Internal Medicine Flashcards

A 58-year-old woman with long-standing rheumatoid arthritis on methotrexate and adalimumab presents with a 3-week history of productive cough, night sweats, and a 4 kg weight loss. Chest CT reveals a right upper lobe cavitary lesion. Her QuantiFERON-TB Gold test is indeterminate. Which is the MOST appropriate next step?

Answer: Perform bronchoscopy with BAL and initiate empiric 4-drug anti-TB therapy pending cultures

This patient has classic features of active pulmonary tuberculosis — cavitary upper lobe lesion, constitutional symptoms, and significant immunosuppression from TNF-α inhibitor therapy. An indeterminate QuantiFERON is common in immunosuppressed patients and is not sufficient to rule out TB. Bronchoscopy with BAL allows microbiologic confirmation (AFB smear, culture, NAAT) while empiric 4-drug therapy (RIPE: rifampin, isoniazid, pyrazinamide, ethambutol) should be started given the high clinical suspicion and the risk of delay in an immunocompromised host. Adalimumab should also be held. Waiting 4 weeks or using monotherapy would be dangerous given active disease concern.

A 44-year-old man is evaluated for recurrent episodes of severe hypertension (BP up to 210/120 mmHg), headache, diaphoresis, and palpitations lasting 15–30 minutes. Between episodes he is normotensive. 24-hour urine metanephrines are elevated at 3.2× the upper limit of normal. CT of the abdomen and pelvis is unremarkable. What is the BEST next imaging step?

Answer: 68Ga-DOTATATE PET/CT

When biochemistry confirms pheochromocytoma/paraganglioma (PPGL) but conventional cross-sectional imaging (CT/MRI) is negative, functional imaging is required to locate the occult tumor. 68Ga-DOTATATE PET/CT is now the preferred first-line functional imaging for PPGL due to its superior sensitivity (>90%) compared to 123I-MIBG scintigraphy (~60–70%), especially for extra-adrenal paragangliomas and metastatic disease. MIBG is no longer the functional imaging of choice for initial localization. 18F-FDG PET is reserved for metastatic/SDHB-related disease. Repeat MRI would not add value after a negative CT.

A 67-year-old man with CKD stage 3b (eGFR 32 mL/min) and type 2 diabetes on metformin presents with worsening dyspnea on exertion. Echo shows an EF of 35% with dilated LV. His current medications include metformin, lisinopril, and amlodipine. Serum potassium is 4.8 mEq/L. Which combination of add-on therapies offers the GREATEST evidence-based mortality benefit in this patient?

Answer: Carvedilol + dapagliflozin + sacubitril/valsartan

For HFrEF (EF ≤40%), the four pillars with the strongest mortality evidence are: ACEi/ARB or ARNI (sacubitril/valsartan), beta-blocker, MRA, and SGLT2 inhibitor. Sacubitril/valsartan reduces mortality significantly over ACEi alone (PARADIGM-HF). Dapagliflozin and empagliflozin both reduce HF hospitalization and CV death in HFrEF (DAPA-HF, EMPEROR-Reduced). This patient is already on an ACEi, so upgrading to ARNI + adding a beta-blocker (carvedilol or bisoprolol) + SGLT2i is optimal. With K+ of 4.8, adding an MRA requires caution in CKD 3b, but the question asks for the combination with GREATEST evidence — the ARNI + BB + SGLT2i triad is best supported. Digoxin has no mortality benefit. Ivabradine is adjunctive. Hydralazine/nitrates are reserved for ACEi/ARB intolerance.

A 72-year-old woman is admitted with altered mental status, hypernatremia (Na 168 mEq/L), and polyuria (8 L/day). She has no history of diabetes mellitus. Serum glucose is 92 mg/dL. After 8 hours of IV hypotonic fluids, urine remains dilute (osmolality 110 mOsm/kg) despite serum osmolality of 348 mOsm/kg. Desmopressin 10 mcg intranasally is given, and 2 hours later urine osmolality rises to 680 mOsm/kg. What does this response MOST indicate?

Answer: Central diabetes insipidus

The water deprivation test (or in this case, the desmopressin challenge during established hypernatremic dehydration) differentiates the causes of diabetes insipidus. A >50% rise in urine osmolality after exogenous desmopressin indicates an intact renal tubular response to ADH — meaning the kidney CAN concentrate urine when given ADH, confirming the problem is ADH deficiency (central DI). In nephrogenic DI, urine osmolality would fail to rise adequately despite desmopressin because the renal tubules are unresponsive to ADH. Primary polydipsia is excluded by the hypernatremia and persistent dilute urine during fluid restriction. Osmotic diuresis from glycosuria is excluded by the normal serum glucose.

A 51-year-old woman with primary Sjögren's syndrome presents with progressive bilateral lower extremity weakness, areflexia, and loss of vibration sense over 6 months. Nerve conduction studies show reduced compound sensory nerve action potential amplitudes with preserved conduction velocities, predominantly in the lower extremities. CSF protein is 78 mg/dL with no pleocytosis. Which pathophysiologic mechanism BEST explains her neurologic presentation?

Answer: Dorsal root ganglionopathy (sensory neuronopathy) from lymphocytic infiltration

Sjögren's syndrome is uniquely associated with sensory neuronopathy (dorsal root ganglionopathy), caused by lymphocytic infiltration of the dorsal root ganglia rather than peripheral nerve axons or myelin. This produces a non-length-dependent, predominantly sensory pattern with reduced SNAP amplitudes and preserved motor conduction — consistent with the NCS findings described. The sensory ataxia and areflexia reflect large fiber proprioceptive loss. Cryoglobulinemic vasculitis produces a length-dependent axonal neuropathy or mononeuritis multiplex. Anti-Ro antibodies are not known to target anterior horn cells. Small fiber autonomic neuropathy presents with pain, anhidrosis, and orthostatic symptoms — not the large-fiber pattern described here.

A 38-year-old man with no prior cardiac history collapses during a basketball game. He is resuscitated from ventricular fibrillation. ECG after resuscitation shows a short PR interval of 100 ms, a slurred QRS upstroke (delta wave), and QRS duration of 130 ms. Echocardiogram is normal. Cardiac MRI shows no fibrosis. During EP study, the accessory pathway has an anterograde effective refractory period (AERP) of 220 ms. Which statement about his risk stratification and management is MOST accurate?

Answer: His cardiac arrest makes him high risk regardless of AERP; catheter ablation is indicated

In Wolff-Parkinson-White (WPW) syndrome, the AERP of the accessory pathway and SPERRI during induced AF are used for risk stratification in asymptomatic patients. However, this patient has already had a WPW-related cardiac arrest (survived VF) — he is by definition HIGH RISK and is a SYMPTOMATIC patient with life-threatening arrhythmia. In survivors of cardiac arrest due to WPW-mediated pre-excited AF degenerating to VF, catheter ablation of the accessory pathway is strongly indicated regardless of EP parameters. AERP and SPERRI thresholds apply to risk stratification of ASYMPTOMATIC WPW, not survivors of cardiac arrest. Flecainide is contraindicated in WPW (can paradoxically accelerate conduction over the AP) and is never preferred over ablation in this setting.