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03 BP1 > 01 Wound Healing > Flashcards

01 Wound Healing Flashcards

1
Q

Mechanisms of tissue repair/healing

A

Regeneration (proliferation of residual cells, maturation of tissue stem cells)
Connective tissue deposition (scar formation)

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2
Q

Characteristics of regeneration

A

Replace damage and return to normal state

Proliferation of cells that survive the injury or stem cells

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3
Q

Characteristics of connective tissue deposition/scar formation

A

Injured structures are incapable of complete restitution or supporting structures are severely damaged
Fibrosis (deposition of collagen; ex. chronic inflammation in organs, ischemic necrosis in MI)

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4
Q

Cell types that proliferate during tissue repair

A

Remnants of injured tissue (restore to normal)
Vascular endothelial cells (create new vessel)
Fibroblasts (for scar formation)

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5
Q

Types of tissues

A 
Labile tissues (dividing cells; hematopoietic cells, epithelium)
Stable tissues (quiescent cells in G0 stage, can divide when injured; parenchyma, endothelial cells, fibroblasts, smooth muscles)
Permanent cells (terminally differentiated, results in scar formation; neurons, cardiac muscle cells, skeletal muscle but has satellite cells)
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6
Q

Signals for cell proliferation

A

Growth Factors

ECM

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7
Q

Characteristics of growth factors

A

Produced by macrophages, epithelial cells, stromal cells
Activates signaling pathways (produces proteins, initiates cells cycle)
Binds to ECM with integrins

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8
Q

Stem cell activation

A

Injury > signal to niches > activate quiescent stem cells > stem cell proliferation and differentiation > mature cells repopulate injured tissue

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9
Q

Characteristics of organs with stable cell populations

A

Limited regeneration, incomplete with scarring

Leads to hypertrophy and hyperplasia

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10
Q

Two mechanisms of liver regeneration

A

Proliferation of hepatocytes following partial hepatectomy

Repopulation from progenitor cells (from canals of Hering)

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11
Q

Steps in regeneration after partial hepatectomy

A

1st phase: priming phase (Cytokines by Kupffer cells act on hepatocytes to make them competent to receive and respond to GF)
2nd phase: GF phase (stimulates metabolism and start of cell cycle G0 to G1 -> replication of non-parenchymal cells)
3rd phasee: termination phase (return to quiescence)

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12
Q

Functions of ECM

A

Mechanical support
Control of cell growth (integrins)
Maintenance of cell differentiation (integrins)
Scaffolding for tissue renewal (basement membrane)
Establish tissue microenvironment (BM)
Storage and presentation of regulatory molecules (FGF and HGF)

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13
Q

Macromolecule groups in ECM

A 
Fibrous structural proteins (collagens and elastins; for tensile strength and recoil)
Adhesive glycoproteins (connects elements and cells)
Proteoglycans and hyaluronan (resilience and lubrication)
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14
Q

Basic forms of ECM

A 
Interstitial matrix (spaces between)
Basement membrane (cell surfaces)
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15
Q

Constituents of interstitial matrix

A 
Fibrillar and nonfibrillar collagen
Elastin
Fibronectin
Proteoglycans
Hyaluronan
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16
Q

Constituents of BM

A

Nonfibrillar collagen (IV)
Laminin
Heparin sulfate
Proteoglycans

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17
Q

Fibrous structural proteins

A

Collagen (framework, three chains forming triple helix, Gly-X-Y)
Elastin (central core of elastic fibers + peripheral network of microfibrils)
Fibrillin (microfibrillar network, connects with self or others)
Elastic fibers (provides elasticity to expand and recoil)

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18
Q

Types of collagen

A

Fibrillar (I, II, III, V, XI)
Basement membrane (IV)
Others (6, 7, 9, 17, 15 and 18)

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19
Q

Main families of adhesive glycoproteins (CAMs)

A

Immunoglobulin family CAMs
Cadherins (plasma membrane-plasma membrane; zonula adherens and desmosomes)
Selectins
Integrins (cell-ECM, cell-cell)

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20
Q

Fibronectin types

A 
Tissue fibronectin
Plasma fibronectin (fibrin; stabilize blood clot; foundation for ECM deposition)
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21
Q

Laminin characteristics

A

Abundant in BM
Binds ECM, cell surface receptors, CT substrates
Collagen IV

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22
Q

Catenin

A

Cadherin-cytoskeleton
Cadherin–B-catenin–a-catenin–actin
Cell motility, proliferation, differentiation, contact inhibition

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23
Q

Cadherin-integrin function

A

Cell surface-cytoskeleton
Mechanism for transmission of mechanical force
Activates intracellular signal transduction
Cross talk in environment

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24
Q

Families of GAGs

A

Heparin sulfate
Chondroitin/dermatan sulfate
Keratan sulfate
Hyaluronan (binds water to resist compression forces, resilience and lubrication, increased in [rheumatoid arthritis, scleroderma, psoriasis])

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25
Q

Effects of severe/chronic injury

A

Damage to parenchymal cells, stromal framework/ECM, epithelial cells, non-dividing cells
Repair and scar formation

26
Q

Basic features of repair

A

Inflammation (contains damage, removes injured tissue, deposition of ECM)
Angiogenesis
Migration and proliferation of fibroblasts
Scar formation
Connective tissue remodeling

27
Q

Major cytokine involved in fibrosis

A

TGF-B

28
Q

Steps in angiogenesis

A

Vasodilation in response to NO
Increased permeability induced by VEGF
Separation of pericytes and breakdown of basement membrane (vessel sprout)
Migration of endothelial cells towards area of tissue injury
Proliferation of endothelial cells
Remodeling into capillary tubes
Recruitment of periendothelial cells to form mature vessel (pericytes or smooth muscle cells)
Suppression of endothelial proliferation and migration
Deposition of BM

29
Q

Components of angiogenesis

A

GFs (VEGF, FGF, Angiopoietins, PDGF and TGF-B)
Notch signaling
ECM proteins
Enzymes (MMPs)

30
Q

Functions of VEGF

A

Stimulates migration and proliferation of endothelial cells (capillary sprouting)
Production of NO = vasodilation
Formation of vascular lumen

31
Q

Functions of FGF

A

Stimulates proliferation of endothelial cells
Migration of macrophages and fibroblasts
Epithelial cell migration (epidermal wounds)

32
Q

Functions of Angiopoietins

A

Structural maturation of vessels

Ang1-Tie2 (RTK) on endothelial cells

33
Q

Functions of PDGF and TGF-B

A

Stabilization process
PDGF: Recruits smooth muscle cells
TGF-B (from granular tissue): suppress endothelial proliferation and migration; fibrosis in lung, liver, and kidneys in chronic inflammation; anti-inflammatory cytokine (inhibit leukocyte proliferation)

34
Q

Functions of notch signaling

A

Cross-talk with VEGF
Regulates vessel formation
Spaces out vessels

35
Q

Functions of ECM proteins

A

Vessel sprouting (interaction with integrin receptors + scaffolding for vessel growth)

36
Q

Function of MMPs

A

Degrades ECM for remodeling and extension of vascular tube
Zymogens -> activated by proteases in site of injury -> MMPs
TIMPs: inhibit activated collangenases
ADAM: family of enzymes related to MMPs

37
Q

Timeline for scar formation

A

24 h: repair (fibroblast emigration and fibroblast and endothelial cell proliferation)
3-5d: granular tissue formation; collagen synthesis by fibroblasts

38
Q

Steps in scar formation

A

Angiogenesis (leaky: incomplete interendothelial junctions; VEGF = increased vascular permeability; edema)
Formation of granulation tissue (fibroblasts, loose CT, vessels, leukocytes; evolves into a scar)
Remodeling connective tissue (maturation and reorganization of CT; stable fibrous scar)

39
Q

Steps in CT deposition

A

Migration and proliferation of fibroblasts into site of injury
Deposition of ECM proteins

40
Q

Regulators of TGF-B

A

Posttranscriptional activation of latent TGF-B
Rate of secretion of active molecule
Factors in ECM (integrins)

41
Q

TGF-B stimulates

A

Fibroblast migration and proliferation
Collagen and fibronectin synthesis
Termination of inflammatory responses

42
Q

TGF-B inhibits

A

Lymphocyte proliferation
Activity of other leukocytes
MMPs
ECM degradation

43
Q

Other serine proteases that can degrade ECM but not metaloenzymes

A

Neutrophil elastase
Cathepsin G
Plasmin

44
Q

Producers of MMPs

A 
Fibroblasts
Macrophages
Neutrophils
Synovial Cells
some epithelial cells
45
Q

Phases of cutaneous wound healing

A

Inflammation (platelet adhesion and aggregation)
Proliferation (granulation tissue, proliferation and migration of CT cels, re-epithelialization of wound surface)
Maturation (ECM deposition, tissue remodeling, wound contraction)

46
Q

Types of skin wound healing

A 
First intention (epithelial layer; regeneration)
Healing by second intention (extensive cell/tissue loss; regeneration and scarring)
47
Q

(First intention) Immediate response

A

Coagulation pathways –> clot
VEGF = increased vessel permeability and edema
Dehydration of external surface of the clot and scabbing

48
Q

(First intention) 24 h

A

Neutrophils migrate towards fibrin clot
Release of proteolytic enzymes to clear debris
Increased mitotic activity of basal cells

49
Q

(First intention) 24-48 h

A

Epithelial cells migrate and proliferate in dermis

Deposition of BM

50
Q

(First intention) Day 3

A

Macrophages replace neutrophils
Granulation tissue invades
Continued epithelial proliferation

51
Q

(First intention) Day 5

A

Peak neovascularization
Increased edema
Chemokines = fibroblast migration
GF = proliferation

52
Q

(First intention) 2nd week

A

Collagen accumulation
Fibroblast proliferation
Decrease leukocytes, edema, vascularity
Blanching = increased collagen deposition

53
Q

(First intention) 1 month

A

Scar (no inflammatory cells, normal epidermis)

Dermal appendages destroyed are lost

54
Q

Timeline for second intention

A

Immediate: Fibrin, collagen, plasma fibronectin, type 3 collagen
Two weeks: type 3 -> type 1
1 month: scar (acellular CT, no inflammation, intact epidermis)

55
Q

Wound strength

A

1 week: 10%
3 mo: 70-80%
Comes from collagen synthesis

56
Q

Systemic factors that influence wound healing

A 
Nutritional status of the host (protein and vit C)
Metabolic status (diabetes = poor perfusion, immunocompromised)
Circulatory status (poor perfusion from diabetes, arteriosclerosis, obstructed veins)
Hormones (steroids = anti-inflammatory, inhibit TGF-B, diminished fibrosis)
57
Q

Local factors that influence wound healing

A

Type and extent of injury
Location of injury and character of the tissue
Infection (delays healing, prolong inflammation)
Mechanical factors (increased local pressure, wounds pull apart)
Foreign bodies

58
Q

Complication: inadequate formation of granulation tissue/scar

A 
Wound dehiscence (rupture, mechanical stress)
Ulceration (inadequate vascularization, non-healing wounds in no sense area)
59
Q

Complication: excessive formation of components of repair process

A 
Hypertrophic scars (raised, within normal margin; accumulation of collagen; involves deep layers of dermis)
Keloid (grows beyond original wound)
60
Q

Complication: exuberant granulation

A

Protrudes above level of skin
Blocks reepithelialization
Desmoids (aggressive fibromatoses, neoplasms)

61
Q

Complication: contracture

A

Develops in palms, soles, anterior aspect of thorax
After serious burns
Compromises movement of joints

03 BP1 (18 decks)

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