DNB CET Pharmacology Syllabus

Pharmacology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Pharmacology in DNB CET, not a summary of it.

1. 1

   General Pharmacology

   4 topics

   • Pharmacokinetics - absorption, distribution, metabolism, excretion
   • Pharmacodynamics, receptors and dose-response
   • Drug interactions and adverse drug reactions
   • Pharmacovigilance and clinical trial phases
2. 2

   Autonomic and CNS Pharmacology

   5 topics

   • Cholinergic and adrenergic agonists and antagonists
   • Sedative-hypnotics and antiepileptics
   • Antipsychotics, antidepressants and lithium
   • Opioid analgesics and general anesthetics
   • Drugs for Parkinsonism and neurodegeneration
3. 3

   Cardiovascular, Endocrine and Autacoid Pharmacology

   4 topics

   • Antihypertensives and antianginal drugs
   • Antiarrhythmics and heart failure drugs
   • Antidiabetics, insulin and thyroid drugs
   • Histamine, NSAIDs and prostaglandins
4. 4

   Chemotherapy

   4 topics

   • Beta-lactams, macrolides and aminoglycosides
   • Antitubercular and antiretroviral drugs
   • Antifungal, antimalarial and antihelminthic agents
   • Anticancer drugs and mechanisms of resistance

Pharmacology flashcards for DNB CET

25 of 52 cards from the Pharmacology deck — real questions with worked answers.

1. Define bioavailability (F) and explain why oral bioavailability is often less than 100%.

   Bioavailability is the fraction of an administered dose that reaches the systemic circulation unchanged. For IV drugs F = 1 (100%). Oral F is reduced by incomplete absorption across the gut wall and by first-pass (presystemic) metabolism in the gut wall and liver. F = (AUC oral / AUC IV) for equal doses.

2. What is the apparent volume of distribution (Vd), its formula, and what does a very large Vd indicate?

   Vd = amount of drug in body / plasma concentration. It is the theoretical volume needed to contain the total drug at the measured plasma concentration. A very large Vd (e.g. >42 L, body water) indicates extensive tissue binding/sequestration (e.g. digoxin, chloroquine), meaning little drug stays in plasma.

3. Distinguish zero-order from first-order kinetics of drug elimination.

   First-order: a constant fraction of drug is eliminated per unit time; rate is proportional to concentration; t1/2 is constant (most drugs). Zero-order: a constant amount is eliminated per unit time because enzymes are saturated; rate is independent of concentration; t1/2 increases with dose. Examples of zero-order: ethanol, phenytoin (high dose), aspirin (high dose), theophylline.

4. Compare Phase I and Phase II drug metabolism reactions.

   Phase I reactions (oxidation, reduction, hydrolysis; mainly cytochrome P450) introduce or unmask a functional group, often producing a more polar and sometimes active/toxic metabolite. Phase II reactions are conjugation (glucuronidation, sulfation, acetylation, glutathione, methylation) that attach an endogenous moiety to make the drug water-soluble and usually inactive for excretion.

5. Give the formula relating half-life (t1/2) to clearance (CL) and volume of distribution (Vd).

   t1/2 = 0.693 x Vd / CL. Half-life is directly proportional to volume of distribution and inversely proportional to clearance. It takes about 4-5 half-lives to reach steady state and to eliminate a drug after stopping.

6. Name important CYP450 enzyme inducers and inhibitors and the clinical significance.

   Inducers (decrease drug levels, may cause failure): rifampicin, phenytoin, phenobarbitone, carbamazepine, chronic alcohol, St John's wort, griseofulvin. Inhibitors (increase drug levels, risk of toxicity): ketoconazole/azoles, erythromycin/clarithromycin, cimetidine, ciprofloxacin, grapefruit juice, ritonavir, valproate, isoniazid.

7. What is the difference between drug affinity, efficacy, and potency?

   Affinity is the tendency of a drug to bind its receptor (reflected by Kd; higher affinity = lower Kd). Efficacy (intrinsic activity) is the maximal effect a drug can produce once bound (full agonist = 1, antagonist = 0). Potency is the amount of drug needed to produce a given effect (lower EC50/ED50 = more potent); potency depends largely on affinity.

8. Differentiate a full agonist, partial agonist, inverse agonist, and antagonist.

   Full agonist: binds and produces maximal response (efficacy = 1). Partial agonist: binds but produces submaximal response even at full occupancy; can antagonize a full agonist (e.g. buprenorphine, pindolol). Inverse agonist: produces an effect opposite to the agonist at a constitutively active receptor (e.g. some beta-carbolines). Antagonist: binds with affinity but zero efficacy, blocking agonist action.

9. How do competitive and non-competitive (irreversible) antagonists differ on a dose-response curve?

   Competitive antagonist: shifts the agonist dose-response curve to the right in parallel; Emax is unchanged (surmountable by more agonist). Non-competitive/irreversible antagonist: reduces Emax and the curve cannot be fully restored by more agonist (insurmountable); apparent potency may also fall.

10. Define therapeutic index (TI) and explain why a high TI is desirable.

    Therapeutic index = TD50 / ED50 (or LD50/ED50 in animals), the ratio of the dose causing toxicity to the dose producing the therapeutic effect. A high TI means a wide safety margin. Drugs with a narrow TI (digoxin, warfarin, lithium, theophylline, phenytoin, aminoglycosides) require monitoring.

11. Classify adverse drug reactions into the main pharmacological types (Rawlins-Thompson A-F).

    Type A (Augmented): dose-dependent, predictable extension of pharmacology, common (e.g. bleeding with warfarin). Type B (Bizarre): dose-independent, unpredictable, immunologic/idiosyncratic (e.g. anaphylaxis, malignant hyperthermia). Type C (Chronic/continuous use). Type D (Delayed, e.g. teratogenesis, carcinogenesis). Type E (End of use/withdrawal). Type F (Failure of therapy).

12. Describe the mechanism of a pharmacokinetic vs a pharmacodynamic drug interaction with an example of each.

    Pharmacokinetic interaction alters absorption, distribution, metabolism, or excretion of a drug, changing its concentration (e.g. rifampicin induces CYP and lowers oral contraceptive levels). Pharmacodynamic interaction occurs at the site of action without changing concentration (e.g. additive CNS depression with alcohol plus benzodiazepines; synergistic bleeding with aspirin plus warfarin).

13. What are the phases of clinical trials (Phase 0 to Phase IV) and their purpose?

    Phase 0: microdosing pharmacokinetic/pharmacodynamic exploration in a few subjects. Phase I: safety, tolerability, PK in healthy volunteers (20-80). Phase II: efficacy and dose-finding in patients (100-300). Phase III: large randomized controlled efficacy/safety trials for marketing approval (1000s). Phase IV: post-marketing surveillance for long-term/rare adverse effects.

14. Define pharmacovigilance and explain the WHO scale for assessing ADR causality.

    Pharmacovigilance is the science of detecting, assessing, understanding, and preventing adverse effects of drugs after marketing. The WHO-UMC causality categories are: Certain, Probable/Likely, Possible, Unlikely, Conditional/Unclassified, and Unassessable. Spontaneous reporting (e.g. yellow card) is a key tool.

15. Compare the actions of muscarinic agonists and the effects of muscarinic blockade (atropine).

    Muscarinic agonists (pilocarpine, bethanechol, ACh) cause miosis, accommodation for near vision, bradycardia, bronchoconstriction, increased glandular secretions (sweat, saliva), increased gut/bladder motility (SLUDGE). Atropine (antagonist) causes mydriasis, cycloplegia, tachycardia, bronchodilation, dry mouth, urinary retention, and antagonizes these effects.

16. What is the treatment of organophosphate (anticholinesterase) poisoning and the rationale?

    Atropine to block excess muscarinic effects (give until secretions dry/atropinization), plus pralidoxime (2-PAM) to reactivate acetylcholinesterase by removing the phosphate group (must be given before 'aging' of the enzyme). Supportive: airway, oxygen, diazepam for seizures. Atropine does not reverse nicotinic (muscle) effects.

17. Classify adrenergic receptors and the main physiological effect of each subtype.

    Alpha-1: vasoconstriction, mydriasis, GU smooth muscle contraction. Alpha-2: presynaptic inhibition of NA release, central sympatholysis, decreased insulin. Beta-1: increased heart rate/contractility, renin release. Beta-2: bronchodilation, vasodilation, uterine relaxation, glycogenolysis. Beta-3: lipolysis, bladder relaxation. Dopamine D1: renal/mesenteric vasodilation.

18. Distinguish non-selective, beta-1 selective (cardioselective), and beta-blockers with intrinsic sympathomimetic activity (ISA).

    Non-selective (propranolol, timolol) block beta-1 and beta-2 (risk of bronchospasm). Cardioselective/beta-1 (atenolol, metoprolol, bisoprolol, esmolol) safer in asthma/diabetes. ISA agents (pindolol, acebutolol) are partial agonists causing less bradycardia/lipid changes. Labetalol and carvedilol also block alpha-1.

19. Compare benzodiazepines and barbiturates in their mechanism on the GABA-A receptor and safety.

    Both potentiate GABA-A chloride channels. Benzodiazepines increase the frequency of channel opening (require GABA present), have a ceiling effect, and a specific antidote (flumazenil), making overdose relatively safe. Barbiturates increase the duration of channel opening and at high dose directly open the channel without GABA, so they have no ceiling, cause severe respiratory depression, and have no specific antidote.

20. Match antiepileptic drugs to their primary mechanism of action.

    Sodium channel blockers: phenytoin, carbamazepine, lamotrigine, lacosamide. Enhance GABA: benzodiazepines, phenobarbitone, tiagabine, vigabatrin. T-type calcium channel block: ethosuximide (absence seizures). Multiple mechanisms: valproate (Na channel, GABA, T-type). SV2A binding: levetiracetam. Glutamate/Ca: gabapentin, topiramate.

21. Which antiepileptic is first-line for absence seizures, and which drugs can worsen absence seizures?

    Ethosuximide is first-line for pure absence seizures (valproate preferred if generalized tonic-clonic also present). Carbamazepine, phenytoin, gabapentin, and vigabatrin can worsen or precipitate absence and myoclonic seizures.

22. Differentiate typical from atypical antipsychotics in mechanism and side-effect profile.

    Typical (haloperidol, chlorpromazine) are potent D2 antagonists with strong extrapyramidal symptoms (EPS) and hyperprolactinemia; better for positive symptoms. Atypical (risperidone, olanzapine, clozapine, quetiapine) block D2 and 5-HT2A, causing fewer EPS but more metabolic effects (weight gain, diabetes, dyslipidemia); they also help negative symptoms.

23. What is unique about clozapine and what monitoring does it require?

    Clozapine is the most effective antipsychotic, reserved for treatment-resistant schizophrenia, and does not cause significant EPS. It carries a risk of agranulocytosis, requiring regular white blood cell/absolute neutrophil count monitoring. Other risks: myocarditis, seizures (dose-related), metabolic syndrome, sedation, and excessive salivation.

24. Compare SSRIs, SNRIs, TCAs, and MAOIs as antidepressant classes.

    SSRIs (fluoxetine, sertraline) inhibit serotonin reuptake, are first-line, safe in overdose. SNRIs (venlafaxine, duloxetine) inhibit serotonin and noradrenaline reuptake. TCAs (amitriptyline, imipramine) block both plus muscarinic/H1/alpha-1 receptors causing anticholinergic, sedative, and cardiotoxic (overdose-fatal) effects. MAOIs (phenelzine, tranylcypromine) inhibit monoamine oxidase; risk of hypertensive crisis with tyramine foods.

25. List the key features of lithium therapy: monitoring, narrow therapeutic range, and toxicity.

    Lithium is a mood stabilizer for bipolar disorder; therapeutic range is 0.6-1.2 mEq/L (narrow TI) requiring blood level monitoring. Excreted unchanged by the kidney; toxicity is increased by NSAIDs, thiazides, ACE inhibitors, and dehydration. Adverse effects: tremor, hypothyroidism, nephrogenic diabetes insipidus, weight gain, Ebstein anomaly (teratogen). Toxicity signs: ataxia, confusion, seizures, arrhythmias.

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