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MHD Exam 1 > Healing Repair > Flashcards

Healing Repair Flashcards

1
Q

Possible outcomes of injury to cells

A
  • adaptation (reversible)
  • repair (heal)
  • death
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2
Q

repair is initiated when _____

A

inflammation begins

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3
Q

healing occurs via ____ and/or ____

A

regeneration and/or scar formation (can both happen at once or just one)

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4
Q

regeneration

A

replacement of damaged cells by replicating cells of the same type

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5
Q

scar formation

A

replacement of damaged tissue by CT

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6
Q

regeneration requires _____ and _____

A

1) a CT framework (ECM) intact to serve as scaffolding for orderly replacement of residual uninjured cells
2) cells must have the capacity to divide

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7
Q

extracellular matrix

A

network of interstitial proteins: interstitial matrix and basement mb

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8
Q

protein composition of ECM

A
  • fibrous structural proteins- collagen, elastins
  • water hydrated gels - proteoglycans and hyaluronan
  • adhesive glycoproteins
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9
Q

labile tissues

A
  • continuously dividing
  • lost cells replaced by maturation from stem cells and/or proliferation of mature cells
  • ex. - hematopoietic cells of bone marrow; squamous epithelium of skin, oral cavity, cervix, and vagin; and columnar epithelium of GI tract
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10
Q

stable tissue

A
  • low/no level of replication (G0 cell cycle)
  • rapidly divide when stimulated (G1 cell cycle and beyond)
  • ex- liver, kidney, pancreas, smooth muscle cells, and fibroblasts
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11
Q

Permanent tissues

A
  • terminally differentiated, non proliferative in postnatal life
  • ex heart and brain
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12
Q

epidermal growth factor (EGF)

A
  • source= activated macrophages, keratiocytes, and other cells
  • functions- mitogenic for keratinocytes and fibroblasts. It stimulates keratinocyte migration
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13
Q

Transforming growth factor a (TGF-a)

A
  • source- activated macrophages, keratinocytes, and other cells
  • functions- stimulates proliferation of hepatocytes and other epithelial cells
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14
Q

Vascular endothelial growth factor (VGF)

A
  • source- mesenchymal cell

- function - stimulates proliferation of endothelial cells and increases vascular permeability

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15
Q

Platelet derived growth factor (PDGF)

A
  • source- platelets, macrophages, endothelial cells, smooth muscle cells, keratinocytes
  • functions- chemotactic, activates and stimulates the proliferation of fibroblasts and endothelial cells, and it stimulates ECM protein synthesis
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16
Q

Fibroblast Growth Factors (FGF)

A
  • source- macrophages, mast cells, endothelial cells, etc

- function- chemotactic, mitogenic for fibroblasts, stimulates angiogenesis, ECM protein synthesis

17
Q

Transforming growth factor (TGF-B)

A

source- platelets, macrophages, endothelial cells, fibroblasts
-function- chemotactic for leukocytes and fibroblasts, stimulates ECM synthesis, and suppresses acute inflammation

18
Q

why are damaged tissues replaced with fibrous CT

A
  • injured tissues can’t regenerate

- supporting structures are severely damaged and stem cells are lost

19
Q

Pro/con of scar formation

A

pro- scar usually provides enough structural stability for injured tissue to continue function
-con- fibrous tissue can’t perform the function of lost parenchymal cells

20
Q

steps in repair by scar formation

A

1) angiogenesis
2) migration and proliferation of fibroblasts
3) formation and deposition of ECM by fibroblasts
4) maturation and organization of fibrous tissue elements

21
Q

angiogenesis

A
  • new blood vessel development from existing vessels

- roles in healing, development of collaterals at sits of ischemia, and tumor growth

22
Q

important mediators of angiogenesis

A

-VEGF, FGFs, PDGF, and TGFB

23
Q

VEGF

A
  • family of growth factors that promote angiogenesis, increase vascular permeability, and stimulate endothelial cell migration and proliferation
  • expressed at low levels in most adult tissues with some exceptions where it is in high amounts (podocytes in glomerulus and pigment epithelium of retina)
  • important inducer of VEGF is hypoxia
  • mutations in VEGF can cause defective angiogenesis and vasculogenesis
24
Q

fibroblasts

A
  • synthesize CT proteins

- their recruitment and activation is driven by many growth factors like PDGF, FGF, and TGF-B

25
Q

granulation tissue

A
  • specialized tissue that fills in defects in organs when non-regenerative cells and/or CT framework is destroyed
  • consists of proliferating fibroblasts laying down immature CT (type III collagen) and proliferating new blood vessels
  • present only during healing
26
Q

organization

A
  • process of transforming granulation tissue into a dense scar
  • with time, blood vessels become less prominent and collage mature (type III collagen is replaced by type I collagen)
27
Q

steps in healing of skin wounds

A

1) laceration occurs
2) inflammatory reaction is incited
3) blood clot (fibrin, fibronectin) forms
4) epithelium regenerates to cover defect
5) cells proliferate and migrate into defect (macrophages remove debris and secrete cytokines, fibroblasts produce extracellular CT matrix, and myofibroblast contract the wound)
6) simultaneously capillaries (endothelium) at the edge of the defect proliferate and extend into the defect under the influence of chemical mediators
7) over weeks to months, the defect is filled with granulation tissue and becomes remodeled into mature collagen and the wound acquires strength through this process

28
Q

healing by first intention

A
  • clean, uninfected surgical incision approximated by surgical sutures
  • epithelial regeneration principle mechanism of repair
  • small scar and minimal contraction of the wound
29
Q

healing by second intention

A
  • large skin wound with extensive destruction, contamination, or infected where the edges aren’t approximated
  • larger clot and more intense inflammation
  • wound granulates in without closing the gap with sutures
  • process of healing is the same but takes longer because of size of the injury
  • wound contraction by myofibroblasts
30
Q

myofibroblasts

A
  • contract wounds

- modified fibroblasts with functional features of contractile smooth muscle cells

31
Q

wound strength by time

A
  • 1 week — 10% normal with collagen synthesis and modification and cross linking to increase fiber size
  • 3 months — 70-80% normal
32
Q

fibrosis

A
  • excessive deposition of collagen and other ECM components in tissue
  • fibrosis has bad effects while scar formation does not
33
Q

factors that influence repair

A
  • infection
  • nutrition
  • glucocorticoids (anti-inflammatory, inhibit TGF-B, can inhibit scar formation)
  • poor perfusion
  • diabetes mellitus (associated with underlying vascular disease)
  • foreign bodies
  • stable or labile cells vs permanent cells
  • location of injury
34
Q

vitamin C

A
  • cofactor for hydroxylation reactions (cross linking of lysine and proline in collagen synthesis)
  • deficiency - scurvy causes impaired wound healing and blod vessel fragility
  • scurvy caused by diets lacking in fruits and veggies
35
Q

zinc

A
  • function- cofactor for metalloenzymes (collagenase)
  • deficiency - poor wound healing and growth impairment
  • caused by inadequate intake, alcoholism, chronic diarrhea, and inflammatory disease
36
Q

copper

A

-cofactor for lysyl oxidase- cross links lysing and hydroxylysine
deficiency- abnormal collagen cross-linking, poor would healing, muscle weakness, and neurological deficits
-caused by total parenteral nutrition (from an IV)

37
Q

keloid

A
  • accumulation of exuberant amount of collagen
  • raised scars, grow beyond wound boundaries
  • more common in African Americans
38
Q

hypertrophic scar

A

excess production of scar tissue localized to the wound (raised scar) which may regress

39
Q

trichrome stain

A

stains mature collagen blue

MHD Exam 1 (6 decks)

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