Systemic allergic reactions
Systemic manifestations affect the entire body and often require emergency care. They include:
- Anaphylactic shock. Triggered by the administration of sera, medications, or insect venoms. The main route of entry is parenteral (intravenous is especially hazardous). Secondary targets are blood cells and the vascular endothelium. Symptoms include severe vasodilation, increased vascular permeability, fluid extravasation into tissues, and severe hypotension.
- Urticaria. Occurs in response to food products and insect venoms when the allergen enters subcutaneously or per os. Affects the vascular endothelium and blood cells. Clinically manifested by hyperemia, pruritic wheals, erythema, and skin rash.
Predominantly local manifestations
These reactions are localized to specific organs, depending on the route of entry and the type of allergen:
- Allergic rhinitis and conjunctivitis. Caused by the inhalation of pollen. The mucosal epithelium and vascular endothelium are affected. Characterized by hypersecretion of mucus, rhinorrhea, and hyperemia.
- Food allergy. Develops upon the intake of allergens per os. Targets include enterocytes, smooth muscles, and the endothelium. Symptoms: diarrhea, nausea, vomiting, urticaria, and sometimes anaphylaxis.
- Angioedema. Triggered by drugs and venoms (parenterally or per os). Affects the vascular endothelium, causing edema of the face and neck.
A distinction is made between hay fever and allergic rhinitis. Hay fever has a strictly seasonal character, as it is exclusively associated with the plant pollination period (manifested by lacrimation and rhinoconjunctivitis). Allergic rhinitis, by contrast, is caused by the constant presence of triggers (house dust, animal dander), occurs without time limitations with constant nasal congestion, and often progresses to bronchial asthma.
Atopic bronchial asthma
This is the most frequent and severe inflammatory disease of an allergic nature. The immunological basis of the disease is due to the structure of the bronchial lymphoid tissue: it is rich in mast cells, and immune processes are shifted towards a Th2 orientation.
- Pathogenesis: The lesion is dominated by eosinophilic infiltration and the secretion of Th2 cytokines (IL-4, IL-5, IL-13). Due to the chronic course, late-phase factors play a leading role rather than mast cell degranulation. The main consequence is bronchial hyperreactivity, i.e., a tendency toward smooth muscle spasm.
- Remodeling: Over time, the bronchial epithelial layer atrophies, while the muscle layer and connective tissue hypertrophy. The lumen narrows, and the barrier weakens.
- Complications: Due to the weakness of the barrier, infection frequently supervenes. This changes the response profile to Th1-dependent. In severe cases, emphysema and damage to the lung interstitial tissue develop.
Atopic dermatitis
A chronic process involving the skin. Often occurs in response to drugs and dyes (route of entry is contact or per os).
A cellular infiltrate consisting of eosinophils, mast cells, and CD4+ T lymphocytes forms in the dermis. Lymphocytes actively secrete interleukins (IL-4, IL-5, IL-13). The main cause of debilitating pruritus is histamine released during mast cell degranulation.
Morphologically, the epidermis undergoes atrophic and degenerative changes, while the dermis hypertrophies and becomes filled with inflammatory cells. Scratching and atrophy promote secondary infection, which, as in asthma, switches the immune response to the Th1 pathway, making the pathogenesis mixed.
Principles of pharmacotherapy
Modern therapy only affects the realization (effector) stage, but cannot eliminate the root cause—the sensitization of the organism.
Main drug groups:
- Antihistamines: block H1 receptors, neutralizing the effects of histamine.
- Smooth muscle drugs: β2-adrenergic receptor agonists, muscarinic receptor blockers, and theophylline (increases intracellular cAMP).
- Leukotriene antagonists: relieve bronchial spastic reactions.
- Membrane stabilizers: block the release of mediators from mast cells.
- Glucocorticoids: possess potent anti-inflammatory effects, suppress histamine synthesis, and increase cAMP. Due to systemic side effects, attempts are made to apply them locally (ointments, sprays).
Briefly: answers to topical questions
Which inflammatory mediators, besides histamine, are released during mast cell degranulation?
In addition to histamine, other preformed factors are released during mast cell degranulation. These include:
- Vasoactive amines — serotonin.
- Proteoglycans — heparin, chondroitin sulfates A and C.
- Enzymes — dehydrogenase, peroxidase, RNase, histidine decarboxylase.
- Proteases — tryptases, chymases, carboxypeptidase A.
- Acid glycosaminoglycans.
- Chemotactic factors — eosinophil chemotactic factor and neutrophil chemotactic factor.
What are the stages of the pathogenesis of an allergic reaction?
The dynamics of the development of an allergic reaction distinguish three consecutive stages.
- Immunological (immunogenic) — the interaction of the allergen with receptors on the surface of mast cells, cross-linking of complexes, and triggering of an activating signal.
- Pathochemical (pathobiochemical) — mast cell degranulation with the release of histamine and other substances, as well as the synthesis of eicosanoids.
- Pathophysiological (stage of clinical manifestations) — the response of surrounding tissue cells (vascular endothelium, smooth muscles, mucous membranes), determining the external manifestations of allergy.
To which type of hypersensitivity according to the Gell and Coombs classification do atopic asthma and anaphylactic shock belong?
Atopic asthma and anaphylactic shock belong to type I hypersensitivity (anaphylactic) according to the classification of P. Gell and R. Coombs. This type of reaction is also known as immediate hypersensitivity, atopic, or reaginic reactions. The main mediators are IgE antibodies (less commonly IgG4). The interaction of antigen with these antibodies leads to the release of biologically active substances from mast cells and basophils, which determines the development of anaphylactic and atopic processes.
Hay fever is seasonal (starts with S), while allergic rhinitis is regular (constant).
Class and exam questions
How does hay fever differ from common allergic rhinitis?
Hay fever is strictly seasonal and depends on the flowering time (pollen), whereas allergic rhinitis is triggered by constant triggers (dust, dander) and proceeds without time limitations.
Why does severe pruritus occur in atopic dermatitis?
In the lesion (dermis), mast cell degranulation occurs. They massively release histamine, which is the main culprit of pruritus.
Can medications completely cure an allergy?
Modern drugs excellently control symptoms by suppressing the effector stage of allergy. However, they do not eliminate the underlying cause (organism sensitization).
What else to study on this topic
- Mechanisms of formation of bronchial hyperreactivity.
- The role of Th2 cytokines (IL-4, IL-5, IL-13) in maintaining allergic inflammation.
- The process of mucosal remodeling in bronchial asthma.
- Changes in the immune response (Th2 to Th1 switch) upon the addition of a secondary infection.
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