Lung - nontumor
Chronic obstructive pulmonary disease (COPD)

Topic Completed: 1 August 2011

Minor changes: 23 August 2019

Copyright: 2003-2019,, Inc.

PubMed search: asthma [title] lungs pulmonary COPD

Elliot Weisenberg, M.D.
Page views in 2019: 5,185
Page views in 2020 to date: 2,568
Cite this page: Weisenberg E. Asthma. website. Accessed May 28th, 2020.
Definition / general
  • 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
  • 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
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;66:942)
  • Nonatopic or Intrinsic: nonimmune; 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
Gross description
  • Overdistended lungs, small areas of atelectasis, thick mucus plugs in proximal bronchi containing whorls of shed epithelium
Gross images

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Mucus plugs

Status asthmaticus

Microscopic (histologic) 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
Microscopic (histologic) images

Contributed by Bobbi Pritt, M.D., Dr. Neil Harris and Dr. Stacy Beal

Curschmann spirals

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Smooth muscle hypertrophy and inflammatory cells

Eosinophils and Charcot-Leyden crystals

Curschmann spirals

Differential diagnosis
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