Wound healing Flashcards
(10 cards)
what are the 4 time dependant phases of wound healing?
Haemostasis phase
Inflammation phase
Proliferation or granulation phase
remodelling phase
(these steps overlap so not one after the other)
What are the 3 steps of the haemostasis phase and how they work?
- 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 - 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 (increase)
serotonin - vasoconstriction (increase)
thromboxane A2 - platelet aggregation (increase)
- Secondary haemostasis - 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
finally thrombus formation
What is the inflammation 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 24-48rs)
Macrophages replace neutrophils, which undergo cell death
Neutrophiles clearance -> critical for inflammation resolution
Neutrophil persistence -> chronic wounds
Macrophage exert many essential activities
What are the aims of the inflammation phase?
minimizes infections and removes debris
activates keratinocyte regeneration
promotes new vessel formation -> Angiogenesis
What are the steps of the proliferation phase?
a. Granulation - fibroblasts migrate and synthesise ECM (collagen III and proteoglycans)
b. Angiogenesis - mediated by macrophages (producing VEGF, PDGF)
Formation of new blood vessel to provide nutrients and oxygen to the affected area
Endothelial cells are activated to proliferate toward hypoxia and differentiate into capillaries
c. Wound contraction
Myofibroblasts contract reducing the size of the wound
d. Re-epithelialisation of wound surface
Keratinocytes at the wound edge are activated (by IL-1, IL-6, and TNF-α) to:
lose cell adhesions to migrate over the wound bed
divide and undergo keratinisation to reform the epidermal layer in the gap
Stem cells proliferate to form also hair follicles, sebaceous glands and melanocytes
what are the aims of proliferation?
Formation of granulation tissue
Angiogenesis/neovascularization
Wound contraction
Epidermal resurfacing/re-epithelialisation
Steps of remodelling phase?
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 I
Granulation tissue retracts, scar matures and fades
Tissue regains up to 80% of the initial strength and functionality
aims of remodelling phase?
Further wound contraction
Scar maturity
What are chronic wounds and the clinical challanges?
They fail to progress through a timely repair sequence
clinical challanges:
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
Summary of the wound assessment management TIME?
T - tissue management
I - Control of infection and inflammation
M - Moisture balance
E - Advancement of the epithelial edge of the wound
