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