Exams

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Exams

  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)

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