Was Hamlet Mad Essays - Characters In Hamlet, Prince Hamlet, Hamlet

Was Hamlet Mad? Hamlet is a complex character in the play. His character is always changing in some way, and he never seems to be the same person. In some scenes, he appears to be mad, while in others he is perfectly sane. Therefore, a question that has become a major argument for those who analyze the Shakespearean text is : was Hamlet mad or sane in the play? There are several arguments as to why Hamlet was mad. The first occurrence of his madness is found after his encounter with the ghost, his father. Hamlet appears to be act insanely when he speaks to his friends about what he saw. He speaks "wild and whirling words,"(Act 1, Scene V, lines 127-134). Horatio and the others are mystified when Hamlet talks like they have never heard him before. Another argument for his madness can be supported in his treatment towards Ophelia. When he first encounters her after speaking to the ghost, he is courteous at first, but then suddenly turns against her. He completely denies ever having loved her, attacks the womankind, and orders her to go to a nunnery. If this is not mad behavior, what is? Another point where Hamlet acts madly is when he had Rosencrantz and Guildenstern killed even though they had nothing to do with the plan to murder his father. Granted they were carrying letters to England with orders to kill him, but they were not aware of wh at was written in them. The argument can be further supported when Hamlet is in his mother's chamber. Hamlet alone sees his father's ghost. Every other time the ghost appeared someone else could see it. During this scene, the argument for Hamlet's madness can be strongly supported because his mother could not see it. Gertrude even says, "Alas, how is't with you-That you do bend your eye on vacancy,"(Act 3, Scene 4, lines 133-134). IN that same scene, Hamlet acts violently to his mother. He tells her that she is a whore and to abandon his uncles' bed. Finally, Hamlet's madness can be seen in his actions after killing Polonius. Hamlet even tells Laertes that he killed Polonius in "a fit of madness." When Hamlet is confronted about the murder, he will not tell anyone where the body is and seems very happy about it. These are all strong arguments for Hamlet being mad. However, one must look at the other side of the argument before making the decision about whether Hamlet was sane or not throughout the play. For example, Hamlet, after meeting the ghost, tells Horatio that he is going to "feign madness" and that if Horatio notices any strange behavior from Hamlet, it is because he is putting on an act. A pattern also emerges on when Hamlet is "mad" and when he is not. Hamlet's "madness" only manifests itself when he is in the presence of certain characters. When Hamlet is around Polonius, Claudius, Gertrude, Ophelia, Rosencrantz and Guildenstern, he behaves irrationally. However, when Hamlet is around Horatio, Bernardo, Francisco, the Players, and the Gravediggers, he behaves rationally. Several characters also admit to believing that Hamlet is not mad. Even Claudius confesses that Hamlet's "actions, although strange, do not appear to stem from madness,"(Act III, Scene 1, lines 177-180). Polonius admits that Hamlet's actions and words have a "method " to them, and there appears to be a reason behind them, and they are logical in nature. A powerful example that supports this argument is Ophelia's true madness. Ophelia's insanity and Hamlet's are entirely different from one another. In fact, Hamlet's actions contrast them. Ophelia acts mad no matter who is around, and she acts different than Hamlet. Finally, Hamlet believes in his sanity at all times. He never doubts his control over his psyche. He even tells his mother that he is not mad, "but mad in craft," (Act III.Scene IV. Line 210). Therefore, one can see that this argument is also strong. It is up to the audience to decide whether or not Hamlet was truly mad or not. However, it seems that the argument for Hamlet being sane is stronger. Hamlet tells his best friend that he is going to pretend to be mad.

THE USE OF STEROIDS BY ATHLETES essays

THE USE OF STEROIDS BY ATHLETES essays Steroids are drugs that many athletes use to enhance their abilities in sports. The use of steroids can be dangerous to both your body and mind. The drug also can give athletes unfair advantages which could propel them to victory. The use of steroids should not be permitted What is a steroid? Steroids are a synthetic version of the human hormone testosterone. Testosterone stimulates and maintains the male sexual organs. It also stimulates the development of bones and muscle, promotes skin and hair growth, and can influence emotions. In males, testosterone is produced by the testes and the adrenal gland. In the 1930's, researchers first developed steroids to rebuild and prevent the breakdown of body tissues from disease. The first use of steroids in sports was recorded in 1954 at the world championships in Vienna, Austria (Snyder 72). Russian weight lifters were using steroids and were merely invincible in their competition against other countries (Snyder 72). The U.S. coach asked the Russians how they were accomplishing this, and they told him they were given steroids (Snyder 72). This started the craze for steroids around the world especially in the United States (Snyder 72). Many scientists believe it can increase strength and body size, but others believe that using the drug makes you hostile and aggressive which makes you train harder therefore resulting in gained body size and strength (Snyder 74). Many people that take them are athletes and people with body image issues (Steroids). Others such as police officers and bouncers use them because they work in physical fighting environments (Steroids). The use of steroids may cause many serious mental side effects. The drug produces a change in the electroencephalogram, an image of the brain activity (Macmillan 94) . Mood swings are common which are caused by increased hostility and aggressiveness (Steroidsinfo). Som...

Cardiovascular Diseases

Thanks to the rising health awareness and government programmes this number significantly reduce during last 30 years. Coronary heart disease and cardiovascular disease Cardiovascular diseases are diseases of the heart (cardiac muscle ) or blood vessels (vasculature). Cardiovascular disease (CVD) means all the diseases of the heart and circulation (blood vessels disease) including coronary heart disease (angina and heart attack) and stroke, as well as coronary and periphery blood vessels disease (problems with circulation). Diseases from this group are the biggest killer in Europe and USA, but developing and non-develop countries too. The final and most tragic consequence of different types of heart disease is heart attack with tragic consequences. Heart diseases are caused by atherosclerosis, a disease of arterial blood vessels resulted from atheroma i. . plaques accumulated (forming; sticking) on artery walls which makes the blood vessels nonelastic and narrowed and leads to decreased blood flow. For the atherosclerosis doctors very often use alternative name chronic cardiovascular disease. The opposite group acute heart disease made group of diseases which are dangerous for patients lives. Acute heart diseases include conditions or illnesses wh ich usually have a rapid onset of symptoms and may resolve within days with or without treatment. A condition or illness that is sudden or severe. On the other hand a condition or illness that arises slowly over days or weeks and may or may not resolve with treatment made a group of chronic heart disease. Both of them are caused by atheroma and the most known are next: a) Acute heart disease Heart attack is caused by lack of O2 in heart muscle cells. Very often it is caused by rupture of â€Å"hard plaques† patches which result in blood clots and partially or completely block blood flow and cause a heart attack. When a fiber cap becomes thin, these â€Å"hard plaques† can suddenly rupture, spilling their contents, resulting in blood clots that partially or completely block blood flow and cause a heart attack http://www. authorstream. com/Presentation/nitin-35423-heart-diseases-science-technology-ppt-powerpoint/ Cholesterol glossary. http://www. mybwmc. org/library/28/000225 Stroke Stroke is death of brain cells caused by obstructed blood flow to parts of the brain. Since the level of LDL cholesterol is main cause of narrowed of blood vessels, it is necessary control it. If not treated properly, high LDL cholesterol can cause a stroke. Cholesterol glossary. http://www. mybwmc. org/library/28/000225 b) Coronary heart disease Heart disease (coronary heart disease), When the plaque build up in th conorary arteries heart does not get sufficient blood, the condition is called coronary artery disease or coronary heart disease. Atherosclerosis is a disease of arterial blood vessels in which plaques form on artery walls. This is a consequence of different substances circulating in the bloodstream (inflammatory cells, proteins, cholesterol and calcium) sticking inside the vessel walls. Plaque patches influence on narrowing blood flow in the artery. ttp://www. bodybuilding. com/fun/gastelu5. htm Peripheral artery disease (reduced blood flow in the limbs, usually the legs Coronary plaque Coronary plaque is a term which use in practice as a synonym for atheroma or atherosclerosis. Patches of atheroma are formed from substances that circulate in the bloodstream. They consist of lipid, or fat, cores covered by collagen fiber cap s which are sticking to the inside of the vessel walls. Over time plaque or patch of atheroma increases making an artery narrower and the blood flow through the artery is reducing. We can see the changes in blood vessels caused by plaque in the Figure 1. Figure 1 Artery with the patches of atheroma – plaque Preventing Cardiovascular Diseases. Patient. co. uk. emis www. patient. co. uk/health/Preventing-Cardiovascular-Diseases. htm (March 13, 2013) http://medicineworld. org/blogs/heart/blog/permalinks/Jan-2006/coronary-plaque-detection-by-molecular-imaging. html (March 13, 2013) Mature plaques typically consist of two main components: soft, lipid-rich atheromatous â€Å"gruel† and hard, collagen-rich sclerotic tissue. Lipid-rich and soft plaques are more dangerous than collagen-rich and hard plaques because they are more unstable and rupture-prone and highly thrombogenic after disruption. Researchers have found that many people who have heart attacks do not have arteries narrowed by plaque. Many heart attacks are now known to be caused by soft or vulnerable plaques, located on an inflamed part of an artery. This plaque can burst, leading to the formation of a blood clot that can cause a heart attack. The 2009 issue of â€Å"The American Journal Pathology† edited explanation of those relations discovered by Olga Ovchinnikova and er colleagues. They found that inflammation results in the formation of soft (vulnerable) plaque which is filled with different cell types that promote blood clotting. This leads to a reduction of mature collagen, resulting in thinner caps that are more likely to rupture, even in the cases when total level of plaque isn’t extremely high. The authors advocate d ifferent viewpoints about relations between the plaque level and structure, i. e. its influence on heart attack. The first group claims that described types of blockages cause only about 30 percent of heart attacks. On the other hand, some sources state that more than two-thirds of acute coronary events result from rupture of coronary plaques. However problems that plaque creates are extremely dangerous for people’s life and it is very important to prevent and monitor its appearance and changes. Graphs of vulnerable plaque and rupture of plaque which causes a heart attack is presented below. Figure 2 Vulnerable atherosclerotic plaques. Vulnerable atherosclerotic plaques. A. Atherosclerosis in a chronic disease that leads to plaque rupture and vascular occlusion. B. Cross-section of a lethal coronary plaque rupture. Adapted from Heistad D. Unstable coronary-artery plaques. N Engl J Med. 2003. Atherosclerosis Modeling In-vitro. http://www. remedi. uzh. ch/research/disease. html Figure 3 Plaque Rupture and Heart attack http://hon. nucleusinc. com/generateexhibit. php? ID=30468A=1027 Factors influencing plaque growth and stability Based on everything mentioned above and medical experience the conclusion about relations between heart attack and other cardiovascular disease and the level of plaque increasing are found. The higher the level of plaque the higher risk of heart disease will be. The level of plaque will increase as the result of high level of cholesterol, type LDL, so called â€Å"bad cholesterol† in blood. When the level of LDL is normal, blood can pass in and out of the blood vessels without problems, but if it significantly increase particles of the blood will accumulate and sooner or later provoke trigger (cause) heart attack. Other very important factors influencing plaque level increasing are high blood pressure and cigarette smoking. Both factors accelerate the plaque formation changing (damaging) artery walls and even more, helping cholesterol forming. Medical experience proved that plaque composition and vulnerability (hard or soft plaque) is more responsible for the conversion of a stable disease to a life-threatening condition than the plaque size. Except the plaque vulnerability the risk of plaque disruption is are consequence of rupture triggers (extrinsic forces). Soft plaque – lipid-rich one is more dangerous because of its instability and higher probability for rupture. Even (IAKO) Although â€Å"hard plaque† that one having higher level of calcium influence on the blood vessels walls and their â€Å"hardness† experience show that heart attacks are mostly caused by soft plaque disruption. Figure 4 Plaque rupture and its consequences in the form of heart diseases http://www. nature. com/nrg/journal/v7/n3/fig_tab/nrg1805_F2. html Risk factors of coronary heart disease Risk factors influencing cardiovascular disease we can group based on their stability into the three groups: a) Modifiable risk factors In this group hypertension is the most dangerous risk factor for heart attacks, but even more for stroke. It is forming as the result of abnormal blood lipid levels which means high total cholesterol, high levels of triglycerides and high levels of low-density lipoprotein or low levels of high-density lipoprotein (HDL). Smoking, physical inactivity, Type 2 diabetes, and a diet full with saturated fats are risk factors strongly influencing the heart disease. All of them are treatable and patients (individuals) belonging into the different types of risk customers’ groups should avoid practice them. b) Non-modifiable risk factors The factors from this group mostly are constant, like the case in gender or family history. Others are changing when time is passing, like age and lifestyle and personal habits. Older people have more chance to get heart attack and the man, especially those having â€Å"bad medical history†. Ration between man and woman are changing when women past the menopause. After that the level of risk is similar as the men’s one. As I’ve presented there is direct correlation between cardiovascular disease and condition and health of blood vessels, more precisely of developing atheroma, means level and structure of plaque in vessels. On the other development of plaque and its level is directly influenced by level of cholesterol and some other elements which are connected with individual person and his/her life and genetic predispositions. As with the other diseases everybody has some risk of developing atheroma, but some risk factors increase the risk level for several categories. Those risk factors include: fn 12 †¢Fixed risk factors – factors that person cannot change: oA strong family history which means close relatives who developed heart disease or a stroke before they were 55 (for males) or 65 (for female). Severe baldness in men at the top of the head. oAn early menopause in women. oAge. Older people have more risk to develop atheroma. oEthnic group. Medical data show that people from different ethnic group have different risk for heart diseases. †¢Treatable or partly treatable risk factors include different health problems caused basically by the same causes as the: oHypertension (high bl ood pressure). oHigh cholesterol blood level. oHigh triglyceride (fat) blood level. oDiabetes. oKidney diseases causing diminished kidney function. All factors from this group have to be controlled and monitor. Any kind of their complication probably will trigger more serious problems such as heart attack or stroke. †¢Lifestyle risk factors that can be prevented or changed. Actually these factors PRETHODE precede to those belonging to the second group. Except the genetic factors way of life and daily habits are the more responsible for different kind of heart diseases. Those factors are: oSmoking (Smoking cigarette increase blood pressure, decrease HDL; damages arteries and blood cells and increases heart attacks. Passive smoking is also a risk factor for cardiovascular disease ) oLack of physical activity. Obesity (People who are overweight (10-30% more than their normal body weight) have 2 to 6 times the risk of developing heart disease. ) oAn unhealthy diet and eating too much salt. oExcess alcohol. Looking on those three groups one can easily conclude that people with â€Å"bad predisposition† having high fixed risk factors have to think about their lifestyle risk factors ev en more, in order to try to decrease the second group of factors (treatable or partly treatable risk factors). On the other hand some of risks are more dangerous than the others; for example smoking increases risk for heart disease more than obesity. And of course combination of two or more risk factors increases significantly the level of risks; older man (or woman) who smokes, without physical activity and with bad eating habits has more chance to get some of previously explained disease than the one who have â€Å"just one of bad habits†. The more risk factors someone has the greater is the likelihood that he/she will develop cardiovascular disease, unless taking action to modify his/her risk factors and working to prevent them compromising his/her heart health. That doesn’t mean that people with â€Å"good genes† can be irresponsible and ZANEMARITI risk factors from other groups. With or without genetic predisposition modern life significantly increases a risk of heart disease for everybody. Hormones impact on lipids and other risk factors Different numbers of man and women died from heart attack initiated a lot of research about hormones’ influence on the risk factor and heart disease development. Number of men died from the heart attack outnumbered the number of women in pre-menopause period, but in the post-menopause data show completely opposite situation. A percentage of women in post-menopause having heart disease and dying from heart attack increase dramatically and now outnumbered the men. The main reasons for those changes are connected to the level of hormones and their influence on level and structure of cholesterol and consequently on risk factors and heart disease. As mentioned before total cholesterol actually is made of two different types of cholesterol: LDL – low density lipoprotein (LDL), so called bad cholesterol and high density lipoprotein (HDL). High levels of LDL cholesterol lead to atherosclerosis increasing the risk of heart attack and ischemic stroke. HDL cholesterol reduces the risk of cardiovascular disease as it carries cholesterol away from the blood stream. http://www. walgreens. com/marketing/library/careguides/careguide. jsp? docid=000225=28=High%20Cholesterol Estrogen, a female hormone, raises HDL cholesterol levels, partially explaining the lower risk of cardiovascular disease seen in premenopausal women. But after menopause (natural or surgical) when a level of estrogen significantly decreases total cholesterol rises, low density lipoprotein (LDL) cholesterol rises, and high density lipoprotein (HDL) cholesterol does not change or decreases slightly. This is the reason why negative hormones’ effect after menopause increasing more than proportionally. Some authors argue that even influence of estrogen on LDL and HDL level is proved it is yet unclear whether increase in risk is caused, at least partially, by increased level of androgen (the other of hormones belong to steroid as estrogen too), which is characteristics of menopause too. This sexual dimorphism means a lower incidence in atherosclerotic diseases in premenopausal women, which subsequently rises in postmenopausal women to eventually equal that of men. These observations point towards estrogen and progesterone playing a lifetime protective role against CAD in women. As exogenous estrogen and estrogen plus progesterone preparations produce significant reductions in low-density lipoprotein (LDL) cholesterol levels and significant increases in high-density lipoprotein (HDL) cholesterol, this should in theory lower the risk of CAD. UKLOPITI U ONO GORE Among estrogen’s positive effects on the heart are: †¢Reducing the LDL (â€Å"bad†) cholesterol in the blood. †¢Increasing the HDL (â€Å"good†) cholesterol in the blood. †¢Helping to keep blood vessels open. †¢Lowering blood pressure at night. †¢Reducing blood viscosity (how sticky the blood is), a property that may cause blood clots which could result in a heart attack or stroke. Estrogen’s effects on clotting are complicated, however, since there also is an increased risk for thromboembolism (a blood clot that blocks a vessel) in women taking estrogen. Possibly enhancing fibrinolysis, which is the body’s natural process for breaking down blood clots. Read more: http://ehealthmd. com/content/what-are-benefits-hrt#ixzz2NbWR3MxY http://ehealthmd. com/content/what-are-benefits-hrt#axzz2NbW1GJJN Nutrition guidelines As presented before three different groups of risk factor exist. Some of them people can cha nge but the other are fixed, non-changeable because they caused by genetic heritage ( ) influences. Controllable factors are connected to the lifestyle of person. Lifestyle changes can prevent or slow the development of coronary plaque and heart disease. In order to prevent a disease development one have to keep track of his/her blood pressure and cholesterol levels. Choosing a heart-healthy diet is vital in controlling weight, which helps keep blood pressure and cholesterol levels down. Foods high in cholesterol and saturated fat should be avoided, and quitting smoking is imperative. Regular exercise and an increased overall activity level contribute to heart health and help reduce stress. The risk of cardiovascular disease is possible to reduce following recommendation for lifestyle changing: Cessation of smoking and avoidance of second-hand smoke. Nutrition should ensure a healthy diet wiht total diet no more than 8% of saturated + trans fatty acids of total energy intake. All people, especially ones with high risk factors should lower alcohol consumption As the prevention physical activities are recommended – at least 30 minutes of moderate intensity physical activity per day or three days week (i. e. 150 mins/week minimum). Currently practiced measures to prevent cardiovascular disease include: †¢A low-fat, high-fiber diet including whole grains and plenty of fresh fruit and vegetables (at least five portions a day)[29][30] †¢Tobacco cessation and avoidance of second-hand smoke;[29] †¢Limit alcohol consumption to the recommended daily limits;[29] consumption of 1-2 standard alcoholic drinks per day may reduce risk by 30%[31][32] However excessive alcohol intake increases the risk of cardiovascular disease. [33] †¢Lower blood pressures, if elevated, through the use of antihypertensive medications[citation needed]; †¢Decrease body fat (BMI) if overweight or obese;[34] Increase daily activity to 30 minutes of vigorous exercise per day at least five times per week;[29] †¢Decrease psychosocial stress. [35] Stress however plays a relatively minor role in hypertension. [36] Specific relaxation therapies are not supported by the evidence. [37] Routine counselling of adults to advis e them to improve their diet and increase their physical activity has not been found to significantly alter behaviour, and thus is not recommended. [38] http://www. news-medical. net/health/What-is-Cardiovascular-Disease. aspx http://www. barnesandnoble. om/w/prevent-halt-and-reverse-heart-disease-joseph-piscatella/1100260037 Primary and secondary prevention of heart disease It is necessary start with prevention from heart disease as early as possible. Changes in the number of people killed by heart attack in developed countries show that prevention and awareness about this group of disease help to http://circ. ahajournals. org/content/123/20/2274/F2. expansion. html health plans must continue to drive cardiovascular care further along the continuum toward primary prevention of cardiovascular disease (CVD). CVD risk factors should be managed not only after a coronary event has occurred, but also before the onset of such and event. Ideally, health lifestyles should be promoted with all patients so that risk factors for CVD never develop. In this way, CVD care can be moved from the inpatient setting to the outpatient setting. Sidney C. Smith Jr, MD. Focus on Cardiovascular Disease; A Word About the Quality of Care in Cardiovascular Disease. Director, Center for Cardiovascular Science and Medicine University of North Carolina at Chapel Hill. http://www. qualityprofiles. rg/leadership_series/cardiovascular_disease/cardiovascular_introduction. asp Key priorities for implementation Primary prevention of CVD †¢For the primary prevention of CVD in primary care, a systematic strategy should be used to identify people aged 40–74 who are likely to be at high risk †¢People should be prioritised on the basis of an estimate of their CVD risk before a full formal risk assessment. Thei r CVD risk should be estimated using CVD risk factors already recorded in primary care electronic medical records †¢Risk equations should be used to assess CVD risk People should be offered information about their absolute risk of CVD and about the absolute benefits and harms of an intervention over a 10-year period. This information should be in a form that: opresents individualised risk and benefit scenarios opresents the absolute risk of events numerically ouses appropriate diagrams and text (See www. npci. org. uk) †¢Before offering lipid modification therapy for primary prevention, all other modifiable CVD risk factors should be considered and their management optimised if possible. Baseline blood tests and clinical assessment should be performed, and comorbidities and secondary causes of dyslipidaemia should be treated. Assessment should include: osmoking status oalcohol consumption oblood pressure (see ‘Hypertension’, NICE clinical guideline 34) obody mass index or other measure of obesity (see ‘Obesity’, NICE clinical guideline 43) ofasting total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides (if fasting levels are not already available) ofasting blood glucose orenal function oliver function (transaminases) thyroid-stimulating hormone (TSH) if dyslipidaemia is present †¢Statin therapy is recommended as part of the management strategy for the primary prevention of CVD for adults who have a 20% or greater 10-year risk of developing CVD. This level of risk should be estimated using an appropriate risk calculator, or by clinical assessment for people for whom an appropriate risk calculator is not available or approp riate (for example, older people, people with diabetes or people in high-risk ethnic groups) †¢Treatment for the primary prevention of CVD should be initiated with simvastatin 40 mg. If there are potential drug interactions, or simvastatin 40 mg is contraindicated, a lower dose or alternative preparation such as pravastatin may be chosen. Secondary prevention of CVD †¢For secondary prevention, lipid modification therapy should be offered and should not be delayed by management of modifiable risk factors. Blood tests and clinical assessment should be performed, and comorbidities and secondary causes of dyslipidaemia should be treated. Assessment should include: osmoking status oalcohol consumption oblood pressure (see ‘Hypertension’, NICE clinical guideline 34) obody mass index or other measure of obesity (see ‘Obesity’, NICE clinical guideline 43) ofasting total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides (if fasting levels are not already available) ofasting blood glucose orenal function oliver function (transaminases) othyroid-stimulating hormone (TSH) if dyslipidaemia is present. Statin therapy is recommended for adults with clinical evidence of CVD †¢People with acute coronary syndrome should be treated with a higher intensity statin. Any decision to offer a higher intensity statin should take into account the patient’s informed preference, comorbidities, multiple drug therapy, and the benefits and risks of treatment †¢Treatment for the secondary prevention of CVD should be initiated with simvastatin 40 mg. If there are potential drug interactions , or simvastatin 40 mg is contraindicated, a lower dose or alternative preparation such as pravastatin ay be chosen †¢In people taking statins for secondary prevention, consider increasing to simvastatin 80 mg or a drug of similar efficacy and acquisition cost if a total cholesterol of less than 4 mmol/litre or an LDL cholesterol of less than 2 mmol/litre is not attained. Any decision to offer a higher intensity statin should take into account informed preference, comorbidities, multiple drug therapy, and the benefit and risks of treatment http://www. eguidelines. co. uk/eguidelinesmain/guidelines/summaries/cardiovascular/nice_lipid_modification. php How to lower the risk of cardiovascular disease The risk of cardiovascular disease is possible to reduce following recommendation for lifestyle changing: Cessation of smoking and avoidance of second-hand smoke. Nutrition should ensure a healthy diet wiht total diet no more than 8% of saturated + trans fatty acids of total energy intake. All people, especially ones with high risk factors should lower alcohol consumption As the prevention physical activities are recommended – at least 30 minutes of moderate intensity physical activity per day or three days week (i. . 150 mins/week minimum). Cessation of smoking The aim of this measure is complete cessation of smoking and avoidance of second-hand smoke. Patient and their families need to stop smoking. Those who are unable to quit may need professional help in form of counselling, behavioral therapy and even pharmacological therapy. Nicotine replacement therapy (NRT) is the first line choice of medication. Nutrition The aim of thi s measure is to ensure a healthy diet. Total diet should have no more than 8% (of total energy intake) of saturated + trans fatty acids. All patients are advised to take approximately 1g Eicosapentaenoic acid (EPA) and Docosahexaenoic acid (DHA) and more than 2g Alpha Linolenic Acid (ALA) daily. Diet should have vegetables, fruits and legumes, grain-based foods, moderate amounts of lean meats, poultry, fish and reduced fat dairy products. EPA and DHA can be obtained from oily fish and marine n-3 (fish oil) capsule supplements. Alcohol consumption All patients should be advised to lower alcohol consumption. Men should drink no more than 2 standard drinks per day and women no more than 1 standard drink per day. Physical activity The aim of this measure is to raise physical activity and exercise to the recommended goal of at least 30 minutes of moderate intensity physical activity on most, if not all, days of the week (i. e. 150 mins/week minimum). Maintaining a healthy body weight The aim should be to achieve a waist measure of less than or equal to 94 cm in men and less than or equal to 80 cm in women. The body mass index (BMI) should be maintained at 18. 5–24. 9 kg/m2 Lowering blood cholesterol The aim of therapy should be to maintain blood cholesterol at: †¢Low density lipoprotein (LDL) at – less than 2. mmol/L †¢HDL – more than 1. 0 mmol/L †¢Triglyceride (TG) less than 1. 5 mmol/L The blood cholesterol can be maintained with the use of pharmacotherapy. Statins are commonly used lipid lowering drugs. Those with diabetes and atherosclerosis need stringent blood cholesterol control as well. Other lipid lowering drugs include fibrates like gemfibrosil, clofibrates etc, Eze timiber and niacin. Lowering blood pressure High blood pressure is one of the important risk factors for cardiovascular disease. Those with coronary heart disease, diabetes, kidney disease or stroke need tight blood pressure control. The aim should be a blood pressure of less than 130/80 mm of Hg. Diabetes and blood sugar control Those diagnosed with diabetes need stringent blood sugar control to prevent cardiovascular damage. HbA1c levels should be maintained at less than 7%. Other drugs to lower risk of cardiovascular disease Other drugs used to lower risk of cardiovascular diseases include: †¢Antiplatelet agents – this includes Aspirin and Clopidogrel. These drugs when given to patients with risk of heart attacks may prevent such attacks and events. †¢ACE inhibitors like Enalapril, Captopril, Lsinopril and Cardiovascular Diseases Thanks to the rising health awareness and government programmes this number significantly reduce during last 30 years. Coronary heart disease and cardiovascular disease Cardiovascular diseases are diseases of the heart (cardiac muscle ) or blood vessels (vasculature). Cardiovascular disease (CVD) means all the diseases of the heart and circulation (blood vessels disease) including coronary heart disease (angina and heart attack) and stroke, as well as coronary and periphery blood vessels disease (problems with circulation). Diseases from this group are the biggest killer in Europe and USA, but developing and non-develop countries too. The final and most tragic consequence of different types of heart disease is heart attack with tragic consequences. Heart diseases are caused by atherosclerosis, a disease of arterial blood vessels resulted from atheroma i. . plaques accumulated (forming; sticking) on artery walls which makes the blood vessels nonelastic and narrowed and leads to decreased blood flow. For the atherosclerosis doctors very often use alternative name chronic cardiovascular disease. The opposite group acute heart disease made group of diseases which are dangerous for patients lives. Acute heart diseases include conditions or illnesses wh ich usually have a rapid onset of symptoms and may resolve within days with or without treatment. A condition or illness that is sudden or severe. On the other hand a condition or illness that arises slowly over days or weeks and may or may not resolve with treatment made a group of chronic heart disease. Both of them are caused by atheroma and the most known are next: a) Acute heart disease Heart attack is caused by lack of O2 in heart muscle cells. Very often it is caused by rupture of â€Å"hard plaques† patches which result in blood clots and partially or completely block blood flow and cause a heart attack. When a fiber cap becomes thin, these â€Å"hard plaques† can suddenly rupture, spilling their contents, resulting in blood clots that partially or completely block blood flow and cause a heart attack http://www. authorstream. com/Presentation/nitin-35423-heart-diseases-science-technology-ppt-powerpoint/ Cholesterol glossary. http://www. mybwmc. org/library/28/000225 Stroke Stroke is death of brain cells caused by obstructed blood flow to parts of the brain. Since the level of LDL cholesterol is main cause of narrowed of blood vessels, it is necessary control it. If not treated properly, high LDL cholesterol can cause a stroke. Cholesterol glossary. http://www. mybwmc. org/library/28/000225 b) Coronary heart disease Heart disease (coronary heart disease), When the plaque build up in th conorary arteries heart does not get sufficient blood, the condition is called coronary artery disease or coronary heart disease. Atherosclerosis is a disease of arterial blood vessels in which plaques form on artery walls. This is a consequence of different substances circulating in the bloodstream (inflammatory cells, proteins, cholesterol and calcium) sticking inside the vessel walls. Plaque patches influence on narrowing blood flow in the artery. ttp://www. bodybuilding. com/fun/gastelu5. htm Peripheral artery disease (reduced blood flow in the limbs, usually the legs Coronary plaque Coronary plaque is a term which use in practice as a synonym for atheroma or atherosclerosis. Patches of atheroma are formed from substances that circulate in the bloodstream. They consist of lipid, or fat, cores covered by collagen fiber cap s which are sticking to the inside of the vessel walls. Over time plaque or patch of atheroma increases making an artery narrower and the blood flow through the artery is reducing. We can see the changes in blood vessels caused by plaque in the Figure 1. Figure 1 Artery with the patches of atheroma – plaque Preventing Cardiovascular Diseases. Patient. co. uk. emis www. patient. co. uk/health/Preventing-Cardiovascular-Diseases. htm (March 13, 2013) http://medicineworld. org/blogs/heart/blog/permalinks/Jan-2006/coronary-plaque-detection-by-molecular-imaging. html (March 13, 2013) Mature plaques typically consist of two main components: soft, lipid-rich atheromatous â€Å"gruel† and hard, collagen-rich sclerotic tissue. Lipid-rich and soft plaques are more dangerous than collagen-rich and hard plaques because they are more unstable and rupture-prone and highly thrombogenic after disruption. Researchers have found that many people who have heart attacks do not have arteries narrowed by plaque. Many heart attacks are now known to be caused by soft or vulnerable plaques, located on an inflamed part of an artery. This plaque can burst, leading to the formation of a blood clot that can cause a heart attack. The 2009 issue of â€Å"The American Journal Pathology† edited explanation of those relations discovered by Olga Ovchinnikova and er colleagues. They found that inflammation results in the formation of soft (vulnerable) plaque which is filled with different cell types that promote blood clotting. This leads to a reduction of mature collagen, resulting in thinner caps that are more likely to rupture, even in the cases when total level of plaque isn’t extremely high. The authors advocate d ifferent viewpoints about relations between the plaque level and structure, i. e. its influence on heart attack. The first group claims that described types of blockages cause only about 30 percent of heart attacks. On the other hand, some sources state that more than two-thirds of acute coronary events result from rupture of coronary plaques. However problems that plaque creates are extremely dangerous for people’s life and it is very important to prevent and monitor its appearance and changes. Graphs of vulnerable plaque and rupture of plaque which causes a heart attack is presented below. Figure 2 Vulnerable atherosclerotic plaques. Vulnerable atherosclerotic plaques. A. Atherosclerosis in a chronic disease that leads to plaque rupture and vascular occlusion. B. Cross-section of a lethal coronary plaque rupture. Adapted from Heistad D. Unstable coronary-artery plaques. N Engl J Med. 2003. Atherosclerosis Modeling In-vitro. http://www. remedi. uzh. ch/research/disease. html Figure 3 Plaque Rupture and Heart attack http://hon. nucleusinc. com/generateexhibit. php? ID=30468A=1027 Factors influencing plaque growth and stability Based on everything mentioned above and medical experience the conclusion about relations between heart attack and other cardiovascular disease and the level of plaque increasing are found. The higher the level of plaque the higher risk of heart disease will be. The level of plaque will increase as the result of high level of cholesterol, type LDL, so called â€Å"bad cholesterol† in blood. When the level of LDL is normal, blood can pass in and out of the blood vessels without problems, but if it significantly increase particles of the blood will accumulate and sooner or later provoke trigger (cause) heart attack. Other very important factors influencing plaque level increasing are high blood pressure and cigarette smoking. Both factors accelerate the plaque formation changing (damaging) artery walls and even more, helping cholesterol forming. Medical experience proved that plaque composition and vulnerability (hard or soft plaque) is more responsible for the conversion of a stable disease to a life-threatening condition than the plaque size. Except the plaque vulnerability the risk of plaque disruption is are consequence of rupture triggers (extrinsic forces). Soft plaque – lipid-rich one is more dangerous because of its instability and higher probability for rupture. Even (IAKO) Although â€Å"hard plaque† that one having higher level of calcium influence on the blood vessels walls and their â€Å"hardness† experience show that heart attacks are mostly caused by soft plaque disruption. Figure 4 Plaque rupture and its consequences in the form of heart diseases http://www. nature. com/nrg/journal/v7/n3/fig_tab/nrg1805_F2. html Risk factors of coronary heart disease Risk factors influencing cardiovascular disease we can group based on their stability into the three groups: a) Modifiable risk factors In this group hypertension is the most dangerous risk factor for heart attacks, but even more for stroke. It is forming as the result of abnormal blood lipid levels which means high total cholesterol, high levels of triglycerides and high levels of low-density lipoprotein or low levels of high-density lipoprotein (HDL). Smoking, physical inactivity, Type 2 diabetes, and a diet full with saturated fats are risk factors strongly influencing the heart disease. All of them are treatable and patients (individuals) belonging into the different types of risk customers’ groups should avoid practice them. b) Non-modifiable risk factors The factors from this group mostly are constant, like the case in gender or family history. Others are changing when time is passing, like age and lifestyle and personal habits. Older people have more chance to get heart attack and the man, especially those having â€Å"bad medical history†. Ration between man and woman are changing when women past the menopause. After that the level of risk is similar as the men’s one. As I’ve presented there is direct correlation between cardiovascular disease and condition and health of blood vessels, more precisely of developing atheroma, means level and structure of plaque in vessels. On the other development of plaque and its level is directly influenced by level of cholesterol and some other elements which are connected with individual person and his/her life and genetic predispositions. As with the other diseases everybody has some risk of developing atheroma, but some risk factors increase the risk level for several categories. Those risk factors include: fn 12 †¢Fixed risk factors – factors that person cannot change: oA strong family history which means close relatives who developed heart disease or a stroke before they were 55 (for males) or 65 (for female). Severe baldness in men at the top of the head. oAn early menopause in women. oAge. Older people have more risk to develop atheroma. oEthnic group. Medical data show that people from different ethnic group have different risk for heart diseases. †¢Treatable or partly treatable risk factors include different health problems caused basically by the same causes as the: oHypertension (high bl ood pressure). oHigh cholesterol blood level. oHigh triglyceride (fat) blood level. oDiabetes. oKidney diseases causing diminished kidney function. All factors from this group have to be controlled and monitor. Any kind of their complication probably will trigger more serious problems such as heart attack or stroke. †¢Lifestyle risk factors that can be prevented or changed. Actually these factors PRETHODE precede to those belonging to the second group. Except the genetic factors way of life and daily habits are the more responsible for different kind of heart diseases. Those factors are: oSmoking (Smoking cigarette increase blood pressure, decrease HDL; damages arteries and blood cells and increases heart attacks. Passive smoking is also a risk factor for cardiovascular disease ) oLack of physical activity. Obesity (People who are overweight (10-30% more than their normal body weight) have 2 to 6 times the risk of developing heart disease. ) oAn unhealthy diet and eating too much salt. oExcess alcohol. Looking on those three groups one can easily conclude that people with â€Å"bad predisposition† having high fixed risk factors have to think about their lifestyle risk factors ev en more, in order to try to decrease the second group of factors (treatable or partly treatable risk factors). On the other hand some of risks are more dangerous than the others; for example smoking increases risk for heart disease more than obesity. And of course combination of two or more risk factors increases significantly the level of risks; older man (or woman) who smokes, without physical activity and with bad eating habits has more chance to get some of previously explained disease than the one who have â€Å"just one of bad habits†. The more risk factors someone has the greater is the likelihood that he/she will develop cardiovascular disease, unless taking action to modify his/her risk factors and working to prevent them compromising his/her heart health. That doesn’t mean that people with â€Å"good genes† can be irresponsible and ZANEMARITI risk factors from other groups. With or without genetic predisposition modern life significantly increases a risk of heart disease for everybody. Hormones impact on lipids and other risk factors Different numbers of man and women died from heart attack initiated a lot of research about hormones’ influence on the risk factor and heart disease development. Number of men died from the heart attack outnumbered the number of women in pre-menopause period, but in the post-menopause data show completely opposite situation. A percentage of women in post-menopause having heart disease and dying from heart attack increase dramatically and now outnumbered the men. The main reasons for those changes are connected to the level of hormones and their influence on level and structure of cholesterol and consequently on risk factors and heart disease. As mentioned before total cholesterol actually is made of two different types of cholesterol: LDL – low density lipoprotein (LDL), so called bad cholesterol and high density lipoprotein (HDL). High levels of LDL cholesterol lead to atherosclerosis increasing the risk of heart attack and ischemic stroke. HDL cholesterol reduces the risk of cardiovascular disease as it carries cholesterol away from the blood stream. http://www. walgreens. com/marketing/library/careguides/careguide. jsp? docid=000225=28=High%20Cholesterol Estrogen, a female hormone, raises HDL cholesterol levels, partially explaining the lower risk of cardiovascular disease seen in premenopausal women. But after menopause (natural or surgical) when a level of estrogen significantly decreases total cholesterol rises, low density lipoprotein (LDL) cholesterol rises, and high density lipoprotein (HDL) cholesterol does not change or decreases slightly. This is the reason why negative hormones’ effect after menopause increasing more than proportionally. Some authors argue that even influence of estrogen on LDL and HDL level is proved it is yet unclear whether increase in risk is caused, at least partially, by increased level of androgen (the other of hormones belong to steroid as estrogen too), which is characteristics of menopause too. This sexual dimorphism means a lower incidence in atherosclerotic diseases in premenopausal women, which subsequently rises in postmenopausal women to eventually equal that of men. These observations point towards estrogen and progesterone playing a lifetime protective role against CAD in women. As exogenous estrogen and estrogen plus progesterone preparations produce significant reductions in low-density lipoprotein (LDL) cholesterol levels and significant increases in high-density lipoprotein (HDL) cholesterol, this should in theory lower the risk of CAD. UKLOPITI U ONO GORE Among estrogen’s positive effects on the heart are: †¢Reducing the LDL (â€Å"bad†) cholesterol in the blood. †¢Increasing the HDL (â€Å"good†) cholesterol in the blood. †¢Helping to keep blood vessels open. †¢Lowering blood pressure at night. †¢Reducing blood viscosity (how sticky the blood is), a property that may cause blood clots which could result in a heart attack or stroke. Estrogen’s effects on clotting are complicated, however, since there also is an increased risk for thromboembolism (a blood clot that blocks a vessel) in women taking estrogen. Possibly enhancing fibrinolysis, which is the body’s natural process for breaking down blood clots. Read more: http://ehealthmd. com/content/what-are-benefits-hrt#ixzz2NbWR3MxY http://ehealthmd. com/content/what-are-benefits-hrt#axzz2NbW1GJJN Nutrition guidelines As presented before three different groups of risk factor exist. Some of them people can cha nge but the other are fixed, non-changeable because they caused by genetic heritage ( ) influences. Controllable factors are connected to the lifestyle of person. Lifestyle changes can prevent or slow the development of coronary plaque and heart disease. In order to prevent a disease development one have to keep track of his/her blood pressure and cholesterol levels. Choosing a heart-healthy diet is vital in controlling weight, which helps keep blood pressure and cholesterol levels down. Foods high in cholesterol and saturated fat should be avoided, and quitting smoking is imperative. Regular exercise and an increased overall activity level contribute to heart health and help reduce stress. The risk of cardiovascular disease is possible to reduce following recommendation for lifestyle changing: Cessation of smoking and avoidance of second-hand smoke. Nutrition should ensure a healthy diet wiht total diet no more than 8% of saturated + trans fatty acids of total energy intake. All people, especially ones with high risk factors should lower alcohol consumption As the prevention physical activities are recommended – at least 30 minutes of moderate intensity physical activity per day or three days week (i. e. 150 mins/week minimum). Currently practiced measures to prevent cardiovascular disease include: †¢A low-fat, high-fiber diet including whole grains and plenty of fresh fruit and vegetables (at least five portions a day)[29][30] †¢Tobacco cessation and avoidance of second-hand smoke;[29] †¢Limit alcohol consumption to the recommended daily limits;[29] consumption of 1-2 standard alcoholic drinks per day may reduce risk by 30%[31][32] However excessive alcohol intake increases the risk of cardiovascular disease. [33] †¢Lower blood pressures, if elevated, through the use of antihypertensive medications[citation needed]; †¢Decrease body fat (BMI) if overweight or obese;[34] Increase daily activity to 30 minutes of vigorous exercise per day at least five times per week;[29] †¢Decrease psychosocial stress. [35] Stress however plays a relatively minor role in hypertension. [36] Specific relaxation therapies are not supported by the evidence. [37] Routine counselling of adults to advis e them to improve their diet and increase their physical activity has not been found to significantly alter behaviour, and thus is not recommended. [38] http://www. news-medical. net/health/What-is-Cardiovascular-Disease. aspx http://www. barnesandnoble. om/w/prevent-halt-and-reverse-heart-disease-joseph-piscatella/1100260037 Primary and secondary prevention of heart disease It is necessary start with prevention from heart disease as early as possible. Changes in the number of people killed by heart attack in developed countries show that prevention and awareness about this group of disease help to http://circ. ahajournals. org/content/123/20/2274/F2. expansion. html health plans must continue to drive cardiovascular care further along the continuum toward primary prevention of cardiovascular disease (CVD). CVD risk factors should be managed not only after a coronary event has occurred, but also before the onset of such and event. Ideally, health lifestyles should be promoted with all patients so that risk factors for CVD never develop. In this way, CVD care can be moved from the inpatient setting to the outpatient setting. Sidney C. Smith Jr, MD. Focus on Cardiovascular Disease; A Word About the Quality of Care in Cardiovascular Disease. Director, Center for Cardiovascular Science and Medicine University of North Carolina at Chapel Hill. http://www. qualityprofiles. rg/leadership_series/cardiovascular_disease/cardiovascular_introduction. asp Key priorities for implementation Primary prevention of CVD †¢For the primary prevention of CVD in primary care, a systematic strategy should be used to identify people aged 40–74 who are likely to be at high risk †¢People should be prioritised on the basis of an estimate of their CVD risk before a full formal risk assessment. Thei r CVD risk should be estimated using CVD risk factors already recorded in primary care electronic medical records †¢Risk equations should be used to assess CVD risk People should be offered information about their absolute risk of CVD and about the absolute benefits and harms of an intervention over a 10-year period. This information should be in a form that: opresents individualised risk and benefit scenarios opresents the absolute risk of events numerically ouses appropriate diagrams and text (See www. npci. org. uk) †¢Before offering lipid modification therapy for primary prevention, all other modifiable CVD risk factors should be considered and their management optimised if possible. Baseline blood tests and clinical assessment should be performed, and comorbidities and secondary causes of dyslipidaemia should be treated. Assessment should include: osmoking status oalcohol consumption oblood pressure (see ‘Hypertension’, NICE clinical guideline 34) obody mass index or other measure of obesity (see ‘Obesity’, NICE clinical guideline 43) ofasting total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides (if fasting levels are not already available) ofasting blood glucose orenal function oliver function (transaminases) thyroid-stimulating hormone (TSH) if dyslipidaemia is present †¢Statin therapy is recommended as part of the management strategy for the primary prevention of CVD for adults who have a 20% or greater 10-year risk of developing CVD. This level of risk should be estimated using an appropriate risk calculator, or by clinical assessment for people for whom an appropriate risk calculator is not available or approp riate (for example, older people, people with diabetes or people in high-risk ethnic groups) †¢Treatment for the primary prevention of CVD should be initiated with simvastatin 40 mg. If there are potential drug interactions, or simvastatin 40 mg is contraindicated, a lower dose or alternative preparation such as pravastatin may be chosen. Secondary prevention of CVD †¢For secondary prevention, lipid modification therapy should be offered and should not be delayed by management of modifiable risk factors. Blood tests and clinical assessment should be performed, and comorbidities and secondary causes of dyslipidaemia should be treated. Assessment should include: osmoking status oalcohol consumption oblood pressure (see ‘Hypertension’, NICE clinical guideline 34) obody mass index or other measure of obesity (see ‘Obesity’, NICE clinical guideline 43) ofasting total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides (if fasting levels are not already available) ofasting blood glucose orenal function oliver function (transaminases) othyroid-stimulating hormone (TSH) if dyslipidaemia is present. Statin therapy is recommended for adults with clinical evidence of CVD †¢People with acute coronary syndrome should be treated with a higher intensity statin. Any decision to offer a higher intensity statin should take into account the patient’s informed preference, comorbidities, multiple drug therapy, and the benefits and risks of treatment †¢Treatment for the secondary prevention of CVD should be initiated with simvastatin 40 mg. If there are potential drug interactions , or simvastatin 40 mg is contraindicated, a lower dose or alternative preparation such as pravastatin ay be chosen †¢In people taking statins for secondary prevention, consider increasing to simvastatin 80 mg or a drug of similar efficacy and acquisition cost if a total cholesterol of less than 4 mmol/litre or an LDL cholesterol of less than 2 mmol/litre is not attained. Any decision to offer a higher intensity statin should take into account informed preference, comorbidities, multiple drug therapy, and the benefit and risks of treatment http://www. eguidelines. co. uk/eguidelinesmain/guidelines/summaries/cardiovascular/nice_lipid_modification. php How to lower the risk of cardiovascular disease The risk of cardiovascular disease is possible to reduce following recommendation for lifestyle changing: Cessation of smoking and avoidance of second-hand smoke. Nutrition should ensure a healthy diet wiht total diet no more than 8% of saturated + trans fatty acids of total energy intake. All people, especially ones with high risk factors should lower alcohol consumption As the prevention physical activities are recommended – at least 30 minutes of moderate intensity physical activity per day or three days week (i. . 150 mins/week minimum). Cessation of smoking The aim of this measure is complete cessation of smoking and avoidance of second-hand smoke. Patient and their families need to stop smoking. Those who are unable to quit may need professional help in form of counselling, behavioral therapy and even pharmacological therapy. Nicotine replacement therapy (NRT) is the first line choice of medication. Nutrition The aim of thi s measure is to ensure a healthy diet. Total diet should have no more than 8% (of total energy intake) of saturated + trans fatty acids. All patients are advised to take approximately 1g Eicosapentaenoic acid (EPA) and Docosahexaenoic acid (DHA) and more than 2g Alpha Linolenic Acid (ALA) daily. Diet should have vegetables, fruits and legumes, grain-based foods, moderate amounts of lean meats, poultry, fish and reduced fat dairy products. EPA and DHA can be obtained from oily fish and marine n-3 (fish oil) capsule supplements. Alcohol consumption All patients should be advised to lower alcohol consumption. Men should drink no more than 2 standard drinks per day and women no more than 1 standard drink per day. Physical activity The aim of this measure is to raise physical activity and exercise to the recommended goal of at least 30 minutes of moderate intensity physical activity on most, if not all, days of the week (i. e. 150 mins/week minimum). Maintaining a healthy body weight The aim should be to achieve a waist measure of less than or equal to 94 cm in men and less than or equal to 80 cm in women. The body mass index (BMI) should be maintained at 18. 5–24. 9 kg/m2 Lowering blood cholesterol The aim of therapy should be to maintain blood cholesterol at: †¢Low density lipoprotein (LDL) at – less than 2. mmol/L †¢HDL – more than 1. 0 mmol/L †¢Triglyceride (TG) less than 1. 5 mmol/L The blood cholesterol can be maintained with the use of pharmacotherapy. Statins are commonly used lipid lowering drugs. Those with diabetes and atherosclerosis need stringent blood cholesterol control as well. Other lipid lowering drugs include fibrates like gemfibrosil, clofibrates etc, Eze timiber and niacin. Lowering blood pressure High blood pressure is one of the important risk factors for cardiovascular disease. Those with coronary heart disease, diabetes, kidney disease or stroke need tight blood pressure control. The aim should be a blood pressure of less than 130/80 mm of Hg. Diabetes and blood sugar control Those diagnosed with diabetes need stringent blood sugar control to prevent cardiovascular damage. HbA1c levels should be maintained at less than 7%. Other drugs to lower risk of cardiovascular disease Other drugs used to lower risk of cardiovascular diseases include: †¢Antiplatelet agents – this includes Aspirin and Clopidogrel. These drugs when given to patients with risk of heart attacks may prevent such attacks and events. †¢ACE inhibitors like Enalapril, Captopril, Lsinopril and Cardiovascular Diseases

Contractual Agreement for an Architect in Canada Research Paper

Contractual Agreement for an Architect in Canada - Research Paper Example The general architect is entirely responsible for the construction in accordance with this kind of agreement and for every compensation made for the expenses and performance connected to the subcontractors. The advantages associated with kind of contractual arrangement include: A single prime deal is regularly simpler to manage since it has a centralized task for the architect and client. The transactions made by the client are transferred to one architect, reducing the possibility of confusion, unlike multiple prime contractors. Design plans for the construction are originally arranged by a planning expert. The client then selects one architect to perform the work, following a bidding procedure grounded on the design plans. This is the most widespread of architectural deal used in Canada. This is because another major advantage lays in the plans and requirements being prepared by design experts turning out to be part of the bidding credentials. This way, the client is bound to recei ve high quality outcomes of the construction from the contractors (Quatman and Dhar 342). ... 2. Design-build contractual agreement The Design-build agreement is an accord between a client and an architectural firm that offers design and building services (Hopper 134). An expansion of this kind of contract is a â€Å"turnkey† project where the contractor gets project funding, acquires land, offers blueprint and construction services, and delivers the final product to the client, available for occupancy. The advantages of using this kind of contractual agreement include: Saving time, an aspect of the sort of  contract an architect might go into when offering archetypal Design-Bid-Build services. Nevertheless, time is not considered a major factor in architecture in comparison with the expenses, construction and quality of the project. The association with a quick track program, able to eliminate the possibility of incorporated designs. The programs frequently imply that each period of the building phase is spent with the occupants to determine their requirements in th e new building (OAA 2011). When the designer operates for the builder, instead of working directly for the client, checks and balances existing in other techniques’ are mislaid. The architect and contractor’s engineer, otherwise known as the ‘clerk of the works’ in Canada, are normally depended upon to maintain the trend made by the construction. This approach of the contract assures that the builder sticks to the plans and regulations of the contract. Under such an observation, the client is guaranteed adherence and honor to the contract made with the construction organization (Quatman and Dhar 342). Certain disadvantages may arise from this kind of contractual agreement depending on the organization and builders the client has awarded. The demerits

The Foreign Corrupt Practices Act Research Paper

The Foreign Corrupt Practices Act - Research Paper Example INTRODUCTION This paper shall discuss the Foreign Corrupt Practices Act of 1977 (FCPA), which is a United States federal law passed mainly to ensure accounting transparency as mandated by the Securities Exchange Act of 1934. It also includes provisions meant to address the bribery of foreign officials. This paper shall discuss the act, including its pertinent details and essential provisions, as well as its reasons for passage and application. II. BODY The Foreign Corrupt Practices Act is a law which includes specific provisions on accounting and prohibitions on bribery (Cook and Connor, p. 2). The accounting provisions of the law are meant to prohibit illegal accounting practices which are often carried out to conceal corrupt practices. The provisions are also meant to guarantee that company shareholders, including the Securities and Exchange Commission are given an accurate picture of corporate status and finances (Cook and Connor, 2010). This law covers two groups of corporate per sonalities, first are â€Å"those with formal ties to the United States and those who take action in furtherance of a violation while in the United States† (Cook and Connor, 2010, P. 2). The US issuers and domestic concerns are required to heed the provisions of the FCPA, regardless of their actions being within or outside the US territories. Issuers are companies with securities in the US or those which are legally called for to regularly report with the US SEC (Cook and Connor, 2010). On the other hand, those under domestic concerns have a wider coverage, and include individuals or residents of the US. Corporations, partnerships, business trusts, sole proprietorships, and like entities are also covered under domestic concerns, for as long as their main place of business is in the US or their governing provisions are under the US laws (Cook and Connor, 2010). This act holds corporations and other entities legally liable for bribing foreign officials even if such act was carr ied out beyond American shores and throughout the years, various violators have been prosecuted under these provisions. The basic provisions of this law hold the following practices as illegal: â€Å"1) a payment, offer, authorization, or promise to pay money or anything of value; 2) to a foreign government official (including a party official of manager of a state owned concern), or to any other person knowing that the payment of promise will be passed on to a foreign official; 3) with a corrupt motive; 4) for the purpose of (a) influencing any act or decision of that person, (b) inducing such person to do or omit any action in violation of his lawful duty, (c) securing an improper advantage, or (d) inducing such person to use his influence to affect an official act or decision; 5) in order to assist in obtaining or retaining business for or with, or directing any business to, any person† (FCPA, in Cook and Connor, 2010, p. 2). Individuals and corporate entities violating th e provisions of this law can be held criminally liable and may be imprisoned and/or fined for their actions (Biegelman and Biegelman, 2010). The law also provides a generalized definition for what is to be qualified as ‘payment’ punishable under the FCPA. The FCPA defines these payments to cover any benefits (monetary or otherwise) given or gifted to a foreign official in order to curry favorable treatment in business activities with the involved foreign official (Cook and Connor,

Blood clotting enzyme Essay Example for Free

Blood clotting enzyme Essay Serine protease proteins are important enzymes involved in the process of blood coagulation. Blood coagulation is an importance defense mechanism that prevents the host mammal organism from losing excess blood or from forming unwanted blood clot. The process of coagulation can be initiated by both intrinsic factors and extrinsic factors. A cascade of event is followed which activate these enzymes; normally the enzymes are inactive state a condition called zymogens. Zymogens by their virtual condition of being inactive prevent unwanted blood clotting which may have a far reaching consequence such as thrombosis. Blood clotting in a series of processes, in which the zymogens’ need to be activated by reacting with its glycoprotein co-factors. Among the serine protease is the thrombin enzyme factor five (v) responsible for clearing clot in the blood. The enzyme is usually present circulating in plasma which is made up of a single monomer chain, it life span can range from 12 to 36 hours. In human the main regulator in blood coagulation is erythrocytes leukemia cells which activate adenylate cyclase, the process is reversible by the interaction of Aalpa-thrombin with glycoprotein while b alpha enhance the platelets interaction which initiate the proteolytic process. Fibrin-bound thrombin is cleaved by thrombin at a very specific site at the extracellular N-terminal, PAR-1 regulates a number of endothelial cell biology, vascular development but more so is a mediator of thrombin signaling. The human thrombin consist of two gamma chains namely the gamma A and gamma’ the final stage of coagulation of mammalian blood involves the cleavage of the four arginine and glycine bond. Binding studies shows both fibrin 1 and fibrin 2 with low affinity to the E domain and high binding affinity at the extreme end of 408 to 425 on the gamma chain The mode of action involves conversion of fibrinogen to fibrin by breaking the bonds in the fibrinogen at a precise position of arginine and glycine where the fibrin peptides are released. The serine proteases require restructuring itself in order to fit the key and lock model. The glycine at the position five is highly conserved because it is the one which occupy the active site which is determine by the acryl group during the substrate conformation. Asparagines 189 help the enzyme to easily recognize the substrate. The active site is entirely made of histidine 57, asparagines 102, serine 195 and serine 214. The reaction on many a times prefers position 1 to position 4 during remodeling, therefore the type of protein presence to a large extend determine the kind protease and also the kind of cleavage to take place. Thrombin activation is regulated by pentapeptide of the COOH terminus of the factor (v) heavy chains. Thrombin and thrombin receptors is another regulatory point where they both posses strong protective barrier and at the same time cancerous cells were eliminated by apoptosis. A study carried out using mitochondrial membranes which were depolarized using attenuated Catalase lead to controlled cell death. Statistical finding indicate that 30% of the population carried world wide indicated that activated peptide segment at position 4 of factor eight caused a substitution in V34L after binding the structure and analyzing the interaction according to (Brenda 2010). The switching of receptor is PAR-1-dependent signaling specifically to thrombin resulting inhibition of adhesion cell surface which activate thrombin the ligand occupancy position switches the protease receptor by signaling specifically to the thrombin. Human cell in culture indicated low amount of thrombin and receptor PAR-1 agonist induced strong anti-inflammatory activities which was secondary effect of the low concentration of thrombin after activation by P13 kinase and PAR-1. Thrombin like other enzymes is very specific in the binding domain and the insertion loop which is determined by the residues involved in ligand binding as result of interaction glycoprotein and protease receptor on the platelet membrane. This uniqueness makes it very efficient in it task according to (Webert 2006). The enzyme play vital role in homeostasis, cell differentiation, thrombosis and activation of blood cell types, on exposure to phosphatidylserine on the outer surface the platelets were stimulated. A study done using heparin indicated an overlap of the active site, which was attributed to the interaction of thrombin and the gamma peptide chains to the external and the interaction to the active site in close proximity to the Na+ of the substrate. The role of the enzyme can be explained in terms of NA+ binding to thrombin on the basis of prothrombotic and procoagulant. The cascade is a continuous cycle of events that are activated by two factors ,factor (ix) and factor (viii) to form tenase complex which is discontinued by down regulation that occur in the following mechanism which include; serpin (serine protease inhibitors) which function to degrade thrombin and other activation factors, it can also be regulated by protein C where thromodulin bind to it and is inactivate in the presence of protein S, limiting the action of tissue factor by the tissue factor pathway inhibitors by inhibiting excessive TF mediated activation of factor (ix) and factor (x), plasmin help to degrade fibrin hence preventing more fibrin being formed and lastly but not the least regulation through adenylate cyclase pathway by inhibiting platelet activation by decreasing cytosol level of calcium which ultimately result to decreased release of granules which are responsible for the activation of more platelets and coagulation cascade. In conclusion the work play by thrombin enzyme is of paramount importance considering the complexity of the enzyme kinetics involved in the human body. References Brenda Enzyme database retrieved on 13 August 2010 from http://www. brenda-enzymes. org/php/result_flat. php4? ecno=3. 4. 21. 5 Furie B, Furie BC (2005). Thrombus formation in vivo. J. Clin. Invest. 115 (12): retrieved on 12 August 2010 from http://www. jci. org/cgi/content/full/115/12/3355. Webert KE, Cook RJ, Sigouin CS, (2006). The risk of bleeding in thrombocytopenic patients with acute myeloid leukemia. haematologica .

NAFTA and Mexico Essay -- essays research papers fc

Mexico’s economy is undergoing a stunning transformation. Seven years after the launch of the North American Free Trade Agreement, it is fast becoming an industrial power. Free trade with the U.S. and Canada is turning the country from a mere assembler of cheap, low-quality goods into a reliable exporter of sophisticated products from auto breaks to laptops computers. Although Mexico has seen economic growth lately, it still faces tremendous problems in the aftermath of the 1995 recession and the revolution that took place in the Chiapas which still wages on today. The purpose of this paper is to explore the effects that NAFTA has had on the economy and it’s people during the implementation of NAFTA and in what NAFTA will bring in the future. The North American Free Trade Agreement was designed to open borders and promote free trade between three countries: Canada, the United States and Mexico. Signed in 1992, ratified by the U.S. Congress in November 1993 and implemented January 1, 1994, NAFTA reduced some tariffs immediately while others are scheduled to fall to zero over a 15-year period. NAFTA follows the prescription of liberalization- including the deregulation of government restrictions to allow increased trade, direct foreign investment, and foreign ownership of businesses.   Ã‚  Ã‚  Ã‚  Ã‚  On January 1, 1994, a Mexico still sleepy from New Year’s celebrations awoke to discover a passionate new revolution sweeping across the state of Chiapas. The Zapatistas, a small, yet powerfully forceful group of indigenous people, exhausted from centuries of oppression, poverty and corruption, rose up to end this societal injustice, and most specifically, to battle the new tyrant that would be born that very day: The North American Free Trade Agreement. This revolt was viewed by the indigenous population of Chiapas as an essential act to stop the debilitating cycle of injustice and to prevent future harm to the Mexican people by opposing NAFTA. â€Å"The Zapatistas have pulled back the curtain that covered up the other Mexico. It is not the Mexico of eager entrepreneurs lined up to open Pizza Hut franchises or consumers eager to shop at Wal-Mart, but rather the Mexico of malnourished children, illiteracy, landlessness, poor roads, lack of health clinics, and life as a permanent struggle.† (Quoted in Russell, p. 1)   Ã‚  Ã‚  Ã‚  Ã‚  NAFTA was ... ...nmental Issues Under the NAFTA. Canadian – American Committee. Toronto: 1993. Marinez, Elizabeth and Arnoldo Garica. (No Date). What is â€Å"Neo Liberalism†? [Online]. Avaible:   Ã‚  Ã‚  Ã‚  Ã‚  http://www.corpwatch.org/trac/corner/glob/neolib.html (June 27-29, 1997). NAFTA’s Failure to Deliver [Online]. Available:   Ã‚  Ã‚  Ã‚  Ã‚  http://www/coha.org/pressr/naftapr/html Nelan, Bruce W. (April 4, 1994). Days of Trauma and Fear [Online]. Available:   Ã‚  Ã‚  Ã‚  Ã‚  http://www.time.com/time/magazine/archieves/1994/940404/940404.mexico.html Perlo, Vicotr. (March 4, 1995). The Rape of Mexico [Online]. Available:   Ã‚  Ã‚  Ã‚  Ã‚  http://www.hartford-hwp.com/archives/46/031.html â€Å"The President, the peso, the market and those Indians.† The Economist 24 Dec 1994: 43. Russell, Philip. The Chiapas Rebellion. Mexico Resource Center. Austin: 1995 Shadows of Tender Fury: The Letters and Communiques of Subcomandante Marcos and the Zapatista Army of National Liberation. Monthy Review Press. New York: 1995 Wise, Carol. â€Å"The Post-NAFTA Political Economy.† Mexico and the Western Hemisphere. Pennsylvania State University Press: September 1998.