ENDOCRINE SYSTEM PART II DENNIS STEVENS CRNA, MSN, ARNP

ENDOCRINE SYSTEMPART II

DENNIS STEVENS CRNA, MSN, ARNPNOVEMBER 2007

FLORIDA INTERNATIONAL UNIVERSITYADVANCED BIOSCIENCE IN ANESTHESIOLOGY II

NGR 6145


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.


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


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


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


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


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


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


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


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…!


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…!


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


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


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


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


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…!


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


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


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…!


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


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


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…!


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


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…!


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…!


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.

ENDOCRINE SYSTEM PART II DENNIS STEVENS CRNA, MSN, ARNP

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