Divorce Essays (1064 words) - Family Law, Childhood, Parenting

Divorce It seems that more and more marriages are falling apart everyday. Divorce rates seen to be climbing astronomically. In so many of these divorces there are children to be considered. What is best for the child? Who will get custody? Will the child be scarred for life? Its really hard to say. The overall effects on our children vary according to the factors involved. I am going to attempt to discuss a few of the problems that can occur with children of divorced families and what parents can do to ease the transition. I will limit this discussion to infantile age thru early elementary aged children. Lets start with understanding the parents role concerning being together or being apart. Obviously, two parents can provide children with far more guidance, sustenance, and protection than one, and are more likely to prevent the kinds of psychological disturbance that may result from deprivations of these necessities ...When one parent is temporarily absent from the intact home, it is likely that the other will be available to ratify the childs needs in a loving way. This is not so readily the situation in the divorced home. ( Gardner, 1977). In this statement he illustrates the importance of having both parents together. This can be emphasized further with a statement from Buchanan, Maccoby, and Dornbusch (1996). Childrens parents are their anchors. Parents provide the structure for childrens daily lives, and even when parents are not functioning very well, children depend on them for a sense of security that enables them to cope with their developmental tasks. When one parent leaves the home, the child realizes a shattering possibility; parents are not always there. It is not hard to realize that divorce can have a devastating effect on children. Lets brake it down by age groups; infants, toddlers, and so on. DeBorg (1997) states that infants do not understand conflict, but may react to changes in parents energy level and mood. She goes on to list possible reactions like loss of appetite; upset stomach - may spit up more; more fretful or anxious. She says that parents should keep their normal routines, and stay calm in front of the child. Toddlers understand that a parent has moved away, but doesnt understand why. I know that my son was very confused. He was only two when my wife and I separated. He seemed to display allot of anger and insecurity. DeBorg says that a toddlers reactions could include more crying, clinging; problems sleeping; regression to infant behaviors; and worry when parent is out of sight. My son, his name is Cody, definitely fits this profile. He cried constantly. It seemed that nothing would calm him down. If you got him to go to sleep, good luck keeping him there. As far as infant behaviors go, his biggest problems were wanting to be rocked like when he was younger and trying to go back to the bottle. DeBorg say to allow some return to infantile behaviors, but set clear limits. Easier said than done I can assure you. Pres choolers dont understand what separation or divorce means, they realize one parent is not as active in his or her life (DeBorg, 1997). Their reactions could include pleasant and unpleasant fantasies; feeling uncertain about the future; feeling responsible; and they may hold their anger inside. Deborgs first strategy listed for parents is to encourage the child to talk. This makes sense if you are concerned with straitening out these issues of anger and feeling responsible. It seems to be the only way to really understand your childs problems. Gardner (1977, p. 42) talks of something called the oedipal phase. He explains that this occurs between ages three and five. This is the period... when a child develops a strong possessive attachment to the opposite-sexed parent. Gardner says that at times the attraction can take on mildly sexual overtones toward the opposite-sexed parent..., but the sexual desires are generally not for intercourse, the child being too young to appreciate that act. He explains that if a boy begins sleeping in Mothers bed thoughout the night, an a continual basis, the likelihood that oedipal problems will arise is great... this holds true for

Fossil Fuels essays

Fossil Fuels essays We get energy from sunlight, wind, nuclear plants, and damns... However, most of the energy that we use comes from fossil fuels. There are three major fossil fuels: Coal, oil and natural gas. These are composed of carbon, hydrogen, nitrogen, oxygen and sulfur. Carbon is the major element in fossil fuels. We obtain energy from fossil fuels by burning them. Coal is the most abundant fossil fuel in the U.S. Yet it has a major disadvantage. It is a strong pollutant. When it is burned, it releases impurities like nitrogen and sulfur, which combine with water vapor to create acid rain. Also, coal is a major contributor to the imbalance of the carbon cycle. When coal burns, it forms carbon dioxide. Scientists believe that carbon dioxide traps the earths heat in a process called the greenhouse effect. However, scientists have developed new methods to burn coal more efficiently, filter impurities before they are released in the atmosphere, and cut down on the release of carbon dioxide. Oil is another important fossil fuel. It is found under tons of rock, deep in the earths crust. Precisely, oil is found in rocks, trapped in little pores. When an oil well is dug in the earth, pressure from the reservoirs will make the oil spurt to the top of the well. When oil is pumped out of reservoirs, about only  ¼ of the oil available will be accessible to the pumps. Scientists and engineers have yet to discover a method to collect the remaining  ¾ of oil. Often, natural gas is found with oil. In some cases, oil companies separate the two fossil fuels and inject the natural gas back into the reservoir, creating enough pressure to allow more oil to spring to the surface. Natural gas is a colorless, odorless gas. It is responsible for fueling over half of the United States homes appliances. Some countries have discarded natural gas because they think it is worthless. Precisely, there isnt enough natural g ...

LM3 Assignment Example | Topics and Well Written Essays - 2000 words

LM3 - Assignment Example The major characteristics that make it difficult to define leadership include; people from both public and private organization barely know the components of leadership whether it exist or it doesn’t. According to Denhardt, Denhardt & Aristigueta, p-189 â€Å"leadership is becoming one of the most widely debated but least clearly understood concepts† Secondly people have not yet understood that leadership has become so dynamic whereby, society has been described as â€Å"highly turbulent subject to sudden and dramatic shift† (Denhardt, Denhardt & Aristigueta, pp-189). Thirdly, people have not yet understood leadership requires corporation among all the concern parties, whereby, according to Denhardt, Denhardt & Aristigueta, pp-190, â€Å"Moreover, clients or citizens also want to participate, as well they should†. Additionally, lack some aspect of creativity and innovativeness with respect to leadership style has made it quite challenging to define leaders hip (Denhardt, Denhardt & Aristigueta, pp-190-192). This is because leadership style that may be applied in a particular organization may not be effective in another organization. Additionally, different organizations have different structures and may require different leadership styles (Denhardt, Denhardt & Aristigueta, pp-189-195). In above connection, future leadership is more of a shared process because current leadership was build based on the past leadership theories. This is according to Denhardt, Denhardt & Aristigueta, p-190 â€Å"we need to understand how leadership has been studied and practiced in the past†. Therefore, through past leadership, future leadership can have a reference point as well as a fundamental base of formulating the appropriate leadership styles to be applied in future organizations (Denhardt, Denhardt & Aristigueta, pp 189-192). However, it is important to consider that â€Å"leadership is changing in many ways, and we should be attentive to those changes† (Denhardt, Denhardt & Aristigueta, pp-190). In above connection, it can be scrutinized that, â€Å"In the past, a leader was considered the person who held a formal position of power in an organization or a society† (Denhardt, Denhardt & Aristigueta, p-190). However, through evolution of leadership, people have come to understand that leadership is a process that requires corporation and integration among all people within and outside the organization (Denhardt, Denhardt & Aristigueta, pp190-193).Additionally, leadership has taken a certain angle, whereby, decision makers should not only involve people from top management but should also involve those from lower levels of management (Denhardt, Denhardt & Aristigueta, pp 190-195).This is because when everybody is involved in decision making, people feel that they own those decision(Denhardt, Denhardt & Aristigueta, pp 190-195 2. How to our text authors define â€Å"moral imagination†? When is this t o be used? Why? What does it involve? The author has employed the concept of moral imagination to explain what moral leadership entails as well as moral issues. According to Denhardt, Denhardt & Aristigueta, pp 224-225, moral imagination entails â€Å"not just heightening attention to moral con-cerns, but rather carefully and thoughtfully understanding and evaluating

The Import-substitution Industrialisation (ISI) Failure in Argentina Essay

The Import-substitution Industrialisation (ISI) Failure in Argentina - Essay Example Center of discussion in this paper is import substitution industrialization in Argentina that depended on the exchange rate and trade restrictions. They included several exchange rates, import licenses, quotas, protective tariffs, and export taxes. The main aim was to limit external trade and prepared the domestic market for local manufactures. Further, another aim was to protect the domestic industries from stiff competition arising from external industries. The domestic industries were expected to compete internationally. However, these policies typically led to inefficient firms and high cost industrial substitutes. The consequences were diverse, for instance, the local industries could not pose any competitive challenge internationally. As a result, Latin Americans had to pay high prices for substandard goods that could not satisfy their need for quality. Further, Argentina was not able to have foreign exchange to pay for the much required imports; they had spent much time de-emp hasizing exports. ISI had actually led to some economic gains, however, by 1980s, it had been exhausted. During 1980s and 1990s, Argentina was forced to injstitute a number of policies with the aim of opening its economy, decrease the size of the government as well as improving efficiency. Other countries in the Latin America such as Brazil and Paraguay experience government involvement in infrastructure development and in the production sectors. However, the major difference between these countries and Argentina was the issue of funding. This issue was not well addressed in Argentina. The country began to use inflation taxation as the best solution to their problems. Inflation taxation occurs when the government decides to print money to pay the state bills. From the mid 1940s, Argentina witnessed huge difference in its rising inflation figures from the low inflation figures in other countries of the world (Zanetta, 2004). High inflation rates, high fiscal deficits and huge governm ent debts were the main challenges facing Argentina from 1940s to the end of the century. Several argentine citizens argued that the excessive government interference in the economy and the fiscal laxness were not the only problems that led to economic down turn in Argentina. Another challenge that faced Argentina was the relatively trained administrative personnel. The argentine government was not prepared to put in place policies that could lead to stable economic growth. Corruption also affected this problem as well (Birkbeck, 2011). President Peron’s earlier economic gains in Argentina quickly ran into a number of challenges. In 1949, Peron’s government witnessed inflation of about 31percent. This was due to Peron’s strategy of demand expansion through wage increases. At this time, employment was already high. Further, the controlling of imports and the stronger purchasing power siphoned off exports and led to inflation in Argentina (Birkbeck, 2011). In 1949 , Argentina was affected by its first foreign trade deficit since the First World War. In addition, the drought that affected Argentine’s agricultural export further affected argentine’s economy. Further, the terms of trade had started to work against the country. The terms of trade included the rising prices of imports and the decreasing prices of exports. Peron’s approach to economic growth was making the problems worse. For instance, in giving artificially low prices to farmers, to ensure that urban food

Political science Essay Example | Topics and Well Written Essays - 1500 words - 2

Political science - Essay Example In fact, national democracy is one of the key sources of such transactional cost, since it provides sovereign risk and regulates rules at the border. In addition, national democracy reduces chances of global risks by providing regulations and supervision of financial intermediaries (Rodrik, 212). Therefore, it is important that global federalism be adopted where democratic politics is aligned with global markets. Consequently, it is important that the national state is maintained and the needs of international economy are also catered for. As a result of this, the nation will in most cases pursue the objective of achieving global economic integration before considering other objectives. The national democracy can also be used in order to reduce the goals and visions of the international economic integration and going for limited globalization as was witnessed in post war in Bretton Woods’s regime where there was more capital control and minimal trade liberalization (Rodrik, 102). Although, this system led to failure of the approach given, it is thus important that for more globalization to be achieved, national democracy or national sovereignty must be reduced. Furthermore, this clearly illustrates that national democracy is one of the factors that determine the state and pace of globalization in a country. The potential effect of globalization is the reduction of national democracy, which also reduces global fiscal competition. In that sense, it is important that democracy be provided in a way that promotes civil rights, although this will lead to low economic growth but cause high social stability. In addition, this can help in expanding global civil rights (Rodrik, 110). This also clearly indicates that economics is an important political decision-making processes that requires global order. Furthermore, although globalization is one of the factors for economic growth in both rich and poor countries, it is currently producing a different result

Case Summary On The Effects Of Unstable Angina Nursing Essay

Case Summary On The Effects Of Unstable Angina Nursing Essay Mr AR is a 41 years old male. His calculated BMI was 20.9kg/m2. His presenting complaint was chest pain which has lasted for three days before being admitted into the hospital. His chest pain was of pressing type, it occurred even at rest and lasted for 5-10 minutes each time. It was relieved slightly by rest and it was always accompanied by numbness on his left hand. He had shortness of breath, orthopnea, headache and low effort tolerance. He complained of abdominal discomfort also. He had stopped taking all his medications for the past three days. He had a pacemaker fixed 16 years ago for his atrial fibrillation (AF), but the pacemaker stopped functioning 3 years ago. Due to financial constraint, he did not go for a new pacemaker replacement. He underwent an angiogram last year and was found that he has 2 blocked vessels. He has a history of hypertension too. Before being admitted into the hospital, he has been taking frusemide 40mg twice daily, hydrochlorothiazide 25mg once daily, perindopril 8mg once a day and amlodipine 10mg once a day for his hypertension. For his AF, he has been taking warfarin 5mg once daily and digoxin 125microgram once daily. In addition, he took simvastatin 40mg at night for the prevention of cardiovascular events. Mr AR was found to have poor compliance. He always missed the dose, took the medications at the wrong time and was unsure the reason behind taking all his medications. He was first admitted to the acute and emergency department. ECG was carried out and there was no ST-elevation. His blood pressure was found to be high, 172/126mmHg. No troponin test was done on Mr AR, the only available test results on cardiac enzymes were that of creatine kinase (CK), aspartate amino transferase (AST) and lactate dehydrogenase (LDH). All three were not elevated. Hence, he was diagnosed with unstable angina, gastritis and hypertensive urgency. He was given nifedipine 10mg, aspirin 300mg, Sublingual GTN and plavix 300mg in the acute and emergency department. His management plans were to monitor his vital signs every hourly for two hours followed by every two hourly and to carry out dextrostix test three times daily. He was given 60mg enoxaparin subcutaneously immediately and twice daily thereafter, intravenous ranitidine 50mg three times daily, sublingual glyceryl trinitrate (GTN) one tablet when required and IV frusemide 20mg twice daily. He was restricted to fliud intake of 800mL per day and started on fliud input and output monitoring. He will also be started on low salt diet for the management of his hypertension. On day 2, he no longer complained of chest pain. His potassium level was found to be slightly lower than normal range (3.3mmol/L). His BP was still high throughout the day, fluctuating at around 150/120mmHg. He was started on tablet clopidogrel 75mg once daily. On day 3, IV frusemide was changed to oral frusemide. On day 4 his blood pressure has already dropped to around 120/90 mmHg. He was planned for discharge and enoxaparin was to be stopped on that day. Disease overview and pharmacological basis of drug therapy Mr AR was diagnosed with 3 diseases. Only unstable angina will be discussed. Unstable angina (UA) is categorized under acute coronary syndrome (ACS) which is very common in the UK. According to the hospital episode statistic year 2002-2003, there were 83842 cases of UA in England and 4421 cases in Wales.1 UA happened when there is insufficient myocardial oxygen supply to meet the oxygen demand of the heart. The reduction in the oxygen supply is due to the disruption of artherosclerotic plaque, causing the formation of intracoronary thrombus and hence narrowing of artery. Abnormal vasospasm of the coronary arteries or coronary dissection may also lead to UA. UA is closely related to non-ST elevated myocardial infarction (NSTEMI) as they have the same pathogenesis and both are presented as chest pain. The only difference between them is that in NSTEMI, there is a rise in the cardiac biomarkers such as cardiac troponin or the MB isoenzyme of creatine phospokinase (CK-MB), which indicate s myocardial injury. In UA, the ischemia is not severe enough to cause damage to the myocardial cells and thus releasing these biomarkers in detectible amount. For the diagnosis of unstable, the patients history of anginal symptoms should be obtained. Physical examination like cardiac examination and vital signs monitoring may also be done. Patient with ongoing chest discomfort should have a 12-lead ECG performed within 10 minutes of onset to check if there is any ST-elevation or depression. If there is no ST elevation, STEMI will be ruled out and the level of serum cardiac biomarkers will be used to determine if the patient has UA or NSTEMI. Troponin I or T are normally the biomarker chosen for detecting myocardial cell death as it is detectable in the serum 3-6 hours after a myocardial infarction and remained raised for 14 days. If the serum troponin level is less than 0.01 Ã‚ ­g/L, then the patient will be diagnosed to have unstable angina. CK-MB may also be used when troponin test is not available. In Mr AR case, the results on the cardiac enzymes available, namely AST, CK and LDH are all non specific cardiac biomarkers as those enzy mes can also be elevated in skeletal muscle injury or liver disease. The treatment of UA can be divided into emergency treatment and secondary prevention treatment.2,3 Patients must rest in bed and ECG monitoring should be continued during the early phase of hospital stay. Sublingual glyceryl trinitrate (GTN) tablet or spray should be given for the relief of angina symptoms. GTN is a fast acting coronary vasodilators. Dilatation of veins going to the heart reduces ventricular volume and preload, while dilatation of systemic conductive arteries together with the decrease in ventricular volume causes a reduction in afterload. These effects will all reduce the myocardial oxygen demand.4 GTN also found to dilate collateral vessels, thus the areas of ischemia will receive a higher blood flow. If the chest pain is not relieved by GTN, intravenous morphine sulphate can be given to ensure patient comfort. Patient with ongoing chest pain or high risk patients should be given inravenous beta-blockers followed by oral route if there is no contraindication. Inter mediate or low risk patients can be given oral beta-blockers. If beta-blocker is contraindicated such as the in presence of uncontrolled heart failure, or the chest pain is not relieved by GTN and beta-blocker, nondihydropyridine calcium channel blocker can be given. Antiplatelet therapy should be given immediately by giving aspirin 300mg initially, followed by 75mg once daily for long term secondary prevention. In addition, clopidogrel 300mg should be given initially and 75mg daily thereafter for 3 months. Aspirin works by inhibiting the cyclooxygenase (COX) 1 enzyme on the platelet, thus preventing the production of thromboxane which stimulates platelet aggregation.5 Clopidogrel is an antiplatelet which acts by inhibiting adenosine diphosphate (ADP) from binding to its receptor, hence blocking the activation of ADP-mediated glycoprotein GPIIb/IIIa complex, a step involved in aggregation of platelets.6 Unfractionated heparin (UH) or low molecular weight heparin (LMWH) is an important antithrombotic agent in the management of UA. LMWH is normally preferred over UH as it can be given subcutaneously and no coagulation monitoring is needed. LMWH like enoxaparin should be given for 2-8 days. Heparin binds to antithrombin and the complex formed deacti vates a series of enzymes involved in the coagulation process. Thus thrombus formation will be inhibited.7 Patients with high risk of MI or death should also be given glycoprotein IIb/IIIa antagonist such as eptifibatide, tirofiban or abciximab. For the secondary prevention treatment, in addition to aspirin and clopidogrel, beta-blockers should be continued indefinitely. Statins can be started regardless of the patients cholesterol level for the preventing cardiovascular events. Statins are 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, which act by inhibiting the biosynthesis of cholesterol.8 Angiotensin converting enzyme (ACE) inhibitors are useful in patients with UA also. They work by inhibiting the production of angiotensin II which is a potent vasoconstrictor and reducing the breakdown of bradykinin which is a potent vasodilator.9 Evidence for the treatment of the conditions When the patient was admitted to the acute and emergency department, he was given clopidogrel 300mg, aspirin 300mg immediately and was then continued with long term treatment of 75mg of clopidogrel. The use of clopidogrel for the long term treatment of unstable angina was supported by two large trials. First, the CAPRIE trial which compare the beneficial effect of clopidogrel versus aspirin in patients at high risk of ischaemic event.10 In this trial, patients were either given 75mg clopidogrel once daily or 325mg of aspirin once daily. The clopidogrel group has a marginally lower risk of ischaemic stroke, myocardial infarction, or vascular death (5.32%) compared to the aspirin group (5.83%). The side effects reported were similar in both groups, indicating that clopidogrel has a comparable safety profile to that of aspirin. The second trial is the CURE Trial which investigate the beneficial effect of adding clopidogrel to aspirin therapy in patients with non-ST elevation acute coronary syndrome.11 In this trial, 12,562 patients were given either 300 mg clopidogrel innitially, then 75 mg once daily or placebo plus aspirin for 3 months to a year. It was found that there was a lower rate of death from cardiovascular causes, nonfatal MI or stroke in the clopidogrel group. However, the risk of major bleeding was significantly higher in clopidogrel group. Hence, it can be concluded that long term clopidogrel should be used in patients with acute coronary syndrome in addition to aspirin. In addition, according to a meta-analysis done by the Antithrombotic Trialists Collaboration, long term treatment of aspirin in the range of 75-150mg was found to be beneficial in patients with acute coronary syndrome. In cases where antithrombotic effect is needed immediately such as during acute attack of MI or UA, aspirin at a dose of 300mg should be given.12 In Mr AR case, only 300mg of aspirin was given in the acute and emergency department, no long term treatment of aspirin was given. This might be due to his newly diagnosed gastritis. NSAIDs were found to cause or worsen gastritis.13 According to the AHA/ACC guideline, clopidogrel will be the alternative for patients intolerant to aspirin due to gastrointestinal problems. According to a study done by Harker LA et al. where the tolerability and side effects of aspirin and clopidogrel were compared using the results from the CAPRIE trial, it was found that the group of patients receiving clopidogrel has a lower percentage of gas trointestinal side effects, with a rate 27.1% compared to 29.8% in those taking aspirin (p < 0.001).14 This finding support the reason behind clopidogrel being the only antiplatelet given to Mr AR. However, The difference in the incidence of side effects between the two treatment group was small and higher rate of occurrence of gastrointestinal problem in aspirin group might be due to the high dose of aspirin used (325mg). The policy of the ACC/AHA guideline of using clopidogrel instead of aspirin in patient with a history of GI complication was also refuted by Chan and colleagues.15 In this study, 320 patients who had recovered from aspirin-induced upper GI bleeding were given either 75 mg of clopidogrel daily or 80 mg of aspirin daily together 20mg of proton-pump inhibitor esomeprazole twice daily. When the patients were followed up after one year, it was found that patients in the aspirin group has a lower rate of recurrent upper GI bleeding compared to those receiving clopidogrel plus esomeprazole (8.6% versus 0.7%, P=0.001). No protective effect was conferred by esomeprazole in aspirin-induced lower GI bleeding. Hence, low dose aspirin is still deemed appropriate in Mr ARs case if given with a proton pump inhibitor or H2-antagonist like ranitidine. On day 1 Mr AR was given 60mg of enoxaparin immediately and twice daily thereafter. A comparison between the efficacy of UH and LMWH was carried out in the ESSENCE trial.16 In this trial, patients were allocated either subcutaneous enoxaparin plus placebo bolus and infusion or bolus and infusion unfractionated heparin plus placebo subcutaneous injection. In addition, they were all given oral aspirin. It was found that the enoxaparin group has a lower rate of recurrent angina, MI or death and also the need of revascularization process. Hence it was concluded that enoxaparin is more advantageous than UH, as there is little protein binding, longer plasma half life and more resistant to neutralisation by platelet factor IV as compared to UH. The dose given to Mr AR is justified according to a trial where the dose of enoxaparin was adjusted according to the weight of the patients. 17 It was found that giving 1mg/kg of enoxaparin to patients with UA or non-Q wave MI resulted in a lower ris k of major bleeding compared to giving a dose of 1.25mg/kg (6.5% versus 1.9%). Mr ARs weight was 59kg, thus a dose of 60mg is appropriate and evidence based. Sublingual GTN was given to Mr AR for the relief of his chest pain. According to the British Medical Journal evidence centre, no good evidence was found on the angina. There is one randomized placebo controlled study done by Karlberg et al. where they compared the effectiveness of intravenous GTN versus placebo in reducing ischaemic attack in unstable angina.18 In this trial, they found that patients given GTN have a fewer new onset of chest pain compared to placebo group. No trial was done to investigate the effectiveness of sublingual GTN in preventing ischaemic attack. However, according to a methodological study done by G Nyberg to determine the time of onset of sublingual GTN, it was found there was a significant reduction in the intensity of exercise induced chest pain and an improvement in the ST-depression when 0.5mg of GTN was given sublingually at the onset of chest pain.19 Hence, there is a consensus that sublingual GTN can be used for symptomatic control of unstable angin a. Mr ARs previous medications were continued during the hospital stay. Among those medications, perindopril, an ace-inhibitor, is also proved to be beneficial in the prevention of MI. There are two well known studies done on the effect of ace-inhibitors in preventing cardiovascular event in patients with cardiovascular disease, namely the HOPE trial and the EUROPA trial.20,21 In the HOPE trial, ramipril was chosen as the treatment drug. As for the EUROPA trial, perindopril was chosen to investigate if there is any beneficial effect in preventing MI, cardiac arrest or mortality in patients with stable coronary disease. It was found out that in the group of patients receiving perindopril, there was a 20% relative risk reduction in the primary end point as compared to the placebo group. Hence, it was concluded that perindopril should be given to all patients with coronary heart disease, including Mr AR who has unstable angina. In addition, Mr AR was continued with 40mg simvastatin once daily at night. According to a trial on simvastatin, it was found that giving simvastatin to high risk patients lowers their cholesterol level and reduces the incidence of cardiovascular events.22 In this trial, 20536 adults in the UK with high risk of getting cardiovascular event were given simavastatin 40mg daily or placebo. It was found that the simvastatin group has a lower percentage of all cause of death (12.9%) and major vascular event (19.8%) compared to the placebo group (14.7% and 25.2% respectively). There was a difference of about 1.0mmol/L in the LDL cholesterol level between the two groups after treatment regardless of the initial cholesterol level. This indicates that there is a reduction in the LDL cholesterol level in the simvastatin group which is independent on the initial cholesterol level. For patient given simvastatin, the risk reduction of the first major vascular event is similar no matter the patient s were taking ace inhibitors, aspirin, beta blockers or antihypertensive drugs or not. This shows that simvastatin provides additional benefits when added to the existing treatment with these drugs. Thus, it can be concluded that simvastatin will be beneficial to Mr AR who was taking ace inhibitor and antihypertensive drugs concurrently. Mr Ar was newly diagnosed with gastritis and was commenced on IV ranitidine. In a double blind clinical study, patients diagnosed with gastritis were given 300mg ranitidine daily for 4 weeks or placebo only.23 It was found that patients from the ranitidine group improved significantly faster than the placebo group and 80% of the patients had their symptoms completely resolved. Only 45% of the patients from placebo group achieved improvement in their symptoms while the remaining showed no change in their gastritis. Hence, it was concluded that ranitidine is an effective treatment option for gastritis. However, this trial only involved 52 patients and this small sample size renders the finding from trial inconclusive. In another trial where the effectiveness of ranitidine and sucrafate was compared, it was found out that both have a similar activity in relieving the symptoms of gastritis.24 77.6% of the patients receiving sucralfate and 79.4% from the ranitidine group had their symptom s completely resolved at the end of the study period (8 weeks). However, ranitidine was found to act faster in relieving pain compared to sucralfate. Hence, it can be concluded that the management of Mr ARs gastritis with ranitidine is justified. Mr AR was given nifedipine 10mg for the treatment of his hypertensive urgency. Even though nifedipine was found to be effective in reducing blood pressure within 20 minutes, this fast release, short-acting calcium channel blocker are not recommended in this case as Mr AR did not receive any beta-blocker before. According to the results obtained from the Holland Interuniversity Nifedipine/metoprolol Trial (HINT), monotherapy with nifedipine in patients with unstable angina naà ¯ve to beta blockers was associated with a higher risk of recurrence ischaemic attack or MI.25 The event rate ratio compared to placebo for beta blocker naà ¯ve, nifedipine only group was 1.15. As for the group receiving both nifedipine and metoprolol, the ratio was lower (0.80). Patients who were already receiving beta blockers and were added with nifedipine also showed lower rate ratio (0.68). Hence, it was concluded that nifedipine was only beneficial in patients who were treated with beta blocker at the sa me time. Moreover, it was found from the Trent study that nifedipine does not show any beneficial effect in patients with MI.26 In this trial, the death rate for patients receiving nifedipine 10mg four times daily and placebo was similar. When the number of death and MI were compared among patients taking beta blocker and not taking beta blocker among admission, it was found that the latter group has a higher rate of death and MI. This result is comparable to those from the HINT trial. Hence, the use of nifedipine in treating Mr ARs hypertensive urgency is not justified, other drug should be chosen. Conclusion The immediate treatment of UA with high dose of antiplatelet agent aspirin and clopidogrel together with the antithrombotic agent LMWH are justified as they help preventing the progression of UA to MI. Sublingual GTN on the other hand helps relieving his chest pain. As for his previous perindopril and simvastatin that were continued, these help in preventing recurrent angina also. Choosing clopidogrel for the long term prevention treatment of UA due to the presence of gastritis might not be the best option for Mr AR. Once his gastritis has resolved, life-long aspirin at the dose of 75mg should be added in with oral ranitidine 300mg twice daily prescribed as prophylaxis against NSAID induced gastritis. However, the use of nifedipine in the management of his hypertensive urgency is not justified. Instead, he should be given labetalol, atenolol or clonidine which were found to be better alternatives to nifedipine in treating hypertensive urgency.27 PATIENT MEDICATION PROFILE Patient details Name: AG Consultant: General Practitioner: Address: Gender: Male Weight: 59kg Height: 168cm Community pharmacist: Age: 41 Known sensitivities: NKDA Social history: Non-smoker, No alcohol abuse. Patient hospital stay Reason for admission Admission date: Chest pain. Discharge date: Relevant medical history Relevant drug history Date Problem description Medication Comments 1994 Pacemaker fixed Warfarin 5mg OD Atrial fibrillation 2007 Pacemaker not functioning, did not go for replacement due to financial constraint T digoxin 125mcg OD Atrial fibrillation 2007 Angiogram, 2 blocked vessels T frusemide 40mg BD Hypertension Hypertension Perindropil (coversylƒ’) 8mg OD Hypertension T amlodipine 10mg OD Hypertension Hydrochlorthiazide 25mg OD Hypertension T simvastatin 40mg ON Prevention of cardiovascular event Prescribed medication Route of administration Start Stop Nifedipine (adalat) 10mg PO Day 1 Aspirin 300mg PO Day 1 Day 1 Clopidogrel (plavixƒ’) 300mg PO Day 1 Day 1 Clopidogrel (plavixƒ’) 75mg OD PO Day 2 Enoxaparin (Clexaneƒ’) 60mg stat, BD subcutaneous Day 1 GTN 1 tablet PRN sublingual Day 1 Simvastatin 40mg ON PO Day 1 Amlodipine 10mg OD PO Day 1 Hydrochlorothiazide 25mg OD PO Day 1 Warfarin 5mg OD PO Day 1 Furosemide (Lasix) 40mg stat, BD IV Day 1 Day 3 Furosemide 40mg BD PO Day 3 Perindopril (Coversylƒ’) 8mg OD PO Day 1 Ranitidine (zantac) 50mg tds IV Day 1 Digoxin 125mcg OD PO Day 1 Clinical/ Laboratory Tests Date Results Potasium (3.5-5.0 mmol/L) Day 2 3.3 BP Day 2 150/118 Day 3 134/100 Day 4 122/86 Pharmaceutical Care Plan Care Issue Action Actual output/ Desired output Long term treatment with aspirin. Patient should be given 75mg of aspirin for the secondary prevention of UA. Patient has gastritis. He should be started on long term treatment of aspirin once his gastritis has resolved and ranitidine should be prescribed as prophylaxis against NSAIDs induced GI complications. Long term treatment with beta blockers. Beta blocker should be given to the patient as the secondary prevention treatment. Patient should be started on labetalol 100mg twice daily and titrate up to 200mg twice daily. Inappropriate use of nifedipine for the management of hypertensive urgency. Nifedipine should be substituted with labetalol 200-300mg every 3-4 hours when required. Not taken. Interaction between digoxin and diuretics when hypokalaemia occur. Potasium level should be monitored. Inform the patient on signs and symptoms of digoxin toxicity. Patients potassium level was lower than the normal range on day 2. He should be given potassium sparing diuretics or potassium supplement if the potassium level keeps going down. Monitoring should be continued. High risk of bleeding due to warfarin, aspirin, clopidogrel and enoxaparin. Bleeding tendency should be monitored. Patient should be told to inform the GP if there is any unusual bleeding like blood in the stool. Patients INR and prothrombin time were within the normal range. Monitoring was continued. Changing of IV ranitidine to oral ranitidine. Patient should be switched to oral ranitidine150mg twice daily after being discharged. Not taken. GTN for relief of angina symptoms. Patient should be prescribed GTN spray or sublingual tablet for the relief of chest pain shoul the patient has another angina attack. GTN sublingual tablet was prescribed as discharge medication. Poor patient compliance Patient should be informed on the reason behind taking his medication, the importance of compliance. Compliance aid should be given. Patient was counselled on the importance of compliance. Side effects of simvastatin -muscular side effects -liver disease Patient should be advised to report immediately any unexplained muscle pain, weakness nor tenderness. Regular LFT monitoring should be done. No monitoring of cholesterol level. Cholesterol level should be monitored suring the hospital stay so that the dosage of simvastatin can be adjusted accordingly. Cholesterol level should be maintained below 5.2mmol/L. Patient education on healthy lifestyle. Patient should be told on the importance of low salt diet for his HT and encouraged to exercise more. Patient was counselled on the importance of healthy lifestyle before being discharged.

The Death Penalty Is Dead Wrong :: Capital Punishment

Why the Death Penalty is Dead Wrong Most people argue that the death penalty is not a form of cruel and unusual punishment. However, this is extremely inaccurate. Electric chair victims can take up to 14 minutes to die, maintaining full consciousness as their flesh begins to scorch and burn off. During lethal injection, "even a slight error in dosage or administration can leave a prisoner conscious but paralyzed with pain, serving as a witness for his own demise." The following is an eye witness account of an Arizona gas chamber execution given by Supreme Court Justice John Paul Stevens: "When the fumes enveloped Don's head he took a quick breath. A few seconds later, he looked again in my direction. His face was red and contorted as if he were attempting to fight through tremendous pain. His mouth was pursed shut and his jaw was clenched tight. Don then took several more quick gulps of the fumes. His body started convulsing violently and his skin turned a deep red...the viens in his temple and neck began to bulge until I thought they might explode. After about a minute, Don's face leaned partially forward, but he was still very conscious. He was shuddering uncontrollably and his body was racked with spasms. His head continued to snap back. His fists were clenched tightly. After several more minutes, the most violent of the convulsions subsided. At this time, the muscles along Don's left arm and back began twitching in a wavelike motion under his skin. Spittle drooled from his mouth. Don Harling took exactly ten minutes and 31 seconds to die. Approximately three months later, he was found innocent." And it wasn't the first time. Amnesty International sites that "from 1900 to 1985 over 350 people sentenced to death were later found to be innocent of the crimes charged. Some excaped execution by only minutes, but 23 were actually executed. Within the last 20 years, 54 Americans under sentence of death have been released because of evidence of their innocence." Unlike a life imprisonment, death offers no second chance. If new evidence surfaces after the person has been executed, it's too late to do anything about it. The death penalty doesn't save tax payers any money, either. Many people have the misconception that criminals should not be allowed to "rot in jail" wasting tax payers money. However, a study conducted by the Death Penalty Information Center (DPIC) concludes that tax payers pay an average of $3.2 million dollars per each death penalty case -- enough to sentence someone to 120 years in a maximum security facility. The death penalty is also not a detterent to crime.