DOCSLIB.ORG

Internal Medicine Exam Questions; 3Rd Dep. 3 Rd Year, 2Nd Semester 08/09

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Internal Medicine Exam Questions; 3Rd Dep. 3 Rd Year, 2Nd Semester 08/09 Internal Medicine exam questions; 3 rd dep. 3 rd year, 2 nd semester 08/09 Exam Questions - 3rd Year, 2nd Semester Academic Year 2008/2009 Tests of the anterior pituitary function. Hypopituitarism. Syndromes of anterior pituitary hyperfunction. Disorders of the posterior pituitary. Diabetes mellitus. Hypoglycemic disorders. Pancreatic islet Diseases of the hypothalamus. cell tumors. Evaluation of the adrenal function. Adrenocortical hypofunction. Cushing's syndrome. Mineralocorticoid excess states. The adrenogenital syndromes. The disorders of the adrenal medulla. Tests of thyroid function and thyroid regulation. Hyperthyreoidism. Hypothyroidism. Thyroiditis. Sporadic and endemic goiter. Benign and malignant tumors of the Hyperparathyroidism. thyroid. Hypoparathyroidism. Diseases of the breast. The carcinoid syndrome. The disorders of lipid metabolism. Principles of alimentation and hyperalimentation. Protein-calory undernutrition. Anorexia nervosa and bulimia nervosa. Obesity. Disorders of purine metabolism. Gout. Alcoholism. Amenorrhea. Hypogonadism in males. Hirsutism. Acid-base disorders. Volume disorders. Osmolality disorders. Vitamine deficiencies and hypervitaminoses. Budapest, 17. January, 2009. Dr. Katalin Keltai English Tutor ECH 1 Tests of the anterior pituitary function -Basal pituitary hormones: ACTH; TSH; LH, FSH; GH; PRL -Target gland hormones: cortisol (circadian); thyroxine, T3; testosterone or estradiol; IGF-1 Stimulation tests -stimulation of the hypothalamus: -INS hypoglycemia test stimulates ACTH, GH, PRL synthesis. Contraindicated in patients >65yrs, pt.’s with CHD, uncontrolled HTN or epilepsy -clonidine/arginine: stim. release of GH -clomiphene: test LH, FSH. It inhibits the action of estrogen on the hypothalamus by binding to estrogen Rs for a long time prevents normal R recycling, in hypothalamic R no loss of FB FSH & LH -metoclopramide: test PRL. It binds to DA D2-Rs antagonistically inhibits DA PRL. Contraindicated in pheochromocytoma -stimulation of the ant. pit. with hypophysiotropic hormones: CRH; TRH; GnRH, GHRH; TRH (theoretical, rarely of practical clinical significance) -stimulation of the target gland with tropic hormones: -Short Synacthen test (short ACTH stim. test): to assess adrenal axis: do plasma cortisol before and 30 min after tetracosactide (=Synacthen) 250 g IM. Addison’s is excluded if 2nd cortisol >550 nmol/L -hCG test: LH, FSH Other dynamic tests: -INS tolerance test (ITT): in specialist centers, to assess adrenal and GH axes. Contraindications: epilepsy, heart disease, adrenal failure. Done in the morning by injecting IV INS to induce hypoglycemia, causing stress to ACTH and GH secretion. Glc must fall below 2.2 mM, normal is GH >20 mU/L and peak cortisol >550 nmol/L -when ITT is contraindicated: arginine + GHRH test; glucagon stimulation test -glucose tolerance test (OGTT): with GH measurement; done if acromegaly is suspected; test is done at 09.00 with fasting from midnight. GH and glc samples taken at 0, 30, 60, 90, 120, 150 min. Normally GH secretion is inhibited by a rice in glc, and GH should be undetectable – in acromegaly there is failure to suppress GH release (false positive results are seen in puberty, pregnancy, hepatic and renal disease, anorexia nervosa, and DM) -dexamethasone suppression test: screening test to diagnose and differentiate among types of Cushing’s and other hypercortisol states. Give dexamethasone 1mg PO at midnight; check serum cortisol before, and at 8AM. In normal pt.’s this high dose of steroid ECH 2 causes neg. FB ACTH and cortisol secretion to <50 nmol/L; in Cushing’ syndrome, there is a failure to suppress cortisol secretion ACTH Cortisol Interpretation Undetectable/ Not suppressed Adrenal Cushing’s sy. is likely / Not suppressed Ectopic ACTH prod. is likely Pituitary Cushing’s d. should be / Suppressed considered (do MRI) Hypopituitarism -diminished secretion of ant. pituitary hormones (loss or absence of >75% of anterior pituitary parenchyma -affected in the following order: GH, gonadotropins (FSH, LH), PRL, TSH, ACTH -panhypopituitarism is usually caused by irradiation, surgery or pituitary tumor -hypopituitarism accompanied by posterior pituitary dysfunction (diabetes insipidus) is almost always of hypothalamic origin Causes are from 3 levels: -Hypothalamus: Kallman’s sy. (gonadotropin releasing hormone def., often with anosmia and color blindness secondary hypogonadism), tumor, inflammation, infection (meningitis, TB), ischemia -Pituitary stalk: trauma, surgery, mass lesion (craniopharyngioma – from Rathke’s pouch, commonest childhood cranial tumor), meningioma, carotid artery aneurysm -Pituitary: tumor, irradiation, inflammation, infiltration (hemochromatosis, amyloidosis, metastatic cancer), ischemia (apoplexy, Sheehan sy. – postpartum pituitary necrosis) Features: -GH lack: central obesity; atherosclerosis; dry wrinkly skin; dec. strength, balance, CO; osteoporosis; dec. glc; growth failure (pituitary dwarfism) in children -gonadotropin lack: ♀: oligomenorrhea/amenorrhea, osteoporosis, breast atrophy, dyspareunia, dec. fertility and libido. ♂: erectile dysfunction, dec. libido and muscle bulk, hypogonadism -thyroid lack: tiredness, lethargy, depression, cold intolerance, weight gain, constipation, menorrhagia, hoarse voice, poor cognition/dementia, myalgia -corticotropin lack: nonspecific symptoms: fatigue, weakness, anorexia etc. -prolactin lack: rare – failure of lactation -pallor from loss of stimulatory effects of MSH on melanocytes -If the cause is pituitary tumor mass effect, or hormone secretion with dec. secretion of other hormones (eg. prolactinoma, acromegaly, Cushing’s) ECH 3 Tests: -Basal: LH & FSH or Testosterone or estradiol TSH or T4 Prolactin May be due to loss of DA from hypoth. IGF-1 cortisol Na+ - dilution Hb (normochromic, normocytic) -Dynamic tests: -Short Synacthen test: ACTH stim. test, to assess the adrenal axis -ITT: assess adrenal and GH axes; IV INS hypoglycemia ( cortisol and GH secretion) -Arginine + GH releasing hormone test -Glucagon stim. test -MRI to look for lesion Treatment: -hormone replacement, treatment of underlying cause -Hydrocortisone for secondary adrenal failure -Thyroxine for hypothyroid - For symptoms of hypogonadism and to prevent osteoporosis: ♀estrogen (estradiol implants, patches, pills) ♂ testosterone enanthate (IM, gels, tablets) -Gonadotropin therapy to induce fertility (-Somatropin for GH def.) !Hypopituitary coma: usually develops gradually in a person with known hypopituitarism (rarely due to infarction of pituitary tumor – pituitary apoplexy) -symptoms: headache, meningism (DDx: subarachnoid hemorrhage) -pt present with headache, ophthalmoplegia, consciousness, hypotension, hypothermia, hypoglycemia -tests: T4, cortisol, TSH, ACTH, glc. Pituitary fossa CT/MRI -Rx: hydrocortisone sodium succinate + T3 (after hydrocortisone); surgery if the cause is pituitary apoplexy Syndromes of anterior pituitary hyperfunction ECH 4 -adenohypophysis; originates from invagination of oral ectoderm (Rathke’s pouch); peptide hormones; pars distalis, tuberalis, intermedia; ACTH, TSH, FSH, LH, GH, PRL, -endorphin -10% of intracranial neoplasms (almost always benign adenomas); peak incidence from 30s to 50s -chromophobe: 70%, PRL (ACTH, GH); local pressure effect in 30% -acidophil: 15%, GH, PRL; local pressure effect in 10% -basophil: 15%, ACTH; local pressure effect rare -local pressure effects: headache, bilateral temporal hemianopsia, CN palsies, disturbance of hypothalamic centers of T, sleep, and appetite, CSF rhinorrhea (erosion through floor of sella) -investigations: MRI, assessment of visual fields, screening tests (PRL, IGF-1, ACTH, cortisol, TFTs, LH/FSH, testosterone in males, short Synachten test, OGTT (acromegaly), water deprivation test (DI) -water deprivation test: to see if the kidneys persist in producing dilute urine despite dehydration -treatment: surgery (trans-sphenoidal, trans-frontal), post-op radiotherapy if complete removal has not been possible -pituitary apoplexy: acute hemorrhage into an adenoma rapid enlargement of the lesion, depression of consciousness; may cause sudden death (Rx: steroids) -functional (hormone excess, clinical manifestation of hyperproduction) vs. silent (immunohistochemical demonstration of hormone production at tissue level only; without clinical manifestation of hormone excess) -approx. 40% of somatotropic adenomas and a minority of corticotropic adenomas bear GNAS1 mutations (chr. 20q13; mutation in -subunit of Gs GTPase activity, constitutive activation of Gs, persistent activation of cAMP, unchecked cellular proliferation) -cellular monomorphism, absence of reticulin network Prolactinoma with hyperprolactinemia -most common pituitary tumor (30%) -PRL >5000 mU/L is likely to be due to a prolactinoma (N=♂<450 mU/L, ♀<600 mU/L (<900 pmol/L)) -chromophobic staining -hyperprolactinemia can be caused by hypothalamic lesions or by medications (methyldopa, reserpine) that interfere with dopamine (prolactin-inhibitory factor) secretion. Can be associated with estrogen therapy -DDx: pregnancy, high-dose estrogen therapy, renal failure, hypothyroidism (TRH), stalk effect (mass in suprasellar compartment disturb normal inhibitory influence of hypothalamus on prolactin secretion) -loss of libido, infertility, amenorrhea, galactorrhea in women -loss of libido, infertility, impotence, sometimes galactorrhea in men ECH 5 -management: dopamine agonists (bromocriptine, cabergoline) Somatotropic adenoma with hypersecretion of GH -2nd
Load more

Recommended publications
  • Endocrinopathy in the Etiology of Obesity
    University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1935 Endocrinopathy in the etiology of obesity Forrest B. Spieler University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Spieler, Forrest B., "Endocrinopathy in the etiology of obesity" (1935). MD Theses. 411. https://digitalcommons.unmc.edu/mdtheses/411 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. Endocrinopathy in the Etiology of Obesity by Forrest B. Spieler Senior Thesis Uni vers! ty of Itebraska College of Medicine 1935 ,. TABLE OF CONTENTS Introduction ••••••••••••••••••••••• 1 Endoerinppathy as a Cause •••••••••• 3 Classification. • • • • • • • • • • • • . •• • • • •• 6 The pituitary types of Obesity •••••• 7 a. Froehlich's Syndrome •••••••••• 10 b. Adiposis Dolorosa ••••••••••••• 14 b. Basophilism •••••.••••.•.•••••• 2l ThyroidalObesity •••••••••••••••••• 26 AdrenalOb.slty •••••••••••••••••••• 30 GonadalObesity ••••••••••••.••.•••• 32 Pancreatic Obesity •••.••..•...••.•• 36 Conclusions •••••••••••••••••••.•••• 40 Bibliography 480728 ENDOCRINE OBESITY Introduction The movies with their Marlene Dietrichs and Jean Harlows have made the public figure-conscious. People in all walks of life, from the young coed to the elderly spinster, are doing their utmost to make their figures approximate that Of their favorite movie heroine. Even wives are at­ tempting to make the husbands'figure Jook like that of some Greek god swaggering across the silver screen.
    [Show full text]
  • Froehlich's Syndrome and Homoeopathy
    Froehlich’s Syndrome and Homoeopathy Dr. Rajneesh Kumar Sharma MD (Homoeopathy) Dr. Swati Vishnoi BHMS Dr. Preetika Lakhera BHMS Dr. Mohammad Tayyab Daud BHMS Dr. Mohammad Tayyab Amir BHMS Dr. Vaishnavi Rathore BHMS Froehlich’s Syndrome and Homoeopathy Froehlich’s Syndrome and Homoeopathy © Dr. Rajneesh Kumar Sharma MD (Homoeopathy) Dr. Swati Vishnoi BHMS Dr. Preetika Lakhera BHMS Dr. Mohammad Tayyab Daud BHMS Dr. Mohammad Tayyab Amir BHMS Dr. Vaishnavi Rathore BHMS Homoeo Cure Research Institute NH 74- Moradabad Road Kashipur (UTTARANCHAL) - INDIA Ph- 09897618594 E. mail- [email protected] www.treatmenthomeopathy.com www.homeopathyworldcommunity.com Contents Definition .............................................................................................................................................. 2 Etymology ............................................................................................................................................. 2 Pathophysiology ................................................................................................................................... 2 Anatomy of Hypothalamus ............................................................................................................... 2 Preoptic region ................................................................................................................................. 3 Supraoptic or anterior region ..........................................................................................................
    [Show full text]
  • The Lateral Hypothalamic Parvalbuminimmunoreactive
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE Published in "7KH-RXUQDORI&RPSDUDWLYH1HXURORJ\ GRLFQH" provided by RERO DOC Digital Library which should be cited to refer to this work. The lateral hypothalamic parvalbumin-immunoreactive (PV1) nucleus in rodents* Zoltán Mészár1, Franck Girard1, Clifford B. Saper2 and Marco R. Celio1,2** 1Anatomy Unit and “Program in Neurosciences”, Department of Medicine, University of Fribourg, Rte. A. Gockel 1, CH-1700 Fribourg, Switzerland 2 Neurology and Neuroscience, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA Running title: Parvalbumin-positive nucleus in the lateral hypothalamus Associate Editor: Paul W. Sawchenko Key Words: medial forebrain bundle, lateral tuberal nucleus, glutamate, projection neurons, neuropeptides, vocalization Corresponding author: Marco R. Celio, Anatomy and “Program in Neuroscience”, Department of Medicine, University of Fribourg, Rte. A. Gockel 1, CH-1700 Fribourg, Switzerland. Phone: +41 26 300 84 91; Fax: +41 26 300 97 33. E-mail: http://doc.rero.ch [email protected]. **MRC spent sabbatical leaves at HMS in 1997 and 2008. Supported by the Canton of Fribourg, an grant of the Swiss National Science Foundation (no.: 3100A0-113524), the Novartis Foundation and USPHS grants NS33987 and NS072337. *Dedicated to Emilio Celio (1927-2011), founder of Swant. Abbreviations: Anatomic: IIn: optic nerve 3dV: third ventricle 2 A: amygdala AHA: anterior hypothalamic area Cer: cerebellum cp: cerebral peduncle DMH: dorsomedial hypothalamic
    [Show full text]
  • Pharmacy Edition
    Mythbusters: Pharmacy Edition University of Washington School of Pharmacy Residents February 2012 Quarterly news- Myth: The human chorionic gonadotropin (hCG) is a weight loss miracle cure By Elina Baskina, PharmD (Valley View Clinical Pharmacy) letter developed by the University Finding: BUSTED stricted caloric intake. Proponents of the diet of Washington Explanation: claim that although calories are highly re- The ―hCG diet‖ (as it‘s commonly known) was stricted, it is the hCG that prevents patients School of Phar- developed by a British endocrinologist Dr. from feeling hungry and weak. If this were macy Residents. Albert T.W. Simeons in the 1950s. He believed true, a greater drop out rate would have been in the use of hCG as a treatment modality for noted in the placebo arm of the randomized Please enjoy our adiposogenital dystrophy – a pituitary disor- trials. However, as the authors of the meta- ―mythbusters‖ der that causes severe obesity and a delay analysis noted, this was not the case. edition. in puberty in young men. Dr. Simeons went on to perfect his hCG weight loss protocol The hCG diet should not be recommended to Edited by Sheila Song and and his method was largely sought after by patients. There is no data backing the efficacy Morgan Adams the society‘s elite and old Hollywood. The of hCG as a weight loss supplement. The highly tenets of the ―hCG diet‖ are as follows: dura- restrictive diet puts the patient at risk for Inside this issue: tion of 3.5-6 wks; fat-free, 500 kcal/day malnutrition. Sustainable weight loss must be diet; daily injections of 125 IU of hCG.
    [Show full text]
  • At the Staff Meeting of the Department of Pediatrics №4
    Ministry of Health of Ukraine Bogomolets National Medical University “APPROVED” At the staff meeting of the Department of pediatrics №4 Chief of the Department of Pediatrics №4 Academician, Professor, MD, PhD Maidannyk V.G. __________________________(Signature) “_____” ___________________ 2020 y. Methodological recommendations for students Subject Pediatrics, Children’s infectious diseases. Module 1 Pediatrics Topic Thyroid gland diseases in children. Course 5 Faculty Medical №2 Kyiv -2020 1 AUTHORSHIP Head of the Department - Doctor of Medical Sciences, MD, PhD, Academician of the NAMS of Ukraine Professor V.G. Maidannyk; MD, PhD, Associate Professor Ie.A. Burlaka; MD, PhD, Associate Professor R.V. Terletskiy; MD, PhD, Associate Professor O.S. Kachalova O.S.; MD, PhD Assistant T.D. Klets; MD, PhD Assistant T.A. Shevchenko. Topic: Thyroid gland diseases in children. Classification of thyroid diseases in children. Etiology, pathogenesis, clinical presentation, diagnostics, differential diagnostics, treatment, prophylaxis of diffuse toxic goiter, hypothyroidism, autoimmune thyroiditis, Prognosis. І. Topic Relevance. Thyroid functions disturbances is the common state among children. Thyroid diseases is quite various in children age. Thyroid diseases problems are the main relating to Chernobyl disaster because of morbidity increasing among children in autoimmune thyroiditis, hypothyroidism, good- quality and malignant tumors of thyroid. One of major places occupies congenital hypothyroidism that meets in frequency of 1 case to 5000 newborns. Congenital hypothyroidism in 85 – 90% of cases is primary and related to the iodine deficit or thyroid dysgenesis. Thus, the aplasia, hypogenesis or dystopia of thyroid are the more frequent states. Primary hypothyroidism in 5 – 10% of cases unconditioned by dyshormonose (autosomal – recessive inheritance).
    [Show full text]
  • X-Linked Kallman's Syndrome: a Molecular Genetic And
    X-LINKED KALLMANN'S SYNDROME: A MOLECULAR GENETIC AND DEVELOPMENTAL ANALYSIS. BY VERONIQUE MICHAL DUKE B.Sc (Hons) A thesis submitted to the University of London in fulfdment of the requirement for the degree of Doctor of Philosophy. Academic Department of Medicine, Division of Endocrinology Royal Free Hospital School of Medicine, Rowland Hill Street, LONDON NW3 2QG. 1996 ProQuest Number: U090189 All rights reserved INFORMATION TO ALL USERS The quality of this reproduction is dependent upon the quality of the copy submitted. In the unlikely event that the author did not send a complete manuscript and there are missing pages, these will be noted. Also, if material had to be removed, a note will indicate the deletion. uest. ProQuest U090189 Published by ProQuest LLC(2016). Copyright of the Dissertation is held by the Author. All rights reserved. This work is protected against unauthorized copying under Title 17, United States Code. Microform Edition © ProQuest LLC. ProQuest LLC 789 East Eisenhower Parkway P.O. Box 1346 Ann Arbor, Ml 48106-1346 ABSTRACT Kallmami's syndrome (KS) is defined as the association of hypogonadotrophic hypogonadism (IHH), caused by hypothalamic gonadotrophin releasing hormone (GnRH) deficiency, and anosmia, due to malformation of the olfactory bulbs and tracts. Patients most commonly present with delayed puberty and may also present in childhood with cryptorchidism. Renal agenesis seen in 40% and synkinesis observed in up to 90% of patients with X-linked KS (XKS) are likely to originate in the aberrant expression oîKAL (Xp22.3) during early foetal development. Failure of the olfactory axons in the accessory ol&ctory nerves to project through the cribriform plate and estabhsh synaptic contact with the developing olfactory bulb is thought to be central to the pathogenesis of these clinical features.
    [Show full text]
  • Typical Disorders of the Endocrine System 1. Choose the Correct Option of Transpituitary Regulation of the Endocrine Glands: A) the Cerebral Cortex – Peripheral Gland
    Typical disorders of the endocrine system 1. Choose the correct option of transpituitary regulation of the endocrine glands: a) the cerebral cortex – peripheral gland. + b) the cerebral cortex - the hypothalamus-pituitary – peripheral gland. c) the cerebral cortex - the hypothalamus - the nerve conductors - peripheral gland. d) the cerebral cortex - pituitary - hypothalamus – peripheral gland. e) subcortical centers - nerve agents – peripheral gland. 2. Transpituitary regulation is the basis for: a) pancreas; + b) thyroid gland; + c) gonads, d) parathyroid glands; + e) adrenal cortex. 3. Violations of transpituitary regulation are the basis of changes in production of a) insulin; b) glucagon; c) parathyrin; d) catecholamines; + e) thyroid hormones. 4. Violation of transpituitary regulation is the basis of changes in production of + a) TSH; b) aldosterone; c) insulin; d) parathyroid hormone; e) glucagon. 5. Basis of the violation of feedback mechanism is + a) reducing the sensitivity of hypothalamic centers sensing fluctuations in hormone concentrations in the blood; b) the decrease in the production of liberins; c) the increase in the production of statins; d) an increase in anterior pituitary hormone production; e) reduction of the production of statins. 6. Metabolism of hormones is disrupted in diseases of + a) liver; b) the spleen; c) heart; d) lungs; e) nervous system. 7. Hypoproteinemia is accompanied by + a) an increase in the fraction of free hormone and increasing their effects; b) an increase in the fraction of free hormone and a decrease in their effects; c) a decrease in the fraction of free hormone and a decrease in their effects; d) a decrease in the fraction of free hormone and an increase in their effects; e) the perverse effect of hormones.
    [Show full text]
  • B Disorders of Autonomic Nervous System
    Application of the International Classification of Diseases to Neurology \ Second Edition World Health Organization Geneva 1997 First edition 1987 Second edition 1997 Application of the international classification of diseases to neurology: ICD-NA- 2nd ed. 1. Neurology - classification 2. Nervous system diseases - classification I. Title: ICD-NA ISBN 92 4 154502 X (NLM Classification: WL 15) The World Health Organization welcomes requests for permission to reproduce or translate its publications, in part or in full. Applications and enquiries should be addressed to the Office of Publications, World Health Organization, Geneva, Switzerland, which will be glad to provide the latest information on any changes made to the text, plans for new editions, and reprints and translations already available. ©World Health Organization 1997 Publications of the World Health Organization enjoy copyright protection in accordance with the provisions of Protocol 2 of the Universal Copyright Convention. All rights reserved. The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the Secretariat of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. The mention of specific companies or of certain manufacturers' products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of
    [Show full text]
  • Absence of Pituitary Failure in Fat Boys with Testicular Deficiency
    T. E. JONES AND R. W. KEHM Actually each instance presented a difficult diagnostic problem. In not one case could an absolute diagnosis of hernia as the cause of the obstruction be made, although hernia was suspected in all but the second case. In any occasion of acute, intestinal obstruction where there is a history of previous hernia or any masses in the inguinal or femoral region, the possibility of strangulation with incarceration of the hernia should be excluded. The incision should be in a region where the suspected hernia is easily accessible. Decision as to where the incision should be made, however, is often difficult when the etiologic factor is not localized. Clinical diagnosis of high or low obstruction may help since the jejunum and proximal portion of the ileum usually lay high in the abdomen and to the left, while the distal portion of the ileum is apt to be in the lower part of the abdomen or pelvis. In the first case there was some difficulty in freeing the incarcerated bowel because the in- cision was distant from the site of herniation. A small incision is preferable. It may be enlarged if indicated. Through a small wound a collapsed loop of intestine can be picked up and traced back to the point of obstruction. A large incision presents the problejn of coping with an open abdomen full of distended loops of bowel. With a small incision shock from exposure and handling is mini- mized, and closure of the wound is greatly facilitated. ABSENCE OF PITUITARY FAILURE IN FAT BOYS WITH TESTICULAR DEFICIENCY E.
    [Show full text]
  • Pathophysiology of the Reproductive System and Sex Hormones
    PATHOPHYSIOLOGY OF THE REPRODUCTIVE SYSTEM AND SEX HORMONES Martina Šalomová Department of Pathological Physiology, Faculty of Medicine in Pilsen Infertility and male or female phenotype disorders represent the main disorders of reproductive system. Sex hormones Estrogens - estron (E1), estradiol (E2), estriol (E3) - steroid hormones (precursors – androstenedione, testosterone) - sources: ovary, placenta, testes, fat tissue in case of estrone (after menopause, the estrone constitutes the main estrogen), exogenous estrogens, phytoestrogens, endocrine active tumors Estrogens are feminizing hormones and their production and plasma levels fluctuate during the ovarian cycle. Estradiol, the main estrogen in fertile females, is produced by cells of theca interna and granulosa (follicular) cells (+ corpus luteum). Its secretion is regulated by gonadotrophin hormones of the adenohypophysis (FSH and LH). Effects of estrogens: - Development and growth of reproductive organs - Increase blood flow in reproductive organ and stimulate lubrication of the vagina - Stimulate neuroplasticity processes and affects mood - Neuroprotective action - Increase of NO and prostacyclin production → short-term vasodilatation - ↓ cholesterol and vasodilatation by local increase of NO production - Stimulation of blood coagulation (higher concentrations increase the risk of thrombosis) - Mildly increase of water and salt retention; increases angiotensinogen production - stimulate osteoblasts, inhibit osteoclasts. As a result, they prevent osteoporosis, accelerate body
    [Show full text]
  • Loss of NSCL-2 in Gonadotropin Releasing Hormone Neurons
    The Journal of Neuroscience, June 19, 2013 • 33(25):10459–10470 • 10459 Development/Plasticity/Repair Loss of NSCL-2 in Gonadotropin Releasing Hormone Neurons Leads to Reduction of Pro-Opiomelanocortin Neurons in Specific Hypothalamic Nuclei and Causes Visceral Obesity Thomas Schmid,1 Stefan Gu¨nther,1 Luca Mendler,2 and Thomas Braun1 1Max Planck Institute for Heart and Lung Research, D-61231 Bad Nauheim, Germany, and 2Institute of Biochemistry, Faculty of General Medicine, University of Szeged, H-6720 Szeged, Hungary Regulation of sexual reproduction and energy homeostasis are closely interconnected, but only few efforts were made to explore the impact of gonadotropic neurons on metabolic processes. We have used Nscl-2 mutant mice suffering from adult onset of obesity and hypogonadotropic hypogonadism to study effects of gonadotropin releasing hormone (GnRH) neurons on neuronal circuits controlling energy balance. Inactivation of Nscl-2 in GnRH neurons but not in pro-opiomelanocortin (POMC) neurons reduced POMC neurons and increased visceral fat mass, suggesting a critical role of GnRH cells in the regulation of POMC neurons. In contrast, absence of POMC processing in the majority of Nscl-2-deficient POMC neurons had no effect on energy homeostasis. Finally, we investigated the cellular basis of the reduction of GnRH neurons in NSCL-2 mutants using a lineage tracing approach. We found that loss of Nscl-2 results in aberrant migration of GnRH neurons in Nscl-2 mutant mice causing a lineage switch of ectopically located GnRH neurons. Introduction well as in multiple areas of the CNS and PNS. In adult mice, Onset of puberty is controlled by awakening of gonadotropin NSCL-2 is found in the paraventricular (PVN) and arcuate (Arc) releasing hormone (GnRH) neurons, which start to release nuclei of the hypothalamus (Kru¨ger et al., 2004), in which its GnRH in a pulsatile manner, leading to activation of GnRH- expression is stimulated by food intake and leptin injection (Vella dependent hypothalamic–pituitary–gonadal axis, gametogene- et al., 2007).
    [Show full text]
  • Laurence-Moon-Biedl Syndrome
    LAURENCE-MOON-BIEDL SYNDROME A Report, of Four Cases in One Family E. Perry McCullagh, M.D., and E. J. Ryan, M.D. The Laurence-Moon-Biedl syndrome was first described by Laurence and Moon in the British Journal of Ophthalmology in 1866. Further reports by Bardet1 in 1920 and by Biedl2 in 1922 resulted in the application of the terms Biedl-Bardet syndrome and Laurence- Biedl syndrome in some instances. The condition is uncommon, only 129 cases having been reported until the middle of 1940, according to Schwartz and Boudreau3. The following features are characteristic of the condition: (1) Mental retardation, (2) pigmentary degeneration of the retina, (3) adiposo- genital dystrophy, (4) familial occurrence, and (5) polydactylism or syndactylism. The presence of all of these characteristics is not a funda- mental necessity in the establishment of the diagnosis, but when one or more is absent, a familial occurrence would appear to be a reasonable requirement, as mentioned by Molitch, et al.4 Of the 77 cases (includ- ing 4 of their own) in the world literature until 1932, reviewed by Reilly and Lisser5, only 25 presented all of the typical findings. Other anomalies have been reported by various observers, and include nystagmus, night blindness, atresia ani, various additional skeletel abnormalities, and deafness, among others. The pathogenesis of the disorder is incompletely understood. The familial occurrence is significant. Numerous reports are available in which are recorded the finding of one or more characteristics of the condition in antecedents of affected individuals. There have been no instances reported indicating inheritance of the entire complex, al- though, as mentioned by Sorsby, Avery and Cockayne6, there have been case records which indicate that patients with this syndrome may not necessarily be sterile.
    [Show full text]