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Seasonal variation in the incidence of infection

There are predisposing factors, other than age and inherent susceptibility, that are associated with the precipitation of clinical furunculosis in hatchery stocks throughout the year. These include physical damage, poor water quality, presence of ectoparasites and other diseases, diet and physical and psychological stresses, such as grading, tagging, injection and netting (Olivier, 1997 Pickering, 1997). However, a marked seasonality in the incidence of both clinical and covert furunculosis infections has been observed in hatchery stocks and wild populations. In hatchery stocks, both smolting and high water temperatures have been implicated in this apparent seasonality. The period of smolting is associated with major physiological changes, including chronic cortisol elevation, which can bring about severe depression of the fish's defence system and increased susceptibility to bacterial infections (Maule et al., 1986 Pickering, 1997). In addition, high water temperatures (12-15 C) in...

Preoperative abnormalities

Biochemical abnormalities include hypokalaemic alkalosis, sodium and water retention, hyperglycaemia, lack of diurnal variation in plasma cortisol with failure to decrease at night, and increased urinary free cortisol. 5. Screening by overnight dexamethasone test and 24-h urinary excretion of cortisol (Klibanski & Zervas 1991). 8. Patients with treated Cushing's disease who are considered 'cured' still have an increased risk of cardiovascular disease and atherosclerosis, despite having normal cortisol levels (Colao et al 1999).

Are there other substances that affect bone development What about hormones

Cortisol Secreted by the adrenal glands (located by the kidneys), is needed in small amounts for bone growth. Large amounts of cortisol can interfere with bone growth. The synthetic form of cortisol, or steroids, used in the treatment of some diseases, can cause bone loss. Cortisol, secreted by the adrenal glands (located by the kidneys), is needed in small amounts for bone growth. Large amounts of cortisol can interfere with bone growth. The synthetic form of cortisol, or steroids, used in the treatment of some diseases (see Question 16), can cause bone loss. Insulin, a hormone secreted by the pancreas to help the body use carbohydrates and sugar, and leptin, a newly identified hormone that is found in fat cells, both have effects on bone growth.

Exclusion of Specific Disorders

Approximately 6 of androgen excess patients suffer from a specific disorder, including classic and nonclassic 21-hydroxylase deficiencies, the HAIR-AN syndrome, or an ASN, among others (12). In patients clinically suspected of having an ASN, a computed tomography or magnetic resonance imaging scan of the adrenals and transvaginal ovarian ultrasonography should be obtained to assess for adrenal or ovarian masses, respectively. Importantly, measurement of a basal 17-hydroxyprogesterone serum level should be obtained in the follicular phase of the menstrual cycle, preferably in the morning, to exclude 21-hydroxylase-deficient NCAH (39). In patients suspected of having Cushing's syndrome, it will also include a 24-hour urinary free cortisol level or a cortisol level following an overnight dexamethasone (1.0 mg at 11 pm) test. If the HAIR-AN syndrome is suspected, a basal or preferably a glucose-stimulated insulin level should be obtained. Growth hormone levels should be obtained in...

Clinical And Biochemical Evaluation

Cinomas is similar to that observed in patients with adrenal adenomas. The presence of very high levels of urinary free Cortisol and 17-ketosteroid, or elevated levels of intermediary precursors in the steroid biosynthesis or their metabolites, however, strongly suggests adrenocortical carcinomas.19,20 Tumors secreting multiple hormones, such as cortisol and aldosterone, are usually malignant. Adreno-cortical carcinomas that secrete aldosterone are larger and cause higher blood aldosterone levels and more hypokalemia than the usual small (less than 2 cm) benign aldosteronomas.21,22 Nonfunc-tioning or minimally functioning tumors may be discovered incidentally on ultrasound or computed tomographic (CT) scans performed for unrelated reasons, so-called incidentalomas. Patients with nonfunctional cortical carcinomas, however, usually present with local symptoms, such as pressure, and invasion of contagious structures. Other associated symptoms include unexplained fever, anemia, and weight...

Adrenal Incidentaloma

Incidentalomas comprise a variety of pathologies (Table 12-1). Most incidentalomas are benign cortical adenomas that do not secrete hormones and are termed nonfunctioning tumors. Some tumors, however, are hormonally active and secrete cortisol (Cushing's syndrome), aldosterone (primary hyper-aldosteronism), or catecholamines (pheochromocy-toma). A third group consists of malignant tumors that are either primary adrenocortical carcinomas or metastatic cancers to the adrenal gland. In the workup of incidentalomas, it then becomes important to determine whether the adrenal mass is (1) a functioning or nonfunctioning tumor, (2) a metasta-tic tumor, or (3) an adrenal carcinoma.

Addisonian crisis or acute adrenocortical insufficiency see

A) Cardiac arrest during appendicectomy in a 15-year-old girl responded to cardiac massage, saline, and bicarbonate (Salam & Davies 1974). She was subsequently found to have a normal resting blood cortisol, but no response to adrenal stimulation. f) A patient with severe diarrhoea and vomiting presented with hypotension, tachycardia, and fever (Frederick et al 1991). Despite rehydration and inotropic support on the ITU, he developed acute respiratory distress with hypoxia and died 10 h later. It was later discovered that his brother had primary Addison's disease, and the patient's own plasma cortisol level before death was 2 m gdl-1 (normal

Preoperative Investigations and Preparation for the Procedure

Fasting serum concentration of gastrin, basal acid output off all acid secretory inhibitors for at least 3-7days, secretin test. When indicated, serum concentrations of intact PTH, total or ionized calcium, prolactin, fasting glucose, pancreatic polypeptide, chromogranin A, and serotonin, 24-h urine excretion of free cortisol, and if indicated 5-hydroxyindole acetic acid (HIAA).

Evidence For Monoamine Contributions To Adhdne And 5ht Activity

The results for the 5-HT system are more limited, reflecting in part the methodological issues (see Section 7). However, if one brings the separate findings together, there is an indication of an increase of 5-HT turnover, largely reflecting decreases in 5-HT levels (Table 1). Nonetheless, as with NE, it must be recognized that there will be subgroups, however defined, for which the effects associated with the core symptoms will be masked by other features. One such example is shown by the contrast between ADHD boys brought up in families with or without alcoholic fathers (164). Those with this experience showed a larger cortisol response to a challenge dose of fenfluramine than those without an alcoholic father. This was interpreted as reflecting increased 5-HT receptor sensitivity.

Exposure to Red Tide Planktons

The physiological consequences of the structural changes described above involve both cardiovascular and respiratory systems. Recent work by Ishimatsu and co-workers (Ishimatsu et al., 1990, 1991) with yellowtail corroborates previous data showing a reduction in arterial pH and oxygen tension (POz), with exposure to high densities of red tide plankton. The fall in blood PO2, an increase in ventilatory pulse pressure (Ishimatsu et al., 1990), and a moderate increase in plasma catecholamine concentrations (Tsuchiyama et al., 1992) were the initial changes to C. marina exposure, followed by a relatively stable physiological profile until the final stages of life. After about three hours of exposure, most of the measured variables changed drastically just before death. That stage was characterized by hypoxaemia, hypercapnia, plasma and erythrocytic acidoses, increases in plasma concentrations of Na+, K+, Cl-, Mg2+, Ca2+, bradycardia, and large increases in noradrenaline and adrenaline...

Animal Models of Human Prostate Cancer

Documented in 20-40 of CaP cases 164-166 , Both LNCaP and the CWR22 xenografts bear AR mutations that enable the receptor to be activated by nonandrogenic steroid hormones such as progesterone and estrogen. In addition, in a patient who had failed androgen ablation, it was recently demonstrated that his CaP-cells possessed a mutated AR with altered lig-and affinity. Essentially, the mutant AR functioned as a high-affinity Cortisol receptor, enabling the CaP cells to circumvent the androgen requirement for growth 167 . Another emergent theme is that some hormone refractory cancers have activated the AR signaling pathway through a ligand-independent mechanism. For example, in LAPC-4 cells expressing wild-type AR, the overexpression of Her-2 neu has been shown to activate AR 168 . Not surprisingly, the LAPC-4 xenograft progresses to androgen-independence after androgen ablation and differential gene expression studies reveal a consistent increase in Her-2 neu protein expression in...

Congenital Adrenal Hyperplasia Female Pseudohermaphroditism

Disorder is characterized by a normal 46,XX karyotype. The phenotypic appearance of the patient is due to exposure to excessive endogenous androgens in utero. The amount of virilization can vary from mild clitoral hypertrophy to severe forms where the clitoris resembles a penis. The spectrum of phenotypes is illustrated in Fig. 35.1. This is due to deficiency of one of three enzymes 21-hydroxylase, 11-hydroxylase, or 3-beta hydroxysteroid dehydrogenase. 21-Hydroxy-lase deficiency is seen in 75-91 of patients. The first goal of treatment is to address the steroid deficiencies. Glucocorticoid replacement is given if necessary and patients with the salt-wasting form of the syndrome are given fluorocortisone. Surgery is then advised depending on the amount of virilization present in the external genitalia.

Computed Tomography of ARVCD

Hamada et al. 56 imaged four ARVC D patients who had abnormalities on electrocardiography and angiography using electron bean CT (EBCT). With contrast enhanced volume mode scanning they were able to demonstrate morphologic abnormalities in ARVC D (a) abundant epicardial fat, (b) low attenuation trabeculations, (c) scalloping of RV free wall, and (d) intramyocardial fat deposits. Quantification of ventricular volumes was performed on cine mode scanning, which showed regional dysfunction and depressed global RV function respectively. Tada et al. 57 added ten more ARVC D patients to the above series and compared electron beam CT findings in 16 age-matched, non-ARVC D patients with RV dilation dysfunction with 13 control subjects. Intramyocar-dial fat was defined based on tissue attenuation values. The attenuation value for epicardial adipose tissue is approximately 65 10 Hounsfield units (HU), and 5 to -17 HU for intramyocardial fat, which is far less than that of myocardium. Using the...

Hyposecretion and Hypersecretion

Same Person Different Ages Pictures

Excessive hormone release, called hypersecretion, has multiple causes. Some tumors result in the overgrowth of functional endocrine tissue. A pheochromocytoma (FEE-o-CRO-mo-sy-TOE-muh), for example, is a tumor of the adrenal medulla that secretes excessive amounts of epinephrine and norepinephrine (table 17.8). Some tumors in nonendocrine organs produce hormones. For example, some lung tumors secrete ACTH and thus over-stimulate cortisol secretion by the adrenal gland. While certain autoimmune disorders can cause endocrine hyposecretion, others cause hypersecretion. An example of this is toxic goiter (Graves25 disease), in which autoan- tibodies mimic the effect of TSH on the thyroid, causing thyroid hypersecretion (table 17.8). Endocrine hypersecretion disorders can also be mimicked by excess or long-term clinical administration of hormones such as cortisol.

ApoE4 A case of evolutionary underperformance

Anorectal Malformation Pathophysiology

These multiple screenings led to the identification of several potent apoE-inducing agents. Among the most interesting candidates are 1) indomethacin (Aleong et al. 2003), a potent anti-inflammatory drug used in the past with some success in a placebo-controlled clinical drug trial in mild to moderate AD (Rogers et al. 1993), 2) estrogen (a problematic hormone used recently with disappointing results in elderly women Craig et al. 2005) and 3) cholesterol-lowering drug called probucol (Champagne et al. 2003), the first generation of cholesterol- lowering agents that were used mostly in severe familial hypercholesterolemia (Davignon et al. 1982). We also identified two apoE-reducing agents, 1) cortisol a glucocorticoid hormone associated with stress, known to inhibit synaptogenesis at physiological concentration in vivo and to be markedly up-regulated in MCI subjects (Lupien et al. 1998) , and 2) simvastatin a second-generation cholesterol-lowering drug that can inhibit apoE secretion...

Options for Hormonal Therapy

Another option in hormone therapy is to block the production of androgens, which can be accomplished through the use of oral contraceptives and low-dose glucocorti-coids. This is most commonly used to treat the patient with late-onset congenital adrenal hyperplasia, which is an inherent defect in the 21-hydroxylase or the 11-hydroxylase enzyme. This defect causes a block in the cortisol biosynthetic pathway, which results in a buildup of precursors for potent androgens. Low-dose prednisone (2.5-5 mg a day, at bedtime) is one option. Dexametha-sone can also be used, but the risk of adrenal suppression is higher. To ascertain if the therapy is having the desired effect, the serum DHEAS can be monitored. A decrease or normalization of the blood levels indicates that treatment is successful. To check for adrenal suppression, an ACTH-simulation test can be performed. This consists of injecting ACTH and assessing the plasma cortisol 30 min later. If plasma cortisol has risen by an...

Venous Sinus Obstruction in Pseudotumor Cerebri Syndrome Cause or Effect

Dural Sinus Stenosis Stent

There are various other pathological entities that may be represented in the spectrum of obstructive intrinsic venous sinus lesions. Fat deposits in the dural sinuses on CT was reported by Tokiguchi et al. 173 . These authors reported 8 cases in which macroscopic, non-obstructing fat deposits were demonstrated in the walls of the sinuses. In 5 cases fat was located at the torcular while in 3 it was located in the SSS. Anatomical proof that these lesions did indeed consist of fat was supplied in a later report where 2 of these patients had later undergone autopsy 174 . Finally, nodules of cavernous tissue have been identified in the sinuses, especially at the junction of the straight sinus and vein of Galen 13, 95 . The nodules, distinct from arachnoid granulations, were common at autopsy and were composed of endothelium lined sinusoids resembling erectile tissue.

Anovulation Is A Characteristic Feature Of Pcos. It Manifests As Menstrual Disturbance 80 Amenorrhoea Oligoamenorrhea

Patient With Hyperandrogenism

Weight gain that is primarily centripetal, especially if associated with extremity wasting, purple striae, easy bruisability, moon facies, and rubor, suggests the presence of Cushing's syndrome, and these patients should be appropriately screened using 24-hour urinary-free cortisol levels or a cortisol level following an overnight dexamethasone suppression test. Other information that should be sought includes the patient's awareness of her body fat distribution, as women with PCOS have a greater prevalence of abdominal obesity (29). Weight gain may also be associated with carbohydrate craving and evidence of postprandial reactive hypoglycemia, particularly in mid-afternoons. For example, Holte and colleagues found that although insulin resistance in obese women with PCOS was reduced by weight loss to similar levels as BMI-matched controls, these patients continued to demonstrate an increased early insulin response to glucose, which could stimulate appetite and persistent weight gain...

Review of Key Concepts

Hunger is suppressed by leptin, cholecystokinin, and neurons called glucostats, and is briefly inhibited even by chewing and swallowing. Hunger is stimulated by endocannabinoids, neuropeptide Y, and the hunger contractions of an empty stomach. 4. The postabsorptive state is regulated by multiple hormones. Glucagon, epinephrine, and norepinephrine promote lipolysis, glycogenolysis cortisol promotes fat and protein catabolism cortisol and glucagon promote gluconeogenesis and growth hormone raises blood glucose by antagonizing insulin.

Anterior Pituitary Tumorsnance imaging MRI with gadolinium contrast of

Sella, basal GH, prolactin, and urine free cortisol. by pituitary tumors associated with MEN type I The diagnosis of Cushing's syndrome is made by include GH, GH-prolactin, and ACTH (Figure increased glucocorticoid levels (increased 24-hour 16-5). Rarer tumors associated with MEN type I urine cortisol excretion) or diminished response of include luteinizing hormone feedback. The feedback is most coming hormone (FSH), thyroid-stimulating hormone monly assessed by the overnight dexamethasone (TSH), and nonsecreting adenomas. Patients present suppression test (dexamethasone 1 mg orally at with symptoms and signs secondary to mass effect 11 00 pm should normally suppress cortisol to (headache, visual field loss), hypopituitarism, 5 p,g dL at 8 00 am). The differential diagnosis and or excessive hormone production. includes pituitary-dependent ACTH excess (ade-The evaluation for pituitary tumors includes a noma or hyperplasia), ectopic ACTH from bronchial history of reproductive function...

General Risk Factors for Infectious Diseases in Intensive Aquaculture and Relationship to Noninfectious Disorders

That increased plasma cortisol can increase susceptibility to Hitra disease. However, predicting the effect of management events and non-infectious diseases on resistance to infectious disease, by the use of surrogate physiological indices, is still in its infancy and many conflicting reports exist. For example, during some instances of acute and chronic stress, plasma cortisol levels can recover, but secondary stress responses such as the leucocrit can remain affected (Flos et al., 1988 Pickering and Pottinger, 1989 Maule and Schreck, 1990 Pickering, 1992).

Regulation of the Postabsorptive State

The sympathoadrenal system also promotes glycogenolysis and lipolysis, especially under conditions of injury, fear, anger, and other forms of stress. Adipose tissue is richly innervated by the sympathetic nervous system, while adipocytes, hepatocytes, and muscle cells also respond to epinephrine from the adrenal medulla. In circumstances where there is likely to be tissue injury and a need for repair, the sympathoadrenal system therefore mobilizes stored energy reserves and makes them available to meet the demands of tissue repair. Stress also stimulates the release of cortisol, which promotes fat and protein catabolism and gluconeogenesis (see chapter 17, p. 664).

Hypothalamic and pituitary hormones

The function that prolactin plays in the stallion is unclear. In other animals, prolactin is associated with the function of the accessory glands and Leidig cells, enhancing the effect of LH on spermatogenesis. Such an association has not been found as yet in the stallion, though treatment with bromocriptine is reported to decrease the volume of seminal plasma, and a link has been established between sexual activity, and elevated concentrations of prolactin and cortisol (Nett, 1993 Thomson et al., 1996).

Anti Inflammatory Drugs

Cortisol and corticosterone are used as steroidal anti-inflammatory drugs (SAIDs). They inhibit inflammation by blocking the release of arachidonic acid from the plasma membrane, thus inhibiting the synthesis of all eicosanoids. Their main disadvantage is that prolonged use causes side effects that mimic Cushing syndrome (see p. 668). Aspirin and ibuprofen (Motrin) are nonsteroidal anti-inflammatory drugs (NSAIDs) with more selective effects. They stop the action of cyclooxy-genase, thus blocking prostaglandin synthesis without affecting lipoxygenase or the leukotrienes. For similar reasons, aspirin inhibits blood clotting (see chapter 18). One theory of fever is that it results from the action of prostaglandins on the hypothalamus. Most antipyretic (fever-reducing) drugs work by inhibiting cyclooxygenase.

Androgens and Sebum Production

Acne Vulgaris

Androgen Metabolism within the Skin Dehydroepiandrosterone sulfate (DHEAS) is produced in large quantities by the zona reticularis of the adrenal gland. It circulates in the bloodstream in high levels in relatively high levels compared to other hormones with the exception of cortisol. The enzyme 3P-hydroxyste-roid dehydrogenase (3P-HSD) acts on DHEA to convert it to androstenedione (fig. 1). This conversion may take place in the adrenal gland and tissues such as the sebaceous gland where activity of the 3P-HSD enzyme has been identified by several investigators 16-18 . There are two known forms or isozymes of 3P-HSD. The type I iso-zyme is active in skin, placenta and mammary tissue, whereas the type II isozyme is active in the adrenal gland and the gonads 19 . The major isozymes of steroid-metabolizing enzymes that are active in human sebaceous glands are listed in table 1. Another important enzyme that is found within the skin is 17P-hydroxysteroid dehydrogenase (17P-HSD). This is a...

Hormones And The Emergence Of Endocrinology

During the turbulent years leading up to and following World War II, the major question was whether only ovarian hormones such as progesterone and estrogen were the inducers and controllers of normal breast growth or were there other elements Lyons, in 1958, clearly defined the minimal hormonal growth requirements for normal mammary development in mice as being estrogen, adrenocortical steroids, growth hormone, and cortisol (Lyons, 1958 Lyons et al., 1958). Muhlbock in the Netherlands was particularly interested in the role of the pituitary in mammary gland physiology (Dux and Muhlbock, 1969a,b Muhlbock, 1956).

Subclinical Cushings Syndrome

Preclinical or subclinical Cushing's syndrome is caused by autonomous glucocorticoid secretion in patients who may have no overt, or only minimal, clinical signs and symptoms of full-blown Cushing's syndrome. Subclinical hypercortisolism has been reported in 5 to 20 of patients with adrenal inci-dentalomas. Depending on the amount of glucocor-ticoid secreted by the tumor, the clinical spectrum can vary considerably. Diagnostically, patients often have a slightly attenuated diurnal rhythm of cortisol secretion. They may also have a suppressed contralateral adrenal gland. Removing the hypersecret-ing adrenal gland, even without removing the normal gland, may result in life-threatening acute adrenal insufficiency. The natural history of this condition is unclear because long-term prospective studies are lacking. Subclinical Cushing's syndrome may progress to overt Cushing's syndrome. Some patients with subclinical Cushing's syndrome have subtle biochemical abnormalities that are reversed...

Maintenance of the Body

Fat storage can be regarded as another important maintenance mechanism. In natural environments, the supply of food fluctuates. When it is abundant, some is stored in the form of fat. This is then used up in times of scarcity. Clearly this adaptation benefits survival in harsh or stressful environments. Unfortunately it has bad consequences in any environment where food is always plentiful. In this case fat keeps being added to the body and obesity results. This is an unusual example of a maintenance mechanism failing in an artificial man-made environment, whereas it is effective in a natural environment. Human obesity commonly leads to late-onset diabetes with all its physiological complications, and puts additional stress on the vascular system. Fat storage

Metformin Weight Loss and PCOS

High concentrations of serum LH in the follicular phase are associated with PCOS and with decreased reproductive function (22). Tonic hypersecretion of LH appears to induce premature oocyte maturation, causing problems with fertilization and miscarriage. Van Dam et al. (23) noted that 7 days of calorie restriction on a very-low-calorie diet (VLCD) (471 kcal day) paradoxically increased basal and pulsatile LH secretion, despite reductions in plasma glucose, insulin, leptin, and testosterone concentrations, which decreased by 18, 75, 50, and 23 , respectively. Serum estrone, estradiol, SHBG, and androstenedione concentrations remained unchanged.

Problems Associated with Seawater Transfer

Gill Lamella

The smolt transfer period presents several opportunities for preventing pathogen transfer between companies, and between environments. For example, post-transfer outbreaks of furunculosis are assumed to reflect recrudescence of this bacterial pathogen in carrier smolt, which are stressed by the transfer process. Although generally regarded to be a freshwater protozoal disease, costiasis is also reported in post-transfer smolt (Fig. 12.15) (Ellis and Wooten, 1978 Urawa, 1993). Accordingly, programmes of health checks, stress tests (with cortisol and temperature elevation), saltwater challenges, chemical baths and vaccinations, are used to uncover, treat, or prevent diseases which could affect fish post-transfer. Paradoxically, multiple management events close to the smolt window may not always be beneficial. Treatment chemicals may have increased toxicity (either immediate effects or affecting ability to accommodate seawater challenge) to salmonids during the smolt window because of...

Organ And Tissue Indicators Composition of Blood

Changes in plasma hormone concentrations are widely employed as indicators of the physiological condition of fish. Changes in the levels of hormones associated with reproduction are useful indicators of impaired reproductive function (see above). 'Stress' hormones, such as cortisol, are commonly used as indicators of acute or chronic responses to environmental stressors (see Chapter 11). In addition, hormones that are involved in the regulation of metabolic functions may also lend themselves to diagnostic assessment. For example, in some fishes, a reduction in food consumption (either enforced or by choice) is followed, within a few hours, by a reduction in the production of the thyroid hormone triiodo-L-thyronine (T3), and thus in a fall in blood T3 content (Farbridge et al., 1992 Leatherland and Farbridge, 1992). We have, therefore, employed commercially available assays to measure plasma T3 concentration to assess the nutritional condition of fish species held in culture (e.g....

Adipocyte Dysfunction And Insulin Resistance

Figure 4.6 CD68+ macrophages in human white adipose tissue. A hypertrophic adipocyte is surrounded by macrophages. Adipose tissue recruits macrophages for reasons that are not entirely clear. However, the local inflammatory milieu is thought to (a) increase adipocyte lipolysis as cytokines downregulate insulin signaling and (b) change the secretion of adipokines such as leptin and adiponectin. Photomicrograph courtesy of Barbara Kozak, PhD Figure 4.6 CD68+ macrophages in human white adipose tissue. A hypertrophic adipocyte is surrounded by macrophages. Adipose tissue recruits macrophages for reasons that are not entirely clear. However, the local inflammatory milieu is thought to (a) increase adipocyte lipolysis as cytokines downregulate insulin signaling and (b) change the secretion of adipokines such as leptin and adiponectin. Photomicrograph courtesy of Barbara Kozak, PhD our understanding of fat and carbohydrate metabolism and their interaction. In particular, a large body of...

Documenting Support Group Processes

There is no dearth of hypotheses about the mediating processes or mechanisms at work in support groups. Biological pathways include alterations in immune system function, blood pressure, and urinary cortisol, whereas behavioral changes range from improved adherence to recommended dietary and drug regimens to changes in modes of coping, including the use of community services. The psychological factors that have been cited most frequently as potential mediators include the 10 listed at the bottom of Table I. At present, little is understood about the complex ways in which psychological, biological, and behavioral changes interact to produce durable and important outcomes such as the improvements in mood and survival of the cancer patients who were involved in the support groups organized by Spiegel, Bloom, Kraemer, and Gottheil in 1989.

Colostrum and Milk Synthesis

Milk synthesis is promoted by prolactin, a hormone of the anterior pituitary gland. In the nonpregnant state, dopamine ( prolactin-inhibiting hormone) from the hypothalamus inhibits prolactin secretion. Prolactin secretion begins 5 weeks into the pregnancy, and by full term it is 10 to 20 times its normal level. Even so, prolactin has little effect on the mammary glands until after birth. While the steroids of pregnancy prepare the mammary glands for lactation, they antagonize prolactin and suppress milk synthesis. When the placenta is discharged at birth, the steroid levels abruptly drop and allow prolactin to have a stronger effect. Milk is synthesized in increasing quantity over the following week. Milk synthesis also requires the action of growth hormone, cortisol, insulin, and parathyroid hormone to mobilize the necessary amino acids, fatty acids, glucose, and calcium.

Anterior Lobe Hormones

ACTH is secreted by pituitary cells called corticotropes. ACTH stimulates the adrenal cortex to secrete its hormones (corticosteroids), especially cortisol, which regulates glucose, fat, and protein metabolism. ACTH plays a central role in the body's response to stress, which we will examine more fully later in this chapter.

How are MS attacks treated Why are there different drugs to treat attacks of MS

ACTH (or corticotrophin) is a hormone that is made in the brain and is stored in the pituitary gland, which is situated at the base of the brain. This hormone is normally released in miniscule amounts during the early hours of the morning to stimulate the adrenal glands' production of steroid hormones. Cortisol, the active form of cortisone, is one product of ACTH stimulation. Dr. Leo Alexander began using ACTH a half-century ago at Harvard Medical School. He showed in a series of studies that it speeded recovery from MS attacks. Later, a national study, published in 1970, proved that it did indeed significantly speed the recovery for patients with acute exacerbations of MS. glands secrete steroid hormones that are important in the body's response to stress. Cortisol the stored form of cortisol produced by the adrenal cortex.

Background On Polycystic Ovarian Syndrome Among Adolacents

The mechanism for the growth and development of the zona reticularis during the transition from childhood to adulthood has yet to be determined. The increased production of adrenal androgens is not attributable to any increases in circulating levels of adrenocorticotropic hormone (ACTH) and is not accompanied by alterations in cortisol levels. Although the existence of an adrenal androgen-stimulating hormone has been postulated, no factor has yet been identified that satisfies the expectations for such a substance. It is likely that acute and chronic regulation of steroid secretion in the zona reticularis is dependent on pituitary ACTH, and the functional phenotype (downregulation of 3P-HSD, but enhanced expression of CYP17, cytochrome b5, and hydroxysteroid sulfotransferase) of The adrenals and ovaries contribute variably to the circulating levels of androgens in adult women (15). Generally, it is thought that A4 is derived in roughly equal amounts from the ovary and the adrenal,...

Catecholamine Biosynthesis And Catabolism

Norepinephrine in storage vesicles can diffuse into the cytoplasm. In certain cells (particularly the adrenal medulla), norepinephrine is converted to epinephrine in the cytoplasm, catalyzed by (PNMT). (Once formed, epinephrine may then return to the vesicle, diffuse from the cell, or undergo catabo-lism.) The expression of PNMT is enhanced by cortisol, which is present in high concentrations in areas of the adrenal medulla, owing to venous blood flow from the adjacent adrenal cortex. This accounts for the fact that, in the normal human adrenal medulla, about 80 of the catecholamine content is epinephrine, whereas only 20 is norepinephrine. Serum epinephrine concentrations fall dramatically after resection of both normal adrenals, whereas norepi-nephrine concentrations do not decline.1

Figure 210

Mechanism of aldosterone action in the distal nephron 19 . Aldosterone, the predominant human mineralocorticoid hormone, enters distal nephron cells through the plasma membrane and interacts with its receptor (the mineralocorticoid receptor MR , or Type I receptor). Interaction between aldosterone and this receptor initiates induction of new proteins that, by way of mechanisms that remain unclear, increase the number of sodium channels (ENaC) and sodium-potassium adenosine triphosphatase (Na-K ATPase) pumps at the cell surface. This increases transepithelial Na (and potassium) transport. Cortisol, the predominant human glucocorticoid hormone, also enters cells through the plasma membrane and interacts with its receptor (the glucocorticoid receptor GR ). Cortisol, however, also interacts with mineralocorticoid receptors the affinity of cortisol and aldos-terone for mineralocorticoid receptors is approximately equal. In distal nephron cells, this interaction also stimulates electrogenic...


The central role of StAR was proven by two observations. First, robust steroid hormone synthesis follows co-transfection of StAR and the cholesterol side-chain cleavage system into nonsteroidogenic COS-1 cells (3,4). Second, patients with mutations of StAR have congenital lipoid adrenal hyperplasia, in which all adrenal and gonadal steroidogenesis is disrupted (4,5). Thus, StAR is needed for the rapid flux of cholesterol from the outer to inner mitochondrial membrane to facilitate acute synthesis of aldosterone following angiotensin II stimulation, of cortisol following ACTH stimulation, and of gonadal sex steroids following LH stimulation. Steroidogenic enzymes fall into two broad categories the cytochrome P450 enzymes and the hydroxysteroid dehydrogenases (1). Cytochrome P450 includes a large group of enzymes containing about 500 amino acids and a single heme group their name derives from the characteristic absorption peak at 450 nm. There are two classes of P450 enzymes. Type I...

Figure 316

Mechanism of hypokalemia in the syndrome of apparent mineralo-corticoid excess (AME). Cortisol and aldosterone have equal affinity for the intracellular mineralocorticoid receptor (MR) however, in aldosterone-sensitive tissues such as the kidney, the enzyme 11 p-hydroxysteroid dehydrogenase (11 p-HSD) converts cortisol to cortisone. Since cortisone has a low affinity for the MR, the enzyme 11 p-HSD serves to protect the kidney from the effects of glucocorticoids. In hereditary or acquired AME, 11 p-HSD is defective or is inactiveted (by licorice or carbenoxalone). Cortisol, which is present at concentrations approximately 1000-fold that of aldosterone, becomes a mineralocorticoid. The hypermineralo-corticoid state results in increased transcription of subunits of the sodium channel and the Na+-K+-ATPase pump. The favorable electrochemical gradient then favors potassium secretion 7,15 .


Its development include the magnitude and time course of the hypercapnia, severity of the acidemia, and degree of attendant hypoxemia. Progressive narcosis and coma may occur in patients receiving uncontrolled oxygen therapy in whom levels of arterial carbon dioxide tension (PaCO2) may reach or exceed 100 mm Hg. The hemodynamic consequences of carbon dioxide retention reflect several mechanisms, including direct impairment of myocardial contractility, systemic vasodila-tion caused by direct relaxation of vascular smooth muscle, sympathetic stimulation, and acidosis-induced blunting of receptor responsiveness to catecholamines. The net effect is dilation of systemic vessels, including the cerebral circulation whereas vasoconstriction might develop in the pulmonary and renal circulations. Salt and water retention commonly occur in chronic hypercapnia, especially in the presence of cor pulmonale. Mechanisms at play include hypercapnia-induced stimulation of the...


Adrenal and gonadal maturation are not functionally interdependent. In adult women, the adrenals and ovaries contribute variably to the circulating levels of androgens, although in general A4 is derived in roughly equal amounts from the ovary and the adrenal, whereas testosterone is derived approximately 25 from the adrenal, 25 from the ovary, and 50 from the peripheral conversion of A4. DHT is produced in peripheral tissues from testosterone and circulates at levels of about one-third to one-half that of testosterone. DHEA and DHEAS are almost exclusively of adrenal origin. DHEA is secreted in a pulsatile manner and demonstrates a diurnal rhythm that is similar to that of cortisol in young women.

Figure 622

Role of insulin deficiency and the counter-regulatory hormones, and their respective sites of action, in the pathogenesis of hyper-glycemia and ketosis in diabetic ketoacido-sis (DKA).A, Metabolic processes affected by insulin deficiency, on the one hand, and excess of glucagon, cortisol, epinephrine, norepinephrine, and growth hormone, on the other. B, The roles of the adipose tissue, liver, skeletal muscle, and kidney in the pathogenesis of hyperglycemia and ketone-mia. Impairment of glucose oxidation in most tissues and excessive hepatic production of glucose are the main determinants of hyperglycemia. Excessive counterregula-tion and the prevailing hypertonicity, metabolic acidosis, and electrolyte imbalance superimpose a state of insulin resistance. Prerenal azotemia caused by volume depletion can contribute significantly to severe hyperglycemia. Increased hepatic production of ketones and their reduced utilization by peripheral tissues account for the ketonemia typically...

Figure 1218

And the basolateral sodium-potassium adenosine triphosphatase (Na-K ATPase). Sodium moves from the lumen into the cell and down its electrochemical gradient, thus generating a lumen-negative transepithelial voltage that drives potassium secretion from the principal cells and hydrogen secretion from the intercalated cells. The type I mineralocorticoid receptor (MR) is nonspecific and can bind both aldosterone and cortisol, but not cortisone. The selective receptor specificity for aldosterone is mediated by the kidney isoform of the enzyme, 11- 3-hydroxysteroid dehydrogenase, which oxidizes intracellular cortisol to its metabolite cortisone. Three hypertensive syndromes, glucocorticoid-remedial aldostero-nism (GRA), Liddle's syndrome, and apparent mineralocorticoid excess (AME), share a common clinical phenotype that is characterized by normal physical examinations, hypokalemia, and very low plasma renin activity. The molecular defect in GRA derives from an unequal crossover event...

Figure 421

Adrenal Cushing's syndrome typically is caused by a solitary adrenal adenoma (rarely by carcinoma) producing excessive amounts of cortisol autonomously. The increased levels of cortisol feed back to suppress release of adrenocorticotropic hormone (ACTH) and corticotropin-releasing factor. The finding of very low ACTH levels in the face of elevated cortisol values and a loss of the circadian pattern of cortisol confirm the diagnosis (see Fig. 4-4). Additional anatomic studies of the adrenal (computed tomographic scan and magnetic resonance imaging) usually disclose the source of excessive cortisol production. Surgical removal usually is effective. iCTH Cortisol iCTH Cortisol

Figure 419

Corticotropin-releasing factor (CRF) acts to stimulate the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary. ACTH then stimulates the adrenal zona fasciculata and zona reticularis to synthesize and release cortisol (see Figs. 4-2 and 4-3). The increased levels of cortisol feed back to suppress additional release of ACTH. As shown in Figure 4-4, ACTH and cortisol have circadian patterns.

Figure 420

Pituitary Cushing's disease results from excessive production of adrenocorticotropic hormone (ACTH), typically owing to a benign adenoma. Excess ACTH stimulates both adrenals to produce excessive amounts of cortisol and results in bilateral adrenal hyperplasia. The increased cortisol production does not suppress ACTH release, however, because the pituitary tumor is unresponsive to the normal feedback suppression of increased cortisol levels. The diagnosis usually is made by demonstration of elevated levels of ACTH in the face of elevated cortisol levels, particularly in the afternoon or evening, representing loss of the normal circadian rhythm (see Fig. 4-4). Radiographic studies of the pituitary (computed tomographic scan and magnetic resonance imaging) will likely demonstrate the source of increased ACTH production. When the pituitary is the source, surgery and irradiation are therapeutic options.

Figure 44

Circadian rhythmicity of steroid production and major stimulatory factors. Aldosterone and cortisol and their respective major stimulatory factors, plasma renin activity (PRA) and adrenocorticotropic hormone (ACTH), demonstrate circadian rhythms. The lowest values for all of these components are normally seen during the sleep period when the need for active steroid production is minimal. ACTH levels increase early before awakening, stimulating cortisol production in preparation for the physiologic changes associated with arousal. PRA increases abruptly with the assumption of the upright posture, followed by an increase in aldosterone production and release. Both steroids demonstrate their highest values through the morning and early afternoon. Cortisol levels parallel those of ACTH, with a marked decline in the afternoon and evening hours. Aldosterone demonstrates a broader peak, reflecting the postural stimulus of PRA.

Figure 423

Screening tests for Cushing's syndrome. Whereas elevated evening plasma cortisol levels typically indicate abnormal circadian rhythm, other factors such as stress also can cause increased levels late in the day. Urinary levels of 17-hydroxy corticosteroids may be increased in association with obesity. In such cases, repeat measurement after a period of dexamethasone suppression may be required to distinguish this form of increased glucocorticoid excretion from Cushing's syndrome. The measurement of urinary-free cortisol is the most sensitive and specific screening test.

Figure 48

Localizing tests for primary aldosteronism. Adrenal venous blood sampling with determination of both aldosterone and Cortisol concentrations during adrenocorticotropic hormone stimulation provides the most accurate way to identify unilateral hyperaldos-teronism. This approach minimizes artefact owing to episodic steroid secretion and to permit correction for dilution of adrenal venous blood with comparison of values to those in the inferior vena cava. (see Fig. 4-12). (Data from Weinberger and coworkers 3 .)

Figure 415

Humoral changes in glucocorticoid-remediable aldosteronism with dexamethasone. A-E, Depicted are the changes in plasma cortisol (panel A), urinary aldosterone (panelB), plasma renin activity (PRA) (panel C), plasma aldosterone (panel D), and serum potassium (panel E) before and after dexamethasone administration in the patients in Figure 4-14. Note that before dexamethasone administration, serum cortisol was in the normal range and was markedly suppressed after treatment. Urinary aldosterone was completely normal and plasma aldosterone was

Figure 424

In pituitary Cushing's disease and ectopic forms of Cushing's syndrome, elevated values are observed, especially in the afternoon and evening. The next step in differentiation is an anatomic evaluation of the pituitary. When no abnormality is found, the next step is a search for a malignancy, typically in the lung. The finding of low ACTH levels points to the adrenal as the source of excessive cortisol production, and anatomic studies of the adrenal are indicated. CT computed tomography MRI magnetic resonance imaging.

PHsd Isozymes

Two 11p-HSD isozymes have been identified, 11p-HSD1 and 11p-HSD2 15,16 . 11p-HSD2 is a nicotinamide adenine dinucleotide (NAD) dependent dehydrogenase that catalyzes the reverse reaction of 11p-HSD1 to inactivate cortisol to cortisone 17 . 11p-HSD2 is mainly localized in mineralocorticoid receptor (MR) target tissues such as kidney, colon, and salivary gland. The function of 11 p-HSD2 is critical for protecting the MR from excessive exposure to cortisol and ensuring the normal activity of MR ligand aldosterone. 11 p-HSD2 inhibition by genetic mutations or 18p-glycyrrhetinic acid, the active component of licorice, leads to sodium retention and hypertension 18-20 . Although 11p-HSD1 and 11p-HSD2 are isozymes in terms of their biological function, they share only 16 sequence homology 17 . The structural diversity between the two enzymes provides the potential to develop 11p-HSD1 selective inhibitors. Recent studies have identified several classes of potent, highly specific compounds...

Endocrine Regulation

The prostate is dependent on testicular-derived testosterone despite the presence of the 3p-hydroxysteroid dehydrogenase-a5-a4 isomerase complex,160 the prostate has not been reported to synthesize testosterone de novo. It can reversibly metabolize testosterone to androstenedione (17P-hydroxysteroid dehydrogenase161) and, possibly irreversibly, to estrogens (see below). The prostate's primary metabolite of testosterone is dihydrotestosterone (DHT), an irreversible reaction catalyzed by 5 a-reductase.162 This is a more potent ligand for the androgen receptor than is testosterone, as it binds the receptor with greater affinity, enhances translocation from the cytoplasm to the nucleus, and is more effective in activating many androgen-response elements.163,164 Following 5 a-reduction, DHT and androstanedione are further metabolized by 3a p -hydroxysteroid dehydrogenase to 5 a-androstane-3a p-17P-diol and androsterone.165,166 The reader is referred to the work of Amann and colleagues167...


There are multiple hypotheses on the regulation of hunger and body weight, and they are not mutually exclusive. According to the glucostat hypothesis, the satiety center has neurons called glucostats that rapidly absorb glucose after a meal and send inhibitory signals to the feeding center, thus temporarily suppressing the appetite. According to the lipostat hypothesis, adipocytes secrete a protein hormone called leptin.3 The greater the body's fat stores, the more leptin is secreted. Leptin reduces food intake, partly by inhibiting the synthesis of an appetite stimulant called neuropeptide Y. It also inhibits the storage of additional fat and thus reduces the amount of weight gained for a given caloric intake (see insight 26.1). A reduction in body fat lowers leptin levels, so there is less to suppress the appetite and food intake increases, returning the body weight toward a hereditary set point. Another family of appetite stimulants is the endo-cannabinoids. The...


Adipose tissue is now recognized as an endocrine tissue secreting a series of hormones and regulators such as leptin, adiponectin and TNF-a (Matsuzawa, 2004). NIH 3T3-L1 cells were often used as an adipocyte model, and confluent NIH 3T3 cells (non-adipocytes) were differentiated into adipocytes by the definite stimulation. AM secretion rates from pre-adipocyte and adipocyte were 3.77 and 1.51


Improved expression and decreased liver toxicity has also been observed following gene transfer with an HC-Ad vector expressing the murine leptin cDNA from the human cytomegalovirus (HCMV) promoter 29 . Leptin is a potent modulator of weight and food intake. In leptin-deficient ob ob mice, daily delivery of recombinant leptin protein suppresses appetite, induces weight reduction, and decreases blood insulin and glucose levels. Results from gene transfer experiments with a first-generation vector suggested that delivery of the leptin cDNA might provide therapeutic benefit equivalent to daily leptin protein treatment. However, the effects were only transient in both lean and ob ob mice due to the loss of DNA and due to significant inflammatory changes in liver. Using an HC-Ad vector carrying the same expression cassette, leptin expression and physiological consequences were analyzed following gene transfer. In lean mice, tail vein injection of 1-2 x 1011 particles of the HC-Ad vector...


Negative studies have also been published concerning IGF-1, IGF-1 receptor. IGFBP1, IGFBP3. Leydig insulin-like protein 3. SORBS1, IGF-2 receptor, and PTP1B. Negative linkage and association studies of genes relating to obesity and fuel metabolism in PCOS have been published concerning leptin and leptin receptor, glucocorticoid receptor, glycogen synthase, melanocortin 4 receptor, proopiomelanocortin, and uncoupling proteins 2 and 3. PCOS. polycystic ovary syndrome VNTR, variable number tandem repeat SNP, single nucleotide polymorphism.


Testosterone (ET ratio) in both men and women. Young women naturally have a high estrogen testosterone ratio (a lot of estrogen, very little testosterone), whereas young men have a low estrogen testosterone ratio (very little estrogen, a lot of testosterone). Estrogen levels drop dramatically in women after menopause, and men show a similar decline in the level of testosterone at a corresponding age. As a consequence, men and women approach a similar ET ratio throughout their sixth to ninth decades, a condition that is thought to influence the rate at which genetic instability occurs. In addition, many scientists believe the shift in the ET ratio is largely responsible for the weakening of the human immune system, leading to the increased occurrence not only of cancer but of many other diseases as well.

MR Imaging of ARVCD

Casolo et al. 12 were the first to describe the use of MR imaging to assess ARVC D in 1987. They demonstrated intramyocardial fat deposits in the RV on conventional spin echo imaging. Since that time several authors including our group have reported MR abnormalities in ARVC D 17-26 . Broadly, MR imaging abnormalities in ARVC D can be grouped into two major categories (1) morphological abnormalities, and (2) functional abnormalities. Morphologic abnormalities include intramyocardial fat deposits, focal wall thinning, wall hypertrophy, trabecular disarray, and RV outflow tract enlargement. Functional abnormalities include regional contraction abnormalities,


We need to eat to live and for most people the feeling of hunger is a regular and very familiar occurrence. But the mechanisms that control hunger are a very complex mixture of the physiological and the psychological. There is the intake of necessary energy in the form of calories and there are fat deposits and general metabolic rate. There are also external, psychologically mediated factors such as the sight or the smell of a favourite food. This might well tempt us to eat even though we have recently eaten.

Predisposing factors

Richards and Pickering (1978) noted that fungal lesions were common on the dorsum in mature males and on the caudal fin in mature females. The activation of the pituitary-interrenal axis in teleosts is recognized as an almost ubiquitous component of the response to many different factors, most of which are considered stress related (Pickering, 1981). An increase in circulating corticosteroids has been used to assess the importance of the stress response in fish with Saprolegnia infection (Pickering and Duston, 1983). Prolonged oral administration of cortisol or natural increases in this hormone resulted in a marked increase in the susceptibility of the fish to fungal infection. However, their plasma cortisol levels were within the levels capable of being produced by fish under natural stress (Pickering and Pottinger, 1985). Several authors have reported the immunosuppressive role of raised cortisol in salmonids (Pickering and Pottinger, 1985 Bennett and Wolke, 1987). A chronic...

Prepubertal Acne

Adrenarche presents with high levels of DHEA and DHEAS that start rising at 6-7 years in girls and 7-8 years in boys and follow increasing during mid puberty. Excessive androgen production may result due to adrenal hyperandrogenism (exaggerated adrenarche, exuberant production of adrenal androgens relative to cortisol), congenital adrenal hyperplasia, Cushing's disease, 21-hyroxy-lase deficiency, and more rarely androgen producing tumors. Ovarian contribution to androgens can be through tumors (malignant and benign), but most commonly due to polycystic ovarian disease associated very often with obesity, persistent or resistant acne and insulin resistance 3, 12 .

Adrenal Disorders

Cushing26 syndrome is excess cortisol secretion owing to any of several causes ACTH hypersecretion by the pituitary, ACTH-secreting tumors, or hyperactivity of the adrenal cortex independently of ACTH. Cushing syndrome disrupts carbohydrate and protein metabolism, leading to hyperglycemia, hypertension, muscular weakness, and edema. Muscle and bone mass are lost rapidly as protein is catabolized. Some patients exhibit abnormal fat deposition between the shoulders ( buffalo hump ) or in the face ( moon face ) (fig. 17.26). Long-term hydrocortisone therapy can have similar effects.

Nuclear Receptors

Sec Nursing Colge Anm

Recent advances in imaging techniques, allowing for in vivo monitoring of protein trafficking within live cells, have made it possible to study the events following the binding of hormones to their receptors. These events are described in Sec. 6.2.1 with the example of the hormone cortisol and its receptors, but the characteristics of the cortisol-receptor interactions can be generalized to other steroid and nuclear hormone receptors. Overall, there have been at least 48 nuclear receptors identified in the human genome. They are classified into type I or type II receptors according to their mechanism of action, or subdivided into seven subfamilies based on their amino acid sequence. The subfamilies include receptors for steroid hormones such as cortisol and receptors that are activated by nonsteroidal compounds such as retinoids, thyroid hormones, and vitamin D. Many of the nuclear receptors are still known as orphan receptors, because their in vivo ligands are not yet identified....

Hormone Transport

Thyroid hormone binds to three transport proteins in the blood plasma albumin, an albumin-like protein called thyretin, and an a-globulin named thyroxine-binding globulin (TBG). TBG binds the greatest amount. About 99.8 of T3 and 99.98 of T4 are protein-bound. Bound TH serves as a long-lasting blood reservoir, so even if the thyroid is surgically removed (as for cancer surgery), no signs of TH deficiency appear for about 2 weeks. Steroid hormones bind to globulins such as transcortin, the transport protein for cortisol. Aldosterone is unusual. It has no specific transport protein, but binds weakly to albumin and others. However, 85 of it remains unbound, and correspondingly, it has a half-life of only 20 minutes.

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