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  1. 1. ENDOCRINE SYSTEM PART II <ul><li>DENNIS STEVENS CRNA, MSN, ARNP </li></ul><ul><li>NOVEMBER 2007 </li></ul><ul><li>FLORIDA INTERNATIONAL UNIVERSITY </li></ul><ul><li>ADVANCED BIOSCIENCE IN ANESTHESIOLOGY II </li></ul><ul><li>NGR 6145 </li></ul>
  2. 2. ENDOCRINE SYSTEM PART II <ul><li>OBJECTIVES </li></ul><ul><li>Discuss the importance and physiologic effects of calcium on metabolic functions. </li></ul><ul><li>Explain the primary purposes of parathyroid hormone in relation to calcium regulation and phosphate metabolism. </li></ul><ul><li>State clinical manifestations and treatment modalities associated with hypercalcemia and hypocalcemia. </li></ul><ul><li>Describe significant metabolic effects related to insulin production and secretion. </li></ul><ul><li>Explain the pathologic processes and anesthetic considerations associated with insulin deficiency. </li></ul><ul><li>Discuss anesthetic management of the diabetic patient. </li></ul>
  3. 3. ENDOCRINE SYSTEM PART II <ul><li>CALCIUM REGULATION </li></ul><ul><li>Three principal hormones operate to regulate the plasma concentration of calcium: </li></ul><ul><ul><li>Vitamin D </li></ul></ul><ul><ul><li>Parathyroid hormone (PTH) </li></ul></ul><ul><ul><li>Calcitonin </li></ul></ul><ul><li>Only the free, ionized form of calcium exerts physiologic effects </li></ul><ul><li>Vitamin D and PTH raise serum calcium and calcitonin lowers it </li></ul><ul><li>Normal plasma calcium concentration: 8.5-10.5 mg/dL </li></ul>
  4. 4. ENDOCRINE SYSTEM PART II <ul><li>CALCIUM REGULATION </li></ul><ul><li>PTH is the most important regulator of plasma calcium: </li></ul><ul><ul><li>Decreases in plasma calcium stimulate PTH secretion and increases in plasma calcium inhibit PTH secretion </li></ul></ul><ul><li>Vitamin D augments intestinal absorption of calcium, facilitates action of PTH on bone, and augments renal absorption of calcium in distal tubules </li></ul><ul><li>Calcitonin secreted by parafollicular cells in the thyroid gland; secretion stimulated by hypercalcemia and inhibited by hypocalcemia </li></ul>
  5. 5. ENDOCRINE SYSTEM PART II <ul><li>PARATHYROID GLANDS </li></ul><ul><li>Small oval bodies located on the posterior surface of the thyroid gland </li></ul><ul><li>Most individuals have four parathyroid glands </li></ul><ul><li>Blood supply: inferior thyroid arteries </li></ul><ul><li>Parathyroid hormone (PTH) is secreted from chief cells of the parathyroid gland in response to a low serum ionized calcium concentration </li></ul>
  6. 6. ENDOCRINE SYSTEM PART II <ul><li>PARATHYROID GLANDS </li></ul><ul><li>PTH is the body’s major hormonal regulator of calcium and phosphate metabolism </li></ul><ul><li>Hypertrophy of the parathyroid glands may be produced by a sustained deficit in serum calcium levels </li></ul><ul><li>Elevation in serum calcium ion concentration produces an abrupt decline in PTH synthesis and output </li></ul><ul><li>Parathyroid gland function and PTH secretion are inhibited by severe and chronic hypomagnesemia </li></ul><ul><li>Increase in serum calcium level and decline in serum phosphate level in response to PTH are the result of the hormone’s effect on bone, the kidney, and the intestinal tract </li></ul>
  7. 7. ENDOCRINE SYSTEM PART II <ul><li>PARATHYROID GLANDS </li></ul><ul><li>Effect on bone: </li></ul><ul><ul><li>When ionized calcium levels decline, PTH is released and acts directly on bone to mobilize skeletal calcium stores </li></ul></ul><ul><li>Effect on the intestinal tract: </li></ul><ul><ul><li>When plasma calcium level is low, PTH acts to stimulate the formation of active vitamin D, which in turn increases the intestinal absorption of calcium </li></ul></ul><ul><li>Effect on the kidney: </li></ul><ul><ul><li>PTH has two major effects on the kidney; increases calcium reabsorption and increases phosphate excretion </li></ul></ul>
  8. 8. ENDOCRINE SYSTEM PART II <ul><li>HYPERCALCEMIA </li></ul><ul><li>Can occur as a result of a variety of disorders: </li></ul><ul><ul><li>Primary hyperparathyroidism </li></ul></ul><ul><ul><li>Secondary hyperparathyroidism </li></ul></ul><ul><li>Clinical manifestations: </li></ul><ul><ul><li>Anorexia, nausea, vomiting, weakness, and polyuria </li></ul></ul><ul><ul><li>Ataxia, irritability, lethargy, or confusion can rapidly progress to coma </li></ul></ul><ul><ul><li>Hypertension presents initially </li></ul></ul><ul><ul><li>ECG signs </li></ul></ul><ul><ul><li>Pathological processes can complicate hypercalcemia </li></ul></ul>
  9. 9. ENDOCRINE SYSTEM PART II <ul><li>HYPERCALCEMIA </li></ul><ul><li>Treatment: </li></ul><ul><ul><li>Most effective initial treatment is rehydration followed by brisk diuresis </li></ul></ul><ul><ul><li>Additional therapy; administration of bisphosphonate or calcitonin </li></ul></ul><ul><ul><li>Treat underlying cause </li></ul></ul><ul><li>Anesthetic considerations: </li></ul><ul><ul><li>Monitor ionized calcium levels with serial measurements of K + and Mg + . Avoid hypovolemia and acidosis. Invasive monitoring may be necessary. Responses to anesthetic agents are not predictable </li></ul></ul>
  10. 10. ENDOCRINE SYSTEM PART II <ul><li>HYPOCALCEMIA </li></ul><ul><li>Should be diagnosed only on the basis of plasma ionized calcium concentration </li></ul><ul><li>Hypocalcemia due to hypoparathyroidism is a relatively common cause of symptomatic hypocalcemia </li></ul><ul><li>Clinical manifestations of hypocalcemia: </li></ul><ul><ul><li>Paresthesias, confusion, laryngeal stridor, carpopedal spasm, masseter spasm, and seizures </li></ul></ul><ul><ul><li>Cardiac irritability and decreased cardiac contractility may present </li></ul></ul><ul><ul><li>ECG findings…! </li></ul></ul>
  11. 11. ENDOCRINE SYSTEM PART II <ul><li>HYPOCALCEMIA </li></ul><ul><li>Treatment: </li></ul><ul><ul><li>IV administration; calcium chloride or calcium gluconate </li></ul></ul><ul><ul><li>Serial ionized calcium measurements. Assess plasma magnesium concentration </li></ul></ul><ul><ul><li>Chronic hypocalcemia…! </li></ul></ul><ul><li>Anesthetic considerations: </li></ul><ul><ul><li>Hypocalcemia should be corrected preoperatively </li></ul></ul><ul><ul><li>Monitor ionized calcium levels intraoperatively, avoid alkalosis, and concern with citrated blood products </li></ul></ul><ul><ul><li>Negative inotropic effects of anesthetic agents and responses to neuromuscular blocking agents…! </li></ul></ul>
  12. 12. ENDOCRINE SYSTEM PART II <ul><li>PANCREAS </li></ul><ul><li>Contains both exocrine and endocrine functions </li></ul><ul><li>Acinar cells synthesize and secrete digestive enzymes and bicarbonate into the pancreatic ducts </li></ul><ul><li>Adults normally secrete ~50 units of insulin each day from β -cells of the islets of Langerhans and α -cells secrete glucagon </li></ul>
  13. 13. ENDOCRINE SYSTEM PART II <ul><li>INSULIN </li></ul><ul><li>Insulin and glucagon are crucial in regulating carbohydrate, fat, and protein metabolism </li></ul><ul><li>Rate of insulin secretion is primarily determined by the plasma glucose level and is essential for the maintenance of proper plasma glucose levels </li></ul><ul><li>Insulin stimulates anabolism while its lack is associated with catabolism and a negative nitrogen balance </li></ul><ul><li>Insulin is synthesized within the β -cells of the pancreas, and is packaged and stored in membrane lined vesicles within the β -cell cytoplasm </li></ul>
  14. 14. ENDOCRINE SYSTEM PART II <ul><li>INSULIN </li></ul><ul><li>Metabolic effects: </li></ul><ul><ul><li>Important to many cellular activities related to growth </li></ul></ul><ul><ul><li>Intimately involved in the regulation of carbohydrate, fat, and protein metabolism </li></ul></ul><ul><ul><li>Most cells have insulin receptors, but the major targets of insulin action are the liver, muscle, and adipose tissue </li></ul></ul><ul><ul><li>Key hormone in controlling glucose removal from the plasma </li></ul></ul><ul><ul><li>Facilitates the disposition of glucose by stimulating its uptake into liver, muscle, and adipose tissue </li></ul></ul>
  15. 15. ENDOCRINE SYSTEM PART II <ul><li>INSULIN </li></ul><ul><li>Control of insulin secretion: </li></ul><ul><ul><li>Ingestion of a meal increases rate of insulin secretion </li></ul></ul><ul><ul><li>Plasma insulin levels rise reaching peak levels 30 -60 minutes after eating is initiated </li></ul></ul><ul><ul><li>Between meals, insulin levels drift downward </li></ul></ul><ul><ul><li>Elevated plasma glucose levels directly activate β -cells of the pancreas, stimulating insulin synthesis and secretion. Low plasma glucose concentrations inhibit this response </li></ul></ul><ul><ul><li>Maximal insulin response…! </li></ul></ul><ul><ul><li>Amino acids also are potent stimulators of insulin release </li></ul></ul>
  16. 16. ENDOCRINE SYSTEM PART II <ul><li>GLUCAGON </li></ul><ul><li>Linear polypeptide hormone produced by the α -cells of the pancreatic islets </li></ul><ul><li>Most important role is to enhance hepatic glucose output and increase plasma glucose </li></ul><ul><li>Insulin and glucagon have opposing biologic actions </li></ul><ul><li>Glucagon in concert with other hormones are strong defenders against hypoglycemia and are critical in restoring normal glucose levels during periods of hypoglycemic stress </li></ul><ul><li>Secreted in response to…! </li></ul>
  17. 17. ENDOCRINE SYSTEM PART II <ul><li>INSULIN DEFICIENCY </li></ul><ul><li>Diabetes mellitus (DM) is a complex metabolic derangement </li></ul><ul><li>Glucose is present in abundance but, due to lack of insulin, is unable to reach cells for energy provision </li></ul><ul><li>Recommended guidelines for diagnosing diabetes include a fasting plasma glucose (FPG) of 126 mg/dL or greater </li></ul><ul><li>Incidence of diabetes is increasing and can be attributed to a combination of three factors: </li></ul><ul><ul><li>Overweight population </li></ul></ul><ul><ul><li>More sedentary lifestyles </li></ul></ul><ul><ul><li>Rise in the number of elderly </li></ul></ul>
  18. 18. ENDOCRINE SYSTEM PART II <ul><li>INSULIN DEFICIENCY </li></ul><ul><li>Insulin-dependent diabetes mellitus (IDDM): </li></ul><ul><ul><li>~ 10% of diabetics have type 1 or IDDM </li></ul></ul><ul><ul><li>These patients have an absolute deficiency of insulin </li></ul></ul><ul><ul><li>Disease course may be complicated by periods of ketosis and acidosis </li></ul></ul><ul><ul><li>Type 1 DM is believed to be caused by autoimmune destruction of the β -cells of the pancreatic islets </li></ul></ul><ul><ul><li>Usually develops before the age of 40 years </li></ul></ul><ul><ul><li>Classic symptoms of type 1 DM appear when at least 90% of the β -cells are destroyed </li></ul></ul>
  19. 19. ENDOCRINE SYSTEM PART II <ul><li>INSULIN DEFICIENCY </li></ul><ul><li>Non-insulin dependent diabetes mellitus (NIDDM): </li></ul><ul><ul><li>~ 90% of patients with DM have type II or NIDDM </li></ul></ul><ul><ul><li>NIDDM characterized by: </li></ul></ul><ul><ul><ul><li>Impaired insulin secretion, or </li></ul></ul></ul><ul><ul><ul><li>Peripheral insulin resistance, or both </li></ul></ul></ul><ul><ul><li>Type 2 DM occurs in patients who have some degree of endogenous insulin production </li></ul></ul><ul><ul><li>Typically, type 2 DM occurs in patients who are older than 40 years, obese (80%), and with a family history </li></ul></ul><ul><ul><li>Insidious onset </li></ul></ul><ul><ul><li>Treatment modalities…! </li></ul></ul>
  20. 20. ENDOCRINE SYSTEM PART II <ul><li>INSULIN DEFICIENCY </li></ul><ul><li>DM may be associated with other conditions </li></ul><ul><li>Long-term diabetic complications: </li></ul><ul><ul><li>Extensive arterial diseases </li></ul></ul><ul><ul><li>Cataracts </li></ul></ul><ul><ul><li>Peripheral neuropathies </li></ul></ul><ul><ul><li>Autonomic nervous system dysfunctions </li></ul></ul><ul><li>There is a strong relationship between the hyperglycemia of diabetes and end-organ diseases </li></ul>
  21. 21. ENDOCRINE SYSTEM PART II <ul><li>ANESTHETIC MANAGEMENT OF THE DIABETIC PATIENT </li></ul><ul><li>DM is the most common endocrine disorder encountered in surgical patients </li></ul><ul><li>Diabetic patients have higher morbidity and mortality in the perioperative period </li></ul><ul><li>Elective surgical procedures should be scheduled early in the day if possible </li></ul><ul><li>Preoperative considerations: </li></ul><ul><ul><li>Detailed preanesthetic assessment is warranted </li></ul></ul><ul><ul><li>Examine patient’s history of glycemic control </li></ul></ul><ul><ul><li>Recommended target blood glucose range…! </li></ul></ul><ul><ul><li>Review of oral hypoglycemic and insulin regimens </li></ul></ul>
  22. 22. ENDOCRINE SYSTEM PART II <ul><li>ANESTHETIC MANAGEMENT OF THE DIABETIC PATIENT </li></ul><ul><li>Intraoperative management: </li></ul><ul><ul><li>No specific anesthetic technique is superior overall for diabetic patients </li></ul></ul><ul><ul><li>RA may produce less deleterious changes in glucose homeostasis </li></ul></ul><ul><ul><li>Patients under anesthesia are generally maintained with a mild transient hyperglycemia to avoid the potentially catastrophic effects of hypoglycemia </li></ul></ul><ul><ul><li>Frequent blood glucose determinations during surgery and in the immediate postoperative period are central to safe practice </li></ul></ul><ul><ul><li>Universal goal…! </li></ul></ul>
  23. 23. ENDOCRINE SYSTEM PART II <ul><li>ACUTE DERANGEMENTS IN GLUCOSE HOMEOSTASIS </li></ul><ul><li>Hypoglycemia: </li></ul><ul><ul><li>Medications and certain pathologic disorders are causes of hypoglycemia </li></ul></ul><ul><ul><li>Blood glucose levels in the range of 40-60 mg/dL commonly produce mild symptoms of hypoglycemia </li></ul></ul><ul><ul><li>Acute treatment for the hypoglycemic surgical patient… </li></ul></ul><ul><ul><ul><li>IV administration of 25 mL of 50% glucose </li></ul></ul></ul><ul><ul><li>Hypoglycemia is potentially catastrophic during surgery </li></ul></ul><ul><ul><li>Frequent blood glucose determinations, maintenance of mild hyperglycemia, and careful monitoring help to avoid this serious complication during anesthesia </li></ul></ul>
  24. 24. ENDOCRINE SYSTEM PART II <ul><li>ACUTE DERANGEMENTS IN GLUCOSE HOMEOSTASIS </li></ul><ul><li>Diabetic ketoacidosis (DKA): </li></ul><ul><ul><li>DKA is a medical emergency triggered by a hyperglycemic event </li></ul></ul><ul><ul><li>Major signs and symptoms of DKA include hyperglycemia (>250 mg/dL), volume depletion, tachycardia, metabolic acidosis (arterial pH <7.3) with ketonemia, electrolyte depletion, hyperosmolarity (>320 mOsm/L), N&V, abdominal pain, and lethargy </li></ul></ul><ul><ul><li>Preoperative management of the surgical patient with DKA…! </li></ul></ul>
  25. 25. ENDOCRINE SYSTEM PART II <ul><li>ACUTE DERANGEMENTS IN GLUCOSE HOMEOSTASIS </li></ul><ul><li>Hyperglycemic hyperosmolar nonketotic syndrome (HHNS): </li></ul><ul><ul><li>A hyperosmolar state triggered by a hyperglycemic event </li></ul></ul><ul><ul><li>Commonly occurs in type 2 diabetics </li></ul></ul><ul><ul><li>Hyperglycemic episode overwhelms the pancreas and produces severe hyperglycemia and glucosuria </li></ul></ul><ul><ul><li>Usually not associated with acidosis or significant ketogenesis </li></ul></ul><ul><ul><li>Spectrum of symptoms is associated with HHNS </li></ul></ul><ul><ul><li>Profound dehydration is always present </li></ul></ul><ul><ul><li>Mortality rate…! </li></ul></ul><ul><ul><li>Treatment goals…! </li></ul></ul>
  26. 26. ENDOCRINE SYSTEM PART II <ul><li>REFERENCES </li></ul><ul><li>Morgan, G.E., Mikhail, M.S., and Murray, M.J. (2006). </li></ul><ul><li>Clinical Anesthesiology . (4 th Ed.) New York, NY: </li></ul><ul><li>McGraw-Hill. </li></ul><ul><li>Nagelhout, J.J. and Zaglaniczny, K.L. (2005). Nurse </li></ul><ul><li>Anesthesia . (3 rd Ed.) St. Louis, MO: Elsevier- </li></ul><ul><li>Saunders. </li></ul>