Study day december 13

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Tumor Lysis Syndrome – Teaching Points

Core Concept

  • Tumor lysis syndrome (TLS) occurs due to rapid destruction of tumor cells with release of intracellular contents.

  • TLS is most likely in tumors with high cell burden or rapid turnover, such as diffuse large B-cell lymphoma.

  • TLS typically develops within days after starting chemotherapy or immunotherapy.

Characteristic Laboratory Abnormalities

  • TLS classically causes:

    • Hyperphosphatemia

    • Hyperkalemia

    • Hyperuricemia

    • Hypocalcemia

  • Hypocalcemia occurs because phosphate binds calcium to form calcium-phosphate complexes.

Acute Kidney Injury in TLS

  • The most common cause of AKI in TLS is acute nephrocalcinosis.

  • Acute nephrocalcinosis results from calcium phosphate deposition in the renal tubules and interstitium.

  • Phosphate nephropathy leads to AKI via tubular obstruction and direct tubular injury.

  • Uric acid nephropathy usually requires uric acid levels >15 mg/dL and is now less common due to effective prophylaxis.

Why AKI Occurs Despite Rasburicase

  • Rasburicase lowers uric acid by converting uric acid to allantoin.

  • Despite urate-lowering therapy, AKI still occurs because phosphate nephropathy remains common.

  • In modern TLS, AKI is more often due to calcium phosphate precipitation rather than uric acid stone formation.

TLS Prophylaxis

  • TLS prophylaxis includes aggressive intravenous fluids and urate-lowering therapy.

  • Xanthine oxidase inhibitors used for prophylaxis include allopurinol and febuxostat.

  • Rasburicase is preferred in patients with high-risk TLS or underlying kidney disease.

TLS Management

  • Management of severe TLS includes:

    • Intravenous fluids

    • Continuous cardiac telemetry

    • Frequent electrolyte monitoring and correction

  • Hemodialysis is indicated in severe cases, such as when the calcium–phosphate product is ≥70 mg²/dL².

Differential Diagnosis – Why Other Causes Are Less Likely

  • Cyclophosphamide toxicity typically causes hemorrhagic cystitis, not electrolyte-driven AKI.

  • Renal infiltration by lymphoma usually causes insidious kidney injury, not abrupt electrolyte abnormalities.

  • Rituximab hypersensitivity presents with fever, chills, hypotension, or urticaria, which are absent here.

  • Xanthinuria-related AKI occurs with xanthine oxidase inhibitor therapy, not rasburicase.

High-Yield Clinical Pearl

  • In modern tumor lysis syndrome, the most common cause of acute kidney injury is phosphate-mediated acute nephrocalcinosis, not uric acid nephropathy.

Administer the single-item screening test or Alcohol Use Disorders Identification Test–C (AUDIT-C)

Why this is correct

  • This patient is asymptomatic and presenting for a routine primary care visit.

  • Current guidelines (eg, USPSTF) recommend universal screening for unhealthy alcohol use in adults using brief, validated screening tools.

  • The preferred initial screening tests in primary care are:

    • Single-item alcohol screening question, or

    • AUDIT-C (3-question abbreviated AUDIT)

These tools are:

  • Quick

  • Highly sensitive

  • Designed for initial detection, not diagnosis

What the preferred screening tools look like

Single-item screening question

“How many times in the past year have you had 5 or more drinks in a day (for men), or 4 or more drinks in a day (for women)?”

  • ≥1 = positive screen

AUDIT-C

  • Assesses frequency, quantity, and binge drinking

  • Positive screen → proceed to full assessment (eg, full AUDIT, DSM-5 criteria)

High-yield teaching pearl

Unhealthy alcohol use screening in primary care should start with a brief validated tool (single-item screen or AUDIT-C), not CAGE or laboratory tests.



Emergency Surgery in Severe Aortic Stenosis

Key Diagnosis

  • Free air under the diaphragm on upright chest x-ray indicates intraabdominal (hollow viscus) perforation.

  • Diffuse abdominal tenderness with rebound is consistent with generalized peritonitis, which is a surgical emergency.

Immediate Management

  • The definitive treatment for bowel perforation with peritonitis is emergent exploratory abdominal surgery.

  • Initial stabilization includes intravenous fluids and broad-spectrum antibiotics, but these measures do not replace surgery.

Impact of Severe Aortic Stenosis

  • Severe aortic stenosis is defined by an aortic valve area ≤1.0 cm² (this patient: 0.8 cm²).

  • Severe aortic stenosis increases perioperative risk, including hypotension, myocardial infarction, heart failure, arrhythmias, and sudden cardiac death.

  • Patients with moderate-to-severe aortic stenosis may also have increased bleeding risk due to acquired von Willebrand syndrome.



Surgery Decision-Making Principle

  • A high-risk cardiac condition (eg, severe aortic stenosis) should not delay emergency, life-saving noncardiac surgery.

  • In contrast, nonemergency noncardiac surgery should be postponed until the cardiac condition is treated or optimized.

What Should NOT Delay Surgery

  • Balloon aortic valvuloplasty may be considered before nonemergency surgery in selected patients but should not delay emergency surgery, especially in asymptomatic severe aortic stenosis.

  • Stress testing (eg, dobutamine echocardiography) does not alter acute management and should not delay surgery.

  • Left heart catheterization is useful for preoperative risk stratification in nonemergent settings but should not delay emergency surgery.

Perioperative Management Focus

  • Emergency surgery in severe aortic stenosis should proceed with:

    • Invasive hemodynamic monitoring

    • Maintenance of preload

    • Avoidance of hypotension

    • Preservation of sinus rhythm

High-Yield Clinical Pearl

  • High-risk cardiac conditions require optimization before nonemergency surgery, but never delay emergency, life-saving noncardiac surgery.



Clinical Context

  • This patient has stage 2 hypertension, with repeated blood pressure readings of 145–155/88–95 mm Hg.

  • She prefers lifestyle modification rather than pharmacologic therapy due to prior adverse reactions to antihypertensive medications.

Most Effective Lifestyle Change

  • The lifestyle intervention most likely to produce the greatest reduction in blood pressure is initiation of the low-sodium DASH diet.

DASH Diet – Key Features

  • The DASH diet is characterized by:

    • High intake of fruits and vegetables

    • Low-fat dairy products

    • Whole grains and plant-based proteins

    • Low saturated and total fat

    • Reduced intake of processed meats and sweets

  • Compared with a typical American diet, the DASH diet is lower in sodium and higher in potassium, calcium, and magnesium.

Magnitude of Blood Pressure Reduction

  • The standard DASH diet reduces systolic blood pressure by approximately 8–14 mm Hg (mean ≈11 mm Hg).

  • Combining DASH with more rigorous sodium restriction (≤1500 mg/day) can result in blood pressure reductions approaching those of antihypertensive medications.

Comparison With Other Lifestyle Interventions

  • Regular aerobic exercise lowers systolic blood pressure by approximately 7 mm Hg.

  • Dietary sodium reduction alone lowers systolic blood pressure by 5–8 mm Hg.

  • Alcohol limitation (≤1 drink/day for women) lowers systolic blood pressure by approximately 5 mm Hg.

  • Increased intake of flavonoids lowers systolic blood pressure by only 2–3 mm Hg.

  • Low-carbohydrate diets may reduce systolic blood pressure modestly (~5 mm Hg) but are less effective than the DASH diet.

Patient-Specific Factors

  • This patient’s diet high in processed foods, saturated fat, and sodium and low in fruits and vegetables makes her particularly responsive to the DASH diet.

  • Older age, female sex, Black race, and metabolic syndrome are associated with a greater blood pressure response to DASH-style dietary changes.

High-Yield Clinical Pearl

  • Among lifestyle interventions for hypertension, the low-sodium DASH diet produces the largest and most consistent reduction in blood pressure.

 


High-Yield Clinical Pearl

  • For primary prevention of cardiovascular disease, the Mediterranean-style diet has the strongest and most consistent evidence for reducing cardiovascular mortality, especially when combined with regular physical activity and smoking cessation.


Peri-Infarction Pericarditis (PIP)

Clinical Recognition

  • Peri-infarction pericarditis occurs within days after an acute myocardial infarction.

  • Typical symptoms include pleuritic chest pain that worsens with inspiration and radiates to the shoulder or trapezius ridge.

  • Physical examination commonly reveals a pericardial friction rub.

Risk Factors

  • PIP is more common in patients with large infarcts or no reperfusion therapy.

Pathophysiology

  • PIP results from inflammation of the pericardium overlying necrotic myocardium.

  • It is not immune-mediated, distinguishing it from Dressler syndrome, which occurs weeks to months after MI.

Best Management

  • Symptomatic peri-infarction pericarditis should be treated with high-dose aspirin.

  • Recommended aspirin dosing is 650–1000 mg three times daily.

  • Aspirin is preferred because it controls inflammation without impairing myocardial healing.

Adjunctive Therapy

  • Colchicine or narcotic analgesics may be added for persistent symptoms despite adequate aspirin therapy.

What to Avoid

  • NSAIDs (eg, ibuprofen) should be avoided because they increase the risk of infarct expansion, scar thinning, and myocardial free wall rupture.

  • Glucocorticoids should be avoided as they impair healing and increase recurrence risk.

  • Anticoagulation should be discontinued if a pericardial effusion develops due to risk of hemorrhagic effusion and tamponade.

Antiplatelet Therapy

  • Aspirin and clopidogrel should NOT be discontinued after MI in patients with peri-infarction pericarditis.

Echocardiographic Findings

  • A small or trivial pericardial effusion is common and does not change management in uncomplicated PIP.

High-Yield Clinical Pearl

  • Acute pericarditis within days of MI = peri-infarction pericarditis → treat with high-dose aspirin, avoid NSAIDs, steroids, and unnecessary anticoagulation.





Congenital Long QT Syndrome – Cloze Teaching Cards

Clinical Recognition

  • A normal corrected QT interval (QTc) is 370–440 msec.

  • A QTc is considered prolonged when it is >450 msec in men or >470 msec in women.

  • A QTc of 505 msec with a family history of sudden unexplained death strongly suggests congenital long QT syndrome (LQTS).

  • Normal electrolytes and normal cardiac structure support a diagnosis of inherited rather than acquired QT prolongation.

Pathophysiology & Risk

  • Congenital LQTS predisposes patients to torsades de pointes, which can degenerate into ventricular fibrillation and cause sudden cardiac death.

  • Patients may be asymptomatic or present with syncope, seizures, palpitations, or cardiac arrest.

  • A QTc >500 msec is associated with increased arrhythmic risk, even in asymptomatic patients.

Initial Management

  • All patients with congenital LQTS, whether symptomatic or asymptomatic, should receive beta-blocker therapy.

  • The preferred initial treatment is a nonselective beta blocker, such as propranolol or nadolol.

  • Beta blockers reduce arrhythmic risk by blunting adrenergic stimulation that can trigger ventricular arrhythmias.

Why Other Options Are Incorrect

  • Reassurance alone is inappropriate because congenital LQTS carries a persistent risk of sudden cardiac death.

  • Disopyramide (class Ia antiarrhythmic) can further prolong the QT interval and worsen arrhythmia risk.

  • Diltiazem is used for supraventricular tachyarrhythmias and has no role in LQTS management.

  • Implantable cardioverter-defibrillator (ICD) placement is reserved for patients with:

    • Recurrent syncope or ventricular arrhythmias despite beta blockers

    • Aborted cardiac arrest

    • It is not first-line therapy in asymptomatic patients.

Lifestyle & Safety Counseling

  • Patients with LQTS should avoid:

    • QT-prolonging medications (eg, macrolides, fluoroquinolones, antipsychotics)

    • Electrolyte disturbances (hypokalemia, hypomagnesemia)

    • High-adrenergic triggers (depending on LQTS subtype)

High-Yield Clinical Pearl

  • Congenital long QT syndrome should be treated with beta blockers as first-line therapy, even in asymptomatic patients.

Final Answer

✅ Propranolol



Atrial Fibrillation With Rapid Ventricular Response AF w/ RVR

Clinical Recognition

  • This patient has atrial fibrillation with rapid ventricular response (AF with RVR), evidenced by an irregularly irregular rhythm and heart rate >120/min.

  • Symptoms present for 2 weeks indicate AF duration >48 hours.

  • Echocardiography showing diffuse LV hypokinesis with EF 40% suggests tachycardia-induced cardiomyopathy and decompensated heart failure.

Initial Management

  • First-line therapy for AF with RVR includes:

    • Rate control with AV-nodal blockers (eg, beta blockers)

    • Systemic anticoagulation

  • Failure of escalating beta-blocker therapy indicates inadequate rate control with persistent symptoms.

Need for Rhythm Control

  • In patients with persistent symptoms or heart failure despite rate control, rhythm control (cardioversion) is indicated.

  • However, AF lasting >48 hours carries a risk of left atrial appendage thrombus and systemic embolization with cardioversion.

Best Next Step

  • Before cardioversion in AF lasting >48 hours, the next step is transesophageal echocardiography (TEE) to:

    • Assess for left atrial appendage thrombus

    • Safely guide early cardioversion

  • If no thrombus is seen, the patient can proceed immediately to cardioversion with continued anticoagulation for 4 weeks.

  • If thrombus is present or not excluded, cardioversion should be delayed until ≥3 weeks of therapeutic anticoagulation is completed.

Why Other Options Are Incorrect

  • Flecainide is contraindicated in patients with structural heart disease or LV systolic dysfunction.

  • Sotalol has negative inotropic effects and increases risk of proarrhythmia in patients with reduced EF.

  • Cardiac catheterization and myocardial perfusion imaging are not indicated without evidence of acute ischemia.

High-Yield Clinical Pearl

  • AF lasting >48 hours + need for cardioversion → perform TEE first to exclude atrial thrombus, especially in patients with heart failure or LV dysfunction.



Alcohol Withdrawal



Polyarteritis Nodosa (PAN) – Cloze Teaching Points

Pattern Recognition

  • Recurrent postprandial abdominal pain suggests mesenteric ischemia due to medium-vessel vasculitis.

  • Testicular pain and swelling (orchitis) is a classic but often overlooked feature of polyarteritis nodosa.

  • Uncontrolled hypertension points to renal artery involvement rather than glomerular disease.

Key Risk Factor

  • A history of chronic hepatitis B infection is strongly associated with polyarteritis nodosa.

Systemic Features

  • PAN commonly presents with fever, weight loss, and elevated inflammatory markers (eg, CRP).

  • Multisystem involvement may include:

    • Gastrointestinal ischemia/infarction

    • Renal ischemia and hypertension

    • Peripheral neuropathy (mononeuritis multiplex)

    • Orchitis

    • Myocardial ischemia

Laboratory Clues

  • ANCA is negative, helping distinguish PAN from ANCA-associated vasculitides.

  • Normal urinalysis argues against glomerulonephritis, which PAN typically spares.

  • Rheumatoid factor may be positive due to immune-complex–mediated inflammation.

Pathophysiology

  • Polyarteritis nodosa is a necrotizing vasculitis of small- and medium-sized arteries.

  • It causes segmental transmural inflammation, leading to:

    • Luminal narrowing and thrombosis

    • Tissue infarction

    • Microaneurysm formation

  • PAN spares arterioles, capillaries, venules, and the lungs.

Diagnosis

  • There is no specific serologic test for PAN.

  • Diagnosis is confirmed by:

    • Tissue biopsy showing nongranulomatous vasculitis, or

    • Angiography revealing renal, hepatic, or mesenteric microaneurysms

Treatment

  • Initial treatment includes high-dose corticosteroids.

  • Cyclophosphamide is added for moderate to severe disease.

  • ACE inhibitors are used to manage hypertension.

Why Other Diagnoses Are Less Likely

  • Essential mixed cryoglobulinemia → usually hepatitis C, palpable purpura, and renal disease.

  • Granulomatosis with polyangiitis → upper/lower airway disease, glomerulonephritis, ANCA positive.

  • Microscopic polyangiitis → pulmonary hemorrhage, glomerulonephritis, ANCA positive.

  • Henoch–Schönlein purpura → IgA vasculitis, palpable purpura, typically children.

High-Yield Clinical Pearl

  • Middle-aged patient with hepatitis B + postprandial abdominal pain + orchitis + hypertension + negative ANCA = polyarteritis nodosa.

Final Answer

✅ Polyarteritis nodosa




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