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Hailey - Neuro > Block 2 Extra Stuffiez > Flashcards

Block 2 Extra Stuffiez Flashcards

1
Q

JC polyomavirus

A

immunocompromised, HIV
white matter lesions
demyelination subcortical region

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2
Q

No vertical transmission

A

Rabies
PCPsc (prion diseases)
H influenza B

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3
Q

Selegine

A

MAOI inhibits metabolism* of 5HT

MOA can sell-a-gill

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4
Q

fever, seizure, hx sinusitis next step

A

brain CT

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5
Q

facial nerve NOT involved in _____

A

smell

IS involved in chewing, taste, salivation, smiling

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6
Q

excitotoxicity

A

glutamate and NMDA

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7
Q

cell bodies of 2* STT

A

contralateral dorsal horn nuclei

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8
Q

lateral horn

A

sympathetic

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9
Q

paramedian branch of

A

basilar artery, to pons

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10
Q

STT is outside which horn in SC

A

anterior lateral horn

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11
Q

the decussation of SCP is where

A

above the potato (pons) in section

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12
Q

CN nuclei that are medial in brainstem

A

III, IV, VI, XII (factors of 12 minus 1 and 2)

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13
Q

Haem influenza B

A

Chocolate agar
gram - (pink)
pleomorphic

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14
Q

Photophobia with meningitis/encephalitis, think

A

viral (tendency)

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15
Q

acyclovir

A

prodrug > viral thymidine kinase > acyclovir triphosphate

affects viral DNA polymerase

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16
Q

papilledema

A

enlarged optic disk
sign of increased ICP
increased risk of herniation
don’t do LP

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17
Q

primary measles encephalitis

A

ACTIVE measles infection

Sx: fever, HA, altered mental status, SEIZURES, ATAXIA, weakness, MORBILLIFORM RASH, inc ICP

CSF: marked LMN, mild inc protein, normal glucose
EEG: diffuse slowing
MRI: focal hyperintensities, brain edema

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18
Q

acute post-infectious measles encephalitis

A

RECENT measles inf

Sx: WEAKNESS, SENSORY LOSS

CSF: elevated MBP (myelin basic protein) in CSF, mild LMNs, mild inc protein, normal glucose
EEG: normal
MRI: hyperintensities esp in white matter, DEMYELINATION

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19
Q

subacute sclerosing panencephalitis

A

measles inf in first 2 years of life, ONSET 3-20 YEARS AFTER MEASLES INF

Sx: BEHAVIOR PROBS, progressive DEMENTIA, myoclonus, demyelination, neuronal loss, cellular inclusion bodies

Serum: defective measles virus present, MARKED INC MEASLES SP AB
CSF: MARKED INC MEASLES SP AB, otherwise normal
EEG: period complexes, burst suppression, slow waves
MRI: focal leukodystrophy, diffuse cortical atrophy

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20
Q

CN nuclei location

A

Medial midbrain: III, IV, (III) Edinger-Westphal
Lateral midbrain: mesencephalic of V
Medial pons: VI
Lateral pons: chief sensory of V, spinal nucleus of V, VII, VIII
Medial medulla: XII
Lateral medulla: IX, X

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21
Q

How many CN emerge/have nuclei in brainstem

A

10 of 12

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22
Q

CN brainstem attachments

A

221-3211
Future Male Partner (PMJx) Man Crush Monday
forebrain (I, II) midbrain (III, IV) pons (V)
PMJx = pontomedullary junction (VI, VII, VIII)
medulla (IX, X) cervical cord (XI) medulla (XII)

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23
Q

alar CN nuclei

A

lateral

sensory/dorsal

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24
Q

basal CN nuclei

A

medial

motor/ventral

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25
Q

somatotopic maps in SC and thalamus

A

medial lemniscus: person standing on pyramids
VPL in thalamus: boot in face, person laying down with face near tip of boot
VPM in thalamus: tip of boot to mid boot: taste, oral cavity, face
cortical homunculus: medial (legs) lateral (face)
SMA: orthogonal to cortical homunculus: ventral to dorsal, face to legs

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26
Q

decussation of 2* DC/ML neuron

A

caudal medulla (DCN)

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27
Q

DC/ML fibers

A

large diameter
afferents
touch, vibration, proprioception

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28
Q

decussation of 2* STT neuron

A

anterior white commissure from dorsal horn/lissaur’s tract (where synapse took place)

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29
Q

STT fibers

A

small, afferent
nociceptors, mechanoreceptors, thermoreceptors
pain, temp

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30
Q

cell bodies of motor neurons that innervate skeletal muscle located

A

in CNS (M1)

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31
Q

decussation of 1* efferent UMN

A

motor decussation at caudal medulla

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32
Q

Trigeminal nuclei

A
  1. EFFERENT MOTOR from motor nucleus of trigeminal (muscles of mastication and tensor tympani)
  2. SENSORY mesencephalic (proprioception of jaw, have cell bodies in the nucleus)
  3. SENSORY main/chief sensory trigeminal (normal touch, like DC/ML)
  4. SENSORY spinal (descending) trigeminal (painpathways, like STT)
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33
Q

major input to main (chief) sensory nucleus of V is

A

mechanoreceptors

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34
Q

2* axons project to ______ VPM

A

contralateral

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35
Q

small components projections to ______ VPM

A

ipsilateral

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36
Q

input to “face” region of VPM from

A

contralateral spinal nV

contralateral chief sensory nV

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37
Q

input to “intraoral cavity” area of VPM from

A

bilateral chief sensory nV

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38
Q

mesencephalic trigmenal nucleus cell bodies are where

and what kind of neuron

A

cell bodies in pons and midbrain (not in trigeminal ganglion)
pseudo-unipolar

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39
Q

Facial nerve pathways

A
  1. branchial motor: EFF to IPS muscles face exp and stapedius
  2. visceral motor: PREgang PARAsym to glands
  3. somatic sensory: AFF to IPS outer ear, nasal cav, soft palate
  4. visceral (special) sensory: AFF to IPS taste of ant 2/3 tongue
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40
Q

Branchial motor efferents pathway

A

leave nucleus > up over abducens nucleus (internal genu VII/fascial colliculus) > descend > exit brainstem > inn IPS side of face

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41
Q

Corneal blink reflex pathway

A

touch cornea > sensory afferent to V1 > trigeminal ganglion > descend in spinal trigeminal tract > rostral spinal trigmeinal nV > output to both motor nuclei of VII (BILATERAL) > efferent from motor nuclei VII > orbicularis oculi > BILATERAL BLINK

42
Q

UMN vs LMN VII facial lesion

A

UMN: quadrant
LMN: asymmetry – Bell’s palsy

43
Q

Thujone

A

blocks GABA receptors > solemn, down, drunk

44
Q

clathrins

A

proteins circle vesicle to recycle it, make new vesicle of NT

45
Q

NT classes

A
  1. biogenic amines (aa, nucleotides, monoamines, etc.)

2. neuropeptides (peptides, hormones)

46
Q

Define NT

A
  1. present at nerve terminal
  2. when AP, should be released
  3. receptor for it
  4. abl to be blocked or activated (antagonized, agonized)
47
Q

Distinguishing feature between small molecules and peptide transmitters

A

small: synthesized in presynaptic zone, carried down by dynes, etc.
peptides: synthesized up by neuron cell body, put on RR track of filaments, packaged and carried down later

48
Q

Beware of _____. -Drewes

A

V-ATPase and VGLUT

because they pump the NT against concentration

49
Q

SNAP25, Synaptobrevin, Syntaxin

A

involved in docking, attaching and releasing vesicle contents

50
Q

SNARE proteins and poisons

A

involved in docking of poisons
EX: toxins of clostridium bacteria are actually zinc proteases, are able to hydrolyze SNARE proteins so can’t dock === botox and tetanus toxins ==== tetanus induced seizures/opisthotonos (in brain) and certain paralysis (in spinal cord)

51
Q

opisthotonos

A

classic tetanus reaction: spinal muscles contracted***

art of man bent backwards, head back, also feet contraction

52
Q

metabotrophic receptors

A 
interacts with GTP-binding protein
modulates VG channels
typically increase K or inhibit Ca
typically inhibitory
slow
53
Q

nicotinic receptor is antagonized by

A

curare

54
Q

muscarinic receptor is antagonized by

A

atropine

55
Q

antidote to nerve gas

A

atropine

56
Q

Myasthenia gravis

A

auto-antibodies to nACHR, decreased neurotransmission

57
Q

Excitotoxicity

A

too much glutamate released > binds to NMDA receptor, allows Na and Ca into cell > too much Ca intracell is bad > mito damage, cell swelling and lysis > nuclear damage

excess glutamate > neurons die

(seizures, strokes, head trauma)

58
Q

DA, NE, EPI synthesized from

A

tyrosine

59
Q

5-HT synthesized from

A

tryptophan

60
Q

Endocannabinoids, delta-9-THC, anandamide have same

A

receptor as THC

61
Q

anandamines

A

NT, packaged in vesicles

RETROGRADE: diffuses out

62
Q

NTs of/disease association:

i. motor stimulation
ii. motor inhibition
iii. motor stimulation by inhibition of inhibition
iv. memory
v. psychoses
vi. pain

A

i. glutamate (STIM)
ii. GABA, glycine, NE (INHIB)
iii. DA (DISINHIB)
iv. ACh (INHIB mus, STIM nic)
v. DA D2 receptor, 5-HT2 receptor
vi. opiods (INHIB)

63
Q

lidocaine mech

A

blocks Na+ channels (at AP)

64
Q

L-DOPA mech

A

increase dopamine (synth of NT)

65
Q

reserpine mech

A

depletes NE (storage of NT)

66
Q

MAOIs mech

A

prevent monoamine metabolism (metabolism of NT)

67
Q

methamphetamine mech

A

DA and NE release ( release of NT)

68
Q

cocaine mech

A

prevents dopamine uptake (uptake of NT)

69
Q

anticholinesterase mech

A

prevents ACh degredation (degade NT)

70
Q

__% of brain is inhibitory

A

90%

but glutamate is always excitatory

71
Q

NMDA

A

responds to glutamate, allows Ca into cell
requires membrane to be depolarized for it to be activated
LTP (long term potentiation) memory
ketamine works here

72
Q

cholera toxin

A

overstimulation of GI: diarrhea
G-protein adensoine cyclase > cAMP
increases cAMP

73
Q

prednisone mech

A

transcriptional regulator

74
Q

interferon beta

A

Jak stat pathway/receptor

75
Q

benzodiazepines

A

activated GABA receptors to cause sedation: take away GABA, will get emotions, release of inhibition - Tracte

76
Q

motor and sensory perception pathways are typically _____

A

hierarchical: disruption at any level ablates the system/no redundant mechaisms

77
Q

monoaminergic system tend to be more _____

A

diffuse: NE containing neurons have cell bodies in locus creels projection many other places

78
Q

difference between opiate, opioid, narcotic

A

opiate: drug derived from opium poppy
opioid: all substances (endogenous, exogenous) that bind opioid receptors
narcotic: legal term, illicit drug use

79
Q

opioid receptors:
mu
kappa
delta

A

mu: analgesia, resp depression, decreased GI motility, phys dependence (endorphins, endomorphins)
kappa: analgesia, sedation, decreased GI motility (dynorphins)
delta: modulates mu activity (enkephalins)

80
Q

ascending pain transmission pathway

descending inhibitory pathway

A

ascending: MOR (mu opioid receptor)
1. inhibit VG Ca > reduce release of glutamate and substance P
2. activate VG K > inhibit excitation of POST neuron

descending: (signal to ascending pathway to shut off pain)
1. blocks release of GABA from inhib interneuron, so AP is sent

81
Q

gabapentin

A

directly acts to inhibit VG Ca channels

82
Q

ascending pain transmission pathway sites of action

A

peripheral tissues
spinal cord
thalamus

83
Q

opiiod agonists

A 
receptor binding > effect
MORPHINE
METHADONE
OXYCODONE
HEROIN
84
Q

opioid antagonists

A

receptor binding produces no effect or reverse effects
NALOXONE
NALTREXONE

85
Q

opioid partial agonists

A

less efficacy, lower abuse potential

CODEINE (mu receptor)

86
Q

opioid mixed agonist/antagonists

A

agonist at 1 receptor, antag at other
PENTAZOCINE (ag at K, antag at mu) *may precipitate withdrawal symptoms
BUPRENORPRHINE (partial ag at mu, antag others) *often used with naloxone

87
Q

which opioid less impacted by first pass, so dose x1.5-2 (instead of dose x3-6)

A

METHADONE

88
Q

are opioids lipid soluble

A

yes: cross BBB > “rush”

heroin > morphine (rate of entry to brain)

89
Q

opioid sites of action

therapeutic uses

A

cortex (pain perception, euphoria, sedation)
medulla (respiratory distress, antitussive effects, N/V, thermoregulation)
SC (depressed pain reflex)
eye/CN III (MIOSIS/PINPOINT PUPILS, little tolerance)
CN X (bradycardia, increased GI tone)
GI (constipation, decreased gastric emptying, cramping)
uterus (prolongs labor)
ureter (difficulty urinating)

Therapeutic uses:
analgesia (severe constant pain, cancer)
cough
acute overdose (naloxone)
obstetric labor (crosses placental barrier, slows labor pregression)
diarrhea
anesthesia
90
Q

sudden onset, “thunderclap” headache

A

subarachnoid hemorrhage

91
Q

HA onset with exercise

A

ruptured aneurysm

92
Q

new HA onset after age 50

A

temporal arteritis

intracranial mass

93
Q

HA w fever, stiff neck, photophobia, systemic signs

A

meningitis

encephalitis

94
Q

HA onset hours to weeks after trauma

A

subdural hematoma

95
Q

HA w/ focal neurological signs, symptoms, papilledema

A

tumor
subdural hematoma
epidural hematoma

96
Q

multiple ppl with new, similar onset HA

A

environmental exposure

carbon monoxide

97
Q

triptans

A

5-HT1D receptor agaonist
treats migraines
causes vasoconstriction

98
Q

opioid tolerance

A

rate of tolerance:

fast: analgesia, euphoria, sedation, resp dep, cough, N/V
never: miosis, constipation

99
Q

opioid addiction treatment

A

methadone
buprenorphrine and naloxone (suboxone)
naltrexone

100
Q

tolerance:
dependence:
addiction:
withdrawal:

A

decrease in effect over time w/ repeated delivery
removal of drug > withdrawal syndrome
compulsive use, drug seeking behavior
degree of dependence

Hailey - Neuro (10 decks)

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