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depression > IC4: Antiepileptics & Antimigraine > Flashcards

IC4: Antiepileptics & Antimigraine Flashcards

1
Q

Phenytoin MOA

A

Block voltage-dependent Na+ channels
Prevents Na+ influx into cell and reduce ability for action potential
This reduces excitability for cortex

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2
Q

Phenytoin is used to treat what seizure types?

A

All seizures except absence seizures

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3
Q

Describe the PK properties of phenytoin

A

Narrow TI (plasma conc 40-100mcM)
Saturation kinetics
Non-linear kinetics –> need TDM

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4
Q

Can phenytoin be used in pregnancy?

A

No, teratogenic. Caution in females in reproductive age

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5
Q

Carbamezpine MOA

A

Block voltage-gated Na+ channels (similar to phenytoin)

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6
Q

Carbamazepine can be used to treat what seizure types?

A

All seizures except absence seizures (similar to phenytoin)

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7
Q

Which pharmacogenomic ADR is common a/w Carbamazepine

A

SJS/TEN

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8
Q

Which allele is implicated for SJS/TEN in Asians that require genetic screening?

A

HLA-B*1502

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9
Q

Sodium Valproate MOA

A
  1. Blockade of voltage-dependent Na+ and Ca2+ channels (reduce excitatory tone)
  2. Also inhibits GABA transaminase -> increased GABA (incr inhibitory tone)
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10
Q

Sodium valproate is used to treat which seizure types?

A

All types (incl absence)

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11
Q

List the PK property(s) of Valproate

A
  1. High & strong protein binding (80-90%) - displace other antiepileptics = incr free fraction
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12
Q

List at least 4 Dose-related ADRs for ASMs

A
  1. Drowsiness
  2. Confusion
  3. Nystagmus (repetitive uncontrolled eye movement)
  4. Ataxia (poor muscle coordination)
  5. Slurred speech
  6. Unsual behaviour
  7. mental changes
  8. Coma
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13
Q

List at least 4 NON-dose related ADRs of ASMs

A
  1. Hirsutisms
  2. Acne
  3. Gingivial hyperplasia
  4. Folate deficiency (? megaloblastic anemia)
  5. Osteomalacia (weak bones)
  6. Hypersensitivty eg. SJS
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14
Q

Benzodiazepines MOA

A

Benzodiazepines bind to GABA-A receptors (from a diff side as GABA) to potentiate influx of Cl- ions leading to hyperpolarisation.
This makes it harder for depolarisation and therefore, reduce action potnetials

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15
Q

True or False? Benzodiazepines mimics endogenous GABA to potentiate Cl- influx into the neuron.

A

False. Benzos bind to the benzodiazepine binding site of the GABA-A receptors. In addition, Benzos potentiate the action of GABA. Hence, without GABA, no inhibition can occur.

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16
Q

List 2 short (fast) acting benzodiazepines and state their common indications

A
  1. Midazolam - induction of general anesthesia, procedural sedation
  2. Triazolam - insomnia (fyi?)
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17
Q

List at least 2 intermediate acting Benzodiazepines and their indications

A
  1. Clonazapam - Panic disorder, seizure
  2. Lorazepam - Status epilepticus, anxiety, insomnia
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18
Q

List a long acting benzodiazepine used for epilepsy treatment

A

Diazepam

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19
Q

List 3 unwanted effects of benzodiazepines (BZP)

A
  1. Acute toxicity/overdose (resp depression)
  2. Side effects (ataxia, drowsiness)
  3. Tolerance and dependency
20
Q

List at least 3 ADRs of benzodiazepines

A
  1. CNS: Drowsiness, confusion, amnesia
  2. MSK: Ataxia (impaired muscle coordination)
21
Q

Effects of benzodiazepine toxicity/overdose

A

Severe respiratory depression, esp with concurrent alcohol

22
Q

State the agent used for Benzodiazepine toxicity

A

Flumazenil (benzodiazepine antagonist)

23
Q

State some withdrawal symptoms of benzodiazepines

A
  1. Disturbed sleep
  2. Rebound anxiety
  3. Tremor
  4. Convulsions
24
Q

Why are BZPs less indicate for treating epilepsy

A
  1. Epilepsy needs daily lifelong administration. This can lead to tolerance and eventually dependence.
  2. This requires gradual withdrawal
25
Q

Phenobarbital class of medications and MOA

A

Class: Barbiturate
MOA: Potentiate GABA-A mediated Cl- currents at a site distinct from benzodiazepines

26
Q

Given the similar MOA of phenobarbital and BZPs, can flumazenil be given to treat barbiturate overdose?

A

NO. Flumazenil does not bind to the benzodiazepine binding site

27
Q

List a long, short and ultrashort acting barbiturate & state their indications

A
  1. Long acting- Phenobarbital, anticonvulsant
  2. Short (3-8H)- pentobarbital & amobarbital, sedative & hypnotic
  3. Ultrashort (20min)- Thiopental, IV induction of anesthesia
28
Q

T/F? Barbiturates cause less CNS depression than benzodiazepines

A

False (its the other way round)

29
Q

Levitiracetam place in therapy for seizures

A
  1. Adjunctive therapy for partial (focal) onset seizures
  2. Generalised tonic-clonic seizures
  3. Monotherapy for partial onset seizures in newly diagnosed epilepsy
30
Q

Levitiracetam common and rare ADRs

A

Common
1. Headache,
2. Vertigo (feeling of spinning)
3. Cough
4. Depression
5. Insomnia

Rare
1. Agranulocytosis
2. Suicide
3.Delirium
4. Dyskinesia

31
Q

Lamotrigine MOA

A

Block Voltage-gated Na channels, inhibit release of glutamate -> this impedes sutained repeititve neuronal depolarisation.

32
Q

Indication(s) for lamotrigine in seizure treatment

A
  1. Adjunctive or monotherapy treatment of partial (focal) seizures & generalised seizures (incl tonic-clonic seizures)
  2. Monotherapy for typical absence seizures
  3. Adjunctive or initial ASM for Lennox-Gastaut Syndrome (severe childhood epilepsy)
33
Q

Which ASMs follows linear and non-linear kinetics?

A

Linear: Levetiracetam, Lamotrigine
Non-linear: Phenytoin

34
Q

Lamotrigine common and rare ADRs

A

Common
- Headache, irritability/aggression, tiredness

Rare
- Agranulocytosis, hallucination, movement disorders (worsen PD), SJS/TEN, hepatic failure

35
Q

Topiramate place in therapy

A
  1. Monotherapy of partial (focal) seizures and generalised tonic-clonic seizures
  2. Adjunctive (only) for lennox-gastaut syndrome
  3. Migraine prophylaxis in adults (no tx)
36
Q

PK properties of Topiramate

A
  1. Linear
  2. Oral route
  3. Long plasma half life
  4. Renal clearance, not a potent inducer of drug metabolising enzymes
37
Q

Common and rare ADR of topiramate

A

Common
- Depression, somnolence, fatigue, nausea, weight change

Rare
- Neutropenia, mania, tremor, transient, blindness, SJS/TEN, hepatic failure

38
Q

Cafergot MOA

A
  1. Tonic action on vascular SM in extenal carotid network
  2. This leads to vasoconstriction by stimulating alpha-adrenergic (eg. a1, a2, b1,b2) & 5-HT receptors (5HT1b & 1d especially)
39
Q

ADM(E) of cafergot

A

A: rapid absorption, Tmax 1.5-2H, F=2-5%
D: High plasma protein binding.
M: Inhibit CYP3A4 (avoid macrolides) -> vasospam & tissue ischemia

40
Q

Common and Rare ADR of Cafergot

A

Common: NV
Rare: MI, ergotism (vascular ischemia)

41
Q

What agents should Cafergot be avoided with?

A

Vasoconstrictor agents eg. ergot alkaloids, sumatriptan, 5HT1 agonist

42
Q

Sumatriptan MOA

A

Selective agonist for serotonin (5-HT1B and
5-HT1D) receptors on:
● Trigeminal nerves (CN V):
inhibit neuropeptide release (eg VIP, sub P,
CGRP) → less vasodilation, less activation of nociceptors, reduces neurogenic inflammation

[● Intracranial extracerebral blood
vessels: direct vasoconstriction (relief of
migraine)
● No effect on cerebral blood flow
→ does not affect blood flow to brain]

43
Q

Which enzyme metabolises Sumatriptan?

A

Monoamine Oxidase A (MAO-A)

44
Q

Sumatriptan contraindications

A
  1. Concurrent adm with MAO-i
  2. Myocardial infarction
  3. Hypersensitivty to triptans
45
Q

Sumatriptan common anad rare SE

A

Common:
- Dysgeusia (unplesant taste), transient BP increase, flushing, sensation of cold, pressure, tightness

Rare:
- minor disturbances in LFT

46
Q

Erenumab MOA

A

Mab that blocks CGRP receptor. CGRP is a nociceptive neuropeptide at the trigeminal ganglion (causes pain).

47
Q

T/F? Erenumab is used for the acute treatment of migraine

A

False. Erenumab only for prophylaxis

depression (5 decks)

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