Glucocorticoids: baseline antiallergic drugs
Glucocorticoids (GCs) serve as fundamental baseline therapy. Their spectrum of activity is particularly pronounced in the treatment of immediate-type allergic reactions.
The mechanism of the antiallergic action of glucocorticoids is implemented through a sequential biochemical cascade that reliably suppresses the development of the allergic response:
- First, blockade of the enzyme phospholipase A2 occurs, which is the starting point of their pharmacological effect.
- Consequently, there is a pronounced decrease in the production of arachidonic acid—a crucial precursor of inflammatory agents.
- At the cellular level, the drugs create an obstacle to mast cell degranulation by stabilizing their membranes.
- Ultimately, there is a complete blocking of the release of allergy mediators into the surrounding tissues, which halts the progression of the pathological process.
Dependence of GC formulation on condition severity
The choice of a specific glucocorticoid dosage form strictly depends on the localization of the pathological process and the severity of the patient's condition. A correctly selected route of administration ensures maximum clinical efficacy.
| Dosage form | Indications for use | Condition severity |
|---|---|---|
| Injections | Anaphylactic shock, angioedema (angioneurotic edema) | Severe and moderate conditions |
| Inhalations | Bronchial asthma | Local effect in the respiratory tract |
| Ointments and topical forms | Atopic dermatitis, insect bite reactions | Skin manifestations of varying severity |
Symptomatic drugs in life-threatening conditions
Symptomatic antiallergic drugs are first-line agents for managing acute, life-threatening conditions. The primary and irreplaceable drug in this situation is Epinephrine (Adrenaline).
The main indication for its immediate administration is anaphylactic shock. This critical condition is traditionally accompanied by two life-threatening factors: a sharp drop in blood pressure (hypotension) and pronounced bronchospasm. The routes of administration to achieve the fastest possible effect are intramuscular or intravenous.
Pharmacodynamics of epinephrine in anaphylaxis
The action of adrenomimetics, particularly adrenaline, in anaphylactic shock aims at the immediate elimination of the pathophysiological mechanisms of shock through action on various types of adrenoceptors.
- Combating hypotension: The drug stimulates α-adrenoceptors of blood vessels. The clinical effect of this action is a powerful vasoconstrictor response and, consequently, an increase in blood pressure (BP), which allows overcoming shock-induced hypotension.
- Combating respiratory failure: Simultaneously, β2-adrenoceptors of the bronchi are stimulated. The result of this activation is the relaxation of the smooth muscles of the airways and the complete elimination of bronchospasm, which restores adequate pulmonary ventilation.
Briefly: answers to topical questions
Which specific allergy mediators stop being released under the action of glucocorticoids?
Sources specifically indicate that glucocorticoids block the biosynthesis of cysteinyl leukotrienes. They also prevent the release of allergy mediators and mast cell degranulation, but the specific mediators whose release is blocked specifically by glucocorticoids are not listed.
What is the standard dosage of epinephrine administered intramuscularly in anaphylactic shock?
The standard dosage of epinephrine for intramuscular administration is 0.01 mg/kg of body weight. A 0.1% solution of the drug is used for the injection. Meanwhile, the maximum single dose should not exceed 0.5 mg. In the absence of clinical improvement 5 minutes after the first injection, administration can be repeated every 5–10 minutes until the patient's hemodynamic and respiratory parameters are fully stabilized.
What drugs, other than epinephrine, are used for symptomatic relief of bronchospasm in allergy?
In case of severe asphyxia and bronchial obstruction, additional medications used include inhaled bronchodilators, specifically salbutamol, and topical glucocorticoids, such as budesonide.
To remember the effects of adrenaline, use the association "A-A, B-B": Alpha-receptors — Blood Pressure (increases), Beta-receptors — Bronchi (dilates).
Class and exam questions
Which drug is the agent of choice in anaphylactic shock?
The drug of choice is epinephrine (adrenaline). It is administered intramuscularly or intravenously for the emergency relief of life-threatening symptoms.
What is the mechanism of action of glucocorticoids in allergy?
They block the enzyme phospholipase A2, reduce the production of arachidonic acid, prevent mast cell degranulation, and block the release of allergy mediators.
How does epinephrine relieve bronchospasm?
Epinephrine stimulates bronchial β2-adrenoceptors, leading to the relaxation of their smooth muscle and the restoration of airway patency.
What else to study on this topic
- Detailed biochemical cascade of arachidonic acid
- Differences in the affinity of epinephrine for alpha- and beta-adrenoceptors
- Pharmacokinetics of injectable and inhaled glucocorticoids
- Pathophysiology of anaphylactic shock and angioedema
- Mechanism of mast cell degranulation in immediate-type reactions
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