ch 39: wound healing

skin

the largest organ in the body

skin fxns (5)

- waterproof barrier -> 1st line of defense

- maintain thermoregulation

- minimize water loss

- somatic sensations

- metabolism & activation of vitamin D

layers of the skin

dermis & epidermis

epidermis

upper layer of the skin

cells of the epidermis (6)

- stratified squamous

- keratinocytes

- melanocytes

- dendritic cells (langerhans)

- tactile cells (merkel)

- sensory receptors

keratin

water insoluble protein

keratinocytes

filled w keratin & dead at surface

what does the dermis contain? (4)

- BV

- skin appendages

- sensory receptors for pain, touch, & temp

- smooth & skeletal muscle cells

2 layers of the dermis

- papillary layer (superficial)

- reticular (thicker & deeper)

papillary layer of the dermis

loosely & irregularly organized CT

what does the papillary layer contain? (6)

- fibroblasts

- macrophages

- plasma cells

- mast cells

- endothelial cells

- adipose cells

reticular layer of the dermis

dense CT

dermal epidermal junction (DEJ)

barrier against passage of substances into & out of the body

- framework to restore architecture of tissue

extracellular matrix (ECM)

ground substance for tissue growth & wound healing

what does the ECM contain? (4)

- collagen

- elastin

- adhesive glycoproteins

- GAGs

what molecules are in the cell matrix

integrins, cytokines, & GF which allow cell to cell interactions to occur

integrins fxn (3)

- transmit info bidirectionally

- bind extracellular substances

- adhesion molecules

acute wounds

occurs suddenly

acute wound outcome

restoration in 4-6 weeks

chronic wound

occurs over long period of time

chronic wound outcome

- does not heal in organized & timely manner

- impairment of structural & functional integrity

partial thickness wound

damage extends through epidermis w dermis intact

- reepithelialization

reepitheliazation

epithelial cells migrate to area & replicate my mitosis

full thickness wound

damage extends through epidermis & dermis & possibly extends to subcutaneous tissue, muscle, & bone

- scar formation

chemical mediators of would healing (6)

- neutrophils, macrophages, & lymphocytes

- platelets

- keratinocytes

- fibroblasts

- endothelial cells

- GF & cytokines

what does wound healing depend on? (4)

- type of injury

- extent of tissue loss

- inf, necrotic tissue, or secondary breakdown

- type of cell

primary intention (closure)

surgical closure of wound

primary intention characteristics

- formation of new ECM

- regeneration

- little granulation tissue

secondary intention (spontaneous closure)

full thickness wound heals w/o closure attempt

secondary intention characteristics

- large amt of granulation tissue

- longer healing time & larger scare

- skin grafting & substitutes

tertiary intention (delayed primary closure)

combination of primary & secondary intention

- contaminated wound cleaned & left open drainage

role of cytokines in wound healing

initiate healing process & stimulate expression of GF

- develop the ECM

- coordinate intercellular comminication

role of GF in wound healing

stimulate growth, division, & differentiation of other cells

- regulate intercellular communication

direct effect of nitric oxide in wound healing

bacterial killing

indirect effect of nitric oxide in wound healing

modulate cytokine & GF activity

would healing phases (4)

1. hemostasis

2. inflammation

3. proliferation/granulation

4. remodeling/maturation

hemostasis phase goals (2)

- prevent additional tissue injury

- prepare wound for healing & regeneration

hemostasis phase steps (2)

1. platelet adhesion

2. fibrin clot formation

platelet adhesion phase of hemostasis

platelet activation & platelet plug forms

fibrin clot formation phase of hemostasis

recruitment of phagocytic cells & wound debridement

inflammation phase goals (3)

- clean wound

- prevent additional injury

- prepare wound for healing

inflammation phase

recruitment of phagocytic cells & wound debridement

proliferative phase goal

wound healing guided toward tissue repair

proliferative phase steps (5)

1. granulation tissue

2. fibroblast

3. myofibroblasts

4. endothelial cells

5. reepithelialization

granulation tissue step of proliferative phase

foundation for collages based matrix that replaces fibrin based provisional matrix

fibroblast step of proliferative phase

produce collagen & adhesive proteins for ECM

endothelial cell step of proliferative phase

angiogenesis (neovascularization)

reepithelialization step of proliferative phase

regeneration of keratinocytes

process of vascular endothelial GFs in wound healing

cell mobilization -> VEGF secretion -> angiogenesis -> wound bed

remodeling phase goals (2)

- restoration of structural & functional integrity of skin

- dermal matrix mended not regenerated

remodeling phase steps (5)

1. wound contraction & closure

2. continuous turnover of collagen

3. decrease capillary density

4. declining cellular content

5. mature scare tissue

hypoxia affects on wound healing

delays or stops wound healing process

- cause inf, inhibited fibroblast activity, & collagen deposition in matrix

inf & contamination affect on wound healing

can overwhelm host defenses

essential macronutrients for wound healing

carbs & fats

- play a major role

negative nitrogen balance effects on wound healing (3)

- impaired immune & inflammatory responses

- delayed wound healing & increased inf

- diminished angiogenesis

vitamin & mineral deficiencies effects on wound healing

chronic, non-healing wounds in nutritionally debilitated individuals

corticosteroid effects on wound healing (3)

- promote carb, fat, & protein breakdown

- impedes inflammatory phase of wound healing

- negative effects

what type of drugs are antineoplastics?

potent immunosuppressants

antineoplastic drug effects in wound healing

impair reepithelialization, granulation tissue formation, & angiogenesis

outcomes of hyperglycemia w untreated diabetes (3)

- chronic macrovasculaar disease

- atherosclerosis

- thickening of basement mem -> diabetic lesions

outcomes of atherosclerosis due to DM (2)

- tissue ischemia

- hypoxia

outcome of sensory neuropathy due to DM

reduces pain sensation associated w wounds

excessive abnormal wound healing

abnormally high CT deposition resulting in altered tissue structure & fxn

types of excessive abnormal wound healing (4)

- fibrosis

- keloids

- hypertrophic scars

- contractures

fibrosis

replacement of normal tissue w excessive nonfxnal collagen or scare tissue

fibrosis cause

excess synthesis &/or delayed degradation

keloids

lesions of dermal scar or fibrotic tissue

hypertrophic scar

excess fibrotic tissue

- raised above level of surrounding skin

- grow within boundaries of original injury

contractures

abnormal exaggeration of wound contraction

- shrinking scars deform wound

contracture outcome

reduce mobility

deficient abnormal wound healing

insufficient deposition of dermal CT matrix weakens tissue to wound failure

- includes wound dehiscence

wound dehiscence

when a closed incision splits open

- incudes extrafascial & fascial

extrafacial wound dehiscence

partial or complete separation of outer layers of sutured wound

- underlying fascial layer remains intact

fascial wound dehiscence

evisceration & separation of fascial layers

chronic nonhealing wounds

progress through healing process but cannot maintain structural & functional integrity

what phase are chronic nonhealing wounds arrested?

the inflammatory phase

chronic nonhealing wound characteristics (2)

- harbor bacteria causing an imbalance between neutrophilic proteolytic enzymes & their inhibitors

- increase in inflammatory mediators