exam 2 Flashcards by Janvi Patel

what is a primary headache due to

neurological process (not caused by another disorder)
-most common

How well did you know this?

Not at all

Perfectly

a secondary headache is due to what

specific underlying cause

How well did you know this?

Not at all

Perfectly

what are the examples of primary headache

migraine
tension
cluster

How well did you know this?

Not at all

Perfectly

what are the examples of secondary headache

med overuse headache
temporal arteritis

How well did you know this?

Not at all

Perfectly

what is the diagnostic criteria for secondary HA

HA >15 days
-from reg overuse of 1 or more sx meds for >3 mo

How well did you know this?

Not at all

Perfectly

what are the RF for MOH

genetic
central sensitization
biobehavioral

How well did you know this?

Not at all

Perfectly

what are the drug RF for MOH

opiods
butalbital
apap-asa-caffeine
-apap or asa
triptans and NSAIDS but low

How well did you know this?

Not at all

Perfectly

is abrupt dc of meds recommended for MOH

yes

How well did you know this?

Not at all

Perfectly

what is the bridge therapy for MOH

long NSAID
prednisone

How well did you know this?

Not at all

Perfectly

you must start what kind of therapy for MOH when theres a HA disorder–to prevent relapse

preventive therapy

How well did you know this?

Not at all

Perfectly

what is the max days for triptans and NSAIDs for MOH tx

triptans-9 days/mo
nsaids-14 days/mo
-AVOID anything else bc of high risk of relapse

How well did you know this?

Not at all

Perfectly

what is temporal arteritis

inflammation of arterries

How well did you know this?

Not at all

Perfectly

what are the sx of temporal arteritis

throbbing-continuous
one temporal artery
artery tender, thick, pulseless

How well did you know this?

Not at all

Perfectly

what is the diagnosis of temporal arteritis based on

temporal artery biospy
increased ESR

How well did you know this?

Not at all

Perfectly

what is the biggest sign of temporal arteritis HA

vision loss in one or both eyes–not reversible
-if not treated within week–50% lose vision

How well did you know this?

Not at all

Perfectly

how to treat vision loss for temporal arteritis

prednisone 60mg/day for 2-4 wks WITHOUT pos biopsy results
-if failed to tx, can result in blindness
-tx w prednisone abolishes risk of vision loss

How well did you know this?

Not at all

Perfectly

tension headaches are least studied because why

pt self medicate
-most common primary HA disorder

How well did you know this?

Not at all

Perfectly

what are some characteristics of tension headaches

bilateral–both sides
tightening–muscle tender
not aggravated by physical activity
no n/v

How well did you know this?

Not at all

Perfectly

how long do tension headaches last

30 mins to 7 days

How well did you know this?

Not at all

Perfectly

what is the major goal for tension HA

avoid MOH headache

How well did you know this?

Not at all

Perfectly

what is acute tx for tension HA

ibuprofen–fewest ADE
naproxen
aspirin

How well did you know this?

Not at all

Perfectly

what is prophylactic treatment for tension HA

amitriptyline–strongest evidence
mirtazapine
venlafaxine

How well did you know this?

Not at all

Perfectly

migraines are caused stimulation of what pathways

trigeminal nerve trigeminovascular

How well did you know this?

Not at all

Perfectly

what does activation of trigeminovascular sensory nerve do

releases vasoactive neuropeptides which leads to inflammation

How well did you know this?

Not at all

Perfectly

what are the inflammatory proteins

neurokinin A substance P CGRP

what is elevated during a migraine attack

CGRP

migraines are usually what

one sided aggravated by physical activity

what is the most potent and common triggers of migraine

menstruation

what do menstruation migraines respond better to

triptans

what is first line agent for migraines w/o n/v

NSAIDs

what is the MOA of triptans

5-HT1b and 1d agonists -inhibit release of CGRP promote VC

triptans are first line for what

mod-sev migraines

what are the preferred triptans

almotriptan eletriptan rizatriptan

what triptans have the fastest onset

sumatriptan zolmitriptan

what are CI of triptans

cardio issues cerrebovascular disease pregnancy

what is the only 1st gen triptan

sumatriptan

what is the most lipophilic triptan

zolmitriptan

when is appropriate to use ditans or CGRP antagonist

for pt >18 who are not responsive or intolerant to 2 or more triptans

what are the CGRP antagonist

ubrogepant rimegepant

what is level A tx for migraine prophylaxis

antiepileptic drugs beta blockers triptans

what arre the first and second line antihypertensives for migraine prophylaxis

BB-1st ACE/ARB-2nd`

what are the antiepileptic drugs for migraine prophylaxis

topiramate sodium valproate --no for pregnancy

what is abortive therapy for cluster HA

standard: O2 triptans compress exercise prednisone burst

what is prophylactic therapy for cluster HA

verapamil glucocorticocoids emgality

what are the barbituates

phenobarb primidone

major ADE w barbituates

rash-can progress to SJS

which barbituate has long half life

phenobarb -50-140 hrs

phenytoin protein binding is affected by what factors

-hypoalbuminemia -renal failure -hyperbilirubinemia

what are major ADEs of phenytoin

purple glove (IV) BBW-severe hypotension and cardiac arrhythmia -blurry vision, rash, gingival, blood dyscrasias

fosphenytoin is the water soluble prodrug of what

phenytoin

what are the advantages for fos vs phen

for has lower risk of hypotension/bradycardia and phlebitis

what are ADES with ethosuximide

psych sx rash blood dyscrasias

when should ethosuximide be d/ced

if WBC <3500 target serum concen--40-100 mcg

what are the benzos

lorazepam diazepam midazolam clonazepam clobazam

what are the major ADEs for benzos

sedation dizzy amnesia respiratory and CVD depression

what are the major ADEs with carbamazepine (CBZ)

hyponatremia--RF for seizures BBW--agranulocytosis and aplasic anemia (ANC <1000-d/c) BBW-rash

what are ADEs for oxcarbazepine

hyponatremia (more than CBZ) rash

what is the major active metabolite of eslicarbazepine

oxcarbazepine

what are the ADEs of valproate

tremor weight gain PCOS thrombocytopenia hyperammonemia rash BBW-hep failure--d/c if LFTS >3x and pancreaitis

what are ADEs of lamotrigine

arrhythmias rash--d/c at first sign of rash

what are ADEs of lacosamide

blurry vision PR interval prolongation--monitor ECG

what are ADEs for levetiracetam

asthenia behavioral disturbance

major ade for brivaracetam

behavioral chnges

what are ades for topiramate

weight loss paresthesia nephrolithiasis acidosis--monitor serum bicarb oligohydrosis hyperammonemia rash

ade for zonisamide

weight loss nephro acidosis oligo rash rare: agranulocytosis and aplastic anemia

ade for gabapentin

weight gain edema behavioral change breathing difficulty

ade for pregabalin

weight gain edema blurry eyes breathing difficulty rare: angioedema, thrombocytopenia, rhabdo

ade of cenobamate

fatal hypersensitivtiy QT shortening

aeds have almost a 2 fold increase in what

suicidal behavior/ideation

what are AEDs associated with decreased mineral bone density

phenytoin primidone phenobarb cbz

what are aeds associated with anticonvulsant hypersensitivty syndrome

aromatic AEDS -phenytoin phenobarb primidone cbz lamotrigine rufinamide

how to treat hypersensitivity syndrome

treat with steroids -VPA and benzos safe after rxn

what aeds induce hepatic enzymes so reduce levels of many aeds, benzos and OC

phenobarb primidone phenytoin cbz

treatment should be initiated after how many seizures

2nd unprovoked

aeds for focal seizures

levetiracetam lamotrigine lacosamide oxc cbz

aeds for tonic clonic

levetiracetam lamotrigine cbz oxc vpa topiramate zonisamide

aeds for multiple generalized seizures

vpa lamotrigine topiramate zonisamide

aeds to avoid in pt w multiple seizure types

cbz phenytoin phenobarb

what aed cause neural tube defects

valporate cbz

what aed causes oral cleft

cbz vpa phenytoin phenobarrb

what aed to use in kids

cbz vpa phenytoin phenobarb

what aed to avoid in old ppl

barbituates

how many trials of monotx should be considered in old ppl before to moving to adjunctive tx

a depletion of what monoamines is associated with depression

serotonin NE dopamine

what non pharm thearpy has high response rate and rapid response

electroconvulsive therapy

what are the SSRIs

fluoxetine (20-80) sertraline (50-200) paroxetine (10-60) fluvoxamine (50-300) citalopram (20-40) escitalopram (10-20)

what is moa of SSRI

inhibit 5ht reuptake so increased 5ht in synapse

what is are SE of SSRI

sexual dysfunction anxiety headache insomnia

what SSRI is most likely to cause sedation constipation and dry mouth

paroxetine

what SSRIs are morer likely to have insomnia

sertraline fluoxetine

what SSRI has morer potential for cardiac toxicity

citalopram

SSRIs have what effect with NSAIDs, anticoags, and antiplatelets

increased bleeding

fluoxetine and paroxetine are strong inhibitors of

cyp2d6

what are the SNRIs

venlafaxine duloxetine desvenlafaxine levomilnacipran

what is the moa of SNRI

inhibit reuptake of both 5ht and NE

venlafaxine has more reuptake of what

5ht -doses more than 150 give NE reuptake effect

what are SE from SNRIs

same as ssri but -venla/desven-increase BP levo--can cause tachy

duloxetine inhibits what

2d6 so avoid co admin w 1a2 inhibitors (fluvoxamine and cipro)

bupropion moa

inhibits reuptake of NE and DA

what are bupropion se

dry mouth anixety insomnia increased seizure rrisk NO SEX DYSFXN

bupropion is a strong inhibitor of what

2d6

what is the moa of mirtazapine

5ht and NE 5ht2a/c/3 antagonist

what are se of mirtazapine

somnolence increased appetite dry mouth orthostasis

what are the serotonin reuptake inhibitor

trazodone nefazodone

what is trazadone primarily used for

insomnia

what are the TCAs tertiary drugs

amitriptyline imipramine clomipramine doxepin

what are the TCAs secondary drugs

nortriptyline desipramine protriptyline amoxapine

all tcas have what metabolism

2d6

what drugs to be cautious with 2d6 metabolism

fluoxetine paroxetine bupropion duloxetine

what is the moa of tcas

block NE and 5ht reuptake

clomipramine is more selective for what

5ht

desipramine is more selective for what

what are the SE of TCAs

sex dysfunction antichol weight gain cardiac conduction changes

what is the dose that can be lethal for TCAs

10-15mg/kg

what are the sx of TCA toxicity

hypotension hypothermia urinary retention seizures depression

what are the monoamine inhibitor drugs

phenelzine tranylcypromine isocarboxazid selegiline

what is the moa of MAOs

irreversibly inhibit MAO, enzyme responsible for degradation of 5ht, NE an d DA

with MAO-A being blocked what does that cause

tyramine can cause HTN

exam 2 Flashcards

(118 cards)