General Internal Medicine Flashcards

A 58-year-old man with a history of heart failure (EF 30%) presents with worsening dyspnea. His current medications include carvedilol, lisinopril, and furosemide. Labs show Na 128 mEq/L, K 3.2 mEq/L, creatinine 2.1 mg/dL (baseline 1.4). BNP is 1,800 pg/mL. On exam, JVP is elevated to 14 cm and he has 3+ pitting edema. Which is the most appropriate next step?

Answer: Increase furosemide dose and add metolazone, accepting transient creatinine rise

This patient has decompensated heart failure with cardiorenal syndrome type 1. The elevated JVP, significant edema, and markedly elevated BNP indicate severe volume overload as the primary problem. The hyponatremia is dilutional and the creatinine rise is likely from reduced forward flow due to congestion — not true prerenal azotemia. Aggressive decongestion with furosemide escalation plus metolazone (sequential nephron blockade) is the correct approach; transient worsening of creatinine is acceptable and often reverses with decongestion. Holding diuretics would worsen congestion. Tolvaptan is not indicated for dilutional hyponatremia in heart failure when volume overload is the dominant problem. A rigid urine output target without creatinine trending is unsafe.

A 44-year-old woman with SLE is admitted for pleuritic chest pain and dyspnea. D-dimer is elevated at 4.2 µg/mL. CT pulmonary angiography shows bilateral subsegmental pulmonary emboli. Her platelet count is 62,000/µL, aPTT is prolonged at 68 seconds (1:1 mixing study does NOT correct), and anti-β2-glycoprotein I IgG is markedly positive. Which anticoagulation strategy is most appropriate?

Answer: Warfarin with a target INR of 3.0–4.0, bridged with unfractionated heparin

This patient has antiphospholipid antibody syndrome (APS) confirmed by a positive anti-β2-glycoprotein I and a lupus anticoagulant (suggested by prolonged aPTT not correcting on mixing study). For high-risk APS (triple positivity or anti-β2GP1 positive with lupus anticoagulant), warfarin with a higher target INR of 3.0–4.0 is recommended over standard 2.0–3.0, particularly after arterial events or recurrent VTE. Direct oral anticoagulants (rivaroxaban, apixaban) are contraindicated in high-risk APS due to increased thrombotic recurrence rates demonstrated in the TRAPS trial. Bridging with UFH is necessary because warfarin's effect on APS monitoring (aPTT is unreliable) requires anti-Xa levels during the bridge phase.

A 67-year-old man with type 2 diabetes, stage 3b CKD (eGFR 38), and a recent MI (6 weeks ago) presents for medication reconciliation. His HbA1c is 8.9%. Current medications include metformin 500 mg BID, aspirin, atorvastatin, carvedilol, and lisinopril. Which adjustment to his diabetes regimen is most evidence-based?

Answer: Continue metformin; add semaglutide 0.5 mg weekly

Metformin is acceptable at eGFR 38 (threshold for discontinuation is eGFR < 30). The patient needs an agent with proven cardiovascular benefit post-MI. GLP-1 receptor agonists (semaglutide, dulaglutide, liraglutide) have demonstrated MACE reduction in high-CV-risk patients and are safe in CKD stage 3b. SGLT2 inhibitors (empagliflozin) also carry CV and renal benefits, but their glycosuric efficacy diminishes significantly below eGFR 45 (particularly for glucose lowering), and empagliflozin's heart failure indication threshold is eGFR ≥ 20. At eGFR 38, semaglutide added to metformin provides superior glycemic control and CV benefit. Dulaglutide is also acceptable but discontinuing metformin without a clear contraindication is not indicated. Aggressive insulin targeting HbA1c < 7.0% post-MI carries hypoglycemia risk without proven MACE benefit.

A 71-year-old woman is admitted with confusion, fatigue, and hypercalcemia (calcium 13.8 mg/dL). PTH is suppressed at 4 pg/mL. PTHrP is undetectable. 1,25-dihydroxyvitamin D (calcitriol) is markedly elevated at 210 pg/mL (normal 18–72). 25-hydroxyvitamin D is normal. ACE level is mildly elevated. CT chest reveals bilateral hilar lymphadenopathy and pulmonary nodules. Which is the most likely cause of her hypercalcemia?

Answer: Granulomatous disease with autonomous 1α-hydroxylase activity

The pattern of suppressed PTH, undetectable PTHrP, and markedly elevated 1,25-dihydroxyvitamin D with normal 25-hydroxyvitamin D is classic for granulomatous disease (most likely sarcoidosis here, supported by hilar lymphadenopathy and elevated ACE). Activated macrophages within granulomas express 1α-hydroxylase, which converts 25-OH vitamin D to the active 1,25-OH form without the normal feedback inhibition from PTH or calcium. Vitamin D toxicity raises 25-OH vitamin D, not 1,25-OH (except in granulomatous disease). PTHrP-mediated hypercalcemia (humoral hypercalcemia of malignancy) would show elevated PTHrP, not elevated calcitriol. Primary hyperparathyroidism would show elevated or inappropriately normal PTH.

A 55-year-old man with compensated cirrhosis (Child-Pugh B) presents with new-onset ascites. Diagnostic paracentesis shows: total protein 1.8 g/dL, albumin 0.6 g/dL, SAAG 1.5 g/dL, WBC 180 cells/µL (68% neutrophils). Serum albumin is 2.4 g/dL. He is started on spironolactone and furosemide. 48 hours later, PMN count on repeat tap is 142/µL despite IV cefotaxime started at admission. Which intervention should now be prioritized?

Answer: Add IV albumin 1.5 g/kg on day 1 and 1 g/kg on day 3 to prevent hepatorenal syndrome

The patient has spontaneous bacterial peritonitis (SBP), defined by ascitic PMN ≥ 250/µL. Cefotaxime is the correct first-line antibiotic. The critical co-intervention supported by the SORT trial and incorporated into AASLD/EASL guidelines is IV albumin infusion: 1.5 g/kg on day 1 and 1 g/kg on day 3. This significantly reduces the incidence of hepatorenal syndrome (type 1 AKI) and mortality in SBP, especially in patients with serum creatinine > 1 mg/dL, BUN > 30, or bilirubin > 4 mg/dL. A PMN of 142 on day 2 still represents a treatment response (decreasing from 180 PMN equivalent on baseline × 0.68 = ~122 PMN originally; the original count just met the 250 threshold). Switching to meropenem without culture data suggesting resistance is premature. TIPS is not an acute SBP intervention.

A 63-year-old woman presents with progressive proximal muscle weakness over 4 months, difficulty climbing stairs, and dysphagia. CK is 4,200 U/L. ANA is positive 1:320. Anti-Jo-1 antibody is negative. Anti-MDA5 antibody is strongly positive. Chest CT shows bilateral ground-glass opacities and reticulation in both lower lobes. Muscle biopsy shows perifascicular atrophy with MHC-I upregulation. Which of the following is most accurate regarding her prognosis and management?

Answer: This pattern suggests amyopathic dermatomyositis with high risk of rapidly progressive ILD; aggressive immunosuppression is warranted

Anti-MDA5 (anti-melanoma differentiation-associated gene 5) antibody is associated with clinically amyopathic dermatomyositis (CADM) or dermatomyositis with relatively mild myositis but a very high risk of rapidly progressive interstitial lung disease (RP-ILD), which carries a mortality rate of 30–50% even with treatment. Perifascicular atrophy with MHC-I upregulation is the histologic signature of dermatomyositis (not polymyositis). This patient's presentation — ground-glass opacities + reticulation + anti-MDA5 — requires aggressive combination immunosuppression (high-dose corticosteroids + calcineurin inhibitor such as tacrolimus + possibly rituximab or cyclophosphamide). Hydroxychloroquine monotherapy is wholly inadequate. Anti-Jo-1 is associated with antisynthetase syndrome; anti-MDA5 carries a distinct and more dire pulmonary phenotype.