Etiology: Where Asthma Comes From
Globally, the causes of the disease can be divided into two broad groups, depending on whether an external trigger can be identified.
- Exogenous (atopic) form. Develops when external allergens enter the body of a patient with individual hypersensitivity. Allergens can be extremely diverse:
- Plant-derived (plant pollen).
- Food-derived (eggs, chocolate, strawberries, and other products).
- Household (mold spores, house dust, animal dander).
- Drug impurities.
- Occupational and chemical. Medical history describes classic examples: "pharmacists' asthma" (reaction to ipecacuanha) and "furriers' asthma" (reaction to the chemical ursol).
- Endogenous form. Diagnosed in cases where a specific external allergen cannot be detected. In this situation, the disease is caused purely by internal bodily factors. In modern clinical practice, there is a steady upward trend in the number of such patients.
Clinical and pathogenetic variants
In addition to the classic allergic form, medicine distinguishes a number of special clinical and pathogenetic variants of the disease. These include:
- "Aspirin-induced" asthma (also called prostaglandin-induced).
- Exercise-induced asthma.
- Bronchial asthma in pregnancy.
- Psychogenic form.
- Hypereosinophilic form.
- Infection-dependent form (traditionally classified as a separate category).
Pathogenesis: How an attack develops
The modern concept states: the basis of asthma is chronic inflammation of the bronchial wall, dominated by eosinophils, lymphocytes, and mast cells. It is this inflammation that makes the bronchi hyperreactive—excessively sensitive to any nonspecific irritants.
IgE-dependent immunological mechanism (in the atopic form):
- Sensitization. Upon first contact with the allergen, the immune system produces IgE antibodies. They do not remain in the blood, but firmly bind to the membranes of mast cells.
- Re-exposure. When the allergen enters the body again, it binds to the pre-existing IgE molecules.
- Degranulation. Mast cells are activated and release a potent cocktail of mediators. This includes histamine, chemotactic factors (which attract neutrophils and eosinophils), and the slow-reacting substance of anaphylaxis (a complex of leukotrienes).
- Bronchospasm. The combined action of histamine and leukotrienes causes a sharp contraction of the bronchial smooth muscle.
Phases of the bronchospastic reaction
From a pathophysiological standpoint, the suffocation attack itself proceeds in two consecutive phases.
First (early) phase Characterized by a rapid increase in vascular wall permeability. As a result, fluid leaks into the tissues, and edema of the bronchial mucosa develops instantly.
Second (late) phase Here, chemotactic factors play a key role. They attract effector cells, primarily eosinophils, to the lesion. The recruited cells release aggressive substances that damage the bronchial epithelium. This sustains chronic inflammation and prolongs the period of negative allergen exposure.
The role of arachidonic acid metabolites, which are formed from mast cell membranes, also deserves mention. Leukotrienes are synthesized via the lipoxygenase pathway, and thromboxanes via the cyclooxygenase pathway. These substances exert a colossal spastic effect on smooth muscle cells (SMCs), especially in small bronchi, cementing the obstruction.
Briefly: answers to topical questions
What is the pathogenesis of aspirin-induced bronchial asthma?
The pathogenesis of aspirin-induced bronchial asthma involves impaired arachidonic acid metabolism. The administration of nonsteroidal anti-inflammatory drugs (e.g., acetylsalicylic acid) blocks the cyclooxygenase pathway. This leads to a metabolic shift and the activation of an alternative pathway—the lipoxygenase pathway. As a result, there is an overproduction of leukotrienes (particularly leukotriene $D_4$), which exert a powerful effect on smooth muscle and cause pronounced bronchial spasm.
What medications are used to relieve an acute attack of bronchial asthma?
For relieving acute episodes of suffocation in bronchial asthma, sources indicate formoterol: it combines a long duration of action with a rapid onset of effect (1–3 min).
The single inhaler treatment regimen (MART therapy) is also described: one inhaler is used for both maintenance therapy and symptom relief. Low doses of fixed combinations are used for this purpose:
- budesonide + formoterol;
- beclometasone + formoterol.
Additionally, sources indicate the relief of bronchial asthma attacks with a bronchodilator administered subcutaneously.
What auscultatory findings are detected during an attack of bronchial asthma?
During a bronchial asthma attack, specific auscultatory signs of bronchial obstruction syndrome are detected. The main manifestations include:
- Dry wheezes — scattered sounds during auscultation that significantly increase during expiration.
- Distance wheezes — whistling ("music in the chest"), loud enough to be heard at a distance from the patient.
- Prolonged expiration — a sign of expiratory dyspnea due to impaired airflow.
To remember the main cells involved in asthma inflammation, use the mnemonic LET (airways "let" go into spasm): Lymphocytes, Eosinophils, Tast cells.
Class and exam questions
What is the main difference between obstruction in asthma and other lung diseases?
In bronchial asthma, obstruction occurs acutely and is reversible. The bronchial lumen can recover either spontaneously or under the influence of medications.
Why is asthma called a chronic disease if attacks do not happen all the time?
Because chronic inflammation of the bronchial wall (involving eosinophils and mast cells) persists constantly, even between attacks. It is this inflammation that establishes bronchial hyperreactivity.
What is the "slow-reacting substance of anaphylaxis"?
This is a complex of leukotrienes released during mast cell degranulation. Together with histamine, this complex causes a powerful and prolonged bronchial spasm.
What else to study on this topic
- Arachidonic acid metabolism: lipoxygenase and cyclooxygenase pathways
- Mechanisms of bronchial epithelial damage in the late phase of the reaction
- Features of the pathogenesis of "aspirin-induced" (prostaglandin) asthma
- Differentiation of endogenous and infection-dependent forms of the disease
- The role of chemotactic factors in the formation of the cellular infiltrate
Master the entire topic in the "Propaedeutics" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Bronchial Asthma" and 3,152 more pages of the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 113 video lessons on the subject
Other topics in the "Respiratory System" section
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.