Immunopath Flashcards
type 1 autoimmune rxns
anaphalctic- mediated by mast cells releasing vasoactive/spasmogenic substances
IgE binds to mast cells. next time IgE recognizes Ag, it crosslinks IgE receptors it releases vasoactive substances
type 1 autoimmune rxn types
localized (asthma, hay fever) or systemic (stings, hives)
2 types of substances in mast cells
preformed- granules- histamine
actively formed
2 stages of type 1 rxns
immediate- mast cells release preformed mediators. vasodilation, vasoleakage, muscle contraction
delayed- releases synthesized mediators. infiltration via basophils, neutrophils and T cells; tissue injury and remodeling
eosinophil contribution to type 1 rxns
releases major basic protein, leads to mast cell degranulation and epithelial damage
releases leukotriene 4, platelet activating factor
severe urticaria
induced by heat or cold- no need for IgE
localized
atopic keratoconjunctivitis
type 1 rxn
localized inflammation of eyes
asthma
type 1 rxn abnormal repair response to epithelial injury
over time, causes epithelial shedding, gland hyperplasia, matrix remodeling, muscle hyperplasia, inflammatory infiltrate, and basement membrane thickening
anaphylaxis
systemic type 1 rxn
resipratory and heart rate dramatically increase, BP drastically decreases
type 2 rxns
mediated by Abs
damage defined by where Ab binds
hemolytic transfusion rxns
acute- high levels of preexisting Abs bind and lyse transfused blood. cells destroyed via complement
delayed- low levels of Abs, over 1-2 weeks cause slow hemolysis. cells destroyed via phagocytes
erythroblastosis fetalis
child born anemic, edema, liver hypertrophy
caused by Rh- mom attacking Rh+ child blood cells
goodpasture’s disease
Abs bind basement membrane of glomeruli
visualized w/ stain for IgG
causes renal failure and pulmonary hemorrhages
rheumatic fever
Abs that develop in response to strep throat cross react w/ other host tissue
causes arthritis, endocarditis, chorea, and myocarditis
immune complexes deposit and cause vasculitis
graves disease
cause autoimmune stimulation of TSH receptors- causes massive thyroid hormone relase
myasthenia gravis
autoimmune blockade of AcH receptors in muscle motor plates
type 3 rxns
immune system produces Abs, repeated exposure to Ags, Ag-Ab complexes form and are deposited in the tissues. complement cascade causes attraction and activation of PMNs and macrophages. end result is damage and inflammation
post streptococcal glomerulonephritis
type 3 rxn
Abs form to streptococci Ag form. Ag-Ab complexes form and deposit in glomerulus causing damage
vascullitis
Ab-Ag complexes deposit in blood vessel walls outside epithelium
often seen in Hep B
serum sickness
injection of horse serum caused Ag-Ab complexes to buildup and deposit in many places in the body causing massive complement activation
type 4 rxns
driven by lymphocytes and macrophages
delayed type- CD4 driven
viral- CD8 driven
transplant rejection- both
granuloma formation
result of type 4 rxn where Ag cannot be cleared
