Yes doctor helpful now a days for any treatment this DM is a compkimentry to us
Useful update sir ji
Nice update@Dr. Rajesh Gupta ji
Sir thanks for article. But last para it is said some Rx's and used by us? . From where please and ........
How many cases are at least under control,not cured by any if our Rx?.Includes Scyz jambo Q.?I hope some replies.
Best drug to tret type2 ?
Thank you sir.
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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.Dr. Rajesh Gupta5 Likes4 Answers
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Diabetes Supplements: Vitamins, Minerals, And Antioxidants 1mg TeamSeptember 11, 2018 Diabetes,Eat Well, Health A-Z, Supplements ￼ There is no doubt that diet plays a key role in the management and treatment of diabetes. In addition to taking medications, it is important to follow a nutritious diet to keep your blood glucose level in control. If your diet lacks adequate nutrition, adding dietary supplements might be recommended. Here is a quick guide on the use of vitamin, mineral and antioxidantsupplements for diabetes. Vitamin supplements for diabetes Vitamins play a key role in glucose metabolism and the lack of these nutrients could make supplementation necessary to manage and prevent diabetes-related complications. Due to abnormal glucose metabolism in diabetics, there is an excess production of free radicals. This, in turn, reduces the antioxidants in the blood, which causes a deficiency of vitamins such as A, C, and E, which are potent antioxidants. This may require you to load up on the vitamins to meet your body’s requirements. Certain medicines used to treat diabetes can lower the absorption of Vitamin B9 (folic acid) and Vitamin B12. So, if you are taking diabetes medication for a long time, you may also need to take supplements. -Vitamin A: The active form of Vitamin A is retinol, which is a potent antioxidant that not only helps deal with stress but also improves the functioning of the pancreatic cells. This is important as pancreatic cells produce insulin. -Vitamin C: According to a 2007 study in the Indian Journal of Medical Research, consumption of 1000 mg of Vitamin C supplements on a daily basis was found to lower levels of glucose and lipids in people with type 2 diabetes. Supplements can also help prevent Vitamin C deficiency and thereby reduce the risk of complications associated with diabetes. -Vitamin E: The use of Vitamin E supplements in people with diabetes mellitus for around 24 months was found to prevent the development of diabetic complications. This includes complications like diabetic retinopathy, foot ulcers, and cardiovascular problems. Moreover, vitamin E supplementation slows down the progression of complications in people with uncontrolled diabetes. -Vitamin B1: Many people with Type 1 and type 2 diabetes suffer from Vitamin B1 or thiamine deficiency. Studies have reported that the use of thiamine supplements for at least a month decreases blood glucose level in diabetics, also lowering the risk of diabetic nephropathy. -Vitamin B9: Studies have shown that folate supplementation can help improve glycemic control by reducing HbA1c levels. Additionally, it improves serum insulin and insulin resistance in type 2 diabetes patients. When used in combination with other vitamins like Vitamin B6 and Vitamin B12, it can also improve symptoms of diabetic retinopathy. -Vitamin B12: Supplementation of vitamin B12, along with folate (Vitamin B9) and pyridoxine (Vitamin B6), improves symptoms of diabetic retinopathy such as retinal edema (fluid accumulation in the eyes) and increased sensitivity to light. When supplemented along with lipoic acid, vitamin B12 also improves nerve function, protecting against diabetic neuropathy. Overall, numerous research studies have reported that vitamin supplementation not only improves glycemic control in diabetics but also prevents diabetes-related complications. Mineral supplements for diabetes Minerals play an equally important role in the management and treatment of diabetes. This is because lack of minerals can impair glucose metabolism, raising the risk of health complications. In fact, diabetes patients often suffer from low levels of magnesium and zinc. -Magnesium: Magnesium is needed for the breakdown of glucose by various enzymes. Moreover, low levels of this mineral can impair the secretion of insulin by the pancreas. For this reason, the use of magnesium supplements can improve glycemic control, helping in the management of diabetes. -Zinc: Zinc plays a significant role in the synthesis, storage, and secretion of insulin. Low levels of zinc not only increase the risk of diabetes and associated complications, but it also affects other cellular functions. Hence, to regulate glucose levels and prevent diabetic complications, zinc supplementation may be recommended. -Chromium: Research studies have shed light on the need for chromium, which is a trace mineral. This mineral is required for the metabolism of carbohydrates. Although low doses of this mineral are regarded as safe, there is not enough evidence on the appropriate dosage. Do talk to your doctor before you take any mineral supplements for diabetes. Antioxidants for diabetes Hyperglycemia or high blood glucose levels can lead to auto-oxidation of glucose to form free radicals. An excess of free radicals in the body can lead to vascular damage and dysfunction of the blood vessels and neurons, thus increasing the risk of diabetic neuropathy. Antioxidants help to scavenge free radicals, thereby lowering the risk of complications. Intake of antioxidants such as Vitamin C and alpha lipoic acid (ALA), either through natural food sources or through supplements, can help to prevent the risk of diabetic pathologies. This makes them helpful in the management of diabetes. ALA is a potent antioxidant that lowers fasting blood glucose levels, reduces oxidative stress, and decreases insulin resistance. However, this supplement should be used with caution as it can cause a drastic drop in your blood glucose levels. Before you start using any supplements, keep in mind that certain supplements might interfere with your diabetes medications. This is why it is important to first consult your doctor for the appropriate dosage and usage information, depending on your specific requirements. (The article is reviewed by Dr. Lalit Kanodia, General Physician)Saquib Nomani Microbiologist4 Likes4 Answers
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DIABETIC NEUROPATHIES. Diabetic neuropathies are a family of nerve disorders caused by diabetes. WHAT CAUSES DIABETIC NEUROPATHY. Nerve damage is likely due to a combination of factors. 1.METABOLIC FACTORS. : hyperglycemia, long duration of diabetes, abnormal blood fat levels and low levels of insulin. 2.NEUROVASCULAR FACTORS : Neurovascular factors leading to damage of blood vessels that carry oxygen and nutrients to nerves. 3.AUTOIMMUNE FACTORS : Causes inflammation of nerves. 4.MECHANICAL FACTORS : Injury to nerves as in carpel tunnel syndrome. 5.INHERITED TRAITS : That increase susceptibility to nerve disease. 6.LIFESTYLE FACTORS : Smoking, alcohol. SYMPTOMS. Symptoms depends on the type of neuropathy and which nerves are affected.Symptoms involve sensory,motor and autonomic nervous system. 1.Tingling, numbness or pain in the toes,feet,legs,hands,arms and fingers. 2.Wasting of muscles of hand or feet. 3.Indigestion, nausea, vomiting, diarrhea,c constipation. 4. Dizziness or fainting due to a drop in blood pressure after standing or sitting up. 5.Problems with urination. 6.Erectile dysfunction. 7.Weakness. TYPES OF NEUROPATHY. Diabetic neuropathy can be classified as 1.Peripheral neuropathy. 2.Autonomic neuropathy. 3.Proximal neuropathy. 4.Focal neuropathy. PERIPHERAL NEUROPATHY. Peripheral neuropathy,also called distal symmetric neuropathy or sensorimotor neuropathy ,is nerve damage in arms and legs.Symptoms are *Numbness or insensitivity to pain or temperature. *A tingling,burning or prickling sensation. *Sharp pains or cramps. *Extreme Sensitivity to touch. *Loss of balance and coordination. Peripheral neuropathy also causes muscle weakness and loss of refle guyxes.Blisters and sites may appear on the numb areas of the foot because pressure or injury goes unnoticed.I f an infection occurs and is not treated promptly,the infection may spread to the bone and the foot may need amputation.Many amputations can be prevented if minor problems are treated in time. AUTONOMIC NEUROPATHY. Autonomic neuropathy affects the nerves that control the heart,blood pressure and blood glucose levels.Autonomic neuropathy also affects internal organs causing problems with digestion,respiration. urination,sexual response and vision. 1.HYPOGLYCEMIA UNAWARENESS. Normally,symptoms such as shakiness,sweating and palpitations occurs when the blood glucose levels drop below <<70 mg/dl.In people with autonomic neuropathy,symptoms may not occur making hypoglycemia to be recognized. 2.HEART & BLOOD VESSELS. Damage to the nerves in the cardiovascular system interferes with the body's ability to adjust blood pressure and heart rate. Due to this,blood pressuremay drop sharply after standing or sitting,causing a person to feel light headed or faint. Damage to nerves that control heart rate makes the heart rate to stay high , instead of rising and falling in response to normal body functions and physical activity. 3.DIGESTIVE SYSTEM. Nerve damage to the digestive system most commonly causes constipation. Damage can also cause the stomach to empty slowly,a condition called GASTROPARESIS. Gastroparesis can lead to persistent nausea and vomiting,bloating and loss of appetite. Gastroparesis also makes blood glucose levels to fluctuate widely ,due to abnormal food digestion. Nerve damage to the OESOPHAGUS MAKES SWALLOWING DIFFICULT. Nerve damage to bowels can cause constipation alternating with uncontrolled diarrhea, 3.URINARY TRACT & SEX ORGANS. Autonomic neuropathy often affects the organs that control urination and sexual functions. Nerve damage can prevent the bladder from emptying completely , allowing the bacteria to grow in bladder and kidneys causing urinary tract infections. When the nerves of the bladder are damaged,urinary incontinence may result because a person may not be able to sense when the bladder is full or control the muscles that release urine. Autonomic neuropathy also leads to decreased sexual response in men and women. A man may have erectile dysfunction or may reach sexual climax without ejaculating normally. A woman may have difficulty in arousal,lubrication or orgasm. 5.SWEAT GLANDS. Nerve damage may cause improper working of sweat glands.It can also result in profuse sweating at night or while eating. 6.EYES. Due to autonomic neuropathy,pupils become less responsive to changes in light.A s a result,a person may not be able to see well when light is turned on In a dark room or have trouble driving at night. PROXIMAL NEUROPATHY. Proximal neuropathy//lumbosacral plexus neuropathy //femoral neuropathy //diabetic amyotrophy causes pain in the thighs,buttocks,hips or legs,usually on one side of the body. FOCAL NEUROPATHY. Focal neuropathy appears suddenly and affects specific nerves,most often in the head,torso or leg. Focal neuropathy is painful and unpredictable.and occurs most often in older adults with diabetes. However,it tends to improve itself over weeks or months and does not cause long term damage. Focal neuropathy can cause *Inability to focus the eye. *Diplopia. *Aching behind the eye. *Bell's palsy. *Severe pain in the lower back and pelvis. *Pain in the front of the thigh. *Pain in the chest and stomach. *Pain on the outside of the shin or inside of the foot. *Chest pain and abdominal pain is mistaken for heart attack or appendicitis. CAN DIABETIC NEUROPATHIES BE PREVENTED. THE BEST WAY TO PREVENT NEUROPATHY IS TO KEEP BLOOD GLUCOSE LEVELS AS CLOSE TO THE NORMAL RANGE AS POSSIBLE.MAINTAINING SAFE BLOOD GLUCOSE LEVELS PROTECTS NERVES THROUGH OUT THE BODY.Dr. Suvarchala Pratap16 Likes25 Answers
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You can find here key changes in ADA guidelines. They are published in Diabetes Care once yearly in the month of January. GENERAL CHANGES The field of diabetes care is rapidly changing as new research, technology, and treatments that can improve the health and well-being of people with diabetes continue to emerge. With annual updates since 1989, the ADA has long been a leader in producing guidelines that capture the most current state of the field. To that end, the “Standards of Medical Care in Diabetes” now includes a dedicated section on Diabetes Technology, which contains preexisting material that was previously in other sections that has been consolidated, as well as new recommendations. SECTION 1. IMPROVING CARE AND PROMOTING HEALTH IN POPULATIONS Additional information was included on the financial costs of diabetes to individuals and society. Because telemedicine is a growing field that may increase access to care for patients with diabetes, discussion was added on its use to facilitate remote delivery of health-related services and clinical information. SECTION 2. CLASSIFICATION AND DIAGNOSIS OF DIABETES Based on new data, the criteria for the diagnosis of diabetes was changed to include two abnormal test results from the same sample (i.e., fasting plasma glucose and A1C from same sample). The section was reorganized to improve flow and reduce redundancy. Additional conditions were identified that may affect A1C test accuracy including the postpartum period. SECTION 3. PREVENTION OR DELAY OF TYPE 2 DIABETES This section was moved and is now located before the Lifestyle Management section to better reflect the progression of type 2 diabetes. The nutrition section was updated to highlight the importance of weight loss for those at high risk for developing type 2 diabetes who have overweight or obesity. Because smoking may increase the risk of type 2 diabetes, a section on tobacco use and cessation was added. SECTION 4. COMPREHENSIVE MEDICAL EVALUATION AND ASSESSMENT OF COMORBIDITIES On the basis of a new consensus report on diabetes and language, new text was added to guide health care professionals’ use of language to communicate about diabetes with people with diabetes and professional audiences in an informative, empowering, and educational style. A new figure from the ADA-European Association for the Study of Diabetes (EASD) consensus report about the diabetes care decision cycle was added to emphasize the need for ongoing assessment and shared decision making to achieve the goals of health care and avoid clinical inertia. A new recommendation was added to explicitly call out the importance of the diabetes care team and to list the professionals that make up the team. A recommendation was added to include the 10-year atherosclerotic cardiovascular disease (ASCVD) risk as part of overall risk assessment. The fatty liver disease section was revised to include updated text and a new recommendation regarding when to test for liver disease. SECTION 5. LIFESTYLE MANAGEMENT Evidence continues to suggest that there is NOT an ideal percentage of calories from carbohydrate, protein, and fat for all people with diabetes. Therefore, more discussion was added about the importance of macronutrient distribution based on an individualized assessment of current eating patterns, preferences, and metabolic goals. Additional considerations were added to the eating patterns, macronutrient distribution, and meal planning sections to better identify candidates for meal plans, specifically for low-carbohydrate eating patterns and people who are pregnant or lactating, who have or are at risk for disordered eating, who have renal disease, and who are taking sodium–glucose cotransporter 2 inhibitors. There is NOT a one-size-fits-all eating pattern for individuals with diabetes, and meal planning should be individualized. A recommendation was modified to encourage people with diabetes to decrease consumption of both sugar sweetened and nonnutritive-sweetened beverages and use other alternatives, with an emphasis on water intake. The sodium consumption recommendation was modified to eliminate the further restriction that was potentially indicated for those with both diabetes and hypertension. Additional discussion was added to the physical activity section to include the benefit of a variety of leisure-time physical activities and flexibility and balance exercises. The discussion about e-cigarettes was expanded to include more on public perception and how their use to aide smoking cessation was not more effective than “usual care.” SECTION 6. GLYCEMIC TARGETS This section now begins with a discussion of A1C tests to highlight the centrality of A1C testing in glycemic management. To emphasize that the risks and benefits of glycemic targets can change as diabetes progresses and patients age, a recommendation was added to reevaluate glycemic targets over time. The section was modified to align with the living Standards updates made in April 2018 regarding the consensus definition of hypoglycemia. SECTION 7. DIABETES TECHNOLOGY This new section includes new recommendations, the self-monitoring of blood glucose section formerly included in Section 6 “Glycemic Targets,” and a discussion of insulin delivery devices, blood glucose meters, continuous glucose monitors (real-time and intermittently scanned, and automated insulin delivery devices. The recommendation to use self-monitoring of blood glucose in people who are not using insulin was changed to acknowledge that routine glucose monitoring is of limited additional clinical benefit in this population. SECTION 8. OBESITY MANAGEMENT FOR THE TREATMENT OF TYPE 2 DIABETES A recommendation was modified to acknowledge the benefits of tracking weight, activity, etc., in the context of achieving and maintaining a healthy weight. A brief section was added on medical devices for weight loss, which are not currently recommended due to limited data in people with diabetes. The recommendations for metabolic surgery were modified to align with recent guidelines, citing the importance of considering comorbidities beyond diabetes when contemplating the appropriateness of metabolic surgery for a given patient. SECTION 9. PHARMACOLOGIC APPROACHES TO GLYCEMIC TREATMENT The section on the pharmacologic treatment of type 2 diabetes was significantly changed to align, as per the living Standards update in October 2018, with the ADA-EASD consensus report on this topic. This includes consideration of key patient factors: (a) important comorbidities such as ASCVD, CKD, and HF, (b) hypoglycemia risk, (c) effects on body weight, (d) side effects, (e) costs, and (f) patient preferences. To align with the ADA-EASD consensus report, the approach to injectable medication therapy was revised. A recommendation that, for most patients who need the greater efficacy of an injectable medication, a GLP-1 agonist should be the first choice, ahead of insulin. A new section was added on insulin injection technique, emphasizing the importance of technique for appropriate insulin dosing and the avoidance of complications (lipodystrophy, etc.). The section on non-insulin pharmacologic treatments for DM1 was abbreviated, as these are not generally recommended. SECTION 10. CARDIOVASCULAR DISEASE AND RISK MANAGEMENT For the first time, this section is endorsed by the American College of Cardiology. Additional text was added to acknowledge heart failure as an important type of cardiovascular disease in people with diabetes for consideration when determining optimal diabetes care. The blood pressure recommendations were modified to emphasize the importance of individualization of targets based on cardiovascular risk. A discussion of the appropriate use of the ASCVD risk calculator was included, and recommendations were modified to include assessment of 10-year ASCVD risk as part of overall risk assessment and in determining optimal treatment approaches. The recommendation and text regarding the use of aspirin in primary prevention was updated with new data. For alignment with the ADA-EASD consensus report, two recommendations were added for the use of medications that have proven cardiovascular benefit in people with ASCVD, with and without heart failure. SECTION 11. MICROVASCULAR COMPLICATIONS AND FOOT CARE To align with the ADA-EASD consensus report, a recommendation was added for people with type 2 diabetes and chronic kidney disease to consider agents with proven benefit with regard to renal outcomes. The recommendation on the use of telemedicine in retinal screening was modified to acknowledge the utility of this approach, so long as appropriate referrals are made for a comprehensive eye examination. Gabapentin was added to the list of agents to be considered for the treatment of neuropathic pain in people with diabetes based on data on efficacy and the potential for cost savings. The gastroparesis section includes a discussion of a few additional treatment modalities. The recommendation for patients with diabetes to have their feet inspected at every visit was modified to only include those at high risk for ulceration. Annual examinations remain recommended for everyone. SECTION 12. OLDER ADULTS A new section and recommendation on lifestyle management was added to address the unique nutritional and physical activity needs and considerations for older adults. Within the pharmacologic therapy discussion, de-intensification of insulin regimes was introduced to help simplify insulin regimen to match individual’s self-management abilities. SECTION 13. CHILDREN AND ADOLESCENTS Introductory language was added to the beginning of this section reminding the reader that the epidemiology, pathophysiology, developmental considerations, and response to therapy in pediatric-onset diabetes are different from adult diabetes, and that there are also differences in recommended care for children and adolescents with type 1 as opposed to type 2 diabetes. A recommendation was added to emphasize the need for disordered eating screening in youth with type 1 diabetes beginning at 10–12 years of age. Based on new evidence, a recommendation was added discouraging e-cigarette use in youth. The discussion of type 2 diabetes in children and adolescents was significantly expanded, with new recommendations in a number of areas, including screening and diagnosis, lifestyle management, pharmacologic management, and transition of care to adult providers. New sections and/or recommendations for type 2 diabetes in children and adolescents were added for glycemic targets, metabolic surgery, nephropathy, neuropathy, retinopathy, nonalcoholic fatty liver disease, obstructive sleep apnea, polycystic ovary syndrome, cardiovascular disease, dyslipidemia, cardiac function testing, and psychosocial factors. SECTION 14. MANAGEMENT OF DIABETES IN PREGNANCY Women with preexisting diabetes are now recommended to have their care managed in a multidisciplinary clinic to improve diabetes and pregnancy outcomes. Greater emphasis has been placed on the use of insulin as the preferred medication for treating hyperglycemia in gestational diabetes mellitus as it does not cross the placenta to a measurable extent and how metformin and glyburide should not be used as first-line agents as both cross the placenta to the fetus. SECTION 15. DIABETES CARE IN THE HOSPITAL Because of their ability to improve hospital readmission rates and cost of care, a new recommendation was added calling for providers to consider consulting with a specialized diabetes or glucose management team where possible when caring for hospitalized patients with diabetes. SECTION 16. DIABETES ADVOCACY The “Insulin Access and Affordability Working Group: Conclusions and Recommendations” ADA statement was added to this section. Published in 2018, this statement compiled public information and convened a series of meetings with stakeholders throughout the insulin supply chain to learn how each entity affects the cost of insulin for the consumer, an important topic for the ADA and people living with diabetes.Dr. Peerzada Ovais Ahmad6 Likes7 Answers
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This is a path case. 55yo male, known chronic kidney disease (stage 2) due to “moderately controlled” diabetes mellitus type 2 (diagnosed 7 years ago), presents with a jump in Kreatinine and proteinuria over few months. HbA1C around 7%, Krea = 1.7, Proteinuria = 1.9 g/24h. Nephrology decided to biopsy because of this atypical course. These pictures show the light microscopy of his renal core biopsies. What do you think may the IF look like? Is there evidence of acute disease or is it all chronic? Please feel free to share your thoughts !Dr. Tanish Wadhwa1 Like5 Answers