Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

NPLEX II TIA > Neurology > Flashcards

Neurology Flashcards

1
Q

What is CT scan? When is it used?

A

produces XR similar to conventional XR but produces cross sectional images without superimposing tissues on each other - used in trauma situations due to speed and superiority over plain film

used in initial CVA/neuro studies but NOT preferred over MRI

fat is black on a CT scan (vs white on MRI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is SPECT? When is it used?

A

Single position emission CT; function CT scan of the brain

used in dx of dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is unique about a PET scan?

A

reveals the cellular level metabolic changes occuring in an organ/tissue (important bc this is where disease proceses often begin; earlier detection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

imaging of choice for nervous system

A

MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the procedure of choice in CNS diagnosis?

A

Imaging (MRI) except in cases of meningitis > lumbar puncture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Low Ach =

A

decreased memory, delirium, delusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

high ach =

A

aggression, depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

low dopamine =

A

dementia, movement disorders, depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

high dopamine =

A

psychoses, anxiety, confusion, aggression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

low norepi =

A

depression, dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

low GABA =

A

anxiety

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

high GABA =

A

affective decrease, lethargy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

low glycine =

A

anxiety

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

high glycine =

A

affective decrease, lethargy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

low NO =

A

vasospasm, potential hyperactivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

high NO =

A

sedation, vasodilation, visual hallucinations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

low histamine =

A

depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

high histamine =

A

mania

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

“Downers” (neurotransmitters)

A

GABA
glycine
NO
histamine (special instances)
neurosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

“uppers” (neurotransmitters)

A

serotonin
ach
dopamine
NE
histamine
glycine (special instances)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

neuroleptic MOA and classes

A

dopamine blocking
phenothiazine
benzisoxazole (respiradone)
butyrophenon (haloperidol)
dibenzodazepine (clozapine, quetiapine)
thienebenzodiazepine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

adverse effects of neuroleptics/antipsychotics

A

tremors/parkinsonian effects
spasms/movements you cant control
tardive dyskinease
POTS
blurred vision, dry mouth, constipation, urinary retention
sexual dysfunction
drowsiness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is neuroleptic malignant syndrome? how does it present, and what is the tx?

A

too much neuroleptic drug; catatonia, fluctuating BP, dysarthria, and fever

fatal unless antipsychotic immediately discontinued and tx with dopamine agonist such as bromocriptine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

If you are looking at doing AA therapy with somebody, what is an important consideration?

A

make sure their B vitamin/mineral cofactor levels are at proper level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

supplement for concentration/cognitive support

A

phosphatidylcholine - donates choline for ach syntehesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

supplement for sleep-wake regulation

A

phosphatidylserine - donates choline, supports dopamine production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

supplement for serotonin affected syndromes

A

phosphatidylinositol - sensitizes serotonin receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

NT therapy for the tx of depression

A

catecholamine therapy (need uppers)
serotonin therapy (need leveling)
combination?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

NT therapy for the tx of anxiety/sleep/seizure/mania

A

GABA
glycine
NMDA antagonist
NO
histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

supplements for depression

A

SAMe
phenylalanine
tyrosine

(inc dopamine and norepi)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what nutrients are precursors for catacholeamines and should be avoided if someone is on a dopamine reuptake inhibitor?

A

tyrosine
phenylalanine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

reuptake of dopamine is blocked by:

A

cocaine
buproprion
benzatropine
amphetamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

norepi reuptake is blocked by

A

tricyclics
amphetamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

serotonin comes from the breakdown of ____

A

tryptophan >

> serotonin > melatonin

> niacinamide (low niacin might steal tryptophan for its pathway)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

serotonin is degraded by

A

MOA
aldehyde dehydrogenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is key for SSRI lowering/removing?

A

tryptophan and cofactors (B3, iron, B5, B6, B12, folate)

taper drug almost all the way/fully first before adding nutrients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

signs/sx of serotonin syndrome

A

fever
hyperreflexia
BP changes
coma
death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

tricyclic drugs MOA

A

“combinations” catecholamines AND serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

tricylcic discontinuation considerations

A

watch for rebound insomnia, replace NE and 5HT with SLOW tapering

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

drugs for depression and central pain

A

citalopram (SSRI)
escitalopram (SSRI)
duloxetine (SSNRI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

drugs for fibromyalgia

A

mostly antidepressants raising serotonin, NE, DOPA, or all three

one is an atypical anti-seizure med

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

histamine effects in the brain

A

H1 (stimulating)
H2 (stimulating)
H3 (inhibiting)
H4 (inhibiting)

so h1/h2 blockers can produce somnelesence > used for insomnia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

3 Bs of GABA reception

A

booze
barbiturates
benzodiazepines

GABA overdose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

GABA comes from ____

A

glutamine

glutamine > GABA (relaxing)
glutamine > glutamate (stimulating)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

inhibitory activity of the CNS is caused by

A

chloride channel opening (by GABA or glycine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

why is progesterone considered a neurosteroid?

A

binds to GABA receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is the class effect of barbituates/benzos?

A

amnesia (faster hits ur brain = more amnesia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is an anxiety drug with no GABA effect/addictive qualities?

A

buspirone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

there is a need for extreme caution in patients with what dx in glycine supplementation?

A

bipolar; potential NMDA (glutamate) receptor triggering > mania

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

excitatory action NMDA receptors

A
  • glycine (in some cases)
  • glutamate
  • zinc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

how to dx epilepsy

A

can NOT dx with secondary seizure cause (tumors, organic dz, etc)

MRI image of choice, LP may be done in some cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

simple partial seizure

A

limited to single part of body/one aspect of bx
consciousness preserved
focal motor (convulsive jerks) or somatosensory (paresthesia or tingling)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

jacksonian seizure

A

spread to “march” to diff parts of limb to body
sensory sx (light flashes, smells, buzzing, songs)
autonomic sx (flushing, sweating, epigastric sensations)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

complex partial seizure

A

s/s may change during attach (hallucinations > complex motor acts)
change in or loss of consciousness
deja vu, fear, pleasure, anger

can lead to tonic-clonic/complete seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

generalized seizures

A

may evolve from partial seizures
paroxysmal neuronal d/c generalized to both sides of the brain
usually has alteration or LOC
two major kinds - absence (petit mal) and tonic clonic (grand mal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

absence (petit mal) seizures

A

begin 2-12
+ fhx
two types: simple absence (1-2 sec, blank stare, spacing out), complex absence (15-30 sec, head drops, arms jerk, every 10-100 days, hyperventilating can trigger > can lead to grand mal as adults)

57
Q

tonic clonic (grand mal)

A

most extreme, can begin at any age
triggered by fatigue, fever, low Ca, glucose, magnesium
may be preceded by prodrome of mood change, apprehension, loss of appetite

tonic (10-20 sec) body stiff/arch, cyanotic
clonic (series of jerks, loss of sphincter control, bite tongue)
post ichtal - flaccid relaxation, heavy breathing/salivating
> wake up, sleep for several hours, start new convulsion (status epilepticus)

58
Q

what is an important dietary consideration for a pt on lithium?

A

NEVER low sodium diets! lithium interferes with sodium ions in the brain (and rest of body)

59
Q

common long term kidney adverse effects

A

kidney dz
hypothyroidism

60
Q

what nutrient used with ritalin improves ADHD sx control in children?

A

zinc

61
Q

bacterial meningitis etiology, presentation

A

e coli, h flu, meningococcus
HA with photophobia
purpuric rash on trunk, fever
nuchal rigidity (not always in peds/neonates)
obtundation (dec alertness)
toxic appearance

62
Q

most common organisms and tx for meningitis in ages: 0-4 weeks

A

group B strep, e coli, listeria

ampicillin + cefotaxime

63
Q

most common organisms and tx for meningitis in ages: 4-12 weeks

A

strep pneumo, group B strep, e coli, listeria

ampicillin, third generation cephalosporin

64
Q

most common organisms and tx for meningitis in ages: 3 mo-18 years

A

s pneumo, n meningitidis, h flu

third gen cephalosporins

65
Q

most common organisms and tx for meningitis in ages: 15 years-50 years

A

s pneumo, n meningitis

third generation cephalosporin

66
Q

most common organisms and tx for meningitis in ages: >50 years

A

s pneumo, n meningitis, listeria, aerobic gram - bacilli

third generation cephalosporin + ampicillin

67
Q

encephalitis presentation and etiology

A

severe: HA with systemic sx, focal neuro deficit
sub acute: similar to severe viral illness, HA persists as systemic sx wax and wane

EEE (togaviridae) from bird as reservoir (ppl and horses get the disease)

MMR/chicken pox > AI encephalitis

HSV 1+2

68
Q

what sign/sx can differentiate between meningitis and encephalitis?

A

focal neuro deficit present in encephalitis

69
Q

presentation rabies

A

dog or wild carnivore bite
negri bodies in hippocampus and cerebellum
paresthesias around wound, spasms, hydrophobia

70
Q

presentation poliomyelitis

A

non specific gastroenteritis - flaccid paralysis, hyporeflexia, secondary invasion of LMN

post polio syndrome - progressive weakness 25-35 years later, muscle wasting, pain, virus not found

71
Q

what ddx can commonly be mistaken for vertebral back pain?

A

herpez zoster recurrence

72
Q

bells palsy etiology, presentation, tx

A

unilateral facial paralysis of sudden onset
usu viral infxn with swelling CN7 (facial)
pain behind ear may precede paralysis
no sensory loss, except taste

tx: difficult; steroids, PT, eye patching

73
Q

guillian barre synrome presentation

A

follows flu/recent viral infxn

symmetric weakness with paresthesias, beginning in legs and moving upward (most reach max paralysis in 2-3 weeks), half have facial involvement

DTRs lost, sphincter control maintained
inc CSF protein
generally self limited; supportive care

ddx: botulism

74
Q

botulism presentation

A

descending paralysis
dry mouth, diplopia, ptosis, loss of accomodation and pupillary light reflex
GI sx precede > N/V, cramps, diarrhea
NO FEVER

75
Q

how may infant botulism present differently?

A

most often seen at 2-3 months
caused by colonization of gut (honey, soil, spore contaminated foods)
constipation may preceded other sx
may progress to “flobby baby”

stool analysis confirms dx

76
Q

where do brain/CNS tumors tend to occur?

A

in adults - ABOVE tentorium cerebelli
in children - BELOW

77
Q

astrocytoma

A

grade 1-2: benign
grade 3: malignant
grade 4: glioblastoma multiforme - AGGRESSIVE, MALIGNANT

78
Q

what is the most common primary brain tumor in adults?

A

glioblastoma multiforme (grade 4 astrocytoma)

79
Q

peripheral nerve tumors

A

schwannomas: benign
acoustic neuroma: CN 8 (severe vertigo)
neurofibromas: benign if solitary
neurofibromastosis = von recklinghausens, AD & mutations

80
Q

wernicke korsakoff syndrom

A

thiamine (b1) def due to alcoholism
confabulations, no short term memory
typically reverses with IV B1

81
Q

pellegra

A

niacin/b3 def
dementia, dermatitis, diarrhea (death)

82
Q

b12 def

A

macrocytic anemia
degeneration of spinal cord (spasticity, weakness, dementia, loss of proprioception)
NOT cured by folate supplementation, tho the anemia will clear

83
Q

key points of ischemic cerebrovascular dz/stroke

A

new recurrent, nondescript HA often occur before event: new HA in pts > 50 should be investigated

84
Q

signs of increased ICP

A

papilledema (swelling of disk) and brain herniation

85
Q

cerebral edema

A

brain has no lymphatics, BBB controls fluid transport

edema secondary to inc vascular permeability, altered regulation of fluid or transudation

common after injury, radiation, long term HTN

86
Q

hydrocephalus

A

enlarged ventricles
inc CSF produced in choroid plexus
lateral third and fourth ventricles swell

87
Q

what type of necrosis occurs in cerebral infarction/stroke?

A

liquifaction necrosis

88
Q

most common arteries to be affected in stroke

A

middle cerebral arteries

89
Q

intracranial hemorrhage

A

HTN, rupture of aneurysms (charcot bouchard)
confusion, drowsiness, HA, nausea

90
Q

vascular malformations in the brain

A

AVM = congenital, anywhere, chronic HA
berry = congenital, ant middle and post communicating arteries; sudden excruciating HA with rupture

91
Q

hypertensive encephalopathy

A

DP > 120
grade 4 retinal changes
confusion, drowsiness, HA, nausea
may lead to rupture and hemorrhage

92
Q

CNS vascular compromise

A

various neuro deficits
often from vascular compression (tumors, acute disk compression)
occlusion from remote causes (aortic surgery, dissecting aneruysm)

93
Q

time frame that TIA and RIND affect pt

A

TIA: sx/signs of stroke <24 hours
RIND: sx/signs of stroke >24 hr BUT RESOLVE COMPLETELY

94
Q

most common presentation of TIA

A

acute onset, last 2-30 min
no permanent sequelae
90% affect carotid > ipsilateral blindness, CL hemiparesis
neuro exam normal

95
Q

type of stroke with: speech not impaired

A

right cortical stroke

96
Q

type of stroke with: impaired attention

A

corticol stroke

97
Q

type of stroke with: impaired cognition

A

large cortical or bilateral stroke

98
Q

type of stroke with: total hemiplegia

A

sub cortical stroke

99
Q

type of stroke with: lower CN involved

A

sub cortical stroke

100
Q

type of stroke with: cerebellar signs

A

sub cortical stroke

101
Q

what could be a non-typical presenting sx of stroke?

A

seizures
personality change

102
Q

what is unique bx to a cluster headache?

A

restless behavior (evil lil gnome hitting u with hammer..taking break…hitting again - bc they know pain is coming but dont know when so they are extremely agitated)

103
Q

ddx of headache as a sign

A

infectious (encephalitis, meningitis)
brain tumors
eye
sinus
vascular (AVM, aneurism, HTN, giant cell arteritis)

cluster, tension, migraine
trigeminal neuralgia

104
Q

migraine tx

A

goal is vasoconstriction
triptans are specific 5HT effectors
ergot drugs are alpha effectors

105
Q

consideration for triptans

A

highest action in basilar artery
CI in basilar artery migraine (comes from base of skull, radiates upwards) > can cause rupture (inoperable death sentence)

106
Q

important finding in trigeminal neuralgia to differentiate it from more serious causes

A

no sensory loss or motor weakness

107
Q

giant cell/temporal arteritis presentation and tx

A

malaise, proximal muscle pain, jaw claudication, tender scalp arteries, unilateral HA

untreated > blindness in 50% of those who present with HA (from opthlamic branch)

ESR 100+ biopsy of artery

tx: immediate steroids

108
Q

first ddx of someone waking up in the morning with a headache

A

carbon monoxide poisoning

109
Q

DEA control of pain meds

A
  • central muscle relaxants - nonDEA
  • central pain control - DEA and non DEA scheduled
  • peripheral pain control (NSAIDS, steroids) - non DEA scheduled
110
Q

MOA muscle relaxants

A

work on proprioception; drive to have muscle contraction (why overdose can lead to respiratory depression)

111
Q

all opiates share what SE?

A

PSLYTIC activity
constipation, N/V, rebound insomnia
itching
overdose = death from respiratory distress

112
Q

MOA opiates

A

central (kappa / mu)
disassociation from pain

113
Q

naloxone vs naltrexone

A

naloxone (IV) = EMS opiod overdose tx
naltrexone = same but also used orally low dose in CA and AI

114
Q

adult dose threshold acetominophen

A

4 g / 24 hours
#1 overdose/toxicity in the world

toxicity = hepatotoxic necrosis (etoh inc hepatotoxicity at 3 drinks/day)
no dialysis/way to get out of system. NAC assists in excretion.

115
Q

acetominophen MOA

A

hypothalmic pain threshold

116
Q

peripheral pain control

A

shut down cytokines
NSAIDS, steroids, gout meds

117
Q

main SE aspirin

A

salycism (severe vertigo); tinnitus, hearing loss

118
Q

whats a risk in IV NSAIDS that is more of a long term risk in oral?

A

kidney damage

119
Q

dose calculations b/w prednisone and cortisone

A

prednisone:cortisone = 4:1
(5 mg prenisone = 20 mg prednisone)

120
Q

physiologic cortisone dose

A

25-40 mg orally

121
Q

MS etiology, presentation, workup

A

chronic remitting dz with demyelination of patches in the brain and spinal cord > multiple neuro sx

glove and stocking paresthesias
onset between 20 and 40
weakness, numbness, tingling, unsteadiness, spasticity, diplopia, sphincter disturbance, chronic recurrent optic neuritis

MRI to show plaques (paraventricular white matter lesions)

122
Q

dx in muscular dystrophy

A

muscle biopsy

123
Q

cerebral palsy

A

motor manifestations of nonprogressive brain damage sustained during prenatal/postnatal life (low birth weight, anoxia at birth)

spastic; quadraplegic, hemiplegic, diplegic

124
Q

ALS

A

progressive degeneration of corticospinal tracts and/or anterior horn cells and/or bulbar motor nuclei

both upper AND lower neuron dysfunction

mid and later life; progressive; most die in 3-6 years

125
Q

myasthenia gravis

A

AI disorder caused by ab to ACh receptor of skeletal muscle

women in 20s, men in 40s-50s
weakness (starts in face, head, neck)
weakness on exertion that is progressive!
no sensory loss

126
Q

what is the most common movement disorder?

A

benign essential tumor
fhx
inc with skilled movements (esp with hands) and with tension/stress
absent at rest
tremor of head and voice

127
Q

parkinsons

A

dec dopamine; slowly progressive degenerative dz of CNS
- slow movement (bradykinesia)
- muscular rigidity (affects the face; mask like features), diff initiating movements
- resting tremor/pill rolling tremor (dis with sleep, worse w excitement/fatigue)
- postural instability (shuffling gait, no arm swing)

128
Q

huntingtons

A

dec GABA; manifests in 3rd/4th decade
starts as fidgeting or restlessness > writhing, purposeless movements > dementia > death in 15-20 years

129
Q

alzheimers

A

diffuse cotical atrophy, neurofibrillary tangles
senile plaques in cortex (abnormal tau protein in nerve processes, microglia, and astrocytes)
progressive impairment of higher intellectual function

MUST rule out other causes of dementia; blood sugar, sleep deprivation, etc…

130
Q

dx criteria alzheimers

A

clinical exam and MMSE (deficits in 2+ areas)
SPECT scanning
progressive worsening
no disturbance of consciousness
absence of systemic or other brain dz to acct for sx

131
Q

use of MMSE

A

dx / follow mental deficit disorders (such as alzheimers)

graded by education level

132
Q

what NT is central for memory

A

Ach
for more Ach/chole sparing agents
-inhibit ach esterase (keep it from breaking down, stay in neural synapse)

133
Q

supplement for memory

A

phosphatidylcholine

134
Q

first step in workup for syncope

A

EKG; esp to rule out silent heart block

135
Q

very common cause of syncope

A

too much HTN meds/meds with alcohol

136
Q

NT MOA cannabis

A

dopamine is released: more neuro activity
anti-inhibition of GABA neurons: more relaxed

137
Q

cocaine MOA

A

blocks reuptake of
dopamine (euphoria)
serotonin (confidence)
norepi (energy)

138
Q

ecstasy MOA

A

potentiates norepi and dopamine
STRONG affinity for serotonin transporters (more serotonin = more break from reality)

139
Q
A

NPLEX II TIA (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions