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PR3153 CA1 > IC4: Pharmacology > Flashcards

IC4: Pharmacology Flashcards

1
Q

What molecule synthesises neurotransmitters?

A

ChAT (choline acetyltransferase)

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2
Q

What are the 2 receptors that neurotransmitters bind to?

A

GPCR (mAChR = muscarinic)
Ion channels (nAChR = nicotinic)

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3
Q

What are the 2 receptors that neurotransmitters bind to?

A

GPCR (mAChR = muscarinic)
Ion channels (nAChR = nicotinic)

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4
Q

What are the 4 main neurotransmitters found in the body and what kind of synapses are they usually involved in?

A

Glutamate - excitatory
GABA - inhibitory
Acetylcholine - learning, arousal and reward
Dopamine - motor systems and reward

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5
Q

what are the 3 functions of the blood brain barrier?

A
  1. Modulation of the entry of metabolic substrates (especially glucose)
  2. Control of ion movement → Na-K-ATPase in barrier cells pump Na into the CSF and pumps K out into blood
  3. Prevention of access to CNS by toxins and peripheral neurotransmitters
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6
Q

What is the non-saturable method of crossing the BBB and what characteristics make a drug a good candidate for this method?

A

Transmembrane passive diffusion

Drugs w LMW, high lipid solubility (not too high)

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7
Q

What is the saturable method of crossing the BBB and what are the 4 things that regulate it

A

Transporter systems

Regulated by cerebral blood flow, co-factors, hormones and efflux transporters (eg. P-glycoprotein)

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8
Q

Describe generalised seizures

A

involve the entire brain, will cause loss of consciousness

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9
Q

What are the 4 main types of generalised seizures?

A

Tonic clonic (Grand mal)
Absence (Petit mal)
Myoclonic
Atonic

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10
Q

What are the 2 types of partial seizures

A

Simple (consciousness not impaired)
Complex (impaired consciousness)

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11
Q

What is phenytoin’s MOA

A

Blocks VG-Na+ channels, decreasing Na+ influx hence preventing the formation of an AP

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12
Q

Where can phenytoin be used

A

All but absence seizures

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13
Q

What must be taken note of for PHT monitoring

A

Narrow tp range, w saturation kinetics, non-linear relationship between dose and plasma concentration necessitating titration and monitoring

PHT is also teratogenic

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14
Q

What is CBZ’s MOA

A

Blocks VG-Na+ channels, decreasing Na+ influx hence preventing the formation of an AP

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15
Q

Where can CBZ be used?

A

All but absence seizures

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16
Q

What enzymes are implicated with CBZ?

A

CYP450 inducer
Its own t-half decreases with repeated doses and increases elimination of other drugs

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17
Q

What must be screened for prior to CBZ use?

A

HLA-B*1502 (SJS/TEN risk)

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18
Q

What is valproate’s MOA? (3)

A

Blocks VG-Na+ AND Ca2+ channels, decreasing Na+ influx hence preventing the formation of an AP

Also inhibits GABA transaminase (hence increasing GABA levels)

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19
Q

Where can valproate be used?

A

Suitable for ALL seizure types

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20
Q

What should be taken note of for valproate?

A

Highly protein bound and will displace other ASMs

21
Q

What are the general dose-related SEs for ASMs? (6)

A

drowsiness, confusion, ataxia, slurred speech, mental changes, coma

22
Q

What are the general non-dose-related SEs for ASMs? (6)

A

hirsutism, acne, gingival hyperplasia, folate deficiency, osteomalacia, HS rxns

23
Q

How can ODs occur with benzodiazepines and what should be used to treat it?

A

Overdose and/or concurrent use with alcohol

Treat with flumazenil

24
Q

Why arent benzodiazepines and barbituates used as often?

A

High instances of tolerance and dependence

Barbituates have a worse profile than benzodiazepines

25
Q

How do barbituates differ from benzodiazepines in terms of MOA?

A

Barbituates also potentiate GABA(A) mediated Cl- currents but at a site distinct from benzodiazepines

(hence flumazenil does not work in cases of overdose)

26
Q

What are the 3 other non-first line ASMs?

A

Levetiracetam
Lamotrigene
Topiramate

27
Q

What is levetiracetam used for? (3)

A

Adjunctive therapy for:
partial onset seizures
myoclonic seizures
primary generalised tonic-clonic seizures

28
Q

What are some common and rare SE for levetiracetam? (3+3)

A

Common: HA, vertigo, insomnia
Rare: agranulocytosis, suicide, delirium

29
Q

What is lamotrigene’s MOA?

A

Blocks VG-Na+ channels and inhibits glutamate release

30
Q

What is lamotrigene indicated for? (3)

A

adjunctive or monotherapy treatment of:

partial seizures
generalised seizures (including absence)
lennox-gastaut syndrome

31
Q

What are some rare SEs of lamotrigene? (4)

A

agranulocytosis
movement disorders (worsens Parkinson’s)
SJS/TEN
hepatic failure

32
Q

What is topiramate indicated for? (2 monotx, 1 adj)

A

monotherapy for:
partial
generalised seizures

adjunctive therapy for:
Lennox-Gastaut syndrome

33
Q

Under which 3 circumstances should monitoring for ASMs be done?

A
  1. assess compliance in pts w refractory epilepsy (but claim to be compliant)
  2. assess sx due to ASM toxicity (especially w PHT)
  3. to titrate PHT dose
34
Q

Describe the general pathophysiology of a headache (4) VTNI

A

Vasodilation of intracranial extracerebral blood vessels →

activation of the perivascular trigeminal nerves →

release vasoactive neuropeptides →

promote neurogenic inflammation

35
Q

Which biological molecule has been implicated as an important mediator of migraines?

A

Serotonin (5-HT)

36
Q

What is the general flow in migraine pharmacological management?

A

NSAIDs or paracetamol first

If fail or in cases of moderate to severe migraines, try cafergot, sumatriptan or erenumab

37
Q

What is cafergot and what is its MOA? (3)

A

caffeine + ergotamine

tonic action on vascular smooth muscles in the external carotid network →

stimulates α-adrenergic and 5-HT receptors →

leading to vasoconstriction

38
Q

When is cafergot indicated?

A

Acute tx of migraine, given at first sx of attack

39
Q

What other drugs should cafergot not be given with? (2)

A
  1. other CYP3A4 inhibitors (eg. macrolides)
  2. other vasoconstrictors (ergot alkaloids, sumatriptan, other 5HT-1 agonists)
40
Q

What are the two main severe SE to look out for with cafergot

A

MI and ergotism (vascular ischemia)

41
Q

What is sumatriptan’s MOA (2)

A

selective vascular serotonin (5-HT1d) receptor agonist →

selectively constricts the carotid arterial circulation but does not alter cerebral blood flow →

inhibits trigeminal blood flow

42
Q

What is sumatriptan indicated for?

A

acute treatment of migraine with or without aura

43
Q

What are the contraindications for taking sumatriptan? (3)

A

HS to triptans
MI
concurrent administration with MAOis

44
Q

What is the main rare SE of sumatriptan?

A

minor disturbances in LFTs

45
Q

What is CGRP?

A

Nociceptive neuropeptide at the trigeminal ganglion that acts as a vasodilator (more neuropeptide comes out, causes more pain)

46
Q

What is erenumab’s MOA (2)

A

Monoclonal antibody CGRP inhibitor

blocks nociceptive perception (pain is decreased)
alleviates vasodilation (less neuropeptide is released)

47
Q

What is erenumab indicated for?

A

prophylaxis for migraine in adults who have at least 4 migraine days a month

48
Q

How should erenumab be taken

A

SQ injection monthly, clinical benefit typically seen within 3 months

PR3153 CA1 (5 decks)

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