A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 63-year-old woman is brought to the emergency department because of a 2-day history of severe epigastric pain and nausea. She has a 20-year history of alcohol use disorder. Nine hours after admission, she becomes increasingly dyspneic and tachypneic. Pulse oximetry on supplemental oxygen shows an oxygen saturation of 81%. Physical examination shows diffuse lung crackles, marked epigastric tenderness, and a periumbilical hematoma. Laboratory studies show normal brain natriuretic peptide. An x-ray of the chest shows bilateral opacities in the lower lung fields. Which of the following pathomechanisms best explains this patient's pulmonary findings?
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A
Alveolocapillary membrane leakageCorrect. ARDS in severe pancreatitis results from systemic inflammatory cytokines damaging the alveolocapillary membrane, producing non-cardiogenic protein-rich pulmonary edema.
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B
Increased production of surfactantIncorrect. Surfactant production is DECREASED in ARDS due to type II pneumocyte injury, not increased; reduced surfactant contributes to atelectasis and hypoxia.
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C
Embolic obstruction of pulmonary arteriesIncorrect. Pulmonary embolism (e.g., from DVT) is a possibility, but bilateral diffuse infiltrates with a clear inflammatory precipitant favor ARDS over embolic obstruction.
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D
Inflammation of the bronchial mucosaIncorrect. Bronchial mucosal inflammation describes bronchitis/asthma — not the alveolar-level membrane injury that causes ARDS.
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E
Left atrial pressure elevation causing transudative edemaIncorrect. Elevated left atrial pressure produces cardiogenic pulmonary edema, but this patient's normal BNP and inflammatory precipitant (pancreatitis) point to non-cardiogenic alveolocapillary injury (ARDS).
↑ Tap an answer to reveal the reasoning
Answer: A. Acute pancreatitis in a chronic alcoholic with Cullen sign (periumbilical hematoma — indicating hemorrhagic pancreatitis) who then develops bilateral lower-lobe infiltrates, severe hypoxemia despite supplemental oxygen, and a NORMAL BNP has acute respiratory distress syndrome (ARDS). ARDS is one of the most common pulmonary complications of severe acute pancreatitis. The mechanism is non-cardiogenic pulmonary edema: systemic inflammatory mediators (TNF-alpha, IL-1, IL-6, complement, neutrophil products) injure the alveolocapillary membrane, increasing permeability and allowing protein-rich fluid to flood alveoli. The normal BNP rules out cardiogenic pulmonary edema (CHF).
Berlin criteria for ARDS: acute onset, bilateral opacities not fully explained by effusions/atelectasis, no cardiogenic cause (PCWP <18 or no clinical evidence of left atrial hypertension), and PaO2/FiO2 <300. Treatment is low-tidal-volume ventilation (6 mL/kg ideal body weight) with PEEP, prone positioning for severe ARDS, and treating the underlying cause.
Pearl: pancreatitis-induced ARDS results from systemic cytokine release damaging the alveolocapillary barrier — not from circulating pancreatic enzymes directly.
**Why each option:**
**A.** Correct. ARDS in severe pancreatitis results from systemic inflammatory cytokines damaging the alveolocapillary membrane, producing non-cardiogenic protein-rich pulmonary edema.
**B.** Surfactant production is DECREASED in ARDS due to type II pneumocyte injury, not increased; reduced surfactant contributes to atelectasis and hypoxia.
**C.** Pulmonary embolism (e.g., from DVT) is a possibility, but bilateral diffuse infiltrates with a clear inflammatory precipitant favor ARDS over embolic obstruction.
**D.** Bronchial mucosal inflammation describes bronchitis/asthma — not the alveolar-level membrane injury that causes ARDS.