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125 Cards in this Set
- Front
- Back
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ab structure
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light chains- kappa or lambda
heavy chains (M G A D E) heavy and light chains consist of variable and constant domain |
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variable domain =
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Fab
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constant domain
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Fc
resp for activating C' |
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multiple monomers of IgM and A are linked by
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j chains
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predom serum ab
75% in blood 4 subclasses only Ig that crosses placenta equal conc in serum and tissue |
IgG
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IgG that activ C'
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IgG 1, 2, 3
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5 monomers linked by j chian
1st ab prod against ag best activator of C' (classical) only 1 req only is serum |
IgM
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serum is single, secretory is dimer with j chain
2 subclasses for ag clearance and immune reg in mucous membs to block attachment to viruses, bact, toxins to host cells no C' activ |
IgA
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surface component of B cells
short half life |
IgD
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allergic rxns (type 1)
fc portion binds to receptors on mast cells and basos in parastitc infs |
IgE
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CD 19 and 20
mature in BM diff into plasma cell to prod ab or memory cell membrane bound IgD and M |
B cell
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CD 2, 3, 4 and 8
stim or supress other cells mature in thymus |
T cell
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CD 16 and 56
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NK
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B cell ag receptor
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IgM and IgD
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have CD4 on surface tat interacts with MHC II on APCs
make IL2 |
TH cell
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have CD8 on surface that interact with MHC I on APCs
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TS cell
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med by TH cells, secret cytokines
involve monos and macros, NK cells |
Cell med immun
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begins with B cell activ, when ag binds to ab on surface
process ag and present to TH cell, which prod cytokines cytokines stim B cell to mature and prod ab or memory cell involves AB prod |
Humoral med immun
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C1q, C1r, C1s, C4, C2, C3
activated by immune complexes, 1 IgM or 2 IgG |
Classical pathway
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factors B, D and properdin
begins at C3 req Mg++ activ by ab and microbial components |
Alternative pathway
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C3 conv
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C- C4b2a
A- C3bBb |
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C5 conv
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C- C4b2a3b
A- C3bBbb |
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MAC complex
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C567
binds 8 to form pore binds several 9 to lyse cell |
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anaphylotoxins
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C4a, C3a, C5a
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C3 def
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incr risk for overwhelming infs
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C4 and C3 def
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indicate consumption with Classical pathway activation
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C1 (qrs) C4, C2 def
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collagen disease
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C5,6,7 def
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N. meningitidis inf risks
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anaphylactic rxn
immediate hypersens rxn due to IgE involves histamine, prostaglandins, leukotrines |
type 1 hypersens rxn
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cytotoxic
due to IgM and IgG directed against cell surface ags causes C' med lysis can be from incompat blood transf |
type II hypersens rxn
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immune complexes are deposited in tissues > inflamm
Arthus rxn serum sickness glomerulonephritis vaculitis |
type III hypersen rxn
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cell med
delayed hypersen rxn T cells prod lymphokines TB skin test dermatitis |
type IV hypersen rxn
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marked def of all classes or igs
detected at 6 mos recurrent life threatening infs S. pneumo, H. influ decr or absent B cells an TK grou O, no anti A or B |
Brutons X link hypogammaglobulinemia
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x linked
icr IgM, IgG and A decr or absent resp tract infs autoabs to all cells |
Hyper IgM synd
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small or decr amount of serum and secretory IgA
genetic or drug induced |
Selective IgA def
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spiderweb capillaries on skin
decr motor fnx, metal retardation recurrent pulm infs immune defects can have IgA or IgE def effects B and TH cells |
Ataxia-telangiectasia
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tetany (decr Ca)
undevel of heart and thymus decr to no T cells susc to opportunistic infs, poor prognosis low set ears and fish mouth no thymic shadow on xray |
Di George's Synd
Congenital Thymic Hypoplasia |
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affects T and B cell fnx
low T cells present hypogammaglonulinemia recurrent infs |
SCID
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gene mutation
prevent TH cells from delivering lymphokines to B cells, macros eczema, TTP, incr infs small defective plts thrombocytopenia at birth, bleeding by 6 mo H. influ |
Wiskott Aldrich synd
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lymphoprolif disease, excess immunoglob prod
BJ proteins in urine incr plasma cells in bm sheets of binucleated cells in bm punched out bony lesions (skull) fractures, bone pain M spike incr sed rate |
Multiple Myeloma
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uncontrolled prolif of B cells, excess IgM prod
hyperviscosity of plasma bm has plasmacytoid lymphs pancytopenia incr sed rate and rouleaux |
Waldenstroms macroglobulinemia
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direct detection of Syphilis
from lesions |
darkfield microscopy
with silver stain |
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nontreponemal ag test for Syphilis
only used for screening use cardolipin ag |
VDRL and RPR
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treponemal ag test for Syphilis
highly specific/sensitive confirm test |
FTA-ABS
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initial, painless lesion
lymph nodes enlarge ab prod up to 1 month after chancre spirochetes in lesion |
primary syphilis
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skin rash, fever, swollen lymph nodes
4-6 weeks spirochetes present in all of body ulcers on mucous membs pos serologic tests |
secondary syphilis
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no signs/sympts
nontreponemal and treponemal tests pos |
latent syphilis
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later after 1st inf
gummas throughout body neuro sympts |
tertiary syph
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RPR/VDRL- neg/pos
FTA-ABS pos |
primary syphilis
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RPR/VDRL- pos/pos
FTA-ABS- pos |
secondary syphilis
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RPR/VDRL- pos/neg
FTA ABS- pos |
latent syphilis
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immunofluorescense testing
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abs are labeled with fluor dye and are used to detect an ab or ag
direct= ab to ag indirect= ab to ag/ab complex (antihuman ab) ANA=indirect FTA-ABS |
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ELISA/ELIA
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enzyme labeled reagents used to detect ags or abs
enzymes cant bind to ag/ab independently colorless substrate is metabolized by enzyme to colored compound more intense color= more enzyme present sandwich |
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nephelometry
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measurement of light scattered
scatter directly proportional to # and size of particles |
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spectrophotometry
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measures light transmitted
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turbidomertry
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measures light blocked
uses spectro |
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chronic systemic inflamm disease that primarily affects joins
due to prod of IgM ab against IgG fc region is synovium forms immune complexes and activates C' pos RF ab (IgM) that binds to IgG |
RA
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chronic imflamm disease involving many organs
tissue injury due to ab and immune complexes deposited in tissues causes by depressed TS cells neutropenia |
SLE
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homog ANA
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SLE
anti- dsDNA Crythidia kinetoplast will react with anti dsDNA |
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Centromere ANA
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anti centromere/CREST
CREST small dots, ~46 |
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Nucleolar ANA
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anti RNA
bigger dots, 2-6 blobs scleroderma |
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speckled ANA
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lupus and RA
anti Smith stains all but nucleoli |
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macroscopic flocculation
uses VDRL ag with charcoal particles semi quantitative |
RPR
for syphilis |
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sore throat, fever, lymphadenopathy
lymphocytosis, atypical reactive lymphs, enlarged lymph nodes can last up to 2 months will prod heterophile abs |
EBV
IM |
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Western Blot used to confirm diagnosis
2 of 3 bands must appear to be considered pos, p24, gp41, gp120/160 |
HIV testing
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fecal oral transmission
can be asympt liver Anti HAV (IgM) pos |
Hep A
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transm through mucous membs, body fluids, parenterally
1st marker is HbsAg 2nd is HBeAg 1st ab to appear is anti HBc liver |
Hep B
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chronic hep > 50% asympt
transmitted mucous membs, parenteral anti HCV |
Hep C
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only in Hep B inf
HDV Ag pos |
Hep D
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rare
fecal oral transm |
Hep E
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how to get monoclonal ab
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from hybridomas, neoplastic B cell
used for antisera |
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tests for Rubella
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IgG ab offer lifetime immunity, IgM ab= infection
Rubella virus agglu chick cells- if agglu with test= ab are present (due to pt and Rubella ab/ag complexes) |
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on MHC I cells and most cell surfaces
present ag to CTLs stim ab prod |
HLA A,B,C
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on MHC II cells
on monos, macros, B cells, aciv T cells, present to TH cells stim T cell response |
HLA DP,DQ,DR
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binds to bact and fungi
from liver incr 4-6 hrs post inf indicates acute inflamm activates C' latex agglu reverse passive agglu |
CRP
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APRs
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fibrinogen
alpha 1 anti trypsin ceruloplasmin serum amyloid A |
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neutrophil extravasation
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rolling
activation adhesion |
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false neg test result
due to ab excess |
prozone
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SPE-
alpha 1 and 2 incr |
acute inflam
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SPE-
no alpha 1 |
alpha 1AT def
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SPE-
all decr |
chronic protein loss
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decr albumin, incr alpha 2
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nephrotic synd
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SPE-
decr in albumin, alpha 1, gamma incr alpha 2 |
severe burn
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SPE-
decr gamma |
hypogammaglobulinemia
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SPE-
albumin, alpha 1, alpha 2, beta decr gamma slight incr |
hepatic inflamm
1st 4 prod by liver so decr |
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SPE-
decr albumin incr alpha 1, alpha 2, gamma |
chronic inflamm
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SPE-
decr albumin and alphas beta gamma bridging (due to incr IgA) |
cirrhosis
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SPE-
broad incr gamma |
polyclonal gammopathy
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SPE-
large peak gamma M spike |
monoclonal gammopathy
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causes angioedema
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C1 inhib def
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incr risk for overwhelming infs
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C3 def
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indicate collagen disease
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C1, C4, C2 def
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incr risk for N. minin infs
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C 5,6,7 def
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causes lysis of RBC in vivo, looks like intrav heme or auto ab/ transf rxn
can cause cold auto heme anemia- RBCs coated with IgM and C' |
M. pneumo
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sanwich technique
ab absorbed onto solid surface ad pt serum with ag to bing to ab coated bead/well add enzyme labeled ab to form ag-ab-labeled sanwich ad enzyme susbtrate |
ELISA
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ad pt serum to enzyme-drug conj and anti drug ab
add enzyme substrate for drugs and hormones |
EMIT
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add reagent ab and pt serum w/ ag
if pos, reduces amount of polarized light prod |
FPIA
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current Hep B inf
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HBsAg
HBeAg maybe Anti HBe and Anti HBc (IgM) |
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chronic HepB inf
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HBsAg
HBeAg Anti HBc maybe Anti HBe and Anti HBc (IgM) |
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past HepB inf/recovery
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ANti HBe
Anti HBc Anti HBs |
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Hep B vaccine
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Anti HBs
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pt ag and labeled ag are incubated with known amount of specific ab(anti IgE), compete for binding of ab
wash to remove unbound ag the lower the radioactive count, the higher the conc of pt ag If you have low radioactive count: tells us that a lot of the binding sites were taken up by patient IgE, so the pt has a lot of IgE If we have high count of radioactive IgE: tells us pt IgE level low. sandwich measures total IgE |
RIST
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most people prod ab to
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IgA
due to IgA def |
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test fro anti HLA A,B,C
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use pt serum and known cells with ag
incubate with guinea pig serum an ag/ab rxn indicates C' activation (seen by lysing of lymphs) add dye and lymhps will be large and dark negative ag/ab rxn = no C' activ and refractile lymphs |
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will cause dev of anti I, but in low titer
will last as long as infected opaque spots on chest xray |
M. pneumo inf
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seen mostly in elderly
will have hypertension, purple extremities in cold can > lymphoma/leukemia has high anti I titer |
Cold agglut
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can dev anti i
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Mono
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ab to microsomal structure
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autoimmune thyroid disease
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anti mitochondrial ab
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primary biliary cirrhosis
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can accredit lab but only 2 agencies that can shut you down if not run properly
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JCAHO and CAP
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caused by HLA ab in DONOR
react with WBC in recip lungs |
TRALI
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ab/ag depsit in kidney and lungs
due to autoimmune, ab to glom. basement membs |
Goodpasture synd
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outcome assessment
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compares tests and treatment to see which one is more efficient for best patient care and getting best test results
done by performing studies |
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RPR neg
FTA pos no sympts |
past infection
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how to test in transplant pt is prod ab to HLA ags of donor tissue
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test ab response, not T cell response
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what makes each immunoglob unique?
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Heavy chains don’t have same amino acid sequencing
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advantage to this is it can detect nucleic acid Ags much earlier that we can detect other Ags of viral diseases. Disadvantage: expensive. Not a rapid slide test, it is a nucleic acid test where you go by detailed testing protocol.
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NAT testing
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the reason for testing for both Hepatitis B surface Ag and Ab to HepBcore Ag
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When the surface Ag is present in such great quantities in serum, the pt is frequently asymptomatic, and it’s not until they prod Abs to core Ag that they become symptomatic. If we just tested for Surface Ag and not Abs to the core Ag…we would get false negs and would miss individuals that had ceased to have large quantities of surface Ag in their serum and were producing Ab to the core Ag.
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Assoc with Anti-acetyl choline receptor sites
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Myesthenia gravis
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assoc with ab to the myelin sheath
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Multiple Sclerosis
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Anti-parietal
Ab to intrinsic factor: cannot absorb appropriate vitamins |
Pernicious anemia
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Excellent at activating complement, found only in serum
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IgM
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doing nephlometery
scratched cuvette is used how will result be affected |
false elevated because light will bounce off of scratch
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how to tell is T cells are functioning
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thymic shadow on xray
B cells are stim by IL prob IL 1 is present, stim TH cells NOT ab prod or memb bound IgM/D |
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Nk cells
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they do not have to have been previously exposed to an Ag to mount an effective Ab response
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