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Path Gen 1 > Immunopathology > Flashcards

Immunopathology Flashcards

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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
antigen presentation for antigens that cross-react with body
MHC I
26
alleles for MHC class I
HLA A,B
27
alleles for MHC class II
HLA DR, DQ
28
normal ESR (although increases with age)
15 mm/hr
29
normal CRP level
10 mg/L
30
usually from expansion of tumor --> only one type of Ig made by clonal expansion (1 heavy 1 light chain)
monoclonal
31
many types of Ig made --> nonspecific activation of B cells (infections, vaccinations, SLE, mono)
polyclonal
32
normal immune response --> few clones of lymphocytes responding to specific antigen (*MS, guillain barre*)
oligoclonal
33
acute infections are measured with this titer; what titer are chronic infections measured by?
IgM; IgG
34
normal differential for total PMNs (in total wBC)
65-80%
35
normal differential for lymphocytes (in total WBC)
15-40%
36
approximate number of lymhocytes per microliter
2000
37
two ways type II HS reaction is mediated -> can cause tissue damage/cell lysis, activation/blockage of specific receptors
complement mediated or ADCC
38
what kind of HS reaction: autoimmune hemolytic anemia, Goodpasture's, Grave's disease, Myasthenia Gravis
II
39
what is autoimmune reaction in Grave's disease?
Ab against TSH receptor (II)
40
what is autoimmune reaction in myasthenia gravis?
Ab to ACH receptor at neuromuscular junction (II)
41
this complement protein serves as chemotactic for inflammatory cells -> can cause bystander injury
C5a
42
what mediates ADCC? what specific enzymes/cytokines are involved?
Fc receptors NK cells; IFN-g, granzymes, perforins
43
Ab-mediated activation of disruption of intracellular adhesions in epithelium
pemphigus vulgaris
44
anti-platelet antibodies
ITP, TTP
45
what causes destruction of cells in type II hematology sensitivities?
Ab-mediated phagocytosis, complement lysis (mostly opsonization)
46
this tests for autoimmune hemolytic anemia -> add anti-Ig antibody and cause agglutination of RBC with anti-RBC antibody
Coomb's test
47
test for type II hypersensitivity -> looks for presence of antibodies in serum
indirect Coomb's
48
what makes up immune complexes in III HS?
IgG and soluble antigen, Ab complexing with trapped antigen
49
what is responsible for inflammation in type III HS?
complement activation and PMN
50
once this is reached there is deposition of insoluble lattices in tissue
point of equivalence
51
where do soluble immune complexes typically deposit?
vascular walls, serosal linings (pleura pericardium, synovium), glomeruli
52
3 phases of type III HS
formation Ab-Ag complex, deposition in tissues, local tissue destruction (from complement induced cell infiltration/activation)
53
what causes local tissue destruction in type III HS?
complement induced cell infiltration/activation
54
where do antigens typically become fixed in type III HS (soluble antigens, drugs, infectious antigens)?
blood vessels and glomeruli
55
these both must be present for immune complex to form
multivalent antigen and antibody
56
factors that affect the deposition of immune complexes in tissue
size, localization Ag, vascular permeability (& concurrent inflammation), mechanical factor
57
hallmark morphological features of type III HS
complement consumption, acute inflammation/infiltration of leukocytes, deposition of immune complexes (demonstrated by immunofluoresence)
58
morphological features of vessels damaged by immune complexes
necrotizing fasciitis, fibrinoid necrosis, neutrophilic infiltrate
59
morphological features of kidney damage (glomerular damage) caused by immune complex deposition
immune deposits (by EM and immunofluorescence), hypercellular proliferation, neutrophilic and monocytic infiltration
60
cell types involved in type III HS
PMN, MP, platelets
61
these are released from tissues damaged by immune complexes
release PGs, vasodilator peptides, NO, chemotactic substances, lysosomal enzymes/proteases, free oxygen radicals
62
this occurs from proliferation of cells due to immune complex deposition
tissue thickening and epithelial proliferation in glomeruli
63
how long does it take for serum sickness to occur after foreign protein injection?
7-10 days after initial, 1-3 after subsequent
64
symptoms of serum sickness
fever, arthralgia, rash (vasculitis)
65
what causes arthus reaction?
injection soluble antigen in patient with pre-existing IgG
66
what causes vasculitis associated with arthus reaction?
immune complex deposition in dermal blood vessel, activation of complement and recruitment PMNs
67
morphological features of arthus reaction vasculitis
fibrin necrosis, PMNs, edema, hemorrhage
68
what are the three main things that type II HS causes?
tissue lysis, phagocytosis, interference with receptor function
69
what mediates type IV sensitivity reaction?
Ag specific T cells and cytokines
70
what kind of ells are recruited when cytokines are released in type IV reaction?
monocytes and lymphocytes
71
these cells are responsible for tissue injury in type IV reaction
CD8 and activated MP
72
these are the result of cytolytic action of CD4 cells in type IV reaction
vesicles
73
this amplifies the type IV response (after CD8 activation via MHC I)
CD4 and lymphokine production
74
two mechanisms for cell lysis in type IV reaction
perforins and granzymes (within CTL granules), fas-ligand mediated apoptosis
75
this is responsible for epithelioid cell formation when it acts on MP -> secreted by Ag-specific CD4 cells
IFN-g
76
this is responsible for fibrosis in type IV reaction
TGF-b
77
what do lymphokines cause in type IV HS?
activate lymphocytes, MP, FB, cause local lymphocytic inflammation/infiltrate
78
this is secreted by MP for activation of CD4 cells -> secreted once persistent Ag activates MP
IL-1
79
how does granuloma form?
chronically activated MP secretes IL-1 to activate CD4 lymphocytes, which secretes IFN-g to further activate MP/form epithelioid cells/giant cells
80
this cell responds to tissue specific Ag ->stimulates CD8 and Ab formation -> tissue destruction
CD4
81
what causes reaction in allergy skin test?
Ag-specific IgE degranulation mast cells (release of histamine)
82
reaction seen in positive allergy skin test
wheal/flare
83
time it takes for arthus reaction to occur
4-12 hours
84
things that mediate type IV skin tests
IFN-G, MP cytokines, PGs
85
this causes type IV skin test reaction
activation of Ag specific T cells and MP
86
this skin test reaction is transferred by lymphocytes only (others are by serum)
type IV
87
aka immediate type HS
urticaria
88
domains used to identify B cells
CD10, 19, 20, 30 40 (binds CD40L on CD4)
89
markers used for fluorescent labeling of B cells
CD 19, 20
90
marker used for fluorescent labeling of T cells
CD 3 (CD4/8 also)

Path Gen 1 (6 decks)

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