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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
Leukocyte adhesion deficiency
autosomal recessive defect of integrins (CD18) | clinical: increased circulating neutrophils, lack of pus formation, delayed umbilical cord separation
26
4 substances that attract neutrophils
C5a, LTB4, IL-8, bacterial products
27
2 opsonins, function
IgG, C3b | signals that enhance phagocytosis by neutrophils
28
chediak-higashi syndrome
autosomal recessive defect in protein trafficking = impaired phagolysosome fusion (neutropenia, increased pyogenic infections, giant granules in leukocytes, defective primary hemostats, albanism, peripheral neuropathy)
29
describe the process of O2- dependent killing and the enzymes involved
O2 --> O2.- by NADPH oxidase O2.- --> H2O2 by SOD H2O2 --> HOCl by MPO
30
chronic granulomatous disease
X-linked or autosomal recessive defect in NADPH oxidase | recurrent infection/granuloma formation, especially by catalase+ organisms
31
test for CGD
nitroblue tetrazolium | clear + disease
32
catalase + organisms (5)
staph aureus, Pseudomonas, serratia, nocardia, aspergillus
33
MPO deficiency
unable to generate HOCl, usually asymptomatic, increased risk for candida infections
34
main killing mechanism of macrophages
O2-independent (lysozyme, secondary granules)
35
macrophages peak in tissue at-
2-3 days
36
4 outcomes dictated by macrophages
resolution/healing (IL-10, TBF-b) Continue acute inflammation (IL-8) Abscess formation Chronic inflammation (present antigens to CD4+ t cells)
37
how are CD4 T cells activated
1st signal- bind to MHC II on APC via CD4 | 2nd signal- bind to B7 on APC via CD28
38
TH1 CD4 cells secrete (2)
IFNg- activate macrophages, promote IgM--IgG switching, promote TH1/decrease TH2 IL-2- activate T cells
39
TH2 CD4 cells secrete (4)
IL 4/13- IgE IL5- eosinophils, IgA IL10- decrease TH1
40
how are CD8 T cells activated
1st signal: bind to MHC I on any cell via CD8 | 2nd signal: IL-2 secreted by TH1 CD4 cells
41
2 ways that B cells are activated
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
42
what is the defining cell of a granuloma
epithelioid histiocyte (macrophages)
43
steps in granuloma formation
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
44
digeorge syndrome (defect, symptoms)
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
45
infections related to T cell deficiency
virus and fungus
46
3 causes of SCID
1- ADA deficiency 2- cytokine receptor defects 3- MHC II deficiency
47
infections related to SCID
ALL! fungal, viral, bacterial, protozoan, opportunistic
48
X-linked agammaglobulinemia (defect/cause)
total lack of immunoglobulin due to mutated BTK
49
X-linked agammaglobulinemia presentation
after 6 months with bacterial, enteroviral and giardia infections (after 6 mo because that is when maternal antibodies disappear)
50
common variable immune deficiency
low immunoglobulin production | increased risk for bacterial, enteroviral, giardia infections
51
CVID complications (2)
increased risk of autoimmune, lymphoma
52
selective IgA deficiency
most common Ig deficiency low IgA increased risk of mucosal infections
53
IgA deficiency complications (2)
celiac disease | anaphylaxis with blood transfusion
54
cause of hyper IgM syndrome
defect of CD40 (B cells) or CD40L (CD4 cells) that prohibits class switching = low IgG, IgA, IgE (pyogenic infections, mucosal infections)
55
Wiskott-Aldrich syndrome (gene, triad)
X-linked mutation in WASP gene | triad: thrombocytopenia, eczema, recurrent infections
56
C5-9 completment deficiency
increased risk of neisseria infections
57
C1 inhibitor deficiency
angioedema
58
AIRE
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
AIRE mutations (triad)
result in development of autoimmunity (triad hypoparathyroidism, adrenal destruction, chronic candida infections)
60
2 outcomes of negative selection in B cells
1) receptor editing via re-expression of RAG genes | 2) apoptosis (intrinsic pathway(
61
anergy
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
ALPS
autoimmune lymphoproliferative syndrome - due to failure to initiate apoptosis from defect in FAS/FASL
63
regulatory t cell characteristics (3)
CD4, CD25, FoxP3
64
CD25
IL-2 receptor, participates in activation of regulatory cell
65
FoxP3
transcription factor involved in development and maintenance of regulatory T cells
66
actions of regulatory T cells (2)
1) block T cell activation via CTLA-4 | 2) produce anti-inflam cytokines TGFb and IL-10
67
FOXP3 mutations cause
disorder of T regs = IPEX- immune dysregulation, polyendocrinopathy, enteropathy, X-linked)
68
why are autoimmune disease more common in women?
estrogen may reduce apoptosis of self-reactive B cells
69
HLA with highest assoc with autoimmunity
B27
70
epitope spreading
spreading of immune response to additional antigens that are exposed to immune cells upon tissue destruction
71
most symptoms in lupus are related to
hypersensitivity type III
72
pathogenesis of SLE
poor clearing of apoptotic debris leads to activation of self-reactive lymphocytes that produce antibodies against nuclear antigens in the debris
73
complement deficiency as it relates to SLE
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
most common complement deficiency in SLE
C2
75
criteria needed for SLE diagnosis
4
76
arthritis in SLE
peripheral, no deformity
77
most common cause of death in SLE
renal disease
78
anemia in SLE
type II HST
79
endocarditis in SLE
Libman-sacks, small vegetations on both sides of the mitral valve
80
antibodies in SLE (specific and nonspecific)
specific- anti-dsDNA, anti-Smith | nonspecific- ANA
81
3 types of antiphospholipid antibodies
anticardiolipin anti-B2- glycoprotein I lupus anticoagulant
82
anticardiolipin antibody causes false +
VDRL/ RPR
83
lupus anticoagulant causes
false elevated PTT (actually hypercoaguable)
84
drug induced lupus antibody
anti-histone antibody
85
drugs that are implicated in drug-induced lupus (3)
procainamide, hydralazine, INH
86
course of drug induced lupus
CNS and renal involvement are rare | remission likely with removal of drug
87
sjogren syndrome
T cell mediated autoimmune destruction of salivary and lacrimal glands (type IV HST)
88
antibodies in sjogrens syndrome (4)
anti-ro (SSA) anti-La (SSB) RF ANA
89
antibodies associated with extra glandular manifestations
anti-SSA, SSB
90
antibody associated with neonatal lupus/heart block
anti-SSA
91
dx of sjogrens requires
biopsy of minor salary glands
92
2/3 criteria for sjogrens
dry eyes ANA + Anti-SSA or SSB or RF lymphocytic sialadenitis on biopsy of minor salivary glands
93
sjogrens complication
marginal lymphoma of salivary glands
94
pathogenesis of systemic sclerosis
fibroblast activation leads to collagen deposition = inflammation, vasoconstriction and secretion of growth factors (TGFb, PDGF)
95
CREST syndrome
limited systemic sclerosis | Calcinosis, raynauds, esophageal dysmotility, sclerodactyly, telangectasias of skin
96
m/c site affected in diffuse systemic sclerosis
GI tract
97
antibody of limited SS
anti-centromere
98
antibody of diffuse SS
anti-SCL70/topoisomerase I
99
antibodies in MCTD (2)
ANA + anti-U1 ribonucleoprotein
100
regeneration
replacement of damaged tissue with native tissue
101
repair
replacement of damaged tissue with fibrous scar
102
labile tissues -3
constant turnover (GI tract, skin, bone marrow)
103
stable tissues- 2 examples
in G0 but have capacity to regenerative (liver, proximal renal tubular cells of kidney)
104
permanent tissues-3
will not regenerative (skeletal mm, nerve, cardiac mm)
105
main tissue in repair
granulation tissue
106
3 elements of granulation tissue
type III collagen capillaries myofibroblasts
107
what is the fate of type III collagen in scar?
eventually removed by collagenase and replaced with type I collagen (zinc cofactor)
108
TGF a
epithelial and fibroblast growth
109
TGF b
epithelial and fibroblast growth, anti-inflammatory
110
PDGF
growth factor for endothelium, smooth mm and fibroblasts
111
Fibroblast growth factor
angiogenesis, skeletal development
112
VEGF
angiogenesis
113
type I collagen
bone, strong
114
type II collagen
cartilage
115
type III collagen
pilable (blood vessels, granulation tissue, embryonic tissue)
116
type IV collagen
basement membrane
117
vitamin c in wound healing
cofactor for hydroxylation of proline and lysine
118
copper in wound healing
cofactor for cross-linking of lysine and hydroxylysine
119
zince in wound healing
cofactor for collagenase, replaces type III with type I collagen
120
hypertrophic scar
large, but stays in the boundaries of the original defect
121
keloid
excess type III collagen, outside of the boundaries of the original defect

pathoma (7 decks)

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