Pathophysiology Of Acute Inflammation

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Pathophysiology Of Acute Inflammation

What are the pathophysiology stages of inflammation?

What are the Stages of Inflammation? – G4 Physiotherapy & Fitness

  • Inflammation is a result of damage to body tissues and can be caused by a number of factors including trauma, repetitive use and those conditions affected by age such as Osteoarthritis.
  • The are three main stages of inflammation which can each vary in intensity and duration:
  1. Acute -swelling stage
  2. Sub-acute – regenerative stage
  3. Chronic – scar tissue maturation and remodelling stage

During the acute inflammatory stage, there is evident redness (erythema) and swelling due to vascular changes. Exudation of cells and chemicals cause swelling and pain. A haematoma may form if there is bleeding within the tissues. Secondarily, chemical irritants are neutralized and the area is sealed off from surrounding tissues and circulation is impaired.

  1. There is early fibroblastic cell activity.
  2. Pain is normally present at rest over a diffuse area and can be aggravated by activity.
  3. Secondary muscle spasm and guarding normally restrict passive movement.
  4. During range of movement testing, pain is felt before the tissue resistance is reached.
  5. Injuries to deep structures or poorly vascularised areas can lead to surface swelling and oedema but may not be noticeable.

The sub-acute stage is the commencement of healing and repair. Noxious chemicals are further neutralized and new capillary beds growing into the damaged areas are supported by connective tissue growth (collagen fibres) and together form granulation buds.

  • Visible signs of inflammation start to subside and range of movement increases with pain felt at the point of tissue resistance.
  • The chronic inflammatory stage is the period when tissue remodelling takes place.
  • Signs of inflammation are absent and scar tissue is maturing.
  • Pain is felt further into the range of movement after the tissue resistance has been reached.

Maturation refers to the growth of the fibroblasts to fibrocytes and remodelling refers to the organization of and shrinking of collagen fibres along the lines of stress. The skill of the physiotherapist is to identify the exact stage of the inflammation and then intervene to enhance the healing process with the most appropriate form of treatment.

What are the 5 cardinal signs of inflammation pathophysiology?

Introduction – Based on visual observation, the ancients characterised inflammation by five cardinal signs, namely redness ( rubor ), swelling ( tumour ), heat ( calor ; only applicable to the body’ extremities), pain ( dolor ) and loss of function ( functio laesa ).

  • The first four of these signs were named by Celsus in ancient Rome (30–38 B.C.) and the last by Galen (A.D 130–200),
  • More recently, inflammation was described as “the succession of changes which occurs in a living tissue when it is injured provided that the injury is not of such a degree as to at once destroy its structure and vitality”, or “the reaction to injury of the living microcirculation and related tissues,

Although, in ancient times inflammation was recognised as being part of the healing process, up to the end of the 19 th century, inflammation was viewed as being an undesirable response that was harmful to the host. However, beginning with the work of Metchnikoff and others in the 19 th century, the contribution of inflammation to the body’s defensive and healing process was recognised,

Furthermore, inflammation is considered the cornerstone of pathology in that the changes observed are indicative of injury and disease. The classical description of inflammation accounts for the visual changes seen. Thus, the sensation of heat is caused by the increased movement of blood through dilated vessels into the environmentally cooled extremities, also resulting on the increased redness (due to the additional number of erythrocytes passing through the area).

The swelling (oedema) is the result of increased passage of fluid from dilated and permeable blood vessels into the surrounding tissues, infiltration of cells into the damaged area, and in prolonged inflammatory responses deposition of connective tissue.

  1. Pain is due to the direct effects of mediators, either from initial damage or that resulting from the inflammatory response itself, and the stretching of sensory nerves due to oedema.
  2. The loss of function refers to either simple loss of mobility in a joint, due to the oedema and pain, or to the replacement of functional cells with scar tissue.
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Today it is recognised that inflammation is far more complex than might first appear from the simple description given above and is a major response of the immune system to tissue damage and infection, although not all infection gives rise to inflammation.

  1. Inflammation is also diverse, ranging from the acute inflammation associated with S.
  2. Aureus infection of the skin (the humble boil), through to chronic inflammatory processes resulting in remodeling of the artery wall in atherosclerosis; the bronchial wall in asthma and chronic bronchitis, and the debilitating destruction of the joints associated with rheumatoid arthritis.

These processes involve the major cells of the immune system, including neutrophils, basophils, mast cells, T-cells, B-cells, etc. However, examination of a range of inflammatory lesions demonstrates the presence of specific leukocytes in any given lesion.

  • That is, the inflammatory process is regulated in such a way as to ensure the appropriate leukocytes are recruited.
  • These events are controlled by a host of extracellular mediators and regulators, including cytokines, growth factors, eicosanoids (prostaglandins, leukotrines, etc), complement and peptides.

In fact, it is the discovery of many of these mediators over the past 20 years that has increased our understanding of the regulation of the inflammatory process whilst, at the same time, revealing its complexity. These extracellular events are matched by equally complex intracellular signalling control mechanisms, with the ability of cells to assemble and disassemble an almost bewildering array of signalling pathways as they move from inactive to dedicated roles within the inflammatory response and site.

  • Which cells and mediators come into play depends on wide range of factors.
  • These include: what stage the process of inflation is at; the initiating event, i.e.
  • Type of pathogen, auto-immune, chemical or physical injury, etc.; the tissue or organ involved; whether the inflammation is of an acute, resolving form or chronic, non resolving or long-lasting type; whether formation of granuloma is involved, or whether scarring results.

The role of inflammation as a healing, restorative process, as well as its aggressive role, is also more widely recognised today. Inflammation is now considered as the full circle of events, from initiation of a response, through the development of the cardinal signs above, to healing and restoration of normal appearance and function of the tissue or organ.

  • However, in certain conditions there appears to be no resolution and a chronic state of inflammation develops that may last the life of the individual.
  • Such conditions include the inflammatory disorders rheumatoid arthritis, osteoarthritis, inflammatory bowel diseases, retinitis, multiple sclerosis, psoriasis and atherosclerosis.

In order to study inflammation a multidisciplinary approach is necessary. Classically, it has required the study of the immune system, in order to understand the events involved in initiating and maintaining inflammatory conditions. Today it is recognised that the underlying genetics and molecular biology basis to cellular responses are also important in order to identify genetic predisposition to inflammatory diseases, while pharmacological studies are necessary to identify targets and develop novel treatments to bring relief from chronic life-threatening inflammatory conditions.

Thus research into inflammation includes not only the study of immunological and cellular responses involved but also the pharmacological process involved in drug development. Many of the drugs used in the treatment of inflammatory conditions, predate our current understanding of the biochemical processes involved in the disease.

Traditionally, the standard treatments for rheumatoid arthritis has been to use a non-steroidal anti-inflammatory drug (NSAID), such as aspirin, for pain relief and to use corticosteroids or even disease-modifying anti-rheumatic drugs in an attempt to reduce other symptoms of the disease.

For many years the pharmaceutical industry attempted to develop NSAIDs which shared the therapeutic action of aspirin but which did not cause the main adverse event, namely gastric ulceration. This research led to the development of indomethacin, the fenamates, ibuprofen and many others. However, while all these drugs had clinical utility they also eroded the gastric mucosa.

In addition, this research also led to the development of some of the animal models still used in arthritis research today, such as carrageenin oedema and adjuvant arthritis ). The development of NSAIDs, with reduced potential to cause gastric ulcers, was finally realised with the demonstration that clinically useful NSAIDs inhibited the enzyme cyclo-oxygenase, which was also present in the gastric mucosa.

  1. The finding that cyclo-oxygenase present in inflammatory lesions (COX2) was distinct from that found in the stomach (COX1) led to the development of selective COX2 inhibitors, such as celecoxib.
  2. These drugs provide relief from many of the symptoms of arthritis but have a reduced potential to cause gastric ulceration,
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The differential responsiveness to these, and other, therapeutic agents and, indeed, the induction of the inflammatory response in some patients with asthma by aspirin, has led to the concept of pharmacogenomics to understand individual drug sensitivities with a view to producing therapy tailored to the individual.

Similarly, glucocorticoids are widely used in the treatment of inflammation. Unlike the NSAIDs these agents do not relieve pain but reduce inflammation by inhibiting leukocyte function. The active ingredient responsible for the anti-inflammatory activity of adrenal cortex extracts was discovered in the 1940s.

This led to the use of cortisol as an anti-inflammatory and the development of potent synthetic agents typified by dexamethasone. However, because cortisol, and synthetic glucocorticoids, produce their therapeutic action at supra-physiological concentrations, adverse effects, such as suppression of the HPA-axis and Cushingoid changes are inevitable.

Many of these adverse effects can be avoided by giving glucocorticoids topically. This has led to the development of inhaled glucocorticoids for the treatment of inflammatory diseases of the respiratory tract and steroid containing creams for the treatment of skin inflammation. However, applying this approach to the treatment of rheumatoid arthritis necessitates the use of intra-articular injection.

Thus, there is a clear unmet medical need for a drug that provides relief from the symptoms of inflammation but can be given systemically. The fact that a large number of patients with severe chronic inflammatory disease fail to respond to conventional systemic or topical therapy resulting in a huge clinical and socio-economic burdon underlies the need to develop novel therapies.

Thus, modern research has used molecular techniques to identify which genes are regulated by glucocorticoid receptors in an attempt to identify novel therapeutic targets. This work has attempted to fine tune the immune system through use of agents that inhibit specific pathways and mediators rather than to suppress immune cell activity.

Examples of such approaches include the development of anti-TNFa therapies, anti adhesion molecule therapies and inhibitors of cytokines believed to be pivotal in a given pathology, Furthermore, inhibitors of selective pro-inflammatory intracellular signalling pathways are currently in use e.g.

cyclsporin or under development e.g. NF-κB, p38 MAPK and PDE4 inhibitors, As we understand more about the complexity of the inflammatory response and the actions of the currently available drugs the value of particular clusters of targets becomes apparent. However, the success of anti-TNFα therapy in RA underlines the importance of understanding/discovering the initial driver(s) of the inflammatory response in individual diseases and patients.

While research into inflammation has resulted in great progress in the latter half of the 20th century, we recognise that the rate of progress is accelerating. Furthermore, it is our perception that there is a need for a vehicle through which this very diverse research can readily be made available to the scientific community.

What are the 5 processes of inflammation?

Summary – Inflammation occurs as your body fights infection. And as it wages the fight, you may experience pain, heat, redness, swelling, and loss of function. The symptoms are common enough, but it’s still smart to learn the differences between acute and chronic inflammation. It probably will make a difference in how your particular case of inflammation is treated.

What are 3 features of acute inflammation?

1. What are the Types of Acute Inflammation? – Acute inflammation begins within seconds to minutes following injury to tissues. It is usually characterized by four key features, including redness, heat, swelling and pain. Redness results from secondary to vasodilatation and increased blood flow.

  • Heat is caused by localized increase in temperature, and also due to increased blood flow.
  • Swelling results from increased vessel permeability and allows fluid loss into the interstitial space.
  • Pain is caused by stimulation of the local nerve endings, from mechanical and chemical mediators.
  • Due to the difference of inflammatory factors, the degree of tissue reaction and the different sites of inflammation, the pathological form of acute inflammation is also different.

According to the main components of exudate, acute inflammation is divided into four types, including serous inflammation, fibrinous inflammation, purulent inflammation and hemorrhagic inflammation. The differences of these four types of acute inflammation are shown as follows:

Type Features Prevalent disease or location
Serous inflammation

The main component of the serous exudation is serum; It can cause effusion in the chest cavity, pericardium, joints, and abdominal cavity; It is mild and easy to subside.

Mucosa, serosa, loose connective tissue
Fibrinous inflammation

It is dominated by fibrinogen exudation and the formation of cellulose in the inflammation focus; The blood vessel wall is severely damaged, and the vascular permeability is obviously increased.

Mucosa, serosa, Lung bacillary dysentery, fluffy heart
Purulent inflammation It is characterized by neutrophil exudation, with different degrees of tissue necrosis and pus formation. Appendices, skin, subcutaneous, muscle, internal organs, serous membrane, etc.
Hemorrhagic inflammation It is characterized by severe blood vessel damage, and the exudate contains a large number of red blood cells Epidemic hemorrhagic fever, leptospirosis, plague.
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What is swelling in inflammation pathophysiology?

What happens when you have an inflammation – When an inflammation occurs in your body, many different immune system cells may be involved. They release various substances, known as inflammatory mediators. These include the hormones bradykinin and histamine.

  1. They cause the small blood vessels in the tissue to become wider (dilate), allowing more blood to reach the injured tissue.
  2. For this reason, inflamed areas turn red and feel hot.
  3. The increased blood flow also allows more immune system cells to be carried to the injured tissue, where they help with the healing process.

What’s more, both of these hormones irritate nerves and cause pain signals to be sent to the brain. This has a protective function: If the inflammation hurts, you tend to protect the affected part of the body. The inflammatory mediators have yet another function: They make it easier for immune system cells to pass out of the small blood vessels, so that more of them can enter the affected tissue.

The immune system cells also cause more fluid to enter the inflamed tissue, which is why it often swells up. The swelling goes down again after a while, when this fluid is transported out of the tissue. Mucous membranes also release more fluid when they are inflamed. For instance, this happens when you have a stuffy nose and the membranes lining your nose are inflamed.

Then the extra fluid can help to quickly flush the viruses out of your body.

What is the main characteristic of acute inflammation?

Acute inflammation is the early (almost immediate) response of a tissue to injury. It is nonspecific and may be evoked by any injury short of one that is immediately lethal. Acute inflammation may be regarded as the first line of defense against injury and is characterized by changes in the microcirculation: exudation of fluid and emigration of leukocytes from blood vessels to the area of injury.

Acute inflammation is typically of short duration, occurring before the immune response becomes established, and it is aimed primarily at removing the injurious agent. Until the late 18th century, acute inflammation was regarded as a disease. John Hunter (1728–1793, London surgeon and anatomist) was the first to realize that acute inflammation was a response to injury that was generally beneficial to the host: “But if inflammation develops, regardless of the cause, still it is an effort whose purpose is to restore the parts to their natural functions.” Clinically, acute inflammation is characterized by 5 cardinal signs: rubor (redness), calor (increased heat), tumor (swelling), dolor (pain), and functio laesa (loss of function) ( Figure 3-1 ).

The first four were described by Celsus (ca 30 bc –38 ad ); the fifth was a later addition by Virchow in the nineteenth century. Redness and heat are due to increased blood flow to the inflamed area; swelling is due to accumulation of fluid; pain is due to release of chemicals that stimulate nerve endings; and loss of function is due to a combination of factors.

These signs are manifested when acute inflammation occurs on the surface of the body, but not all of them will be apparent in acute inflammation of internal organs. Pain occurs only when there are appropriate sensory nerve endings in the inflamed site—for example, acute inflammation of the lung (pneumonia) does not cause pain unless the inflammation involves the parietal pleura, where there are pain-sensitive nerve endings.

The increased heat of inflamed skin is due to the entry of a large amount of blood at body core temperature into the normally cooler skin. When inflammation occurs internally—where tissue is normally at body core temperature—no increase in heat is apparent.