DOCSLIB.ORG

Managing Acute & Chronic Hyperkalemia

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Managing Acute & Chronic Hyperkalemia MANAGING ACUTE AND CHRONIC HYPERKALEMIA: SOLVING THE PUZZLE Matthew R. Weir, MD Professor and Chief Division of Nephrology University of Maryland School of Medicine Disclosure Slide Scientific Advisor: Janssen, Astra, BI, MSD, Akebia, Relypsa, Boston Scientific, Lexicon, Bayer, Vifor, CareDx Grant Funding: NIDDK: R01DK066013, U01DK116095,and U01DK106102; NHLBI: R01HL127422, R01HL132732 Outline • Recognition: Review prevalence and risk factors for hyperkaleMia • Management: Review current ManageMent strategies • Treatment: • Describe current approaches for the treatment of hyperkalemia both acutely and chronically • Highlight new option to treat hyperkalemia in patients on renoprotective therapies Overview: Epidemiology of Hyperkalemia • Prevalence in hospitalized patients ranges froM 1%-10% depending on the definition of hyperkaleMia1 • Prevalence in patients with CKD ranges froM 5%-50%, increasing as kidney function declines2 • HyperkaleMia is More coMMon in patients with3 • Reduced kidney function • Multiple medications (especially RAAS inhibitors) • Older age • Diabetes mellitus 1. Hollander-Rodriguez JC, Calvert JF Jr. Hyperkalemia. Am Fam Phys. 2006;73(2):283-290. 2. Reardon LC, Macpherson DS. Arch Intern Med. 1998;158(1):26-32. 3. Lazich I, Bakris G., Semin Nephrol 2014; 34:333-339. Hyperkalemia Varies Widely in Studies and Guidelines • The upper liMit of norMal (ULN) for seruM K+ levels varies across guidelines and publications1-6 Hyperkalemia • Serum K+ levels of 5.0, 5.5, or 6.0 mEq/L are 6.0 commonly used cutoffs for ULN 5.5 • Some studies differentiate hyperkalemia by severity1 + 5.0 • Serum K+ levels ≥5.5-<6.0 mEq/L defined as Normal moderate + (mEq/L) Target Range: K =3.5-5.0 + Serum K 4.0 • Serum K levels ≥6.0 mEq/L defined as severe 3.5 3.0 Hypokalemia K+: potassiuM 1. Einhorn LM, et al. Arch Intern Med. 2009;169(12):1156-1162. 2. Yancy CW, et al. J Am Coll Cardiol. 2017 Apr 21. pii: S0735-1097(17)37087-0. doi: 10.1016/j.jacc.2017.04.025. [Epub ahead of print]. 3. Ponikowski P., et al., Eur Heart J. 2016 Jul 14;37(27):2129-200. 4. National Kidney Foundation. Guideline 11: Use of angiotensin-converting enzyMe inhibitors and angiotensin receptor blockers in CKD. In: K/DOQI Clinical Practice GuidelineS on HypertenSion and AntihypertenSive AgentS in Chronic Kidney DiSeaSe. 2002. http://www2.kidney.org/professionals/kdoqi/guidelines_bp/guide_11.htm. Accessed February 17, 2015. 5. National Institute for Health and Clinical Excellence (NICE) [UK]. Chronic kidney disease (CG73): Early identification and Management of chronic kidney disease in adults in priMary and secondary care. 2008. http://www.nice.org.uk/CG73. 6. Heart Failure Society of AMerica, Lindenfeld J, et al. J Card Fail. 2010;16(6):475-539. Overview: Epidemiology of Hyperkalemia • Prevalence in hospitalized patients ranges froM 1%-10% depending on the definition of hyperkaleMia1 • Prevalence in patients with CKD ranges froM 5%-50%, increasing as kidney function declines2 • HyperkaleMia is More coMMon in patients with3 • Reduced kidney function • Multiple medications (especially RAAS inhibitors) • Older age • Diabetes mellitus 1. Hollander-Rodriguez JC, Calvert JF Jr. Hyperkalemia. Am Fam Phys. 2006;73(2):283-290. 2. Reardon LC, Macpherson DS. Arch Intern Med. 1998;158(1):26-32. 3. Lazich I, Bakris G., Semin Nephrol 2014; 34:333-339. Prevalence of Hyperkalemia Defined as Serum Potassium >5 mEq/l and/or Sodium Polystyrene Use in Diabetic and Non-diabetic Patients with CKD Stages 2, 3 and 4 Loutradis C, et.al. Am J Nephrol 2015;42:351-360 Hyperkalemia Rates in RAASi-Treated Patients in Randomized Trials Patient Population # of Patients Definition Rate AASK1: 417 ≥5.5 7.2% non-diabetic CKD J-LIGHT2: 58 >5.1 ≤6.9 5.2% HTN-CKD RENAAL3: 751 ≥5.5 10.8% diabetic nephropathy IDNT4: 579 >6 18.6 diabetic nephropathy 1. Weinberg JM, et al. Arch Intern Med. 2009;169(17):1587-1594. 2. Iino Y, et al. Hypertens Res. 2004;27(1):21-30. 3. Miao Y, et al. Diabetologia. 2011;54(1):44-50. 4. Avapro [package insert]. Bridgewater, NJ: sanofi-aventis U.S. LLC. 2012. Predictors of Hyperkalemia Before Starting Therapy • eGFR <45 ml/min/1.73m2 • serum potassium of >4.5 mEq/L • eGFR <45 ml/min/1.73m2 + serum [K+] >4.5 mEq/L (HIGHEST PREDICTOR) in the absence of RAAS blockers Lazich I and Bakris G. Sem Nephrol 2014;34:333-339; Khosla N et.al. Am J Nephrol 2009;30:418-423 Hyperkalemia: A Significant Risk Marker for Mortality Spline Analysis Adjusted for Covariates, Showing Serum Potassium as a Continuous Variable with All-Cause Mortality Collins AJ, et al. Am J Nephrol 2017;46:213-221. Serum K+ Concentrations and Survival in Hemodialysis Patients 2.5 Unadjusted Unadjusted Case-mix 2 Case-mix Case-mix and Case-mix and 2 MICS MICS Both incident and Only prevalent* MHD patients prevalent* MHD patients (vintage ≥6 months) n=74,219 1.5 n=53,206 1.5 Ratio 1 Cause Mortality HazardRatio CauseMortality - 1 Cardiovascular Mortality Hazard Mortality Cardiovascular All 0.8 <4.0 4.29 4.59 4.99 5.29 5.59 5.99 6.29 ≥6.3 – – – – – – – <4.0 – 4.29 – 4.59 – 4.99 – 5.29 – 5.59 – 5.99 – 6.29 ≥6.3 4.0 4.3 4.6 5.0 5.3 5.6 6.0 4.0 4.4 4.6 5.0 5.3 5.6 6.0 Potassium (mEq/L) Potassium (mEq/L) Predialysis serum K+ categories in 74,219 Predialysis serum K+ categories in 53,206 MHD patients observed for up to 3 years prevalent MHD patients observed for up to 3 years MHD: maintenance hemodialysis; MICS: malnutrition inflammation complex syndrome. Kovesdy CP, et al. Clin J Am Soc Nephrol. 2007;2:999-1007. Admission Serum K+ Levels and In-Hospital Mortality among CKD Patients With and Without CVD Analysis of 73,983 patients admitted to Mayo Clinic Rochester. A U-shaped curve showed higher in-hospital mortality associated with both hypo- and hyperkalemia 12 10.2 10 7.9 8 6.3 6.3 6 4.1 4.1 4 3.1 3.3 2.8 2.8 3 2.7 hospital Mortality hospital (%) 1.9 - 2 1.7 In 0 <3.0 3.0-<3.5 3.5-<4.0 4.0-<4.5 4.5-<5.0 5.0-<5.5 ≥5.5 Cardiovascular disease Non-cardiovascular disease Serum Potassium at Hospital Admission (mEq/L) Odds Ratio for in-hospital mortality 3.26 2.40 1.38 1 1.13 1.89 3.62 after adjusting for (95%CI 2.03-4.98) (95%CI 1.89-3.04) (95%CI 1.15-1.66) (REFERENCE) (95% CI 0.94-1.37) (95% CI 1.49-2.38) (95%CI 2.73-4.76) potential cofounders* * Adjusted for age, sex, race, GFR, principal diagnosis, Charlson comorbidity score, CAD, CHF, PVD, stroke, DM, COPD, cirrhosis, use of ACEI/ARB, diuretics and potassium supplements CVD = cardiovascular disease Cheungpasitporn W., et al., QJM. 2017 Jun 16. doi: 10.1093/qjmed/hcx118. [Epub ahead of print] Traditional Treatment Options for Hyperkalemia Traditional Treatment Options for Hyperkalemia Membrane stabilization Calcium + Insulin1 K redistribution gluconate salt1 K+ elimination ᵦ-andrenoreceptor Removal/reduction of drugs that ↑ serum K+ agonists1 RAASi Dialysis1 SPS1 reduction2 Sodium Loop diuretics1 Dialysis1 Low K+ diet2 bicarbonate1 Therapy Emergent Intermediate Maintenance Acute management RAASi: renin-angiotensin-aldosterone system inhibitor, SPS: sodium polystyrene sulfonate 1. Weisberg L. Crit Care Med. 2008;36(12):3246-3251. 2. PalMer BF, et al. N Engl J Med. 2004;351(6):585-592. Standard Care of CHRONIC Hyperkalemia • Review medication history • Titrate or discontinue RAAS inhibitors • Diuretic therapy • Potassium binder therapy National Kidney Foundation. Am J Kidney Dis. 2002;39(suppl 1):S76-S110. Palmer BF. N Engl J Med. 2004;351:585-592. Modifiable Risk Factors for Hyperkalemia in Patients on RAAS • Reduce potassium intake: – Low potassium diet – Avoid potassium supplements, including salt substitutes and certain herbs • Avoid Drugs That Concomitantly Interfere With Renal K+ Excretion: – Nonsteroidal antiinflammatory drugs – Beta-blockers – Calcineurin inhibitors: cyclosporine, tacrolimus – Heparin – Ketoconazole – Potassium-sparing diuretics: spironolactone, – eplerenone, amiloride, triamterene – Trimethoprim – Pentamidine Palmer B, N Engl J Med. 2004 Aug 5;351(6):585-92. Medications Associated With Hyperkalemia Class Mechanism Example Inhibit conversion of angiotensin I to ACE inhibitor Captopril, lisinopril, etc. angiotensin II Inhibit activation of angiotensin I receptor by ARB Losartan, irbesartan, etc. angiotensin II Aldosterone Spironolactone, Block aldosterone receptor activation antagonist eplerenone β-Adrenergic Propranolol, metoprolol, Inhibit renin release receptor blocker atenolol Digitalis Inhibit Na+-K+-ATPase; necessary for K+ Digoxin glycoside secretion Heparin Reduces production of aldosterone Heparin sodium K+-sparing Block collecting duct apical Na+ channel, Amiloride, triamterene diuretic decreasing gradient for K+ secretion Inhibit synthesis of prostaglandin E and NSAIDs Ibuprofen prostacyclin, inhibiting renin release Block collecting duct apical Na+ channel, Trimethoprim, Other decreasing gradient for K+ secretion pentamidine Weiner ID, et al. Comprehensive Clinical Nephrology 2015;111-123. Limitations of Diuretic Therapy • Diuretic therapy is commonly used to treat hyperkalemia but has limited effectiveness in patients with advanced CKD • Diuretic-induced kaliuresis is dependent on kidney function, adequate extracellular voluMe, and delivery of sodiuM to the cortical collecting tubule, all of which May be iMpaired in patients with advanced renal insufficiency and/or heart failure • Syncope, orthostatic hypotension, gout, ototoxicity, and increasing azotemia secondary to volume depletion can limit the use of diuretics, especially in high doses or as coMbination strategies • Please consult the reference list in the source article, Weir et al, for background information in the literature. Do not use fludrocortisone! • VoluMe overload • Toxin for MyocardiuM, kidney and vascular beds Low Potassium Diet K+ Quiz Dairy Products Ice cream Yoghurt Cheddar Advising Your Patient About K+ Intake 1.None of these are high in potassium 2.Yoghurt > Ice cream > Cheddar 3.Ice cream > Yoghurt > Cheddar 4.Cheddar > Ice cream > Yoghurt 5.Ice cream > Cheddar > Yoghurt Dairy Products Food Per Serving mEqs Cheddar cheese 1.5 oz.
Load more

Recommended publications
  • Renal Diet for Patients with Diabetes
    Webinar: BDA - Diabetes Specialist Group Renal diet for Patients with Diabetes By Gabby Ramlan Diabetes & Renal Specialist Dietitian Overview • Diabetes Dietitian Vs Renal Dietitian • Problems in individual with kidney disease • Salt • Protein • Phosphate • Potassium • Acute Kidney Injury (AKI) Around 40% people with diabetes eventually develop diabetic nephropathy or diabetes kidney disease. Diabetes is a leading cause of kidney failure in UK – around 20% starting dialysis have diabetes. Kidney Research UK “Dietary requirements for patients with both diabetes and chronic kidney disease (CKD) is more complicated than with each individual condition as it involves multiple nutrients” National Kidney Foundation (NKF) 2007 Diabetes vs Renal Specialist Dietitian Diabetes Renal • Salt • Salt • Lipid control • Lipid control • Carbohydrates • Protein • Glycaemic control • Potassium • OHAs • Fluid • Injectable meds • CKD-MBD • Insulin • Phosphate Binders • Vit D / calcimimetic Kidney’s Functions • Regulation of the composition and volume of body fluids – Na+, K+, Phosphate, Mg – Acid/base balance – BP & volume via renin angiotensin system • Excretion of waste products – Urea (protein metabolism) – Creatinine (muscle metabolism) – Drugs & toxins Kidney’s Fx • Endocrine fx - Erythropoetin & Hb • Metabolic - Control calcium/phosphate/ PTH balance - Vit D metabolism - Excretion of phosphate Common problems with renal patients • Anaemia – no dietary advice CKD – Mineral Bone Disorder (MBD) 1. Vitamin D Fluid Hyperkalaemia 2. Corrected Hypertension 1.
    [Show full text]
  • New Brunswick Drug Plans Formulary
    New Brunswick Drug Plans Formulary August 2019 Administered by Medavie Blue Cross on Behalf of the Government of New Brunswick TABLE OF CONTENTS Page Introduction.............................................................................................................................................I New Brunswick Drug Plans....................................................................................................................II Exclusions............................................................................................................................................IV Legend..................................................................................................................................................V Anatomical Therapeutic Chemical (ATC) Classification of Drugs A Alimentary Tract and Metabolism 1 B Blood and Blood Forming Organs 23 C Cardiovascular System 31 D Dermatologicals 81 G Genito Urinary System and Sex Hormones 89 H Systemic Hormonal Preparations excluding Sex Hormones 100 J Antiinfectives for Systemic Use 107 L Antineoplastic and Immunomodulating Agents 129 M Musculo-Skeletal System 147 N Nervous System 156 P Antiparasitic Products, Insecticides and Repellants 223 R Respiratory System 225 S Sensory Organs 234 V Various 240 Appendices I-A Abbreviations of Dosage forms.....................................................................A - 1 I-B Abbreviations of Routes................................................................................A - 4 I-C Abbreviations of Units...................................................................................A
    [Show full text]
  • 1 Fluid and Elect. Disorders of Serum Sodium Concentration
    DISORDERS OF SERUM SODIUM CONCENTRATION Bruce M. Tune, M.D. Stanford, California Regulation of Sodium and Water Excretion Sodium: glomerular filtration, aldosterone, atrial natriuretic factors, in response to the following stimuli. 1. Reabsorption: hypovolemia, decreased cardiac output, decreased renal blood flow. 2. Excretion: hypervolemia (Also caused by adrenal insufficiency, renal tubular disease, and diuretic drugs.) Water: antidiuretic honnone (serum osmolality, effective vascular volume), renal solute excretion. 1. Antidiuresis: hyperosmolality, hypovolemia, decreased cardiac output. 2. Diuresis: hypoosmolality, hypervolemia ~ natriuresis. Physiologic changes in renal salt and water excretion are more likely to favor conservation of normal vascular volume than nonnal osmolality, and may therefore lead to abnormalities of serum sodium concentration. Most commonly, 1. Hypovolemia -7 salt and water retention. 2. Hypervolemia -7 salt and water excretion. • HYFERNATREMIA Clinical Senini:: Sodium excess: salt-poisoning, hypertonic saline enemas Primary water deficit: chronic dehydration (as in diabetes insipidus) Mechanism: Dehydration ~ renal sodium retention, even during hypernatremia Rapid correction of hypernatremia can cause brain swelling - Management: Slow correction -- without rapid administration of free water (except in nephrogenic or untreated central diabetes insipidus) HYPONA1REMIAS Isosmolar A. Factitious: hyperlipidemia (lriglyceride-plus-plasma water volume). B. Other solutes: hyperglycemia, radiocontrast agents,. mannitol.
    [Show full text]
  • Study Guide Medical Terminology by Thea Liza Batan About the Author
    Study Guide Medical Terminology By Thea Liza Batan About the Author Thea Liza Batan earned a Master of Science in Nursing Administration in 2007 from Xavier University in Cincinnati, Ohio. She has worked as a staff nurse, nurse instructor, and level department head. She currently works as a simulation coordinator and a free- lance writer specializing in nursing and healthcare. All terms mentioned in this text that are known to be trademarks or service marks have been appropriately capitalized. Use of a term in this text shouldn’t be regarded as affecting the validity of any trademark or service mark. Copyright © 2017 by Penn Foster, Inc. All rights reserved. No part of the material protected by this copyright may be reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without permission in writing from the copyright owner. Requests for permission to make copies of any part of the work should be mailed to Copyright Permissions, Penn Foster, 925 Oak Street, Scranton, Pennsylvania 18515. Printed in the United States of America CONTENTS INSTRUCTIONS 1 READING ASSIGNMENTS 3 LESSON 1: THE FUNDAMENTALS OF MEDICAL TERMINOLOGY 5 LESSON 2: DIAGNOSIS, INTERVENTION, AND HUMAN BODY TERMS 28 LESSON 3: MUSCULOSKELETAL, CIRCULATORY, AND RESPIRATORY SYSTEM TERMS 44 LESSON 4: DIGESTIVE, URINARY, AND REPRODUCTIVE SYSTEM TERMS 69 LESSON 5: INTEGUMENTARY, NERVOUS, AND ENDOCRINE S YSTEM TERMS 96 SELF-CHECK ANSWERS 134 © PENN FOSTER, INC. 2017 MEDICAL TERMINOLOGY PAGE III Contents INSTRUCTIONS INTRODUCTION Welcome to your course on medical terminology. You’re taking this course because you’re most likely interested in pursuing a health and science career, which entails ­proficiency­in­communicating­with­healthcare­professionals­such­as­physicians,­nurses,­ or dentists.
    [Show full text]
  • Hyperkalemia Masked by Pseudo-Stemi Infarct Pattern and Cardiac Arrest Shareez Peerbhai1 , Luke Masha2, Adrian Dasilva-Deabreu1 and Abhijeet Dhoble1,2*
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Springer - Publisher Connector Peerbhai et al. International Journal of Emergency Medicine (2017) 10:3 International Journal of DOI 10.1186/s12245-017-0132-0 Emergency Medicine CASEREPORT Open Access Hyperkalemia masked by pseudo-stemi infarct pattern and cardiac arrest Shareez Peerbhai1 , Luke Masha2, Adrian DaSilva-DeAbreu1 and Abhijeet Dhoble1,2* Abstract Background: Hyperkalemia is a common electrolyte abnormality and has well-recognized early electrocardiographic manifestations including PR prolongation and symmetric T wave peaking. With severe increase in serum potassium, dysrhythmias and atrioventricular and bundle branch blocks can be seen on electrocardiogram. Although cardiac arrest is a worrisome consequence of untreated hyperkalemia, rarely does hyperkalemia electrocardiographically manifest as acute ischemia. Case presentation: We present a case of acute renal failure complicated by malignant hyperkalemia and eventual ventricular fibrillation cardiac arrest. Recognition of this disorder was delayed secondary to an initial ECG pattern suggesting an acute ST segment elevation myocardial infarction (STEMI). Emergent coronary angiography performed showed no evidence of coronary artery disease. Conclusions: Pseudo-STEMI patterns are rarely seen in association with acute hyperkalemia and are most commonly described with patient without acute cardiac symptomatology. This is the first such case presenting concurrently with cardiac arrest. A brief review of this rare pseudo-infarct pattern is also given. Keywords: Cardiac arrest, Hyperkalemia, Myocardial infarction, STEMI, ECG Background Case presentation Hyperkalemia that manifests with electrocardiographic A 27-year-old Caucasian male with a past medical his- findings of an ST segment elevation myocardial infarc- tory of hypertension presented to the emergency room tion (STEMI) is very rare.
    [Show full text]
  • Safety and Tolerability of the Potassium Binder Patiromer from a Global Pharmacovigilance Database Collected Over 4 Years Compar
    Safety and Tolerability of the Potassium Binder Patiromer From a Global Pharmacovigilance Database Collected Over 4 Years Compared with Data from the Clinical Trial Program Patrick Rossignol, Lea David, Christine Chan, Ansgar Conrad, Matthew Weir To cite this version: Patrick Rossignol, Lea David, Christine Chan, Ansgar Conrad, Matthew Weir. Safety and Tolerability of the Potassium Binder Patiromer From a Global Pharmacovigilance Database Collected Over 4 Years Compared with Data from the Clinical Trial Program. Drugs - real world outcomes, 2021, 10.1007/s40801-021-00254-7. hal-03236228 HAL Id: hal-03236228 https://hal.univ-lorraine.fr/hal-03236228 Submitted on 26 May 2021 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Distributed under a Creative Commons Attribution| 4.0 International License Drugs - Real World Outcomes https://doi.org/10.1007/s40801-021-00254-7 ORIGINAL RESEARCH ARTICLE Safety and Tolerability of the Potassium Binder Patiromer From a Global Pharmacovigilance Database Collected Over 4 Years Compared with Data from the Clinical Trial Program Patrick Rossignol1,2 · Lea David3 · Christine Chan3 · Ansgar Conrad3 · Matthew R. Weir4 Accepted: 22 April 2021 © The Author(s) 2021 Abstract Introduction The availability of the sodium-free potassium binder patiromer opens new opportunities for hyperkalemia management.
    [Show full text]
  • Electrolyte Disorders and Arrhythmogenesis
    Cardiology Journal 2011, Vol. 18, No. 3, pp. 233–245 Copyright © 2011 Via Medica REVIEW ARTICLE ISSN 1897–5593 Electrolyte disorders and arrhythmogenesis Nabil El-Sherif1, Gioia Turitto2 1State University of NY, Downstate Medical Center and NY Harbor VA Healthcare System, Brooklyn, NY, USA 2Methodist University Hospital, Brooklyn, NY, USA Abstract Electrolyte disorders can alter cardiac ionic currents kinetics and depending on the changes can promote proarrhythmic or antiarrhythmic effects. The present report reviews the mecha- nisms, electrophysiolgical (EP), electrocardiographic (ECG), and clinical consequences of elec- trolyte disorders. Potassium (K+) is the most abundent intracellular cation and hypokalemia is the most commont electrolyte abnormality encountered in clinical practice. The most signifcant ECG manifestation of hypokalemia is a prominent U wave. Several cardiac and + non cardiac drugs are known to suppress the HERG K channel and hence the IK, and especially in the presence of hypokalemia, can result in prolonged action potential duration and QT interval, QTU alternans, early afterdepolarizations, and torsade de pointes ventricu- lar tachyarrythmia (TdP VT). Hyperkalemia affects up to 8% of hospitalized patients mainly in the setting of compromised renal function. The ECG manifestation of hyperkalemia de- pends on serum K+ level. At 5.5–7.0 mmol/L K+, tall peaked, narrow-based T waves are seen. At > 10.0 mmol/L K+, sinus arrest, marked intraventricular conduction delay, ventricular techycardia, and ventricular fibrillation can develop. Isolated abnormalities of extracellular calcium (Ca++) produce clinically significant EP effects only when they are extreme in either direction. Hypocalcemia, frequently seen in the setting of chronic renal insufficiency, results in prolonged ST segment and QT interval while hypercalcemia, usually seen with hyperparathy- roidism, results in shortening of both intervals.
    [Show full text]
  • Medical Term Lay Term(S)
    MEDICAL TERM LAY TERM(S) ABDOMINAL Pertaining to body cavity below diaphragm which contains stomach, intestines, liver, and other organs ABSORB Take up fluids, take in ACIDOSIS Condition when blood contains more acid than normal ACUITY Clearness, keenness, esp. of vision - airways ACUTE New, recent, sudden ADENOPATHY Swollen lymph nodes (glands) ADJUVANT Helpful, assisting, aiding ADJUVANT Added treatment TREATMENT ANTIBIOTIC Drug that kills bacteria and other germs ANTIMICROBIAL Drug that kills bacteria and other germs ANTIRETROVIRAL Drug that inhibits certain viruses ADVERSE EFFECT Negative side effect ALLERGIC REACTION Rash, trouble breathing AMBULATE Walk, able to walk -ATION -ORY ANAPHYLAXIS Serious, potentially life threatening allergic reaction ANEMIA Decreased red blood cells; low red blood cell count ANESTHETIC A drug or agent used to decrease the feeling of pain or eliminate the feeling of pain by general putting you to sleep ANESTHETIC A drug or agent used to decrease the feeling of pain or by numbing an area of your body, local without putting you to sleep ANGINA Pain resulting from insufficient blood to the heart (ANGINA PECTORIS) ANOREXIA Condition in which person will not eat; lack of appetite ANTECUBITAL Area inside the elbow ANTIBODY Protein made in the body in response to foreign substance; attacks foreign substance and protects against infection ANTICONVULSANT Drug used to prevent seizures ANTILIPIDEMIC A drug that decreases the level of fat(s) in the blood ANTITUSSIVE A drug used to relieve coughing ARRHYTHMIA Any change from the normal heartbeat (abnormal heartbeat) ASPIRATION Fluid entering lungs ASSAY Lab test ASSESS To learn about ASTHMA A lung disease associated with tightening of the air passages ASYMPTOMATIC Without symptoms AXILLA Armpit BENIGN Not malignant, usually without serious consequences, but with some exceptions e.g.
    [Show full text]
  • Cerebral Salt Wasting: Truths, Fallacies, Theories, and Challenges
    Journal Article Page 1 of 10 Use of this content is subject to the Terms and Conditions of the MD Consult web site. Critical Care Medicine Volume 30 • Number 11 • November 2002 Copyright © 2002 Lippincott Williams & Wilkins REVIEW ARTICLE Cerebral salt wasting: Truths, fallacies, theories, and challenges Sheila Singh, MD; Desmond Bohn, MB; Ana P. C. P. Carlotti; Michael Cusimano, MD; James T. Rutka; Mitchell L. Halperin, MD From the Departments of Pediatric Neurosurgery (SS, JTR) and Critical Care Medicine (DB), Hospital for Sick Children, Toronto, Canada; the Department of Anaesthesiology, University of Toronto, Toronto, Canada (DB); the Department of Pediatrics, Universidade de Sao Paulo, Ribeirao Preto, Brazil (APCPC); and the Department of Neurosurgery (MC) and Renal Division (MLH), St. Michael’s Hospital, University of Toronto, Toronto, Canada. Supported, in part, by a grant from Physicians Services Incorporated. Address requests for reprints to: Mitchell L. Halperin, MD, Division of Nephrology, St. Michael’s Hospital, Annex, 38 Shuter Street, Toronto, Ontario M5B 1A6, Canada. E-mail: [email protected] Cerebral salt wasting is a diagnosis of exclusion that requires a natriuresis in a patient with a contracted effective arterial blood volume and the absence of another cause for this excretion of Na+ . Background: The reported prevalence of cerebral salt wasting has increased in the past three decades. A cerebral lesion and a large natriuresis without a known stimulus to excrete so much sodium (Na+ ) constitute its essential two elements. Objectives: To review the topic of cerebral salt wasting. There is a diagnostic problem because it is difficult to confirm that a stimulus for the renal excretion of Na+ is absent.
    [Show full text]
  • 205739Orig1s000
    CENTER FOR DRUG EVALUATION AND RESEARCH APPLICATION NUMBER: 205739Orig1s000 MEDICAL REVIEW(S) DIVISION OF CARDIO-RENAL DRUG PRODUCTS Divisional Memorandum NDA: 205739 (pati romer; Veltassa) Sponsor: Re lypsa Review date: 17 October 2015 Reviewer: N. Stockbridge, M.D., Ph.D., HFD-110 (b) (4) (b) Patiromer is a polymer(4) intended as a non-absorbable potassium bi nder. T he appli cation has been the subject of reviews of CMC/Biopharmaceutics by Drs. Frankewich, Sapru, Chikhale, Srinivasachar and others (28 July 2015; 15 October 2015), a pharmacology/toxicology review by Dr. Link (19 June 2015), clinical pharmacology reviews by Drs. Lai, Florian, and Madabushi (23 July 2015; 16 October 2015), clinical review by Dr. Xiao (19 June 2015), and statistical review by Dr. Kong (11 June 2015). There is a CDTL memo by Dr. Thompson (9 October 2015) with which I am in substantial agreement. I note a few selected issues here. At this writing, there are no ope n CMC issues. The drug product must be refrigerated to retard fluoride release, and then used wi thin 3 months of be i ng stored outside a refrigerator at room temperature (25°C ± 2°C [77°F ± 4°F]). However, the sponsor printed carton and container labels with instructions (b) (4) . CMC’s position (email of 15 October) is that the carton and container labels need to be consistent with the PI. I agree that the carton and container labels need to be made consistent, but I believe that this can reasonably be deferred until the next printing. I do not believe that storage under the conditions on the carton and container label is less safe (b) (4) Manufacturing inspe ctions were satisfactory.
    [Show full text]
  • Potassium-Binders.Pdf
    Arch Intern Med Res 2020; 3(2): 141-145 DOI: 10.26502/aimr.0034 Short Communication Potassium Binders Mohammad Tinawi* Department of Internal Medicine and Nephrology, Nephrology Specialists, Munster, IN, USA *Corresponding author: Mohammad Tinawi, Department of Internal Medicine and Nephrology, Nephrology Specialists, P.C., 801 MacArthur Blvd., Ste. 400A, Munster, IN 46321, USA, E-mail: [email protected] Received: 31 May 2020; Accepted: 13 June 2020; Published: 15 June 2020 Citation: Mohammad Tinawi. Potassium Binders. Archives of Internal Medicine Research 3 (2020): 141-145. Abstract Sodium polystyrene sulfonate was approved by the rhabdomyolysis. Potentially fatal cardiac arrhythmias FDA in 1958. It was the only potassium binder available can develop. The treatment of these emergencies on the market until 2015. Patiromer and sodium focuses on myocardial membrane stabilization zirconium cyclosilicate are newly approved potassium (intravenous [IV] calcium gluconate or chloride), binders. They are better tolerated and can be used on a shifting K+ intracellularly (IV regular insulin with IV chronic basis to mitigate hyperkalemia. They allow dextrose, nebulized albuterol, and possibly IV sodium patients to continue to use critical medications such as [Na+] bicarbonate), and elimination of K+ (loop ACE inhibitors even in advanced chronic kidney diuretics, hemodialysis, and K+ binders) [1]. Most K+ disease. binders have a delayed onset of action and should never be the sole treatment of a hyperkalemic emergency. K+ Keywords: Hyperkalemia; Potassium Disorders; binders are used for the management of nonemergent Sodium Polystyrene Sulfonate; Patiromer; Sodium and chronic hyperkalemia. They are combined with Zirconium Cyclosilicate dietary counseling, medication adjustments and elimination of K+ sources such as K+ supplements and + 1.
    [Show full text]
  • Evaluating and Managing Electrolyte Disbalances in the Outpatient Setting Disclosure
    EVALUATING AND MANAGING ELECTROLYTE DISBALANCES IN THE OUTPATIENT SETTING DISCLOSURE There are no conflicts of interest Homeostasis • Potassium • Water Evaluation and Management of Electrolyte TO BE DISCUSSED Disbalances • Hyperkalemia • Hypokalemia • Hypernatremia • Hyponatremia Summary DISORDERS OF POTASSIUM BALANCE: HYPERKALEMIA AND HYPOKALEMIA POTASSIUM HOMEOSTASIS • Aldosterone • High Na+ delivery to distal tubule Increase (diuretics) Renal K+ • High urine flow (osmotic diuresis) Excretion • High serum K+ level • Delivery bicarbonate to distal tubule • Absence, or very low aldosterone • Low Na+ delivery to the distal Decrease tubule Renal K+ • Low urine flow Excretion • Low serum K+ level • Kidney Injury MORTALITY IN DYSKALEMIA Collins et al Am J Nephrol 2017;46:213- 221 HYPERKALEMIA MY PATIENT HAS HYPERKALEMIA, WHAT SHOULD I DO? H&P and Check other medication causes •Changes? Treat review •Send home •Symptoms? Treat •Metabolic acidosis •Obstruction •Hyperosmolarity •K+ increasing meds •CKD Pseudohyperkale EKG and BMP mia CAUSES OF HYPERKALEMIA Increased potassium release from Reduced urinary potassium excretion cells • Pseudohyperkalemia • Acute and chronic kidney disease • Fist clenching • Reduced aldosterone secretion or • Tourniquet use response to aldosterone • Metabolic acidosis • Reduced distal sodium and water • Insulin deficiency, hyperglycemia, delivery and hyperosmolality • Drugs • Increased tissue catabolism • Drugs • Hyperkalemic Periodic Palasysis Biff Palmer A Physiologic-Based Approach to the Evaluation of a Patient
    [Show full text]