Hypersensitivity reactions - Overview: Nursing pathophysiology

Hypersensitivity reactions are immune responses that are excessive or have undesirable effects like disease or damage to the body.

They're categorized as type 123 or four based on the immune response and its effect. Type one hypersensitivity reactions also called immediate hypersensitivity reactions.

Or IgE mediated reactions occur in response to normally harmless triggers like pollen, bee stings or medications. Type one hypersensitivity reactions occur in two steps which involve a primary exposure called sensitization and a subsequent exposure when the inflammatory reaction occurs.

First, the immune system is exposed to an antigen or allergen. Next antigen presenting cells called AP CS present the allergen to T cells which then become helper T cells or th two cells.

The th two cells then release large amounts of cytokines that signal B cells to proliferate and turn into plasma cells that start producing IgE antibodies which bind to mast cells sensitizing them.

Then during subsequent exposure, the antigen forms crosslinks on the IgE antibodies on the mast cell membrane causing mast cell degranulation and release of proinflammatory mediators like histamine resulting in an acute inflammatory reaction because this is an immediate hypersensitivity reaction.

Clinical manifestations typically occur within 15 to 30 minutes of subsequent exposure to the antigen manifestations can include rhinitis characterized by sneezing and nasal congestion hives along with rash, redness and itching, angioedema where swelling occurs in the deep layers of the skin bronchospasm, which is a tightening of the bronchial smooth muscle and even systemic reactions like anaphylaxis characterized by difficulty breathing hypotension and death if left untreated.

Next type two hypersensitivity reactions also called tissue specific or cytotoxic reactions are mediated by IgG or IgM antibodies against target antigens on a specific tissue or cell.

Examples of type two hypersensitivity reactions include complement mediated lysis antibody dependent cell mediated cytotoxicity or ADCC and antireceptor antibodies also called antibody mediated cellular dysfunction.

Each mechanism begins with antibodies binding to tissue specific antigens which are expressed on certain cell surfaces. First, with complement mediated lysis antibody antigen binding activates a complement cascade that ultimately forms membrane attack complexes or max which then bind to the target cell and induce cell lysis.

A common type of complement mediated lysis is an A B transfusion reaction. For example, if a patient with type A blood is given a transfusion from a donor with type B blood, the patient's immune system which has anti B antibodies will attack the donor blood leading to red blood cell hemolysis.

Next A DCC happens when antibodies bind to antigens on target cells. This attracts immune cells like natural killer cells which release toxic substances onto the target cell causing cell lysis, an example of A DC is autoimmune thrombocytopenia where autoantibodies bind to platelet membrane proteins.

The antibody coated platelets attract immune cells which induce platelet destruction and subsequent thrombocytopenia. Finally, with antibody mediated cellular dysfunction, autoantibodies cause cells to malfunction instead of directly killing them.

These autoantibodies bind to the target receptors on cell surfaces and impair their normal activity. An example is graves disease where the body produces autoantibodies that bind to thyroid stimulating hormone receptors on the thyroid gland inappropriately stimulating it to produce thyroid hormones and causing hyperthyroidism.

Type three hypersensitivity reactions are mediated by immune complexes comprised of an antigen and IgG antibodies. These immune complexes are formed within the blood or body fluids and are subsequently deposited in tissues.

The harmful effects occur through complement activation and a traction of neutrophils that attempt to phasis the immune complexes but have a hard time ingesting them.

Since the complexes are bound to tissues as they attempt to phasis the complexes. Lysosomal enzymes leak into the surrounding area causing tissue damage.

An example of type three hypersensitivity reaction is the autoimmune disease. Systemic lupus erythematosus where immune complex deposits can result in dermatologic hematologic renal joint and nervous system effects.

Affected individuals typically have a characteristic butterfly rash across their nose and cheeks. They can also experience autoimmune hemolysis and anemia, glomerulonephritis, joint pain and stiffness fever and fatigue.

Finally type four hypersensitivity reactions also called cell mediated or delayed reactions result from a delayed cellular reaction to an antigen.

These reactions differ from other hypersensitivity reactions because they don't involve antibodies. Instead, cytotoxic T cells directly destroy cellular targets and helper T cells activate phagocytic cells such as macrophages that also release proinflammatory cytokines.

These reactions typically take 24 to 72 hours following exposure to the antigen for the reaction to become clinically evident.

The classic example of a type four hypersensitivity reaction is a tuberculin skin test where a protein from the bacterium, mycobacterium tuberculosis or TB is injected into the skin.

When an individual has been exposed to TB, previously, TB, specific T cells will migrate to the injection site and induce an inflammatory response that creates an induration or a hardened area in the skin.

Other common examples of type four hypersensitivity reactions include exposure to plant oils like poison ivy and contact dermatitis that occurs with exposure to substances such as detergents, latex and metal jewelry.

All right, is a quick recap hypersensitivity reactions are immune responses that are excessive or have undesirable effects like disease or damage to the body.

Type one reactions are IgE mediated. Type two reactions are tissue specific and cytotoxic type three reactions are immune complex mediated and type four reactions are delayed and cell mediated