Introduction to Inflammation & Wounds Flashcards
(12 cards)
What is inflammation? What are the core signs of inflammation?
Inflammation is initiated by tissue injury (cuts, burns, reduction in blood flow, foreign substances etc), infection (bacteria, viruses, fungi) or your immune system. ‘Itis’ means comes with inflammation eg colitis, brochitis.
It is non specific, innate but only happens in vascular tissue (with a blood supply).
Cardinal signs are local eg.
* redness (rubor)
* heat (calor)
* swelling (tumor)
* pain (dolor) and
* sometimes, loss of function (functio laesa)
…and also systemic, eg fever (from liver), high heart rate and blood pressure, malaise, lack of appetite.
Inflammation can be considered both beneficial - in its defensive capacity against infection (seals the area off and stops infection spreading, and supports wound healing) - and harmful in its role in pathogenic processes leading to more systemic disease. We must understand the distinction and support or interrupt the process as appropriate.
A number of different mediators interact to cause the inflammatory response –
* cascades such as the complement system and cytokines
* cells such as neutrophils and eosinophils and
* localised tissue responses such as vascular dilatation and increased vascular permeability
A broad generalisation we can draw is that acute inflammation tends to be beneficial whereas chronic inflammation is harmful.
Considering an example of acute inflammation, that which occurs in acute bronchitis, the
processes involved can be seen to be helpful in combating invading pathogens to resolve the
situation, minimising and hopefully resolving damage to lung tissue. If exposed to persistent irritation, however, bronchitis may become chronic. A constant state of inflammation is undesirable, in itself causing rather than resolving tissue damage.
Which cells are involved in inflammation and how?
- Basophil/mast cell - Release of inflammatory mediators (which trigger a cascade of events that lead to the recruitment of immune cells, increased blood vessel permeability, and pain)
- Eosinophil; Cytotoxicity (death or damage to cells) & release of inflammatory mediators
- Neutrophil; Phagocytosis, release of inflammatory mediators
- Natural killer cell; Cytotoxicity, release of inflammatory mediators
- Macrophage; Phagocytosis, antigen presentation (allows the immune system to recognize and respond to foreign invaders or internal threats like cancer cells) release of inflammatory mediators
- T lymphocyte - Helps to activate B cells and macrophages, cytotoxicity
- B lymphocyte - Antibody production, antigen presentation
What are the stages of acute inflammation?
- Stimulus phase eg thorn in the skin, which causes cell trauma/damage and introduces pathogens, which all causes tissue death
- Mediators phase - cells which sit under the skin (such as macrophages, mast cells, or dendritic cells) pick up the pathogens and release mediators such as prostaglandin, histamine and cytokines to activate the endothelium of blood vessels.
- Vascular phase - This leads to vasodilaton causing more blood flow to the region causing heat and redness (from histamine, prostaglandins, nitric oxide, bradykinin, platelet activating factor (PAF); this then causes shrinkage thus increased vascular permeability of endothelium cells, causing swelling from plasma escape (Histamine, bradykinin, leukotrienes, PAF, nitric oxide, complement)… This is exudate = plasma fluid with things in it to help. Also Bradykinin release makes the pain sensors very sensitive, causing pain.
- Cellular phase - immune cells such as neutophils (most important one for acute inflammation) and macrophages get pushed to the edge of the blood vessels and pop into the tissue to go where the injury is. They start to eat up all the bacteria and dead tissue in the first 6-24 hours (causing pus), and macrophages afterwards (48 hours). Meanwhile cytokines go into the blood causing Interleukin 1, TNF etc to cause systemic effects; eg go to your hypothalamus which elevates your core temperature to help acute inflammation cells work better, also formation of fibroblasts
- Repair/Resolution phase - ideally agent gets taken away, fibroblasts will start to close off the site. However sometimes the body can’t repair like with like and leaves scarring. Finally you have chronic inflammation.
What are the processes involved in chronic inflammation?
Although brilliantly evolved to combat attack by pathogens or damage from injuries, the human body’s inflammatory response cannot overcome all invasion.
Inflammation is essentially an attempt to bring a process to resolution, to neutralise and ideally eradicate a damaging stimulus – should the stimulus persist whether physiologically (think of stomach acid and an area of inflammation in the gut) or pathologically (consider the ongoing presence of urate crystals in the tissues of patients with gout) then the process remains unresolved and the inflamed area reaches an uneasy compromise – chronic inflammation
What occurs in chronic inflammation as a systemic process?
When thinking about systemic, rather than localised, inflammation we are usually considering a chronic rather than an acute picture.
As inflammation persists, the release of pro-inflammatory cytokines triggers the activation of the immune system, with lymphocytes infiltrating tissues
Tissue damage, acute inflammation, granulation tissue, repair and an active immune response are all happening at the same time.
Predisposition to chronic inflammation occurs through:
* a persistent damaging stimulus
* inadequate response to infection
* persistent autoimmune disease
There are variabilities in people’s vulnerability to chronic inflammation – in some it may express in their joints, some in their gut and so on. It is, however, a systemic process affecting the whole body
How do you resolve inflammation?
Resolution of inflammation and the normal function of inflammatory processes is
dependent on the health of the body.
If an individual is not having adequate nutrition, is under persistent stress, doesn’t have sufficient sleep and doesn’t take adequate and appropriate exercise then the body’s capacity to resolve inflammation is reduced.
Specific disease states also contribute to a reduced capacity of the body to resolve
inflammation. These include but are not limited to:
* Circulatory insufficiency (e.g. ischaemic heart disease, chronic hypertension)
* Impaired respiratory function (e.g. asthma, COPD)
* Allergic (atopic) tendency (asthma, hayfever, eczema)
* Autoimmune disease
* Diabetes
How does inflammation help with wound healing?
So far we have considered inflammation as either an acute or chronic systemic process,
looking at infection and autoimmune disease as some precipitating factors respectively.
The process of inflammation is of course also associated with the healing of wounds - this process leads to formation of a scar rather than full resolution of the inflammation. The
size and quality of scarring is related to the size of the area damaged and subsequent
spread of inflammation.
A number of factors can impede the process of wound healing –
* Poor nutrition
* Tissue ischaemia
* Denervation of the damaged area
* Infection during the healing process
* Retention of foreign material in the wound
* Steroid medications
* Radiation exposure e.g. radiotherapy
* Disease states such as diabetes
What are the stages of wound healing?
There are several stages to the process of scarring otherwise known as the organisation and repair stage of the inflammatory process.
1. Debris is removed by macrophages – new
capillaries bud into the damaged area, infiltration by macrophages, fibroblasts and
myofibroblasts
2. Formation of vascular granulation tissue
composed of capillaries, macrophages and
support cells
3. Formation of fibrovascular granulation tissue as fibroblasts proliferate in the capillary network, capillaries regress, fibroblasts synthesise collagen, scar area contracts (myofibroblasts help here)
4. Collagenous scar formation through fibroblasts generating dense collagen
What problems might wounds have with healing?
Keloid scar - An overgrowth of dense fibrous scar tissue, extending beyond the border of the original wound, developing after
the healing of a skin injury. A genetic predisposition is suspected, with trauma and the presence of foreign material in the wound being precipitating factors.
Hypertrophic scar - Hypertrophic scars, common after any injury damaging the
deep dermis, are characterized by itchy, erythematous raised fibrous lesions that don’t extend beyond the boundaries of the initial injury. They may spontaneously
resolve.
Hyperpigmentation
It is important to distinguish post-inflammatory
hyperpigmentation (such as that which may develop after acne scarring) from that caused by an underlying conditions such as Addison’s disease.
It is self evident that if scarring takes place in a restricted and/or motile area, there is a risk that the scar tissue may adhere to neighbouring tissues causing damaging restriction to the form and function of those tissues.
Patients undergoing bowel surgery are at risk of developing post-operative adhesions, which themselves bring the risk of pain, small bowel
obstruction and infertility. Further surgery may be required to address the adhesions, although several preventative treatments and measures continue to be developed.
Patients who suffer from endometriosis are also at risk of intra-abdominal scarring with subsequent bowel adhesions, with surgery being similarly required to address them.
When might we see slow or non healing wounds?
Although we have been considering wound healing from injury to resolution, it is important to note that as well as slowing healing of wounds from trauma, some disease states may actually cause a wound to develop in the first place.
Conditions that can be included here are:
Diabetes – nerve damage and deteriorating integrity of circulation are key factors that may lead to development of foot and leg ulcers. Neuropathy reducing sensation in the feet increases risk of unnoticed and so untreated wounds leading to infection and ulceration
Varicose veins and Raynaud’s syndrome – these are just two examples of conditions impacting on peripheral circulatory sufficiency, reducing integrity of the tissues and so leading to potential skin inflammation. Poor
circulation to the feet may lead to the specific condition of varicose eczema, ultimately predisposing to ulceration
Other relevant factors which may slow or prevent wound healing are:
* Autoimmune conditions
* Certain medications – NSAIDs (non-steroidal anti-inflammatories), anticoagulants and immunosuppressants
How is fever a defence mechanism?
A fever is currently defined as any reading above 38C in both adults and children.
With the advent of temperature reducing medication such as paracetamol and ibuprofen, the view of fever as a process
supportive to be healing has diminished. This can be problematic as fever is a useful mechanism in the body’s array
of defences against infection.
How does fever occur?
Infection with a virus or bacteria can cause the release of pyrogens, which are chemical substances that signal to the
hypothalamus via alteration of the sensitivity of temperature sensing neurons. Essentially, the hypothalamus perceives the temperature of the body to be colder than it actually is, and so
sets the body’s ‘thermostat’ higher.
This promotes lymphocytes to multiply and facilitates their circulation around
the body, and also supports the function of antibodies. A further effect of high temperature is to directly damage and kill
those viruses and bacteria that can only survive in narrow temperature ranges.
How do you manage a fever?
In the instance of fever, the optimal outcome it to assist the patient through the fever to a complete resolution of their symptoms. Patients however will often seek to attenuate their symptoms in order to meet domestic or work commitments.
Why might this be problematic?
* Incomplete disease process – infection becomes sub-clinical and lingers, recurring when the individual becomes run-down
* Inadequate investigation of underlying causes – fever is a symptom rather than a disease, simply suppressing fever means the body’s warning signals are being ignored
* Increased spread of disease – taking fever reducing medication and thus feeling more well means individuals will go to work and other public places while still harbouring the infection that triggered the fever in the first place.
What is the role of convalescence in recovery from fever?
How long is the optimal convalescent period?
Suppression or management? Although in the holistic model of health fever management rather than temperature reduction is usually the desired outcome, it is important to
be realistic in the approach taken.
In the case of very young children especially, although this can extend to any individual with fever, there is little virtue in perpetuating suffering and so a balance between fever management and relief of the pain and discomfort that accompany fever needs to be sought.
Fever management in the holistic context consists of a few simple measures to aid the patient in navigating fever with minimal discomfort and bringing the infection causing the fever to a complete resolution.
Principles:
* Manage rather than suppress temperature – the use of diaphoretic (sweat inducing) herbs is invaluable here to allow the body to release heat and use natural cooling mechanisms
* Maintain optimal hydration
* Avoid food during the active phase of fever
* Provide symptomatic relief according to the specific symptoms associated with the fever e.g. herbs for nausea, cough, pain etc.
* Ensure the underlying cause is being addressed – often bringing fever to adequate resolution will address the cause but it is essential to look at all aspects of the case history
