Year 1 Pathology > Immunopathology I > Flashcards

Immunopathology I Flashcards

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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
what is the cause of GVHD?
donor T cells recognize host HLAs as foreign and mount a type IV (DTH or CTL) reaction against graft elements and tissues
26
what is the crucial component of GVHD?
activation of CD4 cells
27
what characterizes chronic GVHD?
generalized fibrosis of dermis and skin, GI mucosa, and bile ducts
28
what characterizes acute GVHD?
epithelial necrosis in target organs - skin (dermatitis), GI (enteritis), liver (hepatitis, bile duct necrosis, jaundice)
29
how is the diagnosis of AI disease made when autoantibodies are found in healthy individuals and may be formed after tissue damage?
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
30
what are the possible mechanisms of tolerance breakdown?
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
what characterizes failure of T cell anergy?
expression of B7 co stimulatory molecule leads to autoreactivity
32
what characterizes failure of activation induced cell death?
failure of Fas-FasL system - peripheral persistence and proliferation of auto-reactive cells
33
what characterizes failure of T cell mediated suppression?
failure of regulatory T cells to suppress proliferation of other T cells encourages autoreactivity
34
what characterizes molecular mimicry or cross reactivity?
self Ag sharing an antigenic determinant with microbial Ag
35
what characterizes polyclonal lymphocyte activation?
activation of B cells or CD4 cells may induce immune response leading to autoreactivity
36
what characterizes exposure of cryptic antigenic determinants?
hidden epitopes are exposed, leading to self reactivity
37
what is the immune response in SLE?
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
in SLE autoantibodies are directed against which cell components?
antinuclear antibodies (ANAs) - reflect loss of tolerance and act as mediators of tissue injury
39
ANAs are directed against what categories of nuclear antigen?
1. DNA 2. histones 3. proteins bound to RNA 4. nucleolar antigen
40
homogenous ANA staining indicates binding to what antigen? which disease is implicated?
1. chromatin, dsDNA, histone 2. drug induced SLE
41
rim ANA staining indicates binding to what antigen? which disease is implicated?
1. dsDNA 2. SLE
42
speckled ANA staining indicates binding to what antigen? which disease is implicated?
1. histones and ribonucleoproteins 2. SLE, SS, Sjogren
43
nucleolar ANA staining indicates binding to what antigen? which disease is implicated?
1. nucleolar RNA 2. SLE, SS, CREST
44
anti-histone ANAs are indicative of what type of AI disease?
drug induced lupus
45
anti-RNP ANAs are indicative of what type of AI disease?
Sjogren syndrome
46
anti-dsDNA ANAs are indicative of what type of AI disease?
SLE
47
type II SLE mechanism involves what type of lesion? type III?
1. type II - RBC 2. type III - visceral lesions
48
what occurs during lupus vascular changes?
circulating immune complexes deposit in vascular beds, activate complement, type III reaction
49
what are the histologic features of acute and chronic lupus vascular damage?
1. acute - vasculitis with fibrinoid necrosis of arteries / arterioles in any tissue 2. layered fibrous thickening (onion skinning)
50
what is the mechanism of kidney injury during lupus?
immune complex deposition in glomeruli, basement membranes, larger blood vessels, thrbombosis due to antiphospholipid antibody
51
what is the result of lupus nephritis?
1. thickening of membranous part of capillary loops, diffuse proliferative glomerulonephritis 2. proteinuria
52
what are the features of acute and chronic lupus serositis?
1. exudation of fibrin 2. proliferation of fibrous tissue, thickened membranes and adhesions
53
what are the features of acute and chronic lung involvement with lupus?
1. acute - pneumonitis with alveolar damage, edema, hemorrhage 2. chronic - interstitial and vascular fibrosis leads to pulmonary fibrosis and pulmonary hypertension
54
what are the features of chronic discoid lupus?
variety of skin lesions without systemic features, +ANAs, anti dsDNA rare
55
what are the features of subacute cutaneous lupus?
diffuse, superficial, nonscarring photosensitive lesions, mild systemic disease
56
what is the pathogeneis of sjogren syndrome?
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
what is the morphology of sjogren syndrome?
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
patients with sjogren syndrome are at 40% risk of what cancer?
B cell lymphoma
59
what is the clinical course of sjogren syndrome?
systemic vasculitis with extraglandular involvement of kidneys, lungs, skin, CNS, muscle
60
what are the features of systemic sclerosis?
chronic inflammation, destruction of small vessels and progressive tissue fibrosis
61
what is the pathogenesis of systemic sclerosis?
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
what is CREST syndrome?
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
what are the GI changes in systemic sclerosis?
1. esophagus - collagenization and fibrosis of muscularis - esophageal dysmotility, LES dysfunction - reflux 2. small intestine - mucosal thinning, loss of villi, submucosal fibrosis - malabsorption
64
what are the early and late stages of musculoskeletal changes in systemic sclerosis?
1. early - nondestructive hyperplasia and inflammation of synovium 2. late - fibrosis of synovial and peri-articular connective tissue
65
what are the kidney changes associated with systemic sclerosis?
proliferation of intimal cells and deposition of collagenous or mucinous material - thickening of interlobular arteries
66
what are the pulmonary changes associated with systemic sclerosis?
interstitial pneumonitis, alveolar fibrosis, pulmonary hypertension from endothelial dysfunction (cor pulmonale - right heart hypertrophy / failure)
67
what are the heart changes associated with systemic sclerosis?
peridcarditis with effusion, perivascular lymphoid infiltrates, arteriolar thickening, interstitial fibrosis - restrictive cardiomyopathy
68
what is the pathogenesis of RA?
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
what occurs in the joint space during RA?
activated macrophages, lymphocytes, neutrophils release degradative enzymes and inflammation (IL-1, TNF)
70
what is a pannus?
granulation tissue, synovial and inflammatory cells, fibrous CT
71
RA nodules contain what type of tissue?
fibrous tissue with palisading macrophages and central necrosis
72
what is the cause of death with RA?
disease complications of amyloidosis, vasculitis, drug therapy (bleeding, infection)
73
what is mixed connective tissue disease?
1. overlapping features of SLE and systemic sclerosis 2. specific antibody to RNP 3. minimal renal disease
Year 1 Pathology
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