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Chronic obstructive pulmonary disease (COPD)


Reviewers: Elliot Weisenberg, M.D. (see Reviewers page)
Revised: 30 January 2012, last major update August 2011
Copyright: (c) 2003-2012, PathologyOutlines.com, Inc.


● Defined by the National Asthma Education and Prevention Program as a “chronic inflammatory disorder of the airways in which many cells and cellular elements play a role - in particular, mast cells, eosinophils, T lymphocytes, macrophages, neutrophils and epithelial cells
● In susceptible individuals, causes episodes of wheezing, breathlessness, chest tightness and coughing, particularly at night or early morning
● Episodes are usually associated with widespread but variable airflow obstruction that is often reversible, either spontaneously or with treatment
● Inflammation also causes an associated increase in the existing bronchial hyperresponsiveness to a variety of stimuli
● Very common, affects 14-15 million Americans
● Causes 3,000 US deaths annually (American Academy of Allergy, Asthma & Immunology)
● Has increased in Western hemisphere over past 40 years

Clinical features

Atopic or Extrinsic: Type I hypersensitivity, generally due to allergens; begins in childhood, triggered by environmental allergens (dander, dust, pollen, food), often positive family history; more common in African American children; evidence of allergen sensitization; skin test causes wheel and flare reaction (CMAJ 2009;181:E181)
Noneosinophilic (“neutrophilic”) asthma; a subgroup of atopic asthma not associated with eosinophilia; IL8 recruiting neutrophils are an important mechanism; patients tend to be less responsive to corticosteroids (Thorax 2011 Jul 23 [Epub ahead of print])
Nonatopic or Intrinsic: non-immune; due to aspirin ingestion, pneumonia, cold, stress, exercise; follows respiratory infection (rhinovirus, parainfluenza virus); usually not familial; no evidence of allergen sensitization; normal serum IgE, negative skin tests; viral induced inflammation may lower threshold of subepithelial vagal receptors to irritants
Occupational asthma: due to repeated exposure to fumes, dusts, gases, chemicals, often in minute quantities; varying mechanisms of disease depending upon the stimulus
Drug induced asthma: associated with several drugs, but most noteworthy is aspirin use; rare, aspirin related cases are associated with recurrent rhinitis, nasal polyps and urticaria; patients are sensitive to small doses of aspirin; may be due to direct effects of aspirin on cyclooxygenase pathway
Status asthmaticus: unremitting attacks due to exposure to previously sensitized antigen; may be fatal, usually in patients with a long history of asthma


Atopic or Extrinsic: initial sensitization affects T helper 2 cells, which release IL4/5, which promote IgE release by B cells, mast cells, and eosinophils
● Re-exposure to allergen leads to mediator release from mucosal mast cells
● Acute/intermediate response is bronchoconstriction, edema, mucus secretion and vasodilation with increased vascular permeability
● Late phase reaction is due to influx of other inflammatory cells stimulated by chemokines released by mast cells, epithelial cells, T lymphocytes and other cytokines; includes release of major basic protein from eosinophils, which causes epithelial damage and airway constriction
● Putative mediators are leukotrienes C4, D4, E4 and acetylcholine; minor mediators are histamine, prostaglandin D2; associated with serum eosinophilia, sputum eosinophils

Gross description

● Overdistended lungs, small areas of atelectasis, thick mucus plugs in proximal bronchi containing whorls of shed epithelium

Gross images

Mucus plugs

Thickened bronchial walls

Status asthmaticus

Micro description

● Curschmann spirals, eosinophils, extracellular Charcot-Leyden crystals (crystalloids composed of galectin-10, an eosinophil lysophopholipase), increased mucosal goblet cells and submucosal glands, thickened basement membrane, bronchial smooth muscle hypertrophy, airway wall edema

Micro images

Smooth muscle hypertrophy and inflammatory cells

Goblet cells and inflammatory cells

Eosinophils and Charcot-Leyden crystals

Curschmann spirals

Virtual slides


Differential Diagnosis

Allergic bronchopulmonary aspergillosis: important complication of asthma and cystic fibrosis
● Bronchocentric granulomatosis without the granulomatous inflammation

Additional references

Dail and Hammar’s Pulmonary Pathology, 3rd edition

End of Lung-nontumor > Chronic obstructive pulmonary disease (COPD) > Asthma

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