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Equine Medicine > Myopathies > Flashcards

Myopathies Flashcards

1
Q

whatis rhabdomyolysis

A

destruction of striated muscle cells

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2
Q

what are common diagnostic tests for Myopathies?

A
  • Serum Chemistry and CBC
    • Electrolytes
    • BUN and Creatining (increased)
    • Muscle enzyme activities
      • increased creatine kinase (CK)
      • increased aspartate aminotransferase (AST)
  • Vit E/selenium Nutritional- white muscle disease
  • Urinalysis
  • Fractional excretion of electrolytes
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3
Q

Creatine Kinase (CK)

A

source skeletal muscle

Levels increase 4-6 hours following insult.

This increase is very short lived.

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4
Q

AST

A

Many sources: skeletal muscle, cardiac muscle, liver, RBC

Peak levels approximately 12-24 horus following insult

half life is very long, so it remains elevated for longer

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5
Q

what would a differential diagnosis for a Marked increase in CK (10,000-100,000IU)

A

severe rhabdomyolyysis

Persistent elevation indicated continuing myonecrosis

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6
Q

What do you look for on urinalysis for indications of muscle damage?

A

myoglobinuria- indicates severe muscle damage

Assess for secondary renal disease (pigment nephropathy)

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7
Q

Muscle biopsy

A

gluteal, semimembranosus, or other affected muscle

Samples collected percutaneously

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8
Q

what is electromyography used for

A

electrical recording of muscle activity

  • differentiates myopathic vs. neuropathic diseases
  • distribution of disease
  • pathophysiologic mechanism
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9
Q

How is an exercise challenge test utilized in Myopathy cases

A

detects subclinical cases of chronic ER

light exercise 15-30 minutes of trotting

CK evaluation before and 4-6 hours after exercise

There will be >3-4x increase in CK post submas. exercise indicative of exertional rhabdomyolysis

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10
Q

when using a hair sample or whole blood for genetic testing, what inherited muscle diseases can you test for?

A

Hyperkalemic periodic paralysis (HYPP)

Polysaccharide Storage Myopathy (PSSM)

Malignant hyperthermia (MH)

Glycogen branching enzyme deficiency (GBED)

Immune mediated myositis

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11
Q

What are the 2 categories of Exertional Rhabdomyolysis?

A

chronic or sporadic

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12
Q

what are the treatment goals for Rhabdomyolysis?

A
  • releave pain and anxiety
  • correct electrolyte and acid-base abnormalities
  • limit muscle damage
  • maintain perfusion
  • prevent pigment nephropathy
  • provide supportive care
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13
Q

What treatments can you use for Rhabdomyolysis?

A

sedatives, tranquilizers

analgesics (flunixin or phenylbutazone)

IV vluid therapy- LRS, or isotonic saline (HYPP)

antioxidants- Vit E or selenium

Muscle relaxants

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14
Q

What are muscle relaxants used in Rhabdomyolysis

A

methocarbamol, Guaifenesin

Dantrolene

Phenytoin

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15
Q

What are characteristics of Methocarbamol and Guaifenesin?

A
  • centrally acting MR
  • exact mechanism unknown

sedative effects

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16
Q

What are characteristics of Dantrolene?

A
  • interferes with Calcium release of Ca++ from SR
  • used for Malignant hyperthermia, or recurrent rhabdomyolysis
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17
Q

What are characteristics of Phenytoin?

A

acts as ion channels in muscle and nerves (promotes Na+ efflux; membrane stabilizing)

Decreases sensitivity of muscle spindles to stretch

anticonvulsant, antiarrhythmic

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18
Q

PSSM- Polysaccharide Storage Myopathy

A

Form of Exertional Rhabdomyolysis
Quarter Horse related breeds, draft horses etc.

Accumulation of glycogen and amylase-resistant abnormal polysaccharide in skeletal muscle

“Glycogen Storage Disease”

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19
Q

Type 1 PSSM (glycogen synthase 1 mutation)

A

autosomal dominant trait

Gain of function mutation in GYS1 gene -> elevated GS activity

Increased glycogen synthesis within the muscle cell

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20
Q

Type 2 PSSM (non-GYS1 forms) characteristics

A

familial basis is suspected

genetic mutation not yet identified

inconsistent accumulation of abnormal polysaccharide

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21
Q

What are clinical signs of PSSM in Draft horses

A

generally subclinical

abnormal gait, muscle wasting, Exertional RM

Postanesthetic myopathy

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22
Q

What are clinical signs of PSSM in quarter horses

A

Exertional Rhabdomyolysis

abnormal gait

Muscle wasting

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23
Q

What are clinical signs of exertional rhabdomyolysis?

A

Mild form- exercise intolerance, pawing post exercise, muscle fasiculations, sweating stiffness uriation stance

Severe form- severe pain resembling colic, recumbency, renal failure

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24
Q

What do you see on a muscle biopsy for PSSM?

A

Must use Periodic acid-Schiff (PAS) stain for glycogen

  • increased density of glycogen (2x)
  • abnormal PAS pos. inclusions
  • Subsarcolemmal vacuoles
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25
Q

what is the diagnosis for the histopathology sample on the right?

A

PSSM

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26
Q

How do you manage PSSM?

A
  1. dietary management-
    • decrease NS Carbohydrates
      • alfalfa/grass hay mix or grass hay
    • increase fat > 13% Digestible energy from fat
  2. Regular exercise or access to paddock
    • burns muscle glycogen stores
    • Enhances oxidative capacity of muscle by increasing enzymes that utilize fat as fuel
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27
Q

Recurrent Exertional Rhabdomyolysis (RER) overview

A

inherited autosomal dominant trait in TB

Most common in young TB fillies in training

defective intracellular Ca++ regulation

clinical sings: poor performance, muscle stiffness, rhabdomyolysis

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28
Q

How do you prevent RER?

A
  • minimize stress (train before others, stall in quiet barn area)
  • daily exercise, turn-out
  • Decreased carbohydrates
  • fat supplement
  • Acepromazine, dantrolene, phenytoin before training exercise
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29
Q

What is the big difference between PSSM and RER in management?

A

Patients tend to outgrow RER, and can still have a successful career

PSSM is a chronic problem

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30
Q

What is compartment syndrome?

A

this is when the muscle fascia is unable to stretch

Trauma causes increased pressure and ischemia

31
Q

Malignant hyperthermia overview

A
  • Generalized post-anesthetic myopathy
    • sensitivity of muscle cells to
      • halothane
      • succinylcholine
  • Non-anesthetic forms
    • triggering factors
      • exercise, illness, stress, breedign
      • concurrent other myopathies (PSSM!)
32
Q

Pathogenesis for Malignant Hyperthermia

A
  • mutation in Ryanodine Receptor 1 gene
  • Autosomal dominant trait in the horse
    • genetic test
    • part of 5 pannel test for QH
  • Excessive Ca++ release -> muscle contracture -> hyperthermia
33
Q

What are clinical signs of Malignant hyperthermia?

A

anxiety

tacycardia, tachypnea

profuse sweating, hyperthermia

recumbency/struggling to rise

Muscle ragidity, myoglobinuria

death with peracute rigor mortis

34
Q

What is the treatment for Malignant Hyperthermia?

A
  • Continue Rhabdomyolysis treatment in general
  • alcohol/cold water baths (to decrase the temperature)
  • Muscle relaxants (Dantrolene)
  • sodium bicarbonate
    • if metabolic or respiratory acidosis
35
Q

What are methods of preventing post-anesthetic form of malignant hyperthermia?

A
  • correct positioning
  • adequate paddling during anesthesia
  • maintain mean arterial blood pressure > 80-85 mmHg
  • Dantrolene 1-2h before induction to decrease the Ca release
36
Q

Nutritional myodegeneration overview

A

“White Muscle disease”

  • Vit E/Selenium deficiency
  • Mainly in fast growing foals from birth to 11 months of age
  • Mares of affected foals typically on selenium-deficient diet during gestation
37
Q

What are methods of diagnosis for Nutritional myodegeneration?

A

Elevated muscle enzymes (CK and AST)

Myoglobinuria

Severe electrolyte abnormalities (low Na, CL High K and P)

Low blood Se and/or glutathione peroxidase levels

response to Vit E/selenium a swift response is diagnostic

38
Q

what are post mortem diagnosis for Nutritional myodegeneration?

A

bilateral symmetric myodegeneration

Muscle is pale and dry apperance (white in color)

39
Q

what are methods of treatment for Nutritional Myodegeneration?

A
  • exercise restriction*****
  • supportive care
    • correct electrolyte and acid base imbalances
    • Antimicrobial and antiulcer therapy
40
Q

What is the prognosis for Nutritional Myodegeneration?

A

Guarded

30-45% mortality (skeletal form)

95% mortality in th ecardiac form

41
Q

What are methods for prevention of Nutritional Myodegeneration

A
  • Se supplementation
    • pregnant mares
    • foals from birth to 6 months of age
  • Access to good quality green forage
42
Q

True or False

Nutritional myodegeneration is common among adult horses.

A

False

This is rare.

Muscles of mastication, locomotion, or caridac muscle most commonly affected

43
Q

What is seasonal Pasture Myopathy?

A

This is a form of nonexertional Rhabdomyolysis

  • acute, severe rhabdomyolysis
  • pastured horses
  • seasonal
  • High case fatality rates 75%-95%
44
Q

What are the clinical signs of Seasonal Pasture Myopathy

A

Acute weakness/stiffness

Muscle fasciculations

Myoglobinuria

recumbency

45
Q

For seasonal Pasture Myopathy, what clinical pathology data will you find?

A
  • increased CK & AST
  • Hyperglycemia
  • Hypocalcemia
  • metabolic acidosis
  • Increased liver enzymes
46
Q

what is the etiology for Seasonal Pasture Myopathy

A

hypoglycin in seeds/seedlings of maple trees

47
Q

What is the pathogenesis for Seasonal Pasture Myopathy?

A
  • Hypoglycin inhibits mitochondrial enzymes
  • this causes acumulation of secondary metabolites
  • lack of energy supply in tissues utilizing Fa for energy production
48
Q

How do you diagnose Seasonal PAsture Myopathy?

A
  • Muscle biopsy
    • postural and intercostal muscles
      • high oxidative capacity
  • Oil Red O stain
    • fresh frozen muscle
      • paucity of cellular infiltrates
      • Zenker’s necrosis and lipid accumulation
  • Metabolic profiles
  • toxic metabolite of hypoglycin
49
Q

what are risk factors for Seasonal Pasture myopathy

A
  • overgrazed pasture
  • horses at pasture 24/7
  • little/no supplemental feed
  • inclement weather
    *
50
Q

How do you preevent seasonal pasture myopathy?

A
  • prevent access to box elder seeds in the fall/spring
  • supplemental feeding (hay, grain)
    • prevents negative energy balance and foraging for “unusual” feedstuff
  • Prevent stress that could trigger development of clinical signs in subclniical cases
51
Q

Treatment for Seasonal Pasture Myopathy

A
  • symptomatic (muscle relaxants, IV fluids, antimicrobials)
  • 5% dextrose IV (insulin if needed)
  • Frequent, small, carbohydrate rich meals
  • Riboflavin (Vit B2)
  • antioxidants (Vit E/selenium ; Vit C)
52
Q

Clostridial myonecrosis

A
  • rapidly progressive local necrotizing muscle infection
  • within 2 days of intramuscular non-antibiotic injection (flunixin) or injury
  • systemic toxemia
  • Highly fatal
  • C. septicum, chauvoei, perfringens, sore=delli, novii, often mixed infection
53
Q

Clincial signs of Clostridial myonecrosis

A

severe depression

fever

tachycardia, tachypnea

anorexia

ataxia

dyspnea

recumbency

coma, death within 12-24 hours

Painful, hot, soft swelling +/- crepitus

54
Q

Methods of treatment for Clostridial myonecrosis

A

aggressive surgical debridement and fasciotomy to establish drainage and aeration

antibiotics (penicillin and metronidazole)

supportive care such as IV fluids

hydrotherapy

55
Q

Methods of diagnosis for Clostridial myonecrosis

A

history/clinical presentaion

Needle aspiration with a direct smear showing Gram - rods

Anaerobic culture

56
Q

Streptococcus equi associated myopathies

A

Non-exertional rhabdomyolysis

severe acute rhabdomyolysis

infarctive purpura hemorrhagica

Both are rare and highly fatal

57
Q

Muscle atrophy

A

immune mediated myositis

rapid lumbar & gluteal muscle atrophy

stiffness, malaise, weakness

Mild-moderate elevation of CK and AST

CBC is often unremarkable

58
Q

Immune medaited myositis and genetics

A

linked to missense mutation in myoglobin heavy chain 1 gene in QH

autosomal dominant trait with variable penetrance

auto-immun reaction to Type 2x myosin

Exposure to S.equi or other respiratory disease is triggering favtor in 40% fo cases

59
Q

What group of Quarter Horses have a higher prevalence of immune mediated myositis

A

Reigning horses 13.5% of affected quarter horses

60
Q

How do you diagnose immune mediated myositis?

A
  • tru-cut biopsy of the epaxial or gluteal muscle)
    • atrophy of type 2 fibers
    • lymphocytic vasculitis
  • Genetic testing
61
Q

what are treatment methods for immune mediated myositis?

A

immunosuppressive (corticosteroids)

antimicrobials (if bacterial respiratory infection)

62
Q

What is the prognosis for Immune-mediated myositis

A

fair

muscle mass recovery within 2 months

63
Q

Disorders of muscle tone

A

Hyperkalemic Periodic Paralysis (HYPP)

64
Q

HYPP

A
  • autosomal dominant genetic disease associated with QH stud “Impressive”
    • point mutation in voltage gated sodium channel of skeletal muscle
    • Na+ channels fail to inactivate -> abnormal influx of Na+ depolarization and efflux of K+
    • persistent depolarization and temporary weakness
65
Q

what are clinical signs of HYPP?

A
  • Midl episode: muscle fasciculations , muscle cramps, sweating, prolapse of 3rd eyelid, muscular weakness
  • Severe episode: swaying, dogsitting, staggering, recumbency, laryngeal/pharyngeal paralysis, resp.distress, collase, death (cardiac arrest)
66
Q

Clinical signs of HYPP

A
  • foals
    • parallysis of upper respiratory muscles
    • respiratory stridor/distress
    • dysphagia
    • aspiration pneumonia
67
Q

what are precipitating factors for HYPP episodes?

A
  • fasting
  • anesthesia/heavy sedation
  • stress
  • trailer rides
  • dietary changes (increased K+ diet)
68
Q

methods for diagnosis of HYPP

A

hyperkalemia during episodes

mild hyponatremia, hemoconcentration

DNA testing- included in AWHA 5 panel test

69
Q

Treatment of HYPP

A

grain, corn syrup-not mylasses

5% dextrose

sodium bicarbonare

Calcium gluconate

Acetazolamide (K+ wasting diuretic)

70
Q

Preventing of HYPP attacks

A
  1. low K+ diet
  2. feed several times/day
  3. regular exercise or access to a paddock
  4. increased K+ excretion
    1. acetazolamide (K+ wasting diuretic)
    2. Hydrochlorothiazide
71
Q

Glycogen branching enzyme deficiency (GBED)

A

fatal glycogen storage disorder of QH

autosomal recessive disorder

lack of normally configured Glycogen for energy metabolism. These accumulate in the liver, and skeletal and cardiac muscles

72
Q

clincial signs for GBED

A

weakness at birth

congenital limb contracture

inability to rise

decreased f=physical activity

sudden death

73
Q

Methods of diagnosis for GBED

A

presistent mild elevations of CK

elevated GGT

Leukopenia

Hypoglycemia

Genetic testing (part of 5 panel AQHA testing)

Muscle biopsy with lack of normal glycogen stain uptake

Equine Medicine (5 decks)

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