Asthma – is a disease that has allergic and inflammatory basis, as evidenced by the
presence in the mucosa infiltrates, containing eosinophilic granulocytes (EG), mast
cells and lymphocytes (even in mild flow).
Flow of an allergic reaction is immediate and delayed type. In the immediate type
reactions leading role belongs to reagin that interact with antigen. This is
particularly Ig E. It forms a complex with the antigen on the surface membrane of
mast cells bronchial mucosa. This is followed by aggregation of membrane
receptors and Ig E is a trigger of activation of mast cells.
At patochemical stage due to allergen-antibody reactions in membranes of mast
cells are released active substances - histamine, serotonin, bradykinin,
leukotrienes, acetylcholine, prostaglandin F2α addition, bradykinin causing
inflammation.
Aspirin asthma - the development of an asthma attack while taking aspirin
resembles an allergic reaction, but they are based on immune mechanism. Aspirin
inhibits cyclooxygenase, which leads to the metabolism of arachidonic acid. The
synthesis of prostaglandin E is suppressed, which has a bronchodilator effect,
which enhances the action of prostaglandin F2α, as well as histamine and
leukotrienes.
In the human genome are genes that induce disease control response to treatment.
Investigated the following factors responsible for the development of asthma:
1) Interleukin (IL) 3, 4, 5, 9, 13.
2) Β2 - adrenergic receptor.
3) Lymphocyte specific glucocorticoid receptor.
4) Tumor necrosis factor (TNF).
5) Highaffine receptor Ig E, beta subunit.
6) Receptor 1 TNF.
7) Gamma-interferon.
8) Mast cell chymase.
9) T - cell receptor.
However, a great role is assign to environmental risk factors.
Risk factors
Among the factors provoking or can modify the flow of asthma, select:
1. Inductors (inhaled allergens, some food allergens, dermatophytes, chemicals,
heredity).
■ immune response (T-helper type 2, Ig E, Ig G)
■ inflammation (T-helper type 2, EG, basophilic granulocytes)
2. Amplifiers (rhinoviruses, endotoxins)
3. The triggers (exercise, cold air, histamine, methacholine, passive smoking,
sharp smells)
■ difficulty in breathing.
Inductors - foreign proteins and chemical particles with a small molecular weight,
which can trigger an immune response.
Amplifiers - agents that are in the environment and are not able to provoke an
immune response.
The triggers (provocateurs) - agents that are able to enhance bronchial hyper
reactivity in a short period without development of inflammation in the airway
wall.
Today proved that the development of asthma associated with hyper reactivity of
large and shallow bronchi, caused by chronic inflammation, which is coordinated
by T-helper 2-type. T helper type 2 secretes IL-4 and IL-5.
IL-4 is the main cytokine that switch B lymphocytes Ig synthesis in E. IL-5
selectively activates EG, which are two of the main effector cells of allergic
inflammation. In EG activation also participate IL-3, platelet-activating factor.
Mediators of the early phase of allergic reactions 1 - type and their biological effects.
Histamine
Vasodilation, increase vascular penetration,
itching, bronchospasm
Proteases
The destruction of the basement membrane of
blood vessels, increasing histamine release and
migration of EG
Heparin
Formation of complex with proteases,
extracellular matrix destruction, block of the
mediators releasing
Eosinophilic chemotactic factor A
Chemotaxis of EG
Neutrophilic chemotactic factor
Chemotaxis of neutrophilic granulocytes (NG)
Cells and cytokines that are involved in the late phase of allergic inflammation in the
mucosa of the respiratory tract
Cells Cytokines
T-helper cells type 2 IL-4, IL-5, IL-6, IL-9, IL-10, IL-13, GM-CSF
Masts cells and EG are the main effector cells in the pathogenesis of asthma.
Cysteine leukotrienes lead to airway obstruction at humans by stimulating
specific receptors, called receptor cysteine leukotriene type 1 (TsysLT1-
receptors). Today managed to selectively block of only one ferment - 5
lipoxygenase that participates in the synthesis of leukotrienes.
Classification of asthma.
According to the first division distinguished:
Excitation is
Consciousness Typically, Typically,
possible Confusion
excitation excitation
Accelerated
Breathing. Accelerated Accelerated more than 30
in 1 min
Participation of
supporting Almost Paradoxical
Typically, there Typically, there
muscles in always there thoracoabdominal
is no is
breathing is breathing
Wheezing
Moderate,
No wheezing Wheezing is
usually in the Noisily Noisily
Wheezing absent
end of exhale
The presence of
a paradoxical Missing in
Missing Missing Missing
pulse muscle fatigue
PEF after
More than 80% Less than
administration 60 - 80% of the
of the 60% of the
of appropriate
appropriate appropriate
bronchodilators values
values values
≥ 60 mm.
РаО2, mm. Hg.c. ≥ 60 mm. Hg.c.
Norm Hg.c.
Ра СО2, mm.
≥ 45 mm.
Hg.c. ≤ 45 mm. Hg.c. ≤ 45 mm. Hg.c.
Hg.c.
SаО2, %
≥ 90% 91 - 95 % ≤ 90%
Daily performance PEF more than 20% is diagnostic feature of asthma, and
the deviation is directly proportional to the severity of the disease.
There is no Typical
Allergy
Asthma attack