Test 2 Flashcards
RBC transfusions
Type 2
Hemolytic Disease of Newborn
Type 2
prevent with anti-RhD commercial IgG Rhogam shot
idiopathic hemolytic anemia
Type 2
Thrombocytopenia
Type 2
Cole agglutinin disease
IgM aggregates, Type 2
Warm Agglutinins Disease
IgG aggregates (internal body temp)
Type 2
drug induced hemolytic anemia
type 2
pernicious anemia
type 2
good pastures syndrome
type 2
antibody against GBM (glomerular basement membrane) followed by recruitment of PMNs, and NET which damages
tissues
pancreatitis
antibody against islet cells
type 2
rheumatic fever
strep antibody against heart
type 2
thyroiditis
type 2
antibody against thyroglobulin
pemphigoid
type 2
skin basement membrane
primary biliary cirrhosis
type 2
mitochondria ; not disease causing
Sjorgen Syndrome
type 2
salivary glands
myasthenia gravis
acetylcholine receptor
graves’ disease
hyperthyroidism, acts like TSH
type 2
cryoglobulin vasculitis, raynauds
type 3
IgM aggregates
hypersensitive allergic pneumonitis
type 3
starts of as th2 disease
can turn into type 4 granuloma bc organisms have intracellular phase,
lupus
type 3
CIC mediated glomerulonephritus
type 3
cic non-specifically deposits on GBM of kidney
different than good pasteurs syndrome
farmers lung
can be type 3
rheumatoid arthritis
type 3
IgM against IgG
chronic hepatitis
type 3
persistent viral antigen( liver damage impedes CIC clearance)
alcoholic cirrhosis
liver damage and impedes cic clearance
type 3
serum sickness
type 3
anaphylaxis
can be type 1 or 3
occurs when sensitized individual is re-exposed to antigen
if the individual is atopic, type 1 reaction …antigen has direct access to circulation causing IgE and histamine release)
type 3 competent causes histamine r lease
major players in type 2 and type 3
c3b c3a c5a PMNs lysis
skin testing
type 4
details if individual precious encountered antigen or
immune competency of suppressed people
causes of granulomas
can be infections (tb, mumps, leprosy)
or non infections (wood, glass, metals, dust)
irritant contact dermatitis
allergic contact dermatitis
type 4
differentiate by T cell involvement/activation (only in allergic) via elispot assay or patch test
scratch test
patch test
scratch used for type 1 (minutes)
patch used for type 2 (days)
why no antibody response in type 4 allergic contact dermatitis
no free antigen
it’s a chemical, cause hapten formation but no free antigen for sIg to bind
well demarcated lesions
type 4
t/f little to no mast cell activation in type IV acute contact dermatitis
true
also not much complement
histamine release from complement binding mast cell in type 3 and 2 though
treat by removing offending agent or topical anti inflammatory
type IV a b c d
a: th1 cells recruit and activate macrophages…contact dermatitis
b: eosiniphils cause asthma
c: cd8 can cause contact contact dermatitis by hapten on MHC1
d: neutrophils , Behcet disease
formaldehyde
type 4
nickel
type 4
how can you inherit allergies
leaky gap junctions, genes
mhc haplotype
parents have allergies
non inherited characteristics of allergies
class switch from igg to ige , using il4 and il13 cytokines
b cell with il4 and il13 receptors
iga deficiency (allows allergens to bypass mucusol surfaces)
presence and reactivity of Tregs (release il10 which prevents class switch)
environment
anaphylaxis
constriction of bronchial tubes , sometimes rash and fever , life threatening
caused by histamine release from mast cells
either by IgE binding (1) or C3a and C5a binding (3)
wheal and flare
type 1 type 3 (from histamine release from mast cells via complement)
allergic rhinitis
inflammation of the eye nose or throat
c3 convertase
C3bBbP
C1C2bC4b
mutations in C1 inhibitor can cause
vasodilation bc too much C3a and C5a
pleiotropic cytokine
IL4
class switch
macrophage inhibitor
t cell growth factor
redundant cytokines
il4
il5
il2
b cell proliferation
antagonistic cytokines
Il10 and IL4 perfect class switch
IFNy and Il10 macrophage activator and inhibitor
autocrine cytokines
il2
endocrine cytokine
IL1
paracrine cytokine
IL 4 from t cell causes adjacent b cell to class switch
how many types of cytokine receptor families
i
i
iii
iv
type and type ii property
have separating binding and signaling domain
IL2 low intermediate and high
a
by
aby
anakinra
receptor agonist
entanercept and infliximab
tnf soluble receptor
clinical uses of GM-CSF
bone marrow transplant
cytopenias
EPO
kidney dialysis
anemia from chemo
cytokines clinically used for cancer
ifn-a
cytokines clinically used to viral therapy like hep b and c
if a
integrins function
cell cell
cell ecm interactions
chemokines act via what receptor
g coupled protein
chemokines jobs
chemotaxis
degranulation
angiogenesis
