Module 5- Altered healing and mobility Flashcards
How can bed rest affect the body
Decreases the use of muscles and the effects of gravity resulting in kidneys diuresis, changes in lung ventilation and cardiovascular deconditioning
Can reduce muscle and bone mass and cause pressure injuries
What is the acute inflammatory response
Most common form of response, takes around 8-10 days (part of innate immune response)
Defence mechanism of the body
Inflammation is triggered by cells that recognise pattern of molecules associated with cellular damage or pathogens
List the first step of acute inflammatory response
Entry of foreign molecule e.g. bacteria into the body resulting in tissue damage
List the second step of the acute inflammatory response
Mast cells stimulated to release chemical mediators (rapid response within seconds to minutes) which triggers three main actions:
- Vasodilation: increases vessel diameter slowing blood flow and increasing volume of blood flow, allowing for increased inflammatory cells and chemicals to area of injury - leads to swelling and pain
- Increased vessel permeability: retraction of endothelial cells lining vessels causes gaps to open up between these cells allowing leakage of plasma out of vessel (exudation) which causes swelling (oedema). Blood becomes more viscous and flows slowly which increases blood volume and conc. of red blood cells at site of inflammation - causes heat and redness
- Diapedesis and chemotaxis: white blood cells (e.g. leucocytes) adhere to inner walls of capillaries and migrate through enlarged junctions between endothelial cells lining vessels into the surrounding tissue - attracts inflammatory cells such as phagocytes which cause phagocytosis
List the third step of acute inflammatory response
As a result of changes to blood vessels the signs of inflammation are observed:
Redness: increased blood flow from vasodilation and increased permeability
Heat: increased blood flow (blood=warmth)
Swelling: increased blood flow from vasodilation and increased vessel permeability - increased fluid and blood cells to region
Pain: swelling effects leads to increased fluid in region which activates pain receptors, inflammatory mediators also directly activate pain receptors
Describe histamine
Vasoactive amine that acts on blood vessels. Come from platelets, mast cells and basophils and cause increased vasodilation, vascular permeability, vascular smooth muscle contraction and endothelial activation
Describe serotonin
Come from platelets and causes vasodilation and increased vascular permeability
Describe prostaglandin
Come from mast cells and leucocytes, cause vasodilation, pain, chemotaxis and fever
Describe Leukotrienes
Come from leucocytes and mast cells, causes increased vascular permeability, chemotaxis, leucocyte adhesion and activation
Describe platlet-activating factor
Come from leucocytes and mast cells, cause vasodilation, increased vascular permeability, leucocyte adhesion, chemotaxis and degranulation
Describe nitric oxide
Come from endothelium and macrophages, cause vascular smooth muscle relaxation and killing of microbes
Describe cytokines
Come from macrophages, endothelial cells and mast cells, cause local endothelial activation, fever, pain, hypotension, decreased vascular resistance (shock) - common ones include Interleukins and interferons
Describe chemokines
Come from leucocytes and activated macrophages, cause chemotaxis, recruitment of leucocytes to sites of inflammation and migration of cells to normal tissues
Describe tumor-necrosis factor alpha
Strong mediator of fever
Describe wound healing
Begins during acute inflammation and can last up to 2 years
Wounds that heal under conditions of minimal tissue loss e.g. paper cut, are said to heal by primary intention
Wounds that do not heal as easily e.g. pressure injury, are said to heal by secondary intention
What are the steps of wound healing
- Inflammation
- Reconstructive/proliferative phase
- Maturation/remodelling phase
Haemostasis can also be described as first step, then the others follow (controlling the bleeding)
How long do wound healing phases last
Haemostasis initial injury to 3 hrs post injury
Inflammation is 4-6 days
Proliferation is 4-24 days
Remodelling is 21 days - 2 years
Explain the second wound healing phase- reconstructive/proliferation
Macrophages invade dissolving the clot and clear away dead cells and debris, also secrete biochemical mediators that promote healing
Granulation tissue (connective tissue and fibroblasts) grows into wound from surrounding healthy connective tissue which leads to fibrosis
Tissue is filled with new capillaries (process called angiogenesis – meaning growing new blood vessels) derived from capillaries in surrounding tissue which gives tissue red, granular appearance
New lymphatic vessels also grow, as well as an additional extracellular matrix which provides a scaffold to guide cell placement, proteins also direct some cellular functions related to wound healing
How is healing protected during second phase
Through epithelialisation which is where epithelial cells grow into the wound from surrounding healthy tissue
Explain epithelialisation
Epithelial cells do the following:
- Migrate under clot or scab to unravel collagen
- Contact similar cells from all sides of wound and seal it to halt migration and proliferation
-Undergo differentiation to give rise to epidermal layers
Epithelialisation can be quick process if wound is kept moist as it keeps fibrin clot from becoming a scab
What are the most important cells during healing phase
Fibroblasts are most important cells during healing as they secrete collagen and other connective tissue proteins, which are deposited in debrided areas about 6 days after fibroblasts have entered the lesion
Collagen is the most abundant protein in the body (high conc. of amino acids) - as healing progresses, collagen undergoes chemical reactions to form collagen fibres (complete process takes several months)
What is wound contraction
Occurs during second phase of healing process
Wound contraction needed to close wounds (especially those by secondary intention) – noticeable 6-12 days after injury
Granulation tissue contains myofibroblasts (cells specialised for wound contraction (shortening)- functions of both smooth muscle cells and fibroblasts)
Contraction occurs as extensions from plasma membrane of myofibroblasts establish connections between neighbouring cells exerting tension while anchoring themselves to wound bed
Explain the maturation/remodelling phase of wound healing
Continuation of collagen matrix assembly, tissue regeneration
Scar tissue remodelled and capillaries disappear making scar avascular
Takes 2-3 weeks after maturation begins for scar tissue to gain 2/3 of maximum strength
Epidermal secondary intention healing wounds and un-sutured internal lesions not completely restored by healing (at best gains 80% original strength)
Only epithelial, liver and bone marrow are capable of regaining complete strength (this is called compensatory hyperplasia)
In fibrous connective tissue joints and ligaments, injured tissue is replaced with new tissue, however, does not have exactly same structure and function as original tissue (why it can easily become re injured)
Difference between resolution and repair
Resolution: returning injured tissue to the original structure and function
Repair: replacement of destroyed tissue with scar tissue (composed primarily of collagen to restore the tensile strength of the tissue)
Explain primary intention wound healing
Wounds that heal under conditions of minimal tissue loss
Include clean incisions such as paper cut or sutured surgical wound
Heal primarily through process of collagen production
Close proximity of wound edges
Little sealing (epithelisation) and shrinkage (contraction)
Original tissue structure and function restored (capable of regeneration)
Explain secondary healing intention
Wounds that require a great deal more tissue replacement
- Open wounds
- Do not heal as easily- healing process takes longer
- Wounds usually contain extensive tissue loss such as a pressure injury
- Processes take longer
- Tissue cannot regenerate so results in a scar
Example: pressure ulcer
How are antihistamines used for wound healing
Stop binding of histamine to receptors, therefore, decrease inflammation
How is aspirin and other NSAIDs used for wound healing
Block production of prostaglandins inhibiting inflammation, and reducing pain and fever
How can wound healing be dysfucntional during reconstruction phase
Impaired collagen synthesis (keloid scar and hypertrophic scar)
Impaired epithelisation (anti-inflammatory steroids, hypoxaemia and nutritional deficiencies)
Impaired contraction (contracture)
Wound disruption:
- Dehiscence- wound pulls apart at suture line, excessive strain and obesity can be causes, and increases risk of wound sepsis
Which cells in epidermis initiate immune responses and provide protection against environmental antigens
Langerhans cells
What is the term for skin lesions that are elevated, rounded and firm with irregular margins extending beyond site of initial injury
keloid
occur due to excess collagen
What is the first sign of pressure injury and what dressings should be applied to them
Nonblanchable (don’t have to touch it or apply pressure) erythema of intact skin
Flat and moist dressings
What is deep vein thrombosis
When a blood clot develops deep in a vein
Can happen with bed rest
Describe haemostasis stage of wound healing
Adrenaline (vasoconstrictor) released to stop bleeding
Platlet cells aggregate (clot) and cytokines released (line up around wound border). Cytokines call in other cells to help with later phases.
CONTROLS BLEEDING
What is a scab
platelets and red blood cells which have clotted
What causes itching of a wound
Angiogenesis (development of new blood vessels) causes itching which is caused by histamine
