, Chapter: 30 Pharmacology of Reproduction
CONTENT Chapter: 31 Pharmacology of the Endocrine
Pancreas and Glucose Homeostasis
Chapter: 1 Drug–Receptor Interactions Chapter: 32 Pharmacology of Bone Mineral
Chapter: 2 Pharmacodynamics Homeostasis
Chapter: 3 Pharmacokinetics Chapter: 33 Principles of Antimicrobial and
Chapter: 4 Drug Metabolism Antineoplastic Pharmacology
Chapter: 5 Drug Transporters Chapter: 34 Pharmacology of Bacterial
Chapter: 6 Drug Toxicity Infections: DNA Replication, Transcription, and
Chapter: 7 Pharmacogenomics Translation
Chapter: 8 Principles of Cellular Excitability and Chapter: 35 Pharmacology of Bacterial and
Electrochemical Transmission Mycobacterial Infections: Cell Wall Synthesis
Chapter: 9 Principles of Nervous System Chapter: 36 Pharmacology of Fungal Infections
Physiology and Pharmacology Chapter: 37 Pharmacology of Parasitic Infections
Chapter: 10 Cholinergic Pharmacology Chapter: 38 Pharmacology of Viral Infections
Chapter: 11 Adrenergic Pharmacology Chapter: 39 Pharmacology of Cancer: Genome
Chapter: 12 Local Anesthetic Pharmacology Synthesis, Stability, and Maintenance
Chapter: 13 Pharmacology of GABAergic and Chapter: 40 Pharmacology of Cancer: Signal
Glutamatergic Neurotransmission Transduction
Chapter: 14 Pharmacology of Dopaminergic Chapter: 41 Principles of Combination
Neurotransmission Chemotherapy
Chapter: 15 Pharmacology of Serotonergic and Chapter: 42 Principles of Inflammation and the
Central Adrenergic Neurotransmission Immune System
Chapter: 16 Pharmacology of Abnormal Chapter: 43 Pharmacology of Eicosanoids
Electrical Neurotransmission in the Central Chapter: 44 Histamine Pharmacology
Nervous System Chapter: 45 Pharmacology of Hematopoiesis
Chapter: 17 General Anesthetic Pharmacology and Immunomodulation
Chapter: 18 Pharmacology of Analgesia Chapter: 46 Pharmacology of
Chapter: 19 Pharmacology of Drugs of Abuse Immunosuppression
Chapter: 20 Pharmacology of Cholesterol and Chapter: 47 Integrative Inflammation
Lipoprotein Metabolism Pharmacology: Peptic Ulcer Disease
Chapter: 21 Pharmacology of Volume Chapter: 48 Integrative Inflammation
Regulation Pharmacology: Asthma
Chapter: 22 Pharmacology of Vascular Tone Chapter: 49 Integrative Inflammation
Chapter: 23 Pharmacology of Hemostasis and Pharmacology: Gout
Thrombosis Chapter: 50 Environmental Toxicology
Chapter: 24 Pharmacology of Cardiac Rhythm Chapter: 51 Drug Discovery and Preclinical
Chapter: 25 Pharmacology of Cardiac Development
Contractility Chapter: 52 Clinical Drug Evaluation and
Chapter: 26 Integrative Cardiovascular Regulatory Approval
Pharmacology: Hypertension, Ischemic Heart Chapter: 53 Systematic Detection of Adverse
Disease, and Heart Failure Drug Events
Chapter: 27 Pharmacology of the Hypothalamus Chapter: 54 Protein Therapeutics
and Pituitary Gland Chapter: 55 Drug Delivery Modalities
Chapter: 28 Pharmacology of the Thyroid Gland
Chapter: 29 Pharmacology of the Adrenal Cortex
,Chapter 1: Drug–Receptor Interactions
1. A patient is prescribed a β1-selective adrenergic antagonist for hypertension. The
drug primarily inhibits which aspect of receptor function?
A. Receptor synthesis
B. Agonist binding at the orthosteric site
C. Signal transduction downstream of the receptor
D. Ligand-independent receptor internalization
Answer: B
Rationale: β1-selective antagonists block the binding of endogenous catecholamines
(norepinephrine/epinephrine) at the orthosteric site of β1 receptors, preventing receptor activation.
They do not alter receptor synthesis or directly interfere with downstream signaling beyond
preventing activation.
Key words: β1 antagonist, receptor binding, orthosteric site, hypertension
2. A partial agonist at a receptor:
A. Produces maximal effect at full receptor occupancy
B. Blocks effects of a full agonist when co-administered
C. Is unable to bind the receptor
D. Has no effect in the presence of an antagonist
Answer: B
Rationale: Partial agonists have lower intrinsic activity than full agonists. When co-administered with
a full agonist, they compete for binding and reduce the maximal effect of the full agonist.
Key words: partial agonist, intrinsic activity, receptor competition
3. Which statement correctly distinguishes potency from efficacy?
A. Potency depends on receptor reserve; efficacy is independent of dose
B. Efficacy refers to the concentration required to achieve half-maximal effect
C. Potency measures maximal response a drug can produce
D. Efficacy is the maximal effect a drug can elicit regardless of dose
,Answer: D
Rationale: Efficacy is the intrinsic ability of a drug to elicit a maximal response. Potency refers to the
concentration required to achieve a given response (often EC50).
Key words: efficacy, potency, dose-response, EC50
4. A competitive antagonist:
A. Irreversibly inactivates the receptor
B. Shifts the dose-response curve of an agonist to the right without changing maximal response
C. Increases the intrinsic activity of the receptor
D. Produces a response in the absence of agonist
Answer: B
Rationale: Competitive antagonists compete with agonists for the same receptor binding site.
Increasing agonist concentration can overcome inhibition, causing a rightward shift in the dose-
response curve without changing maximal effect.
Key words: competitive antagonist, dose-response, receptor occupancy
5. Which of the following best describes spare receptors?
A. Receptors that cannot be activated by agonists
B. Receptors that exist in excess of what is needed for maximal response
C. Receptors that produce only partial agonist effects
D. Receptors permanently bound by antagonists
Answer: B
Rationale: Spare receptors refer to receptor populations that exceed the number needed to elicit a
maximal response. They allow full effect at submaximal receptor occupancy.
Key words: spare receptors, maximal response, receptor reserve
6. A patient develops tachyphylaxis to a β-agonist. The most likely mechanism
involves:
,A. Receptor downregulation
B. Enhanced agonist binding
C. Upregulation of second messengers
D. Increased intrinsic efficacy
Answer: A
Rationale: Tachyphylaxis is rapid desensitization of a receptor to agonist stimulation, often due to
receptor downregulation or phosphorylation, reducing receptor availability.
Key words: tachyphylaxis, receptor downregulation, desensitization
7. Non-competitive antagonists:
A. Bind only when agonist is bound
B. Reduce maximal response regardless of agonist concentration
C. Can be overcome by increasing agonist concentration
D. Act exclusively at allosteric sites
Answer: B
Rationale: Non-competitive antagonists reduce maximal response by either irreversibly binding the
receptor or modulating receptor function allosterically. Increasing agonist cannot restore maximal
effect.
Key words: non-competitive antagonist, allosteric modulation, maximal response
8. Receptor desensitization typically involves:
A. Increased receptor synthesis
B. Receptor phosphorylation and uncoupling from G-proteins
C. Conversion of antagonist into agonist
D. Depletion of extracellular ligand
Answer: B
Rationale: Desensitization commonly occurs via phosphorylation of receptors, leading to uncoupling
from G-proteins, reducing downstream signaling.
Key words: receptor desensitization, phosphorylation, G-protein uncoupling
,9. A ligand that binds preferentially to a receptor’s inactive state is called:
A. Full agonist
B. Inverse agonist
C. Partial agonist
D. Neutral antagonist
Answer: B
Rationale: Inverse agonists stabilize the inactive conformation of receptors, reducing basal
(constitutive) receptor activity.
Key words: inverse agonist, receptor conformations, basal activity
10. A clinician uses a drug with high receptor selectivity to minimize side effects.
This approach relies on:
A. Drug metabolism differences
B. Targeting specific receptor subtypes in relevant tissues
C. Non-competitive antagonism
D. Altered pharmacokinetics
Answer: B
Rationale: High receptor selectivity allows drugs to act on specific receptor subtypes in target tissues,
reducing off-target effects.
Key words: receptor selectivity, side effects, tissue specificity
11. A drug exhibits a ceiling effect. Which mechanism explains this phenomenon?
A. Saturation of enzymes metabolizing the drug
B. Receptor full occupancy or limited efficacy
C. Increased renal clearance at higher doses
D. Competitive inhibition at transporters
Answer: B
Rationale: The ceiling effect occurs when all receptors are occupied or the drug has limited intrinsic
efficacy, preventing further effect regardless of dose increase.
Key words: ceiling effect, receptor occupancy, intrinsic efficacy
, 12. Agonist efficacy is primarily determined by:
A. Binding affinity alone
B. Intrinsic activity at the receptor
C. Half-life in circulation
D. Route of administration
Answer: B
Rationale: Efficacy depends on the intrinsic activity of the agonist at the receptor, i.e., the ability to
trigger the receptor’s active conformation. Affinity affects potency but not efficacy.
Key words: agonist efficacy, intrinsic activity, receptor activation
13. Which type of antagonist can decrease the effect of both full and partial
agonists?
A. Competitive
B. Non-competitive
C. Reversible
D. Allosteric agonist
Answer: B
Rationale: Non-competitive antagonists reduce maximal response regardless of agonist type,
affecting both full and partial agonists.
Key words: non-competitive antagonist, partial agonist, maximal response
14. G-protein-coupled receptor (GPCR) activation primarily involves:
A. Direct ion channel blockade
B. Conformational change leading to G-protein signaling
C. Covalent receptor modification
D. Nuclear receptor translocation
Answer: B
Rationale: GPCRs transduce extracellular signals via conformational changes that activate G-proteins,
initiating intracellular signaling cascades.
CONTENT Chapter: 31 Pharmacology of the Endocrine
Pancreas and Glucose Homeostasis
Chapter: 1 Drug–Receptor Interactions Chapter: 32 Pharmacology of Bone Mineral
Chapter: 2 Pharmacodynamics Homeostasis
Chapter: 3 Pharmacokinetics Chapter: 33 Principles of Antimicrobial and
Chapter: 4 Drug Metabolism Antineoplastic Pharmacology
Chapter: 5 Drug Transporters Chapter: 34 Pharmacology of Bacterial
Chapter: 6 Drug Toxicity Infections: DNA Replication, Transcription, and
Chapter: 7 Pharmacogenomics Translation
Chapter: 8 Principles of Cellular Excitability and Chapter: 35 Pharmacology of Bacterial and
Electrochemical Transmission Mycobacterial Infections: Cell Wall Synthesis
Chapter: 9 Principles of Nervous System Chapter: 36 Pharmacology of Fungal Infections
Physiology and Pharmacology Chapter: 37 Pharmacology of Parasitic Infections
Chapter: 10 Cholinergic Pharmacology Chapter: 38 Pharmacology of Viral Infections
Chapter: 11 Adrenergic Pharmacology Chapter: 39 Pharmacology of Cancer: Genome
Chapter: 12 Local Anesthetic Pharmacology Synthesis, Stability, and Maintenance
Chapter: 13 Pharmacology of GABAergic and Chapter: 40 Pharmacology of Cancer: Signal
Glutamatergic Neurotransmission Transduction
Chapter: 14 Pharmacology of Dopaminergic Chapter: 41 Principles of Combination
Neurotransmission Chemotherapy
Chapter: 15 Pharmacology of Serotonergic and Chapter: 42 Principles of Inflammation and the
Central Adrenergic Neurotransmission Immune System
Chapter: 16 Pharmacology of Abnormal Chapter: 43 Pharmacology of Eicosanoids
Electrical Neurotransmission in the Central Chapter: 44 Histamine Pharmacology
Nervous System Chapter: 45 Pharmacology of Hematopoiesis
Chapter: 17 General Anesthetic Pharmacology and Immunomodulation
Chapter: 18 Pharmacology of Analgesia Chapter: 46 Pharmacology of
Chapter: 19 Pharmacology of Drugs of Abuse Immunosuppression
Chapter: 20 Pharmacology of Cholesterol and Chapter: 47 Integrative Inflammation
Lipoprotein Metabolism Pharmacology: Peptic Ulcer Disease
Chapter: 21 Pharmacology of Volume Chapter: 48 Integrative Inflammation
Regulation Pharmacology: Asthma
Chapter: 22 Pharmacology of Vascular Tone Chapter: 49 Integrative Inflammation
Chapter: 23 Pharmacology of Hemostasis and Pharmacology: Gout
Thrombosis Chapter: 50 Environmental Toxicology
Chapter: 24 Pharmacology of Cardiac Rhythm Chapter: 51 Drug Discovery and Preclinical
Chapter: 25 Pharmacology of Cardiac Development
Contractility Chapter: 52 Clinical Drug Evaluation and
Chapter: 26 Integrative Cardiovascular Regulatory Approval
Pharmacology: Hypertension, Ischemic Heart Chapter: 53 Systematic Detection of Adverse
Disease, and Heart Failure Drug Events
Chapter: 27 Pharmacology of the Hypothalamus Chapter: 54 Protein Therapeutics
and Pituitary Gland Chapter: 55 Drug Delivery Modalities
Chapter: 28 Pharmacology of the Thyroid Gland
Chapter: 29 Pharmacology of the Adrenal Cortex
,Chapter 1: Drug–Receptor Interactions
1. A patient is prescribed a β1-selective adrenergic antagonist for hypertension. The
drug primarily inhibits which aspect of receptor function?
A. Receptor synthesis
B. Agonist binding at the orthosteric site
C. Signal transduction downstream of the receptor
D. Ligand-independent receptor internalization
Answer: B
Rationale: β1-selective antagonists block the binding of endogenous catecholamines
(norepinephrine/epinephrine) at the orthosteric site of β1 receptors, preventing receptor activation.
They do not alter receptor synthesis or directly interfere with downstream signaling beyond
preventing activation.
Key words: β1 antagonist, receptor binding, orthosteric site, hypertension
2. A partial agonist at a receptor:
A. Produces maximal effect at full receptor occupancy
B. Blocks effects of a full agonist when co-administered
C. Is unable to bind the receptor
D. Has no effect in the presence of an antagonist
Answer: B
Rationale: Partial agonists have lower intrinsic activity than full agonists. When co-administered with
a full agonist, they compete for binding and reduce the maximal effect of the full agonist.
Key words: partial agonist, intrinsic activity, receptor competition
3. Which statement correctly distinguishes potency from efficacy?
A. Potency depends on receptor reserve; efficacy is independent of dose
B. Efficacy refers to the concentration required to achieve half-maximal effect
C. Potency measures maximal response a drug can produce
D. Efficacy is the maximal effect a drug can elicit regardless of dose
,Answer: D
Rationale: Efficacy is the intrinsic ability of a drug to elicit a maximal response. Potency refers to the
concentration required to achieve a given response (often EC50).
Key words: efficacy, potency, dose-response, EC50
4. A competitive antagonist:
A. Irreversibly inactivates the receptor
B. Shifts the dose-response curve of an agonist to the right without changing maximal response
C. Increases the intrinsic activity of the receptor
D. Produces a response in the absence of agonist
Answer: B
Rationale: Competitive antagonists compete with agonists for the same receptor binding site.
Increasing agonist concentration can overcome inhibition, causing a rightward shift in the dose-
response curve without changing maximal effect.
Key words: competitive antagonist, dose-response, receptor occupancy
5. Which of the following best describes spare receptors?
A. Receptors that cannot be activated by agonists
B. Receptors that exist in excess of what is needed for maximal response
C. Receptors that produce only partial agonist effects
D. Receptors permanently bound by antagonists
Answer: B
Rationale: Spare receptors refer to receptor populations that exceed the number needed to elicit a
maximal response. They allow full effect at submaximal receptor occupancy.
Key words: spare receptors, maximal response, receptor reserve
6. A patient develops tachyphylaxis to a β-agonist. The most likely mechanism
involves:
,A. Receptor downregulation
B. Enhanced agonist binding
C. Upregulation of second messengers
D. Increased intrinsic efficacy
Answer: A
Rationale: Tachyphylaxis is rapid desensitization of a receptor to agonist stimulation, often due to
receptor downregulation or phosphorylation, reducing receptor availability.
Key words: tachyphylaxis, receptor downregulation, desensitization
7. Non-competitive antagonists:
A. Bind only when agonist is bound
B. Reduce maximal response regardless of agonist concentration
C. Can be overcome by increasing agonist concentration
D. Act exclusively at allosteric sites
Answer: B
Rationale: Non-competitive antagonists reduce maximal response by either irreversibly binding the
receptor or modulating receptor function allosterically. Increasing agonist cannot restore maximal
effect.
Key words: non-competitive antagonist, allosteric modulation, maximal response
8. Receptor desensitization typically involves:
A. Increased receptor synthesis
B. Receptor phosphorylation and uncoupling from G-proteins
C. Conversion of antagonist into agonist
D. Depletion of extracellular ligand
Answer: B
Rationale: Desensitization commonly occurs via phosphorylation of receptors, leading to uncoupling
from G-proteins, reducing downstream signaling.
Key words: receptor desensitization, phosphorylation, G-protein uncoupling
,9. A ligand that binds preferentially to a receptor’s inactive state is called:
A. Full agonist
B. Inverse agonist
C. Partial agonist
D. Neutral antagonist
Answer: B
Rationale: Inverse agonists stabilize the inactive conformation of receptors, reducing basal
(constitutive) receptor activity.
Key words: inverse agonist, receptor conformations, basal activity
10. A clinician uses a drug with high receptor selectivity to minimize side effects.
This approach relies on:
A. Drug metabolism differences
B. Targeting specific receptor subtypes in relevant tissues
C. Non-competitive antagonism
D. Altered pharmacokinetics
Answer: B
Rationale: High receptor selectivity allows drugs to act on specific receptor subtypes in target tissues,
reducing off-target effects.
Key words: receptor selectivity, side effects, tissue specificity
11. A drug exhibits a ceiling effect. Which mechanism explains this phenomenon?
A. Saturation of enzymes metabolizing the drug
B. Receptor full occupancy or limited efficacy
C. Increased renal clearance at higher doses
D. Competitive inhibition at transporters
Answer: B
Rationale: The ceiling effect occurs when all receptors are occupied or the drug has limited intrinsic
efficacy, preventing further effect regardless of dose increase.
Key words: ceiling effect, receptor occupancy, intrinsic efficacy
, 12. Agonist efficacy is primarily determined by:
A. Binding affinity alone
B. Intrinsic activity at the receptor
C. Half-life in circulation
D. Route of administration
Answer: B
Rationale: Efficacy depends on the intrinsic activity of the agonist at the receptor, i.e., the ability to
trigger the receptor’s active conformation. Affinity affects potency but not efficacy.
Key words: agonist efficacy, intrinsic activity, receptor activation
13. Which type of antagonist can decrease the effect of both full and partial
agonists?
A. Competitive
B. Non-competitive
C. Reversible
D. Allosteric agonist
Answer: B
Rationale: Non-competitive antagonists reduce maximal response regardless of agonist type,
affecting both full and partial agonists.
Key words: non-competitive antagonist, partial agonist, maximal response
14. G-protein-coupled receptor (GPCR) activation primarily involves:
A. Direct ion channel blockade
B. Conformational change leading to G-protein signaling
C. Covalent receptor modification
D. Nuclear receptor translocation
Answer: B
Rationale: GPCRs transduce extracellular signals via conformational changes that activate G-proteins,
initiating intracellular signaling cascades.
