NONSTEROIDAL ANTI-INFLAMMATORY DRUGS ON PLATELET AGGREGATION

Nonsteroidal Anti-Inflammatory Drugs and Platelet Aggregation

Abstract

The research examines the impact of Impact of Non steroidal anti-inflammatory drugs on platelet aggregation). The research methodology used is the secondary research where the literature research is conducted through the online journals, article and books. The research facilitates the current learning in the pharmacology since it extends the impact of the anti-inflammatory drugs on the platelet aggression.

Table of Contents

Introduction4

Problem Statement5

Purpose of the Study6

Literature Review6

Pharmacological Considerations8

Methodology10

Research Design10

Data Collection Procedure10

Inclusion Criteria11

Discussion11

Results13

References15

Appendix18

Nonsteroidal Anti-Inflammatory Drugs and Platelet Aggregation

Introduction

Nonsteroidal anti-inflammatory drugs (NSAIDs for short) are a diverse group and chemically heterogeneous drugs mainly anti-inflammatory, analgesic and antipyretic, thereby reducing the symptoms of inflammation, the pain and fever respectively. All exert their effects by action inhibition of the enzyme cyclooxygenase. The natural anti-inflammatory drugs are secreted by the body itself, and are the derivatives of steroids. Substances of steroidal anti-inflammatory are powerful, but they may also show the significant side effects. In opposition to steroids, the term "nonsteroidal" applies to NSAIDs to emphasize their chemical structure and fewer steroid side effects. As pain is characterized by not belonging to the class of drug and act by blocking the synthesis of prostaglandins (Knijff,Schutand,2003, 68-94).

Nonsteroidal antiinflammatory drugs inhibit the activity of both cyclooxygenase-1 (COX-1) as cyclooxygenase-2 (COX-2) and, therefore, the synthesis of prostaglandins and thromboxanes. It is thought to be the inhibition of COX-2 which in part leads to anti-inflammatory, analgesic and antipyretic activity of NSAIDs; however, those that simultaneously inhibit COX-1 have the ability to cause bleeding and digestive ulcers, particularly aspirin. Thus, it emphasizes the advantages of selective inhibitors for COX-2 (Knijff,Schutand,2003, 68-94).

The prototype NSAID is aspirin that accompanies a variety of organic acids, including derivatives propyl acid (such as ibuprofen and naproxen), derivatives of acetic acid (such as indomethacin) and enolic acids (such as piroxicam) and the arachidonic acid by the active site of cyclooxygenase. The paracetamol is included NSAIDs, despite their lack of anti-inflammatory action. Since anti-inflammatory drugs interfere with prostaglandin adverse effects related to the processes in which they are involved as gastric cytoprotection, they may cause the aggregating platelets, renal vascular auto regulation and mechanism of delivery. Drugs that inhibit COX-2 may have adverse cardiovascular effects in susceptible patients that mat be fatal (Knijff,Schutand,2003, 68-94).

The clinical definition of aspirin resistance has failed a drug to prevent atherothrombotic event despite regular intake of the appropriate dose is a fairly common problem. Definitions of laboratory aspirin resistance participated detects failure of the pharmacological effect of aspirin or aspirin failed to prevent platelet aggregation. Aspirin resistance, defined as the pharmacological effect of a continuous production (Kumar, 2002,15-26). Thus NSAIDs usually cause irritation of the gastric mucosa (the most common adverse effect) and cause peptic ulcer, demonstrating these effects by stomach pain and heartburn. They can also cause bleeding, dizziness, headache, fatigue, sleep, and sometimes cause allergic reactions of consideration. Rarely produce alteration of the blood cells, kidney or renal disease and liver disorders Steroids can cause alterations in adrenocortical secretion coming to ...