Prescription medicine is popular because it relives the symptoms fast and easy but is it the best thing for the cause? In dealing with pain one should pay special attention to the cause of pain as our body is trying to connect to our attention.
Inflammation is the response of living tissue to damage.
The acute inflammatory response has 3 main functions.
The affected area is occupied by a transient material called the acute inflammatory exudate. The exudate carries proteins, fluid and cells from local blood vessels into the damaged area to mediate local defenses. If an infective causitive agent (e.g. bacteria) is present in the damaged area, it can be destroyed and eliminated by components of the exudate. The damaged tissue can be broken down and partialy liquefied, and the debris removed from the site of damage.
The cause of acute inflammation may be due to physical damage, chemical substances, micro-organisms or other agents. The inflammatory response consists of changes in blood flow, increased permeability of blood vessels and escape of cells from the blood into the tissues. The changes are essentially the same whatever the cause and wherever the site.
Acute inflammation is short-lasting, lasting only a few days. If it is longer lasting however, then it is referred to as chronic inflammation. Various examples of acute inflammation that you may be aware of are sore throat, reactions in the skin to a scratch or a burn or insect bite, and acute hepatitis and so on. However, there are occasional historical exceptions such as pneumonia, inflammation of the lung rather than pneumonitis and pleurisy, inflammation of the pleura, rather than pleuritis.
Acute inflammation is a stereotyped response to recent or ongoing injury. Although the process is complex, the principal features are dilatation and leaking of vessels, and involvement of circulating neutrophils.
Acute inflammation is almost completely stereotyped -- over minutes to a few days, blood vessels widen and disgorge protein, and neutrophils leave the bloodstream and circulate through surrounding tissues.
Beneficial and Harmful Effects of Acute Inflammation
Beneficial effects
Both the fluid and cellular exudates may have useful effects. Beneficial effects of the fluid exudate are as follows:
Dilution of toxins. Dilution of toxins, such as those produced by bacteria, allows them to be carried away in lymphatics.
Entry of antibodies. Increased vascular permeability allows antibodies to enter the extravascular space, where they may lead either to Iysis of microorganisms, through the participation of complement, or to their phagocytosis by opsonisation. Antibodies are also important in neutralisation of toxins.
Drug transport. The fluid carries with it therapeutic drugs such as antibiotics to the site where bacteria are multiplying.
Fibrin formation. Fibrin formation from exuded fibrinogen may impede the movement of micro-organisms, trapping them and so facilitating phagocytosis.
Delivery of nutrients and oxygen. Delivery of nutrients and oxygen, essential for cells such as neutrophils which have high metabolic activity, is aided by increased fluid flow through the area.
Stimulation of immune response. The drainage of this fluid exudate into the lymphatics allows particulate and soluble antigens to reach the local Iymph nodes where they may stimulate the immune response.
Harmful effects
The release of Iysosomal enzymes by inflammatory cells may also have harmful effects:
Digestion of normal tissues. Enzymes such as collagenases and proteases may digest normal tissues, resulting in their destruction. This may result particularly in vascular damage, for example in type III hypersensitivity reactions and in some types of glomerulonephritis.
Swelling. The swelling of acutely inflamed tissues may be harmful: for example, the swelling of the epiglottis in acute epiglottitis in children due to Haemophilus influenzae infection may obstruct the airway, resulting in death. Inflammatory swelling is especially serious when it occurs in an enclosed space such as the cranial cavity. Thus, acute meningitis or a cerebral abscess may raise intracranial pressure to the point where blood flow into the brain is impaired, resulting is ischaemic damage, or may force the cerebral hemispheres against the tentorial orifice and the cerebellum into the foramen magnum (pressure coning).
Inappropriate inflammatory response. Sometimes, acute inflammatory responses appear inappropriate, such as those which occur in type I hypersensitivity reactions (e.g. hay fever) where the provoking environmental antigen (e.g. pollen) otherwise poses no threat to the individual. Such allergic inflammatory responses may be life-threatening, for example extrinsic asthma.
Chronic inflammation ("late-phase inflammation") is a response to prolonged problems, orchestrated by T-helper lymphocytes. It may feature recruitment and activation of T- and B-lymphocytes, macrophages, eosinophils, and/or fibroblasts.
Chronic inflammation is more variable, with variable participation by lymphocytes, plasma cells, macrophages, and healing cells (fibroblasts and angioblasts).
Chronic inflammation is an inflammatory response of prolonged duration - weeks, months, or even indefinitely - whose extended time course is provoked by persistance of the causative stimulus to inflammation in the tissue. The inflammatory process inevitably causes tissue damage and is accompanied by simultaneous attempts at healing and repair. (These are dealt with in a separate section). The exact nature, extent and time course of chronic inflammation is variable, and depends on a balance between the causative agent and the attempts of the body to remove it.
Chronic inflammation may develop in the following ways:
As a progression from acute inflammation if the original stimulus persists, after repeated episodes of acute inflammation, if the causative agent produces only a mild acute response.
Aetiological agents producing chronic inflammation
Infectious organisms that can avoid or resist host defences and so persist in the tissue for a prolonged period. Examples include Mycobacterium tuberculosis, Actinomycetes, and numerous fungi, protozoa and metazoal parasites. Such organisms are in general able to avoid phagocytosis or survive within phagocytic cells, and tend not to produce toxins causing acute tissue damage.
Infectious organisms that are not innately resistant but persist in damaged regions where they are protected from host defences. The common example here is of bacteria which grow in the pus within an undrained abscess cavity, where they are protected both from host immunity and from blood-borne theraputic agents, e.g. antibiotics. Some locations are particularly prone to chronic abscess formation, e.g. bone, pleural cavities.
Irritant non-living foreign material that cannot be removed by enzymic breakdown or phagocytosis. Examples include a wide range of materials implanted into wounds (wood splinters, grit, metals and plastics), inhaled (silica dust and other particles or fibres), or deliberately introduced (surgical prostheses, sutures, etc.). Dead tissue components that cannot be broken down may have similar effects, e.g. keratin squames from a ruptured epidermoid cyst or fragments of dead bone (sequestrum) in osteomyelitis.
In some cases the stimulus to chronic inflammation may be a "normal" tissue component. This occurs in inflammatory diseases where the disease process is initated and maintained because of an abnormality in the regulation of the body's immune response to its own tissues, the so called auto-immune diseases.
Many diseases characterised by a chronic inflammatory pathological process the underlying cause remains unknown.
Whole body inflammation, formerly a popular term used especially by surgeons for the patients who they could not save, is going out of fashion in favor of multiple organ failure. Whatever you call it, in super-sick people, various cytokines increase tremendously in the bloodstream; this situation interacts with ischemia, free radical production, and leakage of heatshock proteins from cells to create a vicious downward cycle into irreversible shock.
Some of us have a tendency to equate "inflammation" and infection, at least unconsciously. This is plain wrong. Several infectious diseases feature no inflammation (Creutzfeldt-Jacob disease, yellow fever, and many of the opportunistic infections in AIDS are only three examples.) Noxious, non-infectious things that produce inflammation include trauma, radiation injury, various poisons, chemical or thermal burns, tissue necrosis itself (except apoptosis), and any of the four major types of immunologic injury. A sun burn or a red scratch are inflammation, just like mosquito bites, pimples, plague and leprosy.
Inflammation, Heart Disease and Stroke
The Role of C-Reactive Protein
How does inflammation relate to heart disease and stroke risk?
“Inflammation” is the process by which the body responds to injury. Laboratory evidence and findings from clinical and population studies suggest that inflammation is important in atherosclerosis (ath”er-o-skleh-RO’sis). This is the process in which fatty deposits build up in the lining of arteries.
C-reactive protein (CRP) is one of the acute phase proteins that increase during systemic inflammation. It’s been suggested that testing CRP levels in the blood may be a new way to assess cardiovascular disease risk. A high sensitivity assay for CRP test (hs-CRP) is now widely available.
The American Association and the Centers for Disease Control and Prevention recently published a joint scientific statement about using inflammatory markers in clinical and public health practice. This statement was developed after systematically reviewing the evidence of association between inflammatory markers (mainly CRP) and coronary heart disease and stroke.
What’s the role of CRP in predicting recurrent cardiovascular and stroke events?
A growing number of studies have examined whether hs-CRP can predict recurrent cardiovascular disease and stroke and death in different settings. High levels of hs-CRP consistently predict new coronary events in patients with unstable angina and acute myocardial infarction (heart attack). Higher hs-CRP levels also are associated with lower survival rate of these people. Many studies suggested that after adjusting for other prognostic factors, hs-CRP was still useful as a risk predictor.
Recent studies also suggest that higher levels of hs-CRP may increase the risk that an artery will reclose after it’s been opened by balloon angioplasty. High levels of hs-CRP in the blood seem to predict prognosis and recurrent events in patients with stroke and peripheral arterial disease.
What’s the role of hs-CRP in predicting new cardiovascular events?
Most studies show that the higher the hs-CRP levels, the higher the risk of developing heart attack. In fact, scientific studies have found that the risk for heart attack in people in the upper third of hs-CRP levels is twice that of those whose hs-CRP is in the lower third. These prospective studies include men, women and the elderly. Recent studies also found an association between sudden cardiac death, peripheral arterial disease and hs-CRP. However not all of the established cardiovascular risk factors were controlled for when the association was examined. The true independent association between hs-CRP and new cardiovascular events hasn’t yet been established.
What causes low-grade inflammation?
No one knows for sure what causes the low-grade inflammation that seems to put otherwise healthy people at risk. However, the new findings are consistent with the hypothesis that an infection -- possibly one caused by a bacteria or a virus -- might contribute to or even cause atherosclerosis.
Possible infectious bacteria include Chlamydia pneumoniae (klah-MID'e-ah nu-MO'ne-i) and Helicobacter pylori (HEL'ih-ko-bak"ter pi-LO'ri). Possible viral agents include herpes simplex virus and cytomegalovirus (si"to-meg"ah-lo-VI'rus). Thus, it may be that antimicrobial or antiviral therapies will someday join other therapies used to prevent heart attacks.
This idea clearly needs to be tested in clinical trials. However, the notion that chronic infection can lead to unsuspected disease isn't foreign to most doctors. For example, bacterial infection with Helicobacter pylori is now known to be the major cause of stomach ulcers. The treatment for this condition now routinely includes antibiotic therapy. Patients with autoimmune diseases and cancer also often have elevated CRP levels.
Should I have my CRP level measured?
If a person’s cardiovascular risk score — judged by global risk assessment — is low (the possibility of developing cardiovascular disease is less than 10 percent in 10 years, no test is immediately warranted. If the risk score is in the intermediate range (10-20 percent in 10 years), such a test can help predict a cardiovascular and stroke event and help direct further evaluation and therapy. However, the benefits of such therapy based on this strategy remain uncertain. A person with a high risk score (greater than 20 percent in 10 years) or established heart disease or stroke should be treated intensively regardless of hs-CRP levels.
What is the normal range of hs-CRP level?
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If hs-CRP level is lower than 1.0 mg/L, a person has a low risk of developing cardiovascular disease.
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If hs-CRP is between 1.0 and 3.0 mg/L, a person has an average risk.
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If hs-CRP is higher than 3.0 mg/L, a person is at high risk.
If, after repeated testing, patients have persistently unexplained, markedly elevated hs-CRP (greater than 10.0 mg/L), other evaluation should be considered to exclude noncardiovascular causes.
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