Aspirin - Acetylsalicylic Acid - Term Paper Example

You’re 2-Sep-16 This paper is based on the study of Aspirin, which is also known as acetylsalicylic acid. This paper presents detailed medical properties of it. Additionally this paper examines the various circumstances when Aspirin is prescribed by doctors and the typical patient profile for such drugs. Aspirin is synonymous for acetylsalicylic acid, which functions mainly as pain and fever reliever, and as an anti-inflammatory treatment. Aspirin decreases prostaglandin production which results in decrease in prostaglandin which alleviates inflammation and pain. As with all drugs, aspirin also has side-effects, details of which are discussed in the paper below. Lastly this summary of the literature studied is presented and a list of works cited is included also. Table of Contents Table of Contents 2 Introduction 3 Literature Review 3 Conclusion 7 Works Cited 8 Aspirin Introduction Aspirin is synonymous for acetylsalicylic acid, which functions mainly as pain and fever reliever, and as an anti-inflammatory treatment. Aspirin decreases prostaglandin production which results in decrease in prostaglandin which alleviates inflammation and pain. When therapeutic doses of aspirin are ingested, the drug is rapidly immersed in the stomach, and peak blood levels usually occur within one hour. Following overdose, however, absorption and elimination are drastically altered. Peak levels are frequently delayed, and may occur six hours or more after absorption as a result of pylorospasm, bezoar formation, or the use of extended-release, enteric-coated formulations (Pierce et al,. pp. 65-212 ). In one extreme case, peak levels did not occur until 35 hours after ingestion (Rivera et al., pp. 53-90). Literature Review Aspirin is mostly used for preventing heart attacks, strokes, ease pain, swelling, and fever. It can also be used to treat arthritis and gout attacks. Aspirin is prescribed to patients with indications of rheumatic fever or in order to protect bypass grafts and stents in the heart. Aspirin works by blocking chemicals that cause pain and swelling and lowers fever by changing the bodys thermostat in the brain. It also helps in stopping platelets from getting sticky and clumping, thus preventing blog clogging which result in heart attacks. Doctors recommend aspirin usage at a regular interval and mostly after having food. Doctors warn that aspirin should not be given to children and teenagers for flu signs or chickenpox and unsafe side effects may happen if taken while taking some other drugs. Additionally children younger than 16 years of age for those having flu or chickenpox symptoms should not be prescribed aspirin or if the patient has an allergy to aspirin or any other part of this drug. Patients with acute health problems like asthma, bleeding problems, nose polyps, or rhinitis are also not advised to use aspirin nor is it recommended for ladies who are more than 24 weeks pregnant. Aspirin resistance is a laboratory phenomenon, in which there is the inability of aspirin to constrain one or more in vitro tests of platelet function. While thrombosis is the close cause of almost all occlusive cardiovascular disease events, other factors such as vascular function and possibly interactions with endothelial cells and/or monocytes are also likely to be important. However, mechanistic approaches to investigating "aspirin resistance" have depended to a great extent on ex vivo evaluation of platelet function, using such tests as light transmission platelet aggregometry following addition of arachidonic acid or adenosine diphosphate, the Platelet Function Analyzer, the VerifyNow Aspirin, rapid platelet function assay, or measurement of thromboxane generation in vitro or via serum levels of thromboxane B2 or urinary levels of 11-dehydrothromboxane B2. (Renda et al., pp. 95-209, Gachet and Aleil, pp. 13-38, Sweeny et al., pp. 62-73) Aspirin exacerbated respiratory disease describes patients with asthma and chronic rhinosinusitis with nasal polyposis, who experience acute respiratory tract symptoms following the ingestion of aspirin or other nonsteroidal anti-inflammatory drugs. Aspirin exacerbated respiratory disease affects 5 to 20 percent of all patients with asthma. Reactions to nonsteroidal anti-inflammatory drugs typically begin 30 minutes to 3 hours after ingestion, and present as a sudden worsening of asthma and nasal congestion, sometimes accompanied by other symptoms. Interactions between nonaspirin nonsteroidal anti-inflammatory drugs and aspirin may decrease the potentially beneficial antiplatelet effect, and are one of the causes of aspirin resistance, which is a laboratory phenomenon described by the incapability of aspirin to inhibit one or more in vitro tests of platelet function. Aspirin challenge is the only way to diagnose nonsteroidal anti-inflammatory drugs sensitivity definitively. Definitive diagnosis is important for research protocols involving Aspirin exacerbated respiratory disease patients. In contrast, aspirin challenge is only indicated for clinical purposes if the patient has a specific need for regular nonsteroidal anti-inflammatory drugs therapy (i.e., nonsteroidal anti-inflammatory drugs for rheumatologic disease, aspirin for cardiovascular disease, or aspirin for treatment of Aspirin exacerbated respiratory disease), in which case challenge is often performed as part of a desensitization protocol. Aspirin challenges are generally performed orally in the United States. In other areas (e.g., Europe) a liquid lysylacetylsalicylic acid derivative is available for diagnostic aspirin challenge. This can be administered either as an intranasal or bronchial challenge, although inhaled administration is not adequate for desensitization. (Pierce et al,. pp. 65-212) In preparation for oral aspirin challenge or desensitization, patients with suspected Aspirin exacerbated respiratory disease are usually pretreated with leukotriene modifying agents as these medications have been shown to dramatically reduce the severity of pulmonary reactions during the procedure. Leukotriene modifying agents dramatically reduce the pulmonary symptoms, although nasal and ocular symptoms are still apparent in most patients, such that the outcome of challenge should be apparent to the experienced clinician. Antihistamines are also withheld for a week prior to the procedure. (Sweeny et al., pp. 62-73) Aspirin formulation — the formulation of aspirin — regular, buffered, or enteric coated — should be an individual clinical decision made with the patient. Enteric covered aspirin is intended to repel dissolution in the stomach; thus, health care providers and their patients may believe this to be an attractive alternative to conventional aspirin. Even though this preparation may diminish corrosions on endoscopy, enteric coating does not apparently protect against the clinically pertinent end point of gastrointestinal bleeding (Kelly et al., pp. 21-46). This finding is not surprising, since injury severe enough to induce bleeding is thought to reflect the systemic rather than just the local effects of aspirin. In some (Coxx et al., pp.219-233), but not all (Maree, pp. 112-158) studies, corresponding doses of enteric coated aspirin are not as helpful as plain aspirin. Worse bio-availability of these arrangements and poor absorption from the greater pH environment of the small intestine may cause insufficient platelet inhibition, predominantly in heavier subjects. These data contribute to the formulation of the hypothesis that small quantity of enteric coated aspirin does not produce adequate platelet inhibition. In acute occlusive vascular events (e.g., acute coronary syndrome), the necessity to accomplish a speedy clinical antithrombotic effect precludes the recommendation of enteric coated aspirin because of its delayed absorption. If the only available preparation is enteric coated, the single tablet or multiple tablets necessary to achieve the recommended dose of 325mg should be crushed or chewed. (Gachet and Aleil, pp. 13-38) Aspirin decreases the risk of cardiovascular disease (cardiovascular disease) events in a wide range of patients with established disease. Although the randomized data are sparse, aspirin may also be of net assistance in patients with a coronary heart disease equivalent (such as patients with diabetes). In all patients, the use of aspirin is associated with an increase in the risk of major bleeding, particularly from the gastrointestinal tract. In secondary prevention, the absolute benefit is large compared to the absolute risk of major bleeding. In primary prevention, the absolute benefit is lower and must be weighted on an individual clinical basis against the absolute risk of major bleeding. Doctors recommend long-term antiplatelet therapy (either aspirin or clopidogrel) for the secondary hindrance of cardiovascular procedures in all patients with recognized cardiovascular disease, including those with a history of gastrointestinal bleeding. In patients with a history of gastrointestinal bleeding, prevention with a proton pump inhibitor should be considered. Based on overall benefit to risk and benefit to cost considerations, doctors suggest aspirin rather than clopidogrel for secondary prevention. Patients for whom cost is not an issue could reasonably choose clopidogrel rather than aspirin, given clopidogrels slightly greater efficacy. As the data in primary prevention have far more uncertainties than for secondary prevention, we believe that healthcare providers should make individual clinical judgments about the use of aspirin for principal deterrence in those apparently healthy men and women whose absolute benefit on reducing cardiovascular events will outweigh their risks of major bleeding. For patients at risk of a first cardiovascular event, doctors suggest presenting individual patient specific information about his/her absolute risk, the absolute risk reduction with aspirin, and the increased risk of a major bleed, as opposed to decision making solely based on absolute risk. For patients without established disease but at moderate or high risk (10-year risk, 10 to 19 percent), risk assessment can be accomplished using various approaches. Conclusion Aspirin, acetylsalicylic acid, is a nonsteroidal anti-inflammatory drug with antipyretic, analgesic, and antiplatelet activities, which are dose-dependent. Low doses have antithrombotic effects; intermediate doses have antipyretic and analgesic effects; and high doses have anti-inflammatory effects comparable to other nonsteroidal anti-inflammatory drugs. The mechanisms of action by which aspirin and the nonacetylated salicylates act include both cyclooxygenase-dependent and -independent mechanisms. Nonsteroidal anti-inflammatory drugs may restrict the cardio protective effects of aspirin by interference with aspirin binding to cyclooxygenase or due to their own effects upon cardiovascular risk. Adverse effects of aspirin include gastrointestinal toxicity (nonsteroidal anti-inflammatory drugs gastropathy), anticoagulant effects, Reye syndrome, and effects on pregnancy, renal function, and both allergic and pseudoallergic reactions. Salicylate toxicity may occur when higher salicylate levels are achieved. Works Cited Cox D, Maree AO, Dooley M, Conroy R, Byrne MF, Fitzgerald DJ; Effect of enteric coating on antiplatelet activity of low-dose aspirin in healthy volunteers; Department of Clinical Pharmacology, Royal College of Surgeons, 123 St Stephens Green, Dublin 2, Ireland. (2006) pp.219-233 Gachet C and Aleil B; testing antiplatelet therapy. Eur Heart J (2008); pp. 13-38. Kelly JP, Kaufman DW, Jurgelon JM, Sheehan J, Koff RS, Shapiro S; Risk of aspirin-associated major upper-gastrointestinal bleeding with enteric-coated or buffered product. Slone Epidemiology Unit, School of Public Health, Boston University School of Medicine, Brookline, Massachusetts 21-46, USA (1996) Maree AO, Curtin RJ, Dooley M, Conroy RM, Crean P, Cox D, Fitzgerald DJ; Platelet response to low-dose enteric-coated aspirin in patients with stable cardiovascular disease.; Department of Clinical Pharmacology, Royal College of Surgeons in Ireland, Dublin, Ireland. (2005); pp. 112-158. Pierce RP, Gazewood J, Blake RL Jr; Salicylate poisoning from enteric-coated aspirin. Delayed absorption may complicate management; Department of Family and Community Medicine, University of Missouri--Columbia (1991) pp. 65-212. Renda G, Zurro M, Malatesta G, et al. Inconsistency of different methods for assessing ex vivo platelet function: relevance for the detection of aspirin resistance. Haematologica (2010); pp. 95-209. Rivera W, Kleinschmidt KC, Velez LI, Shepherd G, Keyes DC; Delayed salicylate toxicity at 35 hours without early manifestations following a single salicylate ingestion. Section of Toxicology, University of Texas Southwestern (UTSW) Emergency Medicine, Dallas, TX 8579, USA. (2004) pp. 53-90 Sweeny JM, Gorog DA, Fuster V. Antiplatelet drug resistance. Part 1: mechanisms and clinical measurements. Nat Rev Cardiol (2009); pp. 62-73. Read More