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Diabetes Mellitus Types I & II

Diabetes Mellitus Types I & II. James Bresnahan , MS1 Robert Gyory , MS1. Introduction. How does your body make use of glucose from the food you eat? What is the difference in etiology between type 1 and type 2 diabetes? How does this affect treatment?

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Diabetes Mellitus Types I & II

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  1. Diabetes Mellitus Types I & II James Bresnahan, MS1 Robert Gyory, MS1

  2. Introduction • How does your body make use of glucose from the food you eat? • What is the difference in etiology between type 1 and type 2 diabetes? How does this affect treatment? • What is the homeostatic balance between insulin, glucose, glucagon, and stress hormones? How does this differ between nonaffected individuals vs. type 1 diabetics vs. type 2 diabetcs? • Why does high blood glucose cause other complications? • What are some psychosocial considerations regarding diabetes?

  3. Glycogen is a good form of storage. It’s condensed, easily broken down, and its byproducts are used efficiently to make energy. I thought T1DM is about insulin? α-1,6-linkage α-1,4-linkage

  4. Without insulin…

  5. How do you get Type 1 “Diabeetus?” • No!! • T1DM is AUTOIMMUNE. • Destruction of Pancreatic B-islet cells. • What about T2DM? Ask Rob..

  6. What are B-Islet cells? How are they destroyed? • Genetic predisposition • Environmental stimuli • Lead to antibodies that attack pancreatic Beta cells • Diagnosis is bimodal with peaks at 4-6 years and 10-14 years • 3M:2F?? • 23.6 per 100,000 per year.

  7. What are the general effect

  8. Clinical Presentation

  9. How do you treat T1DM?  Future?

  10. How do Endocrinologists monitor their diabetic patients over long periods of time?

  11. So, high glucose is bad, what about low glucose? -Low blood glucose is FAR more detrimental in terms of short term problems. -Diabetic coma due to Neuroglycopenia - Glucagon is released by a-cells in RESPONSE to b-cells not making insulin (a sign of high BG.) If B-cells are destroyed, a-cells can’t release glucagon.

  12. Future ways to monitor T1DM? http://www.youtube.com/watch?v=w0aalblWfjU Take into consideration different ethical issues ranging from cost of supplies/equipment to the mental demands of current T1DM patients.

  13. Diabetes Mellitus Type II

  14. But first, a biochemical interlude: Downregulation vs. Upregulation Adapted from the common domain of Cornell University

  15. The mechanism of DM II is a complex sequence of biochemical processes • Diet high in fat and carbohydrates + sedentary lifestyle  highly elevated plasma [glucose] • Chronically ↑ plasma [glucose]  chronic overstimulation of β cells and chronic hypersecretion of insulin • Chronic hypersecretion of insulin  down regulation of insulin receptors on adipocytes and skeletal muscles

  16. Down regulation of insulin receptors exhibits a number of negative consequences • ↓ glucose uptake by cells • ↓ glucose for cells to use for energy • ↑↑ plasma [glucose] • Can cause relatively minor symptoms or serious DM I type symptoms Adapted from the University of Arizona Dept. of Biological Sciences

  17. What are the consequences of decreased glucose for cellular energy? • Cells begin to burn fats for energy. • Can cause pH problems (DKA) • Inefficient fuel source leads to fatigue, low energy, etc. *Important: Glucose uptake is severely decreased, but not nonexistent as in DM I

  18. What are the consequences of elevated plasma [glucose]? • DM Type I Symptoms • e.g. polyuria, polydypsia, glycosuria, etc. • Hypertrophy of β cells • Extremely chronic hyperstimulation can lead to β cell destruction • Leads to insulin dependence Beta cells stained in green

  19. What are the symptoms of Type II diabetes mellitus? • Some patients may be asymptomatic for many years • Others experience lighter versions of many of the symptoms of diabetes mellitus I • Rarely, DKA and other complications can occur such as hyperosmotic coma • Why do these symptoms differ from DM I when their mechanisms of pathogenesis are so similar?

  20. How is DM II diagnosed? • Chronically high fasting plasma [glucose] • Elevated glycated hemoglobin pattern (HbA1C) • In difficult cases, insulin immunoassay

  21. Treatments for DM II are widely variable • For most people, diets lower in fats and carbohydrates coupled with exercise will correct the down-regulation of insulin receptors • Others need medications such as biguanides and sulfonylureas (e.g. metformin) to decrease endogenous glucose production • Severe cases in which beta cells have been destroyed will need to supplement with insulin • ‘insulin dependent’ diabetes

  22. Biguanides versus sulfonylureas • Biguanides • Metformin • Phenoformin • Buformin • Proguanil • Sulfonylureas • Carbutamide • Tolbutamide • Chlorpropamide • Acetohexamide • And others….

  23. The prognosis and sequelae of DM II are very similar to DM I Sequelae Prognosis If a person controls their condition well, they can either live an asymptomatic life or go into remission altogether With poor control, however: Myocardial infarction, stroke, blindness, amputation, degenerative brain disorders, renal failure, death • In well controlled diabetics, there are very few resulting problems • With poor control, however: • Poor circulation  vascular disease and cardiovascular problems • Neuropathy • Other metabolic dysfunctions

  24. Diabetes mellitus II is one of the most preventable disease in our society • Obesity is the number one predictor of DM II • Healthy diet and plenty of exercise are needed • Patient education!!! • Prior patient knowledge about the various genetic and medical factors that can increase DMII predisposition

  25. Systemic Insulin Regulation

  26. How do hormones and other factors regulate insulin?

  27. The following hormone pathways work to help regulate the action of insulin • Epinephrine and cortisol inhibit insulin and increase secretion of glucagon in the pancreas • HPA axis • Growth hormone directly acts on the pancreas to cause glucagon secretion • Glucagon inhibits insulin secretion and causes biochemical effects that are opposite those of insulin

  28. Other friends that you’ve met throughout the year that effect insulin secretion • ↓ insulin secretion • Thyroxine and T3 • Norepinephrine • Low ATP • And others • ↑ insulin secretion • High ATP • Somatostatin • Leptin • And others

  29. Learning objectives for this lecture • Review the biochemistry, pathology, and medical treatments of diabetes mellitus 1 and 2 • Provide a general overview of biochemical dysfunction, resulting metabolic derangement, compare and contrast the risks and sequelae, and discuss the treatments for both diseases and why treatments are specific to only one disease and not the other • Discuss the utility of HbA1c measurement as a method of monitoring treatment efficacy • Discuss patient, doctor, and psychosocial issues surrounding diabetes mellitus • Discuss the prevalence of diabetes mellitus, long term risks to patients, and cost of care issues • Discuss quality of life issues • Discuss the importance of primary prevention in diabetes mellitus 2

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