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

PHARM - Headache & NMJ Disorders Flashcards

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
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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
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3
Q

what is the _mainstay treatment_s for LEMS

A
  • amifampridine (3,4 diaminopyridine) - 1st line
  • pyridiostigmine - if in conjunction with amifampridine
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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
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5
Q

when is amifampridine contraindicated?

A

with epilepsy

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6
Q

how is amifampridine deactivated?

A

by an N-acetyltransferase reaction

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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
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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)
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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

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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
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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
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12
Q

what are the treatments for botulism?

A
  • anti-toxin: always used
  • Abx (penicillin G, metronidazole) for wound botulism after anti-toxin administration
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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
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14
Q

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

A

those < 1 year of age

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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
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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

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17
Q

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

A

they are NMJ blockers at the pre-synapse

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18
Q

what are the two major goals when treating headaches?

A
  • to reduce acute pain
  • to provide prophylaxis
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19
Q

which drugs are used in the treatment of acute headache?

A
  • acetaminophen / NSAIDS
  • triptans
  • lasmiditan
  • ergot alkaloids
  • CGRP antagonist
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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
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21
Q

what are the adverse affects of triptan?

A

all cardiovascular (due to vasoconstriction)

  • MI
  • HTN
  • arrtyhmias
  • angina
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22
Q

triptans are contraindicated with what drug? why?

A

MAO inhibitors

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

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23
Q

which enzymes metabolize tryptan into naratryptan?

A
  • MAO-A
  • CYP-3A4
  • CYP-1A4
24
Q

lasmiditan

  • what kind of drug?
  • clinical use
  • MOA
  • AEs
A
  • 5-HT1 agonist
  • clinical use: acute headache -m/c in episodic migraine
  • MOA: stimulates 5-HT1F receptors on cranial vessels
  • AEs: dizziness
25
Q

how do the vascular affects of triptans and lasmiditan differ?

why does this matter?

A

lasmitidan does NOT cause vasoconstriction of dilated cranial vessels - thus, less effective than triptans

26
Q

ergot alkaloids

  • include what drugs?
  • clinical use?
  • MOA?
A
    • 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
Q

how do the vascular affects of ergot alkaloids and triptans differ?

A
  • ergot alkaloid induced vasoconstriction is
    • longer lasting
    • cummulative
    • cerebral
28
Q

diydroergotamine

  • what kind of drug
  • clinical use
  • MOA
  • PK
  • AE/CI
A
  • 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
Q

caffeine improves the absorption of which acute headache drug?

A

dihydroergotamine

30
Q

what are the major AEs of dhydroergotamine?

A
  • GI - diarrhea, N &V: d/t D1, D2 agonism
  • CNS - severe cerebral vasoconsriction
  • CV - angina like sx
  • parasthesia
31
Q

dihydroergotamine is contraindicated in a patient taking what drug?

why?

A

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
Q

use of dihydroergotamine during pregnancy can lead to which effects?

A
  • prematurity
  • low birth weight
  • spontaneous abortion
33
Q

list the receptors bound by each 5-HT1 agonist used to treat acute headache

A
  • triptans: 5-HT1B, 5-HT1D
  • lasmiditan: 5-HT1F
  • ergot alkaloids
    • 5-HT1B, 5-HT1D
    • a1, a2 (partial)
    • D1, D2 (dihdydroerogamine)
34
Q

the efficacy of which acute headache drug can be improved when combined with triptans?

A

NSAIDS

ex - naproxen & sumatriptan

35
Q

anti-emetic agents

  • include which drugs?
  • clinical use
  • MOA
  • AE/CI
A
  • 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
Q

what is the antidote for akthisia & acute dystonic reaction secondary to anti-emetic agents?

A

IV diphenhydramine

37
Q

anti-emetic agents are contraindicated in someone taking what other drugs?

why?

A
  • agents that increase that prolong QT interval
  • anti-emetics increase QT interval, posing risk for torsades
38
Q

metoclopramide

  • what kind of drug?
  • clinical use
  • MOA
  • AE/CI
A
  • 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
Q

chloropromazine

  • what kind of drug?
  • clinical use
  • MOA
  • AE/CI
A
  • 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
Q

list the keys drugs contraindicated with each acute HA drug

A
  • triptans: MAO-A inhibitors
  • dihydroergotamine: beta blockers
  • anti-emetics (metoclopramide, chloropromazine): drugs that prolong the QT interval
41
Q

which drugs are used to provide prophylaxis against headache?

A
  • CGRP antagonists
  • topiramate
  • propanolol
  • cyrpoheptadine
  • botox
42
Q

CGRP (calcitonin gene related peptide) inhibitors

  • include what drugs?
  • clinical use
  • MOA
  • AEs
A
  • 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
Q

rimegrepant is

what kind of drug?

clinically used for?

A

CGRP inhibitor used to treat acute headache pain

44
Q

ubrogrepant is

what kind of drug?

clinically used for?

A

CGRP inhibitor used to treat acute headache pain

45
Q

erenumab

is what kind of drug?

used clinically how?

A

CGRP inhibitor used to prevent headache pain (bind circulating CGRP)

46
Q

fremanezumab

is what kind of drug?

used clinically how?

A

CGRP inhibitor used to prevent headache pain (bind circulating CGRP)

47
Q

topiramate

  • what kind of drug?
  • clinical use
  • MOA
  • AE
A
  • 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
Q

what is the role of propanolol in headache management?

A

headache prophylaxis

those with intrinsic sympathetic activity not affective

49
Q

propanolol is not recommended for which patients?

A
  • those > 60
  • those who use tobacco products
50
Q

cyproheptadine

  • clinical use
  • MOA
  • AEs
A
  • 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
Q

which headache drug is most likely to cause vomiting?

A

dihydroergotamine

ergot alkaloid that stimulates D1 & D2 receptors

52
Q

which headache drug is most likely to cause a myocardial infarction?

A

triptans

53
Q

which headache drugs prolong the QT interval?

A

anti-emetic drugs: metoclopramide, chlorpromazine

54
Q

which headache drugs “decrease the # of headache days”

A

CGRP inhibitors

55
Q

which headache drug has signifiance uteronic effects?

A

dihydroergotamine (ergot alkaloid)

56
Q

which headache drug is a class B preganancy drug?

what does this mean?

A

cyproheptadine

is useful for headache prophylaxis in pregnant women

57
Q

which headache drug is contraindicated with beta blockers?

A

dihydroergotamine (ergot alkaloid)

Week 2 (Neuro 2) (9 decks)

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