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Type 2 Diabetes

ID: ANM10005
MEDICAL ANIMATION TRANSCRIPT: One of the endocrine functions of the pancreas is to secrete a hormone called insulin into the blood. Microscopic regions of beta cells in the pancreas are located in the islets of Langerhans. These beta cells release insulin hormone. The insulin molecules leave the beta cells and travel into the bloodstream to regulate blood glucose levels. After a meal, increasing amounts of glucose in the blood trigger beta cells in the islets to secrete the appropriate amount of insulin hormone, which travels through the bloodstream to target cells where it promotes the transport of glucose into the cells. Certain tissues, such as skeletal muscle and adipose tissue, require insulin to unlock their cells before glucose can enter. Insulin attaches to specific receptors on the cell's surface, causing glucose transporter proteins in the cell membrane to open, which allows glucose to pass into the cells. In type II diabetes, the body usually continues to produce self-made, or endogenous insulin. However, in this case, the target cells resist the effects of the insulin or there is an insufficient amount of insulin to meet the body's needs, or both. Insulin resistance is caused by a decrease in receptors or by the presence of abnormal receptors. In many cases, a defect in insulin receptors prevents the normal effects of insulin on target cells, resulting in inadequate glucose transport into cells. Consequently, rising levels of glucose in the blood result in hyperglycemia. Hyperglycemia stimulates the beta cells in the pancreas to produce more insulin in an attempt to reduce the high blood glucose level. The overworked beta cells try to keep up with the demand but gradually lose their ability to produce enough insulin. Due to the pathophysiology of hyperglycemia and the lack of insulin, the following classic symptoms of diabetes appear: polyphagia, or excessive eating, polydipsia, or excessive thirst, polyuria, or increased urine volume, and unexplained weight loss. Symptoms of type II diabetes that appear over time include fatigue, recurrent infections, changes in vision, pruritus, or itching, and paresthesia, which is a tingling or prickling sensation in the skin. As the insulin deficiency continues, cells are unable to use sugar for energy, so the body breaks down fats and proteins to use them as an alternative source of energy. As fat breakdown continues, acidic byproducts known as ketone bodies accumulate in the blood resulting in a condition called ketosis. If allowed to build up to dangerously high levels, a life-threatening condition called diabetic ketoacidosis results. An acute complication of medications for type II diabetes, called hypoglycemia or insulin shock, usually begins with an excessive dose of insulin or oral hypoglycemic medication. Excessive insulin or oral hypoglycemic medication causes cells to remove too much glucose from the blood, leaving an insufficient amount in the bloodstream for certain organs to acquire the constant energy supply they need to function properly. Because the brain's primary source of energy is glucose, it is the first organ affected by glucose levels below 70 milligrams per deciliter. The neurons starved for glucose start to malfunction, causing symptoms such as nervousness, shakiness, and confusion. If the glucose levels continue to drop, the electrical activity of neurons diminishes significantly, resulting in seizures or diabetic coma. Chronic, poorly controlled type II diabetes can cause degenerative tissue damage resulting in long-term complications such as atherosclerosis, blindness, neuropathy, and renal failure. Licensed health professionals prescribe a variety of oral hypoglycemic drugs to treat type II diabetes. Some treatments increase insulin production in the beta cells of the pancreas. Others decrease insulin resistance in skeletal muscle. Some treatments increase insulin sensitivity in target tissues. Others promote a slight decrease in absorption of glucose in the gut. And finally, some inhibit glucose production in the liver. Patients with type II diabetes can control their glucose levels primarily with diet and exercise. In addition, patients should monitor their glucose levels frequently. Blood glucose levels should fall between 70 and 130 milligrams per deciliter prior to a meal or while fasting, and should be less than 180 milligrams per deciliter 2 hours after starting a meal. When diet, exercise, and oral hypoglycemic drugs fail to control high blood sugar, patients can administer insulin injections. Medication should be continued with the use of non-drug therapy options. [music]
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