Equine Myopathies Flashcards

1
Q

what anatomic components do most myopathies affect?

A

most myopathies on the level of the muscle fiber (cellular level / group of cells)

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2
Q

Musculoskeletal exam components

A
  • Distance examination
    ◦ Posture & stance
    ◦ Muscle mass
    ◦ Muscle symmetry
  • Palpation
    ◦ Muscle tone
  • Presence of fasciculations
  • Motion exam
    ◦ Lameness
    ◦ Ataxia
    ◦ Weakness
    ◦ Stiffness
    ◦ Spasticity
    ◦ Exercise intolerance
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3
Q

myopathies diagnostic tests, generally

A
  • Biochemical analysis
    ◦ Creatine Kinase (CK) > acute
    ◦ Aspartate transamine (AST) > slower to rise and fall
    ◦ Lactate dehydrogenase (LDH)
    ◦ Creatinine
    ◦ BUN
    > renal values relevant to pigment nephropathy
  • Urinalysis
  • Vitamin E and selenium
  • Exercise-Response Testing
  • Imaging
    ◦ Thermography
    ◦ Nuclear Scintigraphy > r/o bony lesions
    ◦ Ultrasonography
  • Electromyography
  • Muscle biopsy > common in field
    ◦ Semimembranosus
    ◦ Gluteus medius
    ◦ Epaxial
    ◦ Sacrocaudalis dorsalis
  • Genetic testing
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4
Q

Non-exertional Myopathies - infectious casues

A

◦ Viral
◦ Clostridium spp.
◦ Streptococcus equi
◦ Anaplasma phagocytophilum
◦ Sarcocystis fayeri

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5
Q

Non-exertional Myopathies - toxin causes

A

◦ Ionophores
◦ Hypoglycin A

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6
Q

Non-exertional Myopathies - nutritional causes

A

◦ Vitamin E deficiency
◦ Selenium deficiency

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7
Q

Non-exertional Myopathies - traumatic causes

A

◦ Compressive
◦ Postanesthetic
◦ Trauma

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8
Q

Non-exertional Myopathies - genetic causes

A

◦ Glycogen branching enzyme deficiency
◦ Hyperkalemic periodic paralysis
◦ Malignant hyperthermia
◦ Myosin heavy chain myopathy

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9
Q

Non-exertional Myopathies - immune-related causes?

A

Immune mediated

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10
Q

Sporadic Exertional Myopathies - causes

A

◦ Overexertion
◦ Exhaustion
◦ Dietary Imbalance

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11
Q

Chronic Exertional Myopathies - causes

A

◦ Polysaccharide storage myopathy type 1
◦ Polysaccharide storage myopathy type 2
◦ Myofibrillar myopathy
◦ Recurrent exertional rhabdomyolysis
◦ Idiopathic exertional rhabdomyolysis

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12
Q

Hypoglycin A myopathy
- what is it? etiology?
- signs
- dx
- prognosis

A
  • Highly fatal lipid storage myopathy
  • Ingestion of seeds from Acer sp. trees (boxelder maple)
    <><>
    Clinical signs
    ◦ Weakness/ stiffness
    ◦ Sweating
    ◦ Fasciculations
    ◦ Tachycardia/ tachypnea
    ◦ Myoglobinuria
    <><>
    Diagnosis – measurement of serum acylcarnitines and urine organic acids
    <><>
    Prognosis - <75% of horses survive
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13
Q

Vitamin E and Selenium deficiency - myopathy
- what is it?
- forms, signs, prognosis?

A

Nutritional myodegeneration
<><><><>
* Cardiac form
◦ Weakness, respiratory distress, tachycardia, arrythmias
◦ Poor prognosis, residual myocardial damage if survive
<><>
* Skeletal form > far more common
◦ Slower onset
◦ Weakness, stiffness, trembling, and recumbency
◦ Painful, firm muscles on palpation
◦ Dysphagia > may be the only sign: foals with weak swallowing muscles
◦ Favorable prognosis with Vitamin E/Se supplementation

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14
Q

Glycogen Branching Enzyme Deficiency
- etiology of myopathy
- signs
- bloodwork
- dx?

A

Fatal autosomal recessive mutation in GBE1 gene
> way less GBE protein (enzyme) in these foals
> foals cant form branched glycogen
<><>
Clinical signs
◦ Hypothermia
◦ Weakness & intermittent collapse
◦ Flexural deformities
◦ Ventilatory failure & cardiac arrhythmias
<><>
Bloodwork
◦ Recurrent hypoglycemia
◦ Increased CK, AST and GGT
<><>
Genetic testing
> these foals cannot go far - euthanize

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15
Q

Malignant Hyperthermia
- etiology of myopathy
- triggers
- clinical signs
- dx
- tx

A

Autosomal dominant mutation in RYR1 gene
<><>
Triggers
◦ Halogenated anesthetics
◦ Depolarizing muscle relaxants
◦ Stress
<><>
Clinical signs
◦ Hyperthermia (> 43 C)
◦ Tachycardia
◦ Muscle rigidity and rhabdomyolysis
<><>
Genetic testing
<><>
Treatment and prevention
◦ Dantrolene

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16
Q

Hyperkalemic periodic paralysis
- myopathy etiology
- clinical signs
- dx
- tx

A

Autosomal dominant mutation > incomplete penetrance, will have different degrees of clinical signs
◦ Voltage-dependent skeletal muscle Na channel
<><>
Clinical signs
◦ Sporadic attacks of muscle tremors (“worms crawling under skin”), weakness, and collapse
◦ 3rd eyelid protrusion
<><>
Serum hyperkalemia
<><>
Diagnosis
◦ Genetic testing
<><>
Treatment
◦ Oral &/or IV dextrose > insulin will drive K into cells
◦ IV calcium
◦ Acetazolamide

17
Q

Myosin Heavy Chain Myopathy
- old name?
- who gets it?
- etiology, progression
- signs

A

Previously: Immune-mediated myositis
<><>
Quarter horses and related breeds
<><>
Autosomal co-dominant MYH1 mutation
* Rapid onset muscle atrophy > can be triggered by vaccine
◦ 30-40% of muscle mass in days
* Nonexertional rhabdomyolysis
◦ Muscle stiffness
◦ Pain
◦ Inability to rise
* 40% of heterozygous horses no clinical signs
- can have recurrence, especially with two copies of gene

18
Q

Polysaccharide Storage Myopathy type 1
- prevalence
- etiology
- what is it?
- who gets it?
- triggers?

A

Autosomal dominant genetic mutation
◦ GYS1 gene
> can cause episodes of muscle stiffness and pain after exercise, also known as “tying up” or exertional rhabdomyolysis
* Prevalence:
◦ European continental drafts (Belgians & Percherons)
◦ Quarter horses & related breeds
- very common
<><>
Most common trigger of clinical signs
* Less than 20min of exercise at one time
◦ Walk and trot
◦ Several days of rest prior

19
Q

Polysaccharide Storage Myopathy type 1
- Acute clinical signs
- dx

A
  • Acute clinical signs
    ◦ Muscle fasciculations
    ◦ Muscle stiffness
    ◦ Tucked up, camped out stance
    ◦ Sweating
    ◦ Reluctance to move forward
  • CK > 35,000 U/L
  • Myoglobinuria
20
Q

Polysaccharide Storage Myopathy type 1
- Chronic clinical signs: light horses
- biochem?

A

◦ Lack of energy
◦ Reluctance to move forward
◦ Frequently stopping and stretching out
◦ Poor performance
◦ Repeated episodes of exertional rhabdomyolysis
◦ Chronic back pain
<><>
Persistent elevation in CK and AST

21
Q

Polysaccharide Storage Myopathy type 1
- Chronic clinical signs: drafts and draft crosses

A

◦ Many are asymptomatic
◦ Progressive weakness and muscle loss
> Difficulty rising
> Normal CK level
◦ Severe rhabdomyolysis and myoglobinuria
> Recumbency and death

22
Q

Polysaccharide Storage Myopathy Type 1
Diagnosis

A

Gold standard
◦ Genetic testing
<><>
Muscle biopsy
◦ PAS+ & amylase-resistant inclusions
◦ False negatives
> Small samples
> Horses < 1 year of age

23
Q

Polysaccharide Storage Myopathy type 2
- etiology?
- prevalence and who gets it?

A

No known genetic mutation
◦ Prevalence:
◦ Warmbloods (Dutch, Swedish, Selle Francois, Hanoveraian)
◦ Quarter horses and related breeds
◦ Morgans, Thoroughbreds & Standardbreds

24
Q

Polysaccharide Storage Myopathy type 2
Acute and chronic clinical signs, who is affected

A

Acute clinical signs
◦ Most common in QHs, TB, STDB and Arabians
◦ Exertional rhabdomyolysis
<><>
Chronic clinical signs
◦ Poor performance
◦ Gait abnormalities
◦ Sore muscles
◦ Unwillingness to work/ low energy

25
Q

Polysaccharide Storage Myopathy type 2
- diagnosis?

A

No glycogenolytic enzyme defects
<><>
Diagnosed by muscle biopsy
◦ Abnormal glycogen aggregates
◦ Amylase-sensitive
◦ PAS +
◦ Increase in normal beta glycogen particles

26
Q

Management of PSSM type 1 & 2

A
  • Exercise
    ◦ Limit stall rest to <48 hours
    ◦ Pasture turnout
    ◦ Regular daily exercise
  • Genetics
  • Diet > lower sugar, higher fat
27
Q

Exertional Rhabdomyolysis
- prevalence
- clinical signs

A

Most common muscle disease of the horse
◦ Sporadic or recurrent
◦ Associated with other muscle diseases
<><>
Clinical signs
◦ Stiff, stilted gait
◦ Excessive sweating
◦ Tachypnea
◦ Reluctance to move/walk
◦ Painful, firm muscles on palpation
◦ Myoglobinuria
◦ Colic
◦ Recumbency

28
Q

Exertional Rhabdomyolysis
Causes

A
  • Overexertion
  • Exhaustion
  • Dietary imbalances
    ◦ High NSC
    ◦ Electrolyte deficiencies
    ◦ Selenium/ vitamin E deficiency
  • Genetics?
    ◦ Recurrent exertional rhabdomyolysis
29
Q

Exertional Rhabdomyolysis
Diagnosis, treatment

A

Diagnosis
◦ History and exam
◦ Elevated CK and AST
◦ +/- myoglobinuria
<><>
Treatment
◦ Fluid therapy > for pigment nephropathy, and if they are painful they dont drink
◦ Correct electrolytes
◦ Pain management > Use caution with NSAIDs
◦ Rest