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PathomaSUN > Ch2 Inflammation > Flashcards

Ch2 Inflammation Flashcards

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
Q

macrophages timing and functions (2)

A

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

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26
Q

hyper IgM syndrome

A

elevated IgM due to mutated CD40L or CD40 receptor (on B cells), so no class switching happens

27
Q

3 infections that immunoglobulins defend against

A
  1. bacterial- opsonize. 2. enterovirus 3. giardia = no IgA so cannot protect gut/mucosa
28
Q

2 steps for CD8 killer T cell activation, and function

A
  1. intracellular antigen presented via MHC class 1
  2. IL-2 is co-signal.
    function: kills via granzyme and perforin and FAS ligand
29
Q

lm-rolling

A

selectin speed bumps upregulated on endothelial cells by histamine, TNF and IL-1. selectin binds sialyl lewis x on leukocyte, causes rolling

30
Q

steps of leukocyte migration (lm)

A

MRATPDR

margination-rolling-adhesion-transmigration and chemotaxis-phagocytosis-destruction-resolution

31
Q

SLE symptoms

A
  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
Q

Th1 and Th2

A

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
Q

Function of LTB4, LTC4, LTD4, LTE4

A

LTB4 attracts and activates neutrophils; the rest mediate anaphylaxis reactions (vasoconstriction, bronchospasm and increased vascular permeability)

34
Q

SCID + 3 etiologies

A

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
Q

Anti-histone antibody

A

drug-induced lupus: procainamide, hydralazine, isoniazid. Rx: remove drug

36
Q

complement deficiency in lupus

A

complements play a role in clearing Ag/Ab complex via opsonization

37
Q

NBT test

A

test to screen for CGD; whether NADPH oxidase is intact

38
Q

AIRE mutations

A

transcription factor that upregulates the self-antigens presented for T-cell education. Autoimmune polyendocrine syndrome triad: hypoparthyroid, adrenal failure and candida infections

39
Q

AA metabolites include what two things?

A

Prostaglandin and Leukotrienes

40
Q

granulation tissue formation components (3)

A
  1. fibroblasts deposit T3 collagen, 2. capillaries provide nutrients. 3. myofibroblasts contract wound
41
Q

central vs peripheral tolerance

A

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
Q

Mixed CTD

A

features of SLE, systemic sclerosis, polymyositis. characterized by ANA and Antibodies to U1 ribonucleoprotein

43
Q

theory why autoimmune disease is more common in women

A

estrogen reduces apoptosis of self-reactive B-cells

44
Q

2 steps for CD4 helper T cell activation

A
  1. extracellular antigen presented via MHC class 2

2. B7-1,2 on APC binds CD28 on helper T cell

45
Q

epitope spreading

A

exposure of new antigens that lead to relapses and remissions

46
Q

Toll-like receptors (TLRs) located where and do what?

A

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
Q

Mast cells are activated by what three things?

A

tissue trauma, complement proteins C3a and C5a, cross linking of cell-surface IgE by antigen

48
Q

lm-destruction of phagocytosed material (equation and two types)

A

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
Q

General pathway of complement activation

A

C3 convertase makes C3 to C3a, then C5–> C5a, then C5a-C9 makes MAC which makes holes on cell membrane

50
Q

lm-margination

A

vasodilation in post-capillary venules cause heavy cells to move out to periphery

51
Q

lm-transmigration and chemotaxis

A

C5a, IL8, LTB4, bacterial products

52
Q

3 criteria for sjogren’s

A
  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
Q

MPO deficiency

A

defective conversion of peroxidase to bleach, increased risk of candida, but most asx

54
Q

4 things that attract neutrophils

A

C5a, LTB4, IL8, bacterial products

55
Q

pathophysiology of fever

A

pyrogens cause macrophages to release IL-1 and TNF, which increase COX activity in hypothalamus, and increased PGE2 raises temp set point

56
Q

SLE patho

A

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
Q

digeorge’s syndrome

A

developmental failure of 3rd and 4th pharyngeal pouches, 22q11 deletion, lack of thymus, parathyroid and great vessels. Lack T cells, hypocalcemia etc

58
Q

lm-resolution

A

neutrophils undergo apoptosis within 24 hrs, and become pus

59
Q

types of collagen

A

Type1: bone, strength. Type2: cartilage Type 3: Blood vessels, granulation tissue, embryonic tissue; pliability. Type4: basement membrane

60
Q

lm-adhesion

A

CAM interacts with integrins (upregulated by C5a and LTB4)

61
Q

wiskott aldrich syndrome

A

triad: thrombocytopenia, eczema, recurrent infections, mutation in the WASP gene

62
Q

IgA deficiency

A

most common Ig deficiency, increased risk for mucosal infection, ex: celiac disease

63
Q

two types of systemic sclerosis

A

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
Q

primary and secondary intention of healing

A

1: edges brought together. 2: granulation tissue fills first, then myofibroblasts contract

PathomaSUN (3 decks)

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