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Small Animal Final Year > SA Muscle Disease > Flashcards

SA Muscle Disease Flashcards

1
Q

Idiopathic polymyositis

  1. Which species are affected?
  2. What is the aetiology?
A
  1. Dogs & cats
  2. Immune-mediated
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2
Q

Idiopathic polymyositis

  1. What is the clinical presentation?
  2. What are some diagnostic procedures and results?
A
  1. Variable: exercise intolerance, progressive weakness, stilted gait, dysphagia. Myalgia and pyrexia can occur. Muscle atrophy develops. Breed related myositis is seen (for example in Vizlas and Newfoundlands).
  2. Histopathology: Variable degree of lymphocytic infiltrates within skeletal muscle (lymphocytic myositis). Other informative tests: negative serologic tests for infectious disease; may be positive for anti-nuclear antibodies (ANA) but this is very non-specific. CK may be normal or elevated. EMG can be helpful.
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3
Q

Idiopathic polymyositis

  1. What is the treatment?
  2. What is the prognosis?
A
  1. Immune suppressive treatment initially with corticosteroids. Additional immune suppressive drugs might be needed.
  2. Generally animals respond well, especially if treated in the acute phase of disease. However, if chronic lesions (for example fibrosis) are present, the prognosis is poor. Cats: spontaneous remission has been reported
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4
Q

Infectious myositis

  1. What species are affected?
  2. What is the aetiology?
A
  1. Dogs & rarely cats
  2. Neospora caninum (dogs); toxoplasma gondii (cats,dogs)
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5
Q

Infectious myositis

  1. What is the clinical presentation?
  2. What are some diagnostic procedures and results?
A
  1. Neospora: young pups (3-8 weeks of age) typically show progressive rigid hind limb hyperextension. Toxoplasma: clinical signs in cats relate more to the CNS, respiratory or GI systems.
  2. Serology (to detect a rising antibody titre)

Histopathology: Variable mixed inflammation with associated segmental myofiber necrosis (necrotizing myositis) and intracytoplasmic protozoal cysts; immunochemistry increases sensitivity.

PCR of CSF fluid to detect N. caninum genomic material

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6
Q

Infectious myositis

  1. What is the treatment?
  2. What is the prognosis?
A
  1. Neospora: clindamycin and trimethoprim/sulpha
    Toxoplasma: clindamycin
  2. To be effective, therapy must be instituted promptly. In chronic cases, prognosis is poor.
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7
Q

Masticatory myositis

  1. What species is affected?
  2. What is the aetiology?
A
  1. Dogs, (very rare in cats)
  2. Immune-mediated
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8
Q

Masticatory myositis

  1. What is the clinical presentation?
  2. What is the diagnostic procedures and results?
A
  1. Acute onset bilaterally symmetrical masticatory muscle swelling and pain. Rapid progression to masticatory muscle atrophy. A severe breed associated disease has been identified in young CKCS.
  2. Serologic tests to detect anti-type 2M myosin antibodies (for example ELISA).
    Histopathology: Only masticatory muscles affected. The degree of inflammation is variable. Lesions range from myositis with muscular necrosis to chronic fibrosis with muscular atrophy. Biopsy can help determine the prognosis.
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9
Q

Masticatory myositis

  1. What is the treatment?
  2. What is the prognosis?
A
  1. Immune suppressive treatment with corticosteroids initially.

Additional immune suppressive drugs might be needed.

Nutritional support should be considered if dogs are unable to eat.

  1. Prognosis is good if treatment is given early and continued for long enough. Chronic fibrosis has an adverse effect on outcome in some cases.
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10
Q

Centrolnuclear myopathy

  1. What species are affected?
  2. What is the aetiology?
A
  1. Dog
  2. Inherited (autosomal recessive)
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11
Q

Centrolnuclear myopathy

  1. What is the clinical presentation?
  2. What are the diagnostic procedures and results?
A
  1. Affects young (2-11 mths old) Labradors. Neuromuscular weakness and atrophy within the first 6 months of age. Exercise intolerance and collapse during prolonged exercise or cold. Loss of triceps and patellar reflexes.
  2. Genetic testing (PCR and sequencing to detect the mutation/s).
    CK can be variable

Histopathology: Clusters of fibres showing atrophy or hypertrophy, some with internal nuclei. No inflammation.

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12
Q

Centrolnuclear myopathy

  1. What is the treatment?
  2. What is the prognosis?
A
  1. There is no treatment
  2. Usually the disease does not progress more after 6-12 months and animals can still be kept as pets.
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13
Q

Steroid myopathy

  1. What species are affected?
  2. What is the aetiology?
A
  1. Dog
  2. Iatrogenic steroid treatment or Cushing’s disease (HAC)
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14
Q

Steroid myopathy

  1. What is the clinical presentation?
  2. What are the diagnostic procedures and results?
A
  1. Long term steroid treatment can be associated with profound muscle weakness and atrophy. With excess of endogenous steroids there are usually other clinical signs of Cushing’s (HAC)
  2. Review the history to check if the dogs is on medication (skin disease, other immune mediated disease) or showing signs of Cushing’s (HAC)

Histopathology shows type II muscle fibre atrophy (biopsy not usually indicated)

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15
Q

Steroid myopathy

  1. What is the treatment?
  2. What is the prognosis?
A
  1. Gradually withdraw treatment with corticosteroid treatment if the underlying disease allows. Additional steroid sparing immune suppressive treatment might be needed to manage the underlying disease. If diagnostic tests for HAC are consistent with this diagnosis- start treatment with trilostane.
  2. Usually good with careful management in the medium to longer term.
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16
Q

Hypokalaemic myopathy

  1. What species are affected?
  2. What is the aetiology?
A
  1. Cat
  2. Numerous causes include poor dietary intake, excessive urinary loss, GI losses, aldosterone producing adrenal tumour (Conn’s Syndrome), iatrogenic (iv fluids without potassium supplementation, diuresis with frusemide). Burmese kittens: inherited episodic hypokalaemia.
17
Q

Hypokalaemic myopathy

  1. What is the clinical presentation?
  2. What is the diagnostic procedures and results?
A
  1. Generalized and dramatic muscle weakness with ventroflexion of the neck, stiff stilted gait, exercise intolerance, muscle pain and reluctance to walk
  2. Serum potassium

Review the history and consider imaging adrenal glands if no other evidence of disease

Histopathology would show variable muscular necrosis and regeneration

18
Q

Hypokalaemic myopathy

  1. What is the treatment?
  2. What is the prognosis?
A
  1. Oral potassium or potassium supplemented iv fluids if the patient is vomiting and oral treatment is not appropriate
  2. Generally good if the underlying problem is addressed
19
Q

Ischaemic neuromyopathy

  1. What species are affected?
  2. What is the aetiology?
A
  1. Cats & less commonly dogs
  2. Aortic thromboembolism 2ry to heart disease in cats (common) or other systemic disease in dogs (less common) such as protein losing nephropathy (PLN)
20
Q

Ischaemic neuromyopathy

  1. What is the clinical presentation?
  2. What are the diagnostic procedures and results?
A
  1. Cats: acute onset pain, hind limb paresis, cold HL extremities, loss of peripheral HL pulses

Dogs: can be acute but more likely gradual onset HL weakness, exercise intolerance, HL ataxia

  1. Physical exam reveals absent or significantly reduced femoral pulses

Ultrasound reveals aortic thrombus

21
Q

Ischaemic neuromyopathy

  1. What is the treatment?
  2. What is the prognosis?
A
  1. Treat the underlying disease.

No safe specific treatment available.

  1. Varies depending on underlying disease and extent of ischaemic necrosis. Euthanasia may be needed.
22
Q

Myasthenia Gravis

  1. What species are affected?
  2. What is the aetiology?
A
  1. Dogs & cats (rare)
  2. Congenital absence of functional acetyl choline receptors (rare) or acquired immune mediated disease
23
Q

Myasthenia Gravis

  1. What is the clinical presentation?
  2. What are the diagnostic procedures and results?
A
  1. Congenital:

Generalised MG: episodic weakness affecting all 4 legs which worsens with exercise and improves with rest.

Fulminant MG: Acute and severe generalised muscle weakness

Focal MG: facial weakness, dysphagia, megoesophagus but no generalised muscle weakness

  1. Acetyl choline receptor antibody blood test. False –ve results occur in some focal forms of disease and in animals already treated with corticosteroids

Edrophonium response test (beware- can cause a cholinergic crisis)

Electrodiagnostic testing

Look for underlying trigger factor such as neoplasia

24
Q

Myasthenia Gravis

  1. What is the treatment?
  2. What is the prognosis?
A
  1. Long acting acetylcholinesterase drugs.

Consider immune suppressive treatment if immune mediated.

Spontaneous remission can occur

  1. Variable- significant risk of aspiration pneumonia secondary to regurgitation and dysphagia
25
Q

Extraocular myositis

  1. What species are affected?
  2. What is the aetiology?
A
  1. Dogs
  2. Immune mediated
26
Q

Extraocular myositis

  1. What is the clinical presentation?
  2. What are the diagnostic procedures and results?
A
  1. Acute: bilateral exophthalmos

Chronic: restrictive strabismus

  1. Rule out other more generalised inflammatory myositis

Ultrasound or advanced imaging shows abnormalities in the extraocular muscles

27
Q

Extraocular myositis

  1. What is the treatment?
  2. What is the prognosis?
A
  1. Immune suppressive treatment with corticosteroids
  2. Prognosis is good with early treatment

Small Animal Final Year (317 decks)

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