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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
what is the diagnosis for the histopathology sample on the right?
PSSM
26
How do you manage PSSM?
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
27
Recurrent Exertional Rhabdomyolysis (RER) overview
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
28
How do you prevent RER?
* minimize stress (train before others, stall in quiet barn area) * daily exercise, turn-out * Decreased carbohydrates * fat supplement * Acepromazine, dantrolene, phenytoin before training exercise
29
What is the big difference between PSSM and RER in management?
Patients tend to outgrow RER, and can still have a successful career PSSM is a chronic problem
30
What is compartment syndrome?
this is when the muscle fascia is unable to stretch Trauma causes increased pressure and ischemia
31
Malignant hyperthermia overview
* 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
Pathogenesis for Malignant Hyperthermia
* 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
What are clinical signs of Malignant hyperthermia?
anxiety tacycardia, tachypnea profuse sweating, hyperthermia recumbency/struggling to rise Muscle ragidity, myoglobinuria death with peracute rigor mortis
34
What is the treatment for Malignant Hyperthermia?
* Continue Rhabdomyolysis treatment in general * alcohol/cold water baths (to decrase the temperature) * Muscle relaxants (Dantrolene) * sodium bicarbonate * if metabolic or respiratory acidosis
35
What are methods of preventing post-anesthetic form of malignant hyperthermia?
* 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
Nutritional myodegeneration overview
"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
What are methods of diagnosis for Nutritional myodegeneration?
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
what are post mortem diagnosis for Nutritional myodegeneration?
bilateral symmetric myodegeneration Muscle is pale and dry apperance (white in color)
39
what are methods of treatment for Nutritional Myodegeneration?
* exercise restriction\*\*\*\*\* * supportive care * correct electrolyte and acid base imbalances * Antimicrobial and antiulcer therapy
40
What is the prognosis for Nutritional Myodegeneration?
Guarded 30-45% mortality (skeletal form) 95% mortality in th ecardiac form
41
What are methods for prevention of Nutritional Myodegeneration
* Se supplementation * pregnant mares * foals from birth to 6 months of age * Access to good quality green forage
42
True or False Nutritional myodegeneration is common among adult horses.
False This is rare. Muscles of mastication, locomotion, or caridac muscle most commonly affected
43
What is seasonal Pasture Myopathy?
This is a form of nonexertional Rhabdomyolysis * acute, severe rhabdomyolysis * pastured horses * seasonal * High case fatality rates 75%-95%
44
What are the clinical signs of Seasonal Pasture Myopathy
Acute weakness/stiffness Muscle fasciculations Myoglobinuria recumbency
45
For seasonal Pasture Myopathy, what clinical pathology data will you find?
* increased CK & AST * **_Hyperglycemia_** * Hypocalcemia * metabolic acidosis * Increased liver enzymes
46
what is the etiology for Seasonal Pasture Myopathy
hypoglycin in seeds/seedlings of maple trees
47
What is the pathogenesis for Seasonal Pasture Myopathy?
* Hypoglycin inhibits mitochondrial enzymes * this causes acumulation of secondary metabolites * lack of energy supply in tissues utilizing Fa for energy production
48
How do you diagnose Seasonal PAsture Myopathy?
* 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
what are risk factors for Seasonal Pasture myopathy
* overgrazed pasture * horses at pasture 24/7 * little/no supplemental feed * inclement weather *
50
How do you preevent seasonal pasture myopathy?
* 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
Treatment for Seasonal Pasture Myopathy
* 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
Clostridial myonecrosis
* 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
Clincial signs of Clostridial myonecrosis
severe depression fever tachycardia, tachypnea anorexia ataxia dyspnea recumbency coma, death within 12-24 hours **Painful, hot, soft swelling +/- crepitus**
54
Methods of treatment for Clostridial myonecrosis
aggressive surgical debridement and fasciotomy to establish drainage and aeration antibiotics (penicillin and metronidazole) supportive care such as IV fluids hydrotherapy
55
Methods of diagnosis for Clostridial myonecrosis
history/clinical presentaion Needle aspiration with a direct smear showing Gram - rods Anaerobic culture
56
Streptococcus equi associated myopathies
Non-exertional rhabdomyolysis severe acute rhabdomyolysis infarctive purpura hemorrhagica Both are rare and highly fatal
57
Muscle atrophy
immune mediated myositis **rapid** lumbar & gluteal muscle atrophy stiffness, malaise, weakness Mild-moderate elevation of CK and AST CBC is often unremarkable
58
Immune medaited myositis and genetics
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
What group of Quarter Horses have a higher prevalence of immune mediated myositis
Reigning horses 13.5% of affected quarter horses
60
How do you diagnose immune mediated myositis?
* tru-cut biopsy of the epaxial or gluteal muscle) * atrophy of type 2 fibers * lymphocytic vasculitis * Genetic testing
61
what are treatment methods for immune mediated myositis?
immunosuppressive (corticosteroids) antimicrobials (if bacterial respiratory infection)
62
What is the prognosis for Immune-mediated myositis
fair muscle mass recovery within 2 months
63
Disorders of muscle tone
Hyperkalemic Periodic Paralysis (HYPP)
64
HYPP
* 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
what are clinical signs of HYPP?
* **_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
Clinical signs of HYPP
* foals * parallysis of upper respiratory muscles * respiratory stridor/distress * dysphagia * aspiration pneumonia
67
what are precipitating factors for HYPP episodes?
* fasting * anesthesia/heavy sedation * stress * trailer rides * dietary changes (increased K+ diet)
68
methods for diagnosis of HYPP
hyperkalemia during episodes mild hyponatremia, hemoconcentration DNA testing- included in AWHA 5 panel test
69
Treatment of HYPP
grain, corn syrup-not mylasses 5% dextrose sodium bicarbonare Calcium gluconate Acetazolamide (K+ wasting diuretic)
70
Preventing of HYPP attacks
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
Glycogen branching enzyme deficiency (GBED)
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
clincial signs for GBED
weakness at birth congenital limb contracture inability to rise decreased f=physical activity sudden death
73
Methods of diagnosis for GBED
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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