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FPP Weeks 1 & 2 > Tissue Repair > Flashcards

Tissue Repair Flashcards

1
Q

What are the two types of regeneration?

A

Regeneration-growth of cells and tissues to replace lost structures

and

Healing with scar-When complete restitution not possible since supporting structures everely damaged and/or injured tissues are incapable. Usually collagen deposition (fibrosis) provides structural support

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2
Q

what organs regenerate vs. heal with scars

A

Regeneration:

Skin, Liver, Intestinal

Healing with scar:

Severe/chronic damage in lung, liver kidneys etc.

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3
Q

What are the 3 types of cell renewel tissues and what types of organs are associated with each?

A
  1. Labile- Continuous renewal

Hematopoietic cells in marrow, surface epithelia, mucosal epithelia (ducts, g.i., bladder respiratory, etc.)

  1. Stable- Parenchyma of most solid organs

Pancrease, adrenal, lung, thyroid, kidney, also liver (except liver has more regenerative capabilities, fxnal mas not form) also almost all hepatocytes participate during regeneration not stem cells.

  1. Non-dividing cells- repair by connective tissue

Neurons, cardiac myofibers

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4
Q

What are the 4 growth factors involved in repair?

A
    1. VEGF (Vascular endothelial growth factors)*
    1. FGF (Fibroblast growth factors)*

3. PDGF (Platelet-derived growth factors)

4. TGF-beta (Transforming growth factor-beta)

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5
Q

Source and fxn of VEGF?

A

Mesenchymal cells

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

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6
Q

Source and fxn of FGF?

A

Macrophages, mast cells, endothelial cells, fibroblasts, and more

Induces angiogenesis; promotes migration of fibroblasts, epithelial cells, and macrophages

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7
Q

Source and fxn of PDGF?

A

Platelets, macrophages, endothelial cells, smooth muscle cells epithelium

Induces fibroblast, smooth muscle, endothelial cell proliferation & migration; stimulates production of ECM

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8
Q

Source and fxn of TGF-beta

A

Platelets, endothelium, epithelium, lymphocytes, macrophages, smooth muscle cells, fibroblasts.

Suppresses endothelial proliferation/migration & acute inflammation; stimulates production of ECM proteins

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9
Q

What are the 2 basic forms of ECM?

A

Interstitial matrix: a 3-D amorphous gel

Basement Membrane: highly organized interstitial matrix present around epithelial cells, endothelial cells, & smooth muscle cells.

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10
Q

What synthesizes interstitial matrix

A

Fibroblasts

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11
Q

What synthesizes basement membrane

A

Mesenchyme and epithelium

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12
Q

What is the role of the extracellular matrix ECM?

A
  • Mechanical support
  • Regulate cell proliferation (through integrins)
  • Provides scaffold essential for healing without scar
  • Storage of growth factors: fibroblast growth factor, hepatocyte growth factor
  • Creates a “microenvironment”
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13
Q

What are the components of ECM

A

I. Fibrous structural proteins:

Collagen and Elastin

II. Proteoglycans & hyaluronan-

Highly hydrated gels that provide compressibility and contain growth factors

III. Adhesive glycoproteins & receptors:

Fibronectin (major component of interstitial ECM), Laminin (Major component of basement membrane), Adhesion molecules (cell adhesion molecules CAMs)

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14
Q

What is collagen?

A

Structural proteins providing tensile strength

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15
Q

What is elastin?

A

Forms elastic fibers with fibrillin allowing for recoil

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16
Q

What is the cause of Ehlers-Danlos syndrome (EDS)

A

Genetic defects in collagen synthesis or structure

17
Q

What are the common clinical features of Ehlers-Danlos syndrome?

A

Tissues containing the type of affected collagen lack tensile strength:

  1. Skin-hyperextensible, fragile, and easily traumatized
  2. Joints and ligaments are hypermobile
  3. Rupture of internal organs (colon) & large arteries
  4. Poor wound healing

* Classic type results in deficient production of collagen type V

18
Q

What is Marfan syndrome? What are some of the symptoms/findings?

A

Mutation affecting fibrillin.

  1. Degeneration of aorta:aneurysm and dilatation
  2. Dislocated lens
  3. Abnormalities of aortic and mitral valves
  4. Long legs, arms, fingers
  5. Hyper-extensible joints
19
Q

What is Fibrillin and where is it present?

A

The major component of microfibrils in ECM, widely distributed in body and abundant in: AORTA, LENS, LIGAMENTS

20
Q

When does repair by connective tissue (scar formation) occur?

A

Severe/chronic injury with destruction of stroma.

Injury of non-dividing cells

21
Q

What are the steps of repair by connective tissue (Scar formation)?

A
  1. Angiogenesis
  2. Fibroblast migration and proliferation
  3. Extracellular matrix deposition (scar formation)
  4. Maturation of fibrous tissue (remodeling)
22
Q

When is granulation tissue present? What is it and what does it contain?

A

3-5 days.

Specialized tissue seen in healing.

Contains new vessels, inflammatory cells, and fibroblasts.

23
Q

What are the important growth factors for Angiogenesis?

A

VEGF and FGF

24
Q

Where does angiogenesis come from? And what are the important key points of each?

A
  1. From pre-existing vessels

Vasodilatation: Nitric oxide (NO), vascular endothelial growth factor (VEGF)

Migration

Proliferation

Eventual inhibition and remodeling

  1. From endothelial precursor cells (angioblasts) in bone marrow

Neovascularization of ischemic organs, wounds and tumors, and re-endothelialization of grafts

25
Q

What are the important growth factors for fibroblast migration and proliferation and deposition of ECM?

A

**TGF-beta **

PDGF

FGF

26
Q

What occurs in the maturation of fibrous tissue?

A

Decreased vessels and some degradation of collagen and other extracellular matrix proteins.

27
Q

What accomplishes the degradation of collagen and other ECM proteins during the maturation of fibrous tissue? What is it secreted by

A

Matrix metalloproteinases (MMP) containing zinc.

Secreted by several cell types: fibroblasts, macrophages, neutrophils etc.

28
Q

What is wound strength at the end of the first week?

A

10%

29
Q

What are the steps to cutaneous wound healing?

A

3 phases;

  1. Inflammation
  2. Granulation tissue formation and re-epithelialization
  3. Wound contraction, ECM deposition, and remodeling
30
Q

Steps of healing by First Intention (or Primary Union) and timeframe

A
  • Immediate*- Incisional space fills with clotted blood
  • Within 24 hrs*- Neutrophils appear at margin of wound, beginning of re-epithelialization
  • By day 3*- Neutrophils replaced by macrophages and granulation tissue fills incisional space
  • By day 5*- Maximal granulation tissue and Collagen fibers begin to bridge incision
  • Weeks*-Scar: connective tissue without inflammation;decreased vessels
31
Q

When does healing by Secondary Intention/Secondary union occur?

A

When more extensive damage leaves a tissue defect: large wounds, abcesses, ulceration.

32
Q

When does wound strength rapidly increase and when does it plateau and to what extent of wound strength?

A

10% at end of first week.

Rapid increase in wound strength over the next four weeks

Plateaus by 3rd month at 70-80%

33
Q

Factors influencing healing

A

Nutrition- Vitamin C deficiency inhibits collagen synthesis

Metabolic status- Diabetic patients have impaired neutorphil and macrophage functions, impaired new vessel formation, impaired collagen synthesis, all leading to persistence of ulcers and infections.

Circulatory status- Poor perfusion or obstructed venous drainage prevents in-flow of needed cells/proteins

Hormones-Steroids inhibit TGFbeta and decreases fibrosis

Infections- Prolongs inflammation and may increase local tissue injury

Mechanical factors- Increased local pressure may lead to dehiscence (rupture of surgical incision or closed wound)

Foreign bodies- Prolongs inflammation

34
Q

Types of wound healing complications

A
  1. Deficient scar formation- Dehiscence and ulceration like on diabetic patients
  2. Excessive repair component formation- Keloid (raised scar due to excess collagen) and Exuberant graulation (protrudes above surrounding skin and prevents re-epithelialization).
  3. Formation of contractures- Excessive contraction resulting in deformity of wound/surrounding tissue such as afer serious burns
35
Q

What is the mechanism of keloids?

A

Not completely understood but

Increased activity of TGF-beta and IL-1 (fibrogenic cytokines) has been described.

Heritable and African-Americans have increased risk.

FPP Weeks 1 & 2 (18 decks)

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