^ Jump up to: a b c d Inzucchi, SE; Bergenstal, RM; Buse, JB; Diamant, M; Ferrannini, E; Nauck, M; Peters, AL; Tsapas, A; Wender, R; Matthews, DR (March 2015). "Management of hyperglycaemia in type 2 diabetes, 2015: a patient-centred approach. Update to a Position Statement of the American Diabetes Association and the European Association for the Study of Diabetes". Diabetologia. 58 (3): 429–42. doi:10.1007/s00125-014-3460-0. PMID 25583541.
Sequelae. The long-term consequences of diabetes mellitus can involve both large and small blood vessels throughout the body. That in large vessels is usually seen in the coronary arteries, cerebral arteries, and arteries of the lower extremities and can eventually lead to myocardial infarction, stroke, or gangrene of the feet and legs. atherosclerosis is far more likely to occur in persons of any age who have diabetes than it is in other people. This predisposition is not clearly understood. Some believe that diabetics inherit the tendency to develop severe atherosclerosis as well as an aberration in glucose metabolism, and that the two are not necessarily related. There is strong evidence to substantiate the claim that optimal control will mitigate the effects of diabetes on the microvasculature, particularly in the young and middle-aged who are at greatest risk for developing complications involving the arterioles. Pathologic changes in the small blood vessels serving the kidney lead to nephrosclerosis, pyelonephritis, and other disorders that eventually result in renal failure. Many of the deaths of persons with type 1 diabetes are caused by renal failure.
Monogenic diabetes is caused by mutations, or changes, in a single gene. These changes are usually passed through families, but sometimes the gene mutation happens on its own. Most of these gene mutations cause diabetes by making the pancreas less able to make insulin. The most common types of monogenic diabetes are neonatal diabetes and maturity-onset diabetes of the young (MODY). Neonatal diabetes occurs in the first 6 months of life. Doctors usually diagnose MODY during adolescence or early adulthood, but sometimes the disease is not diagnosed until later in life.
Type 1 diabetes in pediatric patients has been linked to changes in cognition and brain structure, with a study by Siller et al finding lower volume in the left temporal-parietal-occipital cortex in young patients with type 1 diabetes than in controls. The study also indicated that in pediatric patients, higher severity of type 1 diabetes presentation correlates with greater structural differences in the brain at about 3 months following diagnosis. The investigators found that among study patients with type 1 diabetes, an association existed between the presence of diabetic ketoacidosis at presentation and reduced radial, axial, and mean diffusivity in the major white matter tracts on magnetic resonance imaging (MRI). In those with higher glycated hemoglobin (HbA1c) levels, hippocampal, thalamic, and cerebellar white matter volumes were lower, as was right posterior parietal cortical thickness, while right occipital cortical thickness was greater. Patients in the study were aged 7-17 years. [43]
How does type 2 diabetes progress over time? Type 2 diabetes is a progressive disease, meaning that the body’s ability to regulate blood sugar gets worse over time, despite careful management. Over time, the body’s cells become increasingly less responsive to insulin (increased insulin resistance) and beta cells in the pancreas produce less and less insulin (called beta-cell burnout). In fact, when people are diagnosed with type 2 diabetes, they usually have already lost up to 50% or more of their beta cell function. As type 2 diabetes progresses, people typically need to add one or more different types of medications. The good news is that there are many more choices available for treatments, and a number of these medications don’t cause as much hypoglycemia, hunger and/or weight gain (e.g., metformin, pioglitazone, DPP-4 inhibitors, GLP-1 agonists, SGLT-2 inhibitors, and better insulin). Diligent management early on can help preserve remaining beta cell function and sometimes slow progression of the disease, although the need to use more and different types of medications does not mean that you have failed.
The information contained in this monograph is for educational purposes only. This information is not a substitute for professional medical advice, diagnosis, or treatment. If you have or suspect you may have a health concern, consult your professional health care provider. Reliance on any information provided in this monograph is solely at your own risk.
Jump up ^ Sarwar N, Gao P, Seshasai SR, Gobin R, Kaptoge S, Di Angelantonio E, Ingelsson E, Lawlor DA, Selvin E, Stampfer M, Stehouwer CD, Lewington S, Pennells L, Thompson A, Sattar N, White IR, Ray KK, Danesh J (June 2010). "Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies". Lancet. 375 (9733): 2215–22. doi:10.1016/S0140-6736(10)60484-9. PMC 2904878. PMID 20609967.

Complications of diabetes are responsible for considerable morbidity and mortality. The acute complications of diabetes are hypo- and hyperglycemic coma and infections. The chronic complications include microvascular complications such as retinopathy and nephropathy, and the macrovascular complications of heart disease and stroke. Diabetes mellitus is the commonest cause of blindness and renal failure in the UK and the USA. Other common complications include autonomic and peripheral neuropathy. A combination of vascular and neuropathic disturbances results in a high prevalence of impotence in men with diabetes. Peripheral neuropathy causes lack of sensation in the feet which can cause minor injuries to go unnoticed, become infected and, with circulatory problems obstructing healing, ulceration and gangrene are serious risks and amputation is not uncommon. Evidence from meta-analysis of studies of the relationship between glycemic control and microvascular complications (Wang, Lau, & Chalmers, 1993), and from the longitudinal multicenter Diabetes Control and Complications Trial (DCCT) in the USA (DCCT Research Group, 1993), have established a clear relationship between improved blood glucose control and reduction of risk of retinopathy and other microvascular complications in insulin-dependent diabetes mellitus (IDDM). It is likely that there would be similar findings for noninsulin-dependent diabetes mellitus (NIDDM) though the studies did not include NIDDM patients. However, the DCCT included highly selected, well-motivated, well-educated and well-supported patients, cared for by well-staffed diabetes care teams involving educators and psychologists as well as diabetologists and diabetes specialist nurses.
Aspirin should be used as secondary prophylaxis in all diabetic people with evidence of macrovascular disease, and it should be strongly considered as primary prevention in diabetic subjects with other risk factors for macrovascular disease, such as hypertension, cigarette smoking, dyslipidemia, obesity, and albuminuria (macro or micro).228 Because of the platelet defects associated with diabetes, it is recommended that the dose of aspirin should be 300 mg per day,228–230 although the American Diabetes Association’s position statement (http://www.diabetes.org/DiabetesCare/supplement198/s45.htm) advocates a dose of 81 to 325 mg enteric-coated aspirin per day. If the patient cannot tolerate aspirin, then clopidogrel231 can be used.
High blood glucose sets up a domino effect of sorts within your body. High blood sugar leads to increased production of urine and the need to urinate more often. Frequent urination causes you to lose a lot of fluid and become dehydrated. Consequently, you develop a dry mouth and feel thirsty more often. If you notice that you are drinking more than usual, or that your mouth often feels dry and you feel thirsty more often, these could be signs of type 2 diabetes.