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Week 3 (Neuro 2) > PHARM - Seizures & Alzheimer's > Flashcards

PHARM - Seizures & Alzheimer's Flashcards

1
Q

what is the overarching mechanism by which drugs treat seizures?

A

by decreasing hyperexcitability

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2
Q

what are the methods by which drug decrease hyperexcitability?

A
  • ion channel modulation
  • GABA enhancement
  • Glutamate inhibition
  • modulation of NT release
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3
Q

which cation channels can be modulated to decrease hyperexcitability?

how?

A
  • Na+ channel: blockage
  • Ca++ channel: blockage
  • K+ channel: enhancement
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4
Q

sodium channel modulators

  • includes which drugs?
  • clinical use
  • MOA
  • AE/CI
A
  • drugs: phenytoin, carbapezamine, lacosamide
  • clinical use: seizures - focal, tonic-clonic
  • MOA: bind to Na+ channels in the inactivated state, inhibiting high -frequency firing
    • phenytoin, carbapezamine: fast-inactivation
    • lacosamide: slow inactivation
  • AE: drug-specific
  • CI: absence seizures
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5
Q

phenytoin

  • what kind of drug?
  • clinical use
  • MOA
  • PK
  • AE/CI
A
  • sodium channel modulator
  • clinical use: seizures - focal, tonic clonic
  • MOA: enhance fast-inactivation of inactivated Na+ channels -> inhibitng high-frequency firing
  • PK:
    • narrow therepeutic range - small dose changes can lead to toxicity
    • metabolized by CYP-2C9
    • inhibits CYP-3A4
  • AE:
    • gingival hyperplasia
    • facial feature coarsening
    • mild cerebrovestibular effects - vertigo, ataxia, HA, nausea
  • CI:
    • absence seizures
    • pregnancy & oral contraceptives - is teratogenic
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6
Q

what are the contraindications of phenytoin?

A
  • absence seizure (like all Na modulators)
  • in pregnancy - teratogenic
  • with oral contraceptives - teratogenic
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7
Q

how id phenytoin metabolized?

A

by CYP-2C9

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8
Q

phenytoin inhibits…?

A

CYP-3A4

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9
Q

carbapezamine

  • what kind of drug?
  • clinical use
  • MOA
  • PK
  • AE/CI
A
  • sodium channel modulator
  • clinical use: seizures - focal (simple & complex), tonic clonic
  • MOA: enhance fast-inactivation of inactivated Na+ channels -> inhibitng high-frequency firing
  • AEs:
    • allergic reactions
    • cerebrovestibular - nausea, ataxia
  • CI:
    • absence seizures
    • SLE
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10
Q

what are the contraindications of carbapezamine?

A
  • absence seizures
  • SLE
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11
Q

explain the mechanism behind absence seizures

A

oscillations between the thalamus and cortex that are generated in the thalamus by T-type (transient) Ca++ current

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12
Q

what drugs are used to treat absence seizures?

A
  • Ca++ channel modulators
    • ethosuxamide
    • valproate
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13
Q

Ca++ channel modulators

  • include which drugs?
  • clinical use?
  • MOA?
  • AE?
A
  • drugs: valproate, ethosuximide
  • clinical use: absence seizures
  • MOA: block low threshold-Ca++ channels -> blocking T-type currents
  • AE: drug specific
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14
Q

valproic acid

  • what kind of drug?
  • clinical use?
  • MOA?
  • AE/CI?
A
  • is a calcium channel modulator
  • clinical use: absence seizures
  • MOA: block low threshold-Ca++ channels -> blocking T-type currents
  • AE/CI: more severe than ethosuximide
    • teratogenic / CI in pregnancy
    • hepatoxic / CI in liver disease
    • CNS depression / CI other depressants
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15
Q

ethosuxamide

  • what kind of drug?
  • clinical use?
  • MOA?
  • AE/CI?
A
  • is a calcium channel modulator
  • clinical use: absence seizures
  • MOA: block low threshold-Ca++ channels -> blocking T-type currents
  • AE: safer than valproic acid
    • ​GI
    • anorexia
    • drowisniesss
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16
Q

which drugs are

  • used to treat absence seizures?
  • C/I in a pt with absence seizures?
A
  • treated with:
    • valproic acid
    • ethosuximide
  • C/I drugs:
    • phenytoin
    • carabemazepine
    • lacosamide
17
Q

benzodiazapines

  • includes what drugs
  • clinical use
  • MOA
  • AE
A
  • drugs: -epams: diazepam, lorazepam, clonazepam
  • clinical use: seizures - myoclonic, status epilepticus
  • MOA: positive allosteric GABAA receptor modulators - enhance receptor-GABA affinity
  • AE: drowsiness
18
Q

barbituates

  • includes what drugs
  • clinical use
  • MOA
  • AE
A
  • drugs: phenobarbital, primodone
  • clinical use: seizures - status epilepticus, myoclonic
  • MOA:
    1. ​positive allosteric modulators of GABAA receptors
    • at higher concentrations - a direct GABA antagonist
  • AE: general CNS depression
19
Q

what tolerance risk do benzodiazepnies pose?

A
  • DO lead to tolerance of AED (anti-epileptic effects)
  • do NOT lead to tolerance of anti-hyponotic effects
20
Q

how are benzodiazapenes / barbituates

  • similar
  • different
A

both

  • are postiive allosteric regulators of GABAa receptors
  • are used for myoclonic seizures & status epilepticus
  • can lead to AED tolerance

only barbituates

  • can be a direct GABAa agonist at high concentrations
21
Q

diazepem - is what kind of drug?

A

benzodiazepine

22
Q
  • is what kind of drug?
A

benzodiazepines

23
Q

lorazepam - is what kind of drug?

A

benzodiazepine

24
Q

clonazepam - is what kind of drug?

A

benzodiazepines

25
Q

phenobarbital - is what kind of drug?

A

barbarbituate

26
Q

primidone - is what kind of drug?

A

barbarbituate

27
Q

topiomarate

  • clinical use
  • MOA
  • AE/CI
A
  • clinical use: seizures - complex partial, generalized clonic tonic
  • MOA:
    • blocks Na+ channels
    • blocks AMPA (Glu) channels
    • enhances GAGA transmission
  • AE: teratogenic - cleft palate
  • CI: pregnancy
28
Q

what AES are C/I in pregnancy

which one can lead to a cleft palate?

A
  • phenytoin [Na+ blocker]
  • valproic acid [Ca+ blocker]
  • topiomarate - can cause a cleft palate
29
Q

what is the #1 treatment for status epilepticus?

A

lorazepam

30
Q

describe the imbalance that leads to Altheimers

A
  • deficits in cholinergic signaling
  • excess glutamate signaling
31
Q

what are the three methods by which althzheimers is treated?

what drugs are utilized for each method?

A
  1. increase cholinergic activity: AChE inhibitors - donepezil, endophonium
  2. decrease glutmate activity: NMDA receptor antagonists - memantine
  3. reduce beta amyloid plaques: abudacumab
32
Q

AChE inhibitors in the treatment of parkinsons

  • which drugs are used?
  • which is better tolerated?
  • how are they administered?
  • AEs?
A
  • drugs: ribastigmine, donepezil
  • better tolerated: donepezil
  • administrated: often in combination w/ memantine
  • AE: ACh excess - N &V, cramps, bradycardia, syncope
  • CI: in pts w/ bradycardia / syncope
33
Q

which NDMA antagonist is used to treat Parkinson’s?

A

memantine

(often given in combination with donepezil)

34
Q

which medication potentially reduces plaques in Altzheimers?

A

aducunumab

Week 3 (Neuro 2) (5 decks)

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