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Principles of Wound Healing Flashcards

1
Q

Damage Response

A
  1. Damage to hepatocytes not matrix- no damage, heals
  2. Damage to hepatocytes and matrix- cirrhosis scarring, end stage liver disease
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2
Q

Cirrhosis Due to Hep C

A
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3
Q

Cell Paths

A
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4
Q

Cell Regeneration

A
  1. G0 to G1 phase
  2. G1-S & G2-M checkpoints
  • Labile cells- continuously dividing & dying. Found in blood, surface epith, skin, GI tract, genital tract, urinary tract
  • stable cells- quiescent, Liver, kidney, pancreas
  • Permanent cells- terminally differentiated. Non prolif cardiac m., neurons
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5
Q

Stem Cells in Labile Tissues

A
  • Homeostatic equilib between replication & differentiation of stem cells & death of fully differentiated mature cells
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6
Q

Skin

A
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7
Q

GI stem cells

A
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8
Q

Stem Cell charac

A
  • some stem cells differentiate
  • some undiff- can self renew!
  • Embryonic Stem cells- multiple cell lineages
  • Adult/tissue sstem cells- multiple lineage in BM
  • Differentiation plasticity- embryonic cells
  • transdifferentiation- change in diff program of already committed cell
  • uncommitted progenitor cell- select specific path
  • BM stem cells very broad diff capability (fat, cartilage, bone, endoth & m.)
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9
Q

Stem Cell Niches

A
  • liver stem cells, oval cells, in canals of Hering which connect bile ductules w/ hepatocytes
  • corneal stem cells, in limbus, b/t conjunctiva & cornea
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10
Q

Cell Cycle

A
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11
Q

EGF

A

from activated macrophages, salivary glands, keratinocytes & other cells

  • mitogenic for keratinocytes & fibroblasts, stimulate keratinocyte migration & granulation tissue formation
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12
Q

TGF-a

A

from activated macrophages, T lymphocytes, keratinocytes & other

  • like EGF
  • stim replc of hepatocytes & other epith cells
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13
Q

HB-EGF

A

from macrophages, mesenchymal cells

  • keratinocyte repl
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14
Q

VEGF

A

from mesenchymal cells

  • increase vascular perm, mitogenic for endoth cells
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15
Q

HGF

A

from mesenchymal cells

  • ehances prolif of epith & endoth cells & hepatocytes
  • increase cell motility
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16
Q

PDGF

A

platelets, macrophages, endoth cells, keratinocytes, smooth m. cells

  • chemotactic for PMNs, macrophages, fibrblast & smooth m. cells
  • activate PMNs, macrophage, fibroblast
  • mitogenic for fibroblast, endoth & smooth m.
  • stim production of MMPs, fibronectin & HA
  • stim angiogen & wound remodeling
  • reg integrin expression
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17
Q

FGF 1, 2

A

macrophage, mast cells, T lymph, endoth cells, fibroblast

  • chemotactic for fibrblast
  • mitogenic for fibroblast & keratinocytes
  • stim keratinocyte migration, angiogen, wound contraction & matrix deposition
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18
Q

TGF-B

A

platelets, T lymphocytes, macrophages, endoth cells, keratinocytes, smooth m. cells, fibroblast

  • chemotactin for PMNs, macrophage, lymphocyte, fibroblast, smooth m. cells
  • stim TIMP syn, angiogen, fibroplasia
  • I production of MMPs & keratinocyte prolif
  • reg integrin expression & other cytokines
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19
Q

KGF

A

Fibroblast

  • stim keratinocyte migration, prolif & diff
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20
Q

TNF

A

macrophage, mast cells, t lymph

  • activate macrophage, reg other cytokines, mult f
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21
Q

GF role in carcinogenesis

A
  • EGF & TGF a have similar R (EGFR) w/ intrinsic tyrosine kinase activity
  • EGFR1 over expressed in lung, head/neck & some brain neoplasms- therapeutic target
  • HER-2/NEU is over expressed in brain cancers- Herceptin target
  • HGF binds to c-MET a tyrosine kinase in thyroid & kidney papillary cancer
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22
Q

Organ Regeneration

A
  • parenchymal organs tissue regen
  • pancreas, adrenal, thyroid, lung
  • hypertrophy & hyperplasia of proximal duct cells
  • dramatic regen of liver after surgical removal of hepatic tissue
  • donor liver transplant, partial hepatectomies for tumor removal, prolif response of remaining hepatocytes, replication of hepatic non parenchymal cells
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23
Q

Organ Regen

A
  • TNF & IL-6 prime cells for repli by stim G0 to G1 transition
  • TGFa, HGF & HB-EGF family
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24
Q

Liver Regeneration

A

Partial hepatectomy- 2/3 remove liver

3 wks- R lateral & caudate lobes enlarge to reach original mass

TNF & IL-6 prime normal hepatocytes *not oval cells*

HGF, TGFa, HB-EGF stim primed hepatocytes

NE, SE, insulin, thyroid & GH act as adjuvants facilitation hepatocyte entry into cell cycle

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25
Q

CT of liver regen

A
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26
Q

ECM

A
  • mech support for tissue
  • reg cell growth/scaffolding for tissue
  • maintain cel diff
  • Collagen
  • elastin- recoil
  • cell adhesion prot (ICAM, cadherin, integrin, selectin, fibronectin & laminin)
  • glycosaminoglycans & proteoglycans (heparan sulfate, chondroitin/dermatan sulfate, keratan sulfate & hylauronan)
27
Q

Fibrillar Collagens

A
  • I- hard & soft tissues, **osteogenesis imperfecta, Ehlers-Danlos syndrme type I **
  • II- cartilage, IV disk, vitreous, Achondrogenesis type II, spondyloepiphysea dysplasia syndrome
  • III- hollow organs, soft tissues, Vascular E-D syndrome
  • V- soft tissues, BV, Classic E-D syndrome
  • IX- cartilage & vitreous **Stickler Syndrome **
28
Q

Basement mem collagens

A
  1. IV- basement mem, **Alport syndrome **
29
Q

Other Collagens

A
  1. VI- in microfibris, Bethlem myopathy
  2. VII- anchoring fibrils @ dermal epiderm junction; dystrophic epidermolysis bullosa
  3. IX- cartilage, IV disk; **multiple epiphyseal dysplasia **
  4. XVII- transmem collagen in epidermal cells, Benign atrophic generalized epidermolysis bullosa
  5. XV & XVIII- endostatin forming collagens, endoth cells, **Knobloch syndrome **
30
Q

Proteoglycans f in ECM w/ control prot

A
  • proteoglycans act as reservoir for GF
  • Heparan sulfate binds basic fibroblast GF FGF-2
  • injury to ECM, release FGF-2, stim recruitment of inflamm cells, fibroblast activation & new BV formation
  • syndecan cell surface proteoglycan w/ transmem core prot & attach w/ extracell GAG side chains
  • GAG chains can also bind free FGF-2 from ECM & mediasite interactions w/ cell surface FGF R
  • Cytoplasmic tail of syndecan attach to intracell actin cytoskeleton & maintain architercture of epith sheets
31
Q

Healing by CT fibrosis

A
  1. When regen fails
  2. permanant cells/organs
  3. stable cells in large tissue damage
  4. cutaneous wound healing
32
Q

Healing

A
  1. Inflammation
  2. angiogen- granulation tissue
  3. fibrobalst migration & prolif
  4. scar formation (deposit ECM)
  5. maturation & reorganize fibrous tissue (remodeling)
33
Q

Granulation Tissue

A
  • highly organized & specialized CT made up of
  • proif BV
  • fibroblast
  • inflamm cells: macrophage
  • VEGF & FGF-2
  • replaces necrotic debris w/ fibrous tissue
34
Q

Granulation Tissue

A

Proportional to amt of fibrosis/scarring

35
Q

Angiogenesis

36
Q

Angiogenesis

A
  • EPCs diff & form mature network by linking w/ previous vessels
  • Endoth cells from preexisting vessels become motile
  • Endoth cells prolif to form capillary sprouts
  • angiogen vessel maturation require recruitment of pericytes & smooth m. cells to form periendoth layer
37
Q

VEGF

A
  • produced in low levels in various adult tissue & at higher levels like podocytes in glomerulus & cardiomyocytes
  • induced by hypoxia, TGF-B, PDGF, TGF-a
  • VEGFR-1,-2,-3
  • promote angiogen, increase vascular perm, stim endoth cell migration & prolif, VEGF-C induce hyperplasia of lymphatic vasculature
  • upreg endoth expression of plasminogen (activator, inhibitor & collagenase)
38
Q

Cutaneous Wounds

A
  • CT fibrosis
  • healing by first intention- clean, uninfected
  • second intention healing- excision wounds more intense inflamm, abundant granulation tissue & extensive collagen deposition that contrats. **No sutures! **
39
Q

Wound Healing

40
Q

First Intention

A
  • sharp & clean wound
  • edges close
  • epidermal regen
  • less granulation tissue- less fibrosis
  • less time to heal
41
Q

Secondary Intention

A
  • large surface defect
  • considerable inflamm
  • increase granulation tissue
  • prolong time course to heal
42
Q

Blood Clot

43
Q

Initial Blood Clot Formation

A
  • wounding causes hemorrhage
  • rapid activation of clotting cascade
  • clot has RBCs, fibrin, fibronectin, complement components
  • Clot f to stop bleeding, scaffolding for migrating leukocyte attracted by chemotactic factors
  • release VEGF lead to increase vascular perm in clot- edema
  • neutrophils appear early on periph in first 24 hr releasing proteolytic enz to clean up debris & killbac
44
Q

Early granulation tissue

45
Q

Angiogen

Epith regen

Formation & migration of granulation tissue to site of injury

46
Q

Granulation Tissue Formation Hallmark

A
  1. prolif fibroblast & endoth cells 24-72 hrs
  2. new small BV, myofibroblasts & macrophages
  3. vessels leaky
  4. amt depends on intensity of inflamm
  5. max 5-7 days formed!
47
Q

Collagenous scar & remodel of parenchymal & CT

48
Q

Late granulation tissue

49
Q

Fibroblast migration & ECM deposition

A
  • scar formation- build on granulation tissue
  • fibroblast migrate & prolif
  • deposit ECM by these cells
  • recruit & stim of fibroblasts- PDGF, FGF-2, TGF-B
  • activated endoth & inflamm cells- rich in mast cells w/ appropriate chemotactic lymphocytes
  • macrophages key cell constituent
  • clear extracell debris & fibrin @ injury site
  • elaborate host of mediators induce fibroblast prolif & ECM production
50
Q

GF & cytokines affecting cutaneous wound healing

A
  1. monocyte chemotaxis- chemokines, TNF, PDGF, FGF, TGF-B
  2. Fibroblast migration/replication- PDGF, EGF, TGF-B, TNF, IL-1
  3. Keratinocyte replication- HB-EGF, FGF-7, HGF
  4. Angiogen- VEGF, angiopoietins, FGF
  5. Coll syn- TGF-B, PDGF
  6. collagenase secretion- PDGF, FGF, TNF while TGF-B inhibits
51
Q

Macrophages

A
  • debridement removal of debris & tissue: phagocytosis, collagenase, elastase
  • antimicrobial activity: nitric acid, ROS
  • chemotaxis & prolif of fibroblast & keratinocyte: PDGF, TGF-B, TNF, IL-1, KGF-7
  • angiogenesis: VEGF, FGF-2, PDGF
  • deposition & remodling ECM: TGF-B, PDGF, TNF, OPN, IL-1, collagenase, MMPs
52
Q

ECM Deposition

A
  1. fibroblast progressively assume more synthetic phenotype & increased deposit of ECM
  2. collagen syn critical
  3. Day 3-5 begin syn of collagen by fibroblast
  4. same GF that reg fibroblast prolif also do this
  5. net coll. accumulate depends not only on increase syn but on diminished coll degradation
  6. granulation tissue scaffolding evolves into scar w/ inactive, spindle shpaed fibroblast, dense coll, fragment of elastic tissue & other ECM components
53
Q

Wound Contraction

A
  • granulation tissue
  • healing by secondary intention
  • initiated by myofibroblasts- smooth m. a actinin & vimentin
54
Q

Scar remodeling

A
  • transition from granulation tissue to scar involve shifts in ECM composition
  • scar ECM modified & remodeled
  • outcome @ ea stage balance b/t ECM syn & degradation
  • degrade coll & other ECM components due to metalloproteinases!
55
Q

Tensile strenghts

A
  • 1st week- 40-70% from suture, granulation tissue still there
  • 2nd week- 10% suture, can remove it
  • 4th week- 50% from new coll
  • 12th week- 80% from coll
56
Q

Systemic factors- defective healing

A
  • nutrition- vit C, prot, Zn
  • genetic- E-D syndrome/diabetes
  • circulatory- atherosclerosis, venous stasis
  • hormones- glucocorticoids
57
Q

Local

A
  • infection- persistent injury
  • movement & tension- spearate edges
  • foreign bodies- impediment to healing
  • size, location & type- large size, foot, face etc.
58
Q

Pathology of Repair

A
  1. inadeq granulation tissue & scar- wound dehiscence
  2. excessive formation:
  • fibroblastic prolif (keloid),
  • exuberant granulation tissue (proud flesh, prevent re-epith)
  • contracture
59
Q

Abdomen wound dehiscence

60
Q

Keloid

61
Q

Proud Flesh

A

excess granulation

excision

62
Q

Contracture

63
Q

Fibrosis in injury

64
Q

Interstitial pulmonary fibrosis

Pathology (8 decks)

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