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Path Gen 1 > Immunopathology > Flashcards

Immunopathology Flashcards

1
Q

hypersensitivity reaction –> antibodies to antigens on cells or tissues

A

II

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2
Q

aka ADCC –> tissue damage/lysis from HS II

A

antibody dependent cell-mediated cytotoxicty

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3
Q

mechanism for tissue destruction in hemolytic anemia HS II reaction

A

enhanced phagocytosis (hemolysis)

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4
Q

goodpasture’s syndrome has Ab to this; what does this cause?

A

type IV collagen BM glomerular/pulmonary capillary; glomerulonephritis and pulmonary hemorrhage

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5
Q

treatment for HS II reaction

A

immunosuppression, plasmapheresis, prevention (like Rhogam)

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6
Q

HS caused by immune complexes of IgG and soluble antigen OR complexing Ab with trapped antigen

A

III

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7
Q

this is responsible for type III HS inflammation

A

complement activation and PMNs

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8
Q

biggest cause for decreased complement levels

A

immune complex formation

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9
Q

these are two biggest results from HS III immune complexes

A

decreased complement and PMN mediated damage

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10
Q

places where complexes deposit

A

blood vessels, glomeruli, serosal linings (pleura, pericardium, synovium)

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11
Q

typical time it takes to make multivalent Ab for the first time

A

7-10 days

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12
Q

immune complex mediated skin reaction

A

Arthus reaction

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13
Q

preferred sites of immune complex deposition –> causes vasculitis, serositis, arthritis, GN

A

renal glomeruli, joints, skin, heart, serosal surfaces, small blood vessels

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14
Q

occurs as a result of injection of foreign proteins resulting in antibody formation –> can occur any time person injected with antigen with antibodies present

A

serum sickness

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15
Q

this causes arthus reaction (localized skin response)

A

injection soluble antigen w/ pre-existing IgG Ab

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16
Q

HS that is cell-mediated/delayed-type

A

IV

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17
Q

these mediate type IV HS

A

CD4/CD8 (Ag-specfic T cells) and cytokines

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18
Q

pathogenesis of type IV HS

A

TH1 activation, cytokine release (monocyte/lymphocyte recruitment), CD8 and MP tissue destruction

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19
Q

type of inflammation seen in type IV HS

A

mononuclear

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20
Q

these mediate local inflammation of type IV HS

A

PGs and cytokines

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21
Q

oil from poison ivy complexes with proteins and activates these, which then present via MHC II to CD4

A

dendritic cells

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22
Q

when you see this reaction on skin, know it is cell mediated

A

vesicles

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23
Q

type IV HS skin test initiates over this time period

A

24-48 hours

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24
Q

production of lymphokines in type IV HS skin test causes this to happen

A

activate lymphocytes/MP/fibroblasts, cause local lymphocytic inflammation/infiltrate

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25
Q

antigen presentation for antigens that cross-react with body

A

MHC I

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26
Q

alleles for MHC class I

A

HLA A,B

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27
Q

alleles for MHC class II

A

HLA DR, DQ

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28
Q

normal ESR (although increases with age)

A

15 mm/hr

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29
Q

normal CRP level

A

10 mg/L

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30
Q

usually from expansion of tumor –> only one type of Ig made by clonal expansion (1 heavy 1 light chain)

A

monoclonal

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31
Q

many types of Ig made –> nonspecific activation of B cells (infections, vaccinations, SLE, mono)

A

polyclonal

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32
Q

normal immune response –> few clones of lymphocytes responding to specific antigen (MS, guillain barre)

A

oligoclonal

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33
Q

acute infections are measured with this titer; what titer are chronic infections measured by?

A

IgM; IgG

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34
Q

normal differential for total PMNs (in total wBC)

A

65-80%

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35
Q

normal differential for lymphocytes (in total WBC)

A

15-40%

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36
Q

approximate number of lymhocytes per microliter

A

2000

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37
Q

two ways type II HS reaction is mediated -> can cause tissue damage/cell lysis, activation/blockage of specific receptors

A

complement mediated or ADCC

38
Q

what kind of HS reaction: autoimmune hemolytic anemia, Goodpasture’s, Grave’s disease, Myasthenia Gravis

A

II

39
Q

what is autoimmune reaction in Grave’s disease?

A

Ab against TSH receptor (II)

40
Q

what is autoimmune reaction in myasthenia gravis?

A

Ab to ACH receptor at neuromuscular junction (II)

41
Q

this complement protein serves as chemotactic for inflammatory cells -> can cause bystander injury

A

C5a

42
Q

what mediates ADCC? what specific enzymes/cytokines are involved?

A

Fc receptors NK cells; IFN-g, granzymes, perforins

43
Q

Ab-mediated activation of disruption of intracellular adhesions in epithelium

A

pemphigus vulgaris

44
Q

anti-platelet antibodies

A

ITP, TTP

45
Q

what causes destruction of cells in type II hematology sensitivities?

A

Ab-mediated phagocytosis, complement lysis (mostly opsonization)

46
Q

this tests for autoimmune hemolytic anemia -> add anti-Ig antibody and cause agglutination of RBC with anti-RBC antibody

A

Coomb’s test

47
Q

test for type II hypersensitivity -> looks for presence of antibodies in serum

A

indirect Coomb’s

48
Q

what makes up immune complexes in III HS?

A

IgG and soluble antigen, Ab complexing with trapped antigen

49
Q

what is responsible for inflammation in type III HS?

A

complement activation and PMN

50
Q

once this is reached there is deposition of insoluble lattices in tissue

A

point of equivalence

51
Q

where do soluble immune complexes typically deposit?

A

vascular walls, serosal linings (pleura pericardium, synovium), glomeruli

52
Q

3 phases of type III HS

A

formation Ab-Ag complex, deposition in tissues, local tissue destruction (from complement induced cell infiltration/activation)

53
Q

what causes local tissue destruction in type III HS?

A

complement induced cell infiltration/activation

54
Q

where do antigens typically become fixed in type III HS (soluble antigens, drugs, infectious antigens)?

A

blood vessels and glomeruli

55
Q

these both must be present for immune complex to form

A

multivalent antigen and antibody

56
Q

factors that affect the deposition of immune complexes in tissue

A

size, localization Ag, vascular permeability (& concurrent inflammation), mechanical factor

57
Q

hallmark morphological features of type III HS

A

complement consumption, acute inflammation/infiltration of leukocytes, deposition of immune complexes (demonstrated by immunofluoresence)

58
Q

morphological features of vessels damaged by immune complexes

A

necrotizing fasciitis, fibrinoid necrosis, neutrophilic infiltrate

59
Q

morphological features of kidney damage (glomerular damage) caused by immune complex deposition

A

immune deposits (by EM and immunofluorescence), hypercellular proliferation, neutrophilic and monocytic infiltration

60
Q

cell types involved in type III HS

A

PMN, MP, platelets

61
Q

these are released from tissues damaged by immune complexes

A

release PGs, vasodilator peptides, NO, chemotactic substances, lysosomal enzymes/proteases, free oxygen radicals

62
Q

this occurs from proliferation of cells due to immune complex deposition

A

tissue thickening and epithelial proliferation in glomeruli

63
Q

how long does it take for serum sickness to occur after foreign protein injection?

A

7-10 days after initial, 1-3 after subsequent

64
Q

symptoms of serum sickness

A

fever, arthralgia, rash (vasculitis)

65
Q

what causes arthus reaction?

A

injection soluble antigen in patient with pre-existing IgG

66
Q

what causes vasculitis associated with arthus reaction?

A

immune complex deposition in dermal blood vessel, activation of complement and recruitment PMNs

67
Q

morphological features of arthus reaction vasculitis

A

fibrin necrosis, PMNs, edema, hemorrhage

68
Q

what are the three main things that type II HS causes?

A

tissue lysis, phagocytosis, interference with receptor function

69
Q

what mediates type IV sensitivity reaction?

A

Ag specific T cells and cytokines

70
Q

what kind of ells are recruited when cytokines are released in type IV reaction?

A

monocytes and lymphocytes

71
Q

these cells are responsible for tissue injury in type IV reaction

A

CD8 and activated MP

72
Q

these are the result of cytolytic action of CD4 cells in type IV reaction

A

vesicles

73
Q

this amplifies the type IV response (after CD8 activation via MHC I)

A

CD4 and lymphokine production

74
Q

two mechanisms for cell lysis in type IV reaction

A

perforins and granzymes (within CTL granules), fas-ligand mediated apoptosis

75
Q

this is responsible for epithelioid cell formation when it acts on MP -> secreted by Ag-specific CD4 cells

A

IFN-g

76
Q

this is responsible for fibrosis in type IV reaction

A

TGF-b

77
Q

what do lymphokines cause in type IV HS?

A

activate lymphocytes, MP, FB, cause local lymphocytic inflammation/infiltrate

78
Q

this is secreted by MP for activation of CD4 cells -> secreted once persistent Ag activates MP

A

IL-1

79
Q

how does granuloma form?

A

chronically activated MP secretes IL-1 to activate CD4 lymphocytes, which secretes IFN-g to further activate MP/form epithelioid cells/giant cells

80
Q

this cell responds to tissue specific Ag ->stimulates CD8 and Ab formation -> tissue destruction

A

CD4

81
Q

what causes reaction in allergy skin test?

A

Ag-specific IgE degranulation mast cells (release of histamine)

82
Q

reaction seen in positive allergy skin test

A

wheal/flare

83
Q

time it takes for arthus reaction to occur

A

4-12 hours

84
Q

things that mediate type IV skin tests

A

IFN-G, MP cytokines, PGs

85
Q

this causes type IV skin test reaction

A

activation of Ag specific T cells and MP

86
Q

this skin test reaction is transferred by lymphocytes only (others are by serum)

A

type IV

87
Q

aka immediate type HS

A

urticaria

88
Q

domains used to identify B cells

A

CD10, 19, 20, 30 40 (binds CD40L on CD4)

89
Q

markers used for fluorescent labeling of B cells

A

CD 19, 20

90
Q

marker used for fluorescent labeling of T cells

A

CD 3 (CD4/8 also)

Path Gen 1 (6 decks)

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