Immunopathology I Flashcards

(47 cards)

1
Q

type I hypersensitivity

A

immediate. the injury is caused by TH2 cells, IgE antibodies, mast cells and other leukocytes

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2
Q

type II hypersensitivity

A

antibody-mediated disorders, secreted IgG and IgM antibodies injure cells by promoting their phagocytosis or lysis and injure tissues by inducing inflammation

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3
Q

Type III hypersensitivity

A

immune complex-mediated disorders, IgG and IgM antibodies bind antigens usually in circulation and antigen-antibody complexes deposit in tissues and induce inflammation

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4
Q

Type IV

A

in cell mediated immune disorders sensitized T lymphocytes (TH1, TH17, and CTLs) are the cause of tissue injury

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5
Q

systemic lupus is an example what what type of sensitivity

A

type III

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6
Q

what antigen is involved in lupus

A

nuclear antigens

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7
Q

thematoid arthiritis is an example of what type of hypersensitiviy

A

type IV

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8
Q

isograft

A

from identical twin

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9
Q

transplant rejection

A

immune damage resulting from recipient response to allograft HLA antigens

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10
Q

direct pathway

A

reaction to donor APC

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11
Q

indirect pathway

A

reaction to self APC

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12
Q

cell mediated cytotxicity

A

host cytotoxic lymphocytes destroy graft cells

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13
Q

delayed type hypersensitivy

A

helper lymphocytes secrete cytokines, recuit mononuclear cells which release inflammatory mediators which cause tissue damge

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14
Q

what does kidney rejection most often affect

A

epithelial and vascular cells

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15
Q

type II hypersensity reaction to target graft vascular

A

Ab bind to HLA moecules in graft endothelium, activate complement causing acute inflammation or basculitis

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16
Q

type III hypersensitivity reaction to target graft vasculature

A

Ag-Ab complexes fix complement causing necrotizign, immune complex vasculitis

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17
Q

what are the patterns of rejection

A

hyperacute, acute, chronic

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18
Q

hyperacutre rejection

A

the recipienct has already encountered the donor materal and body views it as foreign.

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19
Q

how can you prevent hyperacute rejection

A

cross-matching recipient serum with donor lymphocytes to determine presence of cytotoxin Ab to donor MHC I and II antigens

20
Q

what is acute rejection mediated by

A

cellular, humoral, or combined/overlapping mechanisms

21
Q

when does acute rejection occur

A

days-months post transplant or after withdrawal of immunosuppressive therapy

22
Q

morphology of acute rejection

A

lymphocytic infilitrates and tubular necrosis

23
Q

what cells predominant in acute cellular rejection

24
Q

what cells predominant in acute cellular rejection

25
how do cytotoxin (CD8+) lymphocytes help with acute cellular rejection
infiltrates tubular and bascular basement membranes cause tubular damage and endothelitis
26
how do hylper T cells (CD4+) help with acute cellular rejection
produce cytokines which cause extensive interstitial inflammation
27
how does acute humoral rejection affect vascularture
necrotizing vasculitis | intimal thickening due to accumulation of fibroblasts, foamy macrophages, myocytes
28
humoral injury of chronic rejection
proliferative vascular lesions
29
cellular injury of chronic rejection
cytokine induced proliferation of bascular smooth muscle and production of collagen in extracellular matrix
30
morphology of chronic rejection
vascular changes, interstitial fibrosis, tubular atrophy, chronic inflammation
31
when does acute liver rejection occur
within 3 months after transplant
32
what is teh triad of freatures of acute liver rejection
portal tract inflammation bile duct epithelial damage endothelitis of protal vein and hepatic a
33
chronic liver rejection
progressive disappearnace of bile ducts due to direct immunologic destruction or loss of blood supply
34
what is the end results of chronic liver rejection
portal and heptaic fibrosis
35
what is heart transplant treatment for
advanced, irreversible myocardial disease
36
what is a major complication of heart transplant
diffuse intimal proliferation, coronary artery disease silent MI infection maligancies
37
what maligancies are assocaited with heart transplant
epstein-barr virus associated B cell lyphmoa
38
what do steroids suppress
macrophage activity and inflammation
39
how does cyclosporine work
block nuclear factor of activated T cell (NFAT)
40
function of NFAT
necessary for IL-2 stimulation of T cells
41
complications of transplantation
infections recurrence of origal disease maligancy MI due to steroids
42
what maligancies are associated with transplant pts
lymphoma and kaposi's sarcoma
43
why does transplantation of hematopoietic cells treat
hematologic disorders non-hematologic malignancies immunodefiences
44
what are complications of transplantation of hematopoietic cells
graft versus host disesea infection immunodeficiency
45
what has to happen to teh hematopoietic transplant pt
you have to completely destroy their bone marrow - very immunosuppresed
46
graft v host disease
donot t cells recognize host HLA antigens as form and mount a type IV reaction against graft elements and tissues
47
what are the targets of graft v. host disease
epithelia of skin, GI, liver