POS Flashcards
1
Q
What is hematocrit
A
Hematocrit also known as Packed cell volume is a measure of the total amount of RBC’s in the blood. MCHC (Mean cell hemaglobin concentration)
2
Q
What does MCV stand for
A
Mean cell volume is a measure of the volume of red blood cells. When RBC count is low cells can be characterized into: normocytic (Mild non regenerative anemia - acute haemorrhage), Microcytic (Extra division of RBC due to Fe defeciency) or macrocytic (Polychromatophils - large purple immature RBC’s, contain ribsomal RNA)
3
Q
What are the two types of anemia
A
Regenerative - either haemorrhage or haemolysis
Non-regenerative - Anemia of inflammatory disease/chronic disease, chronic renal failure or Decrease of BM production
4
Q
What are reticulocytes
A
Seen with a new methylene blue stain, RNA precipitation. Same as polychromatophils.
5
Q
What are the signs of regeneration of a smear
A
Polychromasia
Nucleated RBC’s
Codocytosis (Mexican hats)
6
Q
What is Leukemia and what are the two types
A
Leukemia is neoplasia of the WBC’s. Can be acute or chronic. Can be of myeloid origin ( from bone marrow) causing faulty basophils, neutrophils or eisinophils. Can also be of lymphoid origin affecting the production of lymphocytes. enlargement of LN’s would be seen.
7
Q
What do you use to conduct a biochemistry profile
A
Serum. Plasma contains anticoagulants that interfere with the test.
8
Q
What is azotemia
A
Increase in Nitrogenous waste in circulation
9
Q
What are the different methods of enteral feeding
A
Orogastric feeding tube - not tolerated by small animals, only used for neonates
naso-oesophageal feeding tubes - most common in practice. can be done under local anesthetic. However diameter of tube is small so only liquid based diet
oesophagostomy feeding tube - tube directly in the oesophagus. well tolerated by animal and has a wider diameter so can give significant amounts of food.
Percutaneous Endoscopic-Guided Gastrostomy Tube - needed when the oral cavity and oesophagus need to be bypassed. usually for long term cases lasting months.
10
Q
When is fluid therapy necessary
A
Hemorrhage Diarrhoea & vomiting Polyuria Sequestrial fluid Hypovalaemic shock General anesthesia Azotaemia ( increases GFR which increases removal of renal toxins)
11
Q
What are crystalloid fluids and the different types and when they would be used
A
Water with small molecules that can move freely out of intravascular space.
Isotonic - 0.9% Nacl. distributed evenly between compartments. suitable for shock diarrhoea, diuresis & anesthesia. Complications when too little or too much given
Hypertonic - 7.5% Nacl, draws fluid from interstitium and extracellularly into the intramuscular compartments. Rapid resuscitation with patients in shock. low dose required and can also be used with cerebral oedema. however needs to be followed up by other fluids. Can’t be used with dehydrated patient and can only be used once
Hypotonic - 0.5% Nacl. Only useful with hypernatraemic patients.
12
Q
What are synthetic colloid fluids and what are their purpose
A
Consists of water with and large molecules (gelatin and starch) that are used to treat hypovalaemic shock and restore circulating volume. Generates a colloid osmotic pressure –> delays equilibrium of fluid with other compartments. Useful for resuscitation of intravascular volume. possible complications arise when theres dilution of platelets and clotting factors –>coagulopathy
13
Q
What is mannitol used for
A
Shifts fluid to the intravascular compartment to be excreted by the kidney. Used for head trauma when theres an increase in intracranial pressure & acute glaucoma.
14
Q
What is paraentral feeding and what is total and partial PN.
A
Paraentral feeding is the feeding via fluids via iv. TPN contains 100% of required energy requirements via the jugular vein and Partial paraentral nutrition contains 40-70% energy requirements met
15
Q
What is the first broad spec anthelmintic group, whats its mode of action and why is more potent in some species
A
Benzimidazoles (white drench)(E.g Fenbendazole). Decreased oral availability therefore oral only drug. Binds to tubulin of parasite inhibiting glucose uptake causing glycogen depletion and death.
Activity covers adult worms, larvae and arrested larvae & lungworms. Multiple small doses has a greater potency than single large dose. Also hgiher potency in horse/cow as the caecum & rumen act as reservoir
16
Q
What is the second broad spec group of anthelmentics, whats its mode of action
A
Imidazothiazines (yellow drench)(E.g levamisole). Cholinergic agonist, causing a spastic paralysis due to neuromuscular junction overload.
Very short half life. available as injection, oral or pour on with the latter having the longest residual action (24hours)
17
Q
What is the third broad spec anthelminitic drug group, whats its mode of action, what does it act against and why can it be used metaphalacticly and prophylacticly
A
Macrocyclic lactones (clear drench)(avermectins). Opens specific glutamate chloride channels in the post synaptic membrane causing a flaccid paralysis.
Broad spec killing gut worms (including arrested larvae), lungworms and arthropods. Has a persistent effect so therefore can be used in 2 different ways.
a) Metaphylaxis - treating animals going out on to dirty pasture (minimise EXPECTED outbreak of disease)
b) Prophylaxis - Prevent initial contamination of pasture (prevent disease)
18
Q
What is praziquantel
A
Anthelmintic that acts by disrupting tegument of the helminth altering permeability, causing an iniflux of calcium ions causing muscle spasms. Causes worm to release gut wall and then is digested.
19
Q
What are the possible reasons for anthelmintic treatment failure
A
Under dosing Poor treatment technique Use of incorrect drug Underestimating body weight Inadequate maintenance of equipment Reintroduction onto heavily contamintae dpasture Resistance Failure to follow manufacturers guidance
20
Q
What is the problem associated with anthelmintic resistance
A
By time Anthelmintic resistance is detectable the allele frequency is >25% and resistant parasite population is >5% & by time clinical failure of anthelmintics the allele frequency is >50% and resistant parasites is >95%
21
Q
How can anthelminitic resistance be measured
A
- Drench test - Anthelmintic treatment to a group of animals & F.e.c of 10 samples post treatment
- Fecal egg count reduction tests - Comparing f.e.c before and after treatment with untreated controls. Resistance is indicated if treatment doesnt reduce F.e.c by >95%
22
Q
What is ‘COWS’ and what are their guidelines
A
Control of worms sustainably
- Work out a Strategy
- Treat cattle in quarantine & turn out onto dirty pasture (polution)
- Test for Anthelmintic resistance on farm
- Administer wormer efficiently
- Dose only when needed
- Select appropriate wormer
- Preserve susceptible worm population (Refugia). Some calves are left undosed. This allows them to produce eggs of susceptible worms, diluting the population of resistant ones. Also resistance can come at a cost of fitness, therefore can be out-competed by susceptible worms.
- Reduce dependence on worming. Use grazing management, targeted treatment by F.e.c & quarantine appropriate stock
23
Q
What is an antigen-specific antibody used for and give 3 examples
A
Can be useful when determining: Exposure of an individual/herd to a specific pathogen (BVDV), response to vaccination and diagnosis of antibody mediated hypersensitivity.
- ELISA - Can be used to detect antigen or antibody. Generally if infection had occured in <7days then will look for infectious organism whereas >7days will look for antibodies. So if testing for antigen will have serum antibodies added to well with known antigen, enzyme linked antibody will then bind to any antibody-antigen complexes causing substrate change.
- Immunofluorescence - Same principle as ELISA except instead of enzyme linked antibody will have fluorecent marker.
- Virus neutralising assay - Culture cells deliberately in the presence of virus in question, with and without presence of serum. If patient has no Ig’s then cells become infected and will either be lyses (cytopathic viruses) or will show cytopathic effects. The virus neutralising titre is the greatest dilution in which serum prevents the cells from becoming infected. An advantage of this is that it shows the Ig’s are biologically active
24
Q
Explain and allergy test
A
A serology based test measuring allergen specific IgE. A labelled recombinant Fc-epsilon receptor to detect atopic dermatitis or flea allergic dermatitis.
Important to detect specific IgE and not any other antibodies because the reactivity of another Ig wouldnt necessarily indicate a hypersensitivity, therefore giving a false positive.
25
What is serum protein electrophoresis used for diagnostically
Can tell you if theres a monoclonal gammopathy (Large narrow increase, myeloma) or polyclonal gammopathy (wide peak indicating multiple proteins and a chronic infection)
26
How can you evaluate T cell responces
1. Invitro can be measure by measuring cytokine release following stimulation by specific antigen (bovine IFN gamma ELISA).
2. Can be measure invivo by performing a delayed hypersensitivity test. this is the basis of bovine TB testing in uk. ( single intradermal comparative cervical tuberculin)
27
How are antibodies used as detection reagents
Used to detect pathogen in an clinical sample.
a) Sandwich ELISA (faecal/biological fluids)
b) Immunofluorescence (smears/tissue sections)
c) Immunohistochemistry - tissue section on slide, then an enzyme labelled antibody against the cell surface markers.
28
What is immunophenotyping
Antibodies against cell surface markers can be used to determine cell types present. Can be done on cells in suspension by flow cytometry. An example if this could be a LN aspirate from a dog with lymphoma, determining the cell lineage the cancer
29
What biochemistry results (enzymes) would indicate damage to the liver
ALT, AST, SDH, GLDH are all directly leaked from hepatocytes and indicate damage or necrosis.
ALT and AST are low in large animals so GLDH and SDH are more reliable indicators. AST and ALT also increase due to muscular injury. (therefore creatine kinase can be used to differentiate muscle damage)
ALP is derived from bile duct epithelium and indicates cholestasis when increased. Also increases in growing animals because its found in bones. steroids can induce increase of isoform in DOGS, any increase in cats is significant, often indicating hyperthyroidism or hepatic lipidosis
GGT is derived from bile duct epithelium. More sensitive indicator of cholestasis in large animals as ALP has wide range.
30
What biochemistry results would indicate dysfunction of the liver
Bilirubinuria - in the dog, the kidney can metabolize a small amount of haemoglobin into bilirubin, so a reading of +2 can be normal. However in cats and positive reading indicates liver disease as conjugated bilirubin has exceeded renal threshold.
Urea decreases with liver disease
Cholesterol - Increase with cholestasis and decrease due to hepatic failure.
Bile acids - Endogenous test that involves measuring fasting levels and postprandial levels, as the bile acids should be stored in the gall bladder, released after feeding and then undergo enterohepatic recycling. An increase in bile acids shows one of two things, a) decrease in excretion of bile due to obstructive cholestasis or b) decreased bile acid clearance from portal blood due to portosystemic shunt.
31
What are the 3 main parameters looked at with effusion fluid collected & what are the normal for each
1. Total nucleated cell counts (<3 x 10e9/L)
2. Cell identification & morphology (mesothelial cells/macrophages)
3. Protein concentration (25-30g/L)
32
Define transudate
Clear water like fluid with Low protein and low cellularity. total protein <25g/L, TNCC <0.5 x 10e9, and mesothelial cells, macrophages and low number of non-degenerate neutrophils can be seen.
Thought to be due to decreased colloid osmotic pressure from hypoalbuminemia (which is due to glomerular or hepatic disease).
Hepatic fibrosis/cirrhosis will cause prolonger portal hypertention and the formation of secondary collateral circulation. Local vasodilators released (NO), causing vasodilation and decreased effective blood flow. Also compounded by Renal retention of Na due to RAAS, End result is expansion of plasma volume and leakage of low protein lymph from intestines.
33
Define modified transudate
A yellow serosonguinous fluid. Amount of protein is variable (25-50g/L). can expect a TNCC of 0.3-5.5 x 10e9. Cells present will include macrophages, neutrophils, mesothelial cells & small lymphocytes.
Causes include:
cardiac disease causing congestion and an increase in hydrostatic pressure (especially in hepatic sinusoids)
leakage of protein rich lymph
chylous effusions
34
Define exudate
Turbid fluid thats white/yellow/red. Has high TNCC (3.0 x 10e9) and high total protein (>30g/L). Cells present include macrophages, neutrophils (degenerative and non-degenerative), lymphyctes and eosinophils.
Caused by inflammation of the pleural or abdominal cavity. Can be septic (degenerate neutrophils present and intracellular bacteria) cause or non-septic ( Non degenerate neurtophils and no bacteria e.g FIP)
35
Describe properties of a hemorrhagic effusion
turbid red.
Total protein >30g/L.
TNCC 1.5-10 x 10e9
Cell types dependent on the type of haemorrhage
An ongoing/iatrogenic haemorrhage will have erythrocytes and platelet clumps present
An acute haemorrhage will have erythrophagia, where macrophages can be seen with intact or partially digested RBC's inside.
With a chronic haemorrhage siderophages (haemosiderin containing macrophages) can be seen along with haematoidin (orange-yellow pigment)
36
What are the modes of action or antibiotics with examples of each
> Inhibition of cell wall synthesis - Penicillins & cephalosporins
> Inhibition of cell membrane function - Polymxins imidazoles
> inhibition of protein synthesis - Chloraphenicol, macrolides, linocosamides, tetracyclines and aminoglycosides
> Inhibition of nucleic acid synthesis - Sulphonamides, quinolones and metronidazole
37
What bacteria are present in the following areas: oral, liver, lungs, GIT, urinary tract and skin
Oral - Gram -ve and anaerobes
Liver - Gram -ve, anaerobes and staphylococcus
Lungs - Gram -ve & +ve, and atypical (e.g mycoplasma)
GIT - Gram -ve & anaerobes
Urinary - Gram -ve & staphylococcus
Skin - Staphylococcus
38
What is minimum inhibitory concentration
Lowest concentration of drug that will inhibit bacterial growth
39
Describe a bacteriostatic drug and give examples
```
Effects are reversible once drug is removed. Drug concentration at site of infection must be maintained above MIC throughout dosing interval (therefore adherence to the dosing schedule is key)
Examples include:
> Chloraphenicol
> Lincosamides
> Macrolides
> tetracyclins
```
40
What are the two types of Bacteriocidal drugs with examples
1. Time dependent - Time above MIC over a 24hr period determines therapeutic success. Thus dosing regime must be followed, also can't be used with bacteriostatic drugs. E.gs include penicillins and cephalosporins
2. Concentration dependent - Peak concentration under curve predicts the therapeutic success. Can be given once a day. E.gs include Aminoglycosides, Metronidazole & Fluoroquinolones
41
What antibiotics are recommended for atypical bacteria
Atypical bacteria include mycoplasma and chlamydia.
| Tetracyclins are the most commonly selected, Macrolides, fluoroquinolones and chloraphenicol can also be used.
42
Describe pharmokinetic considerations when administering antibiotics and which areas are hard to treat
```
Distribution of the drug is dependent on the perfusion of that specific tissue. However some tissues have permanently limited drug distribution due to lipid membranes, E.g
> Brain
> Eye
> Prostate
> Bronchus
> Blood-milk
> intracellular
```
43
When is surgical antibiotic prophylaxis justified & what class of antibiotic would you recommend
```
> With high risk dental procedures
> Patient with leukopenia
> Contaminated surgery
> Orthopedic surgery or any major Abdominal/thoracic surgery
> Surgical time >90mins
```
To achieve maximum effect drug must be present at the time of contamination. Likely pathogens from skin (staph) and intestines (anaerobes & gram +ve).
1st gen cephalosporins good choice (if no risk of GI contamination) or 2nd gen (off label)
44
Why must maximum withdrawal times always be used
Withdrawal times are calculated on healthy patients. With sick patients possible to have decreased clearance & half life, therefore maximum withdrawal is recommended
45
What is maximum residue limit
MRL is the maximum concentration of residue accepted in EU food product that have received veterinary medicine.
46
Which antibiotics can not be used on farm animals
> Chloraphenicol (can be used on horses bust document it in the passport to prevent animal going into food chain) - causes aplastic anaemia in humans
> Phenylbutazone - aplastic anaemia
> Metronidazole - carcinogenic
Will be struck off if used
47
What 4 ways can bacteria be resistant to antimicrobials
1. AM cant reach target due to decreased penetration into the bacterial cells
2. AM expelled by special efflux pumps
3. AM inactivated by modification before or after cell penetration
4. AM target modified or protected by another molecule
48
Give an example of intrinsic resistance in bacteria
Gram -ve bacteria are resistant to macrolides as their to large to cross the cell wall and gain access to cytoplasmic target
49
What are the three VFA's and how are they affected by PH changes in the rumen
Acetate - Predominates at high roughage diet and is the precursor for milk fat
Propionate - Predominates at high concentrate diet and provides energy via conversion to glucose in the liver
Butyrate - Provides energy to the rumen wall and used for body fat
Rumen normally maintained at 6-7 PH, when lowered causes an increase in the propionate:acetate ratio causing decrease in milk fat.
50
How is cow comfort measured
Approximately 85% of the herd should be laying down 1 hour before feeding.
51
What is target milk fat and what would a low milk fat in the bulk tank indicate
Ideal is 4.2%. Altered by an increased propionate:acetate ratio caused by increased concentrates. Could indicate SARA
52
What is the target milk protein and why might it fall
3.4% is ideal. Milk protein is due to overflow of bacteria in the rumen into abomasum. must be sufficient energy to allow bacteria proliferation. After periods of inadequate intake possible for milk protein to fall, difficult to correct quickly
53
Why is the drying off period so critical
critical period 6 weeks either side of calving. Problems here cause poor DMI, milk production, fertility and can cause metabolic disease.
Should aim for a BCS of 3 (expect to lose 0.5 at calving. Losing excessive weight during dry period causes excess fat mobilization and increases the risk of fatty liver.
Dry cows should be split into 2 groups to easily manage transition in diets. 1) from drying off to 14 days before calving & 2) 14 days before calving up to calving
54
To get a metabolic profile of a dairy cow when are bloods taken
4 times a year:
1. soon after spring turnout onto grass
2. Mid to late summer when pasture quality is variable
3. Soon after housing
4. Late winter housing period
* also 10 days after any major dietary changes.
55
Why is weight gain an issue in summer
POMC is secreted by the pars intermedia due to increased day length. POMC causes increased adipogenesis and stimulates appetite
56
What conditions are associated with obesity in horses
abnormal reproductive performance and mesenteric lipomas are a direct result of obesity. Insulin dysfunction can also have consequences including:
- Laminitis
- Equine metabolic syndrome
- Hyperlipaemia
- Developmental orthopedic disease
57
What are the implications of a mare being obese during pregnancy
Mare with increased concentrations glucose and NEFA induce epigenetic changes which cause permanent changes:
- Appetite changes
- Neuroendocrine control
- Greater adiposity & risk of obesity later in life
*Sub optimal nutrition in utero can cause impaired pancreatic development causing impaired glucose homeostasis due to decreased Beta cells
58
What can be done to help a horse lose weight
Overall aim is to decrease calories but maintain DMI otherwise problems may occure ( dental disease, gastric ulcer due to decreased fibre or stereotypies).
Horse can consume 3% of their body weight in 3 hours therefore restricting time on pasture is crucial. removing of pasture and feeding 1.5% bw in hay is an alternative.
59
If you suspect an feline injection site sarcoma when should you take an incisional biopsy
> If it increases in size after 1 month post vaccine
> If its larger than 2cm in diameter
> If the mass persists for longer than 3 months
60
Are Feline injection site sarcomas metastatic?
10-25% metastatise to the lungs.
Potentially 75% curable with aggressive therapy.
Local disease is commonly the cause of death, either due to recurrence or unresectable to location
61
What are the treatment options for feline injection site sarcomas
Adjuvant radiation therapy 10-14 days post resection.
62
What are the clinical signs of hypomagnesemia (subacute and chronic) in ruminants and how is it treated & prevented
Subacute - Spasmodic urination and defication and muscle tremors.
Chronic - Poor appetite and depressed milk yield
Can be due to poor Mg in diet (grass grown too quickly has diluted minerals), reduced food intake or poor absorption due to increase K and Na
> Treatment - Magnesium sulphate 25% S/C only
> Prevention - MgO in concentrates or put Mg tablets in drinking water. Also avoid the use of K+ fertilisers
*prevention harder in beef herds as the system is extensive
63
What controls calcium levels, what are the clinical signs of Hypocalcemia(3 stages) and what is the treatment & prevention
Calcium homeostasis is dependant on PTH, vitamin D3 and calcitonin. Also MG is a co-factor required for absorption.
Clinical signs:
> Subclinical - tremors, ataxia and bloat ( due a decrease in ruminal turnover)
> Moderate - Sternal recumbancy, cold extremities, no defication, bloat and delayed or absent pupil response
> Severe - Lateral recumbancy, muscle flaccidity & unresponsive to stimuli
Treatment - 20/40% CaBorogluconate 400ml or low volume maxacal 100ml. Animal should then be encouraged to sit up.
Prevention - Drench at calving and bolus after calving. Also decrease the amount of calcium in dry cow ration and increase in milking cow ration
64
Whats the term for a hypophosphataemic cow
'happy downer' cow. Would also suspect Hypocalcemia and hypomagnesemia
65
what is DCAB and what are the consequences
Dietary cation anion balance.
(K + Na) - (S + Cl) = -100 to -200. Aim to have increased anions, decreases PH of blood thus making PTH more effective (reducing likely hood of milk fever)
However anionic salts are not palatable and excess will cause negative energy balance --> fatty liver.
Can monitor by monitoring PH of urine, should be 5.5-6.5. In the range of 5.0-5.5 shows many anions absorbed.
66
What are the two feedback systems for voluntary feed intake and what is inert fill
1. Distention feedback - As rumen fills stretch receptors send signals to the vagal nerve decreasing VFI
2. Chemostatic feedback - Changes inmetabolic status imacts on the vagal nerve.
Inert fill ie an abscess or pregnancy will cause a decrease in intake and increase in flow rate. food is therefore not fermented to the same degree therefore more digestible feed should be used.
67
explain the glucostatic theory
Glucoreceptors in CNS are sensitive to the rate at which glucose is utilized. Peripheral arterio - venous glucose differences serve as an index for utilization.
*Ruminant plasma glucose is about 1/2 that of non ruminants therefore the CNS is insensitive to changes in blood glucose.
68
Explain the hepatic oxidation theory
Levels of ATP in the liver determine the vagal stimulation, therefore low levels of ATP = hunger.
69
Explain the thermostatic theory
Animals eat to maintain body temperature. in ruminants the rumen is exothermic therefore not really applicable more applicable to poultry.
70
Explain the lipostatic theory
Hypothalamic feedback loop in which body fat reserves modulate the food intake and energy expenditure. The greater the fat store the lower the appetite
71
Describe what NEB is and is consequences
Negative energy balance occurs because the cows metabolism is completely devoted to supporting mammary metabolism. causes a decrease in circulating leptin (which usually has a negative effect on VFI) therefore theres an increase in feed intake, especially in early lactation
72
What are NDF and ADF measure of in feed
> Neutral detergent fibre is best single measure of forage quality. a high NDF --> decreased VFI
> Acid detergent fibre is used to predict the energy content of forage as its inversely related to digestibility
73
Name 4 anti nutritional factors that could effect ruminants
1. Tannins - found in Oak and acorns. eaten in large quantity cause precipitating enzymes which decrease fermentation and DMI
2. Lectins - Glycoproteins found in legumes (peas & beans) cause poor utilization and growth.
3. Glucosinolates - found in cabbage and oilseed rape. effects thyroid function
4. Sapsonins - Found in soybeans
74
What parameters are included in the profitable lifetime index of a bull
```
Milk yield
Fat
Protein
Lifespan
SCC
Locomotion
```
75
What are the routes of infection for mastitis
1. Haematogenous
2. Skin abrasion
3. Galactogenic
76
What are the bodys defences against mastitis, including cellular and soluble factors
> Smooth muscle sphincter
> Keratin - from epithelium contains fatty acids which are bactericidal
> Furstenbergs rosett - Prevents physical entry into the canal, contains fatty acids (bacterialcidal) & subepithelial cells produce Immunoglobulins
Soluble factors:
> Lactoferrin - ion binding protein which inhibits bacteria (more effective in non lactating gland)
> Compliment
> Cytokines
```
Cellular factors:
> Neutrophils - Acute inflammation
> Macrophages - Ingest bacteria
> Natural killer cells
> Lymphocytes - Sensitised to bacteria and retain memory for subsequent infections
```
77
What are the 3 clinical categories of mastitis and their clinical signs
1. Peracute - Life threatening, usually systemic infection. mostly occur around parturition with death within a few hours.oedema, dark blue, blistering, oozing serum and cold to touch. theres death of glandular tissue
2. Acute - Mostly local effects - oedema, fibrin exudation & neutrophilic response. Altered milk quality on histology extensive vacuolisation and extensive interstitial oedema.
3. Chronic - Gland becomes hard and atrophic. Involutio causes temporary loss of secretory function due to obstruction of granulation tissue. Fibrosis causes permanent loss of secretory tissue due to progressive destruction
78
What are the pathogens associated with clinical and subclinical mastitis and what are their pathogenicity factors
50% of clinical mastitis is due to E.coli or Strept uberis, with S.aureus and CNS (coagulase negative staphylococci) making up 11% each
50% of subclinical cases are due to CNS and S.uberis, with S.aureus and coryne make up 16 each
Dry cow mastitis due to trueperella pyogens and streptococci dysgalactiae
Ewe mastitis is due to mannheimia haemolytica, S.aureus and E.coli
S.aureus habitat is skin and mucous membranes, making it contagious. When treated possible to reoccur because some are intracellular. Hypersensitivity can also occur.
Pathogenicity factors:
Alpha toxin - potent nectrotic factor
Beta toxin - Sphingomyelinase digests through host cell membrane
TSST-1 superantigen causing inappropriate cytokine release
Polysacchride capsule in vivo prevent phagocytosis
Fibronectin binding protein - Adherence prevents flushing action of milk
79
Give 3 ways of testing for mastitis
1. California milk test - lyses somatic cells present and denatures and DNA present
2. Electrical conductivity - Ion concentration of milk is changed during mastitis
3. In line SCC
80
What is treatment for mastitis
Either intra-mammary or systemic antibiotic used.
Also anti inflammatory can be given, however generally have withdrawal period of 1-2 months, therefore dont use in dry cow or whole lactation is rendered useless
81
In terms of control, what are the two types of categories of mastitis with examples
1. Contagious - Organisms live in the udder/teat skin. Often cause subclinical infection, spreading from cow to cow. E.g staph aureus & strept agalacticae. main control strategy involves good milking hygiene, culling persistent cases and dry cow therapy.
2. Environmental - Sporadically gain entry to udder via wounds/abrasions. Tend to rapidly eliminated or cause very serious mastitis. E.gs E.coli, Strept uberis, coliforms and klebsiella.
82
What is the 5 point plan to help prevent/reduce mastitis
1. Prompt detection & treatment
2. Post milking teat dipping - teat orifice remains open 30-40 minutes post milking, therefore must keep cows standing by eating
3. Dry cow therapy - Long acting antibiotics to remove existing subclinical cases. Teat sealant can be used. or can infuse antibiotics to those cows with >200,000 SCC (selective dry cow therapy)
4. Cull persistent offenders - 3+ cases in one lactation or persistently high SCC despite treatment
5. Regular servicing & maintenance of milking machine - can cause damage to teats, allowing contagious organisms a portal of entry.
83
What are the initial differentials for a large mass
Inflammatory lesion E.g granuloma or abscess
Haematoma
Seroma - pocket of clear serous fluid that develops after surgery
Cysts
Neoplasia
84
For suspected neoplasm, what diagnostic tests would you conduct
FNA - quick and cheap test that gives you an idea of types cell types and morphology. Can see if its an inflammatory lesion or neoplasia, also if it has benign or malignant properties
Histopathology - Requires a biopsy (incisional, excisional. Gives you more detail, e.g tissue architecture, blood vessels, necrosis, tumour grade and if its invaded into neighboring tissues or contained within a capsule
85
What are the criteria used to help grade a tumour
```
Mitotis index
Degree of cellular differentiation
Amount of necrosis
Invading of surrounding tissues
Invasion of vasculature/lymphatitis
```
*important to assess margins of excised tumour
86
Describe TNM system for staging a cancer patient
```
T = Primary tumour - size is the most important factor. also mobility, ulceration and relationship to surrounding tissue.
N = Node - Assess regional nodes for size increases and can aspirate to decide if theres any metastasis
M = Distant metastasis
```
87
Describe the stages (5) of lymphoma classification
1 - One LN involved
2 - More LN's on one side of the diaphragm
3 - LN's on both side of the diaphragm are effected
4 - Spleen and liver involved
5 - When other systems are involved e.g bone marrow
88
What are the 6 hallmarks of cancer
1. Sustaining proliferative signalling - achieved in 3 different ways. a) Make own growth factors, autocrine and paracrine. b) mutation of growth factor receptors, meaning receptor activated in the abscence of ligand or over expression allows activation with low numbers of ligand ( common in canine MCT, KIT gener mutation). c) mutate intracellular signalling molecules (RAS-->activate MAPK)
2. Evading growth suppressors - mutations to p53 and retinoblastoma genes, predisposed in bull mastif (germline p53 mutation = lymphoma predisposition
3. Resisting cell death - many cancers down regulate death receptors
4. Avoiding senescence - up regulate telomerase
5. Induce angiogenesis - secrete VEGF. tumours often outgrow blood supply causing central core of necrosis
6. Invasion and metastasis - alteration in cell adhesion molecules allow them to detach and migrate. loss of E.cadherin allows cells to detach. matrix metalloproteinases melts ECM
89
What are 3 emerging hallmarks of cancer
1. Tumour surveillance - Tumours down regulate immunogenic antigens, kill infiltrating lymphocytes and produce immunosuppressive mediators
2. Inflammation - Inflammatory cells infiltrating is common however may paradoxically enhance malignancy by releasing immunosuppressive cytokines, growth factors and angiogenic mediators.
3. Reprogramming energy metabolism - upregulation of GLUT-1 receptors for increased uptake of glucose, also limit metabolism to glycolysis.
90
Describe gross differences between benign and malignant tumours
> Benign tumours grow by expansion and malignant by invasion
> Benign are well demarcated whereas malignant are not
> Benign are surrounded by a connective tissue capsule, malignant arent
> Benign are freely moveable and malignant arent
> Benign are homogenous on cut surface, while malignant are often ulcerative on skin and show internal hemorrhage and necrosis
91
Describe microscopic differences between benign and malignant tumours
> Benign will be similar to the tissue of origin whereas malignant display anisocytosis (abnormal cell sizes) and anisokaryosis (variation in size and shape of nucleus)
> Benign has few or no mitotic bodies whereas malignant has variable amount, also have increased nuclear to cytoplasmic ratio
> malignant don't often have a capsule, but when they do often invaded
> malignant cells display malignant fusion = multinucleated cells.
> Benign endocrine tumours can be functional which can cause clinical signs
92
What would you call a benign tumour of epithelial origin
If its on surface epithelium e.g skin known as a PAPILLOMA e.g squamous papilloma
whereas if its from glandular epithelium its known as an ADENOMA e.g thyroid adenoma
93
What would you call a malignant tumour of epithelial origin
if originating from glandular epithelium its given the suffix ADENOCARCINOMA e.g mammary adenocarcinoma
whereas if its a malignant tumour of epithelial origin its known as a CARCINOMA e.g squamous cell carcinoma.
*carcinoma tend to metastasize via the lymphatics
94
what would you name a mesenchymal originating benign tumour?
Would add -oma to the end
| e.g lipoma, fibroma, leiomyoma
95
What would you name a malignant tumour of mesenchymal origin
a sarcoma, e.g osteosarcoma or haemangiosarcoma
*sarcomas tend to metastasize in vasculature by seeding to internal organs
96
Name tumours that frequently metastasise
Mammary carcinoma
osteosarcomas
Pancreatic carcinomas
Digital melanomas
97
Describe different ways in which tumours can be graded
1. Light microscope - e.g with squamous cell carcinoma
2. Immunophenotyping - Lymphoma - loses expression of expected tissue markers
3. Detection of genetic mutations - Lymphoma
4. Use of proliferation markers - Ki-67 stains proliferating cells, used for diagnosis of MCT
98
How can immunohistochemistry be used for diagnosis of tumours
> CD3 - T cell lymphoma
> CD79a - B cell lymphoma
> Vimentin - sarcoma
> cytokeratin - carcinoma
99
What are the indications for chemotherapy
> Treatment of disseminated disease e.g lymphoma, leukamias, myeloma and disseminated MCT
> Adjuvant therapy following surgery of a known metastatic tumour (start after wound has healed)
> Neo-adjuvant chemo to shrink tumour
> Chemosensitive tumours not amenable for surgical resection
* more likely to be sensitive to treatment if mitotic index is high, if in g0 relatively resistant
100
how would you administer chemotherapy
Given intralesionaly or intra cavitary.
A given does of drug will kill a fixed percentage of cells, therefore we pulse dose at intervals allowing normal tissue to recover between doses but not allowing tumour to regrow.
Dosing is done on mg/m2
101
What is chemotherapy protocol?
> Induction - Fairly intense, aim to induce remission (where tumour not clinically detectable)
> Maintenance - Less intense, maintain remission
> Re-induction - When tumour relapses, return to initial protocool
> Rescue - When tumour becomes resistant to current therapy, use different drug
102
What chemotherapy protocol is used for canine lymphoma
COP based:
> Cyclophosphamide
> Vincristine
> Prednisolone
103
Give two alternatives to cytotoxic drugs that can be used for chemotherapy
1. Metronomic therapy - Low dose cytotoxic drugs + NSAIDS = lack of progression of disease. Inhibits angiogenesis & immunodulatory effects (increase in anti tumour immunity)
2. Receptor tyrosine kinase inhibitors - Interfere with cell signaling, inhibiting angiogenesis, reducing proliferation and promoting apoptosis
104
What factors effect success of chemotherapy
> tumour cell type - some tumours are highly sensitive to anti cancer drugs (e.g lymphoma) whereas other are intrinsically resistant
> penetration of drug into the tumour - this is dependent on the blood supply and the barriers E.g BBB
> Drug resistance - mutations convey resistance e.g decreased drug uptake or increase removal, decreased drug activation or the use of alternate signalling pathways
105
name common anti cancer drugs and mode of action
> Alkylating agents - interfere with DNA synthesis by substituting alkyl side chain for H+. E.g cyclophosphamide
> Mitotic spindle inhibitors - cause metaphase arrest by preventing spindle formation e.g Vincristine
> Platinum compounds - Cross link DNA strands e.g Cisplatin
> Anti-tumour antibiotics - Inhibit topoisomerase II - e.g Doxorubicin
Non toxic:
> Prednisilone - Cause apoptosis of lymphoid and mast cells
> L-asparaginase - Breaks down L-aparagine which is needed by neoplastic lymphoid cells
106
Give some general side effects of cytotoxic drugs used for chemo
> Myelosuppression - neutropenia and thrombocytopenia (complete blood count should be monitored) - can prophylacticly use antibiotics
> Gastrointestinal toxicity - Vomiting & diarrhoea - Can give metaclopramide/maripitant. Also bland diet
> poor hair growth - more extensive in curly hair dog breeds
> Drug extravasation - Vincristine and doxorubicin can cause sever tissue damage so must ensure clean catheter placement and flush with saline before and after use.
107
Give some specific drug related toxicities of chemotherapy drugs
> Doxorubicin - Cardiotoxicity in dogs, causing dysryhmias, and chronic use causes DCM. prevent by giving over 20-30 minutes.
> Cyclophosphamide - Cause hemorrhagic cystitis in dogs. prevent by allowing free access to water and oppertunity to urinate. Can give oxybutinin ( causes urination - antispasmodic) and analgeisia
> Cisplatin - nephrotoxic - requires extensive diuresis, also acting on CRTZ to cause vomiting. also can cause fatal pulmonary oedema in cats
Vincristine - Peripheral neuropathies & ileus ( give metoclopramide)
108
What are the indications for radiation therapy
> Local and regional disease
> not surgically resectable
> Treatment of neoplastic cells remaining after surgery
> Incurable tumours causing pain and discomfort
* examples of tumours commonly used on are soft tissue sarcomas, MCT's and brain tumours
109
Explain how radiation therapy is administered and what are the 4 R's
High energy beam of ionizing particles passed through tissue - Direct damage by directly disrupting DNA and indirect damage by formation of oxygen radicals which cause DNA damage. For oxygen radicals to be effective must be good oxygenation - Very large tumours have poorly oxygenated necrotic centers therefore making them resistant.
Given in small doses over 3-4 weeks (fractination - total dose of radiation split into amount of treatments), giving normal cells time to REPAIR & REPOPULATE.
Radiation kills oxygenated cells - therefore better distribution of oxygen to cells within the tissue, RE OXYGENATION AND REDISTRIBUTION
110
Whats the difference between electron and photon beam radiation therapy
Electron beam - Rapid dose reduction - low penetration used for superficial tumours
Photon beam - high penetration and slow dose reduction. CT based planning required
111
What are the 3 volumes used for radiation planning
1. Gross tumour volume - Only include gross tumour
2. Clinical target volume - Gross tumour volume + expansion accounting for regional microscopic disease
3. Planning target volume - clinical target volume + expansion for variation in anatomy (e.g bladder fill)
112
What are the 3 radiation therapy protocols
1. Definitive - Long term tumour control, used as the primary treatment when Radiation therapy is the best therapy option (e.g nasal tumours), also used as adjuvant treatment after surgery. Daily treatments fpr 3-4 weeks
2. Stereostatic - same as definitive but high doses of radiation in a smaller number of treatments.
3. Palliative - Large doses 1/2 x weekly for 1-4 weeks. Used primarily for improvement of clinical signs. Primary treatment used when tumour is non - resectable e.g bone tumours
113
What are the side effects associated with radiation therapy
Acute effects - Reversible side effects affecting the majority of patients, usually resolving in 2-3 weeks after treatment completion. effects rapidly dividing tissue such as skin, mucosa and GI epithelium. Examples include alopecia, conjunctivits, keratitis and dermatitis
Late effects - Permanent, irreversible changes effecting <5% of patients, effecting slowly dividing/non dividing cells. Often permanent and occur months to years later. Examples include fibrosis, non healing ulcerations, necrosis and cataracts.
114
Distinguish the difference between contamination and infection at the surgical site
Contamination - Pathogen present but no multiplying or affecting healing
Infection - Pathogens present and multiplying: disrupting healing, damaging tissues, can spread to adjacent tissues and can cause systemic infection
115
Describe the sterilisation techniques used for instruments
1. Steam - 2 different types
> Gravity displacement - Steam introduced at the top and moves down under pressure. sterilisation in 13 mins at 120 degrees
> Pre-vacuum sterilisation - Actively removes air to create a vacuum before rapidly introducing steam. Sterilisatio in 3 minutes under 131 degrees
2. Ethylete oxide replaced by Hydrogen peroxide gas plasma because it was toxic - Hydrogen peroxide turn into vapour and then with the use of radio waves turned into gas. Gas is then turned into plasma by an electrical field destroying any pathogens. By products are o2 and h20. expensive and done within a hour.
3. Gamma radiation - used for alot of pre-packed sterile items.
116
What antiseptics are used before surgery to prep patient
> Chlorohexidine gluconate (4%) - Broad spec activity (more effective against -ve), enveloped viruses, yeast but not effective against mycobacterium, protozoa and fungi. Rapid initial kill of 96% in 30 secs and 98% in 3 mins. Good residual action as it binds to stratum corneum. contact toxicity to middle ear, meninges, cornea and conjunctiva
> Povidone idodine (10%) - Broad spec, effective against everything including mycobacterium, fungi and protozoa. Rapid kill of 77% in 3 mins and good persistent action. Causes acute dermatitis in 50% of dogs. used for eye surgery at 02% and ear at 1%.
> 70% alcohol - Rapid kill of 98-99% in 30 seconds. however will cause necrosis on open wound and dehydration of skin causing irritation.. combined with 2% chlorohexidine for chloraprep.
117
Describe surgical classification and when antibiotics are indicated
> Clean - Non traumatic elective surgery. Antibiotics if >90mins or where infection would be catastrophic e.g joint replacement
> Clean-contaminated - Entry into hollow organ (bladder), or no significant spillage or infection. no indication for antibiotics.
> Contaminated - Fresh traumatic wound (6-8hrs), spillage from contaminated organ or the presence of infection. a clean surgery but there was a break in aspetic technique. Antibiotics are indicated.
> Dirty - Infected surgical site, or purulent discharge is present. Wound is open and untreated for >6-8 hours. Antibiotics are therapeutic in these cases, should be based on culture sensitivity testing.
118
When is the use of a drain indicated and what are the two typed of drain
> Indications - Contaminated or infected wound. When there is dead space (e.g tumour removal or amputation). this is because theres an accumulation of blood/serum, which prevents adherence of skin to underlying tissue.
1. Pennrose drain (passive) - Exit must always be below/ventral to the wound. also is at risk of ascending infection as its left open. These drains always work, are inexpensive, can be used with contaminated/infected wounds and can be used with wounds that cant be completely closed
2. Jackson pratt drains (active) - closed system therefore no risk of ascending infection. Accurate assessment of fluid production. But wound must be completely sealed and cleaned and failure can occur due to premature loss of vacuum or obstruction in the drain tubing.
119
When is it time to remove a drain
> when theres under 2ml/kg of bw/day being produced
> Inflammation reduces - Cytology daily looking for transition from degenerative neutrophils to non degenerative
> Absence of bacteria
> 1-3 days for penrose drain & 3-5 days for jackson pratts
120
Name a synthetic absorbable multifilament suture and when it would be used
```
Vicryl.
> Closure of vessels/ligation
> Also soft tissue closure
> Rapid absorption + good knot security
> Loss of 33% tensile strength in 7d, and complete loss in 21d
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121
Name a synthetic absorbable monofilament and when it would be used
Monocryl
> Closure of viscera (GIT/bladder), soft tissue closure, subcutaneous and intradermal
> Short term suture
PDS II - Longer duration in comparison to monocryl
> Used on tissue that takes longer to heal but needs to be absorbable E.g linea alba or viscera
122
Name a synthetic non absorbable suture and when it would be used
Prolene/ethilon
> Used for skin closure
> Used for hernia closure where prolong support is needed
> Minimal reaction as its inert
123
Name a natural absorbable multifilament suture and when it cold be used
Catgut
> Generally not used - Variable absorption rate due to phagocytic breakdown + marker tissue reaction
> Knots weaker when wet
> Used to ligate vessels
Mersilk
> Used for portosystemic shunts - Causes marked inflammation therefore closing the shunt
124
What are some general rules when selecting appropriate suture material
> Avoid multifilament in contaminated wounds
> Avoid non-absorbable in hollow organs as it acts as a foreign body
> Non absorbable material used in fascia/tendons
125
What are halsteds principles of surgery
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> Gentle handling of tissue
> Meticulous haemostasis
> Preservation of blood supply
> Strict aseptic technique
> Minimum tension on tissues
> Accurate tissue apposition
> Obliteration of dead space
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126
What are the advantages and disadvantages of doing an inverted and everted suture pattern
Inverted
> Can be used for the closure of the stomach
> However more work because not aligned. Inverted tissue can act as a foreign body
Everting
> Increases the tensile strength and endothelial contact reduces the risk of thrombosis
> However increased risk of leakage, stenosis, incidence of adhesions and prolonged inflammation
127
What are the 3 stages of wound healing
1. Inflammation - Hypoxic conditions cause fibrin clot. Bacteria engulfed by neutrophls cause the release of vasodilators causing increased blood flow and permeability. Adhesion and activation of platelets.
2. New tissue formation - Formation of granulation tissue. Inflammatory cells move away from site and VEGF released allowing angiogenesis, Re epithelialisation under scab (single keratinocyte layer) (2-10d)
3. Remodelling - Disorganised collagen move into the wound. wound contracted near surface. Re-epithelised wound raised. last months/years.
128
What are the 2 phenotypesof macrophages
> M1 - Pro-inflammatory & inhibit proliferation. Use argenine to produce NO which inhibit proliferation. Also secrete TNF-a which promotes inflammation and fibrosis
> M2 - Anti-inflammatory and promote proliferation. Usesargenine to produce ornithine which promotes cell proliferation and repair. Also secretes IL-10 which is anti-inflammatory and Wnt7b (repair)
129
What is the role of fibroblasts in wound healing and what do they transform into
Fibroblasts are responsible for laying down new ECM. they predominate at wound edge.
Transition into myofibroblasts which contract allowing wound closure. Also secrete proteases which degrade non viable tissue and fibrin.
130
What is debridement
Removal of devitalized, infected or contaminated tissues and foreign material. Surgical procedure done under aseptic conditions
131
What are the various debridement dressings and there pros and cons
> Wet to dry - Moist sterile gauze applied to wound then dry sterile gauze/bandage applied. Draws exudate out and bacteria and necrotic tissue cant retain water and dry out.
- Inexpensive, easily available and effective
- Requires changing every 12-24hrs, also painful on removal requires sedation
> Hydrogels - hydrophilic and inoluble, covered by a semi-occlusive layer. Gives up water to wound maintaining moist wound. Wound exudate remains in contact with wound promoting wound healing while endogenous enzymes break down nectrotic tissue and attract macrophages.
- Inexpensive, easy to apply, effective, comfortable, useful in deep pocketed wounds
- Change every 24-48hrs and needs to be flushed every dressing change
> Sugar - Draws water out
> Manuka honey - Decrease inflammatory oedem, attracts macrophages ad increases shedding of devitalized tissues. But must be changed every 24 hours and animal will eat
> Negative pressure wound therapy - Removes exudate and promotes perfusion. Increases granulation and wound edge contraction. Also only has to be changed every 3 days however cant use on infected wounds and there can be a failure/loss of vacuum.
