Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.



Published on

  • Be the first to comment

  • Be the first to like this


  1. 1. Exams & Grading: 85% of the final grade : Exam scores from each of the three Sections will represent one-third of a total of 85% of the final grade for the course. Two exams will be administered in Section I, while one exam each will be given in Sections II & III. Sectional exams will be based on Tuesday-Friday lectures and employ a mix of short answer & essay questions. 10% of the final grade : The Final Exam on the “Integrative Perspective on Diabetes” will comprise 10% of the final grade. 5% of the final grade : The average score for the written responses to pre-assigned topics for Monday Discussions will comprise a total of 5% of the final grade. A traditional numerical scoring system will be used to generate a final letter grade - A= 90-100% B=80-89% C=70--79%, D=60-69%, and F= 59% or less. FIS 2006
  2. 2. diabetes <ul><li>Type I </li></ul><ul><ul><li>Autoimmune destruction of β -cells of pancreas </li></ul></ul><ul><li>Type II </li></ul><ul><ul><li>Insulin resistance coupled with deficient release </li></ul></ul><ul><li>hyperglycemia & hyperlipidemia leading to atherosclerosis, neuropathy & infection </li></ul>
  3. 3. FIS 2006 (Diabetes) Version date: Aug 03, 2006 Final Exam: Integrative Perspective on Diabetes - 1 0% Final Grade Types of Questions: Contrast the etiologies of Type I & Type II diabetes, and discuss the mechanisms for the metabolic derangements leading to hyperglycemia and hyperlipidemia. Focus on a specific organ system (vascular, neural, host-defense) subjected to long-standing hyperglycemia, hyperlipidemia and other abnormalities secondary to poorly controlled Type I or II diabetes: - Discuss the mechanisms for pathology; - Discuss the mechanisms for pharmacological prophylaxis and/or treatment of organ system dysfunction.
  4. 4. FIS Organization: Exam #1- Basic Principles -> diabetes Exam #2- Neurobiology -> diabetes Exam #3- Endocrinology -> diabetes Exam #4- Immunology & Bacterial Pathogenesis -> diabetes ↓ ↓ (Exam #5: final)
  5. 5. FIS 2006 (Diabetes) Lectures: Sept 2 - Diabetes & Polyphagia Oct 06 - Insulin Oct 10 - Counter Regulatory Hormones Oct 18, 18 & 20 - Homeostasis & Responses to External Environment Nov 17 – Immunology of Diabetes Monday Discussions : (student-driven lecture questions, student-driven journal clubs & faculty-driven discussion of relevance of lectures to diabetes). Resource Text: Ellenberg & Rifkin’s DIABETES MELLITUS, sixth edition, Porte et al ., Neurobiology Sept 11 - Diabetes & Neuropathy Journal Club Organization Sept 18 - Diabetes & Neuropathy Journal Club Sept 25 - Diabetes & Neuropathy Journal Club Oct 02 - Diabetes, Erectile Dysfunction & Viagra Basic Principles & Endocrinology Aug 28- Diabetes & Atherosclerosis Oct 09 - Diabetes, Insulin Resistance & Metabolic Syndrome Oct 16 – Pharmacological Management of Diabetes Oct 23 - Diabetes, Insulin Resistance & Polycystic Ovary Syndrome Immunology & Bacterial Pathogenesis: Nov 27 - Immunology of Diabetes Dec 04- Infections & Diabetes
  6. 6. FIS & Diabetes: Type I Diabetes: Autoimmune destruction of β -cells of pancreas Type II Diabetes: Insulin Resistance Pathology of Diabetes: Atherosclerosis Neuropathy Susceptibility to Infection Pharmacological Prevention: Type I- Insulin Replacement Regimens Type II- Insulin Secretogogues - Insulin Sensitizers Pharmacological Treatment: examples: Viagra & Erectile Dysfunction Aldose Reductase Inhibitors & Neuropathy Insulin Sensitizers & Polycystic Ovary Syndrome
  7. 7. Atherosclerosis: Abnormal vascular smooth muscle migration to sub-endothelial space and proliferation <ul><li>Key abnormalities: </li></ul><ul><li>smooth muscle </li></ul><ul><li>lipid </li></ul><ul><li>Significance: </li></ul><ul><li>↓ perfusion </li></ul><ul><li>infarction </li></ul>
  8. 9. Atherosclerosis <ul><li>Insult to Endothelium </li></ul><ul><li>potential mechanisms include non-enzymatic glycosylation </li></ul><ul><li>& lipid-induced macrophage growth factors </li></ul><ul><li>Consequence & Focus for FIS Discussion: </li></ul><ul><ul><ul><ul><li>defective inhibitory proteoglycans of endothelial extracellular matrix in contact with smooth muscle cells </li></ul></ul></ul></ul><ul><ul><ul><ul><li>deficient release of inhibitory NO to smooth muscle cells </li></ul></ul></ul></ul><ul><ul><ul><ul><li>abnormal smooth muscle migration & proliferation </li></ul></ul></ul></ul>
  9. 10. Diabetic Neuropathy
  10. 11. mechanism for diabetes-induced neurodegeneration <ul><li>Sorbitol </li></ul><ul><ul><ul><li>glucose -> sorbitol -> fructose </li></ul></ul></ul><ul><ul><ul><ul><li>osmotic perturbations due to sorbitol (hydroxyated glucose), </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>“ trapped” intracellularly </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>specific to neurons (aldose reductase) </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>elevated intraneuronally in diabetes due to hyperglycemia & insulin-independent neuronal glucose uptake </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>oxidative stress due to depletion in NADPH by aldose reductase </li></ul></ul></ul></ul>
  11. 12. Diabetes & Neuropathy: 4 Journal Clubs <ul><li>Descriptive changes: </li></ul><ul><li>Diabetes-induced changes in morphology & electrophysiology </li></ul><ul><li>Causal role of sorbitol: </li></ul><ul><li>Diabetes-induced intra-neuronal sorbitol, potentially leading to perturbations via osmotic distortion &/or oxidative stress </li></ul><ul><li>3) Abnormal protein phosphorylation of neuronal structure: </li></ul><ul><li>Diabetes-induced abnormal neurophilament phosphorylation, potentially leading to impaired structural/functional integrity and ultimately ↓ conduction & terminal degeneration. </li></ul><ul><li>4) Loss of neurotransmitter synthesis in nerve terminal: </li></ul><ul><li>Diabetes-induced degeneration of nitrergic neurons, specifically loss of NO synthesis, potentially leading to impaired vasodilation & erectile dysfuction </li></ul>
  12. 13. Diabetes & Immunology/Bacterial Pathogenesis <ul><li>Etiology of Type I diabetes: </li></ul><ul><ul><li>Autoimmune destruction of β -cell </li></ul></ul><ul><li>Infections & diabetes </li></ul><ul><ul><li>sensation (neural) </li></ul></ul><ul><ul><li>perfusion (vascular) </li></ul></ul><ul><ul><li>substrate for bacterial growth </li></ul></ul><ul><ul><li>host defense </li></ul></ul>
  13. 14. Version date: 2006 FIS Final Exam: Sample Questions Q: Contrast the etiologies of Type I & Type II diabetes. (Basis for Answer: Type I- Autoimmune & Type II- Insulin Resistance) Q: Discuss the mechanisms for the potential pathological changes in a specific organ system, secondary to long-standing hyperglycemia and/or hyperlipidemia of Type II diabetes. (Basis for Answer: Erectile Dysfunction due to both vascular occlusion (atherosclerosis) & deficient NO release from neurons responsible for vasodilation Q: Review the pharmacological basis, including mechanism of action, for a prophylaxis and amelioration of this specific organ system disease - or its consequences. (Basis for Answer: Prophylaxis- insulin sensitizing drugs; Treatment- Viagra, a cyclic GMP phosphodiesterase inhibitor)