NURS 6013 Module 3 Exam Review | Questions and Answers | 2026/2027 Updated | 100% Correct.
Section 1 – Multiple-choice questions
Question 1: Local anesthetics
Clinical scenario: A 34-year-old patient has an infected tooth with inflamed surrounding tissue.
Lidocaine is being considered for local anesthesia during treatment.
1A. Why can local anesthetics be less effective in infected, acidic tissues?
A. Acidic conditions increase the non-ionized drug fraction and accelerate absorption.
B. Infection increases the number of sodium channels.
C. Acidic conditions completely deactivate epinephrine.
D. Acidic conditions increase the ionized drug fraction, reducing penetration into nerves.
Correct answer: D
Rationale: Lidocaine is a weak base. An acidic environment shifts more of the drug into its
ionized form, which crosses lipid membranes less effectively. Consequently, local anesthesia
may be less reliable in infected tissue.
1B. How does lidocaine interrupt nerve impulse transmission?
A. By blocking voltage-gated sodium channels.
B. By preventing substance P release in the spinal cord.
C. By stimulating mu-opioid receptors.
D. By activating ligand-gated chloride channels.
Correct answer: A
Rationale: Lidocaine blocks voltage-gated Na⁺ channels, reducing sodium entry into neurons.
This prevents the propagation of action potentials necessary for transmitting pain signals.
1C. Why is epinephrine sometimes combined with local anesthetics?
A. It constricts local blood vessels and reduces systemic absorption.
B. It competitively blocks alpha-adrenergic receptors.
,C. It produces vasodilation to accelerate drug absorption.
D. It changes the local anesthetic's pKa.
Correct answer: A
Rationale: Epinephrine promotes local vasoconstriction, which can reduce systemic absorption
of the anesthetic, prolong its local action, and decrease bleeding at the procedural site.
Question 2: Cardiovascular toxicity of local anesthetics
Which serious cardiovascular complication may occur with excessive systemic exposure to
bupivacaine?
A. Severe hypertension alone.
B. Ventricular fibrillation and cardiac conduction blocks.
C. Peripheral vasoconstriction without cardiac effects.
D. Increased cardiac output.
Correct answer: B
Rationale: Systemic local anesthetic toxicity can disrupt cardiac sodium-channel activity, impair
electrical conduction, and produce serious arrhythmias. Bupivacaine is particularly associated
with severe cardiotoxicity.
Question 3: Nerve sensitivity to local anesthetics
Which nerve characteristics influence susceptibility to local anesthetic blockade?
A. Thickness of adjacent skeletal muscle.
B. Acetylcholine receptor density.
C. Axonal diameter and myelination.
D. Total body water.
Correct answer: C
Rationale: Nerve-fiber diameter and myelination influence susceptibility to conduction blockade.
The relationship is complex because myelinated fibers require blockade across successive nodes
of Ranvier.
,Question 4: Morphine pharmacology
Clinical scenario: A 55-year-old postoperative patient receives intravenous morphine for pain
management.
4A. Which receptor is chiefly responsible for morphine's analgesic effects?
A. Kappa-opioid receptor.
B. Alpha-2 adrenergic receptor.
C. Delta-opioid receptor.
D. Mu-opioid receptor.
Correct answer: D
Rationale: Morphine is a mu-opioid receptor agonist. Activation of these receptors produces
analgesia but is also associated with adverse effects, including respiratory depression and
constipation.
4B. What cellular changes follow opioid-receptor activation in pain pathways?
A. Increased calcium entry and reduced potassium exit.
B. Blockade of norepinephrine and serotonin reuptake.
C. Increased presynaptic glutamate release.
D. Reduced calcium entry and increased potassium conductance.
Correct answer: D
Rationale: Mu-opioid receptors are coupled to inhibitory G proteins. Receptor activation reduces
presynaptic calcium influx and increases postsynaptic potassium conductance. These effects
reduce excitatory neurotransmitter release and neuronal excitability.
4C. What does the presence of markedly constricted pupils suggest in a patient exposed to
opioids?
A. Opioid withdrawal.
B. Histamine-mediated vasodilation.
C. A characteristic central nervous system effect associated with opioid exposure or toxicity.
, D. Increased sympathetic stimulation.
Correct answer: C
Rationale: Miosis is a characteristic opioid-associated finding. It can occur with therapeutic
opioid exposure and is also commonly associated with toxicity. It is not, by itself, sufficient to
diagnose overdose.
Question 5: Opioid antagonists
Which medication is a pure opioid-receptor antagonist used clinically to reverse opioid-induced
respiratory depression?
A. Pentazocine.
B. Buprenorphine.
C. Naloxone.
D. Methadone.
Correct answer: C — Naloxone
Rationale: Naloxone is an opioid-receptor antagonist that can reverse opioid-induced respiratory
depression. The other listed medications have opioid agonist or mixed agonist-antagonist
properties.
Question 6: Mixed opioid agonist-antagonists
Why can pentazocine exhibit a lower maximal degree of respiratory depression than a full mu-
opioid agonist?
A. It acts exclusively on gastrointestinal receptors.
B. Its effects can exhibit a ceiling.
C. It increases the brainstem's sensitivity to carbon dioxide.
D. It has no interaction with opioid receptors involved in analgesia.
Correct answer: B
Rationale: Pentazocine has mixed opioid-receptor activity, including kappa agonism and mu
antagonism or partial agonism. Certain effects may exhibit a ceiling, although clinically
important respiratory depression remains possible.
Section 1 – Multiple-choice questions
Question 1: Local anesthetics
Clinical scenario: A 34-year-old patient has an infected tooth with inflamed surrounding tissue.
Lidocaine is being considered for local anesthesia during treatment.
1A. Why can local anesthetics be less effective in infected, acidic tissues?
A. Acidic conditions increase the non-ionized drug fraction and accelerate absorption.
B. Infection increases the number of sodium channels.
C. Acidic conditions completely deactivate epinephrine.
D. Acidic conditions increase the ionized drug fraction, reducing penetration into nerves.
Correct answer: D
Rationale: Lidocaine is a weak base. An acidic environment shifts more of the drug into its
ionized form, which crosses lipid membranes less effectively. Consequently, local anesthesia
may be less reliable in infected tissue.
1B. How does lidocaine interrupt nerve impulse transmission?
A. By blocking voltage-gated sodium channels.
B. By preventing substance P release in the spinal cord.
C. By stimulating mu-opioid receptors.
D. By activating ligand-gated chloride channels.
Correct answer: A
Rationale: Lidocaine blocks voltage-gated Na⁺ channels, reducing sodium entry into neurons.
This prevents the propagation of action potentials necessary for transmitting pain signals.
1C. Why is epinephrine sometimes combined with local anesthetics?
A. It constricts local blood vessels and reduces systemic absorption.
B. It competitively blocks alpha-adrenergic receptors.
,C. It produces vasodilation to accelerate drug absorption.
D. It changes the local anesthetic's pKa.
Correct answer: A
Rationale: Epinephrine promotes local vasoconstriction, which can reduce systemic absorption
of the anesthetic, prolong its local action, and decrease bleeding at the procedural site.
Question 2: Cardiovascular toxicity of local anesthetics
Which serious cardiovascular complication may occur with excessive systemic exposure to
bupivacaine?
A. Severe hypertension alone.
B. Ventricular fibrillation and cardiac conduction blocks.
C. Peripheral vasoconstriction without cardiac effects.
D. Increased cardiac output.
Correct answer: B
Rationale: Systemic local anesthetic toxicity can disrupt cardiac sodium-channel activity, impair
electrical conduction, and produce serious arrhythmias. Bupivacaine is particularly associated
with severe cardiotoxicity.
Question 3: Nerve sensitivity to local anesthetics
Which nerve characteristics influence susceptibility to local anesthetic blockade?
A. Thickness of adjacent skeletal muscle.
B. Acetylcholine receptor density.
C. Axonal diameter and myelination.
D. Total body water.
Correct answer: C
Rationale: Nerve-fiber diameter and myelination influence susceptibility to conduction blockade.
The relationship is complex because myelinated fibers require blockade across successive nodes
of Ranvier.
,Question 4: Morphine pharmacology
Clinical scenario: A 55-year-old postoperative patient receives intravenous morphine for pain
management.
4A. Which receptor is chiefly responsible for morphine's analgesic effects?
A. Kappa-opioid receptor.
B. Alpha-2 adrenergic receptor.
C. Delta-opioid receptor.
D. Mu-opioid receptor.
Correct answer: D
Rationale: Morphine is a mu-opioid receptor agonist. Activation of these receptors produces
analgesia but is also associated with adverse effects, including respiratory depression and
constipation.
4B. What cellular changes follow opioid-receptor activation in pain pathways?
A. Increased calcium entry and reduced potassium exit.
B. Blockade of norepinephrine and serotonin reuptake.
C. Increased presynaptic glutamate release.
D. Reduced calcium entry and increased potassium conductance.
Correct answer: D
Rationale: Mu-opioid receptors are coupled to inhibitory G proteins. Receptor activation reduces
presynaptic calcium influx and increases postsynaptic potassium conductance. These effects
reduce excitatory neurotransmitter release and neuronal excitability.
4C. What does the presence of markedly constricted pupils suggest in a patient exposed to
opioids?
A. Opioid withdrawal.
B. Histamine-mediated vasodilation.
C. A characteristic central nervous system effect associated with opioid exposure or toxicity.
, D. Increased sympathetic stimulation.
Correct answer: C
Rationale: Miosis is a characteristic opioid-associated finding. It can occur with therapeutic
opioid exposure and is also commonly associated with toxicity. It is not, by itself, sufficient to
diagnose overdose.
Question 5: Opioid antagonists
Which medication is a pure opioid-receptor antagonist used clinically to reverse opioid-induced
respiratory depression?
A. Pentazocine.
B. Buprenorphine.
C. Naloxone.
D. Methadone.
Correct answer: C — Naloxone
Rationale: Naloxone is an opioid-receptor antagonist that can reverse opioid-induced respiratory
depression. The other listed medications have opioid agonist or mixed agonist-antagonist
properties.
Question 6: Mixed opioid agonist-antagonists
Why can pentazocine exhibit a lower maximal degree of respiratory depression than a full mu-
opioid agonist?
A. It acts exclusively on gastrointestinal receptors.
B. Its effects can exhibit a ceiling.
C. It increases the brainstem's sensitivity to carbon dioxide.
D. It has no interaction with opioid receptors involved in analgesia.
Correct answer: B
Rationale: Pentazocine has mixed opioid-receptor activity, including kappa agonism and mu
antagonism or partial agonism. Certain effects may exhibit a ceiling, although clinically
important respiratory depression remains possible.
