logging in or signing up Pathophysiology Ch 25 Endocrine Disorders kokodeganurse Download Post to : URL : Related Presentations : Let's Connect Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 141 Category: Entertainment License: All Rights Reserved Like it (0) Dislike it (0) Added: January 23, 2013 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript PowerPoint Presentation: INSULIN AND DIABETES MELLITUS Diabetes mellitus is caused by a relative deficit of insulin secretion from the beta cells in the islets of Langerhans or by the lack of response by cells to insulin (insulin resistance). Insulin is an anabolic hormone (building up or synthesis of complex substances from simple molecules). Deficient insulin results in abnormal carbohydrate, protein, and fat metabolism. Insulin is not required for the transport of glucose into brain cells . This is fortunate, because neurons require glucose constantly as an energy source. In the digestive tract, insulin is not required for glucose absorption . Exercising skeletal muscle can utilize glucose without proportionate amounts of insulin. This can be significant because excessive exercise can deplete blood glucose and result in hypoglycemia.PowerPoint Presentation: Gestational diabetes may develop during pregnancy and disappear following delivery of the child. In many cases, women who have gestational diabetes develop diabetes few years later. The following discussion focuses on types II diabetes.PowerPoint Presentation: Pathophysiology Initial Stage Insulin deficit results in decreased transportation and use of glucose in many cells of the body. Blood glucose levels rise ( hyperglycemia ). Excess glucose spills into the urine ( glucosuria ) as the level of glucose in the filtrate exceeds the capacity of the renal tubular transport limits to reabsorb it. Glucose in the urine exerts osmotic pressure in the filtrate, resulting in a large volume of urine to be excreted ( polyuria ), with the loss of fluid and electrolytes (e.g., sodium) from the body tissues. Fluid loss through the urine and high blood glucose levels draw water from the cells, resulting in dehydration . Dehydration causes thirst ( polydipsia ). Lack of nutrients entering the cells stimulates appetite ( polyphagia ). Progressive Effects Lack of glucose in cells results in catabolism of fats and proteins, leading to excessive amounts of fatty acids and their metabolites, known as ketones or ketoacids , in the blood. Because the liver and other cells have limited capcity to process lipids, fatty acids, or ketones, excessive amounts of ketones in the blood cause ketoacidosis . Some ketoacids are excreted in the urine ( ketonuria ). Some diabetic patients test their urine for ketones. However, as dehydration develops, the glomerular filtration rate in the kidney is decreased, resulting in decompensated metabolic acidosis (diabetic ketoacidosis [DKA] or diabetic coma) .PowerPoint Presentation: Diagnostic Tests Fasting blood glucose level & the glucose tolerance test , At present, a fasting blood sugar equal to or greater than 126 mg/dL , taken on more than one occasion, confirms a diagnosis of diabetes. The test for glycosylated hemoglobin (HbA1c ) is used to monitor long-term control (8 to 12 weeks) of blood glucose levels. The test should be repeated every 3 months. The acceptable level for HbA1c has been lowered to 7.0%, and is likely to be lowered again to 6.0% (normal), in order to reduce the serious long-term effects of hyperglycemia. Self Check : Patients with diabetes can monitor themselves carefully at home by taking a sample of capillary blood from a finger and checking it with a portable monitoring machine ( glucometer ). Urine tests for ketones are helpful for those who are predisposed to ketoacidosis. Arterial blood gas analysis is required if ketoacidosis develops. Serum electrolytes may be checked as well.PowerPoint Presentation: Treatment. Maintenance of normal blood glucose levels is important to minimize the complications of diabetes mellitus, both acute and chronic. Diet. Therapy is based on maintaining optimum body weight as well as control of blood glucose levels. Recommended diets include more complex carbohydrates (minimal amounts of simple sugars are advised) and adequate protein , as well as maintaining low cholesterol and low lipid levels . Increased fiber with meals appears to reduce surges in blood sugar associated with food intake. Exercise. A regular moderate exercise program is very beneficial to the diabetic. Exercise can increase the uptake of glucose by muscles substantially without an increase in insulin utilization. There is a risk that hypoglycemia may develop with exercise , Increasing carbohydrate intake by eating a snack to compensate for exercise can decrease this risk. Oral Medications. For type II, Drugs which stimulate the beta cells to increase insulin release: glyburide (Diabeta) and repaglinide (Prandin).. Drugs such as metformin (Glucophage) act to reduce insulin resistance and to reduce hepatic glucose production. The newer drugs (rosiglitazone- Avandia) increase tissue sensitivity to insulin. 4 . Insulin Injections. Insulin can be used for replacement therapy must be injected subcutaneously because it is a protein that is destroyed in the digestive tract if taken orally. Continuous infusions via a small pump are favored by some diabetics. The primary form of insulin used now is a biosynthetic form of insulin, identical to human insulin (Humulin), synthesized by bacteria using recombinant DNA techniques.PowerPoint Presentation: Complications: I. Acute Complications: Hypoglycemia (insulin shock), diabetic ketoacidosis & Hyperosmolarhyperglycemic nonketotic comaPowerPoint Presentation: Chronic Complications 1- Vascular ProblemPowerPoint Presentation: 2. Neuropathy. Peripheral neuropathy is a common problem for diabetics. This leads to impaired sensation, numbness, tingling, weakness, and muscle wasting. Autonomic nerve degeneration develops as well, leading to bladder incontinence, impotence, and diarrhoea. Impaired vasomotor reflexes may cause dizziness when a person stands up. 3. Infections. Causes : i. Vascular impairment , which decreases tissue resistance, ii. the delay in healing because of insulin deficit, iii. and the increased glucose levels in body fluids that support infection. Diabetics are also susceptible to tuberculosis , which is increasing in incidence. Infections in the feet and legs > gangrene > amputation. Fungal infections such as Candida occur frequently Periodontal disease (infection in the tissues around the teeth) and dental caries. 4. Cataracts. Clouding of the lens of the eye is another degenerative process related to the abnormal metabolism of glucose, and it results in accumulated Sorbitol and water in the lens, destroying the transparency. Cataracts may eventually lead to blindness and should be removed when they impair visual function You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.