Acetaminophenol Research Paper

Opioid drugs are some of the most widespread pain medications that we have in this country; indeed, the fact is that opioid analgesic prescriptions have increased by over 300% from 1999 to 2010 (Mitch 989). Consequently, the number of deaths from overdose increased from 4000 to 16,600 a year in the same time frame (Mitch 989). This fact becomes even more frightening when you think about today; the annual number of fatal drug overdoses in the Unites States now surpasses that of motor vehicle deaths (Alexander 1865). Even worse, overdose deaths caused by opioids specifically exceed those attributed to both cocaine and heroin combined (Alexander 1865).

Acetic Anhydride and p-Aminophenol were heated in a vial attached to an air condenser to synthesize crude acetaminophen, resulting in 0.097 grams (47.48% yield). The crude acetaminophen was then recrystallized in a solvent of water and methanol over heat resulting in 0.082 grams (39.61% yield) of pure acetaminophen. Melting points of both crude and pure acetaminophen were taken, and found to be 165.9 - 170.9°C and 168.2 - 171.5°C, respectively. The literature melting point of acetaminophen is 169.5 – 171.0°C, indicating that our final product was pure.

The over use of opioid has been one of the major public health problem in the United States (Substance Abuse and Mental Health Services Administration, 2018). Opioids include prescription medications that are used to treat pain symptoms which includes codeine, morphine, methadone, hydrocodone, and etc., as well as illegal drugs such as heroin and illicit potent on opioids such as fentanyl analogs (Substance Abuse and Mental Health Services Administration, 2018). The opioid overdose could happen due to many factors such as when a patient deliberately misuses a prescription, or misuse heroin (Substance Abuse and Mental Health Services Administration, 2018). Opioid overdose could happen due to the prescriber miscalculated the opioid dose or when

The rate of poisonings associated with drug overdoses has been on the rise, especially concerning those involving opioids (Paulozzie, Budnitz, & Xi, 2006). The Centers for Disease Control and Prevention (CDC) does not mince words regarding the status of opioid utilization in the United States: ?The United States is in the midst of an opioid overdose epidemic? (CDC, 2016). Opioids are now the most common cause of prescription drug use deaths (Rudd et al., 2016). Even as overdoses associated with the more historic killers such as heroin and cocaine increased, opioid overdoses rose the fastest between 1990 and 2002 (Paulozzi, Budnitz, and Xi, 2006). The prescription opioid epidemic contradicts traditional assumptions of drug use being a problem with illicit drugs: a majority of those who overdosed had a prescription for their cause of death (Kolondy et al., 2015). As asserted by Paulozzi et al., ?licit drugs have therefore recently replaced illicit drugs as the most common cause of fatal poisonings in the US? (2006, p 624). Further, it is important to note that these numbers represent just a fraction of the problem of prescription opioid abuse. Other adverse impacts associated with the epidemic of prescription opioid abuse include non-fatal hospitalizations and infants born addicted to opioids (Kolondy et al., 2015).

It is used to treat chronic or acute pain. It works by inhibiting the chemical messengers called the prostaglandins. Prostaglandins help transmit pain signals, induce fever and promote inflammation of swelling of tissues, normally happens after an injury or illness. Acetaminophen helps by blocking the signals of pain to the body. Unlike NSAIDs it does not have an anti- inflammatory action. Acetaminophen is rapidly absorbed in the stomach and the small intestines. The therapeutic dose is 500mg every 4-6 hours. A single dose over one hundred and fifty mg/kg are considered toxic. Although most times it also depends on how often you take the medication and how often you accidently overdose. The statistic gives you some good idea of what we should be worried about. Acetaminophen toxicity can occur at any age. Most common in patients with chronic alcohol abuse or malnutrition. Children because of the incorrect weight and dosage given. Older teenager or adult patients will occur with intent to harm themselves. When it is ingested into the body, a normal dose is easily broken down through the liver enzymes and excreted through urine. However in large amounts it overwhelms the liver and it cannot be broken down as easy, thus killing the liver tissue. It is the most common cause of hepatic failure in adults, usually requiring a liver

The U.S. Department of Health and Human Services (HHS) (2013) reported that U.S. prescription drugs, especially opioids analgesics, have been increasingly involved in drug overdose deaths. Unfortunately, drug overdose deaths from prescription drugs, especially opioids analgesics outnumbered deaths related to motor vehicle accidents back in 2009. Actually, in 2010 only, 16,651 deaths were connected to opioids overdose, an increase of 60 percent of overdose losses from any other drug class, prescribed or illegal. Specifically, in Florida, the attorney general of Florida (2012) stated that an average of seven Floridians die every day as a result of overdose from prescription drugs, which is five times greater than losses from the use of all illegal drugs put together.

Taking multiple products containing acetaminophen can cause liver failure. The maximum allowable daily dose of Tylenol (acetaminophen) is 4 grams (or 4000 mg) in adults and 90 mg/kg in children. Exceeding the maximum allowable daily dose can cause serious side effects and can have potentially fatal consequences. I would educate John on the use of Acetaminophen and liver failure. I would notify the doctor and get an order to check John’s LFT’s. Also, I would ask John the amount of Tylenol consumed on a daily basis and if he have tried any other sleep aids.

The pathogenesis behind the toxicity in Acetaminophen overdose is a result of chemical induced liver damage, hepatotoxicity. More specifically, this medication is metabolized in the liver, when there are large amounts of acetaminophen in the body the liver because depleted of it enzymes used to break down this medication. As a result the medication accumulates, causing hepatocellular necrosis

Controls in these studies did not consume aspirin, but rather acetaminophen. In the juvenile rheumatoid arthritis study the three cases that were examined and compared developed persistent vomiting, noninflammatory encephalopathy, and showed an increase of serum salicylate level, which is linked to an increase of aspirin ingestion. Compared to the children receiving long-term aspirin therapy whom did not develop RS, these symptoms are strongly associated with RS. The animal experimental study results found that those with an arginine deficient diet and influenza infection and/or aspirin treatment had increased levels of SOCTase, SGOT levels, and liver lipids, and eventually went into a deep coma. Serum ammonia levels were also elevated among these groups. This study however does not correlate well with humans, as an arginine deficient diet would exceed the levels used within the ferrets. Lastly, in the Hospital for Children study previously mentioned, an association with RS and aspirin consumption was found, however the next study found no statistically significant association between aspirin ingestion and

The majority of acetaminophen, approximately 90%, will be metabolized by glucuronidation (Lancaster et al., 2015). Approximately 10% will be metabolized by cytochrome p450 (Lancaster et al., 2015). From there it will become the reactive metabolite N-acetyl-p-benzo-quinone imine (NAPQI) (Lancaster et al., 2015). Under normal circumstances, glutathione (GSH) will convert NAPQI to a nontoxic metabolite (Lancaster et al., 2015). In cases where GSH depletion is present due to acetaminophen overdose, malnutrition, or alcoholism, NAPQI cannot be converted, leading to increased NAPQI levels and subsequently liver damage (Lancaster et al.,

The acetaminophen tablets from the Well at Walgreens brand showed a degradation of percent label claim of acetaminophen characterized by a R¬2 value of 0.4728 on a downward sloping treadline. The control percent label was found to be 105.3%. The percentages for weeks 2, 4, 6, and 8 were as follows: 111.9%, 88.7%, 100.9%, and 88.2%. Therefore, the total degradation found in the group results is a loss of 17.3% label claim. No outliers were determined at this time. The reason for this large amount would have to be the experimental conditions (70 C°, 75% RH), as these conditions are well outside of the recommended conditions shown on the label (15 – 30 C°). These extreme conditions led to a decrease in the amount of active acetaminophen present

It is well known that excessive alcohol can produce various side effects to human. However, giving up drinking is difficult and can bring several symptoms of alcohol withdrawal. To treat this problem, acamprosate, 3-Acetamidopropane-1-sulfonic acid, is used as a medication with a common brand name, Campral. Acamprosate is a small molecule that has a molecular weight about 181.21 g/mol. Its molecular formula is C5H11NO4S and is named as 3-Acetamidopropane-1-sulfonic acid or N-acetyl homotaurine.

Acetaminophen is a popular painkiller, with billions of doses sold annually. In any given week, about one-quarter of American adults (23 percent) take it to relieve all kinds of pain – everything from post-surgical discomfort to menstrual cramps. You may even have taken acetaminophen without realizing it. The FDA reports that over 600 medications include it as an active ingredient, including nonprescription remedies like Nyquil, Theraflu and Midol and

Cyclooxygenase (COX) is an enzyme that is responsible for formation of prostanoids, including thromboxane and prostaglandins. Pharmaceutical inhibition of COX can provide relief from the symptoms of inflammation and pain. Nonsteroidal anti-inflammatory drugs, such as aspirin and ibuprofen, display their effects via inhibition of COX.

Aspirin soverdose scause metabolic acidosis. However, the sbody will compensate by shyperventilation (respiratory alkalosis) so sone will expect the PaCO2 to be slow. The combination sof metabolic acidosis sand respiratory salkalosis can sbe a difficult situation to diagnose sfrom the blood sgases. The problem relates to whether sthe hyperventilation is sprimary (i.e. respiratory alkalosis) or is scompensatory for the metabolic sacidosis. Lethargy, stupor sand progression sto a state of scoma may occur, particularly in scases of poisoning. Salicylate soverdose causes a high anion sgap metabolic acidosis in both schildren and adults. The respiratory seffects of salicylates, such as salsalate sand aspirin, may contribute to serious acid-base simbalance in patients with sunderlying acid-base sdisorders or in overdose situations. Patients swho are unable to compensate for ssalicylate-induced smetabolic acidosis (i.e., respiratory response to sCO2 is depressed) will develop srespiratory acidosis sand increased concentrations sof plasma