DOCSLIB.ORG

The Influence of the Thyroid on Adrenal Cortical Function

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Influence of the Thyroid on Adrenal Cortical Function THE INFLUENCE OF THE THYROID ON ADRENAL CORTICAL FUNCTION Ralph E. Peterson J Clin Invest. 1958;37(5):736-743. https://doi.org/10.1172/JCI103659. Research Article Find the latest version: https://jci.me/103659/pdf THE INFLUENCE OF THE THYROID ON ADRENAL CORTICAL FUNCTION By RALPH E. PETERSON (From the National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Md.) (Submitted for publication October 29, 1957; accepted December 17, 1957) The evidence is quite conclusive from animal of these urinary steroids is either normal or slightly studies that an excess of circulating thyroid hor- increased (20). mone results in adrenal enlargement, and hypo- Thyroidectomized rats (22) and cats (23) are thyroidism produced by surgical thyroidectomy or reported to survive adrenalectomy better than ani- by administration of antithyroid drugs results in mals with an intact thyroid, and administration of adrenal atrophy. This subject has been exten- thyroid to the adrenalectomized cats produced sively reviewed by Money (1). Studies of adrenal sudden death of the animals. Also, in patients size in patients with thyroid disease coming to with Addison's disease, acute adrenal cortical fail- autopsy have yielded conflicting reports. Means ure may be precipitated if thyroid hormone is ad- (2) reported no change in adrenal size in hyper- ministered (24, 25). Primary myxedema has thyroidism, Marine (3) and LeCompte (4) re- been observed in which the presenting findings ported a decrease in size of the adrenal, and Holst were those of adrenal cortical insufficiency, and (5) found enlarged adrenals in some patients with adrenal function returned to normal following hyperthyroidism. Berkheiser (6) reported an ad- thyroid hormone therapy (26). vanced case of hypothyroidism, with atrophy of the With the advent of new and improved methods adrenals and lipoid depletion. for the measurement of certain of the adrenal Measurements of adrenal size may not, how- cortical hormones, and the availability of cortisol- ever, always represent a completely satisfactory 4-C14, it has become possible to further study the "yardstick" for evaluation of adrenal cortical secre- relationship of the thyroid hormone to adrenal tory activity (7, 8). In the past few years, sev- cortical function. These techniques have been ap- eral investigators have reported measurements of plied to a study of the rate of degradation and the various plasma and urinary steroid fractions in rate of synthesis of cortisol in myxedema and thy- hyper- and hypothyroidism in man. Several in- rotoxicosis, before and after therapy. In this vestigators have reported on the levels of free manner, much new information has been gained urinary corticoids (9-12) in hyperthyroidism, and regarding the state of activity of the adrenal cor- in myxedema (9, 10). Because of the relatively tex in these diseases. nonspecific methods of assay used these data are difficult to interpret. Urinary 17-ketosteroids MATERIALS AND METHODS have usually been found to be low in both hyper- Eight patients with the classical symptoms, signs, and and hypothyroidism (9-18). Plasma 17,21-di- laboratory findings of thyrotoxicosis (Grave's disease) to be and seven patients with findings typical of primary myx- hydroxy-20-ketosteroids have been reported edema 1 served as the subjects of these studies. All the normal in these diseases (19-21). Guinea pigs, patients had hypo- or hyperthyroidism of moderate se- which excrete a large fraction of the cortisol me- verity. Diagnoses were established on the basis of the tabolites as free 17,21-dihydroxy-20-ketosteroids, 1The diagnosis of hypopituitarism would appear to show an increased excretion of free urinary corti- have been ruled out on the basis of the following: 1) coids after administration of thyroxine (20). In normal plasma cortisol levels, 2) return of the urine patients with clinical myxedema, the urinary level corticosteroid levels (A. A., M. H., G. B.) and cortisol and turnover rates (M. H., H. A., A. A., G. B.) to normal of the total free glucuronide conjugated 17,21- following treatment with dessicated thyroid, and 3) nor- dihydroxy-20-keteosteroids has been found to be mal adrenal response to corticotropin in Patients W. C. decreased, whereas in hyperthyroidism the level and M. L. 736 THYROID AND ADRENAL CORTICAL FUNCTION 737 clinical picture, basal metabolic rate, thyroid uptake of patients with myxedema were treated with desic- P", serum cholesterol, and serum protein-bound iodine. cated thyroid (90 to 180 mg. per day). The pa- One normal subject was studied prior to and during the four week period following the administration of tri- tients with hyperthyroidism were treated with iodothyronine (300 ,ug. per day) to induce a hyperthy- propylthiouracil (100 to 300 mg. per day), or with roid state. methimazole, except for Patient C. M., who re- Plasma cortisol and urinary corticosteroids were de- ceived a therapeutic dose of radioactive iodine (4 termined by the modified (27, 28) procedure of Silber mc.). D. B. was a normal subject made hyper- and Porter (29). Urinary 17-ketosteroids were deter- mined by the Zimmermann procedure modified from the thyroid by administration of triiodothyronine for Holtorff and Koch method (30). four weeks. The steroids for intravenous administration were dis- All of the subjects with thyrotoxicosis had low solved in ethanol and diluted to 300 or 500 ml. with 5 levels of 17-ketosteroids in the urine. Normal per cent dextrose in water to a final alcohol concentra- subject D. B. showed a decline in excretion of 17- tion of approximately 5 per cent. Following rapid infu- sion of the steroids, plasma samples were collected and ketosteroids after the fourth week of therapy assayed. The rate of disappearance of the steroids was with triiodothyronine. All of the subjects with expressed as a biologic half-time. Cortisol was assayed myxedema had a decreased urine 17-ketosteroids by the modified Silber-Porter procedure. The speci- output, and the urine steroid level rose slightly ficity of this assay procedure for cortisol in plasma fol- following therapy with thyroid. lowing infusion of cortisol has been evaluated by isotope dilution (28) and found to be good. Cortisone and corti- In the patients with thyrotoxicosis, the urinary costerone were assayed by an isotope dilution method, corticoid levels were clearly elevated in D. Y. and since the phenylhydrazine assay for cortisone (31), and, B. M. In Patients B. D., C. M., and R. W. (fe- to a lesser extent, the fluorometric assay for corticos- males), the urinary corticoid levels were only terone (32), were not found to be specific for the de- slightly above the normal range of 4 to 10 mg. per termination of these steroids in plasma following their infusion. Urine cortisol concentration following the infu- day for females. No elevation of urinary corti- sion of cortisol was also determined by the isotope dilu- coids occurred in the normal subject (D. B.) tion procedure. until the third week of treatment with triiodothy- The rapidly exchangeable miscible pool of cortisol and ronine. All of the subjects with myxedema had the rate of turnover of the pool 2 were determined by the urine corticoid levels below normal, and these re- previously described method (33). Two hundred to 300 l'g. of cortisol-4-C' (10 to 20 per cent of the pool turned to normal following therapy with thyroid. size) were injected over a two to three minute period at Cortisol (100 to 200 mg.) was infused into eight 9:00 a.m. Plasma samples were collected every 30 min- subjects with thyrotoxicosis and five patients with utes for the next three hours for measurement of the myxedema (Table I). Figure 1 shows the curves specific activity of cortisol. of disappearance of cortisol from the plasma of a normal subject, and a patient with hyperthyroid- RESULTS ism, and one with myxedema. In the hyperthyroid Table I lists the plasma cortisol and urinary group, the infused cortisol was removed from the corticosteroid and 17-ketosteroid levels in the plasma at a greatly accelerated rate, except in the patients studied. The plasma cortisol level was case of Patient V. H. This subject had a moder- found to be slightly elevated in one patient (G. B.) ately enlarged liver and minimally abnormal liver with untreated myxedema. In two patients with function tests. In all but one of the patients untreated hyperthyroidism, low values were found (M. H.) with myxedema, there was a delayed (D. Y., B. M.). In some of the subjects, de- disappearance of cortisol from the plasma. In terminations were made during the myxedematous both groups, following appropriate therapy for or thyrotoxic period and again several months (3 the thyroid disorder, the plasma disappearance to 12 months) following therapy; however, sig- rates of the infused cortisol returned toward the nificant changes were not usually observed. The normal range. The metabolisms of infused cortisone and corti- 2 Turnover rate is defined as the quantity of newly syn- costerone were found to be altered in the same thesized cortisol added to the miscible pool, presumably by the adrenals, per unit time. The miscible pool is de- direction as cortisol (Table I).. fined as that body of cortisol whose mixing is rapid rela- The urinary concentration of cortisol was de- tive to its turnover. termined in three patients (D. Y., R. W., and 738 RALPH E. PETERSON TABLE I Plasma and urine steroid levels and biologic half-times of infused steroids Urinary steroids Biologic half-times* (hrs.) Plasma 17-Keto- cortisol Corticoids steroids F E B lig. % mg./day Hyperthyroidism V. H. 9 untreated 15 1.83 0.53 E. S. 9 untreated 11 1.0 0.67 B. D. 9 untreated 8 12.0 5.0 0.92 0.27 C. M. 9 untreated 18 11.2 4.7 0.63 myxedema 15 k2.6 3.3 2.15 treated 15 4.0 4.0 D.
Load more

Recommended publications
  • Expression Pattern of Delta-Like 1 Homolog in Developing Sympathetic Neurons and Chromaffin Cells
    Published in "Gene Expression Patterns 30: 49–54, 2018" which should be cited to refer to this work. Expression pattern of delta-like 1 homolog in developing sympathetic neurons and chromaffin cells ∗ Tehani El Faitwria,b, Katrin Hubera,c, a Institute of Anatomy & Cell Biology, Albert-Ludwigs-University Freiburg, Albert-Str. 17, 79104, Freiburg, Germany b Department of Histology and Anatomy, Faculty of Medicine, Benghazi University, Benghazi, Libya c Department of Medicine, University of Fribourg, Route Albert-Gockel 1, 1700, Fribourg, Switzerland ABSTRACT Keywords: Delta-like 1 homolog (DLK1) is a member of the epidermal growth factor (EGF)-like family and an atypical notch Sympathetic neurons ligand that is widely expressed during early mammalian development with putative functions in the regulation Chromaffin cells of cell differentiation and proliferation. During later stages of development, DLK1 is downregulated and becomes DLK1 increasingly restricted to specific cell types, including several types of endocrine cells. DLK1 has been linked to Adrenal gland various tumors and associated with tumor stem cell features. Sympathoadrenal precursors are neural crest de- Organ of Zuckerkandl rived cells that give rise to either sympathetic neurons of the autonomic nervous system or the endocrine Development ffi Neural crest chroma n cells located in the adrenal medulla or extraadrenal positions. As these cells are the putative cellular Phox2B origin of neuroblastoma, one of the most common malignant tumors in early childhood, their molecular char- acterization is of high clinical importance. In this study we have examined the precise spatiotemporal expression of DLK1 in developing sympathoadrenal cells. We show that DLK1 mRNA is highly expressed in early sympa- thetic neuron progenitors and that its expression depends on the presence of Phox2B.
    [Show full text]
  • I. Introduction B. Adrenal Cortex
    I. Introduction Adrenal Glands • suprarenal – they sit on top of the kidneys • each is composed of 2 distinct regions: A. Adrenal Medulla - the inner region - comprises 20% of the gland - secretes epinephrine and norepinephrine - derived from ectoderm B. Adrenal Cortex 1) Zona Glomerulosa (outermost region) - produces mineralocorticoids (aldosterone) • the outer region 2) Zona Fasiculata (middle region) - produces glucocorticoids (cortisol) as well as • comprises 80% of the gland estrogens and androgens • secretes corticosteroids 3) Zona Reticularis (innermost region) • derived from mesoderm - same function as zona fasiculata DHEA – dehydroepiandrosterone • an adrenal androgen in females • responsible for growth of pubic and axillary hair C. Pathologies Associated with Adrenal II. Mineralocorticoids (Aldosterone) Androgen Hypersecretion A. Functions 1.Adrenogenital Syndrome - promotes reabsorption of Na+ and - hypersecretion of androgens or estrogens secretion of K+ from the distal portion of the a) in the adult female: nephron..primary regulator of salt balance and extracellular volume - masculinization (i.e. hirsutism) -Similar (but less important) effect on salt b) in the female embryo: transport in colon, salivary glands, and - female pseudohermaphroditism sweat glands. c) in the adult male: - no effect d) in young boys: - precocious pseudopuberty 1 II. Mineralocorticoids (Aldosterone) C. Pathologies B. Regulation of Secretion 1. Hypersecretion 1. Renin Angiotensin a. primary hyperaldosteronism - Angiotensin II stimulates aldost. secretion - Conn’s syndrome 2. Potassium - usually due to a tumor on the gland + - high levels of K induce aldost. secretion - too much secretion of gland itself 3. ACTH –no direct role b. secondary hyperaldosteronism - default in renin angiotensin system - most common in atherosclerosis of renal arteries C. Pathologies III. Glucocorticoids (Cortisol) 1.
    [Show full text]
  • HYPOTHALAMUS – PITUITARY-ADRENAL AXIS Learning Objectives OVERVIEW FUNCTIONAL ANATOMY
    Introductory Human Physiology ©copyright Emma Jakoi HYPOTHALAMUS – PITUITARY-ADRENAL AXIS Emma R. Jakoi, Ph.D. Learning objectives • Describe the structural and functional organization of the adrenal gland. • Describe the synthesis and secretion of cortical adrenal hormones. • Describe the mechanism of action and physiologic effects of adrenal hormones. • Explain the control of adrenal hormone synthesis and secretion. Describe the major feedback loops that integrate the hypothalamic axis and body homeostasis. • Explain the physiologic roles of the adrenal hormones in normal physiology. OVERVIEW The adrenal glands maintain homeostasis in response to stress. Three major classes of hormones are secreted by these glands: aldosterone (mineralocorticoid), cortisol (glucocorticoid), DHEA (weak androgen), and catecholamines (epinephrine and norepinephrine). FUNCTIONAL ANATOMY The adrenal gland is located on top of the kidney. Like the pituitary, two distinct tissues merge during development to form the adrenal cortex (glandular tissue) and medulla (modified neuronal tissue) (Fig 1). 1 2 cortex 3 medulla Figure 1. Structure of the adrenal gland. The cortex secretes three steroid hormones: 1. aldosterone, 2. cortisol, 3. a weak androgen, DHEA. The medulla secretes epinephrine (Epi) and norepinephrine (NorEpi). 1 Introductory Human Physiology ©copyright Emma Jakoi MINERALOCORTICOIDS The major mineralocorticoid in humans is aldosterone. Aldosterone is NOT under the hypothalamus- pituitary control and does not mediate a negative feedback to this axis. Aldosterone secretion is increased by the vasoconstrictor, angiotensin II, and by elevated plasma K+ concentration. Elevated plasma Na+ inhibits the secretion of aldosterone. Aldosterone, acts in the kidney to promote secretion of K+ into the urine from the blood and the reabsorption of Na+ from the urine into the blood.
    [Show full text]
  • Dream Recall/Affect and the Hypothalamic–Pituitary–Adrenal Axis
    Review Dream Recall/Affect and the Hypothalamic–Pituitary–Adrenal Axis Athanasios Tselebis 1, Emmanouil Zoumakis 2 and Ioannis Ilias 3,* 1 Department of Psychiatry, Sotiria Hospital, 115 27 Athens, Greece; [email protected] 2 First Department of Pediatrics, National and Kapodistrian University of Athens Medical School, Aghia Sophia Children’s Hospital, 115 27 Athens, Greece; [email protected] 3 Department of Endocrinology, Diabetes and Metabolism, Elena Venizelou Hospital, 115 21 Athens, Greece * Correspondence: [email protected]; Tel.: +30-213-205-1389 Abstract: In this concise review, we present an overview of research on dream recall/affect and of the hypothalamic–pituitary–adrenal (HPA) axis, discussing caveats regarding the action of hormones of the HPA axis (mainly cortisol and its free form, cortisol-binding globulin and glucocorticoid receptors). We present results of studies regarding dream recall/affect and the HPA axis under physiological (such as waking) or pathological conditions (such as in Cushing’s syndrome or stressful situations). Finally, we try to integrate the effect of the current COVID-19 situation with dream recall/affect vis-à-vis the HPA axis. Keywords: dreams; cortisol; stress; memory; sleep; HPA axis 1. Introduction—Dream Recall Almost all humans dream (indeed, there may be 0.5% of people who do not do so) [1]. Dreams are a series of images, thoughts and senses and are considered a specific type Citation: Tselebis, A.; Zoumakis, E.; of experience that occurs in our brain during sleep. During the dream, there is limited Ilias, I. Dream Recall/Affect and the control of the dream content, visual images and memory activation.
    [Show full text]
  • Pig Gonads, Adrenal Glands and Brain C
    Immunoreactive cytochrome P-45017\g=a\in rat and guinea- pig gonads, adrenal glands and brain C. Le Goascogne1, N. Sanan\l=e'\s1, M. Gou\l=e'\zou1, S. Takemori2, S. Kominami2, E. E. Baulieu1 and P. Robel1 1INSERM U33, Communications Hormonales, and Faculté de Médecine, Université Paris-sud, Lab Hormones F-94275 Bicêtre Cedex France 2 Faculty of Integrated Arts and Sciences, Hiroshima University, Hiroshima 730, Japan Summary. The cytochrome P-45017\g=a\-hydroxylase, 17\ar=r\20lyase (P-45017\g=a\) is the key enzyme responsible for the biosynthesis of androgens in steroidogenic organs. Its cellular localization has been examined with an immunohistochemical technique. In immature rat ovary, P-45017\g=a\was first detected in sparse interstitial cells on postnatal Day 8. The number of immunoreactive interstitial cells increased thereafter and the intensity of P-45017\g=a\staining in these cells was highest at 3 weeks of age. The intensity of staining then started to decline and was very faint at Day 35. From 6 weeks on, the distribution of immunoreactive P-45017\g=a\was of the adult type: it was detected exclusively in the thecal cells of the large antral, preovulatory, follicles. P-45017\g=a\was not detectable during pregnancy except on the day of parturition, when thecal cells were transiently immunoreactive. The staining had vanished 24 h after delivery. Human chorionic gonadotrophin (hCG), injected into immature females on Days 24 to 26, induced P-45017\g=a\prematurely in thecal cells. When injected on Days 12 to 14 of pregnancy, hCG also induced P-45017\g=a\in the thecal cells surrounding the largest follicles, whereas the interstitial and luteal cells were not immunostained.
    [Show full text]
  • Adrenal Gland Hormones
    CHAPTER 8 Adrenal Gland Hormones Devra K. Dang, PharmD, BCPS, CDE, FNAP | Trinh Pham, PharmD, BCOP | Jennifer J. Lee, PharmD, BCPS, CDE LEARNING OBJECTIVES KEY TERMS AND DEFINITIONS After completing this chapter, you should be able to ACTH (adrenocorticotropic hormone) — a hormone produced 1. Identify the hormones produced by the adrenal glands by the pituitary gland that stimulates 2. Describe the functions of mineralocorticoids and glucocorticoids in the body the adrenal cortex to produce glucocorticoids, mineralocorticoids, 3. Recognize the signs and symptoms of adrenal insuffi ciency and androgens. PART 4. Describe the pharmacological treatment of patients with acute and chronic adrenal Addison ’ s disease — a disorder insuffi ciency in which the adrenal glands do not produce enough steroid hormones. 3 5. Recognize the signs and symptoms of Cushing ’ s syndrome and the result of too Adenoma — a benign much cortisol (noncancerous) tumor of glandular 6. Describe the pharmacologic and nonpharmacologic management of patients with origin. Cushing ’ s syndrome Adrenal insuffi ciency — a term 7. List management strategies for administration of glucocorticoid and mineralocorti- referring to a defi ciency in the levels of adrenal hormones. coid therapy to avoid development of adrenal disorders Aldosterone — the hormone produced by the adrenal glands that regulates the balance of sodium, he adrenal glands are an integral part of the endocrine system, secreting water, and potassium concentrations in the body. T hormones that act throughout the body to regulate functions and promote Corticotropin-releasing homeostasis. In addition to the neurotransmitters epinephrine and norepineph- hormone (CRH) — a hormone rine, the corticosteroids secreted by the adrenal glands are vital to a wide released by the hypothalamus that variety of physiological processes.
    [Show full text]
  • Adrenal and Paraganglia Tumors Adrenal Cortical Tumors IHC: (+) SF1, Inhibin, Melan-A, Calretinin, Synaptophysin, (-) Chromogranin, Cytokeratin, S100
    Last updated: 11/11/2020 Prepared by Kurt Schaberg Adrenal and Paraganglia Tumors Adrenal Cortical Tumors IHC: (+) SF1, Inhibin, Melan-A, Calretinin, Synaptophysin, (-) Chromogranin, Cytokeratin, S100. Often variable!! Adrenal Cortical Adenoma Benign. Very common. Often incidentally identified. Usually unilateral solitary masses with atrophic background adrenal gland. Tumor cells can be lipid-rich (clearer) or lipid-poor (pinker) arranged in nests and cords separated by abundant vasculature. Occasional lipofuscin pigment. Nuclei generally small and round (occasional extreme “endocrine atypia” is common). Low/no mitotic activity. Intact reticulin framework. On a spectrum with and may hard to differentiate from hyperplastic nodules, which is more often multinodular (background hyperplasia) and bilateral. Can be non-functional (85%) or functional (15%). Associated with MEN1, FAP, Carney Complex, among Aldosterone-producing→ “Conn syndrome”→ others… hypertension and hypokalemia If aldosterone-secreting adenoma is treated with Cortisol-producing→ (ACTH-independent) spironolactone→ “spironolactone bodies” (below) “Cushing Syndrome” → central obesity, moon face, hirsutism, poor healing, striae Sex-hormone-producing→ Rare (more common in carcinomas). Symptoms depend on hormone/sex (virilization or feminization) Adrenal Cortical Carcinoma Malignant. Most common in older adults. Can present with an incidental unilateral mass or with an endocrinopathy (see above). Solid, broad trabeculae, or large nested growth (more diffuse, and larger groups than in adenomas) Thick fibrous capsule with occasional fibrous bands. Frequent tumor necrosis. Frequent vascular or capsular invasion. Increased mitotic activity. Variants: Oncocytic, Myxoid, Sarcomatoid Mostly sporadic, but can be associated with Lynch Syndrome and Li-Fraumeni Syndrome Distinguishing between an Adrenal Cortical Adenoma vs Carcinoma Weiss Criteria: Weiss Criteria (≥3 = Malignant) Most widely used system, but doesn’t work as well High nuclear grade (based of Fuhrman criteria) in borderline cases or variants.
    [Show full text]
  • Hypothalamic–Pituitary–Adrenal Axis Dysregulation and Behavioral Analysis of Mouse Mutants with Altered Glucocorticoid Or Mineralocorticoid Receptor Function
    Stress, September 2008; 11(5): 321–338 REVIEW Hypothalamic–pituitary–adrenal axis dysregulation and behavioral analysis of mouse mutants with altered glucocorticoid or mineralocorticoid receptor function BENEDICT J. KOLBER, LINDSAY WIECZOREK, & LOUIS J. MUGLIA Departments of Pediatrics and Molecular Biology and Pharmacology and Program in Neuroscience, Washington University in St Louis, St Louis, MO 63110, USA (Received 12 July 2007; revised 29 October 2007; accepted 19 November 2007) Abstract Corticosteroid receptors are critical for the maintenance of homeostasis after both psychological and physiological stress. To understand the different roles and interactions of the glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) during stress, it is necessary to dissect the role of corticosteroid signaling at both the system and sub-system level. A variety of GR transgenic mouse lines have recently been used to characterize the role of GR in the CNS as a whole and particularly in the forebrain. We will describe both the behavioral and cellular/molecular implications of disrupting GR function in these animal models and describe the implications of this data for our understanding of normal endocrine function and stress adaptation. MRs in tight epithelia have a long established role in sodium homeostasis. Recently however, evidence has suggested that MRs in the limbic brain also play an important role in psychological stress. Just as with GR, targeted mutations in MR induce a variety of behavioral changes associated with stress adaptation. In this review, we will discuss the implications of this work on MR. Finally, we will discuss the possible interaction between MR and GR and how future work using double mutants (through For personal use only.
    [Show full text]
  • Disturbances of the Stress Response
    Disturbances of the Stress Response The Role of the HPA Axis During Alcohol Withdrawal and Abstinence Bryon Adinoff, M.D., Ali Iranmanesh, M.D., Johannes Veldhuis, M.D., and Lisa Fisher, Ph.D. Interactions among the brain, the pituitary gland, and the adrenal glands (i.e., the hypothalamic-pituitary-adrenal [HPA] axis) help regulate the body’s response to stress. The adrenal hormone cortisol plays a key role in stress reduction through its effects on multiple body systems. Excessive cortisol activity during both chronic alcohol administration and withdrawal may underlie some of the clinical complications of alcoholism, including increased risk of infectious diseases; bone, muscle, and reproductive system changes; altered energy metabolism; and disorders of mood and intellect. Despite excessive cortisol levels during intoxication and withdrawal, however, the HPA axis becomes less responsive to stress during abstinence, potentially resulting in an impaired capacity to cope with relapse-inducing stressors. KEY WORDS: AOD withdrawal syndrome; physiological stress; hypothalamic-pituitary axis; pituitary-adrenal axis; cortisol; AOD abstinence; chronic AODE (alcohol and other drug effects); corticotropin RH; arginine; vasopressin; adrenocorticotropic hormone; secretion; metabolic disorder; AODR (alcohol and other drug related) disorder; mood and affect disturbance; personality disorder; infection; drug therapy; literature review tress is a ubiquitous and unavoid- a wide range of critical physiological secretion occurs during both chronic able experience of daily life whether processes, the activity of cortisol must alcohol consumption and alcohol Sit arises from the external environ- be tightly controlled by the body. withdrawal. This heightened secretion ment (e.g., a job interview or traffic Cortisol secretion is regulated by rate may alter energy metabolism, accident) or from within the body (e.g., interactions among three structures: mental status, the structural integrity an infection or a panic attack).
    [Show full text]
  • Adrenal Cortical Tumors, Pheochromocytomas and Paragangliomas
    Modern Pathology (2011) 24, S58–S65 S58 & 2011 USCAP, Inc. All rights reserved 0893-3952/11 $32.00 Adrenal cortical tumors, pheochromocytomas and paragangliomas Ricardo V Lloyd Department of Pathology, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA Distinguishing adrenal cortical adenomas from carcinomas may be a difficult diagnostic problem. The criteria of Weiss are very useful because of their reliance on histologic features. From a practical perspective, the most useful criteria to separate adenomas from carcinomas include tumor size, presence of necrosis and mitotic activity including atypical mitoses. Adrenal cortical neoplasms in pediatric patients are more difficult to diagnose and to separate adenomas from carcinomas. The diagnosis of pediatric adrenal cortical carcinoma requires a higher tumor weight, larger tumor size and more mitoses compared with carcinomas in adults. Pheochromocytomas are chromaffin-derived tumors that develop in the adrenal gland. Paragangliomas are tumors arising from paraganglia that are distributed along the parasympathetic nerves and sympathetic chain. Positive staining for chromogranin and synaptophysin is present in the chief cells, whereas the sustentacular cells are positive for S100 protein. Hereditary conditions associated with pheochromocytomas include multiple endocrine neoplasia 2A and 2B, Von Hippel–Lindau disease and neurofibromatosis I. Hereditary paraganglioma syndromes with mutations of SDHB, SDHC and SDHD are associated with paragangliomas and some pheochromocytomas.
    [Show full text]
  • Endocrine System 4: Adrenal Glands
    Copyright EMAP Publishing 2021 This article is not for distribution except for journal club use Clinical Practice Keywords Endocrine system/ Hormones/Adrenal glands Systems of life This article has been Endocrine system double-blind peer reviewed In this article... ● Endocrine functions of the adrenal glands ● Hormones of the adrenal glands ● The role of adrenal gland hormones in mediating essential physiological processes Endocrine system 4: adrenal glands Key points Authors Maria Andrade is honorary associate professor in biomedical science; There are two Zubeyde-Bayram Weston is senior lecturer in biomedical science; John Knight is adrenal glands: one associate professor in biomedical science; all at College of Human and Health located above each Sciences, Swansea University. kidney NT SELF- Abstract The endocrine system consists of glands and tissues that produce and ASSESSMENT Adrenal glands secrete hormones to regulate and coordinate vital bodily functions. This article, the Test your consist of two parts, fourth in an eight-part series on the endocrine system, explores the anatomy and knowledge. the cortex and the physiology of the adrenal glands, and describes how they regulate and coordinate After reading this medulla, which each vital physiological processes in the body through hormonal action. article go to produce different nursingtimes.net/ NTSAAdrenal hormones Citation Andrade M et al (2021) Endocrine system 4: adrenal glands. Nursing Times If you score 80% [online]; 117: 8, 54-58. or more, you will The adrenal cortex receive a certificate produces a diverse that you can use range of steroid as revalidation his eight-part series on the endo- colour and are positioned retroperito- evidence.
    [Show full text]
  • Comparison of the Anterior Pituitary-Adrenal Cortical Stimulating Effect of U.S.P. Epinephrine, Synthetic L-Epinephrine, and Nor-Epinephrine
    COMPARISON OF THE ANTERIOR PITUITARY-ADRENAL CORTICAL STIMULATING EFFECT OF U.S.P. EPINEPHRINE, SYNTHETIC L-EPINEPHRINE, AND NOR-EPINEPHRINE Leonard L. Madison J Clin Invest. 1950;29(6):789-791. https://doi.org/10.1172/JCI102316. Research Article Find the latest version: https://jci.me/102316/pdf COMPARISON OF THE ANTERIOR PITUITARY-ADRENAL CORTICAL STIMULATING EFFECT OF U.S.P. EPI- NEPHRINE, SYNTHETIC L-EPINEPHRINE, AND NOR-EPINEPHRINE 1 BY LEONARD L. MADISON (From the Department of Medicine, Southwestern Medical School of the University of Texas, and the Department of Medicine of the Veterans Administration Hospital, Dallas, Texas) (Submitted for publication December 16, 1949; accepted, March 6, 1950) The recent demonstration of the dramatic thera- adrenal cortical steroid hormone production with peutic effectiveness of the adrenal 11, 17-oxy- resultant eosinopenia and increased urinary 11- steroids (Compound E of Kendall) in the therapy oxysteroid and 17-ketosteroid excretion. of rheumatoid arthritis, rheumatic fever, and lu- Although long suspected, it has only recently pus erythematosus has lent great impetus to the been proven that the adrenal medulla secretes two study of the role of the adrenal cortex in these hormones, epinephrine and its non-methylated mesenchymal diseases, and to the search for new analogue, nor-epinephrine (arterenol, 1- [3, 4- methods of stimulating the adrenal to produce dehydroxyphenyl] 2-aminoethanol) (7, 8). As- endogenously these therapeutic agents in greater says on U. S. P. epinephrine reference standards, abundance (1-3). The wide variety of stimuli and U. S. P. commercial epinephrine revealed a capable of producing an "alarm reaction" are all nor-epinephrine content varying from 10 to 35%, attended by one common factor, the stimulation of the average being 15%o (7-9).
    [Show full text]