Muscle Diseases, Pt. 3 Flashcards
Rhabdomyolysis vs. myopathy:
Muscle diseases, breeds and genetics:
What history is related to sporadic exertional rhabdomyolysis? What clinical signs are associated?
overexertion and dietary imbalance
- muscle pain associated with unwillingness to move, stiffness, recumbency, posturing to urinate, and colic
- high temperature, sweating
- tachycardia, tachypnea
- pigmenturia
What are the 2 major ways to diagnose sporadic exertional rhabdomyolysis? What consequences are associated?
- CHEM: exponentially increased CK and AST, hyperkalemia
- UA: pigmenturia, casts
dehydration and acidosis
How can sporadic exertional rhabdomyolysis be prevented? What 5 ways of medical management are recommended?
minimize movement and decrease work
- calm horse with sedation: Xylazine, Detomidine
- relieve pain: Banamine, Phenylbutazone (nephrotoxic!)
- stimulate diuresis: Furosemide, Dopamine
- limit muscular lesions: Methocarbamol, Dantrolene
- treat dehydration and electrolyte abnormalities
How can further episodes of sporadic exertional rhabdomyolysis be avoided?
- rest
- progressive return to work
- continue prevention and testing
What is the etiology of recurrent exertional rhabdomyolsysis? In what horses is it most common?
unidentified genetic component (NO TEST) causes abnormal intracellular calcium metabolism
young, fit, nervous, triggered (females) Thoroughbreds —> most common during race season
(+ Standardbreds, Arabians)
What are the most common clinical signs associated with recurrent exertional rhabdomyolysis?
- muscle cramps - stiffness, pain, migrating lameness
- pain - sweating, tachypnea, refusal to move
- myopathy - pain on palpation, increased HR and RR
- hematuria
In a non-symptomatic horse, how many hours after exercise would you draw blood to measure CK to compare to baseline values?
4-6 hours
How is recurrent exertional rhabdomyolysis diagnosed? How does age affect this?
CK and AST measuremen 4-6 hours post exercise should be 3-4x base value
more fluctuation are seen in younger horses up to 2 y/o
What diagnostic is recommended for difficult cases of recurrent exertional rhabdomyolysis? What are other tests performed?
- muscle biopsy
- exercise testing (subclinical cases, guided exercise)
fractional excretion, vitamin E, Se
How are rhabdomyolysis treated and triggers decreased for cases of recurrent exertional rhabdomyolysis?
rest, calm, fluids
- PHARMACOLOGIC: sedation
- MANAGEMENT: regular, timed, free exercise at pasture
In what 4 ways is the diet managed for treatment of recurrent exertional rhabdomyolysis?
- high-quality grass or oat hay forage at 1.5-2% BW
- high fat, low starch diet**
- complete feeds, like Re-Leve and Ultium, to meet high caloric needs
- provide electrolytes
What are the 2 forms of polysaccharide storage myopathy?
PSSM1 = glycogen synthase GYS1 mutation - autosomal dominant with genetic test
PSSM2 = no mutation identified yet - no validated genetic test
What is seen histologically in muscle tissue with polysaccharide storage myopathy?
abnormal energy metabolism causes a deficit, resulting in abnormal aggregates of dark, granular polysaccharides seen on PAS and amylase stain
What is thought to have cause the develpoment of polysaccharide storage myopathy?
European draft forse and a lighter horse breed was crossed to carry men in armor
What 2 breeds are most commonly affected by polysaccharide storage myopathy? What is the known etiology?
- AQH
- European-derived Draft breeds
autosomal dominant mutation in glycogen synthase (GYS1)
What is the most common trigger associated with polysaccharide storage myopathy? What are 5 causes of variability in clinical signs?
rest before exercise
- breed
- diet
- exercise
- environment: stress
- influence of other genes
What are the most common clinical signs seen with polysaccharide storage myopathy?
episodes of rhabdomyolysis in horses at young ages and with little exercise
- tucked abdomen, camped-out stance
- lazy shifting lameness
- muscle fasciculations, tremors, sweating
- gait asymmetry, hindlimb stiffness
- reluctance to move, signs of colic
What clinical signs is specifically seen in Draft horses with glycogen storage myopathy?
loss of muscle mass, progressive weakness, and recumbency
What 2 diseases on the Quarter Horse and Related Breeds Disease Panel are caused by recessive genese?
- glycogen branching enzyme deficiency
- hereditary equine regional dermal asthenia
HYPP, MYHM, MH, and PSSM1 = dominant
What breeds are most commonly affected by glycogen storage myopathy? Etiology?
- Warmbloods
- Arabians
- AQH that take part in barrel racing, reining, and cutting > halter
no genetic mutation identified yet - any horse with clinical signs of exercise intolerance and abnormal aggregates of polysaccharide in muscle fibers without GYS1 mutation
What clinical signs of glycogen storage myopathy is seen in AQH?
- tying up
- muscle atrophy
- <1 y/o = difficulty rising
- increased CK and AST
What clinical signs of glycogen storage myopathy is seen in Warmbloods?
poor performance > tying up and high CK
- gait abnormalities
- soreness
- drop in energy 5-10 mins following exercise
- loss of muscle mass when out of work
