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Equine Flashcards

1
Q

predisposition of colic

A

: neonatate (entercolitis, meconium retention), geriatric (strangulating pedcunculated lipoma, large colon impaction), pregnant mares (uterine torsion, large colon displacement/volvulis)…

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2
Q

signalment of colic

A

age, gender, breed

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3
Q

cause of colic

A

gut “spasm” resulting from a change in diet/routine

twisting of a part of the intestine with consequent strangulation of its blood supply.

Can be impaction, parasites, high in grain, dental issues, feed that is mouldy, dehydration, ingesting sand, NSAID over time

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4
Q

signs of colic

A

respiration: tachypnoea = pain, enlarge nostrils
- bloating, distress, agitation, sweating, stretching, sitting, lack of movement sounds in gut
- mild = dullness, curling up of top lip, straining to urinate
- severe = can cause horse to roll and throw itself about in an uncontrolled and dangerous manner

mild dehydration
- bright/quiet, responsive, HR <48bpm, MM pink, tachy, warm extremities, good jugular refill
moderate dehydration and hypovolemia
- quiet but alert and responsive, HR 62-76bpm, MM variable, tachy to dry, cooler extremities, slow jugular refill, pulse quality variable

severe dehydration and hypovolemic shock
- dull mentation, Hr 8-012bpm, dry/pale MM, cool extremities, peripheral pulse difficult to palpate

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5
Q

diagnosis of colic

A
  • Probing = 5-10x check for fluid, empty the tube and kink it, slowly pull out the tube

Abdominocentesis
- most ventral part of abdomen to the right
- 18G needle, EDTA tube, biochemical test tube, teat cannula

FLASH – fast localised abdominal sonography of the horse
- shortened exam
- 7 key abdominal windows
- final diagnosis made with US
- patient monitoring

US = peritonitis, hemoperitoneum, diaphragmatic hernia, masses, urolithiasis

Lab work = 1st evaluation
- haematological examination = haematocrit, leucocytosis/leukopenia
- biochemistry = urea, creatinine, glucose, TP, albumin
- acid – base status and electrolytes
Lactate
- transition of aerobic to anaerobic metabolism
- decreased renal excretion due to hypoperfusion

Endoscopy – gastroscopy
- oesophagus, stomach, proximal duodenum,
rectum
- fasting 8-12 hr before procedure
- sedation
- through ventral nasal passage, 3 m long endoscope
Faecal tests = parasitology + bacteriology (salmonellosis, clostridiosis)

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6
Q

treatment for colic

A

Medical therapy
- treat visceral pain, re-establish bowel passage, establish acid-base balance, walking
- rehydrate horse, treat endotoxemia, bacterial/parasitic infection
- analgesic, liquid, mineral oil and laxative
- NSAID
o meloxicam, firocoxib, flunixin-meglumine, metamizole sodium
o complication: kidney tubule necrosis, ulceration of the stomach + damage to the MM of the jejunum and colon
- a2, a2 adrenergic agonist
o inability to cure pain with flunixin
o xylazine, detomidine reduce intestinal motility
- Opoiod analgetic
o morphine, buprenorphine, butorphanol = reduce intestinal motility, excitation
- Spasmium
o spasmolytic and analgetic 0.2mg/kg IV, shortened tachycardia, combined with NSAIDs, metamizole sodium
- Laxative
Surgical management

Nasogastric intubation
- in every horse, immediately on admission
- transparent tubes of multiple sizes, 2 buckets of water
- pH measurements + preparing the horse, sedation
- ventral nasal passage to the pharynx, ventroflexion of the neck, push the tube in when swallowed, turning and blowing in the probe

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7
Q

prognosis of colic

A

guarded

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8
Q

simple oesophageal obstruction predisposition

A

freisians

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9
Q

cause of simple oesophageal obstruction

A

ingestion of material that when swallowed, becomes impacted in the oesophagus + doesn’t pass into stomach

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10
Q

signs of simple oesophageal obstruction

A

passage of ingesta and saliva down the nostrils, coughing, stretching of the neck, pain and distress, dysphagia,

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11
Q

diagnosis of simple ossophageal obstruction

A
  • resentment of cranial oesophageal palpation
  • may be obvious swelling
  • resistance to passage of nasogastric tube
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12
Q

treatment of simple oesophageal obstruction

A
  • heavy sedation and lavage via nasogastric tube
  • broad spectrum ATB
  • maintain soft diet for 7 days post relief of obstruction
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13
Q

prognosis of simple oesophageal obstruction

A

mostly good, but depends on severity of the impaction

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14
Q

differential of simple oesophageal obstruction

A

oral foreign bodies, dysphagia due to neurological disease, periodontal disease, periodontal

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15
Q

retropharygneal abscesation (strangles) predisposition

A

all ages – young and elderly at risk of severe disease , poor condition + genera management and general stress factors

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16
Q

cause of strangles

A

strep eqiu

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17
Q

signs of strangles

A

dysphagia, cough, dyspnoea, lymphadenitis, pyrexia, retropharyngeal pain and swelling, maybe guttural pouch involvement/ subcutaneous emphysema

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18
Q

diagnosis of strangles

A

history of colic/nasogastric intubation, endoscopy or radiography, bacteriology, CBC (maybe leukocytes, neutrophils), biochemistry (plasma: fibrinogen)

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19
Q

treatment of strangles

A

attempt to establish drainage, may require tracheotomy, total parenteral nutrition, attempt to gauge severity of trauma and lesions size before starting

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20
Q

prognosis of strangles

A

poor

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21
Q

expected sequelae of strangles

A

dysphagia, fasciitis, aspiration pneumonia, sepsis, potential for mediastinitis, similar signs to oesophageal rupture

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22
Q

recurrent oesophageal obstruction (signs, diagnosis, treatment)

A

Signs: recurrent bouts of choke, tends to deteriorate with age in congenital cases due to poor wall tone
Diagnosis: endoscopy, double contrast oesophageal and radiographic investigation of aspiration
Treatment: cervical pulsatile diverticula can be repaired surgically, can empty manually In some horses, dietary management only for large diverticuli at thoracic inlet

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23
Q

equine gastric disroder

A

Parasitic infection: gasterophilus larvae

Dysmotility: equine dysautonomia, acute gastric dilatation, gastric impaction, chronic gastric dilatation

Ulcerative: equine gastric ulceration syndrome, perforation and rupture

Neoplastic: squamous cell carcinoma

Inflammatory: inflammatory polyps, glandular ulceration and gastritis

Acute gastric distension: acute colic, possible rupture, peristonitis, endotoxemia

Chronic gastric distension: weight loss and reduced rate of feed intake, increased water intake, recurrent mild colic

Chronic inflammation: may be symptom free, progressing to acute colic, change in dietary preference

Chronic ulceration: loss of performance, decreased forward movement, anterior abdominal pain

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24
Q

acute gastric dilation predisposition

A

sporadic

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25
Q

acute gastric dilation associated with

A

reflux of intestinal contents secondary to acute intestinal obstruction, ingestion of excess fluid/feedstuff or acute idiopathic dilation after racing

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26
Q

signs of acute gastric dilation

A

acute abdominal pian, spontaneous nasogastric reflux, progressive acidosis, endotoxemia, colic

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27
Q

diagnosis of acute gastric dilation

A

based on presentation, nasogastric reflux without other identifiable cause

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28
Q

treatment of acute gastric dilation

A

gastric decompression and lavage
- IV fluid support, correction of acidosis + management of endotoxemia

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29
Q

complication of acute gastric dilation

A

endotoxemia sequelae (laminitis, acute renal failure), gastric (transient loss of motility, delayed emptying, serosal tear)

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30
Q

acute gastric impactin

A

Firm accumulation of food in stomach, causes stomach to become enlarged and can rupture

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31
Q

cause of acute gastric imapction

A

poor dentition, old age, trichobezoars, persimmon seeds, inappropriate feeding

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32
Q

signs of acute gastric impaction

A

acute colic at presentation, endotoxemia, possible rupture

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33
Q

diagnosis of gastric impaction

A
  • resistance to stomach tube
  • enlargement gastric outline
  • stomach may be palpable
  • gastroscopy
  • transcutaneous US
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34
Q

treatment of acute gastric impcation

A

Gastric lavage – remove soluble material
Continuous lavage
- 5 L/h as continuous infusion via indwelling tube
- position in terminal oesophagus – connect to overhead hanger
- alternate electrolyte with water to prevent Na overload
- daily mineral oil

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35
Q

prognosis of acute gastric imapction

A

good

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36
Q

predisposition of chronic gastric impaction

A

not known, increased in warmbloods

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37
Q

signs of chronic gastric impaction

A

failure to gain weight/weight loss, change in abdominal silhouette, change in demeanour, ventral oedema, acute colic +/- prior recurrent colic

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38
Q

treatment of chronic gastric impaction

A
  • no forage other than grass, complete pelleted ration if required
  • prolonged continuous gastric lavage
  • aim to empty stomach
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39
Q

prognosis of chronic gastric impaction

A
  • progressive further dilatation of stomach
  • spontaneous rupture possible
  • 2-4 years from presentation
  • dependent on speed of initial diagnosis
  • lifelong diligent management needed
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40
Q

equine gastric ulceration syndrome (EGUS)

A

squamous erosion and ulceration

glandular ulceration (and inflammation)

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41
Q

predisposition of squamous erosion and ulceration

A
  • decreased access to grazing, high intake of concentrate rations, NSAIDs, crib-biting, prolonged periods without forage, pregnancy and other GI disorders
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42
Q

signs of squamous erosion and ulceration

A
  • loss of performance, decreased feed intake, colic as severity increases
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43
Q

diagnosis of squamous erosion and ulceration

A
  • gastroscopy, sucrose absorption may be herd screening tool

Stratified squamous ulceration scores:
- 0-4, with lesions more than 3 of clinical significance
- surface area Is primary determinant of score
- “crater” lesions, superficial erosions may appear due to fasting requirement

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44
Q

management of squamous erosion and ulceration

A
  • increased access to forage and grazing
  • decrease or stop concentrate feeds
  • decreased intensity of exercise
  • chaff feeds prior to exercise
  • reduce other stressors
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45
Q

prevention of squamous erosion and ulceration

A
  • improved management to reduce risk factors
  • gastroguard 1mg/kg at start of training
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46
Q

signs of glandular ulceratoin

A

Signs:
- erythema to ulceration, flat/raised/depressed/haemorrhagic/diphtheritic/proliferative
- raised inflammatory or diphtheritic lesions more significant
Refractory lesions:
- doxycycline 10mg/kg BID in sucralfate carrier, further 4 week course of omeprazole
Equine glandular polyps
- current colic: weight loss, short episodes of acute pain
Inflammatory polyps:
- longer treatment course, strict dietary control, life long management

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47
Q

treatment for EGUS

A
  • omeprazole 4mg/kg SID 4-6 weeks
  • tapered dose for 2 weeks
  • sucralfate 20mg/kg 3-4 x daily
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48
Q

duodenal biopsy technique

A
  • fasted for min of 14 hr
  • detomidine may reduce frequency of small intestinal contractions
  • collection of “bites” from same site with gastroscopic biopsy forceps – increases depth of sample
  • 6 samples from diameter of duodenum
  • submission in biopsy tray in 5% formol saline
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49
Q

equine asthma definition

A

chronic lung disorder that is marked by recurring episodes of airway obstructions manifested by laboured breathing accompanied especially by wheezing and coughing and by a sense of constriction in the chest and is triggered by hyperreactivity to various stimuli

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50
Q

equine asthma predisposition

A

environmental causes, genetics, infection (bacteria, viruses)

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51
Q

cause of equine asthma

A

: organic and inorganic particles, familial predisposition, infections

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52
Q

pathogenesis of equine asthma

A

not fully defined - airway hyperresponsiveness – inhalation allergens

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53
Q

signs of equine asthma

A

inflammation, bronchoconstriction, mucus production, bronchospasm, nasal discharge, exercise intolerance and respiratory difficulty

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54
Q

diagnosis of equine asthma

A

history, clinical exam, T, HR, RR, Ln.N, nasal discharge, cough, nostrils airflow, auscultation of thorax, rebreathing examination, haematology, endoscopy, respiratory endoscopy
Tracheal wash
- transtracheal or endoscopic + cytology and bacteriology
BAL
- blind or endoscope + cytology
- through the scope – 2m scope
- 1% lidocaine for cough suppression – 2 locations x20ml
- 240ml of warm saline
- frothy sample
- cytology

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55
Q

treatment of equine asthma

A

Environment
- 24h/day in the pasture, dust, bedding, ventilation, bring out horse when cleaning
Systemic corticosteroids
- anti-inflammatory effect
- decreases reactiivy + enhances functionality
- prednisolone or dexamethasone

Inhalation corticosteroids
- fluticasone propionate: most potent, long-lasting minimal adrenal suppression, effect lasts 24-48hr
- beclomethasone dipropionate: long lasting effect, cheaper

Bronchoconstriction: bronchodilators always combined with dust control +/- cortisteroids
- b2 adrenergic agonist:
o clenbuterol, salbutamol (albuterol), salmeterol

anticholinergic:
o smooth muscle
o atropine, N-butylscopolamine bromine, ipratropium bromide

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56
Q

prognosis of equine asthma

A

serve asthma: not curable, significant improvement in environmental3 hygiene

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57
Q

IAD 0 inflammatory airwayy disease definition

A

mild to moderate asthma

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58
Q

predisposition of IAD

A

all age and breed, racehorses

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59
Q

diagnosis of IAD

A

clinical exam (poor performance, intermittent cough, nasal discharge)
- mild to moderate increase in neutrophils, eosinophils and mast cell
- clinical signs of lower respiratory tract disease
- endoscopy and cytology of BAL

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60
Q

classification of IAD

A

Upper respiratory tract disease:
- infectious: influenzas, strangles etc
- non-infectious: structural and functional abnormalities of the pharynx, larynx and nasal passage
Lower respiratory tract disease:
- infectious: pneumonia, pleuropneumonia
- non-infectious (asthma, and EIPH)

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61
Q

differentials of IAD

A

ROA, viral infection, bacterial bronchitis, pleuropneumonia, parasitic lung invasion, neoplasia, upper airway inflammation

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62
Q

RAO - recurrent airway obstruction (severe equine asthma) definition

A

recurrent lower airway obstruction

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63
Q

predisposition of RAO

A

6-10 years, uncommon in young

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64
Q

cause of RAO

A

environmental, genetic, horses >8 years, domestic disease, pollen, common resp infections

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65
Q

signs of RAO

A

bronchoconstriction, mucus production and bronchospasms, tachypnoea and cough at rest, poor performance, difficulty breathing at rest, expiratory whistles

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66
Q

diagnosis of RAO

A

clinical signs + history, BAL, tracheal aspirates

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67
Q

treatment of RAO

A

palliative only, remove allergens, improve management, corticosteroids, bronchodilators

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68
Q

prognosis of RAO

A

clinical signs reversible on removal of allergens

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69
Q

differentials of RAO

A

bacterial pneumonia, lungworm infection, lung abscess, pulmonary neoplasia

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70
Q

areas of cardiac auscultation

A
  • mitral valve: left 5th ICS halfway between shoulder and sternum
  • Aortic valve – left 4th ICS just below point of shoulder
  • Pulmonic valve – left 3rd ICS just below point of shoulder
  • Tricuspid valve – right 3rd-4th ICS
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71
Q

heart sounds in horse

A
  • S1, S2, S3, S4 audible in healthy horses
  • S4 audible in nearly all horses
  • S3 audible about 30% of time
  • Splitting of S1/S2 sometimes occurs
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72
Q

ECG in horse

A

base apex ECG lead 1

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73
Q

equine atrial fibrillation

A

Most important arrhythmia affecting performance in athletic horses

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74
Q

predisposition of equine atrial fibrillation

A

horses predisposed to AF due to large atrial mass (size)

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75
Q

cause of equine atrial fibrillation

A

autonomic imbalance during exercise, myocardial disease, atrial dilation

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76
Q

signs of atrial fibrillation

A

poor performance, epistaxis during exercise

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77
Q

AF without heart disease

A
  • poor performance and exercise intolerance
  • CO at rest is normal
  • check for mitral/tricuspid regurgitation, aortic regurgitation
  • CBC and chemistry, heart rate, ECG
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78
Q

AF with heart disease

A
  • myocardial disease or myocardial scarring, valvular disease with heart enlargement, increased HR, grade 3/6 or loud murmur, atrial enlargement
  • treat heart disease
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79
Q

diagnosis of AF

A

ECG (absence of P wave, irregularly irregular), auscultation

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80
Q

treatment of AF

A

standard therapies: digoxin, flecainide (minimal efficacy), quinidine sulphate/gluconate (most used), amiodarone (some efficacy and side effects), transvenous electrical conversion
- <48 h = no treatment; observe for spontaneous conversion
- >48 h but <7 days = consider IV quinidine gluconate if available if not, oral QS or TVEC
- >48 h but < 4 months = consider either oral QS or TVEC
- > 4 months = consider TVEC or oral QS

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81
Q

prognosis of AF

A
  • duration <4 months, HR <60min, murmur <3/6 = 95% conversion rate, 25% recurrence rate, return to racing in 48hr
  • duration > 6 months, HR <60/min, murmur <3/6 = 80% conversion rate, 60% recurrence rate, return to racing in 24- 48hr
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82
Q

atrial/ventricular premature contractions (cause, sign, diagnosis and treatment)

A

Cause: electrolyte depletion, myocardial disease
Signs: premature beat worsens with exercise and reduce CO leading to exercise intolerance, minimal or no symptoms at rest
Diagnosis: chemistry and UA with fractional excretion of electrolytes to assess electrolyte homeostasis, CBC, 24hr ECG
Treatment: rest

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83
Q

cause of equine ventricular tachycardia

A

severe systemic disease (intestinal disease; colic and infectious disease) or underlying heart disease (myocarditis)

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84
Q

pathogenesis of VT

A

most severe myocardial disease, can affect cardiac output at rest, can lead to V-fib

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85
Q

signs of VT

A

exercise intolerance, weakness, loss of consciousness and respiratory distress

86
Q

diagnosis of VT

A

Auscultation – regular rhythm with booming heart sounds, prominent jugular pulses, variable blood pressure, variable peripheral pulse or pulse deficits

87
Q

treatment of VT

A
  • supplement Mg, K, Ca if needed
  • anti-inflammatory drugs in horses with endotoxemia
  • if CO not normal at rest = clinical signs of cardiovascular collapse
  • if HR >100/min or multifocal/polymorphic
  • R on T phenomenon
  • Torsade de points
  • lidocaine (0.5mg/kg boluses) often doesn’t work in horses, quinidine
88
Q

prognosis of VT

A

life threatening in advanced cases, with medication it’s good

89
Q

predisposition of valvular disease

A

most common in older horse

90
Q

cause of valvular disease

A

Acquired valvular incompetency common, affects mitral, aortic and tricuspid valves causing regurgitation

91
Q

pathogenesis of valvular dsiease

A

stenotic congenital lesions extremely, rare in horses.

92
Q

signs of valvular disease

A

degenerative thickening, bacterial endocarditis, rupture of chordae tendinae, cardiomegaly, valvulitis

93
Q

diagnosis of valvular dsiease

A

Valvular insufficiency
- physical exam: auscultation, pulses, vein, ECG, lab testing
Mitral regurgitation
- MR radiates to heart base and can sound louder near AV
- MR commonly produces goose honk
Aortic regurgitation:
- AR produces harsh diastolic murmur
- murmur sometimes cooing or buzzing
- bounding pulse with moderate to severe AR due to left volume overload

94
Q

treatment of valvular dsiease

A

none usually used, unless heart failure – furosemide

95
Q

prognosis of valvular disease

A

asymptomatic = good outlook, with more severe disease shouldn’t be ridden or exercised and have poor outlook

96
Q

cause, signs, diagnosis and treatment of myocardial dysunfction

A

Cause: electrolyte abnormalities, viral disease, endotoxemia, ionophores, ischemia, selenium deficiency, tumours, bacterial embolism, idiopathic cardiomyopathy
Signs: heart murmur, tachycardia, enlarged jugular veins, throbbing of the jugular veins, coughing, rapid breathing, lack of appetite, weight loss, collapse, exercise intolerance
Diagnosis: echo
Treatment: diuretics, ACE inhibitors, beta blockers

97
Q

predisposition of ventricular septal defect

A

most common congenital abnormality, may occur with other abnormalities of the heart present at birth

98
Q

pathogenesis of ventricular septal defect

A

shunting of blood from the LV into the RV due to the higher pressure of the left ventricle  recirculated causig enlargement

99
Q

signs of ventricular septal defect

A

Small defects
- pressure differential adequate – no effect – resistive defect
Large defects
- can die of CHF in first few days of life – non-resistive defects, pressure equilibration/shunt reversal

100
Q

diagnosis of ventricular septal defect

A

echo, chest x-ray

101
Q

treatment of ventricular septal defect

A

small defects don’t usually need treatment, removal of excessive blood cells

102
Q

predisposition of PPID

A

uncommon in equids <15 yr., no apparent breed or sex predilection

103
Q

cause of PPID

A

loss of dopaminergic inhibition of the melanotropes

104
Q

pathogenesis of PPID

A

slowly progressive degenerative disease of hypothalamic dopaminergic neurones
hypothalamus  dopamine  PPID  ACTH  adrenal gland  cortisol
hypothalamus  TRH  PPID  ACTH  Adrenal gland  cortisol

105
Q

signs of PPID

A

hypertrichosis, prone to infections, PUPD, skeletal muscle atrophy, laminitis

Early:
- change in attitude, decreased performance, delayed haircoat shedding, abnormal sweating, infertility, laminitis, regional adiposity, regional hypertrichosis
Advanced:
- dull attitude, altered mentation, exercise intolerance, generalised hypertrichosis, loss of haircoat shedding, topline muscle atrophy, rounded abdomen, PUPD, infertility

106
Q

diagnosis of PPID

A

Lab:
- hyperglycaemia, hyperinsulinemia, hypertriglyceremia, high faecal egg count

TRH stimulation test – early PPID
- horses can be tested after hay but not for 12 hours after grain meal
- be performed before oral sugar test, don’t perform after
- administer -.5 mg (horses <250kg), or 1.0mg (horses >250kg) IV
- collect samples at 0 and 10 minutes after TRH application
- submit sample for TRH in the same manner as
ACTH

Basal ACTH concentration – moderate to advanced PPID (time 0 for TRH stimulation test)
- Glass or plastic tubes containing EDTA (purple top)
- Collect at any time of the day
- Keep samples cool (ice packs or refrigerator) at all times
- Centrifuge and separate plasma before shipping
- Ship overnight with ice packs or frozen

Overnight dexamethasone suppression test
MRI specific for pars intermedia enlargement
Insulin dysregulation
- 30% of PPID will have ID
- increased laminitis risk

107
Q

treatment of PPID

A
  • dopamine agonist
  • pergolide – prascend
    o 0.5mg for horse <250kg, <500kg, 1.0mg/horse
    o side effects: appetite reduction, decrease or discontinue for 5 days or till appetite returns
  • cabergoline – dopamine agonist, cyproheptadine – serotonin antagonist
108
Q

prognosis of PPID

A

> /–75% of cases improve clinically and endocrinologically with treatment

109
Q

definition of equine metabolic sydnrome

A

collection of risk factors highly associated with an increased risk of hyperinsulinemia-associated laminitis (HAL) and other morbidities

110
Q

predisposition of equine metabolic sydnrome

A

pony breeds, domesticated spanish mustangs, etc

111
Q

cause of equine metabolic syndrome

A

obesity, but not every fat horse has EMS

112
Q

pathogenesis of equine metabolic sydnrome

A

alters cortisol metabolism, results from excess production of active cortisol in fat cells, or adipose tissue with normal pituitary gland function. Abnormal fat deposition and laminitis

113
Q

signs of equine metabolic syndrome

A

generalised obesity, regional adiposity, laminitis, altered reproductive cycling in mares

114
Q

diagnosis of equine metabolic syndrome

A

Basal insulin
- resting (basal) insulin concentration
- single blood sample collected
- horse is fed (hay or pasture, no grain)
- plasma/ serum insulin concentrations are measured to detect resting hyperinsulinemia

oral sugar test – corn syrup
- ideally fast horse for 6 hours or feed only low NSC forage
- administer 0.15mls/kg karo syrup by dosing
- 60-90 minutes after dosing, take blood sample twice at 15-minute intervals for measurement of insulin and glucose
- Insulin above reference suggest ID, simple but with great variability in results

Oral sugar test – dextrose
- Ideally fast horse for 6 hours or fed only low NSC forage
- Feed 1g/kg bodyweight powdered dextrose, mixed with 1g/kg bodyweight low sugar chaff and 1ml/kg bodyweight water
- Collect a blood sample for measurement of insulin and glucose 2 hours later
- Oral dextrose powder can be used when corn syrup unavailable
- Test procedure and cut-off values for interpretation differ

Insulin tolerance test
- no fasting, just hay,
- collect baseline blood
- administer insulin IV
- collect blood after 30 minutes and test glucose

115
Q

treatment for equine metabolic syndome

A
  • reduce dietary sugar intake
  • decrease pasture (grazing muzzle)
  • eliminate concentrate
  • low NSC hay (soaking)
  • restrict calorie for weight loss, exercise
  • drugs (levothyroxine, metformin)
116
Q

prognosis of equine metabolic syndrome

A

depends on the severity of laminitis lameness and associated hoof degradation

117
Q

diagnosis of equine myopathies

A

Serum CK
- limited elevations may accompany training or transport
- recumbent animals may also have slightly elevated CK activities

Serum AST
- high activity in skeletal and cardiac muscle and also in liver, RBC and other tissues
- elevations are not specific for myonecrosis and increases could be the result of haemolysis, muscle, liver or otheor organ damage
- AST activity peaks between 12-24 hours after the insult

Vitamin E
- concentration can be measured in serum concentration

Selenium
- whole blood selenium concentration or glutathione peroxidase measured in EDTA or heparain tubes

Urinalysis
- elevations in creatinine or suspected electrolyte imbalance
- USG, protein content, WBC count, RBC count and elevation of cast formation

118
Q

predisposition of exertion rhabdomyolysis

A

racehorses, thoroughbred or trotters

119
Q

cause of exertional rhabdomyolysis

A

intense or prolonged exercise, excess training, exercise during viral illness/electrolyte abnormality

120
Q

pathogenesis of Exertional Rhabdomyolysis

A

syndrome of muscle cramping that occurs during physical exertion or exercise

121
Q

types of exertional rhabdomyolysis

A

Chronic exertional rhabdomyolysis
- horse has underlying myopathy
- underlying pathologic condition of the muscle
- diet plays a role in horse that are predisposed to exertional rhabdomyolysis from several different underlying myopathies

Sporadic exertional rhabdomyolysis
- Horse has been over-exerted physically
- Physical exertion to a state of abnormal exhaustion
- An environment of heat and high humidity can result in multiple organ failure
- Rhabdomyolysis is a common component

Recurrent exertional rhabdomyolysis
- It may affect as much as 5% of the racing thoroughbred population
- Is inherited as an autosomal dominant trait
- Expression of the disorder is multifactorial

122
Q

signs of exertional Rhabdomyolysis

A

Sporadic:
- muscle stiffness, shortened stride of hind limbs, reluctance of move, tight, sore muscles of the back, anxiety, pain, sweating, rapid breathing

Recurrent:
- Mild to moderate signs of muscle cramping
- Affected muscles are firm and painful on palpation
- Mild to severe pain, anxiety, profuse sweating, refusal to move and increased heart and respiratory rates
- In severe cases, the horse cannot stand
- Recovery depends on the amount of necrosis in the muscle fibres. Days to weeks. Months

123
Q

diagnosis of exertional Rhabdomyolysis

A

Elevated CK and AST
- muscle biopsy: chronic changes no signs of PSS<

124
Q

treatmetn of exertional Rhabdomyolysis

A

pain reflief, rehydration

125
Q

prognosis of exertional Rhabdomyolysis

A

generally great, severe episodes can cause collapse and even death, but it’s rare

126
Q

definition of polysaccharide storage myopathy (PSM)

A

accumulation of alpha-crystalline polysaccharides in skeletal muscle

127
Q

signs of PSM

A

mild to severe accumulation of abnormal polysaccharide within the myoplasm, it’s characterised by repeated episodes of exertional rhabdomyolysis that in some cases may be induced with little exercise

128
Q

Type 1 PSM

A
  • H309G mutation- causing abnormal 3D structure of glycogen
  • breeds: Belgian cold-blooded, Percheron, shire, haflinger, quarter horse
  • signs: from asymptomatic to severe, after 20 minutes of light exercise, after a few days of rest
    o acute: similar to those with other forms of Rabb
    o chronic: lack of energy under the saddle, reluctance to move forward, stopping and stretching as if wet and poor attitude towards work
  • diagnosis:
    o elevated CK at rest
    o up to 3x after exercise test
    o PSSM 1 – GYS1 mutation
    o blood or hair follicles
    o biopsy in horses older than 2 years
129
Q

Type 2 PSM

A
  • they’re non GYS1 gene mutation
  • diagnosis: skeletal muscle histopathology
  • breeds: quarter and similar warbloods, araps, connemares
  • signs:
    o sore muscles, undiagnosed lameness, poor performance, unwillingness to move forward under the saddle, unwillingness to collect and in some cases a slow onset of back muscle atrophy, especially if not working
    o increased serum CK activity after exercise is rarely present in warm-blooded horses
130
Q

treatment PSM

A

keep blood insulin levels low and reduce glycogen storage in muscle, NSAIDs

131
Q

prognosis PSM

A

no cure, but can be managed successfully

132
Q

cause of malignant hyperthermia

A

suspected genetic abnormality of skeletal muscle, triggering factors (volatile anaesthetic agents, environmental factors)

133
Q

pathogenesis of malignant hyperthermia

A
  • Cause of autosomal dominant mutation in skeletal muscle of ryanodine receptor 1 (RYR1) gene
  • reduces activation and raises the threshold for deactivation of the ryanodine receptor
  • anaerobic glycogen metabolism is activated
  • lactate and excessive heat are created while massive muscle necrosis occurs
134
Q

signs of malignant hyperthermia

A

Symptoms: respiratory distress, fever, arrhythmias, muscles stiffness, cramps, sweating
Signs: asymptomatic or mild signs of rhabdomyolysis, Possible peracute death, tachycardia, hypertension, tachypnoea, raised HR, metabolic and respiratory acidosis

135
Q

diagnosis of malignant hyperthermia

A

history and clinical signs, biochemistry (hyperkalemia)

136
Q

treatment of malignant hyperthermia

A

remove inciting stimulus, reduce temperature +/- administration of dantrolene sodium solution

137
Q

prognosis of malignnat hyperthermia

A

good if treated early, high mortality if not rapidly diagnosed and treated

138
Q

differentials of malingnat hyeprthermia

A

pyrexia from other cause, heat stroke, hypocalcaemia, hypernatremia

139
Q

predisposition of myofibrillar myopatby

A

6-8 years

140
Q

cause of myofibrillar myopathy

A

trauma to muscle

141
Q

pathogenesis of myofibrillar myopathy

A

: identified disorder in horses with exercise intolerance or intermittent rhabdom
- impaired myofibril deposition, ectopic cytoskeletal protein accumulation and Z-disc degeneration

142
Q

signs of myofibirilary myopathy

A

Lack of endurance and unwillingness to move forward, inability to collect, abnormal hole crossings, and inability to maintain a normal gallop
Signs: mild onset of intolerance to exercise

143
Q

endurance - myofibirllary myoatphy

A
  • occasional increases in serum CK activity after a race or during exercise following a week or more rest
  • pain, sweating, and reluctance
  • Myoglobinuria can be observed in horses only with mild muscle stiffness
  • Between episodes, either, lactate, CK and AST within limits
144
Q

diagnosis fo myofibrilary myopathy

A
  • serum CK and AST activities are usually within normal limits, unless samples are taken during rhabd
145
Q

treatment of myofibrillar myopathy

A
  • correct fluid loss
  • establish diuresis
  • analgesia
    o mild cases: acepromazine (0.04-0.07mg/kg), xylazine (0.4-0.8mg/kg)
    o severe cases: NSPUL: phenylbutazone (2.2-44mg/kg), flunixin meglumine (1.1mg/kg)
  • minimise further muscle damage:
    o rest, limited movement 48hr
    o monitoring of muscle enzymes, gradual return to work
146
Q

management of myofibrillary myopathy

A
  • diet: limit glycogen synthesis by reducing circulating insulin and stimulate glycogen metabolism
  • low carb more fat, Vit E, wet hay
  • exercise: regular exercise, without breaks, avoid stress, gradually increases intensity
  • dantrolene: RYR1 antagonist
  • inhibits caffeine – induced calcium release from ER
  • 2-4 hr before training 1-4mg/kg
147
Q

Equine atypical myopathy (sycamore poisoning ~ helicopter) cause

A

ingesting sycamore seeds, leaves or seedlings

148
Q

pEquine atypical myopathy (sycamore poisoning ~ helicopter) pathogenesis

A

acute, severe rhabdomyolysis associated with ingestion of hypoglicyn A contained in seeds and seedlings of sycamore maple

149
Q

signs of atypical myopathy

A
  • dark MM, MM become dark red, urine has a dark brown colour, general weakness, muscle trembling, heart problems, signs of severe colic (still have appetite though)
150
Q

acute disease of atypical myopathy

A
  • apathy, lethargy, colic, muscle stiffness and tremor are observed
  • significant swearing and muscle weakness
  • few hours, horses affected by EAM cannot stand for more than a few minutes
  • animals often have difficulty breathing and lying down and most die within 72 hours of onset of signs
151
Q

diagnosis of atypical myopathy

A

measuring CK, presence of red/brown urine, history (whether near sycamore tree)

152
Q

treatment of atypical myopathy

A
  • no specific therapy
  • supportive therapy
  • treatment in most cases still unsuccessful
  • emphasis is still on prevention
  • remove the animal from the pasture as soon as possible and place it in a stable with a deep base to prevent hypothermia and further damage to the body
153
Q

prognosis of atypical myopathy

A

fatal for around ¾ of affected horses

154
Q

bacterial dermatitis/ rain scald

A

Bacterial infection of skin that forms matted scabs affecting back and rump, usually lower limbs

155
Q

cause of rain scald

A

dermatophilus congolensis

156
Q

pathogenesis of rain scald

A

prolongged wetting and cracking of skin surface allows bacteria to enter

157
Q

diagnsosi fo rain scald

A
  • clinical picture (dorsum, distal parts of extremity, muzzle, hoof, interdigital, crust) + history
  • typical sites, crusts, rainy weather
  • microscopy: crusts into sterile water
  • staining by gram
  • filaments of thick clumps of cocci
158
Q

treatment of rain scald

A

allow dry condition, topical (iodine and chlorhexidine), antibacterial shampoo/7 days bathing (tetracyclines, TMS, penicillin)

159
Q

prognosis of rain scald

A

will heal but can recur

160
Q

Corynebacterium pseudotuberculosis predispotion

A

all ages, median age of 5 years

161
Q

cause of Corynebacterium pseudotuberculosis

A

intracellular G+ cocci

162
Q

pathogenesis of Corynebacterium pseudotuberculosis

A

caseous lymphadenitis of the goat adnd sheep

163
Q

signs of Corynebacterium pseudotuberculosis

A

superficial and internal abscesses, ulcerative lymphangitis
- fever, lameness, anorexia, depression, anaemia

164
Q

diagnosis of C. pseudoTb

A

CBC, biochemistry, US of muscle mass and aspiration of pus from abscess
- CBC: leucocytosis, neutrophilia, increased plasma fibrinogen, hyperglobulinemia
- Biochem: hyperproteinaemia, anaemia, AST, CK

165
Q

treatment of C.pseudo Tb

A

isolation, surgery and long term ATB

166
Q

prognosis of C.pseudoTb

A

fair to good if single abscess and responds well, guarded for deeper seated/multiple/lymphangitis

167
Q

predispotiion of staph folliculitis

A

hot + humid environment, high insect/ tick population, wounds, poorly groomed horses

168
Q

signs fo staph folliculitis

A

circular alopecia, crusts, edema, pustule, face, ventral, udder

169
Q

diagnosis of staph of folliculitis

A

histology, often around the eyes, bacterial culture, histopathology

170
Q

treatment of staph folliculitis

A

systemic: novobicin local, ATB baths (chlorhexidine), attention to zoohig conditions

171
Q

exudative epidermtiis pig

A
  • greasy pig disease
  • staph hyicus
  • sudden occurrence
  • piglets from 1-4 weeks of age
  • culture 50% and s. aureus
  • clinical picture: no elevated temp, painful, pruritus’, mucus (sebum, sweat)
  • death after 3- 5 days
  • diagnosis: histology and bacterial culture
  • differential: dermatophytosis, Zn, scabies
172
Q

differentials of staph folliculitis

A

dermatophilosis

173
Q

predisposition of dermatophytosis

A

young horses most common, geriatric have increased risk

174
Q

cause of dermatophytosis

A

Microsporum, trichophyton, Epidermophyton (invades and feeds on keratinised tissue)

175
Q

signs of dermatophytosis

A

alopecia, ringworm, crusts, erythema, papules, +/- itching, mostly the cause of folliculitis

176
Q

diagnosis of dermatophytosis

A
  • wood lamp – rarely and on farm animals
  • microscopic examination with paraffin: hyphae or spores
  • biopsy: fast + special colouring
  • mycological search: DX in 90% cases
  • ELISA
177
Q

treatment of dermatopjhytosis

A

Topical
- large surface lime sulphur 5%
- bleach 1:10 solution
- chlorhexidine ideally 3-4%
- enilconazole
- smaller areas: shampoo and miconazole
- ketoconazole + chlorhexidine
Systemic: not practical, grisoflavinein the calves
Vaccine: ringvac

178
Q

prognosis of dermatophytosis

A

spontaneous remission unless concurrent immunodeficiency, or re-infection occurs

179
Q

cause of mud fever

A

multifactorial, bacteria, fungi, parasites, vasculitis, contact irritant or most often a combination of the above – dermatophilus congolensis

180
Q

signs of mud fever

A

alopecia and crusting

181
Q

diagnosis of ud fever

A

microscopic identification

182
Q

treatment of mud fever

A

hair cutting/shaving, drying, ATB and antifungal shampoo

183
Q

allergies

A

Cause: atopic dermatitis, allergies to dust, mould, insects, food or drugs
Treatment:
- allergies can be treated
- intradermal testing
- specific vaccine for a specific allergen
- antihistamines and corticosteroids

184
Q

cause of photosensitiation

A

hazardous combination of certain plants and UV light

185
Q

types of photosensitiation

A

Type 1: ingestion of toxic substances, plants, drugs
- bishops weed, buckwheat
Type 2: abnormal metabolism of porphyria anaemia, discolouration of teeth
Type 3: liver disease, accumulation of phylloerythrin

186
Q

signs of photosensitiation

A

immediate discomfort and agitation when exposed to light, rubbing or scratching of lightly pigmented or exposed skin areas and lesions in exposed areas, hairless, blisters with pus, redness and swelling of the skin

187
Q

diagnosis of photosensitation

A

assess pasture and hay for contaminants
- skin biopsy: to rule out bacterial infections + liver biopsy
- Biochem: assess liver and kidney function

188
Q

treatment of photosensitation

A

minimised exposure to UV light, pasture turnout at night, keep skin wounds clean

189
Q

differentials of photosensitation

A

sunburn, contact dermatitis, infectious condition

190
Q

viral dsiease

A

viral papilloma, bovine papilloma virus 11 BPV, goats and sheep: 1 strain

191
Q

horse lice cause

A

Predisposition: overcrowding, sick ,old/debilitated horses
Cause: damalinia equie (eats skin debris and secretion), haematopinus asini (drinks blood)

192
Q

signs of horse lice

A

cold season, pruritus, hair loss, anaemia, rough coat, weight loss, skin wounds, stress caused by irritation

193
Q

diagnosis of horse live

A

microscopy, nits

194
Q

eatment of horse lice

A

ivermectin (0.2mg/kg SC, 2 x 3 week interval), eprinomectin (0.5mg/kg pour on) and moxidectin (0.5mg/kg) pour ons are approved

195
Q

cause of scabies

A
  • sarcoptes scabieie var. equi (head)
  • chorioptes equi (legs)
  • psoroptes equi (trunk)
  • pyemotes tritici
  • trombicula and eutrombicula species
196
Q

predispostiion of scabies

A

young debilitatd animals

197
Q

signs of scabies

A

: lesions begin on head, neck and ears and can spread over the entire body, itchy, rubbing and biting, hyperkeratosis

198
Q

diagnosis of scabies

A

deep skin scraping, biopsy
KOH digestion
- 10min in 10% KOH in boiling water bath or longer if scraping is placed in hot KOH directly on slide, mites and eggs will be visible

199
Q

treatment of scabies

A

hair cutting/ shaving, antiparasitic products against scabies (permethrin), oral pastes (ivermectin, moxidectin), therapy of all horses in the barn

200
Q

differetnials of scabies

A

psoroptic mange, lice, insect hypersensitivity

201
Q

predispositon of sarcoid

A

genetic predisposition, Arabian, quarterhorse

202
Q

cause of sarcoid

A

bovine papillomavirus 1+2

203
Q

pathogenesis of sarcoid

A

spread by insect bites or trauma

204
Q

signs of sarcoid

A

: occult (flat), verrucous (scaly, warty), nodular or fibroblastic, alopecia, large ulcerated fibromatous and invasive tumours

205
Q

diagnosis of sarcoid

A

biopsy

206
Q

treatment of sarcoid

A

depends on type, size and location, surgically removed, cytostatics

207
Q

prognosis of sarcoid

A

very guarded

208
Q

predisposition o melanome

A

grey and white horses, over 6 years

209
Q

signs of melanoma

A

tail, anus, inside the foreskin and near the parotid salivary gland, hyperpigmented, firm nodular lesions, ulceration with exudation of thick black fluid

210
Q

diagnosis of melnaom

A

pathology, FNA, US, skin biopsy

211
Q

treatment of melanoma

A

surgical removal, chemotherapy, cimetidine, vaccination with a specific vaccine against the tumour itself

212
Q

rognosis of melanoma

A

variable, often benign and cause no problems, multiple tumours = poorer prognosis

Internal (12 decks)

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