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Obstructive pulmonary disease

Asthma

Author: Elliot Weisenberg, M.D.

Last author update: 1 August 2011

Last staff update: 7 July 2022

Copyright: 2003-2024, PathologyOutlines.com, Inc.

PubMed search: asthma [title] lungs pulmonary COPD

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Table of Contents

Cite this page: Weisenberg E. Asthma. PathologyOutlines.com website. https://www.pathologyoutlines.com/topic/lungnontumorasthma.html. Accessed April 16th, 2024.

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

Pathophysiology

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., Neil Harris, M.D. and Stacy Beal, M.D.