Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Week 2 (Neuro 2) > PHARM - Headache & NMJ Disorders > Flashcards

PHARM - Headache & NMJ Disorders Flashcards

(57 cards)

Start Studying
1
Q

drugs used to treat LEMS fit into what major categories?

list the drugs in each.

A
  • K+ channel blockers
    • amifampridine (3,4 - diamanopyridine)
    • guanidine HCl
  • AChE inhibitor
    • pyridostigmine
  • immunosupressants
    • prednisone
    • azothioprine
    • anti-AChE Abs: IVIG, rituximab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

drugs used to treat myasthenia gravis fit into what major categories?

list the drugs in each.

A
  • AChE inhibitor
    • pyridostigmine
    • neostigmine
    • physostigmine
  • immunosupressants
    • prednisone
    • azothioprine
    • anti-AChE Abs: IVIG, rituximab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the _mainstay treatment_s for LEMS

A
  • amifampridine (3,4 diaminopyridine) - 1st line
  • pyridiostigmine - if in conjunction with amifampridine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

amifampridine

  • clinical use
  • MOA
  • PK
  • AEs / CIs
A
  • clinical use: LEMS - first line
  • MOA: K+ channel inhibition on NMJ pre-synapse
    • ​hyperpolarization prevention
    • pre-synaptic membrane depolarized for longer
    • Ca++ release > P/Q channel blockage
    • ACh released
  • PK
    • good gut absorption
    • ​deactivated by N-acyltransferase
  • AE / CI:
    • AE
      • tingling / numbness ​
      • insomnia
      • seizures
    • CI:
      • EPILEPY
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

when is amifampridine contraindicated?

A

with epilepsy

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

how is amifampridine deactivated?

A

by an N-acetyltransferase reaction

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

guanidine hydrochloride

  • clinical use
  • MOA
  • AE/CI
A
  • clinical use: LEMS - NOT first line (avoided unless absolutely necessary)
  • MOA: K+ efflux inhibition
  • AEs:
    • bone marrow suppresion
    • renal toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

pyridostigmine

  • clinical use
  • MOA
  • AES
  • PK
A
  • clinical use:
    • LEMS (as an adjunctive)
    • myasthenia gravis
  • MOA: AChE inhibitor - inceases ACh at NMJ
  • AES: d/t systemic excess of ACh
    • diarrhea, cramping, N & V
    • possible cholinergic crsisis
  • PK: reversible & short duration (3-4 hrs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

contrast the role of AChE inhibitors in the treatment of LEMS vs myasthenia gravis

A

i.e., pyridostigmine

  • LEMS - effective with amifampridine
  • myasthenia - is effective alone

weakness in LEMS is due to decreased ACh release from the pre-synapse, so is best treated by increasing ACh release rather than slowing ACh breakdown

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

what is the tensilon test & its clinical use?

A
  • distinguishes between myasthenia crisis & cholinergic crisis
    • test: administration of endrophonium, an AChE inhibitor
      • paralysis improves: myasthenia crisis
      • paralysis worsens: cholinergic crisis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

which immuno-suppressants can be used to treat LEMS & myasthenia gravis?

when are they utilized?

A

used ONLY in refractory myasthenia gravis / LEMS.

  • prednisone +/- cycling with azothioprine
    • ​prenidone - most effective, but most toxic
    • azothioprine - steroid sparing
  • other steroid sparing agents
    • rituximab
    • plasma exchange / IVIG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the treatments for botulism?

A
  • anti-toxin: always used
  • Abx (penicillin G, metronidazole) for wound botulism after anti-toxin administration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

botulism anti-toxin

  • MOA
  • variations
A
  • MOA: ​circulates in blood, blocking actions of toxin from C. tetanus
  • comes in two variations:
    • for pts < 1 year: human-derived botulisam immune globulin (BIV-G)
    • ​for pts > 1 year: equine serum heptavalent botuslim antitoxin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

BIG-IV should be given to which patients with botulism?

A

those < 1 year of age

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

what is the role of antibiotics in the treatment of botulism?

A
  • recommended: for wound botulism after anti-toxin administration
    1. penicillin G
    2. metronidazole (if b-lactam allergies)
  • NOT recommended: for GI botuslism; i.e., no oral Abx - lyse cells
  • contraindicated: aminoglycosides - are presynaptic NMJ blockers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

why are oral Abx not recommended in the management of botulism?

A

Abx work by lysing cells, which could serve to increase toxin levels in the body

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

why are aminoglycosides C/I in the treatment of botulism?

A

they are NMJ blockers at the pre-synapse

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

what are the two major goals when treating headaches?

A
  • to reduce acute pain
  • to provide prophylaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

which drugs are used in the treatment of acute headache?

A
  • acetaminophen / NSAIDS
  • triptans
  • lasmiditan
  • ergot alkaloids
  • CGRP antagonist
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

triptans

  • what kind of drug
  • clinical use
  • MOA
  • PK
  • AEs / CIs
A
  • 5-HT1 agonists
  • clinical use: acute headache
  • MOA: bind to 5-HT1B & 5-HTD1 receptors on cranial vessels outside the CNS
    • 5-HT1B stimulation: vasoconstiction
    • 5-HT1D stimulation: inhibition of vasoactive peptides release
  • PK: metabolism into naratripan by
    • CYP-1A2
    • CYP-3A4
    • MAO
  • AEs/CI:
    • AEs: cardiovascular (rare)
      • MI
      • HTN
      • arrytmias
      • angina
    • CI: MAO inhibtors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the adverse affects of triptan?

A

all cardiovascular (due to vasoconstriction)

  • MI
  • HTN
  • arrtyhmias
  • angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

triptans are contraindicated with what drug? why?

A

MAO inhibitors

MAO-A is needed to metabolize triptans into naratriptan for excretion

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

which enzymes metabolize tryptan into naratryptan?

Study These Flashcards
A
  • MAO-A
  • CYP-3A4
  • CYP-1A4
24
Q

lasmiditan

  • what kind of drug?
  • clinical use
  • MOA
  • AEs
Study These Flashcards
A
  • 5-HT1 agonist
  • clinical use: acute headache -m/c in episodic migraine
  • MOA: stimulates 5-HT1F receptors on cranial vessels
  • AEs: dizziness
25
how do the vascular affects of triptans and lasmiditan differ? why does this matter?
lasmitidan does NOT cause vasoconstriction of dilated cranial vessels - thus, less effective than triptans
26
ergot alkaloids * include what drugs? * clinical use? * MOA?
* - **gotramines:** ergotamine, dihydroergotamine * clinical use: acute headache * MOA: * **5-HT1 agonists: 5-HT1B, 5-HT1D** * 5-HT1-B**:** long lasting, cummulative cerebral vasoconstrction * ergotamine: arteries & veins * dihydroergotamine: veins \> arteries * 5-HT1D: inhibition of vasoactive peptide release * **partial *alpha* agonists:** a1, a2 -\> vasoconstriction * **D1, D2 (dihydroergotamine ONLY)**
27
how do the vascular affects of ergot alkaloids and triptans differ?
* ergot alkaloid induced vasoconstriction is * **longer lasting** * **cummulative** * **cerebral**
28
diydroergotamine * what kind of drug * clinical use * MOA * PK * AE/CI
* ergot alkaloid * clinical use: acute headache * MOA: * **5-HT1B, 5-HT1D agonist** * ​long lasting, cummulative vasoconstriction * inhibition of vasoactive peptide release * **partial a1, a2 agonists:** -\> vasoconstriction * **D1, D2** * PK: * absorption: poor, enhanced by caffeine * long half life * rapid elimination * AE/CI: * AE: * **GI - diarrhea, N &V: d/t D1, D2 agonism** * **CNS - severe cerebral vasoconsriction** * **CV - angina like sx** * **teratogenic** * C/I * **pregnancy** * **with beta blockers**
29
caffeine improves the absorption of which acute headache drug?
dihydroergotamine
30
what are the major AEs of dhydroergotamine?
* **GI - diarrhea, N &V: d/t D1, D2 agonism** * **CNS - severe cerebral vasoconsriction** * **CV - angina like sx** * parasthesia
31
dihydroergotamine is contraindicated in a patient taking what drug? why?
**beta blockers.** b/c dihydroergotamine is such a powerful vasoconstrictor, vascular B2 receptors need to available for _induction of vasodilation_ in the case of a vasoconstriction crisis (i.e., cerebral vasoconstriction)
32
use of dihydroergotamine during pregnancy can lead to which effects?
* prematurity * low birth weight * spontaneous abortion
33
list the receptors bound by each 5-HT1 agonist used to treat acute headache
* triptans: 5-HT1B, 5-HT1D * lasmiditan: 5-HT1F * ergot alkaloids * 5-HT1B, 5-HT1D * a1, a2 (partial) * D1, D2 (dihdydroerogamine)
34
the efficacy of _which acute headache drug_ can be improved when combined with triptans?
**NSAIDS** ex - naproxen & sumatriptan
35
anti-emetic agents * include which drugs? * clinical use * MOA * AE/CI
* drugs**: metoclopramide, chlorpromazine / pro-chlorpromazine** * clinical use: acute headache * MOA: **dopamine receptor antagonists** * AE/CI: * AE * **akathisia / acute dystonic reaction:** involuntary contractions * **QT interval prolongation (torsades)** * CI: drugs that prolong QT interval
36
what is the antidote for _akthisia & acute dystonic reaction_ secondary to anti-emetic agents?
IV diphenhydramine
37
anti-emetic agents are contraindicated in someone taking what other drugs? why?
* agents that increase that prolong QT interval * anti-emetics increase QT interval, posing risk for torsades
38
metoclopramide * what kind of drug? * clinical use * MOA * AE/CI
* anti-emetic agent * clinical use: acute headache * MOA: **dopamine receptor antagonists** * AE/CI: * AE * **akathisia / acute dystonic reaction:** involuntary contractions * **QT interval prolongation (torsades)** * CI: drugs that prolong QT interval
39
chloropromazine * what kind of drug? * clinical use * MOA * AE/CI
* anti-emetic * clinical use: acute headache * MOA: **dopamine receptor antagonists** * AE/CI: * AE * **akathisia / acute dystonic reaction:** involuntary contractions * **QT interval prolongation (torsades)** * CI: drugs that prolong QT interval
40
list the keys drugs contraindicated with each _acute HA drug_
* triptans: **MAO-A inhibitors** * dihydroergotamine: **beta blockers** * anti-emetics (metoclopramide, chloropromazine): drugs **that prolong the QT interval**
41
which drugs are used to _provide prophylaxis_ against headache?
* CGRP antagonists * topiramate * propanolol * cyrpoheptadine * botox
42
CGRP (calcitonin gene related peptide) inhibitors * include what drugs? * clinical use * MOA * AEs
* drugs: * **- gepants: rimegepant, urogepant** * **- umabs: erenumab, fremanezumab** * clinical use: acute headache (gepants) AND prophylaxis (umabs) * MOA: **lower the # of "headache days" by inhibiting CGRP, which is a**: * potent vasodilator * key neuropeptide * AE: relatively safe - some CV risk (HTN)
43
rimegrepant is what kind of drug? clinically used for?
CGRP inhibitor used to treat acute headache pain
44
ubrogrepant is what kind of drug? clinically used for?
CGRP inhibitor used to treat acute headache pain
45
erenumab is what kind of drug? used clinically how?
CGRP inhibitor used to prevent headache pain (bind circulating CGRP)
46
fremanezumab is what kind of drug? used clinically how?
CGRP inhibitor used to prevent headache pain (bind circulating CGRP)
47
topiramate * what kind of drug? * clinical use * MOA * AE
* anti-seizure medication * clinical use: prophylaxis against headache * MOA: **enhances GABA mediated Cl- influx, slowing pain transmission** * AE: * cognitive disturbances * visual disturbances * anxiety * weuight loss
48
what is the role of propanolol in headache management?
headache prophylaxis those with intrinsic sympathetic activity not affective
49
propanolol is not recommended for which patients?
* those \> 60 * those who use tobacco products
50
cyproheptadine * clinical use * MOA * AEs
* clinical use: **headache prophylaxis, particularly in children & during pregnancy** * MOA: **5-HT2 antagonist & 5-HT1 agonist** * AEs: from anti-cholinergic effects of 5-HT1 stimulation * sedation * dry mouth * urinary retention
51
which headache drug is most likely to cause vomiting?
dihydroergotamine ergot alkaloid that stimulates D1 & D2 receptors
52
which headache drug is most likely to cause a myocardial infarction?
triptans
53
which headache drugs prolong the QT interval?
anti-emetic drugs: metoclopramide, chlorpromazine
54
which headache drugs "decrease the # of headache days"
CGRP inhibitors
55
which headache drug has signifiance uteronic effects?
dihydroergotamine (ergot alkaloid)
56
which headache drug is a class B preganancy drug? what does this mean?
cyproheptadine is useful for headache prophylaxis in pregnant women
57
which headache drug is contraindicated with beta blockers?
dihydroergotamine (ergot alkaloid)

Week 2 (Neuro 2) (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions