DOCSLIB.ORG

Diabetes Insipidus a Matter of Fluids

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Diabetes Insipidus a Matter of Fluids 1.0 ANCC CONTACT HOUR Diabetes insipidus A matter of fluids Nurses in all clinical areas, from pediatrics to large amounts of dilute urine, increased geriatrics, may encounter this relatively rare thirst, and an increased likelihood of de- hydration, this disorder is seen across the disease. Knowing how to identify, monitor, and lifespan, equally among men and treat it can help save patients from potentially women. Diabetes mellitus (DM) and DI life-threatening complications. are neither the same condition, nor are they related. Although they both share By Amanda Perkins, DNP, RN the word diabetes, they are two very dif- ferent disorders. In patients with DM, blood glucose levels are elevated; this Diabetes insipidus (DI) is a rare condition isn’t the case in individuals with DI. affecting approximately 1 out of 25,000 This article provides a description of people. Characterized by the passage of DI, including the different types, signs AODAODAODAOD / SHUTTERSTOCK 28 Nursing made Incredibly Easy! May/June 2020 www.NursingMadeIncrediblyEasy.com Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved. and symptoms, diagnosis, treatment, and nursing care of patients with the disorder. The mechanism of DI The body’s role in fluid balance Relying on a variety of factors, including Anterior Posterior thirst, the kidneys, and the hormone vaso- pituitary pituitary pressin (also known as antidiuretic hor- mone [ADH]), the maintenance of fluid balance in the body is essential. Vasopres- sin plays a significant role in the regula- tion of urination and, in turn, fluid and electrolyte balance. In addition to being produced by the hypothalamus, vasopres- sin is also stored in and secreted by the pituitary gland. ADH deficiency When the body senses that it has a low fluid level, vasopressin is released to tell the kidneys to absorb a smaller amount of fluid from the bloodstream, effectively H2O increasing the amount of fluid in the body. In cases of dehydration or instances in Collecting duct which a person has hypotension, increased amounts of ADH are released to increase the amount of fluid in the body. Impairment of water On the flip side, when the body senses reabsorption that it has a high fluid volume, the release of vasopressin is either decreased or stopped Urine completely, resulting in an increased loss of fluid in the form of urine. Basically speaking, Decreased renal water reabsorption vasopressin or ADH controls the amount of water that’s released by the kidneys as urine. Four types Inappropriately dilute When DI is present, the kidneys are un- urine able to maintain the delicate fluid balance within the body (see The mechanism of DI). An individual with DI makes and passes DI too much urine, which can lead to signifi- Polyuria, polydipsia cant problems including, but not limited to, dehydration and fluid and electrolyte Source: Braun C, Anderson C. Applied Pathophysiology: A Conceptual Approach to the imbalances. The urine of a person with DI Mechanisms of Disease. 3rd ed. Philadelphia, PA: Wolters Kluwer Health; 2017. is said to be insipid, which means dilute and odorless. Normally, an individual will There are four types of DI: central, have a urine output of approximately 1 to nephrogenic, dipsogenic, and gestational. 2 L per day, whereas the individual with DI may pass anywhere from 3 to 20 L per Central DI day. Additionally, these individuals may Central DI is caused by damage to the urinate as often as every 15 to 20 minutes hypothalamus or pituitary gland due to throughout the course of a day. surgery, infection, inflammation, a www.NursingMadeIncrediblyEasy.com May/June 2020 Nursing made Incredibly Easy! 29 Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved. tumor, or a head injury. To review, the kidneys concentrate urine, leading to hypothalamus makes vasopressin, a large amounts of dilute urine. hormone responsible for increasing or decreasing urine output, and the pitu- Dipsogenic DI itary gland stores and releases vasopres- Dipsogenic DI is caused by a defect of sin. Damage to these areas of the brain the thirst mechanism within the hypo- will lead to difficulty with the produc- thalamus. Individuals with this type of tion, storage, and release of vasopressin. DI are very thirsty, and this increased With central DI, the body has lower- thirst correlates with an increase in fluid than-normal amounts of vasopressin, intake. When fluid intake is increased, which can lead to too much fluid be- we see a suppression in vasopressin se- ing removed from the body in the cretion and increased urinary output. form of urine. In many cases, fluid is This condition typically has the following rapidly lost from the body, leading to three phases: polydipsia and polyuria, dehydration. hyponatremia, and water intoxication. The signs and symptoms of water intoxi- Nephrogenic DI cation are nausea, vomiting, delirium, Nephrogenic DI is caused by kidneys ataxia, seizures, and coma. that are unable to concentrate urine. The Disorders associated with dipsogenic kidneys don’t respond appropriately to DI include chronic meningitis, granuloma- vasopressin, resulting in too much fluid tous disease (immune system disorder in being removed from the body. In individ- which phagocytes don’t work properly), uals with this condition, urine production multiple sclerosis, and mental health dis- can be as high as 12 L per day, with uri- orders. When dipsogenic DI is caused by a nation occurring as often as every hour. mental health disorder, it may be referred Children with nephrogenic DI have a to as psychogenic polydipsia or compul- congenital form, whereas adults present sive drinking. Schizophrenia, compulsive with an acquired form. behaviors, affective disorders, psychosis, Causes of nephrogenic DI include an personality disorders, and stress have been inherited gene, gene mutations, chronic associated with psychogenic polydipsia. kidney disease, medications, decreased Although seen in a variety of mental health serum potassium levels, increased serum disorders, this condition is most commonly calcium levels, and/or a blockage in the seen in patients with schizophrenia. In urinary tract. Lithium is the drug most some cases, the medications used to treat commonly associated with the condition. psychiatric disorders can cause dry mouth, In addition, the antiviral medication foscar- leading to an increased intake of fluids. net and the antipsychotic drug cloza pine Note that this type of DI can lead to hypo- have been associated with nephrogenic DI. natremia instead of hypernatremia. When Glucocorticoids and alcohol use may also hyponatremia develops, it can worsen lead to its development. mental health symptoms for the patient. Medications associated with nephro- genic DI can cause damage to kidney Gestational DI cells, which leads to the cells not respond- Gestational DI typically occurs during ing to vasopressin. Individuals taking lith- the third trimester of pregnancy, affecting ium should have kidney function tests 2 to 6 women out of 100,000. The most every 3 months. As is the case with lithi- common signs and symptoms of gesta- um, hypercalcemia can lead to kidney tional DI are polyuria and polydipsia, damage, resulting in nephrogenic DI. both of which are common in pregnancy, Hypokalemia may alter the way that the making diagnosis a challenge in many 30 Nursing made Incredibly Easy! May/June 2020 www.NursingMadeIncrediblyEasy.com Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved. cases. The risk of gestational DI rises A closer look at hypovolemic shock with an increased placental mass, such as occurs with multiple fetuses. Potential In severe cases, DI can lead to hypovolemic causes of gestational DI are hemolysis shock—a loss of fluid so severe that the heart with elevated liver enzymes and low is unable to pump enough blood to perfuse the body. Hypovolemic shock is a medical platelet count, or HELLP syndrome; pre- emergency and must be identified and treated eclampsia; and acute fatty liver of preg- early. Signs and symptoms include: nancy. Gestational DI may also be caused • hypotension • decreased urine because prostaglandin produced during • decreased output pregnancy can reduce the kidney’s sensi- temperature • confusion tivity to vasopressin. • rapid, thready • weakness With this disorder, the enzyme vaso- pulse • anxiety pressinase made in the placenta can break • tachypnea • agitation down the mother’s vasopressin. Dur- • pallor • loss of ing pregnancy, trophoblasts (cells that • cool, clammy skin consciousness. develop into a major part of the placenta) produce large amounts of the enzyme prevents this risk by sending signals that vasopressinase, which inactivates ADH. the person is thirsty. Polydipsia as a result Interestingly, vasopressinase activity of thirst is another key feature of DI; it can increases 40- to 50-fold during pregnancy. be so significant that the patient drinks as The liver’s ability to degrade this enzyme much as 20 L per day. The polyuria and increases fourfold and the release of ADH polydipsia that occur with DI occur both also increases. Although gestational DI day and night, which is a distinguishing can be problematic, this condition is usu- feature. Due to diuresis, patients with DI ally mild with minimal symptoms and can develop hypernatremia, which can resolves spontaneously 2 to 3 weeks after ultimately lead to confusion. Dehydra- delivery. tion and hypernatremia may lead to the development of weakness, fatigue, hypo- Signs and symptoms tension, tachycardia, and a decreased A variety of signs and symptoms are LOC. In addition to dehydration, you’ll associated with DI. Some of the more see increased serum osmolality or concen- common signs and symptoms include: trated blood. Individuals with DI are also • polyuria at risk for hypovolemic shock (see A closer • polydipsia look at hypovolemic shock). • dehydration Young children may experience severe • hypernatremia dehydration, vomiting, constipation, • dizziness fever, irritability, sleep disturbances, poor • weakness growth, excessive crying, and failure to • nocturia thrive. Older children may wet the bed, • fatigue have a decreased appetite, and be • hypotension fatigued.
Load more

Recommended publications
  • Thyroid Gland, Adrenal Glands, and Gonads Anterior Pituitary „ Negative Feedback Mechanism Finishes the Gonadotropin Releasing Hormone (Gnrh)
    The Endocrine System Disease of the Pituitary Gland Endocrine System Diseases of the Thyroid Maria Alonso, CDE, PA-C Disease of the Adrenal Glands Diabetes Mellitus Lipid Disorders UMDNJ PANCE/PANRE Review Course (becoming Rutgers July 1, 2013) UMDNJ PANCE/PANRE Review Course UMDNJ PANCE/PANRE Review Course (becoming Rutgers July 1, 2013) http://commons.wikimedia.org/wiki/File:Illu_endocrine_system.jpg (becoming Rutgers July 1, 2013) UMDNJ PACE/PANRE Review Course becoming Rutgers July 1, 2013 PITUITARY ANATOMY Pituitary Anatomy •Small pea-sized gland at the base of brain •Located in the “Sella Turcica” •Functions as "The Master Gland" •Attached below hypothalamus by stalk •Large anterior lobe (adenohypophysis) PituitaryPituitary GlandGland •Smaller posterior lobe (neurohypophysis) •The optic chiasm lies directly above •Supplied by internal carotid artery UMDNJ PANCE/PANRE Review Course UMDNJ PANCE/PANRE Review Course (becoming Rutgers July 1, 2013) UMDNJ PANCE/PANRE Review Course Public domain available at: (becoming Rutgers July 1, 2013) (becoming Rutgers July 1, 2013) http://commons.wikimedia.org/wiki/File:Grays_pituitary.png UMDNJ PACE/PANRE Review Course becoming Rutgers July 1, 2013 Quick Review Quick Review: Hypothalamic Quick Review Pituitary Axis Hypothalamus Neurosecretory cells send messages from Hypothalamus brain to hypothalamus GnRH GHRH SS TRH DA CRH ++ Hypothalamus sends chemical hormones + ++__+ to the pituitary gland OxytocinPosterior Pituitary ADH Pituitary gland secretes hormones to the FSH/LH GH GH/TSH TSH
    [Show full text]
  • NUR 155.01: Meeting Adult Physiological Needs I
    University of Montana ScholarWorks at University of Montana Syllabi Course Syllabi Fall 9-1-2006 NUR 155.01: Meeting Adult Physiological Needs I LeAnn Ogilvie University of Montana, Missoula, [email protected] Follow this and additional works at: https://scholarworks.umt.edu/syllabi Let us know how access to this document benefits ou.y Recommended Citation Ogilvie, LeAnn, "NUR 155.01: Meeting Adult Physiological Needs I" (2006). Syllabi. 10732. https://scholarworks.umt.edu/syllabi/10732 This Syllabus is brought to you for free and open access by the Course Syllabi at ScholarWorks at University of Montana. It has been accepted for inclusion in Syllabi by an authorized administrator of ScholarWorks at University of Montana. For more information, please contact [email protected]. University of Montana College of Technology Practical Nursing Program NUR 155 Spring 2006 Course: NUR 155 Meeting Adult Physiological Needs Date Revised: September 11, 2006 Instructor: LeAnn Ogilvie, MS, RN [email protected] Office Phone #243-7863 Office Hours.: Thursday 3PM-4PM & by appointment Semester Credits: 3 Co-requisite Courses: NUR 151, NUR 154, & NUR 195-01 (152) Course Design: On-Line Distance Learning Clinical Lab as scheduled Course Description: The focus of this lecture course is the application of nursing theories, principles, and skills to meet the basic human needs of adult clients experiencing more complex, recurring actual or potential health deviations. The nursing process provides the framework which enables students to synthesize aspects of communication, ethical/legal issues, cultural diversity, and optimal wellness. Supervised care of the adult client is provided during the clinical experience in the acute care setting.
    [Show full text]
  • Diabetes Insipidus View Online At
    Diabetes Insipidus View online at http://pier.acponline.org/physicians/diseases/d145/d145.html Module Updated: 2013-01-29 CME Expiration: 2016-01-29 Author Robert J. Ferry, Jr., MD Table of Contents 1. Diagnosis ..........................................................................................................................2 2. Consultation ......................................................................................................................8 3. Hospitalization ...................................................................................................................10 4. Therapy ............................................................................................................................11 5. Patient Counseling ..............................................................................................................16 6. Follow-up ..........................................................................................................................17 References ............................................................................................................................19 Glossary................................................................................................................................22 Tables ...................................................................................................................................23 Figures .................................................................................................................................39
    [Show full text]
  • Endocrine System
    disorders of the endocrine system duke trillanes iii, rn, map endocrine system endocrine glands endocrine system o endocrine glands o secrete their products directly into the bloodstream o different from exocrine glands o exocrine glands: secrete through ducts onto epithelial surfaces or into the gastrointestinal tract hormones o are chemical substances that are secreted by the endocrine glands. o can travel moderate to long distances or very short distances. o acts only on cells or tissues that have receptors for the specific hormone. o target organ: the cell or tissue that responds to a particular hormone. hypothalamus and pituitary gland regulation of hormones: negative feedback mechanism o if the client is healthy, the concentration or hormones is maintained at a constant level. o when the hormone concentration rises, further production of that hormone is inhibited. o when the hormone concentration falls, the rate of production of that hormone increases. diseases of the endocrine system o “primary” disease – problem in target gland; autonomous o “secondary” disease – problem outside the target gland; most often due to a problem in the pituitary gland disorders of the anterior pituitary gland hypopituitarism hyperpituitarism hypopituitarism o caused by low levels of one or more anterior pituitary hormones. o lack of the hormone leads to loss of function in the gland or organ that it controls. causes of primary hypopituitarism o pituitary tumors o inadequate blood supply to pituitary gland o sheehan syndrome o infections and/or inflammatory
    [Show full text]
  • The Encyclopedia of Endocrine Diseases and Disorders
    THE ENCYCLOPEDIA OF lJ z > 0 z Endocrine < I ~ Diseases UJ< I and Disorders UJ ...J '-'- z 0 V'l 1- u '-'-< WILLIAM P ETIT. JR.. M.0. CHRISTINE ADAMEC THE ENCYCLOPEDIA OF ENDOCRINE DISEASES AND DISORDERS THE ENCYCLOPEDIA OF ENDOCRINE DISEASES AND DISORDERS William Petit Jr., M.D. Christine Adamec The Encyclopedia of Endocrine Diseases and Disorders Copyright © 2005 by William Petit Jr., M.D., and Christine Adamec All rights reserved. No part of this book may be reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage or retrieval systems, without permission in writing from the publisher. For information contact: Facts On File, Inc. 132 West 31st Street New York NY 10001 Library of Congress Cataloging-in-Publication Data Petit, William. The encyclopedia of endocrine diseases and disorders / William Petit Jr., Christine Adamec. p. ; cm. Includes bibliographical references and index. ISBN 0-8160-5135-6 (hc : alk. paper) 1. Endocrine glands—Diseases—Encyclopedias. [DNLM: 1. Endocrine Diseases—Encyclopedias—English. WK 13 P489ea 2005] I. Adamec, Christine A., 1949– II. Title. RC649.P48 2005 616.4’003—dc22 2004004916 Facts On File books are available at special discounts when purchased in bulk quantities for businesses, associations, institutions, or sales promotions. Please call our Special Sales Department in New York at (212) 967-8800 or (800) 322-8755. You can find Facts On File on the World Wide Web at http://www.factsonfile.com. Text and cover design by Cathy Rincon Printed in the United States of America VB FOF 10 9 8 7 6 5 4 3 2 1 This book is printed on acid-free paper.
    [Show full text]
  • Of /Endocrinology&Metabolic Medicine
    Log Out Welcome gehad Home Online Revision Courses Books Help Contact Us About Us Blog My Account Online Extras Community FAQs You are here: MyPasTest » MRCP 2 Online - Apr Exam 2014 » Question Question Browser: MRCP 2 Session Progress Q Correct 60 Q Incorrect 256 Q Total 316 Average Q Percentage 18 % A 37-year-old woman has been brought to A&E with a 1-day history of abdominal pain, diarrhoea and vomiting. She has a history of type-1 diabetes mellitus and pernicious anaemia. Her partner tells you that her GP has R Correct 60 recently prescribed amoxicillin for her chest infection and that she has lost 12.5 kg (nearly 2 stone) in weight over R Incorrect 256 the last few months. She does not smoke or drink alcohol. On examination, she is flushed, disorientated, agitated R Total 316 and jaundiced. Her temperature is 42.1 °C, pulse 180 bpm and irregular and BP 180/70 mmHg. You detect a third R Percentage 18 heartsound, her chest is clear and her abdomen generally tender. Her legs are weak proximally and all reflexes % brisk. She has some pitting oedema of her lower limbs. View More Blood tests reveal: Key: Difficulty Levels Na 131 mmol/l K 2.8 mmol/l urea 17.6 mmol/l creatinine 165 µmol/l Ca 2.82 mmol/l Easy Average Difficult bilirubin 64 µ mol/l Correct Incorrect ALT 141 U/l alkaline phosphatase 210 U/l glucose 19.8 mmol/l Reference WBC 17.2 × 109/l neutrophils 15.6 × 109/l Show Normal Values Hb 10.3 g/dl Haematology MCV 102.4 fl Haemoglobin platelets 273 × 109 /l Males 13.5 - Results of an ECG show a fast AF.
    [Show full text]
  • ODESA NATIONAL MEDICAL UNIVERSITY Department of Internal Medicine № 1 with the Course of Cardiovascular Diseases
    ODESA NATIONAL MEDICAL UNIVERSITY Department of Internal Medicine № 1 with the course of cardiovascular diseases METHODIC RECOMMENDATIONS FOR PRACTICAL CLASSES Topic "Disease of the hypothalamic-pituitary system. Diseases of the gonads " Course IV Faculty: international Specialty :222 -"Medicine" The lecture was discussed on the methodical meeting of the department 27.08.2020 Protocol № 1 Head of the department Prof, Yu.I. Karpenko Odesa I. Actuality of the topic. Acromegalyis a syndrome that results when the pituitary gland produces excess growth hormone (hGH) after epiphyseal plate closure at puberty. A number of disorders may increase the pituitary's GH output, although most commonly it involves a GH producing tumor called pituitary adenoma, derived from a distinct type of cell (somatotrophs). Acromegaly most commonly affects adults in middle age, and can result in severe disfigurement, serious complicating conditions, and premature death if unchecked. Because of its insidious pathogenesis and slow progression, the disease is hard to diagnose in the early stages and is frequently missed for many years, until changes in external features, especially of the face, become noticeable. Acromegaly is often also associated with gigantism. Diseases of the sexual glands are a consequence of chromosomal abnormalities, detected when other endocrine glands are affected. In diseases associated with violations of sexual differentiation, sex may be incorrectly defined, which requires its change in the future. II. The purpose of the lecture: 1. To study the method of determination of etiologic and pathogenic factors of diseases of the hypothalamic-pituitary system (HPS). 2. To familiarize students with classifications of diseases of HPS. 3. Determination of variants of clinical picture of HPS diseases.
    [Show full text]
  • Specimen Collection Instructions
    COLLECTION INSTRUCTIONS |TEST NAME |DEPARTMENT |SPECIMEN CONTAINER |CAP COLOUR |COMMENTS 1,25-Dihydoxycholecalciferol Referred Specimens Blood/SST tube Gold Non-rebateable test. Refer to non-rebateable price list. Patient payment consent required. 1,25-Dihydroxy Vitamin D Referred Specimens Blood/SST tube Gold Non-rebateable test. Refer to non-rebateable price list. Patient payment consent required. 16S rRNA PCR (Ribosomal RNA Referred Specimens Blood/ Fluid/Tissue Sterile Non-rebateable test. Refer to non-rebateable price list. gene sequence) Container Patient payment consent required. 17 Ketosteroids (Urine) Biochemistry 24hr urine collection/Urine No preservative (plain). Please note start date / time and collection bottle with no finish date / time on request form. preservative 17-Hydroxy Progesterone Biochemistry Blood/SST tube Gold Specimen ideally collected between 8am & 10am. 17-OH P Biochemistry Blood/SST tube Gold Specimen ideally collected between 8am & 10am. 17-OH Progesterone Biochemistry Blood/SST tube Gold Specimen ideally collected between 8am & 10am. 25 (OH) D Biochemistry Blood/SST tube Gold 25 (OH) D3 Biochemistry Blood/SST tube Gold 25-Hydroxy Cholecalciferol Biochemistry Blood/SST tube Gold 25-Hydroxy Vitamin D Biochemistry Blood/SST tube Gold 5 HIAA (5-Hydroxy Indole Acetic Referred Specimens 24hr urine collection/Urine Acid preservative. Please note start date / time and finish Acid) collection bottle with acid date / time on request form.Dietary restrictions apply for preservative 2 days prior & during test - walnuts, tomatoes, bananas, pineapple, avocado, red plums, egg plant & kiwi fruit. 5 SRT (Serotonin) Referred Specimens Blood/SST tube Gold Tumour marker - carcinoid tumour. 5-HT (Serotonin) Referred Specimens Blood/SST tube Gold Tumour marker - carcinoid tumour.
    [Show full text]
  • Diagnosis and Management of Nephrogenic Diabetes Insipidus
    PBLD – Table #17 Water! Water! Everywhere! Diagnosis and Management of Nephrogenic Diabetes Insipidus Goals: 1. Understand diabetes insipidus and the role of arginine vasopressin production and its role at the kidney 2. Understand how to differentiate nephrogenic diabetes insipidus from central diabetes insipidus and primary polydipsia 3. Understand the etiology of nephrogenic diabetes insipidus 4. Understand the available diagnostic tools and their usefulness in characterizing the picture of nephrogenic diabetes insipidus in the perioperative environement 5. Understand the management plan and/or treatment options for children diagnosed with nephrogenic diabetes insipidus in the perioperative setting Case: A 42-kg 13-year-old female presents with a three-month history of increasing abdominal girth. MRI revealed a cystic retroperitoneal mass. The patient underwent laparoscopic excision of the cyst and drainage of over 7 L of peritoneal fluid. Intraoperative urine output was 0.5 cc/kg/hr. Postoperatively, urine output was 1,050 ml in the first hour and blood pressure (BP) decreased to 68/45. BP responded to fluid resuscitation, however urine output remained elevated. Serum and urine electrolytes and osmolalities were obtained. We will provide a general understanding of diabetes insipidus and then discuss the possible etiologies of acquired nephrogenic diabetes insipidus and its management in the perioperative setting. Questions: 1. What is Diabetes Insipidus? What is the role of arginine vasopressin? 2. What are the three main subgroups? 3. What is the difference between Central and Nephrogenic Diabetes Insipidus? 4. What causes Central vs. Nephrogenic Diabetes Insipidus? 5. What diagnostic tools can be used to determine the cause of polyuria as nephrogenic diabetes insipidus vs.
    [Show full text]
  • Diabetes Insipidus
    www.healthinfo.org.nz Diabetes insipidus If you have cranial diabetes insipidus, it means you don't have enough anti-diuretic hormone (ADH). This hormone is also called arginine vasopressin (AVP). You make ADH in an area of your brain called the hypothalamus, which is just above your pituitary gland. Your pituitary gland releases the ADH into your blood. ADH acts on your kidneys, allowing you to make concentrated urine. If your body doesn't make enough ADH then your kidneys make a lot of dilute urine. As a result, you'll feel thirsty and have to urinate (wee) a lot. These symptoms are similar to those that people have with sugar diabetes (diabetes mellitus). However, people with diabetes insipidus have normal blood sugar levels. Their symptoms are caused by lack of ADH. What causes diabetes insipidus? Almost any disease that affects the pituitary region of the brain can cause diabetes insipidus. Causes include pituitary tumours, and damage caused by surgery or trauma. Sometimes there might be a genetic cause. Sometimes people's kidneys can't respond to ADH. This is called nephrogenic diabetes insipidus (NDI). NDI can be caused by some medications, in particular lithium. If you're taking lithium, it's important that you tell your doctor about any symptoms such as feeling very thirsty and passing lots of urine. You should also have regular blood tests to check your lithium level. Symptoms and diagnosis Feeling very thirsty, drinking lots of fluid (often preferring cold water) and passing lots of urine are the symptoms of diabetes insipidus. We diagnose diabetes insipidus with blood and urine tests.
    [Show full text]
  • PEDIATRIC Emergencymedicinepractice
    PEDIATRIC EmergEnCy medicinE PRACTICE AN EVIDENCE-BASED APPROACH TO PEDIATRIC EMERGENCY MEDICINE s EBMEDICINE.NET April 2011 An Evidence-Based Volume 8, Number 4 Assessment Of Pediatric Author Wesley Eilbert, MD, FACEP Associate Clinical Professor, Department of Emergency Medicine, Endocrine Emergencies University of Illinois College Of Medicine at Chicago, Chicago, IL Peer Reviewers It’s 2:30 am on a slow Thursday night when the triage nurse Laura K. Bachrach, MD brings in an ill-appearing, tachypneic, and febrile 2-year-old Professor of Pediatrics, Stanford University School of Medicine, Stanford, CA; Lucile Packard Children’s Hospital at Stanford, with markedly delayed capillary refill. As you are listening to Stanford, CA inspiratory crackles in the child’s left lung, you notice that her Ara Festekjian, MD, MS medications list includes hydrocortisone and fludrocortisone. Division of Emergency Medicine, Childrens Hospital Los Angeles, Los Angeles, CA; Assistant Professor Of Pediatrics, Keck School Of You ask the child’s mother about these uncommon medications, Medicine Of The University Of Southern California, Los Angeles, CA and she informs you that her daughter has congenital adrenal Martin I. Herman, MD, FAAP, FACEP hyperplasia. As you struggle to recall the specifics of this rela- Attending, Department of Pediatric Emergency Medicine, Sacred Heart Children’s Hospital, Pensacola, FL; Professor of Pediatrics, tively rare condition, the nurse asks you whether this diagnosis Department of Pediatrics, Florida State University College of is going to change the management of this critically ill child. Medicine, Pensacola, FL CME Objectives Most emergency clinicians are quite comfortable treat- Upon completion of this article, you should be able to: ing diabetic ketoacidosis (DKA) in children, but other 1.
    [Show full text]
  • Pituitary Disease in Pregnancy
    Published online: 2019-03-06 GebFra Science | Review Pituitary Disease in Pregnancy: Special Aspects of Diagnosis and Treatment? Hypophysenerkrankungen in der Schwangerschaft: Besonderheiten in der Diagnostik und Therapie? Authors Stephan Petersenn 1, Mirjam Christ-Crain 2, Michael Droste 3, Reinhard Finke 4,JörgFlitsch5, Ilonka Kreitschmann-Andermahr 6, Anton Luger 7, Jochen Schopohl8,GünterStalla8, 9 Affiliations Correspondence 1 ENDOC Praxis für Endokrinologie, Andrologie und Prof. Dr. med. Stephan Petersenn medikamentöse Tumortherapie, Hamburg, Germany ENDOC Praxis für Endokrinologie, Andrologie 2 Endokrinologie, Diabetologie & Metabolismus. und medikamentöse Tumortherapie Universitätsspital Basel, Basel, Switzerland Erik-Blumenfeld-Platz 27A, 22587 Hamburg, Germany 3 Endokrinologie, Diabetologie, Hormonanalytik. [email protected] MEDICOVER MVZ, Oldenburg, Germany 4 Praxis an der Kaisereiche (üBAG), Berlin-Friedenau, Deutsche Version unter: Germany https://doi.org/10.1055/a-0794-7587 5 Klinik und Poliklinik für Neurochirurgie, Kopf- und Neurozentrum, Universitätsklinikum Hamburg- ABSTRACT Eppendorf, Hamburg, Germany The diagnosis and treatment of pituitary disease in pregnancy 6 Neurochirurgische Klinik, Universitätsklinikum Essen, represents a special clinical challenge. Not least because there Universität Duisburg-Essen, Essen, Germany is very little data on the treatment of pregnant patients with 7 Universitätsklinik für Innere Medizin III, Klinische Abteilung pituitary disorders. A selective search of the literature was car- für Endokrinologie & Stoffwechsel, Medizinische ried out with the aim of compiling evidence about the diag- Universität Wien, Wien, Austria nosis and treatment of pituitary disease in pregnancy. The 8 Medizinische Klinik und Poliklinik IV, Klinikum der search covered the databases PubMed/MEDLINE including Universität München, München, Germany PubMed Central and also used the Livivo (ZB MED) search en- 9 Medicover Neuroendokrinologie, München, Germany gine.
    [Show full text]