Acetaminophen: Non-Opioid Analysis

of prostaglandin E2, which lessen the hypothalamic target point to reduce fever, and creating active the descending inhibitory serotonergic pathways to produce analgesia. Even though acetaminophen have similarities with the analgesic and antipyretic properties of other COX inhibitors like the aspirin and the non-steroidal anti-inflammatory drugs (NSAIDs), still it does not possess considerable anti-inflammatory properties. Contrary to aspirin, acetaminophens do not hinder thromboxane and, as such, aggregation of platelet does not change.

Anne is currently taking paracetamol for the pain in her wrist, within healthcare analgesia should always be monitored to assess whether it is achieving elimination of pain and should be adapted to the individual patient (Vargas-Schaffer, 2010). If paracetamol were not effective in eliminating Anne’s pain then practitioners should consider a non-steroidal anti-inflammatory medication [NSAIDS] or a mild opioid medication such as codeine as the next step (Vargas-Schaffer, 2010). However as Anne is asthmatic NSAID medication should be used with caution due to the risk of increased frequency of asthma attacks and breathlessness (Joint Formulary Committee, 2015); if Anne has taken NSAIDS before with no issue then this would be the next choice of analgesia followed by codeine if combined paracetamol and NSAID did not prove effective (Vargas-Schaffer,

As a widely used analgesic and antipyretic agent, acetaminophen (APAP) overdose induced hepatotoxicity is one of the most common causes of acute liver failure in the USA and in most Western European countries [1]. Although a number of studies have forced on the influences of N-acetyl-p-benzoquinone imine (NAPQI), a highly reactive metabolite of APAP that depletes hepatic glutathione, and increases in oxidative stress during APAP toxicity [2], other mechanisms such as immune response also raise the susceptibility in the early stages of APAP-induced liver injury [3]. Accumulating evidence demonstrates a critical role of inflammatory cytokine released in early liver damage after APAP intoxication [4, 5]. Kupffer cells (KCs), the liver resident macrophages, are major sources of reactive oxygen species (ROS) and inflammatory

NSAIDs side effects can differ in individuals. Long use of NSAIDs cause serious side effects. For example, the development of peptic ulcers in the gut. Peptic ulcers occur due to the Cox enzyme being obstructed by the NSAIDs. This obstruction leads to unpleasant results. One benefit of the COX enzyme being obstructed is that it inhibits prostaglandins forming. However, prostaglandins act as a defence mechanism for the lining of the stomach protecting them from stomach acid. Gastrointestinal symptoms are frequent side effects associated with taking NSAIDs. These side effects include diarrhoea, constipation, heart burn, stomach pain and nausea. In cases of taking NSAIDs such as Naproxen, this could affect the lining of the stomach, it could

I read and examined the article, Acetaminophen reduces social pain (DeWall, 2010) and the main purpose seemed to be that Acetaminophen reduced pain from social rejection and physical pain so they wanted to test that in patients so maybe they can further the research into making it a more perscribable drug to help individuals who might be struggling with social rejection issues.

Medications that can cause interactions include anticoagulants, probenecid, bisphosphonates, angiotensin-converting enzyme (ACE) inhibitors, anticoagulants (Warfarin), antiplatelet medicines (Clopidogrel), aspirin, corticosteroids (Prednisone), heparin, other NSAIDs (Ibuprofen), Rivaroxaban, or Selective Serotonin Reuptake Inhibitors (SSRIs) (Fluoxetine) due to the risk of stomach bleeding may be increased. Bisphosphonates (Alendronate), Cyclosporine, Hydantoins (Phenytoin), Lithium, Methotrexate, Quinolones (Ciprofloxacin), Sulfonamides (Sulfamethoxazole), and Sulfonylureas (Glipizide) side effects may be increased by Naproxen. The effectiveness of Angiotensin-converting enzyme (ACE) inhibitors (Enalapril), Beta-blockers (Propranolol), or diuretics (Furosemide, Hydrochlorothiazide) may be decreased by Naproxen (Lexi-Comp,

Most studies only involve Tylenol. Keep in mind, that since acetaminophen is the most commonly used pain reliever and fever reducer, it’s the one most often used in studies.  It is generally considered a weaker pain reliever to ibuprofen, although it is more widely used because it's better tolerated than Aspirin and ibuprofen, which have both been shown to irritate the stomach. (3)

Lysine is the salt of ibuprofen, and ibuprofen is an acid. This extra ingredient makes this medicine stronger than just taking ibuprofen alone, it also increases the rate of absorption. The gastrointestinal is where absorption of most drugs takes place, and this is where ibuprofen is absorbed. Ibuprofen is bound to proteins, The amount of ibuprofen in circulation reaches its peak concentration, 1-2 hours after it has been taken with food. However, when taken without food it reaches its peak 45 minutes after it has been taken. The amount of ibuprofen lysine 400mg in circulation reaches its peak concentration 38 minutes after it has been taken on an empty stomach. (Reckitt Benckiser Healthcare Ltd, 2016). The active ingredient in Nurofen back pain 300mg sustained-release capsules is ibuprofen. Sustained-release tablets are drugs in a capsule form that release the drug steadily. This takes longer in comparison to other doses. The amount of ibuprofen 300mg in circulation in the body reaches its peak concentration, 1-2 hours after it has been

NSAIDs work commonly by blocking the action of cyclooxygenase isoenzymes (COX-1, COX-2). This consequently blocks the production of prostaglandins which are responsible for inflammation9. The COX-2 isoenzyme is the particular enzyme that produces prostaglandins, which cause inflammation. On the other hand, COX-1 isoenzymes do not produce these inflammatory prostaglandins, but have various other effects. An important effect is maintaining a healthy stomach and intestinal lining9. Traditional non-selective NSAIDs block the action of both COX-1 and COX-2. These can lead to harmful side effects such as intestinal damage and peptic ulcers, amongst others. NSAIDs are commonly prescribed with a PPI to counteract these harmful side effects. In comparison to the other NSAIDs, Etoricoxib is an orally active, selective COX-2 inhibitor2. It does not inhibit the cyclooxygenase-1 isoenzyme. Therefore it simply lowers the prostaglandin production, consequently meaning that there are fewer chances of stomach-related side effects9.

| * 90% of customers uses aspirin based analgesics * Many of them are suffering from side effects such as upset stomach, irritation of the stomach lining, or an allergic reaction. * 10% of customers who generally visited doctors and who get prescription use acetaminophen thorough doctor’s recommendation.

have a brand name like Nuprin, Advil, Motrin and so on. Ibuprofen can be used as a fever reliever, antipyretic, and pain reducer,

Puzzled by what was the working force behind this drug, which was known for its healing properties, I did my own reading and discovered the effects of its abuse. Analgesics are known to relievemost conditions such as fever and inflammation. However, at higher dosages, they are known to cause greater complications in the long run. This motivated me to become someone who can guide patients in taking a safe dosage of the right medication by aiding them to understand the mechanism of medicine on different people. Given the credibility as a pharmacist, I will be dealing directly with patients and plan to provide patient-centered care in improving their health. Additionally, my love for ideas will allow me to design, implement and assess initiatives to further ameliorate

However, when misused they can damage the body. More drugs in the last two years have been changed from prescription-only medication to over the counter medication than in the last decade (Blenkinsopp). The major reason for this is because most OTC medications contain acetaminophen, which is a pain and fever reducer. It is currently the most common medicine for pain relief in the United States (Greenlaw). The problem with acetaminophen is that it can severely damage your liver tissue and skin. It damages the Glutathione Pathway, which is necessary for detoxification. This pathway is strongest antioxidant protector in the liver. Acetaminophen breaks down this pathway and in turn decreases the protection from toxins over time. It also accounts for about 460 deaths, 56,000 emergency room visits, and 2,6000 hospitalizations every year due to acute liver failure (University of Texas Medical Center). Acetaminophen in the correct amount can be advantageous, but one must understand the recommended proper dosage and frequency that the medication should be

Just a few weeks ago, it has come to my attention through a study conducted at Copenhagen University Hospital Gentofte led by Cardiology Professor, Gunnar Gislason. Through the study, it has been discovered that common painkillers, such as ibuprofen (Motrin), gives the person an increased risk of cardiac arrest by 31%. It was found that Non-Steroidal Anti-Inflammatory drugs (NSAIDs) have been linked with it as well and the most common is ibuprofen. Gislason says to only take ibuprofen when it is absolutely necessary, be cautious when using it, and to never take more than 1,200 mg a day. Previous studies have shown that NSAIDs are related to the cardiovascular risk. “Naproxen is probably the safest NSAID, and we take up to

Aceclofenac has demonstrated to be potential analgesic and anti-inflammatory drug with same activity that indomethacin and diclofenac, and due to its preferential Cox-2 blockade, it is more safe than traditional Non-steroidal anti-inflammatory drug (NSAIDs) regarding to adverse effect on gastrointestinal and cardiovascular systems. Aceclofenac has selectivity for Cox-2, what makes it stands among others NAIDs. This favorable Cox inhibitor is well tolerated; it is Gastrointestinal (GI) tolerable and safe for cardiovascular system when compared with other selective Cox-2 inhibitor (Solanki et al, 2015).