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9 Cards in this Set

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4 histologic features of normal muscle
1. polygonal fibers all about the same size
2. peripherally located nuclei
3. regular internal structure of the fibers
4. little to no connective tissue in between the fibers
Neurogenic muscular atrophy
-Early sign/1st/round
-Interlude
-Late Sign/2nd round
Early
-Initial partial denervation leads to angular atrophic fibers

Interlude
-Collateral reinnervation from remaining axons leads to fiber type alteration and subsequent grouping

Late
-Subsequent denervation leads to grouped type atrophy
Destructive myopathy degeneration/regeneration steps
-24 hours
-48 hours
-72 hours
-4 days
-3 weeks successful regeneration
-3 weeks unsuccesful regeneration
-24 hours: necrotic palor

-48 hours: myoblast and macrophage invasion

-72 hours: myoblast fusion

-4 days: basophilic regenerating fibers

-3 weeks successful regeneration: regenerated fibers with central nuclei

-3 weeks unsuccesful regeneration: atrophic denervated regenerated fiber
Inflammatory myopathy histological characteristics
-Muscle fibers
-Inflammation
-Muscle fiber degeneration(necrosis) and regeneration

-Inflammation can be perivascular, perimysial, or endomysial. Combined with pattern of muscle atrophy this dinstigues IM's from destructive myopathies like DMD.
Polymyositis
-Age at manifestation
-Female:Male ratio
-Muscles affected
-Serum CK
-Muscle biopsy
-Pathogenesis
>18 years
- 2:1
- proximal, symmetrical
- elevated up to 50x
- fiber necrosis and regeneration, perimysial and endomysial infiltrates with active myofiber invasion, CD8+ T cells
-T cell mediated disorder
Dermatomyositis
-Age at manifestation
-Female:Male ratio
-Muscles affected
-Serum CK
-Other sign
-Muscle biopsy
-Pathogenesis
-Any age, but peaks at 5-15 and 45-65
-2:1
-Normal to elevated (50X)
-RASH distinguishes it clinically from polymyositis
-Biopsy shows fiber necrosis and regeneration. Key feature is PERIFASICULAR ATROPHY +/- perivascular and perifascular infiltrate of B and CD4+ T cells
-Antibody mediated B cell vascular disorder-->ischemic injury.
Inclusion body myositis
-Age at manifestation
-Female:Male ratio
-Muscles affected
-Serum CK
-Muscle biopsy
-Pathogenesis
> 50 years

- 1:3 (so older men)

- distal to proximal, asymmetrical; unlike PM or DM

-Muscle fiber necrosis and degeneration. Inclusion bodies (rimmed vacuoles) in myofibers with prominent endomysial inflammation-->the hallmark of IBM

-Inflammatory process seconday to a yet unknown primary process. However, anti inflammatories don't work thus there is a poor outcome.
Duchenne muscular dystrophy
-Age at manifestation
-Female:Male ratio
-Muscles affected
-Serum CK
-Other sign
-Muscle biopsy
-Pathogenesis
- Onset by 2-4; wheelchair by 12, will be dead by 30's
- boys only??
- Proximal progressive weakness; pseudohyperotrophy
- elevated CK
- complications of cardiomyopathy, respiratory insufficiency, and scoliosis
- Biopsy shows total absence of dystrophin, necrotic muscle fibers with infiltrate ONLY IN THE FIBERS (unlike IM's), lots of small regenerating fibers. In late stage DMD, there will be a lot of fibrosis (cause of the pseudohypertrophy) and atrophic fibers.
-Caused by mutations in dystrophin, usually from deletions of one or more exons. 30% of mutations are de-novo with no family history. Essentially a sarcoplasmic membrane dysfunction.