Lesson 2/Chapter 3 Flashcards

1
Q

Deterrents to expedient wound healing

A

Wound characteristics
Local factors
Systemic factors
Inappropriate wound management

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2
Q

Wound Characteristics

A
Characteristics that affect rate of wound healing:
Mechanism of onset
Time since onset
Wound location
Wound dimensions
Temperature
Wound hydration
Necrotic tissue or foreign bodies
Infection
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3
Q

Mechanism of Onset

A

Surgical wounds
Traumatic wounds
Wounds with an insidious onset

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4
Q

Acute Wound

A

Wound induced by surgery or trauma in an otherwise healthy individual
Progresses through normal phases of wound healing in predictable time and manner

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5
Q

Chronic Wound

A

A wound whose progression through the phases of wound healing is prolonged or arrested due to underlying conditions

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6
Q

Time Since Onset

A

Can assist with predicting healing time in acute wounds

Assessment of limiting factors can also aid in prediction of healing in chronic wounds

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7
Q

Wound Location

A

Vascularity of area
Wounds over bony prominences
Presence of epidermal appendages
Skin thickness

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8
Q

Wound Hydration

A

Dry wound
Moist wound
Wet wound

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9
Q

Necrotic Tissue or Foreign Bodies

A

Necrotic tissue promotes infection

Foreign bodies prolong inflammation

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10
Q

Colonization

A

Presence of microbes

Normal skin microflora, up to 103 per g/tissue

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11
Q

Infection

A

Invasion and multiplication of microorganisms in body tissues
Culture with >105 microbes per g/tissue
Signs and symptoms similar to inflammation but disproportionate to wound

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12
Q

Local factors known to affect wound healing

A

Circulation
Sensation
Mechanical stress

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13
Q

Circulation

A

Inadequate macrocirculation
Inadequate microcirculation
Sympathetic response: vasoconstriction
Edema

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14
Q

Sensation

A

Warns of tissue damage

Prevents continued trauma going unnoticed

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15
Q

Mechanical Stress

A
Pressure
Shear
Friction
Periwound edema
Tension on wound edges
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16
Q

Systemic factors that affect wound healing

A
Age
Inadequate nutrition
Comorbidities
Medication
Behavioral risk taking
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17
Q

Age

A
Slowed immune response
Decreased collagen synthesis and strength
Epidermal/dermal atrophy
Decreased number of sweat and oil glands
Decreased pain perception
Decreased inflammatory response
Greater number of comorbidities
Increased susceptibility of infection
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18
Q

Inadequate Nutrition

A

Increased incidence of wound complications

Delayed healing time

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19
Q

Comorbidities

A

Disease process affecting tissue perfusion/oxygenation
Immunocompromised patients
Activity limitations

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20
Q

Vascular occulsion:

A

venous insufficieny, atherosclerosis, sickle cell disease

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21
Q

Inflammation:

A

Pyoderma gangrenosum, Necrobiosis lipoidica diabeticorum, Panniculitis, Dysproteinemias, Idiopathic leukocytoclastic vasculitis, Periarteritis nodosa, Wegener’s granulomatosis, Lymphomatoid granulomatosis, Erythema elevatum diutinum

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22
Q

Pressure necrosis

A

Decubitus ulcers Neuropathic ulcers

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23
Q

Physical agents

A

Radiation, Heat, Frostbite, Chemicals, Trauma, Factitial

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24
Q

Infection

A

Bacterial, Fungal, Mycobacterial, Tertiary syphilis

25
Tumors
Lymphomas, Metastases, Primary skin tumors
26
Medication
Steroids at doses of >30–40 mg/day Chemotherapy NSAIDs
27
Behavioral Risk Taking | Alcohol abuse
Malnutrition Greater risk for injury Less likely to obtain medical assistance
28
Behavioral Risk Taking | Smoking
``` Decreases tissue perfusion Reduces tissue oxygenation Delays normal cellular response to wounding 3x increased graft/flap necrosis 3–5x increased infection rate ```
29
Patient-Related Issues
``` Home remedies Not following recommended treatment Lack of understanding of information provided Limited financial resources Insufficient caregiver support ```
30
Clinician-Related Issues
``` Failure to adequately asses wounds Failure to properly educate patient Inappropriate dressing Failure to manage wound with appropriate modalities Failure to adequately debride ```
31
Abnormal wound healing
absence of inflammation | chronic inflammation
32
Absence of Inflammation
Use of anti-inflammatory medications | Impaired immune system function
33
Chronic Inflammation
Presence of foreign body in wound bed Repetitive mechanical trauma Cytotoxic agents Heightened inflammatory response
34
Prednisone/steroids
inhibit inflammatory response by stabilizing lysosomal enzyme membranes preventing release of acid hydrases Inhibits granulation, contraction, collagen production, and decreased tensile strength
35
Impaired Proliferation
Hypo-granulation or Non-advancing Wound Edge Hypogranular wound Epibole
36
Chronic Proliferation
Hypergranulation
37
Chronic Remodeling
Hypertrophic Scarring Keloids Contractures Dehiscence
38
Key differences from acute wound healing
Senescent cells Increased number of inflammatory mediators (MMP’s) Reduced number of tissue inhibitors of MMPs (TIMP’s) Reduced or arrested epithelialization Greater bioburden Greater numbers of inflammatory cytokines Arrested current of injury
39
Senescent cells
Cells that have become inactive and cease to divide | May be related to tumor growth and inhibition
40
Matrix Metalloproteases (MMP’s)
Family of protein degrading enzymes Functions in neutral pH Synthesized and secreted by neutrophils, macrophages, fibroblasts, endothelial cells, epithelial cells Allows cells to migrate through tissues Increased production in presence of bacterial endotoxins Important for remodeling In excess, degrades ECM and maintains inflammatory phase Also play a role in tumor formation
41
TIMP’s
Tissue inhibitors of MMP’s Necessary to mediate MMP’s Inadequate levels in chronic wounds, allowing MMP’s to break down collagen faster than it can be produced.
42
Current of Injury
All cells process their own currents Average skin surface charge is –23mV secondary to the sodium pump Dry wounds eliminate the voltage gradient Macrophages and neutrophils are attracted to the positive pole
43
What does positive current inhibit?
mast cells
44
What does a negative pole attract?
neutrophils during the inflammatory phase and fibroblasts, facilitates migration of epidermal cells and suppresses bacterial growth
45
How long is current positive?
Current becomes positive for 48 hours after injury, triggers repair process Returns to negative 8-9 days after injury and fluctuates slightly until recovery
46
Tunneling
Use clock terms to identify position | Common in patients with neuropathic ulcerations and surgical wounds
47
Undermining
Use clock terms to identify position | Common in patients with pressure or neuropathic ulcerations
48
Wound color red:
pale pink to beefy red, granulation tissue
49
Goal for red wound
protect wound maintain warm, moist environment protect periwound
50
Wound yellow color:
moist, yellow slough | may vary in adherence
51
Goal for yellow color:
debride necrotic tissue absorb drainage protect periwound
52
Wound black color
thick, black, adherent eschar
53
Goal for black color:
debride necrotic tissue
54
Type of drainage
``` serous sanguinous serosanguinous purulent seropurulent ```
55
Serous
normal, transudate
56
Sanguinous
normal acutely or in resposne to traume
57
serosanguinous
normal
58
Purulent
possible infection
59
Seropurulent
possible infection