W25 Wound Healing (GN) Flashcards
Structure of the skin:
What are the layers?
Epidermidis - The outermost layer
Dermis- Connective tissues
Hypodermis/subcutaneous layer
What is contained within the dermis? (4)
- Elastin and collagen fibres (stretch & strength)
- Blood vessels and nerve terminations
- Hair follicles
- Sebaceous/sweat gland
What are the different types of wounds? (3)
Superficial – Grade I
-only the epidermis
Partial Thickness – Grade II
-Involves the epidermis and the dermis
Full Thickness – Grade III and IV
-Exposed to tendons, muscles & bone
Physiology of wound healing
What are the 4 time-dependent phases of wound healing?
1 Haemostasis phase
2 Inflammation phase
3 Proliferation or granulation phase
4 Remodelling phase
- The process in not linear - phases which may overlap
What is the Haemostasis phase?
- The body responds quickly to any disruption of the skin’s surface
- It occurs in 3 consecutive steps:
1. Vasoconstriction - Stop bleeding by localised vasoconstriction
2. Primary haemostasis - platelet plug formation
3. Secondary haemostasis - Activation of the coagulation cascade = thrombus formation
Haemostasis phase - vasoconstriction
Immediate response to reduce haemorrhage - 5/10 min post-injury
- The damaged endothelium releases endothelins, prostaglandins
- Induced vasoconstriction in vascular smooth muscle
- Blood flow reduction at the injury site until hypoxia occurs
- Hypoxia triggers nitric oxide release = vascular vasodilation = restore normal blood flow
Primary haemostasis
Platelet plug* Vascular injury exposes dermis extracellular matrix
attracting platelets
* Platelets adhere to damaged endothelium via adhesion
molecules (vWF) Activation
Release of granules containing:
ADP - attracts more platelets
serotonin - vasoconstriction
thromboxane A2 - platelet aggregation
Platelet plug
* In intact skin, endothelial cells release NO2, to prevent platelet activation
Secondary haemostasis:
What does the cascade lead to the conversion of?
- Injured blood vessels expose tissue factor
- Tissue factor activates the extrinsic pathway of coagulation
Cascade leads to the conversion of prothrombin into thrombin, which cleaves fibrinogen into fibrin - Fibrin forms a stable mesh, reinforcing the platelet plug
= Thrombus formation
Inflammation phase
What are the aims? (3)
How long does this phase last?
- minimizes infections and removes debris
- activates keratinocyte regeneration
- promotes new vessel formation = Angiogenesis
- It lasts for the initial 4-6 days
Inflammation phase:
What is it marked by?
- Oedema =localized swelling due to the accumulation of fluid in the tissues
- Erythema =redness in the affected area, caused by enhanced blood flow
- Heat =due to metabolic reactions
- Pain =nociceptors are activated by tissue injury
Inflammatory phase
Early phase - (within 1 day)
- Damaged tissue cells release chemokines activating neutrophiles
produce factors to further neutrophil infiltration
release toxic proteolytic granules to kill microbes
phagocytosis, by engulfing cell debris or microbes
Late phase - (after 24-48 h)
What occurs?
- Macrophages replace neutrophils, which undergo cell death
- Neutrophiles clearance = critical for inflammation resolution
- Neutrophil persistence = chronic wounds
- Macrophage exert many essential activities
Proliferation phase (from 4 to 21 days)
Remodelling phase (from the 21th day to 2 years)
Aims
Further wound contraction
Scar maturity
ECM reorganization
* Macrophages break down ECM excess and engulf ECM tissue debris =tissue reshape
* Replacing collagen III of the granulation tissue with the stronger collagen l
- Granulation tissue retracts, scar matures and fades
- Tissue regains up to 80% of the initial strength and functionality
- Excessive collagen deposition = Abnormal scarring spontaneously regress or not
(Keloid scars)
Wound healing complications:
What are acute wounds?
What are chronic wounds?
acute:
Wound healing complications
* usually heal in an ordered, timely fashion
chronic:
* Impaired wound healing. Wounds that do not heal within 3 months
- Fail to progress through a timely repair sequence
Clinical challenges – Info only
* People over the age of 60
* Diabetic ulcers, pressure ulcers, venous stasis ulcers, etc
* Microbial biofilm formation = impairing debridement and causing necrosis
-Healing cannot proceed until biofilms and necrotic tissue has been removed