You should consult your General Practitioner to discuss methods of lowering this level.
You should consult your General Practitioner to discuss methods of lowering this level.
No specific intervention is required, just maintain a healthy lifestyle.your LDL levels are slightly above optimal. You should discuss appropriate lifestyle changes with your General Practitioner.your LDL level is higher than what is considered optimal. You should consult your General Practitioner to discuss methods of lowering this level. This may include lifestyle changes and/or medication.please enter your LDL Cholesterol level.HDL Cholesterolyour HDL level falls within the optimal range. No specific intervention is required, just maintain a healthy lifestyle.Your HDL cholesterol is in the normal range.your HDL level is lower than what is considered optimal. You should consult your General Practitioner to discuss methods of raising this level. This may include lifestyle changes and/or medication.please enter your HDL cholesterol level.Total Cholesterolyour total cholesterol level is appropriate for your age and gender. However more important than the total level is the individual components, LDL and HDL.
Optimally, your LDL should be low and your HDL high, check above to see that your level for these is optimal.your total cholesterol level is higher than what is considered optimal. You may like to discuss this with your General Practitioner and also assess the level of the individual components, LDL and HDL.please enter your total cholesterol level.Triglyceridesyour level of triglycerides falls within the optimal range. No specific intervention is required, just maintain a healthy lifestyle.your triglyceride level is higher than what is considered optimal. You may like to discuss these results with your General Practitioner.please enter your triglyceride level.ReferenceNational Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation 2002; 106: 3143–3421.This information will be collected for educational purposes, however it will remain anonymous. What is the evidence for using these treatments to lower LDL cholesterol? Many trials have been conducted to look at the benefits for patients of taking cholesterol lowering medications. Some of the results are summarised below: The Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 (PROVE IT-TIMI 22) trial in Boston compared a high-dose statin treatment to a low-dose statin treatment.
The higher dose provided greater protection against death, heart attack, chest pain requiring hospital admission, and stroke; and improved outcomes over two years among patients with acute heart disease.reduslim prezzo Another group of researchers from the United States showed in their trial, the Treating to New Targets (TNT) trial, that intensive lipid-lowering treatment provides more significant clinical benefit compared with a lower dose of statin drug. The Heart Protection Study in the UK showed that lowering LDL cholesterol from below 3 mmol/L to below 2 mmol/L reduced the risk of heart disease by about one quarter. Overall, the results of these trials suggest that intensive therapy to lower LDL cholesterol levels is beneficial in treating both acute and stable heart disease. They also suggest that high-risk patients may benefit from more extensive lowering of LDL-cholesterol than was once thought necessary. More information For more information on cholesterol, including the health effects of high cholesterol and ways to lower cholesterol levels, as well as some useful tools, see Cholesterol. References Brown AS, Bakker-Arkema RG, Yellen L, et al. Treating patients with documented atherosclerosis to National Cholesterol Education Program-recommended low-density-lipoprotein cholesterol goals with atorvastatin, fluvastatin, lovastatin and simvastatin. J Am Coll Cardiol.
1998; 32: 665. Cannon CP, Braunwald E, McCabe CH, et al. Intensive versus moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med. 2004; 350(15): 1495-504. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the third report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III). JAMA. 2001; 285: 2486-97. Heart Foundation Australia. Lipid Management Guidelines 2001.
Medical Journal of Australia. 2001; 175: S57-S88. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high risk individuals: A randomised placebo-controlled trial. Lancet. 2002; 360: 7-22M.
Kastelein JJ, Isaacsohn JL, Ose L, et al. Comparison of effects of simvastatin versus atorvastatin on high-density lipoprotein cholesterol and apolipoprotein A-I levels. Am J Cardiol. 2000; 86: 221. LaRosa JC, Grundy SM, Waters DD, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med.
2005; 352(14): 1425-34. Ray KK, Cannon CP, McCabe CH, et al. Early and late benefits of high dose atorvastatin in patients with acute coronary syndromes: results from the PROVE IT-TIMI 22 trial. J Am Coll Cardiol. 2005; 46(8): 1405-10. Sacks FM, Tonkin AM, Shepherd J, et al, for the Prospective Pravastatin Pooling Project Investigators Group. Effect of pravastatin on coronary disease events in subgroups defined by coronary risk. Circulation. 2000; 102: 1893. Wood D, De Backer G, Faergeman 0, et al. Prevention of coronary heart disease in clinical practice: recommendations of the Second Joint Task Force of European and other Societies on coronary prevention.
Eur Heart. 1998; 19: 1434-503. Drugs used in this treatment: Jezil (Gemfibrozil) Lipitor (Atorvastatin calcium) Nicotinic Acid (Nicotinic acid) Vytorin (Ezetimibe/ Simvastatin) Zocor (Simvastatin) What is Haemorrhoids (Piles; Hemorrhoids) Statistics on Haemorrhoids (Piles; Hemorrhoids) Risk Factors for Haemorrhoids (Piles; Hemorrhoids) Progression of Haemorrhoids (Piles; Hemorrhoids) Symptoms of Haemorrhoids (Piles; Hemorrhoids) Clinical Examination of Haemorrhoids (Piles; Hemorrhoids) How is Haemorrhoids (Piles; Hemorrhoids) Diagnosed? Prognosis of Haemorrhoids (Piles; Hemorrhoids) How is Haemorrhoids (Piles; Hemorrhoids) Treated? Haemorrhoids (Piles; Hemorrhoids) References What is Haemorrhoids (Piles; Hemorrhoids) Haemorrhoids or piles are located in the anus. The term when used in a clinical sense, refers to the internal disruption or downward displacement of the anal cushions. The anal cushions are tissue structures rich in blood supply, that line the anus and contribute to anal closure. They are classified according to their clinical presentation: First degree haemorrhoids occur when the is some bleeding present.
Second degree heamorrhoids refer to spontaneously reducing prolapse of the anal cushions during defaecation. Third degree haemorrhoids refers to prolapse requiring manual replacement. Fourth degree haemorrhoids indicates permanent prolapse. Haemorrhoids may be referred to as internal or external, depnding on the location of the prolapse. Haemorrhoids are often defined as varicosity of the anal veins causing engorgement. This definition is incomplete, as although commonly defined through the clinical presentation of bleeding, haemorrhoids actually refer to the prolapse of the anal cushions. Statistics on Haemorrhoids (Piles; Hemorrhoids) Up to 4% of the population may have haemorrhoids. Many patients often do not present to health care facilities due to embarassment or the fact that the haemorrhoids spontaneously resolve.
The peak age of occurence is 45-65 years, however, they can occur at any age. Risk Factors for Haemorrhoids (Piles; Hemorrhoids) The anal cushion often prolapse due to engorgment of the blood vessels within them. Factors that may predispose an individual to haemorrhoids may include: excessive straining on defecation, constipation, inflammatory bowel disease, pregnancy, colon cancer, liver disease, loss of muscle tone, occupational (prolonged sitting), obesity and chronic diarrhoea. Progression of Haemorrhoids (Piles; Hemorrhoids) First and second degree internal haemorrhoids may present with rectal bleeding, a lump, discharge, or itching. They may not progress to third or fourth degree haemorrhoids, especially if the patient improves the fibre and fluid content of his/her diet. Haemorrhoids may also present acutely with severe pain as they protrude through the anus and cause the anal sphincter to spasm. A positive “vicious cycle” can be responsible for progression of this episode. As the vascular cushions protrude through a tight anus, they become more congested, which may cause further protrusion, eventually causing the haemorrhoids to strangulate (cut off blood supply) – causing further severe pain and become difficult to be reduced. Eventually the haemorrhoids will ulcerate.
External haemorrhoids similarly may suddenly rupture – usually after straining at stool or heavy lifting. This usually causes thrombosis of the vein – and a painful swollen lump. The skin overlying the thrombosed vein can ulcerate – and eventually with healing a “skin tag” may be all that remains. How is Haemorrhoids (Piles; Hemorrhoids) Diagnosed? Full blood count – if anaemia is suspected. Older patients (>50), as well as those with significant family history of colon cancer or significant anaemia also reqiure either: Colonoscopy.
This allows for inspection of the whole of the colon and biopsies of any suspicous lesions; A sigmoidoscopy may be preferrable. Although it only examines the distal 2/3 of the colon – it requires less preparation of the bowel, and any cause of PR bleeding will almost always be in that part of the bowel. A double contrast Barium Enema is often combined with a sigmoidoscopy. Prognosis of Haemorrhoids (Piles; Hemorrhoids) Haemorrhoids are a chronic condition – but they are treatable. Lower degrees of haemorrhoids (first and second) usually resolve but they can progress, especially if the risk factors – (constipation, straining, hard stools) are not addressed. Higher degrees usually require treatment. Acutely strangulated or thrombosed haemorrhoids can subside on their own over a few days – and surgeons are divided on whether to operate on them immediately, as haemorrhoidectomy (surgery to treat haemorrhoids) can have complications. Recurrence rates are estimated to be 10-50% over 5 years. How is Haemorrhoids (Piles; Hemorrhoids) Treated? All patients should be treated conservatively through techniques such as avoiding prolonged straining, increasing fibre and fluid intake and the use of stool softeners. If these technqiues are inadequate, there are many other interventional options ranging from cryotherapy (using liquid nitrogen to freeze off the piles) to haemorrhoidectomy (surgery to remove the pile).
Warm baths, pain relief and bed rest are often a good starting point. Haemorrhoids (Piles; Hemorrhoids) References Davidson S, Haslett C. Davidson’s Principles and Practice of Medicine (19th edition). Edinburgh: Churchill Livingstone; 2002. Book Hurst JW (ed). Medicine for the Practicing Physician (4th edition). Stamford, CT: Appleton and Lange; 1996. Book Longmore M, Wilkinson I, Török E. Oxford Handbook of Clinical Medicine (5th edition). Oxford: Oxford University Press; 2001. Book McLatchie G, Leaper DJ (eds).
Oxford Handbook of Clinical Surgery (2nd edition). Oxford: Oxford University Press; 2002. Book Morris PJ, Wood WC. Oxford Textbook of Surgery (2nd edition). Oxford: Oxford University Press; 2000. Book Raftery AT. Churchill’s Pocketbook of Surgery (2nd edition). Edinburgh: Churchill Livingstone; 2001. Book Weight lifting involves lifting a heavy weight from the floor to a specified position above the ground, holding it for a period and then putting the weight back on the ground.
Weight lifting is mostly used to improve power and stimulate muscle hypertrophy. Leukopoiesis refers to the production of leukocytes or white blood cells of blood. What is Pulmonary oedema Statistics on Pulmonary oedema Risk Factors for Pulmonary oedema Progression of Pulmonary oedema Symptoms of Pulmonary oedema Clinical Examination of Pulmonary oedema How is Pulmonary oedema Diagnosed? Prognosis of Pulmonary oedema How is Pulmonary oedema Treated? Pulmonary oedema References What is Pulmonary oedema Pulmonary oedema is a disease of the lung. The lungs essentially provide the interface between air and blood.
The lungs consist of a series of folded membranes (the alveoli), which are located at the ends of very fine branching air passages (bronchioles). Blood which arrives into the lungs from the pulmonary artery gets into smaller and smaller blood vessels until it ends up in the capillaries located within the walls of the alveoli, which is a very thin membrane. In this moist environment, oxygen diffuses from within the alveoli into the blood stream, while carbon dioxide moves out of the blood stream into the alveoli and is expelled out of the air passages. Pulmonary oedema is the accumulation of fluid in the alveoli of the lungs. This fluid moves from blood vessels, across capillary and alveolar membranes, into the alveoli, causing symptoms such as shortness of breath. Which alveoli are affected depends on the cause and severity of pulmonary oedema: early pulmonary oedema due to heart failure affects the bases of the lungs, whereas severe adult respiratory distress syndrome involves oedema throughout the lung. Statistics on Pulmonary oedema Pulmonary oedema is a very common condition, mainly due left sided heart failure.
With an ageing population and incresing numbers of patients surviving acute myocardial infarcts (heart attacks) there is a growing number of patients presenting with pulmonary oedema. Heart failure is the most common cause of admission to hospital in the Medicare population in the United States, and almost a million patients (978,000) were admitted in the US with the diagnosis of pulmonary oedema in 1998. Other Western countries such as Australia and the UK have a similarly high incidence. Risk Factors for Pulmonary oedema Movement of fluid from blood vessels into air spaces occurs due to either: increased pressure in pulmonary veins – mostly due to heart failure. reduced protein in the blood – usually due to liver or kidney disease, or increased capillary permeability (leaky blood vessels) – see ARDS. Progression of Pulmonary oedema Congestive heart failure is the most common cause of pulmonary oedema. This causes blood to “back up” in the pulmonary veins. Initially fluid is pushed out of the vessels and into the surrounding tissue (interstitial oedema).
Further increase in pressure causes fluid to move into the alveolar spaces, resulting in “alveolar oedema”.