Free practice quiz
ABIM Pulmonary Disease Prep Course (Pulm/CC): free quiz
10 questions from the program. See your score right away, then unlock the explanation of every answer.
- Question 1 of 10
A 62-year-old man with a 45-pack-year smoking history reports progressive exertional dyspnea and chronic cough. Examination shows decreased breath sounds and a prolonged expiratory phase. Spirometry shows FEV1/FVC 0.48 and FEV1 42% predicted. Lung volumes show TLC 128% predicted and RV 215% predicted. DLCO is 44% predicted. Which interpretation best explains this patient’s lung-volume and compliance pattern?
Review Lung Volumes and Compliance
Emphysema destroys alveolar attachments and elastic recoil, increasing compliance and causing expiratory airway collapse, air trapping, high RV/TLC, and low DLCO. A is tempting because dyspnea and low DLCO occur, but fibrosis lowers TLC and compliance. A causes restriction from chest wall load, usually low TLC and normal DLCO. A also restricts lung expansion through pleural mechanics, not obstructive hyperinflation. Clinician Action: Diagnose emphysema when obstruction plus hyperinflation and low DLCO coexist; order full PFTs and imaging when needed; treat with smoking cessation, bronchodilators, vaccination, pulmonary rehabilitation, and oxygen if hypoxemic; escalate for severe exacerbation or advanced disease evaluation.
- Question 2 of 10
A 62-year-old man with a 45-pack-year smoking history reports progressive exertional dyspnea and chronic cough. Examination shows prolonged expiration without crackles. Postbronchodilator spirometry shows FEV1 1.35 L, 42% predicted; FVC 2.15 L, 52% predicted; FEV1/FVC 0.63, below the lower limit of normal of 0.68. Lung volumes show TLC 91% predicted and RV 148% predicted. Which interpretation is most accurate?
Spirometry Pattern
Obstruction is defined by a reduced FEV1/FVC below the lower limit of normal; RV elevation supports expiratory airflow limitation with air trapping. A is correct. D is tempting because FVC is low, but restriction requires reduced TLC, which is absent. C misuses FVC alone; spirometry can suggest but not confirm restriction. B requires a preserved FEV1/FVC, unlike this case. Severity is contextual, but FEV1 42% predicted indicates at least moderate-to-severe physiologic impairment.
Clinician Action: Diagnose obstruction by low FEV1/FVC; order lung volumes when FVC is low; treat suspected COPD with smoking cessation and guideline inhalers; refer/escalate for hypoxemia, frequent exacerbations, or uncertain physiology. - Question 3 of 10
A 68-year-old man with severe COPD presents with 1 day of somnolence and increased dyspnea after taking extra oxycodone for back pain. He is afebrile; respiratory rate is 8/min, oxygen saturation is 88% on 2 L/min nasal oxygen, and wheezes are present. Basic metabolic panel: sodium 140, chloride 98, bicarbonate 33 mEq/L. Arterial blood gas on 2 L/min: pH 7.31, PaCO2 68 mm Hg, PaO2 62 mm Hg. His outpatient bicarbonate last month was 32 mEq/L. Which acid-base disorder is most likely?
ABG Acid Base Analysis
Low pH with high PaCO2 indicates respiratory acidosis. The elevated baseline bicarbonate reflects chronic renal compensation from COPD; new opioid-related hypoventilation raises PaCO2 before further renal compensation, causing acute-on-chronic respiratory acidosis. A is incorrect because bicarbonate is already chronically elevated. B is tempting, but appropriate chronic compensation should have a near-normal pH, not acute somnolent acidemia. C is incorrect because bicarbonate is elevated, not low, arguing against primary metabolic acidosis.
Clinician Action: Diagnose by sequential pH-PaCO2-HCO3 analysis; order repeat ABG after intervention; treat hypoventilation and consider noninvasive ventilation; escalate if mental status or ventilation worsens. - Question 4 of 10
A 45-year-old woman has episodic wheeze and chest tightness. She has chronic rhinosinusitis with recurrent nasal polyps and twice developed severe wheezing within 1 hour of taking ibuprofen. Between episodes, spirometry is normal. Examination today shows scattered expiratory wheezes; blood eosinophil count is 620/µL. Which asthma phenotype best explains this presentation and most directly guides trigger avoidance and add-on therapy?
Asthma phenotype discrimination
AERD reflects dysregulated arachidonic acid metabolism with cysteinyl-leukotriene excess, causing eosinophilic asthma, chronic rhinosinusitis/nasal polyps, and bronchospasm after COX-1 NSAIDs. D is tempting because eosinophilia suggests type 2 inflammation, but the discriminating NSAID reaction plus polyps favors AERD. A causes exertional symptoms, not nasal polyposis or ibuprofen reactions. A requires a work-linked exposure pattern; none is described. Normal interval spirometry does not exclude asthma.
Clinician Action: Diagnose AERD clinically, order spirometry/bronchodilator testing or bronchoprovocation if uncertain, treat asthma plus leukotriene modifier and avoid COX-1 NSAIDs, and refer allergy/ENT for desensitization or biologic consideration.Review Asthma Pathobiology And Phenotypes — focus on phenotype-specific triggers.
- Question 5 of 10
A 34-year-old woman with severe persistent asthma presents with 4 hours of worsening dyspnea despite repeated albuterol. After 90 minutes of continuous albuterol, ipratropium, and IV methylprednisolone, she speaks one-word answers, uses accessory muscles, and is becoming somnolent. Peak expiratory flow is 90 L/min, about 20% predicted. Arterial blood gas on supplemental oxygen shows pH 7.28, PaCO2 52 mm Hg, and PaO2 70 mm Hg. Which is the best next step?
Impending ventilatory failure in acute asthma
Severe asthma usually causes hypocapnia; rising PaCO2 with somnolence, exhaustion, and peak flow near 20% predicted indicates impending respiratory failure. C is correct: escalate immediately to ICU/airway-capable care while continuing inhaled bronchodilators and systemic steroids. A is tempting because magnesium can help severe exacerbations, but it is adjunctive and insufficient with hypercapnic encephalopathy. D delays needed escalation despite poor response and dangerous gas exchange. B may be a bridge in selected alert patients, but somnolence and worsening hypercapnia require supervised airway readiness, not ward NIV.
Clinician Action: Diagnose impending respiratory failure; order repeat ABG/continuous monitoring; treat with bronchodilators, steroids, oxygen, and airway support; escalate to ICU/anesthesia or critical care. - Question 6 of 10
A 58-year-old man with a 40-pack-year smoking history reports progressive exertional dyspnea and daily productive cough. Post-bronchodilator spirometry shows FEV1/FVC 0.56 and FEV1 48% predicted. CAT score is 18. During the past year, he had two COPD exacerbations treated with prednisone and antibiotics as an outpatient and no hospitalizations. Oxygen saturation is 94% on room air. Which classification best describes his COPD?
COPD Diagnosis and Staging
Persistent post-bronchodilator FEV1/FVC <0.70 confirms COPD in the right exposure context. FEV1 48% predicted is GOLD airflow grade 3, and two moderate outpatient exacerbations place him in group E. B is tempting because CAT 18 suggests high symptoms, but FEV1 is not grade 2 and exacerbation risk overrides B grouping. A is wrong: reversibility magnitude is not required to confirm COPD. C is wrong: normal resting oxygenation does not exclude obstructive disease.
Clinician Action: Diagnose with post-bronchodilator obstruction; order exacerbation and symptom assessment; treat with guideline-directed inhaled therapy and smoking cessation; escalate for hypoxemia, frequent exacerbations, or advanced emphysema evaluation. - Question 7 of 10
A 54-year-old woman with long-standing asthma presents with 2 years of chronic cough productive of thick green sputum and recurrent “pneumonias.” Examination shows scattered wheezes. Blood eosinophils are 850/µL, total IgE is markedly elevated, and Aspergillus-specific IgE is positive. High-resolution CT shows upper-lobe predominant central bronchiectasis with mucus plugging and bronchial wall thickening. Which etiology best explains her bronchiectasis?
Review Bronchiectasis Etiologies And Imaging
ABPA causes hypersensitivity to Aspergillus in asthma, producing eosinophilia, very high IgE, mucus plugging, and central upper-lobe bronchiectasis. C is tempting after recurrent infections, but postinfectious disease is usually localized to the damaged region and lacks Aspergillus sensitization. A often affects older women with nodular tree-in-bud opacities and right middle lobe/lingula disease, not marked IgE elevation. A usually has dependent lower-lobe predominance with dysphagia or reflux history.
Clinician Action: Diagnose ABPA by asthma, Aspergillus sensitization, high IgE, eosinophilia, and central bronchiectasis; order HRCT and immunologic testing; treat with systemic glucocorticoids ± azole therapy; refer/escalate for refractory disease or severe bronchiectasis. - Question 8 of 10
A 68-year-old man has 14 months of progressive exertional dyspnea and dry cough. He has no wheezing, edema, or known connective tissue disease. Examination shows bibasilar inspiratory crackles. Spirometry shows FEV1 68% predicted, FVC 60% predicted, FEV1/FVC 0.88, TLC 56% predicted, and DLCO 39% predicted. During a 6-minute walk, oxygen saturation falls from 95% to 86%. HRCT shows basilar, subpleural reticulation with traction bronchiectasis and honeycombing.
Restrictive PFT And Imaging Patterns
Fibrotic parenchymal restriction causes reduced TLC with preserved/increased FEV1/FVC, low DLCO, exertional desaturation, and HRCT fibrosis; basilar subpleural honeycombing is classic for UIP/IPF. D is tempting because obesity lowers TLC, but DLCO is usually normal or mildly reduced and HRCT lacks honeycombing. A can cause restriction, but the discriminating finding is fibrotic HRCT plus markedly reduced DLCO rather than isolated low maximal pressures. A may restrict lung expansion, but pleural thickening/calcification, not subpleural honeycombing with traction bronchiectasis, would dominate imaging.
Clinician Action: Diagnose fibrotic ILD/UIP pattern; order exposure/autoimmune review and multidisciplinary ILD evaluation; treat with antifibrotic therapy when IPF is confirmed; refer/escalate for oxygen assessment, pulmonary rehabilitation, and transplant evaluation when advanced. - Question 9 of 10
A 72-year-old man presents with 18 months of progressive exertional dyspnea and dry cough. He smoked 20 pack-years but quit 25 years ago. He has no bird exposure, mold exposure, connective tissue disease symptoms, or culprit medication use. Examination shows bibasilar end-inspiratory crackles and mild digital clubbing. Spirometry shows restriction, and DLCO is 42% predicted. High-resolution CT shows basal, subpleural reticulation with traction bronchiectasis and honeycombing, without extensive ground-glass opacity. Which diagnosis is most likely?
UIP pattern and IPF
Idiopathic pulmonary fibrosis causes progressive fibrotic remodeling in older adults; basal subpleural reticulation, traction bronchiectasis, honeycombing, crackles, clubbing, and reduced DLCO support UIP/IPF. B is tempting because chronic hypersensitivity pneumonitis can fibrose, but exposure history and upper/mid-lung air trapping or centrilobular nodules are absent. A shares restriction and fibrosis, but NSIP usually has more ground-glass opacity and relative subpleural sparing. A can fibrose, but typically has perilymphatic nodules, adenopathy, and upper-lobe predominance. Review UIP pattern and IPF — focus on honeycombing plus basal subpleural distribution.
Clinician Action: Diagnose probable IPF; order multidisciplinary ILD review and baseline severity testing; treat with antifibrotic therapy and pulmonary rehabilitation; refer for transplant evaluation when appropriate. - Question 10 of 10
A 58-year-old woman has 9 months of progressive exertional dyspnea and dry cough. She reports Raynaud phenomenon, reflux, and tight puffy fingers but has no known rheumatologic diagnosis. Examination shows bibasilar fine crackles and skin thickening of the fingers. Spirometry shows restriction and reduced DLCO. High-resolution CT shows lower-lobe ground-glass opacity with fine reticulation, traction bronchiectasis, and relative subpleural sparing without honeycombing. Which CTD-associated ILD pattern is most likely?
Review CTD-ILD pattern recognition
Systemic sclerosis commonly causes fibrotic NSIP: basilar ground-glass/reticulation, traction bronchiectasis, and subpleural sparing; Raynaud, reflux, and sclerodactyly support the diagnosis and rheumatology comanagement. A is tempting because RA can cause basilar fibrosis, but RA-UIP more often has honeycombing and lacks scleroderma features. A may have myositis/Raynaud, but organizing pneumonia usually shows patchy consolidations. A causes centrilobular nodules/air-trapping in smokers, not scleroderma-associated restriction.
Clinician Action: Diagnose CTD-ILD, order autoimmune evaluation/PFT monitoring, treat with guideline-supported immunomodulation when progressive, and refer to rheumatology.
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