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Year 1 Pathology > Immunopathology I > Flashcards

Immunopathology I Flashcards

1
Q

what causes damage in type I hypersensitivity reactions?

A

th2 cells, IgE, mast cells, other Abs

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2
Q

what causes damage in type II hypersensitivity reactions?

A

IgG and IgM Abs injure cells by promoting phagocytosis, lysis, and inflammation

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3
Q

what causes damage in type III hypersensitivity reactions?

A

antigen-Ab complexes form from IgG and IgM binding antigen in the circulation, and get deposited in tissues

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4
Q

what causes damage in type IV hypersensitivity reactions?

A

cell mediated - sensitized T cells (Th1, Th17, CD8) - stimulation of macrophages and other mediators involved in inflammation

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5
Q

MHC II binds with what T cells? what mediators are released?

A
  1. Th1 - IFNy 2. Th17 - IL-17, 22
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6
Q

definition: transplant rejection

A

immune damage resulting from recipient response to allograft HLA antigens

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7
Q

what is the direct pathway in type IV hypersensitivity graft rejection?

A

donor APCs present proteins to host immune system - cytotoxic T cells (CD8) and macrophages / cytokines cause the damage (CD4)

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8
Q

what is the indirect pathway in type IV hypersensitivity graft rejection?

A

host APCs pick up donor alloantigens and stimulate a CD4 pathway

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9
Q

antibody mediated vasculitis exhibits what type of hypersensitivity? what is the mechanism?

A
  1. type II 2. antibody binds to surface antigen (HLA molecules) in graft endothelium, activates complement, recruits leukocytes - tissue injury
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10
Q

immune complex vasculitis exhibits what type of hypersensitivity? what is the mechanism?

A
  1. type III 2. antibody against graft antigen forms immune complexes, deposit in graft endothelium, fix complement - necrotizing vasculitis
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11
Q

what is the mechanism of hyperacute graft rejection?

A
  1. preformed Ab in recipient 2. targets vessels with immune complex formation / deposition (type III) 3. fibrinoid necrosis, vasculitis, thrombosis, ischemia
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12
Q

acute rejection uses what hypersensitivity types?

A

II, III, IV

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13
Q

what is the mechanism of acute graft rejection?

A
  1. CD8 lymphocytes infiltrate tubular and vascular basement membrane - tubular damage and endothelitis 2. Th cells produce cytokines - interstitial inflammation
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14
Q

what is the histologic appearance of acute rejection?

A
  1. lymphocytic infiltration and tubular necrosis (cellular) 2. necrotizing vasculitis (humoral) 3. intimal thickening due to accumulation of fibroblasts, foamy macrophages, myocytes
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15
Q

what is the mechanism of chronic rejection?

A
  1. humoral - proliferative vascular lesions 2. cellular - cytokine induced proliferation of vascular smooth muscle and production of collagen in ECM
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16
Q

increased BUN, creatinine, and decreased urine output is indicative of what type of rejection?

A

acute

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17
Q

anuria is indicative of what type of rejection?

A

chronic

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18
Q

what is the histologic appearance of chronic rejection?

A

vascular fibrosis with tissue ischemia, tubular atrophy, and interstitial mononuclear cell infiltrates

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19
Q

what are the general features of liver rejection?

A

portal tract inflammation, bile duct epithelial damage, endothelitis of portal vein and hepatic artery

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20
Q

what are the injuries involved in acute liver rejection?

A

bile duct damage and endothelitis of portal vein

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21
Q

what characterizes chronic liver rejection?

A
  1. disappearance of bile duct due to cellular immune damage 2. obliterative arteritis from proliferation of intimal layer - ischemia 3. portal and hepatic fibrosis
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22
Q

what characterizes heart rejection?

A

classic cellular rejection with interstitial and perivascular T cell infiltrates - myocyte necrosis resembling myocarditis

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23
Q

what is the major complication of heart rejection?

A

diffuse intimal proliferation - coronary artery disease

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24
Q

what is graft arteriopathy?

A

inflammatory cells in adventitia and intima drive smooth muscle proliferation and ECM deposition - intimal hyperplasia

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25
Q

what is the cause of GVHD?

A

donor T cells recognize host HLAs as foreign and mount a type IV (DTH or CTL) reaction against graft elements and tissues

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26
Q

what is the crucial component of GVHD?

A

activation of CD4 cells

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27
Q

what characterizes chronic GVHD?

A

generalized fibrosis of dermis and skin, GI mucosa, and bile ducts

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28
Q

what characterizes acute GVHD?

A

epithelial necrosis in target organs - skin (dermatitis), GI (enteritis), liver (hepatitis, bile duct necrosis, jaundice)

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29
Q

how is the diagnosis of AI disease made when autoantibodies are found in healthy individuals and may be formed after tissue damage?

A
  1. reaction is primary to pathogenesis, not secondary to tissue damage 2. immunological reaction to a self-Ag or native (self) tissue 3. no other well-defined cause or identifiable etiology
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30
Q

what are the possible mechanisms of tolerance breakdown?

A
  1. failure of T cell anergy 2. failure of activation induced cell death (apoptosis of self-reactive cells) 3. failure of T cell mediated suppression 4. molecular mimicry or cross-reactivity 5. polyclonal lymphocyte activation 6. emergence of sequestered antigen 7. exposure of cryptic antigenic determinants
31
Q

what characterizes failure of T cell anergy?

A

expression of B7 co stimulatory molecule leads to autoreactivity

32
Q

what characterizes failure of activation induced cell death?

A

failure of Fas-FasL system - peripheral persistence and proliferation of auto-reactive cells

33
Q

what characterizes failure of T cell mediated suppression?

A

failure of regulatory T cells to suppress proliferation of other T cells encourages autoreactivity

34
Q

what characterizes molecular mimicry or cross reactivity?

A

self Ag sharing an antigenic determinant with microbial Ag

35
Q

what characterizes polyclonal lymphocyte activation?

A

activation of B cells or CD4 cells may induce immune response leading to autoreactivity

36
Q

what characterizes exposure of cryptic antigenic determinants?

A

hidden epitopes are exposed, leading to self reactivity

37
Q

what is the immune response in SLE?

A

self reactive Th cells escape tolerance and drive autoantibody production by B cells - defects in elimination of self reactive B cells peripherally and in bone marrow

38
Q

in SLE autoantibodies are directed against which cell components?

A

antinuclear antibodies (ANAs) - reflect loss of tolerance and act as mediators of tissue injury

39
Q

ANAs are directed against what categories of nuclear antigen?

A
  1. DNA 2. histones 3. proteins bound to RNA 4. nucleolar antigen
40
Q

homogenous ANA staining indicates binding to what antigen? which disease is implicated?

A
  1. chromatin, dsDNA, histone 2. drug induced SLE
41
Q

rim ANA staining indicates binding to what antigen? which disease is implicated?

A
  1. dsDNA 2. SLE
42
Q

speckled ANA staining indicates binding to what antigen? which disease is implicated?

A
  1. histones and ribonucleoproteins 2. SLE, SS, Sjogren
43
Q

nucleolar ANA staining indicates binding to what antigen? which disease is implicated?

A
  1. nucleolar RNA 2. SLE, SS, CREST
44
Q

anti-histone ANAs are indicative of what type of AI disease?

A

drug induced lupus

45
Q

anti-RNP ANAs are indicative of what type of AI disease?

A

Sjogren syndrome

46
Q

anti-dsDNA ANAs are indicative of what type of AI disease?

47
Q

type II SLE mechanism involves what type of lesion? type III?

A
  1. type II - RBC 2. type III - visceral lesions
48
Q

what occurs during lupus vascular changes?

A

circulating immune complexes deposit in vascular beds, activate complement, type III reaction

49
Q

what are the histologic features of acute and chronic lupus vascular damage?

A
  1. acute - vasculitis with fibrinoid necrosis of arteries / arterioles in any tissue 2. layered fibrous thickening (onion skinning)
50
Q

what is the mechanism of kidney injury during lupus?

A

immune complex deposition in glomeruli, basement membranes, larger blood vessels, thrbombosis due to antiphospholipid antibody

51
Q

what is the result of lupus nephritis?

A
  1. thickening of membranous part of capillary loops, diffuse proliferative glomerulonephritis 2. proteinuria
52
Q

what are the features of acute and chronic lupus serositis?

A
  1. exudation of fibrin 2. proliferation of fibrous tissue, thickened membranes and adhesions
53
Q

what are the features of acute and chronic lung involvement with lupus?

A
  1. acute - pneumonitis with alveolar damage, edema, hemorrhage 2. chronic - interstitial and vascular fibrosis leads to pulmonary fibrosis and pulmonary hypertension
54
Q

what are the features of chronic discoid lupus?

A

variety of skin lesions without systemic features, +ANAs, anti dsDNA rare

55
Q

what are the features of subacute cutaneous lupus?

A

diffuse, superficial, nonscarring photosensitive lesions, mild systemic disease

56
Q

what is the pathogeneis of sjogren syndrome?

A
  1. initiation - CD4 T cells against glandular epithelial self antigen 2. systemic B cell hyperactivity - ANAs and RF (75%) 3. specific ANAs to RNP SS-A (Ro) and SS-B (La)
57
Q

what is the morphology of sjogren syndrome?

A
  1. T, B, plasma cells infiltrate ducts and vessels in target gland 2. follicle formation with germinal center 3. ductal epithelial hyperplasia - obstruction 4. acinar atrophy, fibrosis, fat replacement of parenchyma
58
Q

patients with sjogren syndrome are at 40% risk of what cancer?

A

B cell lymphoma

59
Q

what is the clinical course of sjogren syndrome?

A

systemic vasculitis with extraglandular involvement of kidneys, lungs, skin, CNS, muscle

60
Q

what are the features of systemic sclerosis?

A

chronic inflammation, destruction of small vessels and progressive tissue fibrosis

61
Q

what is the pathogenesis of systemic sclerosis?

A
  1. activation of CD4 T cells to secrete cytokines that promote fibrinogenesis (TGF beta) 2. microvascular damage 3. activation of B cells to produce ANAs (anti DNA topo I, anti centromere)
62
Q

what is CREST syndrome?

A
  1. limited variant of systemic sclerosis 2. calcinosis, raynaud’s phenomenon (blood vessel spasm in response to heat / cold), esophageal dysmotility, sclerodactyly, telangiectasia (dilation of capillaries - red marks on skin) 3. limited skin involvement of face, forearms, fingers 4. late visceral involvement 5. 90% anti centromere
63
Q

what are the GI changes in systemic sclerosis?

A
  1. esophagus - collagenization and fibrosis of muscularis - esophageal dysmotility, LES dysfunction - reflux 2. small intestine - mucosal thinning, loss of villi, submucosal fibrosis - malabsorption
64
Q

what are the early and late stages of musculoskeletal changes in systemic sclerosis?

A
  1. early - nondestructive hyperplasia and inflammation of synovium 2. late - fibrosis of synovial and peri-articular connective tissue
65
Q

what are the kidney changes associated with systemic sclerosis?

A

proliferation of intimal cells and deposition of collagenous or mucinous material - thickening of interlobular arteries

66
Q

what are the pulmonary changes associated with systemic sclerosis?

A

interstitial pneumonitis, alveolar fibrosis, pulmonary hypertension from endothelial dysfunction (cor pulmonale - right heart hypertrophy / failure)

67
Q

what are the heart changes associated with systemic sclerosis?

A

peridcarditis with effusion, perivascular lymphoid infiltrates, arteriolar thickening, interstitial fibrosis - restrictive cardiomyopathy

68
Q

what is the pathogenesis of RA?

A
  1. mediated by activated CD4 T cells - production of cytokines and activation of macrophages and B cells 2. IgM targets IgG (RF) at the Fc portion (type III) 3. antibodies against citrullinated peptides or T cell response against peptides
69
Q

what occurs in the joint space during RA?

A

activated macrophages, lymphocytes, neutrophils release degradative enzymes and inflammation (IL-1, TNF)

70
Q

what is a pannus?

A

granulation tissue, synovial and inflammatory cells, fibrous CT

71
Q

RA nodules contain what type of tissue?

A

fibrous tissue with palisading macrophages and central necrosis

72
Q

what is the cause of death with RA?

A

disease complications of amyloidosis, vasculitis, drug therapy (bleeding, infection)

73
Q

what is mixed connective tissue disease?

A
  1. overlapping features of SLE and systemic sclerosis 2. specific antibody to RNP 3. minimal renal disease

Year 1 Pathology (25 decks)

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