Repair, Regeneration, and Fibrosis Flashcards Preview

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Flashcards in Repair, Regeneration, and Fibrosis Deck (14):
1

platelets growth factors

- EGF: Growth of epithlial cells and fibroblasts, granulation tissue
- PDGF: Regulates chemotaxis of fibroblasts and monocytes
- FGF: promotes synthesis of ECM pro
- TGF-b: inhibits epithilial cell growth and promotes growth of fibroblasts

2

Fibroblasts (3)
*Fibronectin

- Produce ECM
- Produce collagen which produces fibrils (goes inbetween interstitual spaces)
- Requires vitamin C and zinc

* Fibronectin (foundation): glycoprotein in ECM
- binds collagen and fibrin

3

Myofibroblasts

- Contract wound, closing it
- Secrete collagen, proteases and other ECM
- Removed by apoptosis when wound closes

4

Angioblasts
- Days

Create temporary BV to provide cells w/ nutrients
- 2-3 days: Start to appear
- 5-6 days: At its peak (pink appearance)

5

Macrophages

Release growth factors to aggregate following:
Myofibroblasts, fibroblasts, angioblasts

Produce cytokine (TNF and IL-1)
Produce chemical mediators

6

Things that aggregate fibroblasts:

- Platelets: EGF, TGF-b
- Macrophages

7

ECM functions (4)

- Mechanical support
- Control cell growth (TGF-b)
- Microenvironment
- Stores regulatory molecules

8

Which cells start onset of tissue repair?

Platelets, macrophages, Mast cells

9

Main components of ECM (6)

- Collagen:
IV: sheets of cartilage
I: skin and bones
- Elastin, fibrillin, elastic fibers (elasticity)
- *Laminin - Most abundant glycoprotient
- Integrins form focal adhesion complexes (allow leukocytes to attach and move)
- *Cadherins: mediate Ca interactions (allow lekocytes direction in ECM)
- Proteoglycan: Retention of water (w/ stand compression)

10

Laminin

Most abundant glycoprotient in ECM
Where g-coupled protien recpetors bind (leukocytes crawl on this)

11

Diseases that decrease laminin alters what?

Alters:
Inflammatory
Repair
Immune

12

Wound dehiscence
- Why does it happen
- Risk of what

Parting of layers or failure of wound repair
- Why? Cells need right nutrients, macros, neutros, GFs, etc...
- Risk: Increased risk of infection and necrosis

13

2nd intention
- Inflammation
- Surface
- Granulation
- Wound contraction
- End result

Larger wound
- Inflammation is more intense (tissue injury while being repaired)

- Surface: fibronectin forms at surface. Not designed for mechanical stress, bacteria and water can get in.

- Granulation: B/c fibroblasts cant close wound, their intracellular mechanisms cause excess collagen fibers. Slows down healing process (LoF)

- Wound contraction: Portions can be closed, but big open area. Big clot
- End result: Ends with large scar (LoF). Can turn into keloid (limited jt mobility due to jt contractures)

14

Variables Influencing Wound Healing
- Systemic
- Local

Systemic:
- Nutritional: (GI tract problems)
- Metabolic: burn pts
- Circulatory: diabetes (poor blood circulation)
- Hormones: cortisol slows down healing

Local factors
- Size and location: skin vs heart
- Local factors can also delay wound healing: diseases affecting homeostasis, delay wound healing