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Pathology > Regeneration and Repair Part II > Flashcards

Regeneration and Repair Part II Flashcards

1
Q

Main functions of ECM

A
  1. mechanical support –> anchorage and migration
  2. storage/release of regulatory molecules –> cell proliferation and differentiation control
  3. maintenance of cell shape and stromal integrity
  4. establishment of tissue microenvionments –> basement membrane acts as a boundary between epithelium and underlying connective
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2
Q

what are the 3 main components of ECM

A
  1. fibrous structural proteins
  2. adhesive glycoprotiens
  3. proteoglycans and hyaluronan
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3
Q

fibrous structural proteins of ECM

A

collagens and elastins provide strength and recoil of tissue

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4
Q

adhesive glycoproteins of ECM

A

connect the matrix elements together

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5
Q

proteoglycans and hyaluronan of ECM

A

provide the matrix in which other proteins are organized

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6
Q

the main components of the ECM form

A

the interstitial matrix and basement membranes

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7
Q

—- is most abundant component in ECM

A

collagen

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8
Q

what is collagen composed of

A

3 alpha chains forming a triple helix (procollagen)

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9
Q

procollagen is cleaved by

A

proteases to allow complete triple helix formation = collagen moecule

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10
Q

what does collagen form

A

form fibrils

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11
Q

function of collagen

A

undergo cross-linking which stabilizes the array and provides tensile strength

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12
Q

what are the 2 main types of collagen

A
  1. fibrillar collagens (type I, II, III V)

2. basement membrane collagen (type IV)

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13
Q

what do fibrillar collagens make up

A

most of the interstitial matrix and connective tissue in scar

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14
Q

basement membranes form

A

sheets instead of fibrils and is highly organized

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15
Q

what is required for cross-linking of collagen fibrils

A

vitamin C

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16
Q

vit C deficiency (scurvey) results in

A
  • impaired cross-linking
  • skeletal deformity
  • inadequate wound healing
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17
Q

purpose of tissue elasticity

A
  • allows for expansion and recoil

- is a functional requirement of tissue (iel vessels, skin)

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18
Q

what are elastic fibers

A

elastin, surrounded by a peripheral network of fibrillin microfibrils

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19
Q

Marfan syndrome

A
  • inherited defect in fibrillin

- results in weakness of vessel walls (aortic dissection) and skeletal system

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20
Q

what are Cell Adhesion Molecules (CAM)

A

-diverse group of cellular receptors that bind to adhesion proteins allowing cellular interaction with other cells, with the ECM and btwn ECM components

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21
Q

what are the 4 main families of CAMs

A
  1. integrins
  2. cadherins
  3. Selectins
  4. immunoglobulins
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22
Q

integrins bind to

A
  • adhesion proteins:
  • laminin (basement membrane component)
  • fibronectin (fibrillar component of interstital matrix)
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23
Q

integrins allow for

A

cell-cell and cell-ECM adhesion maintaining cell shape

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24
Q

integrins stimulate

A

cellular motility, proliferation and differentiation

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25
Q

what is the most abundant glycoprotein in basement membrane

A

laminin

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26
Q

laminin forms tight networks with

A

collagen IV

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27
Q

what can laminin bind

A

to integrins and other cell surface receotirs

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28
Q

laminin mutations results in

A

forms of epidermolysis bullosa, (separation of basement membrane and epidermis)

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29
Q

fibronectin is made by

A

connective tissue cells

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30
Q

fibronectin interacts with

A

cell surface integrins

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31
Q

fibronectin has binding sites for

A

collagen and fibrin

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32
Q

when is fibronectin abundant

A

during embryonic development and wound healing

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33
Q

what are cadherins

A
  • calcium-dependent adherence proteins

- family of adhesion receptors that connect the membrane of adjacent cells

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34
Q

what is the function of cadherins during would healing

A

facilitate formation of cellular junctions

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35
Q

what do cadherins mediate

A

cell-cell interactions; regulate cell motility, proliferation and differentiation

36
Q

loss of E-caderin results in

A

metastasis by disrupting intercellular contacts in human carcinomas (breast and gastric)

37
Q

function of proteoglycans and GAGs

A

confer the ability to resist compression

38
Q

what are proteoglyans

A

are extracellular proteins covalently bound to a special class of long-chain polysaccharides called glycosaminoglycans (GAGs)

39
Q

what do proteoglycans and GAGs form

A

huge aggregates that occupy large volumes and entrap water

40
Q

healing of a mild injury occurs through

A

regeneration

41
Q

healing of chronic/severe injury occurs through

A

repair (scar formation, replacement of injured cells with connective tissue)

42
Q

a combination of repair and regeneration is dependent on

A
  1. the proliferative capacity of the cells/tissue
  2. the integrity of the extracellular matrix
  3. the resolution or chronicity of the injury and inflammation
43
Q

what are the basic steps of tissue repair

A
  1. inflammation
  2. granulation tissue formation
  3. scar formation
  4. remodelling of connective tissue
44
Q

function of inflammation

A
  • serves to contain damage
  • remove damaged cells, promote deposition of ECM components
  • stimulate angiogenesis
45
Q

granulation tissue formation

A
  • proliferating fibroblasts
  • newly-formed blood vessels in loose ECM
  • inflammatory cells (macrophage)
46
Q

scar formation

A

progressive maturation of granulation tissue into dense fibrous tissue and scar

47
Q

how does inflammation begin

A
  • through the activation of coagulation pathways

- a blood clot forms containing fibrin, fibronectin and complement components

48
Q

once inflammation is activated what does it do

A
  • stops the bleeding
  • contains damage
  • lays down framework for wound healing
49
Q

within 24 hrs of inflammation what cells enter

A

neutrophils enter at the wound’s margins and release proteolytic enzymes that clean out debris and bacteria

50
Q

what do neturophils release

A

cytokines and GF that stimulate angiogenesis and granulation tissue formation begins to form

51
Q

describe how granulation tissue from

A
  • FIBROBLAST and vascular ENDOTHELIAL CELLS proliferate forming new LEAKY vessels that allow passage of plasma proteins and fluid into the extravascular space –> EDEMA
  • granulation tissue progressively invades the wound space, filling it by day 5-7
  • concurrently, MACROPHAGES replace neutrophils and clear fibrin and extracellular debris at the site of repair
52
Q

what is angiogenesis

A

a physiologic process involving growth of new blood vessel

53
Q

in injury, new vessels form from

A

pre-existing ones

54
Q

what are the growth factors involved in angiogenesis

A

Vascular Endothelial Growth Factor (VEGF)
Fibroblast Growth Factor (FGF)
Angiopoietins (Ang1 and Ang2)

55
Q

growth factors of angiogenesis active what

A

signaling cascades leading to proliferation of endothelial cells and fibroblast migration to injured cells

56
Q

describe the process of scar formation

A
  • collagen fibers first laid down vertically to allow epithelial cell mobilization
  • re-epithelialization occurs when a continuous epithelial layer closes the wound
  • epithelial cell proliferation thickens the layer
57
Q

epithelial cell proliferation stimulated by what

A
  • fibroblast production of FGF-7 (keratinocyte growth factor)
  • HGF
  • EGF
58
Q

what cell becomes abundant and bridges the incision forming a scar

A

collagen fibrils (predominantly type III)

59
Q

what happens by week 2 of scar formation and wound contraction

A

-leukocytic infiltrate, edema and vascularity decreases secondary to continuous collagen deposition

60
Q

what collagen types is most abundant in scar formation

A

collagen type 1

61
Q

what is blanching

A

replacement of original granulation tissue by a pale, avascular scar

62
Q

what type of cells are scars composed of

A
  • spindle-shaped fibroblasts
  • dense collagen
  • fragments of elastic tissue
  • other ECM components
63
Q

how is connective tissue remodeling achieved

A

through concurrent synthesis and degradation of ECM

64
Q

what are matrix metalloproteinases (MMPs)

A

a large family of proteinases that degrade ECM components

65
Q

MMPs are produced by

A
  • fibroblasts
  • macrophages
  • neutrophils
  • synovial cells
  • some epithelial cells
66
Q

what inhibits MMPs

A

inhibitors of metalloproteinases (TIMPs)

67
Q

following wound healing, strength is only –% to –% compared to normal skin

A

70%-80%

68
Q

the recovery or tensile strength depends on

A
  • a greater synthesis over degradation of collagen

- structural changes of collagen fibers (cross-linking, increased fiber size) after collagen synthesis ceases

69
Q

primary intention of cutaneous wound healing

A
  • clean, uninfected would with adjacent borders

- minimal tissue damage allows for epithelial regeneration and minimal scarring

70
Q

primary intention wound healing commonly seen in

A

sutured surgical incision

71
Q

secondary intention of wound healing

A
  • large wound with inflammation/ infection/ischemia and distant borders
  • extensive scarring and wound contraction (repair)
72
Q

what local factors influence wound healing

A
  1. infections
  2. mechanical factors
  3. foreign bodies
  4. size, location, and type of wound
73
Q

how does infection affect wound healing

A
  • cause delay in healing
  • increases tissue injury and inflammation
  • S. aureus can colonize
74
Q

how can mechanical factors affect wound healing

A

Increased pressure/tension makes wounds prone to dehiscence

75
Q

how can foreign bodies affect wound healing

A

persistance of foreign body will prolong infection therefore want to remove foriegn body

76
Q

how can size, location and type of wound affect wound healing

A
  • Vascularized areas (face) heal faster compared to poorly vascularized (foot)
  • Small incisions heal faster than large wounds caused by blunt trauma
77
Q

what systemic factors affect wound healing

A
  • nutrition
  • metabolic status
  • circulator status
  • glycocorticoids
78
Q

how does nutrition affect wound healing

A

vitamin C and copper deficiency inhibt collagen synthesis and cross-linking

79
Q

how does metabolic status affect wound healing

A

microangiopathy associated with diabetes mellitus results in delayed healing

80
Q

how does circulatory status affect wound healing

A

inadequate blood supply or venous drainage (arteriosclerosis or venous abnormalities)

81
Q

how does glucocorticoids (steroids) affect wound healing

A

have anti-inflammatory effects and inhibit collagen synthesis

82
Q

deficient scar formation may lead to

A

wound dehiscence or ulceration

83
Q

excessive production of repair components can form

A
  • hypertrophic scars

- keloids form secondary to excessive collagen

84
Q

what are contractures

A

exaggerated wound especially in the palms, the soles can cause restricted range of motion

85
Q

what is fibrosis

A

excessive deposition of collagen and ECM components (excessive scarring) following a prolonged or chronic injury

Pathology (18 decks)

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