inflammation & wound healing Flashcards
function of the skin
- protects us from microbes and the elements
- helps regulate body temperature
- facilitates the sensations of touch, heat and cold
3 layers of the skin
epidermis, dermis, hypodermis
epidermis
outermost layer of skin, provides a waterproof barrier and creates our skin tone
dermis
mid layer, contains tough connective tissue, hair follicles and sweat glands
hypodermis
subcutaneous tissue which is made of fat and connective tissue
stratum corneum
ontop of the three living layers; made up of dead flattened epidermal cells which is made up of keratin
components of the skin
blood vessels, sebaceous glands, sweat glands, colour, hair follicle
function of blood vessels in the skin
help maintain body temperature, dilate in heat, constrict in response to cold
function of sebaceous glands in the skin
secrete sebum, helps keep skin from drying out- located in the base of hair follicles
function of sweat glands in the skin
evaporates heat in aid to cool you, located mainly in the palm of your hands and in your forehead
function of the colour of the skin
produced by cells called melanocytes which produce the pigment melanin, which are located in the epidermis
4 stages of wound healing
haemostasis, inflammation, proliferation, remodelling
process of haemostasis
- vasoconstriction occurs, limiting blood flow to the injured site
- platelets stick to the site of injury, which closes up, controlling the bleeding
- stabilised by a protein called fibrin, which forms a mesh with the platelets and creates a clot
- bleeding is stopped with the release of prothrombin
process of inflammation
- capillaries dilate to allow more fluid to the injured site
- pyrogens are release to increase temperature
- pain receptors become activated
- phagocytes migrate to the site of injury
purposes of acute inflammation
- limits spread of injury
- dilutes or removes harmful agents
- removes damaged cells
5 cardinal signs of inflammation
pain, heat, redness, swelling, loss of function (only mobile)
2 components to inflammation
vascular and cellular phase
vascular phase
stimulated by the presence of cytokines
what signalling molecules are released in the presence of damaged tissue?
- mast cells which burst releasing histamine, bradykinin and serotonin
- prostaglandins
- platelets
pain is caused by the release of
bradykinin and prostaglandins
redness and heat is caused by the release of
histamine/ serotonin
process of vascular stage of inflammation
- changes to the capillary bed at the site of injury
- this increases blood flow and permeability
- chemical signals are released to get a response from the immune system
cellular stage of inflammation
arrival of white blood cells
function of neutrophils
destroy bacteria
function of macrophages
destroy bacteria, clean up cellular debris, signal for proliferation to start
processes of the cellular phase of inflammation
margination, rolling, adhesion, transmigration, chemotaxis
margination
as blood flow becomes slower, phagocytes drop to the margins
pavementing
weak attraction and rolling along the endothelial surface
adhesion
phagocyte attaches strongly to attachment proteins
transmigration
phagocyte ‘squeezes’ through permeable endothelial membrane into intracellular spaces
chemotaxis
phagocytes move to area of damage
function of macrophages
- continue the release of cytokines, to attract mote macrophages and fibroblasts
- release growth factors
- release anti-inflammatory mediators
proliferation
- wound is rebuilt with new ‘granulation tissue’
- wounds contract due to myofibroblasts which grip the wound edges and pull them together
- angiogenesis occurs
angiogenesis
new network of blood vessels are developed
by the end of proliferation
- epithelial cells have re-covered the site
- blood vessels have invaded new tissue
- fibroblasts have filled the wound site
- macrophages remain
process of remodelling
- collagen is laid down
- water is reabsorbed so the collagen fibres lie closer together
- cells that have been used to repair the wound that are no longer needed are removed
- this new skin has only 80% of the tensile strength of the unwounded skin
function of myfibroblasts in remodelling
move over the collagen bundles, attach and contract reducing its size, which reduces the size of the scar tissue
apoptosis
the process of normal cell death
What type of wounds might we encounter in practice?
Puncture, surgical, open fractures, burns, non-healing wounds such as ulcers
Process of remodelling
- cells used to repair the wound are no longer needed as removed by cell death
- collagen is aligned within the wound
- healed skin will have 80% of the tensile strength of uninjured tissue
Pressure ulcers
Injured to the skin and other underlying tissue due to pressure, shear or friction
Contributing factors to pressure ulcers
-poor nutrition
- incontinence (weight unevenly distributed)
-moisture
- co-existing medical conditions
- inactivity
Stages of pressure ulcers
Stage 1: redness and warmth
Stage 2: shallow ulcer with distinct edges
Stage 3; full thickness loss of skin
Stage 4: involvement of fascia, connective tissue, muscle and bone
Stage 5: area covered with black Eschar scab (dead cells)
debridement
removal of non-viable necrotic tissue.
is achieved by wet to dry dressings, autolytic debridement, chemical debridement, surgical debridement
autolytic debridement
gels/cream
surgical debridement
physically cut away some of the tissue
open fractures
bone is exposed to the external environment through a break in the skin
diabetic foot
cause skin on the feet to become dry and cracked due to nerve and blood vessel damage
clean/dirty Radiographer technique
1 worker moves equipment whilst 1 moves and helps patient, avoids cross contamination
