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Skin - Derm/Plastics > Wound healing > Flashcards

Wound healing Flashcards

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1
Q

What are the timings and stages of healing?

A
  1. Haemostasis - 3 mins
  2. Inflammation - 3 hours
  3. Proliferation - 3 days
  4. Maturation - 3 weeks
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2
Q

What stage do these occur at?

platelets and vasoconstriction

A

haemostasis (1st stage - 3 mins)

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3
Q 
What stage do these occur at?
thrombin, 
clot formation dissipates, 
vasodilation, cellular infiltration, 
pain
A

inflammation (2nd stage - 3 hours)

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4
Q

What stage do these occur at: collagen remodelling, capillary regression?

A

maturation (4th stage - 3 weeks)

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5
Q

What stage do these occur at: granulation tissue forms, epithelialization, fibroplasia, angiogenesis, contraction?

A

proliferation (3rd stage - 3 days)

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6
Q

what is the physiology of platelets in haemostasis part of wound healing?

A

the exposed sub endothelium w/ collagen and tissue factor —> platelet activation
activation = platelets can degranulate and release chemotactic and growth factors (PDGF, proteases, vasoactive e.g. 5HT, histamine)
–> primary plug /clot formation –> clotting cascade then triggered

Overall: platelets aggregate, release cytokines, chemokines & hormones

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7
Q

What is the physiology of vasoconstriction occuring in haemostasis phase of wound healing? (1st stage - 3 mins)

A

Adrenaline, NA, PGs, 5HT, thromboxane
–> vasoconstriction
–> limits blood loss
= temporary blanching of wound

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8
Q

What is the physiology of thrombin occuring in inflammation phase of wound healing? (2nd stage - 3 hours)

A

thrombin

  • -> activates fibrin
  • -> increases vascular permeability, this = for migration of inflam. cells to injury & protein, cells and fluid leak out
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9
Q

What is the physiology of clot formation dissipating in inflammation phase of wound healing? (2nd stage - 3 hours)

A

As stimuli dissipate

plasminogen is converted to plasmin –> destroys blood clots by attacking fibrin

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10
Q

What is the physiology of vasodilation in inflammation phase of wound healing? (2nd stage - 3 hours)

A

vasodilation allows a more persistent flow of inflammatory cells & factors to wounds
– so there is debridement of the wound by inflammatory cells

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11
Q

What are the role of neutrophils, macrophages, lymphocytes in cellular infiltration during inflammation?

A

1 in = neutrophils (48h)

–> cleanse wound, release inflam mediators and O2 free radicals –> bactericidal
#2 = macrophages (crucial)
–> phagocytose debris & bacteria –> collagenases & elastases (breakdown injured tissue), + cytokines, + PDGF –> chemotaxis, fibroblast & SM proliferation & angiogenesis.
#3 = lymphocytes (72hrs)
–> cellular immunity, Ab produced & lymphokines –> heparin-binding epidermal GF, basic fibroblast GF

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12
Q

What causes pain during inflammation phase of wound healing?

A

pain comes from:

  • Swelling
  • Tissue hypoxaemia
  • pH alterations (tissue & bacterial degeneration)
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13
Q

What is the physiology of granulation tissue in proliferation phase of wound healing? (3rd stage - 3 days)

A

Granulation tissue =
Inflammatory cells, fibroblasts and
neovasculature
in a matrix of fibronectin, collagen T3, glycosaminoglycans which make up proteoglycans in connective tissue and elastin
–> when granulation tissue forms = the wound begins to CONTRACT
from combination of capillary loops and myofibroblasts

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14
Q

What is the physiology of epithelialization in proliferation phase of wound healing? (3rd stage - 3 days)

A

epithelialisation = to seal between underlying wound and environment

1) epidermal cell secrete collagenases –> break down collagen (from macrophages/PDGF)
2) & plasminogen activator (clot dissolution)

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15
Q

What is the physiology of fibroplasia in proliferation phase of wound healing? (3rd stage - 3 days)

A

there are less fibroblasts as inflammation disappears…
they migrate & proliferate in response to:
PDGF, FGF, TGF & C5a
Fibroblasts produce –> collagen, elastin, fibronectin, glyosaminoglycans & proteases

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16
Q

What is the physiology of angiogenesis in proliferation phase of wound healing? (3rd stage - 3 days)

A

macrophages stimulate angiogenesis

there is greater blood flow to the wound & increased perfusion of healing factors

17
Q

when does contraction in proliferation phase of wound healing maximally finish? (3rd stage - 3 days)

A

is the movement of wound edges to facilitate closure

maximal 5-15D post injury (~2wks)

18
Q

What is the physiology of Collagen remodelling in maturation phase of wound healing? (4th stage - 3 weeks)

A

1) Collagenases and Matrix metallproteinases remove collegen (the T3) and it is replaced by T1 new collagen (increased strength)
2) fibronectin, hyaluronic acid & glyco are replaced by proteoglycans
3) water resorbed from scar so collagen fibres lie closer together
4) Cross linking to other collagen and w/protein molecules increases scar tensile strength
[NB: only 80% as strong as original tissue]

19
Q

What is the physiology of capillary regression in maturation phase of wound healing? (4th stage - 3 weeks)

A

there is a reduction in blood vessels

TF reducing blood flow

20
Q

What stage is this: the scar flattens and softens?

A

the maturation phase (4)

collagen remodelling

21
Q

What stage is this: the scar pales and itching subsides?

A

the maturation phase (4)

capillary regression

22
Q

What stage is this: red vascular tissue appears in wound?

A

the proliferation phase (3)

the granulation tissue forms (inflam cells, fibroblasts and neovasculature)

23
Q

What stage is this: smooth marginal zone / island of epithelium seen?

A

The proliferation phase (3)

epithelialisation (collagenases and plasminogen activator)

24
Q

What stage is this: the size of defect is reduced?

A

the proliferation phase (3)

contraction

25
Q

What is this clinical effect due to: skin becomes red and hot?

A

The inflammation phase (2)

vasodilation (histamine, PG, kinins, leukotreines)

26
Q

What is this clinical effect due to: swelling, exudate production?

A

The inflammation phase (2)

cellular infiltration = neutrophils, macrophages, lymphocytes

27
Q

What is this clinical effect due to: crust, pus or sloughing?

A

The inflammation phase (2)

cellular infiltration = neutrophils, macrophages, lymphocytes

28
Q

What is this clinical effect due to: haemorrage control?

A

Platelets & vasoconstriction

29
Q

What is this clinical effect due to: clot formed in wound?

A

platelets –> activated by TF etc –> release chemotactic & primary clot –> clotting cascade triggered

30
Q

What are the patient factors affecting wound healing?

A

1) Age
2) Nutritional status - malnutrition, obesity, recent weight loss
3) Infection
4) Immune status - cancer, steroids, immunosuppressant’s, HIV
5) Comorbidities e.g. diabetes, jaundice, uraemia,
6) Smoking
7) Previous irradiation
8) Immobility
9) Incontinence

31
Q

What are the wound factors affecting wound healing?

A

1) Tissue type injured
- -> Cells:
- — labile (good capacity to regenerate e.g. surface epithelial cells),
- —stable (capacity to regenerate slowly e.g. hepatocytes),
- — or permanent (no capacity to regenerate e.g. nerve & striated muscle cells)
- -> Tissue architecture:
- — complex arrangements cannot be reconstructed e.g. renal glomeruli
2) Arterial supply & venous drainage
3) Physical wound factors: Excessive movement, local distension or distal obstruction
4) Internal wound factors: Infection, malignancy, foreign body, necrotic tissue

32
Q

What are the 2 types of abnormal scarring?

A

hypertrophic

keloid

33
Q

What is hypertrophic scarring?

A

soon after operation
within incision boarders
resolves eventually but slowly

34
Q

What is keloid scarring?

A

appears months-years after op
painful / itchy
outside boarders of incision

35
Q

What are the Rx for abnormal scarrring?

A
  • steroid injection

- de-bulk + 1x session of radiotherapy (high recurrence on just de-bulking)

Skin - Derm/Plastics (5 decks)

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