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the best doctors near me Thrombocytopenia is a condition in which you have a low blood platelet count. Platelets (thrombocytes) are colorless blood cells that help blood clot. Platelets stop bleeding by clumping and forming plugs in blood vessel injuries. Thrombocytopenia often occurs as a result of a separate disorder, such as leukemia or an immune system problem. Or it can be a side effect of taking certain medications. It affects both children and adults. Thrombocytopenia may be mild and cause few signs or symptoms. In rare cases, the number of platelets may be so low that dangerous internal bleeding occurs. Treatment options are available. Symptoms Petechiae on leg and abdomen Petechiae Thrombocytopenia signs and symptoms may include: Easy or excessive bruising (purpura) Superficial bleeding into the skin that appears as a rash of pinpoint-sized reddish-purple spots (petechiae), usually on the lower legs Prolonged bleeding from cuts Bleeding from your gums or nose Blood in urine or stools Unusually heavy menstrual flows Fatigue Enlarged spleen Jaundice
heart doctors Doctors in Vidyaranyapura Anti-platelet therapy Unless there is a contraindication (usually gastric intolerance but occasionally allergy) all patients with suspected angina should take aspirin.14 A daily dose of 75 mg is enough to cause irreversible cyclo-oxygenase inhibition of all the patient’s platelets. Recovery occurs only as platelets are replaced. This treatment causes significant reduction in platelet adhesiveness and reduces the risk of thrombosis within the coronary arteries following rupture of an atherosclerotic plaque. There is a definite improvement in mortality when aspirin is used after myocardial infarction and a probable improvement for patients with angina. The use of half an aspirin tablet (150 mg) is the cheapest approach to aspirin use, but 100 mg preparations in coated tablets and calendar packets are available. Patients unable to tolerate aspirin because of gastric side effects can often be treated with the combination of aspirin and a proton pump inhibitor. The relative risk of cerebral haemorrhage increases by 30% for patients taking aspirin but the absolute risk is less than 1 per 1000 patient years of treatment. For patients with aspirin allergy or intolerance, 75 mg of clopidogrel a day is usually a safer but expensive alternative. It is also associated with a small risk of gastrointestinal bleeding (1.99% versus 2.66% for aspirin over two years in the CAPRIE study). Combination (dual anti-platelet/aspirin and clopidogrel) treatment is not currently indicated for stable angina. Aspirin and clopidogrel resistance
heart doctors Doctors in Vidyaranyapura Anti-platelet therapy Unless there is a contraindication (usually gastric intolerance but occasionally allergy) all patients with suspected angina should take aspirin.14 A daily dose of 75 mg is enough to cause irreversible cyclo-oxygenase inhibition of all the patient’s platelets. Recovery occurs only as platelets are replaced. This treatment causes significant reduction in platelet adhesiveness and reduces the risk of thrombosis within the coronary arteries following rupture of an atherosclerotic plaque. There is a definite improvement in mortality when aspirin is used after myocardial infarction and a probable improvement for patients with angina. The use of half an aspirin tablet (150 mg) is the cheapest approach to aspirin use, but 100 mg preparations in coated tablets and calendar packets are available. Patients unable to tolerate aspirin because of gastric side effects can often be treated with the combination of aspirin and a proton pump inhibitor. The relative risk of cerebral haemorrhage increases by 30% for patients taking aspirin but the absolute risk is less than 1 per 1000 patient years of treatment. For patients with aspirin allergy or intolerance, 75 mg of clopidogrel a day is usually a safer but expensive alternative. It is also associated with a small risk of gastrointestinal bleeding (1.99% versus 2.66% for aspirin over two years in the CAPRIE study). Combination (dual anti-platelet/aspirin and clopidogrel) treatment is not currently indicated for stable angina. Aspirin and clopidogrel resistance
Popular Cardiologist in Vidyaranyapura, Bangalore • Anti-platelet therapy Unless there is a contraindication (usually gastric intolerance but occasionally allergy) all patients with suspected angina should take aspirin.14 A daily dose of 75 mg is enough to cause irreversible cyclo-oxygenase inhibition of all the patient’s platelets. Recovery occurs only as platelets are replaced. This treatment causes significant reduction in platelet adhesiveness and reduces the risk of thrombosis within the coronary arteries following rupture of an atherosclerotic plaque. There is a definite improvement in mortality when aspirin is used after myocardial infarction and a probable improvement for patients with angina. The use of half an aspirin tablet (150 mg) is the cheapest approach to aspirin use, but 100 mg preparations in coated tablets and calendar packets are available. Patients unable to tolerate aspirin because of gastric side effects can often be treated with the combination of aspirin and a proton pump inhibitor. The relative risk of cerebral haemorrhage increases by 30% for patients taking aspirin but the absolute risk is less than 1 per 1000 patient years of treatment. For patients with aspirin allergy or intolerance, 75 mg of clopidogrel a day is usually a safer but expensive alternative. It is also associated with a small risk of gastrointestinal bleeding (1.99% versus 2.66% for aspirin over two years in the CAPRIE study). Combination (dual anti-platelet/aspirin and clopidogrel) treatment is not currently indicated for stable angina. Aspirin and clopidogrel resistance
Popular Cardiologist in Amrutha Halli, Bangalore Anti-platelet therapy Unless there is a contraindication (usually gastric intolerance but occasionally allergy) all patients with suspected angina should take aspirin.14 A daily dose of 75 mg is enough to cause irreversible cyclo-oxygenase inhibition of all the patient’s platelets. Recovery occurs only as platelets are replaced. This treatment causes significant reduction in platelet adhesiveness and reduces the risk of thrombosis within the coronary arteries following rupture of an atherosclerotic plaque. There is a definite improvement in mortality when aspirin is used after myocardial infarction and a probable improvement for patients with angina. The use of half an aspirin tablet (150 mg) is the cheapest approach to aspirin use, but 100 mg preparations in coated tablets and calendar packets are available. Patients unable to tolerate aspirin because of gastric side effects can often be treated with the combination of aspirin and a proton pump inhibitor. The relative risk of cerebral haemorrhage increases by 30% for patients taking aspirin but the absolute risk is less than 1 per 1000 patient years of treatment. For patients with aspirin allergy or intolerance, 75 mg of clopidogrel a day is usually a safer but expensive alternative. It is also associated with a small risk of gastrointestinal bleeding (1.99% versus 2.66% for aspirin over two years in the CAPRIE study). Combination (dual anti-platelet/aspirin and clopidogrel) treatment is not currently indicated for stable angina.
Popular Cardiologist in Amrutha Halli, Bangalore Anti-platelet therapy Unless there is a contraindication (usually gastric intolerance but occasionally allergy) all patients with suspected angina should take aspirin.14 A daily dose of 75 mg is enough to cause irreversible cyclo-oxygenase inhibition of all the patient’s platelets. Recovery occurs only as platelets are replaced. This treatment causes significant reduction in platelet adhesiveness and reduces the risk of thrombosis within the coronary arteries following rupture of an atherosclerotic plaque. There is a definite improvement in mortality when aspirin is used after myocardial infarction and a probable improvement for patients with angina. The use of half an aspirin tablet (150 mg) is the cheapest approach to aspirin use, but 100 mg preparations in coated tablets and calendar packets are available. Patients unable to tolerate aspirin because of gastric side effects can often be treated with the combination of aspirin and a proton pump inhibitor. The relative risk of cerebral haemorrhage increases by 30% for patients taking aspirin but the absolute risk is less than 1 per 1000 patient years of treatment. For patients with aspirin allergy or intolerance, 75 mg of clopidogrel a day is usually a safer but expensive alternative. It is also associated with a small risk of gastrointestinal bleeding (1.99% versus 2.66% for aspirin over two years in the CAPRIE study). Combination (dual anti-platelet/aspirin and clopidogrel) treatment is not currently indicated for stable angina.
HEART SPECIALISTS IN YELAHANKA NEW TOWN BANGALORE The causes of coronary symptoms The symptoms of coronary artery disease are caused by the reduction of myocardial perfusion that results from narrowing of the lumen of one or more of the coronary arteries. This narrowing is most often the result of atherosclerosis. Other much less common causes include: 1 coronary artery spasm (often in an already diseased segment of artery but sometimes as a result of the use of cocaine) 2 thrombosis (usually on an already diseased, or occasionally aneurismal, segment) 3 embolism (e.g. from an infected aortic valve) 4 congenital coronary abnormality 5 vasculitis. Numerous other cardiac symptoms and problems can be the eventual result of atheromatous coronary disease. These include myocardial infarction , cardiac failure cardiac arrhythmias and some cardiac valve problems. Risk factor mechanisms of action Atherosclerosis is thought to result primarily from a disturbance of the vascular endothelium. The final common pathway for the effects of endothelial dysfunction is largely through abnormalities of nitric oxide (NO) production. This chemical, released by a healthy endothelium, is a potent vasodilator and has anti-inflammatory and other favourable actions on the arteries. Causes of this disturbance can be: n mechanical (hypertension) n chemical (oxidised lipids, components of cigarette smoke, hyperinsulinaemia) or n due to immunological injury. The damaged endothelium attracts inflammatory mediators, platelets and circulating lipids and promotes fibroblast and smooth muscle proliferation. This results in the formation of a plaque, which may narrow the arterial lumen. Plaques can remain stable (or sometimes regress), enlarge, rupture or erode (more common in diabetics). Most acute ischaemic events (acute coronary syndromes or acute myocardial infarctions) are thought to be the result of further luminal narrowing caused by the formation of partly or fully occlusive thrombus on a ruptured or eroded plaque. Coronary risk factors may therefore operate because they are atherogenic or thrombogenic. Plaque rupture Plaque rupture may be at least partly an inflammatory process involving inflammatory cells, cytokines and even bacteria. This may explain the association between inflammatory markers such as high-sensitivity C reactive protein (hsCRP) and a risk of acute coronary events. Although this association seems well established, there is still uncertainty about its role in overall risk assessment Plaques at risk of rupture are called vulnerable plaques. They typically have a thin fibrous cap. The shoulde of these caps are at risk of rupturing and allowing material from within the plaque to come
Popular Cardiologist in yelahanka New Town, Bangalore • The causes of coronary symptoms The symptoms of coronary artery disease are caused by the reduction of myocardial perfusion that results from narrowing of the lumen of one or more of the coronary arteries. This narrowing is most often the result of atherosclerosis. Other much less common causes include: 1 coronary artery spasm (often in an already diseased segment of artery but sometimes as a result of the use of cocaine) 2 thrombosis (usually on an already diseased, or occasionally aneurismal, segment) 3 embolism (e.g. from an infected aortic valve) 4 congenital coronary abnormality 5 vasculitis. Numerous other cardiac symptoms and problems can be the eventual result of atheromatous coronary disease. These include myocardial infarction cardiac failure cardiac arrhythmias and some cardiac valve problems. Risk factor mechanisms of action Atherosclerosis is thought to result primarily from a disturbance of the vascular endothelium. The final common pathway for the effects of endothelial dysfunction is largely through abnormalities of nitric oxide (NO) production. This chemical, released by a healthy endothelium, is a potent vasodilator and has anti-inflammatory and other favourable actions on the arteries. Causes of this disturbance can be: mechanical (hypertension) chemical (oxidised lipids, components of cigarette smoke, hyperinsulinaemia) or due to immunological injury. The damaged endothelium attracts inflammatory mediators, platelets and circulating lipids and promotes fibroblast and smooth muscle proliferation. This results in the formation of a plaque, which may narrow the arterial lumen. Plaques can remain stable (or sometimes regress), enlarge, rupture or erode (more common in diabetics). Most acute ischaemic events (acute coronary syndromes or acute myocardial infarctions) are thought to be the result of further luminal narrowing caused by the formation of partly or fully occlusive thrombus on a ruptured or eroded plaque. Coronary risk factors may therefore operate because they are atherogenic or thrombogenic.
Popular Cardiologist in yelahanka New Town, Bangalore • The causes of coronary symptoms The symptoms of coronary artery disease are caused by the reduction of myocardial perfusion that results from narrowing of the lumen of one or more of the coronary arteries. This narrowing is most often the result of atherosclerosis. Other much less common causes include: 1 coronary artery spasm (often in an already diseased segment of artery but sometimes as a result of the use of cocaine) 2 thrombosis (usually on an already diseased, or occasionally aneurismal, segment) 3 embolism (e.g. from an infected aortic valve) 4 congenital coronary abnormality 5 vasculitis. Numerous other cardiac symptoms and problems can be the eventual result of atheromatous coronary disease. These include myocardial infarction cardiac failure cardiac arrhythmias and some cardiac valve problems. Risk factor mechanisms of action Atherosclerosis is thought to result primarily from a disturbance of the vascular endothelium. The final common pathway for the effects of endothelial dysfunction is largely through abnormalities of nitric oxide (NO) production. This chemical, released by a healthy endothelium, is a potent vasodilator and has anti-inflammatory and other favourable actions on the arteries. Causes of this disturbance can be: mechanical (hypertension) chemical (oxidised lipids, components of cigarette smoke, hyperinsulinaemia) or due to immunological injury. The damaged endothelium attracts inflammatory mediators, platelets and circulating lipids and promotes fibroblast and smooth muscle proliferation. This results in the formation of a plaque, which may narrow the arterial lumen. Plaques can remain stable (or sometimes regress), enlarge, rupture or erode (more common in diabetics). Most acute ischaemic events (acute coronary syndromes or acute myocardial infarctions) are thought to be the result of further luminal narrowing caused by the formation of partly or fully occlusive thrombus on a ruptured or eroded plaque. Coronary risk factors may therefore operate because they are atherogenic or thrombogenic.
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