Skip to Main Content

We have a new app!

Take the Access library with you wherever you go—easy access to books, videos, images, podcasts, personalized features, and more.

Download the Access App here: iOS and Android


  • Definition: Bleeding into the alveolar space due to disruption of the alveolar–capillary basement membrane

  • Etiologies: See Table 2.5

  • Clinical presentation:

    • - Cough, fever, hemoptysis, or diffuse GGOs + other concerning features (e.g., extrapulmonary signs of vasculitis, known condition associated with DAH, declining hemoglobin without clear reason)

    • - Pearl: Hemoptysis is only present in 50% of cases and absence does not predict hemorrhage severity

    • - Consider alveolar hemorrhage in a patient with GGOs who is failing to progress as expected (e.g., patient with suspected cardiogenic pulmonary edema who is not improving with diuresis)

  • Diagnostics:

    • - Labs: CBC, BUN/Cr, UA, ESR, CRP. Consider rheumatologic w/u, which may include ANA, dsDNA, RNP, C3, C4, RF, CCP, ANCA, MPO, PR3, cryoglobulins, anti-GBM, RVVT, cardiolipin, B2-glycoprotein Ab

    • - Imaging: Noncontrast chest CT (consider contrast if suspect other causes of hemoptysis): Imaging shows patchy or diffuse GGOs

    • - Bronchoscopy: 1) Serial lavage – gets progressively more hemorrhagic; 2) Rule out infection; 3) Check cell count with differential to evaluate for eosinophilia

  • Management:

    • - Capillaritis: Immunosuppression

      • For ANCA-associated vasculitis, typically give pulse-dose steroids first and then adjunctive therapies like cyclophosphamide, rituximab, etc. if lack of response

    • - Bland hemorrhage or diffuse alveolar damage:

      • Treat underlying cause, supportive care


  • Obstructive = ↑compliance, ↓elastance → problem emptying the lung.

    • - ↑TLC, ↑RV, problem pushing air out → air trapping

    • - ↓↓FEV1 ↓FVC = FEV1/FVC ratio <0.7

Chronic obstructive pulmonary disease (COPD)

  • Epidemiology: Most common in former smokers (although can affect persons in cities with air pollution, women may develop with less significant smoking history). Typical onset age >40 yr

  • Definitions:

    • - COPD: Persistent airflow limitation resulting from the consequences of chronic inflammation from smoking. Classic subtypes were chronic bronchitis and emphysema, although these are not included in the current definition

      • Chronic bronchitis: Clinical diagnosis of chronic productive cough for 3 mo/yr for >2 yr. Normal DLCO.

      • Emphysema: Pathologic diagnosis that describes permanent enlargement of the airspaces and destruction of the alveoli, which causes loss of diffusing capacity and reduced elastic recoil. ↓DLCO.

        • - Centrilobular: Tobacco activates PMNs, inhibits α1-antitrypsin, ↑oxidative stress. Upper lung predominant.

        • - Panlobular: Alpha-1 antitrypsin deficiency. Lung bases with bilateral basilar bullae and can also have liver disease (PAS+).

      • Small airway disease: Third characteristic feature of COPD. Small bronchioles are narrowed and reduced in number. Small airway destruction is a hallmark of advanced COPD.

    • - Asthma–COPD overlap syndrome (some reversibility with bronchodilators)

  • Pathogenesis:

    • - Airways: Chronic inflammation, increased numbers of goblet cells and mucous glands; airway collapse due to the loss of tethering caused by alveolar wall destruction

    • - Lung parenchyma: Affects structures distal to the terminal bronchiole

    • - Pulmonary vasculature: Smooth muscle hypertrophy → chronic hypoxic vasoconstriction of the small pulmonary arteries

  • Clinical presentation: Dyspnea, chronic cough, sputum production

  • Physical exam:

    • - Early in disease: Normal or only ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.