August 26th, 2010 by admin

Bronchial Asthma
Classifications and external resources

ICD-10	J45.
ICD-9	493
OMIM	600807
DiseasesDB	1006
MedlinePlus	000141
eMedicine	med/177 emerg/43
MeSH	C08.127.108

Asthma is a disease of the respiratory system in which the airways constrict, become inflamed, and are lined with excessive amounts of mucus, often in response to one or more “triggers,” such as exposure to an environmental stimulant (or allergen), cold air, exercise, or emotional stress. In children, the most common triggers are viral illnesses such as those that cause the common cold.[1] This airway narrowing causes symptoms such as wheezing, shortness of breath, chest tightness, and coughing, which respond to bronchodilators. Between episodes, most patients feel fine.

The disorder is a chronic or recurring inflammatory condition in which the airways develop increased responsiveness to various stimuli, characterized by bronchial hyper-responsiveness, inflammation, increased mucus production, and intermittent airway obstruction. The symptoms of asthma, which can range from mild to life threatening, can usually be controlled with a combination of drugs and enviromental changes.

Public attention in the developed world has recently focused on asthma because of its rapidly increasing prevalence, affecting up to one in four urban children.[2] Susceptibility to asthma can be explained in part by genetic factors, but no clear pattern of inheritance has been found. Asthma is a complex disease that is influenced by multiple genetic, developmental, and environmental factors, which interact to produce the overall condition.

History

The word asthma is derived from the Greek aazein, meaning “sharp breath.” The word first appears in Homer’s Iliad;[3] Hippocrates was the first to use it in reference to the medical condition. Hippocrates thought that the spasms associated with asthma were more likely to occur in tailors, anglers, and metalworkers. Six centuries later, Galen wrote much about asthma, noting that it was caused by partial or complete bronchial obstruction. Moses Maimonides, an influential medieval rabbi, philosopher, and physician, wrote a treatise on asthma, describing its prevention, diagnosis, and treatment.[4] In the 17th century, Bernardino Ramazzini noted a connection between asthma and organic dust. The use of bronchodilators started in 1901, but it was not until the 1960s that the inflammatory component of asthma was recognized, and anti-inflammatory medications were added to the regimen.

Links

• National Heart, Lung, and Blood Institute — Asthma – U.S. NHLBI Information for Patients and the Public page.
• National Heart, Lung, and Blood Institute — Asthma – U.S. NHLBI Information for Health Professionals page.
• MedLinePlus: Asthma – a U.S. National Library of Medicine page.
• American Academy of Allergy, Asthma, and Immunology – a U.S. organization of medical professionals with a special interest in treating and researching conditions such as allergic rhinitis, asthma, atopic dermatitis/eczema, and anaphylaxis.
• Asthma UK – a patient-oriented site with information on asthma and ways that UK residents can help improve asthma-related policy.
• Asthma Foundation of Queensland Information and education for Australian asthma sufferers.
• Children’s Hospital & Regional Medical Center — Allergies, Asthma & Immune System – A Seattle, Washington hospital website with patient-oriented videos on asthma and the immune system.
• Case Studies in Environmental Medicine (CSEM): Environmental Triggers of Asthma – Agency for Toxic Substances and Disease Registry, U.S. Department of Health and Human Services.
• Asthma as Neurogenic Inflammatory Disease Neurogenic aspects of asthma. Pathophysiological links with other inflammatory disorders.

This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia.

August 15th, 2010 by admin

Relative ion flow in cardiac myocyte in relation to features of the ECG.

Antiarrhythmic agents are a group of pharmaceuticals that are used to suppress fast rhythms of the heart (cardiac arrhythmias), such as atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation.

While the use of antiarrhythmic agents to suppress atrial arrhythmias (atrial fibrillation and atrial flutter) is still in practice, it is unclear whether suppression of atrial arrhythmias will prolong life ^[1][2].

In the past, it was believed that suppression of the potentially dangerous ventricular arrhythmias, ventricular tachycardia and ventricular fibrillation would prolong life, but it was found in large clinical trials that suppression of these arrhythmias would paradoxically increase mortality^[3][4], which may happen due to the increased workload these drugs place on the heart.

In individuals with atrial fibrillation, antiarrhythmics are still used to suppress arrhythmias. This is often done to relieve the symptoms that may be associated with the loss of the atrial component to ventricular filling (atrial kick) that is due to atrial fibrillation or flutter.

In individuals with ventricular arrhythmias, antiarrhythmic agents are often still in use to suppress arrhythmias. In this case, the patient may have frequent arrhythmic events or be at high risk for ventricular arrhythmias. Antiarrhythmic agents may be considered the first-line therapy in the prevention of sudden death in certain forms of structural heart disease, and failure of these agents to suppress arrhythmias may lead to implantation of an implantable cardioverter-defibrillator (ICD).

The use of antiarrhythmic agents in this population may be in conjunction with an ICD. In this case, the ICD is used to prevent sudden death due to ventricular fibrillation, while the antiarrhythmic agent(s) are used to suppress ventricular tachyarrhythmias so that the ICD doesn’t shock the patient frequently.

The cardiac action potential

Many attempts have been made to classify antiarrhythmic agents. The problem arises from the fact that many of the antiarrhythmic agents have multiple modes of action, making any classification imprecise.

References

1. ^ Wyse DG, Waldo AL, DiMarco JP, Domanski MJ, Rosenberg Y, Schron EB, Kellen JC, Greene HL, Mickel MC, Dalquist JE, Corley SD; Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med. 2002 Dec 5;347(23):1825-33. (Medline abstract)
2. ^ Nichol G, McAlister F, Pham B, Laupacis A, Shea B, Green M, Tang A, Wells G. Meta-analysis of randomised controlled trials of the effectiveness of antiarrhythmic agents at promoting sinus rhythm in patients with atrial fibrillation. Heart. 2002 Jun;87(6):535-43. (Medline abstract)
3. ^ The Cardiac Arrhythmia Suppression Trial (CAST): The CAST investigators. Preliminary report: effect of encainide and flecainide on mortality in a randomised trial of arrhythmia suppression after myocardial infarction. N Engl J Med 1989, 321:406–412.
4. ^ The Cardiac Arrhythmia Suppression Trial II (CAST II): The CAST II Investigators. Effect of the antiarrhythmic agent moricizine on survival after myocardial infarction. N Engl J Med. 1992 Jul 23;327(4):227-33. (Medline abstract)

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August 10th, 2010 by admin

Micrograph of a coronary artery with the most common form of coronary artery disease

An antianginal is any drug used in the treatment of angina pectoris, a symptom of ischaemic heart disease.

Drugs used are nitrates such as nitroglycerin (glyceryl trinitrate) or pentaerythritol tetranitrate; beta blockers, either cardioselectives such as acebutolol or metoprolol, or non-cardioselectives such as oxprenolol or sotalol; or calcium channel blockers, either Class I agents (e.g., verapamil), Class II agents (e.g., amlodipine, nifedipine), or the Class III agent diltiazem.

Nitrates cause vasodilation of the venous capacitance vessels by simulating the endothelium-derived relaxing factor (EDRF). Used to relieve both exertional and vasospastic angina by allowing venous pooling, reducing the pressure in the ventricles and so reducing wall tension and oxygen requirements in the heart. Short-acting nitrates are used to abort angina attacks that have occurred, while longer-acting nitrates are used in the prophylactic management of the condition.

Beta blockers are used in the prophylaxis of exertional angina by reducing the work the heart is allowed to perform below the level that would provoke an angina attack. They cannot be used in vasospastic angina and can precipitate heart failure.

Calcium ion (Ca++) antagonists (Calcium channel blockers) are used in the treatment of both exertional and vasospastic angina. In vitro, they dilate the coronary and peripheral arteries and have negative inotropic and chronotropic effects – decreasing afterload, improving myocardial efficiency, reducing heart rate and improving coronary blood flow. In vivo, the vasodilation and hypotension trigger the baroreceptor reflex. Therefore the net effect is the interplay of direct and reflex actions. Class I antiarrhythmic agents have the most potent negative inotropic effect and may cause heart failure; Class II agents do not depress conduction or contractility; the Class III agent has negligible inotropic effect and causes almost no reflex tachycardia.

This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia.

August 5th, 2010 by admin

Anti-inflammatory refers to the property of a substance or treatment that reduces inflammation. Anti-inflammatory drugs make up one half of analgesics, remedying pain by reducing inflammation as opposed to opioids which affect the brain.

Steroidal anti-inflammatory drugs

Many steroids, specifically glucocorticoids, reduce inflammation by binding to cortisol receptors. These drugs are often referred to as corticosteroids, though that is a larger category.

Non-steroidal anti-inflammatory drugs

Non-steroidal anti-inflammatory drugs (NSAIDs), alleviate pain by counteracting the cyclooxygenase (COX) enzyme. On its own COX enzyme synthesizes prostaglandins, creating inflammation. In whole the NSAIDs prevent the prostaglandins from ever being synthesized, reducing or eliminating the pain.

In addition to medical drugs, many herbs have anti-inflammatory qualities, including hyssop, Arnica montana which contains helenalin, a sesquiterpene lactone, and willow bark, which contains salicylic acid, a substance related to the active ingredient in aspirin.

On the other hand, there are analgesics like paracetamol, called acetaminophen in the U.S. and sold under the brand name of Tylenol, which are commonly associated with anti-inflammatory drugs but which have no anti-inflammatory effects.

Some are concerned about the long term usage of NSAIDs as they cause gastric erosions which can become stomach ulcers and in extreme cases result in death. The risk of death as a result of use of NSAIDs is 1 in 10,000 for young adults aged 16-45. The risk increases ten fold for those over 75.

Ice treatment

Applying ice to a tissue injury has an anti-inflammatory effect and is often suggested as an injury treatment and pain management technique for athletes.

Anti-inflammatory Foods

Due to concerns over the gastric problems caused by NSAIDs researchers are turning to more natural solutions to dealing with the problem of inflammation. One ingredient with a great future potential is capsaicin, a naturally occurring ingredient in chili peppers. Studies have shown some success in the control of pain and inflammation when capsaicin is applied topically.

Others advocate the consumption of anti-inflammatory foods as a means of controlling inflammation. Anti-inflammatory foods include most colorful fruits and vegetables, oily fish and certain nuts, seeds, herbs and spices. Those following an anti-inflammatory diet will avoid refined oils and sugars, and show a preference for anti-inflammatory foods in their meal choices. Several types of “Smoker’s Paradoxes” [29], i.e. cases where smoking appears to have specific beneficial effects, have been observed; often the actual mechanism remains undetermined. For instance, recent studies suggest that smokers require less frequent repeated revascularization after percutaneous coronary intervention (PCI) [29], [30]. Smoking appears to interfere with development of Kaposi’s sarcoma [31], breast cancer among women carrying the very high risk BRCA gene [32], preeclampsia [33], and atopic disorders such as allergic asthma [34]. A plausible mechanism of action in these cases may be the nicotine in tobacco smoke acting as an anti-inflammatory agent [35] and interfering with the disease process.

Links

• Health advice regarding NSAIDs
• NSAIDs and adverse effects
• List of anti-inflammatory food
• Topical capsaicin for pain relief

This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia.