogenesis and insulation Protective padding and support Maintaining surface contour/shape Small blood supply - susceptible to disease

Question 1069

Functions of the integument

Answer 1069

1. Protection Mechanical protection from chemical, physical and microbial damage Epidermal cells, Hair, Specialised secretions e.g. sebaceous and sweat glands Antibacterial and antifungal activity Immune system Nerve sensors to allow the perception of heat, cold, pressure, pain and itch Pigment production to protect against solar damage 2. Maintenance of homeostasis prevent loss of water, electrolytes and macromolecules Temperature regulation 3. Excretion Sebaceous glands, sweat glands Secretion via epitrichial, atrichial and sebaceous glands 4. Synthesis of vitamin D Calcium homeostasis Conversion of Vitamin D precursor into Vit D3 Synthesis of calcitriol by kidney 5. Storage Energy reserve Storage of vitamins, electrolytes, water, fat, carbohydrates and protein 6. Other Elasticity to allow movement Production of adnexa, e.g. hair and claws Communication as to the health of the individual and sexual identity

Question 1070

structureof hair

Answer 1070

Specialised keratinised tubular structure- Primary (guard hairs)- Bulb deep in dermis Have associated sebaceous glands, sweat glands, arrector pili muscles Secondary (downy hairs)- Small, not as deep in dermis May have associated sebaceous gland but not sweat glands or arrector pili muscles Cortex, medulla & cuticle containing variable pigment Important for Insulation, Signalling, Physical protection

Question 1071

Sebaceous Glands

Answer 1071

Holocrine secretion – produces sebum containing triglycerides, other lipids (e.g. linoleic acid), transferrin, IgA, IgG Functions of sebum Lubricates hair, and skin (glossy sheen) Required for normal hair shaft separation Excreted via squamous duct to the hair follicle

Question 1072

hair follicles

Answer 1072

Simple hair follicles single hair protrudes from the follicular orifice Compound hair follicles multiple hairs use the same follicular orifice (enter at the level of the sebaceous gland) Species differences: Omnivores and herbivores – simple follicles (bar sheep) Dogs – compound – 2-15 hairs per group Cats – compound follicles – 10-12 hairs per group

Question 1073

The hair cycle

Answer 1073

Three phases: Anagen (growing phase) – deep dermis New hair produced under previous hair in deep dermis Distinctive hair bulb containing follicular dermal papilla Catagen (intermediate phase) – mid dermis Rarely seen in normal skin – feature of some skin diseases (e.g. alopecia X) Telogen (resting phase) – mid to upper dermis Regulated by photoperiod, temperature, hormones and growth factors

Question 1074

Trichograms

Answer 1074

a trichogram is the microscopic examination of hair shafts Telogen bulb- spear-shaped rough no pigment Inactive hairs Normally 80-90% often 100% in endocrinopathies- results in allopecia Anagen bulb- rounded smooth pigmented centre +/- bulb may fold around shaft when plucked Actively growing hairs Normally 10-20% But many variations… Breed variations: poodles 80-100% anagen Most dogs/cats telogenic growth patterns Seasonal variation: summer <50% anagen winter 10% anagen NB 100% telogen never normal. Indicates eg: Endocrine disease Telogen effluvium (sudden hairloss 1-2 months post-stress) Post-clipping alopecia Look at the hair tips! Normal hair tips Smooth pointed tips Angular broken ends Indicates self-inflicted hair loss and probable pruritus

Question 1075

Pruritis

Answer 1075

Unpleasant sensation that elicits the desire or reflex to scratch (rub, lick, chew) Classify as Pruriceptive pruritus – due to stimulation of peripheral receptors in skin (in presence of healthy nervous system). Usually due to skin disease Neuropathic pruritus – generated in CNS in response to circulating pruritogens (eg cholestasis) pharmacological mediators (eg intraspinal morphine) anatomical lesion of PNS or CNS, eg syringomyelia in CKCS Psychogenic pruritus recognised in animals/man, poorly understood) Uncommon but need to differentiate from dermatological causes of pruritus Somato-sensory activity of skin involves Mechanoreceptors Thermoreceptors Nociceptors – itch and pain Mainly via unmyelinated slow-conducting C-fibres Some dedicated purely to itch (and temperature change) Also A-delta fibres But complex interaction between itch and pain Painful stimuli can inhibit itch (eg scratching)

Question 1076

Pruriceptive pruritus

Answer 1076

due to stimulation of peripheral receptors in skin (in presence of healthy nervous system). Usually due to skin disease

Question 1077

Neuropathic pruritus

Answer 1077

generated in CNS in response to circulating pruritogens (eg cholestasis) pharmacological mediators (eg intraspinal morphine) anatomical lesion of PNS or CNS, eg syringomyelia in CKCS

Question 1078

Sensitisation in chronic pruritus

Answer 1078

In man: Peripheral sensitisation Scratching ->increase local inflammation -> production of pruritogens by inflammatory cells -> ncrease C-fibre responsiveness Central sensitisation Inflammation of skin -> altered perception of gentle mechanical /other stimuli -> perceived as pruritus (allokinesis) + Emotional, biochemical, central factors alter pruritic neural impulses in the brain Likely occurs in animals too… Therefore in the chronically pruritic animal, marked pruritus may be incited by only minor stimuli (hyperkinesis) Threshold of itch: summation effect – an important clinical concept.... Pruritus from multiple sources may coexist, eg: Allergen concentrations Often seasonally variable in atopy Environmental factors heat enhances itch – lowers threshold of receptors to pruritus effects on skin microclimate and microbial growth Ectoparasites - Flea burden, even if not flea-allergic Stress factors- changes in the family, new pets, new baby, move house Effects summate and may take pruritus over the pruritic threshold -> clinical pruritus. Identification and elimination of as many factors as possible is important -> return below the threshold where able

Question 1079

Skin lesions

Answer 1079

Primary lesions: Those that are a direct result of skin disease. They are usually most obvious in the early stages of the disease and are those upon which a definitive diagnosis should be based. Macule Papule Nodule Vesicle Bulla Pustule Wheals Alopecia Scale Crust Comedone Follicular Cast Secondary lesions: are mostly non specific and are caused by pathological changes which result from the primary disease and its lesions or by self-inflicted damage by the patient. (more common) result of cutaneous, immunological or metabolic abnormality. Erosion Ulcer Lichenification Hyperpigmentation Epidermal collarette

Question 1080

Epidermal responses

Answer 1080

Hyperkeratosis Scale (seborrhoea) Follicular hyperkeratosis Acanthosis Lichenification Vesicle/pustule formation Hyperpigmentation/ hypopigmentation Crusting

Question 1081

Dermal responses

Answer 1081

Erythema Oedema Thickening

Question 1082

Hyperkeratosis

Answer 1082

Increased depth of the cornified layer Scaling = production of abnormal or excessive scale indicates abnormality of keratinisation also known as seborrhoea (older term) can be greasy (“oleosa”) or dry (“sicca”) Can be primary (usually inherited) or secondary compared to Crusting formation of dried exudate variable cellularity, variably coloured may contain organisms always secondary Primary keratinisation defects unusual/rare in domestic animals Ichthyosis (fish scales) of Golden Retrievers secondary defects are common Non-specific sign indicative of increased turnover of epidermis, or imbalance between turnover and desquamation Feature of many different skin diseases Metabolic Infectious Parasitic Immune mediated Neoplastic Follicular Hyperkeratosis

Question 1083

Follicular Hyperkeratosis

Answer 1083

Keratinaceous plugs in hair follicle infundibula = comedo / comedones (plural) particular feature of Demodicosis-parasite lives down hair follicle Endocrinopathies Comedones (black heads) in a hypothyroid dog -skin scrapes and hair plucks for Demodex are essential first tests in dogs which present with comedones. Keratinaceous collar around emerging hair = follicular cast Non-specific finding, often seen in many diseases where increased keratin produced in the hair follicle e.g. Sebaceous adenitis Demodicosis Dermatophytosis Endocrinopathies Vitamin-A associated dermatosis Usually seen on trichogram

Question 1084

follicular cast

Answer 1084

type of Follicular Hyperkeratosis Keratinaceous collar around emerging hair = follicular cast Non-specific finding, often seen in many diseases where increased keratin produced in the hair follicle e.g. Sebaceous adenitis Demodicosis Dermatophytosis Endocrinopathies Vitamin-A associated dermatosis Usually seen on trichogram

Question 1085

comedo / comedones (plural)

Answer 1085

type of Follicular Hyperkeratosis Keratinaceous plugs in hair follicle infundibula = comedo / comedones (plural) particular feature of Demodicosis-parasite lives down hair follicle Endocrinopathies

Question 1086

Acanthosis

Answer 1086

Increased depth of epidermis - inc no. of layers of cells usually due to persistant low grade trauma different from Hyperkeratosis = Increased depth of cornified layer

Question 1087

Lichenification

Answer 1087

Thickening and hardening of the skin characterised by exaggeration of the superficial skin markings Non-specific finding of many diseases with chronic inflammation or friction : different from Hyperkeratosis = Increased depth of cornified layer

Question 1088

Vesicles of the skin

Answer 1088

A small circumscribed elevation of the epidermis containing clear fluid less than 1 cm (“blister”) Short-lived as epidermis is very fragile Subsequently see erosions and ulcers. Usually occur with: Viruses e.g. FMD Feline orthopoxvirus Orf (sheep) Autoimmune diseases Bulla- As above but more than 1 cm diameter

Question 1089

Erosions vs Ulcers

Answer 1089

Erosions (superficial: basal layer of epidermis not breached) ulcers (deeper: dermis exposed)

Question 1090

Papule

Answer 1090

Papule Small solid elevation of skin <1cm diameter Often erythematous May --> crusts of serum, pus or blood Plaque A large flatter elevation of the skin, sometimes formed by papules coalescing

Question 1091

Plaque

Answer 1091

A large flatter elevation of the skin, sometimes formed by papules coalescing

Question 1092

Pustule

Answer 1092

Pustule Small (<1cm) skin elevation, filled with pus Often start as papule But not all papules turn into pustules! Both are always primary lesions… cf scale, crust Usually associated with infection.. ..but some are sterile (eg auto-immune diseases) do impression smear of contents: Helps differentiate bacterial vs sterile pustules (pustules often sterile in immune-mediated diseases eg pemphigus foliaceus) Also used to detect acantholytic keratinocytes Insert a fine (25-27G) needle into pustule (needle parallel to skin so not puncturing tissue below pustule) Impress microscope slide directly onto pustule contents. Air dry and stain.

Question 1093

Nodules

Answer 1093

Nodules A solid elevation of the skin greater than 1 cm in diameter that usually extends into the deeper skin layers. Nodules may result from: Neoplasia (originating from skin cells, or metastatic) Inflammatory cell accumulation (especially chronic granulomatous inflammation associated with infections or sterile processes) or less commonly, tissue dysplasia or hyperplasia or mineral deposition

Question 1094

Pigmentation Disturbances

Answer 1094

Melanocytes in basal layer of epidermis- Important in skin pigmentation But also role in local modulation of cutaneous inflammation Skin damage can result in both hyperpigmentation and hypopigmentation Hyperpigmentation- Skin pigmentation increased beyond what is normal for that area Non-specific - Commonly post-inflammatory Some endocrine skin disorders Hypopigmentation Skin pigmentation decreased beyond what is normal for that area Feature of diseases affecting the basal epidermis and dermo-epidermal junction in dog, eg some immune-mediated disorders epitheliotropic lymphoma (neoplasia) Hypopigmentation Skin pigmentation decreased beyond what is normal for that area Feature of diseases affecting the basal epidermis and dermo-epidermal junction in dog, eg some immune-mediated disorders epitheliotropic lymphoma (neoplasia) But also post-inflammatory, especially after more marked inflammation in the horse Cutaneous lupus erythematosus (immune-mediated) Leucotrichia

Question 1095

Crusting of the skin

Answer 1095

Formed when dried exudate, serum, pus, blood, cells, scales or medications adhere to skin surface Caused by multiple exudative and ulcerative diseases including: Physical damage- mechanical, thermal, chemical Many infectious processes- Viral, bacterial, fungal, parasitic Sterile inflammatory diseases- auto-immune and immune mediated diseases Ulcerating neoplasms

Question 1096

erythema

Answer 1096

dermal response Damage -> release of pro-inflammatory mediators (incl. histamine) -> vasodilation of dermal vessels -> erythema Common in infectious and allergic processes… Epitheliotropic lymphoma Macule A circumscribed flat area of change in colour of the skin <1cm in diameter >1cm = patch Bacterial pyoderma

Question 1097

Oedema of the skin

Answer 1097

dermal reaction Mediated by histamine and other cytokines  increased vascular permeability  leakage of tissue fluid  urticarial lesions ‘Pit’ on pressure Classically Type I hypersensitivity but occasional other causes Wheals: circumscribed, raised lesion consisting of dermal oedema. -> Reflect localised mast cell degranulation

Question 1098

Thickening of the skin

Answer 1098

dermal reaction Associated with: Longer-standing allergic reactions Late-phase reaction  cellular infiltrate Chronic inflammatory conditions Increased collagen/other connective tissue components NB Sometimes nodular – need to differentiate from neoplasms (fine-needle aspirate/biopsy)

Question 1099

Alopecia

Answer 1099

= Loss of hair Partial Complete Due to failure to grow properly Endocrinopathies Hair follicle dysplasias damage to hair follicles/shafts Trauma Follicular infections Follicular parasites Neoplasia Immune-mediated/autoimmune disease Nutritional deficiency Demidocosis (follicular parasite) Dermatophytosis (Fungal follicular infection) Sertoli cell tumour (testicular tumour) -> produces oestrogens -> alopecia

Question 1100

Normal Skin flora

Answer 1100

Skin and hairs are not sterile and have a resident flora. Normal skin is resistant to microorganisms The resident flora can aid in exclusion of pathogens but may also contribute to disease. Disease occurs when virulence of pathogen overwhelms or bypasses the cutaneous defences - or the resident flora is disadvantaged by local conditions and overgrowth occurs. Definitions. Resident - can replicate on the skin and can persist. Nomad organisms that can colonise and reproduce on the skin for short times. Transient - can not replicate so stay for a short time. Pathogens organisms that become established and can proliferate on the skin surface and deeper that are deleterious to normal physiology of the skin. staphelococus intermedius- resident micrococcus - resident pseudomonas- transient

Question 1101

What should be found on skin microscopy?

Answer 1101

some bacteria and yeast. Malassezia, Gram +ve (Staphylococci) Treat only if intractable send to lab staphelococus psuedointermedius not found on skin but hair and hair folicles Gram –ve unexpected Rods unexpected send to lab – C&S! start treatment -

Question 1102

Bacterial Skin disease

Answer 1102

IS OFTEN SECONDARY Primary disease affects defence Atopic dermatitis Endocrinopathy Nutritional deficiencies Trauma/overcrowding Environmental damage Organisms implicated in the dog most commonly Staphylococcus pseudintermedius Canine Pyoderma 1. Surface pyoderma: Secondary bacterial colonisation of lesions on the skin surface. Examples include: acute moist dermatitis, eczemas and intertrigo. 2. Superficial pyoderma. Infection involves skin and hair follicle epithelium. Examples include: impetigo, superficial bacterial folliculitis, dermatophilosis, pyotraumatic folliculitis and mucocutaneneous pyoderma. 3. Deep pyoderma. Infection involves the dermis and subcutaneous tissue. Examples include: furnculosis, cellulitis, and furunculosis, acral lick furnculosis

Question 1103

Surface pyoderma:

Answer 1103

Secondary bacterial colonisation of lesions on the skin surface. Examples include: acute moist dermatitis, eczemas and intertrigo. Diagnostic techniques * Dermatological signs * Bacterial culture and susceptibility testing * Skin biopsies – histology +/- culture Management Treat the primary disease Treat the bacterial infection (usually topically) Anti-Staphylococcal antibacterial Treat the inflammation (usually topically) Usually corticosteroid - short-acting to reduce the inflammation

Question 1104

Superficial pyoderma.

Answer 1104

Infection involves skin and hair follicle epithelium. Examples include: impetigo, superficial bacterial folliculitis, dermatophilosis, pyotraumatic folliculitis and mucocutaneneous pyoderma. Common, often recurrent (SECONDARY) - treat the primary disease Allergy/endocrinopathy, parasites Clinical Signs Often diffuse – ventral abdomen especially Pustules Papules Epidermal collarettes Alopecia Variable pruritus Epidermal collaret is characterisic- circular leasion of crusting, caused by burst pustule Diagnostic Techniques Dermatological signs – main diagnostic Bacterial culture and susceptibility testing - rarely only if recurrent Skin biopsies – histology +/- culture Management Manage any primary cause Systemic anti-staphylococcal antimicrobial Minimum 3 weeks 1 week beyond cure Topical antibacterial shampoo/rinse e.g. Chlorhexidine Long-term maintenance

Question 1105

Deep pyoderma.

Answer 1105

Infection involves the dermis and subcutaneous tissue. Examples include: furnculosis, cellulitis, and furunculosis, acral lick furnculosis Furuncle – (“boil”) – follicle infection spreads into hair follicle which ruptures in the dermis Cellulitis - infection of follicles and surrounding dermis Difficult to manage Often secondary Some breed predispositions? GSD – immunodeficiency? Clinical Signs Papules Pustules Alopecia Nodules – furuncles, palpable lumps in dermis Sinuses Draining tracts Diagnostic techniques: Dermatological signs Cytology - aspirate/impression smear Bacterial culture and susceptibility testing Skin biopsies – histology +/- culture Management * Treat any primary cause * Topical antibacterial shampoo/rinse * Long courses of systemic antibacterials ○ Based on culture and sensitivity ○ Minimum 6 weeks ○ 2 weeks beyond cure

Question 1106

Acute moist dermatitis

Answer 1106

Surface pyoderma IS USUALLY A SECONDARY CONDITION Look for a primary pruritic condition Otitis externa Anal gland impaction Fleas/other ectoparasites ??Function of hair coat ??Breed predosposition – Golden retriever

Question 1107

Intertrigo

Answer 1107

Surface pyoderma skin fold dermatitis Associated with certain breeds Facial fold Vulval fold Lip fold Tail fold Often less acute/chronic

Question 1108

Fungal Skin disease

Answer 1108

Dermatophytes: Microsporum and Trichopyton species Microsporum canis most common isolate in cats and dogs Use keratin to grow. Grow exclusively in the non living tissue of skin nails & hair. Cause inflammation and irritation. Yeast and Yeast-like organisms: Candida Malassezia Trichosporon

Question 1109

Dermatophytosis

Answer 1109

Microsporum canis Cats>dogs Zoonotic! Reservoirs Infected by direct contact with infected animal/contaminated environment/fomite Ringworm spores can survive for many months Contaminated environment. Exposure to infected host. Fomites Two groups: Culture positive (dogs or) cats with subtle active infections. Culture positive (dogs or cats) no active infection Incubation period is approx 1 week. Spores of the fungus invades anagen hairs – hence circular lesions Germinate – produce hyphae - invasion by digestion of keratin New arthrospores produced Hair breaks off due to weakening leading to partial alopecia Inflammatory reaction leads to folliculitis or furunculosis. Inflammatory disease so animals often pruritic. Clinical Signs: Lesions VERY variable Circular, patchy alopecia (broken hairs) Variable erythema (peripheral?) and pruritus Scale, crusts Local/patchy/generalised Nails may be affected, lost and grow back deformed – onychomycosis Diagnostic techniques Trichogram Wood’s lamp examination Fungal culture McKenzie toothbrush culture PCR Skin biopsies – histology +/- culture Zoonotic! Warn re avoiding handling animals and risk from fomites; esp if immunocompromised people Environmental decontamination: Spores very long-lived in environment – essential to clear from here to prevent continuous reinfection Clip hair around lesions with scissors and dispose carefully of hair Physical cleaning (e.g. daily vacuuming, seal and burn bag) Chemical agents Spontaneous resolution? Topical tx  Miconazole/chlorhexidine shampoo Systemic tx  Ketaconazole licensed for dogs only. Do not use in cats. Itraconazole licensed for cats. Off license in dogs. Clinical resolution reached before mycological cure – base assessment of progress on basis of cultures, not clinical appearance of animal. Monitor all animals with coat brushing weekly: treat until 2-3 negative cultures at least 7 days apart.

Question 1110

Malassezia pachydermatis

Answer 1110

Broad based budding organisms- yeast Isolated from skin and mucous membranes of a variety of species M. pachydermatis is a typical on healthy canine skin and mucosa. It is an opportunistic pathogen of cats and dogs. Infection 100-10000 fold increase in numbers on skin. Breed Predisposition for higher levels in some breeds. Bassett, dachshunds, cocker spaniels, WHWT Common to have concurrent Staphylococcus psuedointermedius infection.

Question 1111

Malassezia dermatitis

Answer 1111

Also known as seborrhoea dermatitis (Seborrhoea = "flow of sebum“) Normal commensal organism Secondary condition Usually generalised Scale – “dry” seborrhoea (dandruff) seborrhoea sicca Greasy coat Seborrhoea oleosa Pathogenesis Primary condition allows yeast overgrowth Yeast lipases alter surface lipid (hence smell) Epidermal turnover rises due to damage (hence scale) Immediate (Type 1) hypersensitivity to yeast develops Clinical Signs Variable, usually generalised Most commonly affected regions are hot and moist! Worse in SKIN FOLDS (athlete’s foot) Erythema Scale Greasy coat OTITIS EXTERNA – may be only sign Variable pruritus Variable alopecia “yeasty” smell Diagnostic techniques Dermatological signs Acetate tape prep Impression smear Fungal culture Management TREAT ANY PRIMARY CAUSE Reduce organism numbers Topical treatment very effective Usually aimed at M.p. AND S.p. Itraconazole if topical fails Often use anti fungal shampoos

Question 1112

steps of a hands off neuro exam

Answer 1112

mentation/sensorume posture gait asymetry

Question 1113

steps of a hands onneuro exam

Answer 1113

proprioseption spinal reflexes cranial nerves nociception

Question 1114

MENTATION vs Levels of Consciousness

Answer 1114

mentation means mental activity Normal Dull/Depressed Obtundation Stuporous- still responds to pain Comatose

Question 1115

MENTATION: behaviour

Answer 1115

Compulsive Disorientation Hyperactive Aggressive

Question 1116

posture in a neuro exam

Answer 1116

Head Turn- forebrain problem, head turns to side of problem Head Turn + Body Turn = Pleurothotonus Head Tilt- vestibular muscle weakness and damage- KYPHOSIS- n excessive curve of the spine results in an abnormal rounding of the upper back LORDOSIS- a deep curve in the spine resulting in dipped back SCOLIOSIS- s shape deviation of the spine special postures Decerebrate Rigidity Decerebellate Rigidity Shiff-Sherrington

Question 1117

Decerebrate Rigidity

Answer 1117

Stuporous or Comatose Extension of all limbs Extension of head and neck (opisthotonus) Acute rostral brainstem injury

Question 1118

Decerebellate Rigidity

Answer 1118

Mentation normal- cerebellum not involved Extension of head and neck (opisthotonus) Thoracic limbs extended Hips flexed- back musces contract, almst lordotic Acute rostral cerebellar injury

Question 1119

Shiff-Sherrington

Answer 1119

Extension of thoracic limbs Normal mentation Reduced to normal tone in pelvic limbs Normal postural responses in thoracic limbs Acute thoracolumbar injury- disc herniation

Question 1120

ATAXIA

Answer 1120

uncordinated gait cerebellar- patient strugles to place feet, incordination, hyermetric (exagerated) gaite, hyometria Vestibular- head tilt, problems with baence, staggering, all four limbs cerebello- vestibular- the cerebellum is involved with the vestibular sytem, head tilt, hypermetria General Proprioceptive/Spinal- involves spinal cord, can effect all four legs but also may just effect pelvic limbs

Question 1121

PARESIS

Answer 1121

weakness of guate Spontaneous knuckling Scuffing of nails Inability to support weight Mono – one limb only Para – pelvic limbs only Hemi – one thoracic and one pelvic (same side) Tetra – All four limbs affected

Question 1122

when is lamness neurological

Answer 1122

Shifting of weight to the contralateral limb Reduced protraction of affected limb Musculoskeletal Radicular pain/Nerve root signature Neuropathy

Question 1123

Asymmetry, Spontaneous and Positional abnormalities in a neuro exam

Answer 1123

Pupil size: Sympathetic vs parasympathetic dysfunction Muscles of mastication: drooping (CNVII) or loss (CN V)- drop jaw Eye Position: (CN III, IV and/or VI) Positional nystagmus or strabismus (vestibular)

Question 1124

neuro Tests for Body and Limbs

Answer 1124

Responses- Postural Hopping Placing Nociception Reflexes- Withdrawal Patellar Perineal Cutaneous trunci- (Extensor carpi radialis) (Cranial tibial) (Triceps) (Gastrops) (Biceps)

Question 1125

PROPRIOCEPTION

Answer 1125

Postural responses- Appropriate response: brisk normal placement of paw Abnormal: delayed response or absence Hopping One leg only- TLs only (wheelbarrow) One side only- PLs only ( Ext postural thrust)

Question 1126

NOCICEPTION

Answer 1126

Response to noxious stimuli Appropriate reaction (vocalization or moving away from noxious stimuli) NOT just movement of limb. In cases of paralysis (plegia) or suspected sensory neuropathy

Question 1127

Spinal Reflexes: Patellar Reflex

Answer 1127

Assessment of Femoral Nerve Appropriate reflex: Kicking out of limb Non-neuro causes for abnormal result: Stifle disease Old age Anatomy: Middle patellar lig. Femoral nerve and L4-L6 spinal cord segment

Question 1128

Spinal Reflexes: Withdrawal Reflex

Answer 1128

DO NOT TRAVEL TO BRAIN Does not require noxious stimuli Appropriate reflex: Flexion of all flexors. Anatomy: Afferent nerve, C6-T2 or L4-S1 spinal cord segment, LMN to flexors

Question 1129

Spinal Reflexes: Cutaneous Trunci Reflex

Answer 1129

Start at L4/5 and pinch with fingers or artery forecepts Continue cranially up to T2 if no response Appropriate reflex = bilateral contraction of cutaneous trunci. Anatomy: Afferent nerve, Spinal cord (C8-L4/5), Brachial plexus, Lateral thoracic nerves, Cutaneous trunci mm.

Question 1130

Spinal Reflexes: Perineal reflex

Answer 1130

stroking the spects of the perineaium watch for the anus clamping down Anatomy: S1-S3 spinal cord segments

Question 1131

neuro tests for head

Answer 1131

Responses- Menace Response Nasal septal mucosal response Reflexes- Pupillary Light Reflex Palpebral Reflex Corneal reflex Vestibulo-ocular reflex Gag reflex

Question 1132

Menace Response

Answer 1132

move hand towards face to cause blink Learned response: > 12 weeks in dogs Not reliable in cats Anatomy: Retina, optic nerve optic chiasm, optic tract, lateral geniculate n. (thalamus), optic radiation, visual cortex (occipital cortex), motor cortex, midbrain, cerebellar cortex, facial nucleus (medulla oblongata), facial n (orbicularis oculi mm)

Question 1133

Nasal septal mucosal response

Answer 1133

poke nose with foreceps and watch for dog flinching away- cover eyes for accurate result Anatomy: nasal septum, ophthalmic branch of CN V, sensory cortex (forebrain)

Question 1134

Pupillary Light Reflex

Answer 1134

shine light on pupil and watch for contraction Anatomy: Retina, optic nerve, optic chiasm, optic tract, pretectal n. (midbrain), parasympathetic n of oculomotor, oculomotor n, ciliary ganglion, short ciliary n, pupillary muscle.

Question 1135

Palpebral reflex

Answer 1135

poke next ot eye, watch for blink Anatomy Medial: A = CN V (ophthalmic branch) E = CN VII (orbicularis oculi mm) Lateral: A = CN V (maxillary branch) E = CN VII (obicularis oculi mm)

Question 1136

Corneal reflex

Answer 1136

poke eye with coton bud, watch for blink(trigeminal nerve) and eye drawing back (facial nerve) Anatomy A = CN V (ophthalmic branch) E = CN VII (obicularis oculi mm) = CN VI (retractor bulbi mm)

Question 1137

Gag reflex

Answer 1137

poke dog in back f throat, watch for swallow Anatomy: A= CN IX and X E= CN IX and X

Question 1138

Vestibulo-ocular reflex

Answer 1138

physiological nastagmus move whole body in asur for small animas move the head an watch for corection of eye direction A = CN VIII E = CN III, IV and CN VI

Question 1139

ranges of motion in a neuro exam

Answer 1139

Neck range of motion Palpation of back and neck check for signs of pain

Question 1140

signs of a forebrain leasion

Answer 1140

circling to side of leasion menece response absent on opposite side to leasion visual input affected- dog wont eat food in bowl on side of leasion

Question 1141

signs of bilateral facil nerve leasion

Answer 1141

no palpebral rsponse on both eyes no menace response response ofn nnasal mucosal response ruling out trigeminal nerve

Question 1142

signs of a bilateral trigeminal nerve leasion

Answer 1142

drop jaw corneal reflex absent insensory section injury but present in motor injury

Question 1143

sings of a cerebellar problem

Answer 1143

head tilt on oposite side to leasion delayed postural reflex on same side as leasion

Question 1144

signs of peripheral nervus sytem issue

Answer 1144

muscle wastage head seems fine- less lilkly to be brain signs of senstation but withdrawl reduced no muscle tone in limbs

Question 1145

AUTONOMIC NERVOUS SYSTEM

Answer 1145

Activating emergency mechanism Preservation of the body’s internal environment: homeostasis E.g change blood supply from skin to guts in aid of preservation Mainly LMN (motor and efferent systems) system but higher centers present within brain (hypothalamus and autonomic nuclei) LMN = Two neuron system- differences between sympathetic and parasympathetic- sympathetic longer and releases acetylcholine and eopineferin whie parasympathetic shorter and just uses acetylecholine Target organ= smooth muscle Parasympathetic vs Sympathetic- YING and YANG relationship, symbiotic

Question 1146

Sympathetic Nervous System

Answer 1146

Flight or Fight response Majority in Thoracolumbar Division [T1-L4]- feeds into other ganglia

Question 1147

Parasympathetic Nervous System

Answer 1147

Rest and Digest Craniosacral divisions Cranio part- give rise to function in head area and slightly branches intothoratic and abdominal Sacral division- pelvic pexus and ganglia

Question 1148

autonomic division of PUPIL CONTROL

Answer 1148

PARASYMPATHETIC= CONSTRICTION SYMPATHETIC = DILATION

Question 1149

assesment of Pupil Size….PARASYMPATHETIC

Answer 1149

Pupillary Light Reflex! Target organ = Sphincter pupillae Involves oculomotor nucleaus-> oculomotor nerve -> cillary gangleion

Question 1150

PARASYMPATHETIC: Dysfunction

Answer 1150

Mydriatic pupil -ve on direct PLR of affected eye -ve on indirect PLR when light shone in unaffected eye INTERNAL OPTHALMAPLEGIA- an ocular movement disorder that presents as an inability to perform conjugate lateral gaze and ophthalmoplegia due to damage to the interneuron between two nuclei of cranial nerves (CN) VI and CN III (internuclear).

Question 1151

assesment of Pupil Size….SYMPATHETIC

Answer 1151

1st order- Hypothalamus ->lateral tectotegmentospinal tract ->Spinal cord segment T1-T3 2nd order Brachial Plexus-> Cervical Sympathetic trunk (with the vagus nerve) 3rd order Cranial cervical ganglion -> passes near middle cavity ->base of skull->exits orbital fissure -> dilator pupillae mm SYMPATHETIC DYSFUNCTION = Horner Syndrome Miosis Third eyelid protrusion Ptosis ( reduced palpebral commissure) Scleral congestion Enophthalmos (Warm ipsilateral pinnae)

Question 1152

symathetic bladder control

Answer 1152

STORAGE = SYMPATHETIC TL division Hypogastric nerve + Relaxes the detrusor muscle Tightens the internal urethral sphincter

Question 1153

parasymathetic bladder control

Answer 1153

MICTURITION/PEEING = PARASYMPATHETIC Sacral division Stretch receptors in the bladder wall travel up the pelvic n. to brain. Centers in the brainstem relay information to activate pelvic nerve +- Contracts the detrusor mm

Question 1154

Pudendal nerve

Answer 1154

controls External urethral sphincter Kept closed during Storage phase (mediated by sympathetic) Opened for micturition (parasympathetic phase)

Question 1155

UMN BLADDER: Dysfunction

Answer 1155

UMN lesion T3-L3- Loss of function from hypogastric muscle, no nerve signals to tell detrusor muscle to relax Increase muscle tone to the external urethral sphincter muscle (lack of inhibition) Increased detrusor muscle tone Increased tone in external urethral sphincter CLINICAL SIGNS- Firm turgid bladder Difficult to express

Question 1156

lmn BLADDER: Dysfunction

Answer 1156

LMN lesion S1-S3 relaxed muscle tone to the external urethral sphincter muscle Decreased detrusor muscle tone and loss of contractility CLINICAL SIGNS Flaccid large bladder Easy to express but not fully Constant leaking of urine

Question 1157

Vestibular System

Answer 1157

Controls balance and posture Stops a cat/dog from falling over Consists of receptors and specialised nuclei Affects movements of eyes, head, neck and limbs CENTRAL vs PERIPHERAL

Question 1158

Peripheral (extracranial) nervous system

Answer 1158

Vestibular receptors Vestibular portion of the vestibulocochlear nerve

Question 1159

Central (intracranial) nervous system

Answer 1159

Vestibular nuclei Caudal cerebellar peduncle Flocculonodular lobe Fastigial nuclei

Question 1160

Peripheral vestibular receptors

Answer 1160

Crista Ampullaris -acceleration/deceleration Macula -static changes in posture

Question 1161

Central vestibular apparatus

Answer 1161

Vestibular nuclei Caudal cerebellar peduncle Flocculonodular lobe Fastigial nuclei

Question 1162

Pathology of Head Tilt

Answer 1162

Unilateral loss of anti-gravity tone on the muscles of the head and neck ipsilateral to the lesion. Imbalance of tone leads to head tilt HEAD TILT TO SIDE OF LESION (n.b exception to the rule [paradoxical])

Question 1163

Gait analysis

Answer 1163

Vestibular ataxia Uncoordinated gait Circling: Circles to the side of the lesion

Question 1164

Clinical Evaluation: Mentation and Posture

Answer 1164

Peripheral: Normal Disorientated Central: Normal  Comatose (Decerebellate Rigidity)

Question 1165

Jerk Nystagmus

Answer 1165

Involuntary rhythmic oscillations of the eyes Fast phase and slow phase NOT spontaneous Elicited via vestibulo-ocular reflex Physiological nystagmus is a normal finding Abnormal finding associated with vestibular disease Spontaneous and positional Fast phase and slow phase Fast phase away from the lesion (with exceptions) Central and peripheral HORIZONTAL VERTICAL ROTATORY

Question 1166

Pendular Nystagmus

Answer 1166

Not pathological Seen in oriental breeds: Siamese overrepresented Seen often in periods of stress

Question 1167

Strabismus

Answer 1167

Abnormal position of the globe of the eye If spontaneous, consider direct cranial nerve dysfunction; III, IV and/or VI In vestibular dysfunction: Positional ventral or ventro-lateral strabismus

Question 1168

Bilateral Vestibular Dysfunction

Answer 1168

Loss of balance to both sides No postural symmetry noted Crouching posture Wide head excursions E.g. thiamine deficiency, metronidazole toxicity, bilateral otitis media/interna

Question 1169

Paradoxical Vestibular dysfunction

Answer 1169

Dysfunction of: Caudal cerebellar peduncle Fastigial nuclei Flocculonodular lobe Lack of inhibition of the vestibular nuclei on affected side -> Greater activation of affected side

Question 1170

Generalised Tonic-Clonic Seizure

Answer 1170

looses consciousness and has stiffening and jerking of the muscles. These seizures usually are generalized, starting on both sides of the brain. Opisthotonus- amatic abnormal posture due to spastic contraction of the extensor muscles of the neck, trunk, and lower extremities that produces a severe backward arching Piloerection- the contraction of small muscles at the base of hair follicles resulting in visible erection of hair. Urination Defecation Salivation Chewing movements Face twitching Clonic phase- paddling Loss of consciousness Mydriasis- dilation of the pupil of the eye Lateral recumbency Tonic phase- outstreached limbs Apnea

Question 1171

What is a seizure?

Answer 1171

ACVIM Consensus 2016 “A non-specific, paroxysmal event of the body that represents an abnormality of forebrain neurotransmission” International Veterinary Epilepsy Task Force 2015 “a transient occurrence of signs due to abnormal excessive or synchronous neuronal activity” Originated by an imbalance of excitatory and inhibitory influences on the cerebral neurons When too many cells in the cerebral cortex become too excited and synchronise, a seizure can result Seizure threshold

Question 1172

Pre-ictal phenomenon

Answer 1172

behavioral changes or autonomic signs that may precede an observable seizure

Question 1173

Ictus

Answer 1173

a sudden paroxysmal neurologic occurrence

Question 1174

Post-ictal phenomenon

Answer 1174

a transient clinical abnormality of the CNS function that appears or becomes more evident when the clinical signs of the seizure have ended Disorientation Ataxia Central blindness Behavioral changes

Question 1175

Generalised seizures

Answer 1175

involvement of both the cerebral hemispheres. Tonic-clonic seizures Clonic Tonic Atonic Absence seizures

Question 1176

Focal seizures

Answer 1176

activation of only part of a cerebral hemisphere simple focal seizures (consciousness is not impaired) complex focal seizures (with impairment of consciousness)

Question 1177

Cluster seizures:

Answer 1177

:two or more seizures in a 24-hour period or one seizure per day

Question 1178

Status epilepticus

Answer 1178

a seizure that shows no clinical signs of arresting after 5 minutes of activity, or recurrent seizures with no recovery between them give emergency ASD If patient newly seizuring naïve of ASDs Haematology Biochemistry (including glucose and electrolytes) Ammonia Bile acids if appropriate (e.g. patient on phenobarbital with signs of adverse effects or uncertain diagnosis) If returning patient on ASDs CBC Biochemistry (including glucose and electrolytes) Ammonia Bile acids if appropriate (e.g. patient on phenobarbital with signs of adverse effects or uncertain diagnosis) Serum levels of anti-seizure drugs (ASD) when appropriate (phenobarbital and potassium bromide – PLAIN SERUM Treatment of Status Epilepticus: duration 5-30 minutes diazepam- 0.5mg-1mg/kg, IV or 1mg/kg rectally, repeated administration >/= 5 minutes apart up to 3 times within 24 hour period Can double the dose in dogs pre-treated with phenobarbital midazolam- 0.2-0.5mg/kg, IN, IV or IM. Repeated administration >/= 5min apart up to 3 times within 24 hr period. CRI 0.2-0.5mg/kg/hr. Continue for 24 hrs and taper. Treatment of SE: duration 30-60 minutes Phenobarbital: In pre-treated patients: 3-5mg/kg, i/v as a bolus In non-pretreated animals: 3-5mg/kg, i/v as bolus (or orally in the event of a cluster seizure) Loading? 2-4 mg/kg q6-8hours [max 24mg/kg/hr] CRI? 2-4mg/kg/hr (<100mg/min) Levetiracetam Loading dose 40-60mg/kg i/v or rectal Followed by: 20mg /kg i/v q 8hrs Treatment of SE: duration 30-60 minutes Potassium Bromide In non-pre-treated patients loading doses: 400-600mg/kg/24hr 100mg/kg PO q4-6hours or 100mg/kg per rectum q24 hours for 5-6 days 130mg/kg/day orally for 6 days Treatment of SE: 60-120 minutes Levetiracetam (can be used in 30-60min interval) Initial dose 40-60mg/kg, i/v or rectally Following therapy: 20mg/kg q 8 hours until seizure-free for at least 48 hours Propofol 1-6mg/kg i/v propofol bolus CRI: 0.1-0.6 mg/kg/min i/v Refractory/Drug-resistant SE: > 120min Ketamine: 5mg/kg, i/v as bolus CRI: 5mg/kg/hr. If seizure-free for 12-24 hrs, continuous rate infusion under observation can be reduced by ~25% every 2 hours. Inhalant anaesthesia: Isoflurane Sevoflurane

Question 1179

Differential diagnoses for sezure

Answer 1179

Syncope Narcolepsy/Cataplexy Neuromuscular Paroxysmal dyskinesia Vestibular episode Idiopathic Head tremor Pain

Question 1180

Idiopathic epilepsy

Answer 1180

(genetic) Recurrent seizures No identifiable cause Genetic/familial predisposition Age dependent

Question 1181

Symptomatic epilepsy

Answer 1181

(structural-metabolic): result of identifiable intracranial or extracranial disease Intracranial (structural) causes such as brain tumors, encephalitides, infarcts… Extracranial (metabolic) diseases such as toxic or metabolic disorders Cryptogenic epilepsy (epilepsy of unknown cause)

Question 1182

Investigations for seizure activity:

Answer 1182

Signalment: age, breed and gender History: Description of event and events before and after that, how long lasted, interictal periods Vaccinations, toxins, head trauma Family history, littermates Physical and neurological examination Abnormal (post-ictal vs inter-ictal) Lateralised signs (structural?) . Haematology, Biochemistry, Urinalysis 5. More extensive work up: Bile acids, Ammonia Serologic studies (infectious diseases) EEG CSF analysis MRI

Question 1183

When to start Anti-Seizure Medication

Answer 1183

>1 seizure within a 6-month period One period of cluster seizures One period of status epilepticus Prolonged or severe post-ictal signs Suspect structural brain disease

Question 1184

Anti-seizure drugs (ASDs) LICENSED in dogs

Answer 1184

Phenobarbitone / Phenobarbital (Epiphen or Phenoleptil or Epityl®) Imepitoin (Pexion®) Potassium bromide (Epilease, Libromide or Bromilep®)

Question 1185

Anti-seizure drugs (ASDs) ‘off-label’ in dogs and cats

Answer 1185

Levetiracetam Zonisamide Gabapentin Pregabalin Topiramate

Question 1186

Phenobarbitone

Answer 1186

MOA: GABAA receptor agonist (potentiating inhibition) Barbiturate 50% protein bound Metabolised by liver (approx. 75%) Approximately a third excreted unchanged in urine Autoinducer of hepatic microsomal enzymes (p450 system) 10-20 days for steady state Expected side effects Polyphagia - High ALKP Polyuria - High ALT Polydipsia - Ataxia (transient) Sedation (transient) - low T4 Dose: 2-3mg/kg PO BID in dogs, 2mg/kg PO BID in cats Monitoring: 2 weeks: CBC, Biochem, pheno serum levels 6 months: CBC, Biochem, pheno serum levels Yearly: Biochem, pheno serum levels Ideal phenobarbital serum levels 25-30 mg/L [10-40] >35 mg/L associated with hepatotoxicity

Question 1187

Potassium Bromide

Answer 1187

anti sezure med MOA: Bromide hyperpolarises neurons entering via Cl- channels Halide salt Excreted in the kidneys (no biotransformation), Half-life in dogs 15-30 days 2-5 months for steady state NOT FOR CATS- eosinphilic brochitis Expected Polyphagia - Polyuria Polydipsia - Ataxia -Sedation DOSE 20-40mg/kg PO SID or dose split BID as monotherapy 10-20mg/kg PO SID if used with phenobarbital. MONITORING 2 months after starting treatment Yearly assessment of serum level and kidney function MANAGEMENT Dietary chloride intake: Increase Cl- = increase clearance of Br- On Biochemistry: False hyperchloraemia (bromide is read as choride)

Question 1188

Imepitoin (Pexion®)

Answer 1188

anti sezure drug MOA: Partial GABA agonist DOSE: 20-40mg/kg PO BID Linear pharmacokinetic, we are NOT currently monitoring serum levels Expected Side effects - Polyphagia - Ataxia - Sedation - Vomiting Other benefits: Anxiolytic; licensed for noise phobia Not licensed for structural epilepsy or cluster seizuring patients

Question 1189

Levetiracetam

Answer 1189

anti sezure med MOA: Inhibits neurotransmitter release (binds to the synaptic vesicle protein 2A) DOSE: 20mg/kg PO TID in dogs and cats Mostly excreted unchanged by the kidneys (biotransformation enzymatic hydrolysis and hepatic metabolism) EXPECTED SIDE EFFECTS: -Hypersalivation (cats) - Sedation - Anorexia MANAGEMENT Linear pharmacokinetic, we are NOT currently monitoring serum levels

Question 1190

Zonisamide

Answer 1190

MOA: inhibition of T-type Ca channels and VG-Na channels = inhibit excitation! Allosterically bind to GABA R to increase function Regulate transporters to decrease glutamate and increase GABA Metabolised by CYP3A4 (with pheno, increase clearance by 50% and shortens half-life) Free-radical scavenger Weak carbonic anhydrase inhibitor Expected side effects - Sedation - Low TT4 - Ataxia - Low albumin Idiosyncratic - Renal tubular acidosis - Polyarthritis - Keratoconjunctivitis sicca

Question 1191

Benzodiazepines

Answer 1191

MOA: GABAA agonist Diazepam and Midazolam Quick onset of action, short half-life Hepatic metabolism Side effects Avoid oral diazepam in cats = idiosyncratic hepatic necrosis

Question 1192

Anti-seizure drugs in an emergency?

Answer 1192

MIDAZOLAM/DIAZEPAM LEVETIRACETAM POTASSIUM BROMIDE PHENOBARBITAL

Question 1193

Treatment of Status Epilepticus: duration 5-30 minutes

Answer 1193

Diazepam: 0.5mg-1mg/kg, IV or 1mg/kg rectally, repeated administration >/= 5 minutes apart up to 3 times within 24 hour period Can double the dose in dogs pre-treated with phenobarbital Midazolam: 0.2-0.5mg/kg, IN, IV or IM. Repeated administration >/= 5min apart up to 3 times within 24 hr period. CRI 0.2-0.5mg/kg/hr. Continue for 24 hrs and taper.

Question 1194

Treatment of SE: duration 30-60 minutes

Answer 1194

Phenobarbital: In pre-treated patients: 3-5mg/kg, i/v as a bolus In non-pretreated animals: 3-5mg/kg, i/v as bolus (or orally in the event of a cluster seizure) Loading? 2-4 mg/kg q6-8hours [max 24mg/kg/hr] CRI? 2-4mg/kg/hr (<100mg/min) Levetiracetam Loading dose 40-60mg/kg i/v or rectal Followed by: 20mg /kg i/v q 8hrs Potassium Bromide In non-pre-treated patients loading doses: 400-600mg/kg/24hr 100mg/kg PO q4-6hours or 100mg/kg per rectum q24 hours for 5-6 days 130mg/kg/day orally for 6 days

Question 1195

Treatment of SE: 60-120 minutes

Answer 1195

Levetiracetam (can be used in 30-60min interval) Initial dose 40-60mg/kg, i/v or rectally Following therapy: 20mg/kg q 8 hours until seizure-free for at least 48 hours Propofol 1-6mg/kg i/v propofol bolus CRI: 0.1-0.6 mg/kg/min i/v

Question 1196

Refractory/Drug-resistant SE: > 120min

Answer 1196

Ketamine: 5mg/kg, i/v as bolus CRI: 5mg/kg/hr. If seizure-free for 12-24 hrs, continuous rate infusion under observation can be reduced by ~25% every 2 hours. Inhalant anaesthesia: Isoflurane Sevoflurane

Question 1197

The Tapetum

Answer 1197

An aid to vision in dim light for nocturnal animals A highly reflective coloured layer in the inner choroid reflecting light back onto the photoreceptors in horse it terminates before optic nerve in sharp line variabkle in dogs and cats

Question 1198

Aqueous fluid

Answer 1198

Watery Constant production- ciliary body Constant drainage- drainage angle

Question 1199

Vitreous fluid

Answer 1199

Gel No turnover

Question 1200

Iris musculature

Answer 1200

Constrictor muscle- Circular Parasympathetic control Dilator muscle- Radial Sympathetic control Miotic = Drug which constricts the pupil Mydriatic = A drug which dilates the pupil

Question 1201

The tarsal plate

Answer 1201

stiffens the lid marginal areas contains the tarsal/Meibomian glands holds sutures much better then adjacent tissues

Question 1202

Distichiasis

Answer 1202

Hairs growing on the edge of the lid from the tarsal/Meibomian glands within the tarsal plate and emerging at the lid margin treatment- Plucking – they regrow Electrolysis Cryo Tarsoconjunctival resection So nothing simple or easily available

Question 1203

Ectopic (conjunctival) cilia

Answer 1203

Emerge from the conjunctival surface and impinge directly on the eye Much more sporadic and far less common than distichiasis Far more painful Alert - young dog (especially bulldogs) with a severely painful eye, possible shallow ulcer and no obvious cause Ectopic cilia can certainly cause shallow ulcers but distichiasis hairs rarely

Question 1204

Entropion

Answer 1204

In-rolling of the lid margin so that skin hairs abrade the eye Chronic severe hair abrasion can cause large masses of corneal granulation tissue. Once the abrasion is removed they resolve. in cats- Kittens/juveniles- British Short Hairs Lid usually needs shortening Older cats- ?pathogenesis Both groups- Major problem for the patient Often not diagnosed It is not advisable to do excision surgery in young pups as the correction required is difficult to judge. A temporary holding procedure – “Tacking” - will buy some time until the pup is more mature

Question 1205

Ectropion

Answer 1205

Out turning of the lid margin with conjunctival exposure More severe ectropion can be part of the “diamond eye” spectrum

Question 1206

Upper lid trichiasis syndrome

Answer 1206

Not true entropion but definitely trichiasis“Middle-aged cocker spaniel upper eyelid syndrome” Middle-aged cocker spaniels (and other breeds and ages) can suffer from a laxity of the upper lid lashes which angle downwards as a result and abrade the eye causing great discomfort and debility. These patients need a (modified) Stades procedure rather than a standard skin-muscle excision

Question 1207

Sebaceous adenoma/epithelioma in the eye

Answer 1207

The most common eyelid tumour in the dog Arises from the tarsal/Meibomian gland Grows as a: well-defined mass requiring full thickness excision but minimal clearances Very low metastatic potential not commonm in cats

Question 1208

Squamous cell carcinoma of the eye

Answer 1208

Lid tumours are very uncommon in the cat SCCa can occur in pale areas It may be nodular and tumour-like OR erosive and destructive

Question 1209

Functions of the Third Eyelid

Answer 1209

Secretory – 30% of aqueous tears Surface protection Tear film distribution Immunological

Question 1210

Cherry Eye

Answer 1210

prolapse of the nictitans gland English bulldogs more than other breeds Burying but preserving the gland (The Pocket Technique) Preserves function Pocket technique ?not that difficult (Relatively) expensive especially if referred Failure rate Excision of the gland 30% of aqueous tear capacity lost Relatively easy and cheap Recommended by many breeders and some vets Comes with a guarantee

Question 1211

The Pre-Corneal Tear Film

Answer 1211

Air Lipid- tarsal glands Aqueou- lacrimal and nictitans gland- Mucus conjunctival goblet cells Corneal surface

Question 1212

Chronic Dry Eye

Answer 1212

Chronic conjunctivitis Dull appearance to the ocular surface Mucopurulent discharge - tenacious and adherent Discomfort Corneal ulceration (variable) Corneal vascularisation and pigmentation Purulent discharge may be hidden in the fornices Uncomplicatedconjunctivitis- antibiotic responsive clears up in a few days does not affect the cornea does not affect the pupil or vision Tear production can be quantified – not a specialist procedure- tear test

Question 1213

corneal ulcer

Answer 1213

A corneal ulcer is a full thickness defect in the epithelium pain potential for progression In favourable conditions the corneal epithelium heals rapidly but… …the corneal stroma is susceptible to enzymatic destruction Proteolytic enzymes may be released by: Bacteria Pseudomonas β haemolytic streps Inflammatory cells Corneal cells Unexplained/sterile Signs of a perforation Sudden pain Convex protrusion of brown/black tissue with overlying fibrinous material Blood from the eye

Question 1214

Indolent ulcers

Answer 1214

generally don’t: get infected deepen melt They just don’t heal! Minor surgery always needed- dont respond to other treatments Debride away all loose epithelium firmly Treat the exposed surface to encourage proper adhesion Local anaesthetic and sedation preferred Debridement needs to be thorough Rub firmly and keep going till it stops “If it comes off it needs to come off” Don’t repeat too soon… …and only if there are loose edges again If the edges are sharp give it longer to heal Repeats possible, serious complications rare Don’t grid stromal ulcers… pathogenesis different …nor cats risk factor for a sequestrum

Question 1215

Corneal Foreign Bodies- essentially two types

Answer 1215

Adherent to surface embedded in/on surface with little penetration can be wiped off or squirted off with a jet of saline under local anaesthesia Intracorneal = thorns easier with a reasonable amount protruding microsurgical problem in many cases needle(s) for removal

Question 1216

Pigmentary keratitis

Answer 1216

Invasion of the cornea by melanocytes A common non-specific response of the cornea of the dog to a variety of insults Common in the medial quadrant of brachycephalics Brachycephalics more prone generally

Question 1217

Dermoid

Answer 1217

a congenital malformation where a patch of skin differentiates on the ocular surface Currently a French bulldog speciality

Question 1218

Pannus

Answer 1218

inflammatory and vascular tissue advances across the cornea always from the ventrolateral direction. Strong association with GSDs topical cyclosporine/tacrolimus or topical steroids

Question 1219

Paracentral lipid dystrophy

Answer 1219

Not proven to be associated with hyperlipidaemia or any systemic disease Deposits of crystalline fat in the central cornea Not proven to be associated with hyperlipidaemia or any systemic disease Peripheral lipid depositions may well be associated with hyperlipidaemia. Investigate

Question 1220

Glaucoma

Answer 1220

Definition - an abnormal rise in intraocular pressure Always a problem of aqueous flow or drainage and not over-production Acute glaucoma causes great pain It rapidly destroys the retina and optic nerve Glaucoma is ultimately the reason for removing most eyes Primary Closed Angle Glaucoma- Primary abnormality of the drainage angle Inherited in several dog breeds Sudden decompensation in middle age with an acute pressure rise Acute pressure rise is devastating – hours matter Bilateral (but not symmetrical) problem The onset is usually acute Easily confused with other conditions The pain is severe and the damage to the eye rapid As a result the most important eye emergency of all The second eye is at risk although it usually appears perfectly normal at the time

Question 1221

Primary lens luxation

Answer 1221

An insidious degeneration of the apparatus supporting the lens Affecting both eyes but not simultaneously If/when the lens luxates anteriorly through the pupil it causes glaucoma, inflammation and secondary corneal oedema presenting as an acute eye Anterior dislocation Surgical lens removal Return the lens to the posterior chamber by external manipulation (“couching”) Then maintain a constricted pupil to keep it there Subluxated lens Maintain a constricted pupil to prevent anterior dislocation (Surgical lens removal – historical now) But the prognosis will always be guarded

Question 1222

Enucleation

Answer 1222

is a means of pain relief and a good one. Removal of a blind painful eye is a simple procedure with a low complication rate which provides pain relief without functional loss. “Without functional loss” – it is not a question of whether the dog “can manage with one eye”.

Question 1223

Chemosis

Answer 1223

oedma of the conjunctiva occurs readily in the cat conjunctiva looks dramatic no prognostic significance

Question 1224

Symblepharon

Answer 1224

The permanent adhesion of ocular surfaces – conjunctiva/cornea - following herpes infection as kittens The flu may have cleared up when the kitten/cat is seen Very variable Often pain free and functionally minor and can be left Special techniques may be required for cases needing surgery

Question 1225

Corneal sequestrum

Answer 1225

Delayed healing of a corneal ulcer may lead to necrosis of the exposed stroma The necrotic stroma then turns brown/black This then acts as a foreign body and causes pain in its own right very common eye condition of cat

Question 1226

Systemic Hypertension and the Eye

Answer 1226

The eyes of cats appear particularly susceptible to the effects of systemic hypertension Dogs with overt ocular signs are usually in renal failure Cats may be surprisingly well with alarmingly high blood pressures Hyphaema in a teenage cat is almost pathognomonic for hypertension unless there has been trauma. Look in the fellow eye

Question 1227

Corneal response to injury

Answer 1227

Epithelium- very good Stroma- significant cellular infiltration so good Endothelium- limited capacity for regeneration

Question 1228

corneal odema

Answer 1228

blue opacity ocuurs ddue to disruption of epthelium

Question 1229

Cellular infiltration of the eye

Answer 1229

White/ creamy opacity Response to infection Scarring and fibrosis

Question 1230

Pentobarbital Sodium (e.g. Dolethal, Pentoject, Euthasol)

Answer 1230

SCHEDULE 3 Barbiturate class of drug 200 or 400mg/ml Coloured solution Progressive CNS depression Stages: i) sedation, ii) intoxication, possibly with involuntary excitement, iii) anaesthesia, (iv) respiratory arrest and subsequent cardiac failure. Rapid IV injection – 200mg/ml 0.4ml/kg debilitated animals 0.6-0.8ml fit/healthy animal (IP, IC, IM, IT) Dogs, cats, rodents, rabbits, cattle, sheep, goats, horses and mink

Question 1231

Somulose

Answer 1231

(SCHEDULE 2) Quinalbarbitone sodium Depresses CNS inc respiratory centre and causes loss of consciousness Cinchocaine hydrochloride Cardiotoxic effects Brain function and cardiac output should stop AT THE SAME TIME CLEAR Solution Licensed in dogs, cats, horses, cattle HIGHLY TOXIC TO HUMANS IV only - VIA 14G CANNULA Horses and Cattle = 1ml/10KG OVER 10-15 Seconds TOO SLOW = ‘Normal’ collapse but prolonged period until death TOO FAST = Premature cardiac arrest (heart attack)

Question 1232

Captive bolt

Answer 1232

Large Animals Stuns by percussive force. MUST be ‘bled’ or ‘pithed’ immediately following stunning Declassified in 1998 – no firearms license required to purchase or use If used in emergency/casualty situations no slaughter license required either

Question 1233

Bleeding (for euthanasia)

Answer 1233

ASAP after stunning – prevents risk of recovery Ideally in tonic phase Sever carotid arteries and jugular veins Emergency – deep transverse cut across angle of the jaw 2 powerful jets of blood Sharp knife at least 120mm long Carcass will not be permitted for human consumption

Question 1234

Pithing

Answer 1234

Not to be performed in animals intended for human consumption Insert a flexible wire or polypropylene rod through the hole in the head made by a captive-bolt. Disposable pithing canes available – Stay inside the carcass

Question 1235

Firearms (for euthanasia)

Answer 1235

Free Bullet Humane Killer – single shot, barrel in contact with animal Shotgun Rifle Hand-gun Shotgun or Firearms License required Storage – locked gun cabinet. Locked metal box in car, ammunition separate from gun health and saftey- Firearms Legislation People Handling and Restraint Backdrop

Question 1236

How is death confirmed

Answer 1236

Absence of rhythmical breathing Absence of corneal reflex Absence of heart beat/pulse Reflex/Agonal ‘gasps’ common

Question 1237

Disposal of carcases

Answer 1237

Burial - Barbituates make boies toxic and owners must be made aware Cremation - Costs involved Incineration/Collection/Fallen Stock

Question 1238

Euthanasia of dogs and cats

Answer 1238

In practice or home visit Almost always by intravenous injection PLAN Gain informed consent Administer sedation if required Secure IV access – cephalic or saphenous vein most common Inject drug IV Confirm death Other methods: Intra-peritoneal Intra-renal Intracardiac

Question 1239

Euthanasia of hrses

Answer 1239

Considerations - Positioning Disposal Safety Insurance - BEVA guidelines Free bullet most common for companion horses Lethal Injection: Gain informed consent Sedate - detomidine IV LA at cannula site Secure IV access with 14g cannula Inject Somulose IV over 10-15 seconds Confirm death

Question 1240

Euthanasia of cattle

Answer 1240

Lethal Injection : 0.4-0.8ml/kg 200mg/ml pentobarbital sodium via rapid IV injection – Jugular vein 1ml/10KG Somulose IV injection over 10-15 seconds – Jugular vein Sedation not normally required in most cases Firearms:

Question 1241

Euthanasia of sheep

Answer 1241

Lethal Injection: 0.4-0.8ml/kg pentobarbital sodium rapid IV injection – Jugular Vein. Sedation not normally required Firearms

Question 1242

Euthanasia of Pigs

Answer 1242

Very difficult Best option is shotgun Can be done with ga into soft muscle the somulose into peritoneal cavity- death takes time

Question 1243

What are RECOVER Guidelines?

Answer 1243

Series of systematic reviews Conducted by more than 100 specialists in the field Evidence based Divided into 5 major topics (domains) 1.Preparedness and prevention 2.Basic life support (BLS) 3.Advanced life support (ALS) 4.Monitoring 5.Post cardiac arrest (PCA) care A total of 101 clinical guidelines were published Evidence classified using Class and Level system

Question 1244

What to do in a case of Cardiopulmonary Arrest

Answer 1244

Philosophy?- cpr on healthy patient will not do harm, start anyway if in doubt Team Size?- could be alone, ideally 3 people with chest compressions, 2 people on respiration, 2 people drawing up drugs, 1 person calling owner, 1 person coordinating team Should we carry out CPR? DNR? Facilities for PCA care Success of CPR? Dogs acute arrest under GA – almost 100% Hospitalised cases Dogs 3.8-25% Cats 2.3-22% People >20%

Question 1245

domain 1 of RECOVER guidelines

Answer 1245

Equipment & Training Ensure: All staff are familiar with and utilise a standardised crash cart- Regular training? Needed drugs and equipment in logical sequence- labels pointing forward Pre drawn seringes of adrenalin and atropine Ensure: Cognitive aids are available Staff receive comprehensive training (including simulations) plus assessment to ensure comprehension Education & Leadership- Refresher training every 6 months recommended (I-A) Specific leadership training for those leading CPR (I-A) Both vets and nurses are capable of leading CPR (IIb-B) Debriefing after CPR to discuss performance (I-A)

Question 1246

domain 2 of RECOVER guidelines

Answer 1246

Clinical signs of CPA? Discoloured blood at surgical site Bleeding stops 'Gasping' ventilation or apnoea Mucous membranes change colour CRT > 2 s No heart sounds No palpable pulse Central eye Mydriasis Dry cornea Cranial nerve arreflexia Generalised muscle relaxation Response- Respond conservatively- O2  PPV  ECC  IT drugs  indirect DC defibrillation (not very useful) Respond aggressively- O2  PPV  thoracotomy- direct cardiac compressions and deal with sequale ICC  IV / IC drugs  direct DC defibrillation Respond conservatively  aggressive if no response DNR Response depends on; Owner Number of assistants available (time of day) Equipment available Drug availability Size of patient Type of arrest: “acute” vs “chronic” Domain 2: Basic life support (BLS) A – Airway B – Breathing C – Circulation D – Drugs E – Electric defibrillation F – Follow up Accept the fact- Call assistance Position In right lateral recumbency On hard surface In head-down position- Drainage of fliud and good blood flow to brain A: Airway Clear airway Cuffed endotracheal tube Check patency Position accurately Breathing- PPV- Anaesthetic machine + abs 100 % O2 Self-inflating resuscitation bags- Air or 100 % O2   No synchronicity Ensure expiratory pause No PEEP Rate = maximum 10 bpm DO NOT OVERVENTILATE   C: Circulation-  Check pulse External cardiac compression (ECC) - Cardiac pump, Thoracic pump Internal cardiac compression (ICC)

Question 1247

Acute Arrest

Answer 1247

Oxygen runs out In myocytes Good prognosis

Question 1248

Chronic Arrest

Answer 1248

Oxygen runs out and there is lactate build up in myocytes- old dog with comorbidities

Question 1249

Cardiac pump

Answer 1249

Cats Dogs < 15 kg rabbit Narrow chests   Compression ventral third 3rd - 6th ribs Between thumb and forefinger   Compression rate 80 - 100 per minute, musxle needs time o relax

Question 1250

Thoracic pump

Answer 1250

For dogs > 20 kg “Barrel chests” (?In dorsal) Compression widest point Compression rate 80 - 100 per minute Compressions during peak lung inflation are fine HANDS OFF BETWEEN COMPRESSIONS

Question 1251

Internal Cardiac Compressions

Answer 1251

Open-chest CPR may be considered in cases of intrathoracic disease if appropriate resources are available for the intensive PCA care these patients will require If thorax is open When ECC fails (2 minutes but can do alot longer) When ECC futile 'Chronic' arrests in dogs > 20 kg Technique   Rapid clip in long-coats over left 3rd - 6th ic spaces Identify 5th ic space Deflate lungs Boldly incise Blunt scissors sternum to dorsum Open pericardium 'Milk' ventricles at 80 - 120 min-1 Internal cardiac compression: advantages More effective Arrhythmias diagnosis Assessment of contractility Atrial & vena caval filling Lung inflation assessed Aortic cross-clamping Cardiac warming Accurate IC injection

Question 1252

domain 3 of RECOVER guidelines

Answer 1252

Advanced Life Support Have specific list of drug doses Adrenaline- 10 mg kg -1 (low dose) (x3 for Intra Tracheal (IT), follow up with saline) x3 then one High dose if needed Atropine - 40 mg kg -1 (x3 IT) every 2/3 rounds- gets rid of low heart rate ADH (vasopressin) - 0.8IU/kg Lidocaine- 2 – 4 mg kg -1 25 – 75 mg kg -1 min –1- FOR ARYTHMIAS Amiodarone – V/A fib- 5mg/kg- FIBRILATION, last resort NO fluids unless hypovolaemic (Magnesium) (Methoxamine - 500 mg kg -1 (X3 IT)) (Calcium) If in doubt use twice maintanence E: Electrical Defibrillation Energy required Lowest setting External 1 - 5 - joules kg -1 Internal 0.1 - 0.5 Crank up Cardiac massage inter discharge

Question 1253

Domain 4 of RECOVER guidelines

Answer 1253

Monitoring – Diagnosing CPA “Rapid identification of a patient requiring CPR allows more rapid institution of BLS and ALS, which increases the chance of ROSC” Pulse palpation to diagnose CPA is NOT recommended (current human guidelines limit pulse palpation by health care professionals to less than 10 seconds before BLS measures are initiated). Electrocardiography (ECG) or Doppler blood pressure measurement to diagnose CPA is NOT recommended ECG or Doppler blood pressure measurement to detect impending CPA is reasonable to perform in at-risk patients End-tidal carbon dioxide (EtCO2) monitoring is recommended for intubated patients at risk of CPA EtCO2 correlates well with cardiac output and rapidly drops to zero at CPA onset ECG recommended for rhythm evaluation- only during intercycle pauses and NOT delay resumption of chest compressions EtCO2 monitoring during CPR to evaluate efficacy of chest compressions is reasonable - ROSC will cause a sharp increase in EtCO2 10-15 c02 = good cpr Blood gas and electrolyte analysis may be helpful in evaluating CPR effectiveness and identifying underlying causes If underlying electrolyte derangements are suspected or known, electrolyte analysis to guide therapy is recommended In patients with documented hyperkalaemia, treatment is recommended

Question 1254

Domain 5 of RECOVER guidelines

Answer 1254

Post Cardiac Arrest Care Excellent PCA care- Minimises CPA recurrence and maximises patient discharge. >50% of dogs and cats will have another CPA event while hospitalised Following ROSC patients have: Haemodynamic instability (vasopressor therapy during CPR or the underlying cause of CPA) Cardiac ischaemia Systemic inflammatory response syndrome (inflammatory system activation and excess circulating cytokines) Anoxic brain injury Referral to Specialty Centre?- improved survival of patients treated by professionals with experience in PCA care and in facilities with higher staff-to-patient ratios Research has indicated that patients were more likely to survive when drugs, such as dopamine and vasopressin, were available and more staff were involved in resuscitation efforts It is reasonable to refer a PCA patient to a facility with- 24-hour care Higher staff-to-patient ratios Advanced critical care capabilities F: Follow Up Oxygenation & ventilation Fluids and urine output Inotropes & anti-arrhythmics Analgesics Warmth OR therapeutic hypothermia Antibiosis Position Neurological sequelae, i.e. Diazepam Monitor Fee collection

Question 1255

Cardiopulmonary Arrest

Answer 1255

Myocardial disease Myocardial hypoxia- Systemic hypoxia Cardiac overwork Hypotension Extremes of temperature Extremes of pH Altered electrolytes Toxaemia

Question 1256

Primary Assessment for triage

Answer 1256

Done by receptionist, nurse ect Respiration Awareness Perfusion RAP

Question 1257

Triaging airway

Answer 1257

Any change in breathing pattern might be an emergency Step back and look- still has airway? just reverse sneezing? abdominal effort? mouth breathing in cat? ?? Emergency Ballpark – Above 50 Br/min considered emergency finding Mucous membranes Pulse oximeter

Question 1258

Triaging AWARENESS

Answer 1258

It is conscious? Yes? Is it: Alert? Normal behavior and is responsive BAR/QAR Depressed? Awake but subdued. Uninterested in environment QAR? Delirious? Awake but altered perception. Responds inappropriately to stimulus Watch for change – a decline in level of consciousness could be indicative of a worsening prognosis Stuporous: Remains in sleep state. Only roused by strong stimulus Comatose: Deep unconsciousness. Unable to rouse even with strong stimulus What kind of situations are these most relevant? What about an animal in a seizure??

Question 1259

Triaging PERFUSION

Answer 1259

MUCUS MEMBRANES They should be PINK Any colour change could represent an emergency They should have a capillary refil time of less than 2 seconds (CRT<2). Cardiovascular collapse might have a CRT of 3 seconds or more. PULSES Quality – are they weak and hard to feel? Are they bounding or hyperdynamic? Rate – too fast? Too slow? Does it co-ordinate with the heart rate i.e. Synchronous or are there Pulse Deficits Rhythm – regular? Irregular? 3. AUSCULATE THE HEART The Rate – too fast or too slow? The Sounds – murmurs? The Rhythm – regular or irregular?

Question 1260

Secondary Assessments - Respiratory

Answer 1260

OXYGEN – Flowby, mask, oxygen tent, nasal prongs Airway?! Inspiratory or expiratory issue?? Primary Respiratory vs Primary Cardio? b lines- lung rocket- seen on t fast scan with wet lungs pulmonary odema can be seen on radiograph as enlarged radioopaque heart pleural effusion can be seen on radiograph as lifting of lungs or large field of radioopuaque material

Question 1261

Secondary Assessments - Awareness

Answer 1261

What is this about?? Pupil assessment: Pupillary Light Response PLR Miosis (bad)? OR Mydriasis(worse)?- progression of this can indicate herniation (no way back) A change? Oculocephalic Reflexes? Strabismus or Nystagmus? Cerebral Perfusion Pressure = Mean Arterial Pressure – Intracranial Pressure CPP = MAP – ICP OXYGEN MEASURE BLOOD PRESSURE IDENTIFY AND TREAT HYPOVOLAEMIA POSITIONING – Keep head at 30^ to ma Head trauma+ shock= vasodilation, leading to increased icp

Question 1262

Secondary assessment - Perfusion

Answer 1262

Hypovolaemic Shock **NEED TO RECOGNISE AND ADDRESS THIS ** Tachycardic Delayed CRT on pale mucous membranes Progresses to weak pulses Dull mentation Low temp/cool extremities Anaemia- Pale/white mucous membranes Normal CRT? Pulse quality bounding – weak Tachycardia Is it bleeding?? Where?! More chronic? Tachypnoea Cardiac Dysfunction- Acute Heart Failure Tachycardia Tachpnoea/Dyspnoea Weak pulses CARDIAC AUSCULATION – changes in RHYTHM, SOUNDS (murmurs or gallop) LUNG FIELD AUSCULATION – Might hear adventitious lung sounds like crackles MUCOUS MEMBRANES – Pale, with long CRT Sepsis- Aka Septic Shock High rectal temp as in over 40 ^C OR low rectal temp as in less than 38^C Tachycardia (OR bradycardia – typically in cats) Hyperemic (RED) mucous membranes with short CRT (less so in cats) Hypotension Other clinical signs assoc with the disease foci.

Question 1263

Other markers to check with triage

Answer 1263

Glucose- Check with glucometer The bladder- Can they urinate? PAIN- **The 4th vital marker!!!** Pain can confuse your diagnostic picture!! Administer analgesia and re-examine, re-examine, re-examine. Opiods vs NSAIDS vs Others – what is appropriate?

Question 1264

Horse obstetrics

Answer 1264

HEALTH AND SAFETY – PLEASE TAKE CARE Stage 2 labour (after the membranes are passed) is only 20 mins in a normal foaling. Foals not delivered within 30 mins have a much lower survival rate Retained foetal membranes – 6 hour window

Question 1265

What is an emergency in exotics?

Answer 1265

Initial phone call Based on this call need to determine whether an emergency- Signalment Species, breed, sex, neutered/entire, age Clinical signs When did this start? Trauma – when and how? Did owner notice the animal eat anything poisonous/toxic? How much and what? Birds – respiratory toxins? Instructions to client Basic first aid Handling Correct Transport to the surgery Examples of signs noted in small mammals needing immediate attention Anorexia Bloating Haemorrhage Respiratory distress/compromise Collapse Diarrhoea or absence of faeces (particularly herbivores) Dysuria Dystocia Neurological signs Traumatic injuries Vomiting (ferrets) Can be divided into two categories Acute- A sudden, recent event Fight/bite wounds (myiasis), haemorrhage Trauma – falls, crash landings, fractures Prolapses Dystocia Chronic- A more chronic illness that has reached a critical point- Dental disease, GI disease Can be just as life threatening!

Question 1266

First aid and basic information in exotic emergencies for client

Answer 1266

Basic first aid – allows animal to be transported safely to optimise survival Bleeding -> apply pressure Burns -> Cool area immediately Choking -> keep animal calm, if breathing immediate travel to surgery. If partially obstructed allow animal to cough. If airway obstructed a modified Heimlich manoeuvre performed Hypothermia -> bubble wrap & towel to prevent further heat loss. Snugglesafe/hotwater bottle covered -> do not want to burn! Hyperthermia (heat stroke – rabbits/guinea pigs) -> move to cooler area. Cool slowly. Drizzle water over, concentrating on head, stomach, inner thighs and footpads. Seizures -> darken room, remove hazards. Time how long seizure lasts. Do not restrain Prolapse -> dampened substrate – damp kitchen towel (no woodchip or sand), cover with cling film/glove

Question 1267

Procedure for exotics emergencies in practice

Answer 1267

Stable vs unstable? Observe the animal History collection: Reason for concerns Diet and husbandry- Hypocalcaemic tetany -> birds & reptiles. Vaccination history (distemper – ferrets; Myxo/RHD 1& 2 – rabbits) Neutering status (ferrets – oestrus induced anaemia. Rabbits – uterine adenocarcinoma/pulmonary metastases) Assess husbandry 1. What do they feed it? 2. Do they feed vitamin/mineral supplements? 3. Is there UVB provision? 4. What temperature gradient do they keep the vivarium at? 5. What hides/cage furniture is present in the tank? 6. What humidity do they keep the vivarium at? 7. Do they have any other reptiles/pets? 8. If a snake-when did it last shed its skin, and was it a complete shed? Physical examination – primary assessment Basic exam initially until stabilised. Alertness Posture Facial asymmetry/facial changes Locomotion Body condition score Coughing Sneezing Wheezing Dyspnoea Open-mouth breathing Increased respiratory effort Ocular and/or nasal discharge Respiratory noise Poor hair coat Abnormal stance Helps to determine level of urgency Standard clinical exam ABCDE protocol

Question 1268

Reptiles - triage

Answer 1268

Initial Assessment 1. Safety first! Is it potentially hazardous/dangerous to the handler? 2. Is it mouth-breathing and possibly in respiratory distress? 3. Is it a species that can perform autotomy? (many geckos will shed their tails very easily) 4. Is it suffering from metabolic bone disease making it a risk to handle? (deformed limbs, shell, spine and inability to support its own weight may predispose it to pathological fractures) 5. How large is the animal? (many larger species of tortoise are heavy and strong, with the ability to crush fingers. Snakes longer than 3-4 feet require more than one handler).

Question 1269

Birds - triage

Answer 1269

Any bird that is unconscious, seizuring, with evidence of head trauma or respiratory distress should be attended to immediately. Birds that are off colour should be hospitalised in a quiet, warm (29-30°C), dimly lit area with supplemental oxygen if there is any evidence of respiratory distress and should be examined as soon as possible. All birds presenting as an emergency should be assumed to be hypothermic

Question 1270

Primary assement of exotics procedure

Answer 1270

ABCDE Airway -> chest & abdominal movements, respiratory effort, respiratory noise, open mouth breathing. Open mouth breathing = Severe distress for birds. Severe distress for our small mammal patient such as rabbits & guinea pigs-> obligate nasal breathers. Breathing -> depth, frequency, rate and rhythm of respiratory movements. - Nostril flaring. Auscultate for respiratory sounds (wheezing/whistling) or for absence of sounds. Percussion of thorax – pneumothorax/pleural effusion. Circulation ->pulse rate/strength, mucous membrane colour, heart rate and rhythm. Reptiles -> use of a Doppler probe applied over the heart/carotid artery can provide an assessment of blood flow -> can assess intensity of flow and turbulence. Disability/disease -> assess the animals consciousness and responsiveness to the surroundings. Assess reflexes Remember menace response frequently ABSENT in rabbits and rodents Exposure to the environment- Bruises, fractures, wounds, contamination Check body temperature If stable -> proceed to secondary assessment/full physical examination

Question 1271

Handling and Hospitalisation of exotics

Answer 1271

Handling Keep to a minimum Place on a non-slippery surface Visualisation within a clear box  transillumination Towel Constantly monitor for signs of stress  stop! Consider sedation Hospitalisation Appropriate environment Heated vivariums to POTZ Appropriate temperature and humidity Escape proof enclosures Quiet environment – minimise stress – Pet Remedy plug-in or spray (is safe for birds!) Predator/prey

Question 1272

Differential for a down dry cow

Answer 1272

Dystocia- uterine torsion, seen as ime of partuition Metabolic- milk fever (secondary possibly to dystocia), ca drop from parturition- not seen without calving complication Toxaemia- recently dried of cows: toxic mastitis, selective dry off, septic peritonitis (quick drop) Trauma- always possibility, dry cows pregnant and mixed into new groups so increases risk, lamness prevents them form rising Physical- near calving puts pressure on many body systems and so may just be the cause

Question 1273

Differentials for down fresh cows

Answer 1273

Trauma (obstetric)- biggest reason, calving paralysis syndromes (nerve damage): soon or late onset Metabolic- Milk Fever Toxic- Mastitis, Metritis

Question 1274

Differentials for Lactating fresh cows

Answer 1274

Traumatic Toxic Metabolic

Question 1275

Reasons grazing causes a down cow

Answer 1275

Toxin Ingestion Hypomagnasaemia- to treat magnesium goes under skin NOT IN VEIN

Question 1276

Reasons grazing causes a heifer

Answer 1276

Trauma Toxin Ingestion Chronic?- may think its acute however could be a long term management problem: pnuemonia

Question 1277

Treatment of a down cow

Answer 1277

Traumatic Depends on prognosis NSAID Supportive care Slaughter certificate?- for animla sthat do not show any sign of systemic disease of emaciation. Needs to be close to abitoure as slaughter man must get there. Kill on farm- captive bolt and examination. Need to know meds that they’ve had Metabolic Correct underlying challenge Supportive care Toxic Depends on prognosis Fluids, NSAID, +/- Abs Supportive care Continued care essential- farmer input important to prevent sequential conitions. If farmer cannot support cow euthanasia may be option.

Question 1278

IV access exotic mammals

Answer 1278

Rabbits – Lateral saphenous vein, cephalic vein or marginal ear vein Guinea pigs – cephalic vein, lateral saphenous, jugular vein, cranial vena cava Ferrets – cephalic, saphenous, jugular vein Hedgehogs – jugular vein, cranial vena cava

Question 1279

Blood sampling - reptiles

Answer 1279

Can take up to 1ml/100g in a healthy animal Advise to collect 0.5ml/100g- Most patients are compromised Collect in lithium-heparin tubes (birds & reptiles) Prepare a fresh blood smear Edta causes haemolysis

Question 1280

Blood collection - chelonians

Answer 1280

Jugular vein Less chance of lymphodilution Often at level of auricular scale and base of neck Apply pressure after Subcarapacial sinus Haemodilution Potential for damage to spine Dorsal coccygeal vein Haemodilution Potential for damage to coccygeal vertebrae Subcarapacial – situated in the midline below the cranial aspect of the carapace, just above the caudal cervical vertebrae Brachial plexus Useful in larger chelonians Extend front limb Palpate tendon on caudal aspect of radial-humeral joint Insert needle just caudal or ventral to the tendon

Question 1281

Blood collection - lizards

Answer 1281

Ventral tail vein Care with species that perform autotomy Jugular vein Can be considered for leopard geckos

Question 1282

Blood collection - snakes

Answer 1282

Ventral tail vein Recommended site Care not to insert needle into hemipenes or cloacal musk glands Cardiocentesis (ADVISE SEDATION FOR THIS METHOD!) CARE - risks of laceration to ventricle and risk of pericardial haemorrhage

Question 1283

Blood collection - birds

Answer 1283

Venepuncture sites Right jugular vein Can obtain large volumes Gentle pressure to achieve haemostasis Basilic (ulnar/brachial vein) Extend wing and visualise vein Vein runs over the elbow area Care as haematoma formation is common Medial metatarsal vein Vein is very short in psittacines

Question 1284

Assessing hydration In exotics

Answer 1284

Assess hydration  often dehydrated Methods are subjective +/- in combination with lab tests Skin turgor – variable  greater elasticity in mammals compared with birds & reptiles. Greater elasticity in younger and fatter animals. Assess over pectoral muscles in birds & scruff of neck most mammals. <5% = no clear sign of skin tenting/loss of elasticity 5-6% = slight skin tenting & loss of elasticity 7-9% = notable skin tenting % significant loss of elasticity 10-12% = marked skin tenting & complete loss of elasticity 12-15% = marked skin tenting & complete loss of elasticity Mucous membranes – difficult to assess. Tacky at 7-9% and dry at 10-15% CRT (mammals) & venous refill time (birds) - >2 seconds at 7-9% and >3 seconds at 10-15% Eyes – varies with species and bodyweight. Slightly sunken at 7-9%, noticeably sunken at 10-12% and markedly sunken at 12-15% General condition – variable and difficult to assess normal in a wild animal  stress response. 7-9% mild changes in mentation, 10-12% marked changes in mentation, 12-15% moderate shock and moribund

Question 1285

Fluid therapy (birds)

Answer 1285

Ability to maintain IV lines more challenging in wildlife/zoo birds vs pet Direct monitoring often more limited Birds- SC injection  inguinal or precrural folds, wing web (propatagium), axilla, interscapular area- Up to 20ml/kg  I tend to go LOWER Can add hyaluronidase – 1500IU/L added to sterile crystalloid fluids – increases absorption IV or IO (non pneumatised long bone only – ulna or tibiotarsus) Maintenance – varies with size of bird – very small birds require more per body mass Average daily maintenance = 100ml/kg/da

Question 1286

Fluid therapy – IO tibiotarsus

Answer 1286

1. Anaesthetise the bird and administer analgesia 2. Aseptic preparation and administer local anaesthesia 3. Hold the tibiotarsus in one hand 4. Insert the needle into the cnemial crest, through the insertion of the patellar tendon that is aligned with the diaphysis. Gently advance the needle 5. Suture in place

Question 1287

Fluid therapy – IO ulna

Answer 1287

GA and administer analgesia 2. Flex the carpus and identify the needle insertion site on the dorsal surface of the ulna just distal to the condyle. 3. Infuse local anaesthesia 4. Aseptic skin preparation 5. Hold the limb and insert the needle in the mid portion of the condyle and in the same plane as the bone 6. Seat the tip of the needle into the periosteum. Rotate the needle and advance. A gentle ‘pop’ may be felt. 7. Flush catheter and secure with tape and sutures

Question 1288

Crop tubing

Answer 1288

Fluid therapy (birds) Crop tubing into crop or at level of thoracic inlet for species without a well developed crop (owls) General rule = crop volume is calculated as 5% bodyweight  LOWER in debilitated patients

Question 1289

Fluid therapy (reptiles)

Answer 1289

Epicoelomic (chelonians) Between the plastron and coelomic membrane Intravenous Requires surgical cut-down Intraosseous Medial tibial crest (lizards) Tibial crest and gular plastron (chelonians) Epicoelomic route recommended  10-20 ml/kg can be given IO requires sedation. In chelonians also reports of IO on the bony bridge but there is debate whether the bridge communicates with vascular system

Question 1290

Cardiopulmonary Resuscitation in reptiles

Answer 1290

Establish an airway (reptiles) Intubation Glottis situated rostrally (lizards & snakes) Tortoise – more challenging due to fleshy tongue Tortoise – Complete tracheal rings Lizards & snakes – incomplete tracheal rings IPPV required Small animal ventilator Manually

Question 1291

Emergency diagnostics

Answer 1291

Conscious radiography DV – assess for shelled eggs (birds and reptiles) Gas within intestinal tract (gastric dilatation – rabbits/g pigs; GDV guinea pigs) Point-of-Care Ultrasound (POCUS) Detection of free fluid Evaluation of trauma cases – pneumothorax/penetrating injury patients

Question 1292

- Describe a basic anesthetic plan for a routine bitch spay

Answer 1292

- Acp or alpha 2 agonist- give reasons for choice e.g (medetomidine gives good anasthesia and analgesia but produces profound bradycardia. Has effective time of 40 mins (is this enough for op? alpha-2 hump as it wears off once prep is finished- top up alpha 2 or give something else appropriate to give analgesia) - - Opiod- - buprenorphine?- last up to 6 hours. When dog gets light you must top up with ketamine/ something other than an opiod. - Methadone is a better choice as as a full mu agonist opiod you can top up, sicker the patient lower the dose. Start low you can always give more top up with half dose. Also, cheaper -don’t forget recovery- alpha 2s only last 40 mins!!!!.

Question 1293

What is the common arrhythmia associated with alpha 2s-

Answer 1293

2nd degree av block. P wave without qrs Will be herd as missed heartbeats

Question 1294

Can you use lidocaine in cats as an anti arhythmic iv

Answer 1294

Only one bolus!!!! For cats with ventricular dysrhythmias

Question 1295

Recommended sedatives for cvrs/ compromised patients

Answer 1295

Very sick patient (cartiovascular- gdv)- sicker the patient the more likely methadone and only a methadone (opiod) is best. Treat bradycardia with atropine Cavvies with mitral valve disease- acp causes less adrenaline, vasodilation, is an antiemetic and calms the dog Benzodiazapime may be appropriate in very young/ very old patients Alpha 2s good because they can be antagonized

Question 1296

Why is butorphanol good for birds and exotics

Answer 1296

Lots of birds and some reptiles have lots of KAPPA receptors so targeting those is thought to be better

Question 1297

Atropine vs adrenaline-

Answer 1297

Atropine increases vagal tone- should be added in every third round of cpr to combat brady cardia Adenerline increases heart rate and returns blood to heart- drug of choice

Question 1298

Cardiogenic ossilations

Answer 1298

Heart beating againt lungs pushes out small bits of co2 and causes “bumpy lines” on capnograph.

Question 1299

Sail shape on capnograph means….

Answer 1299

obstruction

Question 1300

A capnograph that does not reach the dotted baseline indicates

Answer 1300

This is caused by Non- rebreathing systems - The valve being shut (but only in first few seconds) - Too low flow- flow pushes co2 out Circle - Sodalime running out - Stuck valves in set

Question 1301

- Gas flows are measured in

Answer 1301

- Liters per minute