American Board of Internal Medicine Certification (ABIM Board Certification) Pulmonary & Critical Care Medicine Syllabus

Pulmonary & Critical Care Medicine syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Pulmonary & Critical Care Medicine in American Board of Internal Medicine Certification (ABIM Board Certification), not a summary of it.

1. 1

   Obstructive & Airway Diseases

   3 topics

   • COPD diagnosis, GOLD staging, and management
     • Inhaler therapy escalation
     • Acute exacerbation treatment
   • Asthma classification and stepwise therapy
   • Bronchiectasis and cystic fibrosis
2. 2

   Interstitial & Diffuse Parenchymal Lung Disease

   4 topics

   • Idiopathic pulmonary fibrosis
   • Hypersensitivity pneumonitis
   • Sarcoidosis
     • Pulmonary and extrapulmonary manifestations
   • Connective tissue disease-associated ILD
3. 3

   Pulmonary Vascular & Pleural Disease

   4 topics

   • Pulmonary embolism diagnosis and risk stratification
     • Wells/PERC criteria and D-dimer use
     • Thrombolysis and anticoagulation
   • Pulmonary hypertension classification
   • Pleural effusion: Light's criteria and workup
   • Pneumothorax management
4. 4

   Respiratory Failure & Mechanical Ventilation

   4 topics

   • ARDS recognition and lung-protective ventilation
   • Hypoxemic vs hypercapnic respiratory failure
   • Noninvasive ventilation indications
   • Ventilator settings and weaning
5. 5

   Shock & Critical Illness

   4 topics

   • Sepsis and septic shock management
     • Early resuscitation and source control
     • Vasopressor selection
   • Shock classification and hemodynamic assessment
   • Sleep-disordered breathing and OSA
   • Acid-base interpretation in critical illness

Pulmonary & Critical Care Medicine flashcards for American Board of Internal Medicine Certification (ABIM Board Certification)

21 of 60 cards from the Pulmonary & Critical Care Medicine deck — real questions with worked answers.

1. What spirometry finding is required to diagnose COPD?

   A post-bronchodilator FEV1/FVC ratio < 0.70, confirming persistent, non-fully-reversible airflow obstruction.

2. Describe the GOLD spirometric grades (1-4) of airflow limitation based on post-bronchodilator FEV1 % predicted (in patients with FEV1/FVC < 0.70).

   GOLD 1 (mild): FEV1 >=80%; GOLD 2 (moderate): 50-79%; GOLD 3 (severe): 30-49%; GOLD 4 (very severe): <30% predicted.

3. How does the GOLD ABE assessment tool classify COPD patients?

   By symptoms (mMRC/CAT) and exacerbation history: Group A = low symptoms, 0-1 non-hospitalized exacerbations; Group B = high symptoms, 0-1 exacerbations; Group E = >=2 moderate exacerbations or >=1 leading to hospitalization (regardless of symptoms).

4. Which two interventions have been proven to reduce mortality in COPD?

   Smoking cessation and long-term supplemental oxygen therapy in patients with chronic resting hypoxemia (lung volume reduction surgery also benefits selected upper-lobe predominant patients).

5. What are the criteria for prescribing long-term oxygen therapy in COPD?

   Resting PaO2 <=55 mmHg or SaO2 <=88%; or PaO2 56-59 mmHg (SaO2 89%) with evidence of cor pulmonale, right heart failure, or erythrocytosis (Hct >55%).

6. When should inhaled corticosteroids be added to therapy in COPD?

   Favored when blood eosinophils are elevated (>=300 cells/uL, consider at >=100) and/or frequent exacerbations despite LABA/LAMA; ICS are avoided in patients with low eosinophils due to increased pneumonia risk.

7. What is the role of roflumilast in COPD?

   A PDE-4 inhibitor used to reduce exacerbations in patients with severe COPD, chronic bronchitis phenotype, and frequent exacerbations despite inhaled triple therapy.

8. What young patient or basilar-emphysema presentation should prompt testing for alpha-1 antitrypsin deficiency?

   COPD/emphysema in a patient <45 years, a nonsmoker or minimal smoking history, basilar-predominant emphysema, or associated unexplained liver disease.

9. In asthma, what spirometric change defines significant bronchodilator reversibility?

   An increase in FEV1 (or FVC) of >=12% AND >=200 mL after a bronchodilator.

10. How is asthma severity classified by symptom frequency (intermittent vs persistent)?

    Intermittent: symptoms <=2 days/week, nighttime <=2x/month, FEV1 normal. Mild persistent: >2 days/week but not daily. Moderate persistent: daily symptoms, nighttime >1x/week. Severe persistent: throughout the day, frequent nighttime, FEV1 <60%.

11. What is the preferred reliever therapy in current (GINA) stepwise asthma management for adults?

    As-needed low-dose ICS-formoterol (anti-inflammatory reliever), rather than SABA alone, across steps 1-2; SABA-only treatment is no longer recommended.

12. What is the SMART/MART strategy in asthma?

    Single Maintenance And Reliever Therapy: using a single ICS-formoterol inhaler for both daily maintenance and as-needed relief, which reduces exacerbations.

13. Which biologics target which pathways in severe eosinophilic/allergic asthma?

    Omalizumab (anti-IgE) for allergic asthma; mepolizumab/reslizumab (anti-IL-5) and benralizumab (anti-IL-5R) for eosinophilic asthma; dupilumab (anti-IL-4Ra) for type 2/eosinophilic asthma.

14. What is the classic radiographic and clinical hallmark of bronchiectasis?

    Permanent, abnormal bronchial dilation with chronic productive cough; high-resolution CT shows airways larger than the accompanying artery ('signet ring' sign), lack of tapering, and bronchial wall thickening.

15. What is the most common genetic defect causing cystic fibrosis, and how is it diagnosed?

    The Phe508del (F508del) mutation in the CFTR gene; diagnosed by an elevated sweat chloride >=60 mmol/L and/or two disease-causing CFTR mutations with clinical features.

16. Which organisms most commonly colonize/infect the airways in cystic fibrosis over time?

    Staphylococcus aureus in childhood, then chronic Pseudomonas aeruginosa (associated with worse prognosis); also Burkholderia cepacia complex, which carries a poor prognosis.

17. What class of drugs has transformed cystic fibrosis treatment?

    CFTR modulators (e.g., elexacaftor/tezacaftor/ivacaftor, 'Trikafta') that correct/potentiate the defective CFTR protein, improving lung function and reducing exacerbations.

18. What is the characteristic HRCT pattern of idiopathic pulmonary fibrosis (IPF)?

    Usual interstitial pneumonia (UIP): subpleural and basal-predominant reticulation with honeycombing, with or without traction bronchiectasis, and minimal ground-glass.

19. Which two antifibrotic drugs slow disease progression in IPF?

    Pirfenidone and nintedanib; both slow the decline in FVC. Corticosteroids/immunosuppression are NOT beneficial and may be harmful in IPF.

20. What exposure history and CT features suggest chronic hypersensitivity pneumonitis?

    Exposure to organic antigens (birds, molds, hot tubs, farming); CT shows centrilobular ground-glass nodules, mosaic attenuation/air trapping (three-density 'headcheese' sign), and upper/mid-lung fibrosis. BAL typically shows lymphocytosis.

21. What are the classic chest imaging and biopsy findings of pulmonary sarcoidosis?

    Bilateral hilar lymphadenopathy with reticulonodular opacities (often upper-lobe); biopsy shows non-caseating granulomas. Stage I = hilar adenopathy alone; Stage IV = fibrosis.

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