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Ch 4: Pathophysiology
Cell proliferation and tissue regeneration and repair.
Terms in this set (47)
Refers to the restoration of tissue structures and functions after an injury.
-Involve proliferation of various cells, and close interactions between cells and the extracellular matrix.
-proliferation, differentiation, and apoptosis
Found in all body organs and tissues: type 1.
contains the functioning cells of an organ or body part
Found in all body organs and tissues: type 2
Consist of the supporting connective tissues, blood vessels, fibroblasts, nerve fibers and extracellular matrix.
Refers to the process of increasing cell numbers by mitotic division and cell differentiation, the process whereby a cell becomes more specialized in terms of structure and function.
Are undifferentiated cells that have the capacity to generate multiple cell types.
Is the orderly process in which proliferation cells are transformed into different and specialized cell types. It determines the microscopic characteristic of the cell, its functions, and its life span. Cells that are fully differentiated often have reduced rates of proliferation.
Is a form of programmed cell death that eliminates senescent and some types of injured cells.
(G1, S, G2,) interphase and (M) Mitosis.
Gap 1 is the postmitotic phase during which DNA synthesis occurs and cell growth takes place.
DNA synthesis occurs, giving rise to two separate sets of chromosomes. One for each daughter cell.
Is the premitotic phase and is similar to G! DNA synthesis ceases while RNA and proteins synthesis continue.
This is when nuclear division or mitosis and cytokinesis takes place. continually dividing cells, continue to cycle from one mitotic division to the next.
Proliferative capacity of Tissues
The capacity for regenerations varies with the tissue and cell type. Body tissues are divided into three types dependent on their parenchymal cells to undergo regeneration. 1) continuously dividing 2) stable 3) permanent tissues
Continuously dividing Tissues
or labile tissue are those in which the cell continue to divide and replicate throughout out life, replacing cells that are continually being destroyed.
Contain cells that normally stop dividing when growth ceases. Cells in these tissues remain quiescent in the G stage of the cell cycle. However, these cells are capable of undergoing regeneration when confronted with an appropriate stimulus and are thus capable of reconstituting the tissue of origin.
Do not proliferate. The cells in these tissue are considered to be terminally differentiated and do no undergo mitotic division in postnatal life.
once destroyed they are replaced with fibrous scar tissue that lacks the functional characteristics.
Checkpoints and Cyclins
In most cells there are several checkpoints the cell cycle at which time the cycle can be arrested if previous events have not been completed.
-This is a mediator that can trigger cell proliferation.
-Generally applied to small hormone-like proteins that increase cell size and cell division.
Epidermal Growth Factor (EGF)
-Activated macrophages, keratinocytes, and many other cells
-Mitogenic for keratinocytes and fibroblasts; stimulates keratinocyte migration and granulation tissue formation.
Transforming Growth factors (Alpha) (TGF-A)
-Activated macrophages, T cells, Keratinocytes and many others.
-Similar to EGF; stimulates replication of hepatocytes and many epithelial cells.
Transforming Growth Factors (Beta) (TGF-B)
-Activated by platelets, macrophages, T cells, keratinocytes, smooth muscle cells ad fibroblast.
-Chemotactic for neutrophils, macrophages, fibroblast, and smooth muscle cells; stimulates angiogenesis and production of fibrous tissues; inhibits proteinase production and keratinocyte proliferation.
Vascular Endothelial Cells Growth Factor (VEGF)
- From mesenchymal cells
- Increases vascular permeability; mitogenic for endothelial cells of blood vessels
Platelet-Derived Growth Factor (PEGF)
-From Platelets, macrophages, endothelial cells, keratinocytes, and smooth muscle cells.
- Chemotactic for neutrophils, macrophages, fibroblasts, and smooth muscle cells; stimulates production of proteinases, fibronectin, and hyaluroinic acid; stimulates angiogenesis and wound remodeling.
Fibroblast Growth Factor (FGF)
-From macrophages, mast cells, T cells, endothelial cells, fibroblast, and many other tissues
-Chemotactic for fibroblasts; mitogenic for fibroblasts and keratinocytes; stimulates angiogenesis, would contraction and matrix deposition.
Keratinocyte Growth Factor (KGF)
-Stimulates keratinocyte migration, proliferation, and differentiation.
Healing by Connective Tissue Repair
-This refers to the restoration of injured tissue to its normal structure and function by inflammation, proliferation, and remodeling phase.
-Injured Tissues can be repaired by regeneration of the injured tissue cells with cells of the same tissue or parenchymal type, or by connective repair processes in which scar tissue is used to effect healing
is limited to tissues with cells that are able to undergo mitosis.
Wound Healing impaired by
conditions that diminish blood flow and oxygen delivery, restricting nutrients and other materials needed for healing and depress the inflammatory and immune responses; and by infection, would separation and the presence of foreign bodies.
Phases of repair
Repair by connective tissue deposition can be divided into 2 phases: 1) angiogenesis and ingrowth of granulation tissue
2) emigration of fibroblasts and deposition of extracellular matrix and 3) Maturation and reorganization of the fibrous tissue (remodeling)
by 3-5 days this tissue is apparent and progressively accumulates connective tissue, eventually resulting in the formation of a scar, which is then remodeled.
Angiogenesis and Ingrowth of granulation tissue
connective tissue that fills the injured area while necrotic debris is removed.
It is composed of newly formed capillaries (angiogenesis: a vasodilator), proliferating fibroblasts, and residual inflammatory cells followed by fusion and remodeling of the endothelial cells into capillary tubes.
Emigration of Fibroblasts and Deposition of Extracellular Matrix
Scar formation builds on the granulation tissue framework of new vessels and loose ECM. The process occurs in 2 phases: 1. emigration and proliferation of fibroblasts into the site of injury (formation of new vessels decrease and there is increased synthesis and deposition of collagen) 2. Deposition of extracelluar matrix by these cells.
-Ultimately the granulation tissue evolves into scar tissue.
Maturation and Remodeling of the Fibrous Tissue
The transition form granulation to scar tissue involves shifts in the modification and remodeling of the ECM.
There is a degradation of collagen and other ECM proteins.
Cutaneous woud healing
Healing of the skin: Inflammatory phase, proliferative phase and remodeling phase
Begins at the time of injury with the formation of a blood clot and the migration of phagocytic WBCs into the wound site. The first cells to arrive are neutrophils. they ingest and remove bacteria and cellular debris. Soon the macrophages join and continue to ingest cellular debris adn play an essential role in the production of growth factors for the proliferation stage.
The primary process during this phase focus on the building of new tissue to fill the wound space. Fibroblast are synthesized and glycoproteins are needed.
the final component of this phases is epitheliazation, during which epithelial cells at the wound edges proliferate to form a new surface layer that is similar to that which was destroyed by injury.
This phase begins approximately 3 weeks after injury with the development of the fibrous scar dn can continue for months after.
-there is a decrease in vascularity and there is remodeling of scar tissue by simultaneous synthesis of collagen by fibroblast and lysis by collagenous enzymes.
Scar tissue shrinks and is less visible.
Factors that affect wound healing
Malnutrition; impaired blood flow an oxygen delivery; impaired inflammatory and immune responses; infection; wound separation and foreign bodies and age effects.
Successful wound healing depends on adequate stores of proteins, carbs, fats, vitamins, and minerals. Malnutrition slows down the healing process.
prolong the inflammatory phase of healing and impair fibroblast proliferation, collagen and protein matrix synthesis, angiogenesis, and wound remodeling.
Carbs are needed as an energy source for WBCs. Carbs also have a protein-sparing effect and help to prevent the use of amino acids for fuels when they are needed for the healing process.
Fats are essential components of the cell membrane and are needed for the synthesis of the new cell.
Functions in stimulating and supporting epithelialization, capillary formation, and collagen synthesis.
Can counteract the anti-inflammatory effects of drugs and can be used to reverse there effects in persons who are on chronic steroid therapy.
Is needed for collagen synthesis.
without this there is improper sequencing of AA, proper linking of AA does not take place and the by products of collagen synthesis are removed from the cell causing wounds not to heal properly.
impaired Blood flow and oxygen delivery
For healing to occur, wounds must ahve adequate blood flow to supply the necessary nutrients and to remove the resulting waste, local toxins, bacteria and other debris.
Oxygen is required for collagen synthesis and killing of bacteria by phagocytic WBCs.
Impaired inflammatory and immune Responses
Inflammatory and immune responses are necessary for wound healing. Inflammation is essential to the first phase. and immune is needed to prevent infections that impair wound healing. This is a problem in persons with diabetes mellitus because of poor glucose levels.
Infection, wound separation and foreign bodies
Wound contamination, separation and foreign bodies rely healing. infection impairs all dimensions of healing as it prolongs teh inflammatory phase, impairs the formation of granulation tissue, and inhibits proliferation of fibroblast and deposition of collagen fibers.
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