Adrenocortical Hyperfunction: Excess production of ADRENAL CORTEX HORMONES such as ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and/or ANDROSTENEDIONE. Hyperadrenal syndromes include CUSHING SYNDROME; HYPERALDOSTERONISM; and VIRILISM.Adrenocortical Carcinoma: A malignant neoplasm of the ADRENAL CORTEX. Adrenocortical carcinomas are unencapsulated anaplastic (ANAPLASIA) masses sometimes exceeding 20 cm or 200 g. They are more likely to be functional than nonfunctional, and produce ADRENAL CORTEX HORMONES that may result in hypercortisolism (CUSHING SYNDROME); HYPERALDOSTERONISM; and/or VIRILISM.Adrenal Cortex Neoplasms: Tumors or cancers of the ADRENAL CORTEX.Laryngeal Muscles: The striated muscle groups which move the LARYNX as a whole or its parts, such as altering tension of the VOCAL CORDS, or size of the slit (RIMA GLOTTIDIS).Dysphonia: Difficulty and/or pain in PHONATION or speaking.Voice Training: A variety of techniques used to help individuals utilize their voice for various purposes and with minimal use of muscle energy.Voice Disorders: Pathological processes that affect voice production, usually involving VOCAL CORDS and the LARYNGEAL MUCOSA. Voice disorders can be caused by organic (anatomical), or functional (emotional or psychological) factors leading to DYSPHONIA; APHONIA; and defects in VOICE QUALITY, loudness, and pitch.Phonation: The process of producing vocal sounds by means of VOCAL CORDS vibrating in an expiratory blast of air.Adrenocortical Adenoma: A benign neoplasm of the ADRENAL CORTEX. It is characterized by a well-defined nodular lesion, usually less than 2.5 cm. Most adrenocortical adenomas are nonfunctional. The functional ones are yellow and contain LIPIDS. Depending on the cell type or cortical zone involved, they may produce ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and/or ANDROSTENEDIONE.Adrenal Cortex: The outer layer of the adrenal gland. It is derived from MESODERM and comprised of three zones (outer ZONA GLOMERULOSA, middle ZONA FASCICULATA, and inner ZONA RETICULARIS) with each producing various steroids preferentially, such as ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and ANDROSTENEDIONE. Adrenal cortex function is regulated by pituitary ADRENOCORTICOTROPIN.Voice Quality: That component of SPEECH which gives the primary distinction to a given speaker's VOICE when pitch and loudness are excluded. It involves both phonatory and resonatory characteristics. Some of the descriptions of voice quality are harshness, breathiness and nasality.Fibrous Dysplasia, Polyostotic: FIBROUS DYSPLASIA OF BONE affecting several bones. When melanotic pigmentation (CAFE-AU-LAIT SPOTS) and multiple endocrine hyperfunction are additionally associated it is referred to as Albright syndrome.Vocal Cords: A pair of cone-shaped elastic mucous membrane projecting from the laryngeal wall and forming a narrow slit between them. Each contains a thickened free edge (vocal ligament) extending from the THYROID CARTILAGE to the ARYTENOID CARTILAGE, and a VOCAL MUSCLE that shortens or relaxes the vocal cord to control sound production.

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Adrenocortical Hyperfunction. Adrenal Gland Diseases. Endocrine System Diseases. Fluorodeoxyglucose F18. Radiopharmaceuticals. ...

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Hyperfunction of thyroid:. Increased HR. anxiety. weight loss. Heated body temp. Monitor for: Opposite effect of what drug is ... adrenocortical insufficiency needs replacement therapy. Never stop abruptly. Cushings syndrome. tumors increased ...

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Rare condition in which the plasma levels of adrenocortical hormones are increased, resulting in excess secretion of adrenal ... Adrenal HYPERfunction.. Another name for Addison's Disease. Adrenal HYPOfunction.. Causes of Addison's Disease.. 1. ...

*  Cushing's & Cancer: Ami's Five Lousy Bucks

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... adrenocortical (1) adrenocortical carcinoma (1) adrenocorticotropic (1) adult (1) advocacy (1) anatomy (1) androgen (1) ...

Adrenocortical hyperfunctionAdrenocortical carcinomaPosterior cricoarytenoid muscle: The posterior cricoarytenoid muscles are extremely small, paired muscles that extend from the posterior cricoid cartilage to the arytenoid cartilages in the larynx.Spasmodic dysphonia: Spasmodic dysphonia (or laryngeal dystonia) is a voice disorder characterized by involuntary movements or spasms of one or more muscles of the larynx (vocal folds or voice box) during speech.Belting (music): Belting (or vocal belting) is a specific technique of singing by which a singer brings their chest register above its natural passaggio (break) at a loud volume; instead, an alternative production is developed, often described and felt as supported and sustained yelling. 'Belting' is sometimes described as 'high chest voice' but this is technically incorrect and potentially damaging for the voice.List of voice disorders: Voice disordersTitze, I.R.Janwillem van den Berg: Janwillem van den Berg (20 November 1920 in Akkrum – 18 October 1985 in Akkrum) was a Dutch speech scientist and medical physicist who played a major role in establishing the myoelastic-aerodynamic theoryTitze, I. R.Adrenocortical adenoma: A adrenocortical adenoma (or adrenal cortical adenoma) is a benign tumor of the adrenal cortex.Dysprosody: Dysprosody, which may manifest as pseudo-foreign accent syndrome, refers to a disorder in which one or more of the prosodic functions are either compromised or eliminated completely.Lightwood–Albright syndromeVocal folds: The vocal folds, also known commonly as vocal cords or voice reeds, are composed of twin infoldings of mucous membrane stretched horizontally, from back to front, across the larynx. They vibrate, modulating the flow of air being expelled from the lungs during phonation.

(1/78) Stress-level cortisol treatment impairs inhibitory control of behavior in monkeys.

Most studies of cortisol-induced cognitive impairments have focused on hippocampal-dependent memory. This study investigates a different aspect of cognition in a randomized placebo-controlled experiment with monkeys that were treated with cortisol according to a protocol that simulates a prolonged stress response. Young adult and older adult monkeys were assigned randomly to placebo or chronic treatment with cortisol in a 2 x 2 factorial design (n = 8 monkeys per condition). Inhibitory control of behavior was assessed with a test shown previously in primates to reflect prefrontal cortical dysfunction. Failure to inhibit a specific goal-directed response was evident more often in older adults. Treatment with cortisol increased this propensity in both older and young adult monkeys. Age-related differences in response inhibition were consistent across blocks of repeated test trials, but the treatment effects were clearly expressed only after prolonged exposure to cortisol. Aspects of performance that did not require inhibition were not altered by age or treatment with cortisol, which concurs with effects on response inhibition rather than nonspecific changes in behavior. These findings lend support to related reports that cortisol-induced disruptions in prefrontal dopamine neurotransmission may contribute to deficits in response inhibition and play a role in cognitive impairments associated with endogenous hypercortisolism in humans.  (+info)

(2/78) Glucocorticoid and mineralocorticoid resistance/hypersensitivity syndromes.

Glucocorticoids and mineralocorticoids regulate diverse functions important to maintain central nervous system, cardiovascular, metabolic, and immune homeostasis. The actions of these hormones are mediated by their specific intracellular receptors: the glucocorticoid (GR) and mineralocorticoid (MR) receptors. Pathologic conditions associated with changes of tissue sensitivity to these hormones have been described. The syndrome of familial glucocorticoid resistance is characterized by hypercortisolism without Cushing's syndrome stigmata. The molecular defects of four kindreds and one sporadic case have been elucidated as inactivating mutations in the ligand-binding domain of GR. Two cases developed glucocorticoid resistance at the heterozygous state. In these patients, mutant receptors possessed transdominant negative activity upon the wild type receptor. Insensitivity to mineralocorticoids (which may also be caused by loss of function mutations of the MR gene) was found in one sporadic case and four autosomal dominant cases of Pseudohypoaldosteronism type 1. These included two frameshift mutations and a premature termination codon in exon 2, leading to gene products lacking the entire DNA- and ligand-binding domains, and a single base-pair deletion in the intron-5 splice donor site. Tissue hypersensitivity to glucocorticoids was recently hypothesized in patients with Human Immunodeficiency Virus (HIV) type-1 infection via the accessory proteins Vpr and Tat which enhance GR transactivation. Since HIV-1 long terminal repeat (LTR) and glucocorticoid-responsive promoters use the same set of coactivators, these proteins may stimulate HIV-1-LTR and glucocorticoid-inducible genes concurrently. The former may directly stimulate viral proliferation, while the latter may indirectly enhance viral propagation by suppressing the host immune system through glucocorticoid-mediated mechanisms.  (+info)

(3/78) Uptake ratio of (19-1311) cholesterol by adrenal glands as observed by a scintigraphic method.

The adrenal scintigram was performed after administration of [19-131I] cholesterol. A high/low ratio of both adrenal glands was calculated to evaluate whether there is a difference between the left and right sides in adrenal diseases. During scanning, information was stored in a 64 X 64 matrix and then punched out on a computer compatible paper tape. This paper tape was processed with a small digital computer. The areas of interest were selected over adrenal glands. The computer decided mean counts per unit area. After subtraction of background counts, a high/low ratio of adrenal gland was calculated. In five patients with Cushing's syndrome due to bilateral hyperplasia, a high/low ratio ranged from 1.0 to 2.0. In four patients with primary aldosteronism due to adenoma, a high/low ratio ranged from 1.33 to 4.0. This method may be useful to differentiate bilateral hyperplasia from unilateral adrenocortical adenoma.  (+info)

(4/78) From open to laparoscopic adrenalectomy: a review of 16-year experience.

OBJECTIVE: To review the experience with adrenal surgery which was associated with significant morbidity and notable mortality in the past, although laparoscopic approach is beginning to be accepted as the procedure of choice. METHODS: The indications and results of adrenalectomy in 104 patients (36 men, 68 women) over the past 16 years were reviewed. Any potential improvement of surgical results over time was analyzed. RESULTS: Ninety-three patients (89%) had functional problems while malignancy was present in 11 patients (11%). Anterior approach was employed in 27 patients, posterior in 56, lateral in 10, and laparoscopic in 11. One patient required conversion from laparoscopic to anterior approach. No operative mortality was seen, but the morbidity occurred in 16.7%. Complication rate decreased significantly in this study period (1981-1990 versus 1991-1996, 22% versus 5%; P = 0.02). Laparoscopic adrenalectomy was successfully performed for 59% of the patients requiring adrenalectomy recently, compared to 68% of posterior adrenalectomy in the past. CONCLUSIONS: Adrenal surgery is a safe procedure, associated with acceptable morbidity, which has decreased over time. Laparoscopic adrenalectomy is becoming the preferred approach for the majority of patients requiring adrenalectomy.  (+info)

(5/78) Parathyroid hormone secretion in chronic human endogenous hypercortisolism.

Osteoporosis is a common manifestation of Cushing's syndrome, but the mechanisms responsible for this abnormality have not been defined. With the objective of analyzing parathyroid hormone (PTH) secretion in chronic hypercortisolism (CH), we evaluated 11 healthy subjects and 8 patients with CH, 6 with Cushing's disease and 2 with adrenal adenoma. These volunteers were submitted to tests of PTH stimulation through hypocalcemia (EDTA), PTH suppression through hypercalcemia (iv and oral calcium), and evaluation of bone mineral density (BMD) by DEXA. During the test of PTH stimulation, the calcium and magnesium concentrations of the normal and CH groups were similar. Patients with CH showed an increased PTH response to the hypocalcemic stimulus compared to controls. PTH values were significantly higher in the CH group at 70 (17.5 +/- 3.5 vs 10.2 +/- 1.3 pmol/l, P = 0.04), and 120 min (26.1 +/- 5.9 vs 11.3 +/- 1.9 pmol/l, P = 0.008) of EDTA infusion. The area under the curve for PTH during EDTA infusion was also significantly higher in patients with CH than in normal subjects (1867 +/- 453 and 805 +/- 148 pmol l(-1) 2 h(-1), P = 0.02). During the test of PTH suppression, calcium, magnesium and PTH levels of the patients with hypercortisolism and controls were similar. BMD was decreased in patients with hypercortisolism in the spine (0.977 +/- 0.052 vs 1.205 +/- 0.038 g/cm2 in controls, P<0.01). In conclusion, our results show that subjects with CH present decreased bone mass mainly in trabecular bone. The use of dynamic tests permitted the detection of increased PTH secretion in response to a hypocalcemic stimulus in CH patients that may probably be involved in the occurrence of osteoporosis in this state.  (+info)

(6/78) Arterial lesions in repeatedly bred spontaneously hypertensive rats.

Repeatedly bred male and female rats of many strains develop hyperglycemia, hyperlipidemia, hypertension, and arteriosclerosis spontaneously. The intensity of their arterial disease and related metabolic derangements appear to be related to their reproductive activity. Repeatedly bred spontaneously hypertensive rats (SHR) were found to have severe hypertension, hyperglycemia, hyperlipidemia, elevated creatine phosphokinase (CPK), serum glutamic oxaloacetic and glutamic pyruvic transaminase (SGOT, SGPT), and lactic dehydrogenase (LDH), as well as high circulating corticosterone levels. Despite these atherogenic metabolic derangements and their severe hypertension, the breeder SHR did not develop the severe, generalized arteriosclerosis found in other strains of breeder rats. Instead, the arterial lesions, consisting of intimal hyalinization and fibrosis, medial hypertrophy, and occlusion of the lumen, were found only in male breeder SHR and were confined to the intratubular arteries of the testes. It is suggested that the severe hypertension, genetic influences, or differences in hypothalamic-pituitary-adrenal-gonadal function in breeder SHR may not have been conducive to the development of arteriosclerosis in this particular strain of rats.  (+info)

(7/78) Osteoporosis is more prevalent in adrenal than in pituitary Cushing's syndrome.

Osteoporosis is the most common complication of Cushing's syndrome. We retrospectively examined the prevalence and risk factors for osteoporosis in 42 female patients with Cushing's syndrome. Osteoporosis and atraumatic fractures were assessed by bone mineral density of the lumbar vertebral spine (L2-L4) using dual energy X-ray absorptiometry (DXA) and X-ray examination. The prevalence of osteoporosis and fracture were 54.8% and 21.4%, respectively. The prevalence of osteoporosis (69.6% vs. 37.8%) and atraumatic bone fracture (26.1% vs. 15.8%) were significantly higher in patients with adrenal Cushing's than in those with pituitary Cushing's. AP and lateral BMD was significantly higher in patients with pituitary origin than in those with adrenal origin. Among several variables examined by multiple logistic regression, the etiology of Cushing's syndrome (adrenal vs. pituitary origin) was a significant factor affecting the prevalence of osteoporosis. Neither age, body mass index, duration of amenorrhea, nor extent of hypercortisolism were significant factors in this analysis. Plasma DHEA-S and urinary 17-KS excretion were significantly higher in pituitary Cushing's than in adrenal Cushing's. The present study shows that the prevalence of osteoporosis in patients with Cushing's syndrome is influenced by its etiology. A factor associated with pituitary Cushing's syndrome, such as adrenal androgen, may protect these patients from glucocorticoid-induced osteoporosis.  (+info)


A case of severe hypercalcemia secondary to carcinoma of the lung is described in which hypokalemic alkalosis, renal failure and pancreatitis were also present. The relative importance of the few bone metastases found at autopsy is considered, and a probable endocrine-like effect of the tumour in the development of the hypercalcemia is postulated. Treatment of the hypercalcemia included administration of corticosteroids and disodium EDTA, peritoneal dialysis and subtotal parathyroidectomy; the most effective of these was peritoneal dialysis. Subtotal parathyroidectomy failed to produce a further decrease in serum calcium values. The occurrence of hypokalemic alkalosis in the presence of increased adrenocortical function and its relationship to the carcinoma of the lung are discussed. The possibility that this neoplasm produced two factors which caused systemic effects ordinarily associated with the function of endocrine glands must be considered.  (+info)

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