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Path Q2 > Wound Healing > Flashcards

Wound Healing Flashcards

0
Q

healing

A

occurs when tissue scaffolding (BM) altered or destroyed
–>involves a combination of creation of new tissue cells and collagen deposition (fibrosis/scarring)–>totally normal state never reestablished

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1
Q

regeneration

A

requires intact tissue scaffolding (basement membranes, etc)
–>new cells in tissue/organ derived from division of stable cells or new cells from stem cells–>restores tissues to normal state

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2
Q

cell proliferation regulated by

A

hormonal influences
growth stimuli (during growth years)
pathological stimuli

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3
Q

cell division in most stable cell populations is governed by

A

soluble stimulatory factors
stoluble inhibitory factors
cell-cell contact (contact inhibition)

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4
Q

increasing cell proliferation to repair damage can be through

A

shortening cell cycle
pushing stable cells into cell cycle
stimulating cells to generate parenchymal cells

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5
Q

3 types of cell surface receptors important in inflammation and wound healing

A

kinase coupled receptors
receptors without kinase actiity
GPCR

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6
Q

kinase coupled receptors bind___ and activate____

A

growth factors

PI3, IP3, MAP kinase pathways

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7
Q

receptors without kinase activity bind___and activate ____

A

cytokines

JAK/STAT pathways

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8
Q

GPCR bind___and activate ____

A

chemokines

release Ca2+/generate cAMP

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9
Q

G1/S Checkpoint

A

check for DNA damage

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10
Q

G2/M Checkpoint

A

check for damaged or unduplicated DNA

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11
Q

when cyclin B is phosed

A

CDK1/cyclin B activate kinase so can go from G2–>M

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12
Q

stable cells do not___ because they___

A

enter the cell cycle

need to be stimulated

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13
Q

steps in wound healing

A
  • induction of an inflammatory process in response to initial injury with removal of damaged and dead tissue
  • proliferation and migration of parenchymal and CT cells
  • formation of new blood vessels and granulation tissue
  • synthesis of ECM proteins and collagen deposition
  • tissue remodeling
  • wound contraction
  • acquisition of wound strength
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14
Q

components of extracellular matrix

A 
collagen
elastin, fibrillin, & elastic fibers
adhesive glycoproteins
matricellular proteins
proteglycans
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15
Q

types of collagen in ECM

A

I, II, III, IV, IX

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16
Q

types of adhesive glycoproteins

A

fibronectin, laminin

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17
Q

matricellular proteins

A

SPARC (osteonextin), thrombospondins, osteopontin, tenacin

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18
Q

types of proteoglycans in ECM

A

heparan, condrotin, dermatan sulfates

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19
Q

how to make collagen

A

mRNA–>ER–>short units of collagen–>caps on them–>export to extracellular –>cross links between chains after ends are clipped–>collagen trimer

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20
Q

chains of collagen type I

A

aI, a2

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21
Q

collagen type I

A

most abundant collagen

ubiquitous- skin, bone,etc

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22
Q

collagen type II chains

A

aII

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23
Q

collagen type II

A

most cartilage collagen: cartilage, vitreous humor

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24
Q

collagen IV chains

A

AI (IV), a2 (IV)

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25
Q

collagen IV

A

all basement membrane

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26
Q

basement membrane components

A

type IV collagen
laminin
entactin
heparan sulfate proteoglycan

27
Q

type IV collagen job

A

network structural

28
Q

laminin job

A

cell attachment

29
Q

heparan sulfate proteoglycan job

A

electrostatic charge

30
Q

binding sites on laminin

A

type IV collagen binding site
cell-binding domain
proteoglycan binding site

31
Q

fibronectin binding

A

heparan
fibrin
collagen
integrin

32
Q

What does FGF receptor bind?

A

heparan sulfate

33
Q

chemokines work..

A

on a gradient–>as progress back, density gets more and more

34
Q

wound

A

nonspecific- any area of damage

35
Q

scab

A

proteins mixed with blood

36
Q

sccar

A

collagenous tissue repair

37
Q

cicatrix

A

scar

38
Q

Scarring

A

angiogenesis
-migration and proliferation of fibroblasts
-deposition of extracellular matrix
maturation of fibrous tissue (remodeling)

39
Q

coagulation factors

A

active in wound repair

  • hageman factor fragments
  • bradykinin
  • complement activation
  • fibrin clot
40
Q

hageman factor fragments

A

vasopermeability

41
Q

bradykinin

A

vasodilation
vasopermeability
pain

42
Q

complement activation

A

leukocyte recruitment

vasopermeability

43
Q

fibrin clot

A

hemostatic plug
reservoir of growth factors
provisional matrix for cell migratin

44
Q

role of platelets in wound repair

A

adhesion
aggregation
mediator release

45
Q

adhesion

A

plug small leaks in blood vessels

46
Q

aggregation

A

plug large leaks in blood vessels

induce coagulation

47
Q

mediatior relase

A

vasoconstriction
stimulate additional platelet aggregation
growth factor release

48
Q

growth factor 1 and 2 (FGF)

A

fibroblast and epidermal cell proliferation

angiogenesis

49
Q

PDGF (isoforms AA,AB, BB)

A

fibroblast chemotaxis

proliferation & contraction

50
Q

TGF-B (B1, B2, B3)

A

fibroblast chemotaxis: extracellular matrix deposition, protease inhibitor secretion (because collagen is a protein)

51
Q

VGEF

A

vascular permeability

angiogenesis

52
Q

macrophages in wound repair

A

recruitment and maturation
phagocytosis and killing of microorganisms
phagocytosis of tissue debris
growth factor release

53
Q

TGF-B inhibits

A

collagenase secretion

54
Q

fibroblast function in wound repair

A 
growth factor production
proliferation and migration
protease release
ECM production
dynamic linkage between actin bundles and ECM
program cell death
55
Q

epithelial cell function in wound repair

A 
growth factor production
migration and proliferation
protease release
ECM production
terminal differentiation
56
Q

endothelial cell in tissue repair

A

thrombomodulin & syndecan surface expression, prostacyclin release, plasminogen activator release–>needed to prevent thrombosis
metalloproteinase release (basement membrane degradation)
growth factor production
migration and proliferation
ECM production
tube formation

57
Q

endothelial cell activities in tissue repair

A

proteolysis ECM
migration & chemotaxis
proliferation
lumen formation, maturation, and inhibition of growth
increased permeability through gaps and trancytosis

58
Q

fibroblasts make..

A

collagen

59
Q

healing by first intention

A

pinches wound together

60
Q

healing by second intention

A

has to do with extensive tissue damage that you cant just pinch together

61
Q

complications and pathological outcomes of tissue damage

A 
scar formation and loss of function
keloid formation
desmoid (aggressive fibromatosis)
ulceration
wound dehiscence (separation)
scar contraction
62
Q

kelloid are not..

A

hypocellular, they have a lot of cells

63
Q

ALK is elevated in

A

liver stuff

64
Q

troponin i

A

marker of acute myocardial damage

65
Q

Ormond’s Disease

A

idiopathic retroperitoneal fibrosis

–>diffuse retroperitoneal process that involves chronic inflammation, extensive proliferation of fibroblasts, and widespread extracellular matrix deposition

Path Q2 (10 decks)

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