Step 2 CK Practice Questions: Diagnostic Reasoning & Board Strategy

Scleroderma renal crisis (SRC) is a life-threatening complication of systemic sclerosis characterized by acute onset of malignant hypertension, rapidly progressive acute kidney injury, and microangiopathic hemolytic anemia. Angiotensin-converting enzyme (ACE) inhibitors, specifically oral captopril, are the absolute treatment of choice regardless of baseline creatinine elevation.

1. The patient has diffuse cutaneous systemic sclerosis and presents with acute severe hypertension (210/118 mm Hg), hypertensive retinopathy (papilledema, cotton-wool spots), oliguric acute renal failure (creatinine 3.4 mg/dL from 0.8 mg/dL), and microangiopathic features (schistocytes). This is classic scleroderma renal crisis (SRC).
2. Pathophysiology: SRC is driven by intimal thickening and proliferation of the renal arcuate and interlobular arteries, leading to severe renal ischemia and massive activation of the renin-angiotensin-aldosterone system (RAAS).
3. High-dose oral captopril (a short-acting ACE inhibitor) specifically reverses the profound angiotensin II-mediated renal vasoconstriction. Although ACE inhibitors cause a mild initial decrease in glomerular filtration rate in normal physiology, in SRC they halt the ischemic cascade and are lifesaving. Treatment must NOT be delayed due to elevated serum creatinine.

• Scleroderma renal crisis typically occurs in patients with diffuse cutaneous systemic sclerosis, often precipitated by systemic corticosteroid therapy.
• ACE inhibitors (particularly short-acting captopril) are the primary, lifesaving pharmacotherapy, even in the presence of acute kidney injury and elevated serum creatinine.

Spinal epidural abscess (SEA) presents with the classic triad of fever, focal spinal tenderness, and neurologic deficits (e.g., motor weakness, sensory level, sphincter dysfunction). Urgent contrast-enhanced MRI of the entire spine is the diagnostic modality of choice to delineate the extent of cord compression before surgical decompression.

1. The patient has multiple predisposing risk factors for bacteremia and hematogenous seeding (diabetes mellitus, hemodialysis with an indwelling central venous catheter).
2. He presents with the classic clinical progression of spinal epidural abscess (SEA): (1) focal spinal back pain, (2) systemic signs (fever, leukocytosis, markedly elevated ESR), and (3) signs of acute thoracic spinal cord compression (bilateral lower extremity weakness, hyperreflexia, upgoing toes, sensory level at T8, urinary retention with overflow incontinence, decreased rectal tone).
3. This is a neurosurgical emergency. Urgent contrast-enhanced MRI of the complete spine must be performed immediately to confirm the diagnosis, evaluate the exact craniocaudal extent of the abscess (as skip lesions or multi-level involvement occur in up to 20% of cases), and plan prompt surgical decompression (laminectomy) combined with targeted IV antibiotics.

• Spinal epidural abscess most commonly arises from hematogenous spread (frequently Staphylococcus aureus) in patients with diabetes, injection drug use, or vascular access catheters.
• Any patient with back pain, fever, and progressive neurologic deficits requires urgent MRI of the spine to prevent permanent paraplegia.

IgA nephropathy (Berger disease) classically manifests in young adult men as recurrent gross hematuria occurring concurrently with or within a few days (synpharyngitic) of an upper respiratory or gastrointestinal infection, characterized by normal serum complement (C3/C4) levels.

1. The patient is a young male presenting with gross hematuria (cola-colored urine with dysmorphic RBCs and RBC casts, indicating glomerulonephritis) that developed 2 days after an upper respiratory infection.
2. The key distinguishing factors in glomerulonephritis following an infection are timing and complement levels:

• IgA nephropathy is synpharyngitic (occurs within 1–3 days of onset of viral infection) and typically features normal serum complement levels.
• Poststreptococcal glomerulonephritis (PSGN) is post-infectious, occurring 1–3 weeks after pharyngitis (or 3–6 weeks after impetigo), and is associated with low serum C3 levels.

3. The short interval (1–2 days) and normal complement levels strongly confirm IgA nephropathy.

• IgA nephropathy: gross hematuria develops within 5 days of upper respiratory infection; complement levels are normal.
• Poststreptococcal glomerulonephritis: gross hematuria develops 10–21 days after pharyngitis; complement (C3) levels are decreased.

First-line therapy for acute idiopathic or viral pericarditis consists of a combination of a nonsteroidal anti-inflammatory drug (NSAID) such as high-dose ibuprofen or indomethacin plus colchicine to reduce symptoms and prevent recurrence.

1. The patient presents with classic features of acute viral pericarditis: sharp retrosternal chest pain radiating to the trapezius ridge, pleuritic character, relief with leaning forward, a scratchy triphasic pericardial friction rub, and diffuse ST elevations with PR depressions.
2. The underlying pathophysiology is acute inflammation of the pericardial layers, frequently triggered by a preceding viral upper respiratory infection (e.g., Coxsackievirus, adenovirus).
3. Standard practice guidelines dictate that acute pericarditis without myocardial involvement (normal troponin) is treated with high-dose NSAIDs (e.g., ibuprofen 600–800 mg three times daily) combined with weight-adjusted colchicine for 3 months to accelerate symptom resolution and decrease recurrence rates.

• Acute pericarditis classically presents with pleuritic chest pain that improves leaning forward, a pericardial friction rub, and diffuse concave ST elevations with PR depressions.
• High-dose NSAIDs plus colchicine represent first-line therapy; corticosteroids are reserved for contraindications, refractory cases, or specific autoimmune etiologies due to increased recurrence risk.