WGU D116 Advanced Pharmacology HIGH-YIELD MASTERY BANK 2025: 542 Expert-Curated Q&A with Detailed Rationales, NCLEX/APRN-Aligned Case Studies, and System-Based Clinical Applications

a1 receptor -->

Gq --> vasoconstriction (^BP), pupil dilation

*sympathetic receptor

Drugs: phenylephrine, midodrine

CX: Severe HTN, closed-angle glaucoma

Gq receptor does what

activates phospholipase C --> IP3 + DAG = ^ intracellular Ca+ = smooth muscle contraction

a2 receptor -->

Gi --> decrease NE release

*sympathetic receptor (works via neg feedback on presynaptic neuron)

Drugs: Clonidine, Methyldopa (safe in pregnancy)

Risks: Rebound HTN if suddenly stopped

Gi receptor does what?

inhibits adenylate cyclase --> decrease cAMP --> decreased NT release (blood pressure decreases?)

B1 receptor -->

Gs --> ^ HR (chronotropy), ^contractility (inotropy), ^ Renin release

*sympathetic receptor

Drugs: Dobutamine, Isoproterenol

Caution:causes arrhythmias, angina in CAD

Gs receptor does what?

Activates adenylate cyclase --> ^ cAMP --> smooth muscle relaxation = ^ HR! (^BP/^HR!! - emergency like dobutamine!)

B2 receptor -->

Gs --> Bronchodilation, vasodilation, uterine relaxation

*sympathetic receptor

Drugs: Albuterol, Salmeterol

Risks: Hypokalemia, tachycardia

M2 receptor -->

Gi --> decrease HR

*parasympathetic receptor

Affected by: Atropine (antagonist/anticholinergic)

Risk: tachy <3, dry mouth, blurred vision

**M2/Gi found in heart (SA/AV nodes)

M3 receptor -->

Gq --> ^ secretions, bronchoconstriction, miosis, bladder contraction

*parasympathetic receptor

Drugs: Bethanechol (used for urinary retention), pilocarpine (for glaucoma)

CX: asthma, COPD, PUD, dont give in obstruction!

**found in smooth muscle & glands

D1 receptor -->

Gs --> renal vasodilation = ^ renal perfusion & natriuresis

*dopamine receptors

Drug: Low-dose dopamine

Risk: hypotension, tachy, tissue necrosis

*can be used in shock

CYP450 Inducers (decrease drug levels) CRAPGPS

Carbamazepine

Rifampin

Alcohol (chronic)

Phenytoin

Griseofulvin

Phenobarbital

Sulfonylureas

*causes failure of OCP, Warfain

CYP450 Inhibitors (increase drug levels) SICKFACES.COM

Sodium Valproate

Isoniazid

Cimetidine

Ketoconazole

Fluconazole

Amiodarone

Chloramphenicol

Erythromycin

Sulfonamides

Ciprofloxacin

Omeprazole

Metronidazole

*cause toxicity!! (ex: warfarin = bleeding)

fluoroquinolones black box

tendon rupture, QT prolongation

SSRI black box in teens

suicidal

Antipsychotics black box in elderly

increased mortality in dementia

ACEi/ARBs black box

fetal toxicity esp. in 2/3 trimester

Amiodarone black box

pulmonary fibrosis, hepatotoxicity, thyroid dysfunction

Methotrexate black box

hepatotoxicity, myelosuppression

Carbamazepine black box

SJS/TEN (Esp in asians with HLA-B*1502)

monitor what with warfarin?

INR

(goal 2-3)

monitor what with lithium?

lithium levels (0.6-1.2), renal, thyroid (can cause hypothyroidism, nephrogenic DI)

*narrow TI.. monitor kidney & thyroid

monitor what with amiodarone?

LFT, TFT, PFTs

monitor what with clozapine and why?

ANC - high risk of agranulocytosis

monitor what with digoxin?

dig level, K+, ECG (toxicity = vision changes, arrhythmia)

what drugs have zero-order elimination?

phenytoin, ethanol, aspirin

what drugs have first pass effect?

nitroglycerin, propranolol (oral)

Loading dose equation

(Cp x Vd) / F

maintenance dose equation

(Cp x CL) / F

what toxicity can aminoglycosides cause?

ototoxicity, nephrotoxic

what toxicity can vancomycin cause?

red man syndrome (prevent by giving slow!! + an antihistamine)

what toxicity can methotrexate cause?

Mucositis, myelosuppression (rescue with leucovorin)

what toxicity can lithium cause?

tremor, hypothyroid, teratogenic (ebstein anomaly)

what toxicity can ACEi/ARBs cause?

hyperkalemia, angioedema

ACEI are important why:

first line in diabetes, CKD; avoid in pregnancy

Thiazides can cause:

cause hyperglycemia, hyperuricemia, hypercalcemia

loop diuretics can cause:

hypokalemia, ototoxicity

beta-blockers need to know:

contraindicated in asthma, bradycardia

metformin (antidiabetic) need to know:

lactic acidosis risk, stop if eGFR <30

SGLT2 inhibitors (antidiabetic) need to know:

increase UTI risk, DKA risk.. decrease CV events

GLP-1 agonists (antidiabetic) need to know:

weight loss, GI side effects, avoid in hx of medullary thyroid CA

insulin (antidiabetic) need to know:

hypoglycemia risk

SSRI need to know

1st line depression, anxiety, sexual dysfunction

antipsychotics need to know

EPS, metabolic syndrome (esp atypicals)

carbidopa/levodopa need to know

on/off phenomenon, dyskinesias

dopamine agonists need to know

impurse control disorders

anticholinergics need to know

dry mouth, blurry vision, urinary retention

antidote for opioids

naloxone

antidote for benzos

flumazenil

antidote for acetaminophen

N-acetylcysteine (NAC)

antidote for heparin

protamine sulfate

antidote for warfarin

vit K + PCC/FFP

antidote for digoxin

digiband (fab fragments)

antidote for iron

deferoxamine

antidote for

organophosphates

atropine + pralidoxime

antidote for methotrexate

Leucovorin (folinic acid)

A patient with BPH and resistant hypertension is prescribed doxazosin. Which receptor and second messenger pathway does it target, and how might this impact cardiac output?

A. Alpha-1 receptor; inhibits Gq → PLC → IP3/DAG → ↓Ca²⁺; lowers preload and afterload.

B. Beta-2 receptor; activates Gs → cAMP → ↑PKA.

C. Alpha-2 receptor; inhibits Gi → ↓cAMP.

D. Muscarinic M2 receptor; activates Gi → ↓cAMP.

A. Alpha-1 receptor; inhibits Gq → PLC → IP3/DAG → ↓Ca²⁺; lowers preload and afterload.

Rationale: Doxazosin blocks alpha-1 receptors, reducing intracellular calcium and vascular tone.

First-dose syncope with doxazosin is due to:

A. Reflex bradycardia due to baroreceptor activation.

B. Sudden vasodilation via alpha-1 blockade.

C. Direct cardiac suppression.

D. Central vasomotor suppression.

B. Sudden vasodilation via alpha-1 blockade.

Rationale: Profound vasodilation with initial dosing can cause orthostatic hypotension.

Clonidine discontinuation leads to hypertensive crisis because:

A. Persistent beta-adrenergic blockade.

B. Rebound increase in sympathetic tone due to alpha-2 receptor withdrawal.

C. Blockade of aldosterone secretion.

D. Excessive natriuresis.

B. Rebound increase in sympathetic tone due to alpha-2 receptor withdrawal.

Rationale: Clonidine suppresses CNS sympathetic outflow via alpha-2 agonism; stopping it abruptly reverses this.

Hemolytic anemia with methyldopa is best identified via:

A. Elevated bilirubin and LDH only.

B. Positive Coombs test indicating autoimmune destruction.

C. Reduced haptoglobin alone.

D. Negative reticulocyte count.

B. Positive Coombs test indicating autoimmune destruction.

Rationale: Methyldopa can trigger an autoimmune response against RBCs.

Dobutamine increases cardiac contractility by activating:

A. Gq → PLC → IP3 → ↑Ca²⁺

.B. Gi → ↓cAMP.

C. Gs → ↑cAMP → ↑PKA → ↑Ca²⁺.

D. Tyrosine kinase receptor → PI3K pathway.

C. Gs → ↑cAMP → ↑PKA → ↑Ca²⁺.

Rationale: Dobutamine’s β1-agonist action increases cAMP, enhancing calcium entry and contractility.

A patient on lithium develops tremor, polyuria, and hypothyroidism. Which drug could worsen lithium toxicity?

A. Ibuprofen

B. Acetaminophen

C. Azithromycin

D. Lorazepam

A. Ibuprofen

Rationale: NSAIDs like ibuprofen decrease lithium clearance by reducing renal perfusion.

A pregnant patient with autoimmune disease requires corticosteroids. Which agent is safest?

A. Dexamethasone

B. Prednisone

C. Triamcinolone

D. Methylprednisolone

B. Prednisone

Rationale: Prednisone is inactivated by placental 11β-HSD2, minimizing fetal exposure.

A patient on ketoconazole develops gynecomastia. This is most likely due to:

A. Inhibition of androgen receptors

B. Aromatization of testosterone to estradiol

C. Inhibition of steroid synthesis via CYP450 inhibition

D. Increased LH/FSH levels

C. Inhibition of steroid synthesis via CYP450 inhibition

Rationale: Ketoconazole inhibits CYP450 enzymes involved in steroid biosynthesis, including testosterone.

Which antifungal has a black box warning for cardiomyopathy and CHF exacerbation?

A. Fluconazole

B. Itraconazole

C. Voriconazole

D. Amphotericin B

B. Itraconazole

Rationale: Itraconazole is contraindicated in patients with ventricular dysfunction due to its negative inotropic effects.

A patient is treated with acetylcholinesterase inhibitors for myasthenia gravis and develops muscle fasciculations and bradycardia. How do you distinguish myasthenic vs. cholinergic crisis?

A. Increase dose and observe; if symptoms improve, it's cholinergic crisis.

B. Decrease dose and re-evaluate.

C. Give edrophonium; improvement = myasthenic, worsening = cholinergic.

D. Check serum acetylcholine levels.

C. Give edrophonium; improvement = myasthenic, worsening = cholinergic.

A patient on long-term glucocorticoid therapy requires surgery. Which action best prevents adrenal crisis?

A. Continue normal dose only.

B. Administer high-dose hydrocortisone perioperatively.

C. Substitute dexamethasone preoperatively.

D. Stop glucocorticoids 24 hours before surgery.

B. Administer high-dose hydrocortisone perioperatively.

Rationale: Patients on chronic steroids require "stress dosing" during physiological stress (surgery) to prevent adrenal insufficiency.

Which glucocorticoid has the highest anti-inflammatory potency with minimal mineralocorticoid activity?

A. Prednisone

B. Hydrocortisone

C. Dexamethasone

D. Fludrocortisone

C. Dexamethasone

Rationale: Dexamethasone has strong glucocorticoid effects and negligible mineralocorticoid activity.

A patient with hepatic failure and esophageal candidiasis needs antifungal treatment. Best choice?

A. Fluconazole

B. Ketoconazole

C. Itraconazole

D. Caspofungin

D. Caspofungin

Rationale: Caspofungin is not hepatically metabolized like the azoles and is safer in liver dysfunction.

Which azole antifungal is most associated with QT prolongation and CYP3A4 inhibition?

A. Fluconazole

B. Voriconazole

C. Clotrimazole

D. Terbinafine

B. Voriconazole

Rationale: Voriconazole strongly inhibits CYP3A4 and prolongs the QT interval.

Which antifungal may antagonize amphotericin B’s action?

A. Nystatin

B. Fluconazole

C. Ketoconazole

D. Flucytosine

B. Fluconazole

Rationale: Azoles inhibit ergosterol synthesis, decreasing the target for amphotericin B.

A patient on dopamine infusion develops tachyarrhythmia. What receptor-mediated mechanism is most likely responsible?

A. Beta-2 stimulation → vasodilation B. D1 activation → renal vasodilation C. Beta-1 activation → increased HR/contractility

D. Alpha-1 activation → reflex

C. Beta-1 activation → increased HR/contractility

Rationale: At moderate doses, dopamine stimulates beta-1 receptors leading to tachycardia.

Which muscarinic receptor is primarily responsible for bladder contraction in overactive bladder?

A. M1

B. M2

C. M3

D. M4

C. M3

Rationale: M3 receptor activation causes detrusor muscle contraction in the bladder.

Which drug is used as an antidote for cholinergic crisis due to organophosphates?

A. Atropine only

B. Pralidoxime and atropine

C. Neostigmine

D. Pilocarpine

B. Pralidoxime and atropine

Rationale: Atropine blocks muscarinic effects, and pralidoxime reactivates acetylcholinesterase.

A patient with Parkinson’s is treated with carbidopa/levodopa. Carbidopa’s role is:

A. Stimulates dopamine receptors in CNS

B. Prevents dopamine breakdown in brain

C. Inhibits peripheral decarboxylation of levodopa

D. Enhances dopamine reuptake

C. Inhibits peripheral decarboxylation of levodopa

Rationale: Carbidopa inhibits peripheral DOPA decarboxylase, increasing CNS levodopa availability.

Which drug increases cholinergic tone and is used in Alzheimer’s disease?

A. Atropine

B. Donepezil

C. Scopolamine

D. Ipratropium

B. Donepezil

Rationale: Donepezil is an acetylcholinesterase inhibitor used to improve cognition in Alzheimer’s.

A patient with chronic heart failure is started on spironolactone. Which potential complication should be most closely monitored?

A. Hyponatremia

B. Hyperkalemia

C. Hypoglycemia

D. Hypomagnesemia

B. Hyperkalemia

Rationale: Spironolactone is a potassium-sparing diuretic and aldosterone antagonist; it increases serum potassium.

A patient taking fluconazole develops hallucinations and tachycardia after starting haloperidol. What is the most likely mechanism? A. Additive serotonergic toxicity

B. QTc prolongation due to CYP450 inhibition

C. Dopaminergic receptor downregulation

D. Muscarinic antagonism

B. QTc prolongation due to CYP450 inhibition

Rationale: Fluconazole inhibits CYP3A4, reducing haloperidol metabolism, increasing QTc risk.

A patient with pheochromocytoma is undergoing surgery. Which drug is critical to administer preoperatively? A. Beta-blocker first

B. Phenylephrine

C. Alpha-blocker (e.g., phenoxybenzamine)

D. ACE inhibitor

C. Alpha-blocker (e.g., phenoxybenzamine)

Rationale: Alpha blockade is initiated first to avoid hypertensive crisis from unopposed alpha stimulation.

Which of the following best explains the mechanism of action of metoclopramide?

A. Serotonin 5HT3 antagonist

B. Muscarinic receptor agonist

C. Dopamine D2 receptor antagonist

D. Histamine H1 receptor antagonist

C. Dopamine D2 receptor antagonist

Rationale: Metoclopramide blocks D2 receptors in the chemoreceptor trigger zone and gut.

Which of the following medications is most likely to cause lactic acidosis? A. Metformin

B. Pioglitazone

C. Glipizide

D. Sitagliptin

A. Metformin

Rationale: Metformin can cause lactic acidosis, especially in renal or hepatic impairment.

Which of the following medications is most likely to cause lactic acidosis? A. Metformin

B. Pioglitazone

C. Glipizide

D. Sitagliptin

A. Metformin

Rationale: Metformin can cause lactic acidosis, especially in renal or hepatic impairment.

A patient with narrow-angle glaucoma should avoid which of the following? A. Pilocarpine

B. Atropine

C. Acetazolamide

D. Timolol

B. Atropine

Rationale: Atropine dilates the pupil and can worsen angle closure in glaucoma.

What is the primary action of suxamethonium at the neuromuscular junction?

A. Antagonizes nicotinic receptors

B. Inhibits acetylcholinesterase

C. Causes sustained depolarization of the motor end plate

D. Blocks sodium channels directly

C. Causes sustained depolarization of the motor end plate

Rationale: Succinylcholine is a depolarizing neuromuscular blocker.

A patient on lithium presents with confusion, tremor, and ataxia. The most appropriate next step is:

A. Increase dose for symptom control

B. Switch to valproic acid

C. Obtain serum lithium level immediately

D. Prescribe NSAIDs for headache

C. Obtain serum lithium level immediately

Rationale: These are signs of lithium toxicity; a serum level is essential for diagnosis.

Which drug class does NOT increase cholinergic activity?

A. Acetylcholinesterase inhibitors

B. Muscarinic agonists

C. Nicotinic antagonists

D. Direct cholinergic agonists

C. Nicotinic antagonists

Rationale: Nicotinic antagonists block cholinergic signaling.

A child accidentally ingests a large amount of pilocarpine. What symptom would most likely occur?

A. Tachycardia

B. Mydriasis

C. Bronchoconstriction

D. Dry mouth

C. Bronchoconstriction

Rationale: Pilocarpine is a muscarinic agonist; it causes parasympathomimetic effects like bronchoconstriction.

A patient is being treated for tuberculosis. Which drug in the regimen is most likely to cause optic neuritis? A. Isoniazid

B. Rifampin

C. Pyrazinamide

D. Ethambutol

D. Ethambutol

Rationale: Ethambutol can cause dose-related optic neuritis, characterized by decreased visual acuity and red-green color blindness.

Which of the following antibiotics inhibits protein synthesis by binding to the 50S ribosomal subunit?

A. Doxycycline

B. Azithromycin

C. Gentamicin

D. Linezolid

B. Azithromycin

Rationale: Macrolides like azithromycin bind to the 50S ribosomal subunit, inhibiting bacterial protein synthesis.

A patient on warfarin is prescribed fluconazole. What is the expected interaction?

A. Increased warfarin metabolism

B. Decreased INR

C. Increased bleeding risk due to CYP2C9 inhibition

D. No significant interaction

C. Increased bleeding risk due to CYP2C9 inhibition

Rationale: Fluconazole inhibits CYP2C9, the enzyme responsible for warfarin metabolism, increasing INR and bleeding risk.

Which of the following medications acts as a selective beta-1 blocker?

A. Propranolol

B. Labetalol

C. Metoprolol

D. Carvedilol

C. Metoprolol

Rationale: Metoprolol selectively blocks beta-1 receptors, primarily affecting the heart without significant bronchial beta-2 blockade.

Which antihypertensive agent should be avoided in pregnancy due to teratogenicity?

A. Labetalol

B. Methyldopa

C. Enalapril

D. Nifedipine

C. Enalapril

Rationale: ACE inhibitors like enalapril are teratogenic and can cause renal dysgenesis and fetal demise.

Which of the following drugs can cause serotonin syndrome when combined with MAO inhibitors?

A. Levodopa

B. Linezolid

C. Carbamazepine

D. Phenytoin

B. Linezolid

Rationale: Linezolid is a weak MAOI and can precipitate serotonin syndrome when combined with other serotonergic agents.

A Parkinson’s patient develops psychosis. Which antipsychotic is most appropriate?

A. Risperidone

B. Clozapine

C. Haloperidol

D. Olanzapine

B. Clozapine

Rationale: Clozapine is less likely to worsen motor symptoms and is used in Parkinson’s-related psychosis under close monitoring.

What is the mechanism of action of valproic acid?

A. Blocks sodium channels only

B. Inhibits GABA transaminase and blocks sodium channels

C. Enhances NMDA receptor activity

D. Inhibits calcium channels only

B. Inhibits GABA transaminase and blocks sodium channels

Rationale: Valproic acid increases GABA by inhibiting its breakdown and also blocks sodium channels.

A patient presents with dry mouth, flushing, blurred vision, and urinary retention after taking an unknown medication. Most likely cause?

A. Cholinesterase inhibitor

B. Muscarinic antagonist

C. Beta-blocker overdose

D. Nicotinic agonist

B. Muscarinic antagonist

Rationale: These are anticholinergic toxidrome symptoms, commonly caused by muscarinic antagonists like atropine or TCAs.

Which medication should be avoided in patients with G6PD deficiency due to risk of hemolysis?

A. Ceftriaxone

B. Nitrofurantoin

C. Azithromycin

D. Ciprofloxacin

B. Nitrofurantoin

Rationale: Nitrofurantoin can precipitate hemolysis in patients with G6PD deficiency.

What is the difference between potency and efficacy?

potency: amount of drug needed to produce effect (more potent drug requires lower dose to achieve same effect as less potent drug) shown as EC50 - concentration that produces 50% of max effect

efficacy: max effect a drug can produce regardless of dose. drug can be highly potent but have low efficacy

ex: morphine = lower potency than fentanyl but higher efficacy than tramadol

Two drugs, A and B, are compared in a clinical trial. Drug A produces a 75% maximal effect at 5 mg, and drug B produces a 100% effect at 20 mg. Which is more potent and which is more efficacious?

A. Drug A is more potent; Drug B is more efficacious

B. Drug A is more efficacious; Drug B is more potent

C. Drug A is more potent and efficacious

D. Drug B is more potent and efficacious

A. Drug A is more potent; Drug B is more efficacious

Rationale: Drug A reaches a moderate effect at a lower dose (greater potency), but Drug B reaches a higher maximum effect (greater efficacy).

On a dose-response curve, what would a leftward shift indicate?

A. Increased efficacy

B. Decreased efficacy

C. Increased potency

D. Decreased potency

C. Increased potency

Rationale: A leftward shift indicates that a lower concentration of the drug is needed to achieve the same effect—i.e., increased potency.

Potency on the graph: If the curve is more to the left, it means the drug needs a smaller dose to work → it's more potent.

Efficacy on the graph: The taller the curve goes on the y-axis, the more effect the drug can give → it's more efficacious.

If a partial agonist has high potency but low efficacy compared to a full agonist, what clinical effect might be observed when both are given concurrently?

A. Increased total receptor activation

B. Enhanced full agonist response

C. Competitive inhibition leading to decreased total effect

D. No change in effect

C. Competitive inhibition leading to decreased total effect

Rationale: Partial agonists can competitively inhibit full agonists and reduce the total maximal effect, acting as functional antagonists.