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Med/Surg II Wound Care Unit > Overview and Assessment > Flashcards

Overview and Assessment Flashcards

1
Q

Three layers of human skin

A

epidermis, dermis, subcutaneous tissues

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2
Q

Dermis is ___ layers of ____________ tissue

A

2 layers; vascular

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3
Q

The epidermis is (avascular, vascular)

A

avascular

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4
Q

Adipose and fascia are in which layer of skin?

A

subcutaneous

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5
Q

Which skin layer is for protection?

A

subcutaneous

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6
Q

Epidermis has how many layers?

A

5

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7
Q

What is the “horny” layer of the epidermis?

A

stratum corneum

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8
Q

Which layer of the epidermis is the physical barrier from trauma and infection?

A

stratum corneum

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9
Q

The outermost layer of the epidermis

A

stratum corneum

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10
Q

Skin layer beneath the stratum corneum

A

stratum lucidum

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11
Q

How did the stratum lucidum get its name?

A

looks clear under a microscope

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12
Q

Skin layer beneath the stratum lucidum

A

stratum granulosum

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13
Q

Skin layer beneath the stratum granulosum

A

stratum spinosum

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14
Q

Skin layer beneath the stratum spinosum

A

stratum basal

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15
Q

Stratum spinosum consists of several rows of _______________ that appear __________ under a light microscope

A

mature keratinocytes; spiny

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16
Q

Skin layer beneath the stratum basal

A

basement membrane

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17
Q

Keratin is produced by what layer of epidermis?

A

stratum basal

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18
Q

As the basal membrane begins breaking down, what happens?

A

skin becomes more susceptible to wounds (blisters, friction)

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19
Q

Since the epidermis is avascular, how does it receive blood supply?

A

from the dermis through the basement membrane via diffusion

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20
Q

Melanocytes produce ___________ protecting from _______________.

A

melanin; UV rays

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21
Q

What do the melanocytes do?

A

produce melanin protecting from UV rays

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22
Q

Merkel cells are ___________ for _____________.

A

mechanoreceptors; light touch

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23
Q

Langerhans cells present in ______________ that help _________________ by _______________________________.

A

deeper layers; fight infection; attacking and engulfing foreign materials

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24
Q

What do hair follicles help with?

A

temperature regulation

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25
Q

Each hair follicle contains ______________ secreting ____________ to ____________________________.

A

sebaceous gland; sebum; lubricate the skin and hair

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26
Q

Hair follicles are what kind of keratin?

A

soft

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27
Q

Nails are what kind of keratin?

A

hard

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28
Q

Epidermis provides what kind of protection? (functional vs. non-functional)

A

functional

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29
Q

Sudiferous glands are

A

sweat glands

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30
Q

Where are sudiferous glands located?

A

everywhere but lips and ears

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31
Q

Epidermal functions

A
  • barrier to injury, contaminants and light
  • prevents dehydration / retains fluid
  • produces melanin / coloration
  • light touch sensation
  • assists with excretion
  • temperature regulation
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32
Q

Dermal functions

A
  • Houses epidermal appendages
  • Assists with infection control
  • Hair production
  • Assists with infection control
  • Houses sensory receptors
  • Supplies nutrients and oxygen to epidermis
  • Vitamin D production in response to sunlight
  • Supplies sebum to lubricate
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33
Q

Structural changes with aging

A
  • flattening of dermal-epidermal junction pegs
  • epidermal thinning
  • loss of elastin fibers
  • dermal atrophy
  • diminished vascularization
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34
Q

Stratum corneum is how much thickness of the epidermis?

A

3/4 - it is the thickest layer!

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35
Q

Subcutaneous tissue functions

A
  • insulation
  • support
  • padding
  • energy storage for other layers of the skin
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36
Q

Functional changes with aging

A
  • Increased skin permeability
  • Decreased inflammatory response
  • Decreased elasticity
  • Decreased sweat and sebum production
  • Decreased synthesis
  • Impaired sensory perception
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37
Q

Why do you get poor blood supply with aging?

A

nutrition, weight, gravity

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38
Q

The very first thing (phase) that happens when a wound is opened

A

inflammatory phase

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39
Q

How long does the inflammatory phase last?

A

3-7 days

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40
Q

What is the goal of the inflammatory phase?

A

to provide hemostasis and clear away bacteria, foreign material and dead tissues

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41
Q

Inflammatory phase - hemostasis

A

platelet function

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42
Q

Inflammatory phase - vasodilation

A

meet metabolic demands

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43
Q

Inflammatory phase - mast cells

A

histamine response

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44
Q

Inflammatory phase - neutrophils

A

phagocytic, fight bacteria and enhance antibiotic function

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45
Q

Inflammatory phase - macrophages

A

phagocytic, stimulates fibroblast activity for proliferative phase

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46
Q

Why do the macrophages have to show up?

A

to call in the next phase

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47
Q

Inflammation - vascular response

A
  • injury
  • transudate leaks into interstitial spaces
  • vasoconstriction
  • platelets aggregate at injury site
  • activated platelets release chemical mediators
  • vasodilation (within 30 min of vasoconstriction)
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48
Q

What causes exudate in the vascular response of inflammation?

A

vasodilation

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49
Q

What do macrophages call in?

A

fibroblasts

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50
Q

Define margination

A

slower moving PMNs are pushed to sides of vessel walls

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51
Q

Define diapedesis

A

PMNs adhere to endothelium forcing their way into interstitial spaces by extending footlike projections (pseudopods) through narrow openings with vessel walls

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52
Q

Define chemotaxis

A

PMNs migrate toward zone of injury guided by chemical gradient formed by bacterial toxins, dead or dying cells and changes in local pH

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53
Q

PMNs stands for

A

Polymorphonuclear Neutrophils

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54
Q

PMNs secrete

A
  • chemotactic agents and mediators of inflammation

- enzymes to break down damaged tissues and kill bacteria

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55
Q

PMNs secrete chemotactic agents and mediators of inflammation in order to

A
  • attract more PMNs
  • stimulate fibroblast migration
  • induce vascular growth
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56
Q

When do the monocytes come in?

A

after the PMNs

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57
Q

Once in the interstitium, monocytes are called

A

macrophages

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58
Q

How do monocytes direct the repair process?

A
  • Signal extent of injury
  • Attract more inflammatory cells
  • Produce growth factors
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59
Q

Monocytes secrete

A
  • nitrous oxide

- bactericidal enzymes

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60
Q

Mast cells produce

A

chemical mediators that attract and activate inflammatory cells

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61
Q

When should we use hydrogen peroxide?

A

only during the inflammatory phase

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62
Q

cytokines mediate multiple process including

A
  • cell growth
  • migration
  • activation
  • demolition
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63
Q

cytokines are

A

growth factors

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64
Q

What does fibrinolysin do?

A

dissolves clots and plugs

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65
Q

After how many days should you start to see less “red hot and swollen”

A

3-7 days

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66
Q

What does hemosiderin indicate?

A

poor circulation from the veins ???

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67
Q

What are the “stars” of the proliferative phase?

A

fibroblasts

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68
Q

What phase is stimulated by the inflammatory phase?

A

proliferative/granulation phase

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69
Q

The proliferative/granulation phase is stimulated by

A

the inflammatory phase

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70
Q

True/False: The proliferative/granulation phase overlaps with the inflammatory phase.

A

True

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71
Q

Fibroplasia

A

fibroblast synthesis for granulation tissue

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72
Q

Endothelial budding

A

vessels from surrounding tissue migrate to supply nutrients

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73
Q

Myofibroblasts

A

wound contraction at margins

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74
Q

Collagen matrix consists of

A
  • collagen
  • hyaluronic acid
  • fibronectin and elastin formation
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75
Q

Angioblasts

A

endothelial cells that make up blood vessel walls adjacent to zone of injury

76
Q

Angioblasts bud and grow into affected area directed by

A
  • local tissue ischemia
  • vascular endothelial growth factor
  • chemical mediators
77
Q

MMPs stands for

A

Matrix Metalloproteases (MMPs)

78
Q

What produces MMPs?

A
  • neutrophils
  • macrophages
  • fibroblasts
  • keratinocytes
79
Q

What do MMPs do?

A

degrade debris formed during inflammatory phase leaving a defect

80
Q

What kind of tissue is granulation tissue?

A

vascularized connective tisue

81
Q

ECM stands for

A

Extracellular Matrix

82
Q

Surface cell receptors called _______________ help cells _______________ and ______________ to the ____________.

A

integrins; recognize; reversibly bind; ECM

83
Q

Myofibroblasts

A

actin-rich fibroblasts with contractile proteins to pull on ECM and draw wound edges closer together

84
Q

Drawing wound edges closer together is called

A

contraction

85
Q

What is wound contraction? What is responsible for this?

A

Drawing wound edges closer together; myofibroblasts

86
Q

What guides the epithelial cells at the wound margins to migrate to the center of the wound?

A

chemotactic agents

87
Q

If granulation tissue is not “bumpy”, pt is deficient in

88
Q

In the epithelialization/maturation phase, what migrates?

A

epithelial cells

89
Q

In the epithelialization/maturation phase, there is a balance between

A

collagen lysis and collagen synthesis

90
Q

There is a balance between collagen lysis and collagen synthesis in what phase?

A

epithelialization/maturation phase

91
Q

In the epithelialization/maturation phase, collagen aligns how?

A

to applied stress

92
Q

Since collagen aligns to applied stress in the epithelialization/maturation phase, what is important to do?

A

ROM and positioning

93
Q

Scar formation and remodeling occurs in what phase?

A

epithelialization/maturation phase

94
Q

How long does the epithelialization/maturation phase last?

A

6 months to 2 years

95
Q

Tensile strength of wound will not exceed

A

70-80% of the original skin

96
Q

Inadequate stimulus for repair results in

A

gradual loss of tissue, leading to inadequate response

97
Q

Reasons for impaired inflammation

A
  • Inadequate stimulus for repair

- Inadequate perfusion / ischemia

98
Q

At what phase of the inflammatory process should ROM and positioning begin?

A

day 1 of inflammatory

99
Q

Reasons for impaired proliferation/granulation

A
  • Increased amounts of inflammatory cytokines
  • Low levels of growth factor cytokines
  • Inadequate substrate availability (protein, vitamins, minerals)
  • Inadequate oxygenation
  • Disruption of pH and temperature
100
Q

Intrinsic factors affecting healing

A
  • Age
  • Chronic disease
  • Immunosuppression
  • Sensory impairment
  • Presence of foreign body
  • Tissue perfusion
  • Malnutrition
101
Q

Extrinsic factors affecting healing

A
  • Smoking
  • Medications
  • Nutrition
  • Chemotherapy / Radiation Rx
  • Stress
  • Trauma
  • Infection or microbial overload
102
Q

In normal wound healing, full-thickness loss heals how?

A

by scar tissue formation

  • inflammation
  • granulation / proliferation
  • epithelialization
  • maturation / remodeling
103
Q

Reasons for impaired remodeling/maturation

A
  • imbalance of lysis / synthesis activity
104
Q

What types of ulcers are staged? graded?

A

pressure; diabetic

105
Q

What is undermining?

A

Where the wound edge is detached and Q-tip can be slipped in and wiggled around.

106
Q

Iatrogenic factors affecting healing

A
  • local ischemia
  • treatment choices
  • trauma
107
Q

Wound measurements are universally recorded in what order?

A

Length x width x depth

108
Q

Wounds are universally measured in what scale?

A

centimeters

109
Q

Clock vs Perpendicular method of measuring wound size.

A

Clock is more objective and consistent

110
Q

What is tunneling?

A

When two wounds “communicate”

111
Q

What is a fistula?

A

A tunnel with no “exit” - may go straight to an organ or bone

112
Q

Scab vs. eschar

A

A scab is just dried blood, eschar is dead tissue

113
Q

Types of drainage

A
  • serous
  • serosanguinous
  • sanguinous
  • purulent
114
Q

Sanguinous drainage is

115
Q

Serous drainage is

A
  • clear
  • thin
  • watery
116
Q

Serosanguinous drainage is

A

clear with a bloody tint

117
Q

Wound closure - primary intention

A

edges of incision are physically approximated and held in place

118
Q

Wound closure - secondary intention

A
  • granulation tissue matrix must be built and wound contraction achieved
  • unable to approximate wound edges
119
Q

Wound closure - delayed primary intention (tertiary intention)

A
  • combination of primary and secondary intentions

- contaminated wounds

120
Q

Short term goals in wound healing

A
  • Promote moist clean wound environment
  • Reduce / localize erythema - measure
  • Reduce / control edema with elevation or compression - measure
  • Shift drainage from purulent to serous
  • Reduce drainage from copious to mod/min
  • Pain control with dressing or positioning choices
  • Improve periwound integrity to promote wound contraction
  • Soften necrosis to prepare for debridement
  • Reduce risk factors for infection
  • Control drainage with dressing choices to protect periwound
  • Education
121
Q

Long term goals in wound healing

A
  • Reduce necrosis by percentage
  • Promote granulation by %
  • Reduce size of undermining, tract, or tunnel
  • Reduce wound size by cm
  • Tissue perfusion and oxygenation are enhanced
  • Wound and soft tissue healing is enhanced
  • Complications are reduced
122
Q

Examples of linear wounds

A

paper cut, surgical incision, small cutaneous wounds

123
Q

Signs of infection

A
  • Induration
  • Fever
  • Erythema
  • Edema
  • Odor
  • Purulence
  • Increased pain
  • Friable tissue
  • Change in color
124
Q

What is induration?

125
Q

What is friable tissue?

A

wipes away, has too much bacteria

126
Q

What does a change in color of a wound indicate?

A

too much bacteria

127
Q

Long term goals in healing diabetic wounds

A
  • Loading on a body part is decreased
  • Protection of a body part is increased
  • Tolerance to activities is increased
  • Weight bearing status is improved
  • Awareness and use of community resources is improved
128
Q

Long term goals in healing wounds caused by vacular insufficiency

A
  • Pain decreased
  • Protection of a body part is increased
  • Sense of well-being is increased
  • Soft tissue swelling, inflammation, or restriction is reduced
  • Tolerance to positions and activities is increased
129
Q

Purulent drainage is

A
  • cloudy

- white

130
Q

What happens in epiboly?

A

Edges of wound have rolled under and healing has plateaued

131
Q

What is it called when the edges of a wound have rolled under and healing has plateaued?

132
Q

Maceration results in

A
  • moist wound edges
  • white
  • fragile
  • peeling
133
Q

The epidermis contains what types of cells?

A

melanocytes, melanin, Langerhans’ cells

134
Q

The dermis contains what types of cells?

A

fibroblasts, macrophages, WBCs, mast cells

135
Q

What are the fat tissues of the subcutaneous layer for?

136
Q

In which skin layer are hair follicles, sebaceous, and sweat glands located?

137
Q

A localized build up of cells in the stratum corneum due to pressure or friction is called

138
Q

In what layer of skin does a callus occur?

A

stratum corneum

139
Q

2 Layers of the dermis

A
  • papillary

- reticular

140
Q

The papillary dermis is the ground substance that

A

conforms to the contours of the stratum basal

141
Q

What is the purpose of a callus?

A

protection from trauma

142
Q

What is a callus?

A

a localized build up of cells in the stratum corneum due to pressure or friction

143
Q

Layers of the epidermis from superficial to deep

A
  • Stratum corneum
  • Stratum lucidum
  • Stratum granulosum
  • Stratum spinosum
  • Stratum basal
144
Q

What is the “last layer” of the epidermis to contain living keratin cells?

A

stratum granulosum

145
Q

The basement membrane is the “scaffolding” between what 2 skin layers?

A

epidermis and dermis

146
Q

The papillary dermis helps the _______________ to _____________ the dermis and _________________.

A

basement membrane; anchor; protect epidermal appendages

147
Q

Blisters occur at which area layer of skin? Why?

A

papillary dermis; due to friction between layers

148
Q

What does the reticular layer of the dermis provide?

A

structural support

149
Q

Fascia and muscles beneath the subcutaneous tissue provide

A

further structure and padding

150
Q

Regarding the vascular response of inflammation, what happens when transudate leaks from vessels into interstitial spaces?

A

localized edema

151
Q

Regarding the vascular response of inflammation, what is vasoconstriction mediated by?

A

serotonin, norepinephrine, ANS

152
Q

Regarding the vascular response of inflammation, what activates the platelets to aggregate at the injury site?

A

damaged endothelial cells and exposed collagen

153
Q

cytokines

A

signaling proteins

154
Q

What do growth factors control?

A

cell growth, differentiation, and metabolism

155
Q

What do chemotactic agents do?

A

attract cells necessary for repair

156
Q

Regarding the vascular response of inflammation, what triggers vasodilation?

A
  • histamine
  • plasma-active substances
  • platelet-derived vasoactive substances
157
Q

Regarding the vascular response of inflammation, histamine released by mast cells increases

A

vessel wall permeability for short term vasodilation

158
Q

Regarding the vascular response of inflammation, why are prostaglandins released?

A

for long term vasodilation

159
Q

In the cellular response of inflammation, increased vessel wall permeability causes

A

decrease in blood volume

160
Q

Macrophages stimulate what phase?

A

proliferative

161
Q

Enzymes that accelerate the demise of damaged cells are called

A

mast cells

162
Q

Regarding the cellular response of inflammation, what adheres to vessel walls and moves into the interstitial spaces?

A

leukocytes, erythrocytes, and platelets

163
Q

Neutrophils and macrophages phagocytize microorganisms, then excrete

A
  • ascorbic acid
  • lactic acid
  • hydrogen peroxide
164
Q

What is the goal of the proliferative/granulation phase?

A

to replace lost dermal tissue with scar tissue

165
Q

What occurs during the proliferative phase?

A
  • Fibroplasia
  • Endothelial budding
  • Collagen matrix of collagen, hyaluronic acid, fibronectin and elastin formation
  • Myofibroblasts
  • Angiogenesis
  • Granulation tissue formation
166
Q

Fibroblasts secrete __________________ and lay down the ____________________.

A

hyaluronic acid and fibronectin; ECM

167
Q

Fibroblasts are guided by

A
  • chemotactic agents

- low oxygen tension

168
Q

What does the ECM “technically” do?

A

mediates wound contraction

169
Q

What provides a scaffolding for contact guidance to move cells into the wound area?

170
Q

Inadequate perfusion / ischemia leads to

A

vascular insufficiency leading to muted hemostasis and a muted cascade initiation

171
Q

In normal wound healing, partial thickness / superficial loss heals by

A

re-epithelialization / regeneration

172
Q

In normal wound healing of full-thickness loss, how will the wound edges be?

A

soft and gradually adhering

173
Q

When assessing skin, what can hair pattern tell you?

A

where blood is flowing to

174
Q

ABI stands for

A

Ankle-Brachial Index

175
Q

ABI =

A

ankle systolic pressure / brachial systolic pressure

176
Q

ABI values

A

1 = normal
.8-.9 = intermittent claudication
.5-.8 = significant occlusion (compression contraindicated)
>1 - non-compressible arteries, calcification

177
Q

The ABI is invalid for what types of pts?

178
Q

What ABI values contraindicate compression

179
Q

Wounds besides pressure and diabetic ulcers are “graded” how?

A
  • superficial thickness
  • partial thickness
  • full thickness
180
Q

superficial thickness

A

epidermis removed

181
Q

partial thickness

A

epidermis and part of dermis removed

182
Q

full thickness

A

epidermis and dermis removed to/through subcutaneous tissue or deeper

183
Q

What must be done in the case of epiboly?

A
  • must promote inflammatory phase by releasing edges

- debridement or silver nitrate

184
Q

Options for correction of maceration

A
  • choose more absorptive dressing
  • increase frequency of dressing change
  • utilize skin barriers / skin prep
185
Q

Long term goals in healing pressure ulcers

A
  • Loading on a body part is decreased
  • Protection of a body part is improved
  • Sense of well-being is improved
  • Tolerance to positions and activities is increased
186
Q

Long term goals in wound healing in all patients

A

Look it up I’m sick of typing these long-winded goals that are all the same and mostly common sense - p. 16 slide 3

Med/Surg II Wound Care Unit (11 decks)

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