lecture viii wound healing
TRANSCRIPT
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Wound Healing
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A. Types of Wound Closure
1. Primary Closure approximate
disrupted tissues by sutures, staples,
or tapes. With time there will be
a. synthesis
b. depositionc. cross-linking of collagen to
provide the tissue with strength.
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2. Delayed Primary Closure alsocalled tertiary closure. Wound closureis delayed for several days to prevent
wound infection where there is:a. bacterial contamination
b. foreign bodies
c. extensive tissue trauma* Cleaning of the wound is done daily using
NSS
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3. Secondary or Spontaneous Closure- wound closes by contraction of the
wound edges. Usually takes 4-10 days
to close.
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B. Mechanism Involved in Wound Healing
1. Epithelialization
a. keratinocytes migrate thendivide to resurface partial thickness loss of
skin or mucosa.
b. responsible for coverage
c. cells migrate from side to side
d. does not originate from the center
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Examples:
a. partial thickness skin graftdonor site
b. abrasions
c. blisters
d. 1stand 2nddegree burns
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2. Contraction
- the process whereby there isspontaneous closure of full thickness
skin wounds or constriction of tubular
organs such as the CBD or esophagus.
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3. Connective Tissue Matrix Deposition
- the process whereby fibroblasts arerecruited to the site of injury and
produce a new connective tissue
matrix. The cross-linked collagen
provides the strength and integrity to all
tissue.
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C. Phases of Healing
1. Coagulation vasoconstriction
occurs immediately because of the
release of:
a. catecholamines
b. bradykininc. serotonin
d. histamine
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Steps:
i. diapedesis
ii. hemostatic clot formed by plateletes
iii. fibrin clot formation formed byfibroblasts
- plateletes 1stcells to produce essentialcytokines which modulates most of thesubsequent steps in wound healing
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2. Inflammation migration ofleukocytes into the wound. 1st24 hours,polymorphonucleocytes followed bymacrophages.
3. Fibroplasia increases wound strength,hence tissue integrity is restored. Within 10hours after injury, there is increased wound
collagen synthesis. Within 5-7 days, collagenhas peaked and will decline gradually.
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4. Remodeling inflammatory cellsdecrease, angiogenesis and fibroplasia end.
D. Cytokines provides communication for cellto cell interaction. Roles include:
1. Regulation of Fibrosis
2. Healing of wounds and skin grafts.
3. Vascularization
4. Bone and Tendon Strengthening
5. Control of Malignancy
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E. Extracellular Matrix Metabolism
* Collagen the major component of the cellular
matrix of all soft tissues, tendons, bones, and
ligaments.1. Steps in Synthesis
a. Transcription control of mRNA
b. Translational
synthesis whichoccurs on the ribosomes of the rough
endoplasmic reticulum.
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2. Degradation breakdown of collagen
which is initiated by collagenase secreted
by the ff. cells:a. inflammatory cells
b. fibroblasts
c. epithelial cells- collagenase is activated by other proteases
like plasmin
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3. Ground Substance made up ofglycosaminoglycan subunits. Theyfunction as:
a. molecular shock absorberstogether with cartilage
b. provide for moisture storage
c. sequester cytokines
- ground substance releases the cytokinesfollowing injury signaling the repair processto start
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COMPONENTS OF EXTRACELLULAR MATRIX ANDFUNCTION
Component Function
1. Collagen -strength, support, structure
2. Elastin - allows tissue to expand and contract
3. Fibronectin - mediates cell matrix adhesion
4. Laminin - binds cells to type ivcollagen and heparin sulfate
5. Proteoglcans - moisture stores, shock absorption,
sequestration of cytokines6. Hyaluronic acid - provide a fluid environment for cell movement
and differentiation; binds to cytokines
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F. Wound Contraction movement of skin
edges towards the center
- may result in a contracture
1. appears in 2nddegree burns or skin
loss
2. hollow organs will result in stricture
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G. Epithilialization ex. Skin, mucous
membranes. Function:
1. prevents fluid loss
2. protection from radiation
3. protection from trauma
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a. epidermis act as a barrier
b. dermis provides strength
c. partial thickness wounds heal byepithelialization
d. after epithileal destruction, a blood clotis formed and dries up forming a scab
e. the basal layer in the epithilium and deeperhair follicles and sweat glands is wheremigration is initiated. This process is
enhanced by keeping the area moist
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H. Nutrition malnutrition affects wound
healing by inhibiting the immune response
(opsonization)
- lack of vit. C (scurvy) is the most
common cause of wound healing
deficiency
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H. Immunosupression- chemotherapeutic drugs inhibit woundhealing
II. Specific problems for Wound Healing
A. Gastrointestinal Tract
1. Bowel anastomotic strengthdevelops more rapidly than that of theskin.
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2. Ulcers are caused by penetration into thebasement layer by acid and pepsin.
3. Major complications of intestinalanastomoses are
a. leak
b. disruption
4. The submucosa provide the majorstrength in anastmotic closure because itcontains the majority of the fibrousconnective tissue.
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B. Skin
1. Keloids and hypertrophic scars -
occur after injury or surgery
- caused by an overabundance of
collagen
2. Treatment
a. Hypertrophic scar no
treatment necssary
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b. Keloids
i. Triamcinolone
ii. Excision
high recurrence rate
C. Tendon composed mainly of type I
collagen with significant amounts ofproteoglycan. After disruption tendon and
sheath have to be sutured.
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D. Bone
1. soft callus formation
2. mineralized as cartilage3. repalced by osteoid or bone
beginning of remodeling
E. Chronic Wounds failure of healing
because of an underlying pathology
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III. Wound Dressings
A. Films mimics skin
B. Hydrocolloids
- absorbs fluid
- debrides necrotic tissue- protects wounds
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C. Hydrogels- creates moist environment
D. Foams
- debrides, high absorbancy rate
E. Impregnates
- does not adhere to wound
- promotes epithelialization
F. Absorptive Powder and Pastes- debrides necrotic tissue
G. Calcium Alginate
- high absorbancy
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IV. Mechanical ClosureA. Absorbable
1. Synthetic polyglycolic acid
2. Plain Cat Gut
3. Chromium Treated Cat Gut
B. Non Absorbable
1. Cotton or Silk2. Nylon
3. Stainless Steel Wire