Ch2 Inflammation Flashcards

(64 cards)

1
Q

2 ways for B-cell activation

A
  1. IgM binds antigen and becomes IgM producing plasma cell
  2. MHC class 2 presentation to CD4+ helper cell + CD40 cosignal produces IL4 and IL5, which promotes class switching and plasma cell formation
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2
Q

Keloid

A

excess production of scar tissue composed of T3 collagen seen out of proportion to the wound

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3
Q

Mechanism of regeneration and repair and its mediators

A

paracrine signaling, growth factors produced by macrophages: TGF-a (epithelial and fibroblast growth factor), TGF-b (FGF and antiinflammatory), PDGF (endothelium sm muscle and fibroblasts), FGF (angiogenic), VEGF

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4
Q

Sjrogen’s syndrome: def and symptoms

A

autoimmune destruction of lacrimal and salivary glands, dry eyes, dry mouth and recurrent dental caries (no saliva/mucus to protect), can lead to high risk of B-cell lymphoma

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5
Q

Chronic granulomatous disease

A

lack of NADPH oxidase, so recurrent infection and granuloma formation with catalase positive organisms: staph aureus, pseudomonas cepacia, serratia, nocardia, aspergillus

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6
Q

Two phases of mast cell response and action?

A

Immediate: preformed histamine granules; delayed: leukotriene production

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7
Q

Antiphospholipid antibody

A

auto antibody to protein attached to phospholipids, most are non-SLE. anticardiolipid, lups anticoagulant, anti-B2 glycoprotein I, causes hypercoagulable state

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8
Q

Steps of granuloma formation (3)

A
  1. Macrophage presents antigen to CD4 via MHC class 2 presentation. 2. Macrophages secrete IL-12 so CD4 becomes Th1 polarized. 3. Th1 secretes IFN-y which makes epitheliod histiocytes and giant cells
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9
Q

CVID

A

low Ig due to B cell or helper T-cell defects, increased risk of autoimmune and lymphoma

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10
Q

leukocyte adhesion deficiency

A

AR defect of integrins (CD18); neutrophils cannot migrate so stuck circulating in blood. recurrent infections without pus

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11
Q

lm-phagocytosis

A

opsonins (IgG and C3b) help target the targets and pseudopods extend to engulf it

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12
Q

pathogenesis of systemic sclerosis

A

autoimmune damage to mesenchyme. then endothelial dysfunction leads to vasoconstriction which leads to ischemia and secretion of TGF-B and PDGF which activates fibrosis and scarring

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13
Q

systemic sclerosis def and symptoms

A

autoimmune disease characterized by sclerosis of skin and visceral organs, commonly in females 30-50yrs

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14
Q

Vitamins and minerals required for wound healing

A

Vitamin C: hydroxylation of proline and lysine residues on procollagen. Zinc: cofactor for collagenase which replaces T3 with T1 collagen. Copper: cofactor for lysyl oxidase, which crosslinks lysine

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15
Q

x-linked agammaglobulinemia

A

complete lack of immunoglobulin due to BTK defect- B cell does not mature. Presents after 6 months of life because mom’s antibodies are gone

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16
Q

what is hageman factor?

A

proinflammatory protein produced in liver, activates coagulation and fibrinolytic systems, completment, and kinin system (bradykinin- works similar to histamine + pain)

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17
Q

hallmark of granulomatous inflammation

A

epithelioid histiocyte, surrounded by giant cells and outer rim of lymphocytes can be caseating or non-caseating

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18
Q

Function of PGI2, PGD2 and PGE2

A

Vasodilation at arteriole, increase vascular permeability at post-cap venule and PGE2 mediates pain and FEEEEver

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19
Q

Treg (the three factors present)

A

block T cell activation via IL-10 and TGF-B. also use CTLA-4 to block B7 from connecting with CD28. CD4, CD25 (polymorphisms a/w MS and type 1 DM), FoxP3 (mutations a/w IPEX syndrome)

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20
Q

complement deficiencies

A

C5-C9 def: susceptible to Neisseria infection, c1 inhibitor deficiencies lead to hereditary angioedema; SLE development

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21
Q

3 pathways of complement activation

A
  1. Classical- immunoglobulins; 2. Alternative- microbial products. 3. MBL- MBL binds to mannose on microorganisms.
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22
Q

Rx of Lupus (2)

A
  1. avoid sunlight 2. glucocorticoids/immunosuppresives for flare
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23
Q

chediak-higashi syndrome

A

MT defect, which prevents phagolysosome formation. Leads to neutropenia, giant granules, defective primary hemostasis, albinism and peripheral neuropathy

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24
Q

3 types of tissues + regeneration and repair

A

labile, stabile, permanent; existing tissue vs scar tissue when stem cells are lost

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25
macrophages timing and functions (2)
enter into scene after neutrophils 2-3 days, 1. Kill using lysozyme. 2. Manage chronic inflammation and/or healing. If good, IL-10 and TGF-B; If bad, IL-8 to call for reinforcements of neutrophils. presents antigen to CD4 cell
26
hyper IgM syndrome
elevated IgM due to mutated CD40L or CD40 receptor (on B cells), so no class switching happens
27
3 infections that immunoglobulins defend against
1. bacterial- opsonize. 2. enterovirus 3. giardia = no IgA so cannot protect gut/mucosa
28
2 steps for CD8 killer T cell activation, and function
1. intracellular antigen presented via MHC class 1 2. IL-2 is co-signal. function: kills via granzyme and perforin and FAS ligand
29
lm-rolling
selectin speed bumps upregulated on endothelial cells by histamine, TNF and IL-1. selectin binds sialyl lewis x on leukocyte, causes rolling
30
steps of leukocyte migration (lm)
MRATPDR | margination-rolling-adhesion-transmigration and chemotaxis-phagocytosis-destruction-resolution
31
SLE symptoms
1. fever, weight loss, fatigue, LAD, raynaud's 2. Malar rash, discoid (wolfbite) rash, sunlight rash 3. oral/nasopharyngeal ulcers 4. polyarthritis 5. serositis (pleuritis, pericarditis) 6. seizures or psychosis 7. Renal: diffuse proliferative GN or membranous nephropathy 8. anemia, thrombocytopenia or leukopenia 9. LS endocarditis 10. ANA 11. Anti-dsDNA or anti-sm Ab
32
Th1 and Th2
T-cell polarization; Th1 makes IL-2, which activates CD8, and also Interferon gamma which activates macrophages and makes IgG and targets intracellular organisms. Th2 secretes IL-4, IL-5 and IL-13. IgE, recruits eos and targets parasites
33
Function of LTB4, LTC4, LTD4, LTE4
LTB4 attracts and activates neutrophils; the rest mediate anaphylaxis reactions (vasoconstriction, bronchospasm and increased vascular permeability)
34
SCID + 3 etiologies
defective cell and humoral immunity because 1. cytokine receptor defects 2. ADA deficiency (adenosine is bad for lymphocytes) 3. MHC class II deficiency. Tx: bubble and stem cell transplant
35
Anti-histone antibody
drug-induced lupus: procainamide, hydralazine, isoniazid. Rx: remove drug
36
complement deficiency in lupus
complements play a role in clearing Ag/Ab complex via opsonization
37
NBT test
test to screen for CGD; whether NADPH oxidase is intact
38
AIRE mutations
transcription factor that upregulates the self-antigens presented for T-cell education. Autoimmune polyendocrine syndrome triad: hypoparthyroid, adrenal failure and candida infections
39
AA metabolites include what two things?
Prostaglandin and Leukotrienes
40
granulation tissue formation components (3)
1. fibroblasts deposit T3 collagen, 2. capillaries provide nutrients. 3. myofibroblasts contract wound
41
central vs peripheral tolerance
central tolerance: in thymus or BM, T cells and B cells go through positive and negative selection and dendritic cells present stuff to them. if they do not pass, they undergo apoptosis. peripheral: leads to anergy and apoptosis due to lack of cosignal
42
Mixed CTD
features of SLE, systemic sclerosis, polymyositis. characterized by ANA and Antibodies to U1 ribonucleoprotein
43
theory why autoimmune disease is more common in women
estrogen reduces apoptosis of self-reactive B-cells
44
2 steps for CD4 helper T cell activation
1. extracellular antigen presented via MHC class 2 | 2. B7-1,2 on APC binds CD28 on helper T cell
45
epitope spreading
exposure of new antigens that lead to relapses and remissions
46
Toll-like receptors (TLRs) located where and do what?
Macropahges and dendritic cells; activated by PAMPs and upregulates NF-KB (the switch) which produces immune mediators. Also found on lymphocytes so mediates chronic inflammation
47
Mast cells are activated by what three things?
tissue trauma, complement proteins C3a and C5a, cross linking of cell-surface IgE by antigen
48
lm-destruction of phagocytosed material (equation and two types)
O2 >O2^->H2O2>HOCl. Enzymes: NADPH oxidase, SOD, MPO. Can be O2 dependent (more efficient) or O2 independent using lysozyme in macrophages and major basic protein in eosinophils
49
General pathway of complement activation
C3 convertase makes C3 to C3a, then C5--> C5a, then C5a-C9 makes MAC which makes holes on cell membrane
50
lm-margination
vasodilation in post-capillary venules cause heavy cells to move out to periphery
51
lm-transmigration and chemotaxis
C5a, IL8, LTB4, bacterial products
52
3 criteria for sjogren's
1. dry eyes. 2. ANA or SSA/SSB (present for extraglandular manifestations) or RF. 3. Lymphocytic sialadenitis on lip biopsy to exclude amyloid/sarcoid
53
MPO deficiency
defective conversion of peroxidase to bleach, increased risk of candida, but most asx
54
4 things that attract neutrophils
C5a, LTB4, IL8, bacterial products
55
pathophysiology of fever
pyrogens cause macrophages to release IL-1 and TNF, which increase COX activity in hypothalamus, and increased PGE2 raises temp set point
56
SLE patho
UV light damages cells, nuclear antigens activate self-reactive B-cells and make Ag/Ab complex. Ag/Ab complexes activate dendritic cell toll like receptors and amplify immune response
57
digeorge's syndrome
developmental failure of 3rd and 4th pharyngeal pouches, 22q11 deletion, lack of thymus, parathyroid and great vessels. Lack T cells, hypocalcemia etc
58
lm-resolution
neutrophils undergo apoptosis within 24 hrs, and become pus
59
types of collagen
Type1: bone, strength. Type2: cartilage Type 3: Blood vessels, granulation tissue, embryonic tissue; pliability. Type4: basement membrane
60
lm-adhesion
CAM interacts with integrins (upregulated by C5a and LTB4)
61
wiskott aldrich syndrome
triad: thrombocytopenia, eczema, recurrent infections, mutation in the WASP gene
62
IgA deficiency
most common Ig deficiency, increased risk for mucosal infection, ex: celiac disease
63
two types of systemic sclerosis
limited type: CREST- calcinosis, raynaud's, esophageal dysmotility, sclerodactyly and telangiectasias diffuse type: skin involvement with early visceral involvement, a/w antibodies to DNA topoisomerase I (anti-scl-70)
64
primary and secondary intention of healing
1: edges brought together. 2: granulation tissue fills first, then myofibroblasts contract