hypersensitivity Flashcards
hypersensitivity definition
inappropriate and excessive response of the immune system
types of hypersensitivity
I: anaphylactic or immediate
II: cytotoxic rxn
III: immune complex rxn
IV: cell mediated or delayed
type I hypersensitivity examples
allergens
bee sting
anaphylactic shock
selective IgA deficiency
drug sensitivity
Ig mediation of type I hypersensitivity
IgE
cell receptors of type I hypersensitivity
mast cells
basophils
chemical mediators of type I hypersensitivity
histamine
other vascoactive amines
clinical course of type I hypersensitivity
exposure to allergen or antigen
B lymph activated to prod IgE Ab
IgE attaches to mast cells/basophils
basophils release granules
immunologic response of type I hypersensitivity
re-exposure= response in mins
mast cells release vasoactive cmpds
vasodilation, mucus secretion, edema, bronchospasms
vasoactive compounds from granules in mast cells contain
from granules: histamine, heparin, proteases
vasoactive compounds from membrane of mast cells contain
from membrane: leukotrienes, prostaglandins, soluble cytokines
symptoms of type I hypersensitivity
itching
hay fever
asthma
eczema
urticaria (hives)
testing for type I hypersensitivity
total IgE levels
RAST testing
RIST testing for type I hypersensitivity
radioimmunosorbent immunoassay
competitive binding
double Ab technique
correlates w/ increased eosinophil count
RAST testing for type I hypersensitivity
radioallergosorbent test
disks w/ specific allergen
allergen panel varies
direct double Ab
common antigens tested for type I reactions
pollen
food
drugs
insect products
animal hair
in vivo skin testing for type I hypersensitivity
scratch test
allergen placed on skin and punctured
if IgE Ab to allergen hive will appear w/in 15 mins
type I hypersensitivity summary
too much IgE
binds to mast and basophils
upon re-exposure of the immunogen, mast and basos release histamine and other factors
Ig mediation in type II hypersensitivity
IgG
some IgM
type II hypersensitivity examples
Rh autoimmunehemolytic anemia
Thrombocytopenia purpura
autoimmune hemolytic anemia
hemolytic disease of the newborn
transfusion rxns
Graves disease
cells involved in type II hypersensitivity
RBC
WBC
Plts
chemical mediators of type II hypersensitivity
complement cascase leading to cell lysis and destruction
clinical course of type II hypersensitivity
cell damage from Ag-Ab rxns
signs and symptoms specific to etiology
transfusion rxn (type II hypersensitivity)
ABO incompatability
intravascular hemolytic transfusion rxn
IgM anti-A and IgM anti-B coat RBCs
C’ bind to RBCs
lysis occurs intravascularly
hemolytic disease of the newborn (type II hypersensitivity)
mother’s IgG Ab cross placenta
rx w/ Ag on baby’s RBCs
RBCs bind C’
cells are destroyed by baby’s RES (extracellular hemolysis)
causes in utero hemolysis and anemia
type II hypersensitivity summary
Ab formed against self
Ab usually IgG maybe IgM
Ab binds to body cells (RBC, WBC, Plt)
C’ activated
makes cells either sensitive to removal by RES or susceptible to decreased fx due to blockage of fx sites by Ab
type III hypersensitivity examples
glomerulonephritis
rheumatoid arthritis
Arthus Rxn
systemic lupus erythematosus
rheumatic fever
type III hypersensitivity Ig mediation
IgG or IgM
cells involved in type III hypersensitivity
host tissue cells
chemical mediators in type III hypersensitivity
C’
immune complexes
clinical course of type III hypersensitivity
formation of immune cmplxs in normal host fx
(facilitates clearance of foreign Ag and invading organ. by phagocytosis)
complications: Innocent bystander process
(cells in the immediate area of cmplxs r destroyed by phagocytes
acute glomerulonephritis (type III hypersensitivity)
Ag-Ab cmplx
soluble cmplx lodges in tissues w/ large filtration area
Arthus reaction (type III hypersensitivity)
Ab rx w/ Ag injected into interstitial fluid
(2nd time rxn)
Rhematic fever (type III hypersensitivity)
Ab rx w/ Ag on cell surfaces
type III hypersensitivity summary
immune cmplxs form in blood after exposure to foreign Ag or in response to self determinants
cmplxs trapped as they pass thru basement mem. of blood vessels/ glomerulus of kidney
trapped cmplxs activate C’
phagocytic cells migrate to area and damage tissue
“innocent by stander” destruction
type IV hypersensitivity examples
contact sensitivity: poision ivy, allergic rxns
graft vs host disease
immunity to viral/fungal Ag
imminity to intracellular organ.
elimination of tumor cells bearing neoantigens
formation of chronic granulomas (syphilis)
TB skin test
Hashimoto’s thyroditis
graft vs host disease (type IV hypersensitivity)
immunologically competent lymphs are transfused from donor to recipient
recipient is incapable of rejecting lymps
grafted lymphs recognize Ag of the host as foreign and rx against them
may cause uncontrolled destruction of host cells
Ig mediation of type IV hypersensitivity
none- T cell mediated
cells involved in type IV hypersensitivity
host tissue cells
chemical mediators of type IV hypersensitivity
lymphokines
clinical course of type IV hypersensitivity
mediated by T lymphs and phagocytic cells
Ag sensitized T cell release lymphokines
lymphokines attract macrophages to site of inflamm
inflamm rxn and tissue damage
type IV hypersensitivity summary
caused by abnorm. in normal T cell mech
T cells inappropriate response to self or over enthusiastic response to foreign Ag
T cells attract macrophages which destroy foreign and normal cells
