Overview and assessment Flashcards
Layers (stratum) of the Epidermis
- Corneum-3/4 of thickness (20-30 cells), dead keratinocytes, provides physical barrier
-Lucidum- flattened, dead keratinocytes
-Granulosum- 3-5 flattened cells c increased keratin (cells still alive)
-Spinosim- mature, active keratinocytes
-Basal- single row of keratinocytes-produces keratin
Basement membrane-scaffolding
Epidermis
- cells travel from basal to corneum in 2-3 wks
- avascular-nutrients via diffusion from basement membrane
Cells in Epidermis
- Melanocytes: produce melanin, protect from UV
- Merkel cells: mechanoreceptors (light touch)
- Langerhans cells: in deeper layers, fight infection
- Hair follicles-soft keratin (temp. regulation)
- Sudiferous glands-sweat, everywhere but lips/ears. oily sebum slows growth of bacteria
- Nails: hard keratin: arise from cells in stratum germinativum, protects digits.
Dermis
- Papillary layer: ground substance that conforms to stratum basale-anchors dermis and protects epidermal appendages (blisters at junction 2* friction)
- Reticular: dense connective tissue, provides structural support-deeper
Epidermal Functions
- Physical/Chemical barrier to injury, light, etc
- Regulates Fluid
- Produces melanin and coloration
- Light touch sensation
- Assists with excretion
- Temperature regulation
Dermal Function
- Houses epidermal appendages
- Assists with infection control
- Hair production
- Temperature regulation
- Houses sensory receptors
- Supplies nutrients to epidermis
- Supplies sebum
- Vitamin D production
SubQ tissue
- Insulation
- Support
- Padding
- Energy storage
Structural changes with Aging (skin)
- Flattening of dermal-epidermal junction
- Epidermal thinning
- Loss of elastin
- Dermal atrophy
- Decreased vascularization
Function changed with aging (skin)
- Increased permeability
- Decreased inflammatory response
- Decreased elasticity
- Decreased sweat and sebum
- Decreased syntehsis
- Impaired sensory perception
Inflammatory phase of wound healing
- Normal and essential
- Immediate till 3-7 days
- Goal is to provide hemostasis and clear bacteria
Cells of inflammatory phase
- Platelets: hemostasis
- Mast Cells: provide histamine (causes redness)
- Neutrophils (PMN): phagocytic, enhance antibody function
- Macrophages: phagocytic, stimulates fibrobalst activity for proliferative phase-fibrobasts ESSENTIAL for progress to proliferative phase
Inflammation (vascular response)
-Injury
-Transudate into intersitial space causes local edema
-Vasoconstriction-mediated by serotonin, norep, ANS
-Platelets aggregate at inj (activated by damaged endothelial cells and exposed collagen)
-Platelets and fibrin form plugs
-Activated platelets release chemical mediators (cytokines=signaling proteins; growth factors=control cell growth, differnetiation and metabolism; Chemotactic agents attract cells necessary for repair)
-Vasodilation (within 30 min of vasoconstriction) triggered by histamine, plasma/platelet derived substances–causes exudate
(histamie from mast cells for short term, prostaglandins from injured cells for long term
Inflammation (cellular response)
-Increased permeability causes decrease in blood volume (slows flow of PMN)
PMN road out of blood vessels
Margination: slow moving PMN’s are pused to side of vessel walls
Dispedesis: adhere to endothelium forcing their way into interstitial space using pseudopods
Chemotaxis: migrate toward zone of injury, guided by chemical gradient
Cell responsibilities in inflammation
PMN-secrete chemotaxic agents/mediators of inflammation (attract more PMN, stimulate fibroblasts, induce vascular growth.-secrete enzymes to break down damaged tissues and kill bacteria-phagocyte bacteria and debris
Monocytes: after PMN, once in interstitium called macrophages-secrete NO and bactericidal enzymes-Phagocytosis-Direct repair process (signal extent of injury, attract more inflammatory cells, produce growth factors)-Stimulate proliferative phase
Mast Cells: Histamine, Enzymes that accelerate removal of damaged cells, Produce chemical mediators to attract active inflammatory cells.
h2o2: released by PMN and macrophage-kills good and bad cells
Proliferative/Granulation Phase
- Stimulated by inflammatory phase
- overlaps with inflammatory phase
- time frame depends on extent of damage
- goal is to minimize scar tissue
- fibroplasia-fibroblast syntesis for granulation tissue
- endothelial budding-vessels from surrounding tissue migrate to supply nutrients
- granulation tissue: matrix of collagen, hyaluronic acid, fibronectin and elastin
- myofibroblasts: wound contraction at margins
angiogenesis in proliferation phase
-angioblasts: endothelial cells that make up blood vessel walls adjacent to injury bud and grow into affected area directed by: local ischemia, vascular endothelial growth factor, and chemical mediators
Granulation tissue formation
-PMN, macrophages, fibroblasts, and keratinocytes produce Matrix Metalloproteases (MMP) to degrade debris from inflammatory phase, leaving a defect-Continued production of MMP delays wound healing
Granulation tissue fills void
Fibroblasts proliferate the injury, secreting hyaluronic acid and fibronectin to lay down extracellular matrix (area between collagen and elastin)
Extracellular matrix
- provides scaffolding for contact guidance
- integrins (surface cell receptors) help cells recognize/bind to ECM
- mediates wound contraction
Proliferation
myofibrobalsts: actin rich fibroblasts contract to pull ends of wound closer
epithelial cells from edges migrate to center via chemotaxis
Keratinocytes secrete enzymes to break down debris
Clean wound needed
Issues with granulation tissue
Not red enough=decreased blood vessels
Decreased bumpiness=not enough protein
Too much collagen=hypergranulation
Decrease granulation tissue will make area weaker, increase reinjury risk
Epithelialization/maturation phase
- epithelial migration
- caollagen lysis/synthesis balanced
- collagen aligns to applied stress: ROM day 1!!
- Lasts 6 mo to 2 years
- wound only 70-80% normal strength
Impaired Inflammation
- inadequate stimulus for repair=gradual loss of tissue, leading to inadequate response
- inadequate perfusion/ischemia=muted hemostasis and cascade initiation.
Impaired Proliferation
- increase inflammatory cytokines (MMP’s)
- Low levels of growth factor cytokines
- inadequate substrate (protein, viatmins, minerals)
- inadequate o2
- pH disruption
Impaired Remodeling
-imbalance of lysis/synthesis=dehiscence or hypertrophy
partial thickness wound healing
- heals by re-epithelialization/regeneration
- proliferation by mitosis
- no scar formation
- normal function returns
Full thickness wound healing
- via scar tissue
- wound edges will be soft and gradually adhering
Intrinsic factors affecting healing
age chronic disease immuno-suppression sensory impairment presence of foreign body tissue perfusion malnutrition
Extrinsic factors affecting healing
smoking meds nutrition chemotherapy trauma stress infection (edema can lower blood supply by up to 40%)
Iatrogenic factors affecting healing
local ischemia
treatment choice
trauma
Loss of hair on extremity
sign of arterial insufficiency
Physical exam for wound
skin assessment sensation-(protective) pulses rubor of dependency ABI=ankle systolic/brachial systolic
ABI values
> 1 non-compressable arteries (diabetes, use other test such as toe pressure)
1=normal
.8-.9=correlates c intermittant claudication, compress c caution
.5-.8=significant occlusion, compression contraindicated
<.5 refer to vascular specialist
stages/grading
- pressure ulcers are staged
- diabetic ulcers are graded
- others described as partial/full thickness
wound measurement
clock method-pt head is 12
lengthwidthdepth (in cm)
Undermining
-describe with clock
tunneling
- clock method
- connecting wounds
sinus tracts
-tunneling that doesnt connect wounds
granulation tissue physical exam
beefy red bumpy bleeds easily can be painful fragile
be gentle with it
eschar
necrotic tissue
dont debride if it provides physical barrier
Types of drainage
serous: clear, thin, watery
sanguinous: bloody
purulent: thick, cloudy, pus-like
epiboly
edges of the wound have rolled under and healing has plateaued
releasing edges promotes new inflammatory phase
Maceration
moist wound edges
white
fragile
peeling
need to keep wound drier
s/s of infection
induration (hardening) fever erythema edema odor purulence friable tissue
Types of wound closure
primary intention: physical approximation (sx, paper cut, etc)
secondary intention: granulation tissue, edges not approximated
delayed primary (tertiary): combo (contaminated wounds)
Goals for wounds
short term=2-4 wks-optimize environment for wound healing, not actually decreasing size
long term=4-6 wks-reduce wound size
