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Neuro > Peripheral Nervous System > Flashcards

Peripheral Nervous System Flashcards

1
Q

Dermatomyositis -presentation

A

-Progressive, painless symmetrical proximal muscle weakness/ myalgias sometimes -Skin factors *Heliotrope rash *Gottron Nodules- on joints *Erythema of the knees, neck, elbows, shoulders (shawl sign) *Scaly hands

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2
Q

Dermatomyositis- dx

A

-Often r/u -Increased anti-jo -ESR levels

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3
Q

Dermatomyositis-tx

A

-Oral steroids followed by immunosuppresents (azathioprine, methotrexate, IVIG) -ESR, [bx of peri-fasicular atrophy]

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4
Q

Dermatomyositis- etiology

A

-Any age, subacute onset (days-weeks) -Anti-Jo antibodies -Increased risk of malignancy (esp ovarian cancer, NHL) -Macrophages and CD4 -May also be associated with temporal arteritis

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5
Q

Polymyositis-clinical

A

-More gradual onset -Adults (>18) -Dysphagia more common -Progressive, painless symmetrical proximal muscle weakness -Limb girdle distribution, common to have cardio involvement

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6
Q

Polymyositis-dx

A

-often r/u -Ck level 50x elevated -CRP, ESR etc -[bx]

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7
Q

Polymyositis-tx

A

-oral steroids followed by immunosuppresents (azathioprine, methotrexate, IVIG)

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8
Q

Polymyositis-etiology

A

-2nd dec of life, -Increased risk of malignancy (NHL 7 others depending on age, sex) -CD8 cells breakdown myofibrils

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9
Q

Inclusion body myositis (IBM)-clinical

A

-Affects distal muscles of hands and feet and may be asymmetrical -Occurs over years

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10
Q

IBM-etiology

A

->50

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11
Q

IBM-diagnosis

A

-CK normal or mildly elevated -[bx-eosinophilic cytoplasmic inclusions, vacuoles rimmed with basophilic granules, and foci that stain positively for congo red consistent with amyloid deposits,

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12
Q

IBM-tx

A

-none, neuro-degenerative disease

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13
Q

Myasthenia Gravis-clinical

A

-ptosis, proximal muscle weakness, fatiguability of the muscles -Esp ocular, bulbar, facial, respiratory, and limb muscle weakness better with rest; nystagmus, diplopia; difficulty holding up head

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14
Q

Myasthenia Gravis-etiology

A

-F:M 3:2 -Peak in women in 2nd and 3rd decade of life, , 2nd peak during 8th decade of life -M during 6th and 7th decade of life.

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15
Q

Myasthenia Gravis-dx

A

-Anti-Achr antibodies or anti-MuSK -tensilon, ice tests - EMG-repetitive = decremental response - Single-fiber EMG= most sensitive; shows muscular jitter

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16
Q

Myasthenia Gravis -tx

A

-Anticholinesterase inhibitors (pyridostigmine) and immunosuppression -If thymoma, thymectomy may be warranted

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17
Q

Lambert Eaton-clinical

A

Paraneoplastic syndrome, usually spares eye muscles, and brief improvement w/ exercise

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18
Q

Lambert Eaton-etiology

A

-antibodies against pre-synaptic CChannels -Usually small cell lung carcinoma

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19
Q

Lambert Eaton-dx

A

-Incremental response to repeated stimuli

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20
Q

Lambert Eaton-tx

A

-Underlying malignancy

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21
Q

ALS-clinical

A

-Skeletal muscle atrophy and weakness, culminating in respiratory insufficiency -Insidious over months with limb onset occurring in 56-75% of patients -common to have dysphagia/ dysarthria -Degeneration of both UMN/LMN - M>F -Age of onset is a prognostic factor , improved survival with limb onset and slow progression ( poorer with bulbar onset and faster rate of progression

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22
Q

ALS-etiology

A

-90% sporadic, 10% genetic -SOD1 mutation (Cu/Zn) on Chr 21. - Gain of toxin function rather than loss of function

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23
Q

ALS-dx

A

-Strongly associated with LMN/UMN in one limb -Multitude of tests to r/u other causes (EG.NCV, MRI, labs etc)

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24
Q

ALS-tx

A

-No cure -Riluzole

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25
Q

Guilliane Barre -clinical

A

-Ascending weakness with minimal sensory loss -Days-weeks -significant back pain due to inflammation of the nerve roots -+/- autonomic dysfunction -Peak 12 days; bad arrythmias

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26
Q

Guilliane Barre-etiology

A

-Autoimmune, often following GI ( with C. jejuni) -Miller Fisher variant: ophthalmoplegia, areflexia, ataxia. Anti-GQib antibodies

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27
Q

Guilliane Barre-dx

A

-EMG/NCS: conduction block and decreased conduction velocity (demyelinating process) - LOSS OF REFLEXES -Albuminocytologic dissociation - antibodies

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28
Q

Guilliane Barre-tx

A

-IVIG (faster) then plasmapharesis -Supportive care esp respiratory support if needed

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29
Q

Autonomic Dysfunction

A

-k

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30
Q

Autonomic Dysfunction

A

-k

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31
Q

Autonomic Dysfunction

A

-k

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32
Q

Autonomic Dysfunction

A

-k

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33
Q

Spinocerebellar Ataxia

A

-k

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34
Q

Spinocerebellar Ataxia

A

-k

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35
Q

Spinocerebellar Ataxia

A

-k

36
Q

Spinocerebellar Ataxia

A

-k

37
Q

Duchenne Muscular Dystrophy -clinical

A

-Boys -Calf hypertrophy, dilated cardiomyopathy, mild mental retardation

38
Q

Duchenne Muscular Dystrophy -etiology

A

-AR x-linked -Dystrophin mutation– molecule that connects muscle to outside ECM

39
Q

Duchenne Muscular Dystroph-dx

A

-ck may be 100x normal

40
Q

Duchenne Muscular Dystroph-tx

A

-Avoid exercise; -Weekly steroid injections might keep ambulatory for extra 2-3 years

41
Q

Becker’s Muscular Dystrophy

A

-Similar to DMD, but milder; its can walk into their early adulthood

42
Q

Familial Dysautonomia

A

-Mostly pronounced autonomic symtoms

43
Q

Multi-system atrophy

A

-Autonomic symptoms, ataxia, and parkinsonianism

44
Q

-Progressive, painless symmetrical proximal muscle weakness/ myalgias sometimes -Skin factors *Heliotrope rash *Gottron Nodules- on joints *Erythema of the knees, neck, elbows, shoulders (shawl sign) *Scaly hands

A

Dermatomyositis -presentation

45
Q

-Often r/u -Increased anti-jo -ESR levels

A

Dermatomyositis- dx

46
Q

-Oral steroids followed by immunosuppresents (azathioprine, methotrexate, IVIG) -ESR, [bx of peri-fasicular atrophy]

A

Dermatomyositis-tx

47
Q

-Any age, subacute onset (days-weeks) -Anti-Jo antibodies -Increased risk of malignancy (esp ovarian cancer, NHL) -Macrophages and CD4 -May also be associated with temporal arteritis

A

Dermatomyositis- etiology

48
Q

-More gradual onset -Adults (>18) -Dysphagia more common -Progressive, painless symmetrical proximal muscle weakness -Limb girdle distribution, common to have cardio involvement

A

Polymyositis-clinical

49
Q

-often r/u -Ck level 50x elevated -CRP, ESR etc -[bx]

A

Polymyositis-dx

50
Q

-oral steroids followed by immunosuppresents (azathioprine, methotrexate, IVIG)

A

Polymyositis-tx

51
Q

-2nd dec of life, -Increased risk of malignancy (NHL 7 others depending on age, sex) -CD8 cells breakdown myofibrils

A

Polymyositis-etiology

52
Q

-Affects distal muscles of hands and feet and may be asymmetrical -Occurs over years

A

Inclusion body myositis (IBM)-clinical

53
Q

->50

A

IBM-etiology

54
Q

-CK normal or mildly elevated -[bx-eosinophilic cytoplasmic inclusions, vacuoles rimmed with basophilic granules, and foci that stain positively for congo red consistent with amyloid deposits,

A

IBM-diagnosis

55
Q

-none, neuro-degenerative disease

A

IBM-tx

56
Q

-ptosis, proximal muscle weakness, fatiguability of the muscles -Esp ocular, bulbar, facial, respiratory, and limb muscle weakness better with rest; nystagmus, diplopia; difficulty holding up head

A

Myasthenia Gravis-clinical

57
Q

-F:M 3:2 -Peak in women in 2nd and 3rd decade of life, , 2nd peak during 8th decade of life -M during 6th and 7th decade of life.

A

Myasthenia Gravis-etiology

58
Q

-Anti-Achr antibodies or anti-MuSK -tensilon, ice tests - EMG-repetitive = decremental response - Single-fiber EMG= most sensitive; shows muscular jitter

A

Myasthenia Gravis-dx

59
Q

-Anticholinesterase inhibitors (pyridostigmine) and immunosuppression -If thymoma, thymectomy may be warranted

A

Myasthenia Gravis -tx

60
Q

Paraneoplastic syndrome, usually spares eye muscles, and brief improvement w/ exercise

A

Lambert Eaton-clinical

61
Q

-antibodies against pre-synaptic CChannels -Usually small cell lung carcinoma

A

Lambert Eaton-etiology

62
Q

-Incremental response to repeated stimuli

A

Lambert Eaton-dx

63
Q

-Underlying malignancy

A

Lambert Eaton-tx

64
Q

-Skeletal muscle atrophy and weakness, culminating in respiratory insufficiency -Insidious over months with limb onset occurring in 56-75% of patients -common to have dysphagia/ dysarthria -Degeneration of both UMN/LMN - M>F -Age of onset is a prognostic factor , improved survival with limb onset and slow progression ( poorer with bulbar onset and faster rate of progression

A

ALS-clinical

65
Q

-90% sporadic, 10% genetic -SOD1 mutation (Cu/Zn) on Chr 21. - Gain of toxin function rather than loss of function

A

ALS-etiology

66
Q

-Strongly associated with LMN/UMN in one limb -Multitude of tests to r/u other causes (EG.NCV, MRI, labs etc)

A

ALS-dx

67
Q

-No cure -Riluzole

A

ALS-tx

68
Q

-Ascending weakness with minimal sensory loss -Days-weeks -significant back pain due to inflammation of the nerve roots -+/- autonomic dysfunction -Peak 12 days; bad arrythmias

A

Guilliane Barre -clinical

69
Q

-Autoimmune, often following GI ( with C. jejuni) -Miller Fisher variant: ophthalmoplegia, areflexia, ataxia. Anti-GQib antibodies

A

Guilliane Barre-etiology

70
Q

-EMG/NCS: conduction block and decreased conduction velocity (demyelinating process) - LOSS OF REFLEXES -Albuminocytologic dissociation - antibodies

A

Guilliane Barre-dx

71
Q

-IVIG (faster) then plasmapharesis -Supportive care esp respiratory support if needed

A

Guilliane Barre-tx

72
Q

-k

A

Autonomic Dysfunction

73
Q

-k

A

Autonomic Dysfunction

74
Q

-k

A

Autonomic Dysfunction

75
Q

-k

A

Autonomic Dysfunction

76
Q

-k

A

Spinocerebellar Ataxia

77
Q

-k

A

Spinocerebellar Ataxia

78
Q

-k

A

Spinocerebellar Ataxia

79
Q

-k

A

Spinocerebellar Ataxia

80
Q

-Boys -Calf hypertrophy, dilated cardiomyopathy, mild mental retardation

A

Duchenne Muscular Dystrophy -clinical

81
Q

-AR x-linked -Dystrophin mutation– molecule that connects muscle to outside ECM

A

Duchenne Muscular Dystrophy -etiology

82
Q

-ck may be 100x normal

A

Duchenne Muscular Dystroph-dx

83
Q

-Avoid exercise; -Weekly steroid injections might keep ambulatory for extra 2-3 years

A

Duchenne Muscular Dystroph-tx

84
Q

-Similar to DMD, but milder; its can walk into their early adulthood

A

Becker’s Muscular Dystrophy

85
Q

-Mostly pronounced autonomic symtoms

A

Familial Dysautonomia

86
Q

-Autonomic symptoms, ataxia, and parkinsonianism

A

Multi-system atrophy

Neuro (12 decks)

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