INI 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 INI CET, not a summary of it.

1. 1

   General Pharmacology

   5 topics

   • Introduction to pharmacology
     • Definitions
     • Scope
     • Branches of pharmacology
   • Pharmacokinetics
     • Absorption
     • Distribution
     • Metabolism
     • Excretion of drugs
   • Pharmacodynamics
     • Mechanisms of drug action
     • Drug-receptor interactions
     • Dose-response relationships
     • Drug potency
   • Pharmacogenetics and personalized medicine
     • Genetic variation in drug response
     • Pharmacogenomic testing
     • Implications for drug therapy
   • Drug development and regulation
     • Preclinical studies
     • Clinical trials
     • Drug approval process
     • Drug scheduling
2. 2

   Autonomic Nervous System Pharmacology

   4 topics

   • Introduction to autonomic pharmacology
     • Neurotransmitters and receptors in the autonomic nervous system
   • Cholinergic drugs
     • Agonists
     • Antagonists
     • Cholinesterase inhibitors
   • Adrenergic drugs
     • Agonists
     • Antagonists
     • Adrenergic neuron blockers
   • Ganglionic and neuromuscular blocking drugs
     • Mechanism of action
     • Uses
     • Adverse effects
3. 3

   Central Nervous System Pharmacology

   7 topics

   • Introduction to CNS Pharmacology
     • Blood-brain barrier
     • Neurotransmitters in the CNS
     • Receptors in the CNS
   • Sedative-hypnotic Drugs
     • Benzodiazepines
     • Barbiturates
     • Non-benzodiazepine sedative-hypnotics
   • Antiepileptic Drugs
     • Mechanisms of action
     • Classification
     • Therapeutic uses
   • Antipsychotic Drugs
     • Typical antipsychotics
     • Atypical antipsychotics
     • Dopamine receptor antagonists
     • Serotonin-dopamine antagonists
   • Antidepressant Drugs
     • SSRIs
     • TCAs
     • MAOIs
     • Atypical antidepressants
     • Serotonin-norepinephrine reuptake inhibitors (SNRIs)
   • Analgesic and Anti-inflammatory Drugs
     • NSAIDs
     • Opioids
     • Adjuvant analgesics
   • Anxiolytic Drugs
     • Benzodiazepines
     • Buspirone
     • Selective serotonin reuptake inhibitors (SSRIs)
4. 4

   Introduction to cardiovascular pharmacology

   3 topics

   • Hemodynamics
   • Cardiac electrophysiology
   • Regulation of blood pressure
5. 5

   Endocrine Pharmacology

   5 topics

   • Introduction to Endocrine Pharmacology
     • Hormone replacement therapy
     • Hormone antagonists
     • Hormone synthesis inhibitors
   • Thyroid and Antithyroid Drugs
     • Thyroid hormones
     • Antithyroid drugs
     • Iodine preparations
   • Glucocorticoids and Mineralocorticoids
     • Mechanism of action
     • Therapeutic uses
     • Adverse effects
   • Insulin and Oral Hypoglycemic Agents
     • Mechanism of action
     • Classification
     • Therapeutic uses
   • Gonadal Hormones and Contraceptives
     • Estrogens
     • Progestins
     • Androgen receptor antagonists
     • Contraceptive methods
6. 6

   Introduction to chemotherapy

   3 topics

   • Principles of antimicrobial therapy
   • Mechanisms of antimicrobial action
   • Drug resistance
7. 7

   Chemotherapy of Neoplastic Diseases

   3 topics

   • Introduction to cancer chemotherapy
     • Principles of cancer therapy
     • Cell cycle-specific vs. cell cycle-nonspecific drugs
   • Anticancer drugs
     • Alkylating agents
     • Antimetabolites
     • Antitumor antibiotics
     • Mitotic inhibitors
     • Targeted therapies
   • Hormonal therapy
     • Hormone receptor antagonists
     • Aromatase inhibitors
     • Gonadotropin-releasing hormone analogs
8. 8

   Principles of toxicology

   3 topics

   • Mechanisms of toxicity
   • Factors affecting toxicity
   • Toxicokinetics

Pharmacology flashcards for INI CET

25 of 59 cards from the Pharmacology deck — real questions with worked answers.

1. Define pharmacokinetics and pharmacodynamics.

   Pharmacokinetics is what the body does to the drug (Absorption, Distribution, Metabolism, Excretion - ADME). Pharmacodynamics is what the drug does to the body (mechanism of action and effects, including receptor binding, dose-response).

2. What is bioavailability (F) and how is it calculated for an oral drug?

   Bioavailability is the fraction of administered drug reaching systemic circulation unchanged. F = (AUC oral / AUC IV) x (Dose IV / Dose oral). IV drugs have F = 1 (100%).

3. Define volume of distribution (Vd) and give its formula.

   Vd is the apparent volume needed to contain the total drug in the body at the plasma concentration. Vd = Total amount of drug in body / Plasma drug concentration. High Vd indicates extensive tissue distribution.

4. What is drug clearance (CL) and its relationship to half-life?

   Clearance is the volume of plasma cleared of drug per unit time. CL = Rate of elimination / Plasma concentration. Half-life t1/2 = (0.693 x Vd) / CL.

5. Differentiate zero-order from first-order kinetics.

   First-order: a constant fraction of drug is eliminated per unit time (rate proportional to concentration); most drugs. Zero-order: a constant amount is eliminated per unit time (saturable enzymes); examples include phenytoin, ethanol, aspirin (high dose), warfarin, theophylline.

6. What is the loading dose formula?

   Loading dose = (Target plasma concentration x Vd) / Bioavailability (F). It rapidly achieves therapeutic concentration and is independent of clearance.

7. What is the maintenance dose formula?

   Maintenance dose = (Target plasma concentration x Clearance x dosing interval) / Bioavailability (F). It replaces eliminated drug to maintain steady state.

8. How many half-lives are needed to reach steady state and to eliminate a drug?

   Approximately 4-5 half-lives are needed to reach ~94-97% of steady state on a constant infusion, and ~4-5 half-lives to essentially eliminate a drug after stopping.

9. Differentiate Phase I and Phase II drug metabolism reactions.

   Phase I (oxidation, reduction, hydrolysis; mainly CYP450) makes drugs more polar/often introduces functional groups. Phase II (conjugation: glucuronidation, sulfation, acetylation, glutathione) attaches endogenous substrate to increase water solubility for excretion.

10. What is first-pass metabolism?

    First-pass (presystemic) metabolism is the metabolism of an orally absorbed drug in the gut wall and liver before reaching systemic circulation, reducing bioavailability (e.g., propranolol, lidocaine, nitroglycerin, morphine).

11. Define affinity, efficacy, and potency in pharmacodynamics.

    Affinity is the tendency of a drug to bind its receptor (reflected by Kd). Efficacy is the maximal effect a drug can produce (Emax). Potency is the amount of drug needed to produce an effect (reflected by EC50/ED50); lower EC50 = more potent.

12. Differentiate a competitive from a non-competitive antagonist on a dose-response curve.

    Competitive antagonist: surmountable, shifts the agonist curve right (increased EC50), Emax unchanged. Non-competitive (irreversible/allosteric) antagonist: insurmountable, decreases Emax, often no rightward shift.

13. What is the therapeutic index (TI) and how is it calculated?

    TI measures drug safety. TI = TD50 / ED50 (or LD50/ED50 in animals). A higher TI means a wider safety margin; drugs like warfarin, digoxin, and lithium have a narrow TI.

14. Differentiate a partial agonist from a full agonist and an inverse agonist.

    Full agonist: maximal response (high efficacy). Partial agonist: submaximal response even at full receptor occupancy; acts as antagonist in presence of a full agonist (e.g., buprenorphine). Inverse agonist: produces effect opposite to the agonist on constitutively active receptors.

15. What is the role of pharmacogenetics in personalized medicine? Give a classic example.

    Pharmacogenetics studies genetic variation affecting drug response, enabling individualized therapy. Example: slow vs fast acetylators of isoniazid (NAT2); CYP2C9/VKORC1 affecting warfarin dosing; TPMT deficiency increasing azathioprine/6-MP toxicity.

16. What are the four phases of clinical drug trials?

    Phase 1: safety/PK in healthy volunteers (20-100). Phase 2: efficacy and dosing in patients (100-300). Phase 3: large randomized controlled efficacy/safety trials (1000-3000). Phase 4: post-marketing surveillance (pharmacovigilance).

17. What neurotransmitter and receptors mediate the parasympathetic and sympathetic systems?

    All preganglionic fibers and parasympathetic postganglionic fibers release ACh (nicotinic at ganglia, muscarinic at target). Sympathetic postganglionic fibers release norepinephrine (adrenergic receptors), except sweat glands (cholinergic) and adrenal medulla (nicotinic).

18. List the muscarinic receptor subtypes and their main G-protein coupling.

    M1, M3, M5 couple to Gq (increase IP3/DAG, excitatory). M2, M4 couple to Gi (decrease cAMP, inhibitory). M1 = CNS/stomach, M2 = heart (slows HR), M3 = glands/smooth muscle (secretion, contraction).

19. What are the effects of muscarinic agonists (cholinergic stimulation)?

    DUMBELS: Diarrhea, Urination, Miosis, Bradycardia/Bronchoconstriction, Emesis, Lacrimation, Salivation/Sweating. Also decreased intraocular pressure and increased GI/bladder tone.

20. What is the mechanism and antidote for organophosphate (irreversible AChE inhibitor) poisoning?

    Organophosphates irreversibly inhibit acetylcholinesterase, causing cholinergic crisis. Treatment: atropine (blocks muscarinic effects) plus pralidoxime (2-PAM) which reactivates AChE if given before aging.

21. Name an AChE inhibitor used for myasthenia gravis and one used for Alzheimer disease.

    Myasthenia gravis: neostigmine, pyridostigmine (edrophonium for diagnosis). Alzheimer disease: donepezil, rivastigmine, galantamine (centrally acting reversible AChE inhibitors).

22. Classify adrenergic receptors and their primary signaling/effects.

    Alpha-1: Gq, vasoconstriction, mydriasis. Alpha-2: Gi, decreased NE release/decreased BP centrally. Beta-1: Gs, increased HR/contractility/renin. Beta-2: Gs, bronchodilation/vasodilation/uterine relaxation. Beta-3: lipolysis.

23. Differentiate the cardiovascular effects of epinephrine, norepinephrine, and isoproterenol.

    Epinephrine (alpha+beta): increases HR, SBP rises, DBP may fall (beta-2). Norepinephrine (alpha1+beta1): increases BP, reflex bradycardia. Isoproterenol (beta1+beta2): increases HR, decreases DBP, lowers mean BP.

24. What is the mechanism of selective beta-1 blockers and name examples?

    Selective beta-1 blockers (cardioselective) reduce HR, contractility, and renin with less bronchospasm. Examples: metoprolol, atenolol, bisoprolol, esmolol, nebivolol, acebutolol (the 'A through M' beta-blockers are beta-1 selective).

25. What is the mechanism of action of ganglionic blockers and neuromuscular blockers?

    Ganglionic blockers (e.g., hexamethonium, trimethaphan) block nicotinic Nn receptors in autonomic ganglia. Neuromuscular blockers act at Nm receptors of the motor end plate: non-depolarizing (competitive, e.g., vecuronium) or depolarizing (succinylcholine).

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