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chapter 2 Flashcards

1
Q

2 triggers of acute inflammation

A

infection and necrosis

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2
Q

toll like receptors

A

recognized PAMPs and activate innate immune system

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3
Q

example of TLR action

A

CD14 on macrophages recognizes LPS on gram - bacteria, TLR is activated, increased NFkB, activation of immune response genes and increased immune mediators

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4
Q

prostaglandins

A

synthesized by COX

I2, D2, E2- vasodilation, increased permeability

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5
Q

PG that mediates pain and fever

A

PGE2

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6
Q

site of vasodilation

A

arteriole

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7
Q

site of increased permeability

A

post-capillary venule

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8
Q

Leukotrienes

A

synthesized by 5-LPO
B4- attracts neutrophils
C4, D4, E4- mediate vasoconstriction, bronchospasm and increase vascular permeability

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9
Q

3 things that activate mast cells

A

tissue trauma
C3a, C5a
cross linking of IgE

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10
Q

immediate mast cell response

A

release of pre-formed histamine granules

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11
Q

delayed mast cell response

A

synthesis of arachidonic acid metabolites, mainly LTs (long acting substances of anaphylaxis)

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12
Q

C3a, C5a

A

anaphylatoxins- trigger mast cell degranulation

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13
Q

C3b

A

opsonization (PMNs recognize and phagocytose)

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14
Q

Hageman factor

A

Factor XII

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15
Q

what activates hangman factor?

A

exposure to subendothelial collagen

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16
Q

3 actions of hangman factor

A

start coagulation cascade
activate complement
kinin system = increase bradykinin

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17
Q

3 effects of bradykinin

A

pain, vasodilation, increase vascular permeability

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18
Q

2 key pain medications

A

bradykinin and PGE2

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19
Q

fever pathophysiology

A

macrophages release IL-1 and TNF = increased COX activity in perivascular cells of the hypothalamus = increased PGE2 = increased thermo set point

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20
Q

7 steps of neutrophil arrival and function

A 
margination 
rolling
adhesion 
chemotaxis/transmigration
phagocytosis
destruction of phagocytosed material 
resolution
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21
Q

describe rolling

A

selecting speed bumps on the endothelium interact with sialyl lewis X on WBC to slow WBC down

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22
Q

2 types of selectins, sources, mediators

A

P- selectin, WP bodies, histamine triggers

E- selectin, TNFa/IL-1 trigger

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23
Q

describe adhesion

A

ICAM/VCAM on the endothelium firmly attach to WBCs via integrins

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24
Q

what up-regulates intern expression on WBCs? (2)

A

C5a, LTB4

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25
Q

Leukocyte adhesion deficiency

A

autosomal recessive defect of integrins (CD18)

clinical: increased circulating neutrophils, lack of pus formation, delayed umbilical cord separation

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26
Q

4 substances that attract neutrophils

A

C5a, LTB4, IL-8, bacterial products

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27
Q

2 opsonins, function

A

IgG, C3b

signals that enhance phagocytosis by neutrophils

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28
Q

chediak-higashi syndrome

A

autosomal recessive defect in protein trafficking = impaired phagolysosome fusion (neutropenia, increased pyogenic infections, giant granules in leukocytes, defective primary hemostats, albanism, peripheral neuropathy)

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29
Q

describe the process of O2- dependent killing and the enzymes involved

A

O2 –> O2.- by NADPH oxidase
O2.- –> H2O2 by SOD
H2O2 –> HOCl by MPO

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30
Q

chronic granulomatous disease

A

X-linked or autosomal recessive defect in NADPH oxidase

recurrent infection/granuloma formation, especially by catalase+ organisms

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31
Q

test for CGD

A

nitroblue tetrazolium

clear + disease

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32
Q

catalase + organisms (5)

A

staph aureus, Pseudomonas, serratia, nocardia, aspergillus

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33
Q

MPO deficiency

A

unable to generate HOCl, usually asymptomatic, increased risk for candida infections

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34
Q

main killing mechanism of macrophages

A

O2-independent (lysozyme, secondary granules)

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35
Q

macrophages peak in tissue at-

A

2-3 days

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36
Q

4 outcomes dictated by macrophages

A

resolution/healing (IL-10, TBF-b)
Continue acute inflammation (IL-8)
Abscess formation
Chronic inflammation (present antigens to CD4+ t cells)

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37
Q

how are CD4 T cells activated

A

1st signal- bind to MHC II on APC via CD4

2nd signal- bind to B7 on APC via CD28

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38
Q

TH1 CD4 cells secrete (2)

A

IFNg- activate macrophages, promote IgM–IgG switching, promote TH1/decrease TH2
IL-2- activate T cells

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39
Q

TH2 CD4 cells secrete (4)

A

IL 4/13- IgE
IL5- eosinophils, IgA
IL10- decrease TH1

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40
Q

how are CD8 T cells activated

A

1st signal: bind to MHC I on any cell via CD8

2nd signal: IL-2 secreted by TH1 CD4 cells

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41
Q

2 ways that B cells are activated

A

1) bind antigen via surface antibody and being secreting IgM or IgD
2) 1st signal: bind CD4 on CD4 T cells via MHC II
2nd signal: bind CD40L on CD4 via CD40 = CD4 cell secretes IL4, IL5

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42
Q

what is the defining cell of a granuloma

A

epithelioid histiocyte (macrophages)

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43
Q

steps in granuloma formation

A

1) macrophages present antigen to CD4 cells via MHC II
2) macrophages secrete IL-12, promoting TH1 cells
3) TH1 cells scorer IFNg, converting macrophages to epithelioid histiocytes and giant cells

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44
Q

digeorge syndrome (defect, symptoms)

A

22q11.2 micro deletion leads to lack of development of the 3rd and 4th pharyngeal pouches CATCH
Cleft lip, abnormal facies,thymic hypoplasmia, cardiac, hypocalcemia

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45
Q

infections related to T cell deficiency

A

virus and fungus

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46
Q

3 causes of SCID

A

1- ADA deficiency
2- cytokine receptor defects
3- MHC II deficiency

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47
Q

infections related to SCID

A

ALL! fungal, viral, bacterial, protozoan, opportunistic

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48
Q

X-linked agammaglobulinemia (defect/cause)

A

total lack of immunoglobulin due to mutated BTK

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49
Q

X-linked agammaglobulinemia presentation

A

after 6 months with bacterial, enteroviral and giardia infections (after 6 mo because that is when maternal antibodies disappear)

50
Q

common variable immune deficiency

A

low immunoglobulin production

increased risk for bacterial, enteroviral, giardia infections

51
Q

CVID complications (2)

A

increased risk of autoimmune, lymphoma

52
Q

selective IgA deficiency

A

most common Ig deficiency
low IgA
increased risk of mucosal infections

53
Q

IgA deficiency complications (2)

A

celiac disease

anaphylaxis with blood transfusion

54
Q

cause of hyper IgM syndrome

A

defect of CD40 (B cells) or CD40L (CD4 cells) that prohibits class switching = low IgG, IgA, IgE (pyogenic infections, mucosal infections)

55
Q

Wiskott-Aldrich syndrome (gene, triad)

A

X-linked mutation in WASP gene

triad: thrombocytopenia, eczema, recurrent infections

56
Q

C5-9 completment deficiency

A

increased risk of neisseria infections

57
Q

C1 inhibitor deficiency

A

angioedema

58
Q

AIRE

A

transcription factor that is in the nucleus of medullary epithelial cells of the thymus, responsible for presentation of various self antigens during negative selection

59
Q

AIRE mutations (triad)

A

result in development of autoimmunity (triad hypoparathyroidism, adrenal destruction, chronic candida infections)

60
Q

2 outcomes of negative selection in B cells

A

1) receptor editing via re-expression of RAG genes

2) apoptosis (intrinsic pathway(

61
Q

anergy

A

cell tries to become active in the absence of a second signal, shuts down; if it does this repeatedly, then apoptosis via FAS/FASL

62
Q

ALPS

A

autoimmune lymphoproliferative syndrome - due to failure to initiate apoptosis from defect in FAS/FASL

63
Q

regulatory t cell characteristics (3)

A

CD4, CD25, FoxP3

64
Q

CD25

A

IL-2 receptor, participates in activation of regulatory cell

65
Q

FoxP3

A

transcription factor involved in development and maintenance of regulatory T cells

66
Q

actions of regulatory T cells (2)

A

1) block T cell activation via CTLA-4

2) produce anti-inflam cytokines TGFb and IL-10

67
Q

FOXP3 mutations cause

A

disorder of T regs = IPEX- immune dysregulation, polyendocrinopathy, enteropathy, X-linked)

68
Q

why are autoimmune disease more common in women?

A

estrogen may reduce apoptosis of self-reactive B cells

69
Q

HLA with highest assoc with autoimmunity

A

B27

70
Q

epitope spreading

A

spreading of immune response to additional antigens that are exposed to immune cells upon tissue destruction

71
Q

most symptoms in lupus are related to

A

hypersensitivity type III

72
Q

pathogenesis of SLE

A

poor clearing of apoptotic debris leads to activation of self-reactive lymphocytes that produce antibodies against nuclear antigens in the debris

73
Q

complement deficiency as it relates to SLE

A

common in SLE because most symptoms of SLE are due to type III HST (immune complexes), thus decreased complement = decreased removal of immune complexes

74
Q

most common complement deficiency in SLE

A

C2

75
Q

criteria needed for SLE diagnosis

A

4

76
Q

arthritis in SLE

A

peripheral, no deformity

77
Q

most common cause of death in SLE

A

renal disease

78
Q

anemia in SLE

A

type II HST

79
Q

endocarditis in SLE

A

Libman-sacks, small vegetations on both sides of the mitral valve

80
Q

antibodies in SLE (specific and nonspecific)

A

specific- anti-dsDNA, anti-Smith

nonspecific- ANA

81
Q

3 types of antiphospholipid antibodies

A

anticardiolipin
anti-B2- glycoprotein I
lupus anticoagulant

82
Q

anticardiolipin antibody causes false +

A

VDRL/ RPR

83
Q

lupus anticoagulant causes

A

false elevated PTT (actually hypercoaguable)

84
Q

drug induced lupus antibody

A

anti-histone antibody

85
Q

drugs that are implicated in drug-induced lupus (3)

A

procainamide, hydralazine, INH

86
Q

course of drug induced lupus

A

CNS and renal involvement are rare

remission likely with removal of drug

87
Q

sjogren syndrome

A

T cell mediated autoimmune destruction of salivary and lacrimal glands (type IV HST)

88
Q

antibodies in sjogrens syndrome (4)

A

anti-ro (SSA)
anti-La (SSB)
RF
ANA

89
Q

antibodies associated with extra glandular manifestations

A

anti-SSA, SSB

90
Q

antibody associated with neonatal lupus/heart block

A

anti-SSA

91
Q

dx of sjogrens requires

A

biopsy of minor salary glands

92
Q

2/3 criteria for sjogrens

A

dry eyes
ANA + Anti-SSA or SSB or RF
lymphocytic sialadenitis on biopsy of minor salivary glands

93
Q

sjogrens complication

A

marginal lymphoma of salivary glands

94
Q

pathogenesis of systemic sclerosis

A

fibroblast activation leads to collagen deposition = inflammation, vasoconstriction and secretion of growth factors (TGFb, PDGF)

95
Q

CREST syndrome

A

limited systemic sclerosis

Calcinosis, raynauds, esophageal dysmotility, sclerodactyly, telangectasias of skin

96
Q

m/c site affected in diffuse systemic sclerosis

A

GI tract

97
Q

antibody of limited SS

A

anti-centromere

98
Q

antibody of diffuse SS

A

anti-SCL70/topoisomerase I

99
Q

antibodies in MCTD (2)

A

ANA + anti-U1 ribonucleoprotein

100
Q

regeneration

A

replacement of damaged tissue with native tissue

101
Q

repair

A

replacement of damaged tissue with fibrous scar

102
Q

labile tissues -3

A

constant turnover (GI tract, skin, bone marrow)

103
Q

stable tissues- 2 examples

A

in G0 but have capacity to regenerative (liver, proximal renal tubular cells of kidney)

104
Q

permanent tissues-3

A

will not regenerative (skeletal mm, nerve, cardiac mm)

105
Q

main tissue in repair

A

granulation tissue

106
Q

3 elements of granulation tissue

A

type III collagen
capillaries
myofibroblasts

107
Q

what is the fate of type III collagen in scar?

A

eventually removed by collagenase and replaced with type I collagen (zinc cofactor)

108
Q

TGF a

A

epithelial and fibroblast growth

109
Q

TGF b

A

epithelial and fibroblast growth, anti-inflammatory

110
Q

PDGF

A

growth factor for endothelium, smooth mm and fibroblasts

111
Q

Fibroblast growth factor

A

angiogenesis, skeletal development

112
Q

VEGF

A

angiogenesis

113
Q

type I collagen

A

bone, strong

114
Q

type II collagen

A

cartilage

115
Q

type III collagen

A

pilable (blood vessels, granulation tissue, embryonic tissue)

116
Q

type IV collagen

A

basement membrane

117
Q

vitamin c in wound healing

A

cofactor for hydroxylation of proline and lysine

118
Q

copper in wound healing

A

cofactor for cross-linking of lysine and hydroxylysine

119
Q

zince in wound healing

A

cofactor for collagenase, replaces type III with type I collagen

120
Q

hypertrophic scar

A

large, but stays in the boundaries of the original defect

121
Q

keloid

A

excess type III collagen, outside of the boundaries of the original defect

pathoma (7 decks)

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