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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
Guilliane Barre -clinical
-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
26
Guilliane Barre-etiology
-Autoimmune, often following GI ( with C. jejuni) -Miller Fisher variant: ophthalmoplegia, areflexia, ataxia. Anti-GQib antibodies
27
Guilliane Barre-dx
-EMG/NCS: conduction block and decreased conduction velocity (demyelinating process) - LOSS OF REFLEXES -Albuminocytologic dissociation - antibodies
28
Guilliane Barre-tx
-IVIG (faster) then plasmapharesis -Supportive care esp respiratory support if needed
29
Autonomic Dysfunction
-k
30
Autonomic Dysfunction
-k
31
Autonomic Dysfunction
-k
32
Autonomic Dysfunction
-k
33
Spinocerebellar Ataxia
-k
34
Spinocerebellar Ataxia
-k
35
Spinocerebellar Ataxia
-k
36
Spinocerebellar Ataxia
-k
37
Duchenne Muscular Dystrophy -clinical
-Boys -Calf hypertrophy, dilated cardiomyopathy, mild mental retardation
38
Duchenne Muscular Dystrophy -etiology
-AR x-linked -Dystrophin mutation-- molecule that connects muscle to outside ECM
39
Duchenne Muscular Dystroph-dx
-ck may be 100x normal
40
Duchenne Muscular Dystroph-tx
-Avoid exercise; -Weekly steroid injections might keep ambulatory for extra 2-3 years
41
Becker's Muscular Dystrophy
-Similar to DMD, but milder; its can walk into their early adulthood
42
Familial Dysautonomia
-Mostly pronounced autonomic symtoms
43
Multi-system atrophy
-Autonomic symptoms, ataxia, and parkinsonianism
44
-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
Dermatomyositis -presentation
45
-Often r/u -Increased anti-jo -ESR levels
Dermatomyositis- dx
46
-Oral steroids followed by immunosuppresents (azathioprine, methotrexate, IVIG) -ESR, [bx of peri-fasicular atrophy]
Dermatomyositis-tx
47
-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
Dermatomyositis- etiology
48
-More gradual onset -Adults (\>18) -Dysphagia more common -Progressive, painless symmetrical proximal muscle weakness -Limb girdle distribution, common to have cardio involvement
Polymyositis-clinical
49
-often r/u -Ck level 50x elevated -CRP, ESR etc -[bx]
Polymyositis-dx
50
-oral steroids followed by immunosuppresents (azathioprine, methotrexate, IVIG)
Polymyositis-tx
51
-2nd dec of life, -Increased risk of malignancy (NHL 7 others depending on age, sex) -CD8 cells breakdown myofibrils
Polymyositis-etiology
52
-Affects distal muscles of hands and feet and may be asymmetrical -Occurs over years
Inclusion body myositis (IBM)-clinical
53
-\>50
IBM-etiology
54
-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,
IBM-diagnosis
55
-none, neuro-degenerative disease
IBM-tx
56
-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
Myasthenia Gravis-clinical
57
-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.
Myasthenia Gravis-etiology
58
-Anti-Achr antibodies or anti-MuSK -tensilon, ice tests - EMG-repetitive = decremental response - Single-fiber EMG= most sensitive; shows muscular jitter
Myasthenia Gravis-dx
59
-Anticholinesterase inhibitors (pyridostigmine) and immunosuppression -If thymoma, thymectomy may be warranted
Myasthenia Gravis -tx
60
Paraneoplastic syndrome, usually spares eye muscles, and brief improvement w/ exercise
Lambert Eaton-clinical
61
-antibodies against pre-synaptic CChannels -Usually small cell lung carcinoma
Lambert Eaton-etiology
62
-Incremental response to repeated stimuli
Lambert Eaton-dx
63
-Underlying malignancy
Lambert Eaton-tx
64
-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
ALS-clinical
65
-90% sporadic, 10% genetic -SOD1 mutation (Cu/Zn) on Chr 21. - Gain of toxin function rather than loss of function
ALS-etiology
66
-Strongly associated with LMN/UMN in one limb -Multitude of tests to r/u other causes (EG.NCV, MRI, labs etc)
ALS-dx
67
-No cure -Riluzole
ALS-tx
68
-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
Guilliane Barre -clinical
69
-Autoimmune, often following GI ( with C. jejuni) -Miller Fisher variant: ophthalmoplegia, areflexia, ataxia. Anti-GQib antibodies
Guilliane Barre-etiology
70
-EMG/NCS: conduction block and decreased conduction velocity (demyelinating process) - LOSS OF REFLEXES -Albuminocytologic dissociation - antibodies
Guilliane Barre-dx
71
-IVIG (faster) then plasmapharesis -Supportive care esp respiratory support if needed
Guilliane Barre-tx
72
-k
Autonomic Dysfunction
73
-k
Autonomic Dysfunction
74
-k
Autonomic Dysfunction
75
-k
Autonomic Dysfunction
76
-k
Spinocerebellar Ataxia
77
-k
Spinocerebellar Ataxia
78
-k
Spinocerebellar Ataxia
79
-k
Spinocerebellar Ataxia
80
-Boys -Calf hypertrophy, dilated cardiomyopathy, mild mental retardation
Duchenne Muscular Dystrophy -clinical
81
-AR x-linked -Dystrophin mutation-- molecule that connects muscle to outside ECM
Duchenne Muscular Dystrophy -etiology
82
-ck may be 100x normal
Duchenne Muscular Dystroph-dx
83
-Avoid exercise; -Weekly steroid injections might keep ambulatory for extra 2-3 years
Duchenne Muscular Dystroph-tx
84
-Similar to DMD, but milder; its can walk into their early adulthood
Becker's Muscular Dystrophy
85
-Mostly pronounced autonomic symtoms
Familial Dysautonomia
86
-Autonomic symptoms, ataxia, and parkinsonianism
Multi-system atrophy

Neuro (12 decks)

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