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Type 2 Diabetes Mellitus

Risk Factors

The risk factors include family history (parents or siblings with diabetes), lack of physical activity, race or ethnicity (more prominent in some groups of Native Americans, Hispanic American, Asian American, African American and Pacific Island people), previously identified impaired glucose tolerance or impaired fasting glucose, history of gestation DM, history of vascular disease, hypertension (≥140/90 mm Hg in adults), HDL cholesterol ≤1.0mmol/L and/or triglyceride level ≥2.3mmol/L, obesity (≥20% over ideal body weight or ≥25 kg/m2 BMI) (1,2). Obesity is a major risk factor for diabetes as increases in weight is associated with increases in insulin resistance (1). Age greater than 45 years increases the risk for diabetes as there is diminished insulin sensitivity and decline in the body’s responsiveness to carbohydrates (1).

Pathophysiology and Etiology

In the fasting state, the pancreatic α cells secrete glucagon to stimulate hepatic glucose production to prevent hypoglycemia or restore normogylcemia if hypoglycemia has occurred (3). In the fed state, after the ingestion of carbohydrates, insulin is released from the pancreatic β in response to the increases in the plasma glucose concentration (3). This increase in insulin stimulates the glucose uptake by the peripheral tissues and suppresses hepatic glucose production, as a result preventing hyperglycemia (2,3).

Patients that have type 2 DM exhibit a defect in both insulin secretion and insulin action (1,2,3). This contributes to a progressive increase in plasma glucose levels (3). Insulin resistance typically occurs in the hepatic tissue and the muscle cells (3). The consequence of the inability of these cells to respond to insulin include the failure to suppress hepatic gluconeogenesis and elevated plasma glucose concentrations as the muscle cells represent up to 80% of the total body glucose uptake (3). Insulin resistance also occurs in the adipocytes, which due to the increase in free fatty acids in the plasma and triglyceride stores in the muscle and liver, leads to a defect in insulin secretion (3).

At some point, the β cells will no longer be able to secrete enough insulin to compensate for the insulin resistance. (3) A lack of insulin will request in subsequent hyperglycemia (3). As time progresses, during some point, the blood glucose levels will meet the criteria for diagnosis of type 2 DM (2). Many patients with type 2 DM remain asymptomatic for months of years after this point as the hyperglycemia is quite moderate and the symptoms are not as easily noticeable as the symptoms that accompany type 1 DM (2,3).

Diagnosis

The presence of diabetes in a patient can be confirmed by the following: A fasting plasma glucose (FPG) ≥ 7 mmol/L, which needs to be confirmed with another test on a different day (1,3). Fasting is defined to be having no caloric intake for at least 8 hours (1). A casual (random) plasma glucose ≥ 11.1 mmol/L with symptoms of hyperglycemia (1,3). Random plasma glucose is defined to be any time of day without respect to the time since the last meal (1,3). Typical symptoms of hyperglycemia include unexplained weight loss, polyuria, and polydipsia. An oral glucose tolerance test of ≥ 11.1 mmol/L in the 2 hour sample (1,3). This test uses a glucose solution that contains 75 g of anhydrous glucose dissolved in water and or an A 1C value ≥ 6.5% (3).

Symptoms

It is a common occurrence for many patients that have type 2 DM to be asymptomatic and diagnosed only through routine blood tests (1,3). Around 40% of patients are relatively asymptomatic at diagnosis (1,3). The onset of the symptoms is gradual (1,3). Overtime, symptoms of hyperglycemia may manifest (1). These may include lethargy, blurry vision, polyuria, polydipsia, frequent infections and failure of wounds to heal (1). Signs of complications of diabetes may also be present at the time of diagnosis (1). Ocular signs include cataracts, vitreous hemorrhage, macular degeneration, and soft exudates (1,3). Cardiac signs may include previous myocardial infarctions, and congestive heart failure (1,3). Podiatric signs include decreased peripheral pulses, absent ankle-jerk reflex and ulcers (1,3).

Monitoring Parameters

The American Diabetes Association recommends a goal of <7% for the A1C level (4). However, this value needs to be individualized, especially in specific patient populations, such as elderly patients (4). The incidence of microvascular and macrovascular complications of diabetes can be reduced with tight blood pressure control in patients with type 2 DM (4). However, the mortality rate does not appear to be reduced (4). The American Diabetes Association recommends a target blood pressure goal of <130/80 mm Hg in patients with diabetes (4). Reduction in LDL cholesterol, raising HDL cholesterol levels and lowering triglyceride levels has been shown to reduce the chance of cardiovascular events and death (4). The American Diabetes Association recommends the LDL cholesterol level <100 mg/dl, HDL cholesterol level >40 mg/dL, and triglyceride level <150 mg/dL (4). Furthermore, the patient’s feet should be examined on a regular basis (1,5). A visual inspection should be done and an annual neurological examination and measure of pedal pulses should be undertaken (1,5). Dilated eye examination should be done by an expert and then on an annual basis (1,5). Dental examinations should be done twice a year (1,5).

Prognosis

Patients that have diabetes are at an increased risk for cardiovascular disease, peripheral vascular disease, and stroke. They are also at risk of developing specific complications, which include diabetic retinopathy, diabetic nephropathy and diabetic neuropathy (1).

References

  1. Olansky L, Levinson P. Diabetes. MD Consult [online]. Maryland Heights MO: Elsevier Inc. 2011 [cited 2011 Sept 25]. Available from: www.mdconsult.com
  2. Chisholm-Burns MA, Wells BG, Schwinghammer TL, Malone PM, Kolesar JM, Rotschafer JC, Dipiro JT. Pharmacotherapy: Principles and Practice. McGraw-Hill: 2008. p. 643-65.
  3. DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, editors. Pharmacotherapy: A Pathophysiologic Approach, 7th ed. New York: McGraw-Hill; 2007. p. 1205-36.
  4. American Diabetes Association. Standards of Medical Care in Diabetes – 2011. Diabetes Care. 2011; 34 (suppl 1): S11-S61. DOI: 10.2337/dc11-S011
  5. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. Canadian Diabetes Association 2008 clinical practice guidelines for the prevention and management of diabetes in Canada. Can J Diabetes. 2008; 32(suppl 1): S1-S201.

Disclaimer

This information is presented for informational purposes only and is not meant to be a substitute for advice provided by qualified health care professionals. You should contact your qualified health care provider if you have or suspect any health problems. This article is not intended to provide medical advice for its readers


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