DOCSLIB.ORG

Diabetes Insipidus: Overview

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Diabetes Insipidus: Overview Asian Pac. J. Nursing and Health Sci., 2019; 2(1):13-18 e-ISSN: 2581-7442 ____________________________________________________________________________________________________________________________________________ Diabetes insipidus: Overview Seema Sharma*, Karam Singh ASBASJSM College of Pharmacy, Bela, Ropar, Punjab, India ___________________________ *Correspondence Seema Sharma ASBASJSM College of Pharmacy, Bela, Ropar, Punjab, India Email: [email protected] Received: 20-11-2018 / Revised: 28-02-2019 / Accepted: 24-03-2019 Abstract Diabetes insipidus is mainly characterized by polyuria, urinary volume over 3 L/day or 40mL/kg/day in adults, leading to subsequent polydipsia; these features are also present in most cases of diabetes mellitus. But today we can use natural treatment to remedy our problems concerning diabetes. This review is about diabetes insipidus which is entirely different from diabetes mellitus. We have read much about diabetes mellitus but now we must know about the diabetes insipidus. Diabetes insipidus is a uncommon condition, in which the kidneys are unable to conserve water. The amount of water which is conserved by the kidney is controlled by anti diuretic hormone (ADH) also called as vasopressin. In this disease there is lack of vasopressin in the body. In this overview there is a full disease profile of diabetes insipidus, so we came to know about the causes, sign & symptoms, treatment and medication for this diease. Keywords: Diabetes insipidus, Diabetes mellitus, Overview. This is an Open Access article that uses a fund-ing model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. Introduction When most people hear "diabetes," they think of opposed to Diabetes Mellitus, where the urine is diabetes mellitus. That's a condition in which blood hypertonic and sweet (mellitus means honey in Greek), sugars are chronically elevated. In fact, diabetes is a DI is defined as having urine that is hypotonic and general term for conditions that cause increased urine bland, in the setting of polyuria. There are various production. And when it comes to increased urine mechanisms of pathogenesis of DI, all leading to the production, diabetes insipidus takes the cake[1]. same clinical manifestation. In cases where the Diabetes insipidus results in excessive thirst and disorder is due to inadequate secretion of ADH, the urination. The reason is problems with a particular disorder is termed Central DI, whereas when the hormone or its receptor. Diabetes insipidus increases disease is a result of renal insensitivity to ADH, the the risk for dehydration. Diabetes insipidus is a disease is termed Nephrogenic DI [3]. In cases where condition in which the body cannot retain enough polyuria is due to vast amounts of ingested fluids water. The patient is excessively thirsty and excretes driven primarily by behavioral or thirst disorders, it is large amounts of extremely diluted urine - a reduction called Primary Polydipsia (PP). Pregnant women can in fluid intake does not reduce amounts and metabolize ADH in an accelerated manner leading to consistency of urine excretion. Diabetes insipidus is Gestational DI [2]. Overall, there are 3 cases of DI per not related to diabetes mellitus (sugar diabetes). 100,000 in the general population [4].With regard to Inappropriate secretion or action of serum antidiuretic some familial forms of nephrogenic DI, incidence hormone (ADH) is termed Diabetes Insipidus (DI), varies and some regions with common ancestry have characterized by polyuria (defined as 24 hour urine higher incidence than other in the general population output in excess of 40 ml/kg) and polydipsia [2]. As [5]. ____________________________________________________________________________________________________________________________________________ Sharma and Singh ASIAN PACIFIC JOURNAL OF NURSING AND HEALTH SCIENCES, 2019; 2(1):13-18 www.apjnh.com 13 Asian Pac. J. Nursing and Health Sci., 2019; 2(1):13-18 e-ISSN: 2581-7442 ____________________________________________________________________________________________________________________________________________ • Insipidus - "without taste or perceptible flavor," from Fr. insipide, from L.L. inspidus Cause "tasteless," from L. in- "not" + sapidus "tasty," DI is an uncommon condition that occurs when the from sapere "have a taste" kidneys are unable to conserve water as they perform This is because patients experience polyuria (an their function of filtering blood. The amount of water excretion of over 2.5 liters of urine per day), and that conserved is controlled by ADH, also called the urine content does not have an elevated glucose vasopressin. concentration, as opposed to diabetes mellitus.[6] ADH is a hormone produced in a region of the brain Causes called the hypothalamus. It is then stored and released Acquired : NDI is most common in its acquired from the pituitary gland, a small gland at the base of forms, meaning that the defect was not present at birth. the brain. These acquired forms have numerous potential causes. DI caused by a lack of ADH is called central diabetes The most obvious cause is a kidney or systemic insipidus. When DI is caused by a failure of the disorder, including amyloidosis, polycystic kidney kidneys to respond to ADH, the condition is called disease, electrolyte imbalance, or some other kidney nephrogenic diabetes insipidus. defect. Central diabetes insipidus can be caused by damage to The major causes of acquired NDI that produce clinical the hypothalamus or pituitary gland as a result of: symptoms (e.g. polyuria) in the adult are lithium • Head injury toxicity and hypercalcemia.Chronic lithium ingestion - • Infection appears to affect the tubules by entering the collecting • Loss of blood supply to the gland tubule cells through sodium channels, accumulating • Surgery and interfering with the normal response to ADH • Tumor (ADH Resistance) in a mechanism that is not yet fully understood.Hypercalcemia causes natriuresis Sign and symptoms (increased sodium loss in the urine) and water diuresis, Diabetes Insipidus leads to frequent urination, and this in part by its effect through the calcium sensing is the most common and clear symptom. receptor (CaR). [7] Frequent urination, unusual thirst, and dehydration are Osmotic : Other causes of acquired NDI include: all symptoms of DI. hypokalemia, post-obstructive polyuria, sickle cell Children suffering from the condition may become disease/trait, amyloidosis, Sjogren syndrome, renal irritable or listless, with fever and vomiting also cystic disease, Barter syndrome and various drugs possible. (Amphotericin B, Orlistat, Ifosfomide, Ofloxacin, Different types of diabetes insipidus Cidofovir, Vaptanes). Central Diabetes insipidus: occurs when the pituitary In addition to kidney and systemic disorders, gland is damaged resulting in ADH deficiency. It is nephrogenic DI can present itself as a side-effect to treated with desmopressin, a synthetic hormone. some medications. The most common and well known Gestational Diabetes insipidus : is associated with of these drugs is lithium, although there are numerous pregnancy, and occurs when an enzyme created by the other medications that cause this effect with lesser placenta destroys ADH in the mother. frequency. [8] Nephrogenic Diabetes insipidus : is a form of Hereditary : This form of DI can also be hereditary: diabetes insipidus due primarily to pathology of the means if a father is having this type of diabetes kidney. This is in contrast to central/neurogenic insipidus so a son or a daughter can also suffer from diabetes insipidus, which is caused by insufficient of the same disease because it is heriditary disease. ADH/AVP. Nephrogenic diabetes insipidus is caused Diagnosis by an improper response of the kidney to ADH, leading Differential diagnosis includes nephrogenic diabetes to a decrease in the ability of the kidney to concentrate insipidus, neurogenic central diabetes insipidus and the urine by removing free water. psychogenic polydipsia. They may be differentiated by Etymology using the water deprivation test. Recently, lab assays • Diabetes - from L. diabetes, from Gk. diabetes for ADH are available and can aid in diagnosis. "excessive discharge of urine," lit. "a passer- If able to rehydrate properly, sodium concentration through, siphon," from diabainein "to pass should be nearer to the maximum of the normal range. through," from dia- "through" + bainein "to This, however, is not a diagnostic finding, as it depends go" on patient hydration. ____________________________________________________________________________________________________________________________________________ Sharma and Singh ASIAN PACIFIC JOURNAL OF NURSING AND HEALTH SCIENCES, 2019; 2(1):13-18 www.apjnh.com 14 Asian Pac. J. Nursing and Health Sci., 2019; 2(1):13-18 e-ISSN: 2581-7442 ____________________________________________________________________________________________________________________________________________ DDAVP can also be used; if the patient is able to trait. It is now more widely recognized, although the concentrate urine following administration of DDAVP, precise number of people affected
Load more

Recommended publications
  • Thursday 23 June 2016 – Morning A2 GCE HUMAN BIOLOGY F225/01 Genetics, Control and Ageing *5884237032* Candidates Answer on the Question Paper
    Oxford Cambridge and RSA Thursday 23 June 2016 – Morning A2 GCE HUMAN BIOLOGY F225/01 Genetics, Control and Ageing *5884237032* Candidates answer on the Question Paper. OCR supplied materials: Duration: 2 hours None Other materials required: • Electronic calculator • Ruler (cm/mm) *F22501* INSTRUCTIONS TO CANDIDATES • Write your name, centre number and candidate number in the boxes above. Please write clearly and in capital letters. • Use black ink. HB pencil may be used for graphs and diagrams only. • Answer all the questions. • Read each question carefully. Make sure you know what you have to do before starting your answer. • Write your answer to each question in the space provided. If additional space is required, you should use the lined page(s) at the end of this booklet. The question number(s) must be clearly shown. • Do not write in the bar codes. INFORMATION FOR CANDIDATES • The number of marks is given in brackets [ ] at the end of each question or part question. • The total number of marks for this paper is 100. • Where you see this icon you will be awarded marks for the quality of written communication in your answer. • You may use an electronic calculator. • You are advised to show all the steps in any calculations. • This document consists of 24 pages. Any blank pages are indicated. © OCR 2016 [K/500/8502] OCR is an exempt Charity DC (NH/SW) 119808/4 Turn over 2 Answer all the questions. 1 Excretion is the removal of metabolic waste products from the body. The kidney is one of the organs involved in excretion.
    [Show full text]
  • Prenatal Growth Restriction, Retinal Dystrophy, Diabetes Insipidus and White Matter Disease: Expanding the Spectrum of PRPS1-Related Disorders
    European Journal of Human Genetics (2015) 23, 310–316 & 2015 Macmillan Publishers Limited All rights reserved 1018-4813/15 www.nature.com/ejhg ARTICLE Prenatal growth restriction, retinal dystrophy, diabetes insipidus and white matter disease: expanding the spectrum of PRPS1-related disorders Almundher Al-Maawali1,2, Lucie Dupuis1, Susan Blaser3, Elise Heon4, Mark Tarnopolsky5, Fathiya Al-Murshedi2, Christian R Marshall6,7, Tara Paton6,7, Stephen W Scherer6,7 for the FORGE Canada Consortium9, Jeroen Roelofsen8, Andre´ BP van Kuilenburg8 and Roberto Mendoza-Londono*,1 PRPS1 codes for the enzyme phosphoribosyl pyrophosphate synthetase-1 (PRS-1). The spectrum of PRPS1-related disorders associated with reduced activity includes Arts syndrome, Charcot–Marie–Tooth disease-5 (CMTX5) and X-linked non-syndromic sensorineural deafness (DFN2). We describe a novel phenotype associated with decreased PRS-1 function in two affected male siblings. Using whole exome and Sanger sequencing techniques, we identified a novel missense mutation in PRPS1. The clinical phenotype in our patients is characterized by high prenatal maternal a-fetoprotein, intrauterine growth restriction, dysmorphic facial features, severe intellectual disability and spastic quadraparesis. Additional phenotypic features include macular coloboma-like lesions with retinal dystrophy, severe short stature and diabetes insipidus. Exome sequencing of the two affected male siblings identified a shared putative pathogenic mutation c.586C4T p.(Arg196Trp) in the PRPS1 gene that was maternally inherited. Follow-up testing showed normal levels of hypoxanthine in urine samples and uric acid levels in blood serum. The PRS activity was significantly reduced in erythrocytes of the two patients. Nucleotide analysis in erythrocytes revealed abnormally low guanosine triphosphate and guanosine diphosphate.
    [Show full text]
  • DDAVP Nasal Spray Is Provided As an Aqueous Solution for Intranasal Use
    DDAVP® Nasal Spray (desmopressin acetate) Rx only DESCRIPTION DDAVP® Nasal Spray (desmopressin acetate) is a synthetic analogue of the natural pituitary hormone 8-arginine vasopressin (ADH), an antidiuretic hormone affecting renal water conservation. It is chemically defined as follows: Mol. wt. 1183.34 Empirical formula: C46H64N14O12S2•C2H4O2•3H2O 1-(3-mercaptopropionic acid)-8-D-arginine vasopressin monoacetate (salt) trihydrate. DDAVP Nasal Spray is provided as an aqueous solution for intranasal use. Each mL contains: Desmopressin acetate 0.1 mg Sodium Chloride 7.5 mg Citric acid monohydrate 1.7 mg Disodium phosphate dihydrate 3.0 mg Benzalkonium chloride solution (50%) 0.2 mg The DDAVP Nasal Spray compression pump delivers 0.1 mL (10 mcg) of DDAVP (desmopressin acetate) per spray. CLINICAL PHARMACOLOGY DDAVP contains as active substance desmopressin acetate, a synthetic analogue of the natural hormone arginine vasopressin. One mL (0.1 mg) of intranasal DDAVP has an antidiuretic activity of about 400 IU; 10 mcg of desmopressin acetate is equivalent to 40 IU. 1. The biphasic half-lives for intranasal DDAVP were 7.8 and 75.5 minutes for the fast and slow phases, compared with 2.5 and 14.5 minutes for lysine vasopressin, another form of the hormone used in this condition. As a result, intranasal DDAVP provides a prompt onset of antidiuretic action with a long duration after each administration. 1 2. The change in structure of arginine vasopressin to DDAVP has resulted in a decreased vasopressor action and decreased actions on visceral smooth muscle relative to the enhanced antidiuretic activity, so that clinically effective antidiuretic doses are usually below threshold levels for effects on vascular or visceral smooth muscle.
    [Show full text]
  • Endocrinology Test List Endocrinology Test List
    For Endocrinologists Endocrinology Test List Endocrinology Test List Extensive Capabilities Managing patients with endocrine disorders is complex. Having access to the right test for the right patient is key. With a legacy of expertise in endocrine laboratory diagnostics, Quest Diagnostics offers an extensive menu of laboratory tests across the spectrum of endocrine disorders. This test list highlights the extensive menu of laboratory diagnostic tests we offer, including highly specialized tests and those performed using highly specific and sensitive mass spectrometry detection. It is conveniently organized by glandular function or common endocrine disorder, making it easy for you to identify the tests you need to care for the patients you treat. Comprehensive Care Quest Diagnostics Nichols Institute has been pioneering state-of-the-art endocrine testing for over four decades. Our commitment to innovative diagnostics and our dedication to quality and service means we deliver solutions that enable you to make informed clinical decisions for comprehensive patient management. We strive to remain at the forefront of innovation in endocrine testing so you can deliver the highest level of patient care. Abbreviations and Footnotes NDM, neonatal diabetes mellitus; MODY, maturity-onset diabetes of the young; CH, congenital hyperinsulinism; MSUD, maple syrup urine disease; IHH, idiopathic hypogonadotropic hypogonadism; BBS, Bardet-Biedl syndrome; OI, osteogenesis imperfecta; PKD, polycystic kidney disease; OPPG, osteoporosis-pseudoglioma syndrome; CPHD, combined pituitary hormone deficiency; GHD, growth hormone deficiency. The tests highlighted in green are performed using highly specific and sensitive mass spectrometry detection. Panels that include a test(s) performed using mass spectrometry are highlighted in yellow. For tests highlighted in blue, refer to the Athena Diagnostics website (athenadiagnostics.com/content/test-catalog) for test information.
    [Show full text]
  • Diabetes Insipidus
    Your feelings about Infertility conditions series: › Diabetes insipidus The Pituitary Foundation Information Booklets Working to support pituitary patients, their carers & families The Pituitary Foundation is a charity working About this booklet in the United Kingdom and Republic of The aim of this booklet is to provide information Ireland supporting patients with pituitary about diabetes insipidus. conditions, their carers, family and friends. You may find that not all of the information Our aims are to offer support through the applies to you in particular, but we hope it helps pituitary journey, provide information to the you to understand your condition better and community, and act as the patient voice to raise offers you a basis for discussion with your GP awareness and improve services. and endocrinologist. What is diabetes insipidus and why do we get it? 3 The two forms of diabetes insipidus 5 How is DI diagnosed and treated? 7 How is DI diagnosed? 7 What tests are carried out and how will they feel? 7 How is DI treated? 7 Aftercare 9 How will diabetes insipidus affect my life? 10 Prescriptions 10 Driving 10 Employment problems 10 Insurance & pensions 10 Personal medical identification 11 Toilet facilities card 11 National key scheme 11 Common questions 12-13 What DI means to me - a patient's story 14 Membership & donation information 15 2 Diabetes insipidus What is diabetes insipidus (DI) and why do we get it? Diabetes insipidus (DI) is caused by a problem with either the production, or action, of the hormone vasopressin (AVP). If you have DI your kidneys are unable to retain water.
    [Show full text]
  • Oral Desmopressin in Central Diabetes Insipidus
    Arch Dis Child: first published as 10.1136/adc.61.3.247 on 1 March 1986. Downloaded from Archives of Disease in Childhood, 1986, 61, 247-250 Oral desmopressin in central diabetes insipidus U WESTGREN, C WITTSTROM, AND A S HARRIS Department of Pediatrics, University Hospital, Lund, and Faculty of Pharmacy, Biomedicum, Uppsala, Sweden SUMMARY Seven paediatric patients with central diabetes insipidus were studied in an open dose ranging study in hospital followed by a six month study on an outpatient basis to assess the efficacy and safety of peroral administration of DDAVP (desmopressin) tablets. In the dose ranging study a dose dependent antidiuretic response was observed. The response to 12-5-50 mcg was, however, less effective in correcting baseline polyuria than were doses of 100 mcg and above. Patients were discharged from hospital on a preliminary dosage regimen ranging from 100 to 400 mcg three times daily. After an initial adjustment in dosage in three patients at one week follow up, all patients were stabilised on treatment with tablets and reported an adequate water turnover at six months. As with the intranasal route of administration dosage requirements varied from patient to patient, and a dose range rather than standard doses were required. A significant correlation, however, was found for the relation between previous intranasal and present oral daily dosage. No adver-se reactions were reported. No clinically significant changes were noted in blood chemistry and urinalysis. All patients expressed a preference for the oral over existing intranasal copyright. treatment. Treatment with tablets offers a beneficial alternative to the intranasal route, particularly in patients with chronic rhinitis or impaired vision.
    [Show full text]
  • Distal Renal Tubular Acidosis and Diabetes Insipidus Leading to the Diagnosis of Sjögren's Syndrome
    The Medicine Forum Volume 17 Article 15 2016 Distal Renal Tubular Acidosis and Diabetes Insipidus Leading to the Diagnosis Of Sjögren's Syndrome Loheetha Ragupathi, MD Thomas Jefferson University, [email protected] Elijah Grillo, MD Thomas Jefferson University, [email protected] Jonathan Yadlosky, MD Thomas Jefferson University, [email protected] Ravi Sunderkrishnan, MD Thomas Jefferson University, [email protected] Follow this and additional works at: https://jdc.jefferson.edu/tmf Part of the Internal Medicine Commons, and the Nephrology Commons Let us know how access to this document benefits ouy Recommended Citation Ragupathi, MD, Loheetha; Grillo, MD, Elijah; Yadlosky, MD, Jonathan; and Sunderkrishnan, MD, Ravi (2016) "Distal Renal Tubular Acidosis and Diabetes Insipidus Leading to the Diagnosis Of Sjögren's Syndrome," The Medicine Forum: Vol. 17 , Article 15. DOI: https://doi.org/10.29046/TMF.017.1.016 Available at: https://jdc.jefferson.edu/tmf/vol17/iss1/15 This Article is brought to you for free and open access by the Jefferson Digital Commons. The Jefferson Digital Commons is a service of Thomas Jefferson University's Center for Teaching and Learning (CTL). The Commons is a showcase for Jefferson books and journals, peer-reviewed scholarly publications, unique historical collections from the University archives, and teaching tools. The Jefferson Digital Commons allows researchers and interested readers anywhere in the world to learn about and keep up to date with Jefferson scholarship. This article has been accepted for inclusion in The Medicine Forum by an authorized administrator of the Jefferson Digital Commons. For more information, please contact: [email protected].
    [Show full text]
  • Congenital Nephrogenic Diabetes Insipidus Presenting After Acute Pyelonephritis
    IJCRI 201 2;3(11 ):25–27. Castillo et al. 25 www.ijcasereportsandimages.com CASE REPORT OPEN ACCESS Congenital nephrogenic diabetes insipidus presenting after acute pyelonephritis Christian Castillo, Poonam Bherwani, Evelyn Erickson, Gerard Prosper ABSTRACT of neurological and developmental complications associated with NDI. Introduction: Diabetes insipidus (DI) is characterized by the inability to concentrate Keywords: Congenital Diabetes Insipidus, urine. While central DI is caused by failure to Nephrogenic Diabetes Insipidus, Acute release enough functional vasopressin, Pyelonephritis nephrogenic DI (NDI) is due to the insensitivity of the distal nephron to the effect of antidiuretic ********* hormone (ADH). Case Report: A 5­day­old newborn male was admitted for isolated fever Castillo C, Bherwani P, Erickson E, Prosper G. and a questionable early right upper lobe Congenital nephrogenic diabetes insipidus presenting infiltrate. He gradually developed after acute pyelonephritis. International Journal of Case hypernatremia and increased osmolality. As Reports and Images 2012;3(11):25–27. part of his work up for fever, he had a urine culture of 30K colonies of Enterococcus faecalis. ********* His vasopressin test was negative. Conclusion: The polyuria and polydipsia associated with doi:10.5348/ijcri­2012­11­215­CR­8 genetic NDI usually presents within the first several weeks of life but may only become apparent after weaning or with longer periods of nighttime fasting. The acute pyelonephritis of this newborn may have been the initial trigger INTRODUCTION for the congenital NDI. Accurate diagnosis of this patient helped to also diagnose his maternal Diabetes insipidus is characterized by the inability to uncle and provide clues to the current condition concentrate urine.
    [Show full text]
  • X Inactivation, Female Mosaicism, and Sex Differences in Renal Diseases
    BRIEF REVIEW www.jasn.org X Inactivation, Female Mosaicism, and Sex Differences in Renal Diseases Barbara R. Migeon McKusick-Nathans Institute of Genetic Medicine, Department of Pediatrics, Johns Hopkins University, Baltimore Maryland ABSTRACT A good deal of sex differences in kidney disease is attributable to sex differences expressed only in the testes, they have to do in the function of genes on the X chromosome. Males are uniquely vulnerable to with testicular function and fertility. With mutations in their single copy of X-linked genes, whereas females are often mosaic, one X chromosome, males have only a sin- having a mixture of cells expressing different sets of X-linked genes. This cellular gle copy of their X-linked genes. mosaicism created by X inactivation in females is most often advantageous, pro- On the other hand, even though fe- tecting carriers of X-linked mutations from the severe clinical manifestations seen males have two copies of these genes, in males. Even subtle differences in expression of many of the 1100 X-linked genes both are not expressed in the same cell. may contribute to sex differences in the clinical expression of renal diseases. Only one X is programmed to work in each diploid somatic cell. All of the other J Am Soc Nephrol 19: 2052–2059, 2008. doi: 10.1681/ASN.2008020198 X chromosomes in the cell become inac- tive during fetal development. Briefly, compensation for X dosage in our spe- Although being female conveys a protec- with normal kidney function. This re- cies is accomplished by a process that en- tive effect on the progression of chronic view addresses the genetic and epigenetic sures only a single X is active in both renal disease, the basis for this sex differ- programs that contribute to the sex dif- sexes.
    [Show full text]
  • Tests…But Maybe You Transports Don’T 2
    11/12/15 Some things you should When lab tests are useful know about laboratory 1. Managing patients during critical care tests…But maybe you transports don’t 2. While transporting patient to medical facilities for evaluation of laboratory Steve Faynor, CCEMT-P abnormalities HCA Chippenham Medical Center Richmond Ambulance Authority Objectives 1. Review some basic laboratory tests. Treat the patient, not the 2. Appreciate how patterns of laboratory test results can offer insight into etiology. laboratory values. 3. Learn how laboratory test calculations can add additional clinical information. 4. Review some limitations of laboratory tests. ELECTROLYTES & A case of “bad labs” RENAL FUNCTION TESTS 1 11/12/15 Hypernatremia & Renal Failure Hypernatremia • 89 year old white female • Hyperaldosteronism • Coming from nursing home due to • Cushing’s disease or syndrome abnormal labs • Diabetes insipidus (deficiency of ADH) • Sodium 172 mmol/L • Dehydration • Potassium 4.2 mmol/L • Chloride 137 mmol/L • Carbon dioxide 21 mmol/L • What are some causes of hypernatremia? • BP 122/66, SBP 99 later • BUN 212 mg N/dL • HR 64/min • Creatinine 6.10 mg/dL • RR 21/min • What do these values indicate? • SpCO2 98% on 4 L oxygen per min • Does this change your therapy? • Tongue dry, skin turgor poor • What is the cause of the hypernatremia in this patient? Treatment? Acute Renal Failure Use of the BUN/creatinine ratio • Intrinsic renal disease • In intrinsic causes of acute renal failure, the – Acute tubular necrosis: ischemia, toxins BUN/creatinine ratio is typically 10-15. – Acute glomerulonephritis • In pre-renal causes of acute renal failure, – CKD with missed dialysis the BUN/creatinine ratio is typically >20.
    [Show full text]
  • Diabetes Insipidus a I C E L E F Y B
    CE Article #3 s a r a P Diabetes Insipidus a i c e l e F y b n Tracey A. Rossi, DVM o i t a a r t Linda A. Ross, DVM, MS, DACVIM s u l l I Cummings School of Veterinary Medicine at Tufts University ABSTRACT: Diabetes insipidus is a metabolic disorder caused by a deficiency in the production of or response to arginine vasopressin (AVP). The lack of , or inability to appropriately respond to , AVP results in a lack of tubular reabsorption of water and in urine of low specific gravity. Two main categories of diabetes insipidus are recognized in veterinary medicine : central and nephrogenic. iabetes insipidus is a metabolic disorder compulsive consumption of more water than the caused by decreased production of or kidneys can normally excrete. Primary polydipsia inadequate response to arginine vaso - caused by a dysfunction of the thirst center has D 1 pressin (AVP). A deficiency of AVP, or an not been reported in dogs or cats . Psychogenic inability of the distal tubule or collecting ducts polydipsia has been reported in dogs, with no spe - to respond to AVP appropriately, results in a cific breed or gender predisposition; it has not lack of tubular reabsorption of water and urine been documented in cats .4 When considering dia - of low specific gravity .2 betes insipidus as a diagnostic differential in a The main categories of diabetes insipidus rec - patient that has PU/PD, it is important to first ognized in veterinary medicine are central dia - rule out the more common causes (see the box on betes insipidus (CDI) and nephrogenic diabetes page 44 ).
    [Show full text]
  • Neurologic Complications of Electrolyte Disturbances and Acid–Base Balance
    Handbook of Clinical Neurology, Vol. 119 (3rd series) Neurologic Aspects of Systemic Disease Part I Jose Biller and Jose M. Ferro, Editors © 2014 Elsevier B.V. All rights reserved Chapter 23 Neurologic complications of electrolyte disturbances and acid–base balance ALBERTO J. ESPAY* James J. and Joan A. Gardner Center for Parkinson’s Disease and Movement Disorders, Department of Neurology, UC Neuroscience Institute, University of Cincinnati, Cincinnati, OH, USA INTRODUCTION hyperglycemia or mannitol intake, when plasma osmolal- ity is high (hypertonic) due to the presence of either of The complex interplay between respiratory and renal these osmotically active substances (Weisberg, 1989; function is at the center of the electrolytic and acid-based Lippi and Aloe, 2010). True or hypotonic hyponatremia environment in which the central and peripheral nervous is always due to a relative excess of water compared to systems function. Neurological manifestations are sodium, and can occur in the setting of hypovolemia, accompaniments of all electrolytic and acid–base distur- euvolemia, and hypervolemia (Table 23.2), invariably bances once certain thresholds are reached (Riggs, reflecting an abnormal relationship between water and 2002). This chapter reviews the major changes resulting sodium, whereby the former is retained at a rate faster alterations in the plasma concentration of sodium, from than the latter (Milionis et al., 2002). Homeostatic mech- potassium, calcium, magnesium, and phosphorus as well anisms protecting against changes in volume and sodium as from acidemia and alkalemia (Table 23.1). concentration include sympathetic activity, the renin– angiotensin–aldosterone system, which cause resorption HYPONATREMIA of sodium by the kidneys, and the hypothalamic arginine vasopressin, also known as antidiuretic hormone (ADH), History and terminology which prompts resorption of water (Eiskjaer et al., 1991).
    [Show full text]