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53 > 4. Pharmaco > Flashcards

4. Pharmaco Flashcards

1
Q

Seizure

A

a paroxysmal (unexpected) event due to abnormal, hypersynchronous discharge from a mass of CNS neurons

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2
Q

manifestation of seizure

A

Diverse manifestation: convulsion (observable) to an experience (subjective)

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3
Q

is a single seizure due to correctable or avoidable circumstance (ie provoked) considered an epilepsy?

A

not an epilepsy (eg due to alcohol, hypoglycaemia, pyrexia, sleep deprivation)

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4
Q

epilepsy pathophysiology

A

a seizure occurs when there is excessive synchronous depolarisation due to unbalanced excitatory and inhibitory receptor/ ion channel function which favours depolarisation → dysregulated/ unregulated discharge

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5
Q

types of seziure

A
  • generalised (both hemisphere affected, consciousness affected) -> tonic clonic, absence
  • partial seizures (half hemisphere affected) -> simple (consciousness not impaired), complex (consciousness impaired)
  • status epilepticus
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6
Q

rationale for anti-epileptics

A
  • decrease membrane excitability by altering Na+ and Ca2+ conductance during action potential
  • enhanced effects of inhibitory GABA NT (GABA when bind to receptor opens Cl- channels allowing Cl- ions to enter)
  • drugs should be individualised and started on monotherapy initially
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7
Q

phenytoin MOA

A

block voltage-dependent Na+ channels → decreases Na+ entry → decrease AP discharge → decrease excitation of neuron

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8
Q

phenytoin indication

A

for all types of seizures except absence seizures

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9
Q

characteristics of phenytoin

A
  • relative narrow therapeutic range
  • teratogenic
  • non-linear saturation kinetics profile (need TDM)
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10
Q

MOA of carbamazepine

A

blockade of voltage-dependent Na+ channels (similar to phenytoin)

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11
Q

Indiction of carbamazepine

A

for all types of seizures except absence seizures

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12
Q

characteristics of carbamazepine

A

Autoinduction: hepatic CYP450 enzyme inducer, T1/2 shortens with repeated/increasing doses → accelerate metabolism of carbamazepine and other drugs

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13
Q

carbamazepine pgx

A

HLA-B*1502 positive - increased risk of SJS/ TEN (require PGx testing before drug initiation)

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14
Q

MOA of valproate

A
  • blockade of voltage-dependent Na+ and Ca2+ channels
  • inhibit GABA transaminase (enzyme that breakdown GABA) → increase GABA (inhibitory NT)
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15
Q

indication for valproate

A

for all types of seizures including absence seizures

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16
Q

characteristics of valproate

A

strongly bound to plasma proteins, displaces other antiepileptics/ drugs (ie DDI)

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17
Q

Adverse effects of antiepileptics (dose related)

A

drowsiness, confusion, nystagmus (shifty eyes), ataxia (unable to keep balance), slurred speech, nausea, unusual behaviour, mental changes, coma

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18
Q

Adverse effects of antiepileptics (non dose related)

A

hirsutism, acne, gingival hyperplasia (swollen gums), folate deficiency, osteomalacia (softening of bone), hypersensitivity (eg SJS)

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19
Q

MOA of benzodiazepines

A

bind to regulatory site of of GABA receptors (different binding site from GABA) → increase GABA mediated Cl- ions influx → hyperpolarisation → neurons not firing

  • potentiates inhibitory effect of GABA (only works when GABA is present)
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20
Q

acute toxicity/overdose of benzodiazepines

A

acute toxicity/ overdose - cause severe respiratory depression, especially when used concurrently with alcohol

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21
Q

tx of benzodiazepine overdose

A

flumazenil (benzodiazepine competitive antagonist)

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22
Q

SE of benzodiazepine

A

drowsiness, confusion, amnesia (memory loss), impaired muscle coordination, tolerance and dependence

23
Q

MOA of phenobarbital

A

potentiates GABA mediated Cl- ions entry (inhibitory effects) but different site from benzodiazepines (flumazenil not effective for overdose of barbiturate)

24
Q

SE of phenobarbital

A

Severe withdrawal symptoms (more severe than benzodiazepines), greater risk of causing CNS effects especially at higher doses as compared to benzodiazepines

25
Q

Levetiracetam indication

A
  • adjunctive tx
  • can be used as monotherapy for partial onset seizures
  • not effective for absence seizures
26
Q

PK characteristics of levetiracetam

A
  • highly soluble and permeable
  • PK profile is linear with low and intra and inter subject variability (different from phenytoin)
27
Q

route of administration for levetiracetam

A

IV infusionor PO

28
Q

SE of levetiracetam

A
  • common: headache, vertigo, cough, depression, insomnia
  • rare: agranulocytosis, suicide, delirium, dyskinesia (involuntary movement)
29
Q

MOA of lamotrigine

A
  • blocks voltage-gated sodium channels
  • inhibit release of glutamate
30
Q

indication of lamotrigine

A
  • adjunctive/ monotherapy tx
  • can be used as monotherapy for absence seizures (alternative to valproate)
31
Q

PK of lamotrigine

A
  • linear PK, oral route (chewable)
  • shorter half-life in children
  • half-life reduced with co-administration with carbamazepine and phenytoin and increased with valproate
32
Q

SE of lamotrigine

A
  • common: headache, irritability/ aggression, tiredness
  • rare: agranulocytosis, hallucination, movement disorders, SJS/TEN, hepatic failure
33
Q

indication of topiramate

A
  • monotherapy for partial seizures and generalised seizures (tonic clonic)
  • Prophylaxis of migraine headaches in adults (not for acute tx)
34
Q

PK characteristics of topiramate

A
  • linear PK, oral route, long plasma half life
  • renal clearance
  • not a potent inducer of drug-metabolising enzymes
35
Q

SE of topiramate

A
  • common: depression, somnolence, fatigue, nausea, weight change
  • rare: neutropenia, mania, tremor, transient blindness, SJS/TEN, hepatic failure
36
Q

when are TDM needed?

A
  1. Assess compliance
  2. Assess symptoms due to ASM toxicity
  3. Titration of phenytoin dose (phenytoin needs TDM)
37
Q

headache/migraine pathophysiology

A

vasodilation of intracranial extracerebral blood vessels → activation of perivascular trigeminal nerves → release vasoactive neuropeptides → neurogenic inflammation

38
Q

sx of headache/migraine

A

nausea, vomiting, photophobia, phonophobia (scared of loud noises)

39
Q

role of serotonin in migraine

A

serotonin is an important mediator of migraine
- Serotonin agonist for vascular and neuronal 5HT1 receptor cause vasoconstriction of meningeal blood vessels and inhibit vasoactive neuropeptide release and pain signal transmission.

40
Q

MOA of cafergot

A

tonic action on vascular smooth muscles in the intracranial extracerebral blood vessels → vasoconstriction by stimulating alpha-adrenergic and 5HT (1B & 1D) receptors

41
Q

indication of cafergot

A

for ACUTE tx of migraine

42
Q

PK of cafergot

A
  • oral/rectal, rapidly absorbed (max plasma conc in 1.5-2hr)
  • high plasma protein binding, low F
  • inhibit CYP3A4 (avoid use with other 3A inhibitors like macrolides → can elevate ergot toxicity causing vasospasm and tissue ischemia)
43
Q

SE of cafergot

A
  • common: nausea and vomiting
  • rare: hypersensitivity, MI, ergotism (vascular ischemia)
44
Q

DDI

A

Should not be used with other vasoconstrictor agents (eg ergot derivatives, sumatriptan, 5HT1 agonists)

45
Q

MOA of sumatriptan

A
  • selective 5HT 1B/1D receptor agonist → selectively constricts carotid arterial circulation (does not affect cerebral blood flow)
  • inhibit trigeminal nerve activity (eg vasoactive peptides and inflammatory mediators)
46
Q

Indication of sumatriptan

A

acute tx of migraine with or without aura

47
Q

PK of sumatriptan

A
  • oral, nasal, IV
  • rapidly absorbed, low plasma binding, eliminated primarily by MAO (type A)
48
Q

CI of sumatriptan

A

hypersensitivity to triptans, concomitant use with MAOi, MI

49
Q

SE of sumatriptan

A
  • common: dysgeusia (unpleasant taste), transient BP rise, flushing, cold, pressure, tightness, serotonin syndrome
  • rare: minor disturbances in liver function tests
50
Q

MOA of erenumab

A

is a monoclonal antibody that inhibits CGRP receptors
- CGRP are nociceptive neuropeptide at the trigeminal ganglion, a vasodilator
- CGRP increase with migraine

51
Q

indication of erenumab

A

prophylaxis of migraine in adults who have at least 4 migraine days per mth

52
Q

PK characteristics of erenumab

A
  • SC q monthly, benefit seen within 3mths
  • linear kinetics at therapeutic doses (CGRP receptor binding is saturated)
53
Q

SE of erenumab

A

hypersensitivity reactions, injection site reactions, constipation, prutitis

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