Rosiglitazone, a thiazolidinedione, has not been found to improve long-term outcomes even though it improves blood sugar levels. Additionally it is associated with increased rates of heart disease and death. Angiotensin-converting enzyme inhibitors (ACEIs) prevent kidney disease and improve outcomes in those with diabetes. The similar medications angiotensin receptor blockers (ARBs) do not. A 2016 review recommended treating to a systolic blood pressure of 140 to 150 mmHg.
Jump up ^ McBrien, K; Rabi, DM; Campbell, N; Barnieh, L; Clement, F; Hemmelgarn, BR; Tonelli, M; Leiter, LA; Klarenbach, SW; Manns, BJ (6 August 2012). "Intensive and Standard Blood Pressure Targets in Patients With Type 2 Diabetes Mellitus: Systematic Review and Meta-analysis". Archives of Internal Medicine. 172 (17): 1–8. doi:10.1001/archinternmed.2012.3147. PMID 22868819.
Originally described in approximately 30% of patients with type 1 diabetes mellitus, limited joint mobility occurs in 50% of patients older than age 10 years who have had diabetes for longer than 5 years. The condition restricts joint extension, making it difficult to press the hands flat against each other. The skin of patients with severe joint involvement has a thickened and waxy appearance.
The good news is that prevention plays an important role in warding off these complications. By maintaining tight control of your blood glucose—and getting it as close to normal as possible—you’ll help your body function in the way that it would if you did not have diabetes. Tight control helps you decrease the chances that your body will experience complications from elevated glucose levels.
The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus (IDDM). Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus (NIDDM). Beyond these two types, there is no agreed-upon standard nomenclature.
Diabetes is suspected based on symptoms. Urine tests and blood tests can be used to confirm a diagnose of diabetes based on the amount of glucose found. Urine can also detect ketones and protein in the urine that may help diagnose diabetes and assess how well the kidneys are functioning. These tests also can be used to monitor the disease once the patient is on a standardized diet, oral medications, or insulin.
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.
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.
For example, the environmental trigger may be a virus or chemical toxin that upsets the normal function of the immune system. This may lead to the body’s immune system attacking itself. The normal beta cells in the pancreas may be attacked and destroyed. When approximately 90% of the beta cells are destroyed, symptoms of diabetes mellitus begin to appear. The exact cause and sequence is not fully understood but investigation and research into the disease continues.
FIGURE 19-1 ■. This figure shows the hyperbolic relationship of insulin resistance and beta cell function. On the y-axis is beta cell function as reflected in the first-phase insulin response during intravenous (IV) glucose infusion; on the x-axis is insulin sensitivity and its mirror image resistance. In a subject with normal glucose tolerance (NGT) and beta-cell reserve, an increase in insulin resistance results in increased insulin release and normal glucose tolerance. In an individual for whom the capacity to increase insulin release is compromised, increasing insulin resistance with partial or no beta-cell compensation results in progression from normal glucose tolerance, to impaired glucose tolerance (IGT), and finally to diabetes (T2D). Differences between these categories are small at high insulin sensitivity, which may be maintained by weight reduction, exercise, and certain drugs. At a critical degree of insulin resistance, due to obesity or other listed factors, only a further small increment in resistance requires a large increase in insulin output. Those that can increase insulin secretion to this extent retain normal glucose tolerance; those who cannot achieve this degree of insulin secretion (e.g., due to a mild defect in genes regulating insulin synthesis, insulin secretion, insulin action, or an ongoing immune destruction of beta cells) now unmask varying degrees of carbohydrate intolerance. The product of insulin sensitivity (the reciprocal of insulin resistance) and acute insulin response (a measurement beta-cell function) has been called the “disposition index.” This index remains constant in an individual with normal beta cell compensation in response to changes in insulin resistance. IGT, impaired glucose tolerance; NGT, normal glucose tolerance; T2D, type 2 diabetes.
Type II is considered a milder form of diabetes because of its slow onset (sometimes developing over the course of several years) and because it usually can be controlled with diet and oral medication. The consequences of uncontrolled and untreated Type II diabetes, however, are the just as serious as those for Type I. This form is also called noninsulin-dependent diabetes, a term that is somewhat misleading. Many people with Type II diabetes can control the condition with diet and oral medications, however, insulin injections are sometimes necessary if treatment with diet and oral medication is not working.
Because people with type 2 diabetes produce some insulin, ketoacidosis does not usually develop even when type 2 diabetes is untreated for a long time. Rarely, the blood glucose levels become extremely high (even exceeding 1,000 mg/dL). Such high levels often happen as the result of some superimposed stress, such as an infection or drug use. When the blood glucose levels get very high, people may develop severe dehydration, which may lead to mental confusion, drowsiness, and seizures, a condition called hyperosmolar hyperglycemic state. Currently, many people with type 2 diabetes are diagnosed by routine blood glucose testing before they develop such severely high blood glucose levels.
The blood vessels and blood are the highways that transport sugar from where it is either taken in (the stomach) or manufactured (in the liver) to the cells where it is used (muscles) or where it is stored (fat). Sugar cannot go into the cells by itself. The pancreas releases insulin into the blood, which serves as the helper, or the "key," that lets sugar into the cells for use as energy.
Because both yeast and bacteria multiply more quickly when blood sugar levels are elevated, women with diabetes are overall at a higher risk of feminine health issues, such as bacterial infections, yeast infections, and vaginal thrush, especially when blood sugar isn't well controlled. And a lack of awareness about having prediabetes or diabetes can make managing blood sugar impossible.