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EXPLAINS

EXPLAINS. Hypoglycemia. EX PLAINS. Exogenous Insulin . Bolus Novolg Humolog Apidra Regular Exubera(inhaled Insulin ). Basal: Lantus Levemir NPH. ex p lains. Pituitary tumor (adrenal Insuficency, GH deficency ). exp l ains. Liver disease (Cirrhosis,Tumor)

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EXPLAINS

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  1. EXPLAINS Hypoglycemia

  2. EX PLAINS • Exogenous Insulin • Bolus • Novolg • Humolog • Apidra • Regular • Exubera(inhaled Insulin) • Basal: • Lantus • Levemir • NPH

  3. explains • Pituitary tumor (adrenal Insuficency, GH deficency )

  4. explains • Liver disease (Cirrhosis,Tumor) • Decresed gluconeogenesis and glycogenlysis)

  5. explains • Adrenal insuficency(lack of steroid for sustained glycemic control)

  6. explains • Insulin Resistance: • Most common reason for hypoglycemia • Overweight, family history of DM • Mainly postprandial:after meal ,peak in insulin secretion led to hypoglymia • Labs: high insulin level,possible hyperglycemia • TX: Metformin, TZD , precose, Glyset

  7. Insulinomas • Incidence: 0.4/100.000 • Median age: 47 years (8-82), 59% females • Clinical Features: • Fasting hypoglycemia, but can also present as post-prandial hypoglycemia • 20% of patients misdiagnosed with a neurologic or psychiatric disorder

  8. Insulinomas • Weight gain has been described in 18% of patients • Median duration of symptoms before diagnosis is less than 1.5 years • Tumor distribution: • 87% single benign tumor • 7% multiple benign tumors • 6% malignant insulinoma (77% males, median age 48 years)

  9. Insulinomas • MEN-I: • 8% of inulinomas have MEN-I • median age 25 years • 53% females • All have primary hyperparathyroidism, few have prolactinomas, gastrinomas or Cushing’s • 59% have multiple islet cell tumors

  10. Insulinomas (diagnosis) • Blood glucose<45 mg/dl • Insulin level > 6 mcu/ml (RIA) or 3 mcu/ml (ICMA) • C-Peptide > 200 pmol/l (0.6 ng/ml) • Proinsulin > 5pmol/l (ICMA) • Betahydroxybutyrate < 2.7 mmol/l • Increased BG at least 25 mg/dl after glucagon injection (10, 20, 30 min)

  11. explains • Neoplasm: mainly pelvic tumor ,IGF-2 mediated)

  12. explains • Secretatogue(glyburide,glipizide,amaryl, prandin, starlix) • Sepsis

  13. Functional Hypoglycemia • Presentation:young female with spells • Etiology: rapid gastric emtying leading to peak in insulin secretion.especialy high carb meals • Treatment: low carb meal, precose , glyset.

  14. Workup for hypoglycemia • When BG <45, draw the following labs: • Insulin(>6 indicating insulinoma) • C-peptide(>0.6 –insulinoma) • Cortisol(>20) • GH • LFT,BMP,TSH

  15. * * * * * * * The Incretin Effect Beta-Cell Response to Oral vs IV Glucose Incretin Effect

  16. GLP-1 Effects in HumansUnderstanding the Natural Role of Incretins

  17. S e c t i o n 12, 12.2 Mechanism of Action of Sitagliptin Glucose dependent Insulin (GLP-1andGIP) Glucose uptake by peripheral tissue Ingestion of food Pancreas Release of active incretins GLP-1 and GIP Beta cells Alpha cells GI tract  Blood glucose in fasting and postprandial states Glucose- dependent X JANUVIA (DPP-4 inhibitor) DPP-4 enzyme Hepatic glucose production Glucagon (GLP-1) Inactive GLP-1 Inactive GIP • Incretin hormones GLP-1 and GIP are released by the intestine throughout the day, and their levels  in response to a meal. GLP-1=glucagon-like peptide-1; GIP=glucose-dependent insulinotropic polypeptide.

  18. Impairedinsulin secretion Oral Antidiabetic Agents: Sites of Action SulfonylureasRepaglinide Acarbose Miglitol Pancreas Gut Adipose tissue  Glucose uptake  Glucose Absorption Rosiglitazone Pioglitazone Hyperglycemia HGO* Muscle Glucoseuptake Liver Rosiglitazone Pioglitazone Metformin Metformin Rosiglitazone Pioglitazone *HGO, hepatic glucose output.

  19. Natural History of Type 2 DiabetesProgression of Complications Pre-diabetic state Onset of diabetes Environmental factors e.g. nutrition physical inactivity Complications Disability Genetic susceptibility IFG* Death Insulin resistance Hyperinsulinemia Obesity  cell dysfunction  Proinsulin Hypertension Dyslipidemia Atherosclerosis Hyperglycemia Retinopathy Nephropathy Neuropathy Blindness Renal failure CHD† Amputation Abnormal glucose levels Adapted from International Diabetes Center (IDC) Minneapolis, Minnesota *IFG = impaired fasting glucose †Coronary heart disease

  20. Type 2 Diabetes is a Cardiovascular Risk Factor Diabetes and prior myocardial infarction (MI) carry the same mortality risk 45.0%* No Prior MI Prior MI Fatal or Nonfatal MI 20.2% 18.8%* 3.5% Nondiabetic Subjects (n=1373) Type 2 Diabetic Subjects (n=1059) Seven-year incidence in a Finnish-based cohort. *P<.001 Haffner SM, et al. N Engl J Med. 1998;339:229-234.

  21. 9 Conventional 8 ADA action Insulin Median HbA1c (%) Chlorpropamide Glibenclamide (glyburide) 7 ADA goal Metformin 6 Upper limit of normal range (6.2%) 0 10 3 6 9 0 Time From Randomization (years) Intensive Treatments and Increase in HbA1c Over Time United Kingdom Prospective Diabetes Study (UKPDS) UK Prospective Diabetes Study (UKPDS 34) Group. Lancet. 1998;352:854-65.

  22. Normal Mealtime Insulin Response Breakfast Lunch Dinner Plasma insulin 4:00 8:00 12:00 16:00 20:00 24:00 4:00 8:00 Time

  23. No hypoglycemia: TZD(Actos, Avandia) Metformin/glucophage) Alpha glucosidase inhibitor(Precose, Glyset) Combo(avandamet, actoplusmet) DPP IV inhibitor: Januvia Galvus Can Cause Hypoglycemia: SU(glyburide,Amaryl) Prandin/Starlix Combo(glucovance, avandaryl, duetact) Pills available for DM 2

  24. Non insulin injection for DM2 GLP-1 analog(byetta) Amylin(Symlin)

  25. Basal: Lantus Levemir NPH Bolus Novolg Humolog Apidra Regular Exubera(inhaled Insulin) Insulin treatment for DM

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