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4 phases of wound healing and main cells involved
Coagulation
Platelets
Inflammation
Neutrophils
Migration/proliferation
Macrophages
Remodeling
Fibroblasts and lymphocytes
When do neutrophils peak post wounding?
Peak of inflammation = 2 days post wounding
What 3 substances are released upon platelet degranulation?
TGF-beta (promotes ECM)
PDGF
Fibronectin (makes ECM by forming dimers)
Major proinflammatory enzyme for prostaglanding production
COX-2
Promotes TNF which recruits neutrophils + monocytes
5 roles of macrophages in wound healing
Phagocytosis of microbes and wound debris (via collagenase/elastase)
Cell recruitment and activation
Angiogenesis (VEGF)
Matrix synthesis regulation (GF, cytokines, enzymes, PGs)
2 types of macrophages and role in wound healing
M1 → inhibits proliferation with arginine
M2 → stimulates proliferation with arginine
Shifts from M1
Why is wound healing harder in old age? (2)
Slower epithelial outgrowth from sweat glands
Proliferation is unaltered
Lower keratinocyte cohesion and greater cell spacing
Thinner keratinised tissue
3 things produced by the neodermis during the proliferation phase
ECM
Growth factors and TNF-a (cytokines)
Proteases
3 things which are formed when growth factors interact with ECM
Collagens
Fibronectin
Heparin rich proteoglycans (sequester GFs and release them when needed)
Describe how angiogenesis happens in a new wound. (6)
Pericytes surround endothelial cells
Nearby cells make FGF/VEGF (from inflammatory phase of hypoxia) → new capillaries sprout
Endothelial cells make proteases to digest matrix → ‘drill hole’ making way to blood vessels
Endothelial cells migrate towards stronger concentrations of growth factors (where hypoxia is)
Leaky angiogenesis tissue changes integrity
Initially leaky → therefore granulation tissue is usually oedematous
Fibrin clot degraded via matrix metalloproteinase
5 roles of fibroblasts
ECM production (bond intracellular actin)
Growth factor and cytokine production (EGF, FGF, CTGF, PDGF, activin)
Angiogenesis (EGF, FGF, activin)
Protease release
Trigger migration and proliferation
List 2 factors contributing to proud flesh formation on a horse.
Proud flesh = granulation tissue due to aborted wound healing process
Constant movement of limbs
Poor vascularisation → oxidative stress
Therefore cells constantly stuck in angiogenesis and constantly make matrix
8 types of wound aetiology
Incision = aseptic scalpel blade cut
Laceration = sharp tearing and cutting
Abrasion (graze)
Puncture
Degloving = skin sheared and stripped from extremity
Crushing = often delayed effect
Decubital ulcers = body prominence (shoulder/hip) compresses and necroses tissue
Burns = systemic stability more worrying
3 classes for wound duration
Class 1 = <6h (min. contamination of clean laceration)
>6h = infection → >10000 bacteria/gram
Class 2 = 6-12h (significant contamination)
Class 3 = >12h
2 characteristics of clean surgery
Surgical wound
No break in asepsis
3 characteristics of clean contaminated surgery
Minor break in asepsis
Little to no associated leakage
Opening of respiratory, GI, or urogenital system
3 characteristics of contaminated surgery
GI or urogenital system infectious spillage
High bacterial burden wound (e.g. mouth or perineum)
Major break in asepsis
2 characteristics of dirty surgery
Presence of infection, foreign material or necrosis
(Accidental) perforation into respiratory, GI or urogenital tracts
Deliberate opening = clean contaminated
4 things to do for patient wound stabilisation
Control haemorrhage with firm pressure
Temporarily cover wound with sterile dressing and secure with bandage
NOT tourniquet
Systemic antimicrobials
If patient stable = do swab first
Address wound once the CV system is stable
3 ways to clean a wound
Grossly contaminated = tap
Volume > substance
Isotonic saline
Hartmans
3 types of wound irrigation solutions
Prontosan (polyhexamethylene biguanide)
Good V biofilm, lingers in wound for lasting effect
HOCL
Free radicals V microbes
(Chlorhexidine or iodine)
Cytotoxic = don’t use even when dilute!
3 nonselective and 3 selective ways of debridement
Nonselective
Surgical removal
Irrigation
Mechanical debridement (wet to dry)
Selective
Biological (maggots)
Enzymatic (collagenase)
Autolytic (use body moisture = used in dressings for smooth degranulation)