Case Study Of A Patient With Diabetes Mellitus Nursing Essay

Case Study Of A Patient With Diabetes Mellitus Nursing Essay Patient Mr. NCS is a 53 year old Chinese man with the height of 1.72m, and weighs 82kg where his BMI is 27.7kg/m2 (overweight). Patient runs his own business and is currently staying with his wife and 3 children. He claims that he does not smoke and does not drink at all. According to the patient, the paternal side of his family has family history of hypertension and kidney failure where else for the maternal side, hypertension was known to be the family history. Patient has no known drug or food allergy. Patient was known to have had hypertension 15 years ago and also a history of pulmonary tuberculosis 35 years ago. Patient denied of being diagnosed with diabetes mellitus in the past. As for drug history, patient was only on 10mg of lovastatin (tablet) once at night and according to the patient, he was compliant to the medication. 1.2 Clinical Progress Patient was admitted into Accident and Emergency department and complained of shortness of breath (SOB) and mild giddiness. He also complained of having chest pain and a first episode of shortness of breath earlier before he was admitted into the hospital. On examination, he was found to be alert and conscious. Venous blood gas sampling was done and pH was found to be 7.306 (low), pCO2 was 44.2mmHg, pO2 was 45.8mmHg and HCO3 was 24.7mmol/L. Blood pressure was found to be 157/95mmHg, pulse rate was 72bpm, SPO2 was 97%, body temperature was 35.4 °C and respiratory rate was 21 breaths per minute. Reflo value was also obtained and it was found to be 17.1mmol/L and blood ketone was 0.9. Lungs were clear and abdominal was soft and non tender. Cardiovascular testing was done and it showed dual rhythm no murmur. The initial impression of this patient by the general practitioner in the hospital was impending diabetes ketoacidosis. Patient was immediately given 6 units Actrapid subcutaneousl y and the GP also planned to give O2 3L/min and to prescribe GTN 1/1 subcutaneously and Aspirin 1/1. Later on day 1 of admission, patient complained of increased in sweating, shortness of breath, body weakness and vomiting for 3 times in the morning. Patients blood pressure was 123/76, pulse rate was 82bpm, SPO2 was 99% and respiratory rate was 20 breaths per minute. When patient was asked, he mentioned that he has not done body check up and blood pressure measurement for at least 5 years now. Later in the afternoon, patient complained of excessive sweating and lack of appetite for the past 3 days. Patient then denied of having any chest discomfort or shortness of breath, headache and abdominal pain. Besides that, patient also complained of having polyuria and needed to wake up more than 3 times at night for micturation. He also complained of having polydypsia, lethargic and vomiting for 2 times in the morning. Patient was examined and he was found to be alert and conscious where he responded fully to Glasgow Coma Scale (GCS). Patient was also found to have good hydration and his ca pillary refill time (CRT) was less than 2 seconds. Vital signs were obtained and temperature was back to normal, 37 °C, blood pressure was 151/69, SPO2 was 97%, pulse rate was 88bpm and reflo value was 14.6. The management plan by the local GP was to continue monitoring the reflo value, prescribe 10mg lovastatin (tablet) once at night and 10mg amlodipine (tablet) once daily and have the patient to rest in bed. As patient was able to tolerate orally, IV drip was off and patient was allowed to take fluid orally. On day 2, patient was found to be comfortable. However, patient complained of having poor oral intake and that he was sweating profusely. He was still feeling mild giddiness and lethargic but no more chest or abdominal pain. Vital signs were observed and temperature was 37 °C, blood pressure was 128/84, pulse rate was 96bpm and reflo was 14.9mmol/L. Fundoscopy was also done and patient was found to not have any signs of retinopathy and chest X-ray was found to be clear. The management plan for day 2 was to continue 10mg amlodipine once daily, allow fluid intake orally, continue reflo monitoring 4 hourly and to trace and review the fasting blood sugar (FBS). On examination, patient was found to be alert and responded well to the GCS with the score of 15/15. Blood pressure was taken and it was 145/100 when patient was lying down and 130/90 when patient was standing. Renal profile was normal except for low potassium level of 3.0mmol/L. Impression for this patient was newly diagnosed d iabetes mellitus. Further management plan for this patient was to conduct a stress test on patient after discussing with the specialists and to monitor patients blood pressure for both lying down and standing up position 4 hourly for a day. Further plan was to start 500mg metformin (tablet) twice daily, 150mg aspirin (tablet) once daily, 20mg lovastatin (tablet) once at night, trace urine full examination microscopic examination and to refer the patient for diabetic counseling. Besides that, local GP also decided to off amlodipine and to change it to 4mg perindopril (tablet) once daily. Table 1 : Patients laboratory findings on Day 2. Sodium 129 mmol/L à ¢Ã¢â‚¬  Ã¢â‚¬Å" [135 145mmol/L] Potassium 3.0 mmol/L [ 3.5 5.0mmol/L] Creatinine 83  µmol/L [27 62  µmol/L] Glucose fasting 14.1 mmol/L [3.9-5.0mmol/L] Total Cholesterol 5.7 HDL 0.82 Triglycerides 6.7 AST 24 IU/I [10-37IU/I] ALT 45 IU/I [10-65IU/I] Bilirubin 11  µmol/L [2-24  µmol/L] INR 1.03 Trop I 0.02 CKMB 0.5 Disease Overview and Pharmacological Basis of Drug Therapy. Disease Background The prevalence of diabetes mellitus (DM) varies vastly from population to population and throughout the whole wide world. In United Kingdom (UK) itself, diabetes prevalence increased from 2.8% in the year of 1996 to 4.3% in the year of 2005. The incidence of type 2 DM showed an increase from 2.60/1000 person-years in 1996 to 4.31/1000 person-years in 20059. As much as the incidence of DM is increasing, it was estimated that up to half a million more have not had their condition diagnosed and treated10. Diabetes mellitus (DM) is a disorder in which blood glucose level is persistently above the normal range. This hyperglycaemia is thought to be due to either deficiency of insulin secretion or resistance to the action of insulin, or it could also be a combination of these6,7. DM is classified into four different types which include Type 1 DM, Type 2 DM, DM due to specific mechanisms and diseases and lastly, gestational DM8. Only type 2 DM will be discussed further here. Type 2 DM is normally caused by a combination of insulin resistance and decreased insulin secretion to overcome the resistance. It is the more common form of DM and it comprises of approximately 90-95% of the total DM cases8. The common risk factors associated with type 2 DM include increasing age, high caloric intake, overweight, central adiposity and sedentary lifestyle8. In type 2 DM patients, insulin secretory peaks every 5-10 minutes seen in normal subjects are hardly or absolutely not seen. In normal cases, when intravenous glucose is administered into a humans body, this will stimulate normal insulin secretion and is illustrated by a biphasic pattern, with an initial peak rising immediately 3-5 minutes after the administration, and lasted for 10 minutes, then followed by a deliberat e and more progressive phase, which lasts throughout the glucose infusion period. In type 2 DM, initial phase insulin secretion is not seen and the late phase occurs later and to a lesser extent11. For the diagnosis of DM, hyperglycaemia must be established before confirming that the patient has DM. Persistent hyperglycaemia needs to be confirmed and in order to do so, at least two plasma glucose measurements must be taken on separate days. There are three different types of plasma glucose test that can be used which include casual plasma glucose, fasting plasma glucose and oral glucose tolerance test (OGTT). According to WHO, there are three main criteria to be met to confirm diabetes in patients. The first would be symptoms of diabetes which include thirst, polydipsia, loss of weight and polyuria are seen in patients and their casual plasma glucose à ¢Ã¢â‚¬ °Ã‚ ¥ 11mmol/L. The other two would be if patients fasting plasma glucose à ¢Ã¢â‚¬ °Ã‚ ¥ 7.0mmol/L and patients 2-hours plasma glucose à ¢Ã¢â‚¬ °Ã‚ ¥ 11.1mmol/L during OGTT being conducted by giving the patient 75g of glucose load6. OGTT is the most effective test to detect glucose metabolism disorder where it assesses the rate of glucose excretion after administration of glucose. OGTT is strongly recommended when fasting blood glucose is within 7.0-7.8 mmol/L in the diabetic range where OGTT is practical to clarify the diagnosis6,8. Summary of Drugs Pharmacology Aspirin Aspirin with the dose of 150mg is used as an anti-platelet agent or as prophylaxis to cardiovascular events. The mechanism of action of aspirin as an anti-platelet agent is strongly associated with the permanent inactivation of prostaglandin synthase and cyclooxygenase12. It also inhibits the formation of thromboxane in the platelet concurrently. The common side effects of aspirin include bronchospasm, gastrointestinal haemorrhage and also other forms of haemorrhage13. Lovastatin Statin reduces the risk of cardiovascular disease events without taking into account of the serum cholesterol concentration and is often used as the drug of first choice in the primary and secondary prevention of cardiovascular disease. The mechanism of action of statins involves competitive inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, which is the enzyme involved in the synthesis of cholesterol13. As liver is the major site of cholesterol biosynthesis, it appears to be the main target organ for the statins14. Statins can cause several muscular adverse effects which include myositis and other side effects include gastrointestinal disturbances, sleep disturbances, dizziness, paraesthesia, fatigue, sexual dysfunction and alopecia13. Metformin Metformin is so far the only biguanide available in the market now. It is an antihyperglycemic agent that improves glucose tolerance in patients with type 2 DM by decreasing both the intestinal absorption of glucose and the hepatic glucose production, and improves insulin sensitivity in the tissues. Metformin was also found to have potentially favourable effects on decreasing serum lipid levels and fibrinolytic activity15. Gastrointestinal side effects such as nausea, abdominal pain and diarrhoea are common with metformin and may persist in some patients13. Lactic acidosis due to metformin is rare, and the risk of this complication is higher in patients with renal impairment13,15. Amlodipine Amlodipine falls in the calcium channel blockers group which act by interfering with the inward entrance of calcium ions via slow channels present in the active cell membranes. They act mainly on the myocardial cells and the vascular smooth muscle cells which then lead to reduction of myocardial contractility. It affects both the electrical impulses and vascular tone within the heart where they may be depressed or diminished13. 2.2.5 Perindopril Perindopril is an angiotensin converting enzyme (ACE) inhibitor where it acts by inhibiting the conversion of angiotensin I to angiotensin II. ACE inhibitors are the preferred initial drug to be used for hypertension13. ACE is the enzyme that converts angiotensin I to angiotensin II where angiotensin II causes increase blood pressure, systemic vasoconstriction, Na2+ and fluid retention and etc16. Thus, ACE inhibitors act by directly blocking the formation of angiotensin II and also increase the bradykinin level at the same time. This results in reduced vasoconstriction and increased vasodilation through the release of bradykinin. The common side effects of perindopril include profound hypotension, dry cough, angioedema, rash and gastrointestinal disturbances13. Actrapid (Soluble Insulin) Insulin plays an important role in the regulation of carbohydrate, protein and fat metabolism where it helps to increase the glucose utilization in human body. Actrapid, soluble insulin, is a short acting form of insulin where it is normally injected into patients 15 to 30 minutes pre-meal. Actrapid is normally given in emergency cases especially in patients suspected with diabetic ketoacidosis4. It is normally administered subcutaneously as it gives a rapid onset of action (30 to 60 minutes) and a longer duration of action of up to 8 hours. One of the potential problems of insulin is hypoglycaemia where patients can be advised on how to avoid it13. 2.2.7 Glyceryl Trinitrate (GTN) Nitrate plays a key role in the prophylaxis and treatment of angina. It causes direct relaxation on vascular smooth muscles and also dilation of the coronary vessels which improves oxygen supply to the heart. Dilation of the blood vessels results in reduction of preload and afterload and thus, myocardial oxygen consumption is reduced17. Sublingual form of GTN is one of the most effective drugs to provide a fast symptomatic relief of chest pain but it is of short duration of action. Dose of 300mcg is appropriate as the starting dose for patients who have not used GTN before previously. Side effects of nitrates include postural hypotension, tachycardia, dizziness, throbbing headache and possible nausea, vomiting, flushing and heartburn13. 2.2.8 Oxygen Oxygen is normally prescribed for patients experiencing hypoxia to raise the alveolar oxygen tension and to lessen the workload of breathing in patients. There are generally four types of oxygen therapy which include long term oxygen therapy, short burst oxygen therapy, emergency oxygen and ambulatory oxygen. It is commonly given in emergency cases to achieve oxygen saturation within the normal range, just like in this case. The administration of the correct oxygen concentration is important as inappropriate concentration of oxygen may result in serious or fatal outcomes13. Evidence for Treatment of The Condition. Metformin Metformin is one of the main therapeutic drugs used in managing Type 2 DM and many clinical studies have been conducted to support the clinical use of metformin in the management of type 2 DM. In one of the Cochrane Review, it confirms that metformin as a single agent is one of the key therapeutic options for type 2 DM in patients with overweight or obesity problems, as it may prevent some cardiovascular complications events and mortality as well. Just as mentioned in this patient, he is a newly diagnosed diabetes patient who is overweight and he was given metformin 500 mg twice daily. In the study, 29 trials with 5259 participants were included in the analysis, comparing metformin (2007 participants) with sulphonylureas (1167), placebo (702), diet (493), thiazolidinediones (132), insulin (439), meglitinides (208), and glucosidase inhibitors (111). Obese patients who are given metformin as blood glucose control agent showed a superior benefit than glibenclamide, chlorpropamide, or insulin for any diabetes-related consequences (P = 0.009), and for mortality (P = 0.03). Besides that, patients assigned to metformin as a single therapy showed a significant greater benefit for blood glucose control, weight, dyslipidaemia, and blood pressure18. Besides that, the Comparative Outcomes Study of Metformin Intervention versus Conventional (COSMIC) study was done to compare the incidence of serious adverse effects, mortality and hospitalization in patients receiving metformin and also those who are on other usual care treatments. Among the patients, 7,227 of them received metformin and another 1,505 of the patients received usual care. To the end of the study, there were only 89.7% of the metformin group and 76.9% of the usual care group remained receiving their initial intended treatment. Serious adverse events were reported in 10.3% of the metformin group and in 11.0% of the usual care group, where both the groups reported similar adverse events. Cardiovascular events were found to be the most ordinary cause of death in DM patients where 0.7% occurred in metformin group while 0.9% in usual care group19. A population-based cohort study was also done to study on the mortality rates with the use of sulphonylureas compared to metformin. The mean age of the patients was 66.3 ±13.4 years old where 43.4% were female and their mean length of follow-up was 4.6 ±2.1 years. A greater risk of mortality was observed with higher daily doses of the first-generation sulfonylureas and glyburide but not metformin20. 3.2 Insulin secretagogues (Sulphonylureas and Meglitinides) Sulphonylureas is another group of antidiabetic treatment used after metformin in Type 2 DM. Patients blood glucose level remained high on day 2 and thus should be monitored closely after administering metformin. If blood glucose level has not been brought down, addition of sulphonylureas or meglitinides should be considered. The sulphonylureas act by enhancing insulin secretion. The sulphonylureas act at the pancreatic ÃŽÂ ²-cell membrane by causing closing of ATP-sensitive potassium (K+) channels. Closure of the channels occurred when sulphonylurea binds to the sulphonylurea receptor (SUR) subunit of the K+ channel. Meglitinides, which is not a sulphonylurea, act through the same mechanism where it also binds at the sulphonylurea binding site. Examples of sulphonylureas include tolbutamide, gliclazide, glibenclamide and glimepiride. Meglitinides is referred as an alternative to sulphonylureas as it does not cause additional stimulation of insulin excretion when patient failed to respond to maximal dosage of sulphonylureas. Examples of meglitinides include repaglinide and nateglinide21. Adding on a sulphonylurea or meglitinide to metformin as a therapy to type 2 DM was found to have a better control of blood glucose level. 318 patients (61 from metformin group, 126 from glimepiride group and 131 from glimepiride + metformin group) completed the study to compare the effectiveness of metformin monotherapy, glimepiride monotherapy and the combination treatment in controlling blood glucose level. It was found that the greater efficacy of combination treatment in reducing HbA1c levels than either glimepiride alone (p Comparison was conducted in a study where 124 patients were randomly given either repaglinide 1 mg daily or glimepiride 1 mg daily. The dose of study drug was given over an 8 week titration duration, which then followed by a 12 months treatment length. FPG levels, HbAlc values and PPG levels significantly fall from baseline in both groups after 6 and 12 months of treatment. However, after 12 months, fasting plasma insulin (FPI) levels on the other hand were significantly increased in the repaglinide group (p So far, the most commonly reported adverse event in sulphonylureas was hypoglycaemia. 605 people over 34,052 person-years were diagnosed with hypoglycemia during sulphonylurea therapy, which equals to an annual risk of 1.8%24. There is also high risk of hypoglycaemia in diabetic patients who are taking ACE inhibitors at the same time. Therefore, the use of sulphonylureas in this patient should be used in caution as he is currently taking perindopril as his anti-hypertensive drug. Several studies suggested that there is an increase in mortality due to cardiac events in patients treated with sulphonylureas. In one of the studies, 120, 4138 and 1537 patients were given a first-generation sulfonylurea, glyburide monotherapy and metformin monotherapy respectively. 24.8% of the total deaths were found to be due to an acute ischaemic event. Those given first-generation sulfonylurea monotherapy had the highest mortality (67.6 deaths per 1000 person-years), compared with metformin monotherapy users (39.6 deaths per 1000 person-years). As higher doses are used, higher rates of death are observed as compared to those who are on lower doses20. Other less common side effects of sulphonylureas include weight gain, nausea, diarrhoea, gastrointestinal pain and cutaneous reactions such as rashes, urticaria and pruritus21. Further Management Thiazolidinediones, gliptins (GLP-1) mimetic, also known as exenatide and insulin administrations are the further management in type 2 DM if the above oral anti-diabetic agents are not able to control the high blood glucose level. Pioglitazone and rosiglitazone are examples of thiazolidinediones where they are the newer oral anti-diabetic agents which are more expensive but present better adverse effects profiles. A thiazolidinedione can be added on instead of a sulfonylurea as second-line therapy if sulphonylurea is contraindicated or not well tolerated or it can be added on to the sulphonylurea therapy if metformin is contraindicated. Another recommendation is to add on a thiazolidinedione to metformin plus sulphonylurea when the blood glucose is not well controlled and the use of insulin therapy is not suitable25. Two randomised trials were conducted and in the first study, 317 patients who are already on metformin received an add-on therapy of pioglitazone at the dose 15-45 mg/day and another 313 patients received gliclazide at the dose 80-320 mg/day instead. In the second study, 319 patients who are already on sulphonylurea therapy were randomly assigned to receive add-on therapy of pioglitazone at the do se 15-45 mg/day and another 320 with metformin at the dose of 850-2,550 mg/day. After 2 years, the mean reduction in HbA1c from baseline was found to be 0.89% for pioglitazone and 0.77% for gliclazide addition to metformin. The reduction in mean FBG after 2 years was statistically significant between the two add-on therapies where a decrease of 1.8 mmol/L for pioglitazone and a decrease of 1.1 mmol/L for gliclazide was seen (p Another option is adding on a GLP-1 mimetic agent as third-line therapy to first-line metformin and a second-line sulfonylurea25. Effectiveness of exenatides in bringing down the blood glucose level in type 2 DM patients was extensively studied. One of the studies includes patients at the age of 22-76 years old and had type 2 DM treated with at least the maximally effective dose of a sulfonylurea as monotherapy for at least 3 months. After a 4 weeks single-blind, placebo period, 377 patients were randomized (60% men, age 55 ±11 years, BMI 33 ±6 kg/m2, HbA1c 8.6 ±1.2%) and began either at 5  µg subcutaneous exenatide twice daily(before breakfast and dinner; arms A and B) or placebo for 4 weeks. Patients in arm B were then increased to 10  µg bd of exenatide. At week 30, HbA1c changes from baseline were -0.86 ±0.11, -0.46 ±0.12, and 0.12 ±0.09% ( ±SE) in the 10- µg, 5- µg, and placebo arms respectively (p à ¢Ã¢â‚¬ °Ã‚ ¤ 0.001). FPG values also showed a significan t reduction in the 10- µg arm compared to the placebo arm (P à ¢Ã¢â‚¬ °Ã‚ ¤ 0.05) 28. If all else fails to control blood glucose, insulin therapy should be introduced in patients with poorly controlled type 2 DM. It was believed that there is possibility that the oral anti-diabetic agents mentioned above might be useful in combination with insulin therapy in enhancing better blood glucose control, reducing insulin dose requirement, or minimizing side effects of insulin therapy. A study was conducted to compare the efficacy of adding once-daily basal insulin with switching to twice-daily premixed insulin in type 2 DM patients uncontrolled by oral anti-diabetic agents (OADs). It was a 24 weeks period clinical trial where 371 patients with poor glycaemic control (FBG à ¢Ã¢â‚¬ °Ã‚ ¥120 mg/dl, HbA1c 7.5-10.5%) were randomized to once-daily morning insulin glargine plus glimepiride and metformin or to only 30% regular/70% human NPH insulin (70/30) twice daily without any OADs. It was found that mean HbA1c decrease from baseline was significantly better in the presence of O ADs than the one without OADs (p = 0.0003). More patients reached HbA1c à ¢Ã¢â‚¬ °Ã‚ ¤7.0% without confirmed nocturnal hypoglycemia (45.5 vs. 28.6%, p = 0.0013) with glargine plus OAD than with only 70/30 NPH insulin. In addition, decrease in FPG was greater with glargine plus OAD (p Conclusion In this patient, he was newly diagnosed with type 2 DM and was given metformin 500mg twice daily initially to control his high blood glucose level, which was appropriate according to the guideline. If blood glucose is still not well controlled, changing of medication or further management as above should be considered. As hypertension and overweight are risk factors of DM, hypertension should be well managed in this patient and the patient should be advised on complying with his medication. Besides that, patient should also be advised on healthy diet and lifestyle to control his weight.

Advancements in Medical Research Due to Hela Cells

Katrina Samborski Honors English 1100 Dr. Nicole Caswell November 10, 2012 Advancement of Medical Research from HeLa Cells HeLa simply stands for Henrietta Lacks, a young mother in the 1951 who went to the doctor complaining of vaginal bleeding and discovered she had cervical cancer. Henrietta’s cells were taken for a biopsy and were found to be like nothing ever seen before; her cells were immortal. Her cancer cells double every 20 to 24 hours and have lived on for the past 60 years. Since HeLa cells were created, our world of modern medicine has been completely changed.We now vaccines for once incurable diseases and have used the cells for cloning and other biomedical research. Although the cells have done a great deal of good, they have also caused substantial harm to Henrietta Lacks, her family, and potential trial research participants. Therefore, though some may think it was ethically wrong of Henrietta Lacks’ doctors to not inform her that they were using her cel ls, she is the reason we have been able to save thousands of lives. It was at Johns Hopkins Hospital when Dr.Gey, a prominent cancer and virus researcher, discovered Henrietta’s cells were immortal. Since cancer cells will die outside the body without the right mix of chemicals, Dr. Gey created the roller tube. This contraption held glass tubes containing samples in nutrient-rich fluids, turned slowly – sometimes just two revolutions an hour, exposing the cells to just the right mix of air and nutrients. When Henrietta’s cells were placed in this device, they never stopped dividing. While their research value is unquestioned, the tumor cells had created havoc in Henrietta Lacks' body.Skloot recounts the lab technician Mary Kubicek who was present at the autopsy. â€Å"The tumors had completely blocked her urethra, leaving doctors unable to pass a catheter into her bladder to empty it. Tumors the size of baseballs had nearly replaced her kidneys, bladder, ovarie s and uterus. And her other organs were so covered in small white tumors it looked as if someone had filled her with pearls† (Williams). Although her cells are cancerous, HeLa cells share many traits with normal cells, making them useful in studying protein synthesis, the human genome and how viruses work. Dr.Gey sold the cells to researchers around the world, who used them to develop a variety of medicines. HeLa cells were the first to travel into space in an unmanned satellite to see if humans could survive zero gravity. â€Å"This cell line is used all around the world and revolutionized cell biology because they grew so well in culture, said William Earnshaw, principal research fellow at the University of Edinburgh's Centre for Cell Biology. â€Å"They yielded a huge amount of information,† Earnshaw said (Sharp). In the early 1950s, the world experienced the biggest polio pandemic in history.Jonas Salk devised the world's first polio vaccine, but testing it would r equire huge supplies of live cells that, at the time, would have involved the sacrifice of thousands of monkeys. HeLa cells proved to be technically more suitable for testing, and much less expensive and messy, than using monkeys. Moreover, HeLa cells grew virtually anywhere and on any surface, including while floating on liquid. A HeLa mass production and distribution center was therefore established at the Tuskegee Institute, ironically at exactly the same time that the infamous Tuskegee syphilis study on black subjects was being carried out.Soon HeLa cells were to enable the first disaggregation of chromosomes, numerous discoveries from genetic and viral studies, and the first-ever cloning of a cell, gene mapping, in vitro fertilization and much, much more. (Ncayiyana) HeLa cells have had a positive influence on medicine in many ways including with giving us knowledge about the human papillomavirus (HPV) DNA and HPV18-positive. HeLa cells have been linked to changes in microRNA e xpression. Since HPV18 has been associated with very aggressive adenocarcinomas, this finding may explain why Dr.Gey was surprised by the prolific growth of HeLa cells in culture. Routine Papanicolaou smear screening may not detect rapidly progressive cervical carcinomas; the new HPV vaccine holds the promise of preventing these tumors. (Hutchins). The problem of possible contamination of other long-term cultured tumor cell lines with HeLa cells not only caused an international embarrassment, but also raised the concern of misattributing a specific property so another cell line, for example, a virus or a tumor-specific marker, which actually belongs to HeLa.With the continued and growing use of tissue culture in biochemist research, intra- and interspecific contamination becomes a significant risk. The determination of stable genetic markers on cultured cells is a powerful tool for monitoring such contamination. Recent experiments in which cultured cells and innumerable clones of so matic cell hybrids have been used for genetic analysis have shown that, with the proper use of polymorphic markers to characterize the cells, the possibility of undetected cross contamination of cultures is no longer the problem it once may have been.Therefore, in an effort to clarify the characteristics of the HeLa cell and establish its probable genotype for better-known polymorphisms, we studied HLA and other markers, in the surviving husband and children of Henrietta Lacks. (Hsu) Not only were there several negative effects for Henrietta Lacks, but the general public has found flaws with HeLa cells as well. The Drug Information Association sponsored a workshop that brought together people who deal with facilitating or regulating the collection of clinical specimens for genetic analyses to complement drug trials.Genetic studies of clinical samples have for years had to negotiate a tricky path through informed consent, confidentiality, and regulatory-oversight, but according to a couple of speakers who noted the Henrietta Lacks story, the 19 months since the book's publication have made some people even more wary of this research. â€Å"I think it was disconcerting to people who are not used to thinking about how specimens are handled, that their specimens could outlive them,† said the meeting's main organizer and chair, Amelia Wall Warner, Ph. D. who heads clinical pharmacogenomics and clinical specimen management for the drug company Merck. The Skloot book seems to be creating a lot of conversation, with patients often asking for a menu of consent that large-scale trials with many thousands of patients can't accommodate, she noted. (Zoler) Although there are accusations against doctors and corporations that bought these cells stating they did so without Henrietta Lacks’ consent, we owe our world of modern medicine to her. Her cells allowed us to research and experiment countless diseases and opened the door to learn about the human enome and cancer cells. Dr. Gey said, â€Å"It was the best of times, it was the worst of times. † It was the best of times for science in that this very peculiar tumor gave rise to the HeLa cell line, which has been available for the various studies referred to by others. For Mrs. Lacks and the family she left behind, it was the worst of times. Scientific progress and indeed progress of all kinds is often made at great cost, such as the sacrifice made by Henrietta Lacks† (Jones). While her family has yet to be compensated, HeLa cells continue to be used everyday in the medical field.Works Cited: Ncayiyana, Daniel J. â€Å"The extraordinary story of the life after death of Henrietta Lacks. †Ã‚  South African Medical Journal  101. 3 (2011): 141. Health Reference Center Academic. Web. 12 Nov. 2012. Grover M. Hutchins, Brendan P. Lucey, and Walter A. Nelson-Rees. Archives of Pathology & Laboratory Medicine. 133. 9  (Sept. 2009)  p1463. Word Count: 4083. Jones HW Jr â₠¬â€œÃ‚  Am J Obstet Gynecol  Ã¢â‚¬â€œ 01-JUN-1997; 176(6): S227-8 MEDLINE ® is the source for the citation and abstract of this record   Susan H.Hsu, Bernice Z. Schacter, Nancy L. Delaney, Thomas B. Miller, Victor A. McKusick, R. H. Kennett, J. G. Bodmer, D. Young and W. F. Bodmer Science  , New Series, Vol. 191, No. 4225 (Jan. 30, 1976), pp. 392-394 Published by:  American Association for the Advancement of Science Article Stable URL: http://www. jstor. org/stable/1741942 Mitchel Zoler. Internal Medicine News. 44. 17  (Oct. 15, 2011)  p63. Word Count: 433. Williams, Nigel. â€Å"Prize For the HeLa Cell Story. †Ã‚  Current Biology  20. 23 (2010): n. ag. Sciverse. com. Web. 11 Nov. 2012. Manfuso, Jamie, and Stephanie Desmon. â€Å"Honoring the Henrietta Lacks Legacy at Hopkins. †Ã‚  Hopkins Medicine Magazine. Johns Hopkins, 20 May 2011. Web. 11 Nov. 2012. Hepworth, Jeri, PhD. â€Å"Advocacy for Henrietta Lacks and Family Medicine. † Editorial. Fam ily Medicine  Sept. 2011: 595-96. Society of Teachers of Family Medicine. Web. 11 Nov. 2012. Sharp, Rob. Life and afterlife of a women who will live for ever. The Independent. November 10 2010. Web. Nov 12 2012.

An Analysis of the Social Gradient of Health Essay

â€Å"The demonstration of a social gradient of health predicts that reducing inequality itself has health benefits for all, not simply for the impoverished or deprived minorities within populations. † (Devitt, Hall & Tsey 2001) The above quote from Devitt, Hall and Tsey’s paper is a relatively well grounded and well researched statement which draws on contemporary theoretical sociological concepts to support the assertion that reducing inequality is the key to improving health for all. However the assertion that the demonstration of a social gradient of health predicts that a reduction in inequality will lead to health benefits for all is a rather broad statement and requires closer examination. The intention of this essay is to examine the social gradient of health, whose existence has been well established by the Whitehall Studies (Marmot 1991), and, by focusing on those groups at the lower end of the social gradient, determine whether initiatives to address inequalities between social classes will lead to health benefits for those classes at the lower end of the social scale. The effectiveness of past initiatives to address these social and health inequalities will be examined and recommendations made as to how these initiatives might be more effective. The social gradient described by Marmot and others is interrelated with a variety of environmental, sociopolitical and socioeconomic factors which have been identified as key determinants of health. These determinants interact with each other at a very complex level to impact directly and indirectly on the health status of individuals and groups at all levels of society; â€Å"Poor social and economic circumstances affect health throughout life. People further down the social ladder usually run at least twice the risk of serious illness and premature death of those near the top. Between the top and bottom health standards show a continual social gradient. † (Wilkinson & Marmot 1998) In Australian society it is readily apparent that the lower social classes are at greater disadvantage than those in the upper echelons of society; this has been discussed at length in several separate papers on the social gradient of health and its effects on disadvantaged Australian groups (Devitt, Hall & Tsey 2001, Robinson 2002, Caldwell & Caldwell 1995). Within the context of the social gradient of health it can be inferred that Indigenous groups, for example, are particularly susceptible to ill health and poor health outcomes as they suffer inordinately from the negative effects of the key determinants of health. A simple example of this is the inequality in distribution of economic resources: â€Å"Average Indigenous household income is 38% less than that of non-Indigenous households. † (AHREOC 2004). The stress and anxiety caused by insufficient economic resources leads to increased risk of depression, hypertension and heart disease (Brunner 1997 cited in Henry 2001). Higher social status and greater access to economic resources is concomitant with a reduction in stress and anxiety levels, as individuals in these groups have more control over economic pressures which create this stress. This simple comparison proves that the social gradient of health accurately reflects how socioeconomic determinants affect the health of specific social classes at the physiological level. An extension of the research into the social gradient and the determinants of health is the examination of the pathways through which specific social groups experience and respond to these determinants. These ‘psychosocial pathways’ incorporate psychological, behavioural and environmental constraints and are closely linked to the determinants of health; â€Å"Many of the socio-economic determinants of health have their effects through psychosocial pathways. † (Wilkinson 2001 cited in Robinson 2002). These pathways have been demonstrated by Henry (2001) in the conceptual model of resource influences (Appendix A), a model which illustrates the interaction between the constraints mentioned above and their impact on health outcomes. Henry states that a central differentiator between classes is the amount of control an individual feels they have over their environment. Whereas an individual from a lower class group holds a limited sense of control over their well being and consequently adopts a fatalistic approach to health, those in higher classes with a stronger sense of control over their health are more likely to take proactive steps in ensuring their future wellbeing. This means that both individuals will cope differently with the same health problem. This is partly as a result of socioeconomic or environmental determinants relative to their situation, but it is also a result of behavioural/physical constraints and, most importantly, the modes of thought employed in rationalising their situation and actions. In essence these psychosocial pathways occupy an intermediate role between the social determinants of health and class related health behaviours. This suggests that, while the social gradient of health is a good predictor of predisposition to ill health among specific classes, it cannot predict how reducing inequality in itself will affect health outcomes or how a specific social class will respond to these changes. An examination of some initiatives aimed at reducing inequality in the indicators of health outcomes reveals this problem; â€Å"In 1996 only between 5% and 6% of NT Aboriginal adults had any kind of post secondary school qualification compared with 40% of non-Aboriginal Territorians. † (ABS 1998). Within the context of the social gradient of health, education is an important indicator of health outcomes. It is evident from the quote above that there exists huge inequality within the Northern Territory education system; this suggests an increased likelihood of ill health for Aboriginal people in later life. Even though there have been initiatives to address this inequality in one of the indicators of health outcomes (Colman 1997, Lawnham 2001, Colman & Colman 2003), they have had only a minimal impact on Indigenous second level education rates (ABS 2003). This is partly due to the inappropriateness of these initiatives (Valadian 1999), but it is also due to the disempowerment and psychosocial malaise (Flick & Nelson 1994 cited in Devitt, Hall & Tsey 2001) which are a feature of Indigenous interaction and responses to the social determinants of health. Research has also been carried out into how effecting change in the inequalities in other indicators of health might affect health outcomes. Mayer (1997) cited in Henry (2001) examined the effects of doubling the income of low income families and concluded it would produce only modest effects. Henry believes that this points to the strong influence of the psychological domain in influencing health behaviours. This suggests that the key to better health for all lies not just in reducing inequality between the classes but also in changing those elements of the psychological domain which influence health behaviour. Another example of the gap between initiatives to reduce inequality and their impact on those inequalities is evident in an examination of economic constraints experienced by Indigenous Australians on social welfare. Price and McComb (1998) found that those in Indigenous communities would spend 35% of their weekly income on a basket of food, compared to just 23% of weekly income for those living in a capital city for the same basket of food. To combat this inequality it would seem logical to reduce the price of food in Indigenous communities or else increase the amount of money available to those living in remote communities, i. e. a socioeconomic approach. It has already been established that increasing income has only modest effects and in combination with the fact that smoking, gambling and alcohol account for up to 25% of expenditure in remote communities (Robinson 2002), how can it be guaranteed that the extra funds made available through either of the two suggestions above would be employed in achieving a desirable level of health? One possible suggestion is that a socioeconomic approach must be complemented by a psychosocial approach which addresses those abstract modes of thought, cultural norms and habits and health related behavioural intentions which dictate healthful behaviours. â€Å"Culture and culture conflict are factors in Aboriginal health. But instead of the emphasis being placed on Aboriginal failure to assimilate to our norms, it should rather be put on our failure to devise strategies that accommodate to their folkways. † (Tatz 1972 cited in Humphrey & Japanangka 1998) Any initiative which hopes to resolve inequality in health must incorporate a sound understanding of the influence of the psychosocial pathways relative to the class level and cultural orientation of that group, otherwise its success will be modest at best. Using Henry’s model of resource influences provides a framework for understanding how addressing these psychosocial pathways can lead to greater uptake of initiatives designed to address these inequalities. An analysis of the National Tobacco Campaign (NTC 1999) reveals how this initiative failed to impact significantly on Indigenous smoking rates. This was a purely educational initiative which aimed to raise awareness of the effects of smoking on health. One of the primary flaws of its design was its failure to even acknowledge those Indigenous groups at the lower end of the social scale; it also failed to communicate the relevance of its message to Indigenous people; â€Å"The only thing is that when it comes to Aboriginal people, they will not relate to Quit television advertisements because they don’t see a black face†¦. I’ve heard the kids say ‘Oh yeah, but that’s only white fellas’. They do. † (NTC 1999) Not only did this initiative fail to connect with Indigenous people, it also failed to influence the elements of the psychological domain which legitimate such high rates of smoking. Within Indigenous culture smoking has become somewhat of a social practice, with the emphasis on sharing and borrowing of cigarettes (Gilchrist 1998). It is ineffectual to put across messages about the ill effects of smoking if the underlying motivation of relating to others is not addressed. In a report conducted on Indigenous smoking (AMA & APMA 2000 cited in Ivers 2001), it was suggested that one of the key themes of an initiative aimed at reducing indigenous smoking rates should be that smoking is not a part of Indigenous culture. The ‘Jabby Don’t Smoke’ (Dale 1999) is an example of an initiative whose design attempted to influence accepted social norms. Its focus was primarily on children, thereby acknowledging the importance of socialization and the instillation of cultural norms at an early age. Unfortunately no data is available detailing its impact on smoking rates. As mentioned earlier in this essay, another feature of the psychological domain which has an effect through the psychosocial pathways is the modes of thought employed in rationalising actions and responses to various determinants and constraints. Self efficacy or the amount of perceived control over one’s situation is an important contributor to health status; â€Å"Empowered individuals are more likely to take proactive steps in terms of personal health, whilst disempowered individuals are more likely to take a fatalistic approach† (Henry 2001) Examples of initiatives which have strived to empower Indigenous people in being responsible for their own health include ‘The Lung Story’ (Gill 1999) and various health promotion messages conveyed through song in traditional language ( Castro 2000 cited in Ivers 2001, Nganampa Health Council 2005). By encouraging Indigenous people to address these issues in their own way, the amount of perceived control over their own health is increased thereby facilitating a greater degree of self efficacy. The intention of this essay has not been to deny that the social gradient of health does not exist or that it is not an effective tool in creating understanding of where social and health inequalities lie. Unfortunately programs and initiatives which have been guided by the social gradient of health and have been purely socioeconomic in their approach have failed to have a significant, sustainable effect on health inequalities. In the US, despite socioeconomic initiatives to resolve inequality, the gap between upper and lower class groups has actually widened in recent times (Pamuk et al 1998 cited in Henry 2001). The scale of the intervention required to ensure a sustained impact on health inequalities has been discussed by Henry (2001), he also highlights the need to garner substantial political will in order for these changes to happen and makes the point that those in the upper classes are relatively content with the present status quo. This essay has attempted to demonstrate that in an environment where well grounded, evidence based socioeconomic initiatives are failing to have the desired out comes, it is perhaps time to focus more on altering those strongly held health beliefs which not only dictate responses to social determinants of health but also dictate responses to initiatives designed to address these inequalities; â€Å"Healthful behaviours are due to more than just an inability to pay. A mix of psychological characteristics combines to form distinctive behavioural intentions†. (Henry 2001) In the current environment of insufficient political will and finite resources it would be prudent to use every tool available to ensure initiatives aimed at reducing inequality between the classes will have the maximum amount of benefit. This approach is not a long term solution, but until it is possible to achieve the large scale social remodelling necessary to truly remove social inequality, and consequently health inequality, it is the most viable solution available. REFERENCES. ABS, 2003. ‘Indigenous Education and Training’, Version 1301. 0, A Statistical Overview, Australian Bureau of Statistics, Canberra, viewed 22nd August 2005, http://www. abs. gov. au/Ausstats/abs@. nsf/Lookup/FC7C3062F9C55495CA256CAE000FF0D6 A statistical overview of Aboriginal and Torres Strait Islander peoples in Australia 2004, Australian Human Rights and Equal Opportunities Commission (AHREOC), Sydney, viewed 20th August 2005, http://www. hreoc. gov. au/social_justice/statistics/. Brunner, E. 1997. ‘Stress and the Biology of Inequality’. British Medical Journal. No. 314, pp 1472-1476. Castro, A. 2000. ‘Personal Communication’. No other details available. Caldwell, J. & Caldwell, P. 1995. ‘The cultural, social and behavioural component of health improvement: the evidence from health transition studies’, Aboriginal Health: Social and Cultural transitions: Proceedings of a Conference at the Northern Territory University, Darwin 28-30th September. Colman, A. 1997. ‘Anti-racism Course’, Youth Studies Australia, Vol. 16, Issue 3, p. 9, viewed 22nd August 2005, EBSCOhost Database Academic Search Premier, item: AN 12878155. Colman, A. & Colman, R. 2003. ‘Education Agreement’, Youth Studies Australia, Vol. 22, Issue 1, p. 9, viewed 22nd August 2005, EBSCOhost Database Academic Search Premier, item: AN 9398334. Dale, G. 1999. ‘Jabby Don’t Smoke, Developing Resources to Address Tobacco Consumption in Remote Aboriginal Communities’, Paper presented to the Eleventh National Health Promotion Conference, Perth. 23-26th May. Devitt, J. , Hall, G. , Tsey, K. 2001. ‘An Introduction to the Social Determinants of Health in Relation to the Northern Territory Indigenous Population’, Occasional Paper. Co-operative Research Centre for Aboriginal and Tropical Health. Darwin. Flick, B. , Nelson, B. 1994. ‘Land and Indigenous Health’, Paper No. 3, Native Titles Research Unit, Australian Institute of Aboriginal and Torres Strait Islander Studies, Canberra. Gilchrist, D. 1998. ‘Smoking Prevalence among Aboriginal Women’, Aboriginal and Islander Health Worker Journal, Vol. 22, No. 4, pp. 4-6. Henry, P. 2001. ‘An Examination of the Pathways through Which Social Class Impacts Health Outcomes’. Academy of Marketing Science Review, vol. 3, pp 1-26. Humphery, K. , Japanangka, M. D. , Marrawal, J. 1998. â€Å"From the Bush to the Store: Diabetes, Everyday Life and the Critique of Health Service in Two Remote Northern Territory Aboriginal Communities. † Diabetes Australia Research Trust and Territory Health Services, Darwin. Ivers, R. 2001. ‘Indigenous Australians and Tobacco; A Literature Review’, Menzies School of Health Research and the Cooperative Research Centre for Aboriginal and Tropical Health, Darwin. pp. 67-80, 93-107. Lawnham, P. 2001. ‘Indigenous Push at UWS’, The Australian, 27th June, 2001. p. 34, viewed 22nd August 2005, EBSCOhost Database Academic Search Premier, item: AN 200106061025662941. Marmot, M. G. , Davey Smith, G. , Stansfield, S. , Patel, C. , North, F. , Head, J. , White, I. , Brunner, E. and Feeney, A. 1991. ‘Health Inequalities among British Civil Servants: the Whitehall II Study’, Lancet, 337, 1387. reading 1. 5. Mayer, S. 2001. What Money Can’t Buy: Family Income and Children’s Life Chances. Harvard University Press, Cambridge, Massachusetts. National Tobacco Campaign. 1999. ‘Australia’s National Tobacco Campaign: Evaluation report Volume 1’. Commonwealth Department of Health and Aged Care, Canberra. Nganampa Health Council. 2005. Nganampa Health Council, Alice Springs. Viewed 23rd August 2005, http://www. nganampahealth. com. au/products. php Pamuk, E. , Makuc, D. , Heck, K. , Reubin, C. , Lochner, K. 1998. ‘Socioeconomic Status and Health Chartbook’. Health, United States. National Centre for Health Statistics, Maryland. Price, R. , & McComb, J. 1998. ‘NT and Australian Capital Cities Market Basket Survey 1998’. Food and Nutrition Update, THS, Vol. 6, pp. 4-5. Robinson, G. 2002. ‘Social Determinants of Indigenous Health’, Seminar Series, Menzies School of Health Research. Co-operative Centre for Aboriginal Health. Valadian, M. 1999. ‘Distance Education for Indigenous Minorities in Developing Communities’, Higher Education in Europe, Vol. 24, Issue 2, p. 233, viewed 22nd August 2005, EBSCOhost Database Academic Search Premier, item: AN 6693114. APPENDIX A. CCONCEPTUAL MODEL OF RESOURCE INFLUENCES. [pic] Henry, 2001. .

Essay Pro Euthanasia - 711 Words

Pro Euthanasia Most people want to live their life with dignity and die with dignity. People make important choices and decisions through out their life. Some of these decisions are very difficult and even life changing. We live in a democratic society where we are free to make these decisions. Death is an unavoidable event and happens to everyone. Death can be quick or it can make our love ones suffer miserably. Some people become very ill or have devastating physical problems they must deal with daily. They have a constitutional right to refuse treatment. Most patients trust in their doctor to help them deal with their illness. As their suffering increases, their self-respect decreases. A person should have the freedom to end their life†¦show more content†¦These events are also described in (1 Chronicles 10:3-7). Saul took his life because of his injuries. He knew when the Philistines arrived; he would be tortured and brutally killed by them. Saw knew his death would be dragged out l ike a helpless person, slowly and painfully dying, so he quickly killed himself. Think if someone you cherished was dying due to an organ failure or the need of a new organ. There are long waiting lists for hearts, kidneys, livers, and other organs that are necessary to save the lives of people who can be saved. Doctor-assisted suicide allows physicians to preserve vital organs that can be donated to others. However, if certain diseases are not stopped quickly and spread, the organs may weaken or stop working all together. Friends and family of the patient suffers just as much or more than the patient themselves. Death should not be a dragged out painful thing and Assisted suicide shows compassion for the dying(Rifkin 18). Right now there is a shortage of medical staff in this country, especially nurses. 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