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

Block 1 Chronic Inflammation & Repair Flashcards

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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
Components of ECM
Fibrous structural proteins: collagen, elastin, fibrillin Adhesive glycoproteins Proteoglycans, hyaluronan (gels for resilience/lube)
26
Forms of ECM
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
27
Structure of collagen
Triple helix of pre-procollagen -> 3 procollagen chains -> collagen; need vit C for hydroxylation of procollagen
28
Types of collagen
I, II, III, V = fibrillar (interstitial, wound healing) IV = nonfibrillar (BM) VII = nonfribrillar (epidermal/dermal jxn)
29
Ehlers-Danlos Syndrome
Defect in type I, III, V collagen
30
Osteogenesis imperfecta
Defect in type I collagen
31
Epidermolysis bullosa
Defect in type VII collagen
32
Elastic fibers
Elastin: for recoil, forms central core of elastic fibers, in large vessels, skin, ligaments, uterus Fibrillin: form peripheral microfibrillar network of elastic fibers
33
Marfan syndrome
Defect in fibrillin
34
Scurvy
Lack of vitamin C = defective hydroxylation of procollagen
35
Proteoglycans
Protein core linked to GAG (heparan, chondroitin/dermatan sulfate); assembled in Golgi, RER; regulate CT structure and permeability; modulate cell growth/diff
36
Hyaluronan
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
Hyaluronidases
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
Hyaluronan concentration increased in what pathologies?
RA, scleroderma, psoriasis, osteoarthritis
39
Fibronectin
Binds fibrin, collagen, cells, etc.; exists in tissue & plasma forms; receptor is integrin; chemotactic for other cells; promotes wound contraction and epithelial migration
40
Tissue vs. plasma form of fibronectin
Tissue - synthesized locally in wound by fibroblasts | Plasma - binds fibrin in clot formation
41
Laminin
Most abundant GP in BM, binds cells to ECM
42
Cadherins
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
Zonula adherens & desmosomes
ZA: spot-like jxns near apical surface epith cells D: stronger jxns in epith and mm tissues
44
Catenins
Link cadherins to cytoskeleton | b-catenin links cadherin -> a-catenin, which links to actin cytoskeleton
45
Integrins
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
Selectins
WBC/endothelial interaction
47
Regeneration vs. repair vs. fibrosis
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
Granulation tissue & scar
GT: angiogenesis and fibroblast prolif with collagen deposition Scar: tissue replaced by collagen after would healing in skin or replacement of parenchyma
49
Vasculogenesis
Embryonic formation vessels from endoth precursors (angioblasts) derived from hematopoietic/endoth cell precursors (hemangioblasts)
50
Angiogenesis
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
Physiologic and pathologic causes of angiogenesis
Phy: wound healing, regeneration, menstruation, vascularization of ischemic tissue Path: tumor dev/metastasis, diabetic retinopathy, chronic inflam
52
1st intention healing
Primary union, clean wound repaired by epithelial regeneration, small, thin scar results
53
2nd intention healing
Gap filled with granulation tissue, fills in from sides; scab, wound contracts (myofibroblasts), may be complicated by infection, heals more slowly, larger scar
54
Steps of repair
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
Blood clotting mechanism (1st step of repair)
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
Factors involved in epithelial cells depositing BM in wound
FGF-7, IL-6: enhance keratinocyte migration/proliferation | HGF, HB-EGF (heparin-binding)
57
Components of granulation tissue matrix
Initially: fibrin, fibronectin, type III collagen Later: type I collagen mostly
58
What happens in week two of repair
Fibroblasts make collagens and deposit other ECM elements (elastin, PGs, hyaluronan), vessels regress ("blanching") = scar
59
Fibroblast recruitment in scar formation
TGF-b (from MF, platelet, endoth), PDGF, EDGF, FGF, IL-1, TNF
60
Maturation of healed area
Increase matrix secretion with decrease in degradation -> remodeling (MMPs) & wound contraction (myofibroblasts)
61
Wound strength following healing
10% normal by 1 week, 70-80% max by 3 months
62
MMPs
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
Stromelysins
MMP-3,10,11 degrade PGs, laminin, fibronectin, amorphous collagen
64
Gelatinases
MMP-2,9 degrade amorphous collagen, fibronectin
65
Interstitial collagenases
MMP-1,2,3 degrade collagen 1,2,3
66
Wound contraction
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
Influences on wound healing
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
Dehiscence & ulceration
Deficient granulation tissue or scar formation D: rupture U: inadequate vascularization
69
Excessive scar formation
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
Contractures
Excessive contraction of a wound
71
Fibrosis
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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