Paracetamol – Synthesis and Uses Discovered in 1877 by Harmon Northrop Morse at the John Hopkins University, Paracetamol was one of several aniline deriviatives that was found to have analgesic and antipyretic properties (Brodie 23). It was first synthesized by the reduction of p-nitrophenol with tin in glacial acetic acid; however was not used classified as a medication until ten year later (Bertolini 264). Initially, phenacetin, a closely related compound that exhibited similar physiological effects, became the popular over the counter drug for headaches (Bertolini 251). However, later research by Brodie and Axelrod in 1949 found that phenacetin was in fact metabolized into paracetamol within the body (Brodie and Axelrod 60). Subsequently, paracetamol quickly took the place of phenacetin and remains one of the most common over the counter medication for fever reduction and pain relief. Found in drugstores worldwide, paracetamol is commonly known by its American brand name, Tylenol. Paracetamol is chemically named N-acetyl – p – aminophenol. The chemical structure is an aromatic six-membered ring with a hydroxyl substituent placed para to the N-acetyl substituent. As the use of paracetamol increased, scientists and reserachers have looked into the most efficient methods of synthesizing the compound. In 1997, demand for paracetamol in the United States was estimated at 30-35 thousand tons per year(IARC 73). Global demand was similarly heavy in many other countries. There are numerous synthetic pathways that are presently known that seek to produce the compound most efficient manner. In determining efficiency, the many factors must be taken into account. The most important ones include the cost of the reagents,... ... middle of paper ... ...light of paracetmol’s physiological effects. The compound exhibits characteristics that mirror other analgesics and anti-pyretics but also displays unique properties that can be advantageous in certain treatment plans. Its anti-inflammatory activity is not as strong as other similar medications known as NSAIDS; fully refereed to as non-steroidal anti-inflammatory drugs. The main mechanism proposed for paracetamol involves the highly selective inhibition of an enzyme called cyclooxygenase; abbreviated COX. There are two isoenyzmes of cyclooxygenase are of similar molecular weight and structure but each take on different functions. They are labeled COX-1 and COX-2. COX-1 is present in most tissues and but functions more specifically on maintaining the lining of the stomach. It also plays other vital roles within the body such as platelet and kidney function.
This paper discusses pharmacology and terminology related to “Pharmacology” which is the branch of medicine concerned with the uses, effects, and modes of action of drugs“ pharmacology. 2015. In Merriam-Webster.com. The study of different classes of drugs, routes of absorption, and drugs have effects on those consuming them. There are drugs that are necessary for illnesses and healing but, there are medicines that cause concern regarding interaction and harming the body.
Ropivacaine is homologous to Bupivacaine . If local anaesthetics are administered into the vein or artery it results to very high systemic levels possibly causing CNS and CV toxicity due to rapid penetration into these regions. Both bupivacaine and ropivacaine are amide linked esters. They are extensively bound in the plasma. Amides extensively bind to the alpha-1 acid glycoprotein (AAG) with ~94% ropivacaine bound to it; it has a higher affinity even though albumin binds to greater amount due to its relative abundance in the human plasma. AAG concentration increases after operative surgery. Ropivacaine is metabolised by the cytochrome P450 isoenzymes CYP1A2 and CYP3A4 to four metabolites, 3-OH-2’6’-pipecoloxylidide, 4-OH-ropivacaine, 3-OH-ropivacaine, and N-dealkylated PPX. Reduced protein binding means that there is higher fraction of the unbound drug circulating in the plasma. Furthermore, amides are hepatically metabolised by amidases. Amidase metabolism is much slower than plasma hydrolysis in which ester linked local anaesthetics undergo. This means that amides are prone to accumulation when administered by continuous infusion. Drug accumulation is also influenced by reduced hepatic perfusion and hepatic dysfunction. It has been reported that high concentrations of unbound bupivacaine are linked with higher rates of early symptoms of CNS toxicity.
Renak, Judith. “Tylenol made a hero of Johnson and Johnson: The recall that started them all,” The New York Times. March 22, 2002. Retrieved May 3, 2011 from: http://www.nytimes.com/2002/03/23/your-money/23iht-mjj_ed3_.html
Its ability to inhibit phosphodiestarase type 1 leading to an increase in the concentration of cyclic AMP which is thought to result in its vasodilator effects
Granted, opioid based Pain killers like OxyContin have been invented and used for centuries. It was Hippocrates who first used opioids as a form of medicine. He used opium to stop the pain of internal illnesses, like "women’s diseases" (Blachford and Krapp). But as time went on chemists were able to actually separate and isolate more compounds from the opium plant, such as the chemical Thebaine, the main substance used to make Oxycodone (Meier 57). Oxycodone is the chemical in OxyContin that gives it the pain killing effects, it was developed in Germany circa 1916, and they labeled it under the name Eukodal (Blachford and Krapp). From there, the FDA first approved the use of Oxycodone in 1976 (Blachford and Krapp). Then In 1996 a drug manufacturer by the name of Purdue Frederick started the sale of Oxycodone under the brand name OxyContin, in order to sell the drug he opened a special unit known as Purdue Pharma (Meier 12). Following the release in 1996, it became highly sou...
In the late 1800’s it was discovered that papa-amino-phenol, could reduce fever, but the drug was too toxic to use. A less toxic extract called phenacetin was later found to be just as effective but also had pain-relieving properties. In 1949, it was learned that phenacetin was metabolized into an active but also less toxic drug, acetaminophen. Since then, acetaminophen has been sold under many over the counter brand names, most popular being Tylenol.
Percocet is a prescription drug made up of two different components; acetaminophen (pain reliever and fever reducer) and oxycodone (an opioid that binds to opioid receptors to produce morphine like effects). The initial use of percocet results in an euphoric sensation for the user. The drug causes the brain to receive a different signal about the pain and therefore will release dopamine to the body (“How Long Does Percocet Stay in your System?”). When percocet is prescribed in higher doses, the chances of addiction increases. The more frequent a patient takes percocet, the effect on the liver and kidney functions increases as well. It may result in a longer time for the drug to be fully excreted from the body (“Percocet Half-Life: How Long Does it Stay in Your System”). Once a patient becomes addicted to percocet, medical treatment may be needed in order to help the user withdraw from using the drug.
Almost overnight one such venerable substance (or class of substances) has been catapulted into the national spotlight: prescription painkillers, namely those derived from the opium poppy. This class of analgesic encompasses everything from the codeine in prescription cough syrup to the morphine used in the management of sever pain. These compounds are commonly referred to as opiates and are produced naturally by the poppy. The sub-class of this type that has gotten all of the attention recently is the opioids, which are semi-synthetic compounds derived from the opiates (Wade 846). Opioids were developed for a variety of reasons, such as reducing the cost of production (morphine is expensive to synthesize) and attempting to reduce the addictiveness of the drugs.
Paracetamol: 1.Amide: contains nitrogen and carbonyl so it’s hydrophilic.2. Hydroxyl: hydrophilic because of the presence of Oxygen that can H-bond with water.3.benzene ring: lipophilic because of non-polar hydrocarbon ring. 4. Methyl is lipophilic because of the nonpolar hydrocarbon group.
Quinine, a special anti-parasite used in pills and tonic water, and gives it a unique bitter taste. It was a common product in the over the counter pharmacy product until it was banned by the Food and Drug Administration. Why? The side effects of the pill could be deadly unless used under professional medical attention. Yet it’s still used in tonic water? To find out why we have to go deeper into the topic of quinine and it’s history.
The Tylenol crisis occurred in October of 1982 when seven people died in Chicago after immediately taking extra-strength Tylenol capsules. Tylenol was the leading non-prescription pain reliever medicine at that time. The capsules were popular in particular because they were slicker and easier to swallow. It was later found out that the capsules that were taken by these people were laced with a very lethal dose of cyanide. The Tylenol brand name is owned by McNeil Consumer Healthcare, which is a subsidiary of Johnson & Johnson.
Ketamine Hydrochloride is an anethetic developed in 1962 by Dr Calvin Stevens. In the 1960's and 1970's, it was used on the battlefields of the Vietnam War. It had a strong painkilling effect, that did not affect the patients breathing. It's currently used as a human anesthetic and in veterinary medicine, most commonly used on horses. In its illegal form, ketmine is used to get high or even used for drink spiking.
Tylenol's 1982 ordeal has become a classic example of a successful crisis management. Johnson & Johnson faced a major crisis when their leading pain-killer medicine, extra-strength Tylenol, was found to have caused the fatalities of seven people in Chicago, Illinois. It was reported that unknown suspect or suspects took the product off store shelves, tampered it with deadly cyanide and returned to the shelves. As a result, seven people died and consumers lost confidence and panicked over hearing the news of this incident. Tylenol received massive media coverage which led to an expeditious communication of event to the public. Johnson & Johnson (J & J) took a huge financial hit when it had to recall and destroy approximately $100 million dollars worth of inventory in addition to the loss incurred by the company when the public reacted to the incident (Campbell et. al., n.d.). Tylenol's approach was to pull off the products as quickly as possible, stopped production, cooperated with the investigation and the media and halted all forms of advertisement or marketing of the product. Furthermore, Johnson's & Johnson's took the initiative to protect and improve their product packaging which allowed them to regain the public's confidence and paved the way for improved tamper-resistant packaging now used by myriad of manufacturing companies. The fatalities occurred between September 29th to October 1st of the year 1982 and by November, Tylenol had already reintroduced the product with improved tamper-resistant packaging. To regain the public's attention and confidence, Johnson's & Johnson's launched a dynamic marketing campaign to put the product's name before the public.
Analysis of Aspirin Tablets Aim --- To discover the percentage of acetylsalicylic acid in a sample of aspirin tablets. ----------------------------------------------------------------- In order to do this, the amount of moles that react with the sodium hydroxide must be known. This is achieved by using the method of back titration.
Thus, foreign substances undergo so-called first-pass metabolism before they reach other organs in the body. Some hepatotoxins, including carbon tetrachloride (CCl4) and many commonly used drugs, directly cause damage to hepatocytes. However, other toxins become toxic only as a result of enzymatic modification by the liver’s detoxification machinery—the Cytochrome P450 enzymes. For example, acetaminophen (Tylenol) has no toxic properties by itself but becomes noxious upon conversion to the mitochondrial toxin NAPQI (N-acetyl-p-benzoquinone imine) through the activity of the P4502E1 enzyme (14). Toxins can cause injury to hepatocytes, BECs, or both. Cytochrome P450 enzymes are most abundant in zone 3 hepatocytes, accounting for the higher rate of drug toxicity in that portion of the lobule. Toxins can cause either acute or chronic damage, with the most common offenders being alcohol, acetaminophen, galactosamine, CCl4, antibiotics, and nonsteroidal anti-inflammatory