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Neuro II > HA and migraines pharm > Flashcards

HA and migraines pharm Flashcards

1
Q

acute migraine drugs

A 
serotonin agonists
ergot alkaloids
analgesics
combo analgesics
NSAIDs
antiemetics
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2
Q

migraine prophylatics

A

beta blockers
CaCh blockers
antidepressents
anticonvulsants

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3
Q

primary HA disorders

A

migraine
tension
cluster

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4
Q

secondary HA disorders

A

d/t other underlying cause
infection
brain mass or swelling etc

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5
Q

classic migraine

A

30%
aura of variable duration which may involve nausea, vomiting, visual scotomas or hemianopsia, speech abnormalities
followed by sever throbbing, u/l HA lasts for hours to days

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6
Q

common migraine

A

70%

lacks aura

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7
Q

pathophys of migaines

A

trigeminal n and maybe extracranial aa involed

nn release CGRP which is an extremely powerful vasodilatation -> inflammation and edema

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8
Q

food triggers for migraine

A 
alcohol
caffeine/caffeine withdrawl
chocolate
MSG
aspartame
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9
Q

environmental triggers of migraine

A 
flickering lights
high altitude
strong smells/fumes
tabacco smoke
weather
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10
Q

Behavioral triggers of migraine

A 
excess/insufficient sleep
fatigue
menstruation
skipped meals
strenuous activity
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11
Q

tension type HA (TTH)

A

most common type of primary HA disorder
least studied, pathophys not understood
simple analgesics and NSAIDs
amitripyline prophylaxisis

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12
Q

cluster HA

A

rare, but most severe primary HA
pain excruciating, associated with cranial autonomic symptoms
best Tx is prevention

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13
Q

serotonin agonists

A

sumatriptan

-triptan

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14
Q

ergot alkaloids

A

dihyroergotamine (DHE)

ergotamine (+/- caffeine)

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15
Q

combo analgesics

A

excedrin migraine: aspirin, acetaminophen, caffeine

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16
Q

antimemtics

A

metoclopramide

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17
Q

CaCh blockers

A

verapamil

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18
Q

antidepressents

A

antitriptyline

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19
Q

anticonvolssants

A

topiramate

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20
Q

synthesis of serotonin

A

from L-tryptophan
stored in vesicles
over 90% in in enterochromaffin cells in GI tract
in blood in platelets

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21
Q

metabolism of serotonin

A

MAO oxidizes and inactivates it

further metabolized to 5-HIAA which can be collected in 24-hr urine to evaluate serotonin synthesis

22
Q

CNS actions of serotonin

A 
mood
sleep
appetite
temp
pain
BP
vomiting
depression, anxiety, migraine
23
Q

CV effects of serotonin

A

contraction of vascular smooth mm, except skeletal mm and heart where is vasodilates
promotes platelet aggregation

24
Q

skeletal mm effect of serotonin

A

contraction

25
Q

triptans MOA

A

activates serotoninRs on presynaptic trigeminal nn -> inhibitis release of vasodialting peptides
stimulates vasoconstriction

26
Q

triptan disadvantages

A

short half life so often must be dosed multiple times w/in course of HA

27
Q

triptan use

A

first line acute mild-severe migraines in most people

28
Q

ADRs of triptans

A 
most are mild
altered sensations
dizziness
mm weakness
fatigue
drowsiness
nausea
sweating
neck pain
if IV- injection site rxn
1-5% chest discomfort
29
Q

CIs of triptans

A 
CAD
angiina
ischemic heart disease
uncontrolled DM 
DO NOT use w/in 24hrs of ergotamine 
MOA inhibitors
30
Q

ergot alkaloids MOA

A

constiction of peripheral and cranial blood vessels
may also have presynaptic trigeminal nn ending effects
inhibit release of vasodilating peptides
agonists at serontonin Rs

31
Q

ergot PK

A

absorption and rate of action improved when in combo w/caffeine

32
Q

uses of PK

A

migraine
triptans preferred
usually preserved for prolonged attacks

33
Q

ADRs of ergots

A

GI
prolonged vasospasm- gangrene, amputation, bowel infarction
weakness, fatigue, paresthesias, drowsiness

34
Q

butalbital

A

can be mixed with NSAIDs
increases GABAaCh opening time -> membrane hyperpolarization
potential for abuse and tolerance

35
Q

antiemetics MOA

A

block D2,3,4 Rsin chemoreceptor trigger zone and solitary nucleus tract

36
Q

uses of antiemetics

A

adjuncts to Tx nausea and vomiting or migraine

has been used as monotherapy with unknown mechanism

37
Q

ADRs of antiemetics

A

drowsiness and dizziness

extrapyramidal symptoms

38
Q

betal blockers MOA

A

may raise migraine threshold by modulating adrenergic or serotonergic transmisison in Cx or subCx pathways

39
Q

beta blocker uses

A

most used prophylaxis for migraines

40
Q

ADRs of beta blockers

A

drowsiness, fatigue, sleep disturbances, vivid dreams, memory disturbance, depression

41
Q

caution of beta-blockers

A

CHF, peripheral vascular disease, AV conduction disturbances, asthma, depression, DM

42
Q

CaCh blockers MOA

A

inhibits Ca entry -> smooth mm relaxation

43
Q

uses of CaCh blockers

A

migraine prophylaxis, but off label

can also be used as prophylaxis of cluster HAs

44
Q

antidepressents MOA

A

beneficial effects independent of antidepressent activity

may result in down-regulation of central serotonin Rs, increased levels or synaptic NE, and enhances opioid R actions

45
Q

antidepressent ADRs

A

tricyclic- sedating

GI

46
Q

anticonvulsants MOA

A

enhance GABA mediated inhibition, modulate excitatory glutamate transisison
inhibit Na and Ca Ch activity

47
Q

uses of anticonvulsants

A

migraine prophylaxis, particularly useful with comorbid, seizures, anxiety disorders, bipolar disorder

48
Q

ADRs of anticonvulsatns

A

topiramate: paresthesias, fatigue, anoreia, diarrhea, weight loss, taste perversion
balporate: GI, tremor, somnolence, weight gain

49
Q

mild-moderate migraine attacks

A

NSAIDs, if response is poor try actaminophen, aspirin, caffeine combo (excedrin)

50
Q

mild-severe migraine

A

triptans, if unrespnsive try erogts

51
Q

tension HA

A

simple analgesics +/- caffeine

prevention w/tricyclic antidepressent

52
Q

cluster HA

A

oxygen, triptan, ergots

prevention w/ verapamil, lithium, prednisone, topiramate, frovatriptan

Neuro II (22 decks)

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