DOCSLIB.ORG

493 © Springer Science+Business Media LLC 2018 A.S. Reddi

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
493 © Springer Science+Business Media LLC 2018 A.S. Reddi Index A endogenous acid, 312 ABG. See Arterial blood gas (ABG) endogenous base, 312 Absolute deficiency, 222 NAE, 320 Acetylsalicylic acid (ASA). See Aspirin pH, maintenance of, 314 Acid-base balance, 172 buffer, 312–314 Acid–base disorders definition, 311 − ABG kidneys (see Bicarbonate (HCO3 )) arterial vs. venous blood sample, 321 lungs, 314 evaluation, 322 Acquired hypoparathyroidism, 221 AG, 336–337 Active vitamin D3, 214, 255, 270, 287 − ∆AG/∆HCO3 , 326 Acute decompensated heart failure (ADHF), calculation, 323 66–67 causes of, 325 Acute Dialysis Quality Initiative clinical use, 324 (ADQI) group, 469 high AG metabolic acidosis, 325 Acute kidney injury (AKI), 237, 274, 340 hyperglycemia, 324 acid–base disorders, 471 low AG metabolic acidosis, 326 Ca imbalance, 471 low serum albumin, 326 definitions, 469 normal values, 324 fluid imbalance, 470 unmeasured anions and cations, 323 K imbalance, 470 AKI, 471 Mg imbalance, 471 analysis of, 334 phosphate imbalance, 471 characterization, 333, 335 Acute Kidney Injury Network (AKIN), 469 CKD, 477 Acute metabolic acidosis, 339 evaluation, 329, 330 Acute respiratory acidosis, 438, 455 Henderson–Hasselbalch equation, 322, 323 causes, 432, 433 hydration, 332–333 clinical manifestations, 432 liver disease diagnosis, 433 AG metabolic acidosis, 486 treatment, 434 hyperchloremic metabolic acidosis, 486 Acute respiratory alkalosis, 442, 447 metabolic alkalosis, 486 cardiovascular effects, 443 respiratory alkalosis, 486 causes, 442, 443 mixed acid–base disorders, 330, 331 CNS effects, 443 pathogenesis of, 328–329 diagnosis, 444 proximal RTA, 481 metabolic effects, 443 respiratory alkalosis, 491 secondary response, 442, 448 secondary response, 321, 327 Addison disease, 196, 197, 385 terminology, 322 Adrenal hyperplasia, 196 Acid–base physiology, 311–314 Adrenal insufficiency, 138 © Springer Science+Business Media LLC 2018 493 A.S. Reddi, Fluid, Electrolyte and Acid-Base Disorders, DOI 10.1007/978-3-319-60167-0 494 Index Adrenergic agonists, 71 treatment, 77 Adult respiratory distress syndrome Aspirin, 350, 355, 360 (ARDS), 44, 45, 353 Atorvastatin, 69, 89 AKI. See Acute kidney injury (AKI) Autoimmune hypoparathyroidism, 221 Albright’s hereditary osteodystrophy Autosomal dominant hypophosphatemic (AHO), 221 rickets (ADHR), 262, 270 Albumin, 38, 39, 42, 43, 46, 66, 78, 80–83, 90, Autosomal recessive hypophosphatemic 219, 223, 251, 326 rickets (ARHR), 262, 270 Alcoholic ketoacidosis, 348 Alcoholism, 231, 304 Aldosterone, 169, 171, 178, 179, 186–189, B 196, 197, 317, 423 Balanced electrolyte solution, 38 Aluminum hydroxide, 277 Bartter syndrome, 179, 296, 422–424 Amiloride, 29, 89, 172, 178, 186, 189, 301, Beer potomania, 117, 137 − 423 Bicarbonate (HCO3 ), 314–318, 407 Amphotericin B (Amp B), 304 drug-induced acid–base disorders, 464 Angiotensin II, 171 hyperchloremic metabolic acidosis, 393 + Anion gap (AG), 337 NH4 , 319–320 − ∆AG/∆HCO3 , 326 reabsorption calculation, 323 collecting duct, 317 causes of, 325 daily filtered load, 314 clinical use, 324 distal tubule, 316 diarrhea, 401 Henleʼs loop, 316 high metabolic acidosis, 325 proximal tubule, 315 (see also Metabolic acidosis) regulation, 317, 318 hyperglycemia, 324 renal mechanism, 407 low serum albumin, 326 titratable acid excretion, 317–319 metabolic alkalosis, 413, 417 Body fluid compartments, 7–10 mixed acid–base disorder, 449, 452–454, 457–459, 461 mnemonic for, 325 C normal values, 324 CA. See Carbonic anhydrase RTA, 384 (CA) deficiency unmeasured anions and cations, 323 Ca2+-sensing receptor (CaSR), 213, 221 Antidiuretic hormone (ADH), 171 Calcitonin, 214–215 actions, 101 Calcitriol, 227, 239, 268 mechanism, 100 Calcium (Ca2+), 211, 212, 215–217 receptor, 67 active vitamin D3, 214 release, control of, 98 calcitonin, 214 structure and synthesis, 98 factors Apparent mineralocorticoid excess Ca2+ transport, 216 (AME) syndrome, 178 TRPV5, 217 Aquaporins, 100 homeostasis, 212 Arginine vasopressin (AVP), 98 imbalance Arterial blood gas (ABG), 445 AKI, 471 acute respiratory acidosis, 434 CKD, 476 arterial vs. venous blood sample, 321 liver disease, 485 diarrhea, 401 PTH, 213 evaluation, 322 renal handling mixed acid–base disorder, 450, 452–455, collecting duct, 216 458, 459 distal and connecting tubule, 215 values for, 321 proximal tubul, 215 Ascites, 484 TAL, 215 formation of, 76–77 Calcium chloride, 225 Index 495 Calcium disorder Chronic obstructive pulmonary disease (COPD), hypercalcemia, 233 336, 437, 439, 440, 449, 454, 455 calcium-alkali syndrome, 237 Chronic respiratory acidosis, 439, 440, 455 clinical manifestations, 240 causes, 435 diagnosis, 240, 241, 245 clinical manifestations, 435–436 FHH, 236 diagnosis, 436 granulomatous diseases, 239 treatment, 436 Jansen’s disease, 236 Chronic respiratory alkalosis, 441 malignancy, 238 cardiovascular effects, 444 MEN type 1 and type 2a, 235 causes, 442, 443 neonatal severe CNS effects, 444 hyperparathyroidism, 236 diagnosis, 444 pathophysiology, 245 hyperventilation, 444 PHPT, 234 metabolic effects, 444 renal failure, 236 secondary response, 442, 448 treatment, 242–243 Chvostek’s and Trousseau’s signs, 302 vitamin D overdose, 239 Cinacalcet, 220, 243, 268, 280, 284 hypocalcemia, 219 Cirrhosis, 59, 82, 83 clinical manifestations, 225–226 clinical evaluation of, 75 diagnosis, 222–225 edema, treatment of, 75–77 hypoparathyroidism, 221–220 HRS, 79 PsHPT, 221–222 Cisplatin, 144, 294, 301, 302, 304 treatment, 225–227 Cisplatin-induced hyponatremia, 144 vitamin D deficiency, 222 Citrate toxicity, 230 Calcium gluceptate, 226 Cl− reabsorption, 25, 30 Calcium gluconate, 225 Clenbuterol, 188 Calcium pyrophosphate dehydrate Collecting duct, 29, 30, 100 (CPPD), 185 calcium, 216 Calcium-alkali syndrome, 237–238 CCD, 29, 168, 169 Carbonic anhydrase (CA) IMCD, 29, 169 deficiency, 371 Colloid, 35, 38 Cardiogenic shock, 44 Congenital chloride diarrhea, 411 Cardiorenal syndrome (CRS), 67–68 Congestive heart failure (CHF), 59, 63, 65–67 Cations, 3 clinical evaluation, 64 Central chemoreceptors, 430 CRS, 67 Central diabetes insipidus edema, management, 65–67 (CDI), 150, 157, 163 treatment, 65 Cerebral salt wasting (CSW), 113, 138 Conivaptan, 126 Chloroquine, 239, 249, 250 Connecting tubule (CNT), 27, 168, 215 Cholestyramine, 398 Continuous venovenous hemofiltration Chronic hyponatremia, 485 (CVVH), 364 Chronic kidney disease COPD. See Chronic obstructive pulmonary (CKD), 271, 274, 284 disease (COPD) acid–base disorders, 477–478 Copeptin, 98, 99, 113 Ca imbalance, 476 Cortical collecting duct (CCD), 29, 168, 169 definition, 473–474 Corticosteroids, 261, 268 K+ imbalance, 475 Countercurrent exchange, 102 Mg imbalance, 477 Countercurrent multiplication, 102 Na imbalance, 474 Crystalloid, 35–38 phosphate imbalance, 476–477 balanced electrolyte solutions, 38 RTA, 382 dextrose stages 4–5, 339, 341 saline, 38 water imbalance, 474 water, 36–37 Chronic metabolic acidosis, 478 NaCl solutions, 36–38 496 Index Cysteine, 98 toluene ingestion, 377 Cytokines, 239 Distal tubule, 167, 215, 316 Diuresis, 50, 69, 126, 479 Diuretics, 65, 78, 409 D abuse, 399, 422 Dehydration, 91 classification, 51 causes, 92 clinical uses, 53–54 clinical evaluation, 93 complications, 54 treatment, 94 physiologic effects, 53–54 Demeclocycline, 485 potassium, 172 Developmental hypoparathyroidism, 221 resistance, 89 Dextrose DKA. See Diabetic ketoacidosis (DKA) saline, 38 Dobutamine, 71 water, 36 Drug-induced acid–base disorders Dextrose in water (D5W), 95, 129, 137 metabolic acidosis, 463, 464 Diabetes insipidus (DI), 16, 150–152, 157, metabolic alkalosis, 465 158, 162, 490 Diabetic ketoacidosis (DKA), 347, 382 Diarrhea E acidic urine pH, 399 Ecstasy, 116 complications, 400 Edema, 484 diagnosis, 395 ascites electrolyte and ABG pattern, 401 formation of, 76 mixed acid–base disorders, 396 treatment, 77 treatment, 397 diuretics, 78 types, 394–395 formation of, 60–61 water and electrolyte loss, 394 LVP, 78 Dichloroacetate, 346 management Diet, 277 ADH, inhibition of, 67 Dietary phosphate, 256 ADHF, 66 DiGeorges’s syndrome, 221 ambulatory patient, 65 Diluting segment, 26 renin–AII–aldosterone, inhibition of, 67 Dilutional acidosis, 382 sympathetic nervous system, inhibition Distal convoluted tubule (DCT), 27, 28, 32, of, 67 217, 290 refractory ascites, 79 Distal nephron, 31 salt restriction, 78 Distal renal tubular acidoses, 373–381 Effective arterial blood volume (EABV), 59, autosomal dominant inheritance, 386–387 63, 69, 95 hyperkalemia, 387–388 Effective osmolality, 6 causes of, 378, 379 EG. See Ethylene glycol (EG) characteristics, 378 Electrolyte therapy, 42 diagnosis, 379–381 Electrolyte-free-water clearance, 18, 104, 105 subtypes, 377 Endogenous acid, 312 − treatment, 381 Endogenous base (HCO3 ), 312 type IV with urine pH, 378 Epithelial Na+ channel (ENaC), 28 urine pH below 5.5, 378 Ethanol, 351 hypokalemia, 376 Ethylene glycol (EG) causes, 374, 375 clinical manifestations, 353 characterization, 373 diagnosis, 353 diagnosis, 375 lethal dose, 353 nephrocalcinosis, 376 oral ingestion, 352 nephrolithiasis, 376 oxalic acid, 362 pathophysiology, 374 sources, 352 treatment, 376–377 treatment, 353, 354 Index 497 Exercise-induced hyponatremia (EIH), 117 Gitelman syndrome, 179, 180, 185, 296, Extracellular buffering, 313 422–424 Extracellular fluid (ECF), 57–60, 63–68, 73, Glomerular filtration rate (GFR) 85–96 chronic respiratory acidosis, 436 CHF, 63–68 CKD, 474, 475 cirrhosis pregnancy, 489, 490 clinical evaluation of, 75 Glucocorticoid-remediable edema, treatment of, 75–77 hyperaldosteronism (GRH), 178, HRS, 79 425 compartment, 7, 8, 11, 13 Glutathione
Load more

Recommended publications
  • Electrolyte and Acid-Base
    Special Feature American Society of Nephrology Quiz and Questionnaire 2013: Electrolyte and Acid-Base Biff F. Palmer,* Mark A. Perazella,† and Michael J. Choi‡ Abstract The Nephrology Quiz and Questionnaire (NQ&Q) remains an extremely popular session for attendees of the annual meeting of the American Society of Nephrology. As in past years, the conference hall was overflowing with interested audience members. Topics covered by expert discussants included electrolyte and acid-base disorders, *Department of Internal Medicine, glomerular disease, ESRD/dialysis, and transplantation. Complex cases representing each of these categories University of Texas along with single-best-answer questions were prepared by a panel of experts. Prior to the meeting, program Southwestern Medical directors of United States nephrology training programs answered questions through an Internet-based ques- Center, Dallas, Texas; † tionnaire. A new addition to the NQ&Q was participation in the questionnaire by nephrology fellows. To review Department of Internal Medicine, the process, members of the audience test their knowledge and judgment on a series of case-oriented questions Yale University School prepared and discussed by experts. Their answers are compared in real time using audience response devices with of Medicine, New the answers of nephrology fellows and training program directors. The correct and incorrect answers are then Haven, Connecticut; ‡ briefly discussed after the audience responses, and the results of the questionnaire are displayed. This article and Division of recapitulates the session and reproduces its educational value for the readers of CJASN. Enjoy the clinical cases Nephrology, Department of and expert discussions. Medicine, Johns Clin J Am Soc Nephrol 9: 1132–1137, 2014.
    [Show full text]
  • Hypercalcemia and Hyponatremia
    Hypercalcemia and Hyponatremia Santosh Reddy MD FACP Assistant Professor Scott & White/Texas A&M Etiology of Hypercalcemia Hypercalcemia results when the entry of calcium into the circulation exceeds the excretion of calcium into the urine or deposition in bone. Sources of calcium are most commonly the bone or the gastrointestinal tract Etiology Hypercalcemia is a relatively common clinical problem. Elevation in the physiologically important ionized (or free) calcium concentration. However, 40 to 45 percent of the calcium in serum is bound to protein, principally albumin; , increased protein binding causes elevation in the serum total calcium. Increased bone resorption Primary and secondary hyperparathyroidism Malignancy Hyperthyroidism Other - Paget's disease, estrogens or antiestrogens in metastatic breast cancer, hypervitaminosis A, retinoic acid Increased intestinal calcium absorption Increased calcium intake Renal failure (often with vitamin D supplementation) Milk-alkali syndrome Hypervitaminosis D Enhanced intake of vitamin D or metabolites Chronic granulomatous diseases (eg, sarcoidosis) Malignant lymphoma Acromegaly Pseudocalcemia Hyperalbuminemia 1) severe dehydration 2) multiple myeloma who have a calcium- binding paraprotein. This phenomenon is called pseudohypercalcemia (or factitious hypercalcemia) Other causes Familial hypocalciuric hypercalcemia Chronic lithium intake Thiazide diuretics Pheochromocytoma Adrenal insufficiency Rhabdomyolysis and acute renal failure Theophylline toxicity Immobilization
    [Show full text]
  • Pathophysiology of Water Electrolyte Metabolism
    PATHOPHYSIOLOGY OF WATER ELECTROLYTE METABOLISM. PATHOPHYSIOLOGY OF MINERAL METABOLISM. I. PLAN OF STUDY OF THE TOPIC. 1. Changes in water distribution and water volume. 2. Types of dehydration, causes and mechanisms of development. 3. Effect of dehydration on the body. 4. Edema and dropsy: definition, classification. 5. Mechanisms of edema development: pathogenic factors and pathogenesis of different types of edema. 6. Significance of edema for organism. 7. Etiological and pathogenetic principles of edema and dehydration treatment. 8. Disturbance of trace elements metabolism. 9. Disturbance of macronutrients metabolism. II. QUATIONS FOR SELFCONTROL. 1. Types of water balance disturbances. 2. Extracellular water sector. 3. Basic mechanisms of volume water sectors changes. 4. Types of dehydration according to mechanisms of development. 5. Mechanisms of dehydration caused by primary absolute lack of water. 6. Types of dehydration according to speed of water losing. 7. Types of dehydration according to degree of water or electrolyte lack. 8. Pathological conditions when develops " water deficiency due to of limited water supply." 9. Manifestations of intracellular dehydration. 10. Main mechanisms of dehydration from due to a lack of electrolytes. 11. Main causes of hyperosmolar dehydration in the loss of electrolytes through the gastrointestinal tract. 12. Phenomena arising from the violation of the blood supply to the nervous tissue during dehydration. 13. Definition of edema. 14. Classification of edema according to prevalence. 15. Classification of edema according to speed of development. 16. Classification of edema according to pathogenesis. 17. Classification of edema according to etiology. 18. Definition of dropsy. 19. Types of dropsy. 20. Types of lymphatic insufficiency. 21.
    [Show full text]
  • The Journey of Kidney Disease
    2/8/2021 THE JOURNEY OF KIDNEY DISEASE • BY LORETTA DICAMILLO DNP, MSN,RN • RENAL SPECIALISTS • FEBRUARY 6, 2021 FUNCTIONS OF THE KIDNEY The most Vascular organ of the body… Maintenance of body fluids Excretion of wastes Regulation of blood pressure Production of hormones 1 2/8/2021 STATISTICS U.S Department of Health and Human Services More than 726 thousand Americans in 2016 were on dialysis or living with a kidney transplant. Each day over 240 individuals on dialysis pass away. Chronic kidney disease (CKD) is more common in people age 65 and older. 40% of hospitalizations for acute kidney injury (AKI) were among persons with diabetes. The total number of hospitalizations have increased from 900 thousand in the year 2000 to over 3 million in the year 2014. RISKS OF AKI NON-MODIFIABLE MODIFIABLE CHRONIC LIVER DISEASE ANEMIA, HYPERTENSION CONGESTIVE HEART HYPONATREMIA FAILURE, DIABETES HYPOALBUMINEMIA > 65 YEARS OF AGE DRUG USAGE, SEPSIS PERIPHERICAL VASCULAR RHABDOMYOLYSIS DISEASE RENAL ARTERIAL STENOSIS 2 2/8/2021 STAGES OF AKI KDIGO GUIDELINES STAGE 1 STAGE 2 STAGE 3 CREATININE X 1.5 CREATININE X2 CREATININE X 3 BASELINE BASELINE BASELINE OR AN INCREASE TO > 4.0 >0.3 MG/DL URINE OUTPUT < 0.5 MG/DL OLIGURIA < 0.5 MG/KG/HR. FOR > 12 MG/KG/HR. X 6-12 HRS. HRS. ANURIA FOR >12 HRS. BY STAGE THREE PROBABLY NEED RENAL REPLACEMENT THERAPY (RRT) ETIOLOGIES OF AKI PRERENAL – 25% INTRINSIC - 65% PRE-RENAL INTRINSIC POST- ATI- 45% RENAL AKI ON CKD -13% Etiology Hypoperfusion True Kidney Obstruction GN OR VASCULITIS -4% Injury ATHEROEMBOLIC - 1% POSTRENAL – 10% FENa 1% 3.4% Low Yield 3 2/8/2021 PATHOPHYSIOLOGY COMMON ENDPOINT IN ALL TYPES OF ATI IS CELLULAR INSULT SECONDARY TO ISCHEMIA OR DIRECT TOXINS, EFFACEMENT OF THE BRUSH BORDER AND EVENTUALLY CELL DEATH, WHICH SHUTS DOWN THE FUNCTION OF TUBULAR CELLS.
    [Show full text]
  • Electrolytes Imbalance I (Sodium ​&​Water)
    PLEASE CHECK Editing file BEFORE! ​ ​ ​ ​ Electrolytes Imbalance I (Sodium & water) ​ ​ ★ Objectives: ​ 1. Recognize the systems that control body sodium and water contents. 2. Understand the difference between body volume status and serum Sodium concentration. 3. Recognize the different types of intravenous fluids used at bedside. 4. Know the workup for Hyponatremia. 5. Know how to calculate the water deficit in Hypernatremia. ★ Resources Used in This lecture: Slides and Davidson’s Extra Explanation ​ Done by: Mohammad Alkharraz Contact us at: [email protected] ​ Revised by: Nouf Almasoud In this lecture, our goal is to understand sodium and water disorders. The key to unlocking this subject is clearly distinguishing between total body sodium and serum sodium concentration First we will brush on the concepts of body fluids and osmolarity and other basic principles. ★ Body Fluids ● Total body water (TBW)= ○ 60% of weight in males ○ 50% of weight in females ○ It decreases as we increase in age (babies have more TBW than the elderly) ● TBW is divided into ○ ICF (⅔ of TBW) ○ ECF (⅓ of TBW). ECF is divided into ■ Interstitial fluid (¾ of ECF) ■ Plasma (¼ of ECF) ★ Osmosis ○ What is osmosis? ■ It is the movement of WATER from an area of LOW osmolarity to an area of HIGH osmolarity ○ What is osmolarity? ■ It depends on the amount of solutes in the liquid ○ Listen I am a medical student not a chemistry student please get to the point ■ OK Our plasma has a certain osmolarity. This osmolarity depends on two things: the solutes in the plasma, and the amount of water in it. The major electrolyte in the plasma is sodium.
    [Show full text]
  • CARDIOLOGY Antithrombotic Therapies
    CARDIOLOGY Antithrombotic Therapies Anticoagulants: for Vitamin K antagonists Warfarin (Coumadin) -Impairs hepatic synthesis of thrombin, 7, 9, and 10 treatment of venous -Interferes with both clotting and anticoagulation = need to use another med for first 5 days of therapy clots or risk of such -Must consume consistent vit K as factor V Leiden -Pregnancy X disorder, other -Monitor with INR and PT twice weekly until stable, then every 4-6 weeks clotting disorders, Jantoven -Rarely used, usually only if there is a warfarin allergy post PE, post DVT Marvan Waran Anisindione (Miradon) Heparin -IV or injection -Short half-life of 1 hour -Monitored with aPTT, platelets for HIT -Protamine antidote LMWH Ardeparin (Normiflo) -Inhibit factors 10a and thrombin Dalteparin (Fragmin) -Injections can be done at home Danaparoid (Orgarin) -Useful as bridge therapy from warfarin prior to surgery Enoxaparin (Lovenox) -Monitor aPTT and watch platelets initially for HIT, then no monitoring needed once goal is reached? Tinzaparin (Innohep) -Safe in pregnancy Heparinoids Fondaparinux (Arixtra) -Direct 10a inhibitor Rivaroxaban (Xarelto) -Only anticoagulant that does not affect thrombin Direct thrombin Dabigatran (Pradaxa) -Monitor aPTT inhibitors Lepirudin (Refludan) Bivalirudin (Angiomax) Antiplatelets: used COX inhibitors Aspirin -Blocks thromboxane A-2 = only 1 platelet pathway blocked = weak antiplatelet for arterial clots or -Only NSAID where antiplatelet activity lasts for days rather than hours risk of such as ADP receptor inhibitors Ticlopidine (Ticlid)
    [Show full text]
  • Electrolyte Abnormalities in Neonatesneonates
    Electrolyte Abnormalities in NeonatesNeonates Jon Palmer, VMD, DACVIM Director of Neonatal/Perinatal Programs Graham French Neonatal Section, Connelly Intensive Care Unit New Bolton Center, University of Pennsylvania ElectrolyteElectrolyte abnormalities abnormalities CriticallyCritically ill ill neonates neonates • Frequently occur • Usually mild disturbances can be life-threatening • Epiphenomena Reflecting organ dysfunction • Gastrointestinal • Renal • Endocrine Reflecting global insult • Iatrogenic Fluid therapy errors Feeding mishaps • Fetal to neonatal physiology transition ElectrolyteElectrolyte Abnormalities Abnormalities • Sodium/Water Balance • Hyponatremia/Hypernatremia • Hypokalemia/Hyperkalemia • Hypocalcemia/Hypercalcemia • Hypomagnesemia/Hypermagnesemia Sodium/WaterSodium/Water Balance Balance • Transition from fetal physiology Late term fetus High FxNa Transition – to low FxNa • Most species during 1st day • Fetal foal - before birth • Sodium conserving mode Na requirement for growth • Bone growth • ↑body mass Increase in interstitial space Milk diet • Fresh milk is sodium poor 9-15 mEq/l Sodium/Water Balance SodiumSodium Conservation Conservation • Neonatal kidney less able to excrete Na load rapidly • ↓GFR • Glomerulotubular balance Absorption Na in proximal tubule balanced with snGFR Adult – distal tubule modulated based on Na balance Neonate – both proximal and distal tubules Distal important compensatory mechanism • Retention Na for growth • No autoregulation GFR at neonatal BP • Disruption Na reabsorption capacity
    [Show full text]
  • Alluru S. Reddi an Essential Q & a Study Guide
    Alluru S. Reddi Absolute Nephrology Review An Essential Q & A Study Guide 123 Absolute Nephrology Review Alluru S. Reddi Absolute Nephrology Review An Essential Q & A Study Guide Alluru S. Reddi Professor of Medicine Chief, Division of Nephrology and Hypertension Rutgers New Jersey Medical School Newark, NJ, USA ISBN 978-3-319-22947-8 ISBN 978-3-319-22948-5 (eBook) DOI 10.1007/978-3-319-22948-5 Library of Congress Control Number: 2015959706 Springer Cham Heidelberg New York Dordrecht London # Springer International Publishing Switzerland 2016 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made.
    [Show full text]
  • Electrolytes Imbalance: Na+ & Water
    Electrolytes imbalance: Na+ & Water Objectives : 1. Recognize the systems that control body sodium and water contents 2. Differentiate between total body sodium content (volume status) and serum sodium concentration (Hypo- and Hypernatremia) 3. Use the different types of IV fluids in clinical practice 4. Calculate the water deficit in Hypernatremia 5. Explain the workup of Hyponatremia Done by : Team leader: Rahaf AlShammari Team members: Suliman AlThunayan, Abdurhman AlHayssoni Sulaiman AlZomia, Meaad AlNofaie Revised by : Aseel Badukhon Resources : Dr. Tarakji’s handout & notes, Team 436. Important Notes Golden Notes Extra Book Basic Information: Total Body Water: Percentage of TBW decreases with age and increasing obesity (TBW decreases because fat contains very little water): ● Men: Total body water (TBW) = 60% of body weight. In a 70 kg 30 y/o man; TBW will be 42 L in which 28 L will be intracellular and 14 L extracellular (10.5 L in the interstitium and 3.5 plasma) ● Women: TBW = 50% of body weight. TBW will be 60% for adult male. Around 50 to 55% for female. For pediatric around 80%. Geriatric around 50% Distribution of water: Intracellular (ICF) (2/3 of TBW) (0.4 x Body weight) Total Body Water Interstitial Fluid (ISF) (0.6 x Body Weight) (3/4 x ECF) Extracellular (ECF) Venous fluid (1/3 of TBW) “Venous capacitance” (0.2 x Body weight) (85% of plasma) Plasma (1/4 x ECF) For body fluid compartments, remember the 60–40-20 rule: ∙ TBW is 60% of body weight =42 L(50% for women). ∙ ICF is 40% of body weight =28L Arterial fluid ∙ ECF is 20% of body weight=14L (interstitial fluid 15% =10.5 and plasma 5% =3.5L).
    [Show full text]
  • Hyponatremia!!!
    Hyponatremia!!! Sunil Agrawal, MD, FASN Disclosures • Employed by Nephrology Specialist of Oklahoma • Otsuka Speaker Bureau for Jynrque • Local DaVita Medical Director - In-Center and Home Dialysis HYPONATREMIA!!! Confused? PTSD from training!! NOW WHAT????? HYPONATREMIA!!! Natural Inclination: FLUID RESTRICTION THIS NOT THE ANSWER MOST OF THE TIME!!! (ignores causation) USUALLY HAVE TO RESITRICT: < 800 ml/Day!!! Outline • Introduction • Brief Physiology of Water Handling • Diagnosis • Special Cases of Hyponatremia • Treatment → Acute vs. Chronic • Summary Introduction • What is Hyponatremia? • Serum Sodium : <135 • Acute <48 hours • Chronic >48 hours or duration unkown • Why do we care? • 15-22% of Hospital Patients • Substantial Morbidity and Mortality • Growing Geriatric Population at Risk • “Companion Diagnosis” with many Disease States Introduction • Hyponetremia → Free water intake > water secretion • Serum [Na+]∝ Na + K / Total Body Water • Decrease in numerator • Increase in denominator Water Physiology Water Physiology • Concentrating and Diluting Capacity: • Concentration → 1200 mOsm/kg, UOP <1 L/ day • Diluting → 50 to 100 mOsm/kg, UOP ~ 14 L / day • Kangaroo Rat → concentration capacity of 6,000 mOsm/kg! Water Physiology • What is responsible for changes in urine volume and tonicity? • ADH → vasopressin • Made in hypothalamus • Cleaved to active ADH, neurophysin II, & copeptin • Stored in posterior pituitary Water Physiology Stimulated by: • ADH ✓ Hypertonicity • Releases due to ✓ Hypovolemia increase in Posm • >285 mOsm/kg
    [Show full text]
  • Fluid and Electrolyte Management Billie Bartel and Elizabeth Gau
    © Jones & Bartlett Learning, LLC. NOT FOR SALE OR DISTRIBUTION Chapter 7 Fluid and Electrolyte Management Billie Bartel and Elizabeth Gau L EARNING OBJECTIVES 1. Identify and understand basic fluid and electrolyte abnormalities in critically ill patients. 2. Differentiate between the types of fluids used for fluid replacement in different disease states commonly seen in the intensive care unit. 3. Recognize the causes of electrolyte abnormalities in critically ill patients. 4. Understand when and how to replace or replete electrolytes in critically ill patients. INTRODUCTION Fluid and electrolyte abnormalities are common in critically ill patients and often represent complications from underlying disease states or medication therapies. Critically ill patients often experience alterations in absorption, distribution, and excretion of fluids and electrolytes. Changes in hormonal and homeostatic processes and fluid status are also common in intensive care unit patients. 1 04783_CH07_PASS01.indd 1 11/2/11 3:16:52 PM © Jones & Bartlett Learning, LLC. NOT FOR SALE OR DISTRIBUTION 2 Chapter 7: Fluid and Electrolyte Management Significant complications can result from fluid and electrolyte abnormali- ties, and the severity of these complications usually parallels the magnitude of the disorder. Fluid and electrolyte disorders occurring acutely and rap- idly are often associated with increased symptoms and complications when compared to chronically occurring imbalances; these symptomatic abnor- malities require more urgent treatment. Recognizing the cause of fluid and electrolyte abnormalities is important when making treatment decisions. Critically ill patients often require very frequent monitoring and evaluation of fluid status and serum electrolyte concentrations throughout their treat- ment course. Pharmacists often assist in the management of fluid and electrolyte ab- normalities in the intensive care unit.
    [Show full text]
  • Fluid and Electrolytes in Adult Parenteral Nutrition by Theresa Fessler, MS, RD, CNSC
    Fluid and Electrolytes in Adult Parenteral Nutrition By Theresa Fessler, MS, RD, CNSC Suggested CDR Learning Codes: 2070, 3040, 5440; Level 3 Body fluid and serum electrolyte concentrations often become imbalanced in patients who require parenteral nutrition (PN) due to one or more factors, such as physiologic stress, wound drainage, blood loss, gastrointestinal fluid loss, organ malfunction, hormonal abnormalities, IV fluid use, various medications, and even unavoidable shortages of parenteral electrolyte products. It’s important to discuss each patient’s clinical status with the physicians, pharmacists, and nurses involved in the patient’s care to become fully informed about his or her clinical situation. With knowledge of fluid and electrolyte requirements, the conditions in which these needs are altered, and the physical signs of excesses or deficits, RDs can determine safe and reasonable adjustments to PN electrolyte content. This continuing education course focuses on the role of fluid and electrolytes in PN and the clinical situations in which water and electrolytes may need to be adjusted in PN. It’s intended for practitioners who have a good basic knowledge of and experience with PN. Part 1: Requirements for Water and Electrolytes and Units of Measurement The Institute of Medicine lists the Dietary Reference Intakes for oral nutrients in milligrams or grams.1 Parenteral and oral requirements are, of course, different because intravenous administration bypasses normal digestion and absorption. For IV fluids and PN, the milliequivalent (mEq) is the unit of measurement used for sodium (Na), chloride (Cl), potassium (K), magnesium (Mg), calcium (Ca), and acetate, while the millimole (mM) or the milliequivalent can be used for phosphorus (P).2,3 Electrolytes are compounds or substances that dissociate in the solution to release positively and negatively charged ions that can carry electric current—thus, the term electrolyte.
    [Show full text]