Stress and Wound Healing Flashcards
Define normal healing
Healing represents an attempt by the organism to restore integrity to an injured tissue - a multistage process in which sequential elements overlap
What are the 4 types of wound healing?
- Regeneration - complete recovery of function eg. superficial wounds, foetal repair, liver regeneration
- Fibroplasia - recovery of function, but remains distinct from uninjured tissues
- Impaired healing - original function is not recovered, healing remains incomplete
- Fibrosis - inappropriate quantities of connective tissue -> blockage eg. gut
What are the 2 types of repair?
Primary - eg. surgical wounds - two edges entirely opposed, minimal gap to reform
Secondary - eg. trauma - large gap, separate wound edges, fills with clot -> granulation tissue -> scar tissue
Extensive re-epithelialisation
Contraction by myofibroblasts and long term collagen remodelling
What are the 4 phases of wound healing?
- Vascular repsonse
- Lag phase
- Proliferative phase - production of connective tissue
- Remodelling phase - attempt to recover original function
What does the vascular response consist of?
Change in vese ldiamete - inital constriction, later dilation
Decreased blood flow -> transient ischeamia
Increased stickiness of vessel wall (cell adhesion molecules)
Increased vascular permeability - plasma protein and fluid leave vessel -> swelling/oedema
Which cells are involved in the inflammatory or lag phase?
Initially neutrophils (mins-hours) working as “decontaminating phagocytes” to remove damaged tissue and kill micro-organisms
Monocytes>Macrohpages (hours) - highly phagocytic, release growth factors and cytokines - orchestrate later repair process
Granulocytes also
Lymphocytes responding to specific antigen stimulation
Plasma cells - derived from B cells - mediating specific humeral response to antigen
Eosinphils - phagocytic granulocytes release cytotoxic granular contents to attack large targets
Give 3 examples of chemical mediators released from cells
Cytokines - eg. interleukins, tumor necrosis factor, IFN. Regulate cell function
Histamine - Esp. from mast cells, also basophils, platelets, eosinophils. Vascular effects.
PGs - derived from arachidonic acid (COX) Vascular effects, platelet aggregation - regulate cell function
Which are the main cells involved in the proliferative phase? What is the outcome of the proliferative stage?
Fibroblasts (present in tissue and circulating stem cells) and blood capillaries - proliferate
Clot degraded by plasmin
New ECM produced in excess
-> granulation tissue forms
Outline re-epithelialisation
Keratinocytes spread over wound - early closure prevents over granulation and fibrotic healing
Keratinocytes differentiate and the epidermis is regenerated (Basal keratinocytes -> corneocytes)
What occurs during the remodelling phase?
Capillary growth is halted, fibroblasts differentiate to myofibroblasts (contractile) and macrophages begin to die by apopotosis
ECM matirx remodelling returns tissue to normal
Weak collagen replaced by stronger fibres
Contractino reduces wound size
Elevated matrix remodelling continues in the long term
What does scurvy cause?
v collagen synthesis - old scars open due to defective collagen incorporated into scar tissue during remodelling
What are wounds usually infected by?
Bacteria, but can be virus or fungal
What are the 3 types of wound infection?
> Putrid - destructive to cells, breaks down proteins -> H2S and ammonia
Pyogenic - Supparative, toxins promote cell necrosis or destroy WBCs, produce proteases
Anearobic - highly potent toxins and aggressive proteases, infections eg. gas gangrene and tetanus (life threatening)
What are the two forms of gangrene?
Wet - Tissue necrosis -> Septic shock -> death (days)
Dry - No infection, caused by ischeamia (usually hands and feet) - peripheral vascular disease/frostbite
What are the 3 types of fibrosis associated with problem wound healing?
- Hypertrophic scars - forces applied during healing - eg. gut due to peristalsis, Chrons disease
- Keloid scars - proliferation of matrix deposition not limited to the site of injury - able to spread. Genetic component. Poor cross linking of collagen -> water absorption
- Proud flesh - common in horses. Excessive granulation, usually distal limbs. Epidermis doesn’t cover wound properly -> ^ production of granulation tissue.
Caustic chemicals eg. creosote have been advocated to remove excess tissue but this is likely to damage healthy tissue aswell.
