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Equine Medicine > Unit 1 - Myopathies (Intro to Exertional Rhabdomyolyisis) > Flashcards

Unit 1 - Myopathies (Intro to Exertional Rhabdomyolyisis) Flashcards

1
Q

When you have a potential myopathy patient, what questions do you want to ask about their history?

A

duration of illness, recurring problem, precipitating factors, exercise schedule, diet, vaccination history, number of animals affected, and familial relationships

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2
Q

What will you find on a general physical exam in a patient with a myopathy?

A

tachycardia, tachypnea, excessive sweating, and anxiety

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3
Q

What will you find on a muscular system evaluation in a myopathy patient?

A

firm, painful, and swollen muscles, muscle fasciculations, muscle atrophy, gait abnormalities, reluctance/refusal to move, recumbency, and inability to rise

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4
Q

What differential diagnoses should be considered along with myopathies?

A

gastrointestinal disease (colic), respiratory disease (pleuropneumonia), musculoskeletal disease (laminities or other lameness, fracture), neurologic disease ( a lot) electrolyte imbalance, and aorto-iliac thrombosis

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5
Q

What diagnostic tests are important for myopathy diagnosis?

A

serum chemistry and urinalysis

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6
Q

What ancillary tests help with confirming myopathy diagnosis?

A

CBC, vitamin E/selenium, blood gas analysis, fractional excretion of electrolytes

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7
Q

What will a serum chemistry show in a patient with a myopathy?

A

Electrolyte changes - increase P and K, decreased Na, Cl, and Ca
Increase BUN and Creatinine
Increase in creatine kinase (CK) and aspartate aminotransferase (AST)

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8
Q

What secretes creatine kinase?

A

skeletal muscle, myocardium, and the brain

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9
Q

When do increases in CK occur due to insult?

A

4-6 hours post insult

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10
Q

What is the 1/2 life of CK?

A

very short - 2-9 hours

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11
Q

What secretes AST?

A

skeletal muscle, cardiac muscle, the liver, RBC, and others

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12
Q

When do increases in AST occur due to insult?

A

12-24 hours post insult

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13
Q

What is the 1/2 life of AST?

A

very long - 7-10 days

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14
Q

What is creatine kinase a sensitive indicator for?

A

myonecrosis

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15
Q

What can cause a mild increase (<5000) in CK?

A

IM injection, strenuous exercise, recumbency/colic, and transport

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16
Q

What can cause a marked increase (10,000 to greater than 100,000)?

A

severe rhabdomyolosis

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17
Q

What does persistent elevation in CK indicate?

A

continuing myonecrosis

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18
Q

What will you see in a UA from a myopathy patient?

A

myoglobinuria

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19
Q

What does myoglobinuria indicate?

A

severe muscle damage

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20
Q

Why would electromyography help in diagnosing myopathies?

A

it will help determine whether the cause is myopathic or neuropathic and will aid in determining the distribution of the disease

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21
Q

What does thermography do?

A

it measures the skin surface temperature and alterations in blood flow

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22
Q

What does the exercise challenge test detect?

A

subclinical cases of chronic ER

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23
Q

How do you do an exercise challenge>

A

Have the patient do light, submax exercise (15-30 minutes) and evaluate CK before and 4-6 hours after it

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24
Q

What result on an exercise challenge test is indicative of exertional rhabdomyolysis?

A

> 3-4x increase in CK post submax exercise

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25
Q

What is used for genetic testing in regards to myopathies?

A

mane or tail hairs (with roots) or whole blood

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26
Q

What diseases can be detected with genetic testing?

A

hyperkalemic periodic paralysis (HYPP), polysaccharide storage myopathy (PSSM), malignant hyperthermia (MH), glycogen branching enzyme deficiency (GBED), immune-mediated myositis (MYH1M)

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27
Q

What are the two different ways myopathies are classified?

A

by cause or by clinical signs

28
Q

What are the different types of rhabdomyolysis?

A

exertional and non-exertional

29
Q

What is rhabdomyolysis?

A

destruction of striated muscle cells

30
Q

What are the different types of exertional rhabdomyolysis?

A

chronic or sporadic

31
Q

What are the different causes of non-exertional myopathies?

A

infectious, nutritional, toxic, and traumatic

32
Q

What are the treatment goals for rhabdomyolysis?

A

relieve pain and anxiety, correct electrolyte and acid-base abnormalities, limit muscle damage, maintain perfusion, prevent pigment nephropathy, and provide supportive care

33
Q

What treatments can be used for rhabdomyolysis?

A

sedatives, tranquilizers, analgesics, IV fluid therapy, antioxidants, muscle relaxants

34
Q

What muscle relaxants can be used to treat rhabdomyolysis?

A

Methocarbamol, Guaifenesin, Dantrolene, and Paenytoin

35
Q

How does methocarbamol and Guaifenesin work?

A

they are centrally acting, with the exact mechanism unknown - sedative effects

36
Q

How does dantrolene work?

A

interferes with release of Ca from the SR

37
Q

How does phenytoin work?

A

it acts on ion channels in muscles and nerves (promotes Na efflux) which decreases the sensitivity of muscle spindles to stretch
It is an anticonvulsant and antiarrhythmiac

38
Q

What are the types of chronic exertional rhabdomyolysis?

A

PSSM, recurrent ER, and idiopathic

39
Q

What are the causes of sporadic exertional rhabdomyolysis?

A

dietary and overexertion

40
Q

What dietary changes can cause sporadic exertional rhabdomyolysis?

A

increased CHO, decreased Vitamin E/Se, decreased Na or K, and Ca/P imbalance

41
Q

What breeds is polysaccharide storage myopathy (PSSM) common in?

A

quarter horse related breeds, draft horses, and warmbloods

42
Q

What is polysaccharide storage myopathy?

A

When there is an accumulation of glycogen AND amylase-resistant abnormal polysaccharide in skeletal muscle leading to repeated episodes of exertional rhabdomyolysis

43
Q

What gene is associated with type 1 PSSM?

A

GYS1 gene - there is a gain of function mutation (an autosominal dominant trait) that leads to elevated GS activity

44
Q

What is type 2 PSSM?

A

The genetic mutation has not been identified, but there is an inconsistent accumulation of abnormal polysaccharide

45
Q

What is the prevalence of PSSM in quarter horses and of that percentage, what percentage of those cases is type 1?

A

10% prevalence - 72% of those cases is due to type 1

46
Q

What is the age of onset of PSSM in quarter horses and clinical signs?

A

average onset is 5 years (1-14 years) - exertional RM, abnormal gait, and muscle wasting

47
Q

What is the prevalence of PSSM in draft breeds and of that percentage, what percentage of those cases is type 1?

A

40% prevalence - 87% of those cases is due to type 1

48
Q

What is the age of onset of PSSM in draft breeds and clinical signs?

A

8 years - subclinical clinical signs, abnormal gait, muscle wasing, exertional rhabdomyolysis, and postanesthetic myopathy

49
Q

What is the prevalence of PSSM in warmbloods and of that percentage, what percentage of those cases is type 1?

A

The prevalence is unknown, but 18% of the diagnosed cases is due to type 1

50
Q

What is the age of onset of PSSM in warm bloods and clinical signs?

A

8-11 years - firm/painful hindquarters, abnormal gait, and exertional rhabdomyolysis in less than 15% of the cases

51
Q

What are the clinical signs of mild forms of rhabdomyolysis?

A

exercise intolerance, pawing post exercise, muscle fasciculations, sweating, stiffness, urination stance, tucked-up abdomen

52
Q

What are the clinical signs in severe forms of exertional rhabdomyolysis?

A

severe pain resembling colic, recumbency, and renal failure

53
Q

What mutations leads to more severe and occasionally fatal forms of exertional rhabdomyolysis?

A

PSSM mutation with malignant hyperthermia

54
Q

How is PSSM diagnosed?

A

genetic testing for the mutation and gluteal or semimembranous muscle biopsy with periodic acid-schiff stain for glycogen

55
Q

What will a periodic acid-schiff stain show if a patient has PSSM?

A

2 fold increased density of glycogen, abnormal PAS positive inclusions, and subsacrolemmal vacuoles

56
Q

Which fibers are mainly affected with PSSM?

A

type 2 fibers (fast twitch)

57
Q

What are the two management techniques for PSSM?

A

dietary and exercise management

58
Q

What are the recommended changes for dietary management of PSSM?

A

decrease the NSC carbohydrates (should be less than 10%) with alfalfa/grass hay mix or grass hay, and increase the fat content (greater than 13%)

59
Q

What are some products with a high fat content?

A

Re-Leve, envision classic, nutrena empower, purina ultium, moorman’s natural glo or moorglo, equi-jewel, and corn oil

60
Q

What do you want to do for exercise management of PSSM?

A

give them regular exercise or access to the paddock

61
Q

Why would you want to increase exercise in PSSM patients?

A

burn their glycogen stores and enhance the oxidative capacity of muscle by increasing enzymes that utilize fat as fuel

62
Q

What causes recurrent exertional rhabdomyolysis (RER)?

A

an inherited autosomal dominant trait in thoroughbreds that causes defective intracellular Ca regulation

63
Q

What thoroughbred patients is RER the most common in?

A

fit young fillies in training at the racetrack

64
Q

What clinical signs are assoicated with RER?

A

nervous temperament, poor performance, muscle stiffness, and rhabdomyolysis

65
Q

How do you prevent RER?

A

minimize stress, daily exercise, turn-out, decreased carbs, fat supplementation, and give Acepromazine, dantrolene, and phenytoin before training exercise

Equine Medicine (27 decks)

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