Free USMLE Step 2 CK Pulmonary and Critical Care practice questions

This tall, thin young male smoker has a primary spontaneous pneumothorax, caused by rupture of apical subpleural blebs in a patient without known lung disease. The pneumothorax is small (rim under 2 cm at the hilum by BTS criteria, under 3 cm apex to cupola by ACCP criteria) and he is clinically stable with minimal symptoms and normal oxygenation.

A small, minimally symptomatic primary pneumothorax is managed conservatively. He is observed for several hours, and a repeat chest x-ray confirms the pneumothorax is not enlarging before discharge with clear return precautions and early follow-up. Supplemental high-flow oxygen, if he is observed in hospital, lowers the nitrogen partial pressure in the blood, creating a gradient that speeds reabsorption of pleural air severalfold compared with the normal rate of about 1.5% of the hemithorax volume per day. He should also be counseled that smoking cessation is the most effective way to lower his high risk of recurrence and should avoid air travel until resolution is confirmed.

B. Needle aspiration is used for large or symptomatic primary pneumothoraces; this one is small and he is stable. C. A chest tube is indicated for large or symptomatic pneumothorax after failed aspiration, secondary pneumothorax, tension (after decompression), or ventilated patients. D and E. Thoracoscopic bleb resection and pleurodesis are recurrence-prevention procedures reserved for a recurrent pneumothorax, a persistent air leak, a first secondary pneumothorax, or high-risk occupations; they are not indicated after a first small primary episode.

The combination of a middle-aged woman with asthma, a subacute illness of weeks to months with constitutional symptoms (night sweats, fever, weight loss), peripheral blood eosinophilia, BAL eosinophils well above 25%, and bilateral peripheral upper-zone consolidations is classic for chronic eosinophilic pneumonia. The peripheral distribution is often called the photographic negative of pulmonary edema, which is central. Treatment is prednisone about 0.5 mg/kg/day, which relieves symptoms within days and clears the film within weeks; the taper lasts at least 6 months, and about half of patients relapse, usually responding again to steroids.

A is wrong because acute eosinophilic pneumonia evolves over days, typically after new smoking or vaping in a young adult, causes hypoxemic respiratory failure resembling ARDS with diffuse ground glass, and often has a normal blood eosinophil count at onset. C is wrong because ABPA requires Aspergillus sensitization and usually a total IgE above 1000 IU/mL (500 or more in the 2024 ISHAM criteria), with central bronchiectasis and mucus plugs; her Aspergillus-specific IgE is undetectable. D is wrong because Loeffler syndrome is a transient, migratory infiltrate with mild symptoms that resolves within about 2 weeks, usually after Ascaris exposure, not a 2-month illness. E is wrong because tuberculosis can cause upper-lobe disease and night sweats but does not cause marked blood and BAL eosinophilia, and her AFB studies are negative.

This patient meets the definition of a bronchiectasis exacerbation: at least 48 hours of worsening in three or more symptoms (cough, sputum volume, sputum purulence, dyspnea) that warrants a change in treatment. He is clinically stable, with normal oxygenation and blood pressure, no new consolidation, and good oral intake, so he can be managed as an outpatient.

The approach is to send sputum for culture before starting antibiotics and then treat empirically according to the patient's previous isolates, adjusting when results return. Because he has grown Pseudomonas aeruginosa, the empirical agent must be antipseudomonal. Ciprofloxacin (or levofloxacin) is the only oral antipseudomonal option, and his isolates are susceptible. The ERS and BTS guidelines recommend a 14-day course for bronchiectasis exacerbations, which are driven by a high bacterial load in damaged airways; shorter courses are considered only in selected patients with mild disease.

A. Amoxicillin-clavulanate is the usual choice when Haemophilus influenzae is the known organism, but it has no Pseudomonas activity, and 5 days is shorter than recommended. B. IV antipseudomonal beta-lactams are for severe exacerbations or failure of oral therapy; this patient is stable and can take oral medication. C. A short azithromycin course does not cover Pseudomonas and is not exacerbation treatment; long-term macrolides are a preventive strategy. D. Withholding antibiotics is inappropriate once an exacerbation is established, because untreated exacerbations perpetuate the infection and inflammation cycle.

Sudden syncope, hypoxemia, and sustained hypotension with distended jugular veins and clear lungs describe obstructive shock. In a patient 4 days after knee arthroplasty with inadequate thromboprophylaxis, the cause is acute pulmonary embolism with right ventricular failure (high-risk PE, previously called massive PE: systolic pressure below 90 mm Hg for at least 15 minutes). The echocardiogram shows the signature of acute RV pressure overload: a dilated, hypokinetic RV with apical sparing (McConnell sign) and a small, underfilled LV from septal bowing and reduced RV output. A new right bundle branch block and sinus tachycardia support acute right heart strain.

In an unstable patient who cannot safely travel to CT, bedside echocardiographic RV dysfunction justifies treating as high-risk PE, which means systemic thrombolysis if there is no major contraindication (recent surgery is a relative one), with catheter-directed therapy or surgical embolectomy when lysis is contraindicated or fails. Fluids should be given cautiously, and norepinephrine is the vasopressor of choice.

A. Tamponade also causes hypotension and jugular venous distension, but echocardiography would show a pericardial effusion with RV diastolic collapse. B. Tension pneumothorax causes unilateral absent breath sounds and tracheal deviation. C. RV infarction causes hypotension with clear lungs and elevated JVP, but it accompanies an inferior STEMI with ST elevation in V4R, which is absent. E. Hypovolemic or hemorrhagic shock produces flat neck veins and a falling hemoglobin, not a dilated RV.

This man has obesity hypoventilation syndrome (OHS). The diagnosis requires three elements: obesity (BMI 30 kg/m2 or more), daytime hypercapnia while awake (PaCO2 above 45 mm Hg), and no other explanation for hypoventilation. He has all three: a BMI of 46, an awake PaCO2 of 56 mm Hg with a near-normal pH, and normal airflow ratio, chest x-ray, and thyroid function. The raised serum bicarbonate is the renal compensation for chronic hypercapnia and is a useful screening clue in obese, sleepy patients. Chronic hypoxemia explains his secondary polycythemia, and the edema with elevated JVP suggests pulmonary hypertension with cor pulmonale, a recognized complication. About 90% of patients with OHS also have obstructive sleep apnea, which fits the snoring and sleepiness.

The ATS guideline recommends polysomnography to characterize the coexisting sleep-disordered breathing and positive airway pressure therapy (CPAP for those with severe OSA, or noninvasive ventilation such as BiPAP), together with substantial weight loss. Untreated OHS carries high rates of hospitalization, cor pulmonale, and death.

A. COPD causes hypercapnia through airflow obstruction, but he has never smoked and his FEV1/FVC ratio is normal. B. Central sleep apnea with Cheyne-Stokes breathing occurs mainly in heart failure with low or normal daytime PaCO2; it does not produce chronic awake hypercapnia with a high bicarbonate. D. Neuromuscular weakness can cause hypoventilation, but there are no clinical findings of myopathy or neuropathy, and obesity fully explains his restrictive pattern. E. Primary metabolic alkalosis would raise the pH with a compensatory rise in PaCO2; his pH is low-normal, which shows the primary process is respiratory acidosis with renal compensation.

This patient has immune checkpoint inhibitor pneumonitis: new cough and dyspnea within the first months of PD-1 blockade, with bilateral ground-glass and organizing-pneumonia-type opacities. Infection has been reasonably excluded with negative viral, COVID-19 and blood testing and a low procalcitonin, and the imaging shows no tumor progression. Severity is graded by symptoms and extent. He is grade 2: symptomatic, with involvement of 25% to 50% of the lung and limitation of instrumental activities of daily living such as shopping, but no hypoxemia requiring hospital-level oxygen and preserved self-care. ASCO and NCCN guidance for grade 2 is to hold the checkpoint inhibitor and start prednisone 1 to 2 mg/kg/day, then taper over at least 4 to 6 weeks once symptoms improve to grade 1 or less, with reassessment in 48 to 72 hours and escalation to IV steroids and admission if he worsens. Rechallenge can be considered after full resolution.

B is the approach for grade 1 disease (imaging changes only); this patient is symptomatic. C is wrong because permanent discontinuation is reserved for grade 3 to 4 pneumonitis, and infliximab is added only when severe pneumonitis fails to improve after 48 hours of IV methylprednisolone. D is wrong because infection has been excluded and continuing the drug would allow pneumonitis to progress. E is wrong because inhaled glucocorticoids do not treat immune-mediated parenchymal inflammation.

Her pulmonary function shows an isolated low DLCO: normal spirometry (no obstruction), normal TLC (no restriction) and a markedly reduced hemoglobin-corrected diffusing capacity. When the airways and lung volumes are normal, a low DLCO points to loss of pulmonary capillary blood volume, that is, pulmonary vascular disease, or to very early ILD. Here the history of pulmonary embolism, exertional desaturation, a loud P2, edema and enlarged central pulmonary arteries make chronic thromboembolic pulmonary hypertension (CTEPH) the most likely cause. Guidelines advise evaluating patients with persistent dyspnea 3 or more months after PE with echocardiography and a V/Q scan, the preferred screening test because a normal scan essentially excludes CTEPH; right heart catheterization and pulmonary angiography confirm it. CTEPH is important to identify because it is potentially curable with pulmonary endarterectomy.

B. Emphysema lowers the DLCO but also causes airflow obstruction (FEV1/FVC below 0.70) and hyperinflation, and she has never smoked.

C. Idiopathic pulmonary fibrosis lowers both TLC and DLCO and produces basilar crackles and reticular opacities; her volumes and lung fields are normal.

D. Obesity hypoventilation lowers TLC with a normal or high DLCO and raises PaCO2; nothing suggests obesity.

E. Diaphragmatic weakness causes a restrictive pattern, especially supine, with a normal DLCO because the lung itself is healthy.

Several clues point to alpha-1 antitrypsin deficiency: emphysema before age 45 with a modest smoking history, lower-lobe panlobular distribution, and a father who died of emphysema in his 50s. His AAT level is in the low-normal range, but it was drawn during acute pneumonia with a markedly elevated CRP. AAT is an acute-phase reactant, so infection, inflammation, pregnancy, or estrogen can raise the level of a deficient patient (particularly MZ or SZ, and occasionally severe genotypes) into the normal range. When clinical suspicion is high and the level is borderline or was measured during inflammation, the next step is to identify the allele pair directly with isoelectric focusing phenotyping or SERPINA1 genotyping, which is unaffected by inflammation. Many laboratories now offer combined level plus genotype panels for exactly this reason.

A is wrong because a single low-normal value drawn with a CRP of 168 mg/L does not exclude deficiency in a patient with a classic phenotype. C is wrong because liver biopsy is invasive, is used to stage liver disease rather than diagnose AATD, and it adds nothing that a blood genotype cannot provide. D is wrong because cystic fibrosis causes upper-lobe bronchiectasis and pancreatic insufficiency, not basilar panlobular emphysema. E is wrong because a serum IgE level evaluates allergic asthma or allergic bronchopulmonary aspergillosis, neither of which explains fixed basilar emphysema.