Metformin (Glucophage) Reactions

Metformin (Glucophage) Reactions Metformin (Glucophage) is available in the Pakistan since 1998. It falls in the same drug class as phenformin. Metformin is considered a first line agent and is significantly useful in people with known insulin resistance GLUCOPHAGE ® (metformin hydrochloride tablets) and GLUCOPHAGE ® XR (metformin hydrochloride extended-release tablets) are oral antihyperglycemic drugs used in the management of type 2 diabetes. Metformin hydrochloride (N,N-dimethylimidodicarbonimidic diamide hydrochloride) is not chemically or pharmacologically related to any other classes of oral antihyperglycemic agents. The structural formula is as shown: Glucophage (metformin hydrochloride tablets) Structural Formula Illustration Metformin hydrochloride is a white to off-white crystalline compound with a molecular formula of C4H11N5 †¢ HCl and a molecular weight of 165.63. Metformin improves hyperglycemia primarily through its suppression of hepatic glucose production, especially hepatic gluconeogenesis[1]. The average person with type 2 diabetes has three times the normal rate of gluconeogenesis; metformin treatment reduces this by over one third.[2] Metformin activates AMP-activated protein kinase (AMPK), a liver enzyme that plays an important role in insulin signaling, whole body energy balance, and the metabolism of glucose and fats;[3] activation of AMPK is required for metformins inhibitory effect on the production of glucose by liver cells.[4] Research published in 2008 further elucidated metformins mechanism of action, showing that activation of AMPK is required for an increase in the expression of SHP (Small heterodimer partner), which in turn inhibits the expression of the hepatic gluconeogenic genes PEPCK and Glc-6-Pase.[5] Metformin is frequently used in research along with AICAR as an AMPK agonist. The mechanism by which biguanides increas e the activity of AMPK remains uncertain; however, research suggests that metformin increases the amount of cytosolic AMP (as opposed to a change in total AMP or total AMP/ATP).[6] In addition to suppressing hepatic glucose production, metformin increases insulin sensitivity, enhances peripheral glucose uptake, decreases fatty acid oxidation, and decreases absorption of glucose from the gastrointestinal tract.[8] Increased peripheral utilization of glucose may be due to improved insulin binding to insulin receptors.[9] AMPK probably also plays a role, as metformin administration increases AMPK activity in skeletal muscle.[10] AMPK is known to cause GLUT4 translocation, resulting in insulin-independent glucose uptake. Some metabolic actions of metformin do appear to occur by AMPK-independent mechanisms; a recent study found that the metabolic actions of metformin in the heart muscle can occur independent of changes in AMPK activity and may be mediated by p38 MAPK- and PKC-dependent mechanisms.[11] Metformin causes a few gastrointestinal side effects including nausea, metallic taste, diarrhea and abdominal discomfort[7] . These can be avoided if the dose is increased slowly, and taking the drug with meals. A small amount of weight loss, possibly due to drop in net caloric intake due to appetite repression and/or a reduction in hyperinsulinemia is suggested. Falling in the same drug class as phenformin, the reported incidence of lactic acidosis is surprisingly low, 0.03 per 1000. In a US double-blind clinical study of GLUCOPHAGE in patients with type 2 diabetes, a total of 141 patients received GLUCOPHAGE therapy (up to 2550 mg per day) and 145 patients received placebo. Most Common Adverse Reactions (>5.0 Percent) in a Placebo-Controlled Clinical Study of GLUCOPHAGE Monotherapy The occurrence can further be avoided if contraindications are followed. It is contraindicated in people with a high risk of lactic acidosis: renal serum creatinine levels over 150 ÃŽ ¼mol/l[14}or hepatic impairment, respiratory insufficiency, severe infection and alcohol abuse. Any pharmacological therapy that alters either of the factors mentioned before is also considered. It should also be used cautiously in elderly especially those above 80 years of age. It is recommended to monitor renal function upon initiation and at least once a year thereafter. It should be withheld immediately before a person has a procedure with a radiocontrast dye, as the dye increases the risk of renal failure and therefore lactic acidosis [15] [16]. It should also be discontinued before and surgery and can be started immediately after if the renal function is normal and the patient is stable. It is also recommended to monitor hematological parameters as it alters vitamin B12 absorption [12] [13] and therefore cause anemia (7% in clinical trials). The mechanism of action is unknown but can be reversed by discontinuation of the drug. Daily dosage should be 500 mg orally twice daily with meals. The dose can be increased every 2 weeks to 2000 mg daily. References Kirpichnikov D, McFarlane SI, Sowers JR (2002). Metformin: an update. Ann Intern Med 137 (1): 25-33. PMID 12093242. Hundal R, Krssak M, Dufour S, Laurent D, Lebon V, Chandramouli V, Inzucchi S, Schumann W, Petersen K, Landau B, Shulman G (2000). Mechanism by which metformin reduces glucose production in type 2 diabetes (PDF). Diabetes 49 (12): 2063-9. doi:10.2337/diabetes.49.12.2063. PMID 11118008. Towler MC, Hardie DG (2007). AMP-activated protein kinase in metabolic control and insulin signaling. Circ Res 100 (3): 328-41. doi:10.1161/01.RES.0000256090.42690.05. PMID 17307971. Zhou G, Myers R, Li Y, Chen Y, Shen X, Fenyk-Melody J, Wu M, Ventre J, Doebber T, Fujii N, Musi N, Hirshman M, Goodyear L, Moller D (2001). Role of AMP-activated protein kinase in mechanism of metformin action. J Clin Invest 108 (8): 1167-74. doi:10.1172/JCI13505. PMID 11602624. Kim YD, Park KG, Lee YS, et al. (2008). Metformin inhibits hepatic gluconeogenesis through AMP-activated protein kinase-dependent regulation of the orphan nuclear receptor SHP. Diabetes 57 (2): 306-14. doi:10.2337/db07-0381. PMID 17909097. Zhang L, He H, Balschi JA (2007). Metformin and phenformin activate AMP-activated protein kinase in the heart by increasing cytosolic AMP concentration. Am J Physiol Heart Circ Physiol 293 (1): H457-66. doi:10.1152/ajpheart.00002.2007. PMID 17369473. Bolen S, Feldman L, Vassy J, et al (2007). Systematic review: comparative effectiveness and safety of oral medications for type 2 diabetes mellitus. Ann Intern Med 147 (6): 386-99. PMID 17638715. Royal Pharmaceutical Society of Great Britain and the British Medical Association. Chapter 6:Endocrine system—6.1.2.2 Biguanides, British National Formulary, 54. Bailey CJ, Turner RC (1996). Metformin. N Engl J Med 334 (9): 574-9. doi:10.1056/NEJM199602293340906. PMID 8569826. Musi N, Hirshman MF, Nygren J, et al. (2002). Metformin increases AMP-activated protein kinase activity in skeletal muscle of subjects with type 2 diabetes. Diabetes 51 (7): 2074-81. PMID 12086935. Saeedi R, Parsons HL, Wambolt RB, et al. (2008). Metabolic actions of metformin in the heart can occur by AMPK-independent mechanisms. Am J Physiol Heart Circ Physiol 294 (6): H2497-506. doi:10.1152/ajpheart.00873.2007. PMID 18375721 Andrà ¨s E, Noel E, Goichot B (2002). Metformin-associated vitamin B12 deficiency. Arch Intern Med 162 (19): 2251-2. doi:10.1001/archinte.162.19.2251-a. PMID 12390080. Gilligan M (2002). Metformin and vitamin B12 deficiency. Arch Intern Med 162 (4): 484-5. doi:10.1001/archinte.162.4.484. PMID 11863489 Jones G, Macklin J, Alexander W (2003). Contraindications to the use of metformin. BMJ 326 (7379): 4-5. doi:10.1136/bmj.326.7379.4. PMID 12511434 Weir J (March 19, 1999). Guidelines with Regard to Metformin-Induced Lactic Acidosis and X-ray Contrast Medium Agents. Royal College of Radiologists. Retrieved on 2007-10-26 through the Internet Archive. a b Thomsen HS, Morcos SK (2003). Contrast media and the kidney: European Society of Urogenital Radiology (ESUR) guidelines. Br J Radiol 76 (908): 513-8. doi:10.1259/bjr/26964464. PMID 12893691.  

Motives for Iraq War through Realism and Neo-Conservatism Lenses Essay

The invasion on Iraq by the United States in 2003 has become the biggest, lengthiest, and most expensive use of armed force since the Vietnam War. It is the first major post-Cold War U.S. military action taken unilaterally, without an international coalition, and the first U.S. experience as an occupying power in a Middle Eastern country. Although the invasion decision was distinctive (U.S. military connection in an Arab or Muslim country), the argument here is that the Iraqi invasion deals with motives related to natural security, power, and resources. Both realism and neo-conservatism claim to capture the motives behind the war, but only through a comprehensive comparison of the two can a synthesis be achieved. On March 20th, 2003, the United States military invaded Iraq with the ground campaign lasting almost three months. According to then-President of the United States, George W. Bush, and then-Prime Minister of the United Kingdom, Tony Blair, stated reasons for the invasion included the disarmament of â€Å"Iraq, especially with respect to weapons of mass destruction; the ending of Saddam Hussein's support for terrorism; and the liberation of the Iraqi people† (White House Archives). On May 1, the end of major combat operations was declared, ending the invasion period and beginning the military occupation period. However, was this war really needed to put an end to Saddam Hussein's regime in Iraq—a regime that, at that time, had been considered a threat to the United States, as the neo-conservatives claim? Moreover, did Iraq really possess weapons of mass destruction, or was control of Iraq's oil the reason for the United States to invade it, as realists may posit? Often termed the â€Å"pessimistic view† of international politics... ...ospect.org/cs/articles?article=the_road_to_aqaba>. Lieberfeld, Daniel. "THEORIES OF CONFLICT AND THE IRAQ WAR." International Journal of Peace Studies 10.2 (2005): 1-20. Print. Lowbeer-Lewis, Nathaniel. "A Neo World? NEOCONSERVATISM, INTERNATIONAL RELATIONS AND THE IRAQ WAR." Diplomat & International Canada 2009: 72-75.Diplomat & International Canada. 2009. Web. 4 Dec. 2010. . "President Discusses Beginning of Operation Iraqi Freedom." White House Archives. 22 Mar. 2003. Web. 04 Dec. 2010. whitehouse.archives.gov/news/releases/2003/03/20030322.html>. Walt, Stephen. â€Å"International Relations: One World, Many Theories.† Foreign Policy. Spring 1998: pg. 29-45. Waltz, Kenneth. â€Å"The Anarchic Structure of World Politics† International Politics. New York: Pearson, 2009. 37-58.

Elderly Drivers Outline

Elderly Drivers Specific Purpose: We want our audience to agree that the physically disabled elderly people need to retake their test or prove that they can drive before actually getting behind the wheel of a car. Thesis Statement: These elderly drivers, who are physically disabled, should not be driving without retaking the test or doing something to prove they are still capable to drive. I. Elderly are terrible drivers. A. The elderly are an increasing population of bad drivers, because of their health. B.Those include medical conditions like diabetes, having heart problems, having poor eyesight and being delusional. C. People with health risk or even something simple as just wearing glasses should â€Å"renew† their license, and to pass should have to take a small series test as simple as an eye exam. D. Overall, people over the age of 70 should have to perform a simple test to renew their license. II. Problem: According to the U. S. Census Bureau, the population of drivers 70 and older is expected to increase from 27. 8 million in 2010 to 51. 7 million in 2030 and 67 million in 2050.The rapid increase in the older driver population has led to concerns about the potential effects on traffic safety associated with this trend. A. Based on data reported by states to the Federal Highway Administration, there were approximately 22. 3 million licensed drivers 70 and older in 2010. B. A NHTSA study of 1995 FARS (Fatal Accident Reporting System) data reports that senior citizens accounted for: * 5% of all people injured in traffic crashes * 13% of all traffic fatalities * 13% of all vehicle occupant fatalities * 18% of all pedestrian fatalities C.If the elderly continue to drive as their health problems increase, they will not only be putting their selves at risk, but the rest of the population as well. III. Criteria for Solution: The solutions cannot be physically, mentally, or emotionally harmful to the driver. It has to be fair, affordable, and feasible. I V. Possible Solutions: There are a number of solutions that could help prevent harm to drivers of old age. A. Re-test the people over the age of 70+ in every state. B. Give mid-year health check-ups on the elderly to check their capability to drive an automobile. C.On the license plate of an elderly driver, have an identifier on it to signify that it is an elderly driver. D. Make it mandatory to have a passenger with a license to ride in the car with them. E. Check for any diseases, and health risks that would put the driver at risk or being hurt. F. Make sure the person knows the area they drive in. It has to be familiar to them. V. Best Possible Solution: Re-Test the elderly after a certain age. A. Maryland state law allows police, doctors, and residents including relatives to refer potentially unfit drivers to the Motor Vehicle Administration's Medical Advisory Board.B. A 2004 Florida law requiring that older drivers pass a vision test before getting a license renewed has helped cut the death rate among drivers 80 and older by 17%, according to researchers at the University of Alabama at Birmingham. Conclusion: In conclusion, we believe people should have to retake a driving test and vision and hearing test every few years to prove they are still safe and capable drivers. Reflective Thinking Sequence 1. Elderly drivers cause younger drivers to have road rage and put their self at risk. We can limit the problem by making drivers at the age of 70 retake the driving test. . The causes of the problem are the elderly’s vision and hearing getting bad. As they get older, they face more problems. 3. The effects of the problem are people getting hurt or put into danger. The driver puts their self into danger and then gets hurt by other drivers or other drivers hurt them. 4. The criteria in which the solutions should be judged are: Health checkups every few years, have another responsible driver in the car with the elderly, and/or retake the driving test at th e age of 70. 5. A possible solution is to have the driver retake the driving test at the age of 70.A strength would be better drivers on the road. A weakness is they may not want to retake the test. 6. The best solution is to make it mandatory for drivers at the age of 70 to retake the test. 7. We can put it into effect by making the retest a requirement at the age of 70. It’s not illegal because some states already put this into effect. Citations â€Å"Elderly Driving. † Elderly Driving. N. p. , n. d. Web. 29 Nov. 2012. ;http://www. stritch. luc. edu/depts/injprev/Transprt/tran3. htm;. â€Å"Fatality Facts: Elderly. † Fatality Facts: Elderly. Transsaftey Inc, n. d.Web. 29 Nov. 2012. ;http://www. usroads. com/journals/rilj/0101/ri010102. htm;. Copeland, L. (2009, July 6). States seek tests for older drivers. . Retrieved from http://usatoday30. usatoday. com/news/nation/2009-07-05-older-drivers_N. htm Taira, E. D. , M. Maynard, and M. J. Madigan. Assessing the dr iving ability of the elderly, a preliminary investigation. Binghampton, New York: Routledge, 1991. 215. Print. Rothe, John, Peter Cooper, and Brian De Vires. The Safety Of Elderly Drivers: Yesterdays Young, Todays Traffic. Transaction Publishers, 1990. 435. Print.

Health Care Systems For Every Country - 1042 Words

Health care systems are institutions and resources whose main purpose is to improve health. There are different health care systems for every country. The United Kingdom (U.K) has a universal health care that is called the National Health Service (NHS). In the U.K everyone that is a resident has access to the same health care. It is free for people who are not residents (visitors) only if in an emergency or if the person has some infectious disease. One pro of the U.K health care system is that all the records are digital and can be shared between medical systems. This makes it easier for doctors to access records. Although the health care system is great the citizens have to pay extra taxes in order to maintain having a good quality†¦show more content†¦This health care system may sound ideal but the conditions in Cuba compared to other countries are not well off. They have very limited resources, poor equipment and old facilities. But there health care helps its citizens. Unlike the universal health provided by the other 3 nations, the United States (U.S) has a private health care system. This system is not funded by taxes and a citizen would need health insurance to access it. It is not guaranteed for all citizens; in fact the system does not guarantee coverage for the entire population. Some low income people are provided with insurance but not always. More than 50 million Americans do not have health insurance and are really suffering without it. We as Canadians are very blessed when it comes to have our health care system when compared with the U.S. Canada has a single-pay mostly funded system while the U.S has a multi-payer, private system. Canadian health care is universal and is guaranteed for all citizens, but in America there about 50 million people that are uninsured. In 2013 Canada’s life expectancy was 81 years and the infant mortality rate was 5 deaths/1000 live births, while the U.S was at the bottom in infant mortality and life expectancy. In 2012 the gross domestic product (GDP) for Canada was 10.4 % and the GDP in the U.S was 16%, meaning the U.S spent more on health care than Canada. One pro of the U.S health care system is that there are not long waits, in Canada non-emergency surgery