MCQ on Mechanism of Drug Action and Pharmacodynamics

🟒 Easy Level (1–20)

  1. Pharmacodynamics is the study of:
    a) What the drug does to the body βœ”οΈ
    b) What the body does to the drug
    c) Drug absorption
    d) Drug metabolism
    Explanation: Pharmacodynamics focuses on drug effects and mechanisms.
  2. The main site of drug action is the:
    a) Liver
    b) Receptor βœ”οΈ
    c) Kidney
    d) Intestine
    Explanation: Drugs usually act by binding to receptors.
  3. An agonist is a substance that:
    a) Blocks a receptor
    b) Activates a receptor βœ”οΈ
    c) Destroys a receptor
    d) Has no action
    Explanation: Agonists mimic the effect of endogenous substances.
  4. An antagonist:
    a) Stimulates a receptor
    b) Blocks receptor activity βœ”οΈ
    c) Enhances metabolism
    d) Is an enzyme
    Explanation: Antagonists prevent the action of agonists.
  5. Drug-receptor binding follows:
    a) Linear kinetics
    b) Lock-and-key model βœ”οΈ
    c) Random chance
    d) Osmotic flow
    Explanation: Specificity and affinity define this interaction.
  6. Potency refers to:
    a) Maximum effect
    b) Dose required to produce an effect βœ”οΈ
    c) Duration of action
    d) Half-life
    Explanation: Lower dose = higher potency.
  7. Efficacy refers to:
    a) Maximum effect a drug can produce βœ”οΈ
    b) Dose of drug
    c) Speed of onset
    d) Absorption rate
    Explanation: High efficacy = greater therapeutic effect.
  8. EC50 is the concentration at which:
    a) 50% of maximal effect is achieved βœ”οΈ
    b) Drug is eliminated
    c) Receptors are saturated
    d) Toxicity appears
    Explanation: It’s used to measure drug potency.
  9. Which of the following is an example of a receptor?
    a) DNA
    b) Beta-adrenergic receptor βœ”οΈ
    c) Plasma
    d) Ribosome
    Explanation: Receptors are proteins that drugs target.
  10. A partial agonist:
    a) Fully activates receptor
    b) Produces sub-maximal response βœ”οΈ
    c) Blocks receptor
    d) Is inactive
    Explanation: It binds but produces less than full effect.
  11. Which is a type of drug action?
    a) Radiation
    b) Enzyme inhibition βœ”οΈ
    c) X-ray scattering
    d) Hemolysis
    Explanation: Drugs can inhibit enzymes to produce effects.
  12. The therapeutic index (TI) is:
    a) Ratio of toxic dose to effective dose βœ”οΈ
    b) A potency scale
    c) Drug half-life
    d) Duration of therapy
    Explanation: TI indicates drug safety margin.
  13. Tachyphylaxis refers to:
    a) Rapid decrease in drug response βœ”οΈ
    b) Steady effect
    c) Drug accumulation
    d) Tolerance
    Explanation: Repeated doses lead to reduced effect.
  14. Tolerance is:
    a) Hypersensitivity
    b) Reduced response after repeated use βœ”οΈ
    c) Toxicity
    d) First-pass metabolism
    Explanation: More drug needed over time to achieve effect.
  15. Inverse agonist:
    a) Has no effect
    b) Produces opposite effect to agonist βœ”οΈ
    c) Blocks receptor
    d) Enhances agonist
    Explanation: It reduces basal receptor activity.
  16. Which of the following interacts with DNA?
    a) Beta-blockers
    b) Anticancer drugs βœ”οΈ
    c) Antacids
    d) Antihistamines
    Explanation: Many chemotherapeutic agents bind DNA.
  17. Non-specific drug actions include:
    a) Receptor binding
    b) Changing pH βœ”οΈ
    c) Enzyme activation
    d) G-protein stimulation
    Explanation: Antacids and osmotic diuretics act non-specifically.
  18. Dose-response curve plots:
    a) Time vs. concentration
    b) Dose vs. effect βœ”οΈ
    c) Effect vs. toxicity
    d) Receptor vs. DNA
    Explanation: It visualizes the drug’s effect range.
  19. Allosteric modulators bind to:
    a) Active site
    b) Alternate site βœ”οΈ
    c) DNA
    d) Blood proteins
    Explanation: They enhance or reduce receptor activity.
  20. A competitive antagonist:
    a) Competes with agonist for receptor βœ”οΈ
    b) Binds irreversibly
    c) Enhances effect
    d) Activates G-proteins
    Explanation: Can be overcome with higher agonist concentration.

🟑 Moderate Level (21–40)

  1. Non-competitive antagonists:
    a) Compete for active site
    b) Bind irreversibly to receptor βœ”οΈ
    c) Increase potency
    d) Act as prodrugs
    Explanation: Their effect cannot be reversed by agonist.
  2. Drugs acting through ion channels:
    a) Alter membrane permeability βœ”οΈ
    b) Bind to DNA
    c) Change protein synthesis
    d) Inhibit blood cells
    Explanation: Ion channels regulate ion flow, affecting cell function.
  3. Second messengers include:
    a) DNA and RNA
    b) cAMP and IP3 βœ”οΈ
    c) Na+ and Cl-
    d) Glucose and lipids
    Explanation: They mediate intracellular effects of drugs.
  4. G-protein-coupled receptors (GPCRs) involve:
    a) Direct DNA binding
    b) Activation of intracellular signaling βœ”οΈ
    c) Plasma degradation
    d) Albumin synthesis
    Explanation: GPCRs trigger signal cascades.
  5. Drug selectivity means:
    a) Drug acts on specific receptor βœ”οΈ
    b) Drug binds all tissues
    c) Drug shows no effect
    d) All receptors are activated
    Explanation: Selectivity reduces side effects.
  6. Intrinsic activity of an agonist is:
    a) Zero
    b) 1 βœ”οΈ
    c) -1
    d) 0.5
    Explanation: Full agonists have intrinsic activity = 1.
  7. Irreversible antagonists:
    a) Permanently block receptors βœ”οΈ
    b) Require lower doses
    c) Dissociate easily
    d) Increase receptor number
    Explanation: Covalent or strong binding makes it irreversible.
  8. Drug action at enzyme level may involve:
    a) DNA synthesis
    b) Enzyme inhibition βœ”οΈ
    c) ATP storage
    d) O2 transport
    Explanation: Common in antimicrobials.
  9. Tolerance due to enzyme induction is:
    a) Pharmacokinetic βœ”οΈ
    b) Pharmacodynamic
    c) Receptor mutation
    d) Genetic
    Explanation: Body increases metabolism capacity.
  10. The ceiling effect relates to:
    a) Increased toxicity
    b) Maximal effect of a drug βœ”οΈ
    c) Minimum dose
    d) Time to onset
    Explanation: Dose beyond which no effect increases.
  11. Drug with low therapeutic index:
    a) Very safe
    b) Requires close monitoring βœ”οΈ
    c) Highly selective
    d) Short-acting
    Explanation: Narrow margin between therapeutic and toxic dose.
  12. Receptor downregulation leads to:
    a) Hypersensitivity
    b) Decreased response βœ”οΈ
    c) Faster metabolism
    d) Enhanced effect
    Explanation: Fewer receptors reduce response.
  13. Which is a nuclear receptor?
    a) Beta-2 receptor
    b) Estrogen receptor βœ”οΈ
    c) Histamine receptor
    d) Muscarinic receptor
    Explanation: Steroid hormones act via nuclear receptors.
  14. Placebo effect is:
    a) No effect
    b) Psychological benefit from inert substance βœ”οΈ
    c) Drug side effect
    d) Enzyme inhibition
    Explanation: Belief causes perceived improvement.
  15. The therapeutic window is:
    a) Cost-effective range
    b) Range between effective and toxic dose βœ”οΈ
    c) Storage temperature
    d) Drug purity
    Explanation: Safe and effective dosing range.
  16. GPCRs have how many transmembrane segments?
    a) 4
    b) 9
    c) 7 βœ”οΈ
    d) 10
    Explanation: It’s a hallmark of this receptor class.
  17. Biased agonism refers to:
    a) Incorrect drug use
    b) Selective pathway activation βœ”οΈ
    c) Antagonism
    d) Tolerance
    Explanation: Activates only certain receptor functions.
  18. Desensitization occurs due to:
    a) Drug degradation
    b) Liver failure
    c) Receptor internalization βœ”οΈ
    d) Overdosing
    Explanation: Receptors become less responsive.
  19. Which drug acts through enzyme induction?
    a) Digoxin
    b) Rifampicin βœ”οΈ
    c) Aspirin
    d) Propranolol
    Explanation: Rifampicin induces liver enzymes.
  20. Inhibiting acetylcholinesterase leads to:
    a) Increased acetylcholine βœ”οΈ
    b) Muscle paralysis
    c) Decreased heart rate
    d) DNA damage
    Explanation: Acetylcholine is broken down slower.

πŸ”΄ Hard Level (41–50)

  1. Dose-response curve of partial agonist shows:
    a) Lower maximum response βœ”οΈ
    b) No response
    c) Steep increase
    d) Inverse response
    Explanation: It never reaches full effect.
  2. Spare receptors exist when:
    a) All receptors are occupied
    b) Maximal effect occurs without full receptor occupancy βœ”οΈ
    c) Receptors are downregulated
    d) Potency is low
    Explanation: Indicates receptor reserve.
  3. Which receptor is ligand-gated?
    a) Insulin receptor
    b) Nicotinic acetylcholine receptor βœ”οΈ
    c) Estrogen receptor
    d) GPCR
    Explanation: Opens ion channels upon ligand binding.
  4. A sigmoid dose-response curve implies:
    a) Graded effect βœ”οΈ
    b) All-or-none response
    c) Fixed potency
    d) Constant slope
    Explanation: Typical of most drug responses.
  5. ED50 refers to:
    a) Effective dose for 50% population βœ”οΈ
    b) Toxic dose
    c) Minimum dose
    d) Bioavailability
    Explanation: Used to measure drug effectiveness.
  6. Inverse agonists act on:
    a) Constitutively active receptors βœ”οΈ
    b) Non-functional receptors
    c) Non-competitive sites
    d) G-proteins directly
    Explanation: They reduce basal receptor activity.
  7. G-proteins act as:
    a) Molecular switches βœ”οΈ
    b) DNA replicators
    c) Enzymes
    d) Hormones
    Explanation: Activate or inhibit intracellular pathways.
  8. A high-affinity drug:
    a) Binds strongly to its receptor βœ”οΈ
    b) Is non-specific
    c) Is toxic
    d) Is hydrophilic
    Explanation: Needs lower concentrations to bind.
  9. A low KD (dissociation constant) means:
    a) High affinity βœ”οΈ
    b) Low efficacy
    c) Poor selectivity
    d) Fast clearance
    Explanation: KD is inversely related to affinity.
  10. Signal transduction starts with:
    a) Enzyme action
    b) Ligand-receptor binding βœ”οΈ
    c) DNA binding
    d) Protein breakdown
    Explanation: First step in cellular response.