Pharmacodynamics Practice Questions
78 multiple-choice questions on Pharmacodynamics for paramedic and EMT students, from Chapter 13 (Principles of Pharmacology). Read each question, pick your answer, then tap Show answer to check it and read the explanation.
78 practice questions
Pharmacodynamics describes:
- A. How a drug produces its effects
- B. How a drug is absorbed into the blood
- C. How a drug is excreted from the body
- D. How a drug must be stored and handled
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Answer: A. How a drug produces its effects
Most drugs act at receptors.
A receptor is:
- A. An enzyme that breaks down drug molecules
- B. A carrier protein circulating in the blood
- C. The active molecule of the drug itself
- D. A cell site where a drug binds to act
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Answer: D. A cell site where a drug binds to act
Think of a lock that fits a specific key. Receptors are specific sites on or in a cell.
An agonist is a drug that:
- A. Permanently destroys the receptor it binds
- B. Increases the number of cell receptors
- C. Binds a receptor and activates it
- D. Binds a receptor and blocks its response
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Answer: C. Binds a receptor and activates it
Albuterol is a beta-2 agonist. Activation produces the expected response.
An antagonist is a drug that:
- A. Increases the number of available receptors
- B. Binds a receptor and blocks its response
- C. Binds and produces a partial response
- D. Binds a receptor and stimulates it
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Answer: B. Binds a receptor and blocks its response
Naloxone is an opioid antagonist.
A partial agonist:
- A. Binds and blocks the receptor completely
- B. Binds and produces a weaker response
- C. Has no measurable affinity for the receptor
- D. Binds and produces a full maximal response
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Answer: B. Binds and produces a weaker response
Buprenorphine is a common example. Its response is weaker than that of a full agonist.
Affinity refers to:
- A. How strongly a drug binds a receptor
- B. The dose required to produce an effect
- C. The strength of the response produced
- D. How long the drug remains in the body
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Answer: A. How strongly a drug binds a receptor
A drug with high affinity can displace one with lower affinity.
A competitive antagonist:
- A. Binds irreversibly to the receptor
- B. Can be overcome by more agonist
- C. Binds at a separate allosteric site
- D. Enhances the effect of the agonist
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Answer: B. Can be overcome by more agonist
Increasing agonist concentration shifts the balance. It competes for the same receptor site.
A noncompetitive antagonist:
- A. Always binds the agonist's own site
- B. Is overcome by giving more agonist
- C. Has no recognized clinical applications
- D. Cannot be reversed by more agonist
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Answer: D. Cannot be reversed by more agonist
Its effect persists until new receptors are made. It binds elsewhere or irreversibly.
Potency refers to:
- A. The maximum effect the drug can produce
- B. The amount needed for a given effect
- C. The margin between effective and toxic doses
- D. How long the drug's effect lasts after dosing
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Answer: B. The amount needed for a given effect
A more potent drug achieves the same effect at a lower dose.
Efficacy refers to:
- A. The rate at which a drug is eliminated
- B. The maximum effect a drug can produce
- C. The dose needed for a given effect
- D. How tightly a drug binds its receptor
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Answer: B. The maximum effect a drug can produce
A drug can be potent but have low efficacy.
The therapeutic index describes:
- A. The fraction of drug bound to protein
- B. The dose that produces half of the maximal effect
- C. The rate at which a drug is absorbed
- D. The effective dose compared with the toxic dose
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Answer: D. The effective dose compared with the toxic dose
A narrow therapeutic index means small dosing errors can be dangerous. The dose producing half the maximal effect is a potency measure, one input to the index but not the index itself.
A drug with a narrow therapeutic index, such as digoxin, requires:
- A. Careful dosing and monitoring
- B. Rapid IV push to reach effect quickly
- C. No monitoring once a dose is set
- D. Higher doses to reach a therapeutic effect
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Answer: A. Careful dosing and monitoring
Many toxic presentations involve these drugs. Toxicity occurs near therapeutic levels.
The therapeutic threshold is:
- A. The minimum level for the desired effect
- B. The maximum safe dose that can be given
- C. The time for levels to fall by half
- D. The level at which toxicity begins
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Answer: A. The minimum level for the desired effect
Below it, the drug produces little benefit.
Up-regulation of receptors occurs when:
- A. A receptor is chronically blocked
- B. A receptor is chronically stimulated
- C. A drug is excreted by the kidneys
- D. A drug is given once at a high dose
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Answer: A. A receptor is chronically blocked
This helps explain rebound effects when a blocker is stopped abruptly. The cell responds to chronic blockade or understimulation by making more receptors.
Down-regulation occurs when:
- A. The dose of a drug is gradually reduced
- B. Receptors are chronically blocked by a drug
- C. Chronic stimulation reduces receptors
- D. A drug is withheld for several days or weeks
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Answer: C. Chronic stimulation reduces receptors
Long-term beta agonist use is one example. Fewer receptors produce tolerance.
A drug's action may also occur through:
- A. Chemical, osmotic, or pH effects
- B. Absorption into the blood and nothing else
- C. Receptor binding and nothing else
- D. Binding to plasma proteins and nothing else
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Answer: A. Chemical, osmotic, or pH effects
Antacids and activated charcoal work without receptors.
Ketorolac 10 mg IV relieves pain about as well as 30 mg, while the higher dose adds side effects. This illustrates:
- A. Rapid tachyphylaxis to ketorolac
- B. An analgesic ceiling effect
- C. Competitive antagonism
- D. A wide therapeutic index
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Answer: B. An analgesic ceiling effect
Above a certain dose, NSAIDs such as ketorolac give no further pain relief, only more risk: a ceiling effect, shown in ED trials of 10, 15, and 30 mg. Rapid tachyphylaxis is loss of response with repeated doses, competitive antagonism needs a second drug at the receptor, and a wide therapeutic index describes a safety margin, not a plateau in benefit.
Benzodiazepines are called positive allosteric modulators of the GABA-A receptor because they:
- A. Bind a separate site and boost GABA's effect
- B. Open the chloride channel with no GABA present
- C. Compete with GABA for its own binding site
- D. Block glutamate at the NMDA receptor
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Answer: A. Bind a separate site and boost GABA's effect
Benzodiazepines bind a site distinct from GABA's and make the chloride channel open more often when GABA binds. They cannot open the chloride channel with no GABA present (high-dose barbiturates can), they do not compete with GABA for its own binding site, and blocking glutamate at the NMDA receptor is ketamine's mechanism.
Corticosteroids take hours to reduce airway inflammation because they act through:
- A. Membrane ion channels that open instantly
- B. G proteins that raise cyclic AMP
- C. Receptors that change gene expression
- D. Enzymes in the synaptic cleft
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Answer: C. Receptors that change gene expression
Steroids cross the cell membrane and bind intracellular receptors that change gene expression, so new anti-inflammatory proteins take hours to appear. Membrane ion channels open within milliseconds, G proteins that raise cyclic AMP act within seconds to minutes (as with beta agonists), and enzymes in the synaptic cleft such as acetylcholinesterase are not their target.
The nicotinic acetylcholine receptor at the neuromuscular junction is an example of a:
- A. G protein-coupled receptor
- B. Intracellular nuclear receptor
- C. Enzyme-linked tyrosine kinase
- D. Ligand-gated ion channel
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Answer: D. Ligand-gated ion channel
When acetylcholine binds the nicotinic receptor, the receptor itself opens as an ion channel within milliseconds: a ligand-gated ion channel. Muscarinic and adrenergic receptors are G protein-coupled receptors, steroids act on intracellular nuclear receptors, and insulin acts on an enzyme-linked tyrosine kinase receptor.
A patient has taken high-dose opioids for years. To which opioid effects does little tolerance develop?
- A. Euphoria and pain relief
- B. Constipation and pupil constriction
- C. Nausea and drowsiness
- D. Sedation and respiratory depression
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Answer: B. Constipation and pupil constriction
Tolerance develops to opioid euphoria and pain relief, to nausea and drowsiness, and (incompletely) to sedation and respiratory depression, which is why tolerant patients need larger doses yet can still stop breathing. Little tolerance develops to constipation and pupil constriction, so chronic users stay constipated and miotic.
A patient who stopped his clonidine abruptly 2 days ago has BP 210/120, tachycardia, and anxiety. The best explanation is:
- A. Rebound sympathetic activity after withdrawal
- B. An allergic reaction to clonidine
- C. Clonidine toxicity from accumulation
- D. Alpha-2 receptors blocked by leftover clonidine
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Answer: A. Rebound sympathetic activity after withdrawal
Clonidine suppresses sympathetic outflow through central alpha-2 stimulation, and the body adapts. Stopping it abruptly removes that brake, and rebound sympathetic activity after withdrawal causes hypertension, tachycardia, and agitation. This is not an allergic reaction to clonidine; clonidine toxicity from accumulation causes bradycardia and hypotension instead; and clonidine stimulates rather than blocks alpha-2 receptors.
A graph plots the percentage of patients who respond at each dose of a drug. This is a:
- A. Graded dose-response curve
- B. Plasma concentration-time curve
- C. Quantal dose-response curve
- D. Receptor saturation curve
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Answer: C. Quantal dose-response curve
A quantal curve shows the fraction of a population that responds (an all-or-none outcome) at each dose; ED50 and LD50 come from it. A graded dose-response curve shows how the size of the effect grows in one patient, a plasma concentration-time curve shows drug levels over time, and receptor saturation describes binding, not the share of patients responding.
A patient's alcohol withdrawal has become worse with each withdrawal episode over the years, with earlier seizures each time. This is called:
- A. Tachyphylaxis
- B. Cross-tolerance
- C. Down-regulation
- D. Kindling
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Answer: D. Kindling
Kindling is the progressive worsening of withdrawal (earlier seizures, more delirium) after repeated withdrawal episodes, so these patients need early, adequate benzodiazepine treatment. Tachyphylaxis is rapid loss of a drug's effect, cross-tolerance is tolerance extending to related drugs, and down-regulation is loss of receptors with chronic stimulation.
Buprenorphine binds mu receptors more tightly and works at a lower dose than morphine, yet morphine can relieve more severe pain at full doses. Morphine has greater:
- A. Potency
- B. Efficacy
- C. Affinity
- D. Selectivity
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Answer: B. Efficacy
Efficacy is the maximal effect a drug can produce; morphine, a full agonist, has a higher ceiling than the partial agonist buprenorphine. Buprenorphine has greater potency (it works at a lower dose) and greater affinity (it binds more tightly). Selectivity refers to which receptor types a drug acts on.
Carfentanil overdoses may need several naloxone doses mainly because carfentanil:
- A. Is not a true opioid receptor agonist
- B. Is cleared from the body faster than naloxone
- C. Prevents naloxone from being absorbed
- D. Is very potent with high receptor affinity
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Answer: D. Is very potent with high receptor affinity
Carfentanil is roughly 10,000 times as potent as morphine and binds mu receptors with high affinity, so more naloxone is needed to compete it off the receptors; support ventilation while titrating. It is a true opioid receptor agonist, it is not cleared faster than naloxone (it lasts longer), and nothing about it prevents naloxone from being absorbed.
Drug A has a therapeutic index of 2, and Drug B has a therapeutic index of 50. Which statement is correct?
- A. Drug B is more potent than Drug A
- B. Drug A has the smaller margin of safety
- C. Drug A is more efficacious than Drug B
- D. Drug B needs regular blood-level monitoring
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Answer: B. Drug A has the smaller margin of safety
The therapeutic index (toxic dose divided by effective dose) measures the margin of safety: a toxic dose only twice the effective dose leaves Drug A little room for error. The index does not tell you which drug is more potent or more efficacious, and it is the narrow-index drug (A), not Drug B, that would need blood-level monitoring.
Which home medication is most likely to cause toxicity from a modest dose change or a new interacting drug?
- A. Loratadine
- B. Warfarin
- C. Omeprazole
- D. Docusate
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Answer: B. Warfarin
Warfarin has a narrow therapeutic index: small changes in dose, diet, or interacting drugs can push the INR into the bleeding range. Loratadine, omeprazole, and docusate have wide margins between effective and toxic doses.
ED50 is:
- A. The dose that is toxic to 50% of a population
- B. The dose effective in 50% of a population
- C. Half of the usual adult maintenance dose
- D. The dose lethal to 50% of a population
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Answer: B. The dose effective in 50% of a population
ED50 = median effective dose.
LD50 is:
- A. The dose lethal to 50% of a test animal population
- B. Half of the drug's total daily dose
- C. The dose effective in 50% of a population
- D. The loading dose that fills 50% of receptors
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Answer: A. The dose lethal to 50% of a test animal population
LD50 is used in animal toxicity studies.
Mannitol lowers intracranial pressure mainly by:
- A. Blocking receptors on cerebral vessels
- B. Pulling water from brain tissue by osmosis
- C. Constricting cerebral arteries directly
- D. Sedating the patient to lower brain metabolism
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Answer: B. Pulling water from brain tissue by osmosis
Mannitol works without a receptor: it stays in the blood and creates an osmotic gradient that pulls water out of brain tissue. It does not act by blocking receptors on cerebral vessels or constricting cerebral arteries directly, and it has no effect from sedating the patient to lower brain metabolism. Its diuresis can cause hypotension, so volume status matters.
The dose-response curve shows:
- A. Time from dosing to onset of effect
- B. Plasma level over time after one dose
- C. How effect size changes with dose
- D. The drug's elimination half-life
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Answer: C. How effect size changes with dose
Plateau indicates maximal effect. Plasma level over time is a concentration-time curve, a pharmacokinetic graph.
Tachyphylaxis is:
- A. Rapid loss of response to closely repeated doses
- B. Tolerance that develops over months
- C. Increased sensitivity to repeat doses
- D. An immediate allergic reaction to a drug
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Answer: A. Rapid loss of response to closely repeated doses
Example: diminishing response to repeated doses of some sympathomimetics. It develops over a short time.
Tolerance means:
- A. Reduced response needing larger doses
- B. Physical dependence with withdrawal signs
- C. An increased response with each new dose
- D. An allergic reaction after repeated doses
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Answer: A. Reduced response needing larger doses
Chronic opioid users develop tolerance to analgesic effects. The decrease develops over time.
Cross-tolerance occurs when:
- A. Two drugs cancel out each other's effects
- B. A drug is given by two different routes
- C. A single drug produces two separate effects
- D. Tolerance extends to related drugs
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Answer: D. Tolerance extends to related drugs
Tolerance to one benzodiazepine usually extends to others.
Physical dependence is characterized by:
- A. An allergic reaction with each new dose
- B. A reduced drug effect at the same dose
- C. Psychological craving with no physical signs
- D. Withdrawal symptoms when the drug is stopped abruptly
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Answer: D. Withdrawal symptoms when the drug is stopped abruptly
Dependence produces a physiologic withdrawal syndrome.
A patient has used oxymetazoline nasal spray several times a day for 2 weeks and is now more congested than before. The best explanation is:
- A. A delayed allergy to the spray
- B. A sinus infection from the nozzle
- C. Rebound congestion from receptor adaptation
- D. An idiosyncratic genetic reaction to the spray
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Answer: C. Rebound congestion from receptor adaptation
Constant alpha-agonist vasoconstriction leads to receptor adaptation, so congestion rebounds as each dose wears off (rhinitis medicamentosa); labeling limits use to 3 days. A delayed allergy to the spray, a sinus infection from the nozzle, or an idiosyncratic genetic reaction would not explain worsening tied to overuse.
A patient who has taken prednisone daily for 6 months stops it abruptly and becomes weak and hypotensive. The most likely cause is:
- A. Up-regulated beta receptors on the heart
- B. A delayed allergic reaction to prednisone
- C. Rebound histamine release from mast cells
- D. Suppressed adrenal cortisol production
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Answer: D. Suppressed adrenal cortisol production
Months of steroid therapy suppress the hypothalamic-pituitary-adrenal axis, so the adrenal glands cannot make enough cortisol when the drug stops, causing adrenal insufficiency. Up-regulated beta receptors on the heart explain rebound tachycardia after stopping a beta blocker, not hypotension; a delayed allergic reaction to prednisone and rebound histamine release from mast cells do not explain this pattern.
Idiosyncratic reaction refers to:
- A. An immune-mediated allergic reaction
- B. A toxic response to an excessive dose
- C. An unpredictable individual response
- D. An expected, dose-related side effect
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Answer: C. An unpredictable individual response
Example: paradoxical agitation from benzodiazepines in some patients. It is often genetic.
A synergistic drug effect means:
- A. Combined effect equals the sum of each
- B. One drug blocks the other's receptor
- C. Combined effect is greater than the sum of each
- D. The drugs' effects cancel each other out
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Answer: C. Combined effect is greater than the sum of each
Example: opioids + benzodiazepines on respiratory depression.
Potentiation describes:
- A. Two agonists acting at the same receptor
- B. One drug blocking another's receptor
- C. One drug enhancing another's effect
- D. Reduced response after repeated doses
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Answer: C. One drug enhancing another's effect
Promethazine potentiates opioid sedation. The potentiating drug does not have that effect itself.
An additive effect means:
- A. Combined effect equals the sum of each
- B. The drugs' effects cancel each other out
- C. Neither drug's effect changes at all
- D. Combined effect exceeds the sum of each
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Answer: A. Combined effect equals the sum of each
Two drugs with similar actions sum together.
Second messengers in drug action are:
- A. Molecules that relay signals inside cells
- B. A second dose given to boost the effect
- C. Hormones released after the first drug
- D. A second receptor that binds the drug
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Answer: A. Molecules that relay signals inside cells
G-protein-coupled receptors use second messengers. Example: cAMP.
Drug action by enzyme inhibition is illustrated by:
- A. Aspirin blocking cyclooxygenase
- B. Albuterol at beta-2 receptors
- C. Epinephrine at alpha and beta receptors
- D. Naloxone at opioid receptors
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Answer: A. Aspirin blocking cyclooxygenase
Enzyme inhibitors block a biochemical pathway. ACE inhibitors are another example.
Which best describes 'mechanism of action'?
- A. How a drug produces its effect
- B. How the body eliminates the drug
- C. Where in the body the drug is stored
- D. How fast the drug begins to work
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Answer: A. How a drug produces its effect
Understanding mechanism predicts effects and side effects. Mechanism is described at the molecular or cellular level. Elimination and storage are pharmacokinetic properties; mechanism of action is what the drug does at its target.
A drug's side effect is:
- A. A predictable unintended effect
- B. An error in calculating the dose
- C. An immune-mediated allergic reaction
- D. An effect that is always dangerous
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Answer: A. A predictable unintended effect
Side effects may be benign or harmful; many are expected.
The plateau of the dose-response curve indicates:
- A. The maximal effect of the drug
- B. The onset of toxic effects
- C. The dose with no measurable effect
- D. The time of onset of action
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Answer: A. The maximal effect of the drug
Beyond the plateau, higher doses only add toxicity.
Placebo effect is:
- A. An expected side effect of a drug
- B. An allergic reaction to inactive fillers
- C. A toxic effect of an inactive drug
- D. Benefit arising from expectation alone
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Answer: D. Benefit arising from expectation alone
Placebo effects are real and relevant even in field care.
Naloxone reverses opioid toxicity because it is a:
- A. Competitive antagonist at mu opioid receptors
- B. Physiologic antagonist at beta receptors
- C. Noncompetitive enzyme inhibitor
- D. Partial agonist at GABA receptors
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Answer: A. Competitive antagonist at mu opioid receptors
Naloxone has high affinity for opioid receptors with no intrinsic activity, displacing agonists.
Buprenorphine is best described as a:
- A. Full mu receptor agonist of low potency
- B. High-affinity partial mu agonist
- C. Pure competitive mu receptor antagonist
- D. Agonist at benzodiazepine receptors
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Answer: B. High-affinity partial mu agonist
Its high affinity means it binds tightly, while partial activity limits its maximal effect.
A patient dependent on heroin takes buprenorphine and develops sudden withdrawal. Why?
- A. It speeds the liver's metabolism of heroin
- B. It blocks GABA receptors in the brainstem
- C. It is a pure opioid antagonist like naloxone
- D. It displaces heroin but activates receptors less
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Answer: D. It displaces heroin but activates receptors less
Replacing a full agonist with a partial agonist suddenly lowers receptor activation, precipitating withdrawal.
Buprenorphine causes less respiratory depression at high doses than full agonists because it has:
- A. A ceiling on respiratory depression
- B. Antagonist activity at GABA receptors
- C. A very short elimination half-life
- D. No affinity for mu opioid receptors
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Answer: A. A ceiling on respiratory depression
As a partial agonist, buprenorphine plateaus in respiratory effect, though combining it with sedatives remains dangerous.
Drug A produces a given effect at 0.1 mg, while Drug B needs 10 mg for the same effect. Drug A is:
- A. More potent
- B. More efficacious
- C. Less potent
- D. More toxic
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Answer: A. More potent
Potency compares the dose needed for an effect; it says nothing about maximal effect.
Fentanyl is about 100 times more potent than morphine. This means:
- A. Fentanyl's half-life is about 100 times longer than morphine's
- B. A far smaller dose of fentanyl gives equivalent analgesia
- C. Fentanyl produces 100 times more pain relief at maximum dose
- D. Fentanyl causes far less respiratory depression per dose
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Answer: B. A far smaller dose of fentanyl gives equivalent analgesia
Higher potency means a smaller dose is needed, not a greater maximal effect.
A drug has an LD50 of 200 mg/kg and an ED50 of 10 mg/kg. Its therapeutic index is:
- A. 0.05
- B. 20
- C. 2,000
- D. 190
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Answer: B. 20
Therapeutic index equals LD50 divided by ED50: 200 / 10 = 20.
Which drug requires blood-level monitoring because of its narrow therapeutic index?
- A. Diphenhydramine
- B. Lithium
- C. Ondansetron
- D. Albuterol
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Answer: B. Lithium
Lithium's toxic level is close to its therapeutic level, so serum levels are monitored.
A drug with high affinity for a receptor but no intrinsic activity is a(n):
- A. Partial agonist
- B. Prodrug
- C. Full agonist
- D. Antagonist
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Answer: D. Antagonist
Antagonists bind receptors but do not activate them, blocking agonists.
An inverse agonist is a drug that:
- A. Enhances the response to an agonist at the same receptor
- B. Binds the receptor but has no effect of its own
- C. Neutralizes an agonist by binding it chemically in plasma
- D. Opposes the agonist's effect at that receptor
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Answer: D. Opposes the agonist's effect at that receptor
Inverse agonists reduce a receptor's baseline (constitutive) activity, unlike neutral antagonists. It binds the receptor and produces an effect opposite to that of an agonist.
Epinephrine reversing histamine-induced bronchoconstriction is an example of:
- A. Partial agonism
- B. Chemical antagonism
- C. Physiologic antagonism
- D. Competitive antagonism
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Answer: C. Physiologic antagonism
The two drugs act on different receptors to produce opposing effects on the same organ.
Protamine reversing heparin is an example of:
- A. Competitive antagonism at a receptor
- B. Chemical antagonism
- C. Inverse agonism
- D. Physiologic antagonism
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Answer: B. Chemical antagonism
Protamine binds heparin directly to form an inactive complex, with no receptor involved.
Barbiturates differ from benzodiazepines at the GABA-A receptor in that barbiturates:
- A. Increase only the frequency of chloride channel opening
- B. Block GABA binding and close the chloride channel
- C. Lengthen channel opening and can open it without GABA
- D. Act on sodium channels rather than chloride channels
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Answer: C. Lengthen channel opening and can open it without GABA
Barbiturates' ability to act without GABA explains their greater risk of respiratory depression. Barbiturates prolong the duration of chloride channel opening and can open the channel directly at high doses.
Flumazenil reverses benzodiazepine sedation by acting as a:
- A. Inhibitor of acetylcholinesterase in the synapse
- B. Competitive antagonist at the mu opioid receptor
- C. Benzodiazepine-site competitive antagonist
- D. Direct agonist at the GABA-A chloride channel
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Answer: C. Benzodiazepine-site competitive antagonist
Flumazenil blocks benzodiazepines from enhancing GABA but does not reverse opioids or alcohol. It binds the benzodiazepine site on the GABA-A receptor.
Beta-adrenergic receptors produce their effects through G proteins that increase intracellular:
- A. Cyclic AMP (cAMP)
- B. Inositol triphosphate (IP3)
- C. Chloride ion concentration
- D. Cyclic GMP (cGMP)
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Answer: A. Cyclic AMP (cAMP)
Beta-receptor activation stimulates adenylyl cyclase, raising cAMP as the second messenger.
Glucagon helps in beta-blocker overdose because it:
- A. Raises cAMP via its own receptors, bypassing beta blockade
- B. Speeds hepatic metabolism and excretion of the beta blocker
- C. Directly stimulates alpha-1 receptors to raise vascular tone
- D. Competitively displaces the beta blocker from beta receptors
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Answer: A. Raises cAMP via its own receptors, bypassing beta blockade
Glucagon receptors activate adenylyl cyclase independently of beta receptors, improving heart rate and contractility.
In the presence of a competitive antagonist, the agonist dose-response curve:
- A. Shifts to the left with a higher maximum
- B. Is unchanged because the agonist binds first
- C. Shifts to the right with the same maximal effect
- D. Shifts to the right with a lower maximal effect
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Answer: C. Shifts to the right with the same maximal effect
More agonist is needed to compete for receptors, but enough agonist can still reach the full effect. A rightward shift with a lower maximum is the pattern of a noncompetitive antagonist.
Abruptly stopping a long-term beta blocker can cause rebound tachycardia and angina because:
- A. Beta receptors were destroyed by prolonged drug binding
- B. Beta receptors were up-regulated during chronic blockade
- C. Alpha receptors were down-regulated during chronic therapy
- D. The drug remains active in tissues for several weeks
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Answer: B. Beta receptors were up-regulated during chronic blockade
Chronic blockade increases receptor numbers, so normal catecholamines produce an exaggerated response when the drug stops.
A patient using an albuterol inhaler many times daily notices it works less well. A likely reason is:
- A. Beta-2 receptor desensitization and down-regulation
- B. Development of a true allergy to albuterol
- C. Up-regulation of beta-2 receptors from repeated use
- D. Faster hepatic conversion of albuterol to an inactive form
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Answer: A. Beta-2 receptor desensitization and down-regulation
Repeated agonist exposure reduces receptor number and responsiveness.
At higher doses, a beta-1 selective blocker such as metoprolol:
- A. Begins to act as a partial beta-1 agonist
- B. Gains alpha-1 blocking effects similar to carvedilol
- C. Becomes more cardioselective and spares beta-2 receptors
- D. Loses selectivity and can block beta-2 receptors
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Answer: D. Loses selectivity and can block beta-2 receptors
Receptor selectivity is relative and dose-dependent.
Diphenhydramine's sedation is called a side effect when it is used for an allergic reaction, but a therapeutic effect when used:
- A. For anaphylaxis
- B. For urticaria
- C. As a sleep aid
- D. For allergic rhinitis
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Answer: C. As a sleep aid
Whether an effect is a side effect depends on the reason the drug was given.
Aspirin's antiplatelet effect lasts the lifespan of the platelet (about 7 to 10 days) because it:
- A. Has an elimination half-life of about 10 days
- B. Irreversibly acetylates cyclooxygenase
- C. Reversibly binds platelet ADP receptors for days
- D. Is stored in body fat and released slowly
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Answer: B. Irreversibly acetylates cyclooxygenase
Platelets cannot make new COX, so irreversible inhibition lasts until new platelets are formed.
The 'lock and key' model of drug action illustrates that:
- A. Drugs act mainly by inducing liver enzymes
- B. Receptors are found only on nerve cell membranes
- C. All drugs bind equally well to all receptor types
- D. A drug's shape determines which receptor it fits
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Answer: D. A drug's shape determines which receptor it fits
Like a key in a lock, a drug must fit the receptor's binding site to bind and act. Shape determines both a drug's fit and its specificity for a receptor.
Chronic heavy alcohol use can produce metabolic (pharmacokinetic) tolerance, which results from:
- A. Decreased absorption of alcohol from the gut
- B. Faster hepatic metabolism from enzyme induction
- C. Down-regulation of brain receptors from chronic exposure
- D. Increased renal excretion of unchanged alcohol
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Answer: B. Faster hepatic metabolism from enzyme induction
Enzyme induction lowers blood levels; this differs from pharmacodynamic tolerance at the receptor. Increased liver enzyme activity metabolizes the drug faster.
Which describes pharmacodynamic tolerance?
- A. Increased renal excretion of the active drug
- B. Faster drug metabolism by induced liver enzymes
- C. Reduced oral absorption with repeated dosing
- D. Reduced receptor responsiveness to the drug
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Answer: D. Reduced receptor responsiveness to the drug
Pharmacodynamic tolerance happens at the target (receptor adaptation), not through drug handling. A higher concentration is then needed for the same effect.
Ketamine produces dissociative anesthesia mainly by:
- A. Stimulating alpha-2 receptors
- B. Antagonizing NMDA glutamate receptors
- C. Blocking mu opioid receptors
- D. Stimulating GABA-A receptors
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Answer: B. Antagonizing NMDA glutamate receptors
NMDA blockade disconnects thalamocortical and limbic systems while airway reflexes are largely preserved.
Calcium given in calcium channel blocker overdose works mainly by:
- A. Displacing the blocker from plasma albumin binding sites
- B. Directly stimulating beta-1 receptors on the heart
- C. Accelerating hepatic clearance of the channel blocker
- D. Raising extracellular calcium to overcome blockade
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Answer: D. Raising extracellular calcium to overcome blockade
More extracellular calcium increases calcium entry through the remaining open channels.
A partial agonist given alone acts as an agonist, but given with a full agonist it can act as a(n):
- A. Enzyme inducer, speeding the agonist's metabolism
- B. Antagonist, reducing the full agonist's effect
- C. Inverse agonist, lowering baseline receptor activity
- D. Synergist, doubling the full agonist's effect
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Answer: B. Antagonist, reducing the full agonist's effect
By occupying receptors with lower intrinsic activity, a partial agonist reduces the total response to a full agonist.
Intrinsic activity (efficacy) refers to:
- A. The speed at which a drug reaches its receptor
- B. How well a bound drug activates the receptor
- C. The dose needed to produce half the maximal effect
- D. How tightly a drug binds to its receptor site
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Answer: B. How well a bound drug activates the receptor
Affinity is binding strength; intrinsic activity is how much the bound drug activates the receptor. Intrinsic activity is the drug's ability, once bound, to produce a response.
Two drugs reach the same maximal effect, but Drug X does so at a lower dose. Compared with Drug Y, Drug X has:
- A. Greater potency and equal efficacy
- B. Greater efficacy and equal potency
- C. Equal potency and lower efficacy
- D. Lower potency and greater efficacy
Show answer
Answer: A. Greater potency and equal efficacy
Equal maximum means equal efficacy; a lower dose for the same effect means greater potency.
More Principles of Pharmacology practice questions
- Drug names, sources, and regulation (73)
- Pharmacokinetics (80)
- Pharmacodynamics
- Autonomic pharmacology (82)
- Drug classifications (85)
- Adverse effects and interactions (77)
- Special populations (72)
- Legal and safety aspects (70)
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