Block 2 Extra Stuffiez Flashcards Preview

Hailey - Neuro > Block 2 Extra Stuffiez > Flashcards

Flashcards in Block 2 Extra Stuffiez Deck (100):
1

JC polyomavirus

immunocompromised, HIV
white matter lesions
demyelination subcortical region

2

No vertical transmission

Rabies
PCPsc (prion diseases)
H influenza B

3

Selegine

MAOI inhibits metabolism* of 5HT
MOA can sell-a-gill

4

fever, seizure, hx sinusitis next step

brain CT

5

facial nerve NOT involved in _____

smell

IS involved in chewing, taste, salivation, smiling

6

excitotoxicity

glutamate and NMDA

7

cell bodies of 2* STT

contralateral dorsal horn nuclei

8

lateral horn

sympathetic

9

paramedian branch of

basilar artery, to pons

10

STT is outside which horn in SC

anterior lateral horn

11

the decussation of SCP is where

above the potato (pons) in section

12

CN nuclei that are medial in brainstem

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

13

Haem influenza B

Chocolate agar
gram - (pink)
pleomorphic

14

Photophobia with meningitis/encephalitis, think

viral (tendency)

15

acyclovir

prodrug > viral thymidine kinase > acyclovir triphosphate
affects viral DNA polymerase

16

papilledema

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

17

primary measles encephalitis

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

18

acute post-infectious measles encephalitis

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

19

subacute sclerosing panencephalitis

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

20

CN nuclei location

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

21

How many CN emerge/have nuclei in brainstem

10 of 12

22

CN brainstem attachments

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)

23

alar CN nuclei

lateral
sensory/dorsal

24

basal CN nuclei

medial
motor/ventral

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