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Endocrine and Hematology

Endocrine and Hematology. Objectives. SAME AS USUAL Recognize (Diagnose) Evaluate Status Treat Evaluate your treatment. Diabetes Mellitus. Type I (AKA Juvenile, IDDM) Absolute insulin deficiency Often more rapid progression of end organ Dx. Mean age of onset 8-12 years old

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Endocrine and Hematology

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  1. Endocrine and Hematology

  2. Objectives • SAME AS USUAL • Recognize (Diagnose) • Evaluate Status • Treat • Evaluate your treatment

  3. Diabetes Mellitus • Type I (AKA Juvenile, IDDM) • Absolute insulin deficiency • Often more rapid progression of end organ Dx. • Mean age of onset 8-12 years old • “think and act like a beta cell” Rick Carlton, MD • Incidence 12-14 per 100,000/year (not many) • Usually at puberty • Increased incidence in late fall • Genetics: there are 20 independent genes • MHC on chromosome, HLA-DR3 or DR, HLA-DQ • ?Is HLA testing coming? • Subtypes • Autoimmune, idiopathic, chronic pancreatitis, neonatal

  4. Diabetes Mellitus • Type II (AKA adult, NIDDM) • No absolute insulin deficiency...insulin resistance • Relative lack of insulin production as it progresses • Causes • Genetic/familial • Family Hx, 1st degree relative • begin screening at age 30 • Lifestyle • Gestational Diabetes • Obesity • esp. with increasing age • CVD mortality risk • macro vascular • HA1c = Glucose attaches irreversibly to beta chain of Hgb A. Average glucose over 6-12 weeks (life span of the RBC).

  5. Diabetes Mellitus Gestational (Type II variant) • Pregnancy unmasks glucose homeostasis problems • Likely to develop type II later • Encourage lifestyle changes • Secondary Diabetes • Usually related to pancreatitis/ Cushing's syndrome • Starts at a defined event • Heavy long-term glucocorticoids

  6. Goals of Therapy • HgBA1C <6.5 • Directly related to 2hour post-Prandial glucose • Fasting glucose <120 ADA or <110 ACE • Post-Prandial <180 ADA or <140 ACE • HgbA1C <7 ADA or <6.5 ACE • Suggested action >8 ADA or >7 ACE • HgbA1C important to microvascular disease • Post-prandial glucose spikes important to macrovascular disease

  7. Type I Treatment • INSULIN-absolute deficiency • NPH • Lantus • Regular • Delivery • Subcutaneous • Intravenous • Inhaled--Exubera

  8. Alternative Routes- Insulin Pumps • Frequent use by Endocrinology • Super-compliant patients and a lot of education • Requires problem-solving and critical thinking • More flexibility/freer lifestyle • Improves control • Good for brittle DM, Dawn phenomenon • Basal Rate- changes based on stress, exercise, intake, type of foods---suppress production between meals • Boluses at meals • self adjust dosing based on caloric intake • best to calculate intake • In-patient, even if DKA, don’t stop pump—use it

  9. Alternative Routes • Inhaled insulin-Exubera • New, but in use • Regular insulin equivalent • Limited doses available currently-1&3mg • At mealtimes/snacks • Pancreas Transplant • Islet Cell Transplants (in research) • Continuous glucose sensors (in research)

  10. Type II Treatment • Lose Weight (80% are overweight) • Strict Dietary Control • Low Carbs • Avoid simple sugars • Exercise • Burn calories and glucose • Some believe…avoid oral agents… • Multidisciplinary Team-proven to work better

  11. Type II Treatment • <200 NO symptoms • Diet and Exercise alone • 200-300 +/- symptoms • Diet and Exercise • One Oral Agent • >300 + symptoms • Diet and Exercise • Insulin (at least acutely) • Oral Agents

  12. Patho-Specific Treatment INCREASED HEPATIC GLUCOSE OUTPUT GLUCOSE INTAKE Alpha-glucosidase inhibitors-inhibits pancreatic alpha amylase & intestional alpha glucoside hydrolase, delaying absorption Metformin-decreases hepatic production and intestional absorbtion INCREASED HEPATIC GLUCOSE OUTPUT DECREASED INSULIN SECRETION PLASMA GLUCOSE TZDs-Increase insulin sensativity DECREASED PERIPHERAL GLUCOSE UPTAKE Januvia Meglintinides Sulfonylureas Insulin

  13. Type II Treatment • With Time…all with DM will loose β-cell function and require increases in oral agents and insulin • Add NPH insulin initially at bedtime • Shuts down unregulated gluconeogenesis • Start 5-15 u and titrate up • Base treatment on fasting glucose of <110

  14. Patho-Specific Treatment INCREASED HEPATIC GLUCOSE OUTPUT GLUCOSE INTAKE Alpha-glucosidase inhibitors-inhibits pancreatic alpha amylase & intestional alpha glucoside hydrolase, delaying absorption Metformin-decreases hepatic production and intestional absorbtion INCREASED HEPATIC GLUCOSE OUTPUT DECREASED INSULIN SECRETION PLASMA GLUCOSE TZDs-Increase insulin sensativity DECREASED PERIPHERAL GLUCOSE UPTAKE Januvia Meglintinides Sulfonylureas Insulin

  15. Oral Agents • Biguanide (Metformin) • Inc. periph. Glucose uptake and utilization; inhibits hepatic glucose over-production • Can cause lactic acidosis in the setting of CKD • Contraindicated in CHF/Elderly • Sulfonylureas-2nd generation • Increased insulin production and improve beta-cell sensitivity • Glipizide, Glyburide, glimepiride • Mild diuresis (potentiate ADH) • Hypoglycemia (stimulates insulin release) • Great to combine with metformin

  16. Patho-Specific Treatment INCREASED HEPATIC GLUCOSE OUTPUT GLUCOSE INTAKE Alpha-glucosidase inhibitors-inhibits pancreatic alpha amylase & intestional alpha glucoside hydrolase, delaying absorption Metformin-decreases hepatic production and intestional absorbtion INCREASED HEPATIC GLUCOSE OUTPUT DECREASED INSULIN SECRETION PLASMA GLUCOSE TZDs-Increase insulin sensativity DECREASED PERIPHERAL GLUCOSE UPTAKE Januvia Meglintinides Sulfonylureas Insulin

  17. Oral Agents • Alpha-Glucosidase Inhibitors • Inhibit absorption of complex CHO in bowel • Lower post-prandial glucose • acarbose (Precose), miglitol (Glyset) • Take with 1st bite/each meal • GI side effects • Thiazolidinediones (TZDs) • Improve insulin action intracellular/utilization of insulin by gene-expressed proteins • Pioglitazone, rosiglitazone (note new issues) • Well-tolerated

  18. Patho-Specific Treatment INCREASED HEPATIC GLUCOSE OUTPUT GLUCOSE INTAKE Alpha-glucosidase inhibitors-inhibits pancreatic alpha amylase & intestional alpha glucoside hydrolase, delaying absorption Metformin-decreases hepatic production and intestional absorbtion INCREASED HEPATIC GLUCOSE OUTPUT DECREASED INSULIN SECRETION PLASMA GLUCOSE TZDs-Increase insulin sensativity DECREASED PERIPHERAL GLUCOSE UPTAKE Januvia Meglintinides Sulfonylureas Insulin

  19. Oral Agents • Meglintinides • Insulin secretogogues • repaglinide • Great as single agent or to combine with metformin • Hypoglycemia • DPP-4 inhibitor • Januvia-new • Boosts hormones that maintain active insulin in circulation • Also comes combined with Metformin

  20. Patho-Specific Treatment INCREASED HEPATIC GLUCOSE OUTPUT GLUCOSE INTAKE Alpha-glucosidase inhibitors-inhibits pancreatic alpha amylase & intestional alpha glucoside hydrolase, delaying absorption Metformin-decreases hepatic production and intestional absorbtion INCREASED HEPATIC GLUCOSE OUTPUT DECREASED INSULIN SECRETION PLASMA GLUCOSE TZDs-Increase insulin sensativity DECREASED PERIPHERAL GLUCOSE UPTAKE Januvia Meglintinides Sulfonylureas Insulin

  21. Insulin-chronic • We now use human insulin usually instead of beef/pork (less allergy) • Patients must be compliant with FSG • Titrate slowly to FSG 80-120/day and 100-150/bedtime and HgbA1C <6.5 • NPH must be BID • Lantus/Ultralente QD at night • Hypoglycemia risk • PATIENT EDUCATION

  22. Sliding Scale Regular • Needs to be patient specific • Regular insulin only-up to QID • Do not write it and leave-evaluate the patient’s response

  23. Prevent Hypoglycemia • Especially with increased age (>70) • Titrate up slowly • Any lower glucose is an improvement • It takes time to lower HgbA1C • Use shorter acting agents initially • Watch for drug interactions (some are protein bound) • Renal clearance-decrease dose with CKD progression

  24. Complications (Esp. with noncompliance) • Macro vascular disease (inc. risk even if tight control)…MI/CVA • Diabetic Retinopathy • Nephropathy (#1 cause MS, #2 Cause US) • Gastroparesis • Polyneuropathies (peripheral and autonomic)

  25. Preventing complications • Follow recommended guidelines for tight control • Educate and engage patients • Identify At-risk patients (i.e. co-existing risk factors like HTN, hyperlipidemia) • Diet and Exercise • Diet and Exercise • Diet and Exercise

  26. Preventing complications • PCP visits q 3months • HgbA1C • UA with Protein/Creatinine Ratio (microalbuminuria) • Lipid Evaluation and Treatment • Foot exam • Annual Opthamology and Dental • Screen for HTN, Cardiovascular Disease, Smokers

  27. DM in the Acute Care Setting • Try not to screw up good control-harder than you may think • Stress increases glucose • Avoid hypoglycemia—can lead to DEATH • Fasting patients • Remember our discussion of pt specific sliding scales • Watch out for cardiovascular complications • Use the opportunity to evaluate control with good FSGs and compliance

  28. Hyperglycemic Hyperosmotic Syndrome • High glucose =hyperosmosis • Watch Intake and Output-osmotic diuresis • Likely dehydrated at presentation • Super high glucose because there are no ketones • Common to have fever on presentation

  29. Diabetic Ketoacidosis • Occurs 46/100,000 DM pt’s. • 16% of DM fatalities • Same hyperglycemia + ketonemia and ketonuria • Relative deficiency of insulin + excess stress hormones • High osmolarity dehydrates and kills cells • Acidosis and related respiratory problems

  30. DKA, Diagnosis (Laboratory) • Glucose 250-800 • Serum ketosis • Lactic acidosis • Urine ketosis • Glycosuria • Hyponatremia • Increased BUN/creatinine • HCO3 <=15 mEq/L • Metabolic Acidosis by ABG • Increased serum osmolality • Increased anion gap • Elevated base deficit

  31. DKA S/S • Fruity breath • Hypotension • Fever or hypothermia • Abdominal pain • Dry mucus membranes • Poor skin tugor • Kussmaul respirations

  32. Treatment for Both • O2 • IV • Admit for pH < 7.3, glucose >250, HCO3 <=15 • FSG Q1-2 hours until stable • Rapid Fluid Replacement (N/S) • 9-12 L over 24 hours; at least 2L 1st hour • 1/2 over the first 12 hours • D5½NS with any glucose <250 only if insulin given • Treat Electrolytes and monitor closely • K then CO2, Mag, pH Q 2 hrs till stable • Treat underlying cause • DM, steroids, infections, noncompliance, MI, etc

  33. Insulin for DKA/HHS • Regular insulin IV drip • Go slow • Slow to wean-watch for rebound • Requires close RN monitor (ICU) • Aspart insulin SC • Hourly • Frees up RN more • Few studies/more stable patients

  34. Thyroid Disorders • Hyperthyroidism to Thyroid Storm • Graves Disease • Tumors • Hypothyroidism

  35. Thyroid Gland Pathology

  36. Thyroiditis • Thyroid inflammation • Hyperthyroidism followed by hypothyroidism. • Some are painful • Some cause goiter • Causes • Infection, radiation, trauma, post-partum, drugs (i.e. amiodorone, lithium), Reidel’s fibrous dz

  37. Thyroiditis Diagnosis • Radioactive Iodine Uptake scan, Ultrasound (better for suspected cyst rupture) • Labs • Hashimoto’s Dx elevated antithyroid antibodies, autoimmune disorder • Free thyroxine index <5, TSH >5 • Variable thyroid radioactive iodine uptake • Granulomatous thyroidtis • Elevated ESR • Normal or elevated WBC with granolocyte shift to band forms • Early • Free thyroxine index >12, TSH undectable • Radioactive iodine uptake <5% • Late • Free thyroxine <4.5, iodine uptake >35%

  38. Hyperthyroidism Reaction to excess thyroid hormone • Grave’s Dx most common-autoimmune disorder • TSH receptor auto-antibodies • Toxic Nodular Goiter • Solitary nodule with autonomous function; almost always benign • Multi-iodine deprivation then repletion • Single-unknown • Iodine-induced hyperthyroidism • Rare causes pituitary tumors • Sub clinical hyperthyroidism • Suppressed TSH and normal T4

  39. Hyperthyroidism • Varying degrees of sx • Tachycardia (75%), anxiety (85%), fever, heat intolerance (70%), exopthalmus (34%), psychosis, mania, weight loss (52%), apathy, dyspnea (75%) • S/S • Goiter (87%) and opthalmopathy (34%) are common • Diagnosis • Low or normal TSH • High free/total T4(thyroxine); especially high T3(triodothyronine)

  40. Hyperthyroidism Management • Out-patient except in Thyroid Storm • Opthalmologist for exopthalmous • β-blockers-tachycardia • Radioiodine • NSAIDS-thyroiditis • Propylthiouracil- inhibits sythesis of thyroid hormone • Fluids

  41. Thyroid Storm • Uncommon, but life-threatening (cardiac) • Fever can be a hallmark between hyperthyroidism and storm • Untreated hyperthyroidism +/- • Stress, trauma, heart dz, infection, med OD • Presentation-exaggeration of hyperthyroid. Sx • Fever, tachycardia to arrhythmias, agitation to psychosis, low BP, shock • Labs—TSH, T3, T4 (may be nl) • Initial Treatment-start immediately • Sedation, Tylenol, hydration, cardiac monitor • Beta-blockers-propranolol, esmolol • Calcium Channel blockers • PTU or Methinazole; high dose dexamethasone, plasmapheresis, cholesystyramine • Death rate of 20%

  42. Thyroid Goiter • Simple enlargement • Caused by Iodine deficiency • Check TSH, T3, T4-may have accompanying thyroid dz • Sx: occasional tenderness, “lump in throat”, rare tracheal compression • Tx: subtotal thyroidectomy, radioiodine, thyroxine • Urgency of treatment based on severity of sx

  43. Hypothyroidism • Decreased circulating levels of free thyroid hormones or resistance to hormone action • Primary-autoimmune (idiopathic) • Secondary- frequently resulting from treatment of Grave’s • Female > males 5:1 • 5-10/1000 • Symptoms • Fatigue, weakness, cold intolerance, weight gain, dry skin, thinning eyebrows, prolonged DTRs, HTN, high cholesterol, pericardial effusion, anemia; sx of decreased cardiac output, puffy eyes, bradycardia, edema to hands and feet, hypothermia, slow reflexes • Causes • Post ablation therapy • Idiopathic, thyroiditis • Secondary from deficient thyroid releasing hormone • Diagnosis • High TSH, low T4, primary • Low TSH, and low T4 in central • TSH elevated, normal T4 in subclinical • Drug induced • Treatment • Levothyroxine • Titrate to normal TSH • Do not change medication brands

  44. Myxedema Coma • Uncommon-60% mortality • Hypothyroidism + • Pulmonary infections, CVA, trauma, surgery, CNS suppressents • Presentation • Low temp, low HR, hyporeflexia, flat affect, slowing mental status to unconscious • Lab—TSH, CK may be high (not cardiac) • Initial Treatment • Cardiac monitor, Passive rewarming, monitor and treat electrolytes (low Na and gluc common) • Replace hormone; IV hydrocortisone • NO sedation

  45. Anemia • Reduced percentage of RBC in comparison to total cell count • Hematocrit-number • Hemoglobin-O2 carrying capacity • Compare to reference range for “normal” • “Normal” • Women-12-15g/dL (HCT 36-45) (slightly lower if menstruating) • Men-13-15g/dL (HCT 40-45) • Δ in intravascular volume show in HCT

  46. History Drugs Alcohol Blood loss Jaundice Diarrhea Chronic disease ROS Fatigue SOB Sometimes chest pain Palpitations Syncope/dizziness Tinnitus Anemias

  47. Physical Pallor to mucous membranes Tachycardia Edema Systolic Ejection Murmur (maybe) Other Anemia-type specific findings FOBT Lab. Evaluation CBC with differential Platelet count Iron studies Ferritan – body stores, Transferrin – represents iron absorption and transport, Iron, Tsat Reticulocyte count-marrow production Anemias

  48. Microcytic (small celled) Anemias • Decreased iron stores • MOST common in USA • Low MCV • May have elevated platelets • Differential • Iron Deficiency • Lead poisoning • Anemia of Chronic Disease • Thalassemia • Sideroblastic Anemia

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