prep for clinical practice spot exam Flashcards

(263 cards)

1
Q

Total body water =

A

2/3 body weight

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2
Q

Aims of fluid therapy

A

Maintenance of normal physiology – e.g. during anaesthesia
Improvement of organ function e.g. kidney, heart, liver
The correction of electrolyte disturbances
The correction of hypovolaemia
The correction of acid base disturbances
(Total parenteral nutrition (TPN) - usually partial parenteral nutrition (PPN) used in animals)

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3
Q

what is the fluid defecit of a patient with tacky muscous membranes

A

5-6%

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4
Q

what is the fluid defecit of a patient with skin tenting and shrunked eyes

A

6-8%

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5
Q

what is the fluid defecit of a patient with increased pulse rate and colde peripheries

A

8-10%

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6
Q

what is the fluid defecit of a patient with weak pulses

A

10-12%

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7
Q

what is the fluid defecit of a patient with collapse

A

12-15%

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8
Q

What is the daily maintenance rate for an animal?

A

≈2.5ml/kg/hour
≈60ml/kg/day
{Or (30 x Kg) + 70 ???}

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9
Q

Types of fluid

A

Crystalloids (hypotonic, isotonic, hypertonic)

Colloids

Blood products
HBOCS (hemoglobin-based oxygen carrying solutions) –££ & problems….

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10
Q

Crystalloids- Isotonic-Lactated Ringer’s solution (LRS) aka Hartmann’s

A

If in doubt, choose Hartmann’s!

Inadequate potassium for long term therapy
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

Na+ 130 mEq/l , Cl– 109mEq/l
Buffered, contains lactate as a bicarbonate precursor

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11
Q

Crystalloids- Hypotonic

A

0.18% NaCl
0.18% NaCl + 5% glucose

Do you really want to use this ???

Hypotonic losses occur when the type of fluid being lost has a higher concentration of water than plasma, such as with diabetes insipidus and panting.

Hypotonic crystalloids are useful for treating patients with hypotonic fluid losses that result in hypernatremia or patients that have renal disease and cannot excrete the salt load of balanced isotonic solution

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12
Q

Crystalloids- Hypertonic saline

A

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 ICP

used during resuscitation in hypovolemic shock and to decrease intracranial pressure.

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13
Q

colloids

A

Colloid solutions contain large molecules (>10,000 Da) and tend to remain in the intravascular space longer than crystalloids

Support circulating blood volume
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

HES solutions are thought to be most effective in treating hypovolemia because the colloid should theoretically remain in the intravascular space

includes-
artificial -gelatins, dextrans, starches, HBOCs
Oxypolygelatin
Dextran 40
Pentastarch
Hetastarch
Albumin
Whole blood
Plasma

artificial -gelatins, dextrans, starches, HBOCs
natural colloids e.g. albumin, plasma

However, no evidence of clinical superiority
over crystalloids

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14
Q

Colloids – Gelatins (ntk)

A

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

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15
Q

Colloids – starches (ntk)

A

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

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16
Q

blood products

A

Natural’ colloids
Chosen according to clinical requirement
Whole blood
pRBCs
Ffp
Cryoprecipitate

Match the fluid to the loss

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17
Q

Oxyglobin Solution

A

Oxyglobin is a solution for infusion (drip into a vein). What is Oxyglobin used for? Oxyglobin is used to increase the oxygen content of the blood in dogs with anaemia (low red-blood-cell count). Oxyglobin should be used for at least 24 hours.

0 ml per kilogram body weight, administered at a rate of up to 10 ml/kg per hour. The most appropriate dose depends on the severity of the anaemia and how long the dog has been anaemic, as well as the desired duration of the medicine’s effect. Oxyglobin is intended for a single use only. Oxyglobin does not need to be matched to the dog’s blood type

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18
Q

Intravenous access for fluid therapy

A

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)

Complications can & do occur:
Extravasation
Thrombosis
Thrombophlebitis
Infection
Emboli
Exsanguination

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19
Q

burette

A

will deliver 60 drops per ml (more accuratethan giving set) for fluid therapy

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20
Q

giving set

A

it will deliver 15 or 20 drops per ml (check on the packet)
for fluid therapy
less accurate than burrette

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21
Q

how to calculate Volume and rate of fluid therapy

A

Calculate total deficit (% fluid deficit + losses )
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!!

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22
Q

Why Give Fluids during anesthesia?

A

maintain circulating volume to ensure adequate perfusion and oxygen delivery to organs

Allows an ‘open vein’
Ancillary drugs/PIVA
Emergency situations

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

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23
Q

Stranguria

A

difficulty/straining to urinate

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

Stranguria + large bladder may be obstructed = emergency!

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24
Q

Dysuria

A

difficult +/or painful urination

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25
Pollakiuria
abnormally frequent urination (little & often)
26
Haematuria
present of blood in 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)
27
Periuria
urination at inappropriate sites
28
Anuria
failure of urine production by the kidneys
29
Oliguria
reduction in urine production
30
Polyuria
Increase urine production
31
Pigmenturia
The presence of a component that imparts an abnormal colour to urine. Haemoglobinuria pink-red urine Intravascular lysis of RBCs Lysis of RBCs within the urinary excretory pathway e.g. USG <1.008, pH>7 Myoglobinuria rare in dogs and cats (seen more in horses) Extensive skeletal muscle damage/myopathies Creatinine Kinase
32
tests for the function of the distile tubule and loop of henle
Urine Specific Gravity
33
tests for the function of the proximal tubes
Dipstick
34
tests for the function of the Glomerular function
Biochemistry Dipstick
35
dog urine specific gravity
1.015 to 1.045
36
cat urine specific gravity
1.035 to 1.060
37
what does a dipstick test for
Protein pH Blood/Haem Ketone Bilirubin Glucose also measures Leucocytes Nitrite Urobilinogen USG but these should not be used
38
Renal Tubular Casts
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
39
pyuria
pus in your pee Leucocytes Cystocentesis sample - <3/HPF <8/HPF catheter/voided High counts = pyuria +/- bacteria
40
Magnesium ammonium phosphate struvite
Most commonly seen in dogs and cats Neutral-alkaline urine UTI’s Diet thin long, pyramidal
41
Cystine
Hexagonal Acidic Urine Abnormal finding Inherited defect in proximal renal tubular transport of AA’s Concentrated, acidic urine Radiolucent
42
Calcium oxalate dihydrate
Cross-striations, “envelope” Acidic urine Can be seen in clinically normal animals or storage artefact Or urolithiasis, hypercalcuria, hyperoxaluria..
43
Calcium oxalate monohydrate
Picket fence Abnormal in cats/dogs Ethylene glycol ingestion Not 100% sensitive Can be seen in normal horse
44
Calcium Carbonate
Alkaline Urine Yellow-brown or colourless Common in equine Not seen in dogs and cats
45
Bilirubin in the urine
Orange-reddish brown Low number routinely observed in dogs
46
Ammonium biurate Crystals
Acidic urine Abnormal finding in most breeds Routine finding in Dalmations
47
Amorphous Crystals
Aggregates/no defining shape Urates - acidic Phosphates – alkaline Xanthene
48
Urolith
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 Renomegaly – uni/bilateral +/- pain Renal failure if bilateral “big kidney-little kidney” cats
49
Nephroliths
Kidney stones Asymptomatic Incidental finding on x-rays Associated with pyelonephritis Pain, pyuria, pyrexia
50
Eupnoea
Normal respiration
51
Tachypnoea
Increased respiratory rate (not necessarily depth) Primary cardiac disease Neurological disease- Damage to respiratory control centre Pain Stress Hyperthermia- Cooling mechanism Metabolic disease Acidosis/alkalosis Increased PaCO2 Abdominal discomfort Restricted movement of diaphragm Primary respiratory disease
52
Apnoea
Absence of respiration
53
Hypoventilation and Hyperventilation are both...
Alterations in ventilation at the alveolar level
54
Hypercarbia
Increased CO2 in blood Hypoventilation Inc prodn of CO2 Primary drive for respiration
55
Hypoxaemia
Decreased O2 in blood Poor O2 intake Hypoventilation Increased O2 consumption Decreased O2 carrying capacity
56
STRIDOR
noisy breathing that occurs due to obstructed air flow through a narrowed airway. as compared to stertor, which sounds like a snore, stridor is a high-pitched sound that results from rigid tissue vibrations. It is typically associated with laryngeal or tracheal disease. Laryngeal paralysis and tracheal collapse are two common presentations in companion animal practice.
57
STERTOR
This term implies a noise created in the nose or the back of the throat. It is typically low-pitched and most closely sounds like nasal congestion you might experience with a cold, or like the sound made with snoring
58
Upper RT Obstruction respiritory pattern
Causes marked inspiratory effort Dynamic collapse of soft tissues due negative pressure associated with inspiration Inspiratory STRIDOR or STERTOR
59
Lower RT Obstruction
Thickening, inflammation and mucus Causes increased expiratory effort Small airways held open during inspiration Early collapse during expiration
60
Restrictive Respiratory Pattern
Expansion of the thorax restricted Decreased tidal volume Tachypnoea / short-shallow breaths Hypoventilation
61
Paradoxical Respiratory Pattern
Paradoxical movement of the chest wall Trauma – “Flail” chest Terminal respiratory failure – fatigue of muscles
62
serous nasal discharge
Inc. nasal secretions Allergic rhinitis Acute Inflammation Viral infection
63
mucoid nasal discharge
Inc. mucus prodn Chronic disease
64
puralent nasal discharge
Bacterial infection 1o or opportunistic pathogen
65
haemorraghic nasal discharge
Trauma Clotting disorder Vascular disease
66
unilateral nasal discharge can be from
Nasal cavity Paranasal sinuses Guttural Pouch (horses)- sometimes bilateral Nasopharyngeal- sometoimes bilateral
67
bilateral nasal discharge can be from
URT Origins- Guttural Pouch (horses) Nasopharyngeal Trachea LRT Origins- Bronchoalveolar space Oedema, Pneumonia Pulmonary vasculature Haemorrhage
68
Laryngeal Hemiplagia (recurrent laryngeal neuropathy
a disease that affects the upper airway in horses. It causes a decrease in airflow to the lungs and can cause exercise intolerance. Horses with the disease are called “roarers” because they make a characteristic respiratory noise that sounds like “roaring” when exercised Common cause of poor performance in race horses Also occurs in dogs, in association with hypothyroidism
69
Radiographic Patterns- Interstitial
Interstitium is the space between the alveoli and capillaries Interstitium becomes more prominent Air still present in alveoli and normal vessels seen Diffuse (unstructured) - e.g. oedema/ diffuse lymphoma Nodular – e.g. soft tissue mass ie neoplasia/abscess Underexposure, expiration or obesity can look similar – often misdiagnosed
70
Radiographic Patterns- Bronchial
Thickened bronchi Infiltration/mineralisation of bronchial walls or due to peribronchial changes thickning/ mineralisation of the brochial walls or peribrochial changes result in Classical ‘donuts’ or ‘tramlines’ Bronchi may be more obvious in the periphery of the lungs where normally wouldn’t be seen
71
Radiographic Patterns- Alveolar
Consolidation or collapse of alveoli Air in alveoli is replaced by fluid (oedema/haemorrhage) or cells Air bronchogram is commonly seen Can be focal or diffuse Examples; bronchopneumonia, aspiration pneumonia, oedema, haemorrhage, neoplasia, lung lobe collapse or torsion
72
Radiographic Patterns- Vascular
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
73
Pleural effusion
Fluid in the pleural space Transudate, exudate, haemorrhage, chyle lung edges to move away from the thoracic wall
74
Pneumothorax
Air in the pleural space
75
TRACHEAL WASH
Sampling of tracheal mucus Trans-endoscopic Trans-tracheal Representative of tracheal secretions and ascending lower airway secretions Cytology + Culture
76
BRONCHALVEOLAR LAVAGE
Sampling of bronchoalveolar space Trans-endoscopic Blind Cytology on
77
TYPES OF SYNCOPE
Neurocardiogenic Cardiogenic
78
neurocardiogenic syncope
Bradyarrhythmia and vasodilation - Vasovagal- occurs when you faint because your body overreacts to certain triggers, - Tussive- known also as laryngeal vertigo or laryngeal epilepsy, is a. syndrome in which fainting and vertigo with or without convulsions follows. a paroxysm of coughing - Situational- when a patient faints in response to a specific trigger, or a specific situation. Some triggers can include: Swallowing. Coughing. Prolonged periods of straining
79
cardiogenic syncope
Hypotension-inducing arrhythmias - Sinus arrest - V Tach - AV block Combination of structural heart disease & less hypotensive inducing arrhythmias +/- excitement/ exertion 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
80
Pre-syncope/ episodic weakness
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
81
Bradycardias
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
82
Tachycardias
Supraventricular and ventricular tachycardias Dogs >160bpm and cats >200bpm Supraventricular tachycardia Most common is atrial fibrillation (AF) New onset – weakness, collapse or syncope SVT is an umbrella term AF, accessory pathways, atrial flutter… Regular SVT less common cause of syncope Ventricular tachycardia Boxers and Dobermanns Can drop CO dramatically Sudden death – more so when abnormal function of LV
83
Cyanosis
Blue or grey skin or lips (cyanosis) happens when there's not enough oxygen in your blood,
84
Right parasternal long-axis view
displays the right ventricular outflow tract which is usually a third of the normal left ventricle.
85
Right parasternal short-axis view
e define several short-axis views, each cutting the heart at a different level between the base and the apex. The entire heart can be scanned using these short-axis views
86
Fractional Shortening
FS (%) = (Left ventricular internal diameter during diastole – Left ventricular internal diameter during systole)/ LVDd calculated by measuring the percentage change in left ventricular diameter during systole. It is measured in parasternal long axis view (PLAX) using M-mode. The end-systolic and end-diastolic left ventricular diameters are measured. if there are no abnomalities fractional shortening correlates with ejection fraction- the amount of blood that the heart pumps each time it beats FS% is affected by many external factors therefore has its limitations
87
Cornell formula
Left ventricular internal diameter during diastole cm/Body Weightˆ0.294 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
88
E-point to septal separation (EPSS)
Using Echocardiography, the mitral Valve E-Point to Septal Separation (EPSS) is a straightforward approach that roughly corresponds to the status of left ventricular (LV) function, but its use has been limited to echocardiography and without solid quantitative correlation to left ventricular ejection fraction (LVEF) he minimal distance between the anterior leaflet of the mitral valve and the septal endocardium over several cardiac cycles.
89
Bacterial causes of farm animal respiritory disease
Mannheimia haemolytica Pasturella multocida Histophilus somnus Mycoplasma spp. Others
90
parasitic causes of respiritory disease in farm animals
Parasitic bronchitis, commonly known as husk, is caused by lungworm, Dictyocaulus vivaparus, invasion. Unlike most respiratory disease, which tends to be seen in winter months, this disease is only seen from late spring until early autumn. Like other parasitic diseases, its aetiology is dictated by its lifecycle. Once infection occurs by ingestion the infective larvae penetrates the gut wall, migrating through the body to the lung where it reaches adulthood and begins egg laying. The eggs are coughed up, swallowed and pass out through faeces
91
Fog fever
Trypthophan toxicity respiritory disease in cattle 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.
92
Farmers lung
an allergic reaction to the inhalation of fungal spores usually from mouldy silage
93
Differential diagnosis – bovine pneumonia
Enzootic calf pneumonia Pneumonic pasteurellosis (shipping fever) Mycoplasma bovis IBR RSV PI3 Verminous pneumonia Fog Fever Farmers lung Aspiration pneumonia Embolic pneumonia (vena caval abcess) ?Stridor - Calf diptheria (Fusobacterium necrophorum) ?Tachypnoea - Septicaemia (eg salmonella Dublin)
94
What is heart disease vs. failure?
Heart disease is any condition affecting the cardiovascular system - chronic in nature e.g. cardiomyopathy - acute in nature e.g. myocarditis - may or may not have clinical signs associated with it e.g. syncope, exercise intolerance - abnormalities on physical examination usually present e.g. heart murmur Heart failure is a syndrome where the heart can no longer meet the metabolic demand of the body - Usually acute onset - Clinical signs present e.g. exercise intolerance, syncope, lethargy, anorexia etc. - Physical examination abnormalities present e.g. fluid thrill, dyspnoea, crackles, jugular pulsation etc.
95
Gallop sounds
audible s3 and s4 sounds Normally heard in dogs and cats; Occur during systole S1 ‘lub’ Closure of AV valves S2 ‘dub’ Closure of semilunar valves Not normally heard in dogs and cats Gallop sounds (occur in diastole) S3 Early diastolic filling Not heard in compliant ventricle Systolic dysfunction S4 Atrial contraction Forceful atrial ejection into a noncompliant ventricle Hypertrophic/ restrictive cardiomyopathy
96
describe the grades if a heart murmer
1 – barely audible, need quiet room 2 – audible but quieter than heart sounds 3 – clearly audible and as loud as heart sounds 4 - louder than heart sounds 5 – THRILL (PALPATION) present 6 – Audible with stethoscope lifted off chest Mild/ moderate/ loud/ thrilling (Ljungvall 2014)
97
Apical systolic murmurs
Mitral regurgitation- Grade can correlate with severity (MMVD not DCM) Pansystolic worse (MMVD) Can be musical/ whooping Often radiates to right a type of heart valve disease in which the valve between the left heart chambers doesn't close completely, allowing blood to leak backward across the valve. Tricuspid regurgitation- Difficult to distinguish from radiating left sided murmurs Vary with respiration Tricuspid valve dysplasia Pulmonary hypertension Degeneration of valve occurs when the valve's flaps (cusps or leaflets) do not close properly.
98
Basilar systolic murmurs
Harsh sounding Radiate widely to thoracic inlet Low grade are difficult to distinguish from physiologic/ innocent (Cats – HOCM dynamic) The valve between the lower left heart chamber and the body's main artery (aorta) is narrowed and doesn't open fully. Pulmonic stenosis Left heart base Radiate dorsally he narrowing of the pulmonary valve, which controls the flow of blood from the heart's right ventricle into the pulmonary artery
99
Innocent/ functional murmurs
Innocent- Puppies and kittens No structural heart disease Grade 1-3 Systolic Left heart base Don’t radiate widely Functional- Associated with disease process Anaemia Hyperthyroidism Fever Hypertension Pregnancy No structural heart disease Grade 1-3 Systolic Left heart base Don’t radiate widely
100
Ventricular septal defect (VSD)
Usually left to right Smaller defect louder murmur Right sternal border Increased right side pressure Quieter Bi-directional Right to left Absent
101
Atrial septal defect (ASD)
Murmur not directly related to ASD Only large defects Increased blood flow Relative pulmonic stenosis Left heart base
102
Differentials for heart disease
Respiratory disease – cyanosis, dyspnoea/ tachypnoea, muffled heart sounds, crackles, dull percussion, cough, syncope Neoplasia – ascites, muffled heart sounds, dyspnoea/tachypnoea, dull percussion, weakness Hypoproteinaemia – ascites, muffled heart sounds Neurological disease – paresis, paralysis, weakness, syncope Metabolic disease – syncope, weakness, tachypnoea
103
clinical signs of heart disease
Heart murmur (dog vs cats) Arrhythmia (dogs vs cats) Gallop sound Cat with cold hindlimbs Cyanosis Presence of goitre Retinal detachment Some neurological signs
104
clinical signs of heart faliure
Dyspnoea/ tachypnoea Crackles in lungs Ascites (fluid thrill) Jugular distension Significant jugular pulsation Muffled heart or lung sounds Positive hepatojugular reflux Pulsus alternans/ paradoxus Peripheral oedema Plus usually signs of heart disease
105
Two Main Causes of Coughing
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)
106
cardiac faliure aetiologies
Chronic Myxomatous Mitral Valve Dz/CMVD - Dilated Cardiomyopathy/DCM - Hypertrophic Cardiomyopathy/HCM - Pericardial Effusion/PE - Restrictive Cardiomyopathy/RCM Patent Ductus Arteriosus * Mitral Valve Dysplasia * Tricuspid Valve Dysplasia * Pulmonic Stenosis
107
diagnosing congestive heart failure
horacic rads with echo are the gold standard Echocardiography will also diagnose the underlying disease, provide chamber size (prognosis) and identify any effusions
108
VHS
vertebral heart scale measured on VD and DV radiographs a method for measuring heart size in thoracic radiograph 8.5 – 10.5 in dog 7.5 in cat
109
NT-proBNP
diagnostic test for heart failure and its management. It has a very high diagnostic sensitivity for HF Non-cardiac causes of rraised NT-proBN-  Systemic hypertension  Hyperthyroidism  Renal failure
110
What is LA (left atrium) to AO (aorta) ratio?
the most commonly used method to evaluate left atrial (LA) size in dogs Normal LA dimension was defined as an LA/Ao ratio <1.6
111
appearence of the diaphram on a vetrodorsal thoratic x ray
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​
112
Normal Heart Size - Dog
Normal width (DV) ○ < 2/3 width of thorax * Normal width (lateral) ○ 2.5 – 3.5 intercostal spaces wide  Significant breed variation * Normal height (lateral – 5th rib) ○ 2/3 height of thorax
113
Normal Heart Size - Cat
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
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norma; cardiac silhouette
O’Clock: Aortic Arch = 11-1 Right Atrium = 9-11 Main PA = 1-2 Left aurical = 2-3 Left ventricle = 2-5 Right Ventricle = 5-9
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Pink Camels collect extra large apples
1. Assess technical quality Good technique is essential to obtain diagnostic radiographs Positioning Centring Collimation Exposure factors Labelling Artefacts
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what are the uses for different radiograph views
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
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Right lateral radiograph
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 Lateral view: Centre beam slightly caudal to caudal border of scapula Collimate to thoracic inlet, thoracic spine, sternum and diaphragm (cranial abdomen)
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ventral dorsal radiograph
Heart rotates to one side and distorts shadow May produce better pulmonary detail Can see more of the lung fields 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.
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dorsal ventral radiograph
Safer in dyspnoeic patient Heart lies in anatomically correct position – easier to interpret cardiac silhouette 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
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Equine Premedication
Aim to produce a horse ‘sedated enough’ for ketamine induction Healthy horses often receive ACP I/M Associated with improved outcome and better oxygenation Place IV cannula Alpha-2 agonist IV Xylazine shortest acting and can ‘top up’ - ? Good choice with colics Detomidine intermediate action (45 minutes), small volumes Romifidine longest acting (up to 90 minutes) and ? Less ataxia – standing sx? Less common technique – infuse GGE until ‘knuckling’ then induce Centrally acting muscle relaxant Infused immediately prior to induction until horse is ataxic & as part of TIVA often called ‘Triple Drip’ Currently licensed and produced by Dechra Best to use to 5% or 10% solution Can substitute benzodiazepines (BZD) midazolam, diazepam (zolazepam) Used in combination with induction agents to improve relaxation Good in foals alone, don’t use in adults alone
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Guaifenesin (GGE)
Centrally acting muscle relaxant Infused immediately prior to induction until horse is ataxic & as part of TIVA often called ‘Triple Drip’ Currently licensed and produced by Dechra Best to use to 5% or 10% solution Can substitute benzodiazepines (BZD) midazolam, diazepam (zolazepam) Used in combination with induction agents to improve relaxation Good in foals alone, don’t use in adults alone
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Equine Induction Agents
Ketamine - Dissociative anaesthetic Excellent anaesthesia combined with other drugs Must not be used alone (seizures) Eyes remain open and central, less cumulative than thiopentone Can be used as ‘top ups’ (don’t exceed induction dose) Takes up to 2 minutes to ‘go down’ Used in combination with acepromazine, alpha 2 agonists, BZDs or guaifenesin (GGE)
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Example Recipe forfeild anesthesia in a horse
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) Ketamine iv top ups q 8-15 mins (0.1-0.2mg/kg) OR ‘triple drip’ (GGE, ketamine, alpha-2) Add ¼ dose detomidine after 4/5 doses if using ketamine alone DO NOT leave until horse standing Field recoveries usually smoother than hospital Advice to owner and arrange follow up Flies Bleeding Swelling
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Example recipe for General equine Anasthetic Hospital
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
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Anaesthesia of Ruminants
LEGAL ASPECTS – check licenced drugs Many procedures done standing Induction of anaesthesia usually achieved iv (calves can be masked induced) Some cows may drink chloral hydrate...
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pig anaesthesia
Can be achieved with drugs given im (deep), iv or via mask with inhalant Ketamine, alfaxalone, propofol Ketamine combinations Malignant hyperthermia (rare condition of pigs will manifest itself soon after exposure to inhalant usually), rapidly fatal, can be treated with dantrolene
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Common anaesthetic problems
Hypotension- Reduce IAA, fluid boluses, pressors/anticholinergics Inadequate anaesthesia and poor recovery- Is usually inadequate analgesia and premedication! Anaesthetic overdose- Use of alpha-2s, adding CRIs and not reducing vaporiser Equipment/monitor issues- Check first! Hypothermia – delayed recovery and arrhythmias Maintain body temp (warming devices) Low glucose Cardiac dysrhythmias- Bradycardia: Alpha-2s, hypothermia, anaesthetic overdose Tachycardia: Nociception, hypovolaemia, drugs
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what happens when the pop off valve is closed
Increased intra-thoracic pressure Gas flow from flowmeters has nowhere to escape Increased intra-thoracic pressure as lungs inflate Increased alveolar pressure causes: Compression (collapse) of pulmonary capillaries (reduced preload) Compression of heart chambers (decreased filling) Compression of aorta (increased afterload) => Dramatic reduction in cardiac output Circulatory arrest  Alveolar damage / rupture
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subcutaneous emphysema
air becoming trapped in tissues beneath the skin. The condition is rare, but it can occur as a result of trauma, injury, infection, or certain medical procedures. Doctors sometimes refer to subcutaneous emphysema as crepitus, tissue emphysema, or subcutaneous air. can result from ruptured trachea caused by et tube
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Intra-vascular injection of local anaesthetic
can cause cardiovascular arrest Start CPR Specific treatment for local anaesthetic overdose- Lipid infusion: Intralipid 20% Bolus 1 ml/kg over 1 min Q 3-5mins Total dose 3-4 ml/kg CRI: 0.25 ml/kg/min “until haemodynamic recovery” Initial research in dogs Expt overdose of bupivacaine 10 mg/kg i/v Cardiac massage unsuccessful for 10 mins 6/6 lipid treated dogs survived; 0/6 untreated dogs survived Normal sinus rhythm returned w/in 5 mins of lipid infusion
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Why do we Encounter Dysrhythmias?
Older/sick patients Multiple underlying conditions Cardiovascular depression Vasoactive drugs (which?), inhaled anaesthetic agents (effects?) Hypothermia Fluid loss Overstimulation Nociception
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Dysrhythmia Interpretation
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?
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Sinus arrhythmia
seen as longer streaches between each PQRST complex 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
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(1st degree) and 2nd Degree A-V Block
multiple p waves without a PQRS complex 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 Treatment? If necessary, antagonise the alpha-2 agonist (or administer naloxone?) Decrease anaesthetic depth If still no response and reduced cardiac output? Consider atropine/glycopyrrolate
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3rd degree AV block
very strange p waves very deep s waves large t waves Treatment – Stop further deterioration, ensure all other parameters are normal
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AF and ventricular ectopic
ocational very deep s waves coupled with large t waves 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
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Ventricular premature complexes (VPCs) plus compensatory pause
occasional very large qrs waves with pause after Check physiology – often due to hypoxia or hypercapnia. Sometimes low blood pressure Add analgesia – may be due to nociception Possible lidocaine if becoming frequent
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Supra-ventricular tachycardia (SVT)
very squshed look of whole line no visibel p waves with frequent qrs complexes and strange t waves Causes? Anything that causes tachycardia! Nociception, hypotension, hypercapnia, hypoxia, hypokalaemia, drugs – which? Treatment? Underlying cause Lidocaine/magnesium/amiodarone
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Ventricular tachycardia (V tach)
small pqr very deep s wave and large t wave 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
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Ventricular escape
qrs without p wave with large qrs complex 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
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infraorbital nerve blocks
upperlip, roof of nose, skin rostral to canal Transbuccal Transdermal Place needle into canal
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maxillary nerve blocks
maxilla, upper teeth, nose, upper lip Transorbital approach Transdermal approach Ventral to notch in zygomatic arch Transmucosal – cannula into infra-orbital canal
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ophthalmic/ trigeminal nerve block
akinesia of globe, desens, eye and orbit Auriculopalpebral Supraorbital 3 point Petersen block Retrobulbar
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mental nerve block
lower lip, insisors Mandibular nn Mental foramen
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mandibular nerve block
mandible, teeth,skin mucosa Medial mandible Just rostqral to angular process Or transmucosal – medial aspect mandible
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Pulse Oximetry
Displays percentage oxygen saturation of haemoglobin Accuracy is affected by poor circulation (common in critical patients) ambient light movement of the probe chow-chows Useful post-op saturating on room air? Limitations- High/low heart rates Probe design 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) 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 Remember, >95% saturation tells us nothing about blood oxygen content- could be anamic
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Capnography
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 and side-stream machines are available Normal ET CO2 = 35–45 mm Hg Hyperventilation – Decreased ETCO2 Hypoventilation - Increased ETCO2 Cardiovascular status CVS depression / arrest Reduced delivery CO2 to lungs can also show airway obstruction and rebreathing Other indicators Oesophageal intubation Leak at cuff/Patient disconnection Adequacy of resuscitation
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Minimum 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 MAC not affected by Stimulation, duration, species, sex, CO2, NSAIDs Isoflurane 1.28 (dog) 1.63 (cat) Halothane 0.87 (dog) 1.14 (cat) Sevoflurane 2.2 (dog) 2.58 (cat) Desflurane 10.3 (dog) 9.8 (cat) Nitrous oxide 188-297 (dog) 255 (cat)
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TIVA
total intravenous anaesthesia Can be used for short procedures in small animals/aggressive patients E.g. ‘quad’ anaesthesia for cat neuters 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
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PIVA
partial intravenous anaesthesia Goals of PIVA Reduce MAC Reduce cardiopulmonary depression Provide additional analgesia Improve environmental impact ideal drugs- 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
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Scald/Ovine Interdigital Dermatitis
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
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Footrot
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 feet Characterised by lameness which can be severe, often recumbent leading to reduced feeding time, weight loss, poor wool quality Very 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
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CODD
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
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White line separation in sheep
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
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Toe Granuloma
Painful red swellings caused by: Over-trimming Chronic untreated lesions Chemical irritation
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ORF
viral disease usually seen around mouth of ewes/lambs – causes proliferative lesions around coronary band
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SFR
– ongoing research into aetiology – can appear similar to orf lesions
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Laminitis in sheep
lame in all 4 feet, often after grain gorging or over-fat rams, can lead to longer term hoof deformation Broken leg bottom left
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neuro disease presenting as lameness
spinal abscess as a result of any systemic bacterial infection can initially present as lameness before progressing to ataxia
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Joint Ill
Most common = septic arthritis ‘Joint-ill; Streptococcus Dysgalactiae Transmission still unknown – cord/tagging/tailing/castrating/oral/vaginal canal? Swollen joints, ill thrift, death 1-2% of flocks, can be up to 50% of lambs in severe outbreaks control- Lamb outdoors!- Reduces bacterial load for newborn lambs Wear long gloves for each assisted lambing Maintain clean dry lambing shed and pens Consider if tailing/castration necessary for the particular system Check colostrum intake Research evidence suggests that wearing long disposable gloves for lambing will be the most effective method to reduce the prevalence within a flock
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Sole Ulcers
Disruption to horn growth due to pressure on the corium underneath P3 Risk Factors: Standing time Surfaces Foot trimming Fat mobilisation Inflammation 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
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Digital Dermatitis
Multifactorial Strong bacterial component Treponeme spp Genetic susceptibility Hoof hygiene!
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Foul in the foot
Bacterial infection of interdigital tissue F. Necrophorum et al Painful, swollen ID space Characteristic fragrance Treatment Systemic antimicrobials NSAID Local treatments Prevention Similar to DD Minimise risk of interdigital trauma
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Heel horn erosion
Prevention: Hygiene and trimming of loose heel horn v shaped lesions
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Footbathing cows
3-4x/week Not too strong/acidic (below pH3) No more than 200 cows Effective design required Commonest ingredients – formalin, CuSO4
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Denitrogenation
using oxygen to wash out the nitrogen contained in lungs after breathing room air, resulting in a larger alveolar oxygen reservoir. With any rebreathing system where carrier gas is oxygen Use higher flows for ~10 minutes Risk of alveolar hypoxia N.B also after short disconnections – movement between theatres etc
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Non-rebreathing systems
High gas flow requirements Loss of heat and moisture Cheap to purchase, expensive to run Low resistance to respiration Suitable for very small patients Rebreathing circuits use a carbon dioxide absorber to trap and remove CO2 so the patient can breathe gases that have been recycled through the machine. Non-rebreathing circuits use high gas flows to washout expired CO2 from the circuit before the patient takes its next breath. t piece bain lack mcgill
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Working out gas flow requirements
Based on multiples of minute volume, where minute volume is; Respiratory rate x Tidal volume OR 200 ml per kg
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Magill
non-rebreathing Reservoir bag at fresh gas inlet Awkward to use circute factor of 1 1 x Vm (Vm = Vt x RR) or (Vm =200ml/kg) resivour bag is attached to one limbs >5kg not sutible fopr ippv
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Lack
Co-axial Magill circut factor is 1 1 x minute volume (tvxrr) Damage to inner limb results in rebreathing resivour bag is attached to two limbs >10 to <25-30kg not sutible for ippv
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Mini Lack
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
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T-piece
Suitable for very small patients, < 8 kg 2-3 x Vm circute factor is 2-3 Suitable for IPPV resouvouir back further from gass inlet than lack, attached to one limb, with another limb coming form gass outlet
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Bain
Co-axial T-piece Suitable for 7 – 10 kg circute factor of 2-3 2- 3 X Vm Beware – damage to inner tube like magil but with inner tube
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Humphrey ADE
versitile circle unit has sodalime can be converted form circle to lack to t- piece 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
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Breathing system checks
Inspect system Connect to common gas outlet Test system for leaks Check unidirectional valves on circle Specific tests to check integrity of co-axial lack and co-axial Bain
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main types of bone in birds
Pneumatic Medullary
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Blood collection - lizards
Ventral tail vein Care with species that perform autotomy Jugular vein Can be considered for leopard geckos
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Blood collection - snakes
Ventral tail vein Recommended site Care not to insert needle into hemipenes or cloacal musk glands Cardiocentesis CARE  risks of laceration to ventricle and risk of pericardial haemorrhage
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Blood collection - birds
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
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Anaesthetic Machine Components
back bar- 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 Oxygen failure warning device If fitted (Ritchie whistle or electronic) Vaporiser- Expensive and need servicing See maintenance lecture Common gas outlet- Anaesthetic mixture attaches to breathing system Non-return valve Oxygen flush - Bypass vaporiser 35l/min CARE with breathing system valves – expiratory = open
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Intermittent positive pressure ventilation (IPPV)
uses a mechanical respirator to deliver a controlled pressure of a gas to assist in ventilation or expansion of the lungs, thereby providing an increased tidal volume for patients with a variety of pulmonary conditions. 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.
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Breathing system check steps
Visual check Leak test; If pop-off valve, close and inflate with thumb over end until no balloon creases Bain – occlude end with syringe with oxygen at 2l/min – flow should drop With no IAA – BREATH into circle to check valves (or use 2 bag method)
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Soda Lime
used to absorb carbon dioxide 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.
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Pre-Anaesthetic Fasting for common species
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 (gas distension) – controversial Ruminants withdraw 6 hours and reduce concentrates 12-24 hours Small exotics/furries – shorter times depending on species
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Endotracheal Tubes (ETT)
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 (cats, why not dogs?) and WAIT Try largest but have a range available Cut to length – minimise dead space Not possible with armoured tubes 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 More popular 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
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Cole Pattern Tubes
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
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V-gels
veterinary specific (rabbits and cats) 2 species where ETT placement can be challenging Designed to anatomical standards
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Complications of Airway Management
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
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Aims of premedication
Sedation and anxiolysis facilitating handling of the animal Reduction of the stress for the animal 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
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Alpha2 Adrenoceptor Agonists (Alpha-2s)
Potent sedative and analgesic drugs Xylazine was the first 2 agonist to be used in veterinary practice Superseded by medetomidine & dexmedetomidine (cats & dogs), both lasting about 45 minutes Xylazine (30minutes), detomidine (45 minutes)and romifidine (60 minutes, less ataxia) used in horses Xylazine and detomidine used in cattle The superior selectivity of dexmedetomidine makes it the theoretical 2 agonist of choice for use in small animals can be injectable or oral gel Sedation is profound & dose related Alpha 2 agonists provide good analgesia through an agonist effect at spinal cord 2 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 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 2 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 Endogenous insulin secretion is reduced leading to a transient hyperglycaemia 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 #reversable- atipamezole
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reversal of Alpha2 Adrenoceptor Agonists (Alpha-2s)
Alpha 2 sedation and analgesia is rapidly antagonised by the administration of atipamezole, a specific alpha2 adrenergic receptor antagonist 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
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Phenothiazines
Acepromazine commonest/only licensed one Sedation and anxiolysis that is initially dose dependent 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 1 adrenoreceptors and can cause peripheral vasodilation and a fall in arterial blood pressure 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 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 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 Acepromazine gel (horses) & tablets
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Benzodiazepines
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
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Premedication drug combinations (dogs and cats)
Acepromazine + opioid Alpha 2 agonist + opioid Alpha 2 agonist + BZD Alpha 2 agonist + Ketamine BZD + Ketamine Opioid + BZD Alpha 2 agonist + BZD + opioid How to choose.... 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
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Propofol
Injectable Induction Agent Quick recovery with no hangover Apnoea if given too quickly 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 Rapid onset of action -rapid uptake by CNS Short period of unconsciousness (5-8 mins) Large volume of distribution (lipophilic) Rapid smooth emergence due to redistribution & efficient metabolism (hepatic and extra hepatic) metabolites inactive Respiratory depression (apnoea) - IPPV - Speed of injection? Cardiovascular depression Rapid and smooth recovery Suitable for top ups or TIVA Muscle relaxation usually ok Anticonvulsant ?? Not irritant, pain reported Analgesia ?? probably not ↓ ICP (patients with raised and normal ICP) 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)
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Alphaxalone
Injectable Induction Agent Predictable Single use vials Apnoea Rough recoveries
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Dissociative agent & benzodiazepine
Injectable Induction Agent IM or IV Long recovery? Can be rough recovery Controlled drug
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Thiobarbiturates -Thiopentone Sodium
Ultra short acting However difficult (impossible) to source Use currently in horses to ‘top up’ Prolonged recovery in sighthounds - metabolism and body fat Massive skin sloughing if injected extra-vascularly
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Injectable Steroid Anaesthetics
Steroid Anaesthetics – ‘Saffan’ – no longer available in UK in this form Alphaxalone(6mg/ml)/alphadolone(3mg/ml) Alphaxalone more potent Solubilised by Cremaphor EL Didn’t give it to dogs Used in ruminants & pigs Formulation without Cremaphor (instead a 2-hydroxypropyl-beta-cyclodextrin (HPBCD)) Alfaxan  (Alfaxalone) Is suitable for cats and dogs (& other spp) Alfaxalone is a clear colourless neuroactive steroid Causes anaesthesia by activating the GABA (inhibitory) receptor Alfaxalone 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
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Ketamine
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 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 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 ↑ ICP, ocular surgery, fever, hyperthyroidism Schedule 2 CD
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types of colic
Smooth muscle spasm- Inflammation Colitis / Ulceration- Distension Impaction Gas accumulation- Obstruction Impaction Tension on the mesentery- Displacement Tissue congestion/infarction/necrosis- Torsion/volvulus Strangulation
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Clinical Signs of Colic
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 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
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“False” colic
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 Other Non-abdominal, pain mistaken for colic Oesophageal obstruction Rhabdomyolosis (tying-up) Laminitis Pleuroneumonia
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Assessment of Gastrointestinal Tract of a horse
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
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Nasogastric Intubation for colic
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
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palpable structures in a transrectal exam of a horse
ventral band of cecum great vessels caudal pole of left kidney caudodorsal aspect of spleen nephrosplenic space and ligament fecal balls in small colon inguanal rings in stallion bladder when distended Abnormalities: - Impaction - Distension (Gas accumulation) - Displacement - Masses
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Abdominocentesis
Assess for presence of changes in peritoneal fluid Serosanguineous colour change/ 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
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analgesia for colic in the horse
Analgesia Imperative to provide some form of analgesia to a colic case NSAIDs 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
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fluid therapy for colic
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)
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indicators of prognisis in olic in horses
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
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Loading dose
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
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Pharmacodynamics
Effect of drug on the body Drugs are chemicals and as such interact chemically with biological/cellular molecules – most often proteins 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)
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Meyer-Overton hypothesis
the theory of anaesthetic action which proposes that the potency of an anaesthetic agent is related to its lipid solubility. Potency is described by the minimum alveolar concentration (MAC) of an agent and lipid solubility by the oil:gas solubility coefficient.
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Endogenous agonist
a compound naturally produced by the body which binds to and activates that receptor. For example, the primary endogenous agonist for serotonin receptors is serotonin, and the primary endogenous agonist for dopamine receptors is dopamine.
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Efficacy:
the maximum therapeutic response that a drug can produce (example: morphine vs buprenorphine)
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Agonism
Drug Target Interaction 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 Agonist: molecule/drug that binds and activates the receptor Affinity: the tendency of a drug to bind to the receptor Efficacy: the tendency of a drug to activate the receptor once bound
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Affinity
the tendency of a drug to bind to the receptor
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Efficacy:
the tendency of a drug to activate the receptor once bound
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Antagonism
Drug Target Interaction 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
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Competitive Antagonism
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)
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Non-competitive Antagonism
Non-competitive antagonists either bind to a different receptor site OR Block the chain of events “post” binding - acting “downstream” of the receptor. shift the efficacy of the agonist down
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Irreversible Antagonism
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 – why? BUT……Some irreversible enzyme inhibitors are used in practice – e.g. aspirin, omeprazole
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Inverse agonism
Inverse agonist: drug that reduces the activation of a receptor with constitutive activity (example: GABAA receptor) Can be regarded as drugs with negative efficacy.
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EC50
Effective concentration. The dose required for an individual to experience 50% of the maximal effect.
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ED50
Effective dose. The dose for 50% of the population to obtain the therapeutic effect.
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Therapeutic index
toxic dose (or LD50) ÷ effective dose (or ED50) Large TI is safer!
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Drug receptor types
Ion channel cell surface transmembrane receptor Ligand regulated enzyme E.g. insulin receptor G-protein coupled receptors Protein synthesis regulating receptor
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Tachyphylaxis
(“rapid protection”). Reduction in drug tolerance which develops after a short period of repeated dosing. Not common. Often due to a lack of a co-factor
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Self-Antagonism
When a drug becomes antagonistic to its own effects
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Loss of target sensitivity is caused by
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
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Who oversees UK veterinary medicine legislation?
The Veterinary Medicines Directorate (VMD), which is an executive agency, sponsored by the Department for Environment, Food & Rural Affairs VMD is responsible for; monitoring and taking action on reports of adverse events from veterinary medicines testing for residues of veterinary medicines or illegal substances in animals and animal products assessing applications for and authorising companies to sell veterinary medicines controlling how veterinary medicines are made and distributed advising government ministers on developing veterinary medicines policy and putting it into action making, updating and enforcing UK legislation on veterinary medicines
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POM-V
Prescription-only Medicine – Veterinarian must be prescribed by a veterinary surgeon, who must first carry out a clinical assessment of the animal under his or her care.
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POM-VPS
Prescription-only Medicine – Veterinarian, Pharmacist, Suitably Qualified Person medicines may be prescribed in circumstances where a veterinary surgeon has carried out a clinical assessment and has the animals under his or her care. However, the Veterinary Medicines Regulations provide that POM-VPS may be prescribed in circumstances where the veterinary surgeon, pharmacist or SQP has made no clinical assessment of the animals and the animals are not under the prescriber’s care.
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NFA-VPS
Non-Food Animal – Veterinarian, Pharmacist, Suitably Qualified Person medicines may be supplied in circumstances where the veterinary surgeon or SQP is satisfied that the person who will use the product is competent to do so safely, and intends to use it for the purpose for which it is authorised.
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AVM-GSL
Authorised Veterinary Medicine – General Sales List
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the cascade
The cascade is a risk-based decision tree to aid prescribing on a case-by-case basis. Initially a VS should prescribe a medicine authorised in the jurisdiction where they are practising, for use in the target species, for the condition being treated, and used at the manufacturer's recommended dosage. If no such product exists, follow the cascade. Nb. There is separate guidance on the Cascade for veterinary surgeons practising in England/Wales/Scotland, and for those in Northern Ireland. Please refer to VMD website The treatment in any particular case is restricted to animals on a single holding Any medicine imported from another country must be authorised for use in a food-producing species in that country The pharmacologically active substances contained in the medicine must be listed either for use in NI – in table 1 of the Annex to Regulation (EU) No. 37/2010 (this table replaces Annexes I, II or III of Council Regulation (EEC) 2377/90); for use in GB – in the GB MRL Register as part of the VMD’s Product Information Database. The veterinary surgeon responsible for prescribing the medicine must specify an appropriate withdrawal period The veterinary surgeon responsible for prescribing the medicine must keep specified records
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What are controlled drugs(CDs)?
Controlled drugs (CDs) are listed in Schedules 1 to 5 of the Misuse of Drugs Regulations 2001 Veterinary medicines only contain CDs in Schedules 2, 3, 4 and 5 Schedule 1 drugs include drugs such as cannabis or LSD – highly addictive, no therapeutic value Schedule 2 CDs have therapeutic value but are highly addictive Licenced examples; Methadone Fentanyl Pethidine Ketamine Schedule 3 includes buprenorphine, barbiturates and some benzodiazepines which are also subject to special prescription writing requirements. Some are also subject to special storage requirements Schedule 4 and schedule 5 drugs have no additional special controls Ketamine WAS Schedule 4 Since November 2015 reclassified as Schedule 2 Now subject to full schedule 2 legal requirements Schedule 2s: Obtained from wholesalers providing a signed prescription has been issued by the requesting veterinary surgeon Must keep requisition records for at least 2 years Schedule 2 or 3 CDs ; written prescription must be signed by the person issuing it which may be hand-written, typed in a computerised form or computer generated. This prescription is only valid for 28 days. Repeat dispenses on the same prescription are not allowed with schedule 2 or 3 drugs Recommended that you keep a copy of a CD requisition to assist in complying with the law on wholesale supply RCVS considers that a veterinary nurse may draw up and administer a CD Provided the veterinary surgeon Prescribed the drug to a specific animal Decided on the dose Authorised that it be drawn up and is confident that the veterinary nurse is competent to draw up and administer the prescribed dose A veterinary surgeon does not need to be present when the drugs are drawn up or administered but the legal responsibility for the supply of the CDs remains with the veterinary surgeon Recommended to have a standard operating procedure Veterinary nurses may administer CDs out of hours when there is no vet on the premises A veterinary nurse is not able to decide to give a CD or change the dose (i.e. make prescribing decisions) without the instructions of a veterinary surgeon
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records of Schedule 2 CDs
Complete records of Schedule 2 CDs must be kept in a Controlled Drugs Register (CDR) CDR = either a computerised system or a bound book separated into each class of drug with a separate page for each strength and form of that drug at the top of each page. Loose leaf registers or card index systems are not allowed CDR entries must be In chronological order, made in ink or in a computerised form in which every entry can be audited, and made on the day of the transaction The book must be kept at the premises to which it relates and be available for inspection at any time It must be kept for a minimum of two years after the date of the last entry The CDR must record for all CD purchased and supplied The date supply received, name and address of supplier and quantity received The CDR must record for all CDs administered or supplied The date supplied, name and address of person supplied, details of the authority to possess (prescriber or licence holder’s details) and the quantity supplied
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storage of Schedule 2 and Schedule 3 CDs
Schedule 2 and Schedule 3 CDs containing buprenorphine must be kept in a locked container which is constructed and maintained to prevent unauthorised access to the drugs and can only be opened by a veterinary surgeon or other authorised person The room housing this container should be lockable and tidy to avoid drugs being misplaced CD container keys should not be kept with keys to other parts of the building The room should not normally be accessible to clients Any returned CDs should not be re-used and should be destroyed according to regulations.
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Pain pathways
Analgesics may act at different sites 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)
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Opioids
Natural (opiate) and synthetic (opioid) drugs Endogenous opiates Opioid receptors identified; mu, delta, kappa, 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
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Morphine
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
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Methadone
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
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Pethidine (Meperidine)
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 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 ≈ 90 minutes
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Fentanyl
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)
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Codeine
has been used in dogs (often with paracetamol) for mild to moderate pain (post op)
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Naloxone
antagonism of pure mu opioids
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Tramadol
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
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Buprenorphine
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 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)
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Butorphanol
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- suppress coughing LIMITED ANALGESIA
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list 9 Local anaesthetic agents
Lidocaine Prilocaine (+lidocaine) Bupivicaine Mepivicaine Ropivicaine Etidocaine Amethocaine Proparacaine Cocaine
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Local anaesthetic agents
Lidocaine Prilocaine (+lidocaine) Bupivicaine Mepivicaine Ropivicaine Etidocaine Amethocaine Proparacaine Cocaine 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.
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Non-Steroidal Anti-Inflammatory Drugs (NSAID)
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, poSome licensed for pre-operative use Carprofen and meloxicam have revolutionized perioperative pain management in UK in last 3 decades Carprofen Firocoxib Meloxicam Deracoxib Etodolac – Ketoprofen Cimicoxib Mavacoxib Robenacoxib Grapiprant Paracetamol ? and codeine (opioid) Phenylbutazone Tolfenamic acid Tepoxalin* Vedaprofen Keterolac Aspirin Licensed NSAIDs for horses- Phenylbutazone Suxibuzone Firocoxib Meloxicam Flunixin meglumine Vedaprofen Carprofen 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
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COX 1
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
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Grapiprant (Galliprant™)
Piprant class NSAID Non-cyclooxygenase inhibiting non-steroidal anti-inflammatory drug 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
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Naloxone
antagonism of pure mu opioids
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paracetamol
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
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Alpha-2 Adrenoceptor Agonists
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 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 Sedation including standing sedation for equine/large animal Premedication PIVA/TIVA Epidural Rescue analgesia One of the few classes of drugs with an antagonist- atipamazole
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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 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)
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penicillin mechanism of action and target
inhibits cell wall synthesis and gram positive bacteria
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ampicillin mechanism of action and target
inhibits cell wall cynthesis broad spectrum
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bacitracin mechanism of action and target
inhibits cell wall synthesis skin ointment for gram positive bacteria
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cephalosporin mechanism of action and target
inhibits cell wall synthesis broad spectrum