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Pathology Exam III > Immunopathology I > Flashcards

Immunopathology I Flashcards

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

A

lymphocytes

24
Q

what cells predominant in acute cellular rejection

A

lymphocytes

25
Q

how do cytotoxin (CD8+) lymphocytes help with acute cellular rejection

A

infiltrates tubular and bascular basement membranes cause tubular damage and endothelitis

26
Q

how do hylper T cells (CD4+) help with acute cellular rejection

A

produce cytokines which cause extensive interstitial inflammation

27
Q

how does acute humoral rejection affect vascularture

A

necrotizing vasculitis

intimal thickening due to accumulation of fibroblasts, foamy macrophages, myocytes

28
Q

humoral injury of chronic rejection

A

proliferative vascular lesions

29
Q

cellular injury of chronic rejection

A

cytokine induced proliferation of bascular smooth muscle and production of collagen in extracellular matrix

30
Q

morphology of chronic rejection

A

vascular changes, interstitial fibrosis, tubular atrophy, chronic inflammation

31
Q

when does acute liver rejection occur

A

within 3 months after transplant

32
Q

what is teh triad of freatures of acute liver rejection

A

portal tract inflammation
bile duct epithelial damage
endothelitis of protal vein and hepatic a

33
Q

chronic liver rejection

A

progressive disappearnace of bile ducts due to direct immunologic destruction or loss of blood supply

34
Q

what is the end results of chronic liver rejection

A

portal and heptaic fibrosis

35
Q

what is heart transplant treatment for

A

advanced, irreversible myocardial disease

36
Q

what is a major complication of heart transplant

A

diffuse intimal proliferation, coronary artery disease
silent MI
infection
maligancies

37
Q

what maligancies are assocaited with heart transplant

A

epstein-barr virus associated B cell lyphmoa

38
Q

what do steroids suppress

A

macrophage activity and inflammation

39
Q

how does cyclosporine work

A

block nuclear factor of activated T cell (NFAT)

40
Q

function of NFAT

A

necessary for IL-2 stimulation of T cells

41
Q

complications of transplantation

A

infections
recurrence of origal disease
maligancy
MI due to steroids

42
Q

what maligancies are associated with transplant pts

A

lymphoma and kaposi’s sarcoma

43
Q

why does transplantation of hematopoietic cells treat

A

hematologic disorders
non-hematologic malignancies
immunodefiences

44
Q

what are complications of transplantation of hematopoietic cells

A

graft versus host disesea
infection
immunodeficiency

45
Q

what has to happen to teh hematopoietic transplant pt

A

you have to completely destroy their bone marrow - very immunosuppresed

46
Q

graft v host disease

A

donot t cells recognize host HLA antigens as form and mount a type IV reaction against graft elements and tissues

47
Q

what are the targets of graft v. host disease

A

epithelia of skin, GI, liver

Pathology Exam III (10 decks)

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