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Hailey - Neuro > Block 2 Extra Stuffiez > Flashcards

Block 2 Extra Stuffiez Flashcards

(100 cards)

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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
somatotopic maps in SC and thalamus
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
26
decussation of 2* DC/ML neuron
caudal medulla (DCN)
27
DC/ML fibers
large diameter afferents touch, vibration, proprioception
28
decussation of 2* STT neuron
anterior white commissure from dorsal horn/lissaur's tract (where synapse took place)
29
STT fibers
small, afferent nociceptors, mechanoreceptors, thermoreceptors pain, temp
30
cell bodies of motor neurons that innervate skeletal muscle located
in CNS (M1)
31
decussation of 1* efferent UMN
motor decussation at caudal medulla
32
Trigeminal nuclei
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)
33
major input to main (chief) sensory nucleus of V is
mechanoreceptors
34
2* axons project to ______ VPM
contralateral
35
small components projections to ______ VPM
ipsilateral
36
input to "face" region of VPM from
contralateral spinal nV | contralateral chief sensory nV
37
input to "intraoral cavity" area of VPM from
bilateral chief sensory nV
38
mesencephalic trigmenal nucleus cell bodies are where | and what kind of neuron
cell bodies in pons and midbrain (not in trigeminal ganglion) pseudo-unipolar
39
Facial nerve pathways
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
40
Branchial motor efferents pathway
leave nucleus > up over abducens nucleus (internal genu VII/fascial colliculus) > descend > exit brainstem > inn IPS side of face
41
Corneal blink reflex pathway
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
UMN vs LMN VII facial lesion
UMN: quadrant LMN: asymmetry -- Bell's palsy
43
Thujone
blocks GABA receptors > solemn, down, drunk
44
clathrins
proteins circle vesicle to recycle it, make new vesicle of NT
45
NT classes
1. biogenic amines (aa, nucleotides, monoamines, etc.) | 2. neuropeptides (peptides, hormones)
46
Define NT
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
Distinguishing feature between small molecules and peptide transmitters
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
Beware of _____. -Drewes
V-ATPase and VGLUT | because they pump the NT against concentration
49
SNAP25, Synaptobrevin, Syntaxin
involved in docking, attaching and releasing vesicle contents
50
SNARE proteins and poisons
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
opisthotonos
classic tetanus reaction: spinal muscles contracted*** | art of man bent backwards, head back, also feet contraction
52
metabotrophic receptors
``` interacts with GTP-binding protein modulates VG channels typically increase K or inhibit Ca typically inhibitory slow ```
53
nicotinic receptor is antagonized by
curare
54
muscarinic receptor is antagonized by
atropine
55
antidote to nerve gas
atropine
56
Myasthenia gravis
auto-antibodies to nACHR, decreased neurotransmission
57
Excitotoxicity
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
DA, NE, EPI synthesized from
tyrosine
59
5-HT synthesized from
tryptophan
60
Endocannabinoids, delta-9-THC, anandamide have same
receptor as THC
61
anandamines
NT, packaged in vesicles | RETROGRADE: diffuses out
62
NTs of/disease association: i. motor stimulation ii. motor inhibition iii. motor stimulation by inhibition of inhibition iv. memory v. psychoses vi. pain
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
lidocaine mech
blocks Na+ channels (at AP)
64
L-DOPA mech
increase dopamine (synth of NT)
65
reserpine mech
depletes NE (storage of NT)
66
MAOIs mech
prevent monoamine metabolism (metabolism of NT)
67
methamphetamine mech
DA and NE release ( release of NT)
68
cocaine mech
prevents dopamine uptake (uptake of NT)
69
anticholinesterase mech
prevents ACh degredation (degade NT)
70
__% of brain is inhibitory
90% | but glutamate is always excitatory
71
NMDA
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
cholera toxin
overstimulation of GI: diarrhea G-protein adensoine cyclase > cAMP increases cAMP
73
prednisone mech
transcriptional regulator
74
interferon beta
Jak stat pathway/receptor
75
benzodiazepines
activated GABA receptors to cause sedation: take away GABA, will get emotions, release of inhibition - Tracte
76
motor and sensory perception pathways are typically _____
hierarchical: disruption at any level ablates the system/no redundant mechaisms
77
monoaminergic system tend to be more _____
diffuse: NE containing neurons have cell bodies in locus creels projection many other places
78
difference between opiate, opioid, narcotic
opiate: drug derived from opium poppy opioid: all substances (endogenous, exogenous) that bind opioid receptors narcotic: legal term, illicit drug use
79
opioid receptors: mu kappa delta
mu: analgesia, resp depression*, decreased GI motility*, phys dependence (endorphins, endomorphins) kappa: analgesia, sedation*, decreased GI motility* (dynorphins) delta: modulates mu activity (enkephalins)
80
ascending pain transmission pathway descending inhibitory pathway
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
gabapentin
directly acts to inhibit VG Ca channels
82
ascending pain transmission pathway sites of action
peripheral tissues spinal cord thalamus
83
opiiod agonists
``` receptor binding > effect MORPHINE METHADONE OXYCODONE HEROIN ```
84
opioid antagonists
receptor binding produces no effect or reverse effects NALOXONE NALTREXONE
85
opioid partial agonists
less efficacy, lower abuse potential | CODEINE (mu receptor)
86
opioid mixed agonist/antagonists
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
which opioid less impacted by first pass, so dose x1.5-2 (instead of dose x3-6)
METHADONE
88
are opioids lipid soluble
yes: cross BBB > "rush" | heroin > morphine (rate of entry to brain)
89
opioid sites of action therapeutic uses
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
sudden onset, "thunderclap" headache
subarachnoid hemorrhage
91
HA onset with exercise
ruptured aneurysm
92
new HA onset after age 50
temporal arteritis | intracranial mass
93
HA w fever, stiff neck, photophobia, systemic signs
meningitis | encephalitis
94
HA onset hours to weeks after trauma
subdural hematoma
95
HA w/ focal neurological signs, symptoms, papilledema
tumor subdural hematoma epidural hematoma
96
multiple ppl with new, similar onset HA
environmental exposure | carbon monoxide
97
triptans
5-HT1D receptor agaonist treats migraines causes vasoconstriction
98
opioid tolerance
rate of tolerance: fast: analgesia, euphoria, sedation, resp dep, cough, N/V never: miosis, constipation
99
opioid addiction treatment
methadone buprenorphrine and naloxone (suboxone) naltrexone
100
tolerance: dependence: addiction: withdrawal:
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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