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Immunopathology Flashcards

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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
What do CD4 cells do in acute cellular rejection?
help cells produce cytokines, causing interstitial inflammation
26
What are the two morphological patterns if acute humoral rejection?
Necrotizing vasculitis | Initimal thickening d/t accumulation of fibroblasts, foamy macrophages
27
What are the two possible mechanisms behind chronic rejections?
Humoral injury = proliferative vascular lesions | Cellular injury = cytokine induces proliferation of vascular smooth muscle
28
Is there lesser or higher requirement for immunosuppression for livers?
Lesser
29
What is the triad of features of acute liver rejection?
1. Portal tract inflammation 2. Bile duct epithelial damage 3. Endotheliitis of portal vein and hepatic artery branches
30
What cells are involved in acute liver rejection?
Mixed inflammatory cells infiltration with eosinophils
31
What happens histologically in chronic liver rejection?
Progressive disappearance of bile ducts d/t direct immunologic destruction or loss of blood supply
32
What causes the ischemic changes seen in chronic liver rejection?
Obliterative arterities from proliferation of intimal layer
33
What is the end result of chronic liver rejection? (2)
Portal and hepatic fibrosis
34
What is the major complication with heart transplantation?
Diffuse intimal proliferation --> CAD
35
What happens with heart transplant rejection?
Cellular rejection with interstitial and perivascular T cell infiltrates
36
What does heart transplant rejection resemble histologically?
Myocarditis
37
What are the histological characteristics of acute cardiac rejection?
Tons of lymphocytes, with destroyed myocytes
38
What is graft arteriopathy?
Vascular proliferation by immune cell lead constriction of a vessel via hypertrophy
39
What are the infections that cause malignancies in Cardiac transplants? What causes this?
EPV B cells lymphoma from the immunosuppression
40
What does transplantation of hematopoietic cells treat? (3)
1. Hematological disorders 2. Non-hematologic malignancies 3. Immunodeficiency
41
What is GVHD?
Donor T cells recognize the host HLA antigens as foreign, and mount a type IV reaction against graft elements and tissues
42
What are the usual targets of GVHD?
Epithelial skin GIT Liver
43
Asthma is what type of hypersensitivity rxn?
Type I
44
Bronchial asthma is what type of hypersensitivity rxn?
Type I
45
Allergic rhinitis is what type of hypersensitivity rxn?
Type I
46
Food allergies are what type of hypersensitivity rxn?
Type I
47
What portion of immunoglobulins bind to phagocytes?
Fc bit
48
What are the three ways in which antibodies in type II hypersensitivity reactions cause cell damage?
Phagocytosis Complement activation ROS production
49
What are the antigen involved in SLE?
Nuclear antigens
50
What are the major clinical manifestations of SLE?
Nephritis, skin lesions, arthritis
51
What is the MOA of type IV hypersensitivity?
APCs present tissue antigen to CD8 (or CD4) cells, causing activation of T cells
52
What is the specificity of T cells in RA?
Collagen/circulating self proteins
53
What is the principal MOA of RA?
Inflammation mediated by Th17 cytokine releasing
54
What are the clinical manifestations of RA?
Chronic arthritis with inflammation, destruction of articular cartilage
55
What is the cell mediated cytotoxicity in type IV hypersensitivity rxns?
host cytotoxic lymphocytes destroy graft parenchymal cells,
56
What is the MOA of delayed type hypersensitivity?
Helper lymphocytes secrete cytokines, causing recruitment of PMNs
57
What do CD8 cells stimulate? CD4?
``` CD8 = CTLs CD4 = Activated macrophages, B cells ```
58
What do CD4 cells secrete to stimulate macrophage action/activation?
IFN-gamma
59
What are the two main types of hypersensitivity reactions involved in graft rejection?
Type II | Type III
60
How do you avoid hyperacute rejection?
Cross-matching recipient MHC with donor lymphocytes
61
What are the gross characteristics of graft rejection in a kidney?
Areas of infarct/hyperemia
62
What are the histological changes seen in acute rejection?
Fibrinoid necrosis and thrombosis
63
What type of hypersensitivity are involved in acute rejection?
II, III, and IV
64
What are the gross characteristics of acute rejection?
Hyperemia
65
What is the MOA of acute cellular rejection?
CD8 lymphocytes infiltrate BMs CD4 cells produce cytokintes
66
What are the cells types involved in acute cellular rejection? (4)
T cells B cells Macrophages **lymphocytes**
67
What are the two morphological patterns seen in acute humoral rejection?
1. Necrotizing vasculitis | 2. Intimal thickening d/t accumulation of cells
68
What are the two possible mechanisms of chronic rejection?
Humoral injury | Cellular injury
69
What is the morphology seen in chronic rejection?
Vascular changes Interstitial fibrosis Chronic inflammation
70
Which types of hypersensitivity rxns occur with heart transplants?
Type II, III, IV
71
What is the MOA of cyclosporin? (what does it block, and what is this needed for)?
Blocks nuclear factor of activated T cells (NFAT), which is ncessary for IL-2
72
What is the MOA of steroids in immunosuppressive therapy?
Suppress macrophage activity
73
What is the triad of symptoms seen in acute GVHD?
Dermatitis Enteritis Hepatitis
74
What are the symptoms of chronic GVHD? (3)
FIbrosis of the dermis Esophageal stricture Liver/bile damage
75
What is the MOA of primary graft failure?
Host natural killer cells or T cells survive irradiation

Pathology (32 decks)

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