immune system as a whole is protective as well
immunological mechanisms that protect the host from time to time
lead to serious damage of tissues and, sometimes, may
lead to death. Cellular and Coombs classified these
destructive reactions, immunological (also called
hypersensitivity reactions) into four basic types:
immediate hypersensitivity type (type I) reactions cytotoxic
(type II) reactions , mediated by immune complexes (type III)
response and delayed-type hypersensitivity (cellular,
type IV) reactions. A. Type I:
anaphylaxis or immediate hypersensitivity reactions of immediate hypersensitivity reactions
associated with the release of
pharmacologically active substances or mediators from mast cells
and basophils, a mechanism that works
antigens react with pre-, cell associated IgE
molecules. Allergens are antigens
that cause production of specific IgE antibodies in people
. IgE antibodies (reahynov). IgE production under the strict control of specific IgE
T cells that can do both IgE-potentiating and IgE-suppressing factors. Mediators
1. Histamine. This results in smooth muscle >> << and increased permeability of capillaries
2. Slow-reacting substance of anaphylaxis
(MRS-A) contracts smooth muscles and increases capillary permeability
in a long-term basis. 3. Bradykinin. This leads to
smooth muscle in a slow, long way
increases vascular permeability and increased mucus secretion
mucous glands. 4. Serotonin (5-hydroxy)
important mediator in anaphylaxis and other animals >> << than men. 5. Eosinophil chemotaxis
factor of anaphylaxis (ECF-A). It attracts eosinophils to areas
allergic inflammation. 6. Platelet activating factor
(PAF). This leads to platelet aggregation and release of vasoactive amines
, which leads to increased vascular permeability
. , smooth muscle and bronchial
7. Prostaglandins are products
cyclooxygenase metabolism of arachidonic acid. Prostaglandin E
1 (PGE 1) and
PGE 2
powerful bronchodilators and vasodilators. PGI
, 2 (also called prostacyclin) disaggregates platelets. Genetic factors: Hay fever, asthma, food allergy
show the family trend. Clinical signs: 1. Anaphylaxis refers to a >> << immediate hypersensitivity reactions that are induced in normal
owner of a species to the appropriate >> << antigenic effect (called sensitization). A >> << can be either systemic (anaphylactic shock) and local, but
in all, above all, characterized by smooth reduction >> << muscles and increase permeability capillaries. 2. Atopy refers to >> << immediate hypersensitivity reaction that occurs only >> << genetically susceptible host sensitivity to specific allergens
. This condition differs from
anaphylaxis is that it can not be induced in normal hosts. Treatment: 1. Avoiding 2. Hiposensybilizatsiyi 3. Administration changes
allergens or allerhoidy. 4. Drug treatment. Diphenhydramine b. Corticosteroids in. Adrenaline, the sodium kromolin E. Theophylline B. Type II: Cytotoxic antibody cytolytic >> << reactions associated primarily as a combination of IgG
or IgM antibodies to epitopes on the cell surface or fabric> > << or adsorption of antigens or haptenov on fabric or
cell membrane, with subsequent attachment of antibodies >> << to adsorbed antigens. Any mechanism can lead to
one of these destructive processes. Activation of complement >> <<, followed by lysis or inactivation of cells
goal. Phagocytosis
target cells, with or without activation of complement. Lysis or inactivation
target cells by effector lymphoid cells
(eg, ADCC)
Type II
hypersensitivity reactions: 1. Transfusion reactions:
intravascular hemolysis of red blood cells usually
associated with ABO incompatibility system. 2. Extra vascular hemolysis cells
red blood almost always associated with Rh incompatibility.
3. Hemolytic disease of newborn
: erythroblastosis fetalis occurs when Rh-negative mother gives birth >> << Rh-positive child, >> << Rh antigen that were purchased from Rh-positive father. Sensitization can occur during pregnancy, when fetal blood
leak in the maternal circulation. After sensitization
IgG antibodies to Rh
0 (D) antigen is carried out, which can penetrate the placenta
and destroy the cells of the fetus. The first child is usually not affected by
, but the possibility of sensitization increases with subsequent pregnancies
. 4. Autoimmune hemolytic disease >>. << Warm antibody hemolytic anemia, cold antibody hemolytic anemia
, paroxysmal hemoglobinuria cold. 5. White blood cell lysis. System Red
erythematosus (SLE) b. Granulocytopenia with. Idiopathic thrombocytopenic purpura
(ITP) 6. Nephrotoxic nephritis. Goodpasture's Syndrome
7. Bullous diseases. Characterized antibodies and complement deposition in
squamous intercellular spaces and along foundation >> << membranes of the skin. Therapy for
cytotoxic reactions: 1. The suppression of the immune response >>. << 2. Removal of antibodies offenses.
3. Removing offenses antibodies.
4. Nephrectomy. C. Type III: immune complex mediated reactions
pathogenesis of lasix 40 mg ivp immune disorders include complex interactions >> << antigens, antibodies, complement and neutrophils. Soluble immune complexes
: usually occurs in the region of excess antigen >>. << Virtually any antigen that induces antibodies to detect >> << will serve. Antibodies involved mainly
deposition of IgG and IgM can fix complement
. Immune adherence:
Being soluble, immune complexes escape phagocytosis,
penetrate the endothelium of blood vessel walls (perhaps
using vasoactive amines released from platelets and basophils
), and deposited on the vascular shell >> basement. Appendix
<< Activation: When the formation of immune complexes
application is activated with the release of factors that are
chemotaxis for neutrophils (ie S5a and C5b67);
neutrophils, we get in area and production
lysosomal enzymes that destroy the basement membrane
courts. A. Arthus reaction 2. Serum sickness 3. Hypersensitivity pneumonitis
4. Poststreptokokovyy glomerulonephritis
5. Autoimmune disease. Rheumatoid arthritis and SLE. D. Type IV: delayed reaction cell
hypersensitivity (cell), tissue damage results
interaction of sensitized T cells and
specific antigen, which leads to release of solvent
effector substances called lymphokines , direct
cytotoxicity, or both. This reaction does not depend on
antibodies and complement, but it depends on two types
functioning T-cells: T4 + cells. Cages for delayed hypersensitivity and
cells that can produce cytotoxic / suppressor >> << and T8 + cells. Mediators
delayed-type hypersensitivity: is known as
biochemically different lymphokines exists, however, >> << next among those functionally recognized:
1. Migration inhibition factor
(MIF) inhibits macrophage migration. 2. Activation of macrophages
factor (IRF) enhances bactericidal and cytolytic activity of macrophages
(IFN g). 3. Macrophage chemotaxis
factor stimulates the infiltration of macrophages. 4. Transfer factor of 5. Leukocyte inhibition factor
(LIF) inhibits random migration of neutrophils. 6. Interleukin-2 stimulates growth
activated T cells, a mitogenic factor. 7. Limfotoksyn can
lyzyrovat certain tumor cells. 8. Gamma interferon functions
same MAF. . Refusal of vaccination
tissues and organs. would. Contact dermatitis with. Autoimmune disease modulation
delayed-type hypersensitivity. A. Suppressant agents. Corticosteroids have. Antilymphocyte or
antytymotsytarnyy, serum
p. Cytotoxic immunosuppressive drugs
2. Raising
agents.
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