Internal Diseases and Therapy · MU Sofia

132. Asthma: epidemiology, pathogenesis, clinical features, diagnosis and

Covers the definition of asthma as three components: recurrent reversible airway obstruction, airway hyperresponsiveness and airway inflammation. It then takes epidemiology and heritability, the pathology of acute and chronic airway change, and the roles of acetylcholine, histamine, leukotrienes and nitric oxide. Clinical features, examination findings, lung function and peak flow diagnostic criteria, and a list of differential diagnoses follow. A stepwise chronic and acute management outline with drug doses closes the note, which is partly marked as removed from the syllabus.

Inside: 2 sections · 3 labelled pictures · 13 flashcards · 6 min

Topic 133 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 2 sections, about 722 words (6 min of reading), with 13 flashcards.

In this note

  1. Asthma: epidemiology, pathogenesis, clinical features, diagnosis and differential diagnosis.
  2. Treatment of asthma.

Asthma: epidemiology, pathogenesis, clinical features, diagnosis and differential diagnosis.

Definition: Clinical syndrome characterised by three distinct components

  1. 1. Recurrent episodes of airway obstruction that resolve spontaneously or as a result of treatment
  2. 2. Exaggerated bronchoconstrictor responses to stimuli that have little or no effect in nonasthmatic subjects (airway hyperresponsiveness)
  3. 3. Inflammation of the airways

Note, airway obstruction is almost always reversible, however it is now thought that some changes in asthmatic airways may be irreversible.

Asthma affects boys more than girls, although women more than men after puberty. Around 8% of the pop have diagnosed asthma in the developed world, and it can develop at any time in life. Asthma is one of the most common reasons to seek medical treatment.

There is 60% heritability in asthma, with chromosome 17q21 heavily implicated as an important gene.

The pathology of asthma is edema and hyperemia of the mucosa mediated by infiltration with mast cells, eosinophils and TH2 lymphocytes. In acute attacks these inflammatory mediators cause smooth muscle constriction of the bronchi, along with increased glandular secretions.Chronically, these inflammatory stimuli lead to deposition of type III and V collagen below the true basement membrane, along with chronic smooth muscle constriction with hypertrophy and hyperplasia of the airway glands, these can lead to long term, chronic, airway remodelling in asthmatics.

Image: “Asthma attack-illustration NIH” by United States-National Institute of Health: National Heart, Lung, Blood Institute, Public domain, via Wikimedia Commons.

There are some important mediators of the acute asthmatic response that I want to address individually:

  • Acetylcholine
  • Released from intrapulmonary motor neurons causing constriction of airway smooth muscle through direct stimulation of muscarinic receptors of M3 subtype
  • Histamine
  • An endogenous broncho active agent, released from mast cells that mediate airway obstruction
  • Leukotrienes (lipoxins, by contrast, are anti-inflammatory)
  • Nitric oxide

The physiological change as a result of these structural changes should be as plain as day, increased airway resistance due to smooth muscle constriction, thickening of the epithelium and/or free fluid within the airway lumen. Obstruction occurs at all levels of the airway, as it resolves, the changes are reversed, first in the large airways, then in the smaller.

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