NUR 521 ADVANCED PHARMACOLOGY COMPLETE EXAM 4 | COMPLETE
EXAM 2026/2027 | QUESTIONS AND 100% VERIFIED ANSWERS | PASS
GUARANTEE
1. Q: What are the four processes of pharmacokinetics? ANSWER
Absorption, distribution, metabolism, and excretion (ADME).
2. Q: What is the "first-pass effect"? ANSWER The metabolism of a drug
in the liver after absorption from the GI tract before it reaches systemic
circulation.
3. Q: Which route of administration bypasses the first-pass effect?
ANSWER Parenteral routes (IV, IM, subcutaneous), sublingual,
transdermal, and inhalation.
4. Q: What is the volume of distribution (Vd)? ANSWER A theoretical
volume that relates the amount of drug in the body to the plasma
concentration.
5. Q: How does protein binding affect drug distribution? ANSWER Only
unbound (free) drug is pharmacologically active; highly protein-bound
drugs have smaller Vd and longer duration.
6. Q: What is the primary organ for drug metabolism? ANSWER The
liver, primarily via cytochrome P450 enzymes.
7. Q: What is a prodrug? ANSWER An inactive compound that is
metabolized in the body to produce an active drug.
8. Q: What does "bioavailability" mean? ANSWER The fraction of an
administered dose that reaches systemic circulation unchanged.
9. Q: What is the therapeutic index (TI)? ANSWER The ratio of the toxic
dose to the therapeutic dose (LD50/ED50); a narrow TI indicates a small
margin of safety.
10. Q: What is a drug's half-life (t½)? ANSWER The time required for
plasma drug concentration to decrease by 50%.
,11. Q: How many half-lives does it take to reach steady-state
concentration with repeated dosing? ANSWER Approximately 4–5 half-
lives.
12. Q: What is the difference between agonist and antagonist? ANSWER
An agonist binds to a receptor and activates it; an antagonist binds but
does not activate and blocks the receptor.
13. Q: What is a partial agonist? ANSWER A drug that binds to a receptor
and produces a submaximal response compared to a full agonist.
14. Q: What is the difference between pharmacokinetic and
pharmacodynamic drug interactions? ANSWER Pharmacokinetic
interactions affect ADME; pharmacodynamic interactions affect drug
action at the site of activity.
15. Q: What is enzyme induction? Give an example. ANSWER Increased
synthesis of drug-metabolizing enzymes, leading to faster metabolism.
Example: Rifampin induces CYP3A4.
16. Q: What is enzyme inhibition? Give an example. ANSWER Decreased
activity of drug-metabolizing enzymes. Example: Fluconazole inhibits
CYP3A4.
17. Q: What is the "ceiling effect" in pharmacology? ANSWER The dose
beyond which increasing the dose does not produce greater response
(common with partial agonists and some analgesics).
18. Q: What is tachyphylaxis? ANSWER Rapidly decreasing response to a
drug after administration of a few doses.
19. Q: What is the difference between tolerance and dependence?
ANSWER Tolerance requires increased doses for the same effect;
dependence is an adaptive state causing withdrawal symptoms upon
cessation.
20. Q: What is the P-glycoprotein transporter? ANSWER An efflux pump
that transports drugs out of cells, affecting absorption and distribution
(e.g., in the blood-brain barrier and GI tract).
21. Q: What does "loading dose" accomplish? ANSWER Rapidly achieves
therapeutic plasma concentrations by filling the volume of distribution.
22. Q: What is the formula for maintenance dose? ANSWER Maintenance
dose = Clearance × Target plasma concentration / Bioavailability.
, 23. Q: What is zero-order kinetics? ANSWER A constant amount of drug
is eliminated per unit time regardless of concentration (e.g., phenytoin at
high doses, ethanol).
24. Q: What is first-order kinetics? ANSWER A constant fraction of drug
is eliminated per unit time; most drugs follow this.
25. Q: What is the significance of the blood-brain barrier in
pharmacology? ANSWER It limits drug entry into the CNS; lipid-soluble,
small, and uncharged drugs cross more easily.
UNIT 2: Autonomic Nervous System Pharmacology (Questions 26–45)
26. Q: What neurotransmitter is released by postganglionic
parasympathetic neurons? ANSWER Acetylcholine.
27. Q: What neurotransmitter is released by most postganglionic
sympathetic neurons? ANSWER Norepinephrine (except sweat glands,
which release acetylcholine).
28. Q: What is the primary cholinergic receptor in the neuromuscular
junction? ANSWER Nicotinic receptor (Nn/Nm).
29. Q: What effect do beta-1 agonists have on the heart? ANSWER
Increased heart rate, contractility, and conduction velocity.
30. Q: What effect do beta-2 agonists have on the lungs? ANSWER
Bronchodilation.
31. Q: What is the antidote for organophosphate poisoning? ANSWER
Atropine (antimuscarinic) and pralidoxime (2-PAM, regenerates
acetylcholinesterase).
32. Q: What are the clinical uses of atropine? ANSWER Bradycardia,
preoperative reduction of secretions, organophosphate poisoning,
mydriasis.
33. Q: What are the "SLUDGE" symptoms of cholinergic excess? ANSWER
Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis.
34. Q: What is a major side effect of non-selective beta-blockers?
ANSWER Bronchospasm in asthmatics (due to beta-2 blockade).
EXAM 2026/2027 | QUESTIONS AND 100% VERIFIED ANSWERS | PASS
GUARANTEE
1. Q: What are the four processes of pharmacokinetics? ANSWER
Absorption, distribution, metabolism, and excretion (ADME).
2. Q: What is the "first-pass effect"? ANSWER The metabolism of a drug
in the liver after absorption from the GI tract before it reaches systemic
circulation.
3. Q: Which route of administration bypasses the first-pass effect?
ANSWER Parenteral routes (IV, IM, subcutaneous), sublingual,
transdermal, and inhalation.
4. Q: What is the volume of distribution (Vd)? ANSWER A theoretical
volume that relates the amount of drug in the body to the plasma
concentration.
5. Q: How does protein binding affect drug distribution? ANSWER Only
unbound (free) drug is pharmacologically active; highly protein-bound
drugs have smaller Vd and longer duration.
6. Q: What is the primary organ for drug metabolism? ANSWER The
liver, primarily via cytochrome P450 enzymes.
7. Q: What is a prodrug? ANSWER An inactive compound that is
metabolized in the body to produce an active drug.
8. Q: What does "bioavailability" mean? ANSWER The fraction of an
administered dose that reaches systemic circulation unchanged.
9. Q: What is the therapeutic index (TI)? ANSWER The ratio of the toxic
dose to the therapeutic dose (LD50/ED50); a narrow TI indicates a small
margin of safety.
10. Q: What is a drug's half-life (t½)? ANSWER The time required for
plasma drug concentration to decrease by 50%.
,11. Q: How many half-lives does it take to reach steady-state
concentration with repeated dosing? ANSWER Approximately 4–5 half-
lives.
12. Q: What is the difference between agonist and antagonist? ANSWER
An agonist binds to a receptor and activates it; an antagonist binds but
does not activate and blocks the receptor.
13. Q: What is a partial agonist? ANSWER A drug that binds to a receptor
and produces a submaximal response compared to a full agonist.
14. Q: What is the difference between pharmacokinetic and
pharmacodynamic drug interactions? ANSWER Pharmacokinetic
interactions affect ADME; pharmacodynamic interactions affect drug
action at the site of activity.
15. Q: What is enzyme induction? Give an example. ANSWER Increased
synthesis of drug-metabolizing enzymes, leading to faster metabolism.
Example: Rifampin induces CYP3A4.
16. Q: What is enzyme inhibition? Give an example. ANSWER Decreased
activity of drug-metabolizing enzymes. Example: Fluconazole inhibits
CYP3A4.
17. Q: What is the "ceiling effect" in pharmacology? ANSWER The dose
beyond which increasing the dose does not produce greater response
(common with partial agonists and some analgesics).
18. Q: What is tachyphylaxis? ANSWER Rapidly decreasing response to a
drug after administration of a few doses.
19. Q: What is the difference between tolerance and dependence?
ANSWER Tolerance requires increased doses for the same effect;
dependence is an adaptive state causing withdrawal symptoms upon
cessation.
20. Q: What is the P-glycoprotein transporter? ANSWER An efflux pump
that transports drugs out of cells, affecting absorption and distribution
(e.g., in the blood-brain barrier and GI tract).
21. Q: What does "loading dose" accomplish? ANSWER Rapidly achieves
therapeutic plasma concentrations by filling the volume of distribution.
22. Q: What is the formula for maintenance dose? ANSWER Maintenance
dose = Clearance × Target plasma concentration / Bioavailability.
, 23. Q: What is zero-order kinetics? ANSWER A constant amount of drug
is eliminated per unit time regardless of concentration (e.g., phenytoin at
high doses, ethanol).
24. Q: What is first-order kinetics? ANSWER A constant fraction of drug
is eliminated per unit time; most drugs follow this.
25. Q: What is the significance of the blood-brain barrier in
pharmacology? ANSWER It limits drug entry into the CNS; lipid-soluble,
small, and uncharged drugs cross more easily.
UNIT 2: Autonomic Nervous System Pharmacology (Questions 26–45)
26. Q: What neurotransmitter is released by postganglionic
parasympathetic neurons? ANSWER Acetylcholine.
27. Q: What neurotransmitter is released by most postganglionic
sympathetic neurons? ANSWER Norepinephrine (except sweat glands,
which release acetylcholine).
28. Q: What is the primary cholinergic receptor in the neuromuscular
junction? ANSWER Nicotinic receptor (Nn/Nm).
29. Q: What effect do beta-1 agonists have on the heart? ANSWER
Increased heart rate, contractility, and conduction velocity.
30. Q: What effect do beta-2 agonists have on the lungs? ANSWER
Bronchodilation.
31. Q: What is the antidote for organophosphate poisoning? ANSWER
Atropine (antimuscarinic) and pralidoxime (2-PAM, regenerates
acetylcholinesterase).
32. Q: What are the clinical uses of atropine? ANSWER Bradycardia,
preoperative reduction of secretions, organophosphate poisoning,
mydriasis.
33. Q: What are the "SLUDGE" symptoms of cholinergic excess? ANSWER
Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis.
34. Q: What is a major side effect of non-selective beta-blockers?
ANSWER Bronchospasm in asthmatics (due to beta-2 blockade).
