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Endocrinology I

Endocrinology I. Sarah E. French, MD July 19, 2014. Diabetes Lipids Calcium disorders MEN I and II. Diabetes. Diagnostic criteria for diabetes. Random glucose >200 mg/ dL with symptoms Polyuria , polydipsia , unexplained weight loss Fasting glucose > 126 mg/ dL on 2 different days

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Endocrinology I

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  1. Endocrinology I Sarah E. French, MD July 19, 2014 Diabetes Lipids Calcium disorders MEN I and II

  2. Diabetes

  3. Diagnostic criteria for diabetes • Random glucose >200 mg/dL with symptoms • Polyuria, polydipsia, unexplained weight loss • Fasting glucose > 126 mg/dL on 2 different days • 2 hour glucose >200 mg/dL during 75-gram oral glucose tolerance test • A1c > 6.5 (new)

  4. Secondary causes of diabetes • Chronic pancreatitis • Cystic fibrosis • Hemochromatosis • Polycystic ovarian syndrome • Cushing’s syndrome • Acromegaly • Drugs: glucocorticoids, thyroid hormone, thiazides, dilantin, alpha interferon • Somatostatinoma Pancreatic failure Insulin resistance

  5. A1c • Goal <7% • Can be unreliable if • Blood transfusion • Decreased RBC lifespan • Hemoglobinopathies • Alternative is fructosamine

  6. Oral agents in diabetes • Need to know contraindications and most side effects of different agents • Metformin, TZDs and sulfonylureas are roughly equivalent on ability to decrease A1c • Metformin, TZDs and sulfonylureas are FDA approved for combination with insulin • DDP-4 inhibitors (sitagliptin, etc) are NOT FDA approved for combination with insulin

  7. Metformin • Only oral agent that is weight loss/weight neutral • Generally first line agent • Contraindicated if Cr >1.5 in men, >1.4 in females • Sulfonylurea • Insulin secretagogue • Contraindicated in renal failure • TZDs • Can have fluid retention and edema • Contrainidicated in NYC Class III and IV heart failure • DDP-4 inhibitors • Increases insulin production and sensitivity • Delays gastric emptying • Can be used in CKD with dose reduction

  8. Indications for insulin • Significant hyperglycemia at presentation • Acute decompensation • Surgery • Pregnancy • Renal disease • Poor control despite oral agents

  9. Diabetic ketoacidosis • Total body potassium is low • Even if patient presents with hyperkalemia • Monitor potassium and replace • Follow bicarb and anion gap • Generally no need to follow ketones

  10. Diabetes is not just hyperglycemia • Keep blood pressure <130/80 • ACE inhibitor or ARB if proteinuria • Manage any dyslipidemia • If age >40, start statin even if LDL at goal • Screen for complications • Urine microalbumin, dilated eye exam • Smoking cessation • Immunizations

  11. Lipid goals in diabetes • LDL • < 100 for every diabetic • < 70 if DM with CAD or CAD equivalent (PAD, AAA) • First choice is statin • Triglycerides • <150 • First treatment is glycemic control • Fenofibrate safer than gemfibrozil when in combo with statin (less rhabdo) • Secondary target (treat LDL first) unless >500

  12. Complications of diabetes • Acute complications • DKA • Hyperosmolar hyperglycemic nonketotic state (HHNS) • Microvascular • Retinopathy • Neuropathy • Nephropathy • Macrovascular • CAD • PVD • CVD • Atherosclerosis is most common cause of death

  13. Diabetes in pregnancy • Glargine and detemir are contraindicated • Use NPH for basal insulin • Can use regular for prandial/bolus insulin • A1c < 7% before conception and keep it there • Retinopathy may worsen during pregnancy • Remember: statins, ACEIs, and ARBs are contraindicated

  14. Adjusting insulin

  15. Adjusting insulin • Basal insulin—controls fasting glucoses • If fasting hyperglycemia—increase dose • If fasting hypoglycemia—decrease dose • Prandial insulin—controls post-prandial glucoses • If post-prandial hyperglycemia—increase dose • If post-prandial hypoglycemia—decrease dose • Adjustments should be 10-20% of dose

  16. A 58 yo WM with HTN and DM is followed in your clinic and previously had good control of his diabetes with A1c of 6.9 on Novolog 70/30, taking 35 units before breakfast and supper. Has had recently begun complaining of highly variable blood sugars: Pre-breakfast FSG – 200-250 Pre-Lunch FSG – 135-160 Pre-Supper FSG – 130-150 Which of the following is the best next step in his management? • Increase Novolog 70/30 dose in the evening to 40 units. • Begin acarbose therapy • Increase Novolog 70/30 dose in the morning to 40 units • Check blood sugar at 3 AM • Change the patient’s regiment to Lantus and Regular Insulin before each meal for better compliance.

  17. Early morning hyperglycemia • Dawn phenomenon • Rise in GH and cortisol lead to morning hyperglycemia • No associated hypoglycemia • Somogy effect • Nocturnal hypoglycemia leads to morning hyperglycemia • Only way to differentiate is to check 3 AM FSG

  18. 23-year-old man with 13-year history of type 1 DM is preparing for racquetball tournament. The first game of his tournament is at 8 AM and he asks for advice about his insulin regimen because he has never attempted to play racquetball so early in the day (usually plays late afternoon). Usual insulin dosage is 6 units NPH with 10 units insulin lispro with breakfast at 7 AM, 4 units insulin lispro with lunch at 12 PM, and 8 units NPH with 12 units insulin lispro with dinner at 6 PM. His last A1c was 6.4 and his fasting fingerstick readings at 7 AM ranges between 160 and 200 mg/dL. Assuming that his 7 AM glucose concentration is in usual range, which one of the following should he do? A. Not take his insulin or eat breakfast but drink 8oz of orange juice just before the game B. Take his usual insulin and eat his usual breakfast C. Omit the insulin lispro but take the usual dose of NPH with breakfast • Omit the NPH but take the usual dose of insulin lispro with breakfast • Decrease the insulin lispro and NPH and eat his usual breakfast

  19. Glucose Patterns

  20. 250 200 150 100 50 8AM Noon 6PM Normal

  21. Increased insulin requirement Steroid Effect 250 200 150 100 50 8AM Noon 6PM Postprandial Hyperglycemia

  22. 250 200 150 100 50 8AM Noon 6PM Somogyi or Dawn Phenomena

  23. 250 200 150 100 50 8AM Noon 6PM Dietary/Medical noncompliance

  24. Hypoglycemia

  25. Definition of hypoglycemia • Whipple’s triad • Symptoms, signs or both consistent with hypoglycemia • A low plasma glucose concentration • Resolution of symptoms/signs after raising plasma glucose • “In the absence of Whipple’s triad, the patient may be exposed to unnecessary evaluation, costs and potential harms, without expectation of benefit.” • From “Evaluation and Management of Adult Hypoglycemic Disorders: An Endocrine Society Clinical Practice Guidelines”

  26. Insulinoma • Extremely rare • Typically fasting hypoglycemia • Whipple’s triad • Symptoms associated with hypoglycemia • Glucose <70 at time of symptoms • Relief with glucose administration • Have elevated insulin and C-peptide levels • Negative sulfonylurea screen

  27. 18 yo woman evaluated for syncope. Has had 3 episodes in past month that resolved after she drank fruit juice with sugar. Has history of depression treated with citalopram and occasional insomnia treated with zolpidem as needed. Her mother has type 2 diabetes treated with NPH and glyburide. • Several minutes into presentation, patient becomes confused and agitated with tachycardia and profuse sweating. Blood is drawn. IV glucose given with resolution of her symptoms. • Vitals are normal and physical exam is unremarkable. • Lab studies: C peptide 0.4 (0.5-2.5), glucose 34, insulin 26 (2-20), sulfonylurea screen negative. • What is most appropriate next step in management? • Abdominal CT • Abdominal octreotide scanning • Gastric emptying study • Psychiatric evaluation

  28. Interpreting laboratory data • Remember that hypoglycemia is result of low glucose production rather than high glucose utilization. • Plasma insulin, C-peptide, and pro-insulin concentrations don’t have to be high relative to normal values. • Can be “inappropriately normal” for hypoglycemia • Generally, only interpret results if glucose is <55 mg/dL. • A concurrent illness can complicate interpretation of results.

  29. Interpreting laboratory data

  30. Lipids

  31. Lipid profile • Ideally after 14 hour fast and no alcohol for 3 days • LDL is calculated • Total cholesterol – HDL – triglycerides/5 • Not accurate if triglycerides > 400 • VLDL and chylomicrons are rich in triglycerides

  32. Hyperlipidemias • May be primary (genetic) or secondary (meds, other diseases). • Hypercholesterolemia—elevated cholesterol with normal triglycerides • Hypertriglyceridemia—elevated triglycerides with normal cholesterol • Mixed hyperlipidemia—elevated cholesterol and triglycerides

  33. Familial hyperlipidemia • Familial hypercholesterolemia • Reduction or absence of LDL receptor • Tendinousxanthomas • Lipoprotein lipase (LPL) deficiency • Cannot degrade chylomicrons and VLDL • Triglycerides > 1000

  34. Familial hyperlipidemia • Familial combined hyperlipidemia • Most common genetic hyperlipidemia (1%) • Increase ApoB 100 → ↑LDL and ↑ VLDL • Premature CAD • No risk for xanthomas • Familial dysbetalipoproteinemia • Elevated IDL (total cholesterol and triglycerides) • Associated with diabetes, obesity and alcohol abuse • Palmarxanthomas (“yellow hands”)

  35. Tendon xanthoma Elevated LDL Familial hypercholesterolemia

  36. Eruptive xanthomas Elevated triglycerides

  37. Tuberous xanthomas Elevated triglycerides

  38. Palmarxanthomas Elevated IDL Familial dysbetalipoproteinemia

  39. Normal retina Lipemiaretinalis Elevated triglycerides

  40. Lipid disorder scenarios Young child with TG of 8000, pancreatitis, eruptive xanthomas, lipemiaretinalis, positive family history. Most likely diagnosis? 32 yo man with CAD, LDL 350, TG normal and tendon xanthomas. +Famillyhx of premature CAD. Diagnosis? 48 yo woman with premature CAD and severe PVD. +Tuberous and palmarxanthomata. TC 380, TG 400, LDL 50. Diagnosis? Lipoprotein lipase deficiency – unable to degrade VLDL and chylomicrons. Familial hypercholesterolemia (LDL receptor defect; LDL >300). Autosomal dominant with variable penetrance. Familial dysbetalipoproteinemia—High levels of IDL cause severe PVD and early CAD. Treat with statins and fibrates. TC and TG roughly equal with low LDL.

  41. Secondary hyperlipidemia • Increased LDL • Hypothyroidism • Increased triglycerides • Poorly controlled diabetes • Oral estrogens • Alcohol • Increased LDL and triglycerides • Nephrotic syndrome • HCTZ • Beta blockers • Glucocorticoids

  42. Secondary hyperlipidemia • Treat secondary causes FIRST! • If hypothyroid, normalize TSH and then repeat lipid profile. • If uncontrolled diabetes, normalize A1c and repeat lipid profile. • If oral estrogens, change to patch or change method of birth control. • If excessive alcohol intake, work on cessation

  43. Treatment of hyperlipidemia • LDL • Statins +/- ezetimibe • Bile acid resins • Triglycerides • Fibrates • Combined hyperlipidemia • Statin and fenofibrate (safer than gemfibrozil) • Niacin (best for HDL)

  44. Other points • Unless triglycerides >500, LDL is first target. • In patients on HAART, use pravastatin. • Not metabolized through cytochrome P450s. • Statins are contraindicated in pregnancy.

  45. Calcium disorders

  46. Hormonal regulation of calcium Parathyroid hormone (PTH) Vitamin D Increases serum calcium Intestinal absorption Increases phosphorus • Increases serum calcium • Bone resorption • Renal resorption • Decreases phosphorus • PTH = “phosphorus trashing hormone” • Indirectly increases renal hydroxylation of 25-OH vitamin D to active form

  47. Clinical manifestations of hypercalcemia • GI symptoms • Anorexia • Nausea • Vomiting • Constipation • Nephrogenic diabetes inspidius • Dehydration • Myopathy • Cardiac arrhythmias • Sinus bradycardia • AV block • Shortening QT interval • Nephrolithiasis • Nephrocalcinosis • Band keratopathy • Pruritus • Altered mental status • Pancreatitis

  48. Differential diagnosis of hypercalcemia • Primary hyperparathyroidism • Malignancy • Granulomatous diseases • Thyrotoxicosis • Drugs • HCTZ • Lithium • Hypervitaminosis A • Hypervitaminosis D • Tertiary hyperparathyroidism • Familial hypocalciurichypercalcemia • Immobilization • Milk-alkali syndrone

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