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2014-02-10 21:01:42
inflammation tissue healing

inflammation and tissue healing
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  1. an immediate respsonse to help prevent loss of red blood cells and remove damaged tissues is called:

    a series of rxns or events occuring in vascularized tissues in response to injury, foreign body, antigen, or pathogen:
    inflammatory response

    can speed or delay with modalities
  2. why is the inflammatory response essential for tissue repair:
    it helps to establish vasuclar supply to support repair
  3. what are the 3 main purposes of the inflammatory process:

    describe each:
    • destroy: prevents further spreading of bacteria or "invaders" or injury
    • dilute: protects the injured area - cushinoning effect
    • isolate: help prevent loss of red blood cells and remove damaged tissue
    • helps to establish vascular supply to support repair
  4. list the 3 phases of the healing process:
    • (acute) inflammatory: response phase
    • fibroblastic (proliferation): repair phase
    • maturation: remodeling phase
  5. describe the following in injury induced trauma...

    primary trauma:
    primary trauma: traumatic force that cuases irreversible damage
  6. describe the following in injury induced trauma...

    secondary trauma:
    • secondary trauma: damaged caused by lack of oxygen (cell death), enzymatic damage, and mitochondrial failure
    • modalities are most effective
  7. list and describe the 5 cardinal signs of the inflammatory-response phase:

    functio Laesa:
    • inflamer: to set on fire
    • calor: Heat; increased vascularity (hypermia) increased blood flow
    • rubor: redness; incrased vascularity (hypermia)
    • tumor: swelling; blockage of lymphatic drainage and venous
    • dolor: pain; physical pressure or chemical irritation of pain-sensitive structures
    • functio laesa: loss of fxn; pain and swell
  8. what are the 4 components of inflammation:
    • vascular response: capillaries are altered, direct disruption of response from other site
    • hemostatic: controls blood lost; clots
    • cellular: specialized cells
    • immune: celluar and hormonal
  9. the movement of cells away from or towards a chemical stimulus is called:
    • chemotaxis
    • the attraction or repelling of chemical mediators
    • positive or negative energy
  10. as a result of an injury... disruption (direct or indirect) of micro-vascular system (capillaries, venules, lymphatics) is which response of the inflammation phase:
    • vascular response
    • bleeding, fluid loss, cell injury, exposure to foreign materials
  11. transient vasoconstriction of the vascular response...

    mediated by:
    prolonged by:
    • mediated by: norepinepherine, lasts 5-10 minutes
    • prolonged by: serotonin

    • released by Mast cells and platelets
    • detect the presence of injury
    • both NE and serotonin
  12. subsequent vasodilation of the vascular response....

    list the 5 stimulating chemical mediators:
    how long does this last post injury:
    increased capillary permeability of surrounding vessels

    • injury and stimulating (by NE and Seratonin) chemical mediators
    • histamine
    • hageman factor
    • bradykinin
    • prostaglandin
    • complement factors

    lasts up to: 1 hour post injury
  13. Histamine...

    released by:
    inital edema:
    chemotactic for:
    active for how long:
    • released by: mast cells, platelets and basophils at the site
    • fxn: increased permeability and vasodilation leads to swelling and edema
    • initial edema: has few cells and proteins and low specific gravity (=transudate)
    • chemotatic: for leukocytes (white blood cells)
    • active: ~1 hour
  14. chemical mediator of vascular response.. Hageman factor (clotting factor XII)...

    activated by:
    2 fxns:
    • enzyme in blood
    • activated by: exposed injured endothelial cells

    • activates coagulation
    • system to stop bleeding (discussed during hemotactic response)

    • causes vasoconstriction and increased permeability
    • activates other plasma proteins
    • plasminogen to plasmin
    • kallikrinin to kinins
    • generates Bradykinin (effects similar to histamine) increases vascular permability
  15. chemical mediator in vasuclar response...Prostaglandins (PGE):

    fxn in the early stages:
    inhibited by:
    responsible for:
    • produced in nearly all cells including mast cells
    • released with injury to cell membrane
    • fxn: increases permeability and attracts leukocytes and synergist of other mediators (kinins)
    • fxn in early stages: regulates repair process
    • sensitizes pain receports; lowers nerves threshold to pain, so bradykinin can act more quickly
    • also active in later stages of inflammation
    • inhibited by: cortical steroids and NSAIDS
    • responsible for: febrile states (fever)
  16. chemcial mediators in the vascular response phase.... anaphylatoxins (C3a,4a,5a)

    list 2 fxns:
    • complement systems that increase permeability
    • induces mast cell degranulation and furthers histamine response
  17. describe the change of charges that occur at the vessel wall during the vascular response phase:
    • normal vessel wall and inflammatory mediators have negative charges and are repulsed
    • injury occurs
    • vasoconstriction occurs
    • the charges are reversed and the vascular wall attracts and adheres mediators
    • leukocytes (WBC) move from central of vessel wall (extravasation) leaks out of the vessel
  18. describe the role of leukocytes as changes of charges occur at the vessel wall during the vascular response:

    • leukotaxin: mediator that is responsible for margination (on the cell walls) and lining up of leukocytes along the cell wall and increase permeability
    • leukocytes line endothelium of vessel: margination; within 1 hour
    • this process leads to pavementing (cells start to stack in layers)   and subsequent attraction of more WBC
    • leukocytes being to squeeze thru the endothelium: diapedesis (movement of WBC thru intact capillary wall to surrounding tissues) (low gravity; more viscous fluid)
    • the escaping of leukocytes thru the basement membrane: known as emigration
  19. define edema formation of the vascular response:

    list the 5 factors that contribute to edema formation:
    edema formation: fluid within extravascular space and interstitial spaces

    • 5 contributing factors
    • direct endothelial injury (inital vasoconstriction)
    • increased vascular permeability
    • increased hydrostatic pressure (from vasodilation)
    • increased interstital osmotic pressure (from RBC, WBC emigration)
    • overwhelmed lymphatics
  20. list and describe the 4 types of edema:
    • transudate: inital edema, has few cells and proteins and low specific gravity (clear)
    • exudate: as permeability increases cells leak making more viscous and higher specific gravity (more leukocytes, more yellow and thick)
    • pus or "supportive exudate": if high level leukocytes are present
    • abscess: localized collection of pus buried in confined space (needs to be cleaned in a steril space; not usually ATR)
  21. describe the mechanism of increased permeability (leakage) in the vascular response:
    • direct endothelial injury
    • endothelial cell contraction (creates gaps)
    •    - chemcial mediated (so gaps dont haveppen for too long)
    •    - 15-30 minutes
    • leukocyte dependant endothelial injury
    •    -releasing damaging chemicals
    • leakage by regnerating capillaries (new not meshing with old)
  22. describe in general the hemostatic response:
    • controls blood loss when vessels are damaged
    • platelets are first cell to bind releasing fibrin to stimulate clotting
    • platelet derived growth factors (PDGF) is chemotactic substance stimulating fibroblast (create fibers)
    •    -chemotactic to macrophages (mature monocytes) and neutrophils (WBC)
    •    - controls fibrin deposition, proliferation and angiongenesis
  23. describe the 9 steps of coagulation, or the blood clots:
    • thromboplastin (Factor X) combines with free floating prothrombin (normally floating thru the vessel)
    •   - broken down to thrombin
    • presence of thrombin causes fibrinogen unwind to fibrin
    • fibrin deposits over injured site
    • traps RBC, WBC, and Platelets
    • fibrin and fibronectin forms cross links to form fibrin lattice
    • provides temporary plug limiting bleeding and fluid loss
    • confines inflammatory rxn
    • reopens later in healing process
    • would is only form of tensile strength
    •    -scab
  24. describe heparin's role in the hemostatic response:

    common drugs:
    • inflammation delivers prothrobin to area
    • a chemical mediator that acts as an anticoagulant
    • must be balanced
    • common drugs: coumadin, warafin, lovenox
  25. list and describe the 3 steps that hematoma plays a role in the hemostatic response:

    define hematoma:
    • inflammatory exudate that contains RBC indicates vascular interruption
    • hematoma: accumulation of blood in tissue
    • hemarthrosis: blood within a joint
  26. what is the main fxn of the cellular response:

    list the polymorphonucleocytes:

    list the mononuclear cells:
    • main fxn: clear site of debris and microorganisms
    • critical fxn of inflammation is deliverance of leukoctyes (WBC)
    • classified according to size

    • polymorphonucleocytes
    • neutrophils
    • eosinophils
    • basophils

    • mononuclear cells
    • monocytes
    • lymphocytes
  27. ingestion and digestion of bacteria or cells (either waste or energy) is called:
    • phagocytosis
    • migration to injury within hours
  28. describe the neutrophils role in the cellular response:
    • initally highest concentrations
    • rid site of bacteria and debris
    • remain for 24 hours, then disintergrate
    • perpetuate inflammation (chemotactic fxn, leukocytes) (by leaving waste)
  29. list the roles of the following in the celluar response:

    • basophils: release histamine (more swelling)
    • eosinophils: phagocytic (more swelling)
    • monocytes: predominate for 24-48 hours; convert to macrophages when leave blood vessel
  30. the most important cell of inflammation and wound healing, that destroys bacteria and cells is:

    what does this cell leave behind:
    when are they most effect:
    list 2 tissue oxygen tension factors:

    • what does this cell leave behind: useful bi-products chemotactic for fibroblasts
    • most effective: in presence of oxygen significant b/c increased blood flow; secondary trauma; hypoxic death
    •     - can tolerate low O2 as in chronic inflammation

    • tissue oxygen tension factors
    • atmospheric O2 available (hyperbaric)
    • O2 absorbed by respiratory and circulatory systems (disease implications)
  31. list the 3 things that macrophages leave behind as bi-products:

    why is this important for inflammation:
    • release
    • hydrogen peroxide: inhibits bacterial growth
    • ascorbic and lactic acid: concentration interrupted by body for need of increase macrophages

    important: chemotactic for fibroblasts!! (without - low fibroblastic activity)
  32. list in summary the 4 steps in the inflammatory - response phase:
    • 1. injured area is walled- off
    • 2. leukocytes phagocytize foreign debris
    • 3. sets stage for proliferation/fibroblastic repair phase
    • 4. lasts 2-4 days after initial injury (depends on the extent of the injury)

    • purpose:
    • foundation for the next phase
    • walls off the area
    • takes care of bacteria, dead material
  33. what role do NSAIDs and corticosteroids play in inflammation:
    • nsaids: not to stop inflammation; body does way too much inflammation, so nsaids decrease the over abundance of swelling, ect.
    • corticosteroids: stops the process all together; no foundation to heal
  34. list the 3 chemical mediators of the inflammatory response that increase vasodilation:
    • histamine
    • prostaglandins
    • serotonin
  35. list the 6 mediators of the inflammatory stage that increase vascular permeability:
    • bradykinin
    • Anaphylatoxins (C3a, C5a)
    • PAF (platelet-activating factor)
    • histamine
    • serotonin
    • prostaglandins
  36. list the mediator of the inflammatory phase that increases fever:
  37. list the 3 mediators of the inflammatory phase that increases pain:
    • prostaglandins
    • Hageman factor
    • bradykinin
  38. the fibroblastic (proliferative) repair phase..

    lasts how many days:
    involves which tissues and cells:
    • lasts: 3-20 days (bulk of the phase) starts about 24hrs after injury; can last 4/6 to 10/12 weeks
    • involves: epithelial cells and connective tissue
    • purpose: to cover wound and gain strenght
  39. of the fibroblastic (proliferative) repair stage..

    covering of mucous and serous membranes; the epidermis of the skin is called:

    consists of fibroblasts, ground substance, and fibrous strands:
    • epithelial cells
    • connective tissue
  40. the process is the fibroblastic (proliferative) repair stage is:

    what are the signs of this stage on an eval:
    the process is the fibroblastic (proliferative) repair stage is: unorganized; random fashion

    • signs during an eval:
    • stiff
    • decreased ROM
    • .. from collagen
  41. list the 4 processes of the proliferation phase that occur simultaneously:
    • epithelialization: true scab, covering top of wound
    • collagen production: new strands of collagen
    • wound contraction: pull edges of wound together
    • neovascularization: new blood vessels to healing tissue
  42. of epithelialization of proliferation phase..

    superficial (scrape):
    deep (surgical scar):
    contact inhibition:
    approximated wound cover:
    • fxn: uninjured cells form margins, reproduce and migrate covering wound
    •    - prevent fluid loss
    •    - decrease risk of infection (blister)
    • superficial (scrape): reestablishment of epidermis within hours
    • deep (surgical scar): later in process after collagen production and neovascularization
    • contact inhibition: when 2 sides meet, movement
    • approximated wound cover: in 48 hours but takes weeks for layer of epidermis to differentiate (stitches/scrapes)
  43. list the 5 steps of epithelialization of the proliferation phase:
    • with injury basal cells detach from basement membrane
    • the cells migrate while holding on to their "parent" cells and pull them into the center to close the wound
    • contact inhibition: when the two sides meet, movement ceases
    • basal cells differentiate and proliferate
    • become multilayer and restore the epidermis
  44. of collagen production in the proliferation phase...

    what makes the collagen:

    describe the process of how collagen is synthesized: (procollagen, tropocollagen, fibrils, filaments)
    • fibroblasts make collagen:
    • migrate to area from chemotactic response (macrophages byproducts are chemotactic for fibroblasts)
    • adequate O2, ascorbic acid and cofactors such as zinc, iron, manganese, and copper needed

    • how collagen is synthesized
    • fibroblasts synthesize procollagen
    • procollagen: yields tropocollagen (collagenase)
    • tropocollagen: weaves together to form fibrils
    • fibrils: make up filaments
    • filaments: combine to form collagen (makes the bundle, strongest)
    • crosslinking between collagen strand provides further strenght
  45. fibroblasts are chemotactic for:
    GAG: draws H2o into the area, facilitates cellular migration
  46. collagen production of the proliferation phase..

    granulation tissue:
    as granulation increases:
    Day 7:
    Day 12:
    Day 21:
    • granulation tissue: made up of new capillaries , fibroblasts, and myofibroblasts (similar to muscle, smooth muscle; wound contraction)
    • as granulation increases: fibrin clot decreases
    • day 7: significant amount of collagen; initially weak from Type III collagen with no consistent organization
    • day 12: type III begins to be replaced by Type I
    • day 21: highest physical amount of collagen (mostly type III) ; yet strength as low as 20%
  47. describe the following stages of collagen production in terms of strength:

    Days 7-12
    Day 21:
    6 weeks:
    • Days 7-12: 10% of normal strength, can take stitches out; collagen is being produced but weak; steri strips in place of stitches
    • Day 21: 20% strength, no longer needs steri strips, ROM increasing, increasing intensity, much more active
    • 6 weeks: Type III to Type I fibers 80% of normal strength; required for return to play
  48. which of the 3 phases.. inflammation, fibroblastic repair, or maturation remolding  is the most important for TRUE tissue healing:
    fibroblastic repair phase
  49. wound contraction of the proliferation phase...

    which cells are responsible for wound contraction:
    what do uncontrolled contractions result in:
    • fxn: contraction pulls edges of injured site together, shrinking effect
    • cells responsible for wound contraction: myofibroblasts (just below epithelial level)
    • uncontrolled contractions result in: contracture
  50. how does the shape of the wound impact the speed of contraction in wound healing during the proliferation phase:
    • linear
    • edges are close together; heals nicely

    • square
    • pulls corners together

    • round
    • no edges to pull together; skin grafs- something to pull together for larger wounds
  51. a condition of fixed high resistance to passive stretch in the proliferative phase is called:

    describe 4 things this could be the result of:

    • result of:
    • fibrosis of tissue around joint
    • adhesions: filaments no longer slide
    • muscle shortening: voluntary/involuntary protection
    • tissue damage: lack of ROM leads to tissue damage; atrophy or tissue lysis (breakdown)
  52. of the wound contraction stage of proliferation phase...

    primary intention:

    secondary intention:
    • primary intention: wounds that are highly approximated and heal without contraction; closes quickly with minimal scar tissue
    • secondary intention:  wound healing with significant tissue loss or infection; more scar tissue; try to avoid this
    • to minimize contraction skin grafting is often performed (in the inflammatory phase)
  53. during the proliferation phase, scars are observed as which 3 things:

    what is this a result of:
    • scars
    • tender
    • red swollen

    • result of:
    • increased vascularity
    • immaturity
    • very sensitive nerve endings; chem mediators sensitize for pain
  54. during which phase does neovascularization occur:

    what is the definition of neovascularization:

    what initiates this process:
    • neovasularization occurs: proliferation phase
    • definition: development of new blood supply
    • initiates the process: macrophages
  55. during what phase does angiogenesis occur:

    what is the definition of angiogenesis:

    list 2 mechanisms:
    • anigiogenesis occurs in: proliferation phase (neovascularization)
    • angiogenesis: growth of new blood vessels (new capillary beds layed down)

    • 2 mechanisms:
    • generation of new network
    • anastomosis 9(surgical connection between two structures) to preexisting vessels

    • too much rehab too soon- network disturbed; so more swelling and more edema 
  56. list the 3 steps of neovasuclarization:
    • vessels in periphery bud into wound area, eventually coming into contact,  to form capillary loop
    • new vessels give pink to red scar
    • as wound heals, some capillaries close and give more of a whitish scar, similar to adjacent tissue
  57. how long does the maturation phase last:

    how does scar tissue change during the maturation phase (4):

    list the structures that are decreasing in # during the maturation phase:
    maturation phase lasts: 9 days to 2 years

    • changes of the scar:
    • size
    • form 
    • strength
    • scar tissue becomes whiter as it matures and vascularity decreases

    • structures decreasing in# during maturation:
    • fibroblasts
    • macrophages
    • myofibroblasts
    • capillaries
  58. list 2 things that determine the rate of maturation:
    • fiber orientation (how will they align) gives strength; mess of proliferation starts to form; controlled ROM ; forms lines according to the stressed placed on it
    • balance of synthesis and lysis (breakdown)
  59. describe how the synthesis and lysis of maturation is balanced:

    what type of collagen is synthesized during maturation:

    what happens if synthesis is greater than lysis:
    • synthesis/lysis balanced by: hormonal stimulation from inflammation causes collagenasae to increase and cause collagen destruction (tropocollagen bonds)
    • type of collagen synthesized: majority of collagen synthesized and deposited is Type I
    •    - type I is stronger with much less mass (as opposed to type III)
    • if synthesis is greater than lysis: a keloid or hypertrophic scar can develop
  60. define the following of the maturation phase..


    inhibition of lysis is the result of:

    treatment of keloids or hypertrophic:
    • keloids: scars extend beyond original boundaries
    • hypertrphoic: scar remains in boundaries but significantly raised
    • inhibition of lysis is the result of: genetic defect

    • treatment
    • surgery
    • medications
    • pressure
    • irradiation
  61. collagen synthesis in the maturation phase is dependent on:

    what type of therapy is helpful to encourage this:
    • collagen synthesis in the maturation phase is dependent on: O2 if O2 is available more collagen will be synthesized
    • therapy : compression
  62. how does collagen in scar tissue compare to collagen in normal tissue:

    because scars are inelastic, what is needed for mobility:

    if there is an adhesion in a scar:

    what will determine the final structure of a scar:
    • how does collagen in scar tissue compare to collagen in normal tissue:  will always be less organized
    • scars are inelastic: folds are needed for mobility (ROM over scar yield tension) (spring example)
    • if adhesions in scar: mobility will be restricted
    • determine final structure: induction theory/tension theory
  63. define the induction theory of the maturation phase:

    give an example:
    • dense tissue types have preferential (favored) status when compared to adjacent loss tissue
    • scar mimic tissue it is healing
    • surgeon design repair fields (distinct layers: skin, adipose, fascia, muscle, bone)
    • example of pathological scar tissue: open/closed femur fx - myositis ossificans
  64. define and describe the tension theory (5):
    • internal and external stresses on scar determine final structure
    • length and mobility may be modified with appropriate stresses during appropriate phases
    • response best to low load, long duration stretches (promotes collagen production)
    • studies show appropriate forces increase tensile strength
    • immobilization reduces tensile strength and favors excessive cross bridging
    •   - 2-4 week of immobilization can give effects that take (3-4) months of reverse
  65. bone and soft tissue will respond to the physical demands placed on them causing them to remodel along lines of tensile force is known as:
    wolff's law

    you must expose injured structures to increasing loads during the maturation/remodeling phase
  66. list 4 reasons why controlled mobilization is superior to immobilization:
    • decreases (excessive) scar tissue
    • increases revascularization (new blood supply)
    • facilitates muscle regeneration
    • reorientation of muscle and ligament fibers (stronger)