Equine medicine Flashcards

Question

What is recurrent airway osbtruction?

Answer 1

Airway inflammatory response to pro inflammatory agents in inhaled organic dust, originating from poorly conserved hay and straw. Controlled exposure to hay/straw may be done to exacerbate clinical signs and thereby aid diagnosis of mild clinical signs. Risk factors include >5yo, poor stable hygiene, genetic predisposition, respiratory infections and exposure to hay /straw early in life. Coughing is most sensitive indicator of equine pulmonary disease and most frequent presenting sign. Clinical signs reflect airway inflammation and obstruction, especially of the bronchioles. coughing is most sensitive indicator of equine pulmonary disease and most frequent presenting sign for RAO. coughing is usually exacerbated by exercise and poor exercise tolerance is common. Bilateral mucopurulent nasal discharge is present in 55% of cases. the remainder have o nasal discharge because they swallow the increased volumes of mucopus. Overt expiratory dyspnoea leads to tachypnoea, expiratory heaving and development of heave lie. Severely affected horses have audible wheezes or crackles.

Answer 2

This is essential and highly effective. All sources of airborne organic dust may be eliminated, ideally by keeping horses permanetly at pasture. when this is not possible, shavings or paper bedding must be used and all wet bedding removed daily. do not use deep litter shavigs or paper as they rapidly develop mould and bacterial cotamination. haylage, chopped dried alfalfa, silage or complete cubed diets are suitable low dust feedstuffs. Feeding soaked hay is ineffective as the dust challenge is not fully eliminated and additionally the nutritive content of the hay is reduced. To provide adequate ventilation the top door is kept open permanently and a louvered vent inserted in the back wall of the stable. Affected horses should be housed as far as possible from potential sources of organic dusts, such as stables containing hay and straw, waste bedding and barns. Treatment of acute RAO - tur out or house in dust free evironment, best rescue drug is atropine, but adverse effects preclude its repeated use, follow up with clenbuterol or inhaled sallbutamol, inhaled beclomethasone or oral prednislone. maintain hydration to avoid respiratory secretion becoming tenacious.

Answer 3

Similar clinicopathological features to RAO, but affects pastured horses with no access to hay/straw. clinical disease occurs between spring and autumn, with remission during winter. Some horses have both SPAOPD and RAO. Severe and potentially fatal dyspnoea rather than coughing and nasal discharge is the usual presenting sig. Crackles and whezes commonly detected on auscultation. Diagnosis usualy made on basis of history and clinical findings although marked neutrophilia of tracheal mucus and BALF may be helpful. Aetiology is unknown, but likely represents a pulmonary hypersesitivity to inhaled pollens or outdoor moulds. Intradermal antigen testing with a wide variety of antigens has failed to identify the cause. management is more problematic than for RAO. Some horses may improve when moved to a different environment. If this is not feasible. horses should be housed in a dust free environment as for RAO. Bronchodilators in combination with oral or inhaled glucocorticoids are usually administered as bronchodilators alone commonly give only a partial and temporary improvement.

Answer 4

A syndrome characterised by coughing, exercise intolerance, increased volumes of neutrophiilic mucopus within lower airways and occasionally nasal discharge. Horses are not depressed, sick or pyrexic and do not have the overt airway obstruction that characterises RAO. In contrast to RAO, which invariably affects older horses, all ages of horse may develop IAD. IAD is commonly identified at the start of traiing. Syndrome may self resolve within a couple of weeks or may persist for months ot years with chronic cases being frustrating to manage. Many affected horses have a history consistent with a preceding, acute onset infectious respiratory disease. Aetiology is unclear but appears multifactorial,including bacteria and inhaled dust/edotoxin. Treatment is largely symptomatic, including rest and provision of a dust free environment. While those horses with significant bacterial infections may benefit from antibiosis, antibiotic therapy alone is ineffective in many cases. Antibiotics should ideally be selected based on culture and sensitivity of tracheal aspirates. Oxytetracycline, ceftiofur, cefquinome, enrofloxacine or TMPS are commonly used. Some horses with chronic IAD respond favourably to oral or inhaled glucocorticoids. Oral alpha interferon has been shown to be effective in some studies but is expensive. IAD does not cause overt airway obstruction so bronchodilators probably not indicated.

Answer 5

Normally with dictyocaulus arfieldi - uncommon today because of widespread use of effective athelmintics. Occurs in summer or autumn, in horses pastured with donkeys, which are atural and usually asymptomatic, reservoir hosts. Infectios in horses are usually no patent and consequetly the baermann faecal flotation technique is unreliable for diagosis. Diagnosis confirmed by demonstrating eosiophilia in tracheal mucus or BALf, rarely by endoscopic visualisation of larvae within the trachea or in respiratory secretions or by positive response to anthelminics. Affected horses and in contact horses and donkeys should be given an avermectin or bezimidazole and moved to a clean pasture.

Answer 6

Most eosinophilic lung diseases which affect horses in the UK are unrelated to lungworm. These include eosiophil dominated acute alveolitis, chronic small airway diseases and chronic interstitial diseases. these are of unknown aetiology but often respond favourably to corticosteroids.

Answer 7

Poorly understood and uncommoly recognised. Characterised by acute or chronic inflammatory alveolitis with i njury to type I epithelial cells and endothelial cells. Serum proteins leak into alveoli leadig to pulmonary oedema in acute cases. inflammatory cells infiltrate alveoli and interstitium. If horses survive this early injurious phase inflammatory response resolves or interstitial fibrosis and granuloma develop over a period of weeks to years. Cause is not identified in majority of cases. Interstitial disease reduces lung compliance, causing predominantly inspiratory dyspnoea. Crackles, especially end inspiratory and wheezes are common. Nasal discharge and coughing are uncommon. Radiography reveals interstitial or mixed interstitial /alveolar pattern. Early inflammatory phase must be treated aggressively to prevent development of fibrosis. Putative causal agents should be eliminated. Immunosuppressive dosages of glucocorticoids are usually indicated. Frusemide may reduce pulmonary oedema. Bronchodilators are rarely effective.

Answer 8

Causes include acute URT obstruction, cardiac failure, alveolitis/interstitial lung disease, smoke inhalation, neoplasia, plant and drug toxicity, immune mediated and volume overload. Sings include frothy nasal discharge, increased inspiratory effort and widespread fine crackles on auscultation. Endoscopy - frothy fluid within airways. Radiography - diffuse interstitial or mixed interstitial. Treatment - correct underlying cause where possible eg for URT obstruction insert tracheostomy tube, frusemide, intranasal oxygen, and where appropriate, antibiotics and corticosteroids.

Answer 9

Rare. Most cases have lymphosarcoma or metastatic disease, with primary lung neoplasia being rare. Clinical signs are variable and include weight loss, anorexia, pyrexia, dyspnoea, chronic coughing, pleural effusion, ventral oedema and jugular distension. thoracic radiography, ultrasonography, thoracocentesis, pleuroscopy and cytology of pleural fluid or a tracheobronchial aspirate may aid diagnosis.

Answer 10

Often follows prolonged transport, when pulmonary defences are compromised or as a sequel to aspiration of saliva and food. A wide range of aerobic and anaerobic bacteria may be involved, commonly mixed infections. Initially bacteria colonise lung causing localised pneumonia. Extension of inflammatory response to adjacet pleura causes sterile inflammatory effusion termed a parapeumonic pleural effusion. systemic antibiosis alone may be effective at this stage. Extension of bacterial infection into pleura induces production of larve volumes of infected purulent effusion which requires drainage. Large amounts of fibrin are formed lining the pleural surfaces and resulting in locule formation. The organisation phase is characterised by significant fibrin deposition resulting in a thick pleural peel which limits thoracic expansion. Affected horses are sick with lethargy, anorexia, pyrexia, ventral oedema and varying degrees of respiratory distress. Pleural pain causes reluctance to move, base narrow stance, elbow abduction, soft muffled coughing and fast shallow ventilation. These signs may be misinterpreted as signs of colic, laminitis or hypocalcaemia. Malodorous breath suggests anaerobic infection or lung necrosis and is a poor prognostic sig.

Answer 11

Causes include thoracic neoplasia, b acteerial leuropneumonia, penetrating chest wall wounds, concurrent peritonitis, congestive heart failure, hypoproteinaemia, chylothorax ad diaphragmatic hernia. Identify effusion by auscultation, percussion and ultrasoography. Pleural fluid analysis can facilitate differentiation of transudate, modified transudate and exudate. Perform cytological examination for neoplastic cells and aerobic and anaerobic culture and gram smear for bacteria. Treat underlying cause and perform thoracocentesis.

Answer 12

During very fast exercise most horses bleed from dorsocaudal lung, because of very high pulmonary capillary pressures, sub atmospheric inspiratory pressures and presence of other predisposiing URT, LRT and cardiac disorders. Most bleeds are asymptomatic however marked EIPH can cause epistaxis, poor exercise perforamce, pulling up and very rarely, death. Excessive coughing is not a feature of EIPH. Diagnosis is confirmed by bronchoscopy, fresh blood is visible in trachea and large bronchi for a few days following a bleed, while Haemosiderin tinted secretions are visible in trachea and large bronchi for a few days following a bleed, while haemosiderin tinted secretions are visible for up to 1 week. Haemosiderophages can be identified in tracheal aspirates and BALF for many months following a bleed. Treatment is largely unsatisfactory but includes rest treatment of underlying cardiac URT and LRT disorders, nsaids to reduce interstitial lung fibrosis, dust free environment and training at slower speeds. Pre race administration of frusemide is permitted in some countries but is of questionable efficacy. Non responsive horses should be retired to less demanding disciplines.

Answer 13

Passage of faecal material with increased water content. In adult horses - almost exclusively due to disorders of the large intestines, although may be a secondary response to another disease process e.g edotoxaemia, liver disease. Acute diarrhoea may result in sigificat water and electrolyte losses and acid base disturbances.

Answer 14

Malabsorption; decrease i functioal absorptive surface area (decreased fluid absorption and retention), increased secretion: increased solute and water secretion by inflamed colon. Abnormal motility: decreased transit time eg stress/excitement. Osmotic overload e.g carbohydrate overload/magnesium sulphate administration. Increased hydraulic pressure from blood to intestinal lumen e.g congestive cardiac failure, inflammatory bowel disease.

Answer 15

Infectious; salmonella typhiumurium, clostridium difficile, clostridium perfringens, parasitic cyathostomiasis, toxic - NSAIDS, others - atbiotic usage, carbohydrate overload.

Answer 16

Chronic salmonellosis, chronic cyathostomiasis, lawsonia intracellularis, sand, NSAID toxicity, granulomatous eteritis, lymphocytic plasmacytic enteritis, multisystemic eosinophilic epitheliotrophic disease. Disruption in normal physiological processes 9abnormal VFA synthesis or absorption). Non GI- Liver disease, congestive heat failure, renal disease.

Answer 17

Fluid/ electrolyte / protein replacement - orally via indwelling nasogastric tube if no small intestinal ileus, 4-8L every 20-30 min. IV fluids preferred in most cases - isotonic sodium chloride or lactated ringers: volume ad rate depends on degree of fluid and electrolyte losses. Hypertonic NaCl - if severe hyponatraemia, contraindicated if severely dehydrated ad should always be followed by administration of isotonic solutions. Colloids - protein losses may result in interstitial oedema formation, drop in oncotic pressure may worsen with crystalloid fluid administration. Colloids - more effective and longer duration of plasma volume expansion. When using synthetic colloids - plasma protein may be poor indicator of plasma oncotic pressure. Control of colonic inflammation and reduction in fluid secretion - prostaglandins likely play a large role in infectious diarrhoea, COX inhibitors - anti secretory effects however PGE2 and PGI2 are critical for mucosal repair therefore NSAID use is controversial. Other anti inflammatory drugs - metronidazole, bismuth subsalicylate. Control of endotoxaemia with low dose NSAIDS. Promotion of mucosal repair - sucralfate, misoprostol, psyllium mucilloid increases productio of SCFAs. Control of pain - alpha2 agonists, butorphanol, lidocaine. Antibiotics indicated in neutropaenic horses. Increased risk of septicaemia either from primary bacterial cause or GI bacteria breaching a compromised mucosal barrier.

Answer 18

Change diet: hay and alfalfa good source of easily digestible protein. Stop NSAID and antibiotic therapy if this could be possible cause. Caecal traunsfaunation or probiotics. Larvicidal dose anthelmintics & corticosteroids if suspect cyathostomiasis. May need to wait several weeks to determine whether this is effective. Corticosteroids - last resort, may improve inflammatory enteritis. Since may have malabsorption best to give injectable dexamethasone therapy for first week then 1.1g/kg prednisolone every other day orally. Taper dose off over at least a 2 week period. May need intermittent or long term low dose therapy. Not a high success rate.

Answer 19

Clinical signs consistent with abdominal usually gastrointestinal pain. Be aware of false colics - origin of pain from non GI structures. colic is not a diagnosis. Commonly encountered problem in equine practice.

Answer 20

Mild colic - stretching of the abdomen, looking at flanks, teeth grinding, yawning. Moderate colic - pacing up the box, pawing the ground, kicking at belly, crouched stance, grunting, frequent getting up and down, prolonged periods in lateral recumbency. Severe colic: includes many of the above signs in addition to generalised sweating, rolling and self inflicted trauma.

Answer 21

History - when were the clinical symptoms first noticed, how rapidly have the symptoms proressed, what when ad how much feed an water intake, how much faeces urine, repeated episodes of colic? weight loss?, worming programme? at grass:grass sickness, intestinal parasitism, tympanic colic, recent changes in diet? stages of work? (horses in work that are given time off commonly get mild immpactions), bedding: horses that eat their bedding may get impactios, season: incidence of grass sickness peaks in spring/summer, in the winter season there is often an increased frequency of primary impactions.

Answer 22

Intermittent, cotinuous, increasing or decreasing. Visceral pain - most commo: increased peristalsis, distension, ischaemia, stretching of mesentery. Parietal pain: less common, inflammation of the pareital peritoneum, tend to be immobile, boarding of the abdomen, resent external abdominal compression. Abdominal distension - indicates large colon and or Caecal distension in the adult horse. Rectal temperature - increase with anterior enteritis, colitis, peritoitis, and intestinal abscessation. decrease coupled with a rapid weak pulse indicates shock - grave prognosis.

Answer 23

Pink - seen with mild impactions, simple colics. Pale - anaemic, seen with intrabadominal haemorrhage Red /injected: haemoconcentration and vasodilation, results from endotoxaemia. Brick red - further deterioration toxic/dirty brown - later stages of endotoxic shock, may show toxic lie in periodontal region, cyanotic suggests grave prognosis, euthanasia probably best. CRT best assessed from oral mucous membranes, reflects circulatory status. Normal <2 seconds. Increasing CRT indicates a progressively inadequate peripheral perfusion.

Answer 24

Auscultate for several minutes i each of 4 sites (right/left/orsal/ventral). Note site ad nature of the sounds heart - haustral short duration,2-4 per minute, peristaltic longer duratio once every 2-4 minutes, caecal filling, caecal emptying. Increased gut sounds may be heard with spasmodic or tympanitic colics. Decreased gut sounds usually heard with most other types of colic, grass sickness and various metabolic systemic disorders. Generally the quieter the abdomen the more serious the problem. Percussing the abdomen will often elicit a ping over the tympanitic areas especially over a distended caecum.

Answer 25

Only the caudal 1//3 of the abdominal cavity is palpable. Foals and small ponies too small to permit examination. Adequate restraint - necessary to ensure the safety of the personnel and horse. It is not possible to palpate small intestinal loops in a normal horse. The jejunum has a long mesenteric attachment and moves away from the hand. Palpation of distended loops of small intestine is one indication in which referral should be considered. It may be necessary to perform rectal examinations at hourly or two hourly intervals. Specific abnormal rectal findings include; Impaction of the pelvic flexure - very common, often easily diagnosed on rectal examiatio, feels like a doughy mass. Secondary impaction of the pelvic flexure occurs in some conditions with colonic stasis. Absorption of fluid from the colon. Small intestinal distension: may be palpable in grass sickness, enteritis, strangulating obstructions, small intestinal impactions, intussusceptions and non strangulating infarctions. Caecal intussusception - may be palpated as a mass within the caecum. Ileocaecal intussusception may be detected as a paiful, oedematous ass within the caecal base, likely to also result in small intestinal distension. Large intestinal gaseous distension - occurs in a number of conditions including primary flatulent colic, transverse or small colon obstructioon, large colon displacements, large colon torsions. nephrosplenic entrapment of large colon - occurs when the left large colon migrates dorsally between the spleen and the body wall and ultimately hooks over the nephro splenic ligament. colon may be palpated in left/dorsal abdominal quadrant running in a dorsoventral direction. May palpate colon overlying the nephrosplenic ligament. Intra abdominal abscess formation or neoplasia - may be palpable per rectum if situated in a suitable position. Can range in size from golf ball sized to football sized.

Answer 26

For diagnosis of gastric distension with as or liquid, since gastric reflux is nor normally spontaneous it is always necessary to pass a stomach tube to determine if excessive fluid/gas is present. Relief of gastric distension, administration of therapeutic agents directly into the stomach. Conditions that result in gastric dilation/reflux include: acute grass sickness, ileus, small intestinal strangulating obstruction, proximal jejunitis, some cases of large intestinal obstruction.

Answer 27

should be considered in most cases of colic unless confident they are simple medical colics. Interpretation - initial response of the peritoneum to inflammation or ischaemia is an increase in protein and fibrinogen levels. Fibrinogen >0.1g/l is suggestive of an acute inflammatory response or haemoabdomen. With progressive insult - leukocyte counts WBC increase. Acute Ischaemia is characterised by a Neutrophilia and increased erythrocytes due to diapedesis. Acute inflammatory responses such as Abscessation or bacterial peritonitis may increase neutrophils counts without increasing red blood cell numbers. chronic inflammatory conditions show increases in both neutrophils and mononuclear cells. Peritoneal fluid may remai ormal in horses with devitalised bowel if inflammatory debris is trapped, as occurs in epiploic entrapment and intussusceptions. Purulent fluid see in peritonitis. Serosanguinous fluid indicative of infarction in which there is leakage of HB and RBCs from the intestine. Fresh blood from intra abdominal haemorrhage or iatrogeic haemorrhage. Digesta - ruptured viscus.

Answer 28

Severe continuous pain showing no or only short duration improvement with analgesia. Pulse >60, progressively rising and weakening. Progressive cardiovascular collapse: PCV >55, injected or cyanotic mms despite fluids, rectal findings positive for acute abdominal diseas.e progressive reduction in the intestinal motility or continual gas reflux. incraesing abdominal distension. Serosanguinous peritoneal fluid with increased protein and WBCs. If none of the seven criteria are preset, treat medically but reassess at short intervals so that any subsequet development of indications for surgical therapy can be detected early and treated appropriately.

Answer 29

Avoid large volumes of fluids/liquid paraffin orally if intestinal motility is reduced. NSAIDS - act peripherally by inhibiting prostagladin production, do not depress gut motility some have potent endotoxin properties. Excess usage side effects include gastrointestinal ulceration, renal papillary necrosis and blood dyscrasias. options include phenylbutazone, flunixin, ketoprogen. Opioids - very potent analgesics, temporarily prolong gut transit time, cause respiratory and cardiovascular depressio, do nto mask the clinical signs of endotoxaemia. options include butorphanol, morphine. Sedatives - provide good sedation along with varying degrees of visceral analgesia. side effects include reduced gut motility, ataxia and bradycardia. often used in combination with a opioid. options include romifidine, xylazine, detomidine. Spasmolytic drugs; buscopan compositum contains metamizole and butylscopolamine- commonly used first line of treatment. Laxatives best used in conjunction with fluid therapy when treating impactions. important to ensure good intestinal motility before administration. Optios include liquid paraffin, dioctyl sodium sulfosuccinate, oral magesium sulphate. IV fluids - often essential in cases of severe dehydration nor endotoxic shock, administration in the field often quite difficult. very effective in softening intestinal impactions. Options include polyionic fluid, isotonic glucose salie, sodium bicarbonate, hypertonic saline.

Answer 30

Yellow coloration of the sclera and mucous membranes resulting from increased tissue and serum bilirubin. Usually indicative of; decreased excretion of bilirubin with liver or biliary tract disease, increased production of bilirubin with haemolytic anaemia, impaired hepatic uptake or conjugation of bilirubin with liver disease. Accumulation of conjugated bilirubin results in more pronounced jaundice than unconjugated bilirubin therefore most pronounced jaundice seen with hepatic or biliary obstructive disease. Icterus more likely with acute liver disease compared with chronic liver disease. Fasting/anorexia in the horse can result in an increase in unconjugated bilirubin.

Answer 31

Develop only when 60-70% of hepatocytes are destroyed, signs of hepatic failure may appear suddenly, often history of gradual weight loss, decreased appetite and recurrent bouts of photosensitisation before hepatic failure develops. Most die within a few weeks. Most signs are non specific; depressin, anorexia, weight loss, mild to severe abdominal pain. Some signs are more suggestive; icterus, photosensitisatio, pruritus, hepatic encephalopathy, coagulopathy, petechiae, bilateral laryngeal paralysis.

Answer 32

Largely supportive util adequate liver function returns or regeneration occurs. acute failure best progosis. chronic liver disease with extensive fibrosis - hopeless prognosis. treatment of horses with hepatic ecephalopathy rarely warranted. General principles - remove from source of hepatotoxins. Dietary mangement with high carbohydrate diet, low protein, antibiotics only indicated when suppurative cholangitis or abscesation suspected, tracheostomy may be required if bilateral laryngeal paralysis corticosteroids - no evidence to indicate inhibit development of liver fibrosis. may be contraindicated as increase metabolic load on liver. May be indicated in cases of chronic non suppurative cholangiohepatitis. Treatment of hepatic encephalopathy - sedation; only if horse is uncontrollable and poses a danger to handlers. Correction of metabolic, fluid and electrolyte abnormalities, reduction in GIT production/absorption of potential neurotoxins - reduce number of anaerobes and gram negative urea splitting organisms. Lactulose - reduces intestinal neurotransmitter production and absorption.

Answer 33

By eye, Body condition scoring e.g method of carroll and huntigdo, point score, weight tape and calculations - based on algorithms calculated from girth and or other anatomical points, weigh bridge - most accurate and least available, regular calibration required. Owners should be encouraged to regularly condition score their horses.

Answer 34

Management, physiology etc; Poor nutrition; amouts and or types/quality Increased metabolic demads: exercise, pregnancy, vices Hierarchy/pecking order Inability to access Old age Disease: Dysphagia Maldigestion and malabsortion - parasites, IBDz, neoplasia, liver disease Increased consumption or loss (parasites, IBDz, Neoplasia, PPID, EGS, renal disease, liver disease, cardiac disease, infections and sepsis, chronic pain)

Answer 35

Age - parasitism occurs more often in the young and problems like equine proliferative enteropathy are only features of weanlings living in relatively crowded coditions. Neoplasia more common i older animals. History of dental disease/routine floating - many abnormalities such as diastema, caudal hooks may be missed without a proper examination. Feeding history - amounts and types - are they matched nutritionally to the metabolic needs. Medicatio history; any history of repeated or cotinual NSAID use? antibiotics? worm history - very important, best case scenario is to obtain information relating to faecal egg worm counts, but remember that these do not reflect encysted cyathostome numbers, only adults. Even though the owner thinks they have a good worming regime, that may not be the case. Any diarrhoea noted by the owner? Diarrhoea generally means large intestinal problem i the hose. Any lethargy? water intake?

Answer 36

Rectal examination - obtain a fresh faecal sample. Abdominal paracentesis - peritonitis, neoplastic masses. Faecal analysis - blood, mucous, presence of small redowmr larvae, assessment of fibre length, indicatio of poor mastication. Haematology - significant neutrophilia with neoplasia and other inflammatory disease. Biochemistry - initial panel for evaluation of weight loss should include proteins, fibrinoge, alkaline phosphatase, liver screen - GLDH and GGT, assessment of urea and creatinine.

Answer 37

Assess weight and set date for re evaluation. Dietary change - ad lib good quality grass, hay, haylage. High energy feed e.g sugar beet young stock, mix, veteran diets, add oil to ration. Stop/start any long term medication for example phenylbutazone may be a potential cause of colitis or protein loss. Anthelmintic therapy: probably always worth giving a larvicidal dose of anthelmintics despite apparent adequacy of an anthelmintic regime. If high suspisio of cyathostome infestation then using either a single dose of moxidectin or the older regimen of repeating regime of 5 day fenbedazole followed by ivermectin may be used.

Answer 38

Term currently used to describe and explain obese horses or ponies prone to laminitis. Also known as peripheral cushings disease and obesity dependent laminitis. Insulin resistance may be a key factor. If an animal is obese and suffers recurrent bouts of laminitis then it probably has underlying metabolic predisposition to the obesity and the laminitis.

Answer 39

Insulin resistance is thought to play a major role in EMS. Fasting glucose and insulin test may be carried out in conjunction with tests to rule out ECF. starve of concentrations for 12 hours prior to testing. water ad grass hay may still be fed up until the sampling without invalidating the test. Increased levels of insulin provide evidence of insulin resistance, while increased glucose levels in a non stressed individual suggest severe IR/type 2 DM. Oral glucose tolerace test - horse or pony is starved of concentrates for 12 hours before test. Water is removed for 1 hour prior to test. Glucose is administered and blood glucose and insulin levels are tested prior to administration and at various points after. Blood gluocose should double within two hours and reduce to normal levels within 6 hours. Increased peak in glucose or delay to return to normal levels is indicative of relative insulin resistance.

Answer 40

Control of calorific intake with judicious exercise in those individuals where this is possible. If there is an identifiable underlying cause then this should be treated appropriately. for example those animals with ECF should be treated with pergolide.

Answer 41

Feeds with a low glycaemic index should be chosen. Complete starvation should be avoided. Rich grass should be avoided as the sugar content can be very high. Restricted grazing practice must be balanced with the need for exercise therefore use of grass muzzles or night grazing may be advantageous. Grass hay is generally good but may be variable in soluble carbohydrate /sugar content therefore best practice is to encourage owners to have it analysed for non structural carbohydrate. Soaking hay may also reduce the soluble CHO as it gets trapped in the water. If further feeding is required then use other low GI foods. Alfalfa chaff is good extra ration.

Answer 42

May improve insulin sensitivity. Can be difficult if active laminitis. Placing an animal out to grass in theory is beneficial but can be difficult at the high risk times of year. Night grazing may be beneficial.

Answer 43

rhabdomyolysis, botulism, equine motor neurone disease, hyperkalaemic period paralysis, hypocalcaemia, myasthenia gravis. Fasiculuation/muscle twitchig, narrow based stance, icreased periods of recumbency, low head carriage at rest and during exercise, reluctance to bear weight when a limb is raised sudden rapid recumbency, dysphagia.

Answer 44

Rhabdomyolysis, tetanus, hypocalcaemia, shivering and stiff horse syndrome. Key historical findigs: fasciculation, trismus, stiff and stilted gait, other bizarre gait abnormalities.

Answer 45

Caused by the toxin of clostridium botulinum, a gram positive anaerobic spore forming bacteria found ubiquitously in soil. toxin is thought to block acetylcholine release at the neuromuscular junction, peripheral cholinergic nerve terminals in autonomic ganglia, and post ganglionic parasympathetic nerve endings. C botulinum grows best in eutral or alkaline pH and grows ad produces toxin anaerobic environments such as decaying vegetable matter and animal carcasses. Silage provides a suitable medium for growth and toxin production. animal carcasses may be accidently baled into bales or chopped into cubes or pellets. Three modes of intoxication possible; Ingestion, of preformed toxin, growth of the agent in the GI system, or contamination of wounds. In adult horses in the UK, botulism is usually secondary to eating big bale silage.

Answer 46

May be acute in onset with dyspnoea, severe diffuse paresiis and rapid progression to recumbency. In some horses the onset and progression are slower, occuring over several days. Weakness and trembling which improves during periods of recumbency. Inability to fully retract the tongue, dysphagia and drooling of the saliva, flaccidity of the tail, gradual onset of clinical signs is associated with a better prognosis cf acute onset. In fatal cases, death occurs quietly, in non fatal cases, recovery takes weeks to months.

Answer 47

Initially appear alert, progression is associated with paresis, stilted gait and most prominent and generalised muscle trembling - shaker foals. ptosis and decreased tail tone is frequently evident. dysphagia is present despite a normal appetite. May show slow PLR, ileus, constipation and urine retention. Death is caused by respiratory paralysis or complications such as pneumoia. Mortality in this form >90%.

Answer 48

Definitive diagnosis by identification of toxin in serum, GI contents or food. Treatment mainly symptomatic. in cases of wound contamination or toxicoinfectious botulism, antibiotic therapy is indicated. Antibiotics associated with neuromuscular weakness should be avoided if possible e.g aminoglycosides, tetracyclines and procaine penicillin. Antitoxin not widely available for clinical use in the UK. Preention with good husbandry, vermin control, adequate disposal of carcasses, avoiding the use of spoiled foodstuff and poor quality silage.

Answer 49

Caused by clostridium tetani - a large gram positive spore forming bacillus. found in soil and is a commensal in the GI tract of man and domestic animals. the spores of C tetani can persist in the environment for many years. In the body, requires anaerobic conditions to survie. The common sites of contamination includes; puncture wounds, surgical wouds, mucosal wounds and ulers, umbilical cord, retained placenta and Haematogenous spread to devitalise tissue. It produces a potent exotoxin - tetanospasm causes spastic contractions of striated muscles. Tetanospasm acts primarily on the CNS transported partly by the vascular system and partly by retrograde axonal migration along the motor nerves to the ventral horns of the spinal cord grey matter. Thought to act mainly by preveting the release of inhibitory neurotransmitters from the intereurons at the motor synapses in the spinal cord. Locally further tissue necrosis and exudation is aided by another toxin, tetanolysin.

Answer 50

Horse very susceptible to toxin but may take a few days to several weeks to appear. first signs are usually a change in the horses gait (stilted action) and demeanour. May also notice a difficulty in eating at this stage (spasm of muscle of prehension, mastication and swallowing). Generalised spastic muscular contractions are provoked by external stimuli, especially evident in the third eyelid when the cheek is tapped or when fingers are snapped infront of the eye. The disease may worsen dramatically over the ext 24 hours or take several days, the horse will stand square on four stiff limbs with its head and neck extended and the tail raised. it will have an anxious expression with the nostrils flared, eyelids retracted and ears erect. Sweating and tachycardia may result. Drooling may be seen due to involvement of the pharyngeal and laryngeal muscles - food and water may be regurgitated down the nose or pass into the lungs. progression to recumbency and death often from convulsions leading to respiratory and cardiac arrest.

Answer 51

in each case - consider the prognosis and the welfare aspects, recumbent adult animals should be destroyed. Cases with the best prognoses show mild clinical signs over several days and are still able to eat and drink. Quiet dark stable, peat or shavings bedding, elevate food and water soft moist food quiet gentle handing, acetyopromazine, sodium benzylpenicillin, procaine penicillin, antitoxin, hydrogen peroxide in wound. Prevention with vaccinatio.

Answer 52

Common in working horses and ponies. Vast majority sporadic and associated with exercise. excessive glycogen > lactic acid and 02 radicals > coagulative necrosis > further muscle hypoxia > prevents muscular relaxation. Signs occur during or sometimes immediately following exercise. A minority of cases signs may eve occur on leaving the stall/box or following minimal exercise. With acute tying up both hind limbs are usually affected - especially gluteal, femoral and lumbar muscles. Affected horses develop a stiff gait and may refuse to move. Palpation reveals affected muscle groups to be painful, hard and swollen. The animal is frequently distressed, sweating, wiht increased temperature, HR and Rr. In severe cases the urine may be red/brown in colour due to the presence of myoblobin. The excess myoglobin may lead to renal failure due to the accumulation within the renal tubules. If the horse is oliguric, poor prognostic sign.

Answer 53

Elevations in the serum levels of enzyme creatinine kinase, aspartate aminotrasnferase and lactate dehydrogenase. the degree of increase reflects the degree of muscle damage. CK is the most specific for skeletal muscle damage. CK rises first and disappears first followed by LDH and then AST. LDH peaks at approximately 15 hours and may reach several thousant. AST peaks at 24 hours and may reach many thousand. The presence of myoglobin in the urine. When using a dipstick this cannot be distinguished from blood. Pathological findings - extensive pale discolouration of affected muscles.. Degeneration and swelling of muscle fibres histologically.

Answer 54

Rest - further muscular activity exacerbates the disease therefore doo not move the hors. Some very mild cases have been reported to respond to walking out but if in doubt, do not move. Analgesics - NSAIDs highly recommended. Fluids - consider oral fluids for mild cases, i/v for more severe. may of these cases are alkalotic, therefore HCO3 would be contraindicated. If unable to check the elctrolyte and acid base status best to give a balanced electrolyte solution. Diuretics are usually contra indicated unless despite vigorous fluid therapy the horse is still oliguric. Sedatives - ACP, may help alleviate anxiety and muscle spasm. Corticosteroids - short acting steroids may play a useful role in stabilising cellular membranes, however be aware of the risks of laminitis with high doses of potent corticosteroids. Calcium carbonate and calcium gluconate have been cited as being useful in severe cases as calcium may be depleted.

Answer 55

Reduced carbohydrate, increased intake of food AFTER increased workload, Continual exercise with adequate warm ups and without breaks in routine, turnout is beneficial, stress avoidance especially important in recurrent ER cases. Acepromazine to reduce stress of training, dantrolene - reducing post exercise levels of CK. Salt - may sweat profusely resulting in loss of sodium and chloride. Vitamin E and selenium - believed to be useful due to their suspected involvement in oxidative reduction reactions within the cells.

Answer 56

Seizures, Cervical vertebral stenosis, narcolepsy, inappropriate sleep, botulism, arrhthmias, haemorrhage, heart failure, aorto iliac thrombosis, neurocardiogenic collapse, hypocalcaemia, hypoglycaemia, monensin toxicosis, systemic anaphylaxis, air emboli, musculoskeletal abnormality, severe myopathy.

Answer 57

control seizures with diazepam, if hypothermic provide heat lamp or blankets ( blood culture vial. Treat navel with 0.05% chlorhexidine if moist - repeat for several days. Give tetanus antitoxin if mare not vaccinated within the last 4-6 weeks of gestation. LAsts approx 3 months.

Answer 58

Pansystolic murmur at cranial left heart base for up to 7 days in a oal, due to PDA or functional murmur. Palpate thorax for fractured ribs.

Answer 59

Measure neonatal serum IgG from 8-24h onwards. Cannot do when >2 weeks since foals own IgG production will affect results. Single radial immunodiffusion kits - most accurate, highly specific. CITE test - accurate and suitable for field use. Normal IgG at 21 hours old >8g/l. FPT is partial or complete. Partial FPT (4-8g/l) may not need treatment if foal is clinically normal and in clean environment. Treat complete FPT <4g/l otherwise foal susceptible to sepsis.

Answer 60

If 24 hours old - intestinal absorption of IgG ceased, so give 1-2L equine plasma IV. First litre over 60 minutes and slower rate subsequently. Rare complications include tachypnoea, shivering, aaphylaxis, volume overload.

Answer 61

An immune mediated haemolytic anaemia. destruction of the foals RBCS by Colostral antibodies which are directed against foals RBC membrane alloantigens. Most incompatibilities are due to alloantigens Aa and Qa. Problem occurs when foal inherits Aa or Qa alloantigens from Aa or Qa +ve stallion and when RBC of mare are negative for these antigens - during birth of the foal, foetal blood often leaks into maternal 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, however in subsequent pregnancies mare produces increasing amounts of these antibodies which are excreted in colostrum. If subsequent foals are Aa or Qa positive these antibodies cause NI. Normal at birth, signs begin from 6-8 hours, anaemia with weakness, icterus and rarely haemoglobinuria, depressio, anorexia, progressing to collapse and death.

Answer 62

Prevent further absorption of mares colostral Ig - give alternative milk until foal is >24hours old. Milk mare thoroughly and regularly and discard colostrum. Blood transfusion equired if PCV <10-12% or if PCV reducing rapidly. Can transfuse thoroughly washed RBC from mare - wash 3x in saline, then administer 1-21 of 50% suspension of RBCs in saline. Alternatively transfuse whole blood from Aa, Qa alloantigen negative horse or stallion or gelding that has never had a transfusion. Collect blood into transfusion bags as plasma and administer whole blood via iline filter. Prevention - dont mate Aa or Qa ive mares with Aa or Qa +ve stallions. Test at risk mares serum for alloatibodies. in last 2 weeks of gestation when levels are increasing.

Answer 63

The major cause of neonatal mortality, prognosis guarded. prompt therapy critical for success. portal entry GIT, lung, umbilicus, iatrogenic. Rarely acquired in utero, if so are sick at birth. Most acquired post partum - sigs develop 48-96 hours. Bacteria are usually ubiquitous environmental bacteria - maiinly gram negative, E. coli, salmonella, Klebsiella, actinobacillus, pseudomonas. And less often gram +ve streps, staphs, rhodococcus equi, clostridia. Initially have non specific signs reduced apeptiet, decreased sucking, dullness, increased recumbency, pyrexia, rapid progression to signs of multisystem involvement - meningitis, diarrhoea, colic, tachypnoea, resp distress, lameness, swollen joints, omphalophlebitis, uveitis, petechiae, scleral injection.

Answer 64

Blood or body fluid cultures vry useful. collect samples before administration of antibiotics, ideally when foal is pyrexic. do not collect blood from indwelling iv catheter since may have surface contaminants. Do aerobic and anaerobic cultures. WBC counts may be normal, increased or decreased depending on stage of infection may need to follow progress of counts. Presence of bad and toxic neutrophils is suggestive of sepsis. Septic foal are often thrombocytopenic. Fibrinogen increased after 24hours. IgG may be low. Hypglycaemia, low pao2, metabolic acidosis.

Answer 65

While awaiting culture results - use broad spectrum antibiotics e.g penicillin plus getamici, cetiofur or cefquinome. change therapy if necessary after culture and sensitivity results obtained . Treat for 1-2 weeks after clinical signs of sepsis have resolved. often need antibiotics for 1-2 months especially if persistent infection. Local therapy eg joint lavage, pleural drainage, umbilical surgery etc. IgGs - may need supplementing since may will have FPT.

Answer 66

Occurs at 6-14 days. Due to alteration in colonic microflora and epithelium as they adapt from milk to grass diet and perform corpophagy. Transient self curing diarrhoea. No Treatment required but watch in case it isn't foal heat diarrhoea - reconsider diagnosis if becomes sick with pyrexia, depression, dehydration.

Answer 67

Main cause of foal diarrhoea. Widespread in equine population. Adults probably source for foals. survives for over 9 months in enviroment. Many foals 1 month have mild enteritis only. Profuse watery, non foetid diarrhoea, depression. Mainly affects small intestine - stunting of villi & loss of absorptive capacity together with increased intestinal secretion. Diagnosed using ELISA or latex agglutination -submit faecal sample. Treat with specific antisera orally or treat symptomatically. Avoid overstocking. Vaccinate mare in ,9,10th month of gestation with inactivated equine rotavirus to provide Colostral protection.

Answer 68

Salmonellosis: mare is most likely source.commonly mild enteritis but may cause severe septcaemia. Clostridium perfringens type A B & C causes foetid necrotising haemorrhagic enteritis in 1-2 day old foals. commonly causing death within 48 hours. Septicaemia; dairrhoea is commoon presenting sign in septicaemia. Aeromonas spp probable primary cause of diarrhoea in foals. E. coli. Coronavirus and adenovirus. Cryptosporidium. Strongyloides westeri.

Answer 69

Fluid therapy - critical since likely have dehydration, metabolic acidosis, and reduced Na, Cl, K. For mild dehydration administer isotonic electrolyte solutions orally little and often. Severe dehydration usually requires IV fluids. Antibiotics controversial and probably overused. Not idicated in nutritional, viral and parasitic diarrhoea. Only give in foals 1 day only as get undernutrition

Answer 70

Probably multifactorial. Stress important - consequently most sick foals are given GDU prophylaxis. Can be iatrogenic - foals susceptible to NSAID toxicity. NSAIDs inhibit PG synthesis causing gastric mucosal vasoconstriction and ischaemia. Most foals have a few ulcers on the non glandular side of the margo plicatus without symptoms. Symptomatic ulcers occur from day 1 onwards causing anorexia, salivation, colic after sucking, dorsal recumbency, odotopresis, regurgitation of mucoid/watery gastric fluid. Proton pump inhibitor most effective and most commonly used.

Answer 71

Meconium usually voided within a few hours. Retentio mainly in males due to narrow pelvis. Signs start at 6-24 hours, restless, straining, lifting tail, rolling, lying on back, attempts to urinate. Straining may reopen urachus - drip urine in conjunction with straining. Treatment using warm soapy water as enema using soft tube inserted 10-12''. Forceps or rectal spoons not recommended.

Answer 72

Uncommon in the UK - infectious necrotic hepatitis caused by clostridium piliformis. Affects foals 1-6 weeks old, sudden death or acute abdominal pain, depression. Penicillin recommended, b ut most foals die. Usually PM diagnosis.

Answer 73

Urine leakage from ruptured bladder or rarely from patent urachus or ureters. common in colt foals. ladder defect always on dorsal midline. probably ruptures when foals abdominal pressure increases during delivery. signs onset 3-7 days old. Usually only some of urine passes into peritoneal cavity so most foals still urinate exteernally. PRogressive onset of abdominal distension lethargy, tachypnoea, tachycardia, circulatory failure, mild abdominal pain. Diagnosis made on signs, ultrasonography of abdomen and bladder and peritoneal fluid analysis. Uro peritoneum confirmed by demonstrating ratio of creatinine in peritoneal fluid: serum >2:1. Most foals develop azotaemia, hyperkalaemia, hyponaetramemia, hypochloraemia and metabolic acidosis. due to metabolic derangements this is a medical emergency - attempt to drain abdomen via catheter, administer IV saline to correct Na loss and hyperkalaemia. correct hypoglycaemia, administer abx. Once stabilised performs surgical bladder closure.

Answer 74

Exact pathogenesis unclear and likely multifactorial but involves peripartum cerebral hypoxia/ischaemia. Signs of cerebral dysfunction appear after several hours to 1 day - localised seizures of face and limbs, disorientation, ataxia, loss of righting and suck reflexes, loss of affinity for dam, central blindess, barking vocalisation, loss of thermoregulation, erratic breathing pattern, increasing recumbecy, coma or general seizures, o specific treatment. Steroids often administered but no evidence of efficacy. cotrol seizures using diazepam slow IV. Many stabilise by 2-3 days but flul recovery takes several weeks.

Answer 75

2 umbilical arteries which connect internal iliac arteries to placenta and which after birth become round ligaments of the bladder. 1 umbilical vein which connects placenta to hepatic portal vein which becomes the round ligament lying within the falciform ligament after birth. Urachus - connects foetal bladder to allantoic cavity.

Answer 76

Infection occurs usually <1 week old. Most commonly have infection confined to external umbilicus with local heat, pain, swelling and commonly no systemic effects. These can be effectively drained or treated with systemic antibiotics. More concerning is infection of internal umbilicus - ultrasound useful to detect infection - often have secondary septicaemia. usually require surgical removal as rarely respond to antibiotics alone.

Answer 77

Associated with navel ill, septicaemia, increased abdominal pressure due to straining or prolonged recumbency. usually occurs soon after when dried umbilical stump drops off. easily recognised because urine drips from umbilicus and urethra when urinate. perform ultrasound examination to determine if urachus is infected. Infected urachus requires surgical removal, while uncomplicated patent urachus usually resolves simply with correction of underlying cause eg retained meconium.

Answer 78

Strep equi subspp equi, subsolar abscess,diarrhoea, purely viral infections. Sulphonamides are ineffective in purulent and necrotic tissue. Aminoglycosides are ineffective in an abscess.

Answer 79

equitrim an norodine. Both inhibit folic acid synthesis, individually are bacteriostatic but synergistically are bactericidal. Act against gram positive and gram negative but not anaerobes. Purulent and necrotic tissue inactivate sulphonamides. Time dependent. give BID not SId. Fatal cardiac dysrhythmias may occur with concurrent use of A2 agonists and IV TMPS.

Answer 80

Inhibits cell wall synthesis, bactericidal, gram positive,g ram negative and anaerobic effective. Time depedent. Benthazine penicillin G - give single long acting injection. Do not use as fails to reach MIC. Adverse effects to penicillin - inadvertent IV injection - ataxia/seizure like activity, hypersensitivity - urticaria, angiooedema, rapid IV administration - colic, loose faeces.

Answer 81

Active against gram +ve, Gram-ve, aaerobes. Inhibits cell wall synthesis. Bactericial. Time dependent.

Answer 82

Amikacin - pumped across cell membrane & inhibit protein synthesis. Are bactericidal. active against gram ive. Concentration dependent. Side effects include Nephrotoxicity especially if dehydrated and NSAIds, ototoxicity, muscle irritation if IM.

Answer 83

Inhibit bacterial protein synthesis, are bacteriostatic, concentration and time dependent, Active against gram positive, gram negative and anaerobes. Effective against intracellular pathogens - ehrlichia, rickettsial organisms, lawsonia. Oxytetracycline - Ca binding = treatment for flexural limb deformity in foals.

Answer 84

Inhibit DNA gyrase responsble for supercoiling bacterial DNA, bactericidal, concentration dependent, active against gram =ve, gram -ve, not anaerobes. active against rickettsia ehrlichia.

Answer 85

Cause severe and fatal colitis. Hyperthermia with concurrent respiratory distress. Rhodococcus equi highly susceptible. Bacteriostatic. Very active against gram positive. Inhibit bacterial protein synthesis.

Answer 86

Inhibits RNA polymerase. Bactericidal. Gram positive. Anaerobes. synergistic with macrolides - for rhodococcus equi. Always use in combination with another class of Antibiotics. rapidly develop resistance.

Answer 87

Active vaccination induces an antigen specific immune response in the vaccinated animal by administration of dead or live antigen or DNA capable of expressing protein antigens n vivo. Success of vaccination often depends on the effective use of an adjuvant, a compound capable of amplifying and directing immune responses. Passive vaccination is accomplished by administering preformed antibodies either as a plasma transfusion or in a concentrated form.

Answer 88

Equine influenza - 5-6 months of age, 4-6 weeks later, 5 months later. Equine herpes virus - EHV1, EHV4 Tetanus - toxoic 2 vaccines 1 month apart then boosters every 2-3 years. Equine viral arteritis - establishment of EVA negative status of stallions prior to vaccination is important. Streptococcus equi - 2 vaccines 4 weeks apart. Booster every 3-5 months. live modified strain of S equi, submucosal. reduces clinical sigs only. Serological ELISA test positive.

Answer 89

Cyathosomes small strongyles/redworms Large strongyles large redworms e.g strongylus vulgaris Ascarids (large roundworm) - immunity by 2 years Aoplocephala (tapeworm) - 6 month cycle Gasterophilus bots - 12 months to mature, tx once yearly Strongyloides weteri - natural immunity by 6 moths, acquired via mares milk. Oxyuris (pinworm) - irritation only. the most pathogenic equine nematode worldwide = cyathostome. Encysted larvae in large colon with subsequent en masse emergence later winter/early spriing.

Answer 90

FWEC - strongyles and ascarids, doesn't detect immature or encysted strongyles. Tapeworm ELISA - measures atibody, levels take at least 16 weeks to decline.

Answer 91

Febendazole Pyratel Ivermectin Moxidectin

Answer 92

Fenbendazole - 5 day course for encysted redworms. Pyrantel - double dose for tapeworm. Ivermectin - bots and lungworms. Moxidectin - bots and encysted cyathostome larvae.

Answer 93

Moxidectin & praziquantel - safe for foals > 6.5 months old but not pregnant/lactating mares.

Answer 94

Avoid high stocking density/overgrazing, avoid horses with high faecal egg counts, avoid presence of young horses, twice weekly removal of faeces from pasture, alternative species grazing.

Answer 95

failure of anthelmintic to perform as expected. Ca be due to suboptimal dsiing - encourage owners to use weigh tapes. increasingly due to resistance - particularly Benzimidazoles in relation to cyathstomes. over worming using interval programme promotes resistance. importance of refugia in retaining susceptible population of worms. at moment no new wormers in manufacture - can not fully rely on chemotherapeutic.

Answer 96

342 days - range 321 -385 days. Do not induce parturition in the mare. Even if the mare has gone over her expected due date the foal is almost certainly not viable until normal parturition is ready to take place.

Answer 97

Enlarged abdomen Mammary development - 3-6 weeks prepartum, major changes within 2 weeks of term, initially straw coloured discharge, udder distends with colostrum 2-3 days prepartum, teat waxig lasts up to 48 hours, increase in calcium and magnesium content of milk, at term calcium >10mmol/l. Relaxation of sacrosciatic ligaments over last few weeks and vulva in last few hours. Relaxation of cervix. Foaling aids - measurement of milk calcium can be useful. Mares may wear a monitoring alert that sets of an alarm when the mare is recumbent for prolonged periods. this can result i false alarms and miss foalings. Some people have cameras in the stable that can be programmed into the tV in the house or an iphone. Foalert is a small magnetic device that is sutured to the vulva - when parturition begins the magnet is opened and sets off an alarm that rings a mobile phone.

Answer 98

Lasts approximately 2-4 hours, uterine contractions start, cervix relaxes and dilates, restlessness, colicky signs, patchy sweating. In some mares delivery of the foal may be delayed for several hours or days. the end of 1st stage labour is marked by rupture of the allantochorion at an avascular area, the cervical star, and release of straw coloured watery allantoic fluid. The foal rotated to a dorso sacral position just before birth. The amnion should protrude through the vulvar lips within 5 minutes of the rupture of the allantoochorion.

Answer 99

Lasts less than 30 minutes; Assume lateral recumbec, abdominal contractios, foal is delivered covered by amnion, the equine placenta separates from the endometrium rapidly and foetuses not delivered within a relatively short time of onset of 2nd stage labour are deprived of oxygen. Prolonged 2nd stage labour is an emergency. Normal presentation is anterior, dorso sacral, extended. Do not cut the umbilical cord - you may allow excessive bleeding.

Answer 100

Expulsion of the placental membranes usually occurs within 1 hour with the allantoochorion turned inside out. NB always examine the placenta for completeness.

Answer 101

Dystocia exists when 1st or second stage labour is prologed or not progressive and should always be considered an emergency. if o progress occurs within 10 minutes of onset of straining, a veterinary examination is needed. The foal will need to be delivered within an hour. Dystocia is most often caused by abormal presentation with long foetal extremities predisposing the mare to problems with delivery. Examination of the birth canal and feotus is necessary to determine the cause of the dystocia. The foetus is particularly at risk from placental detachment, hypoxia and damage to the respiratory centre.

Answer 102

Primary uterine inertia - usualy due to voluntary suppression of foalig caused by disturbance. Cervix is partially ope. chorioallantois intact. Leave the mare alone for 20 minutes. Mare can have dilated cervix for 12 hours and foal normally. Important to remember that progress needs to be quick when mare on stage II. Can induce parturitio. Secondary uterine inertia - usually caused by foetal malpresetation. Failure of abdominal expulsive effort or obstruction of the birth canal. fetopelvic disproportion is rarely a problem in mares.

Answer 103

Transverse presetatio, uterine torsio, malposture of living foetus which cannot be corrected rapidly, oversized foetus, and maternal pelvic deformities. The time from induction of anaesthesia to foal removal s hould be less than 20 minutes. usual approach is by midline laparotomy. Until the foetus is removed general anaesthesia should be maintained in a light plane to avoid respiratory depression. The uterus is incised along its greater curvature. Uterine contents should be treated as contaminated and carefully drained to the outside. the live foal should be placed alongside the mare with the umbilical cord left intact. The use of a continuous interlocking suture through all the layers of the uterine wall and around the entire margin of the incision controls intraluminal haemorrhage - a significant cause of maternal mortality. The uterus is closed with invertig sutures taking care to exclude any placenta. Administer oxytocin if the placenta was not removed.

Answer 104

Klebsiella and pseudomonas are difficult to treat - often treated with combination of topoical washings with pevidine followed by drying and packing the penis with gentamicin cream or 1% silver nitrate daily for 1-2 weeks. collect serial swabs over several weeks for cultural examination to monitor success of treatment. taylorella is sensitive to most antibiotics and antiseptics. Wash penis daily for 3-5 with 2% chlorhexidine followed by topical application of nitrofurazone or penicillin ointment. can treat penis with broth culture of normal microflora at end of treatment.

Answer 105

Signs may vary from none at all to severe systemic illness including fever, depression, filling of the lower limbs, conjunctivitis with periorbital oedema, nasal discharge, urticarial rashes, and oedematous plaques and ventral oedema. Infected mares may abort 7-10 days later. Infection is via the respiratory or venereal route. virus localises in the accessory sex glands of stallion and 30% of infected stallions continue to shed the virus indefinetly. shedder stallions are always seropositive but not all seropositive stallions are shedders. Mares do not become carriers. seropositive mares with a stable or declining antibody titre are thought not to infect stallions or in contact animals.

Answer 106

Primary psychogenic polydipsia, PPID, Primary renal disease. Less common; pscyogenic salt consumption, diabtes insipidus, drug induced

Answer 107

Urinalysis very important. USG normal 1.020-1.050. Isothenuric 1.008-1.014. Hyposthenuric 75% loss of total tubular function. Protein levels: albumin may decrease with glomerular disease or tubular diseases. Electrolytes - sodium decrease, chloride decrease, calcium increase, phosphate decrease, potassium increase may. Glycaemic status: glucose, insulin and ACTH. Ideally done on resting sample after starving of concentrates for 12 hours for accurate interpretation.

Answer 108

Water deprivation tests - tests the ability of the kidneys to concentrate urine in the face of water deprivation. Complete water deprivation test involves taking all fluid sources away and measuring USG gravity over succeeding hours. Important to evaluate hydration status . Must check renal function before carrying this out : to omit this would be negligent and dangerous.ADH stimulation test - animals which fail to concentrate after both Water deprivation tests have diabetes insipidus - either central or nephrogenic. Aimals with central DI should rapidly concentrate urine when given ADH analogue.

Answer 109

Due to the overproduction of proopiomelanocortin (POMC) peptides from pars intermedia. (PI) . the resultant increase in adrenocorticotrophin levels, coupled with the possible potentiating effects of other POMC Peptides e.g endorphins, insulin like molecules on ACTH causes dysregulated cortisol secretion.

Answer 110

Hirsutism - increased cortisol may lead to increased androgen production from the adrenal glands. Hyperhidrosis due to hirsutism and effects of compression on thermoregulatio. Laminitis due to effects of glucocorticoids on metabolism, vascular function, skin function, bone function. Lethargy & poor demeanour, fat redistribution due to cortisol dysfunction, predisposition to infections, weight loss due to muscle wastage, PUPD due to hyperglycaemia (secondary diabetes mellitus), polyphagia blindness, seizures.

Answer 111

Demonstration of clinical signs described may be justification alone in making a diagnosis of ECD, particularly the pathognomonic sign of hirsutism. Other tests can be used including - basal glucose, basal insulin, basal cortisol (too poor sensitivity) and basal ACTH.

Answer 112

May be no need to provide specific medication to some cases of ECD. sensible conservation measures to manage ECD cases include those recommended for aged animals in genreal. Good attention should be paid to feeding, dentistry, anthelmintic regimes and the early detectio of clinical abnormalities. Clipping the excessively long haircoat may be advantageous. Regular farriery is paramount and horses or ponies should be monitored for signs of laminitis, chronic or acute. In the absence of chronic orthopaedic disease, continued exercise may be beneficial in enhancing insulin sensitivity and offsetting any effects of abnormal cortisol status. Cases of particular concern are those that have a history of laminitis or evidence of chronic laminitic changes in the feet. In these cases early therapy may be sensible. All cases with evidence of resting hyperglycaemia and signifcant increases in insulin should be treated as these have a poorer prognosiis long term without therapy.

Answer 113

reflex/upper motor neurone bladder, eg EHV-1 infection, EPM Paralytic/lower motor neurone bladder e.g polyeuritis equi, EHV1, trauma Non neurogenic (most common)- inflammatory/irritant e.g cystitis, urolithiasis, myogenic (detrusor atony leading to sabulous urolithiasis), neoplasia, ectopic ureter, breeding trauma, hypo oestrogenism.

Answer 114

Generally futile with the exception of EHV1, EPM infection and cystitis. Palliative care - drainage and flushing, washing and vaseline, antibiotics vs secondary cystitis. Some mares have responded to oestrogen, A adrenergic blockers: decrease urethral sphincter thus facilitating urination with UMN problems.. Parasympathomimetics; promote detrusor function.

Answer 115

The clinical signs associated with increased nitrogenous compounds in the blood stream: signs include anorexia, weight loss, bedraggled hair coat.

Answer 116

Azotaemia refers to the abnormal increase in biochemical parameters (urea creatinine and other non protein nitrogenous compounds) that occur in renal disease. This can be further defied in the following; pre renal azotaemia (decreased real perfusion), renal Azotaemia (acute/chronic renal failure), post renal azotaemia (obstructive disorders, uroperitoneum)

Answer 117

Acute tubuler necrosis; toxicity due to drugs: aminoglycosides, NSAIDS, polymixinB, pigments Hb, Mb, vitamins D and K3, heavy metals, acorns. Aminoglycosides accumulate in interstitial cells, NSAIDs cause papillary ecrosis, may affect vascular function, Vitamin D causes tissue mieralisation. Vascular: vasomotor nephrotpathy - dehydration, shock, hypotension, adverse drug reactions. Acute glomerulonephropathy: immune mediated e.g purpura haemorrhagica, bacterial mediated e.g strep E coli acute interstitial nephritis - unknown cause - adverse drug reactions. Primary bacterial - leptospirosis. - L interrogans pomona

Answer 118

Glomerular disease - proliferative glomerulonephritis, membranous glomerulonephritis, membrano proliferative glomerulonephritis. Disease affecting the glomeruli predominantly. types differ in histological changes. Probably immune mediated. Chronic interstitial nephritis - sequel to acute tubuler necrosis, vascular abnormalities and pyelonephritis. Histological changes to tubule cells and interstitial inflammatory cells predominate. End stage kidney disease - gross and histological severe changes comprising both tubular and glomerular disease - primary cause unidentifiable.

Answer 119

Fluid therapy - balanced fluids with regular monitoring of electrolyte status. care regarding over hydration and oedema formation. Monitor urination - if the hors remains oliguric within the first 24 hours of therapy then this must be addressed. Poor prognosis for these cases. Ideally creatinine should decrease by at least 30% in the first 24 hours of therapy, otherwise prognosis poor. animals which respond should be slowly weaned off fluid therapy but may need continued electrolyte supplementation at least in the short term.

Answer 120

Fluid therapy foor 24-48 hours to evaluate for response to therapy with decreases in creatinine. Identify any primary abnoralities and treat if possible e.g urinary stones, pyelonephritis. Dietary - correct any electrolyte or acid base abnormalities, small frequent varied meals encourage appetite. Avoid high calcium foodstuffs e.g alfalfa. Poor renal function leads to hypercalcaemia. Increase CHO intake e.g using oils, but maintain adequate protein. Anabolic steroids - may stimulate appetite. Blood ad plasma transfusions for anaemia and hypoalbuminaemia respectively. Horses with a plasma creatinine 400mol/l and a BUN <15:1 may have an acceptable existence for some months or even years.

Answer 121

Urethral tears - in geldings and stallions, quarter horses, at the end of urination. Cystitis/UTI/Urolithiasis - other clinical signs concurrent e.g stranguria, pollakiuria. Idiopathic renal haematuria - mostly arabs, sudden onset, observe blood from one/both ureters. Neoplasia - e bladder, urethra, penis, sheath. Drugs - NSAIDS Vaginal varicosities - mares, especially multiparous Exercise induced haematuria - usually microscopic, may see bladder lesions. Non urinary systemic disease - haemolysis, acute mypathiies, coagulopathy.

Answer 122

Differentiate haematuria from Hburia/ Mburia. Smal amounts of Rbcs will lead to scattered spots on the dipstick. microscopic evaluation may reveal numerous red cells. spin down urne and look for pellet of cells rather than discoloured urine. Separate glomerular from non glomerular bleeding - evaluate morphology of cells: numerous numbers of more variable appearance are noted in glomerular disease. Evaluate timing of haematuria; throughout urination; kidneys, ureters, bladder. Begiinning of urination; distal urethra. end of urination: proximal urethra and bladder neck.

Answer 123

Lice infestation with biting louse Damalinia equi and sucking louse haematopinus asini. Very common an cause pruritus scaling and alopecia. Often occurs in winter on poorly managed/congregated horses. Common in cushingoid horses. Diagnosis: demonstration of lice or ites. Treatment: insecticidal shampoos, sprays or powders usually containing pyrethrins or yrethroids. Two applications at 14 day intervals are usually sufficient.

Answer 124

Caused by chorioptes equi, primarily affects distal limbs of heavily feathered horses. Carrier horses with no clinical signs can perpetuate the infection. Infection spread by beddig, brushes, contact. Affected horses stamp and bite limbs. Scaling and exudation are present with secondary bacterial infections. Diagnosis: presence of mites in superficial scrapings. Treatment includes removal of hair and scabs combined with application of insecticides including permethrins and fipronil to affected horses ad in contacts. systemic ivermectin may be useful. Seleen shampoo can reduce pruritis.

Answer 125

T autumnalis (small orange/yellow coloured mites). Sucking mite -disease associated with nymphal form. Pruritus of head/legs of grazing horses in late summer/autumn. Diagnose with groomings. Treatment : topical insecticides.

Answer 126

Adult worms migrate from the small colon/rectum to lay eggs on the perianal skin causing pruritus/tail rubbing. Most modern anthelmintics are effective.

Answer 127

Seasonal dermatitis caused by onchocerca cervicalis microfilaria. Parasite 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. Causes alopeciia and scaling of the head, neck, withers, chest and ventral midline. Can be very pruitic. Severe focal dermatitis with pruritus and exudation may develop following the death of microfilaria in the skin after administration of avermectins. Diagnosis o clinical signs, poor worming history, seaso, response to ivermectin, biopsy may identify microfilaria.

Answer 128

Hypersensitivity to bites of culicoides spp midges. Generally common but not in foals. Usually gets progressively worse with age. Commonly affects the mane and tail but can affect the ventral abdomen too. clinical signs are seasonal. pruritus is always present and worst at dawn and dusk when midges are most active. aggressive rubbing causes self inflicted trauma. Clinical signs are often diagnostic. Biopsies, intradermal skin tests and ELISAS also available. Treatment includes; management of skin lesions, corticosteroids, immunotherapy/desensitisation treatment offered by a number of labs e.g greendale. Fly repellants e.g switch (permethrin), preventing midges biting, oil based liquids eg benzyl benzoate, stabling at daw and dusk, r ugs/hoods, insect proof stables with meshes, fans/winds, avoids river/water/woodlands.

Answer 129

Type 1 hypersensitivity reaction to a number of allergens. Causes extreme pruritus and secondary, self inflicted ski lesions. Diagnosis: exclusion of other differentials, skin biopsies generally non specific. Intradermal skin testing is useful but has limitations as requires availability of specific allergens and experienced personnel. Serum ELISA or RAST tests to specific allergens may be of use in diagnosis. Identification of an allergen may allow prevention of contact or hyposensitisation by immunotherapy. systemic corticosteroids are useful in the treatment of the condition.

Answer 130

Common syndrome with a complex immune mediated allergic aetiopathogenesis. Arises frmo injected drugs, ingestical chemicals or feeds, inhaled polles moulds and dust. Alternativley can arise from direct skin contact or mucous membrane contact. physical urticaria occurs without an immunological component. Clinical signs of wheals occur within variable time following the instigating factor. These typically pit on pressure but can be difficult to assess in smal lesions. Pruritus varies from mild to severe. Angio oedema is a subcutaneous form of urticaria which tnds to be more diffuse owing to lack of restraint of the spread of fluid preset in the subcutis. Diagnosis based on clinical signs but identification of the instigating factor can be challeging and unrewarding in isolated occurrences. Skin tests and serum ELISA or RAST tests may be useful in some cases. Treatment: initial attacks usually respond well to short courses of corticosteroids. Often a single dose of intravenous/intramuscular dexamethasone or oral prednisolone will relieve the clinical signs. Further investigations are warranted in recurrent cases. Identification of an allergen may allow prevention of contact or hyposensitisation by immunotherapy.

Answer 131

An autoimmune disease characterised by an exfoliate dermatitis. Results from a type 2 hypersensitivity due to autoantiboidies directed against the cel membrane of epidermal cells. clinical signs include vesicles, pustules, erythematous scaling, crusting commonly begins around the face and limbs. inflammation around the coronary band, ergot and chestnut is common. Lesions may be painful or pruritic. Systemic signs may include lethargy, inappetance, ventral oedema, pyrexia and weight loss. Treatment; high doses of corticosteroids. Attempts to reduce the dose are often unrewarding and result in deterioration of cases. it is likely that treatment will be lifelong.

Answer 132

Common skin infection caused by dermatophilus congolensis. Causes exudation, matter hairs and scabs in areas wetted by rain - primarily the back quarters. classic paint brush lesios. treatment includes antibiotics and clipping/soaking of the skin with chlorhexidine to remove exudates and scabs. Topical treatments including antibiotic ointments applied as necessary.

Answer 133

Commonly caused by trichophyton equium var equinum. Spores highly resistant and surive in stables/tack for years. infection relies on presence of spores and skin abrasion therefore common around the girth/saddle. Lessions appear as circular areas of erect hairs followed by alopecia and scaling. diagnosis: clinical signs, microscopy of a hair pluck/scrape and culture. Infected hairs do not fluoresce with woods lamp. Lesions resolve spontaneously over a number of weeks but treatment limits spread. Topical fungicidal treatments include enilconazole and natamycin. Sporocidal treatment of the environment is also important. Griseofulvin is of limited use and contra indicated in pregnant mares.

Answer 134

Caused by ingestion of seleniferous plants or by unnecessary or excessieve administration of supplements. Acute poisoning usually results from over supplementatio. cases present with lethargy, weakness, colic, diarrhoea, arrhythmias and dyspnoea. Chronic poisoning causes dramatc loss of mane and tail and thin fragile body hair. Lameness results from laminitis, hoof slippering and sloughing. Diagnosis based on history

Answer 135

congenital papillomatosis - papilloma virus has the ability to pass the mares placenta resulting inn viral papillomata on the skin of newborn foals. Treatments include ligation or surgical removal. Rarely, spontaneous resolution occurs. Viral papillomatosis - generally in horses under 3 years old, caused by equiie papilloma virus. Moderately ontagious by contact between co grazing horses. Lesions appear as small white-grey papules and can be present in huge numbers. Usually affects muzzle and lips but can be present on the yeelid, external genitalia ad limbs. usually spontaneously resolve in 3-4 moths. treatment often unecessary but ca include autogenous vaccines and surgery. Aural papillomas - clinically distinct syndrome caused by a papilloma vius. common i horses of all ages but rarely in animals less than 1 year. lesions begin as small Papules that coalesce into white hyperkeratotic plaques. occur on the inner surface of the pinnae.

Answer 136

Most common skin tumour of the horse. 6 types - occult, verrucose, nodular, mixed, fibroblastic, malevolant. Cause not fully understood but bovine papillomavirus widely accepted as having a role. Diagnosis usually based on clinical appearance and submission of photos via liverpools website. Rarely biopsied. Treatment; Benign neglct, Aw4- LUDES cream, surgery, ligation, BCG injection, several other topical medications.

Answer 137

Melanin pigment depots are common in the linings of the guttoral pouches and on the mucosae. Melanomas are benign tumours of melanocytes and generally cause disruption by space occupying bulk. Melanomas are largely limited to grey horses and are common around the periineum, sheath, parotid region and less commonly in the guttoral pouch, eyelids, lips and iris. Melanosarcomas are rapidly invasive and metastasise but are rare. Diagnosis can oten be made on clinical appearance. FNAC or biopsy if necessary. Treatment options include esurgical excision or cryosurgery, cytotoxic drugs - intralesional cisplatin. Other: cimetidine orally.

Answer 138

cutaneous cysts, most commonly found on the dorsal midline. congenital or hereditary lesions affecting young horses. contain soft cheese like material and sometimes coiled hairs.

Answer 139

An ulcerating cutaneous granulating nodule or wound caused by the larvae of habronema muscae, habronema majus and drachia megastoma. Disease has several forms; opthalmic habronemiasis - presence of yellow granules in conjunctivae and nasolacrimal duct. Cutaneous habronemiasis - larvae penetrate wet area of the face e.g secondary to epiphora, granulating wounds and the urethral process. Diagnosis usually made on impression smears and washes. Treamte: oral/topical ivermectin, surgical removal and control of muscid flies.

Answer 140

Digestion of chlorophyl produces a potent phtodynamic agent, phylloerythrin, which is normally detoxified and excreted by the liver. Liver failure allows the substance to pass into the bloodstream unchanged and it accumulates in the skin. Severe damage to the skin is common.

Answer 141

Dermatophilus congolesis. (same agent as rainscald). Causes exudation, scabs ad matting of hair of distal limbs. Diagnosis can be made on examination fo a smear. mixed infections with staphylococcus and streptococcus are common. Treatmet with antibiotics, anti inflammatories and soaking of the skin with chlorhexidine to remove exudates and scabs. May require clipping of hair. skin should be dried and topical treatments including antibiotic ointments applied. Fuciderm and flamazine are useful. Bandaging not always helpful as it may promote moistness of skin.

Answer 142

A skin condition of the unpigmented distal limb. Aetiopathogenesis uncertain but IgG and C3 portion of complement have been detecetd by direct immunofluorescence in vessel walls. unpigmented ski involvement suggests role of UV light, although this condition is not thought to be true photosensitisation. Treatmet: lipping hair and removal of exudates and scabs with c hlorhexiine. topical antiseptics, antibiotics, corticosteroids and sunblock may be useful. Consider leg wraps if horse turned out in sun and systemic corticosteroids may be necessary in some cases.

Answer 143

Idiopathic /immune mediated defect in cornification of coronary bands. All four hooves show hyperkeratotic changes. The ergots and chestnuts may be involved. Lesions may crack and fissue, bleed and ooze serum.

Answer 144

Inflammation of the cutaneous lymphatics usually but not always secondary to a bacterial infection obtained via a small cut/abrasion. Affects hindlimbs more commonly than forelimbs. USually causes marked swelling of the limb 2-3 times normal size, lameness and serum exudation. Treatment - antibiotics based on culture results, NSAIDS/corticosteroids, Potassium iodide and diuretics. Hydrotherapy, cleaning with antimicrobials, leg wraps and gentle exercise may be beneficial. Ulcerative lymphangitis is commonly associated with corynebacterium paratuberculosis, staphylococcal spp and streptococcal sp infections. Can result in nodules which may ulcerate, abscess-ate and drain pus. If fibrosis occurs, disfigurement may be permanent. Chronic lymphatic nodules can potentially be removed.

Answer 145

Wound infection that rapidly spreads along tissue planes. Caused by a number of bacteria. commonly affects the limbs. Causes acute painful swelling, inappetance ad pyrexia. Treatment - antibiotics based on culture results and NSAIDs. Hydrotherapy, cleaning with antimicrobials and gentle exercise may be beneficial.

Answer 146

An inflammatory reaction involving blood vessel walls. Commonly immune mediated involving type 1 and type 3 reactions. Can result from various infections or the administration of drugs. Causes oedema, necrosis and ulceration of lower limbs and mucosae. Treatment includes corticosteroids & antibiotics and symptomatic treatments.

Answer 147

An immune mediated vasculitis associated with recovery of an upper respiratory tract infection most commonly caused by M protein antigen of streptococcus equi subsp equi. immune complexes deposited in the walls of peripheral blood vessels increase vascular permeability and cause oedema, primarily of the limbs. Serum exudation and skin erosions can be marked. Petechial or ecchymotic haemorrhages can occur in the skin and mucosae. Pulmonary and cerebral oedema can develop in most severe cases. Signs usually occur 2-4 weeks after respiratory infection. horses are depressed, inappetent and reluctant to mvoe. diagnosis can be confirmed with biopsies. Treatment is with systemic corticosteroids and antibiotics, hosing limbs, gentle exercise and leg wraps.

Answer 148

Good - vulval lips are vertical, 80-90 degrees is normal. lips are closely apposed making a good seal. >80Vulvar lips below level of ischium. Fair - vulval lips are inclined 50% vulval commisure is above the bony brim with a sunken anus.

Answer 149

It is relaxed in oestrus, turgid in dioestrus. Made or aged mares may not relax fully in oestrus.

Answer 150

Beta haemolytic streptococci E Coli Other enteroobacter Less common; Pseudomonas auruginosa, klebsiella pneumoniae

Answer 151

Using a small volume uterine flush. 60ml of sterile isotonic saline flushed into the uterus then aspirated. this is then centrifuged and placed onto a slide. using a double guarded swab, which is then rolled onto a slide. it is possible to use the swab also for endometrial culture if the slide is sterile. using a plastic disposable cup to scrape the surface of the endometrium. Stain with Diff quik. Look for sheets of epithelial cells to confirm an adequate sample has bee taken. the presence of neutrophils indicates endometritis. It is not possible to assess stage of cycle using cytology in the mare.

Answer 152

Endometritis, periglandular fibrosis, cystic glandular distension.

Answer 153

Granulosa cell tumour most common, adenocarcinoma/adenoma also reported. Hormones produced by the tumour may cause behavioural changes including stallion like behaviour. normal regular cycling will be altered/cease. Palpation and ultrasonography of an abnormally enlarged ovary with a atrophied contralateral ovary. Negative feedback by the secretion of inhibin on the hypothalamus and pituitary cause regression of the opposite ovary to a small i inactive structure. Ovulation fossa of affected ovary obliterated. Treatment- unilateral ovarioectomy - used to be doe trans vaginal colpectomy but now usually done laparoscopically. May take up to a year for other ovary to regain function but fertility should be normal.

Answer 154

Follicle matures as normal but then fails to ovulate filling with blood and usually eventually developing luteal tissue. May be refractory to prostaglandins for several days or weeks, preventing mare from coming back into season.

Answer 155

Pregnancy, Silent heat - cycle progresses as normal but mare does not show signs of oestrus. Failure of luteal regression: PGF2a from uterus fails to cause luteolysis at day 15. Early embryonic loss: mare conceives but embryo lost before first scan takes place. Dioestrus ovulation: occasionally ovulation takes place i mid Dioestrus during mini wave of follicles, Cl formed too late to b elysed by PGF2a at day 15.

Answer 156

Spring/autumn transitional period - mare develops follicles but they do not ovulate. may last for 2-6 weeks. In scotland about 50% of mares will still be in transitional stage in april. GCT - oestrus is a rare clinical sign of GCT - due to the absence of the hormone aromatase. without this hormone, oestrogen cannot be produced from androgens.

Answer 157

Refers to non inflammatory chronic pathology of the endometrium. Incidence increases with age. Commonly associated with endometritis as reduces resistance to infection. Diagnosed by endometrial biopsy. Decreases ability to conceive and carry a foal to term. No effective treatment available. Histopathological changes include periglandular fibrosis: fibrotic changes surrounding uterine glands, lymphatic lacunae - poor myometrial activity fails to pump the lymph fluid a normal and lacunae develop.

Answer 158

Inflammation of the endometrium. probably most common cause of sub fertility in the mare. can be divided into 3 general types; Veneral disease - sexually transmitted diseases such as contagious equine metritis Chronic uterie infection Persistent mating induced edometritis - a prolonged excessive reaction to mating.

Answer 159

Caused by taylorella equigenitalis. A gram negative microaerophilic coccobacillus. Venereal transmission and contaminated equipment and handling spread. Organism persists in clitoral sinus of carrier mares. clinical signs and pathology - severe endometritis, necrosis and shedding of the epithelial lining of the uterus. Profuse, watery , mucopurulent, o clumping discharge from uterus. Short oestrus cycle (8-12 days). Stallions are inapparent carriers (just have surface contamination). Diagnosis by isolation of taylorella equigenitalis from reproductive tract. culture system chocolate agar with increased Co2. approved laboratories only certified to test for this. Treatment - many cases recover spontaneously but carrier status must be assessed. some fail to recover despite treatment. Some require treatment - uterine infusion for several days with antibiotics. topical wash of clitoral fossa with 2% chlorhexidine. Pack external genitals with nitrofurazone or chlorhexidine ointment. clitoral infections can be hard to treat - consider clitorectomy/sinusectomy in very difficult cases.

Answer 160

Normal resistat mares are able to clear bacteria from the uterus quickly. susceptible mares have decreased uterine resistance and remain persistently infected after bacteria are introduced into the uterus. may be due to failure of uterine contractility or uterine immune defence mechanisms. Failure in the 3 seals (vulval lips, vestibulovaginal junction, cervix) will also allow infection to gain access to uterus. Infection is introduced by pneumovagina, urovagina, parturition, copulation, veterinary procedures. Possible causative organisms include beta haemolytic streptococci, E. coli, pseudomonas aeruginosa, klebsiella pneumonia yeasts, gunfi. Clinical signs include discharge from vulva/uterus, fluid in uterus on ultrasound, but these visual clinical signs can be absent so consider if failing to conceive. May have a shorter dioestrus period than the 15 days usually expected. Diagnosis - culture of uterine swabs, histolorigcal or cytological changes.

Answer 161

Short cycle mare with PGF2 - to bring into oestrus - oestrogens have positive effect on uterine immune defence mechanisms. Administer oxytocin IV or IM. Lavage uterus with 0.5-11 sterile hartmanns solution or saline to manually remove contamination. Infuse uterus with appropriate antibiotics such as neomycin/penicillin, framomycin or ceftiofur. Correct any predisposig conformational abnormalities e.g caslicks vulvoplasty. Maintain good hygiene during examinations and breeding. use AI if possible.

Answer 162

All mares will h ave an immunological reaction to semen and produce uterine fluid but normal mares will expel/absorb this fluid at the same rate as it is produced. free intra uterine fluid accumulates and clinical signs and diagnosis as are for CUI. treatment involves oxytocin, flushing and antibiotics but must be started after sperm have reached the oviduct and before the fertilised ovum descends into the uterus.

Answer 163

Pneumovagina; air in vagina with or without faecal contamination. Aetiology - poor vulvar and perineal conformation. Thin flaccid gaped vulvar lips. Urovagina - accumulation of urine in the vagina due to poor perineal conformation, relaxed ligaments or extreme weight loss.

Answer 164

Artificial control of photoperiod - provide natural or artificial light from 8am to 10pm. Start at end of december to initiate transitional period by end of february. Transitional breeding season lasts 30-40 days. Waves of follicles develop and regress without ovulating, giving prolonged ad irregular periods of oestrus acivity. The end of transition is marked by an LH surge a oulation. Onset of normal cyclicity may be hastened by alrenogest orally for 10-15 days (a synthetic progesterone), human chorionic gonadotrophin IV, exogenous GnRH - deslorelin implant or twice daily injections of buserelin.

Answer 165

Traditionally bred on day 2 or 3 of oestrus then every other day until the end of oestrus. Mares should be bred prior to ovulation when a dominant follicle is present. >30mm. If it is necessary to limit the number of breedings, the ovaries should be palpated daily and breeding should take place just prior to ovulation.

Answer 166

Progestogens; synthetic oral solution. Oestrus occurs 4-5 days after withdrawal. Prostaglandin F2 - used to lyse a CL allowing a mare to return to oestrus 2-5 ays later. CL must be between 5 and 14 ays old to respond. ovulation is variable depending on follicular development at time of treaetment. OEstradiol: not available in the UK. Human chorionic gonadotrophin - LH like activity can hasten ovulation of a mature follicle. GnRH - buserelin - given to cause ovulation of a mature follicle, use IM 6 hours before service, ovulatio is expected within 24 hours. Deslorelin is a GnRH analogue which induces ovulation of a 3mm follicle in 36 hours

Answer 167

Acute trauma - usually a kick from a mare/field companion. Use anti inflammatory measures urgently (icepack, NSAIDS, antibiotics, gentle massage). Intrascortal haemorrhage will lead to permanent testicular damage due to the insulating properties of the resultant fibrous tissue. surgical removal of the organised blood clot or hemi castration can be performed in an attempt to save the unaffected testis. Hydrocoele - abnormal collection of fluid between visceral/parietal vaginal tunics. usually not painful. can accompany scrotal oedema. May self resolve especially with gentle exercise, could be drained if not resolving and if unilateral and persistent, remove affected testis ad tunics to save contralateral testis from heat induced degeneration. Haematocoele - usually following trauma - treat as trauma/hydrocele. Scrotal oedema - may be due to local trauma or systemic disease e.g hypoalbuminaemia - treat underlying condition.

Answer 168

Old age, excess heat, trauma, toxins, anabolic steroid use, radiation exposure. Degeneration may be reversible but may take several months for semen to return to normal. Treatment with GnrH has been tried but remains controversial. because it takes approximately 60 days from development of sperm from spermatogonia until ejaculation it is possible for acute testicular degeneration to be present and yet the ejaculate can be fairly satisfactory. may take 2-6 weeks for infertility to become apparent.

Answer 169

Usually greater than 270 degree to stop blood flow. if only 180 degrees is a developmental abnormality which does not affect fertility. Diagnosis: presents as acute colic. Affected testicle may be enlarged and hot or cold depending on duration. surgery required.

Answer 170

Affected testis is hot, swollen, tense and acutely panfu. Fever and scrotal oedema are common. stiffened hindlimb gait. followed by ischaemic necrosis and abscess formation. Adhesions commonly develop. Treatment: antibiotics, NSAIDs,hydrotherapy, prompt removal of a unilaterally affected testis may save the contralateral testis.

Answer 171

IF >3years of age or a donkey do an hcg stimulation test (basal blood asmple, administer hcg iv, 2nd blood sample after 30-60 mins - look for elevation in testosterone. if >3 years of age, do oestrone suphate assay. Treatment: removal by laparotomy/laparoscopy.

Answer 172

After phenothiazine or other sedative use, following preputial trauma, with chronic grass sickness/botulism. Impairs venous and lymphatic drainage. within hours penis and prepuce become oedematous. if left untreated cellulitis, necrosis, gangrene can develop requiring removal of the penis. Support the penis maually. reduce oedema - hydroterhapy, NSAIDS, diuretics, massage.

Answer 173

Often follows kick from a mare at breeding. Misuse of artificial vagina equipment can cause hamatoma. Haemorrhage from superficial vessels in dorsum of peniis. rapid swelling. can result in paraphimosis. treat as for paraphimosis.

Answer 174

balanitis - inflammation of the glans penis Posthitis - inflammation of the prepuce Uncommon in the stallion the preputial cavity contains a wide variety of microorganisms. Trauma can allow introduction of infection into deeper tissues. results in swelling, iflammation, pain and preputial discharge.

Answer 175

Caused by EHV3 - pox like lesions on the penis. venereally transmited. Self limiting. Complete resolution takes 3-5 weeks.

Answer 176

utritio - too thin or too fat Systemic diseases Age Mangement- harsh handling, poor restraint of mount animal, improper footing, mount animal not in oestrus or wrong height, AV too hot or too cold, low ceilig, overuse. Psychic factors: can result from a previous painful experiece, overuse, excessive discipline. Musculoskeletal - especially fi it involves the hindquarters eg spavin. hormonal factors: impotent stallions tend to have lower blood concentrations of LH and oestradiol whereas concentrations of testosterone are normal.

Answer 177

Often presents as stallion with good libido and normal copulatory behaviour. May appear to ejaculate but does not. may ejaculate after several breeding attempts. Causes; psychogenic (may try diazepam), damage to the dorsal nerve of the peis, malfunction of the ANs, blocked ejaculatory ducts, retrograde ejaculation (semen> bladder).

Answer 178

``` Primary; Head/acrosome defects bent mi pieces proximal cytoplasmic droplets tail stump defects Secondary; distal cytoplasmic droplets Kinked tails Tertiary; Detached heads, Kinked tails ``` Haemospermia may be secondary to infection of the tract, trauma, neoplasia or bladder calculi. Urospermia - urination during ejaculation, aetiology unknown

Answer 179

Mares can be bred by stallioins which would otherwise be geographically inaccesible. mares and foals not subjected to transport stress. mares can remain in work. mares owners save on transport costs. no risk of trauma to mare or stallion from each other. Lower risk of disease transmission. BUT more expensive, success rates may be lower than with natural service, more veterinary intervention.

Answer 180

Inseminate mare within 24 hours prior to ovulation. post ovulation inseminations result in lower pregnancy rates and higher rates of early embryonic loss. Scan mare daily until dominant follicle reaches 35-40mm.

Answer 181

Examine mare daily as for chilled AI but use deslorelin implant as induction agent to give a shorter likely ovulation interval. If implanted at 6pm, should ovulate the next but one day between 8am -12pm. Inseminate within 6 hours of ovulation. before or after is fine but because predicting ovulation time is very difficult, insemination usually takes place when CH seen. Scan mare at least 4 hours after AI and on day following insemination to ensure CH present, no free fluid preset.

Answer 182

``` Day 11- 1cm vesicle day 15 - 1.5cm vesicle day 17 - implantation Day 21 - embryo appears ventrally day 24- heartbeat seen day 35- eCG produced day 60-70 - sexing possible ```

Answer 183

Leaing infetious cause of abortion in mares in the UK. the virus is transmitted via the respiratory tract. repeated exposure leaves horses immune to respiratory disease but susceptible to reinfection causing abortion. usually occurs between 5 months of gestation and term. Usually only a few infected mares in a herd abort. abortion occurs 1-4 months after infection. Fresh foetuses expelled often within placental membranes. foals affected near term are viraemic, weak and die shortly after birth. Treat all abortions as possible EHV abortion. Vaccinate at 3,5,7,9 moths of gestation to prevent.

Answer 184

Causes severe systemic illness in dam which may be followed by abortion 7-10 days later. from 3 months to late pregnancy. typically presents with fever, lethargy, depression, conjunctivitis, nasal discharge, urticarial rashes, oedema. Infection is via the respiratory or venereal route. Virus localises in accessory glands. 30% of infected stallions continue to shed virus after resolution of clinical signs. shedding stallions play a major role in disease transmission. Shedder stallions are always seropositive but not all seropositive stallions are shedders. Mares do not become carriers but 90% of mares become infected after breeding with a shedder stallion.

Answer 185

Foetus is usually small and emaciated. near term premature foals with mycotic placentitis have a good chance of survivinng. Grossly the placenta and foetus are similar in appearance to bacterial causes of abortion although microscopically there are abundant fungal hyphae. Aspergillus is the most frequently encountered fungus.

Answer 186

Occurs by 6-10 days post partum. little tissue is lost at parturition therefore vaginal discharge is scant. excessive discharge may be a sign of uterine infection.

Answer 187

This is an emergency. treatment should be initiated if the placenta is retained more than 3 hours. Mares are likely to be less fertile at foal heat. Use oxytocin IV or IM every 15 mins. repeat as necessary. if retention is prolonged >8 hours - beware of sequelae including laminitis and endometritis. Use more aggressive therapy including anti inflammatories, broad spectrum antibiotics, exercise. Alternatively the allantochorion space may be infused with 10-12 litres dilute povidone iodine or saline. the opening in the foetal membranes is tied shut. the distension of the reproductive tract stimulates uterine contractions via oxytocin release ad the membranes are usually passed within 30 minutes.

Answer 188

Different laboratories - use reference intervals from lab that performed analyses. breed - significant differences in haematological parameters between hot blooded and cold blooded horses. age - important differences between neonates and adults. Factors that influence results and interpretation include - sample collection e.g collection tubes/anticoagulant. Sample handling e.g time delays/inappropriate temperatures (glycolysis, haemolysis) phsyiological factors - excitement/stress,exercise, dehydration.

Answer 189

Usually reflected by changes in PCV and plasma protein. increased PCV and normal plasma protein concentration - frequently seen in acute colitis (dehydraiton and protein loss).

Answer 190

Serum sodium concentration - function of exchangeable cation content (exchangeable in ECF and exchangeable K in ICF) relative to total body water. Changes in Sodium reflect changes in water balance. hyponatraemia - relative water excess. Hypernatraemia - relative water deficit. Still possible to have normal Na in the face of significant sodium loss if isotonic dehydration i.e loss of Na and Water. Hyponatraemia may be seen with sweating, diarrhoea, blood loss, excessive gastric reflux, third space sequestration. Hypernatraemia - pure water loss (deprivation), water loss exceedig electrolyte loss (some cases of diarrhoea, diabetes insipidus).

Answer 191

Affected by factors that alter internal balance (distribution of K between ECF and ICF) or External balance (k intake and output). Can have a major effect on cell membrane potential. Difficult to assess accurately as vast majority is intracellular therefore not measured. Hypokalaemia - diarrhoea, third space sequestration, dietary deficiency, altered internal balance. Hyperkalaemia - false hyperkalaemia eg in vitro haemolysis, altered external balance, hypovolaemia - acute renal failure, altered internal balance - metabolic acidosis.

Answer 192

Maintained within a narrow range by adjustments to intestinal absorption, renal excretion, mobilisation from bone stores. Serum Calcium exists as ionised, complexed, or protein bound. Acid base status influences protein binding (alkalosis increases protein binding - reduces ionised calcium/acidosis reduces protein binding ). Hypocalcaemia due to acute renal fialure, exhaustive disease syndrome, transit, periparturient/lactation. Hypercalcaemia - chronic renal failure especially on high calcium diet, hypervitaminosis D, hyperparathyroidism, pseudohyperparathyroidism.

Answer 193

Hypovolaemia, acute colitis, bowel strangulation, exercise above anaerobic threshold. associated with decreased pH, increased H+ ions, primary - decreased HCO3.

Answer 194

Gastric reflux, excessive sweating, prolonged excessive salivary losses. associated with increased pH, decreased H+, primary - increased HC03

Answer 195

e.g primary upper/lower airway disease, decreased effective alveolar ventilation. associated with: decreased pH, increased H+, primary - increased PCO2.

Answer 196

Eg hyperventilation - stimulated by hypoxaemia, fear, pain, excitemet. Associated with increased pH, decreased H+, primary - decreased PCO2.

Answer 197

An approximation of unmeasured anions - proteins, suphate, phosphate, lactate. Normally 12-16. Decreased AG - hypoproteinaemia, Hyperchloraemic metabolic acidosis. Increased AG - lactic acidosis, anaerobic exercise, grain overload, hypovolaemia.

Answer 198

A Hepatocellular derived enzyme, liver specific, indicative of Hepatocellular damage. Short half life. Persistent elevation indicative of ongoing damage.

Answer 199

A marker of Hepatobiliary disorders and cholestasis. highest activity in periportal region of liver, pancreas renal tubular cells - released into filtrate not blood. normal range - higher in donkeys c.f horses. Elevations reported i thoroughbred racehorses in training. longer half life than GLDH.

Answer 200

High concentrations in skeletal and cardiac muscle, liver, kdiney, erythrocytes. a on specific indicator of tissue damage c.f CK, GLDH, long half life elevations remain for up to 10 days post liver damage.

Answer 201

A marker of intra or extra hepatic obstruction of biliary system. also released from bone, intestine, and neutrophils. used mainly for evaluating the liver damage and biliary stasis. along with GGt.

Answer 202

A specific indicator of skeletal muscle damage. Seen in exertional rhabdomyolysis, recumbency, intramuscular injections, short half life (persistent elevation indicative of ongoing damage.) Usually evaluated along with AST and lactate dehydrogenase to monitor chronicity of skeletal muscle damage.

Answer 203

A breakdown product of heme component of haemoglobin. exists in 2 forms - uncongugated and congugated. Elevations with haemolysis, liver disease (both conjugated and unconjugated), if >25% total = conjugated - suggestive of biliary obstruction.

Answer 204

Hypoglycaemia - fasting in neonates, septicaemia, endotoxaemia, hyperlipaemia Hyperglycaemia - physiological - stress, excitement, endotoxaemia, cushings disease.

Answer 205

Derived from skeletal muscle. when released - distributed throughout body water and not reused. excreted by kidneys (glomerular filtration). elevations in prerenal azotaemia, reverses with fluid therapy/rehydration, high urine:plasma creatinine ratio. Renal azotaemia (comprised renal function). Post real azotaemia (urolithiasis, bladder rupture). Marked and transient elevations observed in newborn foals with normal renal function.

Answer 206

Distributed throughout the body water and not reused, excreted by the kidneys by glomerular filtration. Elevations in prerenal azotaemia, reverses with fluid therapy/rehydration. high urine: plasma creatinine ratio. Renal azotaemia (compromised renal function). Post renal azotaemia (urolithiasis, bladder rupture)

Answer 207

Pahyperprotinaemia - loss of blood fluid component with dehydration Hyperglobuinaemia - most common cause increase in gamma globulins. chronic antigen stimulation often associated with a reduction in albumin synthesis.

Answer 208

Hypoalbuminaemia - decreased production rare with equine liver disease. increased breakdown with increased metabolic demands, chronic antigenic stimulatio, increased loss with gastrointestinal and renal. Panhypoproteinaemia with acute protein losing colitis or acute blood loss.

Answer 209

Anaemia - decreased PCV and RBC count, due to blood loss, increased RBC destruction or inadequate RBC production. Mean cell volume - increase suggests regenerative, decrease suggests iron deficiecy. Mean cell haemoglobin - increase may suggest haemolysis, decrease may suggest iron deficiency. absolute - due to increased erythropoietin, appropriate eg chronic hypoxia at high altitude or innapropriate due to renal neoplasia - rare. Relative - dehydration, splenic contractio.

Answer 210

Adrenaline mediated - stress, excitement. increased blood pressure and splenic contraction> increased lymphocytes, increased neutrophils. Corticosteroid mediated - neutrophilia, lymphopaenia.

Answer 211

Inflammation, bacterial infection, may be associated with a left shift (regenerative left shift = immature neutrophil release into circulation in face of neutrophilia)

Answer 212

Decreased production - very rare. Increased consumption - large surface area inflammation eg colitis. Increased margination - endotoxaemia. May be associated with a left shift (degenerative left shift - immature neutrophil numbers exceed mature neutrophil numbers). some viral diseases may cause neutropaenia eg EHV1, equine influenza.

Answer 213

Indicator of renal function. normal animals can dilute urine to 1.050. normal range = 1.020-1.050. Failure to concentrate urine in response to dehydration is an indication of altered renal function eg primary renal disease, diabetes insipidus, medullary washout. atleast 50% renal function must remain to produce highly concentrated urine. Isosthenuric urine in face of varied hydration status = renal function reduced to less than 1/3 normal. pH normally usually 7-9.

Answer 214

Presence may indicate glomerular loss or urinary tract infection - if associated with increase leukocytes and bacteria.

Answer 215

Cushings disease, glucocorticoids, adrenaline. glucosuria without hyperglycaemia suggests renal tubular disease.

Answer 216

Accumulations of protein and cellular material that form in renal tubules in the face of tubular damage. Very fragile - therefore may not be seen in stored or non refrigerated urine.

Answer 217

1) musculoskeletal problems, 2) conditions of the respiratory tract 3) lack of fitness 4) owners unrealistic expectations of ability 5) inappropriate training 6) cardiovascular abnormalities

Answer 218

It is re entrant rythmn initiated by a premature atrial contraction and maintained as a result of the horses large atrial mass and high vagal tone. It may be caused by atrial dilatation secondary to valvular dysfunction or there may be no obvious underlying pathology. Large horses are predisposed to the development of atrial fibrillation due to their large atrial size. Atrial fibrillation can develop secondary to electrolyte abnormalities or medical conditions eg peritonitis. it may be also associated with the administration of alpha 2 agonist drugs which increase vagal tone. on ECG - irregularly irregular rhthmn, no p waves, fluctuating iso electric line, f waves which may be coarse or fine. anti arrhthymic drug - quinidine sulphate.

Answer 219

Premature systoles may be atrial or ventricular in origin. The underlyig aetiology is often difficult to identify. Premature systoles may be associated with hypoxia, myocardial disease, electrolyte and metabolic disturbances, elevated sympathetic tone, fever, and toxaemia. When all non cardiac causes have been ruled out, a primary myocardial lesion must be suspected. Atrial premature systoles are detected fairly frequently in horses in training and affect performance only if they produce excessive heart rates during exercise. more commonly the premature excitatory focus is over ridden as sinus nodal rate increases and the etra systoles disappear. May predispose to atrial fibrillation. Premature atrial systoles - the ECG trace shows P waves which occur earlier tha expected from the underlying P-P interval. with Premature ventricular systoles - the premature QRS complexes may have a wide bizarre configuration as ventricular depolarisation does not follow normal conduction pathways.

Answer 220

Usually specific anti arrhythmic treatment is not indicated as the premature beats are usually too infrequent to significantly affect cardiac output at rest. however it is important to establish what happens to heart rhythm during exercise.

Answer 221

common and may be of no clinical significance but if maintained during exercise, cardiac output will be inadequate and performance will be limited. abnormalities include third and second degree AV block and sinus block. Sinus block and AV block are normal findings therefore diagnosis of abnormality is based on ECG evidence of an inappropriate heart rate response during exercise. pathological second degree AV block and profound sinus bradycardia occur rarely in horses. Third degree AV block indicates total block in conduction at the AV node and is always a pathological finding, thought to be associated with inflammation or degeneration of the AV node.

Answer 222

Teh commonest cause of heart failure in horses, however a murmur of MR is often detected as an incidental fiding during a clinical examination. It may develop in response to the training induced eccentric hypertrophy and increased blood volume. In these cases, the degree of regurgitation is usually mild, the murmur is localised and low grade, 1-3/6 and may be crescendo in nature suggestive of mitral prolapse. On echocardiographic and post mortem examination the mitral valve appears grossly ormal. this type of condition does not progress and the murmur may disappear if the horse retires from active work. IF the regurgitant fraction is small, the heart compensates for the abnormal flow and athletic performance is not significantly affected. Mitral regurgitation can also occur in response to thickening and fibrosis of the valve leaflets. this is thought to be a progressive condition albeit the progerssio is often very slow. Mitral regurgitation will also develop as a result of rupture of one or more chordae tindenae. Mitral regurgitation will occur secondary to any other condition that causes dilation of the valve annulus e.g secondary to cardiomyopathy, aortic insufficiency and ventricular septal defects. The progression and severity will depend on the degree of regurgitation and progression of the underlying condition. Mitral regurgitation may also occur as a result of congenital dysplasia of ay part of the mitral valve apparatus. Mitral regurgitation may also occur as a result of congenital dysplasia of any of the mitral valve apparatus. Infective endocarditis occurs rarely. there is no pathognomonic sign of endocarditis and therefore diagnosis is difficult.

Answer 223

further diagnostic tests are often carried out if the murmur is clearly audible and present throughout systole to further evaluate the cause of the regurgitation before advising on the suitability of the horse. this often gives the client baseline information against which future progression can be assessed. this can be of value if the client is likely to want to sell the horse. this horse would likely be excluded from loss of use insurance policies as MR may cause atrial enlargement, predispose to atrial fibrillation or may progress to cause cardiac failure. Mitral regurgitation would not increase the risk of sudden death so this should not be an exclusion criterion.

Answer 224

ot associated with thickening of the valve leaflets tends not to progress and if mild/moderate will not affect racing performance. Tricuspid regurgitation does not normally result in cardiac failure although very occasionally primary right sided cardiac failure can occur. Tricuspid regurgitation will develop as a result of pulmonary hypertension caused by a left ventricular failure. If the murmur is nto associated with thickening of the tricuspid leaflets it is ulikely to progress and is unlikely to affect performance. If however a hrose has a high grade band shaped murmur the very rare possibility of primary valvular disease could not be ruled out by auscultation and therefore further diagnostic tests may be neccessary to confirm normal vlave structure before advising on the suitability of the horse. the presence of a murmur may affect resale value. this horse would likely be excluded from loss of use insurance policies as theoretically this may cause atrial enlargement and predispose to atrial fibrillatio. Tricuspid regurgitation would not increase the risk of sudden cardiac death and so this should not be an exclusion criterion.

Answer 225

Progressive disease associated with thickening and fibrosis of the aortic valve leaflets. more common in horses over 01 years of age tends to progress very slowly and in older horses rarely affects performance. aortic insufficiency causes volume oveerload of the left ventricle resulting in dilatation. this occurs gradually over years and may ultimately lead to mitral regurgitation, due to dilatatio of the mitral orifice. MR may then result in cardiac failure. when severe aortic insufficiency is present in a young horse this is likely to be due to dilatation of the aortic root or another cause of early degeneration e.g congenital abnormality of the vale or association with a ventricular septal defect. The preogression of this condition is difficult to predict in young horses and therefore in most cases these animals cannot be considered suitable for ridden work. Horses with dilated ventricles are at increased risk of sudden cardiac death. horses will require regular expensive monitoring if they are to be kept in work. Insurance companies are likely to exclude the heart from both loss of use and sudden death policies. in old horses progession is usually slow. Horses with very low grade localised murmurs could be considered to be suitable for purchase in some cases, although old horses are thought to have an increased risk of sudden death, unrelated to aortic valve disease.

Answer 226

The significance of the condition very much depends on the size of the defect. if the defect is small and is restrictive to blood flow, animals will grow and perform normally. if the defect is large, left ventricular volume overload and cardiac failure will occur. small restrictive defects will not affect performance. large defects are not compatible with life. congenital abnormalities are usually diagnosed in young animals as minor defects may not affect performance they may only become apparent in later life eg during pre purchase examination. In horses- septal deects are usually located in the membranous septum below the aortic and tricuspid valves. they are most commonly found in shetland and welsh mountain ponies. in some cases small defects in the membranous septum can cause distortion of the aortic valve leaflets and result in aortic insufficiency. Less commoly defects are located in the muscular part of the septum. defects int his position can be large and most often occur in arabian or TB breeds. when defects are large the pressure in the right ventricle approaches or equals that of the left ventricle. In these cases there may be little flow across the defect and no audible murmur. valid insurance exclusions include any liability from atrial fibrillation and congestive heart failure but should not include sudden cardiac death.

Answer 227

Musculoskeletal problems, conditions of the respiratory tract, lack of fitness, owners unrealistic expectations of ability, inappropriate training, cardiovascular abnormalities or others (medical, neurological).

Answer 228

Count respiratory rate. tachypnoea will be present in horses with pulmonary oedema caused by pulmonary venous hypertension as a result of left sided cardiac failure. Observe respiratory rythm/effort, will be increased with pulmonary oedema. Observe nares. in horses in congestive left sided failure, rarely a white frothy bilateral discharge may appear at the nostrils. This may only have been present at the onset of the condition therefore carefully question the owners. commonly horses will swallow oedema fluid and a nasal discharge will not be obvious. Coughing is not a sign of cardiac failure unless there is secondary bacterial infection as a result of pulmonary oedema.

Answer 229

Jugular distension above the lower 1/3 of its length with the head held up indicates elevated central venous pressure. Causes include; cranial thoracic obstruction/mass, pericardial effusion, right sided failure. Primary right sided failure is rare, more commonly develops secondary to left sided failure. Look for subcutaneous oedema which is indicative of right sided congestive failure Horses develop subcutaneous oedema in a plaque along the ventral thorax and occasionally extending to the cranial abdomen. In severe cases in horses subcutaneous oedema may extend to the upper forelimbs.

Answer 230

Count heart rate, assess rhythmn and pulse quality. In a horse in congestive heart failure the heart rate will be elevated and there will be no evidence of vagal tone. Assess pulse quality. A bounding arterial pulse may indicate severe aortic insufficiency, in a horse with a diastolic murmur that is not excited. In AI systolic pressure is raised due to the increased stroke volume and diastolic pressure is low due to run off into the left ventricle during diastole. Assess mean pressure. Assessing the area under the pressure waveform or the volume of the pulse to give a subjective assessment of stroke volume. Observe mucous membranes. Palpate the cardiac area - find the apex beat. count heart rate and assess rhythm. Precordial thrills indicate significant cardiac disease. A diastolic thrill on the left hemithorax is most likely caused by aortic insufficiency.

Answer 231

Cardiac arrhythmias are very common in athletic horses due to their high resting vagal tone. second degree AV block is present in approximately 15-18% of horses. Sinus block is also common. These arrhythmias would be considered abnormal if the heart rate cannot increase in response to exercise. similarly ventricular premature beats are common in the initial slowing period following exercise considered abnormal if they occur during exercise when they may result in PP or increase in the risk of exercise associated sudden cardiac death. Atrial fibrillation is the commonest cause of PP in thoroughbreds.

Answer 232

Myocarditis secondary to viral and bacterial infections is suspected to be a cause of poor performance. Dilated cardiomyopathy does occur and will cause poor performance with secondary mitral and tricuspid regurgitation. cardiomyopathy will also occur as part of a generalised myopathy. Toxic damage to the myocardium by salinomycin and monensin has been reported. monensin ingestion causes acute myocardial necrosis leading to fibrosis. Clinical signs and outcome depend on amount consumed. Horses present in various stages of heartfailure, murmurs and arrhythmias.

Answer 233

Isolated pericardial effusions occur sporadically in horses although outbreaks have been reported. main forms are idiopathic fibrinous and idiopathic effusive percarditis however neoplasia, traumatic haemorrhage or septic disease can occur sporadically. The volume of the effusion can vary up to approx 6 litres and in most cases is serofibrinous but eosinophilic and histeocytic effusions have been reported. Causes right sided heart failure as the pressure in the pericardial sac compresses the less muscular right side of the heart and prevents filling.

Answer 234

One of the most common cardiac causes of poor performance in large hunters and thoroughbreds. it is re entrant rhythmn initiated by a premature atrial contraction and maintained as a result of the horses large atrial mass and high vagal tone. may be cause by atrial dilatation secondary to valvular dysfunction or there may be no obvious underlying pathology. If there is no underlying cardiac disease then the horse will continue to perform well during low intensity exercise only showing signs of poor performance during maximum exertion.

Answer 235

The underlying cause of the fibrillation must be determined before treatment is attempted. Treatment should not be attempted in horses if there is evidence of cardiac failure and if there is no compromise to athletic ability. Treatment may not be successful where there is atrial dilatation secondary to valvular disease. Horses should not be treated during the first 3-4 days following diagnosis as they may spontaneously revert to normal rhythm. Quinidine sulphate - an anti arrhythmic drug administered via nasogastric tube. Electric defibrillation - application of a direct current shock under general anaesthesia to stop the atrial fibrillation. it requires right heart catheterisation via the jugular vein to allow electrodes to be placed in the pulmonary artery and right atrium.

Answer 236

May be atrial or ventricular in origin. the underlying aetiology is often difficult to identify. premature systoles may be associated with hypoxia, myocardial disease, electrolyte and metabolic disturbances, elevated sympathetic tone, fever and toxaemia. when all non cardiac causes have been ruled out, a primary myocardial lesion must be suspected. Affect performance only if they produce excessive heart rates during exercise. More commonly the premature excitatory focus is over ridden as sinus nodal rate increases and the extra systoles disappear.

Answer 237

Usually specific anti arrhythmic treatment is not indicated, as the premature beats are usually too infrequent to significantly affect cardiac output at rest. It is important to establish what happens to heart rhythmn during exercise. Insevere life threatening ventricular tachycardia lidocaine is the drug of choice to control ventricular rhythm

Answer 238

may be of no clinical significance but if maintained during exercise, cardiac output will be inadequate and performance will be limited. abnormalities include 3rd and 2nd degree AV block and sinus block. Sinus block and AV block are normal findings in horses therefore diagnosis of abnormality is based on ECG evidence of an inappropriate heart rate response during exercise. Pathological second degree AV block and profound sinus bradycardia occur rarely in horses. Affected horses have an inappropriately slow resting heart rate and may present with collapse. Occasionally horses with profound 2nd degree AV block and sinus bradycardia respond favourably to daily oral administration of alpha 2 adrenoreceptor agonist drugs e.g clenbuterol.

Answer 239

Third degree AV block indicates total block in conduction at the AV node and is always a pathological finding, thought to be associated with inflammation or degeneration of the AV node. ECG examination shows multiple P waves not associated with QRS complexes.

Answer 240

Although rare in yearling thoroughbreds it is present in up to 21% of 2 year olds suggesting it may develop in response to training induced eccentric hypertrophy and increased blood volume. Mitral regurgitation can also occur in response to thickening and fibrosis of the valve leaflets. This is thought to be a progressive condition albeit very slow progression. Mitral regurgitation will also develop as a result of rupture of one or more chordae tendinae. Most commonly the rupture is of a minor chorda of one of the commissural cusps. Occasionally there is a rupture of a number of chordae or one of the major valve leaflets - regurgitant flow is suddenly very large and there is little time for atrial dilatation to occur. Mitral regurgitation will occur secondary to any other condition that causes dilation of the valve annulus e.g secondary to dilated cardiomyopathy, aortic insufficiency and ventricular septal defects. Mitral regurgitation may also occur as a result of congenital dysplasia of any part of the mitral valve apparatus. Infective endocarditis occurs rarely. there is no pathognomonic sign of endocarditis and therefore diagnosis is difficult. odes not increase risk of sudden cardiac death.

Answer 241

Very common in national hunt horses. not associated with thickening of the valve laeflets tends not to progress and if mild/moderate will not affect racing performance. Tricuspid regurgitation does not normally result in cardiac failure although very occasionally primary right sided cardiac failure can occur. Tricuspid regurgitation will develop as a result of pulmonary hypertension caused by a left ventricular failure. More rarely, tricuspid regurgitation may develop as a result of a ruptured chorda or congenital dysplasia of any part of the triscuspid valve apparatus. If the murmur is not associated with thickening of the tricuspid leaflets it is unlikely to progress and is unlikely to affect performance. If however a horse has a high grade band, shaped murmur the very rare possibility of primary valvular disease could not be ruled out by auscultation and therefore further diagnostic tests may be necessary to confirm normal valve structure before advising on suitability. Does not increase risk of sudden cardiac death.

Answer 242

A progressive disease associated with thickening and fibrosis of the aortic valve leaflets. more common in horses over 10 years of age. Tends to progress very slowly and in older horses rarely affects performance. Aortic insufficiency causes volume overload of the left ventricule resulting in dilatation. this occurs gradually over years and may ultimately lead to mitral regurgitation due to dilatation of the mitral orifice. MR may then result in cardiac failure. When severe aortic insufficiency is present in a young horse this is likely to be due to dilatation of the aortic root or another cause of early degeneration e.g congenital abnormality of the valve or association with a ventricular septal defect. Increased oxygen demand and reduced coronary reserve increases susceptibility to ventricular arrhythmias that can result in sudden death.

Answer 243

These are the most common congenital abnormality in large animals. The significance of teh condition very muhc depends on the size of defect. if small and restrictive to blood flow - animals will grow and perform normally. if defect is large, left ventricular volume overload and cardiac failure will occur. small restrictive defects will not affect performance. large defects not compatible with life. In horses, septal defects are usually located in the membranous septum below the aortic and tricuspid valves. They are most commonly found in shetland and welsh mountain ponies although other breeds may be affected. Less commonly defects are located in the muscular part of the septum. Defects in this position can be large and most often occur in arabian or TB breeds. When the defects are large the pressure in the right ventricle approaches or equals that of the left ventricle.

Answer 244

Administer analgesics according to diagnosis, house in a warm loose box with deep inedible beddding, if necessary, put on a muzle to prevent them from eating. Remove all objects on which the horse could injure itself if it were to become painful and begin to thash about. Remove all feed for several hours and make sure the horse passes several piles of normal faeces prior to reintroduction of feed. provide free access to water. Have the owner hand walk the horse 10-15 minutes every 2-3 hours. reassess regularly.

Answer 245

Squamous portion most commonly affected ( no protective mechanisms against gastric acid), Seen in high intensity training, roughage restrictin, excessive concentrate feeding. mucosal ulceration also occurs with NSAId use. Clinical signs vary from inconsequential to severe colic, anorexia, bruxism. Treatment; omeprazole, H2 antagonists, sucralfate. Prevention via management changes.

Answer 246

Primary - from highly fermentable feeds (gas accumulation) Secondary - from mechanical or physical SI obstruction/gastric outflow obstruction Fluid accumulation - gastric reflux Diagnosis: nasogastric intubation. treatment depends on aetiology. May result in gastric rupture.

Answer 247

Develops slowly, predisposing factors include ingestion of beet pulp, bran - dessicates within the stomach, dental disorders, terminal liver failure. Diagnosis difficult - difficulty passing nasogastric tube or may cause caudal and medial displacement of spleen on a rectal exam.

Answer 248

Rare in the Uk - possible bacterial aetiology, results in gastric and proximal small intestinal distension. cliical signs - ooften febrile, increased gastric reflux, decreased gut souns.

Answer 249

Most common type of colic, rapid onset, intermittent mild to moderate pain, increased gut sounds, no rectal findings, often resolve spontaneously, usually complete response to analgesics or analgesic/spasmolytic combination.

Answer 250

As with gastric dilation but affecting the LI or caecum. often see abdominal distension - right flak and paralumbar fossa. Diagnosis by rectal examination reveals gas filled colon/caecum. Treatmet; analgesia, exercise, trocharisation (very occasionally employed in cases of caecal tympany). Very important to distinguish from other conditions resulting in colonic gas accumulation and abdominal distension - these other possible causes may require urgent surgery, consider heart rate and signs of endotoxaemic shock.

Answer 251

Pelvic flexure most common site for impaction. predisposing factors include reduced water intake, poor quality roughage, poor dentition, slow onset for several days, depressed, often low grade pain, HR and RR normal usually, small hard faecal balls or no faeces. gut sounds often preset but reduced especially on RHS. Diagnosis by rectal exam. treatment: feed restriction, anaglesics, intragastric laxatives, or electrolyte solution, some horses require intravenous fluids.

Answer 252

More common in small ponies and arabians. Predisposing factors are as for large colon impactions. Mild colic initially - gas accumulation proximally - increased severity of pain. Diagnosis - reduction in faecal output, rectal examination. Treatment: IV fluid administration, enemas - risk of bowel perforation, surgeyr may be required if medical treatment fails (fever, diarrhoea ad laminitis are common post operative complications, high risk candidates for developing post operative salmonellosis).

Answer 253

Most common site for small intestinal intraluminal obstruction. Reported association with anaplocephala perfolita burden, heavy ascarid burdens in foals (post worming). Clinical signs: moderate progressive colic signs. May palpate impaction during transrectal examination, small intestinal distension, no immediate systemic signs of intestinal compromise, gastric reflux (takes several hours as obstruction is far aborally as possible).

Answer 254

Much less common than colon impactions, predisposing causes as with large colons plus hospitalisation, general anaesthesia, NSAID use. Classified as type 1 impactions of dry ingesta filling the caecum and type 2 (impaired caecal outflow due to motility dysfunction). Treatment- depends on severity, medical management - feed restriction, Iv fluid therapy, oral electrolyte solution and mineral oi.

Answer 255

Usually involves the pelvic flexure or right dorsal colon. treatment; psyllium mucilloid treatment. surgery may be required.

Answer 256

predisposing factors - age >7yo, warmblooods, recent foalig, abrupt change in feeding, previous displacements. May cause strangulation of the large colon or non strangulating colon displacement. Left dorsal displacement of the colon & migration of colon between spleen and body wall - entrapment over nephrosplenic ligament, partial or complete colonic obstruction. Right dorsal displacemet - displacement of colon betweencaecum and right body wall. in craniocaudad then craniad direction most common. may be accompanied by trsion.

Answer 257

most common cause of chronic liver failure in the UK. Generally unpalatable to horses. May eat it when there is poor pasture conditions, overgrazing, hay coontamination or contamination of pasture following cutting. horses mainly eat young shoots - owners do not recognise it at this stage. toxic effects are cumulative - long term low exposure or short term high exposure. Metabolites have antimitotic effects in liver. Megalocytes are classical histopathological feature of the disease. Clinical signs: non specific until hepatic failure. Classical features identified on histopathological examination of biopsy include; megalocytosis, periportal fibrosis, biliary hyperplasia, occlusion of central veins and exposure to massive doses may produce acute centrilobular necrosis.

Answer 258

A condition characterised by excessive iron accumulation in the liver resulting in hepatocyte damage - excessive supplementation, or sporadic form. Pathology; fibrosis, biliary hyperplasia, iron accumulation in hepatocytes.

Answer 259

Primary tumours are rare - cholangiocarcinoma sen in older horses, causes multiple hepatic masses. Hepatocellular carcinoma in young horses, often solitary and multilobulated. secondary metastatic lesions; the liver is frequently involved.

Answer 260

A disorder of lipid metabolism; Hypertriglyceridaemia Fatty infiltration of body organs In response to stress ad negative energy balance - mobilisation of fat reserves, NEFAs esterified to triglycerides. Fatty liver most commoon cause of secondary liver failure. common in small ponys and donkeys. clinical signs; anorexia, depression, CNS signs, ventrla oedema, colic, tachypnoea, tachycardia. Poor prognoosis.

Answer 261

1 - head - check for symmetry, tone, sensation in the nasal septum, tongue strength, symmetry, PLR, swinging light test, menace response, nystagmus, lift head up straight towards you and check foor eyedrop/see if more sclera on one side. 2 - Neck and trunk - thracolaryngeal reflex, local cervical and cervicofacial responses, cutaeous trunci reflex. 3- perineum - Check for response and tone of anus - degrees of hypotona,hypalgesia and hyporeflexia fo tail, anus and perineal region, degrees of urinary bladder paresis ad rectal and anal dilation come with lesions of the cauda equina. 4- gait and posture- ataxia, paresis, pull on the tail while walking, spin around you.

Answer 262

Seen in large, younger horses. various manifestations of developmental orthopaedic disease. Vertebral canal stenosis/wedging/angular fixation. often in c3-c4. Vertebral canal malformation pushes and impinges on spinal cord. Vertebral canal must be >50% for the width of the vertebrae.

Answer 263

Large, older horses, due to arthritis of caudal cervical vertebrae. compression of spinal cord by bone and soft tissues - grave prognosis..

Answer 264

Equine herpes virus type 1 EHV1 causes myelooencephalopathy - often with outbreaks of respiratory disease and abortions. reservoir is latently infected horses in the trigeminal ganlia. Often acute onset symmetrical ataxia & paresis. signs progress rapidly for about 2 days then stabilise. Pelvic limbs > thoracic limbs more commonly. Have ataxia and cauda equina syndrome. CSF often xanthochromic. Infection of respiratory epithelium > cell associated viraemia > endothelial infection ad ischaemia of CNS microvasculature. D752 single ucleotide polymorphism > a substitution of asparagine by aspartic acid at amino acid position 752 is significantly associated with outbreaks in which there are neurological signs. but ALL ehv1 strains can cause neurological disease. d752 strains have higher levels of viraemia ad preferentially infect cd4 lymphocytes > virus transfer to endothelia > relatively uninhibited by virus neutralising antibodies. Causes inflammation ad vasculitis of arterioles in brain and spinal cord > multifocal haemorrhagic myeloencephalopathy. humoral immune responses are not protective, although may shorten the duration of virus shedding. Virus specific T cell responses do appear to be protective.

Answer 265

Early dexamethasone useful, oral antiviral drugs: acyclovir poor bioavailability, pro drugs e.g valacyclovir may be better. Prognosis good if horse able to stand even in a sling throughout disease and convalescence. improvement within a few days - may take a few weeks to a year for severe neurologic deficits to completely recover. Diagnosis, supported by ruling out other conditions, demonstrating xanthochromia, identifying or isolating EHV-1 from the respiratory tract, buffy coat or CSF, demonstrating a 4 fold increase in serum antibiotics. Control ; isolate affected cases - vaccine only killed vaccines available, hygiene.

Answer 266

Caused by sarcocystis neurona - the definitive host is the North American opposum. Intermediate hosts include racoon, armadillo. There is a serum immunoblot test available for antibodies. CSF immunoblot test also available for nantibodies. Treatment; inhibit enzymes which catalyse reduction of folic acid; sulfonamides & pyrimethamine. can cause a huge variety of CNs signs. focal spinal cord signs most commoon.

Answer 267

A flavivirus, enveloped, spherical. Mosquitoos and birds are the reservoir. Horses are dead end hosts. can also affect many other animals. Causes paresis, ataxia, abnormal mentation, increased body temp, anorexia, cranial nerve deficits, fasciculations. (not all in all cases). Diagnosis by ; history (vaccination), clinical signs, CSF mononuclear pleocytosis, serology; IgM antibody capture ELISA, PRNT neutralising IgG antibody or PM.

Answer 268

Often they are not pyrexic, CSF is cloudy with low glucose, have a grave outlook. Due to failure of passive transfer usually gram negative organisms . Forebrain signs / head lowered in rigid extension.

Answer 269

Most common cause of diffuse brain disease of horses in the Uk. Pyrrolizidine - in some plants and causes toxicosis eg ragwort. Treatment of underlying disease. Outlook poor to hopeless if severe signs. hepatic encephalopathy is a metabolic disturbance of the CNS - response to multiple toxic breakdown products from intestinal degradation including ammonia, amino acids, short chain fatty acids, mercaptans. Imbalance of GABA and glutamate (disrupted glutamate transporter and receptor function).

Answer 270

Seen more in TB foals which have rapid parturition. signs more often delayed few hours to 2 days. dummy/barker etc describe the clinical syndromes. attend to passive transfer and nursing care. Have behavioural changes, spinal cord signs. rule out FPT and sepsis.

Answer 271

Rare - due to fusarium sp mycotoxicosis, usually in mouldy feed. Causes acute forebrain necrosis - grave outlook.

Answer 272

goes to cerebral circle then to middle cerebral artery which supplies the majority of the forebrain, almost all recover when water soluble agents are used eg romifidine, outlook is bad with oil based drugs and suspensions. typically forebrain signs are seen.

Answer 273

A 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 - steroids don't help. Sacral trauma far more likely. Life may be prolonged by the use of supportive measures including manual evacuation of the rectum, catheterisation of the bladder, treatment of utis with antibiotics.

Answer 274

Poor nutrition, amounts and or types//quality, increased metabolic demands:exercise, pregnancy, vices. Hierarchy/pecking order, inability to access, old age. Disease, dysphagia, maldigestion and malabsorption, increased consumption or loss (IBDz, parasites, neoplasia, PPID, EGS , renal disease, liver disease, cardiac disease, infections and sepsis, chronic pain)

Answer 275

colic/pain - may be low grade\Rectal temperature - many cases will be within normal range, however in some eg cyathostominosis, peritonitis, or neoplasia there may be a mild pyrexia. Signs of ventral oedema - this may be very subtle ins some cases, comprising on a thin plaque at the sternum. take care especially in the winter and in thick coated horses and ponies. Faecal staining on the tail and perineum - may give some indication as to the presence of diarrhoea and severity. scalding is more likely wit frequent and very loose faces. Any other subtle signs that at first may seem irrelevant/puzzling. Some skin lesions associated with IBDS.

Answer 276

Proteins - total albumin and glovulins. Generally oedema will be expected where the albumin is less than 15g/l, even if the globulins are slightly raised to maintain total protein within the normal range. this is because of its chemical properties and abundance albumin exerts the greatest influence on plasma oncotic pressure. Fibrinogen and other acute phase proteins - provide evidence of inflammation. Alkaline phosphatase - aLP is present in high levels in the intestinal brush border and with significant damage will be raised. however non specific liver biliary cells and bone also release ALP. Intestinal form of ALP may be measured by some labs. Liver screen - GLDH and GGT provide information about hepatocytes and biliary tract damage respectively. Assessment of urea and creatinine.

Answer 277

Assess weight and set date for re evaluation. Dietary change - ad lib good quality grass, hay, haylage. High energy feed eg sugar beet, youngstock mix, veteran diets, add oil to ration. Stop/start any long term medication for example phenylbutazone may be a potential cause of colitis or protein loss. alternatively chronically lame horses will lose weight due to chronic pain or impaired eating habits. In this scenario, some analgesia may improve weight gain. Anthelmintic therapy - probably always worth giving larvicidal doses of anthelmintics, despite the apparent adequacy of an anthelmintic regime. in cases where there is a high suspicion of cyathostome infestation then using either a single dose of moxidectin or the 5day fenbendazole followed by ivermectin may be used. this regime is repeated at ten day intervals for three treatments.

Answer 278

The term currently used to describe obese horses or ponies prone to laminitis. Risk factors for equine laminitis includes Obesity/EMS, ECD, Genetics, Exogenous steroids, Stress. If an animal is obese and suffers from recurrent bouts of laminitis then it probably has underlying metabolic predisposition to the obesity and the laminitis.

Answer 279

Insulin resistance is thought to play a major role in EMs. \Fasting glucose and insulin - may be carried out in conjunction with tests to rule out ECD. starve o concentrates for 12 hours prior to the test. water and grass hay may still be fed up until the sampling without invalidating the test. increased levels of insulin provide evidence of insulin resistance while increased glucose levels in a non stressed individual suggest severe IR/type 2 DM.

Answer 280

Horse or pony is starved of concentrates for 12 hours before test. water is removed 1 hour prior to test. 1g/kg glucose is administered as a 20% solution. Blood glucose and insulin levels are tested prior to administration and at 30,60,90,120,150 180,240 minutes. Interpretation: blood glucose should double within two hours and reduce to normal levels within 6 hours. Increased peak in glucose or delay to return to normal levels i.e longer than 6 hours is indicative of relative insulin resistance. be aware of other conditions which could affect this test e.g GIT function. using the insulin levels as well as glucose gives more information.

Answer 281

Feeds with a low glycaemic index should be chosen. complete starvation should be avoided as it promotes a survival mode of increased insulin resistance, thus potentially worsening the situation. Also care re risk of hyperlipaemia. rich grass should be avoided in these animals as sugar content can be unacceptably high, particularly at some times of the year. the restricted grazing practice must be balanced with the need for exercise, therefore use of grass muzzles or night grazing may be advantageous. Grass hay is generally good but may be variable in soluble carbohydrate/sugar content therefore best practice is to encourage owners to have it analysed for non structural carbohydrate i.e sugar content. soaking hay may also reduce soluble CHO as it gets trapped in the water. if further feeding is required then use other low GI foods for example sugar beet has a very low Gi. alfalfa chaff is similarly a good extra ration and for older ponies with bad dentition the short chopped alfalfa feeds can be useful.

Answer 282

50ml/kg/day. Normal urination 10-30ml/kg/day (5-15litres /horse, 2x4 per day)

Answer 283

Primary/psychogenic polydipsia - (stabled, boredum) ECDz/PPIPD - (aged, hirsute, laminitis, recurrent infections) Renal disease (aged, weight loss, uraemia, isosthenuric Less common; Psychogenic salt consumption Diabetes insipidus Drug induged/iatrogenic

Answer 284

Urinalysis; SG - normal 1.020-1.050 Dipstick - pH 7-9, no glucose, no ketones, no Hb/Mb, no bilirubin. protein often + but greater is abnormal. Electrolytes and creatinine Haematology and biochemistry - decreased rbcs; anaemia of chronic disease or inadequate conversion of erythropoietin by kidneys. Increased white cells; may indicate chronic infection e.g pyelonephritis Urea and creatinine increase reflects >75% loss of total tubular function. Protein levels: albumin may decrease with glomerular diseases or tubular diseases (rarely). Electrolytes; following may indicate renal disease - sodium decrease, chloride decrease, calcium increase, phosphate decrease, potassium increase.

Answer 285

Tests the ability of the kidneys to concentrate urine in the face of water deprivation. Must check renal function before carrying this out. to omit this would be negligent. Complete WDT involves taking all fluid sources away and measuring urine specific gravity over suceededing hours. Important to evaluate hydration status and ideally weigh. Normal horse will concentrate urine >1.025 within 12-24 hours. Stop test if >5% loss of body weight (indicates dehydration). Some horses with prolonged pd will have medullary washout i.e concentrating ability of the renal medulla is lost and unable to concentrate.

Answer 286

Due to the overproduction of propriomelanocortin peptides from pars intermedia. the resultant increase in adrenocorticotrophincauses dysregulated cortisol secretion.

Answer 287

Hisutism - increased cortisol may lead to increased androgen production from the adrenal glands. alternatively adenomatous growth may cause compression of hypothalamic thermoregulatory centres. Hyperhidrosis due to hirsuitism and effects of compression on thermoregulation. Laminitis - effects of glucocorticoids on metabolism, vascular function ,skin funciton bone function and GIT mucosa, lethargy, fat redistrubution, predisposition to infections, weight loss due to muscle wastage, PUPD secondary diabetes mellitus - cortisol antagonism of ADH receptors in the kidney, decreased ADH secretion via impingement in pars nervosa of pituitary.

Answer 288

Biting louse damalinia equi Sucking louse haematopinus asini. Often occurs in winter in poorly managed/congregated horses, treatment with insecticidal shampoos, sprays or powders usually containing pyrethrins or pyrethrooids. two applications at 14 day intervals.

Answer 289

Caused by chorioptes equi. primarily affects distal limbs of heavily feathered horses. Affected horses stamp and bite limbs. scaling and exudation present. Treatment - removal of hair and scabs with application of insecticides including permethrins and fiproonil to affected horses and in coontacts.

Answer 290

Oxyuris equi. Adult worms migrate from the small colon/rectum to lay eggs on the perianal skin causing pruritis/tail rubbing. most modern anthelmintics are effective.

Answer 291

Seasonal dermatitis caused by onchocerca cervicalis microfilaria. the parasite is transmitted by culicoides spp and other biting insects. Larve can be found in capillaries of unaffected horses but clinical cases result from type 1 and type 3 hypersensitivity reactions. Causes alopecia and scaling of the head neck withers chest and midline. Diagnosis on clinical signs, poor worming history, season, response to ivermectin.

Answer 292

Hypersensitivity to bites of culicoides spp midges. generally common but not in foals. usually gets progressively worse with age. commonly affects the Mane and tail but can affect the ventral abdomen too. Pruritus is always present at dusk and dawn when midges are most active. Diagnosis; biopsies, intradermal skint ests and ELISAs. treatment inclues managemet of skin lesions, corticosteroids, immunotherapy/desensitisation treatment offered by a number of lags. Fly repellants and preventing midges biting.

Answer 293

Common sydnrome with a complex immune mediated/allergic aetiopathogenesis. arises from inejcted drugs, ingested chemicals/feeds r inhaled pollens moulds and dusts. alternatively can arise from direct skin or mucous membrane contact. typical signs - wheals occur within variable time following the instigating factor. angio oedema is a subcutaneous form of urticaria which tends to be more diffuse owing to lack of restraint of spread of fluid in subcutis. Anti histamines generally have little effect.

Answer 294

An auto immune disease characterised by an exfoliative dermatitis. It results from a type 2 hypersensitivity due to autoantibodies directed against the cell membrane of epidermal cells. Clinical signs include vesicles pustules, erythematous scaling and crusting, commonly begins around the face and limbs. inflammation around the coronary band, ergot and chestnut is common. Lesions may be painful or pruritic. systemic signs may include lethargy, inappetance, ventral oedema, pyrexia and weight loss. Treatment - immunoesuppresive doses of corticosteroids (prednisolone at 2-4mg/kg). attempts to reduce the dose are often unrewarding and result in deterioration of cases.

Answer 295

Multisystemic diseases often affecting the gastrointestinal tract as well as the skin. skin lesions include ulcerative coronitis, alopecia, hyperkeratosis and exudation. lesions can be intensely pruritic. signs f generalised disease include weight loss, inappetance, diarrhoea, oedema, dullness and lethargy. diagnosis usually requires biopsy of the skin, rectum/intestine. hypoalbuminaemia, hypoprotinaemia and hyperfibrinogenaemia may be present and glucose absorption tests may be indicated.

Answer 296

A common skin infection caused by dermatoophilus congolensis. causes exudation, matter hairs and scabs in areas wetted by rain, primarily the back/quarters. Classic paint brush lesions. treatment includes antibiotics/clipping /soaking of the skin with chlorhexidine to remove exudate and scabs. topical treatments include antibiotic ointments applied as necessary.

Answer 297

Commonly caused by trichophyton equinum var equinum and trichophyton equinum var autotrophicum. Spores are highly resistant and survive in stables/tack for years. infection relies on the presence of spores and skin abrasion therefore common around the girth/saddle. Lesions appear initially as circular areas of erect hairs followed by alopecia and scaling. Diagnosis; clinical signs, microscopy of a hair pluck/scrape (hyphae and endothrix sporeS) and culture. infected hairs do not fluoresce with woods lamp. lesions resolve spontaneously over a number of weeks but treatment limits spread. topical fungicidal treatments include enilconazole and natamycin. sporocidal treatment of the environment also important (natamycin or virkon.) Griseofulvin is of limited use ad contra indicated in pregnant mares.

Answer 298

A clinically distinct syndrome caused by a papilloma virus. common in horses of all ages but a rarely in animals less than 1 year. lesions begin as small Papules that coalesce into white hyperkeratotic plaques, occur on the inner surface of the pina. Spontaneous regression does not seem too occur but treatment is not indicated.

Answer 299

the most common skin tumour of horses. 6 types - occult, verrucose, nodular, mixed, fibroblastic, malevolent. Cause not fully understood but bovine papillomavirus widely accepted as having a roole. diagnosis usually based on clinical appearance and submission of photos via liverpools website. rarely biopsied. Treatment - do nothiig, AW4-LUDES cream, surgery, ligation, BCG injection, other topical medications.

Answer 300

Melanomas are benign tumours of melanocytes and generally cause disruption by space occupyig. melanomas are largely limited to grey horses and are common around the perineum, sheath, parotid region and less commonly in the guttoral pouch, eyelids, lips and iris. Melanosarcomas are rapidly invasive and metasasise but are rare.

Answer 301

Ulcerating cutaneous graulating nodules or wounds caused byt he larvae of habronema muscae. habronema majus and drachia megastoma. disease has several forms - opthalmic - presence of yellow ranuloes in cojunctivae and nasolacrimal duct, cutaneous - larvae penetrate wet areas of face, granulating wounds and urethral process.

Answer 302

Loss of pigment oin skin causing depigmented spots. rarely associated with hairloss except around the eye or perineum and can be idiopathic or secondary to surgery, cryosurgeyr, radiation etc.

Answer 303

Caused by dermatophilus congolensis) - exudation, scabs and matting of hair of distal limbs. diagnosis can be made on examination of a smear. mixed infections with staph and strep are common. treatment: antibiotics, anti inflammatories and soaking of the skin with chlorhexidine to remove exudate and scabs. may require clipping of hair. skin should be dried and topical treatments including antibiotic ointmets applied.

Answer 304

Inflammation of the cutaneous lymphatics usually but not always secondary to a bacterial infection obtained via a small cut/abrasion. affects hindlimbs more commonly than forelimbs. usually causes marked swelling of the limb, lameness and serum exudation. Treatment - antibiotics based on culture results, NSAIDs, corticosteroids, potassium iodide ad diuretics. Ulcerative lymphangitis is commonly associaed with corynebacterium paratuberculosis, staphylococcal sp and streptococcal sp infections. can result in nodules which may ulcerate, abscessate and drain pus.

Answer 305

An immune mediated vasculitis associated with recovery of an upper respiratory tract infection most commonly caused by M prootein antigen of streptococcus equi subsp equi. Immune complexes deposited in the walls of pierpheral blood vessels increase vascular Permeability and cause oedema, primarily of the limbs. Serum exudation and skin erosions can be marked. petechial or ecchymotic haemrrhages can occur in the skin and mucosae. pulmonary and cerebral oedema can develop in the most severe cases and is life threatening. signs usually occur 2-4 weeks after respiratory infection. horses are epressed, inappetent and reluctant to move. diagnosis can be confirmed with biopsies. treatment is with systemic corticosteroids and antibiotics, hosing limbs, gentle exercise and leg wraps.

Answer 306

CEM organism (taylorella equigenitalis) or other venereally transmissible organisms. (klebsiella pneumoniae) and pseudomonas aureginosa.

Answer 307

``` Beta haemolytic streptococci spp E cooli Other enterobacter Less common; Pseudomonas auruginosa Klebsiella pneumoniae Pre heavy growth is more likely to be significant than light mixed growths which are likely to be contaminants. the interpretatioon of culture results is best done with the cytology and or ultrasoound findings in mind to be most useful. ```

Answer 308

Clinical signs - hormones produced by the tumour may cause behaviour changes, including stallion like behaviour. normal regular cycling will be altered/cease. diagnosis by Palpation and ultrasonography of an abnormally enlarged ovary with atrophied contralateral ovary, negative feedback feedback by the secretion of Inhibin on the hypothalamus and pituitary cause regression of the opposite ovary to a small inactive structure. ovulation fossa of affected ovary obliterated. Treatment - unilateral ovariectomy done laparoscopically.

Answer 309

Aetiology - trauma, parturition, caustic agents e.g chlorhexidine/iodine scrub. Diagnosis - uterine endoscopy, bands, sheets or tunnels seen. Treatment - breakdown manually or with laser but may recur. Alternatively use biopsy forceps + endoscope or laser.

Answer 310

Refers to noon inflammatory chronic pathology of the endometrium. incidence increases with age. commonly associated with endometritis as reduces resistance to infection. Diagnosed on endometrial biopsy. Decreases the ability to coonceive and carry a foal o term. no effective treatment is available. histopathological changes include periglandular fibrosis, fibrotic changes surrounding the uterine glands, lymphatic lacunae - poor myometrial activity fails to pump the lymph fluid as normal and lacunae develoop.

Answer 311

Taylorella equigenitalis - a notifiable disease. A gram negative microaerophilic coccobacillus. venereal transmission and contaminated equipment and handling. organism persists in the clitoral sinus of carrier mares. Clinical signs ad pathology; severe endometritis, necrosis ad shedding of the epithelial lining of the uterus profuse watery mucoopurulent, non clumping discharge from uterus, short oestrus cycle (8-12 days). Stallions are inapparent carriers - just have surface contamination. Diagnosis by isolation of taylorella equigenitalis from reproductive tract - culture system chocolate agar with increased Co2 - 5 to 10% co2. Many cases recover spontaneously but carrier status must be assessed. some fail to recover despite treatment. Some require treatment - uterine infusion for several days with antibiotics; topical wash of clitoral fossa with 2% chlorhexidine and pack external genitals with nitrofurazone or chlorhexidine ointment. Clitoral infections can be hard to treat - consider clitorectomy/sinusectomy in very difficult cases.

Answer 312

possible organisms include - beta haemolytic streptococci, E. coli, pseudomoonas aureginosa, kelbsiella pneumonia, yeasts (candida spp), fungi (aspergillus sp). clinical signs include discharge from vulva/uterus, fluid in uterus on ultrasound, but these visual clinical signs can be absent to consider fi failing to conceive, may have a shorter dioestrus period than the 15 days usually expected.

Answer 313

short cycle mare with PGF-2 to bring into oestrus - oestrogens have positive effect on uterine immune defence mechanisms. Administer oxytocin Iv or IM. Lavage uterus for 0.5-11 sterile hartmanns solution or saline to manually remove contamination. Infuse uterus with appropriate antibiotics , such as neomycin/penicililln/framomycin or ceftiofur. Repeat treatment for 3-5 days. Correct any predisposing conformational abnormalities e.g caslicks vulvopasly. Maintain good hygiene during examinations and breeding. use AI if possible.

Answer 314

all mares will have an immunological reaction to semen and produce uterine fluid but normal mares will expel/absorb this fluid at the same rate as it is produced. Free intra uterine fluid accumulates and clinical signs ad diagnosis are as for CUI. treatment involves oxytocin, flushing and antibiotics but must be started after sperm have reached the oviduct or before the fertilised ovum descends into the uterus.

Answer 315

Pneumonovagina - air in vagina with or without faecal contamination. Urovagina - accumulation of urine in the vagina - due to poor perineal conformation, relaxed ligaments or extreme weight loss.

Answer 316

lasts 30-60 days on average. waves of follicles develop and regress without ovulating, giving prolonged irregular periods of oestrus activity. cervix is partially open. mares will irregularly tease positive for long periods. The end of transition is marked by an LH surge and ovulation. the onset of normal cyclicity may be hastened by altrenogest (a synthetic progesterone for 10-15 days), human chorionic gonadotrophin IV, or exogenous GRH - deslorelin implant or twice daily injections of buuserelin.

Answer 317

``` Day 0 - ovulation, CH forms Day 5- fully functional corpus luteum Day 15 - CL lysed by PGF2a, one or two dominant follicles develop Day 18 - Standing oestrus begins Day 0 - ovulation ```

Answer 318

Progestogens - oestrus occurs 4-5 days after withdrawal, may be used short term to synchronise a mare or long term to suppress oestrus behaviour. Prostaglandin F2 - used t lyse a CL allowing mare to return to oestrus 2-5 days later. CL must be between 5 and 14 days old to respond. ovulation is variable (3-10 days) depending on follicular development at time of treatment. Natural PGF2a causes more side effects than synthetic preparations. Oestradiol not available in the UK Human chorionic gonadootrophin - lh like activity, can hasten ovulation of a mature follicle.

Answer 319

Infiltrate the vulvar margins with local anaesthetic from just below the level of the ischium to the dorsal commissure. remove a 0.5 cm strip of mucosa. suture dorsal portion of vulvar lips together. remove sutures after 10 days. MUST be re opened before parturition.

Answer 320

traditionally mares are bred on day 2 or 3 of oestrus and then every other day until the end of oestrus. mares shoul be bred prior to ovulation when a dominant follicle is present. if it is necessary to limit the number of breedings, the ovaries should be palpated daily add breeding should take place just prior to ovulation. if ovulation has occurred, good conception rates may still be achieved by breeding 12-18h after ovulation. Incidence of early embryonic death increases with post ovulation breedings du to fertilisation of an aged ovum.

Answer 321

Given to cause ovulation of a mature follicle. use IM 6 hours before service. ovulation expected within 24 hours.

Answer 322

Usually from a kick from a mare/field companion. use anti inflammatory measures urgently (icepack, NAIDS, antibiotics, gentle massage). Intrascrotal haemorrhage will lead to permanent testicular damage due to the insulating properties of the resultant fibrous tissue. surgical removal of the organised blood clot or hemi castration can be performed in an attempt to save the unaffected testis.

Answer 323

An abnormal collection of fluid between the visceral/parietal vaginal tunics - it is usually not painful, and can accompany scrotal oedema. May self resolve especially with gentle exercise, could be drained if not resolving and if unilateral and persistent, remove affected testis and tunics to save contralateral testis from heat induced degeneration.

Answer 324

Major cause of subfertility/iinfertility. may be due to old age, excess heat, trauma, toxins, anabolic steroid use, radiation exposure. Because it takes approx 60 days from development of sperm from spermatogonia until ejaculation it is poossible for acute testicular degeneration to be present

Answer 325

Primary orchitis is rare. affected testis are hot swollen tense and acutely painful. Fever an scrotal oedema are common, with stiffened hindlimb gait, followed by ischaemic necrosis and abscess formation. Adhesions commonly develop. Treatment- antibiotics, NSAIDs, hydrotherapy. Prompt removal of a unilaterally affected testis may save the contralateral testis.

Answer 326

If 3 years - do an oestrone sulphate assay.

Answer 327

After phenothiazine or other sedative use, or following preputial trauma, or with chronic grass sickness/botulism. It impairs venous and lymphatic drainage. within hours penis and prepuce become oedematous. if left untreated cellulitis, necrosis, gangrene can develop requiring removal of the penis. Treatment: support the penis manually, such as with tights. Reduce oedema - hydrotherapy, NSAIDs, diuretics, massage.

Answer 328

Pox like lesions on the penis. venereally transmitted. self limiting. complete resolution in 3-5 weeks.

Answer 329

``` day 11- 1cm vesicle day 15 - 1.5cm vesicle day 17 - implantation day 21 - embryo appears ventally day 24 - heartbeat seen day 35 - ecg produced day 60-70 sexing possible ```

Answer 330

(equine herpes virus 1, EHV1 or uncommonly EHV4)- a leading infectious cause of abortion in mares in the UK. the virus is transmitted via the respiratory tract. repeated exposure leaves horses immune to respiratory disease but susceptible to reinfection causing abortion. Usually occurs between 5 months gestation and term. usually only a few infected mares in a her abort. abortion occurs 1-4 months after infection. fresh foetuses expelled often within placental membranes. foals affected near term are viraemic, weak and die shortly after birth. Treat all abortions as possible EHV abortion.

Answer 331

A togavirus - Causes severe systemic illness in the dam which may be followed by abortion 7-10 days later from 3 months to late pregnacy. Typically presents with fever, lethargy and depression, conjunctivitis, nasal discharge, urticarial rashes, oedema. Infection is via the respiratory or Venereal route. virus localises in accessory sex glands. 30% of infected stallions continue to shed virus after resolution of clinical signs. Shedding stallions play a major role in disease transmission. shedder stallions are always seropositive but all seropositive stallions are shedders. Mares do not become carriers but 90% of mares become infected after breeding with a shedder stallio. Seropositive mares with a stable or declining antibody titre are thought not to infect stallions or in contact animals.

Answer 332

Foetus is usually small and emaciated. Near term premature foals with mycotic placentitis have a good chance of surviving however. Grossly the placenta and foetus are similar in appearance to bacterial causes of abortion although microscopically there are abundant fungal hyphae. Aspergillus is the most frequently encountered fungus.

Answer 333

This is an equine emergency. treatment should be initiated if the placenta is retained moe than 3 hours. Mares are likely to be less fertile at foal heat. Use oxytocin, repeat as necessary (usually expelled within 30 minutes), if retention is prolonged (>8 hours) beware of sequelae: laminitis and enedometritis. Use more aggressive therapy; anti inflammatories, broad spectrum antibiotics, exercise. Alternatively: the allantochorionic space may be infused with 10-12 litres dilute povidine iodine solution or saline. the opening in the foetal membranes is tied shut. the distension of the reproductive tract stimulates uterine contractions via oxytocin release and the membranes are usually passed within 30 minutes.

Answer 334

Associated with endometrial fibrosis/endometrial scarring in older mares. pregnancies are confined to the uterine body also cause abortion due to decreased placentation into the uterine horns. lack of nutrition to the foal causes foetal stress/hypoxia and starts birthing process.

Answer 335

mares may exsanguinate. survival depends whether haemorrhage is contained within the broad ligament or whether the ligament ruptures. signs of colic with weak rapid pulse and pale membranes. keep mare in dark, quiet stable . tranquillisers may help. do not give oxytocin.

Answer 336

Caused by damage to the birth canal by foals hoof/head etc. Repair surgically after 30 days when damaged tissue has sloughed and swelling has resolved. Three types of perineal tear - type 1 mucosal damage only. type 2 - damage into perineal body. type 3- tear exteds int anus, producing a cloaca.

Answer 337

Rhabdomyolysis, botulism, equine motor neurone disease, hyperkalaemic period paralysis, hypocalcaemia, myasthenia gravis. Horses will have a narrow based stance, increased periods of recumbency, low head carriage at rest and during exercise, reluctance to bear weight when a limb is raised.

Answer 338

Rhabdomyolysis, tetanus, hypocalcaemia, shivering and stiff horse syndrome. key findings - fasciculatioon, trismus, stiff and stilted gait, other bizarre gait abnormalities, dysphagia.

Answer 339

Caused by the toxin costridium botulinum a gram positive anaerobic spore forming bacteria in soil. toxin thought to block acetylcholine release at neuromuscular junctions, peripheral cholinergic nerve terminals in autonoomic ganglia and post ganglionic parasympathetic nerve endings. toxicoinfectious botulism = growth of the agent in the GI system.

Answer 340

Severe diffuse paresis, rapid progression to recumbency, onset can be slower in some horses occurring over several days. weakness and trembling which improves during periods of recumbency. inability to fully retract the tongue, dysphagia and drooling of saliva, flaccidity of the tail, gradual onset of clinical signs is associated with a better prognosis c.f acute onset. in fatal cases, death occurs quietly.

Answer 341

Mainly symptomatic. in cases of wound contamination or toxicoinfectious botulism, antibiotic therapy is indicated (metronidazole/penicillin), antibiotics associated with neuromuscular weakness should be avoided if possible e.g aminoglycosides, tetracyclines and procaine penicillin. Antitoxin - not widely available for clinical use in the UK.

Answer 342

Causal organism - clostridium tetani - large gram positive spore forming bacillus. Found in soil and is a commensal in the GI tract of man and domestic animals. the spores oof C tetani can persist in the environment for may years. In the body, requires anaerobic conditions to survive. The common sites of contamination include; puncture wounds, surgical wounds, mucosal wounds and uclers, umbilical cord, retained placenta and haematogenous spread to devitalised tissue. It produces a potent endotoxiin - tetanospasm causing spastic contractions of striated muscles. Thought to act mainly by preventing the release of inhibitory neurotransmitters from the interneurons at the motor synapses in the spinal cord.

Answer 343

May take several days to weeks to appear. first signs are usually a change in the horses gait and demeaour. May also notice a difficulty in eating at this early stage. Generalised spastic muscular contractions are provooked by external stimuli (touch and sound) especially evident in the third eyelid when the cheek is tapped or w hen fingers are snapped infront of the eye. The disease may worsen dramatically over the next 24 hours or take several days - the horse will stand square on four stiff limbs with its head and neck extended and tail raised. Sweating and tachycardia may result. Drooling may be seen due to involvement of the pharyngeal and laryngeal muscles - food and water may be regurgitated dow n he nose or pass into the lungs. progression to recumbency an death from convulsions leading to respiratory and cardiac arrest. Trismus - spasm of the facial muscles is very characteristic of tetanus.

Answer 344

Young TB fillies .

Answer 345

Excessive glycogen > lactic acid + o2 products > coagulative necrosis > further muscle hypoxia > prevents muscular relaxation. common in working horses and ponies. vast majority sporadic and associated with exercise (sporadic exertional rhabdomyolysis). Large variety in the severity of clinical signs seen from a slight change in gait to a reluctance or inability to move, to in a few cases recumbency and death. severity of clinical signs does not reflect degree of muscular damage. Signs occur duriing or sometimes immediately following exercise. in a minority of cases signs may even occur on leavig the stall/box or following minimal exercise. these cases are often the chronic types. With acute - both hindlimbs are usually affected especially gluteal, femoral and lumbar muscles. Affected horses develop a stiff gait and may refuse to move. palpation reveals affected muscle groups to be painful, hard and swollen. the animal is frequently distressed sweating, with increased HR and RR.

Answer 346

Elevation in the serum levels of enzymes creatinine kinase, aspartate aminotransferase and lactate dehydrogenase. the degree of increase reflects the degree of muscle damage. CK is most specific for muscle damage, CK rises first an disappears first followed by LDH then AST. CK peaks at 2-12 hours after onset and may reach 100,000IU/L or more. LDH peaks at approximately 15 hours and may reach several thousand IU/L.

Answer 347

Rest - further muscular activity exacerbates the disease. Analgesics - NSAIds highly recommened eg flunixin meglumine or phenylbutazone. Fluids - oral fluids for mild cases of iv for more severe cases. many are alkalotic therefore Hco3 would be contraindicated. If unable to check the electrolyte and acid base status - best to give a balanced electrolyte solution eg lactated ringers solution. diuretics are usually contraindicated unless despite vigorous fluid therapy the horse is still oliguric when may give frusemide therefore need to monitor urination. Sedatives - ACP may help alleviate anxiety and muscle spasm. may also promote peripheral vasodilation. alpha arenergic agonists e.g romifidine may be useful in distressed animals. Corticosteroids - short acting steroids may play a useful role ins stabilising cellular membranes, however be aware of the risks of laminitis with high doses of potent corticosteroids therefore their overall use is debatable. Calcium carbonate and calcium gluconate - have been cited as being useful in severe cases as calcium which may be depleted is necessary for the normal aerobic function of the muscles. Take great care when administering i/v calcium - monitor the heart rate during infusion and infuse slowly or preferably add to i/v fluids.

Answer 348

Exercise tests and plasma muscle enzymes - allow you to detect whether the response of muscles to exercise is normal. Carry out approx 3 days after return to exercise. take blood samples before and 2-6 hours post exercise. Muscle biopsy - very useful information in recurrent cases. specifically useful in cases of polysaccharide storage but also in other chronic muscle and neuromuscular diseases. Fractional electrolyte excretion test - measurement of FEE is a means of evaluating a horses electrolyte balance. rarely used nowadays due to high variability.

Answer 349

``` commonly due to septicaemia Neonatal isoerythrolysis hepatitis fasting physiological icterus ```