The role of Singulair in the management of the asthmatic patient: a medicine review for medical assistants.
The panel recommendations were rapidly implemented by the medical community. By 1997, the panel revisited both its work and a body of research done by professionals evaluating its recommendations with clinical trials and studies. It then revised and elaborated on management of the disease as proposed in the original report. The expert panel's second release of the findings (EPR-2) cites the following facts regarding asthma and inflammation:
* Asthma is a chronic inflammatory disorder of the airways
* Environmental and other factors "cause" or provoke the airway inflammation in people with asthma
* Airway inflammation causes recurrent episodes of asthma symptoms
* In asthma, there is variable airflow obstruction that is often reversible
* Inflammation causes an associated increase in the existing airway hyper-responsiveness to a variety of stimuli
* Asthma changes over time and requires active management
Managing the disease as a chronic condition of inflammation required some rethinking about the use of bronchodilators and anti-inflammatory medications. Both have long been mainstays in the management of asthma, however, prior to the survey, asthmatics used bronchodilator medicines at irregular intervals on a PRN basis (in a disturbing majority of case studies, these bronchodilators were being dispensed in hospital emergency departments-often too little, too late). Anti-inflammatory medicines were used on a PRN basis for exacerbations of asthma that were related to upper respiratory infections and allergy. This strategy came from the thinking that asthma was an episodic disease, and only generated treatable symptoms when an "attack" occurred. Once the attack or spasm was broken, most considered the problem as being dealt with until the next episode. Prior to the panel's report, asthma was considered to be extrinsic (triggered by things in the environment), or intrinsic (triggered by internal body processes like allergy or emotions). In between asthma attacks the individual was considered susceptible to asthma, but not requiring medical management or treatment.
The new paradigm of looking at asthma as a chronic inflammatory process, requires that one consider it is always present to some degree. This view mandates addressing the chronic problem with ongoing treatment, as opposed to episodic treatment. Moreover, as the chronic nature of the disease is airways inflammation that leads to varying levels of bronchial tube constriction, physicians must put more emphasis upon treating the cause (inflammation) to prevent the effect (bronchoconstriction). This, indeed, is a recommendation of the committee: using anti-inflammatory therapy medicines daily, instead of on a PRN basis.
Dealing With Inflammation
Some review of this essential process is necessary to better facilitate learning. Inflammation is a vital non-specific response used by the body to maintain homeostasis (Tortora, et al). The term non-specific is used to describe it because many factors can trigger it. It is a standard response to any factors affecting or threatening to affect homeostasis. An injury to a cell, tissue or organ, or an invading pathogen entering the body through an open wound; or an irritated bone-end will cause the local cells to signal for help in starting a process to defend themselves and the area. The signaling process is called chemotaxis. This is a beautiful language of chemicals through which cells and body components speak to each other. Instead of using words, cells secrete chemicals to communicate with other cells. Chemotaxis between certain cells triggers the arterioles in an affected area to dilate, and their distal capillaries to become leaky (permeable).
Chemotaxis signals immune cells like macrophages to migrate to an area and begin their work. The internal effect of these actions is to allow more blood to flow to an affected area, and for the immune cells in that blood to leak out of circulation and into the tissue spaces to repair and defend. The outward effect(s) of more blood rushing into an area is swelling, redness, heat, and in some cases, pain. These we know to be the cardinal signs of inflammation
The Cardinal Signs of Inflammation
* Dysfunction (sometimes)
(Tortora, et al)
At the cellular level, there are cells releasing specific chemicals to dilate blood vessels and make capillaries leak. These are the precursors to inflammation. As such, they are the likely targets to "manage" in diseases like asthma wherein suppressing inflammation is required.
Some Chemical Mediators of Inflammation
Histamine: Found in mast cells, platelets, and basophils. This chemical causes capillary leakage and vasodilatation.
Kinins: Attract phagocytes into the area. They also cause capillary leakage and vasodilatation
Prostaglandins: These intensify the effects of histamine and kinins
Leukotrienes: These are secreted by white cells and function to signal other cells to initiate the inflammatory process. They also signal capillaries to become more permeable
(Tortora, et al)
Managing Inflammation with Medicines
The value of anti-inflammatory type medicines has long been known in health care. Current advances in biochemistry and pharmacology have generated both understanding and synthesis of a variety of medications to reduce inflammation. Fortunately, many of these advances coincide with the expert panel's recommendations for asthma management. Steroids are effective in the suppression of inflammation, but are associated with undesirable side effects. Thus, alternatives in the form of non-steroidals are often utilized as a first measure in managing inflammation. This is the case with the drug montelkast, marketed as Singulair, this drug is not a steroid, but rather it antagonizes the action of leukotrienes (PDR).
The word antagonist is used to describe a particular agent working in opposition to another. Recall from the previous discussion on chemotaxis, that some cells can "call out" by chemical means for blood and lymph vessels to engorge and leak, causing inflammation. These chemical messages reach the cell membranes of inflammatory cells too (like mast cells) and cause them to release other chemicals (mediators) that switch on and accelerate the inflammatory process. Drugs like Singulair compete with the "call out" chemicals (in this case leukotrienes) to occupy a receptor site on a cell membrane of an inflammatory cell (like a mast cell), or on cell membrane of a blood or lymph vessel in and around the airways of the lung. One might say these drugs block, or antagonize the cell membrane receptor site, so it cannot be switched on. If the Singulair gets to the inflammatory cell, or vessel cell membrane receptor site first, it will occupy the receptor site and not allow the cell to participate in the process of inflammation (that is, it antagonizes the action of the "call out" chemical). If there is no Singular molecule to occupy the receptor site, the "call out" chemical will switch the receptor on. That would allow the cell membrane to become leaky and trigger the inflammation process. Thus, a daily dose of Singulair can work to suppress inflammation in the airways.
Leukotriene antagonists like Singulair have become a common adjuvant along with inhaled steroids and slow-acting, long-duration bronchodilators in the management of asthma. This combination of medications is given daily as prescribed by the physician for managing the chronic inflammatory process known as asthma. Fast-acting, short-duration bronchodilators like albuterol are not used unless the individual patient is experiencing dyspnea, wheeze and or congestion. Even then, albuterol is used with specific guidelines (EPR-2).
Singulair is most often prescribed to be taken before bedtime, just once daily. For adults, a 10 mg. tablet is available. Four mg. chewables are available for children 12 months to five years, and there is a five mg. chewable for children six to 14 years. Singulair is not given to "break" or treat an acute asthma attack (status). Singular has been FDA approved for treating seasonal rhinitis as well as asthma (PDR).
Questions for STEP Participants
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In the following, choose the one best answer for each question.
1 According to the expert panel, asthma is considered to be:
A. a neurological disease
B. a chronic inflammatory disease
C. an infectious disease
D. an episodic disease
2 The generic name for Singulair is:
3 Which of the following is NOT a chemical mediator of inflammation?
4 A chemical that occupies a receptor site on a cell membrane and blocks another chemical from occupying the same site is known as a(n):
5 When arterioles, capillaries and lymph vessels become permeable:
A. fluid and immune cells escape from the bloodstream and go into the tissue spaces
B. fluid and immune cells cause swelling and congestion in the tissue spaces
C. Both A and B are correct
D. Neither A nor B is correct
6 Prior to the Expert Panel Report, asthma was considered a chronic disease, NOT episodic.
7 According to the Expert Panel, asthma changes over time and requires active management.
8 Dysfunction is sometimes a sign of inflammation.
9 Inflammation is considered a non-specific response to many conditions affecting the body.
10 Singulair is available in 4 mg. chewables for adults over 18 years of age.
National Institutes for Health, National Heart, Lung and Blood Institute (1991). Expert Panel Report: Guidelines for the Diagnosis and Management of Asthma.(NIH Publication No. 666-222). Washington, DC: U.S. Government Printing Office.
National Institutes for Health, National Heart, Lung and Blood Institute (1997). Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma. Retrieved 7/10/07 http://www.nhbli.nih.gov/nhlbi/lung/asthma/prof/asthgdln.htm
Singulair. (2005). Physician's Desk Reference (59th Ed.). Thomson, NJ
Tortora, G. J., Anagnostakos. (1999) Principles of Anatomy and Physiology. HarperCollins. New York
Neilsen J. Schulz, Associate Professor, MEA Program Chair, School of Health Sciences, Ivy Tech Community College, Anderson, Indiana
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|Author:||Schulz, Neilsen J.|
|Publication:||Journal of Continuing Education Topics & Issues|
|Article Type:||Clinical report|
|Date:||Aug 1, 2007|
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