Pathology Exam Block 1

Front 1

Wound Healing

Back 1

the end stage of the host response to tissue injury and is a phenomenon consisting of sequentially controlled, chemically mediated steps with result in the replacement of dead tissue with regenerated cells and/or scar tissue.

Front 2

Somatic Cell Division

Back 2

movement of a cell through the cell cycle. Beginning in G0 phase, then entering G1 phase where RNA is produced and synthesis of proteins occurs, then into S phase where DNA is duplicated, then through prophase, metaphase, anaphase, and telophase as long as no mutations were identified.

Front 3

Repair by regeneration

Back 3

effective repair is dependent on the regenerative capacity of each cell type.

Front 4

labile cells

Back 4

cells which continuously regenerate throughout life to replace other cells that are lost through normal physiological processes. Replacement of damaged cells is relatively rapid. Ex: all epithelial surfaces.

Front 5

permanent cells

Back 5

cells that do not have the ability to regenerate. Including striated and cardiac muscle cells and neurons of the CNS.

Front 6

PNS neurons

Back 6

capable of regenerating axons along a destroyed axon as long as the cell body is not damaged.

Front 7

stable cells

Back 7

cells which retain the ability to regenerate but do not do so under normal circumstances. What stimulates this cells to reenter the G1 phase and proliferate is not entirely known but there are some theories. Ex: hepatocytes, renal tubular epithelial cells, endothelial cells, etc.

Front 8

Stimulation by growth factors

Back 8

this theory states that these growth factors or mediators may be byproducts of phsiologic or pathologic processes or may be derived from injured tissue, inflammatory cells, or "reactive" native cells.

Front 9

growth factors

Back 9

polypeptide proteins which attach to cell membrane receptor sites on various types of cells and either promote DNA replication or "prime" the cell for DNA replication.

Front 10

Loss of contact inhibition

Back 10

when cells lose physical contact with neighboring cells, they are sometimes stimulated to divide by as yet unknown mechanisms.

Front 11

decrease in cellular density

Back 11

when cells of some tissues sense that the density of cells has fallen below a certain level, they are stimulated to divide (again by unknown mechanisms)

Front 12

repairing by collagenous scar formation

Back 12

the repair of injured tissue involves the production (by fibroblasts) of collagen to produce a scar (cicatrix) that will replace structurally damaged tissue.

Front 13

Type 1 collagen

Back 13

the predominant collagen in skin, bone, and most organs

Front 14

type IV (4) collagen

Back 14

a major component of subepithelial/endothelial basement membranes.

Front 15

healing by first intention

Back 15

refers to the repair process involved with surgical incisions where the margins of the wound are closely coapted by sutures or other methods. there is very little loss of tissue substance and a minimal amount of inflammatory exudate or necrotic debris.

Front 16

clot formation

Back 16

the inflammatory response initiated by tissue injury produces a fibrin-rich exudate (blood clot) which fils the space between wound margins. As it dehydrates, it forms a surface scab which seals the wound against invasion by microorganisms.

Front 17

epithelial regeneration

Back 17

Under the scab, surface epithelial cells from the wound margins begin to proliferate and migrate toward the midline within 24 hrs of the injury, and by 48 hrs a single layered epithelium covers the wound's surface. Then further proliferation occus.

Front 18

inflammation

Back 18

within the first 24 hours, polymorphonuclear leukocytes accumulate at the margins of the wound. Fibrin strands coated by plasma fibronectins, are chemotactic for macrophages and fibroblasts and also act as "scaffolding" to facilitate the influx of these cells to the area of injury.

Front 19

fibroblast activation

Back 19

by day 2, fibroblasts are activated, perhaps by growth factors, macrophages, or damaged tissue. They enter the injured area and alter the composition of the extracellular matrix.They secrete collagen and elastic fibers, as well as other matrix components, each directing different cellular responses.

Front 20

neovascularization

Back 20

on day 3, macrophages replace neutrophils and clean up cellular debris along the wound margins and secrete factors which act in concert with fibronectins secreted by the fibroblasts to promote angiogenesis and neovascularization.

Front 21

granulation tissue

Back 21

the combination of neovascularity, "activated" fibroblasts and mixed inflammatory infiltrate (mostly macrophages) embedded in edematous ground substance

Front 22

healing by second intention

Back 22

the repair process involved when there is sufficient loss of tissue to prevent coaptation of the wound margins (abscesses, ulcers, infarctions, etc)

Front 23

wound contraction

Back 23

a phenomenon that occurs in secondary union. Since the wound margins can not be coapted, myofibroblasts at the edges of the wound contract and can significantly reduce the volume of the area that must be filled with ranulation tissue and subsequent scar. Occasionally, this can be deleterious and may lead to disfiguring scars, "frozen" joints, etc.

Front 24

development of wound strength

Back 24

begins as soon as granulation tissue is established and fibroblasts begin to secrete new collagen, the tensile strength of a wound begins to increase although not in a linear fashion. There is resorption and remodeling of collagen as it is deposited, but the total collagen content of a wound increases faster than the tensile strength of a wound. Early in wound healing, type III (3) collagen is secreted (low tensile strength), but as the scar matures and the collagen is remodeled, Type I collagen becomes predominant.

Front 25

tensile strength

Back 25

depends as much on the type of collagen deposited as the amount.

Front 26

Scar

Back 26

after approximately 100 days, seventy to ninety percent of the original tissue strength is restored, but a scar is never as strong as the original tissue, and is non-functional in terms of parenchymal function.

Front 27

exuberant granulation (proud flesh)

Back 27

refers to the excessive buildup of granulation tissue which protrudes above the surface of the wound and prevents re-epithelialization.

Front 28

keloid formation

Back 28

refers to the excessive amounts of collagen leading to disfiguring scars. May be a genetic predisposition to forming keloid scars. There could be an abnormal response of fibroblasts to growth factors, a delay in fibroblast apoptosis, or a defective communication between fibroblasts and the extracellular matrix.

Front 29

requirements for all proper wound healing

Back 29

A. adequate blood supply
B. adequate nutrition
C. adequate cleansing
D. protection from trauma

Front 30

adequate blood supply

Back 30

an essential factor in order to combat infection and meet the requirements of metabolically active tissue.

Front 31

adequate nutrition

Back 31

protein deficiency interferes with collagen synthesis and the proper formation of ground substance; vitamin C deficiency interferes with the production and tensile strength of collagen; and zinc deficiency interferes with DNA and RNA synthesis.

Front 32

adequate cleansing

Back 32

the removal of dead tissue and foreign debris (debridement) is necessary to prevent infection and will expedite the healing process.

Front 33

protection from trauma

Back 33

granulation tissue is easily disrupted and repeated trauma or movement retards the healing process.