Equine Flashcards
1
Q
What can be used to treat head shaking if you are suspiscious it has a photic/trigeminal component?
A
Cyproheptadine or Carbamazepine.
2
Q
What is the normal temperature of the horse?
A
38C+- 0.5
3
Q
What does EHV 1 usually cause?
A
Abortion in last trimester.
4
Q
What is the pathognomic lesion for EHV1 infection?
A
Histological inclusion bodies in foals liver, lungs and thymus.
5
Q
What does neutrophilia over >5% seen in BAL suggest?
A
RAO, SPAOPD, IAD, pleuropneumonia, acute
6
Q
At what age do foals usually develop signs of rhodococcus equi penumonia?
A
infected as neonates by inhalation or ingestion of environmental bacteria but do not develop clinical signs until 2-6 months old. Bacteria reside intraellularly, particularly in phagocytes, leading to multifocal pulmonary abscessation.
7
Q
What is the treatment for rhodococcus equi?
A
Rifampin and erythromycin for several weeks.
8
Q
What are your differentials for acute infectious respiratory disease in adults?
A
Influenza, EHV1 EHV4 Rhinovirus EVA Strangles. Mycoplasma felis, equirhinis, bordetella bronchiseptica, streptococcus pneumonia, pasteurella spp, actinobacilluus sp.
9
Q
What does EHV1 cause?
A
occasionally respiratory disease, more commonly abortion and encephalomyelopathy.
10
Q
What are the signs of equine viral arteritis?
A
Respiratory disease, severe conjunctivitis, profound depression, periorbital oedema due to vasculitis.
11
Q
What is bastard strangles?
A
A complication whereby abscessation occurs in other tissues including mediastinal and mesenteric lymph nodes and physes. Affected horses present with fever, malaise, weight loss and signs related to local abscesation.
12
Q
Which type of hypersensitivity reaction is Purpura haemorrhaghica?
A
Immune mediated (type 3) - occurs 1-3 months after strangles infection, signs include oedema, petechiation, pyrexia, tx with dexamethasone, penicillin.
13
Q
When can you be sure a horse has recovered from strangles?
A
3 consecutive nasopharyngeal swabs negative at weekly intervals
14
Q
How is dictyocaulus arnfieldi diagnosed?
A
Eosinophilia in tracheal mucous or by response to anthelmintics - infections in horses are usually non patent and consquently the baerman faecal flotation technique is unreliable.
15
Q
What are the clinical signs of pulmonary oedema in horses?
A
Frothy nasal discharge, increased inspiratory effort, widespread fine crackles on auscultation.
16
Q
You are examining a 3-day old neonatal foal for suspected sepsis. Upon review of a blood smear, you notice the blue aggregates in many of the neutrophils (see image). What are these called and what do they suggest?
A
Dohle bodies are bluish-gray inclusions within the neutrophil that are retained aggregates of rough endoplasmic reticulum. Dohle bodies are one manifestation of toxic (i.e. endotoxemia) morphologic change to the leukocytes.
Other changes in neutrophil morphology that occur with toxemia include cytoplasmic basophilia, vacuolation, and toxic granulation. These changes are commonly found in septic foals and may be considered “defects” in the neutrophil during intense cell production and maturation. In this image, there are numerous dark blue aggregates suggestive of Dohle bodies.
17
Q
What breed of horse is predisposed to development of recurrent uveitis and equine night blindness?
A
The correct answer is Appaloosa. Equine night blindness is a congenital disease that is bilateral and nonprogressive, wherein horses have variable degrees of decreased vision in the dark. Recurrent uveitis is a very important condition in the horse and is actually the most common cause of blindness in the horse. Appaloosas are overrepresented, but the disease can occur in any breed. It is thought to be related to certain pathogens including Leptospira, Onchocerca, Toxoplasma, Brucella, and other infections, but these relationships are poorly characterized. Affected horses have recurrent bouts of inflammation, and each episode causes progressively worsening intraocular damage. The condition is sometimes referred to as moon blindness.
18
Q
Which of these tests is most reliable in diagnosing a uterine infection in a mare?
A
the correct answer is uterine cytology. Endometrial cytology will show a more quantitative measure of not only bacteria but of leukocytes. Because there are many commensal organisms found in and around the uterus, culture is neither sensitive nor specific. However, it is often a worthwhile test to determine what organisms are there and to design an appropriate antibiotic plan based on susceptibility results. A cervical swab is less reliable than an endometrial sample. CBC is neither sensitive nor specific for diagnosing endometritis. The presence of a high percentage of neutrophils in an endometrial cytology is very suggestive of uterine infection, especially if bacteria are also seen.
19
Q
Why might a thrill be felt in the cardiac area?
A
A diastolic thrill on the left hemithorax is most likely caused by aortic insufficiency, systolic thrill on left hemithorax by mitral regurgitation, systolic thrill on right hemithorax by tricuspid regurgitation or ventricular septal defect.
20
Q
What is the most common cause of poor performance in thoroughbred racehorseS?
A
Atrial fibrillation
21
Q
Which drugs may cause toxic damage to the myocardium in horses?
A
Salinomycin and monensin. Monensin causes acute myocardial necrosis leading to fibrosis.
22
Q
What treatments are available for Atrial fibrillation?
A
quinidine sulphate - anti arrythmic drug. Sudden death may occur. toxicity incudes urticaria, diarrhoea, anorexia, weakness. Heart rate and rhythm must be monitored throughout treatment.
Conversion of AF to normal sius rythm only occurs in 87%, and sudden death is rare but does occur. if horses fail to revert to sinus rythm during initial regimen then quinidine administration should be continued at six hourly intervals following a period of 24 hours without drug administration. Digoxin should be given every 12 hours until sinus rhythmn is restored.
23
Q
Does aortic insufficiency predispose to sudden death?
A
Aortic insufficiency causes decreased coronary perfusion due to reduced diastolic aortic pressure and oxygen delivery to the myocardium is compromised. increased oxygen demand and reduced coronary reserve increases susceptibility to ventricular arryhthmias that can result in sudden death.
24
Q
What is the most common congenital abnormality in large animals?
A
Ventricular septal defect
25
Where are septal defects most commonly located in horses?
In the membranous septum below the aortic and tricupsid valves. Most common in the shetland and welsh mountain ponies.
26
What are the clinical signs of salmonellosis enterocolitis?
May be precedeed by colic
Diarrhoea usually occurs 24-48 hours following fever
Associated with signs of endotoxaemia and hypotensive shock
Reduced intestinal sounds followed by an increase in intestinal sounds. Transrectal palpation reveals fluid filled colon and caecum.
27
What are the clinical signs of cyathostomiasis?
Clinical disease of diarrhoea caused by intra mural larval stages of the nematode and mass emergence of hypbiotic larvae resulting in mucosal injury and inflammatory reaction. Migration of the larvae into the colonic mucosa and even presence of large larval numbers within the mucosa may also result in significant colonic inflammation and clinical signs. Common cause of chronic diarrhoea, an acute form also recognised. Clinical signs vary from weight loss, ill thrift, ventral oedema and soft faeces to severe acute enterocolitis (mass emergence of larvae). Acute diarrhoea mya progress to chronic diarrhoea. Often hypoalbuminaemic - may have elevated a and B globulins resulting in normal total protein concentration. FWEC likely negative as infection not patent at the time of disease.
28
What is the pathophysiology of carbohydrate overload?
Over eating of soluble carbohydrates - overwhelms the small intestinal digestive capabilities - high percentage enters large intestine - rapid fermentation by gram positive lactic acid producing bacteria - decreased caecal ph - death of gram negative bacteria - endotoxin release and absorption. high osmotic load in large intestine and pro secretory effects of acid luminal contents and inflammatory mediators results in diarrhoea.
29
What acid base status do acute colitis cases have?
Metbaolic acidosis
| With hyponatraemia, hypochloraemia, hypokalaemia.
30
Endotoxemia is a term applied when an animal exhibits multiple adverse clinical signs including one or more of the following: fever or hypothermia, leukopenia, tachycardia, tachypnea, obtundation, and a change in gut motility. These physiologic effects are caused by what?
The cell walls of all Gram negative bacteria contain varying amounts of lipopolysaccharide, which in turn varies in its potency to create adverse reactions in animals. The signals have evolved on monocytes and macrophages to warn the animal when a Gram negative bacterium has gained access. When the reaction to this signal is overzealous, a cascade of adverse physiologic reactions can occur.
31
What is a possible complication associatied with colitis/endotoxaemia?
Hypercoagulability
32
What is the treatment for cyathostomes?
Fenbendazole for 5 days followed by ivermectin on day 6 OR moxidectin,
Give dexamethasone too
33
what are good dietary sourcesof protein for chronic diarrhoea?
Hay and alfalfa
34
What type of colics are large breeds predisposed to?
Large colon displacements
35
What type of colic are recently foaled mares prone to ?
Colonic torsions
36
Which colic conditions would result in gastric dilation/reflux?
acute grass sickness, ileus, small intestinal strangulating obstruction, proximal jejunitis.
37
What parameters on abdominal paracentesis are suggestive of inflammation?
Initial response of the peritoneum to inflammation or ischaemia is an increase in protein and fibrinogen levels in the peritoneal fluid. Fibrinogen >0.1g/l is suggestive of an acute inflammatory response or haemoabdomen. Acute ischaemia is characterised by a neutrophilia and increased erythrocytes. Acute inflammatory responses such as abscessation or bacteiral peritonitis may increase neutrophil counts without increasing RBC numbers. Peritoneal fluid may remain normal in horses with devitalised bowel if inflammatory debris is trapped e.g in epiploic entrapment and intussusception. Abnormalities include turbid, purulent or serosanguinous fluid, or digesta/blood in fluid. Total protein - normal is
38
What are the suggested indications for Surgery/euthanasia of colics?
Severe continuous pain showing no or only short duration of improvement with analgesia, pulse >60 progressively rising and weakening, progressive cardiovascular collapse, PCV >55, rectal findings positive for acute abdominal disease, progressive reduction in intestinal motility or continual gastric reflux, increasing abdominal distension.
39
Which enzymes are liver specific in the horse?
GGT and GLDH
40
What laboratory diagnostics are different in equine liver failure cf small animal?
Ammonia in horses not very useful, only in acute severe or end stage chronic disease. Blood ammonia levelsa re increased only in some cases of hepatic encephalopathy. Most affected horses are hyperglycaemic. but severely affected horses may be hypoglycaemic. Hypoproteinaemia and hypoalbuminaemia is rare in horses - most are hyperproteinaemic.
41
whhich breed does polysaccharide storage myopathy most commonly affect?
Quarter horses.
Horses present typically as a chronic case of tying up with signs often initiated following minimal exercise. there are abnormally high levels of the intracellular polysaccharide glycogen up to 4 levels of normal. Diagnosis based on histopathological findings. Genetic testing for glycogen synthase mutation
42
What is atypical myopathy/myoglobinuria?
Serious and frequently fatal. The recent evidence suggests that the toxic agent for this is Box elder tree and sycamore tree. Mainly occurs in young horses and ponies at grass, not related to exercise. Sudden onset muscle weakness and stiffness, afebrile and appetite and thirst remain, urine is red or chocolate coloured, most cases become recumbent and die. CPK and AST are markedly elevated. Myoglobinuria and haemoglobinuria present.
43
What is hyperkalaemic periodic paralysis in horses?
A syndrome of episodic muscular weakness associated with marked hyperkalaemia. Important problem in american quarter horses. Male horses seem to be affected to a greater extent than females. onset of HPP clinical signs typically between 1-5 yo. Episodes of weakness typically last less than 2 hours and affected horses often recover spontaneously. Muscle fasiculations, weakness, sweating, involuntary recumbency. Hyperkalaemia may only be present during an episode.
44
What is the treatment for hyperkalaemic periodic paralysis?
During episodes - i/v sodium bicarbonate, i/v dextrose, potassium free isotonic fluids, i/v calcium gluconate.
45
What are the most common cause of cystic calculi in the horse?
Calcium carbonate
46
What is the cause of urethral haemorrhage and haemospermia in stallions?
Due to tears in the proximal urethra at the ischial arch into the corpus spongiosum penis which is vascular rich and surrounds the urethra. There may be normal urine flow followed by bleeding at the end of urination due to contractions of the urethra that occur during this time, bleeding following ejaculation.
47
What is the current hypothesis for equine grass sickness?
Toxicoinfection with clostridium botulinum types C and D.
48
What are the clinical signs of grass sickness?
Dull, Anorexic, tachycardia (reflects hypotension and alterations in autonomic control of HR), bilateral ptosis, dysphagia, hypersalivation, slight drying of the mucous membranes, patchy sweating, mild to moderate abdominal pain, ileus due to damage to enteric nervous system, reduced inestinal sounds (absent if acute), muscle tremors over the triceps, flanks and quadriceps. On rectal - firm secondary large colon or caecal impaction.
49
What are the gross pathological findings associated with grass sickness?
Oesophageal erosions associated with reflux oesophagitis, gastric and small intestinal distension with fluid, impaction of the large colon with dry ingesta, black coating over firm ingesta, or if v chronic - lack of ingesta and apparent shrinkage of gastrointestinal tract.
50
What is proximal jejunitis (anterior enteritis)
Possible bacterial aetiology. rare in the UK. results in gastric and proximal small intestinal distension. often febrile, Increased gastric reflux of tomato soup fluid, decreased gut sounds. treatment is by decompression, fluid therapy, antibiotic therapy etc.
51
which Antibiotics and which bacteria are the most common causes of antibiotic associated diarrhoea?
Erythromycin, TMPS, penicillins, tetracyclines, clindamycin, lincomycin.
Bacteria - C perfringens, C difficile, Salmonella.
52
What are the predisposing causes to caecal impaction?
hospitalization, GA, Nsaid use, as well as same as large colon impactions. type 1 - impactions of dry ingesta filling the caecum
and type 2 - impaired caecal outflow due to motility dysfunction.
53
what are the predisposing factors to gastric impaction?
Ingestion of beet pulp, bran, dental disorders (incomplete mastication), terminal liver failure.
54
What portion of the stomach is most commonly affected with ulceration and why?
Squamous portion - no protective mechanisms against gastric acid. more common in high intensity training, roughage restriction, excessive concentrate feeding, NSAID use.
55
what is hyperlipaemia and why does this occur?
Hypertriglyceridaemia, fatty infiltration of body organs in resposne to stress and NEB, mobilisation of fat reserves. Common in small ponys and donkeys. clinical signs ; anorexia, depression, CNS signs, ventral oedema, colic, tachypnoea, tachycardia. dx - elevated blood triglycerides. may visually appreciate fatty appearance to plasma.
56
What are the predisposing factors to pelvic flexure impaction?
Reduced water intake, poor quality roughage, poor dentition
57
what is proliferative enteropathy?
Increasingly recognised in recent years, often occurs as outbreaks on breeding farms (4-6month olds affected), faecal oral transmission, causes profound hyperplasia of jejunal/ileal mucosa, resulting in secretory diarrhoea aand weight loss. cliical signs include ill thrift, weight loss, peripheral oedema, diarrhoea, colic.
58
What are the classical histological features of ragwort toxicity?
```
on biopsy:
Megalocytes
Periportal fibrosis
biliary hyperplasia
occlusion of central veins
Exposure to massive doses may produce acute centrilobular necrosis.
```
59
describe the pathway of the pupilary light reflex?
Retina > optic N > optic chiasm > optic tract> midbrain> oculmotor nuclear > oculomotor n > ciliary ganglion > pupil
60
Describe the pathway of the menace response?
Lateral geniculate nucleus > occipital cortex > optic radiation > motor cortex >interneuron > facial nucleus > facial n > orbicularis oculi
61
What is the cauda equina?
Sacrococcygeal spinal cord segments, spinal nerve rootlets and roots of the cauda equine, sacral plexus and peripheral nerves to the bladder, rectum, anus, tail and perneum.
Lesions in cauda equine - degrees of hypotonia, hypalgesia and hyporeflexia of the tail, anus and perineal region, degrees of urinary bladder paresis and rectal and anal dilatation.
62
Where is the most common site for type 1 cervical vertebral malformation?
C3-C4 - seen in larger young horses. Developmental orthopaedic disease - vertebral canal stenosis/wedging/angular fixation.
63
What are the clinical signs of equine herpes myeloencephalopathy?
Often acute onset symmetrical ataxia & paresis. signs progress rapidly for about 2 days then stabilise. Pelvic limbs > thoracic limbs. Ataxia & cauda equine syndrome present. CSF often xanthochromic. It causes inflammation > vasculitis of arterioles in brain and spinal cord > multifocal haemorrhagic myeloencephalopathy.
64
What is the diagnostic test for EPM?
Serum immoblot test for antibodies, CSF immunoblot test for antibodies.
65
What is the Treatment for EPM?
Sulfonamides & pyrimethamine
66
How is west nile virus diagnosed?
Serum IgM antibody capture ELISA or PRNT (neutralizing IgG antibody) or immunohistochemistry on post mortem.
67
What may a foals CSF look like in septicaemia/meningitis?
Cloudy, with low glucose.
68
What is hypoxic/ischaemic encephalopathy? (neonatal maladjustment syndrome)
Seen more commonly in TB foals, after rapid parturition, but usually have a normal birth and signs delayed for a few hours to 2 dys, then start making noises such as barking, or dummy foals. must attend to passive transfer and nursing care.
69
What does fusarium sp mycotoxicosis cause in horses?
Acute forebrain necrosis.
Usually in mouldy feed.
Grave outlook.
70
What is polyneuritis equi?
Chronic granulomatous inflammation of the extradural nerve roots of many peripheral nerves. PNE can present first with cranial nerve signs. disease is progressive and early euthanasia should be considered. (sacral trauma far more likely),
71
What are the signs of west nile virus?
Most profound in non-vaccinated horses and include fever, anorexia, depression, somnolence (sleeping
sickness) to hyperesthesia, proprioceptive deficits, recumbency and cerebral/cranial nerve signs (head
pressing, propulsive walking, circling, head tilt).
Diagnosis:
• Clinical signs
• Abnormal CSF findings (elevated CSF protein and cell count)
• Definitive diagnosis based on serology or necropsy evaluation
Treatment:
• Primarily supportive and includes anti-inflammatory medications and fluid therapy
72
what are the clinical signs of wobblers?
Typically associated with symmetric ataxia, paresis, and spasticity
• Usually worse in the hindlimbs than the forelimbs
• Wide-base stance may be observed at rest along with proprioceptive deficits
• Stumbling, toe dragging and circumduction of the hindlimbs may also be observed
• Usually affects young horses (
73
How is EPM treated?
1. Trimethoprim-sulfonamide & pyrimethamine: causes blockade of folate
metabolism in protozoa
2. Ponazuril (Marquis®): anti-protozoal drug believed to target protozoal organelle
(plastid)
3. Nitazoxinade (Navigator®): thought to inhibit electron transfer reactions
essential for energy metabolism
74
What is the normal result of the oral glucose absorption test?
1g/kg glucose in a 20% solution. the normal result is doubling or >85% of glucose in 2-3 hours then return to 4-6 hours. LEss than 15% absorption is strongly suggestive of severe SI pathology.
75
What tests can be used to measure insulin sensitivity and glycaemic status?
Fasting glucose and insulin - Increased levels of insulin provide evidence of insulin resistance, while increased glucose levels in a non stressed individual suggest severe insulin resistance/type 2 DM.
Oral glucose tolerance test. - blood insulin and glucose levels tested prior to administration and after administration of glucose 1g/kg. dDelay to return to normal (longer than 6 hours) suggestive of relative insulin resistance.
Combined intravenous glucose and insulin tolerance test - currently recommended as the most suitable dynamic test in clinical practice.
76
What is the normal amount a horse should drink?
50ml/kg / day - Polydipsia is >100ml/kg day = 50L for 500kg. Polyuria >50ml/kg/day = 25 L for 500kg.
77
What is the normal specific gravity in a horse?
1.020 - 1.050
Isosthenuric 1.008-1.014
Hyposthenuric
78
What electrolyte abnormalities would you have in the horse with kidney failure?
Sodium decrease, chloride decrease, calcium increase, phosphate decrease, potassium increase.
79
What is the cause of equine cushing's disease/pituitary pars intermedia dysfunction? (PPID)
It is due to the overproduction of propriomelanocortin (POMC) peptides from pars intermedia. the resultant increase in adrenocorticotropin levels, coupled with the possible potentiating effects of other POMC peptides on ACTH, causes dysregulated cortisol secretion.
80
What are the clinical signs of Equine cushings disease?
Hirsuitism/hair coat changes - increased cortisol may lead to increased androgen production form the adrenal glands.
HYperhidrosis/sweating, Laminitis, lethargy/poor demeanour, fat redistribution, predisposition to infections, muscle wastage, PUPD due to hyperglycaemia (secondary DM), cortisol antagonism of ADH receptors in kidney, decreased ADH secretion via impingement in pars nervosa of pituitary gland.
81
What is the best test for diagnosing equine cushings disease?
Basal ACTH - single resting sample
TRH response test - basal cortisol sample, then inject TRH and cortisol sample 30 mins post injection.
Basal glucose elevated in a single resting fasted sample provides strong supportive evidence.
82
What is pergolide?
ergoline-based dopamine receptor agonist, used to treat equine cushings disease. It controls the output of ACTH.
83
What does pheynoxybenzamine do?
Decreases urethral sphincter tone thus facilitating urination with UMN problems. (a adrenergic blockers)
84
Which drugs are most likely to cause acute renal failure in the horse?
Aminoglycosides, NSAIDs, Polymixin,
| Also - Heavy metals, acorns, Hb, Mb
85
What is idiopathic renal haematuria?
Mostly seen in arabs, sudden onset, blood from one or both ureters. unkown cause.
86
Where does chorioptes equi most commonly affect?
The distal limbs of heavily feathered horses.
87
Why do oxyuris equi cause disease?
Adult worms migrate frmo the small colon/rectum to lay eggs on the perianal skin causing pruritus/tail rubbing.
88
What is onchocercal dermatitis?
Seasonal dermatitis caused by onchocerca cervicalis microfilaria. The parasite is transmitted by culicoides spp and other biting insects. Larvae can be found in capillaries of unaffected horses but clinical cases result from type 1 and 3 hypersensitivity reactions. They cause alopecia and scaling of the head, neck, withers, chest and ventral midline.There is severe focal dermatitis with pruritis and exudation which may develop following the death of microfilaria in the skin after administration of avermectins.
89
What is rain scald?
a common skin infection caused by dermatophilus congolensis, causes exudation, matter hairs and scabs in areas wetted by rain, primarily the back/quarters. Classic paintbrush lesions. Tx with chlorhexidine, clip area, antibiotic ointment.
90
What species cause ringworm in horses?
Trichophyton equinum var equinum. Less commonly trichophyton verrucosum and trichophyton mentagrophytes.
91
What are the six types of sarcoids?
Occult, verrucose, nodular, mixed, fibroblastic, malevolan.
92
What are dentigerous cysts?
Swellings in the temporal region arising frmo tooth germ tissue.
93
What is habronemiasis?
Ulcerating cutaneous granulating nodules or wounds caused by the larvae of habronema muscae, habronema majus and drachia megastoma. The disease has several forms; Opthalmic habronemiasis - presence of yellow granules in conjunctivae and nasolacrimal duct
Cutaneous habronemiasis - larvae penetrate wet areas of the face, granulating wounds and the urethral process.
94
What is mud fever?
Dermatophilus congolensis - causes exudation, scabs and matting of hair of distal limbs. Mixed infections common. tx - chlorhexidine, remove exudate and scabs, fuciderm, flamazine.
95
What is pastern/cannon leucoytoclastic vasculitis?
A skin condition of the unpigmented distal limb. unpigmented skin involvement suggests role of UV light, although this condition is not thought to be a true photosensitisation. clinical signs include erythema, oozing and crusting of the white areas of the distal limbs. Can appear very similar to mud fever. clinical signs are often diagnostic but biopsies reveal leucocytoclastic vasculitis, vessel wall necrosis and thrombosis.
96
What is lymphangitis?
Inflammation of the cutaneous lymphatics usually but not always secondary to a bacterial infection obtained via a small cut/abraision. It affects the hindlimbs more commonly than forelimbs. usually causes marked swelling of the limb, lameness and serum exudation. Treatment is antibiotics based on culture results, NSAIDs/corticosteroids, potassium iodide and diuretics. Ulcerative lymphangitis is commonly associated with corynebacterium paratuberculosis, stpahylococcal spp and streptococcal spp infections.
97
What are the most common isolates from an endometrial swab in a mare?
```
Beta haemolytic streptococci
E coli
Other enterobacter
Pseudomonas aurginosa
Klebsiella pneumonia
```
98
What can be diagnosed on endometrial biopsy of a mare?
Endometritis
Periglandular fibrosis
Cystic glandular distension
99
What is the best current test for granulosa cell tumours?
anti mullerian hormone
100
What is endometrosis?
Non inflammatory chronic pathology of the endometrium, incidence increases with age, commonly associated with entometritis as reduces resistance to infection, diagnosed on endometrial biopsy, decreases ability to conceive and carry a foal to term.
101
What is contagious equine metritis?
Caused by taylorella equigenitalis, a gram negative microaerophilic coccobacillus, venereal transmission and contaminated equipment and handling, organism persists in clitoral sinus of carrier mares. There is a profuse watery mucopurulent non clumping discharge from uterus, severe endometritis, necrosis and shedding of epithelial lining of uterus. stallions are inapparent carriers.
102
How may the onset of normal cyclicity be hastened ina mare?
Altrenogest (synthetic progesterone) orally daily for 10-15 days
Human Chorionic gonadotrophin IV
Exogenous GnRH - deslorelin implant or twice daily injections of buserelin.
103
How long does oestrus/dioestrus last in the mare?
Interovulatory interval of 18-24 days
Oestrus lasts 3-8 days, dioestrus 14-18 days.
PGF2a is released by the endometrium at about day 15 if no embryo is detected.
104
When does a cL respond to Prostaglandin F2?
Must be between 5- 14 days to respond.
105
How can cryptorchidism be confirmed?
if 3yo do oestrone sulphate assay.
106
What size should the follicle be in a mare before AI?
40-45mm before ovulation. Remain round until approx 24 hours prior to ovulation then flatten and point.
107
What will be seen on examination of the mares reproductive tract during pregnancy at which days?
```
day 11 - 1cm vesicle
day 15 - 1.5 cm vesicle
day 17 - implantation
day 21 - embryo appears ventrally
day 24- heartbeat seen
day 35 - ecg produced
day 60-70 - sexing possible
```
108
What is the leading cause of abortion in mares in the UK?
Equine herpes virus 1 (equine viral rhinopneumonitis), virus transmitted via respiratory tract. repeated exposure leaves horses immune to respiratory disease but susceptible to reinfection causing abortion. usual abortion occurs 1-4 months after infection. fresh foetuses expelled often within placental membranes. ly occurs between 5 months of gestation and term.
109
What is equine viral arteritis?
Causes severe illness in the dam which may be followed by abortion 7-10 days later. typically presents with fever, lethargy, depression, cojunctivitis, urticarial rashes, oedema. infection is via the respiratory or veneral route. 30% of infected stallions continue to shed virus after reslution of clinical signs. Mares do not become carriers but 90% of mares become infected after breeding with a shedder stallion.
110
How does abortion with fungal agents appear?
Foetus is usually small and emaciated. Near term premature foals with mycoticp placentitis have a good chance of surviving. Grossly the appaerance of placenta and foetus are similar to bacterial causes of abortion. aspergillus most common.
111
How should a retained placenta in a mare be treated?
Treat if retained more than 3 hours. Use oxytocin every 15 minutes. Repeat as necessary. If retention is prolonged >8hrs beware of sequelae: laminitis/endometritis. use more aggressive therapy e.g anti inflammatories, broad spectrum antibiotics, exercise. The allantochorionic space may be infused with 10-12 litres dilute povidone iodine or saline, which stimulates uterine contractions.
112
Which type of horses are prone to exertional rhabdomyolysis?
Young TB fillies
113
What is spasm of the facial muscles characteristic of ?
tetanus. Third eyelid flickering on menace response common with tetanus.
114
What enzymes will be elevated after acute sporadic rhabdomyolysis?
Creatine kinase, aspartate aminotransferase and lactate dehydrogenase (LDH). Ck is the most specific for skeletal muscle damage. CK rises first and disappears first, followed by LDH then AST. CK peaks at 2-12 hours after onset and may reach 100,00 or more. LDH peaks at 15 hours. AST peaks at 24hrs.
115
When is the menace reflex present in a foal?
absent until 2 weeks old. PLR usually slow at birth.
116
If you hear a pansystolic IV/VI murmur at the left heart base in a foal what does this mean?
Common up to 7 days due to PDA not being closed yet.
117
How can FPT be diagnosed? What is normal level of IgG?
Single radial immunodiffusion kits - most accurate, highly specific but time consuming and expensive.
CITE test - accurate and suitable for field use. Normal IgG at 24 h is >8g/l. FPT is partial at 4-8g/l and complete at
118
How can FPT be treated?
24h - Intestinal absorption of IgG ceased so give 1-2L equine plasma IV. first litre over 60 mins and slower subseuqently.
119
What is neonatal isoerythrolysis?
An immune mediated haemolytic anaemia - destruction of foals RBCS by colostral antibodies which are directed against foals RBC membrane alloantigens. Most commonly problem occurs when foal inherits Aa or Qa alloantigens from Aa or Qa +ve stallion and RBCs of mare are negative for these antigens, during birth of this foal, foetal blood often leaks into matenral circulation and mare makes anti Aa or Qa antibodies. As antibodies peak at 9 days after foaling they are not transferred in colostrum at first pregnancy thus do not get NI in first partum mares.
120
What findings will be present in a septic foal?
WBC may be normal, increased or decreased depending on stage of infection. Presence of band and toxic neutrophils is suggestive of sepsis. septic foals are often thrombocytopenic. fibrinogen increased after 24-48hrs. IgG may be low. Hypoglycaemia, low PaO2 and metabolic acidosis.
121
What is the most common cause of foal diarrhoea?
Rotavirus.
| Profuse watery, non foetid diarrhoea, depression. Diagnosed using ELISA or latex agglutination.
122
How do foals become infected with strongyloides westeri?
Mares milk is major source to foal - egg output 2-3 weeks after parturition. Probably doesn't cause diarrhoea but may contribute to dysfunction in conjunction with other pathogens.
123
What is tyzzers disease?
Infectious necrotic hepatitis cause by clostridium piliformis. Affects foals 1-6 weeks old, sudden death or acute abdominal pain and depression. most foals die.
124
How is uroperitoneum confirmed?
by demonstrating ratio of creatinine in peritoneal fluid:serum > 2:1.
Most foals develop azotaemia, hyperkalaemia, hyponatraemia, hypchloraemia and metabolic acidosis.
125
What is perinatal asphyxia syndrome ? (also termed neonatal maladjusment, hypoxaemic ischaemic encephalomyelpathy)
Likely involves peripartum cerebral hypoxia/ischaemia. most foals appear normal for several hours to 1 day, before developing signs of cerebral dysfunction - localised seizures, disorientation, ataxia, loss of affinity for dam, loss of righting and suck reflexes, barking vocalisation, secondary FPT, hypoglycaemia, recumbency.
No specific treatment. steroids often administered, diazepam, nursing, IgG, oxygen. Poor prognosis if not improving within 48 hours.
126
What is the urachus?
connects foetal bladder to allantoic cavity.
127
What is the anion gap? Why may this be altered?
Na+K - Cl+Hco3
Decreased - hypoproteinaemia, hyperchloraemic metabolic acidosis
Increased AG - lactic acidosis (anaerobic exercise, grain overload, hypovolaemia)
128
What is GLDH?
A hepatocellular - derived enzyme, liver specific indicative of hepatocellular damage.
129
what is GGT?
A marker of hepatobiliary disorders and cholestasis, it has the highest activity in perioportal region of the liver, pancreas.
130
Why may hypoalbuminaemia occur in horses?
Rare in equine liver disease cf small animals - has a long half life. Increased breakdown - due to increased metabolic demands or chronic antigenic stimulation (causes increase in globulins and reduction in albumin)
If panhypoproteinaemia - acute protein losing colitis, acute blood loss.
131
Why may hyper and hypo fibrinogenaemia occur?
Hyper - inflammation (acute phase protein(
| Hypo - liver failure
132
Why may neutropaenia occur in the horse?
Increased margination eg endotoxaemia
| Increased consumption e.g large surface area inflammation.
133
What does the british horseracing authority allow for equine influenza vaccination?
1st - 4-6 months of age
2nd - 21-92 days later
3rd - 150-215 days later
Booster
134
When should horses be vaccinated for equine herpesvirus
Initial course 4 weeks apart, boosters every 6 months, pregnant mares vaccinate 3,5,7&9 months pregnancy.
135
When should horses be vaccinated for tetanus?
All horses hsould be vaccinated for tetanus. owners often think that it is not required as pony doesn't go anywhere. Tetanus toxoid - 2 vaccines 1 montha part, then boosters every 2-3 years depending on manufacturer.
136
What is the vaccination protocol for strangles?
2 vaccines 4 weeks apart. booster every 3-6 months. Live modified strain of S equi, submucosal. Reduces clinical signs only. Are serological ElISA test positive after vaccine.
137
What is fenbendazole used to treat in horses?
a 5 day course can be used to treat encysted redworm.
138
What is pyrantel used to treat in horses?
double dose for tapeworm.
139
What is ivermectin used to treat in horses?
bots and lungworm
140
What is the most likely form of african horse sickness to occur in the UK?
Pulmonary form - pyrexia, acute severe dyspnoea, death within a few hours of onset of clinical signs
Other forms include - cardiac (subcut oedema, death within 4-8 days), horse sickness fever which is often subclinical, or mixed form.
141
How is african horse sickness transmitted?
by culicoides sp, mainly imicola in africa.
142
How is West nile virus transmitted?
Primary transmission cycle between wild birds and culex spp mosquitoes. Horses and humans are dead end hosts. clinical signs include behavioural changes, cranial nerve deficits, ataxia, muscle fasciculations, can progress to complete paralysis of one or more limbs. diagnosis by serology e.g IgM ELISA, PCR, or immunohistochemistry.
143
What is equine infectious anaemia? how is it transmitted and what are the clinical signs?
A lentivirus. Mechanical transmission between horses by transfer of infected blood or blood products. Insect vectors e.g biting flies and very rarely mosquitoes., also vertical transmission.
Signs: recurrent pyrexia, inappetance, signs of depression, weight loss, ventral oedema, anaemia, thrombocytopenia, can be fatal. Diagnosis is by coggins test or ELISA.\
Notifiable - no cure, no vaccination.
144
How does yew cause toxicity in horses?
Contains alkaloids called taxines which block Na movement and depress myocardium. Causes collapse and sudden death occasionally preceded by tremors and weakness.
145
What are the clinical signs of acorn poisoning?
Colic, rectal tenesmus, haemorrhagic diarrhoea, tachycardia, tachypnoea and acorns infaeces. may cause sudden daet.
146
What is blister beetle toxicosis?
Cantharidin intoxication from ingestion of dead beetles entrapped in hay at harvesting, ingested cantharidin causes inflammation and necrosis of the GI tract, primarily causes severe colic in horses. hypocalcaemia as well. can be fatal.
147
How is monensin toxic to horses?
Horses are extremely sensitive - it interferes with the transport of Na and K between the intracellular and extracellular spaces, heart is the primary target/
148
What are the 'stars of winslow' in the equine eye?
Numerous fine dark spots seen in the tapetal fundus representing an end on view of the choroidal arterioles which cross the tapetum to link with the choriocapillaris.
149
What electrolyte concentrations can be used to assess foetal maturity in the mare?
Ca2+ concentrations >40mg/dl, Na concentrations > 30meq/l and K concentrations of >35meg/l, indicate foal readiness for birth.
150
What is equine viral arteritis? what are the clinical signs? how is it spread?
A togavirus - signs include fever, depression, filling of lower limbs, conjunctivitis with periorbital oedema, nasal discharge, urticarial rashes and edematous plaques and ventral oedema. infected mares may abort 7-10 days later. infection is via the respiratory or venereal route. virus localises in accessory sex glands of stallion sand 30% of infected stallions continue to shed the virus indefinitely. shedder stallions are always seropositive but not all seropositive stallions are shedders. mares do not become carriers.
151
Where do overgrowths consequently occur when a horse is overjet/overbite?
Rostral aspect of 106& 206 and caudal aspects of 311&411.
152
What is the dental formula of a horse?
3-1-(3-4)-3
153
List the times in which a horses teeth erupt?
6days - incisor 1 (deciduous)
6 weeks - Incisor 2 (deciduous)
6 Months - incisor 3 - (deciduous)
2 1/2 - I1
3 1/2 - I2
4 1/2 - I3
Galvaynes groove - appears around 8/9/10yo, stars appear.
2 - PM1
3- PM2
41/2 -PM3
1 - M1
2- M2
3 1/2- M3
154
If a horse presents aged 2-5 with quidding/playning with the bit, what should you examine them for?
Retention of the remnants of the deciduous cheek teeth. 'loose caps'.
Prolonged retention of caps has been alleged to cause delayed eruption and development of eruption cysts under the apices of the permanent CT.
155
Why is the horse predisposed to developing overgrowths of the cheek teeth?
Eating too much concentrate - more vertical than lateral mandibular action
Equine maxillary CT rows - further apart than mandible
Absence of complete occlusal contact.
156
What is the curve of spee?
The marked dorsal curvature of the caudal maxillary occlusal surface.
157
What cranial nerve innervates the tongue?
12th - hypoglossal
158
What nerves if damaged would lead to pharyngeal paralysis?
10th and 11th
| 10th - laryngeal
159
What metabolic changes may occur with uncorrected choke?
Dehydration and hypochloraemia.
160
What is the treatment of choke?
Most cases will get better spontaneously or respond to medical treatment with spasmolytics and sedatives and busopan. Convervative treatment for up to 24 hours is safe. if not - gentle lavage of oesphagus. Antibiotics incase of aspiration pneumonia. if all else fails - clearance by lavage under GA.
161
What is anterior enteritis?
Colic of unknown aetiology - marked distension of proximal SI and stomach, may resemble a surgical colic. Treatment is medical by repeated nasogastric intubation or surgical manual decompression of the SI.
162
What are the different gradings of rectal tears?
1 - mucosa only
2 - muscularis only
3 - mucosa and muscularis
4 - all layers
163
What is champignon?
Development of granulation tissue protruding frmo the wound. Such cases should have the scrotal wound opened and evacuated by curretage. + antibiotics.
164
What is infection of the spermatic cord termed? what is it usually infected with?
Funiculitis - strep zoo epidemicus.
165
What is schirrhous cord?
Staphylococcus infection long term., will present many months or years following castration as a very firm scrotal swelling with purulent draining tracts, can temporarily appear and disappear. These need a GA and dissection of the entire fibrous mass.
166
how can cryptorchidism be diagnosed in horses?
if >3yo then resting plasma oestrone sulphate assay. If
167
Passing a NG tube into which meatus will cause epistaxis?
middle meatus. Epistaxis may also occur form the ventral meatus if an excessively wide tube is used, inadequate lubrication or with excessive horse movement.
168
What does epistaxis due to a heavy fall usually mean?
Tear of rectus capitis muscle in guttoral pouches.
169
What is the biological behaviour of equine nasal tumours?
They are usually very malignant e.g adenocarcinomas or osteogenic sarcomas. And usually affect older animals. the clinical signs initially reflect local inflammation and scondary infectin on and around the tumour and may include a purulent nasal discharge, secondary sinus empyema, malodours breath.
170
What is the usual cause of mycotic rhinitis in the UK?
Aspergillus fumigatus or pseudalleschieria boydii
171
What is the treatment for progressive ethmoid haematomas?
Intralesional formalin injections appear to offer the best treatment.
172
List the most common causes of sinusitis in order
```
Primary infective sinusitis
Dental apical infection or oro sinus fistula
Maxillary sinus cysts
Sinus neoplasia
Mycotic sinusitis
Sinus trauma
Intra sinus PEH lesion
```
173
What teeth cause dental related sinusitis?
Infection of the apices of the upper 08s-11s that lie within them maxillary sinuses.
174
what is pharyngeal lymphoid hyperplasia?
Multiple large lymphoid follicles in the nasopharynx are very common in young horses. follicle size regresses with maturity. Normal adult horses usually have small follicles. Pharyngeal lymphoid hyperplasia once believed to cause poor performance - has been definitively disproven.
175
What sort of respiratory noises are heard with intermittent dorsal displacement of the soft palate?
If the soft palate displaces dorsally to the epiglottis, this will cause airflow obstruction with the production of loud abnormal gurgling expiratory and inspiratory noises.
Diagnose by dynamic overground treadmill.
176
What respiratory noise is made with epiglottic entrapment?
Airflow obstruction and abnormal expiratory noises occur as air fills the pouch during expiration. An entrapped epiglottis loses normal flat serrated appearance and becomes rounded, thickened, reddened or ulcerated.
The rostral free aspect of the epiglottis becomes trapped in a pouch of mucosa that develops from the mobile sub epiglottic mucosa.
177
What type of respiratory noise does RLN cause?
Affected horses make an abnormal INSPIRATORY noise at exercise.
178
What is a tie back?
A prosthesis mimics the action of the CAD muscle to permanently abduct the left arytenoid - tie to the muscular process of the arytenoid. complications include loss of surgical abduction, coughing due to aspiration tracheitis, postoperative wound infections.
179
What is arytenoid chronditis?
A condition where the arytenoids are swollen and reddened unilaterally or bilaterally, with possible mucosal ulceration, grnaulomas or draining sinus tracts and reduced motility.
180
What type of respiratory noise does tracheal collapse cause?
If in the cervical trachea this causes an inspiratory obstruction whilst intra thoracic obstructions cause end expiratory obstruction. The tracheal collapse can be diagnosed endoscopically or radiographically.
181
How much sodium bicarbonate must be given to a 470kg horse that has a base deficit of 13 to completely correct this deficit?
The best answer is 2400 mEq. The formula you need to know to calculate how much sodium bicarbonate you need (depending on your reference source) is 0.3 to 0.4 x BW x Base Deficit. Plug and chug (using 0.4) and you get 2444, which is the closest answer.
In practice, you may choose to fix only part (often half) of the total calculated bicarbonate and reassess, but this question asks how much is needed to completely correct the deficit.
If you need a reminder, the base deficit is the amount of base that you would need to add to a solution (i.e. plasma) to achieve a pH of 7.4. In general, the normal HCO3 concentration in blood is around 22-24 mEq/L. The base deficit is simply calculated by subtracting the patient's HCO3 concentration (i.e. 10 from the normal concentration [23]). In the formula, the 0.3 factor that is used to multiply represents the extracellular fluid compartment.
182
A one-month old foal develops fever, icterus, and diarrhea acutely. Bloodwork shows hyperfibrinogenemia, hypoglycemia, and elevated liver enzymes. Which of these conditions is most likely?
The correct answer is Tyzzer's disease. This is the most likely cause because of the age of the foal and the acute nature of the disease. Tyzzer's disease is caused by Clostridium piliformis, which causes an acute necrotizing hepatitis. It affects only foals from about 1-6 weeks of age. Theiler's disease is a condition of adult horses. Clostridium novyi is rare in horses and seen much more in sheep and cattle. Herpesvirus can cause hepatitis but is usually seen at or very soon after birth.
183
What virus is suspected to have some relation to sarcoids?
bovine papilloma virus
184
Which type of sarcoid is BCG injection most successful for?
Periocular
185
What is the duration of action of mepivicaine?
5-10 mins onset, duration 2-3 hours
186
What is the duration of action of bupivicaine?
Onset upto 30 mins, duration 4-6 hours
187
What is the duration of action of lignocaine?
onset 5-10 mins, duration 1-2 hours.
188
what does the palmar digital NB block?
It was traditionally thought to be specific for the palmar 1/3 of the sole and navicular region. But can alleviate pain from most of the sole. Usually do not lose dorsal coronary band sensation.
189
What does the abaxial sesamoid block?
All of the hoof capsule, proximal interphalangeal joint, palmar pastern region including sesamoidean ligaments, DDFt, SDFT, distal part of tendon sheath.
190
What is the location of the low 4 point block?
Block Location: To block the palmar nerves, a small amount of anesthetic is placed dorsolateral
and dorsomedial to the digital flexor tendon (between the suspensory ligament and deep digital
flexor tendon) at the level of the distal metacarpal bone (orange arrows), proximal to the fetlock
joint. The medial and lateral palmar metacarpal nerves course parallel to the 2nd and 4th metacarpal
(splint) bones and can be anesthetized as they emerge distal to the end of the splint bones. The site
of injection for the metacarpal nerves is just distal to the end of the splint bones on each
(medial/lateral) side (purple arrows).
191
What does the low 4 point block?
Entire metacarpophalangeal (fetlock) joint and structures distal to this joint.
192
What is the location of the high 4 point block?
anesthesia of the medial and lateral palmar nerves and the medial and lateral palmar metacarpal
nerves just distal to the carpus.
• Block Location: To block the medial and lateral palmar nerves, anesthetic is placed between the
suspensory ligament and the deep digital flexor at a level just distal to the carpus (blue arrows).
Subsequently, to block the medial and lateral palmar metacarpal nerves, anesthetic is placed axial
to the splint bones and abaxial to the suspensory ligament and then guided to the palmar cortex of
the cannon (third metacarpal) bone.
193
What does a high 4 point block?
: Metacarpal region along with the entire metacarpophalangeal (fetlock) joint
and structures of the digit
194
What is a six point block?
blocks lateral and medial plantar nerves and lateral and medial plantar metatarsal nerves, in the hindlimb, the dorsal metatarsal nerves innervate the dorsal surface, therefore an additional subcutaneous ring block is directed dorsally.
195
How fast does the hoof grow?
7-10mm/month
196
What is the current theory for how navicular disease occurs?
Increased pressure between the DDFT and NB, flat foot with a long toe/low heal leads to remodelling of the NB. There is sclerosis, marginal osteophytes, thickening of sc bone and inflammation of the NB >surface defects.
197
What are the clinical signs of Navicular syndrome?
Insidious onset, frequent stumbles, reluctant to work on circle, may point one foot, short strided at the trot, often bilateral lameness which is accentuated on the hard circle. Wil improve to PDNB, DIP and NB.
198
What does tiludronate do?
Redices osteoclast activity
199
What is the surgical options for treatment of navicular disease?
Desmotomy of the suspensory ligaments.
200
A 9-month old foal presents with difficulty walking. You immediately note that the foal appears to have a flexural deformity of the right forelimb consisting of an increased dorsal hoof wall angle of 80 degrees such that the heel does not contact the ground. The coronary band is prominent. You take radiographs which confirm a broken forward hoof-pastern angle. What is the most appropriate treatment for this type of flexural limb deformity?
This case describes a severe flexural deformity of the distal interphalangeal joint, also known as "clubfoot". This is typically a congenital condition in young horses although it can be acquired. A genetic component is suspected. Mild cases can sometimes be managed conservatively with NSAIDs, farriery, exercise and nutritional changes. Severe cases often require surgery; the surgical procedure of choice is desmotomy of the accessory ligament of the deep digital flexor tendon (also known as inferior check ligament desmotomy). The accessory ligament of the deep digital flexor tendon (inferior check ligament) runs from the palmar surface of the proximal metacarpus to the deep flexor tendon in the mid-metacarpal region.
The superior check ligament originates above the knee and attaches to the superficial flexor tendon, and its primary purpose is to support the tendon. Superior check ligament surgery is used to treat a bowed tendon.
Lateral digital extensor tenectomy is a procedure used to treat stringhalt. Transection of the insertion of the semitendinosus is used to treat fibrotic myopathy.
201
What is seedy toe?
Seedy toe is a separation of the horse’s hoof wall from the underlying sensitive laminae at the white line. This results in a cavity which fills with crumbling dirt, horn and debris and is prone to infection. Produces characteristic hollow sound when percussed.
202
What is thrush?
An infection of the frog caused by wet environment, similar to ovine foot rot - fusobacterium necrophorum. There is a black sticky discharge, terrible smell. Treatment is to trim affected parts of the frog, move to a dry environment, give antiseptic footbaths. contracted heels may predispose to getting thrush.
203
What is canker?
A chronic pododermatitis of the germinal layers - it is a gram negative bacterial infection of the stratum germinatum of the frogs epidermis, which causes hypertrophic dermatitis of the frog and the bulbs of the heels. It mainly affects draft horses. The horns of the heels, bars and frog degenerates into strands of soft tissue with cheesy white discharge. they are lame and frequently stamp.
204
What is quittor?
A result of a hoof wall crack, puncture wound, heel laceration > severe degree of lameness untill adequate drainage is established, difficult to treat due to avascular nature of cartilage, there is chronic sepsis with intermittent purulent discharge above the coronary band.
205
What are sheared heels?
Disparity between the medial and lateral heel lengths of 0.5cm or more.
206
What structures could be involved with a solar penetration?
NB, DIPJ, DFTs, DDFT, Digital cushion
207
With what pressure should you lavage a wound?
30ml syringe 19G needle (10-15PSI)
208
Where are the most common places that horses develop skin rubs?
Accessory carpal bone, medial malleolus, flexor tendons, gastrocnemius tendon
209
What are the most common Isolates from Synovial sepsis in horses?
in adults;
Staphylococcus aurues - highest incidence
Non haemolytic staphlococcus
B haemolytic and non b haemolytic streptococci
Rhodococcus equi
Corynebacterium.
Multiple and gram negative are more frequent in foals, including E coli, pseudomonas, enterobacter, actinobacillus, proteus, klebsiella, salmonella.
210
What are the best indicators of synovial infection in adults?
Heat, swelling and lameness
Severe lameness, usually a wound nearby and joint effusion.
Pyrexia is often absent and is a poor indicator of synovial infection in adults.
211
What fluid tube should you collect synovial fluid in?
EDTA for cytology and a separate smaple collected for aerobic and anaerobic culture.
212
What synovial fluid results are indicative of sepsis?
Total protein values >35g/l, leukocyte counts >30x10^9 >80% neutrophilia. Usually appears serosanguinous/xanthrohromic if chronic.
213
What is the gold standard treatment for septic joints?
Arhtroscopic lavage and debridement followed by closed suction drainage.
214
What are subchondral bone cysts?
Radiolucent areas of bone often accompanied by a thin well demarcated rim of sclerotic bone. usually occur in the subchondral bone underlying a weight bearing surface of the articular cartilage, e.g medial femoral condyle, phalanges. Clinical signs include lameness & joint effusion. lameness in young horses usually occurs at onset of training. Treatment involves arthroscopically guided disruption of cyst lining and injection with corticosteroids.
215
What treatments are available for angular limb deformities?
Periosteal transection and elevation - performed on the short side of the bone.
Transphyseal briding - can be placed across the physis on the side that is growing too rapidly. Take implants out before limb is totally straight as is possible to over correct.
216
What are the possible treatment options for flexor deformity of the DIJ (club foot)
1 - demotomy of the accessory ligament of the deep digital flexor tendon
2 - deep digital flexor tenotomy - salvage.
Conservative management with dietary restriction, NSAIDs, controlled exercise, rasp down heels and place toe extension.
217
What is physitis?
Inflammation and disruption of growth in thephyseal regions. Causes include: overload, over exercise, rapid growth, firm often painful swelling of the physeal areas.
218
What joints and WHERE in the joint is Osteochondrosis seen most commonly?
Tarsus- Cranial end of the distal intermediate ridge of the tibia (DIRT). Distal end of the lateral trochlear ridge of the talus, medial malleolus of the tibia, medial trochlear ridge of the talus.
Stifle - Lateral trochlear ridge of femur, medial trochlear ridge of femur, trochlear groove, distal end of the patella. Subchondral bone cysts of the medial femoral condyle are also a manifestation of OC.
Metacarpophalangeal - dorsal edge of the sagittal ridge of the metacarpus.
219
Which pouch do you enter the tarsocrural joint into when performing arthroscopy?
Into the dorsomedial pouch of the tarsocrural joint and an instrument is placed in the dorsolateral pouch of the joint.
220
Which of these test results would be most consistent with EPI (exocrine pancreatic insufficiency) in a German Shepherd?
The correct answer is low TLI. TLI is a pancreas specific marker of trypsinogen. Because acinar cells are lost in EPI, levels decrease. Protein levels and cholesterol are usually unchanged in animals with EPI.
221
Which of these inhalant anesthetics is the most potent in the dog?
Anesthetic potency is described by the MAC (minimal alveolar concentration) of each drug. In the dog, the MAC of these agents are methoxyflurane-0.29, halothane-0.87, Isoflurane-1.30, sevoflurane-2.36, desflurane-7.2
222
Describe the pathogenesis of Intestinal acidosis causing laminitis?
Excess carbohydrate in caecum > increase in lactic acid producing bacteria > drop in caecal pH damages the gram negative bacteria > endotoxin release into circulation >peripheral vasoconstriction and activation of A-v shunts, decreases laminar perfusion, exacerbated by microthrombi. The dorsal laminae are vascularised last within the foot, so they are most affected, once the laminae are damaged the pull of the DDFT is no longer resisted and the bone rotates. If all laminae are affected at the same time, then complete laminar separation may result and the pedal bone will sink ventrally without rotation.
223
Describe the classification fractures of the pedal bone?
Type I - non articular palmar/planter process
II - complete articular parasagittal
III - complete articular saggital
Type IV - extensor process
Type V - comminuted
Type VI- non articular solar margin
type VII - non articular of palmar/plantar eminences
224
How do ulnar olecranon fractures appear?
Affected animals have characteristic dropped elbow stance due to disruption of stay apparatus.
Usually the result of a kick injury. Can be treated conservatively, but surgical treatment improves prognosis.
225
Which steroids can be used for injection into the joint?
Triamcinolone
| Methyl prednisolone acetate
226
What is hyaluronan?
HA is a large nonsulphated glycosaminoglycan component of synovial fluid responsible for viscoelasticity, boundary lubrication and steric hinderance, it is also an important component of proteoglycan in the cartilage matrix providing compressive stiffness.
227
How does tiludronate work?
It is a bisphosphonate that regulates bone remodelling through inhibition of bone resorption (specifically osteoclastic resorption) and it is therefore postulated that it should ameliorate the remodelling process active in OA.
228
what is IRAP?
Autologous conditioned serum - generated from 50ml of the horses blood that is incubated overnight with chromium coated glass spheres. the spheres stimulate WBC to produce anti inflammatory cytokines. Then injected into joints.
229
Which joints are amenable to surgical arthrodesis in the horse?
Proximal interphalangeal joint and tarsometatarsal joint - low motion.
230
What is the treatment for kissing spines in horses?
Rest, local injections of steroid, surgical removal of impinging processes. A novel new treatment - is ctting of the interspinous ligament through small incisions.
231
What is elastography?
Analysis of tissue motino after application of gradual manual tissue compression using the ultrasound transducer. Quantitative imaging of tissue strain.
232
What is platelet rich plasma?
Component of whole blood that contains concentrated amounts of platelets. Platelets release growth factors and other cytokines that interact with the local cells and send signals that initiate a variety of important events such as cell division and migration. the purpose of PRP treatments is to enhance the bodies own response in messenger substances which in turn exert an effect on the local and distant cell population.
233
What size should the scrotal circumference of a bull be?
15 months >31cm
| Over 2yo >34cm
234
What is the minimum progressive mortility and normal sperm morphology for bull semen?
60% progressive motility and minimum 70% normal morphology.
235
What is the minimum bull/cow ratio?
young bull 20-30 cows
| Mature bull 40-50 cows
236
Describe 2 oestrus synchronisation methods for fixed time AI in beef herds?
Double prostaglandin injections - cow/heifer injected twice with PG, 11 days apart and fixed time AI 72 and 96 hours following second injection. Best restricted to maiden heifers as results may be poor in cows due to anoestrus.
Progesterone releasing devices - inserted for 8-10 days with Prostaglandin injection given 1-2 days before device removed. Ai at 48 and 72 hours after device removed.
237
If a medicine prescribed does not state a withdrawal period for the species then which withdrawal period should be used?
Not less than 7 days for milk and eggs, 28 days for meat and 500 degree days for meat from fish.
238
Describe the 'cascade' for food producing species
If there is a licensed product for that particular condition and species then this should be used > if it does not exist then a product for use in that species for a different condition or a product licensed for that condition in another food producing species may be used > then if no product exists then a product available in another member state may be imported provided that it is licensed for use in a food producing species in that state.
239
which antibiotics are not permitted in food produicng animals?
Metronidazole and chloramphenicol.
240
What values does the ADI assume for average daily intake?
500g meat, 1.5 L milk, 2 eggs and 20g of honey
241
What is the adequate colostrum intake for a calf?
10% body weight by 6 hours old and 3.5% by 12 hours old
242
What is the target for serum total protein with passive transfer for calves?
>5.2g/dl is target
| 5.5 g/dl has been correlated with low levels of disease
243
What does EHV1 infection cause?
Usually leads to abortion in last trimester, occasionally leads to birth of extremely weak foals. Confirmation by PCR or detection of pathognomic histological inclusion bodies in foals liver lung and thymus.Can cause respiratory disease but more commonly abortion and encephalomyelopathy.
244
What does ehv4 cause?
Common respiratory infection. All horses acquire EHV early in life and probably all become asymptomatic carriers of latent virus which may recrudesce following stress. immunity is short lived and horses may be repeatedly infected especially following mixing of horses.
245
What are the clinical signs of equine viral arteritis?
Respiratory disease, severe conjunctivitis, profound depresion, periorbital oedema. Venereal spread.
246
What Electrolyte abnormalities are frequently present in an acute colitis/
Metabolic acidosis, hyponatraemia, hypochloraemia, hypokalaemia. Protein loss in face of dehydration - may have near normal protein conc, elevated PCV due to dehydration, leucopaenia especialy if neutropaenic with a left shift and toxic changes in WBCs.
247
What is the treatment for cyathostomes?
Fenbendazole orally for 5 days followed by ivermectin on day 6 or moxidectin.
