Equine Myopathies Flashcards
what anatomic components do most myopathies affect?
most myopathies on the level of the muscle fiber (cellular level / group of cells)
Musculoskeletal exam components
- Distance examination
◦ Posture & stance
◦ Muscle mass
◦ Muscle symmetry - Palpation
◦ Muscle tone - Presence of fasciculations
- Motion exam
◦ Lameness
◦ Ataxia
◦ Weakness
◦ Stiffness
◦ Spasticity
◦ Exercise intolerance
myopathies diagnostic tests, generally
- Biochemical analysis
◦ Creatine Kinase (CK) > acute
◦ Aspartate transamine (AST) > slower to rise and fall
◦ Lactate dehydrogenase (LDH)
◦ Creatinine
◦ BUN
> renal values relevant to pigment nephropathy - Urinalysis
- Vitamin E and selenium
- Exercise-Response Testing
- Imaging
◦ Thermography
◦ Nuclear Scintigraphy > r/o bony lesions
◦ Ultrasonography - Electromyography
- Muscle biopsy > common in field
◦ Semimembranosus
◦ Gluteus medius
◦ Epaxial
◦ Sacrocaudalis dorsalis - Genetic testing
Non-exertional Myopathies - infectious casues
◦ Viral
◦ Clostridium spp.
◦ Streptococcus equi
◦ Anaplasma phagocytophilum
◦ Sarcocystis fayeri
Non-exertional Myopathies - toxin causes
◦ Ionophores
◦ Hypoglycin A
Non-exertional Myopathies - nutritional causes
◦ Vitamin E deficiency
◦ Selenium deficiency
Non-exertional Myopathies - traumatic causes
◦ Compressive
◦ Postanesthetic
◦ Trauma
Non-exertional Myopathies - genetic causes
◦ Glycogen branching enzyme deficiency
◦ Hyperkalemic periodic paralysis
◦ Malignant hyperthermia
◦ Myosin heavy chain myopathy
Non-exertional Myopathies - immune-related causes?
Immune mediated
Sporadic Exertional Myopathies - causes
◦ Overexertion
◦ Exhaustion
◦ Dietary Imbalance
Chronic Exertional Myopathies - causes
◦ Polysaccharide storage myopathy type 1
◦ Polysaccharide storage myopathy type 2
◦ Myofibrillar myopathy
◦ Recurrent exertional rhabdomyolysis
◦ Idiopathic exertional rhabdomyolysis
Hypoglycin A myopathy
- what is it? etiology?
- signs
- dx
- prognosis
- Highly fatal lipid storage myopathy
- Ingestion of seeds from Acer sp. trees (boxelder maple)
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Clinical signs
◦ Weakness/ stiffness
◦ Sweating
◦ Fasciculations
◦ Tachycardia/ tachypnea
◦ Myoglobinuria
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Diagnosis – measurement of serum acylcarnitines and urine organic acids
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Prognosis - <75% of horses survive
Vitamin E and Selenium deficiency - myopathy
- what is it?
- forms, signs, prognosis?
Nutritional myodegeneration
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* Cardiac form
◦ Weakness, respiratory distress, tachycardia, arrythmias
◦ Poor prognosis, residual myocardial damage if survive
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* Skeletal form > far more common
◦ Slower onset
◦ Weakness, stiffness, trembling, and recumbency
◦ Painful, firm muscles on palpation
◦ Dysphagia > may be the only sign: foals with weak swallowing muscles
◦ Favorable prognosis with Vitamin E/Se supplementation
Glycogen Branching Enzyme Deficiency
- etiology of myopathy
- signs
- bloodwork
- dx?
Fatal autosomal recessive mutation in GBE1 gene
> way less GBE protein (enzyme) in these foals
> foals cant form branched glycogen
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Clinical signs
◦ Hypothermia
◦ Weakness & intermittent collapse
◦ Flexural deformities
◦ Ventilatory failure & cardiac arrhythmias
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Bloodwork
◦ Recurrent hypoglycemia
◦ Increased CK, AST and GGT
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Genetic testing
> these foals cannot go far - euthanize
Malignant Hyperthermia
- etiology of myopathy
- triggers
- clinical signs
- dx
- tx
Autosomal dominant mutation in RYR1 gene
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Triggers
◦ Halogenated anesthetics
◦ Depolarizing muscle relaxants
◦ Stress
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Clinical signs
◦ Hyperthermia (> 43 C)
◦ Tachycardia
◦ Muscle rigidity and rhabdomyolysis
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Genetic testing
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Treatment and prevention
◦ Dantrolene