Term
| Four stages of blood clotting (hemostasis) |
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Definition
1.platelet plug
2.clotting factor
3.fibrin
4.RBC & WBCs |
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Term
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Definition
1.Hemostasis (clotting) & degeneration
2.Inflammation
3.Proliferation & migration
4.Remodeling & maintenance
(these phases significantly overlap & depending on the injury can take days, weeks, months or years to heal. |
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Term
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Definition
(Control bleeding)blood clot formation. Coagulation clumps platelets together. Platelets release growth factors & chemotaxic substances to stimulate an immune response.
Growth factors stimulate epithelial cells, fibroblasts & vascular endothelial cells proliferation. |
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Term
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Definition
| Helps T cell to develop recognition of foreign substance. Sign that can be tested for to show inflammation. |
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Term
| Four signs of acute inflammation |
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Definition
Redness; erythema
Heat; increased temperature
Swelling; edema
Pain
(may also include decreased function, increased tone & spasms & decreased range. |
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Term
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Definition
Begins with hematoma, necrosis of dead cells and inflammatory cell response.
Tissue repair begins in 24 hrs of the injury. Fibroblasts release proteins (fibronectin), elastin, & collagen to form a matrix for tissue repair. |
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Term
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Definition
is the coordinated reaction of body tissues to cell injury & cell death that involves vascular, humoral, neurologic & cellular responses.
The inflammatory reaction is to destroy pathogens, remove dead cells, & initiate healing of tissues. |
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Term
| Chemotaxis in inflammation |
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Definition
| stimulates vasodilation, increased capillary permeability & immune response (leukocytes & macrophages) These immune cells destroy bacteria, release elastin and collagen and secrete additional growth factors. |
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Term
The inflammatory reaction includes
(5 aspects) |
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Definition
1.blood vessels
2.circulating blood cells including immune cells.
3.Connective tissue (fibroblasts, mast cells)
4.Chemical mediators
5. Extracellular matrix primarily collagen and basement membranes. |
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Term
| Three outcomes of acute inflammation |
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Definition
1.restoration of normal tissue
2.healing with scar (scars do not have the same tensil strength. scar tissue in heart, does not pump as effectively)
3.chronic fibrosis
(acute inflammation follows injury. When the injurious agent is removed the process stops) |
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Term
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Definition
| System does not turn off. occurs with repeated acute inflammation or the underlying injurious agents are not removed. A persistent immune reaction can occur. Examples are rheumatoid arthritis, systemic lupus, type I diabetes mellitus. |
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Term
| hallmarks of chronic inflammation |
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Definition
1.accumulation of macrophages, lymphocytes and plasma cells
2.granulation tissue made up on fibroblasts and endothelial cells can accumulate in chronic inflammation.
3.aggregates of macrophages can form into granulomas. one example is tuberculosis which forms granulomas. |
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Term
| Three components of inflammatory response |
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Definition
1.acute inflammation can last a few minutes to a few days.
2.Vascular response--with injury, small arteries supply blood to the injury constrict, platelets aggregate and form a clot.
3.Blood vessel endothelial cells become more permeable resulting in swelling. |
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Term
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Definition
| Transudate and exudate are fluids leaking from tissues. The degree of leakage depends on the severity of the injury. |
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Term
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Definition
*Leukocytes are white blood cells (ex. neutrophils and macrophages) that:
1. adhere to the wall of the endothelium of the blood cell--margination.
2. the leukpcytes then migrate out of the capillary into interstitial space.
(chemotaxis initiates the migration) |
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Term
| Neutrophils v Macrophages |
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Definition
Neutrophils inhibit bacterial growth
Neutrophils are replaced by macrophages within 24-hrs which remove dead cells and necrotic tissue.
*An elevation in leukocyte count (elevated WBCs) is an indication of an active inflammatory reaction.) |
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Term
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Definition
*The lymphatic vessels are thin walled channels of endothelial cells that drain into the subclavian vein via the thoracic duct.
*these channels help to drain fluid & proteins from the interstitial space thereby reducing edema.
*movement of phagocytic cells (macrophages) into the lymph nodes stimulates T & B cells can cause enlargement of lymph nodes that can become painful. |
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Term
| Chemical mediators of inflammation |
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Definition
Chemical mediators responsible for vascular & leukocyte response in the acute inflammatory response include:
*histamine (vasodilator systematically) in lungs it's a vasoconstrictor.
*platelet-activating factors
*arachidonic acid
*cytokines
*blood coagulation |
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Term
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Definition
| causes blood vessel walls to become leaky. (vasoconstriction in lungs) |
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Term
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Definition
| Platelet-activating factor induces platelet activation & the aggregation of leukocytes |
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Term
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Definition
| is important in the synthesis of prostaglandins & leukptrienes. If you have a way of inhibiting arachidonic acid you can inhibit inflammation. |
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Term
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Definition
| Anti-inflammatory medication. block the production of arachidonic acid to block the inflammatory reaction |
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Term
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Definition
| nonsteroidal anti-inflammatory drugs such as asprin (ASA), or COX-2 (celebrex) inhibitors or ibuprofen) block the production of prostaglandins & cyclo-oxygenate to block inflammation. |
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Term
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Definition
interleukin 1 (IL-1) & tumor necrosis factor (TNF). Their presence indicates inflammation.
*IL-1 causes fever
*TNF is present in inflammation in heart disease, diabetes, obesity. |
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Term
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Definition
products stimulate inflammation.
*Intrinsic & extrinsic pathways **ULTIMATELY FORM FIBRIN** which is the last step in blood clotting.
ANTI-COAGULATION medications such as Coumadin (warfarin) slow blood clotting. |
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Term
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Definition
| is an important function of the inflammatory response. Chemical mediator attract the phagocytic cells (neutrophils & macrophages) to ingest foreign micro-organisms & necrotic debris. (Fig 6-17, 6-18) |
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Term
| Proliferation and Migration Phase |
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Definition
Within 2 days after a skin wound or injury, endothelial cells from viable blood vessels near the edge of the necrotic tissue begin to proliferate and from new blood vessels termed neo-vascularization or angiogenesis.
The new blood vessels with the connective tissue matrix from granulation tissue.
Newly formed blood vessels are leaky and cause edema in tissue as it is repairing. When tissue is repaired, excessive blood flow to repair diminishes & the edema diminishes. Edemic fluids leave through veins, lymph & venules. |
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Term
| Remodeling & Maturation Phase |
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Definition
In maturation & remodeling, the scar tissue becomes smoother, stronger, less dense and more like a person's natural skin color.
The remodeling process can take years as the skin first produces collagen fibers which are broken down and re-arranaged to withstand stress. |
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Term
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Definition
Tissue contraction is a normal part of the tissue repair process to allow the margins of the healing tissue to approximate.
The problem is when excessive shrinkage of the tissue occurs forming a pathological condition of skin or soft tissue contractures. |
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Term
| Skin and soft tissue contractures |
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Definition
Burns or skin cuts can result in hyertrophic scarring which limits ROM.
*Arthrofibrosis (joints) is periarticular scarring that can restrict ROM or a thickened fibrotic capsule limits ROM. Arthrofibrosis can result from trauma or post surgery. |
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Term
| When can arthrofibrosis occur? |
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Definition
| occurs with prolonged immobilization, infection or graft malposition after ligament reconstruction such as ACL repair. Best treatment for contractures is prevention. |
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Term
| Soft tissue contracture treatment |
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Definition
Immature scar tissue may be successfully treated with early movement in conjunction with analgesic or anti-inflammatory meds.
*Other methods include strengthening, electrical stimulation, manual therapy, splints, bracing for ROM and positioning. |
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Term
| Forceful manipulation of arthofibrosis |
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Definition
| The scar is thought to be mature by 3-4 months. If ROM is not functional then surgical (arthroscopic) manipulation may be required. However forceful manipulation of a stiff joint is not advised bc of p0tential joint compression leading to articular cartilage damage and fracture. |
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Term
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Definition
with trauma, viable skin epithelial cells adjacent to the injury flatten out to cover the injury. Fibroblasts in the extracellular matrix provide proteins for epithelial cells to grow.
Regeneration is the replacement of dead parenchymal cells with new and is ideal bc it is the restoration of normal structure and function. |
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Term
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Definition
only in tissues that can undergo mitosis and divide. Tissues are classified as permanent, stable or labile based on their ability to divide. Only stable and labile can divide and thus regenerate.
Tissues such as cardia and neural are permanent and will heal with scar tissue and not regenerate-VIP |
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Term
| Stable or labile tissue will regenerate only if |
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Definition
1. the inflammatory process is short
2. basement membrane is intact
3. other extracellular components and vascular structures of other parenchymal cells are intact. |
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Term
| Types of permanent tissue |
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Definition
| Tissues such as cardiac and neural are permanent and will heal with scar tissue and not regenerate, VIP. |
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Term
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Definition
| epithelium of skin and GI tract & hematopoietic (blood forming stem cells of bone marrow) divide and continuously will regenerate. |
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Term
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Definition
| such as liver, kidney and muscle to not normally divide, but may be induced to divide by appropriate stimuli. the liver can regenerate after surgical or viral damage. |
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Term
| Neural tissue regeneration |
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Definition
is limited to certain regions such as the hippocampus & olfactory bulb.
Research attempts to unlock a process of regeneration of the nervous system are on going. |
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Term
Formation of Scar Tissue
Primary healing: |
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Definition
| is the close approximation of the edges of the wound to allow for minimal scarring, & w/o infection. healing time is short. |
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Term
Formation of Scar Tissue
Secondary healing: |
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Definition
| occurs when the edges of the wound cannot approximate or infection is present. Healing is prolonged. |
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Term
| Formation of Scar Tissue after wound closure |
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Definition
Even after wound closure is complete degradation and resynthesis of collagen continues.
With skin, a fully mature fibrosis scar may require 12-18 MONTHS and is 20-30% WEAKER than normal skin.
Excessive scar formation such as keloid or hypertrophic scarring can result from excess collagen formation. |
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Term
| Treatment of keloid scars |
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Definition
| include surgical revision followed by use of form pressure garments, pulsed dye lasers & high-dose brachytherapy (radiation right at the site to break up the scar by damaging the excess epithelium). Corticosteroids are also used, this interrupts the inflammatory process. |
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Term
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Definition
such as pressure ulcers, remain in the inflammatory & proliferation phase. The tissue bed and lack of growth factors prevent closure. The wound bed must be prepared and biochemistry restored to act like an acute wound for the tissue to heal.
Glucose spray to activate ATP. |
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Term
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Definition
*poor circulation
*immobilization
*the sores do not bleed so the necessary components in the blood that prevent infection are not present.
*occurs from the inside out |
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Term
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Definition
| *Regeneration can only occur when basement membrane is present.*Phagocytic removal of necrotic cells. *Adjacent living cells migrate onto the remaining basement membrane and differentiate into type II pneumocytes (produce surfactant).*The cells differentiate into type I pneumocytes (cells that permit gas exchange) |
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Term
| Tissue repair in the digestive tract |
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Definition
*Gut normally completes a complete turnover of cells in 4 weeks.
*A mildly to moderately impaired gut takes 3 to 6 months to heal and 12 to 18 months for a more severe intestinal injury.
*(2/3 of immune system functions in the gut and 90% of serotonin function takes place in the gut.) |
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Term
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Definition
*When a nerve is cut, the peripheral portion rapidly undergoes a myelin degeneration and axonal fragmentation.
*Within 24 hrs of section, new axonal sprouts from the central stump are observed with proliferation of Schwann cells from both the central and peripheral stumps.
*The most important factor in achieving successful nerve regeneration after repair is the maintenance of the neurotubules (basement membrane and connective tissue endoneurium), along which the new axonal sprouts can pass. |
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Term
| Tissue repair in skeletal muscle |
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Definition
*Muscle tissue can regenerate but the restoration of normal structure and function is strongly dependent on the type of injury.
*Growth of new, independent fibers is possible when the basement membrane remains intact through mitotic division of satellite cells=essential to the repair of injured muscle by serving as a source of myoblasts for fiber regeneration.
*If there is no basement membrane the muscle will form a scar. doesn't maintain functional ability. |
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Term
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Definition
*Hematoma brings in whit blood cells, luekocytes and macrophages.
*Formation of soft callus which is replaced by hard callus.
*During this phase (reparative) osteoclasts clear away the necrotic bone while the periosteum and endosteum regenerate and begin to differentiate into hyaline cartilage
*soft to hard callus=enchondral ossification.
*remodeling can take up to a year.
*after 6 to 12 weeks the soft callus becomes a hard callus. |
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Term
| Tissue repair in tendons and ligaments |
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Definition
may heal either as a result of proliferation of the tenoblasts from the cut ends of the tendon or more likely as a result of casfular ingrowth and proliferation of fibroblasts derived from the surrounding tissues that were injured at the time of tendon injury.
*adhesion is common*
Functional restoration requires surgical repair to appose and suture cut ends when rupture occurs (ACL) |
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Term
| Tissue repair in cartilage |
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Definition
*require a source of cells, provision of matrix, removal of stress concentration, and intact subchondral bone plate with some mechanical stimulation.
microfracture techniques to enhance chondral resurfacing have made it possible to stimulate the formation of a durable repair cartilage cap over the lesion.
*In adults without intervention, the healing of articular cartilage occurs by fibrous scar tissue or fails to heal at all. (leads to arthritis) |
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Term
| Tissue repair in the synovial membrane |
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Definition
Injury to any joint structures affects the synovium and results in hemorrhage, hypertrophy and hyperplasia of the synovial lining cells and mild chronic inflammation.
*adhesions can form between synovial membrane and adjacent articular cartilage. |
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