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Equine Medicine > Unit 1 - Myopathies (Non-exertional Myopathies to end) > Flashcards

Unit 1 - Myopathies (Non-exertional Myopathies to end) Flashcards

1
Q

What are the infectious causes of non-exertional rhabdomyolysis?

A

streptococcal and clostridial

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2
Q

What are the toxic causes of nonexertional rhabdomyolysis?

A

seasonal pasture myopathy, white snake root, and ionophores

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3
Q

What is the genetic cause of nonexertional rhabdomyolysis?

A

malignant hyperthermia

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4
Q

What are the traumatic/circulatory causes of nonexertional rhabdomyolysis?

A

compartment syndrome and postanesthetic (local)

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5
Q

What is compartment syndrome?

A

when the muscle fascia is unable to stretch - trauma causes increased pressure and ischemia

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6
Q

Malignant hyperthermia is a generalized post-anesthetic myopathy (usually). What is it due to?

A

sensitivity of muscle cells to halothane and succinylcholine

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7
Q

What are the triggering factors for non-anesthetic forms?

A

exercise, illness, stress, breeding, and concurrent other myopathies

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8
Q

What is the pathogenesis of malignant hyperthermia?

A
  1. mutation in Ryanodine receptor 1 gene
  2. Excessive Ca release from the SR due to the mutation
  3. muscle contracture
  4. hyperthermia
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9
Q

What clinical signs are associated with malignant hyperthermia?

A

anxiety, tachycardia, tachypnea, profuse sweating, hyperthermia, recumbency/struggling to rise, muscle rigidity, myoglobinuria, death with peracute rigor mortis

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10
Q

What signs do survivors of malignant hyperthermia have?

A

residual myscle atrophy, fibrosis, and scarring

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11
Q

What is the treatment for malignant hyperthermia?

A

treatment for rhabdomyolysis, alcohol/cold water baths, muscle relaxants, and sodium bicarbonate

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12
Q

How is malignant hyperthermia prevented (post-anesthetic forms)?

A

correct positioning, adequate padding during anesthesia, maintain mean arterial blood pressure, and dantrolene 1-2 hours before induction

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13
Q

What is nutritional myodegeneration also known as?

A

white muscle disease

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14
Q

What causes nutritional myodegeneration?

A

Vitamin E/Se deficiency

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15
Q

What population of horses typically gets nutritional myodegeneration?

A

fast growing foals from birth to 11 months of age

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16
Q

Mares of nutritional myodegeneration foals are typically on ______-deficient diet during gestation.

A

selenium

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17
Q

What are the two forms of nutritional myodegeneration?

A

skeletal and cardiac form

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18
Q

What are the clinical signs/conditions associated with the skeletal form of nutritional myodegeneration?

A

slow onset of muscle weakness, stiffness, hard/painful muscles, trembling, recumbency, dysphagia, aspiration pneumonia, and secondary sysetmic infections due to decreased immunity

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19
Q

What are the clinical signs/conditions associated with the cardiac form of nutritional myodegeneration?

A

acute onset respiratory distress, arrhythmias, cardiovascular collapse, and death

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20
Q

How is nutritional myodegeneration diagnosed?

A

elevated muscle enzymes, myoglobinuria, severe electrolyte abnormalities (decreased Na and Cl, increasd K and P), low blood Se and/or glutathione peroxidase levels, and response to Vit. E/Se

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21
Q

How is nutritional myodegeneration diagnosed post mortem?

A

bilateral symmetric myodegeneration, pale and dry appearance of muscle, and white streaks

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22
Q

What causes white streaks in muscle?

A

it could be due to coagulation necrosis, calcification, fibrosis

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23
Q

How do you treat nutritional myodegeneration?

A

exercise RESTRICTION, selenium and Vitamin E supplementation, and supportive care

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24
Q

What is the supportive care specifically for nutritional myodegeneration treatment?

A

correct electrolyte and acid base imbalances, antimicrobial and antiulcler therapy, and enteral feeding

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25
Q

What is the prognosis for nutritional myodegeneration?

A

guarded - 30-45% mortality in the skeletal form, and 95% in the cardiac form

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26
Q

How is nutritional myodegeneration prevented?

A

Se supplementation to pregnant mares and foals from birth to 6 months of age, access to good quality green forage

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27
Q

Where does nutritional myodegeneration occur if it does in adult horses?

A

muscles of mastication, locomotion, or cardiac muscle most commonly affected

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28
Q

What is seasonal pasture myopathy?

A

acute, severe rhabdomyolysis in pastured horses that is seasonal

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29
Q

Where has seasonal pasture myopathy been reported?

A

australia, canada, and the US (Minnesota in 2006, and Iowa and Wisconsin in 2009)

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30
Q

What is the case fatality rate associated with seasonal pasture myopathy?

A

75-95%

31
Q

What clinical signs are associated with seasonal pasture myopathy?

A

acute weakness/stiffness, muscle fasciculations, myoglobinuria, recumbency, tachycardia, tachypnea/dyspnea, colic like signs, dysphagia, esophageal obstruction, and death (within 3 days)

32
Q

What clinicopathologic data is associated with seasonal pasture myopathy?

A

very increased CK and AST, hyperglycemia, hypocalcemia, metabolic acidosis, and increased liver enzymes

33
Q

What is the etiology of seasonal pasture myopathy?

A

Hypoglycin in seeds/seedlings of maple trees

34
Q

What is the pathogenesis of seasonal pasture myopathy?

A
  1. hypoglycin inhibits mitochondrial enzymes
  2. Fatty acid beta oxidation is inhibited
  3. There is an accumulation of secondary (toxic) metabolies
  4. There is a lack of energy supply in tissues utilizing FA for energy production affecting postural, respiratory, and cardiac muscles?
35
Q

How is seasonal pasture myopathy diagnosed?

A

muscle biopsy, oil red O stain, metabolic profiles (antemortem), toxic metabolite of hypoglycin

36
Q

What muscles do you want to biopsy to test for seasonal pasture myopathy and why?

A

postural and intercostal muscles because they have a high oxidative capacity/type 1 myofibers

37
Q

What do you look for in an Oil Red O stain?

A

paucity of cellular infiltrates - Zenker’s necrosis and lipid accumulation

38
Q

What is the toxic metabolite of hypoglycin?

A

methylenecyclopropyl acetic acid

39
Q

What are the risk factors of seasonal pasture myopathy?

A

overgrazed pasture, horses at pasture 24/7, little/no supplemental feed, and inclement weather

40
Q

How is seasonal pasture myopathy prevented?

A

Prevent access to box elder seeds in fall/spring, supplemental feeding, and prevent stress that could trigger the development of clinical signs in subclinical cases

41
Q

How do you treat seasonal pasture myopathy?

A

symptomatic with muscle relaxants, IV fluids, antimicrobials, 5% dextrose IV, frequent, small, carbohydrate rich meals, riboflavin, and antioxidants

42
Q

What is clostridial myonecrosis?

A

rapidly progressive local necrotizing muscle infections within 2 days of intramuscular non-antibiotic injection or injury that leads to systemic toxemia

43
Q

What etiologic agents cause clostridial myonecrosis?

A

C. septicum, chauvoei, perfringens (type A), sordelli, and novii - it is often a mixed infection

44
Q

What clinical signs are associated with clostridial myonecrosis?

A

painful, hot soft swelling, severe depression, fever, tachycardia, tachypnea, anorexia, ataxia, dyspnea, recumbency, coma, and deathw ithin 12-24 hours

45
Q

How is clostridial myonecrosis treated?

A

aggressive surgical debridement and fasciotomy to establish drainage and aeration (the preferred method), antibiotics, supportive care, and hydrotherapy

46
Q

How is clostridial myonecrosis diagnosed?

A

history/clinical presentation, needle aspirate for a direct smear or anaerobic culture

47
Q

What is the prognosis for clostridial myonecrosis?

A

guarded to poor

48
Q

What are the Streptococcus equi associated myopathies?

A

severe acute rhabdomyolysis and infarctive purpura hemorrhagic (Henoch-Schonlein purpura)

49
Q

What is immune mediated myositis (or polymyositis)?

A

rapid lumbar and gluteal muscle atrophy

50
Q

What signs are associated with immune-mediated myositis?

A

stiffness, malaise, weakness, mild-moderate elevation of CK and AST, and an unremarkable CBC

51
Q

What is the etiology of immune-mediated myositits?

A

a missense mutation in myoglobin heavy chani 1 (MYH1) gene in quarterhorses - autosomal dominant trait

52
Q

What muscle cells does immune-mediated myositis affect?

A

type 2x myosin

53
Q

What is the triggering factor in 40% of cases of immune mediated myositis?

A

exposure to strep equi or other respiratory disease

54
Q

How is immune-mediated myositis diagnosed?

A

Tru-Cut biopsy of the epacial or gluteal muscle to look for atrophy of type 2 fibers and lymphocytic vasculitis or genetic testing

55
Q

How is immune-mediated myositis treated?

A

corticosteroids and antimicrobials if there is a bacterial respiratory infection

56
Q

What is the prognosis for immune-mediated myositis?

A

fair - muscle mass recovery within 2 months

57
Q

What causes hyperkalemic periodic paralysis (HYPP)?

A

a point mutation in voltage gated sodium channels of skeletal muscle causing Na channels to fail to inactivate leading to an influx of Na and efflux of K

58
Q

What breeds of horses typically get HYPP?

A

quarter horses, paints, and appaloosas

59
Q

What clinical signs are associated with a mild episode of HYPP?

A

muscle fasciculations (neck, shoulder, flank), muscle cramps, sweating, prolapse of the third eyelid, muscular weakness

60
Q

What clinical signs are associated with a severe episode of HYPP?

A

swaying, dogsitting, staggering, recumbency, laryngeal/pharyngeal paralysis, respiratory distress, collapse, and death due to cardiac rest

61
Q

What clinical signs of HYPP are found in homozygous foals?

A

paralysis of upper respiratory muscles, respiratory stridor/distress, dysphagia, and aspiration pneumonia

62
Q

How long do episodes of HYPP last?

A

15-60 minutes, spontaneous recovery is common, and longer if severe and untreated

63
Q

What are the precipitating factors of HYPP?

A

fasting, anesthesia/heavy sedation, stress, trailer rids, dietary changes (increased K)

64
Q

How is HYPP diagnosed?

A

hyperkalemia during episodes, mild hyponatremia, hemoconcentration, and DNA testing

65
Q

How is HYPP treated?

A

gran, corn syrup, 5% dextrose, sodium bicarbonate, calcium gluconate, and acetazolamide

66
Q

How is HYPP prevented?

A

a low K diet, feed several times/day, regular exercise or access to a paddock, and increased K excretion by giving acetazolamide and hydrochlorothiazide

67
Q

What is glycogen branching enzyme deficiency (GBED)?

A

a fatal glycogen storage disorder of QH-related breeds

68
Q

Is GBED caused by a recessive or dominant trait?

A

autosomal recessive trait

69
Q

What does the mutation of GBED cause?

A

an accumulation of long unbranched chains of glucose primarily in skeletal muscle, cardiac muscle, and the liver

70
Q

Who are the carriers of GBED?

A

they are heterozygotes that have half-normal GBE activity, normal histopathology and no clinical signs

71
Q

What are the clinical signs of GBED?

A

Unspecific - weakness at birth, congenital limb contracture, inability to rise, decreased physical activity, respiratory failure, seizures, and sudden death

72
Q

How is GBED diagnosed?

A

persistent mild elevations, elevated GGT, leukopenia, hypoglycemia, and genetic testing

73
Q

What does a muscle biopsy of GBED show?

A

lack of normal PAS staining for glycogen and intracellular PAS-positive globular and crystalling inclusions

Equine Medicine (27 decks)

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