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A. Equine and Camelid Medicine and Surgery > Equine Muscle Disorders > Flashcards

Equine Muscle Disorders Flashcards

1
Q

what is special about muscle physiology in horses?

A

increased muscle mass
greater locomotor efficiency
high mitochondrial volume
high intramuscular store of glycogen
high buffer and lactate transport capacity
can improve all of the above with training

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2
Q

what gene determines whether they are better at distance or sprint?

A

myostatin gene

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3
Q

when does sporadic exertional rhabdomyolysis occur?

A

after very hard exercise
unfit horse

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4
Q

when does recurrent rhabdomyolysis occur?

A

beginning of light exercise
stress

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5
Q

what is recurrent rhabdomyolysis due to?

A

abnormal intracellular calcium regulation causing lower threshold for contracture

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6
Q

what are the chief complaints with rhabdomyolysis?

A

reluctance to move
discolored urine
more in quarter horses and draft horses

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7
Q

what are some distinguishing physical exam findings with rhabdomyolysis?

A

hard muscles
muscles sensitive to touch

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8
Q

what is the main pathogenic mechanism of rhabdomyolysis?

A

myocyte lysis

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9
Q

what can you test to check for rhabdomyolysis?

A

creatine kinase
aspartate transaminase
lactate dehydrogenase

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10
Q

what does creatine kinase do in an injury?

A

increases by 6 hours and peaks at 12 hours after
if ongoing injury, will continue to rise

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11
Q

when does lactate dehydrogenase increase with muscle injury?

A

by 2 days
will continue to rise with ongoing injury

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12
Q

what are some key diagnostic test results with rhabdomyolysis?

A

muscle pain
markedly elevated muscle enzyme activities
myoglobinuria

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13
Q

what are the main treatments for rhabdomyolysis?

A

rest
intravenous fluid therapy for perfusion and kidneys
manage/monitor electrolytes
flunixin meglumine NSAID if well hydrated
acetominophen if worried about AKI
butorphanol or morphine if severe pain
acepromazine as anxiolytic if euvolemic

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14
Q

what are the clinical signs of polysaccharide myopathy?

A

severe cases indistinguishable from exertional rhabdomyolysis
chronic low-grade disease: poor performance

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15
Q

what happens in polysaccharide storage myopathy I?

A

glycogen made all the time but not broken down properly

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16
Q

how can you test for polysaccharide storage myopathy?

A

take creatine kinase before and 6 hours after trotting
genetic test if PSSM-1
muscle biopsy

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17
Q

what are the main treatments for polysaccharide storage myopathy?

A

rest
IV fluids if myoglobinuria
low-nonstructural carbohydrate diet

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18
Q

what are the chief complaints with atypical myopathy?

A

same as exertional rhabdomyolysis but not associated with exercise
more severe
sudden death

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19
Q

what is the pathogenesis of atypical myopathy?

A

hypoglycin A in sycamore and box elder
multiple acyl CoA deficiency

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20
Q

who gets post-anesthesia myopathy?

A

large or heavily muscles horses

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21
Q

who can get nutritional myodegeneration (white muscle disease)?

A

foals
lambs
kids

22
Q

which muscle is affected by white muscle disease?

A

more on red (type I oxidative) muscle fibers: use beta oxidation
skeletal and cardiac muscle

23
Q

how can you treat white muscle disease?

A

inject vitamin E and selenium
add vitamin E and selenium to diet
poor prognosis if heart involvement

24
Q

what is the distinguishing physical exam finding with vitamin E deficiency myopathy in an adult?

A

muscle atrophy

25
Q

what is the main pathogenic mechanism in hyperkalemic periodic paralysis?

A

genetic defect in voltage-gated sodium channel

26
Q

is hyperkalemic periodic paralysis associated with muscle damage?

A

no

27
Q

who is hyperkalemic periodic paralysis traced back to?

A

quarter horse stallion named Impressive

28
Q

what are the main treatments for hyperkalemic periodic paralysis?

A

IV dextrose or calcium
acetazolamide
low-potassium diet

29
Q

which MHC heavy chain is fast twitch?

A

2X

30
Q

which MHC heavy chain is slow twitch?

A

1

31
Q

when does sporadic exertional rhabdomyolysis occur?

A

toward end to extreme exercise
several hours after exercise or next day

32
Q

how common is recurrent rhabdomyolysis?

A

5% thoroughbred racehorses less than a year
complex heritable component

33
Q

which muscles should you especially palpate for rhabdomyolysis?

A

epaxials
gluteals

34
Q

what is released when myocytes rupture?

A

myoglobin
other intracellular proteins
electrolytes

35
Q

why is hypocalcemia seen with rhabdomyolysis?

A

calcium binds free actin and myosin

36
Q

where are isoenzymes for creatine kinase?

A

gut
brain

37
Q

what is lactate dehydrogenase critical for?

A

pyruvate-lactate shuttle

38
Q

why are intravenous fluids given for rhabdomyolysis?

A

improve perfusion
prevent renal failure

39
Q

how can rhabdomyolysis be managed?

A

exercise: consistent daily exercise, slow warm up/cool down
recurrent: short periods exercise- 10 minutes
trace minerals and electrolytes in feed
electrolytes in water to exercising horses

40
Q

why does cell swelling and lysis occur with polysaccharide myopathy?

A

cannot use stored glycogen: insufficient ATP for membrane pumps

41
Q

who usually has polysaccharide storage myopathy type 2?

A

warmbloods

42
Q

which polysaccharide storage myopathy has a known genetic cause?

A

type 1

43
Q

who usually gets polysaccharide storage myopathy type 1?

A

quarterhorse types and continental drafts
documented in 20 breeds

44
Q

what is the dietary management of polysaccharide storage myopathy?

A

lower glycogen production
avoid high-glycemic feeds
feed low-starch, low-sugar
substitute fats for sugars
supplemental vitamin E

45
Q

how can you diagnose atypical myopathy?

A

creatine kinase 100k to millions
severe acidosis
not associated with exercise

46
Q

how can vitamin E deficiency myopathy be diagnosed in an adult?

A

usually no elevated creatine kinase
low plasma vitamin E
responds to treatment: vitamin E

47
Q

which horse breeds are more likely to have hyperkalemic periodic paralysis?

A

quarteerhorses and crosses
paint horses
appaloosas
lineage tracing back to Impressive

48
Q

are heterozygotes usually abnormal or normal in hyperkalemic periodic paralysis?

A

normal
homozygotes abnormal

49
Q

why doess weakness happen with hyperkalemic periodic paralysis?

A

myocytes unable to repolarize fast enough

50
Q

when does hyperkalemia occur with hyperkalemic periodic paralysis?

A

only during episode
some horses remain normokalemic

51
Q

how can hyperkalemic periodic paralysis be treated?

A

regular gentle exercise: epinephrine
oral glucose
intravenous glucose
calcium gluconate
inhaled albuterol or oral clenbuterol
acetazolamide
furosemide if no acetazolamide
low potassium diet

52
Q

what is acetazolamide?

A

carbonic anhydrase inhibitor diuretic
potassium-wasting diuretic

A. Equine and Camelid Medicine and Surgery (47 decks)

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