Equine Flashcards
(212 cards)
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)…
2
Q
signalment of colic
A
age, gender, breed
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
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
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)
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
7
Q
prognosis of colic
A
guarded
8
Q
simple oesophageal obstruction predisposition
A
freisians
9
Q
cause of simple oesophageal obstruction
A
ingestion of material that when swallowed, becomes impacted in the oesophagus + doesn’t pass into stomach
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,
11
Q
diagnosis of simple ossophageal obstruction
A
- resentment of cranial oesophageal palpation
- may be obvious swelling
- resistance to passage of nasogastric tube
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
13
Q
prognosis of simple oesophageal obstruction
A
mostly good, but depends on severity of the impaction
14
Q
differential of simple oesophageal obstruction
A
oral foreign bodies, dysphagia due to neurological disease, periodontal disease, periodontal
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
16
Q
cause of strangles
A
strep eqiu
17
Q
signs of strangles
A
dysphagia, cough, dyspnoea, lymphadenitis, pyrexia, retropharyngeal pain and swelling, maybe guttural pouch involvement/ subcutaneous emphysema
18
Q
diagnosis of strangles
A
history of colic/nasogastric intubation, endoscopy or radiography, bacteriology, CBC (maybe leukocytes, neutrophils), biochemistry (plasma: fibrinogen)
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
20
Q
prognosis of strangles
A
poor
21
Q
expected sequelae of strangles
A
dysphagia, fasciitis, aspiration pneumonia, sepsis, potential for mediastinitis, similar signs to oesophageal rupture
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
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
24
Q
acute gastric dilation predisposition
A
sporadic
25
acute gastric dilation associated with
reflux of intestinal contents secondary to acute intestinal obstruction, ingestion of excess fluid/feedstuff or acute idiopathic dilation after racing
26
signs of acute gastric dilation
acute abdominal pian, spontaneous nasogastric reflux, progressive acidosis, endotoxemia, colic
27
diagnosis of acute gastric dilation
based on presentation, nasogastric reflux without other identifiable cause
28
treatment of acute gastric dilation
gastric decompression and lavage
- IV fluid support, correction of acidosis + management of endotoxemia
29
complication of acute gastric dilation
endotoxemia sequelae (laminitis, acute renal failure), gastric (transient loss of motility, delayed emptying, serosal tear)
30
acute gastric impactin
Firm accumulation of food in stomach, causes stomach to become enlarged and can rupture
31
cause of acute gastric imapction
poor dentition, old age, trichobezoars, persimmon seeds, inappropriate feeding
32
signs of acute gastric impaction
acute colic at presentation, endotoxemia, possible rupture
33
diagnosis of gastric impaction
- resistance to stomach tube
- enlargement gastric outline
- stomach may be palpable
- gastroscopy
- transcutaneous US
34
treatment of acute gastric impcation
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
35
prognosis of acute gastric imapction
good
36
predisposition of chronic gastric impaction
not known, increased in warmbloods
37
signs of chronic gastric impaction
failure to gain weight/weight loss, change in abdominal silhouette, change in demeanour, ventral oedema, acute colic +/- prior recurrent colic
38
treatment of chronic gastric impaction
- no forage other than grass, complete pelleted ration if required
- prolonged continuous gastric lavage
- aim to empty stomach
39
prognosis of chronic gastric impaction
- progressive further dilatation of stomach
- spontaneous rupture possible
- 2-4 years from presentation
- dependent on speed of initial diagnosis
- lifelong diligent management needed
40
equine gastric ulceration syndrome (EGUS)
squamous erosion and ulceration
glandular ulceration (and inflammation)
41
predisposition of squamous erosion and ulceration
- decreased access to grazing, high intake of concentrate rations, NSAIDs, crib-biting, prolonged periods without forage, pregnancy and other GI disorders
42
signs of squamous erosion and ulceration
- loss of performance, decreased feed intake, colic as severity increases
43
diagnosis of squamous erosion and ulceration
- 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
44
management of squamous erosion and ulceration
- increased access to forage and grazing
- decrease or stop concentrate feeds
- decreased intensity of exercise
- chaff feeds prior to exercise
- reduce other stressors
45
prevention of squamous erosion and ulceration
- improved management to reduce risk factors
- gastroguard 1mg/kg at start of training
46
signs of glandular ulceratoin
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
47
treatment for EGUS
- omeprazole 4mg/kg SID 4-6 weeks
- tapered dose for 2 weeks
- sucralfate 20mg/kg 3-4 x daily
48
duodenal biopsy technique
- 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
49
equine asthma definition
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
50
equine asthma predisposition
environmental causes, genetics, infection (bacteria, viruses)
51
cause of equine asthma
: organic and inorganic particles, familial predisposition, infections
52
pathogenesis of equine asthma
not fully defined - airway hyperresponsiveness – inhalation allergens
53
signs of equine asthma
inflammation, bronchoconstriction, mucus production, bronchospasm, nasal discharge, exercise intolerance and respiratory difficulty
54
diagnosis of equine asthma
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
55
treatment of equine asthma
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
56
prognosis of equine asthma
serve asthma: not curable, significant improvement in environmental3 hygiene
57
IAD 0 inflammatory airwayy disease definition
mild to moderate asthma
58
predisposition of IAD
all age and breed, racehorses
59
diagnosis of IAD
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
60
classification of IAD
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)
61
differentials of IAD
ROA, viral infection, bacterial bronchitis, pleuropneumonia, parasitic lung invasion, neoplasia, upper airway inflammation
62
RAO - recurrent airway obstruction (severe equine asthma) definition
recurrent lower airway obstruction
63
predisposition of RAO
6-10 years, uncommon in young
64
cause of RAO
environmental, genetic, horses >8 years, domestic disease, pollen, common resp infections
65
signs of RAO
bronchoconstriction, mucus production and bronchospasms, tachypnoea and cough at rest, poor performance, difficulty breathing at rest, expiratory whistles
66
diagnosis of RAO
clinical signs + history, BAL, tracheal aspirates
67
treatment of RAO
palliative only, remove allergens, improve management, corticosteroids, bronchodilators
68
prognosis of RAO
clinical signs reversible on removal of allergens
69
differentials of RAO
bacterial pneumonia, lungworm infection, lung abscess, pulmonary neoplasia
70
areas of cardiac auscultation
- 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
71
heart sounds in horse
- 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
72
ECG in horse
base apex ECG lead 1
73
equine atrial fibrillation
Most important arrhythmia affecting performance in athletic horses
74
predisposition of equine atrial fibrillation
horses predisposed to AF due to large atrial mass (size)
75
cause of equine atrial fibrillation
autonomic imbalance during exercise, myocardial disease, atrial dilation
76
signs of atrial fibrillation
poor performance, epistaxis during exercise
77
AF without heart disease
- poor performance and exercise intolerance
- CO at rest is normal
- check for mitral/tricuspid regurgitation, aortic regurgitation
- CBC and chemistry, heart rate, ECG
78
AF with heart disease
- myocardial disease or myocardial scarring, valvular disease with heart enlargement, increased HR, grade 3/6 or loud murmur, atrial enlargement
- treat heart disease
79
diagnosis of AF
ECG (absence of P wave, irregularly irregular), auscultation
80
treatment of AF
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
81
prognosis of AF
- 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
82
atrial/ventricular premature contractions (cause, sign, diagnosis and treatment)
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
83
cause of equine ventricular tachycardia
severe systemic disease (intestinal disease; colic and infectious disease) or underlying heart disease (myocarditis)
84
pathogenesis of VT
most severe myocardial disease, can affect cardiac output at rest, can lead to V-fib
85
signs of VT
exercise intolerance, weakness, loss of consciousness and respiratory distress
86
diagnosis of VT
Auscultation – regular rhythm with booming heart sounds, prominent jugular pulses, variable blood pressure, variable peripheral pulse or pulse deficits
87
treatment of VT
- 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
prognosis of VT
life threatening in advanced cases, with medication it’s good
89
predisposition of valvular disease
most common in older horse
90
cause of valvular disease
Acquired valvular incompetency common, affects mitral, aortic and tricuspid valves causing regurgitation
91
pathogenesis of valvular dsiease
stenotic congenital lesions extremely, rare in horses.
92
signs of valvular disease
degenerative thickening, bacterial endocarditis, rupture of chordae tendinae, cardiomegaly, valvulitis
93
diagnosis of valvular dsiease
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
treatment of valvular dsiease
none usually used, unless heart failure – furosemide
95
prognosis of valvular disease
asymptomatic = good outlook, with more severe disease shouldn't be ridden or exercised and have poor outlook
96
cause, signs, diagnosis and treatment of myocardial dysunfction
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
predisposition of ventricular septal defect
most common congenital abnormality, may occur with other abnormalities of the heart present at birth
98
pathogenesis of ventricular septal defect
shunting of blood from the LV into the RV due to the higher pressure of the left ventricle recirculated causig enlargement
99
signs of ventricular septal defect
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
diagnosis of ventricular septal defect
echo, chest x-ray
101
treatment of ventricular septal defect
small defects don’t usually need treatment, removal of excessive blood cells
102
predisposition of PPID
uncommon in equids <15 yr., no apparent breed or sex predilection
103
cause of PPID
loss of dopaminergic inhibition of the melanotropes
104
pathogenesis of PPID
slowly progressive degenerative disease of hypothalamic dopaminergic neurones
hypothalamus dopamine PPID ACTH adrenal gland cortisol
hypothalamus TRH PPID ACTH Adrenal gland cortisol
105
signs of PPID
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
diagnosis of PPID
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
treatment of PPID
- 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
prognosis of PPID
>/--75% of cases improve clinically and endocrinologically with treatment
109
definition of equine metabolic sydnrome
collection of risk factors highly associated with an increased risk of hyperinsulinemia-associated laminitis (HAL) and other morbidities
110
predisposition of equine metabolic sydnrome
pony breeds, domesticated spanish mustangs, etc
111
cause of equine metabolic syndrome
obesity, but not every fat horse has EMS
112
pathogenesis of equine metabolic sydnrome
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
signs of equine metabolic syndrome
generalised obesity, regional adiposity, laminitis, altered reproductive cycling in mares
114
diagnosis of equine metabolic syndrome
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
treatment for equine metabolic syndome
- reduce dietary sugar intake
- decrease pasture (grazing muzzle)
- eliminate concentrate
- low NSC hay (soaking)
- restrict calorie for weight loss, exercise
- drugs (levothyroxine, metformin)
116
prognosis of equine metabolic syndrome
depends on the severity of laminitis lameness and associated hoof degradation
117
diagnosis of equine myopathies
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
predisposition of exertion rhabdomyolysis
racehorses, thoroughbred or trotters
119
cause of exertional rhabdomyolysis
intense or prolonged exercise, excess training, exercise during viral illness/electrolyte abnormality
120
pathogenesis of Exertional Rhabdomyolysis
syndrome of muscle cramping that occurs during physical exertion or exercise
121
types of exertional rhabdomyolysis
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
signs of exertional Rhabdomyolysis
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
diagnosis of exertional Rhabdomyolysis
Elevated CK and AST
- muscle biopsy: chronic changes no signs of PSS<
124
treatmetn of exertional Rhabdomyolysis
pain reflief, rehydration
125
prognosis of exertional Rhabdomyolysis
generally great, severe episodes can cause collapse and even death, but it’s rare
126
definition of polysaccharide storage myopathy (PSM)
accumulation of alpha-crystalline polysaccharides in skeletal muscle
127
signs of PSM
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
Type 1 PSM
- 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
Type 2 PSM
- 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
treatment PSM
keep blood insulin levels low and reduce glycogen storage in muscle, NSAIDs
131
prognosis PSM
no cure, but can be managed successfully
132
cause of malignant hyperthermia
suspected genetic abnormality of skeletal muscle, triggering factors (volatile anaesthetic agents, environmental factors)
133
pathogenesis of malignant hyperthermia
- 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
signs of malignant hyperthermia
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
diagnosis of malignant hyperthermia
history and clinical signs, biochemistry (hyperkalemia)
136
treatment of malignant hyperthermia
remove inciting stimulus, reduce temperature +/- administration of dantrolene sodium solution
137
prognosis of malignnat hyperthermia
good if treated early, high mortality if not rapidly diagnosed and treated
138
differentials of malingnat hyeprthermia
pyrexia from other cause, heat stroke, hypocalcaemia, hypernatremia
139
predisposition of myofibrillar myopatby
6-8 years
140
cause of myofibrillar myopathy
trauma to muscle
141
pathogenesis of myofibrillar myopathy
: identified disorder in horses with exercise intolerance or intermittent rhabdom
- impaired myofibril deposition, ectopic cytoskeletal protein accumulation and Z-disc degeneration
142
signs of myofibirilary myopathy
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
endurance - myofibirllary myoatphy
- 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
diagnosis fo myofibrilary myopathy
- serum CK and AST activities are usually within normal limits, unless samples are taken during rhabd
145
treatment of myofibrillar myopathy
- 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
management of myofibrillary myopathy
- 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
Equine atypical myopathy (sycamore poisoning ~ helicopter) cause
ingesting sycamore seeds, leaves or seedlings
148
pEquine atypical myopathy (sycamore poisoning ~ helicopter) pathogenesis
acute, severe rhabdomyolysis associated with ingestion of hypoglicyn A contained in seeds and seedlings of sycamore maple
149
signs of atypical myopathy
- 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
acute disease of atypical myopathy
- 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
diagnosis of atypical myopathy
measuring CK, presence of red/brown urine, history (whether near sycamore tree)
152
treatment of atypical myopathy
- 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
prognosis of atypical myopathy
fatal for around ¾ of affected horses
154
bacterial dermatitis/ rain scald
Bacterial infection of skin that forms matted scabs affecting back and rump, usually lower limbs
155
cause of rain scald
dermatophilus congolensis
156
pathogenesis of rain scald
prolongged wetting and cracking of skin surface allows bacteria to enter
157
diagnsosi fo rain scald
- 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
treatment of rain scald
allow dry condition, topical (iodine and chlorhexidine), antibacterial shampoo/7 days bathing (tetracyclines, TMS, penicillin)
159
prognosis of rain scald
will heal but can recur
160
Corynebacterium pseudotuberculosis predispotion
all ages, median age of 5 years
161
cause of Corynebacterium pseudotuberculosis
intracellular G+ cocci
162
pathogenesis of Corynebacterium pseudotuberculosis
caseous lymphadenitis of the goat adnd sheep
163
signs of Corynebacterium pseudotuberculosis
superficial and internal abscesses, ulcerative lymphangitis
- fever, lameness, anorexia, depression, anaemia
164
diagnosis of C. pseudoTb
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
treatment of C.pseudo Tb
isolation, surgery and long term ATB
166
prognosis of C.pseudoTb
fair to good if single abscess and responds well, guarded for deeper seated/multiple/lymphangitis
167
predispotiion of staph folliculitis
hot + humid environment, high insect/ tick population, wounds, poorly groomed horses
168
signs fo staph folliculitis
circular alopecia, crusts, edema, pustule, face, ventral, udder
169
diagnosis of staph of folliculitis
histology, often around the eyes, bacterial culture, histopathology
170
treatment of staph folliculitis
systemic: novobicin local, ATB baths (chlorhexidine), attention to zoohig conditions
171
exudative epidermtiis pig
- 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
differentials of staph folliculitis
dermatophilosis
173
predisposition of dermatophytosis
young horses most common, geriatric have increased risk
174
cause of dermatophytosis
Microsporum, trichophyton, Epidermophyton (invades and feeds on keratinised tissue)
175
signs of dermatophytosis
alopecia, ringworm, crusts, erythema, papules, +/- itching, mostly the cause of folliculitis
176
diagnosis of dermatophytosis
- 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
treatment of dermatopjhytosis
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
prognosis of dermatophytosis
spontaneous remission unless concurrent immunodeficiency, or re-infection occurs
179
cause of mud fever
multifactorial, bacteria, fungi, parasites, vasculitis, contact irritant or most often a combination of the above – dermatophilus congolensis
180
signs of mud fever
alopecia and crusting
181
diagnosis of ud fever
microscopic identification
182
treatment of mud fever
hair cutting/shaving, drying, ATB and antifungal shampoo
183
allergies
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
cause of photosensitiation
hazardous combination of certain plants and UV light
185
types of photosensitiation
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
signs of photosensitiation
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
diagnosis of photosensitation
assess pasture and hay for contaminants
- skin biopsy: to rule out bacterial infections + liver biopsy
- Biochem: assess liver and kidney function
188
treatment of photosensitation
minimised exposure to UV light, pasture turnout at night, keep skin wounds clean
189
differentials of photosensitation
sunburn, contact dermatitis, infectious condition
190
viral dsiease
viral papilloma, bovine papilloma virus 11 BPV, goats and sheep: 1 strain
191
horse lice cause
Predisposition: overcrowding, sick ,old/debilitated horses
Cause: damalinia equie (eats skin debris and secretion), haematopinus asini (drinks blood)
192
signs of horse lice
cold season, pruritus, hair loss, anaemia, rough coat, weight loss, skin wounds, stress caused by irritation
193
diagnosis of horse live
microscopy, nits
194
eatment of horse lice
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
cause of scabies
- sarcoptes scabieie var. equi (head)
- chorioptes equi (legs)
- psoroptes equi (trunk)
- pyemotes tritici
- trombicula and eutrombicula species
196
predispostiion of scabies
young debilitatd animals
197
signs of scabies
: lesions begin on head, neck and ears and can spread over the entire body, itchy, rubbing and biting, hyperkeratosis
198
diagnosis of scabies
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
treatment of scabies
hair cutting/ shaving, antiparasitic products against scabies (permethrin), oral pastes (ivermectin, moxidectin), therapy of all horses in the barn
200
differetnials of scabies
psoroptic mange, lice, insect hypersensitivity
201
predispositon of sarcoid
genetic predisposition, Arabian, quarterhorse
202
cause of sarcoid
bovine papillomavirus 1+2
203
pathogenesis of sarcoid
spread by insect bites or trauma
204
signs of sarcoid
: occult (flat), verrucous (scaly, warty), nodular or fibroblastic, alopecia, large ulcerated fibromatous and invasive tumours
205
diagnosis of sarcoid
biopsy
206
treatment of sarcoid
depends on type, size and location, surgically removed, cytostatics
207
prognosis of sarcoid
very guarded
208
predisposition o melanome
grey and white horses, over 6 years
209
signs of melanoma
tail, anus, inside the foreskin and near the parotid salivary gland, hyperpigmented, firm nodular lesions, ulceration with exudation of thick black fluid
210
diagnosis of melnaom
pathology, FNA, US, skin biopsy
211
treatment of melanoma
surgical removal, chemotherapy, cimetidine, vaccination with a specific vaccine against the tumour itself
212
rognosis of melanoma
variable, often benign and cause no problems, multiple tumours = poorer prognosis
