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Wound Care > Overview and assessment > Flashcards

Overview and assessment Flashcards

1
Q

Layers (stratum) of the Epidermis

A
  • 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
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2
Q

Epidermis

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

- avascular-nutrients via diffusion from basement membrane

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3
Q

Cells in Epidermis

A
  • 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.
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4
Q

Dermis

A
  • 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
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5
Q

Epidermal Functions

A
  • Physical/Chemical barrier to injury, light, etc
  • Regulates Fluid
  • Produces melanin and coloration
  • Light touch sensation
  • Assists with excretion
  • Temperature regulation
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6
Q

Dermal Function

A
  • Houses epidermal appendages
  • Assists with infection control
  • Hair production
  • Temperature regulation
  • Houses sensory receptors
  • Supplies nutrients to epidermis
  • Supplies sebum
  • Vitamin D production
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7
Q

SubQ tissue

A
  • Insulation
  • Support
  • Padding
  • Energy storage
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8
Q

Structural changes with Aging (skin)

A
  • Flattening of dermal-epidermal junction
  • Epidermal thinning
  • Loss of elastin
  • Dermal atrophy
  • Decreased vascularization
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9
Q

Function changed with aging (skin)

A
  • Increased permeability
  • Decreased inflammatory response
  • Decreased elasticity
  • Decreased sweat and sebum
  • Decreased syntehsis
  • Impaired sensory perception
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10
Q

Inflammatory phase of wound healing

A
  • Normal and essential
  • Immediate till 3-7 days
  • Goal is to provide hemostasis and clear bacteria
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11
Q

Cells of inflammatory phase

A
  • 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
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12
Q

Inflammation (vascular response)

A

-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

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13
Q

Inflammation (cellular response)

A

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

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14
Q

PMN road out of blood vessels

A

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

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15
Q

Cell responsibilities in inflammation

A

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

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16
Q

Proliferative/Granulation Phase

A
  • 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
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17
Q

angiogenesis in proliferation phase

A

-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

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18
Q

Granulation tissue formation

A

-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)

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19
Q

Extracellular matrix

A
  • provides scaffolding for contact guidance
  • integrins (surface cell receptors) help cells recognize/bind to ECM
  • mediates wound contraction
20
Q

Proliferation

A

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

21
Q

Issues with granulation tissue

A

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

22
Q

Epithelialization/maturation phase

A
  • 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
23
Q

Impaired Inflammation

A
  • inadequate stimulus for repair=gradual loss of tissue, leading to inadequate response
  • inadequate perfusion/ischemia=muted hemostasis and cascade initiation.
24
Q

Impaired Proliferation

A
  • increase inflammatory cytokines (MMP’s)
  • Low levels of growth factor cytokines
  • inadequate substrate (protein, viatmins, minerals)
  • inadequate o2
  • pH disruption
25
Q

Impaired Remodeling

A

-imbalance of lysis/synthesis=dehiscence or hypertrophy

26
Q

partial thickness wound healing

A
  • heals by re-epithelialization/regeneration
  • proliferation by mitosis
  • no scar formation
  • normal function returns
27
Q

Full thickness wound healing

A
  • via scar tissue

- wound edges will be soft and gradually adhering

28
Q

Intrinsic factors affecting healing

A 
age
chronic disease
immuno-suppression
sensory impairment
presence of foreign body
tissue perfusion
malnutrition
29
Q

Extrinsic factors affecting healing

A 
smoking
meds
nutrition
chemotherapy
trauma
stress
infection
(edema can lower blood supply by up to 40%)
30
Q

Iatrogenic factors affecting healing

A

local ischemia
treatment choice
trauma

31
Q

Loss of hair on extremity

A

sign of arterial insufficiency

32
Q

Physical exam for wound

A 
skin assessment
sensation-(protective)
pulses
rubor of dependency
ABI=ankle systolic/brachial systolic
33
Q

ABI values

A

> 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

34
Q

stages/grading

A
  • pressure ulcers are staged
  • diabetic ulcers are graded
  • others described as partial/full thickness
35
Q

wound measurement

A

clock method-pt head is 12

lengthwidthdepth (in cm)

36
Q

Undermining

A

-describe with clock

37
Q

tunneling

A
  • clock method

- connecting wounds

38
Q

sinus tracts

A

-tunneling that doesnt connect wounds

39
Q

granulation tissue physical exam

A 
beefy red
bumpy
bleeds easily
can be painful
fragile

be gentle with it

40
Q

eschar

A

necrotic tissue

dont debride if it provides physical barrier

41
Q

Types of drainage

A

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

42
Q

epiboly

A

edges of the wound have rolled under and healing has plateaued

releasing edges promotes new inflammatory phase

43
Q

Maceration

A

moist wound edges
white
fragile
peeling

need to keep wound drier

44
Q

s/s of infection

A 
induration (hardening)
fever
erythema
edema
odor
purulence
friable tissue
45
Q

Types of wound closure

A

primary intention: physical approximation (sx, paper cut, etc)

secondary intention: granulation tissue, edges not approximated

delayed primary (tertiary): combo (contaminated wounds)

46
Q

Goals for wounds

A

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

long term=4-6 wks-reduce wound size

Wound Care (7 decks)

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