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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
Effects of severe/chronic injury
Damage to parenchymal cells, stromal framework/ECM, epithelial cells, non-dividing cells Repair and scar formation
26
Basic features of repair
Inflammation (contains damage, removes injured tissue, deposition of ECM) Angiogenesis Migration and proliferation of fibroblasts Scar formation Connective tissue remodeling
27
Major cytokine involved in fibrosis
TGF-B
28
Steps in angiogenesis
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
Components of angiogenesis
GFs (VEGF, FGF, Angiopoietins, PDGF and TGF-B) Notch signaling ECM proteins Enzymes (MMPs)
30
Functions of VEGF
Stimulates migration and proliferation of endothelial cells (capillary sprouting) Production of NO = vasodilation Formation of vascular lumen
31
Functions of FGF
Stimulates proliferation of endothelial cells Migration of macrophages and fibroblasts Epithelial cell migration (epidermal wounds)
32
Functions of Angiopoietins
Structural maturation of vessels | Ang1-Tie2 (RTK) on endothelial cells
33
Functions of PDGF and TGF-B
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
Functions of notch signaling
Cross-talk with VEGF Regulates vessel formation Spaces out vessels
35
Functions of ECM proteins
Vessel sprouting (interaction with integrin receptors + scaffolding for vessel growth)
36
Function of MMPs
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
Timeline for scar formation
24 h: repair (fibroblast emigration and fibroblast and endothelial cell proliferation) 3-5d: granular tissue formation; collagen synthesis by fibroblasts
38
Steps in scar formation
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
Steps in CT deposition
Migration and proliferation of fibroblasts into site of injury Deposition of ECM proteins
40
Regulators of TGF-B
Posttranscriptional activation of latent TGF-B Rate of secretion of active molecule Factors in ECM (integrins)
41
TGF-B stimulates
Fibroblast migration and proliferation Collagen and fibronectin synthesis Termination of inflammatory responses
42
TGF-B inhibits
Lymphocyte proliferation Activity of other leukocytes MMPs ECM degradation
43
Other serine proteases that can degrade ECM but not metaloenzymes
Neutrophil elastase Cathepsin G Plasmin
44
Producers of MMPs
``` Fibroblasts Macrophages Neutrophils Synovial Cells some epithelial cells ```
45
Phases of cutaneous wound healing
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
Types of skin wound healing
``` First intention (epithelial layer; regeneration) Healing by second intention (extensive cell/tissue loss; regeneration and scarring) ```
47
(First intention) Immediate response
Coagulation pathways --> clot VEGF = increased vessel permeability and edema Dehydration of external surface of the clot and scabbing
48
(First intention) 24 h
Neutrophils migrate towards fibrin clot Release of proteolytic enzymes to clear debris Increased mitotic activity of basal cells
49
(First intention) 24-48 h
Epithelial cells migrate and proliferate in dermis | Deposition of BM
50
(First intention) Day 3
Macrophages replace neutrophils Granulation tissue invades Continued epithelial proliferation
51
(First intention) Day 5
Peak neovascularization Increased edema Chemokines = fibroblast migration GF = proliferation
52
(First intention) 2nd week
Collagen accumulation Fibroblast proliferation Decrease leukocytes, edema, vascularity Blanching = increased collagen deposition
53
(First intention) 1 month
Scar (no inflammatory cells, normal epidermis) | Dermal appendages destroyed are lost
54
Timeline for second intention
Immediate: Fibrin, collagen, plasma fibronectin, type 3 collagen Two weeks: type 3 -> type 1 1 month: scar (acellular CT, no inflammation, intact epidermis)
55
Wound strength
1 week: 10% 3 mo: 70-80% Comes from collagen synthesis
56
Systemic factors that influence wound healing
``` 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
Local factors that influence wound healing
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
Complication: inadequate formation of granulation tissue/scar
``` Wound dehiscence (rupture, mechanical stress) Ulceration (inadequate vascularization, non-healing wounds in no sense area) ```
59
Complication: excessive formation of components of repair process
``` Hypertrophic scars (raised, within normal margin; accumulation of collagen; involves deep layers of dermis) Keloid (grows beyond original wound) ```
60
Complication: exuberant granulation
Protrudes above level of skin Blocks reepithelialization Desmoids (aggressive fibromatoses, neoplasms)
61
Complication: contracture
Develops in palms, soles, anterior aspect of thorax After serious burns Compromises movement of joints

03 BP1 (18 decks)

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