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Pathology Block 1 > Block 1 Chronic Inflammation & Repair > Flashcards

Block 1 Chronic Inflammation & Repair Flashcards

1
Q

Outcomes of acute inflammation

A

Resolution, fibrosis (scar), abscess formation/liquefaction, chronic inflammation

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2
Q

Non-granulomatous inflam

A

D/t persistent infxn, prolonged exposure to toxins, allergic/immune/AI rxns; peptic ulcer disease, atherosclerosis, bronchial asthma, RA

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3
Q

Granulomatous inflammation

A

Distinct pattern evoked by certain agents (fungal, immune-med processes, foreign bodies, unknown); 1-2 mm nodules with epithelioid cells, lymphocytes +/- necrosis (caseating)

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4
Q

Giant cells

A

Multinucleated epithelioid cells, induced by interferon-gamma; present in granulomatous chronic inflammation

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5
Q

SIRS

A

Systemic inflammatory response syndrome/acute phase response: fever, acute phase proteins, increased pulse/bp, leukocytosis

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6
Q

Sepsis

A

Large amounts LPS -> increased TNF, IL-1, IL-12 -> septic shock: DIC, hypotension, metabolic disturbances (acidosis)

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7
Q

Exogenous and endogenous pyrogens

A

Ex: bacterial LPS stimulate release
End: IL-1, TNF cause COX to convert AA to PGs
*PGE2 -> NTs to reset temp set-point in hypothalamus

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8
Q

Acute phase proteins

A

When hepatic synth unregulated by cytokines (IL-6), make you feel sick (anorexia, somnolence, malaise, rigors, chills)
CRP (opsonin), fibrinogen, serum amyloid A (may cause 2’ amyloidosis in CI)

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9
Q

Types of leukocytosis

A

Neutrophilia (bacterial), lymphocytosis (viral), eosinophilia (parasite, allergy, asthma)

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10
Q

Tissues that heal

A

High proliferative capacity, stems cells not destroyed, ECM intact (scaffold, cell polarity maintained)

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11
Q

Repair

A

Organization & fibrosis; org=replace inflam with fibrosis in parenchymal organs; fib=extensive collage deposition with CI

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12
Q

Factors influencing repair

A

Extent, type of injury (cells involved, proliferative capacity, integrity of ECM), resolution/chronicity of injury/inflam

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13
Q

Embryonic, multipotent, & adult stem cells

A

E: pluripotent -> generate all types of tissue lineages
M: become lineage-committed SCs
A: somatic stem cells, lineage-specific; have niche

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14
Q

Proliferative capacities of tissues

A

Labile: continuously proliferating, replace self; e.g. skin, cervix, vagina, GI tract, uterus, urinary tract, bone marrow, hematopoietic tissues
Stable: arrested in G0 with ability to replace necrotic tissue if normal stroma intact; e.g. liver, kidney, pancreas, SM, endoth, fibroblast, chrondrocyte
Permanent: cannot divide -> scar; e.g. neurons, skeletal mm, cardiac mm

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15
Q

Cyclins

A

Act with CDKs to induce cascade of P -> mitosis

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16
Q

p53

A

Most important regulator of cyclins; TF increasing CDKI p21; loss = uninhibited cell growth

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17
Q

EGF and TGF-a

A

Share common receptor
EGF: overexpressed/mutated in lung, brain cancers; ERB-B2 (Her-2/Neu) overex in some breast ca
Both produced by keratinocytes, WBCs in response to injury, mitogen for epith cells, hepatocytes, fibroblasts

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18
Q

HGF/scatter factor

A

From fibroblasts, endoth, liver nonparenchymal cells; promotes scatter/migration cell during dev, mitogen for epith of lung, liver, breast, skin
Receptor c-MET mut/overex in renal and thyroid papillary cancers

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19
Q

VEGF

A

Promotes vessel formation in early dev (vasculogenesis), new vessel growth (angio-, lymphangiogenesis)

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20
Q

Avastin (bevacizumab)

A

Blocks VEGF, used in metastatic disease; treatment of wet macular degeneration, retinopathy of prematurity, diabetic macular edema

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21
Q

PDGF

A

From endoth, MFs, SM; stored in platelet granules; chemotactic for fibro, MF; GF for fibro, SM; promotes collagen synth

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22
Q

FGF

A

FGF-7 (keratinocyte GF): wound repair/ reepithelialization

2: same as FGF-7 + angiogenesis; chemotactic for fibro, MF, endoth; hematopoiesis; lung, liver, cardiac, sk mm dev

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23
Q

TGF-b

A

From platelet, endoth, MF, lymphos
Pleiotropic - multiple, sometimes opposing effects: fibrogenic; stimulates fibro prolif, SM cells; inhibits endo and WBC growth; anti-inflam by inh lympho prolif
Some tumors lose receptor; high exp in hypertrophic scars, systemic sclerosis, Marfan’s

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24
Q

Functions of ECM

A

Mechanical support, maintenance of cell polarity; control cell prolif/diff via storage & presentation regulatory molecules; scaffolding for tissue renewal; establishment of microenvironments/ boundaries

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25
Q

Components of ECM

A

Fibrous structural proteins: collagen, elastin, fibrillin
Adhesive glycoproteins
Proteoglycans, hyaluronan (gels for resilience/lube)

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26
Q

Forms of ECM

A

Interstitial: between cells, made by mesenchymal cells, 3D amorphous gel; fibrillar and non-fib collagens, elastin, fibronectin, PGs, hyaluronan
Basement membrane: appx cell surface, non-fibrillar collagen (type IV), laminin, heparin sulfate, PGs

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27
Q

Structure of collagen

A

Triple helix of pre-procollagen -> 3 procollagen chains -> collagen; need vit C for hydroxylation of procollagen

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28
Q

Types of collagen

A

I, II, III, V = fibrillar (interstitial, wound healing)
IV = nonfibrillar (BM)
VII = nonfribrillar (epidermal/dermal jxn)

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29
Q

Ehlers-Danlos Syndrome

A

Defect in type I, III, V collagen

30
Q

Osteogenesis imperfecta

A

Defect in type I collagen

31
Q

Epidermolysis bullosa

A

Defect in type VII collagen

32
Q

Elastic fibers

A

Elastin: for recoil, forms central core of elastic fibers, in large vessels, skin, ligaments, uterus
Fibrillin: form peripheral microfibrillar network of elastic fibers

33
Q

Marfan syndrome

A

Defect in fibrillin

34
Q

Scurvy

A

Lack of vitamin C = defective hydroxylation of procollagen

35
Q

Proteoglycans

A

Protein core linked to GAG (heparan, chondroitin/dermatan sulfate); assembled in Golgi, RER; regulate CT structure and permeability; modulate cell growth/diff

36
Q

Hyaluronan

A

Huge GAG of repeating disaccharides, assembled at PM, binds water -> compressible gel in heart valve, skin, cartilage, synovial fluid, vitreous of eye, umbilical cord

37
Q

Hyaluronidases

A

Cleave HA into low molecular weight HA, which binds CD44 on WBC to recruit to site of inflammation, stimulates WBC prod of cytokines/chemokines

38
Q

Hyaluronan concentration increased in what pathologies?

A

RA, scleroderma, psoriasis, osteoarthritis

39
Q

Fibronectin

A

Binds fibrin, collagen, cells, etc.; exists in tissue & plasma forms; receptor is integrin; chemotactic for other cells; promotes wound contraction and epithelial migration

40
Q

Tissue vs. plasma form of fibronectin

A

Tissue - synthesized locally in wound by fibroblasts

Plasma - binds fibrin in clot formation

41
Q

Laminin

A

Most abundant GP in BM, binds cells to ECM

42
Q

Cadherins

A

Ca-dependent adherence proteins, intxns bt cells of same type; play role in “contact inhibition”, dysfunction of E-cadherin in forms of breast, gastric cancer

43
Q

Zonula adherens & desmosomes

A

ZA: spot-like jxns near apical surface epith cells
D: stronger jxns in epith and mm tissues

44
Q

Catenins

A

Link cadherins to cytoskeleton

b-catenin links cadherin -> a-catenin, which links to actin cytoskeleton

45
Q

Integrins

A

Bind cell-cell or cell-ECM (fibronectin, laminin); links to actin intracellularly; transmits signal from neighboring cells, ECM to nucleus for integration of cell prolif, diff, protein synth, attachment, migration

46
Q

Selectins

A

WBC/endothelial interaction

47
Q

Regeneration vs. repair vs. fibrosis

A

Reg: restitution of tissue identical to previous, fxn regained
Rep: replacement of tissue with CT, incomplete fxn regained
Fib: extensive CT in setting of CI

48
Q

Granulation tissue & scar

A

GT: angiogenesis and fibroblast prolif with collagen deposition
Scar: tissue replaced by collagen after would healing in skin or replacement of parenchyma

49
Q

Vasculogenesis

A

Embryonic formation vessels from endoth precursors (angioblasts) derived from hematopoietic/endoth cell precursors (hemangioblasts)

50
Q

Angiogenesis

A

Vessel formation in adults; occurs in physiologic and pathologic states by 2 methods: branching/extension adjacent vessels or recruit endoth progenitor cells from bone marrow

51
Q

Physiologic and pathologic causes of angiogenesis

A

Phy: wound healing, regeneration, menstruation, vascularization of ischemic tissue
Path: tumor dev/metastasis, diabetic retinopathy, chronic inflam

52
Q

1st intention healing

A

Primary union, clean wound repaired by epithelial regeneration, small, thin scar results

53
Q

2nd intention healing

A

Gap filled with granulation tissue, fills in from sides; scab, wound contracts (myofibroblasts), may be complicated by infection, heals more slowly, larger scar

54
Q

Steps of repair

A

Blood clot, neutro/MF invasion, epithelial cells from edge of wound migrate and deposit BM to close wound, capillaries/fibroblasts enter = granulation tissue; MF clean debris, fibrin, promote angiogenesis & ECM deposition; fibro make collagen, vessels regress -> scar

55
Q

Blood clotting mechanism (1st step of repair)

A

Vasc injury -> release P-selectin from endoth cells onto ECM -> platelet adhesion & degranulation -> integrins -> recruit neutro/MF -> fibrin clot fills gap & stabilizes platelet plug

56
Q

Factors involved in epithelial cells depositing BM in wound

A

FGF-7, IL-6: enhance keratinocyte migration/proliferation

HGF, HB-EGF (heparin-binding)

57
Q

Components of granulation tissue matrix

A

Initially: fibrin, fibronectin, type III collagen
Later: type I collagen mostly

58
Q

What happens in week two of repair

A

Fibroblasts make collagens and deposit other ECM elements (elastin, PGs, hyaluronan), vessels regress (“blanching”) = scar

59
Q

Fibroblast recruitment in scar formation

A

TGF-b (from MF, platelet, endoth), PDGF, EDGF, FGF, IL-1, TNF

60
Q

Maturation of healed area

A

Increase matrix secretion with decrease in degradation -> remodeling (MMPs) & wound contraction (myofibroblasts)

61
Q

Wound strength following healing

A

10% normal by 1 week, 70-80% max by 3 months

62
Q

MMPs

A

Contain zinc, degrade ECM; produced by fibro, MF, neutro, synovial cells, epith; secretion induced by PDGF, FGF, IL-1, TNF; inhibited by TGF-b, steroids, TIMPs (tissue inh of MMP, from mesenchymal cells)

63
Q

Stromelysins

A

MMP-3,10,11 degrade PGs, laminin, fibronectin, amorphous collagen

64
Q

Gelatinases

A

MMP-2,9 degrade amorphous collagen, fibronectin

65
Q

Interstitial collagenases

A

MMP-1,2,3 degrade collagen 1,2,3

66
Q

Wound contraction

A

Occurs 1’ in large wounds (2’ intention) by myofibroblasts (from fibro via PDGF, TGF-b, FGF-2), can come from bone marrow or epith, contain smooth muscle actin

67
Q

Influences on wound healing

A

Systemic: nutrition (protein, vit C), metabolic status (diabetes), circulation/perfusion (atheriosclerosis), hormones (steroids)
Local: infection, mechanical factor (motion), foreign bodies, size/location/type of wound

68
Q

Dehiscence & ulceration

A

Deficient granulation tissue or scar formation
D: rupture
U: inadequate vascularization

69
Q

Excessive scar formation

A

Hypertrophic scar: excessive collagen
Keloid: scarring beyond original wound
Exuberant granulation: projects above surrounding skin & blocks re-epithelialization
Desmoids: excessive fibro prolif, CT = may be low grade malignancy

70
Q

Contractures

A

Excessive contraction of a wound

71
Q

Fibrosis

A

Excessive collagen & other ECM components
Causes: repeated acute inflam, persistence of stimuli for acute inflam -> CI (continued release of GFs, cytokines, decreased MMP activity), dev immune/AI response, radiation

Pathology Block 1 (12 decks)

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