Friends today I am discussing about a very common problem known as #Erectile Dysfunction. Erectile dysfunction refers to the situation when a man has difficulty in getting a firm erection or an erection, which is required to achieve sexual penetration. Several cases of erectile dysfunction can cause impotency in a man. Causes: A problem in the blood flow, proper hormone secretion and nervous supply in the body may cause erectile dysfunction. Erectile dysfunction also happens due to vascular causes along with neurological causes. Arthrosclerosis is a disease which often leads to erectile dysfunction. This disease is commonly caused because of smoking and diabetes. The arteries to the penis become narrow and clogged and erectile dysfunction occurs. Neuropathy caused due to diabetes, known as diabetic neuropathy, is a primary neurological cause of erectile dysfunction. Nerve damage on account of surgery around the pelvis area may also lead to erectile dysfunction. High blood pressure or hypertension damages arteries all over the vascular system. Blood flow is impaired and proper erection is prohibited, which signifies erectile dysfunction. Erectile dysfunction also happens due to physical causes such as: High cholesterol and obesity Parkinson's disease and multiple cases of sclerosis Smoking, excessive alcohol consumption and substance abuse Disorder in anatomy or structure of the penis Surgical complications Several prescribed medicines may also lead to erectile dysfunction because of reactions and side effects. Erectile dysfunction may also result due to several psychological causes: Depression makes a person uninterested in sex due to lower libido and may cause erectile dysfunction. Do you experience any sexual health issues - premature ejaculation, erectile dysfunction? (your response is private and anonymous) A large amount of stress, fear, tension or anxiety may also lead to erectile dysfunction. Many men suffer from performance anxiety and feelings of sexual failure. This may result in erectile dysfunction. Poor communication with a partner or pressure from partner regarding sex may also cause erectile dysfunction. Homeopathic Remedies For Impotency (erectile dysfunction): Agnus Castus: Homeopathic medicine Agnus Castus is used in cases where there is complete inability to attain penile erection during the sexual act. Homeopathic medicine Agnus Castus can be used in cases of erectile dysfunction and sexual weakness where the male has a mental aversion to indulge in sex, along with decreased physical strength. Caladium: Homeopathic medicine Caladium is of great help for treatment of erectile dysfunction when the male is unable to have an erection despite having a sexual desire or urge. Lycopodium: Homeopathic medicine Lycopodium is of great help for both young people and elderly people suffering from erectile dysfunction. Tribulus Terrestris: The main indication for using Homeopathic medicine Tribulus Terrestris is the presence of urinary troubles along with erectile Dysfunction. Nuphar Luteum: Homeopathic medicine Nuphar Luteum can be beneficial for all those males with erectile Dysfunction in whom the desire to indulge in sexual activity is totally absent. There is no sexual desire with relaxed genitalia. Erectile dysfunction affects the self-esteem and confidence of a man as he is unable to have sex. Necessary measures should be taken to cure erectile dysfunction. If you wish to discuss about any specific problem, you can consult a Homeopathic. Stress is one of the most common and strong barriers to sex. Far too many people suffer from sexual problems caused by worry, tension, and exhaustion of stressful life - and yet unaware of it. If you want to perform your best, then never try too hard. Sex should happen by itself. Never force it upon you. Stay relaxed. Keep anxiety out of your body's way, for, any trace of anxiety, tension, fear, worry, distraction etc. can burst the sexual arousal - like a tiny pin prick blowing up a huge balloon. "When your body is wracked with stress, tension and anxiety, and your mind wracked with worry and distractions, sweet sex is nearly impossible." Three-way effect: Stress affects you physically, physiologically and mentally. During stress, blood vessels supplying blood to the penis don’t dilate fully and the sphincter that serves to stop the blood flowing back into the body fails to constrict adequately, both contributing to poor erections. Failed erections cause additional stress. And stress causes more erection problem. And a pattern of failure thus gets established. In no time, you are conditioned to get an erectile failure every time you attempt sex. That's how stress operates on your bodily responses. Stress disrupts the hormones as well. With stress, the testosterone levels fall, as do the levels of FSH which promotes sperm production. To add fuel to the fire, cortisol, the main stress hormone makes the testes less responsive to a hormone called LH, which tells the testes to produce testosterone. At an emotional level, stress can lead to anxiety, depression, anger, guilt or a combination of them. Each one of them is a powerful enemy to sex. Together they are an unbeatable combination. The underlying power behind all these reactions is the mind. Reconditioning the brain is the key element in reversing it. Here is what you can do: 1. Sometimes, simply recognizing that it is the stress that's causing the sexual problems is enough to bring about recovery. 2. Share your anxiety with your partner; Don’t try to hide. Sharing the tension, anxiety and worry will relieve you of the burden and guilt. You will be even more at ease when reassurance is coming from the other side. This paves way for speedy recovery. 3. Remember that very often, even the most complex problems have simple causes and simple solutions. Don’t be too Google-dependent. Google undoubtedly is a powerful search tool but you often do not know which information is right and which is wrong or which explains your situation the best. 4. Don’t hesitate to seek professional help even in small matters. The experience and training of a therapist are what helps you most. Most sexual problems at a younger age do not need elaborate tests. Often simple prescriptions will help quick restoration. 5. Exercise regularly. It boosts confidence, improves hormone levels, increases blood circulation, and enhances self-image. A good self-image is equal to good sex. 6. Get enough sleep. Don’t try sex at the end of the day, when you are down with fatigue and exhaustion. Instead, begin your day with sex (Sex early in the morning is a good one). 7. Take nutritional supplements such as Energex to boost energy and libido. 8. Bust the stress through, meditation, yoga, progressive relaxation, laughter football, etc.

72 yr old ,Male presented with acute onset of left sidedweakness on 26 feb 2021 , with the back ground history of systemic hypertension ,CAD with post CABG and Types DM. *Chief Complaints* On 26 feb 2021,while watching the news in the evening, he developed left sided mild weakness. He could get up immediately and was able to walk with mild support An hr later he felt better. The next day morning he noted weakness of left side with difficulty to hold things and unable to walk unassisted.Denied having any headache or vertigo but while taking the history he stated that he is getting headache after attending the OPD. *History* Known case of systemic hypertension 20 yrs CAD post CABG 10 yrs ago ,detected to be diabetic sincec2017 *Vitals* Afebrile,BP 140/ 90 mmhg HR 70/ mt *Physical Examination* Fully concious ,communicating well . Left sided UMN facial weakness noted Left upper limb gr 3/ 5 ,left lower gr4/ 5. DTRs hyperactive left side except absent ankle jerks with upgoing left plantar. Intact sensations. No bruit over the carotids or vertebrals. *Investigations* CBC normal FBS 128 mg / dl,HbA1c 7.4% ,renal functions normal. Lipd panel HDL 27 mg/ dl LDL 148mg/ dl( N <100).Normal other bloid work up. ECG old inferior wall MI changes with normal cardiac markers. *Diagnosis* Stroke, details keeping for conclusion *Management* Cadiac evaluation done. Started stroke management as per stroke protocol. Evaluated by the endocrinologist also.Already started physiotherapy

Friends today I am discussing about a very common disease now a days that is Diabetes mellitus. Diabetes mellitus, disorder of carbohydrate metabolism characterized by impaired ability of the body to produce or respond to insulin and thereby maintain proper levels of sugar (glucose) in the blood. diabetes mellitus diabetes mellitus An overview of diabetes mellitus and advances in treatment. HudsonAlpha Institute for Biotechnology Diabetes is a major cause of morbidity and mortality, though these outcomes are not due to the immediate effects of the disorder. They are instead related to the diseases that develop as a result of chronic diabetes mellitus. These include diseases of large blood vessels (macrovascular disease, including coronary heart disease and peripheral arterial disease) and small blood vessels (microvascular disease, including retinal and renal vascular disease), as well as diseases of the nerves. READ MORE ON THIS TOPIC Prozac therapeutics: Diabetes mellitus Diet is the cornerstone of diabetic treatment whether or not insulin is prescribed. The goal is to regulate… Causes And Types Insulin is a hormone secreted by beta cells, which are located within clusters of cells in the pancreas called the islets of Langerhans. Insulin’s role in the body is to trigger cells to take up glucose so that the cells can use this energy-yielding sugar. Patients with diabetes may have dysfunctional beta cells, resulting in decreased insulin secretion, or their muscle and adipose cells may be resistant to the effects of insulin, resulting in a decreased ability of these cells to take up and metabolize glucose. In both cases, the levels of glucose in the blood increase, causing hyperglycemia (high blood sugar). As glucose accumulates in the blood, excess levels of this sugar are excreted in the urine. Because of greater amounts of glucose in the urine, more water is excreted with it, causing an increase in urinary volume and frequency of urination as well as thirst. (The name diabetes mellitus refers to these symptoms: diabetes, from the Greek diabainein, meaning “to pass through,” describes the copious urination, and mellitus, from the Latin meaning “sweetened with honey,” refers to sugar in the urine.) Other symptoms of diabetes include itching, hunger, weight loss, and weakness. The islets of Langerhans are responsible for the endocrine function of the pancreas. Each islet contains beta, alpha, and delta cells that are responsible for the secretion of pancreatic hormones. Beta cells secrete insulin, a well-characterized hormone that plays an important role in regulating glucose metabolism. The islets of Langerhans are responsible for the endocrine function of the pancreas. Each islet contains beta, alpha, and delta cells that are responsible for the secretion of pancreatic hormones. Beta cells secrete insulin, a well-characterized hormone that plays an important role in regulating glucose metabolism. Encyclopædia Britannica, Inc. There are two major forms of the disease. Type 1 diabetes, formerly referred to as insulin-dependent diabetes mellitus (IDDM) or juvenile-onset diabetes, usually arises in childhood. Type 2 diabetes, formerly called non-insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes, usually occurs after age 40 and becomes more common with increasing age. Type 1 diabetes mellitus Type 1 diabetes accounts for about 5 to 10 percent of cases of diabetes. Most cases of type 1 diabetes develop in children or adolescents, but about 20 percent of new patients are adults. The frequency of type 1 diabetes varies widely in different countries, from less than 1 case per 100,000 people per year in China and parts of South America to more than 20 cases per 100,000 people per year in places such as Canada, Finland, Norway, Sweden, and the United Kingdom. Most patients present with symptoms of hyperglycemia, but some patients present with diabetic ketoacidosis, a clear indication that insulin secretion has significantly deteriorated. diabetes mellitus diabetes mellitus A discussion of type I and type II diabetes mellitus. HudsonAlpha Institute for Biotechnology Type 1 diabetes is usually caused by autoimmune destruction of the islets of Langerhans of the pancreas. Patients with type 1 diabetes have serum antibodies to several components of the islets of Langerhans, including antibodies to insulin itself. The antibodies are often present for several years before the onset of diabetes, and their presence may be associated with a decrease in insulin secretion. Some patients with type 1 diabetes have genetic variations associated with the human leukocyte antigen (HLA) complex, which is involved in presenting antigens to immune cells and initiating the production of antibodies that attack the body’s own cells (autoantibodies). However, the actual destruction of the islets of Langerhans is thought to be caused by immune cells sensitized in some way to components of islet tissue rather than to the production of autoantibodies. In general, 2 to 5 percent of children whose mother or father has type 1 diabetes will also develop type 1 diabetes. Type 2 diabetes mellitus Type 2 diabetes is far more common than type 1 diabetes, accounting for about 90 percent of all cases. The frequency of type 2 diabetes varies greatly within and between countries and is increasing throughout the world. Most patients with type 2 diabetes are adults, often older adults, but it can also occur in children and adolescents. There is a stronger genetic component to type 2 diabetes than to type 1 diabetes. For example, identical twins are much more likely to both develop type 2 diabetes than to both develop type 1 diabetes, and 7 to 14 percent of people whose mother or father has type 2 diabetes will also develop type 2 diabetes; this estimate increases to 45 percent if both parents are affected. In addition, it is estimated that about half of the adult Pima Indian population in Arizona has type 2 diabetes, whereas in the entire United States it is estimated that about 10 percent of the population has type 2 diabetes Many patients with type 2 diabetes are asymptomatic, and they are often diagnosed with type 2 diabetes when routine measurements reveal high blood glucose concentrations. In some patients the presence of one or more symptoms associated with the long-term complications of diabetes leads to a diagnosis of type 2 diabetes. Other patients present with symptoms of hyperglycemia that have been present for months or with the sudden onset of symptoms of very severe hyperglycemia and vascular collapse. Type 2 diabetes is strongly associated with obesity and is a result of insulin resistance and insulin deficiency. Insulin resistance is a very common characteristic of type 2 diabetes in patients who are obese, and thus patients often have serum insulin concentrations that are higher than normal. However, some obese persons are unable to produce sufficient amounts of insulin, and thus the compensatory increase in response to increased blood glucose concentrations is inadequate, resulting in hyperglycemia. If blood glucose concentration is increased to a similar level in a healthy person and in an obese person, the healthy person will secrete more insulin than the obese person. leptin leptin The discovery of the leptin protein in mice and its connection to diabetes and obesity. HudsonAlpha Institute for Biotechnology People with type 2 diabetes can control blood glucose levels through diet and exercise and, if necessary, by taking insulin injections or oral medications. Despite their former classifications as juvenile or adult, either type of diabetes can occur at any age. Gestational diabetes Diabetes mellitus also may develop as a secondary condition linked to another disease, such as pancreatic disease; a genetic syndrome, such as myotonic dystrophy; or drugs, such as glucocorticoids. Gestational diabetes is a temporary condition associated with pregnancy. In this situation, blood glucose levels increase during pregnancy but usually return to normal after delivery. However, gestational diabetes is recognized as a risk for type 2 diabetes later in life. Gestational diabetes is diagnosed when blood glucose concentrations measure between 92 and 125 mg per 100 ml (5.1 and 6.9 millimoles [mmol] per litre) after fasting or when blood glucose concentrations equal or exceed 180 mg per 100 ml (10 mmol per litre) one hour after ingesting a glucose-rich solution. Acute Clinical Manifestation Hyperglycemia itself can cause symptoms but usually only when blood glucose concentrations are approximately 180 mg per 100 ml (10 mmol per litre) or higher. When blood glucose concentrations increase, more glucose is filtered by the glomeruli of the kidneys than can be reabsorbed by the kidney tubules, resulting in glucose excretion in the urine. High glucose concentrations in the urine create an osmotic effect that reduces the reabsorption of water by the kidneys, causing polyuria (excretion of large volumes of urine). The loss of water from the circulation stimulates thirst. Therefore, patients with moderate or severe hyperglycemia typically have polyuria and polydipsia (excessive thirst). The loss of glucose in the urine results in weakness, fatigue, weight loss, and increased appetite (polyphagia). Patients with hyperglycemia are prone to infections, particularly vaginal and urinary tract infections, and an infection may be the presenting manifestation of diabetes. There are two acute life-threatening complications of diabetes: hyperglycemia and acidosis (increased acidity of the blood), either of which may be the presenting manifestation of diabetes. In patients with type 1 diabetes, insulin deficiency, if not recognized and treated properly, leads to severe hyperglycemia and to a marked increase in lipolysis (the breakdown of lipids), with a greatly increased rate of release of fatty acids from adipose tissue. In the liver, much of the excess fatty acid is converted to the keto acids beta-hydroxybutyric acid and acetoacetic acid. The increased release of fatty acids and keto acids from adipose, liver, and muscle tissues raises the acid content of the blood, thereby lowering the pH of the blood. The combination of hyperglycemia and acidosis is called diabetic ketoacidosis and leads to hyperventilation and to impaired central nervous system function, culminating in coma and death. Patients with diabetic ketoacidosis must be treated immediately with insulin and intravenous fluids. In patients with type 2 diabetes, high blood glucose concentrations can lead to very severe and prolonged hyperglycemia and to marked polyuria, with the loss of a large volume of fluid and a very high serum osmolality. These factors place patients with type 2 diabetes at a high risk of developing central nervous system dysfunction and vascular collapse (hyperglycemia coma). Ketoacidosis is usually not a problem in patients with type 2 diabetes because they secrete enough insulin to restrain lipolysis. Patients with hyperglycemic coma should be treated aggressively with intravenous fluids and insulin. Diagnosis And Treatment Many people are unaware that they have diabetes. In 2012, for example, it was estimated that 8.1 million of 29.1 million American cases were undiagnosed. The disease is usually discovered when there are typical symptoms of increased thirst and urination and a clearly elevated blood sugar level. The diagnosis of diabetes is based on the presence of blood glucose concentrations equal to or greater than 126 mg per 100 ml (7.0 mmol per litre) after an overnight fast or on the presence of blood glucose concentrations greater than 200 mg per 100 ml (11.1 mmol per litre) in general. People with fasting blood glucose values between 100 and 125 mg per 100 ml (6.1 to 6.9 mmol per litre) are diagnosed with a condition called impaired fasting glucose (prediabetes). Normal fasting blood glucose concentrations are less than 100 mg per 100 ml (6.1 mmol per litre). While the blood glucose concentrations used to define diabetes and impaired fasting glucose are somewhat arbitrary, they do correlate with the risk of macrovascular and microvascular disease. Patients with impaired fasting glucose are likely to have diabetes later in life. Oral glucose tolerance tests, in which blood glucose is measured hourly for several hours after ingestion of a large quantity of glucose (usually 75 or 100 grams), are used in pregnant women to test for gestational diabetes. The criteria for diagnosing gestational diabetes are more stringent than the criteria for diagnosing other types of diabetes, which is a reflection of the presence of decreased blood glucose concentrations in healthy pregnant women as compared with nonpregnant women and with men. The duration and severity of hyperglycemia can be assessed by measuring levels of advanced glycosylation end products (AGEs). AGEs are formed when hemoglobin molecules in red blood cells undergo glycosylation (binding to glucose), and the bound substances remain together until the red blood cell dies (red blood cells live approximately 120 days). AGEs are believed to inflict the majority of vascular damage that occurs in people with diabetes. A glycosylated hemoglobin called hemoglobin subtype A1c (HbA1c) is particularly useful in monitoring hyperglycemia and the efficacy of diabetes treatments. Treatment Before the isolation of insulin in the 1920s, most patients died within a short time after onset. Untreated diabetes leads to ketoacidosis, the accumulation of ketones (products of fat breakdown) and acid in the blood. Continued buildup of these products of disordered carbohydrate and fat metabolism result in nausea and vomiting, and eventually the patient goes into a diabetic coma. Treatment for diabetes mellitus is aimed at reducing blood glucose concentrations to normal levels. Achieving this is important in promoting well-being and in minimizing the development and progression of the long-term complications of diabetes. Measurements of HbA1c can be used to assess whether an individual’s treatment for diabetes is effective. Target values of HbA1c levels should be close to normal. Diet and exercise All diabetes patients are put on diets designed to help them reach and maintain normal body weight, and they often are encouraged to exercise regularly, which enhances the movement of glucose into muscle cells and blunts the rise in blood glucose that follows carbohydrate ingestion. Patients are encouraged to follow a diet that is relatively low in fat and contains adequate amounts of protein. In practice about 30 percent of calories should come from fat, 20 percent from protein, and the remainder from carbohydrates, preferably from complex carbohydrates rather than simple sugars. The total caloric content should be based on the patient’s nutritional requirements for growth or for weight loss if the patient is obese. In overweight or obese patients with type 2 diabetes, caloric restriction for even just a few days may result in considerable improvement in hyperglycemia. In addition, weight loss, preferably combined with exercise, can lead to improved insulin sensitivity and even restoration of normal glucose metabolism. Insulin therapies Diabetics who are unable to produce insulin in their bodies require insulin therapy. Traditional insulin therapy entails regular injections of the hormone, which are often customized according to individual and variable requirements. Beef or pork insulin, made from the pancreatic extracts of cattle or pigs, can be used to treat humans with diabetes. However, in the United States, beef and pork forms of insulin are no longer manufactured, having been discontinued in favour of human insulin production. Modern human insulin treatments are based on recombinant DNA technology. Human insulin may be given as a form that is identical to the natural form found in the body, which acts quickly but transiently (short-acting insulin), or as a form that has been biochemically modified so as to prolong its action for up to 24 hours (long-acting insulin). Another type of insulin acts rapidly, with the hormone beginning to lower blood glucose within 10 to 30 minutes of administration; such rapid-acting insulin was made available in an inhalable form in 2014. The optimal regimen is one that most closely mimics the normal pattern of insulin secretion, which is a constant low level of insulin secretion plus a pulse of secretion after each meal. This can be achieved by administration of a long-acting insulin preparation once daily plus administration of a rapid-acting insulin preparation with or just before each meal. Patients also have the option of using an insulin pump, which allows them to control variations in the rate of insulin administration. A satisfactory compromise for some patients is twice-daily administration of mixtures of intermediate-acting and short-acting insulin. Patients taking insulin also may need to vary food intake from meal to meal, according to their level of activity; as exercise frequency and intensity increase, less insulin and more food intake may be necessary. Research into other areas of insulin therapy include pancreas transplantation, beta cell transplantation, implantable mechanical insulin infusion systems, and the generation of beta cells from existing exocrine cells in the pancreas. Patients with type 1 diabetes have been treated by transplantation of the pancreas or of the islets of Langerhans. However, limited quantities of pancreatic tissue are available for transplantation, prolonged immunosuppressive therapy is needed, and there is a high likelihood that the transplanted tissue will be rejected even when the patient is receiving immunosuppressive therapy. Attempts to improve the outcome of transplantation and to develop mechanical islets are ongoing. Drugs used to control blood glucose levels There are several classes of oral drugs used to control blood glucose levels, including sulfonylureas, biguanides, and thiazolidinediones. Sulfonylureas, such as glipizide and glimepiride, are considered hypoglycemic agents because they stimulate the release of insulin from beta cells in the pancreas, thus reducing blood glucose levels. The most common side effect associated with sulfonylureas is hypoglycemia (abnormally low blood glucose levels), which occurs most often in elderly patients who have impaired liver or kidney function. Biguanides, of which metformin is the primary member, are considered antihyperglycemic agents because they work by decreasing the production of glucose in the liver and by increasing the action of insulin on muscle and adipose tissues. A potentially fatal side effect of metformin is the accumulation of lactic acid in blood and tissues, often causing vague symptoms such as nausea and weakness. Thiazolidinediones, such as rosiglitazone and pioglitazone, act by reducing insulin resistance of muscle and adipose cells and by increasing glucose transport into these tissues. These agents can cause edema (fluid accumulation in tissues), liver toxicity, and adverse cardiovascular events in certain patients. Furthermore, oral hypoglycemic agents lower mean blood glucose concentrations by only about 50–80 mg per 100 ml (2.8–4.4 mmol per litre), and sensitivity to these drugs tends to decrease with time. There are several other agents that can be highly effective in the treatment of diabetes. Pramlintide is an injectable synthetic hormone (based on the human hormone amylin) that regulates blood glucose levels by slowing the absorption of food in the stomach and by inhibiting glucagon, which normally stimulates liver glucose production. Exenatide is an injectable antihyperglycemic drug that works similarly to incretins, or gastrointestinal hormones, such as gastric inhibitory polypeptide, that stimulate insulin release from the pancreas. Exenatide has a longer duration of action than incretins produced by the body because it is less susceptible to degradation by an enzyme called dipeptidyl peptidase-4 (DPP-4). A drug called sitagliptin specifically inhibits DPP-4, thereby increasing levels of naturally produced incretins. Side effects associated with these drugs are often mild, although pramlintide can cause profound hypoglycemia in patients with type 1 diabetes. Glucometer monitoring All patients with diabetes mellitus, particularly those taking insulin, should measure blood glucose concentrations periodically at home, especially when they have symptoms of hypoglycemia. This is done by pricking a finger, obtaining a drop of blood, and using an instrument called a glucometer to measure the blood glucose concentration. Using this technology, many patients become skilled at evaluating their diabetes and making appropriate adjustments in therapy on their own initiative. Long-Term Complications Of Diabetes Mellitus The prolonged survival of patients with diabetes mellitus has led to an increasing incidence of long-term complications. The most common complications are vascular complications, which may involve large arteries, small arteries, or capillaries. Large-vessel disease generally presents as atherosclerotic vascular disease (atherosclerosis). Atherosclerosis in diabetic patients does not differ from that which occurs in nondiabetic patients, although it may occur sooner and progress more rapidly in diabetic than nondiabetic patients. It involves the coronary arteries, the cerebral arteries, and the large arteries (iliac and femoral arteries) that supply blood to the legs. Thus, nonfatal and fatal myocardial infarction (heart attack), stroke, and ulceration and gangrene of the feet, often necessitating amputation, are common in patients with diabetes. Small-artery disease (microangiopathy) consists of thickening of the walls of small arteries and capillaries, which initially renders them permeable (leaky) to fluids and subsequently renders them prone to obstruction (thrombosis or embolism). These changes occur primarily in the retina (diabetic retinopathy) and kidneys (diabetic nephropathy), and as a result diabetes is the most common cause of blindness and end-stage kidney disease. Vascular complications are aggravated by hypertension and hyperlipidemia (high serum levels of lipids), both of which are common in patients with diabetes. Cataract formation can occur as a complication of diabetes (shown here in a person affected by type I diabetes). Cataract formation can occur as a complication of diabetes (shown here in a person affected by type I diabetes). There are other, nonvascular complications of diabetes, including cataract formation and neuropathy (diabetic neuropathy). The most common type of neuropathy is symmetric polyneuropathy. This causes abnormal sensation (numbness or tingling) or loss of sensation, loss of position sense and vibratory sense, and weakness of the muscles of the feet, lower legs, and hands. Other patients have single-nerve neuropathy, such as loss of function of a nerve to the muscles of one eye, causing visual disturbances, or of a nerve to the muscles of the forearm, causing wrist drop. They may also have autonomic neuropathy, which may result in postural hypotension (fainting upon sitting up or standing), gastric retention, erectile dysfunction, or urinary bladder dysfunction. These complications may be caused by glycosylation of ocular tissue or nervous tissue, accumulation of osmotically active glucose metabolites in these tissues, or disease of the small vessels in these tissues. The development or progression of the small-vessel complications of diabetes, such as diabetic retinopathy, diabetic nephropathy, and diabetic neuropathy, can be slowed or prevented by control of hyperglycemia. It is less clear whether the control of hyperglycemia has a similar effect in controlling large-vessel complications. The onset and progression of the vascular complications of diabetes can be delayed by controlling high blood pressure (hypertension). Many antihypertensive treatments are aimed specifically at preventing the actions of angiotensin II, a peptide that stimulates blood vessel constriction to increase blood pressure. The increase in blood pressure can be prevented by drugs that inhibit angiotensin-converting enzyme (drugs known as ACE inhibitors), which converts inactive angiotensin I to active angiotensin II, or by drugs that block the angiotensin receptor, which prevents angiotensin II from stimulating blood vessels to constrict. Cessation of smoking and lowering serum lipid concentrations are also helpful in slowing progression of vascular disease in patients with diabetes. Prevention Attempts to prevent type 1 diabetes have been unsuccessful. On the other hand, in people with impaired fasting glucose, progression to type 2 diabetes can be prevented by weight loss and exercise and by treatment with metformin, an ACE inhibitor, or a statin (a type of cholesterol-lowering drug). Homeopathic remedies marketed to treat the symptoms of diabetes or prevent complications include: Syzygium jambolanum or S. cumini (black plum) is said to help treat thirst, weakness, skin ulcers, and excessive urination. Uranium nitricum is marketed to treat excessive urination, nausea, swelling, and burning with urination. Conium (hemlock) is purported to treat numbness in the feet and hands as well as diabetic neuropathy (nerve damage). Plumbum (lead) is said to help with numbness in the hands and feet, nerve pain, and tinnitus. Calendula (marigold) is said to treat infected ulcers. Phosphoric acid is promoted to treat impaired memory, confusion or heavy head, frequent urination at night, hair loss, and difficulty maintaining an erection.

38yrs/M with K/c/o CAD with HTN was on irregular treatment for past 3mnths presented to casualty after 8hrs of onset of weakness of left sided upper and lower limbs along with Mild difficulty in breathing. O/e - Patient drowsy,arousable, localising pain,Pupils - B/l Assymetrical non reactive,Vitals unremarkable,CNS - Left sided hemiplegic, extensor plantar on left side,GCS - E3VAM4-5. KINDLY INTERPRET CT AND MRI BRAIN AND SUGGEST MANAGEMENT PLAN TOO?

Dear homeopaths Require your view on this case diagnosed as "MND" 46/f Symptoms towards homeopathic case taking as follows Ascending paralytic weakness began a yr ago with Rt sided foot drop . During investigation it was found that pt also had a benign thyroid nodule which was removed ( hoping it may reverse the case ) but it made no major changes -hence diagnosis of MND was clinched .. Patient always complained of low back ache Used to have reddish urine prior to development of these complains( bil. kidney stones found later in USG ) Currently patient is moving around and managing her activities with help /wheel chair..is experiencing weakness Facial countenance is happy yet..(also she s not aware of exact nature of her prob ), Her preference in food had always been sea food No difficulty in bowel bladder habits Apetite good.. Poor thirst /intake of water has always been der F/h -,mother -brain tumor and sister breasts ca No h/o neurological illnesses While it appears to point towards "lyco " on basis of general . Would still like to take your valuable suggestions on the other probable medicines Kindly share your thoughts and guide me ! Ty !!!