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Terms in this set (10)

0-6 days

Reparative process for injured soft tissues involving complex series of interrelated physical and chemical activities

Rubor: redness
Calor: local heat
Tumor: swelling
Dolor: pain
Function laesa: loss of function

Acute: relatively brief duration, characterized by hemodynamic activity that generates exudate (plasma like fluid composed of protein and granular leukocytes)

Chronic: prolonged duration, characterized by the presence of bo granular leukocytes and the production of scar tissue

Sign and symptoms: redness, swelling, warmth, tenderness, loss of function

Vasodilation is brought on by a local axon reflex and the complement and kinin cascades

Approx 20 proteins that normally circulate in the blood in inactive form become active to promote a variety of activities essential for healing

The attraction of neutrophils and macrophages to rid the injury site of debris and infectious shorts through phagocytosis

The stimulation of mast cells and basophils to release histamine (promotes vasodilation)

The conversion of ye inactive enzyme kallikrein to the activated bradykinin (promotes vasodilation and increases old vessel wall permeability)

Heparin: thins the blood and prolongs clotting

Histamine: promotes further vasodilation

Bradykinin: opens the blood vessel walls; causes pain

Blood from the broken vessels and damaged tissues forms a hematoma which in combination with necrotic tissue forms the zone of primary injury: hematoma forms

Approx 1 hour post injury swelling or edema occurs as the vascular walls become more permeable and increased pressure within the vessels forced a plasma exudate out into the interstitial tissues

Typically exists for only a few minutes in cases of mild trauma with a return to normal permeability in 20 to 30 min

More severe traumas can result in a prolonged state of increased permeability

Tissue exudate provides a critically important part of the body's defense: diluting toxins present in the wound, enabling delivery of the cells that remove damaged tissue and enable reconstruction

As the body continued to react to the inflammatory process reparative cells in the exudate arrive at the injury site

Platelets and basophil leukocytes release enzymes that interact with other chemicals in the cell membranes to produce chemical mediators

This chain of chemical activity produces the zone of secondary injury which includes all of the tissues affected by inflammation, edema, hypoxia

After the debris and wasted products from the damaged tissues are ingested through phagocytosis the leukocytes re-enter the blood stream and the acute inflammatory reaction subsides
Three mechanisms

-local vasoconstriction: lasting from a few seconds to as long as 10 minutes, larger blood vessels constrict in response to signals from neurotransmitters, capillaries and set arterioles and venules constrict due to the influence of serotonin and catecholamines released from the platelets and serum during injury, the resulting reduction in the volume of blood flow in the region promoted increased blood viscosity or resistance to the blow which further reduced blood loss at the injury site

-platelet reaction: provokes clotting as individual cells irreversibly combine with each other with fibrin to form a mechanical plug that occluded the end of a ruptured blood vessel, produces an array of chemical mediators that play significant roles in the inflammatory and proliferation phases of healing, mediators include: serotonin, adrenaline, nonradrenaline, histamine;, also found in platelets is the enzymes adenosine triphosphate (atpase): central in supplying the energy needed for healing

-activation of the coagulation cascade: a cascade is heightened physiologic response consisting of several different interrelated processes, fibrinogen molecules are converted into fibrin for clot formation through two different pathways, extrinsic pathway is activated by thromboplastin which is released from damaged tissue, intrinsic pathway inside the blood vessels is enabled by the interaction between platelets and the hageman factor, both paths result in the formation of the prothrombin activator that converts prothrombin into thrombin
Muscle fibers (form adhesions) are permanent cells that do not reproduce or proliferate in response to either injury or training; there are reserve cells in the basement membrane of each muscle fiber that are able to regenerate muscle fiber following injury.

Severe muscle injury can result in scarring or the formation of adhesions within the muscle, which inhibits the potential for fiber regeneration from the reserve cells; consequence: muscle may regain only about 50% of its preinjury strength.

Because tendons and ligaments (slower heal) have few reparative cells, healing of these structures is a slow process that can take more than a year; regeneration is enhanced by proximity to other soft tissues that can assist with supply of the chemical mediators and building blocks required; isolated ligaments (e.g., anterior cruciate) have poor chances for healing;

If tendons and ligaments undergo abnormally high tensile stress before scar formation is complete, the newly forming tissues can be elongated; if this occurs in ligaments, joint instability may result.

Because tendons, ligaments, and muscles hypertrophy (increase in size) and atrophy (decrease in size) in response to levels of mechanical stress, complete immobilization of the injury leads to atrophy, loss of strength, and decreased rate of healing in these tissues; the amount of atrophy is generally proportional to the time of immobilization; immobilization may be necessary to protect the injured tissues during the early stages of recovery, but strengthening exercises should be implemented as soon as appropriate during rehabilitation of the injury.