NEURO CRAP Flashcards

1
Q

Autonomic hyperreflexia: injury above ___

A

usually T6 or above

always T10 or above

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2
Q

Autonomic hyperreflexia: triggered by ___

A

stimulation of hollow organs below injury
childbirth
bowel movement
cutaneous stimulation

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3
Q

Autonomic hyperreflexia: hemodynamics

A
constrict below
bradycardia, HTN
dilate above (but can't communicate with area below)
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4
Q

Autonomic hyperreflexia: s/s

A
HTN
Brady
nasal stuffiness
blurred vision
headache
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5
Q

ALS: begins where?

A

hands

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6
Q

ALS: patho

A

degeneration of motor neurons

does NOT affect occulor muscles

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7
Q

ALS: most common cause death

A

respiratory failure

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8
Q

ALS: succs/nondepolarizers

A

because of up regulation, DO NOT use succs (hyperkalemia)

extra sensitive to nondepolarizers (they are weak to begin with hello)

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9
Q

MG: patho

A

autoimmune
IgG blocks post junctional Ach nicotinic receptors, so same amount of Ach but not enough working receptors
skeletal muscle weakness late in day

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10
Q

MG: what surgery/body part affected?

A

thymus

thymomectomy

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11
Q

MG and preggo:

A

worse in pregnancy

IgG crosses placenta, neonate can be weak after delivery

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12
Q

MG treatment:

A
anti cholinesterase (pyridostigmine)
overdose can cause cholinergic crisis
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13
Q

Eaton Lambert Syndrome: patho

A

IgG destroy PRE synaptic calcium channel (so less Ach release)
often seen side by side with MG

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14
Q

Eaton Lambert Syndrome: musculature

A

affects proximal muscles first

weakness worse in morning

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15
Q

Eaton Lambert Syndrome: succs/NDMR

A

increased sensitivity to succinylcholine

increased sensitivity to NDMR

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16
Q

Eaton Lambert Syndrome: body part associated/comorbidity seen?

A

small cell carcinoma of lung

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17
Q

MG: succs/NMDR

A

because less post junctional receptors, less NDMR needed
so MORE sensitive to roc/NMDR

prolonged duration of succinylcholine, because pyridostigmine impairs pseudocholinesterase
resistant to succinylcholine

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18
Q

GBS other name:

A

acute idiopathic polyneuritis

19
Q

GBS patho

A

myelin in peripheral nerves destroyed
paralysis follows flu-like illness
paralysis moves distal to proximal
lasts 2-4 weeks

20
Q

GBS most common culprits

A

EBV, CMV, campylobacter

21
Q

GBS treatment

A

plasmapheresis, IV IgG

22
Q

GBS succs/NDMR

A
succs no (upregulation)
increased sensitivity to NDMR (already weak hello)

also increased response to ephedrine

23
Q

Familial Periodic Paralysis treatment

A

could be hypo or hyperkalemic

treatment is acetazolamide for both

24
Q

Familial Period Paralysis succs/NDMR:

A

hypokalemic: NDMR ok but short acting (roc) better, succs questionable
hyperkalemic: NDMR ok, no succs

25
Q

Muscular dystrophy patho

A

no dystrophin
x-linked recessive
predisposed hyperkalemia

26
Q

muscular dystrophy MH

A

NOT linked
increased risk MH like syndrome that’s hyperkalemia and rhabdo
triggered by succs

27
Q

seen with muscular dystrophy

A
kyphoscoliosis
resp muscle weakness
deep Q waves
increased aspiration risk
degeneration cardiac muscle
unstable sarcolemma, leaky muscle cell membrane
28
Q

scoliosis surgery needed when:

A

Cobb angle greater than 40-50

29
Q

myotonic dystrophy management (3)

A

avoid succs
avoid hypothermia
avoid anticholinesterase

30
Q

MS patho

A

demyelination CNS

31
Q

MS anesthesia/succs:

A

avoid hyperthermia
avoid spinals**
NO SUCCS

** spinal could exacerbate symptoms: need to know per apex even though clinically not significant

32
Q

Scleroderma patho/SE:

A
fibrosis
HTN
pulmonary HTN
limited mouth opening
CREST syndrome, raynauds
33
Q

there is NO increased risk MH in what 4 muscular disorders?

A

Becker muscular dystrophy
neuroleptic malignant syndrome
myotonia congenita
myotonic dystrophy

34
Q

MH is definitively linked to:

A

King-Deborough syndrome
Central core disease
Multiminicore disease

35
Q

things that exacerbate SLE

A
PISSED CHIMP
Preggo
Infection
Surgery
Stress
Enalapril
D-penicillamine
Captopril
Hydralazine
Isoniazid
Methyldopa
Procainamide
36
Q

RA three airway issues:

A

TMJ- decreased mouth opening
Cricoarytenoid: decreased diameter glottic opening
C-spine: AO sublaxation, limited extension

37
Q

most common airway problem in RA:

A
AO sublaxation
(AO sublaxation is when distance between interior arch of atlas and the odontoid process is greater than 3mm)
38
Q

RA complications:

A
aortic regurgitation
anemia
pleural effusion
restrictive ventilatory defect
morning stiffness
because NSAIDs first line, may bleed
39
Q

Alzheimers key points/treatment:

A

beta amyloid plaque, dysfunctional synapse (not as much Ach)
apoptosis (programmed cell death)
treatment to restore Ach - give cholinesterase inhibitors

40
Q

Alzheimers and succs:

A

succs prolonged, increased duration of action

41
Q

Parkinsons patho

A

chronic neurodegenerative disorder of the basal ganglia
destruction of dopaminergic neurons
relative increase in Ach
increased GABA activity in thalamus

42
Q

parkinsons diagnosis:

A

pill rolling tremor
skeletal muscle rigidity
postural instability
bradykinesia

43
Q

parkinsons treatment

A

levodopa and carbidopa (need to give together –> potentiation)
anticholinergics

44
Q

Parkinson’s anesthesia key points

A

antidopaminergic drugs bad
risk for autonomic instability, orthostatic hypotension, arrhythmia, aspiration
anticholinergics can be used for exacerbation (Benadryl has these properties)
succs and NDMR fine

ketamine controversial