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CA Pharmacology Flashcards

1
Q

What is the MoA of phenytoin and carbamazepine?

A

Block voltage-dependent Na+ channels → ↓excitability

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2
Q

Phenytoin has a ________ therapeutic range, ________ kinetics, and ____________ PK r/s.
This causes phenytoin to have ____________ clearance, where clearance ________ with ________ concentration

A

Phenytoin has a narrow therapeutic range, saturable kinetics, and non-linear PK r/s (zero order kinetics).
This causes phenytoin to have capacity-limited clearance, where clearance decreases with increasing concentration

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3
Q

Can phenytoin be used in pregnancy?

A

No! Contraindicated!

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4
Q

Phenytoin has ________ bioavailability, and absorption is ________ but _______

A

Phenytoin has high bioavailability (95%), and absorption is complete but slow

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5
Q

Can phenytoin be taken together with enteral feeds? Why or why not?

A

No
↓bioavailability when taken together with enteral feeds (space apart by 2hrs)

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6
Q

True or false?

Taking a lower dose of phenytoin is more effective as compared to taking a higher dose

A

True
Lower bioavailability is observed at high doses >400mg/dose

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7
Q

Does phenytoin require dose adjustment in renal impariment? Why or why not?

A

True
Phenytoin is highly protein bound (90%).
Renal impairment may lead to uremia/ hypoalbuminuria → displace phenytoin and ↓protein binding → ↑free phenytoin and more toxic ADRs

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8
Q

True or false?

Phenytoin dominantly undergoes linear hepatic metabolism

A

False
Though phenytoin does undergo hepatic metabolism (100%), it is non-linear (capacity limited clearance)

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9
Q

Does phenytoin induce or inhibit metabolising enzymes? What enzymes does phenytoin affect?

A

Induce CYP2C9, CYP2C19, CYP3A, UGT

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10
Q

True or false

Carbamazepine is highly protein bound and hepatically eliminated

A

True
75-85% protein binding, 100% hepatic elimination (autoinduction)

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11
Q

Does carbamazepine induce or inhibit metabolising enzymes? What enzymes does phenytoin affect?

A

Induce CYP450, CYP1A2, CYP2C9, CYP2C19, CYP3A, UGT

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12
Q

Carbamazepine undergoes ________. This causes ________ clearance and ________ half-life of carbamazepine with repeated doses → ________ metabolism of other drugs

Maximal effect of the above occurs ________ after initiation.
Hence do not start with desired maintenance dose (risk of dose-dependent SEs), but instead gradually ________ dose over initial few weeks

A

Carbamazepine undergoes autoinduction. This causes increased clearance and shorter half-life of carbamazepine with repeated doses → increases metabolism of other drugs

Maximal effect of the above occurs 2-3 weeks after initiation.
Hence do not start with desired maintenance dose (risk of dose-dependent SEs), but instead gradually increase dose over initial few weeks

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13
Q

What is the MoA of sodium valproate?

A

Block voltage-dependent Na+ and Ca+ channels → ↓excitability
Also inhibits GABA transaminase → ↑GABA → ↑inhibition

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14
Q

HLA alleles associated with carbamazepine are:____________.
These alleles can cause ____ and _____

A

HLA-B1502 and HLA-A3101
Causes SJS and TEN

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15
Q

True or false

Phenytoin, carbamazepine, and sodium valproate can be used in all types of seizures

A

False
Phenytoin and carbamazepine cannot be used in absence seizures.

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16
Q

Sodium valproate experiences ____________. This causes ________ protein binding at ________ concentration.

A

um valproate experiences saturable protein binding. This causes decreased protein binding at increasing concentration.

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17
Q

True or false?

Sodium valproate has ____high/low____ protein binding.

A

High (75-95%)

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18
Q

Does sodium valproate induce or inhibit metabolising enzymes? What enzymes does valproate affect?

A

Inhibit CYP2C9, UGT, epoxide hydrolase

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19
Q

What is the MoA of diazepam?

A

Binding of GABA is ↑by benzodiazepine → ↑binding of GABA on GABA receptors on Cl- channels → Cl- channels open → ↑influx of Cl- ions → hyperpolarization → ↑inhibition

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20
Q

What happens during acute toxicity/ overdose of diazepam? What is used to treat it?

A

SEs: severe respiratory depression, esp when w alcohol
Tx: flumazenil (benzodiazepine antagonist)

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21
Q

True or false?

Diazepam and barbituates are associated with withdrawal symptoms/ tolerance and dependence

A

True

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22
Q

True or false

Benzodiazepines have higher dose-dependent depression of CNS as compared to barbiturates

A

False
Opposite!

Benzodiazepines reaches a peak. Whereas barbiturates just keeps increasing linearly so more dangerous, hence not used often nowadays

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23
Q

Tolerance and dependence occurs due to ______________.
Withdrawal effects involve:____________ (4)
Is important to withdraw ___________

A

Frequency of use
Disturbed sleep, rebound anxiety, tremor, and convulsions
Gradually

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24
Q

Diazepam is a ________ benzodiazepine.

A

Long-acting

Lasts around 1-2 days

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25
What is the MoA of Phenobarbital?
Same MoA as benzodiazepines, but at a site distinct from them ## Footnote Binding of GABA is ↑by benzodiazepine → ↑binding of GABA on GABA receptors on Cl- channels → Cl- channels open → ↑influx of Cl- ions → hyperpolarization → ↑inhibition
26
# True or false? Indication of diazepam is all seizures?
True
27
What are the indications of phenobarbital?
1. Sedative-hypnotic 2. AED for paediatric/ neonatal pts (IV loading dose f/b IV/PO maintenance dose)
28
# True or false? Flumazenil is effective for treating barbiturate overdose
**False** Flumazenil only blocks benzodiazepine sites, not effective for treating barbiturate overdose
29
What are the indications of levetiracetam? State which are monotherapy and which are adjunct.
**Monotherapy:** partial onset seizures in newly diagnosed epilepsy **Adjunct:** partial onset, myoclonic, and primary generalised tonic-clonic seizures
30
What is the MoA of lamotrigine?
Block voltage-gated Na+ channels → inhibit release of glutamate → prevents sustained repetitive neuronal depolarization
31
What are the indications of lamotrigine? State which are monotherapy, adjunct, and initial.
**Adjunct/ monotherapy:** partial and generalised seizures **Adjunct/ initial:** Lennox-Gastaut syndrome **Monotherapy:** typical absence seizures
32
What are the DDIs of lamotrigine? Which anti-epileptic drug increases or decreases t1/2?
↓t1/2: carbamazepine and phenytoin ↑t1/2: valproate
33
What are the indications of topiramate? State which are monotherapy, adjunct, and prophylaxis.
Monotherapy: partial and generalised seizures Adjunct: Lennox-Gastaut syndrome Prophylaxis: migraine headaches in adults ***(not for acute tx!)***
34
# True or false? Topiramate is predominantly cleared renally
True
35
# True or false? Topiramate is a potent inducer of drug-metabolising enzymes
False
36
# True or false All ASM may result in an increase in suicidal ideation and behvaiour. Should discontinue drug when patient experiences/ exhibits such symptoms
**False!** Risk of stopping ASM is greater than the benefit of discontinuing it to reduce SEs Close monitoring done instead
37
List 3 antiepileptic drugs
1. Phenytoin 2. Carbamazepine 3. Sodium valproate 4. Diazepam 5. Phenobarbital 6. Levetiracetam 7. Lamotrigine 8. Topiramate
38
What is the MoA of cafergot?
**Ergotamine:** Alpha-adrenergic and 5-HT receptors (5-HT1B/1D) agonists on intracranial vessels → vasoconstriction Inhibit norepinephrine uptake and adrenoreceptors → prolonged vasoconstriction **Caffeine:** Adenosine A1, A2A and A2B receptor antagonists → vasoconstrict cerebral vasculature May ↑GI absorption of ergotamine by ↑solubility of ergotamine and ↓ gastric pH
39
Cafergot is a combination of ________ and ________
Caffeine and ergotamine
40
What is the indication of cafergot?
Acute tx of migraine (given at 1st symptom of attack)
41
What are the ADRs of cafergot?
Common: N/V, cramps, insomnia, transient lower limb muscle pain Rare: hypersensitivity, MI, ergotism (vascular ischaemia)
42
Where is cafergot contraindicated in?
Pre-existing conditions: * Stroke/ TIA * Ischemic coronary artery disease * Coronary artery vasospasm * Uncontrolled HTN * Peripheral vascular disease * Gastrointestinal ischemia * Hx of hemiplegic/ basilar migraine Concomitant use of triptans within 24hrs Potent CYP3A4 inhibitors (proteases inhibitors, macrolides) ## Footnote (similar to triptans, vasoconstriction)
43
Fill in the blanks, regarding the PK of cafergot: Routes: ________ F = _______ _______ absorbed, max plasma concentrations reached in _______ _______ protein bound CYP_____ __________
Routes: **Oral, rectal** F = **2-5%** *(low)* **Rapidly** absorbed, max plasma concentrations reached in **1.5-2hrs** **Highly** protein bound CYP**3A4 inhibitor**
44
What are the DDIs of cafergot?
CYP3A4 inhibitors (causes increased ergot toxicity → vasospasm and tissue ischaemia) Vasoconstrictor agents: ergot alkaloids, sumatriptan, other 5HT1 agonists
45
# True or false? Triptans have a more potent vasoconstriction effect than ergotamine.
**False!** Ergotamine and dihydroergotamine have more potent vasoconstriction effect (hit more receptors than triptans), hence its place in practice have been mostly replaced by triptans
46
What is the MoA of sumatriptan?
Selective serotonin (5-HT1B and 5-HT1D) receptor agonist →: * Vasoconstriction of intracranial extracerebral blood vessels * Inhibition of vasoactive peptide release by trigeminal neurons * Inhibition of nociception neurotransmission within trigeminocervical complex ## Footnote ↓ neurogenic inflammation/ inhibits trigeminal nerve activity, but does not alter cerebral blood flow)
47
What is the indication of sumatriptan?
Acute tx of migraine, should be taken early when pain intensity is mild
48
What are the ADRs of sumatriptan?
Common: dysgeusia, chills, pressure, tightness, serotonin syndrome (transient ↑BP, flushing) Rare: minor disturbances in LFTs
49
Where is sumatriptan contraindicated in?
Pre-existing conditions: * Stroke/ TIA * Ischemic coronary artery disease * Coronary artery vasospasm * Uncontrolled HTN * Peripheral vascular disease * Gastrointestinal ischemia * Hx of hemiplegic/ basilar migraine Concomitant use of MAOi or within 2w of discontinuation of MAOi therapy Concomitant use of ergotamine-containing/ ergot-type medication within 24hrs ## Footnote (similar to ergotamines, vasoconstriction)
50
What are the routes of administration for sumatriptan?
Oral, nasal, IV
51
Sumatriptan is eliminated by ________ mediated by ______
Oxidative metabolism, MAO
52
# True or false? If sumatriptan is not effective in treating patient's medication, should change drug class.
**False** Lack of response to one triptan does not predict response to other triptans -> trial of another triptan
53
# True or false? Triptans can cause recurrence of migraine, and so an additional dose should be taken to alleviate this.
**True** 20-50% of pts experience recurrence of migraine **48hrs after** 1st dose → **take additional dose of triptan**
54
What is the MoA of CGRP mABs?
Monoclonal Ab CGRP (receptor) inhibitor → prevent signalling CGPR: calcitonin gene-related peptide, is a nociceptive neuropeptide at trigeminal ganglion and causes vasodilation → trigger migraine-like headaches
55
List 2 CGRP mABs. State where do they exert their effect on.
Block CGRP receptor on trigeminal nerve: erenumab Block CGRP: eptinezumab, fremanezumab, galcanezumab
56
CGRP stands for:
Calcitonin gene-related peptide
57
What is the indication of CGRP mABs?
Prophylaxis of migraine in adults
58
What are the ADRs of CGRP mABs?
Hypersensitivity, injection site reactions, constipation, nausea, pruritus, raynaud, HTN, joint pain, nasopharyngitis ? ## Footnote Raynaud: a disorder that causes decreased blood flow to the fingers. In some cases, it also causes less blood flow to the ears, toes, nipples, knees, or nose.
59
Clinical benefits of CGRP mABs can be seen within ________
3 months, but note that long-term partial blockade effect is unknown
60
What is the route of administration of CGRP mABs? How often is the dosing frequency?
SC, monthly
61
Erenumab has ________ kinetrics at therapeutic doses, as CGRP receptor binding is ______
Linear, saturated
62
What is the MoA of NSAIDs?
Inhibit prostaglandin synthesis → prevent neurologically mediated inflammation in the trigeminovascular system
63
What is the indication of NSAIDs?
Mild to moderate migraine attacks
64
What are the ADRs of NSAIDs? When should NSAIDs be used with caution/ avoided?
GI discomfort (dyspepsia, N/V, diarrhoea), CNS (somnolence, dizziness) **Caution/ avoid:** prev PUD, renal disease, severe cardiovascular disease, hypersensitivity to aspirin
65
What are some **CNS** dose-dependent common adverse effects of ASMs?
Headache, drowsiness, fatigue, dizziness, confusion, nystagmus, ataxia, visual disturbances, mental changes ## Footnote can anyhow whack and be correct ~ ML
66
What are some **GI** dose-dependent common adverse effects of ASMs?
N/V ## Footnote can anyhow whack and be correct ~ ML
67
What are some **psychiatric & cognitive** dose-dependent common adverse effects of ASMs?
unusual behaviour (behavioural changes), slurred speech ## Footnote can anyhow whack and be correct ~ ML
68
# What are some strategies to mitigate ASM dose-dependent A/E? * Initiate at ____ dose and slowly ____ dose * Avoid ____ ____ ____ * Restrict therapy to ____ drug only * Administer largest dose at ____ (for bothersome symptoms) * Give in ____ ____ * ____ ____ formulations * Reduce ____ ____ dose
* Initiate at **low** dose and slowly **uptitrate** dose * Avoid **large dosage changes** * Restrict therapy to **one** drug only * Administer largest dose at **bedtime** (for bothersome symptoms) * Give in **divided doses** * **Sustained release** formulations * Reduce **total daily** dose
69
What are some idiocyncratic adverse effects of ASM?
* Blood dyscrasia (aplastic anaemia, agranulocytosis), * Hepatotoxicity (1st Gen ASMs) * Pancreatitis (SV) * Lupus-like rxn * Exfoliative dermatitis * Hypersensitivity (SJS, TEN), rash
70
What PGx testing can be conducted for CBZ-induced SJS/TEN?
**HLA-B*1502** if positive: avoid carbamazepine and phenytoin
71
# Do you know the lamotrigine dosing guidelines? If a patient taking valproate is initiated on lamotrigine, how do you uptitrate his dose?
Week 1-2: Take 25mg EOD Week 3-4: Take 25mg OD Week 5 until maintenance: Increase by 25-50mg per day every 1-2 weeks Usual Maintenance dose (in 1-2 divided doses): With Valproate only: 100-200mg OD With Valproate and other meds (induce glucuronidation): 100-400mg OD ## Footnote im so sorry
72
# Do you know the lamotrigine dosing guidelines? If a patient is initiated on lamotrigine, how do you uptitrate his dose?
Week 1-2: Take 25mg OD Week 3-4: Take 50mg OD Week 5 until maintenance: Increase by 50mg per day every 1-2 weeks Usual Maintenance dose (in 1-2 divided doses): 225-375mg per day ## Footnote im so sorry
73
# Do you know the lamotrigine dosing guidelines? If a patient taking phenytoin is initiated on lamotrigine, how do you uptitrate his dose? ## Footnote or carbamazepine/phenobarbital/primidone
Week 1-2: Take 50mg OD Week 3-4: Take 100mg OD (2 divided doses) Week 5 until maintenance: Increase by 100mg per day every 1-2 weeks Usual Maintenance dose (in 2 divided doses): 300-500mg per day ## Footnote im so sorry
74
List at least 3 common ASMs with aromatic rings
Carbamazepine, Lamotrigine, Oxcarbazepine, Phenytoin, Phenobarbital
75
What component of aromatic ASMs causes immunogenecity through interactions with proteins or cellular macromolecules?
Arene-oxide intermediate
76
Which ASM can cause Gingival Hyperplasia?
Phenytoin
77
Which ASM can cause Hirsutism?
Chronic Phenytoin Therapy
78
Which ASM can cause Alopecia?
Valproate
79
Which ASM can cause Peripheral Neuropathy?
(long term) Phenytoin, Carbamazepine, Phenobarbitone ## Footnote can try folate supplementation
80
Which ASM can cause Osteomalacia?** How?**
Phenytoin, Carbamazepine, Phenobarbitone increased Vit D clearance, leading to secondary hypoparathyroidism, increased bone turnover and decreased bone density
81
Which ASM can cause Increased Weight Gain?
Valproate ## Footnote gradually reversible with discontinuation
82
Which ASM can cause Anorexia / Weight Loss?
Topiramate / Felbamate ## Footnote Reversible with discontinuation
83
Which ASM can cause Suicidal Ideation?
ALL ASMs. Just start ASMs though.
84
Which ASM can cause Tolerance/ Dependence?
Benzodiazapems / Barbiturates
85
What are the associated withdrawal effects of Benzodiazepams / Barbiturates?
Disturbed sleep, rebound anxiety, tremor, convulsions
86
Choose the most appropriate answer regarding **gabapentin and pregabalin**: * hepatic/renal elimination * low/high protein binding * no/have DDIs
* **Renal** elimination * **Low** (0%) protein binding * **No** DDIs
87
Choose the most appropriate answer regarding **clozabam**: * hepatic/renal elimination * low/high protein binding * no/have DDIs
* **Renal** elimination * **High** (80-90%) protein binding * **Have** DDIs
88
What are the 4 pharmacological classes to look out for DDIs w ASM?
* Antidepressants and antipsychotics * Immunosuppressive therapy * Antiretroviral therapy * Chemotherapeutic agents
89
What is the active component of Carbamazepine?
its active metabolite: Carbamazepine-10,11-epoxide (CYP3A4)

PR3153 (10 decks)

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