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Pathology > Immunopathology > Flashcards

Immunopathology Flashcards

1
Q

What is a type I hypersensitivity?

A

Immediate injury caused by Th2 cells, IgE antibodies, and mast cells

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2
Q

What is a type II hypersensitivity?

A

Antibody mediated disorder, secreted IgG and IgM antibodies attack self cells

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3
Q

What is a type III hypersensitivity?

A

Immune complex (IgG and IgM) mediated disorder

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4
Q

What is a type IV hypersensitivity?

A

Sensitized T lymphocytes Th1 and Th17 cells (CTLs) cause injury

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5
Q

Myasthenia gravis is what type of hypersensitivity?

A

Type II

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6
Q

Graves disease is what type of hypersensitivity?

A

Type II

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7
Q

SLE is what type of hypersensitivity?

A

Type III

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8
Q

Poststreptococcal glomerulonephritis is what type of hypersensitivity?

A

type III

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9
Q

Th1 cells secrete what cytokines to induce T cell differentiation?

A

IFN-gamma

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10
Q

Why is the time important in organ transplant?

A

Reperfusion injury

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11
Q

What is an isograft?

A

identical twin graft

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12
Q

What is an allograft?

A

Same species graft

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13
Q

What is a xenograft?

A

Different species graft

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14
Q

What is the direct mechanism of transplant rejection?

A

Antigen-presenting cells in the graft activated class II MHC

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15
Q

What is the indirect mechanism of graft rejection?

A

Recipient’s APCs stimulate T cells

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16
Q

What are the two types of cells that are mainly affected in graft rejection?

A

Vascular and epithelial cells

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17
Q

What are the two humoral mechanisms of hypersensitivity?

A

Ab bind to HLA molecules in graft endothelium

Ag-Ab complexes form in circulation (type iII)

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18
Q

What are the three patterns of rejection? What is the timeframe for each?

A

Hyperacute (minutes)
Acute (weeks to months)
Chronic (years)

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19
Q

What can sensitize a patient to a hyperacute rxn?

A

Prior transplant

Prego

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20
Q

What causes the increased sensitivity in hyperacute rejection?

A

Preformed Abs against Ag in allografts

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21
Q

What are the pathological changes seen in hyperacute rxns?

A

Fibrinoid necrosis and thrombosis

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22
Q

Acute rejection is mediated by what?

A

Cellular, humoral, or combined mechanisms

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23
Q

What are the histologic characteristics of acute rejection?

A

Lymphocytic infiltration

Tubular necrosis

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24
Q

What do CD8 cells do in acute cellular rejection?

A

Lymphocytes infiltrate tubular and vascular BM causing tubular damage and endothelitis

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25
Q

What do CD4 cells do in acute cellular rejection?

A

help cells produce cytokines, causing interstitial inflammation

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26
Q

What are the two morphological patterns if acute humoral rejection?

A

Necrotizing vasculitis

Initimal thickening d/t accumulation of fibroblasts, foamy macrophages

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27
Q

What are the two possible mechanisms behind chronic rejections?

A

Humoral injury = proliferative vascular lesions

Cellular injury = cytokine induces proliferation of vascular smooth muscle

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28
Q

Is there lesser or higher requirement for immunosuppression for livers?

A

Lesser

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29
Q

What is the triad of features of acute liver rejection?

A
  1. Portal tract inflammation
  2. Bile duct epithelial damage
  3. Endotheliitis of portal vein and hepatic artery branches
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30
Q

What cells are involved in acute liver rejection?

A

Mixed inflammatory cells infiltration with eosinophils

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31
Q

What happens histologically in chronic liver rejection?

A

Progressive disappearance of bile ducts d/t direct immunologic destruction or loss of blood supply

32
Q

What causes the ischemic changes seen in chronic liver rejection?

A

Obliterative arterities from proliferation of intimal layer

33
Q

What is the end result of chronic liver rejection? (2)

A

Portal and hepatic fibrosis

34
Q

What is the major complication with heart transplantation?

A

Diffuse intimal proliferation –> CAD

35
Q

What happens with heart transplant rejection?

A

Cellular rejection with interstitial and perivascular T cell infiltrates

36
Q

What does heart transplant rejection resemble histologically?

A

Myocarditis

37
Q

What are the histological characteristics of acute cardiac rejection?

A

Tons of lymphocytes, with destroyed myocytes

38
Q

What is graft arteriopathy?

A

Vascular proliferation by immune cell lead constriction of a vessel via hypertrophy

39
Q

What are the infections that cause malignancies in Cardiac transplants? What causes this?

A

EPV B cells lymphoma from the immunosuppression

40
Q

What does transplantation of hematopoietic cells treat? (3)

A
  1. Hematological disorders
  2. Non-hematologic malignancies
  3. Immunodeficiency
41
Q

What is GVHD?

A

Donor T cells recognize the host HLA antigens as foreign, and mount a type IV reaction against graft elements and tissues

42
Q

What are the usual targets of GVHD?

A

Epithelial skin
GIT
Liver

43
Q

Asthma is what type of hypersensitivity rxn?

A

Type I

44
Q

Bronchial asthma is what type of hypersensitivity rxn?

A

Type I

45
Q

Allergic rhinitis is what type of hypersensitivity rxn?

A

Type I

46
Q

Food allergies are what type of hypersensitivity rxn?

A

Type I

47
Q

What portion of immunoglobulins bind to phagocytes?

A

Fc bit

48
Q

What are the three ways in which antibodies in type II hypersensitivity reactions cause cell damage?

A

Phagocytosis
Complement activation
ROS production

49
Q

What are the antigen involved in SLE?

A

Nuclear antigens

50
Q

What are the major clinical manifestations of SLE?

A

Nephritis, skin lesions, arthritis

51
Q

What is the MOA of type IV hypersensitivity?

A

APCs present tissue antigen to CD8 (or CD4) cells, causing activation of T cells

52
Q

What is the specificity of T cells in RA?

A

Collagen/circulating self proteins

53
Q

What is the principal MOA of RA?

A

Inflammation mediated by Th17 cytokine releasing

54
Q

What are the clinical manifestations of RA?

A

Chronic arthritis with inflammation, destruction of articular cartilage

55
Q

What is the cell mediated cytotoxicity in type IV hypersensitivity rxns?

A

host cytotoxic lymphocytes destroy graft parenchymal cells,

56
Q

What is the MOA of delayed type hypersensitivity?

A

Helper lymphocytes secrete cytokines, causing recruitment of PMNs

57
Q

What do CD8 cells stimulate? CD4?

A 
CD8 = CTLs
CD4 = Activated macrophages, B cells
58
Q

What do CD4 cells secrete to stimulate macrophage action/activation?

A

IFN-gamma

59
Q

What are the two main types of hypersensitivity reactions involved in graft rejection?

A

Type II

Type III

60
Q

How do you avoid hyperacute rejection?

A

Cross-matching recipient MHC with donor lymphocytes

61
Q

What are the gross characteristics of graft rejection in a kidney?

A

Areas of infarct/hyperemia

62
Q

What are the histological changes seen in acute rejection?

A

Fibrinoid necrosis and thrombosis

63
Q

What type of hypersensitivity are involved in acute rejection?

A

II, III, and IV

64
Q

What are the gross characteristics of acute rejection?

A

Hyperemia

65
Q

What is the MOA of acute cellular rejection?

A

CD8 lymphocytes infiltrate BMs

CD4 cells produce cytokintes

66
Q

What are the cells types involved in acute cellular rejection? (4)

A

T cells
B cells
Macrophages
lymphocytes

67
Q

What are the two morphological patterns seen in acute humoral rejection?

A
  1. Necrotizing vasculitis

2. Intimal thickening d/t accumulation of cells

68
Q

What are the two possible mechanisms of chronic rejection?

A

Humoral injury

Cellular injury

69
Q

What is the morphology seen in chronic rejection?

A

Vascular changes
Interstitial fibrosis
Chronic inflammation

70
Q

Which types of hypersensitivity rxns occur with heart transplants?

A

Type II, III, IV

71
Q

What is the MOA of cyclosporin? (what does it block, and what is this needed for)?

A

Blocks nuclear factor of activated T cells (NFAT), which is ncessary for IL-2

72
Q

What is the MOA of steroids in immunosuppressive therapy?

A

Suppress macrophage activity

73
Q

What is the triad of symptoms seen in acute GVHD?

A

Dermatitis
Enteritis
Hepatitis

74
Q

What are the symptoms of chronic GVHD? (3)

A

FIbrosis of the dermis
Esophageal stricture
Liver/bile damage

75
Q

What is the MOA of primary graft failure?

A

Host natural killer cells or T cells survive irradiation

Pathology (32 decks)

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