BOOK
Fluid, Electrolyte and Acid-Base Physiology E-Book
Kamel S. Kamel | Mitchell L. Halperin
(2016)
Additional Information
Book Details
Abstract
With a strong focus on problem solving and clinical decision making, Fluid, Electrolyte, and Acid-Base Physiology is your comprehensive, go-to guide on the diagnosis and management of fluid, electrolytes, and acid-base disorders. This in-depth reference moves smoothly from basic physiology to practical clinical guidance, taking into account new discoveries; new understanding of fluid, acid-base, and electrolyte physiology; and new treatment options available to today’s patients. An essential resource for nephrologists and emergency practitioners, this extensively revised edition helps you make the best management decisions based on the most current knowledge.
- Presents questions and explanations throughout that let you test your knowledge and hone your skills.
- Key point boxes make essential information easy to review.
- Numerous line drawings, diagnostic algorithms, and tables facilitate reference.
- Distinguished authors apply their extensive experience in research, clinical practice, and education to make theoretical and clinical knowledge easy to understand and apply.
- More patient-based problem solving illustrates how key principles of renal physiology, biochemistry, and metabolic regulation are applied in practice, challenging you to test your knowledge and hone your decision-making skills.
- Highlights updated clinical approaches to the diagnosis and management of fluid, electrolyte, and acid-base disorders based on current research and understanding.
- Integrative whole-body physiology provides a more comprehensive grasp of the pathophysiology of fluid, electrolyte, and acid-base disorders.
Table of Contents
| Section Title | Page | Action | Price |
|---|---|---|---|
| Front Cover | Cover | ||
| IFC | ES1 | ||
| Fluid, Electrolyte, and Acid–Base Physiology | i | ||
| Fluid, Electrolyte, and Acid–Base Physiology: A Problem-Based Approach | iii | ||
| Copyright | iv | ||
| Dedication | v | ||
| Acknowledgment | vii | ||
| Preface | viii | ||
| Interconversion of Units | ix | ||
| Contents | x | ||
| List of Cases | xi | ||
| List of Flow Charts | xiii | ||
| One - Acid–Base | 1 | ||
| 1 - Principles of Acid–Base Physiology | 3 | ||
| Introduction | 4 | ||
| OBJECTIVES | 4 | ||
| Acid Balance | 4 | ||
| Base Balance | 4 | ||
| A - CHEMISTRY OF H+ IONS | 5 | ||
| H+ IONS AND THE REGENERATION OF ATP | 5 | ||
| Uncoupling of Oxidative Phosphorylation | 6 | ||
| CONCENTRATION OF H+ IONS | 6 | ||
| QUESTIONS | 6 | ||
| B - DAILY BALANCE OF H+ IONS | 7 | ||
| PRODUCTION AND REMOVAL OF H+ IONS | 7 | ||
| Acid Balance | 7 | ||
| H2SO4 | 8 | ||
| Dietary phosphate | 9 | ||
| Base Balance | 10 | ||
| QUESTION | 11 | ||
| BUFFERING OF H+ IONS | 11 | ||
| Bicarbonate Buffer System | 11 | ||
| Which PCO2 is important for the bicarbonate buffer system to function optimally? | 12 | ||
| Failure of the bicarbonate buffer system | 13 | ||
| QUESTIONS | 15 | ||
| ROLE OF THE KIDNEY IN ACID–BASE BALANCE | 15 | ||
| Reabsorption of Filtered HCO3– Ions | 15 | ||
| Reabsorption of NaHCO3 in the proximal convoluted tubule | 15 | ||
| Regulation of proximal tubular reabsorption of bicarbonate ions | 16 | ||
| Luminal ion concentration | 16 | ||
| Luminal H+ ion concentration | 16 | ||
| Concentration of H+ ions in PCT cells | 17 | ||
| Peritubular ion concentration | 17 | ||
| Peritubular PCO2 | 17 | ||
| Angiotensin II | 17 | ||
| Parathyroid hormone | 17 | ||
| Renal threshold for reabsorption of ions | 18 | ||
| Reabsorption of NaHCO3 in the loop of Henle | 19 | ||
| Reabsorption of NaHCO3 in the distal nephron | 19 | ||
| Excretion of Ammonium Ions | 19 | ||
| Production of ions | 20 | ||
| Transport of ions | 22 | ||
| Proximal convoluted tubule | 22 | ||
| Loop of Henle | 22 | ||
| Collecting duct | 23 | ||
| NH3 secretion | 23 | ||
| H+ ion secretion | 24 | ||
| Net Acid Excretion | 24 | ||
| Titratable acids | 25 | ||
| Alkali loss | 25 | ||
| URINE PH AND KIDNEY STONE FORMATION | 25 | ||
| Low Urine pH and Uric Acid Stones | 25 | ||
| High Urine pH and CaHPO4 Kidney Stones | 26 | ||
| C - INTEGRATIVE PHYSIOLOGY | 27 | ||
| WHY IS THE NORMAL BLOOD PH 7.40? | 27 | ||
| Why Is the Arterial PCO2 40 mm Hg? | 27 | ||
| What Is an Ideal ? | 27 | ||
| What Conclusions Can Be Drawn? | 28 | ||
| METABOLIC BUFFERING OF H+ IONS DURING A SPRINT | 28 | ||
| An Overview of the Acid–Base Changes During a Sprint | 28 | ||
| Recovery from the Sprint | 29 | ||
| QUESTION | 29 | ||
| DISCUSSION OF QUESTIONS | 29 | ||
| Low Venous PO2 | 31 | ||
| High Venous PCO2 | 31 | ||
| 2 - Tools to Use to Diagnose Acid–Base Disorders | 33 | ||
| Introduction | 34 | ||
| OBJECTIVES | 34 | ||
| Case 2-1: Does This Man Really Have Metabolic Acidosis? | 34 | ||
| Questions | 35 | ||
| Case 2-2: Lola Kaye Needs Your Help | 35 | ||
| Question | 35 | ||
| A - DIAGNOSTIC ISSUES | 35 | ||
| DISORDERS OF ACID–BASE BALANCE | 35 | ||
| The Is Influenced by Changes in the ECF Volume | 35 | ||
| Measurement of Brachial Venous PCO2 to Assess Buffering of an H+ Ion Load by BBS | 35 | ||
| Disorders With a High Concentration of H+ Ionsin Plasma | 36 | ||
| Metabolic acidosis | 36 | ||
| Respiratory acidosis | 37 | ||
| Disorders with a Low Concentration of H+ Ions in Plasma | 37 | ||
| Metabolic alkalosis | 37 | ||
| Respiratory alkalosis | 37 | ||
| MAKING AN ACID–BASE DIAGNOSIS | 38 | ||
| LABORATORY TESTS USED IN A PATIENT WITH METABOLIC ACIDOSIS | 38 | ||
| Questions to ask in the clinical approach to the patient with metabolic acidosis | 38 | ||
| Is the Content of Ions in the ECF Compartment Low? | 38 | ||
| Is There an Overproduction of Acids? | 38 | ||
| Is the Metabolic Acidosis due to the Ingestion of Alcohols? | 38 | ||
| Is Buffering of the H+ Ion Load by BBS in Skeletal Muscle? | 39 | ||
| In a Patient with Chronic Hyperchloremic Metabolic Acidosis (HCMA), Is the Rate of Excretion of Ions High Enough So That the Kid... | 39 | ||
| If the Rate of Excretion of Ions Is High, What Is the Anion Excreted with Ions in the Urine? | 39 | ||
| If the Rate of Excretion of Ions Is Low, What Is the Basis for the Low Ion Excretion Rate? | 39 | ||
| Is There a Defect in H+ Ion Secretion in the Proximal Tubule? | 40 | ||
| Laboratory Tests | 40 | ||
| 1. The anion gap in plasma | 40 | ||
| An example | 41 | ||
| Pitfalls in the use of the plasma anion gap | 42 | ||
| Issues related to PAlbumin | 42 | ||
| Issues related to other cations and anions | 42 | ||
| Delta anion gap/delta | 42 | ||
| 2. The osmolal gap in plasma | 43 | ||
| 3. Tests used to estimate the rate of excretion of ions | 44 | ||
| The urine net charge | 44 | ||
| The urine osmolal gap | 45 | ||
| 4. Tests used to evaluate the basis for a low rate of excretion of ions | 45 | ||
| The PCO2 in alkaline urine | 46 | ||
| The fractional excretion of | 47 | ||
| Rate of citrate excretion | 47 | ||
| B - IDENTIFYING MIXED ACID–BASE DISORDERS | 47 | ||
| EXPECTED RESPONSES TO PRIMARY ACID–BASE DISORDERS | 47 | ||
| HOW TO RECOGNIZE MIXED ACID–BASE DISORDERS | 48 | ||
| Evaluate the Accuracy of the Laboratory Data | 48 | ||
| Calculate the Ion Content in the ECF Volume | 48 | ||
| Determine the Quantitative Relationship Between the Fall in and the Rise in the PAnion gap | 49 | ||
| Examine the in the Patient with Respiratory Acidosis or Alkalosis to Identify the Presence of a Metabolic Acid–Base Disturbance | 49 | ||
| OTHER DIAGNOSTIC APPROACHES: THE STRONG ION DIFFERENCE | 49 | ||
| DISCUSSION OF CASES | 50 | ||
| Case 2-1: Does This Man Really Have Metabolic Acidosis? | 50 | ||
| Does this patient have a significant degree of metabolic acidosis? | 50 | ||
| Laboratory data | 50 | ||
| Clinical picture | 51 | ||
| Correlating the clinical and laboratory information | 51 | ||
| What is the basis for the high PAnion gap? | 51 | ||
| Case 2-2: Lola Kaye Needs Your Help | 51 | ||
| What is/are the major acid–base diagnosis/diagnoses? | 51 | ||
| Metabolic acidosis | 51 | ||
| Respiratory acidosis | 51 | ||
| Additional Information about Case 2-2 | 52 | ||
| Questions | 52 | ||
| What Is the Most Likely Basis for the Metabolic Acidosis? | 52 | ||
| What Is the Most Likely Basis for the Respiratory Acidosis? | 52 | ||
| 3 - Metabolic Acidosis: Clinical Approach | 53 | ||
| Introduction | 54 | ||
| OBJECTIVES | 54 | ||
| Case 3-1: Stick to the Facts | 54 | ||
| Questions | 55 | ||
| A - CLINICAL APPROACH | 55 | ||
| EMERGENCIES IN THE PATIENT WITH METABOLIC ACIDOSIS | 56 | ||
| Emergencies at Presentation | 56 | ||
| Hemodynamic emergency | 56 | ||
| Cardiac arrhythmia | 57 | ||
| Failure of adequate ventilation | 57 | ||
| Toxin-induced metabolic acidosis | 57 | ||
| Dangers to Anticipate After Commencing Therapy | 57 | ||
| Dangers related to overly aggressive administration of saline | 57 | ||
| 1. A more severe degree of acidemia | 58 | ||
| i) Dilution of the concentration of in the ECF compartment | 58 | ||
| ii) Loss of more NaHCO3 in diarrheal fluid | 58 | ||
| iii) Back-titration of ions by H+ ions that were bound to intracellular proteins | 58 | ||
| 2. Cerebral edema in children with diabetic ketoacidosis | 59 | ||
| 3. Rapid correction of chronic hyponatremia | 60 | ||
| Hypokalemia | 60 | ||
| Metabolic or nutritional issues | 60 | ||
| ASSESS THE EFFECTIVENESS OF THE | 60 | ||
| DETERMINE THE BASIS OF METABOLIC ACIDOSIS | 61 | ||
| Detect Addition of Acids by Finding New Anions in the Blood and/or the Urine | 61 | ||
| Detect Conditions With Fast Addition of H+ Ions | 62 | ||
| Assess the Renal Response to Metabolic Acidosis | 62 | ||
| QUESTIONS | 63 | ||
| B - DISCUSSIONS | 63 | ||
| Case 3-1: Stick to the Facts | 63 | ||
| What dangers were present on admission? | 63 | ||
| Marked degree of contraction of EABV | 63 | ||
| Severe degree of hypokalemia | 63 | ||
| Hyponatremia | 63 | ||
| Binding of H+ ions to proteins in cells | 63 | ||
| What dangers should be anticipated during therapy? | 64 | ||
| A more severe degree of hypokalemia | 64 | ||
| Rapid rise in PNa | 64 | ||
| Further fall in | 64 | ||
| Plan for initial therapy | 64 | ||
| What is the basis for the metabolic acidosis? | 64 | ||
| DISCUSSION OF QUESTIONS | 65 | ||
| 4 - Metabolic Acidosis Caused by a Deficit of NaHCO3 | 67 | ||
| Introduction | 68 | ||
| OBJECTIVES | 68 | ||
| A - OVERVIEW | 68 | ||
| DEFINITIONS | 68 | ||
| PATHOGENESIS OF METABOLIC ACIDOSIS CAUSED BY NAHCO3 LOSS | 69 | ||
| B - CONDITIONS THAT CAUSE A DEFICIT OF NAHCO3 | 70 | ||
| DIRECT LOSS OF NAHCO3 | 71 | ||
| Loss of NaHCO3 in the Gastrointestinal Tract | 71 | ||
| Secretion of ions by the pancreas | 71 | ||
| Secretion of ions by the late small intestine and the colon | 71 | ||
| Clinical Picture | 73 | ||
| Treatment | 75 | ||
| Renal Loss of NaHCO3 | 75 | ||
| C - DISEASES WITH LOW RATE OF EXCRETION OF NH4+ IONS | 76 | ||
| PROXIMAL RENAL TUBULAR ACIDOSIS | 76 | ||
| CLINICAL SUBTYPES OF PROXIMAL RTA | 77 | ||
| Proximal RTA with Fanconi Syndrome | 77 | ||
| Acquired Isolated Proximal RTA | 77 | ||
| Hereditary Isolated Proximal RTA | 78 | ||
| Possible molecular lesions | 78 | ||
| NBCe1 defect | 79 | ||
| Carbonic anhydrase II defect | 79 | ||
| NHE-3 defect | 79 | ||
| Diagnostic Issues in the Patient with Proximal Renal Tubular Acidosis | 79 | ||
| Treatment of the Patient with Proximal RTA | 80 | ||
| DISTAL RENAL TUBULAR ACIDOSIS | 80 | ||
| Case 4-1: A Man Diagnosed With Type IV Renal Tubular Acidosis | 80 | ||
| Two - Salt and Water | 213 | ||
| 9 - Sodium and Water Physiology | 215 | ||
| Introduction | 216 | ||
| OBJECTIVES | 216 | ||
| A - BODY FLUID COMPARTMENTS | 216 | ||
| Case 9-1: A Rise in the PNa After a Seizure | 216 | ||
| Question | 217 | ||
| TOTAL BODY WATER | 217 | ||
| Distribution of Water Across Cell Membranes | 217 | ||
| Defense of Brain Cell Volume | 219 | ||
| Regulatory decrease in brain cell volume | 220 | ||
| Regulatory increase in brain cell volume | 220 | ||
| Distribution of Water in the ECF Compartment | 221 | ||
| Gibbs–Donnan equilibrium | 221 | ||
| B - PHYSIOLOGY OF SODIUM | 222 | ||
| OVERVIEW | 222 | ||
| CONTROL SYSTEM FOR SODIUM BALANCE | 223 | ||
| Normal ECF Volume | 223 | ||
| Control of the Excretion of Sodium Ions | 223 | ||
| Driving force | 225 | ||
| Transport mechanism | 225 | ||
| Proximal convoluted tubule | 225 | ||
| Quantitative analysis | 225 | ||
| Process | 226 | ||
| Control | 228 | ||
| Glomerulotubular balance | 228 | ||
| Neurohumoral effects | 229 | ||
| Disorders involving the PCT | 229 | ||
| Descending thin limb of the loop of Henle | 229 | ||
| Ascending thin limb of the loop of Henle | 230 | ||
| Quantitative analysis | 230 | ||
| Medullary thick ascending limb of the loop of Henle | 231 | ||
| Quantitative analysis | 231 | ||
| Process | 233 | ||
| Control | 234 | ||
| Role of hormones | 234 | ||
| Inhibitors | 234 | ||
| Disorders involving this nephron segment | 234 | ||
| Cortical thick ascending limb of the loop of Henle | 235 | ||
| Quantitative analysis | 235 | ||
| Process | 236 | ||
| Control | 236 | ||
| Reabsorption of Na+ and Cl− ions in the macula densa | 236 | ||
| Early distal convoluted tubule | 237 | ||
| Quantitative analysis | 237 | ||
| Process | 237 | ||
| Control | 237 | ||
| Three - Potassium | 357 | ||
| 13 - Potassium Physiology | 359 | ||
| Introduction | 360 | ||
| OBJECTIVES | 360 | ||
| Case 13-1: Why Did I Become So Weak? | 361 | ||
| A - PRINCIPLES OF PHYSIOLOGY | 361 | ||
| GENERAL CONCEPTS FOR THE MOVEMENT OF K+ IONS ACROSS CELL MEMBRANES | 362 | ||
| Driving Force for the Shift of K+ Ions across Cell Membranes | 362 | ||
| Pathways for the Movement of K+ Ions across Cell Membranes | 362 | ||
| QUESTION | 364 | ||
| B - SHIFT OF POTASSIUM IONS ACROSS CELL MEMBRANES | 364 | ||
| INCREASING THE NEGATIVE VOLTAGE IN CELLS | 364 | ||
| Raise the Intracellular Concentration of Na+ Ions | 364 | ||
| Electrogenic entry of Na+ ions into cells | 364 | ||
| Clinical implications | 365 | ||
| Electroneutral entry of Na+ into cells | 365 | ||
| Clinical implications | 367 | ||
| Activate Pre-existing Na-K-ATPase | 367 | ||
| Increase in the Number of Na-K-ATPase Units in Cell Membranes | 368 | ||
| Insulin | 368 | ||
| Clinical implications | 369 | ||
| Exercise training | 369 | ||
| Thyroid hormones | 369 | ||
| Four - Integrative Physiology | 467 | ||
| 16 - Hyperglycemia | 469 | ||
| Introduction | 470 | ||
| OBJECTIVES | 470 | ||
| A - BACKGROUND | 470 | ||
| Case 16-1: And I Thought Water Was Good for Me! | 470 | ||
| Questions | 471 | ||
| REVIEW OF GLUCOSE METABOLISM | 471 | ||
| QUANTITATIVE ANALYSIS OF GLUCOSE METABOLISM | 472 | ||
| Pool of Glucose in the Body | 473 | ||
| Input of Glucose | 473 | ||
| From the diet | 473 | ||
| From glycogen stores | 473 | ||
| Glycogen in the liver | 474 | ||
| Glycogen in skeletal muscle | 474 | ||
| Conversion of protein to glucose | 474 | ||
| Removal of Glucose | 474 | ||
| Removal of glucose via metabolism | 475 | ||
| Oxidation of glucose | 475 | ||
| Conversion to storage fuels | 475 | ||
| Excretion of glucose in the urine | 475 | ||
| B - RENAL ASPECTS OF HYPERGLYCEMIA | 477 | ||
| GLUCOSE-INDUCED OSMOTIC DIURESIS | 477 | ||
| IMPACT OF HYPERGLYCEMIA ON BODY COMPARTMENT VOLUMES | 478 | ||
| Hyperglycemia and the Shift of Water Across Cell Membranes | 478 | ||
| Quantitative Relationship Between Rise in the PGlucose and the Fall in the PNa | 478 | ||
| The Impact of an Osmotic Diuresis on Body Fluid Composition | 480 | ||
| Sodium Ions | 480 | ||
| Index | 491 | ||
| A | 491 | ||
| B | 493 | ||
| C | 493 | ||
| D | 495 | ||
| E | 496 | ||
| F | 497 | ||
| G | 497 | ||
| H | 498 | ||
| I | 501 | ||
| J | 502 | ||
| K | 502 | ||
| L | 503 | ||
| M | 504 | ||
| N | 505 | ||
| O | 507 | ||
| P | 508 | ||
| R | 509 | ||
| S | 510 | ||
| T | 511 | ||
| U | 511 | ||
| V | 512 | ||
| W | 512 | ||
| Z | 513 | ||
| IBC | ES2 |