Internal medicine for USMLE Step 2 CK

A 66-year-old man with atrial fibrillation, hypertension, diabetes and prior transient ischemic attack asks about stroke prevention. He has no bleeding history and normal renal function. CHA₂DS₂-VASc score is 5. What is the most appropriate recommendation?

1. Aspirin 81 mg daily Antiplatelet monotherapy is substantially inferior to anticoagulation for stroke prevention in atrial fibrillation and is no longer recommended for this indication.
2. Warfarin with target INR 2.0–3.0 Effective and acceptable, but not preferred in non-valvular disease with normal renal function. Warfarin remains indicated for mechanical valves and moderate-to-severe mitral stenosis, where DOACs are contraindicated.
3. A direct oral anticoagulant correct Correct. At a score of 5 the annual stroke risk clearly justifies anticoagulation, and DOACs are preferred over warfarin in non-valvular atrial fibrillation for comparable efficacy, lower intracranial hemorrhage rate, and no INR monitoring.
4. Aspirin plus clopidogrel Less effective than anticoagulation with a bleeding risk approaching it. Reserved for patients who genuinely cannot take an anticoagulant.
5. No antithrombotic therapy A score of 5 with a prior TIA places him at high annual stroke risk; withholding treatment would be indefensible.

The point: CHA₂DS₂-VASc drives the decision; HAS-BLED identifies modifiable bleeding risk rather than a reason to withhold. DOACs first in non-valvular AF; warfarin for mechanical valves and rheumatic mitral stenosis.

Source: ACC/AHA/HRS guideline for the management of atrial fibrillation American College of Cardiology / AHA · tier 2, specialty society or college

A 58-year-old woman with type 2 diabetes has an eGFR of 38 mL/min/1.73m² and a urine albumin-to-creatinine ratio of 480 mg/g. Blood pressure is 142/86 mmHg on lisinopril 20 mg daily. HbA1c is 7.4%. Potassium is 4.6 mEq/L. Which addition will most reduce her risk of progression to end-stage kidney disease?

1. Tightening glycemic control to an HbA1c below 6.5% Wrong emphasis. At 7.4% she is close to target, and intensive glycemic control in established diabetic kidney disease increases hypoglycemia without proportionate renal benefit.
2. A loop diuretic Useful for volume and blood pressure, but it does not modify progression of diabetic kidney disease.
3. Adding an angiotensin receptor blocker to the ACE inhibitor Wrong, and harmful. Dual renin-angiotensin blockade increases hyperkalemia and acute kidney injury without renal benefit, as shown in ONTARGET and related trials.
4. An SGLT2 inhibitor correct Correct. In diabetic kidney disease with albuminuria, SGLT2 inhibitors reduce progression of kidney disease and cardiovascular events on top of maximally tolerated renin-angiotensin blockade. An initial dip in eGFR after starting is expected and is not a reason to stop.
5. A calcium channel blocker for the blood pressure It will lower her pressure, which helps, but dihydropyridines lack the specific antiproteinuric and renoprotective effect of the alternatives.

The point: The pillars of diabetic kidney disease: renin-angiotensin blockade, an SGLT2 inhibitor, blood pressure control, and increasingly a non-steroidal mineralocorticoid antagonist such as finerenone. Expect and tolerate the early eGFR dip with SGLT2 inhibition.

Source: KDIGO clinical practice guideline for diabetes management in chronic kidney disease KDIGO · tier 2, specialty society or college

A 34-year-old woman presents with 4 months of fatigue, weight gain, cold intolerance and constipation. TSH is 14.2 mIU/L with a free T4 of 0.6 ng/dL (low). Thyroid peroxidase antibodies are strongly positive. She is 9 weeks pregnant. What is the most appropriate management?

1. Defer treatment until after delivery to avoid fetal exposure Wrong. Levothyroxine is safe and necessary in pregnancy; the fetus depends on maternal thyroid hormone, particularly in the first trimester before its own gland functions.
2. Start levothyroxine immediately and check TSH every 4 weeks, targeting a trimester-specific range correct Correct. Overt hypothyroidism in pregnancy is associated with miscarriage, preterm birth and impaired neurodevelopment, and treatment is not deferred. Requirements rise in pregnancy, so frequent monitoring against trimester-specific targets is essential.
3. Recheck thyroid function in 12 weeks before deciding Wrong. This is overt hypothyroidism with a clearly low free T4, and a 12-week delay covers the period of greatest fetal vulnerability.
4. Start liothyronine (T3) as the preferred agent in pregnancy Wrong. Levothyroxine is the agent of choice; T3 does not cross the placenta as effectively and is not recommended in pregnancy.
5. Start carbimazole Wrong direction entirely. She is hypothyroid, not thyrotoxic.

The point: Levothyroxine requirements rise by roughly 25 to 30% in pregnancy, women already on replacement should increase the dose as soon as pregnancy is confirmed. Use trimester-specific TSH ranges, and separate levothyroxine from iron and calcium by at least four hours.

Source: ATA guidelines for the diagnosis and management of thyroid disease during pregnancy and the postpartum American Thyroid Association · tier 2, specialty society or college