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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
collagen IV chains
AI (IV), a2 (IV)
25
collagen IV
all basement membrane
26
basement membrane components
type IV collagen laminin entactin heparan sulfate proteoglycan
27
type IV collagen job
network structural
28
laminin job
cell attachment
29
heparan sulfate proteoglycan job
electrostatic charge
30
binding sites on laminin
type IV collagen binding site cell-binding domain proteoglycan binding site
31
fibronectin binding
heparan fibrin collagen integrin
32
What does FGF receptor bind?
heparan sulfate
33
chemokines work..
on a gradient-->as progress back, density gets more and more
34
wound
nonspecific- any area of damage
35
scab
proteins mixed with blood
36
sccar
collagenous tissue repair
37
cicatrix
scar
38
Scarring
angiogenesis -migration and proliferation of fibroblasts -deposition of extracellular matrix maturation of fibrous tissue (remodeling)
39
coagulation factors
active in wound repair - hageman factor fragments - bradykinin - complement activation - fibrin clot
40
hageman factor fragments
vasopermeability
41
bradykinin
vasodilation vasopermeability pain
42
complement activation
leukocyte recruitment | vasopermeability
43
fibrin clot
hemostatic plug reservoir of growth factors provisional matrix for cell migratin
44
role of platelets in wound repair
adhesion aggregation mediator release
45
adhesion
plug small leaks in blood vessels
46
aggregation
plug large leaks in blood vessels | induce coagulation
47
mediatior relase
vasoconstriction stimulate additional platelet aggregation growth factor release
48
growth factor 1 and 2 (FGF)
fibroblast and epidermal cell proliferation | angiogenesis
49
PDGF (isoforms AA,AB, BB)
fibroblast chemotaxis | proliferation & contraction
50
TGF-B (B1, B2, B3)
fibroblast chemotaxis: extracellular matrix deposition, protease inhibitor secretion (because collagen is a protein)
51
VGEF
vascular permeability | angiogenesis
52
macrophages in wound repair
recruitment and maturation phagocytosis and killing of microorganisms phagocytosis of tissue debris growth factor release
53
TGF-B inhibits
collagenase secretion
54
fibroblast function in wound repair
``` growth factor production proliferation and migration protease release ECM production dynamic linkage between actin bundles and ECM program cell death ```
55
epithelial cell function in wound repair
``` growth factor production migration and proliferation protease release ECM production terminal differentiation ```
56
endothelial cell in tissue repair
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
endothelial cell activities in tissue repair
proteolysis ECM migration & chemotaxis proliferation lumen formation, maturation, and inhibition of growth increased permeability through gaps and trancytosis
58
fibroblasts make..
collagen
59
healing by first intention
pinches wound together
60
healing by second intention
has to do with extensive tissue damage that you cant just pinch together
61
complications and pathological outcomes of tissue damage
``` scar formation and loss of function keloid formation desmoid (aggressive fibromatosis) ulceration wound dehiscence (separation) scar contraction ```
62
kelloid are not..
hypocellular, they have a lot of cells
63
ALK is elevated in
liver stuff
64
troponin i
marker of acute myocardial damage
65
Ormond's Disease
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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