Overview and assessment

Question 1

Layers (stratum) of the Epidermis

Answer 1

• 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

Question 2

Epidermis

Answer 2

• cells travel from basal to corneum in 2-3 wks

- avascular-nutrients via diffusion from basement membrane

Question 3

Cells in Epidermis

Answer 3

• 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.

Question 4

Dermis

Answer 4

• 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

Question 5

Epidermal Functions

Answer 5

• Physical/Chemical barrier to injury, light, etc
• Regulates Fluid
• Produces melanin and coloration
• Light touch sensation
• Assists with excretion
• Temperature regulation

Question 6

Dermal Function

Answer 6

• Houses epidermal appendages
• Assists with infection control
• Hair production
• Temperature regulation
• Houses sensory receptors
• Supplies nutrients to epidermis
• Supplies sebum
• Vitamin D production

Question 7

SubQ tissue

Answer 7

• Insulation
• Support
• Padding
• Energy storage

Question 8

Structural changes with Aging (skin)

Answer 8

• Flattening of dermal-epidermal junction
• Epidermal thinning
• Loss of elastin
• Dermal atrophy
• Decreased vascularization

Question 9

Function changed with aging (skin)

Answer 9

• Increased permeability
• Decreased inflammatory response
• Decreased elasticity
• Decreased sweat and sebum
• Decreased syntehsis
• Impaired sensory perception

Question 10

Inflammatory phase of wound healing

Answer 10

• Normal and essential
• Immediate till 3-7 days
• Goal is to provide hemostasis and clear bacteria

Question 11

Cells of inflammatory phase

Answer 11

• 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

Question 12

Inflammation (vascular response)

Answer 12

-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

Question 13

Inflammation (cellular response)

Answer 13

-Increased permeability causes decrease in blood volume (slows flow of PMN)

Question 14

PMN road out of blood vessels

Answer 14

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

Question 15

Cell responsibilities in inflammation

Answer 15

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

Question 16

Proliferative/Granulation Phase

Answer 16

• 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

Question 17

angiogenesis in proliferation phase

Answer 17

-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

Question 18

Granulation tissue formation

Answer 18

-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)

Question 19

Extracellular matrix

Answer 19

• provides scaffolding for contact guidance
• integrins (surface cell receptors) help cells recognize/bind to ECM
• mediates wound contraction

Question 20

Proliferation

Answer 20

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

Question 21

Issues with granulation tissue

Answer 21

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

Question 22

Epithelialization/maturation phase

Answer 22

• 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

Question 23

Impaired Inflammation

Answer 23

• inadequate stimulus for repair=gradual loss of tissue, leading to inadequate response
• inadequate perfusion/ischemia=muted hemostasis and cascade initiation.

Question 24

Impaired Proliferation

Answer 24

• increase inflammatory cytokines (MMP’s)
• Low levels of growth factor cytokines
• inadequate substrate (protein, viatmins, minerals)
• inadequate o2
• pH disruption

Question 25

Impaired Remodeling

Answer 25

-imbalance of lysis/synthesis=dehiscence or hypertrophy

Question 26

partial thickness wound healing

Answer 26

- heals by re-epithelialization/regeneration - proliferation by mitosis - no scar formation - normal function returns

Question 27

Full thickness wound healing

Answer 27

- via scar tissue | - wound edges will be soft and gradually adhering

Question 28

Intrinsic factors affecting healing

Answer 28

``` age chronic disease immuno-suppression sensory impairment presence of foreign body tissue perfusion malnutrition ```

Question 29

Extrinsic factors affecting healing

Answer 29

``` smoking meds nutrition chemotherapy trauma stress infection (edema can lower blood supply by up to 40%) ```

Question 30

Iatrogenic factors affecting healing

Answer 30

local ischemia treatment choice trauma

Question 31

Loss of hair on extremity

Answer 31

sign of arterial insufficiency

Question 32

Physical exam for wound

Answer 32

``` skin assessment sensation-(protective) pulses rubor of dependency ABI=ankle systolic/brachial systolic ```

Question 33

ABI values

Answer 33

>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

Question 34

stages/grading

Answer 34

- pressure ulcers are staged - diabetic ulcers are graded - others described as partial/full thickness

Question 35

wound measurement

Answer 35

clock method-pt head is 12 | length*width*depth (in cm)

Question 36

Undermining

Answer 36

-describe with clock

Question 37

tunneling

Answer 37

- clock method | - connecting wounds

Question 38

sinus tracts

Answer 38

-tunneling that doesnt connect wounds

Question 39

granulation tissue physical exam

Answer 39

``` beefy red bumpy bleeds easily can be painful fragile ``` be gentle with it

Question 40

eschar

Answer 40

necrotic tissue | dont debride if it provides physical barrier

Question 41

Types of drainage

Answer 41

serous: clear, thin, watery sanguinous: bloody purulent: thick, cloudy, pus-like

Question 42

epiboly

Answer 42

edges of the wound have rolled under and healing has plateaued releasing edges promotes new inflammatory phase

Question 43

Maceration

Answer 43

moist wound edges white fragile peeling need to keep wound drier

Question 44

s/s of infection

Answer 44

``` induration (hardening) fever erythema edema odor purulence friable tissue ```

Question 45

Types of wound closure

Answer 45

primary intention: physical approximation (sx, paper cut, etc) secondary intention: granulation tissue, edges not approximated delayed primary (tertiary): combo (contaminated wounds)

Question 46

Goals for wounds

Answer 46

short term=2-4 wks-optimize environment for wound healing, not actually decreasing size long term=4-6 wks-reduce wound size