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Equine Medicine > Muscle Diseases, Pt. 3 > Flashcards

Muscle Diseases, Pt. 3 Flashcards

1
Q

Rhabdomyolysis vs. myopathy:

A
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2
Q

Muscle diseases, breeds and genetics:

A
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3
Q

What history is related to sporadic exertional rhabdomyolysis? What clinical signs are associated?

A

overexertion and dietary imbalance

  • muscle pain associated with unwillingness to move, stiffness, recumbency, posturing to urinate, and colic
  • high temperature, sweating
  • tachycardia, tachypnea
  • pigmenturia
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4
Q

What are the 2 major ways to diagnose sporadic exertional rhabdomyolysis? What consequences are associated?

A
  1. CHEM: exponentially increased CK and AST, hyperkalemia
  2. UA: pigmenturia, casts

dehydration and acidosis

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5
Q

How can sporadic exertional rhabdomyolysis be prevented? What 5 ways of medical management are recommended?

A

minimize movement and decrease work

  1. calm horse with sedation: Xylazine, Detomidine
  2. relieve pain: Banamine, Phenylbutazone (nephrotoxic!)
  3. stimulate diuresis: Furosemide, Dopamine
  4. limit muscular lesions: Methocarbamol, Dantrolene
  5. treat dehydration and electrolyte abnormalities
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6
Q

How can further episodes of sporadic exertional rhabdomyolysis be avoided?

A
  • rest
  • progressive return to work
  • continue prevention and testing
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7
Q

What is the etiology of recurrent exertional rhabdomyolsysis? In what horses is it most common?

A

unidentified genetic component (NO TEST) causes abnormal intracellular calcium metabolism

young, fit, nervous, triggered (females) Thoroughbreds —> most common during race season

(+ Standardbreds, Arabians)

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8
Q

What are the most common clinical signs associated with recurrent exertional rhabdomyolysis?

A
  • muscle cramps - stiffness, pain, migrating lameness
  • pain - sweating, tachypnea, refusal to move
  • myopathy - pain on palpation, increased HR and RR
  • hematuria
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9
Q

In a non-symptomatic horse, how many hours after exercise would you draw blood to measure CK to compare to baseline values?

A

4-6 hours

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10
Q

How is recurrent exertional rhabdomyolysis diagnosed? How does age affect this?

A

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

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11
Q

What diagnostic is recommended for difficult cases of recurrent exertional rhabdomyolysis? What are other tests performed?

A
  • muscle biopsy
  • exercise testing (subclinical cases, guided exercise)

fractional excretion, vitamin E, Se

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12
Q

How are rhabdomyolysis treated and triggers decreased for cases of recurrent exertional rhabdomyolysis?

A

rest, calm, fluids

  • PHARMACOLOGIC: sedation
  • MANAGEMENT: regular, timed, free exercise at pasture
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13
Q

In what 4 ways is the diet managed for treatment of recurrent exertional rhabdomyolysis?

A
  1. high-quality grass or oat hay forage at 1.5-2% BW
  2. high fat, low starch diet**
  3. complete feeds, like Re-Leve and Ultium, to meet high caloric needs
  4. provide electrolytes
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14
Q

What are the 2 forms of polysaccharide storage myopathy?

A

PSSM1 = glycogen synthase GYS1 mutation - autosomal dominant with genetic test

PSSM2 = no mutation identified yet - no validated genetic test

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15
Q

What is seen histologically in muscle tissue with polysaccharide storage myopathy?

A

abnormal energy metabolism causes a deficit, resulting in abnormal aggregates of dark, granular polysaccharides seen on PAS and amylase stain

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16
Q

What is thought to have cause the develpoment of polysaccharide storage myopathy?

A

European draft forse and a lighter horse breed was crossed to carry men in armor

17
Q

What 2 breeds are most commonly affected by polysaccharide storage myopathy? What is the known etiology?

A
  1. AQH
  2. European-derived Draft breeds

autosomal dominant mutation in glycogen synthase (GYS1)

18
Q

What is the most common trigger associated with polysaccharide storage myopathy? What are 5 causes of variability in clinical signs?

A

rest before exercise

  1. breed
  2. diet
  3. exercise
  4. environment: stress
  5. influence of other genes
19
Q

What are the most common clinical signs seen with polysaccharide storage myopathy?

A

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
20
Q

What clinical signs is specifically seen in Draft horses with glycogen storage myopathy?

A

loss of muscle mass, progressive weakness, and recumbency

21
Q

What 2 diseases on the Quarter Horse and Related Breeds Disease Panel are caused by recessive genese?

A
  1. glycogen branching enzyme deficiency
  2. hereditary equine regional dermal asthenia

HYPP, MYHM, MH, and PSSM1 = dominant

22
Q

What breeds are most commonly affected by glycogen storage myopathy? Etiology?

A
  • 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

23
Q

What clinical signs of glycogen storage myopathy is seen in AQH?

A
  • tying up
  • muscle atrophy
  • <1 y/o = difficulty rising
  • increased CK and AST
24
Q

What clinical signs of glycogen storage myopathy is seen in Warmbloods?

A

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
25
Q

What signs are seen in chronic episodes of glycogen storage myopathy?

A
  • muscle stiffness
  • soreness
  • muscle atrophy
26
Q

How is glycogen storage myopathy prevented? What nutrition is recommended?

A

avoid rest - allow regular, incremental exercise program, limit confinement and allow turn out —> 70% will improve with management, but will remain susceptible

caloric balance, select forage, select fat source (low starch, high fat)

27
Q

What breeds are susceptible to malignant hyperthermia? Etiology?

A

AQH

autosomal dominant mutation inf ruanodine receptor (RYR1) causes dysfunction in calcium release channels

28
Q

What triggers cause malignant hyperthermia?

A
  • anesthesia with halothane
  • stress
  • excitement
29
Q

What clinical signs are associated with malignant hyperthermia? What other disease does it commonly present with?

A
  • tachycardia, hyperthermia, muscle rigidity, lactic acidosis, increased CK, and electrolyte derangements seen while under anesthesia
  • exertional rhabdomyolysis: sweating, tachycardia, tachypnea, hyperthermia, muscle rigidity, sudden death

PSSM1 —> will be less responsive to typical treatment

30
Q

What premedication is recommended in animals that can develop malignant hyperthermia? What else is done?

A

Dantrolene

  • genetic screening
  • cool down patient
  • fluids with sodium bicarbonate
31
Q
A

Equine Medicine (33 decks)

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