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FPP: pre-midterm > Tissue healing and repair > Flashcards

Tissue healing and repair Flashcards

1
Q

Describe the two types of tissue repair

A
  • Regeneration (proliferation or uninjured cells and maturation of stem cells)
    • usual response of skin, liver, intestinal mucosa
    • basement membrane intact; NO SCAR
  • Healing with scar (when complete restitution is not possible)
    • usual response to severe/chronic damage in lung, liver, kidneys, etc
    • supporting structures are severly damaged and/or injured tissues are incapable of dividing
    • usually collagen deposition (fibrosis) provides strucutral support
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2
Q

How does regeneration differ between the epithelia and parenchymal organs?

A

Epithelia/skin= rapid replacement from residual cells and tissue stem cells

Parenchymal organs= more limited proliferation of residual cells in pancreas/adrenal/thyroid/lung (liver has more regenerative capacity driven by cytokines IL6/HGF)

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3
Q

Describe stem cell “self renewal”. What are the two types of stem cells?

A

Asymmetrical replication (a daughter cell differentiates, but the other remains a stem cell)

Two types;

  1. Embryonic (pluripotent; able to differentiate into all tissues)
  2. Adult
    1. Lineage specific (e.g. skin, GI epithelium)
    2. Multipotent progenitor cells (retain broad differentiation capabilities e.g. in BM)
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4
Q

Describe the basement membrane

A

Highly organized interstitial matric present around epithelial cells, endothelial cells, and smooth muscle cells.

**synthesized by mesenchyme and epithelium

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5
Q

What are the roles of the ECM?

A
  • mechanical support
  • regulate cell proliferation (through integrins)
  • provides scaffold essential for healing without a scar
  • storage of growth factors (e.g. for fibroblasts/hepatocytes)
  • creates a “microenvironment”
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6
Q

What are the components of ECM?

A
  1. Fibrous structural proteins
    1. Collagen for tensile strength
    2. Elastin (forms fibers with fibrillin) for recoil
  2. Proteoglycans/hyaluronan (gels for compressibility)
  3. Adhesive glycoproteins and receptors
    1. Fibronectin (in interstitial ECM)
    2. Laminin (in basement membrane)
    3. Cell adhesion molecules (CAMs; e.g. immunoglobulins, cadherins, selectins, integrins)
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7
Q

What are the steps of scar formation?

A
  1. Inflammation (macrophages)
    1. M1s clear microbes/necrotic tissue and promote inflammation
    2. M2s produce growth factors that stimulate cell proliferation
  2. Cell proliferation and angiogenesis
    1. Epithelial/endothelial/vascular cells and fibroblasts
    2. Granulation tissue
  3. Remodeling (reorganization of collagen -> scar)
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8
Q

What are the components/steps of angiogensis from pre-existing vessels?

A
  • Vasodilation (NO and VEGF; vascular endothelial growth factor)
  • Migration of endothelial cells towards injury (VEGF)
  • Proliferation of endothelial cells (VEGF and FGF; fibroblast growth factor)
  • Recruitment of pericytes and smooth muscle cells (PDGF; platelet derived growth factor, and TGF-B)
  • Notch signaling; regulates sprouting and branching of new vessels
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9
Q

What causes fibroblast migration to site of injury?

A

Endothelium and inflammatory cells secrete growth factors (TGF-B, PDGF, FGF)

**fibroblasts deposite ECM; at first loose/immature, eventually dense and inactive (scar)

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10
Q

What is VEGF? Its origin and function?

A

Vascular endothelial growth factor

Source: mesenchymal cells

Function: induces angiogenesis in injury and in tumors (stimulates endothelial cells)

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11
Q

What is FGF? Its origin and function?

A

Fibroblast growth factor

Source: macrophages, mast cells, endothelial cells, fibroblasts (and more)

Function: induces angiogenesis; promotes migration of fibroblasts, epithelial cells, and macrophages

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12
Q

What is PDGF? Its origin and function?

A

Platelet derived growth factor

Source: platelets, macrophages, endothelial cells, smooth muscle cells, epithelium

Function: induces fibroblast, SM, endothelial cell proliferation and migration; stimulates production of ECM

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13
Q

What is TGF-B? Its origin and function?

A

Transforming growth factor beta

Source: platelets, endothelium, epithelium, lymphocytes, macrophages, SM, fibroblasts

Function: suppresses endothelial proliferation/migration and acute inflammation; stimulates production of ECM proteins

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14
Q

What is granulation tissue?

A

“Hallmark” of repair process

**fibroblasts/collagen, connective tissue, new blood vessels, and scattered chronic inflammatory cells

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15
Q

What are the characteristics of scar remodeling?

A
  • decreased vessels
  • some degradation of collagen and other ECM proteins (by zinc containing Matrix Metalloproteinases; MMPs)
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16
Q

What is first intention?

A

“Primary union”; a wound closed by approximation of wound margins, placement of a graft, or surgical incision closed with stitches/stables

**Acute wounds withing 24 hours of injury (before granulation tissue)

17
Q

What is second intention?

A

“Secondary union”; wound is left open and allowed to close by epithelialization, granulation tissue and wound contraction (myofibroblasts) -> substantial scar

*more intense inflammatory response than primary (large fibrin clot and more necrotic material to be removed)

**commonly used in management of large/chronic or infected wounds

18
Q

Describe the steps of healing by first intention

A
  1. immediate filling of incisional space with clotted blood
  2. within 24 hrs neutrophils appear at wound margins (begin re-epithelialization)
  3. by day 3 neutrophils replaced by macrophages and granulation tissue fills incisional space
  4. day 5= maximal granulation tissue, collagen fibers begin to bridge incision
  5. weeks later scar is formed (connective tissue without inflammation; decreased vessels)
19
Q

What factors influence healing?

A
  1. Nutrition (vit C deficiency inhibits collagen synthesis)
  2. Metabolic status (e.g. diabetics have impaired neutrophil/macrophage functions, impaired vessel and collagen synthesis -> persistent ulcers/infections)
  3. Circulatory status/perfusion
  4. Steroids (inhibit TGF-B, decrease fibrosis)
  5. Infection
  6. Mechanical factors (increased local pressure -> bed sore)
  7. Foreign bodies
20
Q

What is a keloid?

A

A raised hypertrophic scar due to excess collagen

Mechanism not completely understood (increased activity of TGF-B and IL1?)

**Heritable (african americans= increased risk)

21
Q

What is exuberant granulation?

A

Tissue protrudes above surrounding skin and prevents re-epithelialization

22
Q

What is ehlers-danlos syndrome (EDS)?

A

Genetic defects in collagen synthesis or structure

Symptoms: fragile/stretchy skin, hypermobile joints/ligaments, rupture of internal organst (colon) and large arteries, poor wound healing

**Classic type results in deficient production of collagen type V

23
Q

What is marfan syndrome?

A

Mutation affecting fibrillin (a major component of microfibrils in ECM; abundant in aorta, lens, ligaments)

Symptoms: aortic aneurysm/dilation, lens dislocation, abnormal aortic/mitral valves, long legs/arms/fingers, hypermobile joints

FPP: pre-midterm (19 decks)

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