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Skeletal Muscle Pathology Flashcards

1
Q

Part of muscle that envelopes single muscles

A

Epimysium

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2
Q

Part of muscle that surrounds groups of muscle fibers

A

Perimysium

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3
Q

Part of muscle that surrounds individual muscle fibers

A

Endomysium

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4
Q

Molecule involved in muscle energy metabolism, has two monomers and three types of dimers

A

Creatine kinase

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5
Q

Elevated total CK suggests this type of injury

A

Skeletal muscle

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6
Q

Molecule involved in muscle oxygen use that is released with muscle damage - also elevated with cardiac injury

A

Myoglobin

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7
Q

Molecule involved in muscle glycolysis that is released with muscle damage

A

Aldolase

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8
Q

This molecule released with muscle damage is sometimes elevated when CK is normal

A

Aldolase

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9
Q

Condition of skeletal muscle weakness due to autoantibodies against muscle acetylcholine receptor complex

A

Myasthenia Gravis

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10
Q

Myasthenia Gravis is due to autoantibodies against this

A

Muscle acetylcholine receptor complex
(or anti-MUSK - muscle specific kinase)

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11
Q

Two age peaks of Myasthenia Gravis

A

20’s and 60’s

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12
Q

Skeletal muscle condition associated with thymic tumors (Thymoma, thymic hyperplasia)

A

Myasthenia Gravis

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13
Q

Myasthenia Gravis is associated with tumors of this organ

A

Thymus

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14
Q

Who is more likely to have Myasthenia Gravis, female or male?

A

Female

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15
Q

Condition involving muscle weakness which worsens with repetition/duration

A

Myasthenia Gravis

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16
Q

Condition that commonly affects eye muscles, so patients can have ptosis and diplopia

A

Myasthenia Gravis

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17
Q

Are deep tendon reflexes preserved in Myasthenia Gravis?

A

Yes

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18
Q

ACHesterase inhibitors results in improved symptoms in this condition

A

Myasthenia Gravis

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19
Q

Condition of weakness due to antibodies against calcium channels

A

Lambert-Eaton Myasthenic Syndrome

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20
Q

Lambert-Eaton Myasthenic Syndrome is due to antibodies against this

A

Calcium channels

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21
Q

Condition where muscle strength increases with repetition/duration

A

Lambert-Eaton Myasthenic Syndrome

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22
Q

Half of Lambert-Eaton Myasthenic Syndrome cases are due to paraneoplastic syndrome, and this is the most common

A

Small cell carcinoma of lung

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23
Q

Small cell carcinoma of lung is the most often paraneoplastic syndrome that can cause this condition

A

Lambert-Eaton Myasthenic Syndrome

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24
Q

Are deep tendon reflexes preserved in Lambert-Eaton Myasthenic Syndrome?

A

No, are decreased
May have autonomic effects

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25
Q

Do ACHesterase inhibitors improve symptoms in Lambert-Eaton Myasthenic Syndrome?

A

No

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26
Q

Condition that leads to impaired acetylcholine release, because there is dysfunction in firing of presynaptic calcium channels

A

Lambert-Eaton Myasthenic Syndrome

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27
Q

Clostridium botulinum can block release of this, causing myasthenic syndrome

A

ACH

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28
Q

Does this describe neuropathic or myopathic muscle atrophy:
End result is clustering of atrophy and hypertrophy

A

Neuropathic

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29
Q

Type II fiber atrophy is associated with prolonged use of these

A

Corticosteroids

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30
Q

What is pathognomonic of muscle denervation/reinnervation?

A

Clusters of type I myocytes and clusters of type II myocytes

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31
Q

Does steroid use result in type I or type II atrophy?

A

Type II atrophy
Type I preservation

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32
Q

Acute necrosis of skeletal muscle

A

Rhabdomyolysis

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33
Q

Levels of creatine kinase and aldolase in Rhabdomyolysis

A

Both high due to release of cytosolic proteins

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34
Q

In Rhabdomyolysis, regeneration may occur via these cells

A

Satellite cells (muscle stem cells)
Remember that part of healing response/regeneration is central nuclei

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35
Q

Central nuclei in muscle indicate this process has occurred

A

Regeneration

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36
Q

In Rhabdomyolysis, this molecule may be released into the urine and damage the kidneys, causing acute renal failure

A

Myoglobin

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37
Q

Autoimmune disease with proximal muscle weakness and skin changes

A

Dermatomyositis

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38
Q

Two age groups that may have Dermatomyositis

A

Peds (7 years) and adults (60’s)

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39
Q

Dermatomyositis is an autoimmune disorder mediated by this type of cell

A

B cell
IgG, IgM and complement deposit in microvascular beds

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40
Q

Condition where IgG, IgM and complement deposit in microvascular beds, and results in microangiopathic ischemia in muscle and skin (rash, telangiectasias)

A

Dermatomyositis

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41
Q

Does Dermatomyositis affect proximal or distal muscle first?

A

Proximal

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42
Q

Condition with muscle aches and weakness with gross motor activities affected first (standing from chair, raising arms above head, climbing stairs)

A

Dermatomyositis

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43
Q

Condition with heliotrope rash on upper eyelids

A

Dermatomyositis

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44
Q

Condition with Gottron’s papules on dorsal knuckles

A

Dermatomyositis

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45
Q

Condition with characteristic skin changes including malar erythema, mechanics hands, periungual telangiectasias, and periorbital edema

A

Dermatomyositis

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46
Q

Perivascular perimysial lymphoid infiltrate is pathognomonic of this condition

A

Dermatomyositis

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47
Q

Microvascular immune complexes and perifascicular atrophy are morphologically seen in this condition

A

Dermatomyositis

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48
Q

Level of CK in Dermatomyositis

A

Elevated

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49
Q

Anti-Jo1 antibodies are against this

A

Histidyl tRNA synthetase

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50
Q

Type of antibodies seen in Dermatomyositis that target histidyl tRNA synthetase

A

Anti-Jo1

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51
Q

Anti-Mi2 antibodies target this

A

DNA helicase

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52
Q

Type of antibodies seen in Dermatomyositis that target DNA helicase

A

Anti-Mi2

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53
Q

Type of antibodies that are most common in paraneoplastic Dermatomyositis

A

Anti-p140

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54
Q

Anti-Jo1 and Anti-Mi2 antibodies are seen in this condition

A

Dermatomyositis

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55
Q

Inflammatory myopathy mediated by cytotoxic T cells

A

Polymyositis

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56
Q

Polymyositis is inflammatory myopathy mediated by this type of cell

A

Cytotoxic T cells

57
Q

What is the age of onset of Polymyositis?

58
Q

Are there skin changes in Polymyositis?

59
Q

What part of the muscle is Polymyositis located in?

A

Endomysium

60
Q

Does Polymyositis involve angiopathy?

61
Q

Condition involving muscle fatigue and cramps, proximal weakness initially - especially shoulder girdle

A

Polymyositis

62
Q

Does Polymyositis affect proximal or distal muscles first?

A

Proximal
Especially shoulder girdle

63
Q

Levels of CK and aldolase in Polymyositis

A

Both elevated

64
Q

Anti-Jo1 and Anti-SRP antibodies are seen in this condition

A

Polymyositis

65
Q

Raynauds, interstitial lung disease, and arthralgias are associated with this condition

A

Polymyositis

66
Q

Inflammatory myopathy with cytoplasmic amyloid inclusions

A

Inclusion body myositis

67
Q

Age of patients with Inclusion body myositis

A

Older adults, >50 years

68
Q

Level of CK in Inclusion body myositis

A

Modest elevation

69
Q

Condition associated with anti-CN1a antibodies

A

Inclusion body myositis

70
Q

Inclusion body myositis is associated with this antibodies

71
Q

Condition with amyloid deposition in muscle fibers with CD8+ T cell response

A

Inclusion body myositis

72
Q

Inclusion body myositis involves deposition of this in muscle fibers with CD8+ T cell response

73
Q

Inclusion body myositis involves amyloid deposition in muscle fibers with response of this type of cell

A

CD8 T cells

74
Q

Beta amyloid, Tau protein, and Synuclein can accumulate and deposit in muscle fibers in this condition

A

Inclusion body myositis

75
Q

Condition with cytoplasmic inclusions of amyloid material, rimmed vacuoles, and endomysial T cell infiltrate

A

Inclusion body myositis

76
Q

Condition with morphology of “rimmed vacuoles”

A

Inclusion body myositis

77
Q

Autoimmune disease against skeletal muscle fibers

A

Immune-mediated necrotizing myopathy

78
Q

Condition that produces subacute symmetric proximal weakness

A

Immune-mediated necrotizing myopathy

79
Q

Condition that is associated with other autoimmune disorders and HMG-CoA reductase inhibitors (statins)

A

Immune-mediated necrotizing myopathy

80
Q

Anti-SRP and anti-HMGCR (HMG CoA reductase) autoantibodies are seen in this condition

A

Immune-mediated necrotizing myopathy

81
Q

Level of CK in Immune-mediated necrotizing myopathy

A

Significantly elevated

82
Q

Condition with myocyte necrosis and regeneration, with minimal inflammatory infiltrate (macrophages present but not pathogenic)

A

Immune-mediated necrotizing myopathy

83
Q

Two types of drugs that can cause Toxin mediated myopathy

A

Statins and Hydroxychloroquine

84
Q

Drugs that cause proximal muscle weakness and type II fiber atrophy

85
Q

Binge drinking may result in this condition as well as myoglobinuria and acute renal failure

A

Rhabdomyolysis

86
Q

Toxin mediated myopathy involving proximal muscle weakness with atrophy, myalgias, CK usually normal

A

Thyrotoxic myopathy

87
Q

Level of CK in Thyrotoxic myopathy

A

Normal usually

88
Q

Toxin mediated myopathy that can cause increased metabolic rate, weight loss, moist skin, diarrhea, palpitations, increased DTRs

A

Thyrotoxic myopathy

89
Q

Toxin mediated myopathy involving proximal muscle weakness and CK elevation

A

Hypothyroid myopathy

90
Q

Level of CK in hypothryoid myopathy

91
Q

Toxin mediated myopathy that can cause decreased metabolic rate, weight gain, dry skin, dry brittle hair, constipation, cold interolance, malaise, fatigue, decreased DTRs

A

Hypothryoid myopathy

92
Q

Effect of Thyrotoxic myopathy on deep tendon reflexes

93
Q

Effect of Hypothyroid myopathy on deep tendon reflexes

94
Q

Progressive muscle weakness due to nucleotide repeat disorder

A

Myotonic dystrophy

95
Q

Inheritance pattern of Myotonic dystrophy

A

Autosomal dominant

96
Q

Two main genes associated with Myotonic dystrophy

A

CTG repeats in DMPK gene
CCTG repeats in ZNF9 gene

97
Q

Myotonic dystrophy may be caused by CTG repeats in this gene

A

DMPK (Myotonic dystrophy protein kinase)

98
Q

Myotonic dystrophy may be caused by CCTG repeats in this gene

A

ZNF9 gene (Zn finger protein)

99
Q

Condition characterized by slow relaxation of muscles after contraction and muscle degeneration

A

Myotonic dystrophy

100
Q

Level of CK in Myotonic dystrophy

A

Not elevated (or minimal)

101
Q

What age does Myotonic dystrophy present?

A

Any age, most patients normal at birth

102
Q

Does Myotonic dystrophy show genetic anticipation?

A

Yes, is due to nucleotide repeat disorder

103
Q

Does Myotonic dystrophy favor proximal or distal musculature?

A

Distal: forearms, hands, facial

104
Q

Inherited form of muscle degeneration with fatty replacement

A

Muscular dystrophy

105
Q

What is the inheritance pattern of Muscular dystrophy?

A

X linked recessive

106
Q

Muscular dystrophy involves this gene

A

Dystrophin (anchoring protein to cytoplasmic structures to sarcolemma)

107
Q

Dystrophin is an anchoring protein to cytoplasmic structures to sarcolemma, and is associated with this condition

A

Muscular dystrophy

108
Q

Condition involving membrane destabilization and muscle fiber atrophy

A

Muscular dystrophy

109
Q

Form of Muscular dystrophy involving an absence of dystrophin due to gene deletion

A

Duchenne MD

110
Q

Form of Muscular dystrophy involving truncation of dystrophin

111
Q

Condition with an abnormal sarcolemma-basal lamina interaction

A

Muscular dystrophy

112
Q

Condition where dead muscle is replaced with fibroadipose tissue

A

Muscular dystrophy

113
Q

In Duchenne Muscular dystrophy, what is the level of CK in the mother?

A

May be elevated

114
Q

In Duchenne Muscular dystrophy, how does the child present at birth?

A

Normal - achieves early gross motor skills normally (sitting, rolling, standing)

115
Q

Condition characterized by lordotic posture to stand, waddling gait, and Gower’s sign (using arms to stand)

A

Duchenne Muscular dystrophy

116
Q

Level of CK in Duchenne Muscular dystrophy

117
Q

Condition of progressive muscular weakness that also effects cardiac and respiratory muscles
Death from respiratory compromise; pneumonia

A

Duchenne Muscular dystrophy

118
Q

Life span of Duchenne Muscular dystrophy

A

25-30 years

119
Q

Condition where muscle fibers degenerate, leading to increased fiber diameter variation, increased internal nuclei, and atrophy and death of fibers

A

Duchenne Muscular dystrophy

120
Q

Condition with eventual replacement of dead muscle fibers with fat and fibrous tissue
Formerly enlarged muscles show “pseudohypertrophy” as they are fatty infiltrated

A

Duchenne Muscular dystrophy

121
Q

Life span of Becker Muscular dystrophy

A

Death may be 40’s or normal life span

122
Q

Group of lower motor neuron diseases with muscle atrophy

A

Spinal muscular atrophy

123
Q

Inheritance pattern of Spinal muscular atrophy

A

Autosomal recessive

124
Q

Spinal muscular atrophy involves a mutation in this gene

A

Survival motor neuron gene (SMN1)

125
Q

Mutation of Survival motor neuron gene (SMN1) is associated with this condition

A

Spinal muscular atrophy

126
Q

This condition is the most common cause of infant mortality

A

Spinal muscular atrophy

127
Q

Is SMA type 1 or 4 the least severe form of Spinal muscular atrophy?

A

Type 4 is least severe (1>2>3>4)

128
Q

Allelic form of Spinal muscular atrophy that is the most common and most severe type

A

Werdnig-Hoffman disease (SMA1)

129
Q

Werdnig-Hoffman disease is a form of this condition

A

Spinal muscular atrophy
(specifically involves SMA1)

130
Q

In Spinal muscular atrophy, SMN1 mutation causes death of these cells

A

Anterior horn cells

131
Q

Does Spinal muscular atrophy affect cranial nerves?

A

No, cranial nerves are spared

132
Q

Flaccid paralysis, fascicultations, hyporeflexia and atrophy are clinical patterns of disease of this

A

Lower motor neurons

133
Q

Morphology of this condition shows groups of atrophic muscle fibers, groups of normal or hypertrophic muscle fibers, and spinal cord shows loss of anterior horn neurons

A

Spinal muscular atrophy

134
Q

What age does a patient with Werdnig-Hoffman disease (SMA1) present?

A

Begins soon after birth
Never learn to roll or sit

135
Q

Spinal muscular atrophy form that begins soon after birth, never learn to roll or sit, and death by age 2 from respiratory compromise

A

Werdnig-Hoffman disease (SMA1)

136
Q

Spinal muscular atrophy form with onset in infancy, patients do learn to sit

137
Q

Spinal muscular atrophy form with childhood onset, patients learn to walk

138
Q

Spinal muscular atrophy form with adulthood onset and normal milestones

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