Along with following your diabetes care plan, you may need diabetes medicines, which may include pills or medicines you inject under your skin, such as insulin. Over time, you may need more than one diabetes medicine to manage your blood glucose. Even if you don’t take insulin, you may need it at special times, such as during pregnancy or if you are in the hospital. You also may need medicines for high blood pressure, high cholesterol, or other conditions.
In animals, diabetes is most commonly encountered in dogs and cats. Middle-aged animals are most commonly affected. Female dogs are twice as likely to be affected as males, while according to some sources, male cats are also more prone than females. In both species, all breeds may be affected, but some small dog breeds are particularly likely to develop diabetes, such as Miniature Poodles.
Another diabetes-related sexual dysfunction symptom in men is reduced amounts of ejaculation, or retrograde ejaculation. Retrograde ejaculation is a condition in which the semen goes into the bladder, rather than out of the body through the urethra. Diabetes and damage to the blood vessels causes nerve damage to the muscles that control the bladder and urethra, which results in this problem.
The major eye complication of diabetes is called diabetic retinopathy. Diabetic retinopathy occurs in patients who have had diabetes for at least five years. Diseased small blood vessels in the back of the eye cause the leakage of protein and blood in the retina. Disease in these blood vessels also causes the formation of small aneurysms (microaneurysms), and new but brittle blood vessels (neovascularization). Spontaneous bleeding from the new and brittle blood vessels can lead to retinal scarring and retinal detachment, thus impairing vision.
Clear evidence suggests a genetic component in type 1 diabetes mellitus. Monozygotic twins have a 60% lifetime concordance for developing type 1 diabetes mellitus, although only 30% do so within 10 years after the first twin is diagnosed. In contrast, dizygotic twins have only an 8% risk of concordance, which is similar to the risk among other siblings.
"Secondary" diabetes refers to elevated blood sugar levels from another medical condition. Secondary diabetes may develop when the pancreatic tissue responsible for the production of insulin is destroyed by disease, such as chronic pancreatitis (inflammation of the pancreas by toxins like excessive alcohol), trauma, or surgical removal of the pancreas.
Diabetes mellitus (DM) is best defined as a syndrome characterized by inappropriate fasting or postprandial hyperglycemia, caused by absolute or relative insulin deficiency and its metabolic consequences, which include disturbed metabolism of protein and fat. This syndrome results from a combination of deficiency of insulin secretion and its action. Diabetes mellitus occurs when the normal constant of the product of insulin secretion times insulin sensitivity, a parabolic function termed the “disposition index” (Figure 19-1), is inadequate to prevent hyperglycemia and its clinical consequences of polyuria, polydipsia, and weight loss. At high degrees of insulin sensitivity, small declines in the ability to secrete insulin cause only mild, clinically imperceptible defects in glucose metabolism. However, irrespective of insulin sensitivity, a minimum amount of insulin is necessary for normal metabolism. Thus, near absolute deficiency of insulin must result in severe metabolic disturbance as occurs in type 1 diabetes mellitus (T1DM). By contrast, with decreasing sensitivity to its action, higher amounts of insulin secretion are required for a normal disposition index. At a critical point in the disposition index curve (see Figure 19-1), a further small decrement in insulin sensitivity requires a large increase in insulin secretion; those who can mount these higher rates of insulin secretion retain normal glucose metabolism, whereas those who cannot increase their insulin secretion because of genetic or acquired defects now manifest clinical diabetes as occurs in type 2 diabetes (T2DM).
Monitoring your caloric intake may be helpful if you’re overweight, but everyone with type 2 diabetes should track how many carbs they’re taking in. That can be tricky because carbs are in many of the common foods you may already eat, but there are both good and bad sources of carbs. Fruits and vegetables, for example, are good sources, while pretzels and cookies are bad sources. (29)
Diabetic peripheral neuropathy is a condition where nerve endings, particularly in the legs and feet, become less sensitive. Diabetic foot ulcers are a particular problem since the patient does not feel the pain of a blister, callous, or other minor injury. Poor blood circulation in the legs and feet contribute to delayed wound healing. The inability to sense pain along with the complications of delayed wound healing can result in minor injuries, blisters, or callouses becoming infected and difficult to treat. In cases of severe infection, the infected tissue begins to break down and rot away. The most serious consequence of this condition is the need for amputation of toes, feet, or legs due to severe infection.
“I don’t think that anybody has put their finger on what the true cause of diabetes is, or that we’re going to find a single cause,” Grieger says. So if you’ve been diagnosed with prediabetes or have other risk factors for the disease, avoiding any one food group entirely — even sugar — won’t completely offset your risk. Rather, it’s important to prioritize proper nutrition, exercise regularly, and maintain a healthy weight — all steps the American Diabetes Association recommends for preventing type 2 diabetes.
There are a range of different symptoms in people with diabetes. They may feel thirsty, pass a large amount of urine, wake up overnight to pass urine, lose weight and have blurred vision. Patients are vulnerable to infections such as thrush and may present with this. Particularly in type 2 diabetes, patients may not be aware of their diabetes for several years and a diagnosis may only be made when they seek treatment for diabetes-related complications such as foot, eye or kidney problems. Some patients may become severely ill and be taken into hospital with an infection and/or very high blood sugar levels.
In the United States alone, more than 8 million people have undiagnosed diabetes, according to the American Diabetes Association. But you don't need to become a statistic. Understanding possible diabetes symptoms can lead to early diagnosis and treatment — and a lifetime of better health. If you're experiencing any of the following diabetes signs and symptoms, see your doctor.
In patients with type 2 diabetes, stress, infection, and medications (such as corticosteroids) can also lead to severely elevated blood sugar levels. Accompanied by dehydration, severe blood sugar elevation in patients with type 2 diabetes can lead to an increase in blood osmolality (hyperosmolar state). This condition can worsen and lead to coma (hyperosmolar coma). A hyperosmolar coma usually occurs in elderly patients with type 2 diabetes. Like diabetic ketoacidosis, a hyperosmolar coma is a medical emergency. Immediate treatment with intravenous fluid and insulin is important in reversing the hyperosmolar state. Unlike patients with type 1 diabetes, patients with type 2 diabetes do not generally develop ketoacidosis solely on the basis of their diabetes. Since in general, type 2 diabetes occurs in an older population, concomitant medical conditions are more likely to be present, and these patients may actually be sicker overall. The complication and death rates from hyperosmolar coma is thus higher than in diabetic ketoacidosis.
Type 2 diabetes is mainly caused by insulin resistance. This means no matter how much or how little insulin is made, the body can't use it as well as it should. As a result, glucose can't be moved from the blood into cells. Over time, the excess sugar in the blood gradually poisons the pancreas causing it to make less insulin and making it even more difficult to keep blood glucose under control.
Diabetes is a serious and costly disease which is becoming increasingly common, especially in developing countries and disadvantaged minorities. However, there are ways of preventing it and/or controlling its progress. Public and professional awareness of the risk factors for, and symptoms of diabetes are an important step towards its prevention and control.
In type 1 diabetes (formerly called insulin-dependent diabetes or juvenile-onset diabetes), the body's immune system attacks the insulin-producing cells of the pancreas, and more than 90% of them are permanently destroyed. The pancreas, therefore, produces little or no insulin. Only about 5 to 10% of all people with diabetes have type 1 disease. Most people who have type 1 diabetes develop the disease before age 30, although it can develop later in life.
Those dark patches on your skin could be more serious than a blotchy tan. In fact, they might be the first sign of diabetes. This darkening of the skin, which usually occurs on the hands and feet, in folds of skin, along the neck, and in a person’s groin and armpits, called acanthosis nigricans, often occurs when insulin levels are high. The high insulin levels in your blood can increase your body’s production of skin cells, many of which have increased pigmentation, giving skin a darkened appearance.
Patients need to ensure that their blood glucose levels are kept as normal as possible so that delicate tissues in the body (especially blood vessels in the eyes, kidneys and peripheral nerves) are not damaged by high glucose levels over a long period of time. To achieve this, patients need to measure their glucose regularly and learn how to adjust their insulin doses in order to optimise their glucose levels (diabetes control). Good diabetes control helps to minimise the risk of long-term diabetes complications, as well as short-term symptoms (such as thirst).
Although this complication is not seen in pediatric patients, it is a significant cause of morbidity and premature mortality in adults with diabetes. People with type 1 diabetes mellitus have twice the risk of fatal myocardial infarction (MI) and stroke that people unaffected with diabetes do; in women, the MI risk is 4 times greater. People with type 1 diabetes mellitus also have 4 times greater risk for atherosclerosis.
a broadly applied term used to denote a complex group of syndromes that have in common a disturbance in the oxidation and utilization of glucose, which is secondary to a malfunction of the beta cells of the pancreas, whose function is the production and release of insulin. Because insulin is involved in the metabolism of carbohydrates, proteins and fats, diabetes is not limited to a disturbance of glucose homeostasis alone.
DM is a strong independent predictor of short- and long-term recurrent ischemic events, including mortality, in acute coronary syndrome (ACS),6,7 including unstable angina and non-ST-elevation MI (NSTEMI),8 ST-elevation MI (STEMI) treated medically,9 and ACS undergoing percutaneous coronary intervention (PCI).10,11 Furthermore, the concomitant presence of cardiovascular risk factors and comorbidities that negatively affect the outcomes of ACS is higher in DM patients.12
Insulin is vital to patients with type 1 diabetes - they cannot live without a source of exogenous insulin. Without insulin, patients with type 1 diabetes develop severely elevated blood sugar levels. This leads to increased urine glucose, which in turn leads to excessive loss of fluid and electrolytes in the urine. Lack of insulin also causes the inability to store fat and protein along with breakdown of existing fat and protein stores. This dysregulation, results in the process of ketosis and the release of ketones into the blood. Ketones turn the blood acidic, a condition called diabetic ketoacidosis (DKA). Symptoms of diabetic ketoacidosis include nausea, vomiting, and abdominal pain. Without prompt medical treatment, patients with diabetic ketoacidosis can rapidly go into shock, coma, and even death may result.
In autoimmune diseases, such as type 1 diabetes, the immune system mistakenly manufactures antibodies and inflammatory cells that are directed against and cause damage to patients' own body tissues. In persons with type 1 diabetes, the beta cells of the pancreas, which are responsible for insulin production, are attacked by the misdirected immune system. It is believed that the tendency to develop abnormal antibodies in type 1 diabetes is, in part, genetically inherited, though the details are not fully understood.
Type I diabetes, sometimes called juvenile diabetes, begins most commonly in childhood or adolescence. In this form of diabetes, the body produces little or no insulin. It is characterized by a sudden onset and occurs more frequently in populations descended from Northern European countries (Finland, Scotland, Scandinavia) than in those from Southern European countries, the Middle East, or Asia. In the United States, approximately three people in 1,000 develop Type I diabetes. This form also is called insulin-dependent diabetes because people who develop this type need to have daily injections of insulin.
Diabetes experts feel that these blood glucose monitoring devices give patients a significant amount of independence to manage their disease process; and they are a great tool for education as well. It is also important to remember that these devices can be used intermittently with fingerstick measurements. For example, a well-controlled patient with diabetes can rely on fingerstick glucose checks a few times a day and do well. If they become ill, if they decide to embark on a new exercise regimen, if they change their diet and so on, they can use the sensor to supplement their fingerstick regimen, providing more information on how they are responding to new lifestyle changes or stressors. This kind of system takes us one step closer to closing the loop, and to the development of an artificial pancreas that senses insulin requirements based on glucose levels and the body's needs and releases insulin accordingly - the ultimate goal.
Sources of processed or added sugar, including condiments, honey, and especially sugary drinks, are just a few of the potential culprits for weight gain, Grieger says, and it’s when they’re consumed in excess that they can contribute to diabetes risk. “The largest source of added sugar comes from sweetened beverages. They run the gamut of soda, sweetened tea, juices with added sugar, sports drinks — it’s a plethora. Just about everything we drink has added sugar in it, except for water,” she explains.
It's not as clear what the rest of the type 1 genes are up to, but researchers are eager to find out. "Even though something accounts for a small part [of the genetic risk], it could have a significant impact," says Stephen Rich, PhD, director of the Center for Public Health Genomics at the University of Virginia School of Medicine. Understanding these genes' role may clue researchers in to less obvious biological pathways involved in type 1 diabetes, and to possible prevention strategies.
Hyperglycemia (ie, random blood glucose concentration of more than 200 mg/dL or 11 mmol/L) results when insulin deficiency leads to uninhibited gluconeogenesis and prevents the use and storage of circulating glucose. The kidneys cannot reabsorb the excess glucose load, causing glycosuria, osmotic diuresis, thirst, and dehydration. Increased fat and protein breakdown leads to ketone production and weight loss. Without insulin, a child with type 1 diabetes mellitus wastes away and eventually dies due to DKA. The effects of insulin deficiency are shown in the image below.
Diabetes Mellitus Diabetes Mellitus Complications Diabetes Mellitus Control in Hospital Diabetes Mellitus Glucose Management Diabetes Resources Diabetes Sick Day Management Diabetic Ketoacidosis Diabetic Ketoacidosis Management in Adults Diabetic Ketoacidosis Management in Children Diabetic Ketoacidosis Related Cerebral Edema Hyperosmolar Hyperglycemic State Metabolic Syndrome Type 1 Diabetes Mellitus Type 2 Diabetes Mellitus Type 2 Diabetes Mellitus in Children
Jump up ^ Cheng J, Zhang W, Zhang X, Han F, Li X, He X, Li Q, Chen J (May 2014). "Effect of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on all-cause mortality, cardiovascular deaths, and cardiovascular events in patients with diabetes mellitus: a meta-analysis". JAMA Internal Medicine. 174 (5): 773–85. doi:10.1001/jamainternmed.2014.348. PMID 24687000.
When you have diabetes, excess sugar (glucose) builds up in your blood. Your kidneys are forced to work overtime to filter and absorb the excess sugar. If your kidneys can't keep up, the excess sugar is excreted into your urine, dragging along fluids from your tissues. This triggers more frequent urination, which may leave you dehydrated. As you drink more fluids to quench your thirst, you'll urinate even more.
DM affects at least 16 million U.S. residents, ranks seventh as a cause of death in the United States, and costs the national economy over $100 billion yearly. The striking increase in the prevalence of DM in the U.S. during recent years has been linked to a rise in the prevalence of obesity. About 95% of those with DM have Type 2, in which the pancreatic beta cells retain some insulin-producing potential, and the rest have Type 1, in which exogenous insulin is required for long-term survival. In Type 1 DM, which typically causes symptoms before age 25, an autoimmune process is responsible for beta cell destruction. Type 2 DM is characterized by insulin resistance in peripheral tissues as well as a defect in insulin secretion by beta cells. Insulin regulates carbohydrate metabolism by mediating the rapid transport of glucose and amino acids from the circulation into muscle and other tissue cells, by promoting the storage of glucose in liver cells as glycogen, and by inhibiting gluconeogenesis. The normal stimulus for the release of insulin from the pancreas is a rise in the concentration of glucose in circulating blood, which typically occurs within a few minutes after a meal. When such a rise elicits an appropriate insulin response, so that the blood level of glucose falls again as it is taken into cells, glucose tolerance is said to be normal. The central fact in DM is an impairment of glucose tolerance of such a degree as to threaten or impair health. Long recognized as an independent risk factor for cardiovascular disease, DM is often associated with other risk factors, including disorders of lipid metabolism (elevation of very-low-density lipoprotein cholesterol and triglycerides and depression of high-density lipoprotein cholesterol), obesity, hypertension, and impairment of renal function. Sustained elevation of serum glucose and triglycerides aggravates the biochemical defect inherent in DM by impairing insulin secretion, insulin-mediated glucose uptake by cells, and hepatic regulation of glucose output. Long-term consequences of the diabetic state include macrovascular complications (premature or accelerated atherosclerosis with resulting coronary, cerebral, and peripheral vascular insufficiency) and microvascular complications (retinopathy, nephropathy, and neuropathy). It is estimated that half those with DM already have some complications when the diagnosis is made. The American Diabetes Association (ADA) recommends screening for DM for people with risk factors such as obesity, age 45 years or older, family history of DM, or history of gestational diabetes. If screening yields normal results, it should be repeated every 3 years. The diagnosis of DM depends on measurement of plasma glucose concentration. The diagnosis is confirmed when any two measurements of plasma glucose performed on different days yield levels at or above established thresholds: in the fasting state, 126 mg/dL (7 mmol/L); 2 hours postprandially (after a 75-g oral glucose load) or at random, 200 mg/dL (11.1 mmol/L). A fasting plasma glucose of 100-125 mg/dL (5.5-6.9 mmol/L) or a 2-hour postprandial glucose of 140-199 mg/dL (7.8-11 mmol/L) is defined as impaired glucose tolerance. People with impaired glucose tolerance are at higher risk of developing DM within 10 years. For such people, lifestyle modification such as weight reduction and exercise may prevent or postpone the onset of frank DM. Current recommendations for the management of DM emphasize education and individualization of therapy. Controlled studies have shown that rigorous maintenance of plasma glucose levels as near to normal as possible at all times substantially reduces the incidence and severity of long-term complications, particularly microvascular complications. Such control involves limitation of dietary carbohydrate and saturated fat; monitoring of blood glucose, including self-testing by the patient and periodic determination of glycosylated hemoglobin; and administration of insulin (particularly in Type 1 DM), drugs that stimulate endogenous insulin production (in Type 2 DM), or both. The ADA recommends inclusion of healthful carbohydrate-containing foods such as whole grains, fruits, vegetables, and low-fat milk in a diabetic diet. Restriction of dietary fat to less than 10% of total calories is recommended for people with diabetes, as for the general population. Further restriction may be appropriate for those with heart disease or elevated cholesterol or triglyceride levels. The ADA advises that high-protein, low-carbohydrate diets have no particular merit in long-term weight control or in maintenance of a normal plasma glucose level in DM. Pharmaceutical agents developed during the 1990s improve control of DM by enhancing responsiveness of cells to insulin, counteracting insulin resistance, and reducing postprandial carbohydrate absorption. Tailor-made insulin analogues produced by recombinant DNA technology (for example, lispro, aspart, and glargine insulins) have broadened the range of pharmacologic properties and treatment options available. Their use improves both short-term and long-term control of plasma glucose and is associated with fewer episodes of hypoglycemia. SEE ALSO insulin resistance
Most cases (95%) of type 1 diabetes mellitus are the result of environmental factors interacting with a genetically susceptible person. This interaction leads to the development of autoimmune disease directed at the insulin-producing cells of the pancreatic islets of Langerhans. These cells are progressively destroyed, with insulin deficiency usually developing after the destruction of 90% of islet cells.
Hyperglycemic hyperosmolar nonketotic syndrome (HHNS). Signs and symptoms of this life-threatening condition include a blood sugar reading higher than 600 mg/dL (33.3 mmol/L), dry mouth, extreme thirst, fever greater than 101 F (38 C), drowsiness, confusion, vision loss, hallucinations and dark urine. Your blood sugar monitor may not be able to give you an exact reading at such high levels and may instead just read "high."
Diabetes mellitus (DM) comprises a group of disorders characterized by hyperglycemia. It is the sixth leading cause of death in the United States and results in $132 billion in total direct and indirect costs. Although the incidence of Type 1 diabetes has doubled over the past 30 years, the increase in Type 2 diabetes has been even more dramatic. An estimated 20–40% of cases in large pediatric diabetes centers are now Type 2, and the rates are expected to rise along with the epidemic of childhood and adolescent obesity (Chapter 11).
FASTING GLUCOSE TEST. Blood is drawn from a vein in the patient's arm after a period at least eight hours when the patient has not eaten, usually in the morning before breakfast. The red blood cells are separated from the sample and the amount of glucose is measured in the remaining plasma. A plasma level of 7.8 mmol/L (200 mg/L) or greater can indicate diabetes. The fasting glucose test is usually repeated on another day to confirm the results.
If sugars in general are not associated with increased diabetes risk, but sodas are, it suggests the possibility that something other than sugar explains this relationship.16 Sodas are often accompanied by cheeseburgers, chicken nuggets, and other unhealthful foods. That is, soda consumption can be a sign of a diet focusing on fast foods or an overall unhealthful diet and lifestyle. And sugary snack foods (e.g., cookies and snack pastries) are often high in fat; the sugar lures us in to the fat calories hiding inside. Some, but not all, observational trials have sought to control for these confounding variables.
According to the American Diabetes Association, a child has a 1 in 7 risk of getting type 2 diabetes if his/her parent was diagnosed with type 2 diabetes before the age of 50, and a 1 in 13 risk of developing it if the parent was diagnosed after the age of 50. To see if you may be at risk for diabetes, consider taking this short and simple Type 2 Diabetes Risk Test from the ADA.
The most common complication of treating high blood glucose levels is low blood glucose levels (hypoglycemia). The risk is greatest for older people who are frail, who are sick enough to require frequent hospital admissions, or who are taking several drugs. Of all available drugs to treat diabetes, long-acting sulfonylurea drugs are most likely to cause low blood glucose levels in older people. When they take these drugs, they are also more likely to have serious symptoms, such as fainting and falling, and to have difficulty thinking or using parts of the body due to low blood glucose levels.
Oral glucose tolerance test (OGTT): With this test you will be required to fast for at least 8 hours and then are given a drink with 75 g of carbohydrate. Your blood glucose is checked at fasting and then 2 hours after drinking the solution. If your blood glucose is 11.1 mmol/L or higher, your doctor may diagnose diabetes. If your blood glucose 2 hours after drinking the solution is between 7.8 to 11.1 mmol/L, your doctor may diagnose prediabetes. This is the preferred method to test for gestational diabetes.
Insulin inhibits glucogenesis and glycogenolysis, while stimulating glucose uptake. In nondiabetic individuals, insulin production by the pancreatic islet cells is suppressed when blood glucose levels fall below 83 mg/dL (4.6 mmol/L). If insulin is injected into a treated child with diabetes who has not eaten adequate amounts of carbohydrates, blood glucose levels progressively fall.
Progression toward type 2 diabetes may even be self-perpetuating. Once a person begins to become insulin resistant, for whatever reason, things may snowball from there. The increased levels of circulating insulin required to compensate for resistance encourage the body to pack on pounds. That extra weight will in turn make the body more insulin resistant. Furthermore, the heavier a person is, the more difficult it can be to exercise, continuing the slide toward diabetes.
Can type 2 diabetes be cured? In the early stages of type 2 diabetes, it is possible to manage the diabetes to a level where symptoms go away and A1c reaches a normal level – this effectively “reverses” the progression of type 2 diabetes. According to research from Newcastle University, major weight loss can return insulin secretion to normal in people who had type 2 diabetes for four years or less. Indeed, it is commonly believed that significant weight loss and building muscle mass is the best way to reverse type 2 diabetes progression. However, it is important to note that reversing diabetes progression is not the same as curing type 2 diabetes – people still need to monitor their weight, diet, and exercise to ensure that type 2 diabetes does not progress. For many people who have had type 2 diabetes for a longer time, the damage to the beta cells progresses to the point at which it will never again be possible to make enough insulin to correctly control blood glucose, even with dramatic weight loss. But even in these people, weight loss is likely the best way to reduce the threat of complications.