Hypersensitivity Flashcards
hypersensitivity
a normal immune response that is
- inappropriately triggered
- excessive response
- produces undesirable effects on the body
triggers of hypersensitivity
- specific antigen-antibody rxn
- specific antigen-lymphocyte interaction
four types of sensitivity
- type I, II, III: mediated by antibodies produced by B cells (specifically plasma cell)
- type IV: mediated by T cells
type I rxn
IgE
type I characteristics
immediate rxn (15-20 mins)
reaction occurs after being sensitized to an antigen
occurs at second exposure
antigens of type I
- env like pet dander, bee stings
- foods like nuts, seafood, eggs
- medications like penicillin, contrast dye
type I etiology
- 1 parent allergic = 30%
- 2 parent allergic = 50%
key cells involved in type I rxn
- B lymphocytes
- IgE antibodies
- mast cells (granulocytes)
type I pathogenesis
- antigen will bind to B cell (first exposure)
- plasma cells will produce antibodies, specifically IgE
- IgE will attach to mast cells
- when exposed again, the antigen will bind to the IgE antibody on mast cell which will trigger the release of chemical mediators from mast cell
- chemical mediators can result in numerous affects
chemical mediators of type I result in
intravascular compartment
- anaphylactic shock
skin
- urticaria, atopic dermatitis, wheal flare rxn, angioedema
respiratory system
- rhinitis, asthma
GI system
- N, V, D, cramping
reasons for type I clinical manifestations mediator activities
- potent vasodilation
stuffy nose
lower bp
wheals on skin
reasons for type I clinical manifestations mediator activities
- inc vascular permeability
edema
runny nose
reasons for type I clinical manifestations mediator activities
- bronchial smooth muscle constrictions
breathing difficulties
wheezing
reasons for type I clinical manifestations mediator activities
- stimulates irritant receptors
itching (pruritus)
type I atopic rxns (local rxn)
inherited tendency to become sensitive to allergens
- ex: allergic rhinitis, asthma, urticaria
most common triggers of atopic rxn
pollen
dust
molds
animal dander
type I systemic rxn
results in anaphylaxis, a systemic release of chemical mediators
why is anaphylaxis life threatening
bronchial constriction
airway obstruction
vascular collapse (shock)
most common triggers of anaphylaxis type 1
medications
bee stings
foods
type II rxn
cytotoxic rxn
etiology of type II
exposure of antigen or foreign tissue/cell (not your own cells)
antigens are located on the cell surface
key characteristics of type II
antigen stimulate antibody production
antibodies recognize and attach to cell surface antigens
direct destruction of targeted cells that contain antigen
- cell lysis
- phagocytosis
immune cells involved type II
antibodies IgG an IgM
complement
WBCs (phagocytosis)
examples of type II antigens
blood
some of your body’s own cells (auto immune conditions)
erythroblastosis fetalis (Rh factor btw baby and mom)
type II pathogenesis
type a will have b antibodies, type b will have a antibodies
- when one blood type is put into the other the antibodies will bind with the blood type and cause clumping
clumping results in
- donor cells burst –> kidney damage
- small vessels blocked –> reduced blood supply
type II response example disorders
- blood transfusion rxn
- newborn/mother Rh incompatibility
- autoimmune disorders (hemolytic anemia, myasthenia gravis, graves disease)
- certain drug rxn
transfusion rxn
- fevers, chills, rushing
- inc HR, dec BP
- chest pain, back pain
- N/V
- restlessness
- anxiety
- headache
type III key characteristics
antigen antibody complex complexes that circulate around the body which will be deposited into tissues causing inflammatory response from tissue damage (often at the joints)
type III antibodies
IgG
IgM
type III possible offending antigens
body’s own tissue and/or DNA
inhaled antigens from mold or contaminated plants
bacteria or viruses
key immune cells involved in type III immunity
antibodies (IgG and IgM) that clumps w antigens
complement
neutrophils (release toxins and chemical mediators)
type III pathogenesis
- antigen-antibody complex forms in the blood which will deposit in the tissue
- the deposition causes activation of complement and chemoattraction of neutrophils which will release enzymes and free radicals
clinical manifestations of type III
depends on where the complexes are deposited in the tissue
- rheumatoid arthritis: whatever joints its deposited in
- glomerulonephritis: kidney failure
- systemic lupus erythematosus: skin and many organs
type II vs type III
- type II: rxn occurs on the cell surface and result in direct cell death or manifestation
- type III: immune complexes are deposited into tissues and the resulting inflammation destroys the tissue
type IV key characteristics
- delayed hypersensitivity response
- no antibody involvement
type IV key immune cells
- T cells (no B cells)
- cytokines
- mast cells and macrophages
etiology of type IV
delayed cellular reaction to an antigen
possible source antigens for type IV
- plant oils
- cosmetics, clothing, dyes, adhesives
- nickel alloys
- TB antigen
- organ transplant or skin graft
- gluten
pathogenesis of type IV
- small, incomplete antigen, called a hapten penetrates the skin
- hapten binds with human protein to form complete antigen
- T cells become aware of antigen
- T cells attack the antigen via direct attack of T cells, release of cytokines (inflammation), macrophages (cell destruction)
type IV pathogenesis image
- exposure to hapten with formation of complete antigen
- recognition and processing of antigen by antigen processing cell
- migration of APC to lymph node where antigens are presented to T cells
- release of cytokines that stimulate proliferation of T cells and activates macrophages
- activated T cells and macrophages migrate to epidermis, release inflammatory mediators ,cause cell destruction
clinical manifestations of type IV
- peaks at 48-72 hrs
- contact dermatitis (redness, edema, itching, blisters)
- tuberculin hypersensitivity (redness, induration, inflammation)
4 different types summary: type I
- allergens
- IgE on mast cells
- mediator release
4 different types summary: type II
- IgG and IgM
- antibodies attach to cells
- cell lysis
4 different types summary: type III
- IgG and IgM
- antibodies complexes
- accumulate in tissues
- inflammation
4 different types summary: type IV
- delayed T cell activation
- cytokines
