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14 Cards in this Set

  • Front
  • Back
What are the types of muscle fibers?
type I (slow twitch): aerobic metabolism (endurance)
type II (fast twitch): anaerobic metabolism (speed & strength)
How is body temperature regulated in horses?
skin vasodilation
-prolonged sweating --> dehydration, electrolyte abnormalities
extrinsic water
What is the importance of electrolyte balance & what are some causes of electrolyte imbalances?
excitation contraction coupling: Na, K, Cl
-resting membrane potential
-action potential/depolarization
contraction (sliding filament): Ca, Mg, ATP

causes of electrolyte imbalances
electrolyte loss: sweating, GI dz, renal dz
membrane abnormalities: Na channels, excitation contraction coupling
What diagnostics are involved in working up muscular dz?
PE for muscle problems: TPR, mm, CRT, sweating?, gait abnormalities, distribution of lesions, evaluation of muscles

clin path
-CK (good for acute problems), LDH, AST
-electrolytes: Na, K, Cl, Ca, Mg
-acid-base status
-serum lactate:ammonia ratio

exercise test: not done very often
-measure CK before & 4-6 hrs & 24 hrs after exercise
-exercise could be lunging, treadmill, or normal exercise routine
-however CK may not change at all w/ exercise

muscle bx: histopath, biochemical analysis, histochemical analysis, caffeine, halothane reactivity

electromyography nerve conduction velocity (not commonly done): electrical silence, insertional activity, motor unit APs, miniature end plate potentials, fibrillation potentials, positive sharp waves
hyperkalemic periodic paralysis (HPP)

a. pathogenesis
b. clinical signs
c. ddx
a.defect in muscle membrane ion channel conductance
-autosomal dominant w/ incomplete penetrance
-episodic: may occur rarely to daily; episodes can last minutes to hours
b. recurrent episodes of muscle fasciculations & weakness
exercise intolerance: less willing to work; greater lactic acid production for a given amt. of work
+/- 3rd eyelid prolapse, recumbency, laryngeal swelling/paralysis
c. colic, tetanus, seizure, choke, rhabdomyolysis, hypocalcemia, neurologic, resp. distress
hyperkalemic periodic paralyis

a. dx
b. tx
c. prevention
a. clinical signs, ↑ serum K, pedigree, genetic testing, electromyogram, KCl provocation test
-CK, AST remain normal, or nearly so
b. drive K+ into cells w/ calcium, bicarb, dextrose, (insulin)
c. avoid high K feeds (alfalfa hay, molasses), regular exercise, acetazolamide
ionophore AB toxicity

a. etiology
b. clinical signs
c. dx
d. tx
a. monensin, salinomycin, lasalocid, narasin
-coccidiostats: poultry, ruminants
-growth promoters: ruminants
b. acute: anorexia, colic, weakness, ↑ muscle enzymes, ataxia, shock, death
-chronic: CV dysfunction, exercise intolerance
c. clinical signs, muscle enzymes, ID drug in feed, necropsy, multiple horses affected
d. if acute, try to prevent further absorption
-supportive care
equine rhabdomyolysis

a. pathogenesis
b. causes
a. type II muscle fibers affected: ischemia, build up of lactic acid, damage to cell mems
↑ cytosolic Ca --> ↑ uptake into sarcoplasmic reticulum & mitochondria, damage to cell mems & organelles
disruption of cell mems --> leakage of myoglobin, K, CK, LDH, AST, etc. into extracellular space --> muscle inflammation & necrosis w/ heat, pain, swelling, loss of function
b. 1º: polysaccharide storage myopathy, glycogen branching deficiency, malignant hyperthermia, defect in excitation contraction coupling
2º: poor management, training errors, carbohydrate loading, vitamin E/Se deficiency, K deficiency, estrous cycle, hypothyroidism, nervous horses, post anesthesia
equine rhabdomyolysis

a. clinical signs
b. clin path
c. dx
a. mild: may be confused w/ lameness
-stiff gait, dragging toes, pain over croup, loin, thigh musculature, “back sore”
severe: reluctance to move, anxiety, tachycardia, tachypnea, sweating, pyrexia, tense swollen painful muscles, myoglobinuria, recumbency
b. ↑ muscle enzymes (CK: 2-6 hrs, LDH: 12 hrs, AST: 12-24 hrs)
electrolyte abnormalities
+/- azotemia
c. b’twn episodes: hx, exercise test, clin path (muscle enzymes, electrolytes, U/A, thyroid status, vitamin E/Se), scintigraphy, thermography, muscle bx
-during acute episode: clinical signs, muscle enzymes, +/- myoglobinuria
What are principles of tx for equine rhabdomyolysis?
limit further muscle damage
control pain: NSAIDs safe to give if making urine, else Torb
control anxiety: xylazine
combat inflammation
flush kidneys
↑ blood flow to muscles: fluids, vasodilators (ex. ace)
restore electrolyte, acid-base balance
supportive care
malignant hyperthermia

a. pathogenesis
b. clinical signs
c. tx
d. prevention
a. inappropriate release of Ca for sarcoplasmic reticulum in anesthetized horses
-halothane & succinylcholine are common inciting agents
-probably a genetic predisposition
b. sudden ↑ in body temp, muscle cramping & fasciculations, sweating, tachycardia, irregular breathing, acute ↑ in serum K
c. turn off inhalation anesthetic
-↓ body temp w/ ice
-↑ IV fluids
-symptomatic: restore electrolyte & acid-base status, etc.
d. no grain prior to elective sx
-keep anesthesia time short
-don’t use halothane or succinylcholine
-pre-treat horses prone to myositis w/ dantrolene (not commonly used in horses) or phenytoin
polysaccharide storage myopathy (PSSM)

a. pathogenesis
b. clinical signs
c. dx
d. prevention of episodes
a. probably inherited, esp. in quarterhorse related & draft breeds
-accumulation of glycogen & unavailable mucopolysaccharide in type II muscle fibers
-↑ insulin sensitivity
b. calm demeanor, low exercise tolerance, signs of recurrent rhabdomyolysis at a young age (vary in duration & severity)
c. clinical signs, muscle bx
d. regular daily exercise
-dietary adjustment: low carb, ↑ fat
chronic intermittent (recurrent exertional) rhabdomyolysis

a. pathogenesis
b. signalment
c. dx
d. prevention
a. familial abnormality in excitation contraction coupling
-signs may be mild
b. young nervous fillies, lame horses more likely to develop dz
c. exercise test, muscle bx
d. consistent daily exercise
-dietary adjustments +/- electrolyte supplementation
-vasodilator sedatives
-control of estrus behavior
Clostridial myonecrosis

a. pathogenesis
b. clinical signs
c. dx
d. tx
a. Clostridium spp. present in environment & on skin surface --> invade at site of injection or puncture --> proliferate in bruised (anaerobic) muscle --> release of necrotizing & hemolyzing toxins
b. swelling, pain, & crepitus (Clostridia --> gas production) at site, depression, fever, tachycardia, progression to severe toxemia & death
c. clinical signs, suggestive hx, ↑ muscle enzymes, CBC (toxemia, inflammation), U/S or rads: gas w/in muscle planes, anaerobic culture of tissue aspirate
d. must be rapid & aggressive
-IV penicillin +/- metronidazole
-surgical debridement or fenestration: must let O2 into wound
-specific antitoxin if available
-supportive care