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WI18 Neuro > Neuro Dz 1 > Flashcards

Neuro Dz 1 Flashcards

1
Q

most freq. cause of acute flaccid paralysis

A

GBS

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2
Q

GBS

A

immune mediated disorder directed against myelin or Schwann cells

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3
Q

variants of GBS

A

AIDP
MFS
AMAN
AMSAN

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4
Q

common antecedent illnesses of GBS

A

campylobacter infection

preceded by URI or GI infection

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5
Q

other potential causes of GBS

A

HIV, Zika, influenza, EBV, CMV etc

vaccinations

PCN, OCs, TNFs

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6
Q

epitropic mimicry

A

found in GBS

following illness, immune system goes into overdrive and begins attacking the myelin sheath and/or Schwann cells on peripheral n.

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7
Q

Pathophys of GBS

A

following epitropic mimicry,

demyelination of the nerve and axon degeneration

unable to pass on nerve impulses

all myelinated nerves are affected + protein movement to CSF = edema

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8
Q

GBS epidemiology

A

Bimodal presentation (50-79 y/o, 15-35 y/o)

Men > Women (pregnant women have increased incidence)

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9
Q

GBS presentation

A

symmetric paresthesias
early loss of DTRs
affecting lower extremities first

ascending weakness (can get to muscles of respiration)

severe pain

sensory changes

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10
Q

what is a significant source of mortality in GBS pts

A

autonomic changes + decreased Lung expansion/respiratory failure

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11
Q

autonomic changes in GBS

A

tachycardia –> bradycardia

paroxysmal HTN/HoTN

Urinary retention, ileum, loss sweating, flushing

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12
Q

cranial nerves affected by GBS

A

facial weakness (VII)

impaired EOMs, dysphagia and dysarthria (VI, III, XII, V, IX, X)

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13
Q

natural progression of GBS

A

rapidly progressive weakness and others peak 14-30 days

plateau phase 2-4 weeks (persistent, non progressive)

recovery time is 7 months

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14
Q

steps in diagnosis of GBS

A
  1. CBC/Chem panel
  2. Imaging
  3. LP
  4. Conduction studies
  5. NIP/FEV (staging)
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15
Q

LP of GBS

A

albuminocytologic findings

high protein levels, normal WBCs

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16
Q

tx of GBS

A

hospitalized +/- intubation, supportive care

plasmapheresis OR IVIG (no steroids)

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17
Q

plasmapheresis

A

HD catheter to filter out and remove Ags attacking the myelin

replace plasma with donor plasma so they don’t attack myelin

6-10 tx

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18
Q

IVIG

A

gives pts donor IVIG to decrease body’s production of bad IG cells

“tames immune system”

caution for renal failure, thrombosis

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19
Q

which tx for unstable GBS pt?

A

`IVIG

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20
Q

CIDP

A

chronic (over 8weeks) demyelination and demyelination of nerves + axon degeneration

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21
Q

CIDP s/s

A

fairly symmetric motor and sensory loss

motor > sensory

large and small muscles affected

diminished DTRs globally

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22
Q

CIDP work up

A

Lab work up
LP
imaging
EMG

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23
Q

CIDP tx

A

glucocorticoids
plasmapheresis
IVIG

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24
Q

distinguishing features of CIPD

A 
Chronic onset 
motor > sensory 
old men 
not as commonly cranial nerves 
Tx with steroids
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25
distinguishing features of GBS
``` acute onset all nerves equally affected bimodal presentation EOM issues steroids don't work ```
26
myasthenia Gravis
autoimmune destruction of nicotinic acetylcholine post synaptic receptors of skeletal muscle abnormality of T cells and thymic function
27
pathophys of MG
1. autoAbs block and destroy Ach Receptors 2. deep folds of motor endplate are flattened = widened gap THEREFORE: normal Ach release but insufficient number of receptors on muscle is triggered so contraction is weak or non existent
28
muscles affected by MG
skeletal muscles ONLY no smooth/cardiac muscles
29
symptoms of MG
most commonly affected areas of small skeletal muscle that are used repeatedly muscle fatigue with REPEATED use due to less contractile force
30
symptoms and staging of MG
at beginning - symptoms occur intermittently eventually = fluctuate in severity, persistent
31
cardinal symptoms of MG
1. ocular 2. bulbar 3. facial weakness (snear/snarl) 4. head drooping 5. limb weakness
32
ocular MG manifestations
ptosis/diplopia are first manifestation pupils are always spared
33
what factors worsen MG symptoms?
end of the day feel more tired sunlight, surgery, immunizations, emotional stress, heat, menstruation, illness
34
alleviating MG symptoms?
rest and relaxation good self care
35
medications that exacerbate MG
1. Abx 2. BB 3. Mg 4. Prednisone 5. Anti-cholinergics 6. Verapamil 7. lithium
36
PE findings of MG
bulbar weakness weakness of facial muscle weakness of limbs
37
which part of exam are unaffected by MG?
DTRs Pupillary reflexes Intact sensation
38
diagnostic tests for MG
1. curtain sign 2. ice pack test 3. tensilon test 4. AcH Ab lab testing 5. MuskAb testing 6. repetitive nerve stimulation/fiber MG
39
disease associated with MG
thymic hyperplasia/thymoma must rule out via contrast CT scan of chest or MRI --> locally invasive and removed surgically associated with other autoimmune dz
40
tensilon test
edrophonium (short acting actylcholinestersase inhibitor) given so that they can move the eye and open eye fully diagnose MG
41
tx of MG
1. Cholinesterase inhibitor 2. Immunosuppressants 3. Surgical
42
cholinesterase inhibitors we use MG
pyridostigmine (mestinon) slow down degradation of ACh
43
mestinon MOA, brand name, dosing
Pyridostigmine individualized dosing blocks acetocholinesterase, so that it allows Ach to remain in the NMJ for longer
44
mestinon | ADR
bradycardia, respiratory suppression, diarrhea, diaphoresis, abdominal cramps/pain
45
immunosuppressants used in MG
high dose prednisone mychophenolate mofetil azitharoprine
46
high dose prednisone MG
begun in hospital bc can exacerbate dz 80% of people are helped while they are on the steroids slowly taper up
47
Mycophenolate mofetil (Myfortic)
alternative to pred, long term EBM data lacking
48
Azathiprine (Imuran)
non glucocorticoid drug of choice interferes with T and B cell production and sustained improvement slowly working, blood dyscrasia, BBW for malignancy risk
49
surgical thymectomy
standard of care 10-55 y/o thymoma removed (transiently post op period) may induce remission in some patients
50
general MG care
avoid drugs that worsen considered immunocompromised pregnancy can worsen (can cross fetus - neonatal)
51
myasthenia crisis
severe exacerbation of MG causes acute respiratory insufficiency due to weakened diaphragmatic and intercostal muscles should be suspected with a cold, recent medication admit to ICU
52
tx of myasthenic crisis
1. plasmapheresis | 2. IV IG
53
essential tremor
MC involuntary movement dz familial tremor that peaks at age 70 autosomal dominant
54
describe the tremor of essential tremor
high frequency, bilateral, symmetric upper extremities and head postural and kinetic (pronator drift)
55
tremor will improve with ___ worsen with ___-
improve with Alcohol worsen with stress, strong emotion, fatigue, hunger, temperature extremes
56
treatment of ET
most cases pharm doesn't work primidone (mysoline) Propanol (inderal)
57
primidone
mysoline metabolized to phenobarbital but more active ADRs common on initiation
58
propanolol
inderal younger pts, MOA for tremor unknown,
59
Pseudotumor Cerebri
aka idiopathic intracranial hypertension NOT benign, intractable, disabling, HA, risk of severe, permanent vision loss
60
S/s of Pseudotumor Cerebri
Elevated ICP (HA, papilledema, seizures, AMS) worsened with bearing down or bend over
61
elevated ICP without (pseudo tumor cerebra)
1. space occupying lesions on imaging | 2. abnormalities of cerebrospinal fluid composition
62
etiology of Pseudotumor Cerebri
obese young women often idiopathic, but may be vascular, otitis media/chronic mastoiditis, endocrine disturbances, medications)
63
symptoms of Pseudotumor Cerebri
HA, visual disturbances, intracranial noise, papilledema, vision loss, sixth cranial nerve palsy
64
work up of Pseudotumor Cerebri
CT of head, LP opening pressure try to eliminate hydrocephalus, mass lesion
65
tx of Pseudotumor Cerebri
dc of associated meds, weight loss for pts, evaluation for other dz, pharm tx, serial LP, surgery
66
pharm tx of Pseudotumor Cerebri
Acetazolamide (Diamox) Furosemide Prednisone
67
surgery options for Pseudotumor Cerebri
VP shunt optic nerve sheath fenestration (vision only, no HA relief)
68
Huntington's chorea
autosomal dominant dz affects lg motor movements onset between 30-50, live 20 yrs abnormal movements, intellectual changes, subtle but progress to severe
69
tx of Huntington's chorea
purely symptomatic progression can't be halted typically Haldol and reserpine to control dyskinesia and behavior
70
Huntington's chorea workup
genetic formation of inclusion bodies in neuron MRI atrophy of caudate nuclei and putamen

WI18 Neuro (16 decks)

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