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How sleeping less than 6 hours affects your health After being awake for almost 14-16 hours, our body demands sleep. Minimum sleeping time required for a healthy mind and body is 7-8 hours. Although, this duration varies according to age. Because generally speaking, where a child can sleep for 12-14 hours, grownups can sleep for not more than 9 hours. Sound sleep is very essential otherwise, it can be harmful for our health. Let’s see how sleeping for less than 6 hours affects our health. Headache, weight gain and poor vision: When you sleep for less than 6 hours a day, it can not only give you headache all the time but can lead to a poor vision also. And if continued for a long time, may hamper your eyesight. The lesser you sleep the more weight you gain. And after-effects of gaining weight could be even more hazardous. Memory loss, heart disease, infection: Sleeplessness can have an adverse effect on one’s memory too. A person may find it difficult to remember even simple things. Also, infections can take a longer time to heal because sleep is something that stabilises and balances everything that goes wrong while we are awake. If we don’t get proper sleep, the process of healing takes longer. Lack of sleep can also elevate blood pressure which ultimately affects the heart. Urine overproduction, stammering and accident: Sleeping slows down urinating process but when you are awake for longer hours, you might have to urinate more than usual. Lack of sleep can also make you stammer while speaking. If lack of sleep continues, you may not be able to communicate properly. When you do not have sound sleep, your mental condition would not be stable because of declining concentration. You can be accident prone if you drive in such a condition. These are just a few of the ill effects. Sleeping for less than 5 hours is far more dangerous than you can even think. From behavioural to mental to physical effects, it can harm you in many more ways, So, have a sound sleep to avoid complications in life.
BEST CARDIOLOGY HOSPITALS IN BANGALORE Cardiac failure Cardiac failure is an increasingly common condition affecting about 1% of the population but much higher proportions of older people. It is responsible for an increasing number of hospital admissions. The various aetiologies have been discussed above, but the most common cause is now ischaemic heart disease rather than hypertensive heart disease. This reflects the improved modern management of hypertension in the population. The definition of heart failure has always included reference to the inability of the heart to meet the metabolic needs of the body. The earliest concepts of heart failure were of inadequate cardiac pump function and associated salt and water retention. Treatment was aimed at improving cardiac contractility and removing salt and water from the body. In the 1970s the concept of after-load reduction was introduced. This was based partly on the realisation that vasoconstriction was part of the problem. This has led to the modern neuro-hormonal concept of heart failure. It is clear that many of the features of cardiac failure are a result of stimulation of the renin-angiotensin-aldosterone system and sympathetic stimulation. These responses of the body to the fall in cardiac output temporarily increase cardiac performance and blood pressure by increasing vascular volumes, cardiac contractility and systemic resistance. In the medium and longer term these responses are maladaptive. They increase cardiac work and left ventricular volumes and lead to myocardial fibrosis with further loss of myocytes. Most recently it has become clear that heart failure is also an inflammatory condition, with evidence of cytokine activation. Work is underway to establish a role for treatment of this part of the condition. Current drug treatment has been successful in blocking many of the maladaptive aspects of neuro-hormonal stimulation. Many of these treatments have become established after benefits have been ascertained in large randomised controlled trials. These trials have also led to the abandoning of certain drugs (often those that increase cardiac performance) that were shown to have a detrimental effect on survival (e.g. Milrinone). The principles of treatment of heart failure are as follows: 1 Remove the exacerbating factors. 2 Relieve fluid retention. 3 Improve left ventricular function and reduce cardiac work; improve prognosis. 4 Protect against the adverse effects of drug treatment. 5 Assess for further management (e.g. revascularisation, transplant). 6 Manage complications (e.g. arrhythmias). 7 Protect high-risk patients from sudden death.
CARDIOLOGY DOCTORS IN HOSUR ROAD Pulmonary embolism This is not quite a cardiac condition and not quite a respiratory condition but it is often managed by cardiologists. Modern CT pulmonary angiography is very sensitive and specific for the diagnosis of PE. A negative scan that is of good quality effectively excludes the diagnosis. The scans are so sensitive that small distal emboli may be detected in patients who do not have convincing symptoms of embolism. This poses a therapeutic problem that may be avoided if scans are not ordered inappropriately. Some patients cannot have a CTPA, usually because of renal impairment that would make the injection of contrast risky. A V/Q nuclear scan is then a reasonable alternative to a CTPA. These scans are less accurate than CT pulmonary angiography but the clinical suspicion of PE and a lung scan reported as intermediate or high probability is an indication for treatment. Patients should be admitted to hospital and treatment begun with intravenous heparin or subcutaneous low molecular weight heparin. The latter has the advantage that the dose is determined by body weight and repeated measurements of clotting times are not required. In some cases it may be possible to treat patients with small pulmonary emboli at home with supervised low molecular weight heparin. Either way, soon after diagnosis patients should be started on oral anticoagulation treatment with warfarin. A stable INR may often be achieved within five days or so, the heparin ceased and the patient discharged. Most patients with dyspnoea as a result of PE begin to feel better within a few days of starting treatment. It is often difficult to know how long to continue treatment with warfarin. The usual recommendation for an uncomplicated first PE is three to six months. Recurrent PE may be an indication for lifelong treatment. It also suggests a need to investigate for clotting abnormalities (e.g. anti-thrombin III deficiency, protein S and protein C deficiency, abnormal Factor V and anti-nuclear antibody). A very large and life-threatening PE which is associated with the sudden onset of severe dyspnoea and hypotension may be an indication for thrombolytic treatment. An echocardiogram may show abnormal right ventricular function in these ill patients and help in the decision. Experience with this is limited and the optimum regimen is not really known. Tissue plasminogen activator (TPA) is now indicated for this purpose and current recommendations are for a 10 mg bolus over two minutes followed by 90 mg over two hours.
THE HEARTDOCTORS IN BANGALORE Pulmonary embolism This is not quite a cardiac condition and not quite a respiratory condition but it is often managed by cardiologists. Modern CT pulmonary angiography is very sensitive and specific for the diagnosis of PE. A negative scan that is of good quality effectively excludes the diagnosis. The scans are so sensitive that small distal emboli may be detected in patients who do not have convincing symptoms of embolism. This poses a therapeutic problem that may be avoided if scans are not ordered inappropriately. Some patients cannot have a CTPA, usually because of renal impairment that would make the injection of contrast risky. A V/Q nuclear scan is then a reasonable alternative to a CTPA. These scans are less accurate than CT pulmonary angiography but the clinical suspicion of PE and a lung scan reported as intermediate or high probability is an indication for treatment. Patients should be admitted to hospital and treatment begun with intravenous heparin or subcutaneous low molecular weight heparin. The latter has the advantage that the dose is determined by body weight and repeated measurements of clotting times are not required. In some cases it may be possible to treat patients with small pulmonary emboli at home with supervised low molecular weight heparin. Either way, soon after diagnosis patients should be started on oral anticoagulation treatment with warfarin. A stable INR may often be achieved within five days or so, the heparin ceased and the patient discharged. Most patients with dyspnoea as a result of PE begin to feel better within a few days of starting treatment. It is often difficult to know how long to continue treatment with warfarin. The usual recommendation for an uncomplicated first PE is three to six months. Recurrent PE may be an indication for lifelong treatment. It also suggests a need to investigate for clotting abnormalities (e.g. anti-thrombin III deficiency, protein S and protein C deficiency, abnormal Factor V and anti-nuclear antibody). A very large and life-threatening PE which is associated with the sudden onset of severe dyspnoea and hypotension may be an indication for thrombolytic treatment. An echocardiogram may show abnormal right ventricular function in these ill patients and help in the decision. Experience with this is limited and the optimum regimen is not really known. Tissue plasminogen activator (TPA) is now indicated for this purpose and current recommendations are for a 10 mg bolus over two minutes followed by 90 mg over two hours. 7
Diabetes clinics in Vidyaranyapura, Bangalore • How is type 2 diabetes treated? Type 2 diabetes is often treated with oral medication because many people with this type of diabetes make some insulin on their own. The pills people take to control type 2 diabetes do not contain insulin. Instead, medications such as metformin, sulfonylureas, alpha-glucosidase inhibitors and many others are used to make the insulin that the body still produces more effective. Some people with type 2 diabetes are treated with insulin. Insulin is either injected with a syringe several times per day, or delivered via an insulin pump. The goal of insulin therapy is to mimic the way the pancreas would produce and distribute its own insulin, if it were able to manufacture it. Taking insulin does not mean you have done a bad job of trying to control your blood glucose—instead it simply means that your body doesn’t produce or use enough of it on its own to cover the foods you eat. One of the key factors in Joslin’s treatment of diabetes is tight blood glucose control, so be certain that your treatment helps get your blood glucose readings as close to normal as safely possible. Patients should discuss with their doctors what their target blood glucose range is. It is also important to determine what your goal is for A1C readings (a test that determines how well your diabetes is controlled over the past 2-3 months). By maintaining blood glucose in the desired range, you’ll likely avoid many of the complications some people with diabetes face. One of the key factors in Joslin’s treatment of diabetes is tight blood glucose control, so be certain that your treatment helps get your blood glucose readings as close to normal as safely possible. Patients should discuss with their doctors what their target blood glucose range is. It is also important to determine what your goal is for A1C readings (a test that determines how well your diabetes is controlled over the past 2-3 months). By maintaining blood glucose in the desired range, you’ll likely avoid many of the complications some people with diabetes face.
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