G03

Pharmacology & Allied Subjects

Human anatomy & physiology, pathophysiology, pharmacology, toxicology

22.4%

of the paper

≈ 112 marks

by weightage

of 5 heads

1799

questions

with explanations

cite a source

reference material

Weightage follows the locked NBEMS GPAT blueprint (docs/12-GPAT-TAXONOMY.md), not an estimate. Question counts are read from the live bank when this page is built.

Subtopics in this bank

Adverse drug reactions, drug interactions, new drug development and pharmacovigilanceAutacoids, NSAIDs, antigout and antirheumatic drugsBioassay: principles, types and bioassay of official substancesBody fluids, blood and the lymphatic system: haemopoiesis, coagulation, blood grouping and blood disordersCardiovascular anatomy and physiology: conduction system, cardiac cycle and output, blood pressure regulation and ECGCardiovascular and haematological pharmacology: heart failure, hypertension, angina, arrhythmia, hyperlipidaemia, shock, coagulation and antiplatelet drugsCell injury and adaptation, inflammation and repairCellular, tissue and musculoskeletal organisation of the body: cell transport, cell signalling, tissues, skin, bone, muscle contraction and jointsCentral nervous system pharmacology: anaesthetics, sedative-hypnotics, antiepileptics, psychopharmacological agents and opioid analgesicsChemotherapy of infectious diseases and malignancy: general principles, antibiotics, antimycobacterial, antifungal, antiviral and antiparasitic agentsDigestive system: GI anatomy, gastric acid secretion, digestion-absorption and energeticsDiuretics and antidiureticsEndocrine and reproductive pharmacology: pituitary, thyroid, calcium-regulating hormones, insulin, corticosteroids, sex hormones and oral contraceptivesEndocrine system: hormone classification, mechanism of hormone action, endocrine glands and their disordersGeneral pharmacology: scope, sources of drugs, routes of administration and drug-response terminologyHepatic and joint disorders, principles of cancer, and infectious/sexually transmitted diseasesImmunopharmacology, principles of toxicology and chronopharmacologyNeurophysiology and the central nervous system: action potential, synapse, neurotransmitters, brain and spinal cordPathophysiology of cardiovascular, respiratory, renal, haematological, endocrine, neurological and gastrointestinal disordersPeripheral nervous system and special sensesPeripheral nervous system pharmacology: autonomic drugs, neuromuscular blockers and local anaestheticsPharmacodynamics: receptor theories, receptor classification, signal transduction and dose-response relationshipsPharmacokinetics: membrane transport, ADME, enzyme induction/inhibition and kinetics of eliminationReproductive physiology and introduction to geneticsRespiratory and gastrointestinal pharmacologyRespiratory and urinary system physiology: lung volumes, gas transport, nephron function, urine formation and acid-base balance

Sample questions, with the reasoning

Every question in the bank is explained like this — including why each wrong option is wrong.

A 32-year-old premenopausal woman with symptomatic uterine fibroids is treated with ulipristal acetate. Which of the following best describes the core pharmacodynamic classification and primary clinical action of this agent?

A)Selective estrogen receptor modulator (SERM) acting as an agonist on bone and lipid metabolism while antagonizing endometrial proliferation
B)Selective progesterone receptor modulator (SPRM) that exerts mixed agonist-antagonist effects on progesterone receptors, inducing apoptosis and reducing leiomyoma volume✓
C)Pure androgen receptor antagonist that suppresses gonadotropin release through negative feedback in the pituitary
D)Long-acting GnRH receptor agonist that causes initial receptor downregulation and desensitization of the pituitary-ovarian axis

Why B is correct

Ulipristal acetate is a selective progesterone receptor modulator (SPRM). It binds to progesterone receptors with tissue-specific partial agonistic and antagonistic effects, effectively blocking progesterone-dependent proliferation in uterine fibroids, inducing apoptosis, and delaying ovulation without causing severe hypoestrogenic menopausal side effects.

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A 35-year-old female presents with recurrent arterial and venous thrombosis and recurrent pregnancy losses. Laboratory evaluations reveal a prolonged activated partial thromboplastin time (aPTT) that fails to correct upon mixing with normal pooled plasma. Further specific assays confirm the presence of circulating lupus anticoagulant. Which of the following components of the coagulation or hemostatic system is the primary molecular target of these circulating autoantibodies?

A)Cellular tissue factor exposed on disrupted vascular endothelial cells.
B)Plasma protein-phospholipid complexes, specifically beta-2-glycoprotein I and prothrombin bound to anionic surfaces.✓
C)Activated protein C and its essential cofactor protein S.
D)Von Willebrand factor multimers mediating platelet adhesion to subendothelial collagen.

Why B is correct

Lupus anticoagulants are a family of autoantibodies directed against plasma proteins bound to anionic phospholipids, most notably beta-2-glycoprotein I and prothrombin. Paradoxically, while they prolong phospholipid-dependent coagulation tests in vitro (like the aPTT), they are strongly associated with clinical thrombosis in vivo.

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A 35-year-old male with treatment-resistant focal epilepsy is evaluated for adjunctive drug therapy. The neurologist prescribes cenobamate. Beyond its primary mechanism of enhancing slow inactivation of voltage-gated sodium channels and positively modulating GABA-A receptors, cenobamate possesses a distinct pharmacological action that distinguishes it from most traditional sodium channel blocking antiepileptic drugs. Which of the following precisely describes this additional mechanism?

A)Inhibition of presynaptic vesicular monoamine transporter 2 (VMAT2), reducing monoamine release in the cortex.
B)Direct antagonism of the NMDA receptor glycine binding site to suppress glutamatergic excitatory neurotransmission.✓
C)Selective antagonism of presynaptic alpha-2 delta calcium channel subunits, mirroring the mechanism of gabapentin.
D)Irreversible inhibition of GABA transaminase, elevating whole-brain gamma-aminobutyric acid levels.

Why B is correct

Cenobamate exhibits a dual mechanism of action for antiseizure activity: it enhances the slow inactivation of voltage-gated sodium channels and acts as a positive allosteric modulator of GABA-A receptors. Additionally, preclinical and clinical pharmacological profiling demonstrates that cenobamate is a positive functional modulator of certain ion channels and inhibits excitatory neurotransmission through blockade of the NMDA receptor glycine binding site.

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