FPGEE Practice Questions (2026) — Free Sample Questions with Answers

Answer: B

Streptococcus pneumoniae.: Pneumococcal defense depends mainly on C3b opsonization and the spleen, which remain intact upstream of C5.

Neisseria meningitidis.: Correct. Blocking C5 prevents the membrane attack complex (C5b-9), the main defense against Neisseria; eculizumab therefore carries a boxed warning for meningococcal infection.

Pseudomonas aeruginosa.: Serious Pseudomonas infection is typical of neutropenia or hospital exposure, not terminal complement deficiency.

Pneumocystis jirovecii.: Pneumocystis is a risk of T-cell deficiency (low CD4 counts, high-dose corticosteroids), not complement blockade.

Terminal complement (C5–C9) deficiency, inherited or from C5 inhibitors, predisposes to Neisseria infections; vaccinate before starting therapy.

Answer: C

Thymidylate synthase: Thymidylate synthase is the main target of fluorouracil (FdUMP); leucovorin actually strengthens that inhibition rather than bypassing it.

Ribonucleotide reductase: Ribonucleotide reductase converts ribonucleotides to deoxyribonucleotides and is the hydroxyurea target, not a folate-dependent step.

Dihydrofolate reductase: Correct. Methotrexate blocks dihydrofolate reductase, so tetrahydrofolate cannot be regenerated; leucovorin (folinic acid) is already reduced and bypasses this step.

Inosine monophosphate dehydrogenase: IMP dehydrogenase in guanine synthesis is the mycophenolate target and does not use folate.

Leucovorin is a reduced folate that enters the folate pool beyond dihydrofolate reductase, the enzyme methotrexate inhibits.

Answer: 132 mg

1. NaCl needed if the solution contained only NaCl: 30 mL × 0.9 g/100 mL = 0.27 g = 270 mg.
2. Ephedrine sulfate present: 30 mL × 2 g/100 mL = 0.6 g = 600 mg.
3. NaCl equivalent of the drug: 600 mg × 0.23 = 138 mg.
4. NaCl to add: 270 mg − 138 mg = 132 mg.

NaCl to add = (0.9% × volume) − (grams of drug × E value). Common wrong paths: reporting the drug's NaCl equivalent (138 mg) or the full 270 mg without subtracting.

Answer: D

Bioequivalent for both AUC and Cmax: Overlooks that the Cmax interval extends beyond the 1.25 upper limit.

Bioequivalent, because the AUC interval passes: Extent (AUC) and rate (Cmax) must both pass; AUC alone is not enough.

Not bioequivalent, because AUC fails the lower limit: The AUC lower bound of 0.84 is above 0.80, so AUC passes; the failure is in Cmax.

Not bioequivalent, because Cmax exceeds 1.25: Correct. Both AUC and Cmax 90% confidence intervals must lie entirely within 0.80–1.25; the Cmax upper limit of 1.27 falls outside, so bioequivalence is not shown.

FDA bioequivalence: the 90% CI for the test/reference ratio of both AUC and Cmax must fall within 80–125%.

Answer: A, D, E

Infliximab: Correct. A chimeric monoclonal antibody that binds soluble and membrane-bound TNF-alpha.

Tocilizumab: Incorrect. Tocilizumab blocks the interleukin-6 receptor, not TNF.

Abatacept: Incorrect. Abatacept (CTLA-4–Ig) binds CD80/CD86 and blocks T-cell costimulation.

Etanercept: Correct. A TNF receptor–Fc fusion protein that acts as a decoy receptor for TNF.

Adalimumab: Correct. A fully human monoclonal antibody against TNF-alpha.

TNF inhibitors include infliximab, adalimumab, golimumab, certolizumab and the decoy receptor etanercept; tocilizumab (IL-6R) and abatacept (costimulation) act elsewhere.

Answer: Weak acid, pKa 3.4 → Weak base, pKa 9.4 → Weak acid, pKa 6.4 → Weak base, pKa 7.4 → Weak acid, pKa 8.4

1. Acid: ionized/un-ionized = 10^(pH − pKa). Base: ionized/un-ionized = 10^(pKa − pH).
2. Acid pKa 3.4: 10^4 → 99.99%. Base pKa 9.4: 10^2 → 99.0%. Acid pKa 6.4: 10^1 → 90.9%. Base pKa 7.4: 10^0 → 50%. Acid pKa 8.4: 10^−1 → 9.1%.
3. Common error: applying the acid equation to the bases, which would wrongly rank the pKa 9.4 base as least ionized.

Weak acid, pKa 3.4: First: for an acid, pH − pKa = 4, so ionized : un-ionized = 10,000 : 1 (about 99.99% ionized).

Weak base, pKa 9.4: Second: for a base, pKa − pH = 2, so ionized : un-ionized = 100 : 1 (about 99% ionized).

Weak acid, pKa 6.4: Third: pH − pKa = 1, so the ratio is 10 : 1 (about 91% ionized).

Weak base, pKa 7.4: Fourth: pH equals pKa, so the compound is 50% ionized.

Weak acid, pKa 8.4: Last: the pH is 1 unit below the acid's pKa, so ionized : un-ionized = 1 : 10 (about 9% ionized).

Acids ionize when pH is above pKa; bases ionize when pH is below pKa. Each pH unit of difference changes the ratio tenfold.

Answer: A

Not significant, because the CI includes 1: Correct. For a ratio, no effect is 1. An interval that crosses 1 means the result is not statistically significant at the 0.05 level.

Not significant, because the RR is below 1: Right conclusion, wrong reason. An RR below 1 points toward benefit. Significance depends on whether the CI includes 1.

Significant, because the CI excludes 0: Zero is the null value for a difference (for example, a mean difference), not for a ratio.

Significant, because the RR shows an 18% reduction: The point estimate alone cannot establish significance. The CI still includes 1.

Ratios (RR, OR, HR) are significant only if the 95% CI excludes 1. Differences are significant only if it excludes 0.

Answer: A

Handwashing with soap and water: Correct. Spores resist alcohol. Handwashing with soap and running water removes them physically, which is why it is preferred in outbreak and hyperendemic settings.

Alcohol-based rub (60–95% alcohol): Alcohol rubs are the general default for hand hygiene, but they do not kill or reliably remove C. difficile spores.

Chlorhexidine–alcohol hand rub: Adding chlorhexidine does not make an alcohol rub sporicidal.

Benzalkonium chloride hand foam: Quaternary ammonium compounds are not sporicidal.

C. difficile spores survive alcohol and quaternary ammonium compounds. Soap-and-water washing removes them from the hands, and sporicidal agents such as bleach are used on surfaces.

Answer: B

A standard invoice kept for 2 years: An invoice is the ordering record for Schedule III–V drugs. Hydrocodone combinations were Schedule III before 2014, which is why this answer is tempting.

DEA Form 222 or its CSOS equivalent: Correct. Hydrocodone combination products have been Schedule II since October 2014, and Schedule II substances must be ordered on DEA Form 222 or electronically through CSOS (21 CFR 1305).

DEA Form 224: Form 224 is the application a pharmacy uses to register with DEA. It is not used to order drugs.

DEA Form 106: Form 106 reports the theft or significant loss of controlled substances. It is not an order form.

Every Schedule II order, hydrocodone combinations included, needs DEA Form 222 or a CSOS electronic order. An invoice is enough only for Schedules III–V.

Answer: C

1. Denominator: 0.2 × 2.0 g/dL + 0.1 = 0.5.
2. Adjusted concentration: 7 mcg/mL ÷ 0.5 = 14 mcg/mL.
3. Interpretation: within 10–20 mcg/mL; do not increase the dose based on the total level alone.

3.5 mcg/mL: Multiplies by the denominator instead of dividing: 7 × 0.5 = 3.5.

7.0 mcg/mL: Reports the measured total concentration with no adjustment, ignoring the higher free fraction in hypoalbuminemia.

14.0 mcg/mL: Correct. 0.2 × 2.0 + 0.1 = 0.5, and 7 ÷ 0.5 = 14 mcg/mL, which is within the usual 10–20 mcg/mL range, so the low total level does not by itself justify a dose increase.

17.5 mcg/mL: Omits the + 0.1 term: 7 ÷ 0.4 = 17.5.

Low albumin raises the free fraction of phenytoin, so a "low" total level may be therapeutic; adjust it (or measure the free level) before changing the dose.

Answer: Systematic review with meta-analysis of RCTs → Single randomized controlled trial → Prospective cohort study → Case-control study → Case series

Systematic review with meta-analysis of RCTs: Strongest. It pools several well-conducted randomized trials.

Single randomized controlled trial: Second. Randomization controls known and unknown confounders.

Prospective cohort study: Third. It is observational but establishes that exposure came before outcome.

Case-control study: Fourth. It is retrospective and prone to recall and selection bias.

Case series: Weakest of these. It has no comparison group.

The evidence hierarchy runs from systematic reviews of RCTs, to RCTs, to cohort studies, to case-control studies, to case series and expert opinion.

Answer: A

Amoxicillin 1 g three times daily: Correct. For healthy outpatients, the ATS/IDSA guideline recommends high-dose amoxicillin (doxycycline is an alternative). A macrolide is used only if resistance is below 25%.

Azithromycin monotherapy: Macrolide monotherapy is advised only where pneumococcal macrolide resistance is under 25%. Here it is 30%.

Levofloxacin monotherapy: Respiratory fluoroquinolones are kept for outpatients with comorbidities, given their adverse-effect and resistance concerns.

Amoxicillin–clavulanate plus azithromycin: Combination therapy is the regimen for outpatients with comorbidities. It is broader than needed here.

Healthy outpatient CAP: amoxicillin or doxycycline, or a macrolide only if resistance is below 25%. Comorbidities: a beta-lactam plus macrolide, or a respiratory fluoroquinolone.

Answer: A

Dapagliflozin: Correct. SGLT2 inhibitors reduce cardiovascular death and HF hospitalization in HFrEF (class 1). They are safe at this eGFR and do not raise potassium.

Spironolactone: MRAs lower mortality in HFrEF, but they should not be started when potassium is above 5.0 mEq/L.

Digoxin: Digoxin can reduce HF hospitalizations but does not lower mortality.

Ivabradine: Ivabradine reduces HF hospitalization in selected patients in sinus rhythm (HR ≥ 70 on a maximal beta-blocker) but has not lowered all-cause mortality.

Guideline-directed therapy for HFrEF has four pillars: ARNI/ACEi/ARB, an evidence-based beta-blocker, an MRA and an SGLT2 inhibitor. Hyperkalemia above 5.0 mEq/L rules out starting an MRA.

Answer: B

Severe diarrhea: Bicarbonate loss from diarrhea causes a normal anion gap (hyperchloremic) acidosis.

Salicylate overdose: Correct. Anion gap = 138 − (102 + 14) = 22 mEq/L, which is elevated. Salicylate toxicity adds organic acids (lactate, ketoacids) and causes a high anion gap acidosis, often with a respiratory alkalosis as well.

Acetazolamide therapy: Carbonic anhydrase inhibition wastes bicarbonate in the urine and causes a normal anion gap acidosis.

Spironolactone therapy: Aldosterone antagonism can cause hyperkalemic, normal anion gap (type 4 RTA-like) acidosis.

AG = Na − (Cl + HCO3-). A high gap means an unmeasured acid has been added (for example salicylates, toxic alcohols, lactate, ketoacids, uremia). A normal gap means bicarbonate has been lost.

Answer: 34 mL/min

1. $\text{CrCl}=\frac{(140-\text{age})\times \text{weight}}{72\times \text{SCr}}\times 0.85$ for women.
2. $(140-72)\times 60=68\times 60=4080$.
3. $72\times 1.4=100.8$; $4080÷100.8=40.48$ mL/min.
4. $40.48\times 0.85=34.4$, which rounds to 34 mL/min.
5. Common wrong path: forgetting the 0.85 factor for women gives 40 mL/min.

Cockcroft-Gault: (140 − age) × weight ÷ (72 × SCr), × 0.85 for women.

Answer: C

Phase 0 (rapid depolarization): Phase 0 is fast sodium influx, the target of class I drugs such as flecainide; dofetilide does not block sodium channels.

Phase 2 (plateau): The plateau is a balance of L-type calcium influx and slow potassium efflux; dofetilide prolongs the action potential through the later rapid repolarizing current, not by acting on calcium entry.

Phase 3 (repolarization): Correct. Dofetilide, a class III drug, blocks the rapid delayed rectifier potassium current (IKr), which drives phase 3 repolarization. Slower repolarization lengthens the action potential and the QT interval, raising torsades risk.

Phase 4 (resting potential): The ventricular resting potential is set by the inward rectifier potassium current (IK1), which dofetilide does not meaningfully block; phase 4 does not determine the QT interval.

Class III antiarrhythmics (dofetilide, sotalol, amiodarone) block IKr, slowing phase 3 repolarization; the longer action potential shows as QT prolongation, so QTc and renal function guide dofetilide dosing.