20 Wound Healing Flashcards

1
Q

Hemostasis

A

1º: Formation of platelet plug
2º: production of fibrin clot; intrinsic (8,9,10,12) and extrinsic (7) pathways-> common->coagulation phase

Intrinsic: APTT
Extrinsic: PT
Common: TT

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2
Q

Inflammation cells

A

Neutrophils: first cells (24-48h), cytokines (TNF), proteases
Macrophage: activate and recruit other cells, chemoattractants, 48-96h
T lymph: bridge, strengthen scar formation (collagen), 1wk

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3
Q

Proliferation

A

Day 4-12

Granulation tissue

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4
Q

Proliferation important cells

A

Endothelial cells: mediated by TGFB, TNFa, VEGF; migrate and form new BV
Fibroblasts: ECM; mediated by PDGF

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5
Q

Proliferation ECM

A

1 Structural proteins: collagen (type I [mature, 90%], type III [repair, 9%]; elastin
2 Proteoglycans: dermatan sulfate, chondroitin sulfate; forms ground substance, provide lattice for collagen
3 Adhesive proteins: fibronectin, laminin
4 Hyaluronic acid: fluid environment

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6
Q

Reoganization

A
Type III -> I
ECM deposition (3 mo)
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7
Q

Wound tensile strength

A

2 wk: 20%
3 wk: 30%
10-12 wk: 70-80% (max)

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8
Q

Scar remodeling

A

12-18 mos

1-1.5 yrs = scar revision

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9
Q

Epithelialization

A

Establish tissue integrity

Superficial = reepithelialization (24-48h, waterproof)

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10
Q

Wound contraction

A

Contracture: inc contraction due to myofibroblasts
Myofibroblast: a-smooth muscle actin in thick bundles (stress fibers)

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11
Q

Stratification of bacterial burden

A

Contamination (no multiply)
Colonization (multiply, no host response)
Infection (host response)

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12
Q

Primary intention healing

A
Clean wounds
Mechanical apposition (sutures, tape glue, staples)
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13
Q

Secondary intention healing

A

Reasons: infection, extensive tissue loss
More extensive healing (contracture)
Close spontaneously

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14
Q

Tertiary intention healing

A

Potentially contaminated

Monitor for several days (clean, 3-5d)

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15
Q

Systemic factors that affect wound healing

A

1 Age: physiologic changes, underlying diseases, medications
2 Nutrition: malnutrition (more infection, less collagen), vit C (no collagen, inc infection), vit A (inc inflammatory response), vit E, zinc (cofactor)
3 Metabolic disorders: DM (dec inflammation, angiogenesis, collagen; growth factors), uremia
4 Steroids: anti-inflammatory, prevents epithelialization and contraction
5 Chemo drugs: attenuates inflammation, delay 2 wks post-op
6 Smoking: vasoconstriction -> hypoxia

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16
Q

Local factors affecting wound healing

A

1 Ionizing Radiation Therapy
2 Low Oxygen tension: hypoperfusion (low BV/cardiac failure; local causes), need for collagen synthesis; low BP = arterial insufficiency and vasoconstriction
3 Wound infections: >10^5 microorganisms per gram of tissue (high risk); staphcoccus

17
Q

Class I: clean wounds

A

clean: no 3 tracts (respi, GI, GU),

Class ID: prosthetic devices

18
Q

Class II: clean contaminated

A

entry into 3 tracts, done in elective procedures

19
Q

Class III: contaminated

A

contaminated by not infected

no time to prepare patient

20
Q

Class IV: dirty/infected

A

inflammatory reaction and frank infectious process

21
Q

Antibiotic prophylaxis

A
Only in class 2 and 3
Must be given before surgery (30 mins)
Know the half-life of antibiotics or double the usual dose

Cefazolin

22
Q

Acute wound (normal)

A

Predictable and result is well-healed wound

Standard inflammation, proliferation, remodeling

23
Q

Chronic wound (impaired)

A

Does not heal for 4 wks
Due to local/systemic factors

Delayed wound: dec strength but gets same integrity as normal wound; cause by reversible factors
Impaired healing: no mechanical strength; pts with compromised immune system

24
Q

Chronic wounds

A

Etiology: repeated trauma, excess inflammation, poor oxygen
Causes: GF breakdown, no synthesis of GFs

25
Q

Ischemic arterial ulcer

A

Arterial stenosis -> obstruction -> peripheral vascular resistance (claudication)

Diagnosis: distal portion of extremities, absent pulse, poor granulation, ankle-brachial index

Treatment: revascularization -> wound care

26
Q

Venous stasis ulcer

A

Aging -> venous stasis -> incompetent superficial/deep venous system -> ulceration
Chronic: incompetence of deep venous system

Diagnosis: shallow wound + lipodermatosclerosis (RBC leaks out)

Treatment: compression therapy

27
Q

Diabetic wounds

A

Neuropathy: sensory and motor loss = unrecognized injury, charcot foot
Peripheral vascular disease

Treatment: control DM

28
Q

Pressure injury

A

Excess pressure -> capillary collapse, muscle wasting
Supine: scarum
Wheelchair: ischial tuberosity

Treatment: prevention (turning schedule), wound care

29
Q

Stages of pressure ulcers

A
1 = intact skin
2 = partial thickness skin loss
3 = full thickness skin loss
4 = with fascia and bone
unstageable = eschar
30
Q

Hypertrophic scars

A

In confines of original wound
4 wks after trauma
Occur when not following relaxed skin tension lines (Langer’s lines)

31
Q

Keloid scars

A

Extend beyond border
Does not extend into subcutaneous
Common: earlobe, deltoid, parasternal, upper back

32
Q

Treatment of excess healing

A

intralesional corticosteroid injections: for younger scars, cannot remove scar just reduce; keloid > HTS; no systemic effects

silicone sheets: 24h/day for 3 mos

excision/surgery: HTS > keloid

radiation: destroys fibroblasts, for older adults
pressure: collagen maturation and flattening; for HTS after burns; pressure garment is worn 23-24 hrs for >1 yr