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Integument > Foundations of Wound and Skin Care > Flashcards

Foundations of Wound and Skin Care Flashcards

1
Q

Epidermis Cell Types and Function

A
  • Kertainocytes: protein keratin filaments, most abundant; at surface
  • Langerhans: Monocyte (WBC) turn into Macrophages
  • Melanocytes: skin pigment
  • Merkel Cell: Mechanosensory receptors for pressure; located on epidermis/dermis interface
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2
Q

What layer of the skin do blisters form? Where is this layer located around the body?

A
  • Layer: Stratum Lucidum
  • Located in Lips, Palms, Soles
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3
Q

Epidermal Skin Layers

A
  • Straum Cornium: Stratified Outer Layer with flattened cells overlapping
  • Stratum Lucidum: Clear/translucent layer that resist shearing
  • Stratum granulosum: layer of granules containing a variety lipids, permeability layer between cells
  • Strautum Spinosum: layers of keratin, which flatten to form granules
  • Stratum basale/germinativum: basal/germinal layer of cells connecting to dermis and pushes cells towards surface forming fingerprints/footprints.
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4
Q

Epidermis

A
  • Rapid regeneration
  • Retains moisture
  • Functional barrier
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5
Q

Dermis

A
  • Cutaneous vasculature
  • Nutrition to epidermis
  • Matrix for fibroblasts
  • Struture support for skin
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6
Q

Dermis - Cell Types

A
  • Macrophages (eat necrotic tissue)
  • Mast cells
  • Fibroblasts (make new tissue)
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7
Q

Subcutaneous Fucntion

A
  • Vascularization to skin/body
  • Insulation
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8
Q

Subcutaneous Tissue Cell Types

A
  • Vascular plexus
  • Lymphatics
  • Adipose tissue
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9
Q

Wound definition

A

An interruption in the continuity of bodily structures

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10
Q

Wound Classification - Intention

A
  • 1st intention: incised - no tissue loss: epithelization
  • 2nd intention: incised - tissue loss: regeneration
  • 3rd intention: trauma - structural loss: replacement
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11
Q

What are the 3 phases of wound healing?

A
  • Phase 1: Inflammatory Phase (1-4 days)
  • Phase 2: Proliferative Phase (4 days to 11 months)
  • Phase 3: Matrix Formation - Remodeling phase (30 days - 2 years)
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12
Q

Phase 1,2 and 3 require what type of interventions?

A
  • Phase 1: Debridement and/or cleaning and compression
  • Phase 2: ROM to promote circulation
  • Phase 3: Stretching tissue
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13
Q

As soon as one phase gets to the middle the ____ begins.

A

next phase; therefore there is overlap

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14
Q

Cells interact with their environment (extracellular matrix) through cell surface receptor proteins or ____

A

cell adhesion molecules (CAMs)

CAMs are cells that glob to help seal wounds

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15
Q

Receptors bind extracellular proteins known as…

A

ligands

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16
Q

Cell Biology Initiates signal transduction to upregulate or down regulate ____

A

mRNA (transcription)

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17
Q

Cell biology regulated ____ production (translation)

A

protein

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18
Q

4 types of ligands:

A
  • Cytokines
  • Growth Factors
  • Hormones
  • Chemokines (Chemotaxis = migration)
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19
Q

____ can be put into wounds to help spead up the healing process.

A

Growth factors

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20
Q

Cardinal Signs

Inflammatory Phase 1

A

Calor: Increased Temp
Dolor: Pain
Rubor: Erythema (Redness)
Tumor: Swelling
Loss of Function

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21
Q

An infection =

A

prolonged inflammatory phase

Sign of infection would be an increase in Cardinal Signs

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22
Q

Cellular Reaction - Hemostasis

Inflammatoy Phase 1

A

Hagemann Factor XII
* Turns Prothrombin -> Thrombin
* Turns Fibrinogen -> Fibrin

Scab Formation (Eschar)
* Platelets are the first cells to arrive to injury site
* Platelets release Serotonin to create Vasoconstriction
* Platelet produces platelet derived growth factor (PDGF) that forms the Fibrin clot (platelet plug)
* Fibrin clot acts as the protection layer for early repairs (leukocytes, endothelial cells, fibroblasts and smooth muscle cells bind)
* Endothelial cells restructure the fibrin matrix producing Matrix Matalloproteases (MMP’s) and plasmin for fibrinolysis (break down fibrin)

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23
Q

Matrix Metalloproteinases (MMPs)

A
  • Normal response to healing
  • 26 zinc-dependent proteolytix enzymes produced by neutrophils, macrophages, fibroblasts, endothelial cells
  • Degrade proteins (collagen and growth factors)
  • High levels in chronic wounds, contribute to “biofilm” causing tissue breakdown and chronic inflammation
  • Regulated by Tissue Inhibitors of Metalloproteinases (TIMPs) which can be insufficent in chronic wounds
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24
Q

Vascular Reaction

Inflammatory Phase 1

A
  • Vasocontriction: Platelets release serotonin (Stop Bleeding)
  • Vasodialation: Mast Cells release Histamine (Get rid of debre)
  • Edema (Transudate and Exudate)
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25
Q

Transudate

A
  • Clear
  • Ex: Blister Fluid
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26
Q

Exudate

A
  • Protein (albumin) and leukocytes (viscous)
  • Yellow
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27
Q

Cellular Reaction - Phagocytic

A
  • Prerequisite for healing
  • Initiated during the first 24-48 hours and lasts up to 2 weeks
  • Purpose: Remove foreign bacteria material, damaged cells, dead tissue

PTs do this through debridement

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28
Q

Polymorphonuclear leukocytes - Cellular Reaction

A
  • 48 to 72 hours
  • Neutrophils: release enzymes for autolytic debridement
  • Eosinophils: phagocytic; WBC
  • Mast Cells: release histamine to create VD and produce chemokines for neutrophil migration to site of injury
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29
Q

Autolytic debridement

A
  • Neutrophils do this!
  • Funtion: Phagocytosis (Eat debris), lysosome degradation, kill bacteria
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30
Q

Mononuclear Leukocytes

A
  • Associated with chronic edema
  • Essential to wound healing
  • Tolerate hypoxia (low O2)
  • Become macrophages
  • Release chemotactic factors
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31
Q

If someone with a long standing wound comes in and it gets biopsied, what on the biopsy would indicate it is still in the inflammatory/acute phase?

A
  • Monocytes!
  • Monocytes should change into macrophages; if they don’t likely becomes a chronic wound
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32
Q

Macrophages

A
  • 72 to 84 hours
  • Function in low O2, highly acidotic environment
  • Phagocytose (eat) matrix and debris
  • Transition between inflammatory phase and proliferative phase
  • Secrete cytokines, growth factors (GF) and MMPs
  • Angiogenessi GF which stimulates endothelial budding from damaged blood vessels
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33
Q

Lymphocytes

A
  • 5-7 days
  • Immune System, WBC, defense
  • Down regulates excessive inflammation
  • Controls prolifration and repair
  • Releases cytokines and GFs
  • Overlaps inflammatory and proliferative phases.
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34
Q

Chemical Mediators

Inflammatory Phase 1

A
  • Histamine: Vasodialation, increase wall “leakiness”
  • Serotonin: Vasoconstriction
  • Kinins: Increase small vessel “leakiness”
  • Prostaglandins: Increase permeability and attract leukocytes
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35
Q

When someone takes anti inflammatory medications, what does it do?

A
  • Prevents chemical mediators from working.
  • Leads to poorer wound healing (medications and autoimmunte conditions can slow Wound Healing)
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36
Q

Patient presents to hospital with a Concussion and road rash would on there calf. How does this effect wound healing?

A
  • Any type of inflammation in the body such as that caused by a concussion will result in slower wound healing
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37
Q

Diseases such as RA, Lupus, Sarcoidosis and AIDS all are affected by….

A

the inflammatory response due to wound, perpetuating chronic inflammation

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38
Q

Complement System has ____ plasma proteins that binds antibodies

A
  • 11
  • CS: leukocytes and extra plasma proteins that fight infection
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39
Q

Chronic Inflammation

Inflammatory Phase 1

A
  • Occurs in sealed wounds
  • Not characterized by cardinal signs of inflammation
  • Adhesions form
  • Draining, wet, hasn’t progressed, no granulation tissue

Intervention: cut layers away to create acute phase again and provide growth factor moisturizer to help with skin growth

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40
Q

Fibroplasia

Proliferative Phase II

A
  • Myofibroblasts migrate into wound space
  • Fibroblasts synthesize (Collagen and Glycosaminoglycans)
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41
Q

Angiogensis/Neovascularization/
Vasculogenesis

Proliferative Phase II

A

Formation of blood vessels

42
Q

What does collagen synthesis require?

A

Collagen is the extracellular matrix

Collagen Requires:
* Oxygen (Exercise increases this!)
* Vitamin C
* Amino Acids
* Zinc
* Magnesium

Smoking delays this process

43
Q

Why is it important to stretch wounds out?

A
  • Allows for the collagen to lay down nicely and is plyable early
  • If you don’t move it becomes stuck (nonmovable)
44
Q

What intervention is used to help reorganize hypertrophic scarring?

A
  • Use of pressure!
  • Ex: Pressure dressing
45
Q

Re-epithalialization

Proliferative Phase II

A
  • Begins within hours in superficial wounds
  • Epithelial cells line skin appendages
  • Epithelial cells begin at wound edges and migrate to the center
  • Contact inhibition stops epithelialization; Ex: ear percings
46
Q

What 4 things signal that wound repait is needed?

A
  • Electric gradient (charges)
  • Pain (stimulates the CNS)
  • Infection
    – decreases O2 gradient at wound bed needed for metabolic demand
    – new tissue synthesis
    – collagen remodeling (anaerobic glycolysis)
  • Hyperlactate environment (Acidic; Ex: Lactic Acid)

These send signals for chemotaxis

47
Q

Skin Surface Charge

A
  • -23 mV (Weak electric potential)
  • “Skin battery”; driven by Na+ pump
48
Q

Current of Injury - How does it heal?

A
  • Na+ transports the water in epithelium to internal body fluid creating charge potential of 50 mV across epithelium
  • Break in the tissue causes ionic flow through the path of lowest resistance
  • Dry wound bed eliminates the voltage gradient
49
Q

What cells are involved in charge related healing?

A
  • Galvanotaxis; cells needed for repair are attracted to the poles
  • Wound infection recreates/sustains the inflammatory phase
  • Mast cells: release histamine, vasodilate, increase cell wall permeability, the release heparin to increase endothelial migration
  • Epithelium: receives a signal to migrate from macrophages, neutrophils and current of injury
50
Q

Tissue has a ____ charge

A

+

51
Q

Skin has a ____ charge

A

-

52
Q

Removing ____ allows for migration to occur faster

A

eschar

53
Q

Electrical Stimulation to promote different types of healing

A
  • Autolysis: + on the wound; - on skin
  • Infection: - on the wound; + on skin
  • Granulation: Alternate everyday
54
Q

Undefined border of redness is a sign of an ____.

A

infection

55
Q

Wound Contraction

Pro Phase II

A
  • Myofibroblasts shrink wounds before or after epithelialization
  • Bring wound edges together at a rate of 0.6-0.7 mm/day
  • Wounds under stress heal faster and more securely
56
Q

Shrinking wounds too much may lead to an ____. To prevent it we put dressings in the space to promote ____.

A
  • abcess
  • epithelialization
57
Q

Factors Complicating Wound Healing - intrinsic factors

A
  • foreign material or eschar (contact inhibition)
  • immunosuppression
  • coagulation disorders
  • nutritional deficiencies (Ex: Zinc or protein)
  • metabolic diseases, i.e., R.A. or diabetes mellitus
58
Q

Factors Complicating Wound Healing - Environmental

Tx applied to wound

A
  • “Wound cleansing”
    – Saline/ surfactants vs. cytotoxic agents (acetic acid, hydrogen peroxide, betadine, Dakin’s solution)

Good Tx:
* Dressings
* Electrical stimulation (bring edges together)

59
Q

Factors Complicating Wound Healing - Iatrogenic factors

physical management of wound

A
  • removal of dressings (skin in dressing)
  • frequency of wound cleansing
  • use of clean or sterile technique
60
Q

Types of abnormal wound repair

A
  • Hypergranulation – granulation above the skin level
  • Hypogranulation – granulation below the skin level
  • Hyperwound contraction with hypogranulation and re-epithelialization (tunneling); Ex: skin graft put on too soon
61
Q

Wound Assessment

A
  • Compile information form pt Hx, Subjective and Objective Exam
  • Determine cause, extent of the wound and any conditions that may delay/complicate wound repair
62
Q

Wound Assessment Subjective

A
  • Pt Hx
  • PMH
  • Family Hx
  • Social Hx
  • Current Medications
  • Last tetanus shot (within last 10 years)
  • Wound Sx w/ activity/rest, elevation, dependency
  • Pain
  • Parathesia, anesthesia
63
Q

Objective Wound Exam

A

Assess and Document:
* Location, size & severity
* Dry or draining - note drainage (amount, color, odor) - Any color is an infection
* Wound edges
* Surrounding tissue
* Evidence of skin nutrition (skin atrophy/dryness)
* Swelling
* Skin discoloration

64
Q

Wound Measurement Sizing

A
  • Length (Anatomical length from top to bottom
  • Width (widest part
  • Depth
  • Undermining (lift skin and is underneath)
  • Tunneling (Entry, NO Exit)
  • Fistula (Entry and Exit)
65
Q

Wound Classification - Color Schemes

A
  • Black: Necrosis
  • Yellow: Slough
  • Red: Beefy Red Granulation Tissue
66
Q

Motion Exam

A
  • ROM
  • Strength
  • General activity/mobility
67
Q

Clinical Signs of Infection vs Inflammation:
Erythema, Fever, Odor
Edema, Drainage, Pain

A
68
Q

Fluid - you smell a sweet smell and the liquid is green, what does this mean?

A
  • Sweet-psudemonas
  • Infected
69
Q

Fluid smells like urine, what does this mean?

A
  • Ammonia (Protease)
  • Infected!
70
Q

Serous Fluid

A
  • Clear drainage
  • Healthy
71
Q

Serosanguinous

A
  • Pink
72
Q

Sangrious Fluid

A
  • Red
  • Likely infected
73
Q

What is performed in a vascular Exam

A
  • Pulses - distal to wound
  • Auscultation to detect a briut-caused by:
    – constriction
    – plaque
    – aneurysm
  • Doppler
  • ABI
74
Q

Causes of Venous Insufficency

A
  • Calf pump failure (don’t have musculature)
  • Decrease in insteristial fibrinolysis (deposits become hard)
  • Harvest vein graft (saphenous for bypass surgery)
  • Trauma
75
Q

What does the Trendelenburg test do?

A

Tests integrity of deep veins (DVTs can form here)

76
Q

What are superficial veins called?

A

Spider veins

77
Q

What are some tests for venous insufficency?

A
  • Percussion test - detect dilated saphenous vein
  • Trendelenburg test
  • Cuff test (40 mm Hg)/ Homan’s sign
  • Doppler ultrasound
  • ABI >1.0
78
Q

Tx - Venous Insufficency

A
  • Cleanse & protect with dressings
  • Elevate to decrease edema (Heart level or higher)
  • Support with compression wrap
  • 40 mmHg
  • Ankle pump exercise
  • Stop smoking
  • Dietary management
79
Q

If someone has a wound why would it be bad to be on a diet?

A
  • They lose out of the oxygen, protein, acetic acid and magnesium in their diet needed for healing
80
Q

What are some ways to help rid edema?

A
  • Elevate feet above heart
  • Avoid prolonged sitting or standing
  • Ankle pumps
  • Schedule frequenct rest breaks
81
Q

Tests for Arterial Insufficiency

A
  • ABI < 1.0
  • Rubor of dependency
  • Venous filling time
  • Claudication time
  • Foot print measurements
  • Sensory testing with monofilament
  • (10 g) 5.07 monofilament
82
Q

Tx - Arterial Insufficency

A
  • Warm whirlpool (max 98°)
  • Dressings to maintain moist environment
  • VAC
  • Bed rest
  • Limit leg elevation & activity
  • Limb protection
  • Preserve ROM and strength
83
Q

Surgical Tx - Arterial Insufficency

A
  • Arterial reconstruction (bypass artery)
  • Endarterectomy (go in and try to open up artery)
  • Angioplasty
  • Sympathectomy (cut to open things up; Increases blood flow and decreases pain)
  • Cold laser
84
Q

Diabetic/Neuropathic Wounds

A
  • Greater risk with DM > 15 years
  • Greater risk with neuropathy (can’t feel pressure)
  • Combination of AI and pressure (Charcot joints)
  • Wound healing depends on DM control
  • Slows wound healing
  • Greater risk of osteomyelitis
  • >1.0 ABI
85
Q

Why do pressure ulcers occur?

A
  • In Soft Tissue
  • Usually over bony prominences
  • Results of unrelieved pressure over time
86
Q

Causes/Risk Factors of Pressure Ulcers

A
  • Time/pressure relationship
  • 2 hour max in one position
  • Capillary closing pressure = 32 mm Hg
  • Friction (external rubbing on a surface)
  • Shear (stretching of one layer over the other)
  • Moisture (Can lead to keratin too wet and masticaiton occurs)
87
Q

Approxmately ____ of decubitis ulcers occur in the pelvic area

A

75%

88
Q

Pressure Ulcer Tx

A
  • Eliminate cause of pressure by reducing or redistributing
  • Use pressure relieving devices (PRD’s)
  • Increase activity, maintain ROM & strength
  • Local wound care
89
Q

What type of pillow is really good in preventing pressure ulcers?

A

RIK Fluid Pillow

90
Q

Heel Protection for wounds

A
  • Non-ambulatory
  • Ambulatory
91
Q

What are 4 important nutritional requirements for wound healing?

A
  • Protein
  • Vitamin C
  • Zinc
  • Mg
92
Q

Trauma wounds have a higher risk of ____

A

infection

93
Q

Traumatic Wound Tx

A
  • Protect healthy tissue
    – Wound bed and surrounding tissue
  • Wound debridement/cleansing
    – Foreign and necrotic tissue
  • Anticipate greater risk of infection
    – Systemic Abx and bactericidal dressing
  • Support wound contraction
    – Compression wrapping, VAC, limit joint ROM, ankle pump
94
Q

Silver is a natural ____

A

antimicrobial

95
Q

Wounds from infection are often ____

A
  • Indurated - tissue swelling, hard to the touch
96
Q

Infection Wound Treatment

A
  • Infection management
    – Systemic antibiotics
    – Reduce bacterial load from wound bed(debride/cleansing)
    – Bactericidal topical dressing
  • Pain management
    – Systemic not topical
  • Improve circulation
    – systemic and local
  • Manage drainage
    – daily dressing changes
    – avoid maceration
97
Q

____ and ____ Trauma will delay healing

A
  • Mechanical and Chemical
  • Mechanical Ex: Shear, pressure, ripping off adherent dressings
  • Chemical Ex: cleansers and carriers
98
Q

If you can’t put it in your eye…

A

don’t put it in your wound

99
Q

What are 4 things to never put in a wound?

A
  • Dakin’s solution
  • Acetic Acid
  • Hydrogen peroxide
  • Iodine solutions

All are toxic to myofibroblasts

100
Q

Goals of Wound Cleansing/Debridement

A
  • Rid wound of necrotic tissue
  • Prevent infection
  • Correct abnormal wound repair

Integument (7 decks)

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