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🇮🇳 PGIMER Entrance · subject

PGIMER Entrance Pharmacology Syllabus

The Pharmacology syllabus for PGIMER Entrance in full: 3 chapters, 13 topics and 4 sub-topics, every one listed below, plus 55 Pharmacology flashcards with answers.

3Chapters
13Topics
4Sub-topics
55Flashcards

Pharmacology syllabus: all 3 chapters

Expand any chapter to see its topics and sub-topics.

  1. General Pharmacology

     4 topics
    • Pharmacokinetics
      • Absorption, bioavailability and distribution
      • Metabolism, clearance and half-life
    • Pharmacodynamics and receptor theory
    • Adverse drug reactions and drug interactions
    • Routes of administration and bioequivalence

  2. Autonomic and CNS Pharmacology

     4 topics
    • Cholinergic and adrenergic drugs
    • Sedative-hypnotics and antiepileptics
    • Antipsychotics and antidepressants
    • Opioid analgesics and general anesthetics

  3. Systemic and Chemotherapy Pharmacology

     5 topics
    • Antihypertensives and antianginal drugs
    • Diuretics and drugs for heart failure
    • Antimicrobial agents
      • Beta-lactams and protein synthesis inhibitors
      • Antitubercular and antiretroviral drugs
    • Anticancer drugs and immunosuppressants
    • Endocrine pharmacology and hypoglycemics

PGIMER Entrance Pharmacology flashcards — 55 questions with answers

  1. Define bioavailability (F) and state its value for an intravenous drug.

    Bioavailability is the fraction of an administered dose that reaches the systemic circulation in unchanged form. For an IV drug, F = 1 (100%) by definition.

  2. What is the formula for volume of distribution (Vd)?

    Vd = Amount of drug in the body / Plasma drug concentration. It is an apparent volume relating total body drug to measured plasma concentration.

  3. What is the relationship between clearance (CL), volume of distribution (Vd), and elimination half-life (t1/2)?

    t1/2 = 0.693 x Vd / CL. Half-life is directly proportional to Vd and inversely proportional to clearance.

  4. Differentiate zero-order from first-order kinetics of drug elimination.

    First-order: a constant fraction is eliminated per unit time (rate proportional to concentration). Zero-order: a constant amount is eliminated per unit time (saturated, rate independent of concentration), e.g. ethanol, phenytoin, aspirin (high dose).

  5. What is first-pass metabolism and which routes avoid it?

    First-pass metabolism is presystemic metabolism of an oral drug in the gut wall/liver before reaching systemic circulation, reducing bioavailability. Avoided by IV, sublingual, rectal (partial), transdermal, and inhalational routes.

  6. How many half-lives are needed to reach steady-state concentration on repeated dosing?

    Approximately 4-5 half-lives (about 94-97% of steady state); the same applies for drug elimination after stopping.

  7. List the four reactions of Phase I metabolism and the main enzyme system involved.

    Phase I reactions are oxidation, reduction, hydrolysis, and cyclization/decyclization, performed mainly by the hepatic cytochrome P450 (CYP) microsomal enzyme system.

  8. What distinguishes Phase II metabolism from Phase I?

    Phase II is conjugation (glucuronidation, sulfation, acetylation, glutathione, methylation) that adds an endogenous polar group, producing usually inactive, water-soluble metabolites for excretion. Phase I introduces/exposes a functional group.

  9. Define the therapeutic index (TI) and give its formula.

    Therapeutic index = TD50 / ED50 (or LD50/ED50 in animals). It measures drug safety; a higher TI indicates a wider safety margin.

  10. Distinguish affinity from efficacy (intrinsic activity) at a receptor.

    Affinity is the tendency of a drug to bind to its receptor (governs potency/EC50). Efficacy/intrinsic activity is the ability of the bound drug to produce a response (full agonist =1, antagonist =0, partial agonist between 0 and 1).

  11. How does a competitive (reversible) antagonist alter the agonist dose-response curve?

    It shifts the curve to the right (parallel) with no change in maximal response; the effect is surmountable by increasing agonist concentration.

  12. How does a non-competitive (irreversible) antagonist alter the agonist dose-response curve?

    It reduces the maximal response (lowers the ceiling) and the effect is not fully surmountable by increasing agonist concentration.

  13. Compare a partial agonist with a full agonist at the same receptor.

    A partial agonist has lower intrinsic activity, producing a submaximal response even at full occupancy; in the presence of a full agonist it can act as an antagonist by competing for receptors.

  14. What is an inverse agonist?

    An inverse agonist binds the same receptor as an agonist but produces the opposite effect by reducing constitutive (baseline) receptor activity, e.g. beta-carbolines at GABA-A benzodiazepine site.

  15. Name the four main receptor superfamilies by signal transduction speed.

    1) Ligand-gated ion channels (milliseconds), 2) G-protein coupled receptors (seconds), 3) Enzyme-linked/kinase-linked receptors (minutes), 4) Intracellular/nuclear (gene transcription) receptors (hours).

  16. Classify adverse drug reactions into Type A and Type B with examples.

    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. penicillin anaphylaxis.

  17. What is the difference between pharmacokinetic and pharmacodynamic drug interactions?

    Pharmacokinetic interactions alter absorption, distribution, metabolism, or excretion (changing drug concentration). Pharmacodynamic interactions alter the response at the site of action without changing concentration (additive, synergistic, or antagonistic effects).

  18. Name two potent CYP450 enzyme inducers and two inhibitors.

    Inducers: rifampicin, phenytoin, carbamazepine, phenobarbitone, chronic alcohol. Inhibitors: ketoconazole, erythromycin/clarithromycin, cimetidine, ciprofloxacin, grapefruit juice.

  19. Define bioequivalence.

    Two pharmaceutically equivalent products are bioequivalent when their rate and extent of absorption (bioavailability: Cmax, Tmax, AUC) are not statistically significantly different under the same conditions.

  20. Which routes of administration produce the fastest onset of systemic drug action?

    Intravenous (instantaneous, 100% bioavailability) and inhalational routes give the fastest onset; IV gives immediate, controllable plasma levels.

Show the other 35 Pharmacology flashcards

  1. Differentiate nicotinic and muscarinic cholinergic receptors.

    Nicotinic: ligand-gated ion channels at autonomic ganglia (NN) and neuromuscular junction (NM). Muscarinic (M1-M5): G-protein coupled, found on effector organs of parasympathetic system and sweat glands.

  2. What are the muscarinic (cholinergic) effects summarized by SLUDGE/DUMBELS?

    Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis (and Miosis, Bronchospasm, Bradycardia). Reflects excess parasympathetic/muscarinic stimulation.

  3. What is the antidote for organophosphate (irreversible anticholinesterase) poisoning?

    Atropine (blocks muscarinic effects) plus pralidoxime (2-PAM), a cholinesterase reactivator given before aging of the enzyme occurs.

  4. Classify adrenergic receptors and their main second messengers.

    Alpha-1 (Gq, IP3/DAG - vasoconstriction), Alpha-2 (Gi, decrease cAMP - presynaptic inhibition), Beta-1/Beta-2/Beta-3 (Gs, increase cAMP - cardiac stimulation, bronchodilation, lipolysis).

  5. Why is adrenaline (epinephrine) preferred over noradrenaline in anaphylaxis?

    Adrenaline stimulates alpha-1 (vasoconstriction, raises BP), beta-1 (cardiac output), and beta-2 (bronchodilation and mast cell stabilization), addressing all features of anaphylaxis.

  6. What is the GABA-A receptor and how do benzodiazepines and barbiturates act on it differently?

    GABA-A is a ligand-gated chloride channel. Benzodiazepines increase the frequency of channel opening; barbiturates increase the duration of channel opening (and at high dose open it directly, causing greater lethality).

  7. Which antiepileptic is the drug of choice for absence (petit mal) seizures?

    Ethosuximide (blocks T-type calcium channels); valproate is an alternative, especially with coexisting tonic-clonic seizures.

  8. What is the mechanism of phenytoin and its key kinetic feature?

    Phenytoin blocks voltage-gated sodium channels (use-dependent), stabilizing neuronal membranes. It shows zero-order (saturable) kinetics at therapeutic doses, so small dose increases can cause toxicity.

  9. Distinguish typical from atypical antipsychotics in mechanism and side effects.

    Typical (e.g. haloperidol) block D2 receptors strongly, causing extrapyramidal symptoms and hyperprolactinemia. Atypical (e.g. risperidone, olanzapine) block 5-HT2A and D2, with fewer EPS but more metabolic side effects.

  10. Which antipsychotic is reserved for treatment-resistant schizophrenia and what is its serious adverse effect?

    Clozapine; its serious adverse effect is agranulocytosis, requiring regular WBC monitoring (also lowers seizure threshold and causes myocarditis).

  11. What is the mechanism of SSRIs and name two examples.

    SSRIs selectively inhibit presynaptic serotonin (5-HT) reuptake, increasing synaptic serotonin. Examples: fluoxetine, sertraline, paroxetine, escitalopram.

  12. What is serotonin syndrome and which drug combinations cause it?

    A potentially fatal syndrome of neuromuscular excitation (clonus, hyperreflexia), autonomic instability, and altered mental status from excess serotonin, e.g. SSRI + MAOI, SSRI + tramadol/triptans/linezolid.

  13. What dietary/drug precaution is essential with MAO inhibitors?

    Avoid tyramine-rich foods (aged cheese, wine, cured meats) which can cause a hypertensive crisis (cheese reaction), and avoid sympathomimetics and serotonergic drugs.

  14. Name the three classes of opioid receptors and the predominant effects of mu-receptor activation.

    Mu, kappa, and delta. Mu activation produces analgesia, euphoria, respiratory depression, miosis, constipation, and physical dependence.

  15. What is the opioid overdose triad and its antidote?

    Triad: respiratory depression, pinpoint pupils (miosis), and coma/CNS depression. Antidote is naloxone, a pure opioid antagonist (short-acting, may need repeat dosing).

  16. Which IV anesthetic is preferred in hypovolemic/shock patients and why?

    Ketamine, because it produces dissociative anesthesia with sympathetic stimulation that maintains blood pressure, heart rate, and bronchodilation; it also provides analgesia.

  17. What determines the speed of induction with an inhalational anesthetic?

    The blood:gas partition coefficient - a low coefficient (e.g. nitrous oxide, desflurane) means low solubility, faster rise in alveolar/brain partial pressure, and faster induction and recovery.

  18. List the major classes of antihypertensive drugs.

    Diuretics, ACE inhibitors, ARBs, calcium channel blockers, beta-blockers, alpha-blockers, central sympatholytics, and direct vasodilators.

  19. What is the characteristic adverse effect of ACE inhibitors and its cause?

    Dry cough (and angioedema) due to accumulation of bradykinin (and substance P) because ACE/kininase II normally degrades bradykinin. ARBs avoid this.

  20. How does nitroglycerin relieve angina?

    It releases nitric oxide, increasing cGMP and causing venodilation that reduces preload (and at higher doses, coronary/arterial dilation), thereby lowering myocardial oxygen demand.

  21. Why are dihydropyridine calcium channel blockers (e.g. amlodipine) and non-dihydropyridines (e.g. verapamil) used differently?

    Dihydropyridines act mainly on vascular smooth muscle (vasodilation, antihypertensive). Non-dihydropyridines (verapamil, diltiazem) act on the heart (negative chronotropic/inotropic), useful in arrhythmias and angina.

  22. Match each diuretic class to its site of action in the nephron.

    Carbonic anhydrase inhibitors - proximal tubule; loop diuretics - thick ascending limb (Na-K-2Cl); thiazides - distal convoluted tubule (Na-Cl); potassium-sparing - collecting duct.

  23. Which diuretics are potassium-sparing and how do they act?

    Spironolactone/eplerenone (aldosterone receptor antagonists) and amiloride/triamterene (epithelial Na channel blockers) in the collecting duct; they retain potassium while promoting sodium loss.

  24. Which four drug classes improve survival (mortality) in chronic heart failure with reduced ejection fraction?

    ACE inhibitors/ARBs (or ARNI), beta-blockers (carvedilol, bisoprolol, metoprolol succinate), mineralocorticoid receptor antagonists (spironolactone), and SGLT2 inhibitors.

  25. What is the mechanism of digoxin in heart failure?

    Digoxin inhibits the Na+/K+-ATPase, raising intracellular Na+ and thus intracellular Ca2+ via Na/Ca exchange, increasing cardiac contractility (positive inotropy); it also increases vagal tone, slowing AV conduction.

  26. Classify antimicrobials by whether they inhibit cell wall synthesis.

    Cell wall synthesis inhibitors include beta-lactams (penicillins, cephalosporins, carbapenems, monobactams), glycopeptides (vancomycin), and bacitracin.

  27. Which antibiotic classes inhibit bacterial protein synthesis and at which ribosomal subunit?

    30S: aminoglycosides and tetracyclines. 50S: macrolides, clindamycin, chloramphenicol, linezolid, and streptogramins.

  28. What is the mechanism and key toxicity of aminoglycosides?

    Aminoglycosides bind the 30S subunit causing misreading of mRNA (bactericidal, concentration-dependent). Key toxicities are nephrotoxicity and ototoxicity (vestibular/auditory).

  29. What is the mechanism of fluoroquinolones and a notable adverse effect?

    They inhibit DNA gyrase (topoisomerase II) and topoisomerase IV, blocking DNA replication. Notable adverse effects include tendinitis/tendon rupture, QT prolongation, and cartilage damage (avoid in children/pregnancy).

  30. What is the cell cycle specificity concept in cancer chemotherapy? Give an example of a cell-cycle-specific drug.

    Cell-cycle-specific (CCS) drugs act on cells in a particular phase (e.g. methotrexate and 5-FU act in S phase; vinca alkaloids in M phase). Cell-cycle-nonspecific drugs (e.g. alkylating agents) act on cells in any phase.

  31. What toxicity is associated with doxorubicin and how is it reduced?

    Doxorubicin (anthracycline) causes dose-dependent cardiotoxicity (cardiomyopathy/heart failure) via free radical generation; dexrazoxane (an iron chelator) is used to reduce it.

  32. Name two calcineurin-inhibitor immunosuppressants and their main toxicity.

    Cyclosporine and tacrolimus inhibit calcineurin, blocking IL-2 production and T-cell activation; both are notably nephrotoxic (tacrolimus also more neurotoxic/diabetogenic).

  33. Differentiate sulfonylureas from biguanides in mechanism for type 2 diabetes.

    Sulfonylureas (e.g. glibenclamide) close pancreatic beta-cell K-ATP channels to stimulate insulin secretion (risk of hypoglycemia/weight gain). Biguanides (metformin) decrease hepatic gluconeogenesis and improve insulin sensitivity (no hypoglycemia, weight neutral).

  34. What is the mechanism of action of insulin on its target cells?

    Insulin binds a receptor tyrosine kinase, triggering autophosphorylation and signaling that recruits GLUT4 transporters to the membrane, increasing glucose uptake into muscle and fat, and promoting glycogen, protein, and fat synthesis.

  35. Compare the effects of thyroid hormone replacement (levothyroxine) with antithyroid drugs (carbimazole/propylthiouracil).

    Levothyroxine (T4) replaces deficient hormone in hypothyroidism. Carbimazole/PTU inhibit thyroid peroxidase to reduce hormone synthesis in hyperthyroidism; PTU additionally blocks peripheral T4-to-T3 conversion and is preferred in first-trimester pregnancy.

PGIMER Entrance Pharmacology FAQ

What is in the PGIMER Entrance Pharmacology syllabus?

PGIMER Entrance Pharmacology is split into 3 chapters: General Pharmacology, Autonomic and CNS Pharmacology and Systemic and Chemotherapy Pharmacology. Together they contain 13 topics and 4 sub-topics.

How many chapters are in PGIMER Entrance Pharmacology?

3 chapters, containing 13 topics and 4 sub-topics. The largest chapter is Systemic and Chemotherapy Pharmacology, with 5 topics.

Are there flashcards for PGIMER Entrance Pharmacology?

Yes — a 55-card Pharmacology deck, printed in full in the flashcards section of this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.