Compare And Contrast Paracetamol And Aspirin

As mentioned above, opioids are extremely helpful in killing acute and cancer pain. Because opioid receptors are G-protein coupled reactions, the inhibitory G-protein is usually coupled or attached with the receptors (Ghelardini et al., 2015, page 219). The onset of reaction in inhibit the pain is rapid and effective due to multiple inhibitory actions at the terminal site (refer to the previous section of mechanism of action). Besides, the interaction of opioids gradually increases the threshold of pain neuron as well as attenuates the pain subjective evaluation (Ghelardini et al., 2015, page 220).

Although the mechanism of action of acetaminophen is unclear, it is generally believed to work the same was as ibuprofen. Ibuprofen and acetaminophen produce therapeutic effects by reversibly inhibiting cyclooxygenase and thus blocking the synthesis of proinflammatory prostaglandins, prostacyclins and thromboxanes from arachidonic acid. The effects of these prostanoids include lowering the pain threshold thereby exaggerating pain perception. Inhibiting the synthesis of these prostanoids increases the pain

The history of aspirin is long beginning in 1763 with Edward Stone and is quite extensive including such names as salicylaldehyde in 1838 and salicylic acid and the white willow tree connection by the English. Kolbe in about 1850 and 1870 were involved. More recently, the Bayer and Hoffman companies were participants in some of the most leading contributors to the wide use and distributive properties of aspirin. The history of aspirin reaches as far back as 330 B.C and its functions in relieving pain have far exceeded any discoverers imaginations. The use and consumption of aspirin continues to grow as new methods of the drug become known.

The low back pain condition is becoming more frequent in industrialized countries. The treatment of this condition is effective using peripherally acting NSAIDs justly in a short-term relief or in acute low back pain.1 At the same time, the use of antidepressants or other drugs such as tramadol have shown efficacy, where tramadol is centrally acting analgesic by inhibiting serotonin and noradrenaline reuptake, and activating nonselective m-opioid receptors via its active metabolite. 1 Moreover, acetaminophen is considered a first-line treatment for chronic pain and commonly used among several years, which effectiveness is due to its analgesic and antipyretic properties. 1 However, acetaminophen may present some hepatotoxic effects when misused.1 Therefore, the concomitant use of both therapies would bring efficacy with a multiple analgesic mechanism of action, since this therapy also shown a synergistic effect in animal models. 1

Commonly, a combination of medications / local anaesthetic techniques is employed for safe and effect pain relief. The World Health Organisation analgesic ladder was introduced to improve cancer pain control. The concept is extrapolated to other pain conditions as well – as the intensity of the pain increases, the complexity of the interventions also increase.

Studies comparing opioids and NSAIDs have shown that NSAIDs (Gajraj et al,2005) are effective than opioids, with some studies suggesting that NSAIDs can achieve greater reductions in pain scores (Holdgate and Pollock,2004). For acute pain, it has been suggested that NSAIDs should be used as the first line of treatment in pain therapy (Gajraji et al,2005ANZAC,2015) and recommend that opioids should be added only if pain is not controlled adequately with NSAIDs alone (Becks et al,2005)

Aspirin is a non-opioid analgesic, non-steroidal anti-inflammatory, antipyretic, and antiplatelet. It acts to block pain impulses by blocking COX-1 in CNS, reduces inflammation by inhibition of prostaglandin synthesis, antipyretic action results from vasodilation of peripheral vessels; decreases platelet

Aspirin is one of the most popular pain killers in the world. Aspirin is used to reduce the painor inflammation. It is sometimes used to prevent heart attacks, strokes, and chest pain.

COX-3 activity appears to be selectively inhibited by acetaminophen as well as a few other analgesic and antipyretic NSAIDs. Further, unlike other NSAIDs, acetaminophen is capable of crossing the blood-brain barrier allowing it to reach concentrations in the brain sufficient to inhibit COX-3. All of these lines of evidence strongly implicate COX-3 as the target of acetaminophen action and partly explain the long-standing mystery of why it is often more efficacious against headache in Humans and fever than some of the other NSAIDs. (Chandrasekharan et al 2002)

Dr Redd, There are two basic ways pain medicines work. They either stop the pain signals from going to the brain or they alter the brain’s interpretation of the signals. Analgesics, such as acetaminophen, prevent the signals from reaching the brain. Narcotics, opioids from the poppy or narcotics synthesized by man, attach to protein opioid receptors in the brain or spinal cord to alter the perception or interpretation of signals to the brain. In the case of anesthetics, some increase Cl- in receptors to lessen the nerves ability to fire and others increase Na+ to reduce the action potential of the nerves.

NSAIDs or non-steroidal anti-inflammatory drugs are a class of drugs which consist several drugs which provide analgesic, anti-pyretic and at higher amount of doses, provides anti-inflammatory therapeutic action. NSAIDs work by inhibition of iso-enzymes COX-1 and COX-2. The process of inhibition is completely reversible as compared to aspirin which is a non-selective NSAID and inhibits COX unselectively. COX isoenzymes catalyses the prostaglandin and arachidonic acid synthesis. When a non-selective COX such as aspirin binds, lowers the levels of prostaglandins which are cytoprotective, leads to formation of more amount of acid and causing ulcers, internal bleeding. The selective COX inhibitors such as celecoxib, rofecoxib prevents such side

Injury or inflammation of a bodily tissue can lead to profound changes in the internal chemical environment. Damaged cells discharge their intracellular components, releasing substances, notably ATP, potassium ions (K+) and acetyl chloine (ACh). Some of these contents act on nociceptors directly, triggering an action potential which will end up in the brain. Other components released from the cells can sensitize the terminals, making them hypersensitive to further stimuli. This allows a pain signal to be transmitted when a seemingly

Acetylsalicylic acid, commonly known as aspirin, has a chemical formula of C9H804. Aspirin is one of the first drugs in the world that came to a common use with about 35,000 metric tons that are annually used and consumed by people all over the world. Aspirin is commonly used to relieve people from pain of headaches and reduces the temperatures of fevers. Aspirin is also used to sooth a scratchy throat, relieving pain from bug-bites, wiping away rust marks, and clearing dandruff problems. Most of these problems consist of aspirin to dissolve in water to create a solution.

The term salicylate refers to any of a group of chemicals that are derived from salicylic acid. The best known is acetylsalicylic acid (Aspirin). Acetylsalicylic acid is metabolized to salicylic acid (salicylate) after ingestion. Salicylates are nonsteroidal anti-inflammatory (NSAI) agents commonly used for their analgesic and antipyretic properties. They act on the cyclooxygenase enzymes to impair peripheral and central prostaglandin biosynthesis. (1)

The suppression of pain and inflammation has been a major goal of medical treatment throughout the ages. Inflammation is an essential response to any noxious stimulus which threatens the host and may vary from a localized response to a more generalized one. [1, 2, 3]