Hypersensitivity reactions Flashcards
Hypersensitivity reactions
exaggerated, inappropriate immunologic reaction that is harmful to the host
4 types
sensitization
first exposure to antigen with immune response (antibody)
subsequent exposures cause hypersensitivity reactions
type I Hypersensitivity reactions
allergy or anaphylaxis
type I mechanism
First exposure to antigen causes IgE formation
IgE binds to mast cells
Subsequent exposure – antigen binds to IgE bound-mast cell
Degranulation of mast cells
Release of mediators
antigens in type I
are substance that most people do not react to pollen animal dander foods drugs
type I timing and result
minutes
result increases vascular permeability edema smooth muscle contraction (throat closing)
type I clinical manisfestionas
edema, erythema, itching, urticaria, eczema, rhinitis, conjunctivitis, asthma
more severely: systemic anaphylaxis
systemic anaphylaxis
severe bronchoconstriction and hypotension
urticaria
hives
allergic response
During sensitization, APC picks up the allergen (antigen) and presents part of it to a T helper 2 cell, which helps a B cell become a effector cell
effector cells produce allergen-specific antibodies called IgE, which binds to mast cells.
When allergen returns, mast cells release histamine and other chemicals
In addition, Th2 cells release many different chemicals that attract inflammatory cells such as eosinophils
This results in allergy symptoms such as sneezing, mucus production, swelling, itching, runny nose, coughing, and wheezing
Slow-reacting substance of anaphylaxis (SRS-A)
consist of leukotrienes
increases vascular permeability and smooth muscle contraction
Eosinophil chemotactic factor of anaphylaxis (ECF-A)
release histamine and arylsulfatsae
arylsulfatase
release by ECF A degrades histamine and SRS-A
serotonin
capillary dilation increase vas perm and smooth muscle contraction
Prostaglandins and thromboxanes
Dilation and increased permeability of capillaries and bronchoconstriction
Aggregate platelets
Aggregate platelets
Prostaglandins and thromboxanes
help with clotting
Platelet-activating factor (PAF)
bronchoconstriction, hypertension and vascular permeability
cross linking
the allergen cross-links the bound IgE on those cells. This causes degranulation and release of mediators
medications of Anaphylactic allergic reaction
epinephrine, corticosteroids, fluids for hydration, diphenhydramine (antihistamine) promethazine (antiemetic)
promethazine (Phenergan
antiemetic anti nausea medication
nauseous due to dump of adrenaline
diphenhydramine (Benadryl)
antihistamine
Systemic histamine release in anaphylaxis causes what symptoms
Hypotension
Nausea
Hives
Swollen hands/feet
type II
Cytotoxic Hypersensitivity
Antibody mediated cytotoxic reaction
antigens on a cell surface combine with IgG antibody this leads to complement mediated lysis of the cells
type II timing
hours to days
clinical manifestations of type II
hemolytic anemia, Rh incompatibility, rheumatic fever
hemolytic anemia
type II
antibody IgG attaches to antien on RBC
Complement mediated lysis via MAC
Complement also attracts phagocytes
Type III
IgG
Immune Complex Hypersensitivity
antibody immune complexes are deposited in tissues, complement is activated, and polymorphonuclear cells are attracted to the site. They release lysosomal enzymes, causing tissue damage
Type III timing
2 to 3 weeks
type III clinical manifestations
Systemic lupus erythematosus, rheumatoid arthritis, poststreptococcal glomerulonephritis
type III steps
Antigen–antibody immune complexes form and deposit in tissue
Inflammatory response induced in tissue wall of blood vessel
C3a and C5a are released
Complement activated, and PMNs attract to the site neutrophils by c5a
Lysosomal enzymes released destroy endothelium and red cells escape
results in Tissue damage
Systemic lupus erythematosus (SLE
type III
antibodies are formed to DNA and cell nuclei ANA
goes through type III steps
causes pleural effusions, heart problems, butterfly rashes, arthritis, raynaud’s phenomenon
Rheumatoid Arthritis
type III
Serum and synovial fluid have “rheumatoid factor” (i.e., IgM and IgG antibodies that bind to the Fc fragment of normal human IgG)
Deposits of immune complexes on synovial membranes and in blood vessels
Activate complement and attract polymorphonuclear cells, causing inflammation.
Rheumatoid Arthritis titers
Patients have high titers of rheumatoid factor and low titers of complement in serum especially during periods when their disease is most active
Type IV Delayed (Cell-Mediated) Hypersensitivity timing
2 to 3 days
Type IV Delayed (Cell-Mediated) Hypersensitivity examples
Contact dermatitis, poison oak/ivy, tuberculin skin test reaction, drug rash, Stevens-Johnson syndrome,
type IV mechanism
the macrophage ingest antigen process and preens on it surface as MHC class II T helper I cell is activated and produced gamma interferon and actives macrophage
berculosis, coccidioidomycosis
CD4 (helper) T cells and macrophages
CD8 (cytotoxic) T cells
Contact dermatitis
