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71 Cards in this Set
- Front
- Back
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angiogenesis
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blood vessel formation in adults (critical to chronic inflammation, tumor growth and to vascularization of ischemic tissues)
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precursor of collagen? comes from?
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PROCOLLAGEN (secreted by cells and cleaved into collagen)
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Firbillar Collagens
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Types I, II, III, and V
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In terms of wound healing, probably the most important type of collagen
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Type IV Collagen, (BM type)
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ubiquitous collagen type, most abundant, found in skin, bone, and many other tissues (hard and soft)
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Type I collagen
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Type II collagen
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CARTILAGE
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Type III cartilage is a component of...
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hollow organs and soft tissues
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Type V collagen is found in what types of tissues?
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soft tissues
and blood vessels |
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BM components
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Type IV collagen
Laminin Entactin Haparin Sulfate Proteoglycan |
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type of collagen found in intervertebral disk cartilage
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Type IX volalgen
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firbonectin
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large protein, binds to many molecules (eg: integrins, heparin, collagen, fibrin, proteoglycans and cell-surface receptors)
2 types: TISSUE FIBRONECTIN and PLASMA FIBRONECTIN |
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protein that forms fibrillar aggregates at wound healing sites
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Tissue fibronectin
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protein that forms initial wound filling clot (serves as substrate for ECM deposition)
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Plasma form of Fibronectin
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most abundant glycoprotein in the BM
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Laminin
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Laminin
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most abundant glycoprotein in the BM
has binding domains for both ECM and cell-surface receptors (binding sites for Type IV collagen, cell, heparin sulfate proteoglycan) |
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granulation tissue
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the perfused, fibrous connective tissue that replaces a fibrin clot in healing wounds
(VEGF promotes angiogenesis and + vascular permeability, exudation and deposition of plasma proteins (eg fibrinogen and plasma fibronectin in the ECM) provides a stroma for fibroblast and endothelial cell growth |
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these trigger migration to site of injury and subsequent proliferation of fibroplasts
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GROWTH FACTORS
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examples of GROWTH FACTORS involved in wound healing:
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TGF-beta, PDGF, EGF, FGF and cytokines IL-1 and TNF.
sources: platelets, MOs and activated endothelial cells |
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regeneration
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requires: INTACT TISSUE SCAFFOLDING (esp. BM) new cells in tissue/organ derived from division of stabile cells or new cells from stem cells **restores tissue to NORMAL STATE
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healing
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occurs when tissue scaffolding has been altered or destroyed, involves combination of creation of new tissue cells and collagen deposition (fibrosis/scarring) **normal state never totally re-established
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scar
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composed of spindle shaped fibroblasts, dense collagen, fragements of elastic tissue and other ECM components
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what happens as a scar matures?
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vascular regression continues, eventually transforming the richly vascular granulation tissue to a pale avascular scar
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what are the 3 normal cell types (in terms of their turnover)
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LABILE: continually replaces
STABILE: not dividing, but can divide PERMANANT: cannot divide |
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cell proliferation is regulated by what 3 factors?
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a) hormonal influences
b) growth stimuli (during growth years) c) pathological stimuli |
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cell devision in most stabile cell populations is governed by what 3 factors?
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a) soluble stimulatory factors
b) soluble INHIBITORY factors c) cell-cell contact (eg: contact inhibition) |
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increasing cell proliferation to repair damage can occur by what 3 mechanisms?
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a) shortening the cell cycle (proliferate faster)
b) pushing stabile cells into the cell cycle c) stimulating stem cells to generate parenchymal cells |
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TRANSMEMBRANE SIGNALING is a critical feature in tissue repair. What kind of membrane receptors are involved?
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-RTKs (receptors with kinase activity, typically bind: GFs)
-Receptors w/o kinase activity (typically bind CYTOKINES and INTERLEUKINS) -GPCRs (7 transmembrane proteins, bind CHEMOKINES) |
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ECM components
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COLLAGENS (I, II and IV)
PROTEINS (that connect cells to ECM, laminin, fibronectin, integrins) GAGs (glycosaminoglycans: heparan suflate, dermitan sulfate, etc..) |
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a FIBROPROLIFERATIVE RESPONSE that PATCHES rather than restores tissue
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HEALING
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Basic Steps in TISSUE REPAIR
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1) CLOTTING (fibrin deposition) if needed; 2) INFLAMMATION and DECONTAMINATION (M0s); 3) RELEASE of CHEMOATTRACTANTS AND GFs; 4) MIGRATION/PROLIFERATION of FIBROBLASTS; 5)PRODUCTION of ECM materals 6)ANGIOGENESIS; 7)REMODELING of ECM/COLLAGEN; 8)CONTRACTION 9) APOPTOSIS of FIBROBLASTS in MATURE SCAR
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Pathways (involved in would healing) associated with Receptors with Tyrosine Kinase Activity
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PI3 Pathway
MAP-Kinase Pathway IP3 Pathway (all affect Transcription Factor activity) |
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cAMP pathway is activated by what type of receptor?
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GPCRs (typically bind CHEMOKINES: eg serotonin, histamine)
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JAK/STAT pathway is activated by what?
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CYTOKINES
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chemokines signal ax membranes via what type of receptors?
what kind of intracellular change results? |
GPCRs
causing release of Ca2+ and/or generation of cAMP |
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stabile cells are in what phase of cell cycle?
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Go
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Where are the two major cell cycle checkpoints for DNA damage?
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G2/M checkpoint: for damaged or unduplicated DNA
G1/S checkpoint: for DNA damage |
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What is CDK1? What does it do?
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Cyclin depedent kinase 1 (produced constituitively, but requires cyclinB for activity)
when bound to cyclin B, works as TRANSCRIPTION FACTOR (pushes cell from S phase to G2) phosphorylation, associated with G2/M checkpoint |
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during what phase is the RESTRICTION POINT of the cell cycle?
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G1 (Pre-synthetic phase)
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Over what timeframe do the following events occur following tissue injury?
INFLAMMATION GRANULATION TISSUE formation WOUND CONTRACTION |
INFLAMMATION (0-3 days)
GRANULATION TISSUE formation (0.3-10 days) WOUND CONTRACTION (3-50 days) |
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What is HEALING BY 1st INTENT?
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wound edges apposed (better result than if apart)
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Healing by "2nd INTENT"
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wound edges apart, or loss of tissue (increased scar)
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TRANSMEMBRANE SIGNALING is a critical feature in tissue repair. What kind of membrane receptors are involved?
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-RTKs (receptors with kinase activity, typically bind: GFs)
-Receptors w/o kinase activity (typically bind CYTOKINES and INTERLEUKINS) -GPCRs (7 transmembrane proteins, bind CHEMOKINES) |
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ECM components
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COLLAGENS (I, II and IV)
PROTEINS (that connect cells to ECM, laminin, fibronectin, integrins) GAGs (glycosaminoglycans: heparan suflate, dermitan sulfate, etc..) |
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a FIBROPROLIFERATIVE RESPONSE that PATCHES rather than restores tissue
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HEALING
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Basic Steps in TISSUE REPAIR
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1) CLOTTING (fibrin deposition) if needed; 2) INFLAMMATION and DECONTAMINATION (M0s); 3) RELEASE of CHEMOATTRACTANTS AND GFs; 4) MIGRATION/PROLIFERATION of FIBROBLASTS; 5)PRODUCTION of ECM materals 6)ANGIOGENESIS; 7)REMODELING of ECM/COLLAGEN; 8)CONTRACTION 9) APOPTOSIS of FIBROBLASTS in MATURE SCAR
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Pathways (involved in would healing) associated with Receptors with Tyrosine Kinase Activity
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PI3 Pathway
MAP-Kinase Pathway IP3 Pathway (all affect Transcription Factor activity) |
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cAMP pathway is activated by what type of receptor?
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GPCRs (typically bind CHEMOKINES: eg serotonin, histamine)
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JAK/STAT pathway is activated by what?
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CYTOKINES
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chemokines signal ax membranes via what type of receptors?
what kind of intracellular change results? |
GPCRs
causing release of Ca2+ and/or generation of cAMP |
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stabile cells are in what phase of cell cycle?
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Go
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Where are the two major cell cycle checkpoints for DNA damage?
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G2/M checkpoint: for damaged or unduplicated DNA
G1/S checkpoint: for DNA damage |
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What is CDK1? What does it do?
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Cyclin depedent kinase 1 (produced constituitively, but requires cyclinB for activity)
when bound to cyclin B, works as TRANSCRIPTION FACTOR (pushes cell from S phase to G2) phosphorylation, associated with G2/M checkpoint |
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during what phase is the RESTRICTION POINT of the cell cycle?
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G1 (Pre-synthetic phase)
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Over what timeframe do the following events occur following tissue injury?
INFLAMMATION GRANULATION TISSUE formation WOUND CONTRACTION |
INFLAMMATION (0-3 days)
GRANULATION TISSUE formation (0.3-10 days) WOUND CONTRACTION (3-50 days) |
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What is HEALING BY 1st INTENT?
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wound edges apposed (better result than if apart)
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Healing by "2nd INTENT"
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wound edges apart, or loss of tissue (increased scar)
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complications of wound healing process
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1) SCAR ITSELF (esp. parencymal scarring of organ)
2) KELOIDS 3) CONTRACTURES (collagen maturation/contraction) 4) ULCERATION (incomplete healing) |
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factors determining outcome/effectiveness of healing
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-extent of damage
-if healing by 1st or 2nd intent |
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definition of wound
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disruption of tissue continuity
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scap
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coagulated mtaerial that has accumulated in a wound
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ESCHAR
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scab-like lesion on the skin following a burn
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GRANuLATION TISSUE
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early scar tissue
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KELOID
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exaggherated type of scar formation
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CICATRAX
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scar
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coagulation factors active in would repair
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HAGEMAN FACTOR FRAGMENTS (vasopermeability)
BRADYKININ (vasodilation, permeability, pain) COMPLEMENT (leuocyte recruitment, vasopermeability) FIBRIN CLOT (hemostatic plug, reservoir of GFs, provisional matrix for cell migration) |
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role of platelets in wound repair
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ADHESION (plug small leaks in vessls)
AGGREGATION (plug large leaks, induce coagulation) MEDIATOR RELEASE (vasoconstriction, stimulates additional aggregation of platelets and GF release) |
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GFs active in wound healing
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FGF1 & 2
PDGF TGF-beta VGEF |
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FGF1&2
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Fibroblast Growth Factors
active in wound healing (fibroblast and epidermal cell proliferation and angiogenesis) |
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PDGF
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platelet derived growth factor
active in wound healing involved in fibroblast chemotaxis, proliferation and contraction |
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TGF-beta
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TRANSFORMING GF beta
involved in wound healing fibroblast chemotaxis ECM deposition protease inhibitor secretion |
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VGEF
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Vascular Endothelial Growth Factor
involved in vascular permeability, angiogenesis |
