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Integumentary > Wound healing > Flashcards

Wound healing Flashcards

1
Q

Skin ound/damage: superficial thickness wound: how it gets damaged and how it regenerates

A
  • shearing, friction
  • healing by regeneration of epithelial cells
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2
Q

Partial thickness wounds where is the damage

A
  • epidermis and uppermost dermis
  • superficial and deep partial thickness wounds (deeper = not as painful because the nerve ending is gone
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3
Q

full thickness wounds

A
  • extending all layers of the skin into subcutaneous tissue
    if there is any slough or eschar = always full thickness
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4
Q

types of wound healing

primary intention/closure

A
  • wound cleaned and edges approximated by sutures, staples or use of adhesives
  • free from contamination; minimal tissue loss, heals in approximately two weeks
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5
Q

Types of wound healing

secondary intentio/closure

A
  • wound edges cannot be approximated
  • granulation must be builty to fill in wound
  • once wounds become chronic/dehiscence you cannot close
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6
Q

Types of wound healing

delayed primary closure/teriary intention

A
  • Dirty wound left open to allow cleaning then closed by surgeon via suturing, graft or flap placement
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7
Q

What are the phases of wound healing

A
  • hemostasis/inflammation
  • proliferation/epithelialization
  • maturation and remodeling
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8
Q

Inflammatory phase of healing

A
  • typically 3-7 days
  • changes: red, warmth, swelling, pain, loss of function
  • begins soon after injury; essential for timely healing
  • vascular and cellular response
    cascade of activities including vasoconstriction and vasodilation
  • goal: hemostasis and breakdon and removal of cellular, extracellular and pathogen debris to produce a clean wound
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9
Q

Hemostasis

A
  • <1 hour
  • clot formation - stop the bleeding, contain invader, begin attracting phagocytes
  • clinical signs: clot formation/fibrous scab, hemostasis achieved, inflammation/edema
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10
Q

Hemostasis: vascular events

A
  • transient arteriole constriction,
  • fibrin from liver to form clot,
  • vascular permeability increases after bleeding is contained
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11
Q

Hemostasis: cellular events

A
  • clotting cascade:
  • influx in neutrophils,
  • platelet aggregation,
  • release of platelets
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12
Q

inflammatory phase: vasoconstriction

A
  • coagulation cause hypoxia that initaties the healing cascade of wound repair
  • control hemorrhage/reduce blood loss
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13
Q

Inflammatory phase: vasodilation

A
  • promts increased perfusion and increased vessel permeability and increased temperature
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14
Q

Inflammatory phase: cellular response

platelet activiation

A
  • initiates the clotting process and secretes cytokines and growth factors
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15
Q

Inflammatory phase: cellular response

neutrophils

A

primary cell for wound cleansing

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16
Q

Inflammatory phase: cellular response

mast cells

A
  • secrete histamine
  • improves vasodilation and permeability
  • also promotes fibroblast recruitment
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17
Q

Inflammatory phase: cellular response

macrophages

A
  • key in inflammatory and proliferation phases
  • releases cytokines
  • ingest debris, debride, initiate angiogensis
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18
Q

Inflammatory phase: cellular response

lymphocytes

A
  • important for immunity
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19
Q

Inflammatory phase: cellular response

fibroblast

A
  • a type of cell that synthesiszes the extracellular matrix and collagen
  • responds to the signals from groth factors ad cytokines that stimulate fibroblast proliferation differentiate into myofibroblasts (not inflammatory phase)
20
Q

Cytokines and growth factors

A

cytokines are signaling molecules - peptide/protein

  • proinflammatory cytokines: signal the system to mount an inflammatory response
  • anti-inflammatory cytokines: inhibit the actions of inflammatory process
  • cytokines/growth factors: respresent the intercellular signaling that orchestrates the complex sequence of cell migration, division, differentiation, and protein expression during wound healing
21
Q

Proliferation phase

A
  • few days post njury - 3 weeks
  • angiogenesis: need to see due to damage t vascular system to nourish and feed tissue
  • fibroplasia: collage synthesis: fibroblasts come into area to depsoite collagen and elastin + some differentiate into myofibroblast
  • myofibroblast - wound contraction
    epithelialization: recover wound
    wound dehiscence occurs most frequently during this phase
  • goal: fill in the wound with new tissue (granulation) nad restory integrity of skin
22
Q

Proliferation phase:

growth factors

A
  • promote cell migration
23
Q

Proliferation phase:

angiogensis

A
  • restore vascular integrity
24
Q

Proliferation phase:

fibroblasts

A
  • heal by fibroplasia
  • participate in biosyntehsis of collage to form ECM
25
Q

Proliferation phase:

collage

A
  • type 3 in early wound healing
  • later replaced by type 1 (most of the collagen in the body)
26
Q

Proliferation phase:

myofibroblast

A
  • wound contraction
  • the process by which the edges of a wound are pulled together during the healing process
27
Q

Epithlelialization phase

A
  • restoring the wound surface
  • funtion of keratinocytes to advance and resurface the open space
  • stem from dermal appendages in partial thickness wounds or from wound edges in full thickness wounds
  • begins within hours of injury
28
Q

remodeling phase

A
  • begins with formation of granulation tissue and can continue for 1-2 years
  • matrix remodeling: takes time to become as strong as original tissue
  • scar formation
  • delicate equilibrium of collagen synthesis and lysis (scare changes from brigh red to pink to grey/white)
  • causes scar/wound to heal (lysis)
    goal: normotrophia or normal scaring
29
Q

Intrinsic factors that can influnce healing

A
  • age: changes in skin
  • comorbidities
  • vascular supply
  • immunosuppression
  • neurological impairment
  • mental status: usually due to ability to take care of wounds
  • nutrition: protein +hydration
  • nature, size, location of injury
  • condition of tissue prior to injury
30
Q

extrinsic factors that can influence healing

A
  • medication: blood thinners, NSAIDs, steriods
  • nutritional status
  • movement
  • bioburden/infection
  • psychophysiological stress
  • lifestyle
31
Q

iatrogenic factors that influence healing

A
  • local ischemia
  • inappropriate care
  • tissue trauma
32
Q

Where can wounds become chronic

A
  • disrupted healing that can occur at any stage
33
Q

chronic wounds: disrupted healing in

inflammatory phase

A
  • inadequate perfusion
  • ischemia
  • decreased levels of cytokines and growth factors
34
Q

chronic wounds: disrupted healing in

proliferation phase

A
  • fibroblast senescence (process of deterioration)
  • often have large tissue gaps or dead space
  • chronic wound fluid that is inhibitory to cell regeneration
35
Q

chronic wounds: disrupted healing in

epithelialization

A
  • decreased keratinocyte migration
    lack of a moist, oxygen rich nutritious ound bed
    failure of cytokines to mediate the healing process
36
Q

chronic wounds: disrupted healing in

remodeling phase

A
  • imbalance of synthesis and lysis
37
Q

What are the most common types of wounds (etiology)

A
  1. venous (55%)
  2. diabetic/neuropathic (16%
  3. pressure (15%)
  4. other (9%)
  5. arterial (7%)
38
Q

What are factors that are seen in all types of chronic wounds

A
  • local tissue hypozia: interventions should try to being blood
  • bacterial colonization
  • repetitive iscchemia-reperfusion injury
  • altered cellular and system stress
39
Q

local tissue hypoxia

A
  • ischemic wounds (poor perfusion or oxygenation) impair healing
  • ischemia and tissue hypoxia are not the same
  • need to consider: atherosclerotic disease, edema (extracellular fluid = no perfusion) , pressure (usually causes hypoxia)
  • ischemia = not getting to the area
  • hypoxia = not getting O2 to the cells itself
40
Q

How can bacteria affect wounds

A
  • an open wound becomes contaminated with bacteria from surrounding skin ithin 48 hours (quicker if more bacteria)
  • inflammation is host immune response
  • fluid from chronic wounds demonstrates increased protease levels
  • increased pro-inflammatory factor levels and reduced growth factor levels (fluid from chronic wounds)
41
Q

ischemia-reperfusion injury

A
  • pressure on a wound = ischemia
  • adverse effects of molecular and cellular events following ischemia
  • in chronic ounds events occur in repetitive fashion
  • tissue damage evident in patients unable to avoid the cyclic dependent injury
42
Q

impaired stress response

A
  • chronic stress can cause cells to constantly replicate and enter replicative senescenece
  • latered response in older adults to ischemic stress contributes to impaired healing response
  • patients with more stress are 4x more likely to heal slower
  • regular physical activity, sleep and nutrition increase wound healing
43
Q

Assessment of healing status

-

A
  • wound healing phase diagnosis is useful to demonstrate medical necessity for interventions

phases of healing overlap

  • benchmarks may indicate multiple phases at the same time
  • wound healing phase diagnosis is defined by the predominant phase appearance
44
Q

Abnormal wound repsonses

A
  • infection
  • moisture
  • wound edges
  • hypergranulation
  • necrotic/non-viable tissue
45
Q

Assess process

A
  • wound tissue attributes
  • peri wound skin attributes
  • other tests and measures
46
Q

assessment process: data collected to

A
  • examine the severity of the lesion
  • determine status of wound healing
  • establish a baseline for wound
  • prepare a plan of care
  • report changes in wound over time
47
Q

PT role in wound healing

A
  • thorough evaluation: examination, comorbid conditions, mobility etc
  • accurate assessment: medical condition, co-morbid conditions, mechanism of injury
  • local wound care: cleansing, debridement, dressings
  • exercise: to facilitate healing, health status and mobility
  • education: wound care, positioning, safety

Integumentary (4 decks)

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