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Equine Medicine and Surgery > Lecture 10: Diseases of Muscle > Flashcards

Lecture 10: Diseases of Muscle Flashcards

1
Q

What two muscle enzymes are evaluated in rhabdomyolysis muscle diseases and what disease are they elevated in

A

Creatinine Kinase (CK)
Aspartame Aminotransferase (AST)

Elevated in rhabdomyolysis

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2
Q

How long is plasma half life for CK and how long does it take to return to normal

A

Plasma half life: <2hrs
Returns to normal 2-3 days later

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3
Q

What is the plasma half life of AST and how long does it take to return to normal

A

Plasma half life: 24hrs
Takes 2 weeks to return to normal

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4
Q

What disease is also known as “typing up”

A

Rhabdomyolysis

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5
Q

What are some clinical signs of Rhabdomyolysis

A
  1. Stiff, unwilling to move
  2. Muscle tremors
  3. Sweating, tachypnea, tachycardia
  4. Pawing
  5. Can progress to recumbency
  6. Wine color urine- myoglobinuria
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6
Q

What muscle is good for biopsy

A

Semimembranosus

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7
Q

Horse presents as very stiff and muscle biopsy shows amylase resistant glycogen accumulation in muscle fibers. What is likely cause

A

Polysaccharide Storage Myopathy type 1 (PSSM1)

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8
Q

Horse presents with muscle stiffness, short stride, muscle fasciculations. What tests do you want to run

A
  1. CK and AST- baseline
  2. Exercise tolerance test- to compare CK and AST
  3. Muscle biopsy
  4. Genetic testing
  5. Vitamin E and Selenium levels
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9
Q

What is the 5+ panel test for muscle diseases

A
  1. Polysaccharide storage myopathy type 1
  2. Malignant hyperthermia
  3. Hyperkalemic periodic paralysis
  4. Glycogen branching enzyme deficiency
  5. Myosin heavy chain myopathy
  6. Hereditary equine regional dermal asthenia
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10
Q

What does the histo for PSSM type 1 look like

A

Increased concentrations of glycogen within the muscle tissue

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11
Q

What breeds are predisposed to PSSM1

A
  1. Stock breeds- quarter horses, paints, Appaloosa
  2. Drafts and their crosses
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12
Q

What pathophysiology of PSSM type 1

A
  1. Base pair mutation in GYS1 gene
  2. Gain of function in glycogen synthase combined with increased insulin sensitivity
  3. Result of large stores of glycogen that are amylase resistant so muscle cells can’t contract
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13
Q

What are the diagnostic tests for PSSM1

A
  1. Genetic test for GYS1 mutation
  2. Muscle biopsy semimebranosus
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14
Q

What is tx for PSSM1

A
  1. Daily exercise
  2. Low starch <14%
  3. High fat >6%
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15
Q

What is prognosis for PSSM1

A

Varies from reasonable to excellent

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16
Q

What are some signs of PSSM type 2

A

Poor performance, undiagnosed gait abnormality, sore muscles, drop in energy levels

Doesn’t have a typing up appearance like type 1

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17
Q

What is the mean onset of PSSM type 2 and what breeds

A

8-11yrs old
Warmbloods >80%
Arabians 100%

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18
Q

How do you diagnose PSSM type 2

A
  1. Abnormal aggregates of periodic acid schiffs positive glycogen within muscle
  2. Negative for GYS1 mutation
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19
Q

Arabian between age of 11-15 years that is extremely fit, ties up mildly. Test muscle enzymes and there is none to minimal elevation. What is likely disease

A

Myofibrillar myopathy

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20
Q

Warmblood between 8-10 years old with extremely vague lameness/soreness issues. There are no changes in muscle enzyme elevation. What muscle disease is likely

A

Myofibrillar myopathy

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21
Q

How do you dx myofibrillar myopathy

A

Muscle biopsy, semimebranosus or middle gluteal

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22
Q

What causes myofibrillar myopathy

A
  1. Weakness in Z-discs and resulting in proliferation of cytoskeletal proteins
  2. Desmin is a cytoskeletal intermediate that maintains parallel alignment of the sarcomeres of the Z discs
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23
Q

What disease was thought to be PSSM type 2 due to pools of glycogen within the disrupted myofibrils but is actually ___, caused by weakness in Z-discs

A

Myofibrillar myopathy

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24
Q

What is tx for myofibrillar myopathy

A
  1. Exercise
  2. Amino acid supplements: purina supersport, progressive nutrition topline xtreme
  3. Feed < 12% NSC
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25
Q

What causes over exertion induced rhabdomyolysis

A

History of increase in work intensity without foundation of consistent training

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26
Q

What does light microscopy vs electron microscopy show for overexertion induced rhabdomyolysis

A

Light microscopy: normal
Electron microscopy: disruption of muscle contractile proteins

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27
Q

How much volume do horses lose in sweat

A

15L/hr

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28
Q

What are some clinical signs of exhaustion

A

Dull, depressed, muscle group spasms, clinically dehydrated, elevated heart and respiratory rate, elevated temperature the thumps

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29
Q

What is thumps and what causes it

A

Hypocalcemia, easily excited muscles so heart and muscles are beating at same time

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30
Q

What is the clinical pathology for exhaustion

A

Hypocalcemia, hypomagnesemia, hypokalemia, hypochloremic metabolic alkalosis, normal CK/AST, but can progress to rhabdomyolysis and multiple organ failure

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31
Q

What causes malignant hyperthermia

A

Autosomal dominant mutation in ryanodine receptor (RYR1) and results in abnormal calcium release within muscles

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32
Q

What are some signs of malignant hyperthermia

A

Increase in body temperature and rhabdomyolysis

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33
Q

What can trigger malignant hyperthermia

A

Exercise or anesthesia

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34
Q

How do you dx malignant hyperthermia

A

Genetic testing

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35
Q

What is tx for malignant hyperthermia

A

Supportive care, avoid anesthesia or pretreat with dantrolene

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36
Q

What is prognosis for malignant hyperthermia

A

Not good

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37
Q

What causes recurrent equine rhabdomyolysis

A

Abnormalities in the regulation of muscle contraction and relaxation

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38
Q

What breeds commonly get recurrent equine rhabdomyolysis

A

Thoroughbreds and Standardbreds

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39
Q

How do horses with recurrent equine rhabdomyolysis present

A

Anxious, lame

40
Q

T or F: fillies are more likely to havre recurrent equine rhabdomyolysis

A

True

41
Q

What diet to horses with recurrent equine rhabdomyolysis tend to be on

A

> 10lb of sweet feed

42
Q

What is pathophysiology for recurrent equine rhabdomyolysis

A

Enhanced storage of intracellular calcium in sarcoplasmic reticulum with excessive release during muscle contraction resulting in prolonged depolarization

43
Q

How do you dx recurrent equine rhabdomyolysis

A

Disease rule out
1. Muscle biopsy normal
2. No genetic test

44
Q

What is tx for recurrent equine rhabdomyolysis

A
  1. Daily exercise
  2. Low stress (acepromazine)
  3. Low starch <20% calories and high fat >20% calories
  4. Muscle relaxants: dantrolene, phenytoin
45
Q

What is a nutritional cause of non-exertional rhabdomyolysis

A

Vitamin E or selenium deficiency “white muscle disease”

46
Q

How do you dx white muscle disease

A
  1. Test whole blood selenium or glutathione perioxidase
  2. Test levels of vitamin E
47
Q

What is tx for white muscle disease

A
  1. Supplement natural source alpha tocopherol 2000 IU/day
  2. Supplement selenium 1-3mg/day
48
Q

What causes myosin heavy chain myopathy

A

Autosomal codominant genetic disorder/ mutation in MYH1

49
Q

What two syndromes does myosin heavy chain myopathy cause

A
  1. Nonexertional rhabdomyolysis
  2. Immune mediated myositis
50
Q

__% of quarter horses test positive for myosin heavy chain myopathy

A

7%

51
Q

__% of reining, working cow, halter horses test positive for myosin heavy chain myopathy

A

16-22%

52
Q

What is MYHM: immune mediated myositis characterized by

A

Episodes of severe muscle atrophy following autoimmune event

53
Q

What are some triggering factors for MYHM: immune mediates myositis

A
  1. S. Equi
  2. Respiratory disease
  3. Vaccination
54
Q

What are some clinical signs for MYHM: immune mediated myositis

A

Rapid onset muscle atrophy of epaxials and gluteals

55
Q

How do you dx MYHM: immune mediated myositis

A

Biopsy of muscles reveal lymphocytic vasculitis

56
Q

How do you tx MYHM: immune mediated myositis

A

Corticosteroids

57
Q

What is prognosis for MYHM: immune mediated myositis

A

Depends on response but down and unable to stand is grave prognosis

58
Q

What signs are seen with MYHM: non-exertional rhabdomyolysis

A

Stiffness, swelling of muscles along back and haunches, difficulty rising

59
Q

What causes toxic rhabdomyolysis

A
  1. Hypoglycemia A ingested from Box Elder (acre negunda) trees
  2. Ionophores
60
Q

How does hypoglycin A cause toxic rhabdomyolysis

A

Metabolized to become inhibitor of multiple acyl-CoA dehydrogenases which damages mitochondria and impairs lipid metabolism, results in cell death

61
Q

What are some clinical signs of toxic rhabdomyolysis

A

Sweating, fasciculations, weakness, recumbency, myoglobinuria, colic, myocardial damage, dysphasia and rhabdomyolysis

62
Q

What is elevated in toxic rhabdomyolysis caused by hypoglycin A

A

CK/AST/ troponin

63
Q

What is tx for toxic rhabdomyolysis from hypoglycin A

A

Supportive care

64
Q

What is prognosis for hypoglycin A toxic rhabdomyolysis

A

Grave, >90% die

65
Q

What is commonly added to ruminant feeds to increase growth, but is very toxic to horses

A

Ionophores

66
Q

How do ionophores cause rhabdomyolysis

A

Form lipid soluble complexes with cations to facilitate cation transport across cell walls, excessive influx of calcium and sodium cause swelling and cell death

67
Q

What are some clinical signs of Ionophores toxicity

A
  1. Sudden death within 24hrs
  2. Inappetance
  3. Tremors
  4. Ataxia
  5. Stumbling
  6. Tachycardia
68
Q

What is prognosis for toxic rhabdomyolysis caused by ionophores

A
  1. If horse survives acute intoxication the damage myocardial and skeletal cells are replaced with fibrosis resulting in permanent dysfunction and will lead to cardiac failure
  2. Typically fatal
69
Q

How do you tx acute rhabdomyolysis

A
  1. IV fluids to prevent pigment nephropathy
  2. Anti-inflammatories (NSAIDS, steroids)
  3. Anxiolytics/muscle relaxation- acepromazine
  4. Muscle relaxants: dantrolene, methocarbamol phenytoin
  5. Analgesics: butorphanol, alpha 2 agonists
  6. Limit exercise
  7. Address inciting cause
70
Q

What do you need to use cautiously when tx acute rhabdomyolysis due to renal insult

A

NSAIDS

71
Q

What disease are steroids absolutely indicated for tx of acute rhabdomyolysis

A

MYHC causing immune mediated myositis

72
Q

How does dantrolene work

A

Exhibits muscle relaxation by activity ryanadine R1 receptor antagonist that decrease release of calcium from sarcoplasmic reticulum

73
Q

How does methocarbamol work

A

Acts on the neurons of the spinal cord and reduce acute skeletal muscle spasm

74
Q

How does phenytoin work

A

Anticonvulsant action from promotion of sodium effluent from neurons and thereby inhibiting spread of seizure activity

75
Q

What typically causes Clostridial myositis

A

Intramuscular injection or penetrating wound

76
Q

__environment is essential for Clostridial myositis

A

Anaerobic

77
Q

What are the toxins for clostridial myositis

A

Lecithinase, hemolysin, Neuroamindases

78
Q

What are the clinical signs associated with clostridial myositis

A

Pain, swelling, crepitus, depression, fever, found dead, rapid progression of signs

79
Q

What are the most common bacterial causes of clostridial myositis

A
  1. C. Perfringens type A- most common in horses
  2. C. Sordellii- fatal
80
Q

What is prognosis for C. Myositis

A

Guarded

81
Q

What is the pathophysiology of myotonia

A

Delayed relaxation of muscle after mechanical stimulation or voluntary contraction, abnormal muscle excitability

82
Q

What are nondystophic myotonas result of

A

Sarcolemmal ion channel dysfunction

83
Q

What myotonia typically appears in first year of life and doesn’t progress

A

Myotonia congenital

84
Q

What causes myotonia congenita

A

Mutation in the gene for the skeletal muscle chloride channel 1 protein (CLCN1)

85
Q

Which myotonia is severe, progressive, and rare

A

Myotonia dystrophica

86
Q

How do you dx myotonia

A
  1. Electromyographic examinations that show repetitive and high frequency
  2. Muscle biopsy in myotonia dystrophica but not congenita
87
Q

What dystrophic changes on muscle biopsy are seen with myotonia dystrophica

A

Ringed fibers, numerous centrally displayed myonucleis, sarcoplasmic masses, increased endometrial and peri trial connective tissue

Fiber type grouping and atrophy of bot type I and II muscle fibers

88
Q

How do you dx myotonia

A
  1. Genetic testing for new forest ponies
  2. PE
  3. Clinical pathology- muscle enzymes normal because no rhabdomyolysis
89
Q

How do the muscle enzymes change in myotonia

A

They dont because this is not rhabdomyolysis

90
Q

What breeds are predisposed to HYPP

A

Quarter horse, Appaloosa’s, paints and crosses

91
Q

What causes HYPP

A

Mutation in defective sodium channel genes SCN4A that results in failure to close following depolarization leading to abnormal muscle contraction and paralysis

92
Q

What are some clinical signs of HYPP

A

Myotonia, muscle fasciculations, muscle cramping, third eyelid prolapse, weakness, recumbency, pharyngeal paralysis

93
Q

What are some clinical pathologies associated with HYPP

A
  1. CSK/AST not elevated- not rhabdomyolysis
  2. Hyperkalemia acutely
  3. Genetic testing
94
Q

What is tx for HYPP

A
  1. Clients have Karo syrup at home
  2. Dextrose IV, Calcium IV
  3. Sometimes tracheostomy
  4. Reduce potassium diet- avoid alfalfa, orchard, brome, boy bean meal
  5. Feed Timothy, Bermuda, oats, corn, wheat, barely, beet pulp, pasture
  6. Increase renal potassium excretion with Acetazolamide
95
Q

How does acetazolamide work is what is dose

A

Potent carbonic anhydrase inhibitor that promotes potassium wasting in urine

Dose: 2-2mg/kg PO q8-12

Equine Medicine and Surgery (27 decks)

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