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MSCT > MSCT Week 3: Skeletal Muscle Pathology > Flashcards

MSCT Week 3: Skeletal Muscle Pathology Flashcards

1
Q

Satellite Cells

A

Myofiber associated stem cells called satellite cells that can contribute to regeneration following injury

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2
Q

ONE SLOW RED OX

A
  • Type 1
  • Dark meat red legs these are high in oxidative activity, low in glycolytic capacity and red grossly because of high myoglobin and mitochondrial content
  • they contract slowly but are capable of continuous and repeated contraction
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3
Q

Two Fast White Sugar

A
  • Type II
  • White meat
  • low in oxidative activity
  • high in glycolytic capacity
  • fast contracting
  • cannot maintain repeated contraction
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4
Q

Neurogenic Atrophy

Clinical Clues

A

Nerve Damage (often associated with sensory features)

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5
Q

Neurogenic Atrophy

Histopathologic Features

2 Listed

A
  • Fiber Type Grouping
  • Group Atrophy
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6
Q

Neurogenic Atrophy

Etiology

A

Motor Nerve Damage

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7
Q

Disuse/Steroid Atrophy

Clinical Clues

3 Listed

A
  • Bedridden/ICU
  • Corticosteroids
  • Hyperthyroidism
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8
Q

Disuse/Steroid Atrophy

Histopathologic Features

A

Type II myofiber atrophy

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9
Q

Disuse/Steroid Atrophy

Etiology

A

Atrophy of Fast Twitch Fibers

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10
Q

Dystrophin Related Myopathy

Clinical Clues

A

Childhood onset

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11
Q

Dystrophin Related Myopathy

Histopathologic Features

5 Listed

A
  • Myofiber size variability
  • Necrosis
  • Regeneration
  • Endomysial fibrosis
  • Fatty Replacement
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12
Q

Dystrophin Related Myopathy

Etiology

A
  • Hereditary abnormalities of dystrophin or related proteins
  • DMD gene
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13
Q

Inflammatory Myopathy

Clinical Clues

2 listed

A
  • Adult-onset
  • associated rheumatologic features
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14
Q

Inflammatory Myopathy

Histopathologic Features

3 listed

A
  • Inflammation (usually T-cells)
  • Necrosis
  • Regeneration
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15
Q

Inflammatory Myopathy

Etiology

A

Autoimmune

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16
Q

Congenital Myopathy

Clinical Clues

2 Listed

A
  • Onset at birth
  • Floppy Infant
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17
Q

Congenital Myopathy

Histopathological Features

A

Wide variety of specific changes or inclusions etc (nemaline rods, central cores)

18
Q

Congenital Myopathy

Etiology

A

Variable

19
Q

Channelopathies

Clinical Clues

2 listed

A
  • Myotonia
  • intermittent symptoms
20
Q

Channelopathies

Histopathologic Features

A

May be normal

21
Q

Channelopathies

Etiology

A

Muscle Sodium channel protein SCN4A defect

22
Q

Patterns of myopathic conditions

A

often associated with scattered myofiber necrosis and regeneration

23
Q

Patterns of Inflammatory myopathic conditions

A

Are myopathic but are also characterized by inflammatory infiltrates and/or intracellular inclusions

24
Q

Patterns of Fiber type Grouping and Grouped Atrophy, target Fibers conditions

A

Neuropathic changes

25
Q

Patterns of Type II Myofiber Atrophy conditions

A
  • Disuse atrophy due to any cause (prolonged bed rest in the sick, casting of a bone, can cause focal or generalized muscle atrophy, which tends to affect type II fibers more than type I
  • Glucocorticoid exposure, whether exogenous or endogenous (Cushing’s Syndrome) can also cause muscle atrophy
  • Hyperthyroidism can also result in Type II myofiber atrophy
26
Q

Muscular Dystrophies

A

include a variety of diseases associated with the dystrophin-glycoprotein complex

27
Q

dystrophin-glycoprotein complex

A

consists of skeletal muscle membrane-associated proteins involved in the mechanical stabilization and signalling interactions between the cytoskeleton, membrane, and extracellular matrix

28
Q

Histology of DMD and BMD

2 listed

A
  • progressive replacement of muscle tissue by fibrosis and fat is the result of degeneration outpacing repair (fibrosis and fatty replacement)
  • As a result of ongoing repair muscles typically show marked variation in myofiber size and abnormal internally placed nuclei
29
Q

DMD and BMD in cardiac muscles

A

BMD and DMD also affect cardiac muscles

30
Q

BMD and DMD pathogenesis

A
  • loss-of-function mutations in the dystrophin gene located on the short arm of the X chromosome (Xp21)
  • Severity of the disease correlates with the degree of the dystrophin deficiency
31
Q

Clinical features of DMD

A
  • Clumsiness and inability to keep up with peers due to muscle weakness
  • weakness usually begins in the pelvic girdle and moves to the shoulder girdle
  • enlargement of calf muscles (pseudohypertrophy)
  • owing to ongoing muscle degeneration, high serum creatine kinase levels at birth but slowly decrease as muscle mass is lost
32
Q

Clinical Features of BMD

A
  • symptomatic later in childhood or adolescence
  • nearly normal life-span
  • cardiac involvement can be the dominant feature and may result in death even in the absence of muscle weakness
33
Q

Other X linked and Autosomal muscular dystrophies

A
  • Myotonic Dystrophy
  • Limb-girdle Muscular Dystrophy
  • Emery-Dreifuss Muscular Dystrophy
  • Fascioscapulohumeral Dystrophy
34
Q

Congenital myopathies examples

A
  • Central Core Disease
  • Nemaline Myopathy
  • Centronuclear Myopathy
35
Q

Channelopathies, Metabolic Myopathies, Mitochondrial Myopathies

A

due to defects in ion channels characterized by myotonmia, relapsing episodes of hypotonic paralysis assocated with abnormal serum potassium levels or both

36
Q

Muscle Sodium Channel Protein and chromosome

A

SCN4A

Chromosome 7

37
Q

Malignant Hyperthermia

A

a rare syndrome that can result in death from anesthetic agents or succinylcholine during surgery

38
Q

Mitochondrial Myopathies

A

stem from mutations in either the mitochondrial or nuclear genomes, usually manifest in early adulthood with proximal muscle weakness and sometimes severe involvement of the ocular musculature

some show aggregates of abnormal mitochondria (ragged red fibers)

39
Q

Glycogen synthesis abnormalities are detected with

A

PAS and myophosphorylase

40
Q

Lipid abnormalities are detected with

A

Oil Red O

41
Q

Inflammatory myopathies

A
42
Q

Myotonia

A

inability to relax voluntary muscle after vigorous effort.

MSCT (30 decks)

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