THIRD BHMS
PHARMACOLOGY QUESTION BANK
question bank according to CBDC syllabus
M - MCQ | S - SAQ | L - LAQ | V - VIVA/PRACTICAL | Ø - NON
PHARMACODYNAMICS
1. Mechanisms of Drug Action on Body Systems
a) Receptor Interaction:
–Agonists and antagonists (e.g., β-blockers, opioids)
b) Enzyme Modulation:
–Inhibition or activation of enzymes (e.g., statins inhibit HMG-CoA reductase, aspirin inhibits COX enzymes)
c) Ion Channel Modulation:
–Channel blockers or openers (e.g., calcium channel blockers, sodium channel blockers)
d) Neurotransmitter Systems:
–Reuptake or enzyme inhibitors (e.g., SSRIs, MAO inhibitors)
e) Hormonal Systems:
–Hormone agonists, antagonists, and synthesis inhibitors (e.g., insulin, tamoxifen)
f) Immune Modulation:
–Vaccines, monoclonal antibodies (e.g., rituximab)
g) DNA/RNA Interaction:
–Agents that target nucleic acids (e.g., anticancer drugs like cyclophosphamide, antivirals like AZT)
h) Physical or Chemical Action:
–Osmotic or neutralizing agents (e.g., mannitol, sodium bicarbonate)
2. Dose-Response Relationships
A) Agonists, Antagonists, and Modulators
a) Full agonist:
–Produces maximal response (e.g., epinephrine on β-receptors)
b) Partial agonist:
–Submaximal effect even at full receptor occupancy (e.g., buprenorphine)
c) Antagonist:
–Binds without activating, blocks agonist action (e.g., naloxone)
d) Inverse agonist:
–Produces opposite effect (e.g., propranolol)
e) Allosteric modulator:
–Alters receptor activity via a secondary site (e.g., benzodiazepines on GABA-A)
B) Variability in Dose–Response
a) Inter-individual variability:
–Influenced by genetics, age, disease, interactions
b) Tachyphylaxis:
–Rapid loss of effect (e.g., nitrates)
c) Tolerance:
–Gradual reduction in response (e.g., opioids)
d) Hypersensitivity:
–Exaggerated effect at small doses
C) Drug Toxicity and Overdose Indicators
-TD₅₀: Toxic dose in 50% of subjects
-LD₅₀: Lethal dose in 50% of population
-Margin of safety / Therapeutic index
-Dose adjustment based on monitoring (e.g., INR-guided warfarin dosing)
D) Clinical Applications
a) Therapeutic drug monitoring:
–E.g., digoxin, lithium
b)Avoiding toxicity:
–Adjusting dose, monitoring side effects
3. Factors Modifying Drug Action
A) Physiological Factors
a) Age:
–Neonates – immature metabolism (e.g., chloramphenicol → gray baby syndrome)
–Elderly – reduced clearance (e.g., digoxin accumulation)
b) Gender:
–Hormonal differences in metabolism (e.g., slower benzodiazepine clearance in women)
c) Body weight:
–Dosing based on weight or surface area (important in chemotherapy)
B) Pathological Factors
a) Genetic polymorphisms:
–e.g., slow acetylators (isoniazid)
b) Liver disease:
–Impaired metabolism (e.g., prolonged warfarin effect)
c) Kidney disease:
–Reduced excretion (e.g., aminoglycoside accumulation)
d) Cardiac disease:
–Decreased perfusion affects distribution (e.g., digoxin)
e) Thyroid dysfunction:
–Hyperthyroidism ↑ metabolism (β-blocker clearance)
–Hypothyroidism ↓ metabolism (digoxin half-life ↑)
C) Pharmacogenetic Factors
a) CYP450 enzymes:
–Variants (e.g., CYP2D6, CYP3A4) affect metabolism (e.g., codeine)
b) Drug transporters:
–P-glycoprotein variations alter absorption (e.g., digoxin)
c) Enzyme deficiencies:
–G6PD deficiency → hemolysis with sulfonamides
D) Environmental Factors
a) Diet:
–Grapefruit juice (CYP3A4 inhibition ↑ statin levels), high-fat meals delay absorption
b) Smoking:
–Induces CYP1A2 (↑ theophylline clearance)
c) Alcohol:
–Acute → inhibits metabolism (↑ sedative effect)
–Chronic → induces metabolism (↓ warfarin levels)
d) Temperature:
–Affects absorption through blood flow
E) Drug Interactions
a) Pharmacokinetic:
a) Absorption:
–Antacids ↓ tetracycline absorption
b) Metabolism:
–Rifampin ↑ clearance of oral contraceptives; ketoconazole ↓ midazolam metabolism
c) Excretion:
–Probenecid ↓ penicillin excretion
b)Pharmacodynamic:
-Synergism (e.g., sulfonamides + trimethoprim)
-Antagonism (e.g., naloxone vs. opioids)
F) Tolerance and Dependence
a) Tolerance:
–Reduced effect with repeated use (opioids, nitrates); cross-tolerance possible
b) Dependence:
–Physical or psychological need (opioids, benzodiazepines)
G) Route of Administration
-Oral: First-pass metabolism ↓ bioavailability (e.g., propranolol)
-IV: Rapid, complete absorption
-IM/SC: Absorption depends on blood flow and solubility
H) Disease-Specific Factors
-Infection/Inflammation: ↓ effectiveness in acidic sites (e.g., aminoglycosides)
-Malnutrition: ↓ plasma proteins → ↑ free drug concentration (e.g., phenytoin)
I) Psychological Factors
-Placebo effect: Positive response due to expectation
-Nocebo effect: Negative outcomes due to belief in side effects