Brainscape's Knowledge GenomeTM

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


See full index

Neuro_week3 > Pharm management of HA > Flashcards

Pharm management of HA Flashcards

1
Q

Tension HA

Abortive treatment

A

NSAIDs +/- acetaminophen
Add caffeine if unresponsive

can add muscle relaxants

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

Tension HA

Prophylaxis

A

Amitryptiline (TCA)
SNRIs
SSRIs
Anticonvulsants

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

Migraine

Abortive treamtent

A

1) triptan
2) ergots = ergotamine or DHE
3) NSAIDs
4) Tramadol
5) isometheptene

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

Migraine

Prophylaxis

A

1) Antihypertensives (beta blocker or CCB)
2) anticonvulsants (topiramate and valproate)
3) antidepressants (amitryptiline)
4) NSAIDs
5) 5-HT2 receptor antagonists (methysergide)

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

Cluster HA

abortive treatment

A

1) ergots (DHE and ergotamine)
2) glucocorticoids (interrupt chain)
3) lidocaine
4) oxygen
5) triptans (sumatriptan)

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

Cluster HA

Prophylaxis

A

1) lithium
2) methysergide
3) verapamil (CCB)

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

Current model of migraine HA

A

1) neuropetpide trigger cascade of neuroinflamm
2) Phase 1 = 5HT release from neurons and platelets periph on to vessels causes vasoconstriction and ischemia
3) Phase 2 = cerebral vasodilation and pain regul by trigeminal neurovasc system

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

how do agonists of serotonin reduce pain in migraine

A

via release of pain inducing neuropeptides (CGRP)

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

5-HT1A
Location

Physiology

A

CNS

decr camp

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

5-HT1A

effects

A

1) neuronal inhib
2) sleep
3) anxiety

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

5-HT1A
agonists
antago

A

agonist= buspirone

antag = ergotamine

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

5-HT1B
Location

Physiology

A

CNS, blood vessel

decr camp

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

5-HT1B

effects

A

1) presynap inhib

2) pulm vasoconstriction

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

5-HT1B

agonists

A

ergotamine

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

5-HT1D
location

physiology

A

CNS, blood vessel

decr camp

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

5-HT1D

effects

A

cerebral vasoconstriction

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

5-HT1D
agonist

antagonist

A

sumatriptan

ergotamine

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

5-HT2A
location

physiology

A

CNS

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

5-HT2A

effects

A

1) behavior effects
2) contraction
3) aggregation

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

5-HT2A
agonist
antago

A

LSD

methysergide

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

5-HT2C
location

physiology

A

CNS

incr IP3/DAG

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

5-HT2C

effects

A

CSF secretion

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

5-HT2C

antagonist

A

methysergide

24
Q

NSAIDs

Mechanism of action

A

COX1/2 inhibitors

interrupts inflamm mediator release caused by CGRP

25
Q

NSAIDs
administration

duration

A

most OTC = oral

indomethacin = suppository

4-6 hrs to 8-12 hrs

26
Q

NSAIDs

uses

A

sufficient for mild to moderate migrates without nausea or diability

used for short term prevention

27
Q

NSAIDs

side effects

A

1) avoid in gastritis, peptic ulcers
2) affects platelet aggreg so avoid in bleeding disorders
3) avoid in renal insufficiency

tylenol = liver tox

28
Q

NSAIDs

DDI

A

incr bleeding risk with antiplatelets or anticoags

29
Q

Triptans

mechanism of action

A

5HT1B and 1D agonists
1) cerebral vasoconstriction

2) inhib release of neuropeptides causing vasodilation, inflamm
3) inhib trigeminal pain fibers

30
Q

Triptans

administration

A

1) oral mainly, nasal, subq
2) sumatriptan = poor CNS distrib

short half life

31
Q

Triptans

uses

A

first line for moderate-severe migraines

decr dilution-induced HA

32
Q

Triptans

side effects

A

paresthesias, flushing, drowsiness, dizzy, chest tightness (worst with sumi)

rarely coronary vasospasm *ASSOC WITH DHE, MI, angina, arrhythmia, stroke, death (avoid with HTN and heart dz)

33
Q

Triptans

DDI

A

additive constriction with ergot

incr risk of 5-HT syndrome with MAOIs (less with SNRI, SSRI)

34
Q

Ergots

mechanism

A

5-HT1B and 1D

same as triptans

35
Q

Ergots

administration

A

dihydroergotamine = oral, sublingal, rectal, incr abs with caffeine

DHE = intranasal and parenteral

36
Q

Ergots

uses

A

less effective than triptans but also used in migraines

37
Q

ergots

side effects

A

n/v (give with anti-emetics)
diarrhea, cramps, paresthesia

serious = vascular occlusion, gangrene via alpha 1 vasoconstriction

38
Q

ergots

ddi

A

severe peripheral ischemia if used with beta blockers

additive constriction with triptans

avoid with CYP3A4 inhib = vaosspasm

39
Q

when should you consider prophylaxis

A

1) severe, long last >12 hrs, frequent- more than 4 or disabling

40
Q

prophylaxis
beta blockers
propranolol
timolol

causes side effect

A

first line for migraine prophylaxis
antihypertensive

causes fatigue, exercise intolerance, depression, ortho hypotension

41
Q

prophylaxis
beta blockers
propranolol
timolol

contraindicated in

A

asthma
diabetes
conduction disturbances

42
Q

prophylaxis
CCB
verapamil

A

third line for migraine prophylaxis

tolerance develops

43
Q

prophylaxis
CCB
verapamil

contraindiction

A

don’t use with beta blocker= heart block

44
Q

prophylaxis
ACEI/ARB
lisinopril
candesartan

A

2nd or 3rd line

45
Q

TCA
amitryptiline

side effect

A

incr monoamine transmission, second line

sedation, dry mouth, tachy, weight gain, urinary retention

46
Q

anticonvulsants
topiramate

side effect

A

effect similar to propranolol

side effect = paresthesias, weight loss, taste perversion, fatigue

47
Q

pathophys of migraine

A

1) trigeminal neurovasc dysfunction
2) trigem neurovasc activ
3) release of vasoactive peptides
4) neuroinflamm and vasodilation of pial and dural vessels
5) pain

48
Q

phase 1 of migraines

A

cerebral vasoconstriction and ischemia

cortical spreading depression (decr CBF from vasoconstrict –> aura)

activate trigem nerve afferents

49
Q

phase 2 of migraines

A

cerebral vasodilation

trigeminal neurons release vasocactive peptides (substance P, CGRP) = vasodilation and neuroinflamm

50
Q

role of sensitization

A

1) throbbing pain
2) worsening pain with coughing-bending-sudden head movements
3) hyperalgesia
4) allodynia

51
Q

abortive treatment of migraine with n/v

A

SC sumatriptan

IV metoclopramide + diphenhydramine

52
Q

abortive treatment of migraine with intractable HA

A

IV DHE

53
Q

severe side effect of triptans, ergots esp DHE

A

vasoconstriction and vasooclusion

but more common in ergots and DHE due to alpha1 blockage

54
Q

frontal lobe lesion causes urinary __

A

urgency

55
Q

spinal cord lesions above S2-S4

spinal cord lesions of S2-S4 or injury to periph nerves innerv bladder

A

spastic bladder (think UMN) –> reflux up ureters

flaccid bladder (think LMN) –> overflow incontinence

Neuro_week3 (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions