ABIM IM Practice Questions (2026) — Free Sample Questions with Answers

Answer: B

Ibuprofen alone: NSAID monotherapy treats pain but, without colchicine, roughly doubles the recurrence rate.

Ibuprofen plus colchicine: Correct. Positional pleuritic pain, a friction rub, diffuse concave ST elevation with PR depression (reciprocal changes only in aVR) and a normal troponin indicate acute viral or idiopathic pericarditis. First-line therapy is a high-dose NSAID or aspirin plus colchicine for about 3 months, which hastens resolution and halves recurrence.

Colchicine alone: Colchicine is an adjunct; without an anti-inflammatory dose of NSAID or aspirin, symptom control is inadequate.

Prednisone plus colchicine: Glucocorticoids are second-line (NSAID contraindication, autoimmune or uremic cause) because they increase recurrence.

Intravenous heparin and aspirin: This treats acute coronary syndrome; diffuse ST elevation with PR depression and a normal troponin point to pericarditis, and anticoagulation risks hemopericardium.

Acute pericarditis: NSAID or aspirin plus colchicine first line; reserve glucocorticoids for specific indications.

Answer: E

Intravenous regular insulin bolus and infusion: Insulin is the core DKA therapy but is unsafe while potassium is below about 3.3 mEq/L; starting it now could cause life-threatening hypokalemia.

Subcutaneous insulin glargine: Basal insulin is started before the infusion is stopped, after ketoacidosis resolves; it is not initial therapy and still requires adequate potassium.

Intravenous sodium bicarbonate: Bicarbonate is considered only at pH below about 7.0, and it would lower potassium further.

Intravenous potassium phosphate with insulin infusion: Routine phosphate replacement has no proven benefit, and adding insulin at this potassium level is still unsafe.

Intravenous potassium chloride before starting insulin: Correct. This is severe diabetic ketoacidosis with a high anion gap and ketonemia, but total-body potassium is very depleted, and serum potassium is already low (2.9 mEq/L) despite acidosis. Insulin drives potassium into cells and can precipitate fatal arrhythmia, so intravenous potassium replacement must begin, and insulin is withheld until potassium rises above about 3.3 to 3.5 mEq/L.

In DKA, check potassium before insulin: if it is below about 3.3 mEq/L, replace potassium first and delay insulin.

Answer: D

Intravenous ceftriaxone alone: The antibiotic choice is right, but omitting albumin in a patient with kidney dysfunction and hyperbilirubinemia forgoes a proven reduction in kidney failure and mortality.

Oral ciprofloxacin: Oral fluoroquinolones are used for prophylaxis or selected uncomplicated cases; she has encephalopathy and kidney injury, which require intravenous therapy plus albumin.

Intravenous vancomycin and meropenem: Broad coverage is reserved for nosocomial SBP or known resistant organisms; this community-acquired infection is treated with a third-generation cephalosporin.

Intravenous ceftriaxone and intravenous albumin: Correct. An ascitic neutrophil count ≥250/µL establishes spontaneous bacterial peritonitis. A third-generation cephalosporin treats it, and because creatinine is >1 mg/dL, BUN >30 mg/dL and bilirubin >4 mg/dL, albumin (1.5 g/kg on day 1 and 1 g/kg on day 3) is added to reduce hepatorenal syndrome and death.

Large-volume paracentesis with albumin replacement: Therapeutic paracentesis treats tense ascites; it does not treat infection, and removing large volumes during SBP with kidney injury may worsen circulatory dysfunction.

SBP (ascitic neutrophils ≥250/µL): third-generation cephalosporin plus IV albumin on days 1 and 3 when creatinine >1 mg/dL, BUN >30 mg/dL or bilirubin >4 mg/dL.

Answer: A

Intravenous ceftriaxone: Correct. Short-term antibiotic prophylaxis (ceftriaxone 1 g/day for up to 7 days) is part of the core bundle for any patient with cirrhosis and gastrointestinal bleeding; it lowers bacterial infection, rebleeding and mortality. He has a vasoactive drug and endoscopy is planned, so the missing element is the antibiotic.

Red cell transfusion to a hemoglobin of 10 g/dL: A restrictive strategy (transfuse below about 7 g/dL, target 7–9 g/dL) improves survival in variceal bleeding; liberal transfusion raises portal pressure and rebleeding.

Fresh frozen plasma to correct the prothrombin time: The prothrombin time does not reflect bleeding risk in cirrhosis, and plasma adds volume that raises portal pressure; it is not recommended for correcting the PT.

Oral propranolol: Nonselective β-blockers are for primary and secondary prophylaxis, started after the acute bleed has been controlled and vasoactive therapy stopped; they worsen hypotension now.

Transjugular intrahepatic portosystemic shunt before endoscopy: Preemptive TIPS is considered after endoscopic control in high-risk patients (Child-Pugh C or B with active bleeding), and rescue TIPS for failed endoscopy; it never replaces initial endoscopy.

Acute variceal bleeding bundle: vasoactive drug (octreotide), antibiotic prophylaxis (ceftriaxone), restrictive transfusion (hemoglobin ~7 g/dL) and endoscopic band ligation within 12 hours.

Answer: B

Fondaparinux: Fondaparinux is an option for HIT with normal kidney function, but it is renally cleared and contraindicated with creatinine clearance below 30 mL/min.

Argatroban: Correct. A >50% platelet fall starting 5–10 days after heparin exposure, new venous thrombosis and a strongly positive PF4 antibody indicate heparin-induced thrombocytopenia with thrombosis. A non-heparin anticoagulant is required; argatroban is hepatically cleared and titratable, making it the preferred agent with severe kidney impairment in an ICU patient who may need procedures.

Enoxaparin: Low-molecular-weight heparin cross-reacts with HIT antibodies and is contraindicated in HIT.

Warfarin: Starting warfarin during acute HIT can cause venous limb gangrene through protein C depletion; it is started only after platelets recover (≥150,000/µL), overlapping a non-heparin anticoagulant.

Unfractionated heparin by continuous infusion: Any heparin, whatever the route or dose, perpetuates HIT; the drug must be stopped completely.

HIT with thrombosis: stop all heparin and start a non-heparin anticoagulant (argatroban if kidney function is poor); delay warfarin until platelets recover.

Answer: D

Dengue NS1 antigen test: Dengue causes fever and thrombocytopenia but not splenomegaly with hemolysis (raised bilirubin and LDH); malaria is the must-not-miss diagnosis and is excluded first.

Salmonella Typhi serology (Widal test): Widal serology is unreliable; typhoid is diagnosed by blood culture and would not explain hemolysis and splenomegaly as well.

Leptospira IgM antibody: Leptospirosis follows freshwater or animal-urine exposure, which he did not have.

Thick and thin peripheral blood smears: Correct. Fever within a month of returning from sub-Saharan Africa without chemoprophylaxis, with thrombocytopenia, hyperbilirubinemia, elevated LDH and splenomegaly, is falciparum malaria until proven otherwise. A single negative rapid antigen test does not exclude it, and childhood immunity wanes after years away. Thick and thin smears are needed immediately to confirm infection, identify the species and quantify parasitemia, which determines severity and treatment.

Repeat rapid malaria antigen test: A rapid antigen test can miss low parasitemia, non-falciparum species and parasites with HRP2 gene deletions, and it cannot quantify parasitemia; microscopy is required.

Fever after travel to a malaria-endemic area requires urgent thick and thin smears, even after a negative rapid antigen test, repeated every 12–24 hours for a total of 3 sets if negative.

Answer: D

Vancomycin, ceftriaxone and ampicillin: The antibiotic coverage is right, but omitting adjunctive dexamethasone forgoes its benefit in pneumococcal meningitis, and it must be given now, with the first dose.

Dexamethasone, vancomycin and ceftriaxone: This regimen suits adults aged 18 to 50 years; at 63 years Listeria must be covered with ampicillin.

Dexamethasone, vancomycin and cefepime: Cefepime-based regimens are for postneurosurgical or penetrating-trauma meningitis with gram-negative bacilli including Pseudomonas; they omit Listeria coverage.

Dexamethasone, vancomycin, ceftriaxone and ampicillin: Correct. Neutrophilic pleocytosis, low CSF glucose (ratio about 0.13) and high protein indicate acute bacterial meningitis. In adults older than 50 years, empiric therapy covers Streptococcus pneumoniae (including resistant strains: vancomycin plus a third-generation cephalosporin), Neisseria meningitidis and Listeria monocytogenes (ampicillin), and dexamethasone given with or just before the first antibiotic dose reduces mortality and neurologic sequelae in pneumococcal meningitis.

Intravenous acyclovir alone: Herpes simplex encephalitis causes a lymphocytic pleocytosis with normal glucose; this CSF is bacterial.

Bacterial meningitis after age 50: dexamethasone plus vancomycin, a third-generation cephalosporin and ampicillin.

Answer: E

1. 1. Read event rates: placebo 12%, study drug 9%.
2. 2. Absolute risk reduction = 0.12 − 0.09 = 0.03.
3. 3. NNT = 1 ÷ ARR = 1 ÷ 0.03 = 33.3.
4. 4. Round up: 34 patients must be treated for 3 years to prevent one event; the relative risk reduction (25%) sounds larger but does not change the NNT.

3: This is the absolute risk reduction in percentage points (12% − 9%), not the number needed to treat.

4: This is 1 ÷ relative risk reduction (1 ÷ 0.25); the NNT uses the absolute, not the relative, reduction.

8: This is 1 ÷ the placebo event rate (1 ÷ 0.12), which ignores the treated group.

11: This is 1 ÷ the treated-group event rate (1 ÷ 0.09).

34: Correct. Absolute risk reduction = 12% − 9% = 3% = 0.03; NNT = 1 ÷ 0.03 = 33.3, rounded up to 34 patients treated for 3 years to prevent one composite event (relative risk reduction 25%).

NNT = 1 ÷ absolute risk reduction, over the trial's time frame, rounded up; do not divide by the relative risk reduction.

Answer: C

1. Formula: anion gap = Na − (Cl + HCO₃); corrected AG = AG + 2.5 × (4.0 − albumin); delta ratio = (corrected AG − 12) ÷ (24 − HCO₃).
2. Substitution: AG = 136 − (93 + 18) = 25; corrected AG = 25 + 2.5 × (4.0 − 2.0) = 30; ratio = (30 − 12) ÷ (24 − 18) = 18 ÷ 6.
3. Result: 3.0.
4. Interpretation: ratio <1 suggests an added normal-gap acidosis, 1–2 a pure anion gap acidosis, >2 a concurrent metabolic alkalosis (here from vomiting) superimposed on ketoacidosis.

1.8: Using the upper reference bicarbonate (28) as normal makes the bicarbonate change 10 and the ratio 1.8.

2.2: Forgetting the albumin correction gives an anion gap of 25, a change of 13 and a ratio of 2.2, which hides the size of the ketoacid load.

3.0: Correct. Anion gap = 136 − 93 − 18 = 25; corrected for albumin = 25 + 2.5 × 2 = 30. Change in anion gap = 30 − 12 = 18; change in bicarbonate = 24 − 18 = 6; ratio = 3.0. A ratio above 2 means bicarbonate is higher than the ketoacidosis alone would leave, so a coexisting metabolic alkalosis from vomiting is present, which explains the near-normal pH.

3.7: Including potassium in the anion gap (34 after correction) gives a change of 22 and a ratio of 3.7; the standard gap omits potassium and its range assumes that.

5.0: Dividing the whole corrected gap (30) by the bicarbonate change, without subtracting the normal gap of 12, gives 5.0.

Correct the anion gap for albumin, then compare ΔAG with ΔHCO₃; a ratio above 2 reveals a hidden metabolic alkalosis.

Answer: A

Cardioembolism: Correct. The strip shows an irregularly irregular rhythm without P waves and with a fibrillatory baseline: atrial fibrillation. Simultaneous cortical infarcts in more than one arterial territory (anterior and posterior circulation, both hemispheres) without arterial stenosis point to emboli from the heart, typically from the left atrial appendage.

Large-artery atherosclerosis: Artery-to-artery embolism from a stenotic carotid would affect one territory downstream of the lesion; CT angiography shows no stenosis, and it could not explain infarcts in both anterior and posterior circulations.

Small-vessel (lacunar) disease: Lacunar infarcts are small, deep (basal ganglia, internal capsule, pons) and do not cause cortical signs such as aphasia or hemianopia.

Embolic stroke of undetermined source: This label applies to nonlacunar embolic-appearing strokes when no major cardioembolic source is found; atrial fibrillation is a major source, so the mechanism is determined.

Hypercoagulable state from cancer: Cancer-associated (Trousseau) strokes also cause multiterritory infarcts, but a cardiac source is already evident and there are no clues to malignancy.

Infarcts in more than one arterial territory without arterial stenosis suggest a cardioembolic source; atrial fibrillation on the rhythm strip confirms one and calls for anticoagulation rather than antiplatelet therapy.

Answer: D

Systemic alteplase: Systemic thrombolysis is indicated for high-risk (massive) embolism with sustained hypotension or shock; she is normotensive with normal lactate.

Inferior vena cava filter placement: Filters are for acute venous thromboembolism when anticoagulation is contraindicated; she can be anticoagulated.

Discharge on oral apixaban: Outpatient treatment suits low-risk embolism (normal RV, normal biomarkers, no hypoxemia); RV dysfunction and positive troponin require admission.

Inpatient heparin anticoagulation with close monitoring: Correct. She is normotensive with right ventricular dysfunction on imaging and elevated troponin, which is intermediate-high–risk (submassive) pulmonary embolism. Anticoagulation alone with close monitoring is recommended; routine systemic thrombolysis reduces hemodynamic decompensation but increases major and intracranial bleeding without lowering mortality, so it is reserved for rescue if she becomes hypotensive.

Surgical embolectomy: Embolectomy is for high-risk embolism when thrombolysis is contraindicated or has failed.

Normotensive PE with RV dysfunction and positive troponin: admit, anticoagulate and monitor; thrombolysis only if she decompensates.

Answer: A

1. Formula: PAO₂ = FiO₂ × (Patm − PH₂O) − PaCO₂/RQ; A–a gradient = PAO₂ − PaO₂.
2. Substitution: PAO₂ = 0.21 × (760 − 47) − 30/0.8 = 149.7 − 37.5 = 112.2 mm Hg.
3. Result: A–a gradient = 112.2 − 62 = 50.2 ≈ 50 mm Hg.
4. Interpretation: expected gradient ≈ age/4 + 4 ≈ 13 mm Hg; an elevated gradient means hypoxemia from V/Q mismatch or shunt, not hypoventilation.

50: Correct. PAO₂ = 0.21 × (760 − 47) − 30/0.8 = 149.7 − 37.5 = 112.2 mm Hg; the gradient is 112.2 − 62 ≈ 50 mm Hg. This is well above the expected value for her age (about 13 mm Hg), indicating ventilation–perfusion mismatch; with a normal radiograph and risk factors, pulmonary embolism must be excluded with CT pulmonary angiography.

58: Subtracting PaCO₂ without dividing by the respiratory quotient (149.7 − 30 − 62) gives 58.

60: Omitting water vapor pressure (0.21 × 760 = 159.6; 159.6 − 37.5 − 62) gives 60.

64: Multiplying PaCO₂ by 0.8 instead of dividing (149.7 − 24 − 62) gives 64.

88: Omitting the PaCO₂/0.8 term entirely (149.7 − 62) gives 88.

PAO₂ = FiO₂(Patm − 47) − PaCO₂/0.8; an increased A–a gradient points to V/Q mismatch, shunt or diffusion impairment rather than hypoventilation.

Answer: B

Intravenous nicardipine: Calcium channel blockers may be added once the ACE inhibitor is at maximal dose, but they do not reverse the renin-mediated process and should not replace ACE inhibition.

Captopril: Correct. Abrupt severe hypertension with acute kidney injury and microangiopathic changes in early diffuse systemic sclerosis, after high-dose glucocorticoids, is scleroderma renal crisis. A short-acting ACE inhibitor, titrated rapidly and continued even as creatinine rises, is the treatment that transformed survival; other agents are only add-ons.

Plasma exchange: Plasma exchange treats thrombotic thrombocytopenic purpura; the mild hemolysis here is secondary to renal crisis and does not respond to it.

Intravenous methylprednisolone: High-dose glucocorticoids are a recognized trigger of scleroderma renal crisis and would worsen it.

Intravenous labetalol: β-blockers lower pressure but do not address the renin-angiotensin drive; outcomes depend on ACE inhibition.

Scleroderma renal crisis (early diffuse disease, often after glucocorticoids): treat with an ACE inhibitor titrated to blood pressure control, and continue it even if dialysis becomes necessary.

Answer: C

Indomethacin: NSAIDs are avoided in advanced kidney disease and with anticoagulation because of bleeding risk and loss of residual kidney function.

Colchicine 1.2 mg followed by 0.6 mg 1 hour later: This is the standard flare regimen with normal kidney function; colchicine is not removed by dialysis, and in patients on dialysis a single reduced dose at most, not repeated within 2 weeks, is advised because of neuromuscular and marrow toxicity.

Oral prednisone: Correct. This is a polyarticular gout flare (negatively birefringent needle crystals). In a patient on dialysis who is anticoagulated, NSAIDs are contraindicated and standard colchicine dosing is unsafe, so a short course of systemic glucocorticoid is the treatment of choice for flares involving more than one joint.

Allopurinol: Urate-lowering therapy does not treat an acute flare; starting it now without anti-inflammatory therapy would leave the flare untreated.

Intra-articular triamcinolone in the ankle only: Joint injection is excellent for one or two accessible large joints, but injecting only the ankle leaves the inflamed wrist untreated; systemic therapy covers both.

Choose gout-flare therapy by comorbidity: in advanced CKD or dialysis, especially with anticoagulation, use glucocorticoids (oral, or intra-articular when only one or two joints are involved).