10 results
Chapter 32 - Disorders of calcium metabolism
- from Section 9 - Endocrinology
- Edited by Michael F. Lubin, Emory University, Atlanta, Thomas F. Dodson, Emory University, Atlanta, Neil H. Winawer, Emory University, Atlanta
-
- Book:
- Medical Management of the Surgical Patient
- Published online:
- 05 September 2013
- Print publication:
- 15 August 2013, pp 366-372
-
- Chapter
- Export citation
-
Summary
Calcium is an abundant mineral and has diffuse cellular functions in bone metabolism, cell division, coagulation, enzyme regulation, glycogen metabolism, muscle contraction, neurotransmission, protein synthesis, and degradation. Calcium is ingested in the diet and absorbed in the small intestine. It is distributed throughout the body, but 99% appears in the bone [1–3]. Adult humans contain more than 1 kg of calcium, of which over 99% is skeletal and dental and only 0.1% is in extracellular fluids. About half the calcium in serum is bound to protein, primarily of which is albumin. Decreases in serum albumin are accompanied by decreases in calcium (a drop of 1 g/dL of albumin lowers the calcium by about 0.8 mg/dL). Several calcium determinations and measurement of ionized (physiologically active) calcium levels may be needed to accurately assess calcium status..
Calcium is maintained in a very narrow range by a redundant system of parathyroid hormone (PTH), vitamin D, and calcitonin; all acting at multiple target organs, including bone, kidneys, and the gastrointestinal tract. As ionized (free, metabolically active) calcium levels decrease, the parathyroid glands secrete PTH, which raises calcium levels by stimulating bone resorption, renal calcium reabsorption, phosphate excretion, and renal 1,25-dihydroxycholecalciferol (1,25-[OH]2D3) synthesis. Vitamin D, in turn, promotes bone resorption, increases intestinal absorption of dietary calcium and phosphate, and inhibits PTH secretion [1,4–14]. Finally, calcitonin, released by parafollicular cells of the thyroid in response to hypercalcemia, has been shown to transiently inhibit bone resorption [5].
Chapter 30 - Disorders of the thyroid
- from Section 9 - Endocrinology
- Edited by Michael F. Lubin, Emory University, Atlanta, Thomas F. Dodson, Emory University, Atlanta, Neil H. Winawer, Emory University, Atlanta
-
- Book:
- Medical Management of the Surgical Patient
- Published online:
- 05 September 2013
- Print publication:
- 15 August 2013, pp 350-357
-
- Chapter
- Export citation
-
Summary
Because thyroid hormones exert regulatory effects on multiple organ systems, thyroid function should be aggressively evaluated and abnormal function treated in patients who require surgery. Thyroid hormones also significantly affect the metabolism of many drugs, and dose adjustments may be required when function is abnormal. Medical consultants performing preoperative evaluations should include clinical assessments of thyroid function and perform confirmatory tests when indicated.
The adult thyroid gland weighs 15–20 g, typically consists of two lobes connected by an isthmus, and is located just below the cricoid cartilage. A remnant of the thyroglossal duct, the pyramidal lobe may be noted arising superiorly from the isthmus or medial side of a lobe. Enlargement of the pyramidal lobe indicates a diffuse thyroidal abnormality. The thyroid gland consists of follicles, which are spheres lined by a single layer of cuboidal cells and are filled with a colloid that is composed primarily of thyroglobulin. A rich capillary network surrounds the follicles, explaining why a bruit is sometimes heard over hyperactive, enlarged thyroid glands. Scattered throughout the thyroid are calcitonin-secreting perifollicular cells. Hyperplasic or malignant transformation of these cells does not result in abnormalities of thyroid function [1–3].
Chapter 29 - Diabetes mellitus
- from Section 9 - Endocrinology
- Edited by Michael F. Lubin, Emory University, Atlanta, Thomas F. Dodson, Emory University, Atlanta, Neil H. Winawer, Emory University, Atlanta
-
- Book:
- Medical Management of the Surgical Patient
- Published online:
- 05 September 2013
- Print publication:
- 15 August 2013, pp 343-349
-
- Chapter
- Export citation
-
Summary
Surgery has major effects on carbohydrate metabolism and thus presents special risks for patients with diabetes. Surgical mortality rates for patients with diabetes have declined but the successful perioperative care of these patients requires close cooperation between surgeons, anesthesiologists, and primary physicians to prevent complications. There are 25.8 million children and adults in the USA with diabetes – 8.3% of the population [1]. Diabetes is listed as a diagnosis on 23% of hospital discharges [2]. At least half of these patients will require surgery at some point in their lives. In addition to surgical conditions typical of the general population, patients with diabetes have an increased incidence of occlusive vascular disease; cholelithiasis; ophthalmic disease (i.e., cataract extraction, vitrectomy); renal disease; and infection. Three of four patients with diabetes are older than 40 years and are approaching a time of life when surgical indications increase. The presence of diabetes typically is known prior to surgery, although a new diagnosis of diabetes is made in the perioperative period in as many as 12% of cases [3].
Hyperglycemia in the hospital is common and may result from stress, infection, effect of procedures, or is iatrogenic [4]. Previously, glucose levels between 100 and 200 mg/dL were not treated in the perioperative period. This practice was challenged by studies suggesting that more aggressive treatment of elevated glucose levels with insulin reduces infectious complications, decreases mortality, and decreases length of hospital stay [5–7]. Many hospitals developed programs, and started treating both medical and surgical patients with intensive insulin therapy to maintain blood glucose at or below 110 mg/dL, particularly in ICU settings. But, following studies performed in other ICUs, particularly medical ones, failed to reproduce the beneficial effects of intensive insulin therapy. In fact, intensive insulin therapy increased the risk of death [8–11]. One study demonstrated a 2.6% absolute increase in 90-day mortality in patients randomized to tight glucose control [10]. This may have been related to the increased risk for hypoglycemia in the intensive insulin group [12].
Chapter 31 - Disorders of the adrenal cortex
- from Section 9 - Endocrinology
- Edited by Michael F. Lubin, Emory University, Atlanta, Thomas F. Dodson, Emory University, Atlanta, Neil H. Winawer, Emory University, Atlanta
-
- Book:
- Medical Management of the Surgical Patient
- Published online:
- 05 September 2013
- Print publication:
- 15 August 2013, pp 358-365
-
- Chapter
- Export citation
-
Summary
During surgery there is a coordinated response to stress that includes the nervous, endocrine, and immune systems. Inappropriately low response or inappropriately excessive response to stress may lead to disease and possible premature death [1,2]. The hypothalamic–pituitary–adrenal (HPA) axis and the sympathetic nervous system react to stress by releasing hypothalamic CRH and vasopressin (AVP). These hormones synergistically stimulate systemic ACTH secretion, which, in turn, stimulates the adrenal cortexes to secrete glucocorticoids. Central activation of the sympathetic neurons leads to activation of both the systemic sympathetic nervous system and the adrenal medullae [2,3]. The immune system through inflammatory mediators, especially cytokines, stimulates the release of corticotropin-releasing factor from hypothalamic neurons. This central activation of the HPA axis and the direct stimulation of the adrenal glands by the sympathetic system may be a regulatory mechanism for preventing an excessive immune reaction [4,5].
Adrenocorticotropic hormone (ACTH) is released in quick, pulsatile bursts followed by a slower, more sustained rise in cortisol and metabolites [6,7]. Free cortisol is the active hormone and acts directly on tissues [6]. Normal ACTH release and production of cortisol follows a circadian rhythm and is connected to light. It is the highest on awakening in the morning (peaking about 8 hours after the onset of sleep), declines over the day, and is lowest in the middle of the night [7]. The cortisol secretory pattern is usually resistant to acute change. Prolonged bed rest, continuous feeding, or 5 days of fasting, do not alter the rhythm [8]. Occasionally, abrupt time changes of the sleep–awake cycle, as during shift work rotations and jet lag, may have some effect on the 24-hour cortisol patterns [9–11]. Critical illness, chronic inflammatory conditions, chronic insomnia, coronary artery disease, and severe stress often alter the daily rhythm [12–14]. These conditions exert their effect by cytokines, interleukins, and tumor necrosis factors. Circulating interleukin-6 is a potent activator of the HPA axis. By stimulating pituitary ACTH and therefore cortisol, response to inflammation can enhance resistance to inflammatory disease, while a decreased or defective response can increase susceptibility [4,5,13].
Chapter 33 - Pheochromocytoma
- from Section 9 - Endocrinology
- Edited by Michael F. Lubin, Emory University, Atlanta, Thomas F. Dodson, Emory University, Atlanta, Neil H. Winawer, Emory University, Atlanta
-
- Book:
- Medical Management of the Surgical Patient
- Published online:
- 05 September 2013
- Print publication:
- 15 August 2013, pp 373-376
-
- Chapter
- Export citation
-
Summary
Pheochromocytomas are not a common medical/surgical problem. They are estimated to cause only 0.1–0.5% of all cases of hypertension [1,2], and are seen in 4–7% of patients with incidentally found adrenal adenomas [2,3]. That being said, at some time in their careers medical consultants are likely to be asked to evaluate a patient with a suspected pheochromocytoma. Because catecholamines have major regulatory effects on many different body systems, it is vital that these be anticipated and properly managed in the perioperative period. Pheochromocytomas are associated with an increased risk of adverse reactions to many commonly prescribed drugs and clinicians must also be aware of this potential hazard. The removal of a pheochromocytoma has great potential for complications, both during and after surgery because of the release of catecholamines during manipulation or stimulation of the tumor.
Pathophysiology
Pheochromocytomas arise from chromaffin cells of the neural crest that migrate to form the adult adrenal medulla and sympathetic ganglia. These cells synthesize catecholamines through a series of enzymatically controlled steps, starting with the conversion of tyrosine to dihydroxyphenylalanine (dopa) by tyrosine hydroxylase. This is the rate-limiting step in catecholamine synthesis. Dopa is then converted to dopamine, which is subsequently decarboxylated to norepinephrine. The methylation of norepinephrine to epinephrine is accomplished through the action of phenylethanolamine-N-methyl transferase, an enzyme that is induced by glucocorticoids that reach the adrenal medulla in high concentrations through the corticomedullary venous sinuses from the adrenal cortex. Norepinephrine and epinephrine are the major products of most pheochromocytomas [4]. Epinephrine is produced mainly in the adrenal medulla; thus, a pheochromocytoma that produces epinephrine is nearly always located in the adrenal gland. Norepinephrine is produced and secreted in the central nervous system and the sympathetic post-ganglionic nerve endings as well as in the adrenal medulla. Dopamine is also produced and secreted by some pheochromocytomas. The metabolism of catecholamines takes place mostly in the same cells where the catecholamines are synthesized [4]. Once catecholamines reach the plasma, they have a half-life of only 1–2 minutes before they are taken up by cells or enzymatically degraded [5]. Metanephrine, normetanephrine, and vanillylmandelic acid are the major metabolites.
30 - Pheochromocytoma
-
- By Pamela T. Prescott, University of California at Davis Division of Epidemiology, Sacramento, CA
- Edited by Michael F. Lubin, Emory University, Atlanta, Robert B. Smith, Emory University, Atlanta, Thomas F. Dodson, Emory University, Atlanta, Nathan O. Spell, Emory University, Atlanta, H. Kenneth Walker, Emory University, Atlanta
-
- Book:
- Medical Management of the Surgical Patient
- Published online:
- 12 January 2010
- Print publication:
- 10 August 2006, pp 383-386
-
- Chapter
- Export citation
-
Summary
Although pheochromocytomas are not a common medical/surgical problem (they are estimated to cause only 0.1% to 0.5% of all cases of hypertension, and are operated on only once or twice per year in most centers), medical consultants are likely to be asked to evaluate and prepare for surgery patients with suspected pheochromocytomas at some time during their careers. Because catecholamines have major regulatory effects on many different body systems, it is vital that these be anticipated and properly managed in the perioperative period. Pheochromocytomas are associated with an increased risk of adverse reactions to many commonly prescribed drugs and clinicians must also be aware of this potential hazard. The surgical removal of a pheochromocytoma has great potential for intra- and postoperative complications because of the release of catecholamines during manipulation or stimulation of the tumor.
Pathophysiology
Pheochromocytomas arise from chromaffin cells of the neural crest that migrate to form the adult adrenal medulla and sympathetic ganglia. These cells synthesize catecholamines through a series of enzymatically controlled steps, starting with the conversion of tyrosine to dihydroxyphenylalanine (dopa) by tyrosine hydroxylase. This is the rate-limiting step in catecholamine synthesis. Dopa is then converted to dopamine, which is subsequently decarboxylated to norepinephrine. The methylation of norepinephrine to epinephrine is accomplished through the action of phenylethanilamine-N-methyl transferase, an enzyme that is induced by glucocorticoids that reach the adrenal medulla in high concentrations through the corticomedullary venous sinuses from the adrenal cortex. Norepinephrine and epinephrine are the major products of most pheochromocytomas.
27 - Disorders of the thyroid
-
- By Pamela T. Prescott, University of California at Davis Division of Endocrinology, Sacramento, CA
- Edited by Michael F. Lubin, Emory University, Atlanta, Robert B. Smith, Emory University, Atlanta, Thomas F. Dodson, Emory University, Atlanta, Nathan O. Spell, Emory University, Atlanta, H. Kenneth Walker, Emory University, Atlanta
-
- Book:
- Medical Management of the Surgical Patient
- Published online:
- 12 January 2010
- Print publication:
- 10 August 2006, pp 367-373
-
- Chapter
- Export citation
-
Summary
Because thyroid hormones exert regulatory effects on multiple organ systems, thyroid function should be aggressively evaluated and abnormal function treated in patients who require surgery. Thyroid hormones also significantly affect the metabolism of many drugs, and dose adjustments may be required when function is abnormal. Medical consultants performing preoperative evaluations should include clinical assessments of thyroid function and perform confirmatory tests when indicated.
The adult thyroid gland weighs 15 to 20 g, typically consists of two lobes connected by an isthmus, and is located just below the cricoid cartilage. A remnant of the thyroglossal duct, the pyramidal lobe may be noted arising superiorly from the isthmus or medial side of a lobe. Enlargement of the pyramidal lobe indicates a diffuse thyroidal abnormality. The thyroid gland consists of follicles, which are spheres lined by a single layer of cuboidal cells and are filled with a colloid that is composed primarily of thyroglobulin. A rich capillary network surrounds the follicles, explaining why a bruit is sometimes heard over hyperactive, enlarged thyroid glands. Scattered throughout the thyroid are calcitonin-secreting perifollicular cells. Hyperplasic or malignant transformation of these cells does not result in abnormalities of thyroid function.
Inorganic iodide is actively transported from the blood into the follicular cells, immediately oxidized by perioxidase, and is rapidly incorporated into the tyrosine residues of thyroglobulin. These monoiodotyrosine and diiodotyrosine residues couple to form the iodothyronines thyroxine (T4) and triiodothyronine (T3), which are stored in the follicles.
26 - Diabetes mellitus
-
- By Pamela T. Prescott, University of California at Davis Division of Endocrinology, Sacramento, CA
- Edited by Michael F. Lubin, Emory University, Atlanta, Robert B. Smith, Emory University, Atlanta, Thomas F. Dodson, Emory University, Atlanta, Nathan O. Spell, Emory University, Atlanta, H. Kenneth Walker, Emory University, Atlanta
-
- Book:
- Medical Management of the Surgical Patient
- Published online:
- 12 January 2010
- Print publication:
- 10 August 2006, pp 361-366
-
- Chapter
- Export citation
-
Summary
Surgery has major effects on carbohydrate metabolism and thus presents special risks for patients with diabetes. Surgical mortality rates for patients with diabetes have declined but the successful perioperative care of these patients requires close cooperation between surgeons, anesthesiologists, and primary physicians to prevent complications. More than 20 million people in the USA have diabetes and at least half of them will require surgery at some point in their lives. In addition to surgical conditions typical of the general population, patients with diabetes experience increased intervention for occlusive vascular disease; cholelithiasis; ophthalmic disease (i.e., cataract extraction, vitrectomy); renal disease; and infection. Three of four patients with diabetes are older than 40 years and are approaching a time of life when surgical indications increase. The presence of diabetes typically is known before operation, although a new diagnosis of diabetes is made in the perioperative period in as many as 20% of cases.
Pathophysiology
The endocrine pancreas, which consists of the islets of Langerhans, accounts for less than 3% of the total pancreatic mass in adults. The islets are unevenly distributed through the pancreas and contain four cell types: A (α) cells, which secrete glucagons; B (β) cells, which secrete insulin; D (δ) cells, which secrete somatostatin; and F cells, which secrete pancreatic polypeptide. Insulin, the major secretory product, is synthesized as a precursor molecule, preproinsulin, in the endoplasmic reticulum and is cleaved by microsomal enzymes to proinsulin. Proinsulin is then converted by proteolysis to insulin and an amino acid residue, c-peptide.
29 - Disorders of calcium metabolism
-
- By Pamela T. Prescott, University of California at Davis Division of Endocrinology, Sacramento, CA
- Edited by Michael F. Lubin, Emory University, Atlanta, Robert B. Smith, Emory University, Atlanta, Thomas F. Dodson, Emory University, Atlanta, Nathan O. Spell, Emory University, Atlanta, H. Kenneth Walker, Emory University, Atlanta
-
- Book:
- Medical Management of the Surgical Patient
- Published online:
- 12 January 2010
- Print publication:
- 10 August 2006, pp 379-382
-
- Chapter
- Export citation
-
Summary
Both hypercalcemia and hypocalcemia may be associated with life-threatening cardiac arrhythmias as well as morbidity affecting other organ systems. Effective treatment is available and clinicians should be alert to abnormalities in serum calcium, which are present in more than 2% of hospitalized patients. Furthermore, both hypercalcemia and hypocalcemia suggest significant underlying pathology, and efforts to diagnose and treat these conditions should be instituted.
Adult humans contain more than 1 kg of calcium, of which over 99% is skeletal and dental and only 0.1% is in extracellular fluids. About half the calcium in serum is bound to protein, primarily albumin. Decreases in serum albumin are accompanied by decreases in calcium (a drop of 1 g/dl of albumin lowers the calcium by about 0.8 mg/dl). Several calcium determinations and measurement of ionized (physiologically active) calcium levels may be needed to accurately assess calcium status.
Serum ionized calcium levels are tightly controlled by the interplay of parathyroid hormone, calcitonin, and 1,25-dihydroxycholecalciferol (1,25-[OH]2D3). Parathyroid hormone is synthesized in the parathyroid glands and, after cleavage of precursor molecules, is released into the circulation as an 84-amino-acid polypeptide and small fragments.
The amino-terminal 1–34 amino acids compose the biologically active portion of the molecule. Highly specific immunoradiometric assays are available that measure the intact hormone, permitting accurate diagnosis. Parathyroid hormone release is primarily controlled by serum calcium levels, although modest hypomagnesemia also evokes a parathyroid hormone response, whereas severe hypomagnesemia impairs release.
28 - Disorders of the adrenal cortex
-
- By Pamela T. Prescott, University of California at Davis Division of Endocrinology, Sacramento, CA
- Edited by Michael F. Lubin, Emory University, Atlanta, Robert B. Smith, Emory University, Atlanta, Thomas F. Dodson, Emory University, Atlanta, Nathan O. Spell, Emory University, Atlanta, H. Kenneth Walker, Emory University, Atlanta
-
- Book:
- Medical Management of the Surgical Patient
- Published online:
- 12 January 2010
- Print publication:
- 10 August 2006, pp 374-378
-
- Chapter
- Export citation
-
Summary
Serum cortisol levels rise within 30 minutes of the induction of anesthesia and remain elevated for hours to days in the face of postoperative stress. Because of cortisol's critical role in the successful handling of stress, a careful clinical assessment of adrenal function is necessary before surgery. Either deficiency or excess of cortisol can adversely affect surgical outcome. The physiology and metabolism of the adrenal cortex are briefly reviewed in this chapter to help clarify the appropriate selection of tests to verify a clinical diagnosis of adrenal cortex disorder. The adrenal medulla is discussed in Chapter 30.
Human adult adrenal glands weigh 4 to 5 g each and reside in the retroperitoneal space supermedial to the kidneys. The cortex, of mesodermal origin, occupies the outer 90% of the gland. It consists of three concentric histologic zones, two of which have apparently identical function. The outermost zona glomerulosa produces aldosterone but, because it lacks 17 α-hydroxylase activity, is unable to synthesize cortisol or androgens. The middle zona fasciculate is the largest area of the adrenal cortex, and the small innermost zona reticularis encircles the medulla. These two zonae produce cortisol, androgens, and small amounts of estrogen but lack the 18-hydroxysteriod dehydrogenase required for aldosterone synthesis. Histologic evidence suggests that the zona fasciculata responds to acute adrenocorticotropic hormone (ACTH) stimulation, whereas the zona reticularis responds to prolonged stimulation.
Adrenal steroid synthesis is controlled by the hypothalamic–pituitary–adrenal (HPA) axis.