The Washington Manual of Surgery (Lippincott Manual Series (Formerly known as the Spiral Manual Series)) by Klingensmith Mary E. & Aziz Abdulhameed & Bharat Ankit & Fox Amy C. & Porembka Matthew R

Author:Klingensmith, Mary E. & Aziz, Abdulhameed & Bharat, Ankit & Fox, Amy C. & Porembka, Matthew R. [Klingensmith, Mary E.]
Language: eng
Format: epub
ISBN: 9781451180800
Publisher: Lippincot (Wolters Kluwer Health)
Published: 2012-03-05T00:00:00+00:00

ENDOCRINE PANCREAS

I. EMBRYOLOGY, ANATOMY, AND PHYSIOLOGY

A. Embryology. The pancreas originates from two diverticula in the foregut to develop the final adult form around the fifth and sixth weeks of gestation. The endocrine cells that form the pancreatic islets also originate from the foregut endoderm.

B. Anatomy. In the adult, the pancreatic islets are scattered throughout the pancreas and are composed of four major cell types: A, B, D, PP cells. Beta cells occupy the center of the islets with the remainder of the cells scattered in the periphery.

C. Physiology. Each of the various pancreatic endocrine cells produces different hormones with a variety of local and systemic actions

1. A cells produce glucagon that is a polypeptide whose main function is to promote the conversion of hepatic glycogen to glucose and increase the systemic glucose levels.

2. B cells produce insulin whose main function is to promote glucose transport into cells and therefore decrease systemic glucose levels.

3. D cells produce somatostatin that functions to inhibit the release of other gastrointestinal hormones, gastric acid secretion, and small bowel electrolyte secretions.

4. D2 cells produce vasoactive interstitial peptide that serves as an enteric vasodilator.

5. G cells produce gastrin whose actions increase the secretion of gastric acid and pepsinogen.

II. PANCREATIC ISLET CELL TUMORS are rare tumors that produce clinical syndromes related to the specific hormone secreted. Insulinomas are the most common of these tumors, followed by gastrinoma, then the rarer VIPoma, glucagonoma, and somatostatinoma. Islet cell tumors are often occult, and their localization may be difficult, especially for small, multifocal, or extrapancreatic tumors. Islet cell tumors may occur sporadically or as a component of MEN type 1 or von Hippel–Lindau disease (nearly always multifocal) and may be benign or malignant, although prediction may be based on the hormone produced rather than the tumor size.

A. Insulinoma

1. Clinical features. Patients with insulinoma develop profound hypoglycemia during fasting or after exercise. The clinical picture includes the signs and symptoms of neuroglycopenia (anxiety, tremor, confusion, and obtundation) and the sympathetic response to hypoglycemia (hunger, sweating, and tachycardia). These bizarre complaints initially may be attributed to malingering or a psychosomatic etiology unless the association with fasting is recognized. Many patients eat excessively to avoid symptoms, causing significant weight gain. Whipple’s triad refers to the clinical criteria for the diagnosis of insulinoma: (1) hypoglycemic symptoms during monitored fasting, (2) blood glucose levels less than 50 mg/dL, and (3) relief of symptoms after administration of intravenous glucose. Factitious hypoglycemia (excess exogenous insulin administration) and postprandial reactive hypoglycemia must be excluded.

2. Diagnosis. A supervised, in-hospital 72-hour fast is required to diagnose insulinoma. Patients are observed for hypoglycemic episodes and have 6-hour measurement of plasma glucose, insulin, proinsulin, and C peptide. The fast is terminated when symptoms of neuroglycopenia develop. Nearly all patients with insulinoma develop neuroglycopenic symptoms and have inappropriately elevated plasma insulin (>5 μU/mL) associated with hypoglycemia (glucose <50 mg/dL). Elevated levels of C peptide and proinsulin are usually present as well (Curr Probl Surg. 1994;31:79).

3. Localization. Insulinomas typically are small (<2 cm), solitary, benign tumors that may occur anywhere in the pancreas.

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