Fluid, Electrolyte and Acid-Base Physiology

A Problem-Based Approach
 
 
Elsevier (Verlag)
  • 5. Auflage
  • |
  • erschienen am 7. Oktober 2016
  • |
  • 590 Seiten
 
E-Book | ePUB mit Adobe DRM | Systemvoraussetzungen
E-Book | PDF mit Adobe DRM | Systemvoraussetzungen
978-0-323-35908-5 (ISBN)
 

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.
    • Englisch
    • Philadelphia
    • |
    • USA
    • Höhe: 260 mm
    • |
    • Breite: 184 mm
    • |
    • Dicke: 0 mm
    • 8,06 MB
    978-0-323-35908-5 (9780323359085)
    0323359086 (0323359086)
    weitere Ausgaben werden ermittelt
    • Front Cover
    • IFC
    • Fluid, Electrolyte, and Acid-Base Physiology
    • Fluid, Electrolyte, and Acid-Base Physiology: A Problem-Based Approach
    • Copyright
    • Dedication
    • Acknowledgment
    • Preface
    • Interconversion of Units
    • Contents
    • List of Cases
    • List of Flow Charts
    • One - Acid-Base
    • 1 - Principles of Acid-Base Physiology
    • Introduction
    • OBJECTIVES
    • Acid Balance
    • Base Balance
    • A - CHEMISTRY OF H+ IONS
    • H+ IONS AND THE REGENERATION OF ATP
    • Uncoupling of Oxidative Phosphorylation
    • CONCENTRATION OF H+ IONS
    • QUESTIONS
    • B - DAILY BALANCE OF H+ IONS
    • PRODUCTION AND REMOVAL OF H+ IONS
    • Acid Balance
    • H2SO4
    • Dietary phosphate
    • Base Balance
    • QUESTION
    • BUFFERING OF H+ IONS
    • Bicarbonate Buffer System
    • Which PCO2 is important for the bicarbonate buffer system to function optimally?
    • Failure of the bicarbonate buffer system
    • QUESTIONS
    • ROLE OF THE KIDNEY IN ACID-BASE BALANCE
    • Reabsorption of Filtered HCO3- Ions
    • Reabsorption of NaHCO3 in the proximal convoluted tubule
    • Regulation of proximal tubular reabsorption of bicarbonate ions
    • Luminal ion concentration
    • Luminal H+ ion concentration
    • Concentration of H+ ions in PCT cells
    • Peritubular ion concentration
    • Peritubular PCO2
    • Angiotensin II
    • Parathyroid hormone
    • Renal threshold for reabsorption of ions
    • Reabsorption of NaHCO3 in the loop of Henle
    • Reabsorption of NaHCO3 in the distal nephron
    • Excretion of Ammonium Ions
    • Production of ions
    • Transport of ions
    • Proximal convoluted tubule
    • Loop of Henle
    • Collecting duct
    • NH3 secretion
    • H+ ion secretion
    • Net Acid Excretion
    • Titratable acids
    • Alkali loss
    • URINE PH AND KIDNEY STONE FORMATION
    • Low Urine pH and Uric Acid Stones
    • High Urine pH and CaHPO4 Kidney Stones
    • C - INTEGRATIVE PHYSIOLOGY
    • WHY IS THE NORMAL BLOOD PH 7.40?
    • Why Is the Arterial PCO2 40 mm Hg?
    • What Is an Ideal ?
    • What Conclusions Can Be Drawn?
    • METABOLIC BUFFERING OF H+ IONS DURING A SPRINT
    • An Overview of the Acid-Base Changes During a Sprint
    • Recovery from the Sprint
    • QUESTION
    • DISCUSSION OF QUESTIONS
    • Low Venous PO2
    • High Venous PCO2
    • 2 - Tools to Use to Diagnose Acid-Base Disorders
    • Introduction
    • OBJECTIVES
    • Case 2-1: Does This Man Really Have Metabolic Acidosis?
    • Questions
    • Case 2-2: Lola Kaye Needs Your Help
    • Question
    • A - DIAGNOSTIC ISSUES
    • DISORDERS OF ACID-BASE BALANCE
    • The Is Influenced by Changes in the ECF Volume
    • Measurement of Brachial Venous PCO2 to Assess Buffering of an H+ Ion Load by BBS
    • Disorders With a High Concentration of H+ Ionsin Plasma
    • Metabolic acidosis
    • Respiratory acidosis
    • Disorders with a Low Concentration of H+ Ions in Plasma
    • Metabolic alkalosis
    • Respiratory alkalosis
    • MAKING AN ACID-BASE DIAGNOSIS
    • LABORATORY TESTS USED IN A PATIENT WITH METABOLIC ACIDOSIS
    • Questions to ask in the clinical approach to the patient with metabolic acidosis
    • Is the Content of Ions in the ECF Compartment Low?
    • Is There an Overproduction of Acids?
    • Is the Metabolic Acidosis due to the Ingestion of Alcohols?
    • Is Buffering of the H+ Ion Load by BBS in Skeletal Muscle?
    • In a Patient with Chronic Hyperchloremic Metabolic Acidosis (HCMA), Is the Rate of Excretion of Ions High Enough So That the Kid...
    • If the Rate of Excretion of Ions Is High, What Is the Anion Excreted with Ions in the Urine?
    • If the Rate of Excretion of Ions Is Low, What Is the Basis for the Low Ion Excretion Rate?
    • Is There a Defect in H+ Ion Secretion in the Proximal Tubule?
    • Laboratory Tests
    • 1. The anion gap in plasma
    • An example
    • Pitfalls in the use of the plasma anion gap
    • Issues related to PAlbumin
    • Issues related to other cations and anions
    • Delta anion gap/delta
    • 2. The osmolal gap in plasma
    • 3. Tests used to estimate the rate of excretion of ions
    • The urine net charge
    • The urine osmolal gap
    • 4. Tests used to evaluate the basis for a low rate of excretion of ions
    • The PCO2 in alkaline urine
    • The fractional excretion of
    • Rate of citrate excretion
    • B - IDENTIFYING MIXED ACID-BASE DISORDERS
    • EXPECTED RESPONSES TO PRIMARY ACID-BASE DISORDERS
    • HOW TO RECOGNIZE MIXED ACID-BASE DISORDERS
    • Evaluate the Accuracy of the Laboratory Data
    • Calculate the Ion Content in the ECF Volume
    • Determine the Quantitative Relationship Between the Fall in and the Rise in the PAnion gap
    • Examine the in the Patient with Respiratory Acidosis or Alkalosis to Identify the Presence of a Metabolic Acid-Base Disturbance
    • OTHER DIAGNOSTIC APPROACHES: THE STRONG ION DIFFERENCE
    • DISCUSSION OF CASES
    • Case 2-1: Does This Man Really Have Metabolic Acidosis?
    • Does this patient have a significant degree of metabolic acidosis?
    • Laboratory data
    • Clinical picture
    • Correlating the clinical and laboratory information
    • What is the basis for the high PAnion gap?
    • Case 2-2: Lola Kaye Needs Your Help
    • What is/are the major acid-base diagnosis/diagnoses?
    • Metabolic acidosis
    • Respiratory acidosis
    • Additional Information about Case 2-2
    • Questions
    • What Is the Most Likely Basis for the Metabolic Acidosis?
    • What Is the Most Likely Basis for the Respiratory Acidosis?
    • 3 - Metabolic Acidosis: Clinical Approach
    • Introduction
    • OBJECTIVES
    • Case 3-1: Stick to the Facts
    • Questions
    • A - CLINICAL APPROACH
    • EMERGENCIES IN THE PATIENT WITH METABOLIC ACIDOSIS
    • Emergencies at Presentation
    • Hemodynamic emergency
    • Cardiac arrhythmia
    • Failure of adequate ventilation
    • Toxin-induced metabolic acidosis
    • Dangers to Anticipate After Commencing Therapy
    • Dangers related to overly aggressive administration of saline
    • 1. A more severe degree of acidemia
    • i) Dilution of the concentration of in the ECF compartment
    • ii) Loss of more NaHCO3 in diarrheal fluid
    • iii) Back-titration of ions by H+ ions that were bound to intracellular proteins
    • 2. Cerebral edema in children with diabetic ketoacidosis
    • 3. Rapid correction of chronic hyponatremia
    • Hypokalemia
    • Metabolic or nutritional issues
    • ASSESS THE EFFECTIVENESS OF THE BICARBONATE BUFFER SYSTEM
    • DETERMINE THE BASIS OF METABOLIC ACIDOSIS
    • Detect Addition of Acids by Finding New Anions in the Blood and/or the Urine
    • Detect Conditions With Fast Addition of H+ Ions
    • Assess the Renal Response to Metabolic Acidosis
    • QUESTIONS
    • B - DISCUSSIONS
    • Case 3-1: Stick to the Facts
    • What dangers were present on admission?
    • Marked degree of contraction of EABV
    • Severe degree of hypokalemia
    • Hyponatremia
    • Binding of H+ ions to proteins in cells
    • What dangers should be anticipated during therapy?
    • A more severe degree of hypokalemia
    • Rapid rise in PNa
    • Further fall in
    • Plan for initial therapy
    • What is the basis for the metabolic acidosis?
    • DISCUSSION OF QUESTIONS
    • 4 - Metabolic Acidosis Caused by a Deficit of NaHCO3
    • Introduction
    • OBJECTIVES
    • A - OVERVIEW
    • DEFINITIONS
    • PATHOGENESIS OF METABOLIC ACIDOSIS CAUSED BY NAHCO3 LOSS
    • B - CONDITIONS THAT CAUSE A DEFICIT OF NAHCO3
    • DIRECT LOSS OF NAHCO3
    • Loss of NaHCO3 in the Gastrointestinal Tract
    • Secretion of ions by the pancreas
    • Secretion of ions by the late small intestine and the colon
    • Clinical Picture
    • Treatment
    • Renal Loss of NaHCO3
    • C - DISEASES WITH LOW RATE OF EXCRETION OF NH4+ IONS
    • PROXIMAL RENAL TUBULAR ACIDOSIS
    • CLINICAL SUBTYPES OF PROXIMAL RTA
    • Proximal RTA with Fanconi Syndrome
    • Acquired Isolated Proximal RTA
    • Hereditary Isolated Proximal RTA
    • Possible molecular lesions
    • NBCe1 defect
    • Carbonic anhydrase II defect
    • NHE-3 defect
    • Diagnostic Issues in the Patient with Proximal Renal Tubular Acidosis
    • Treatment of the Patient with Proximal RTA
    • DISTAL RENAL TUBULAR ACIDOSIS
    • Case 4-1: A Man Diagnosed With Type IV Renal Tubular Acidosis
    • Questions
    • Case 4-2: What Is This Woman's "Basic" Lesion?
    • Questions
    • Nomenclature
    • Clinical Approach: Initial Steps
    • Assess the rate of ion excretion
    • Determine the basis of the low rate of excretion of ions
    • SUBTYPES OF DISORDERS CAUSING LOW ION EXCRETION
    • Pathophysiology
    • Clinical features
    • Hyperkalemia
    • Consequences of a persistently low urine pH
    • Treatment
    • Emergency management
    • Acid-base management
    • Subtype With Low Net Distal H+ Ion Secretion
    • Pathophysiology
    • Low number of H+ ATPase pumps in the distal nephron
    • Inhibition of existing H+-ATPase pumps by an alkaline cell pH (Figure 4-7)
    • Back-leak of H+ ions in the distal nephron
    • Distal secretion of ions
    • Clinical features
    • Associated findings
    • Hypokalemia
    • Nephrocalcinosis
    • Consequences of a high urine pH
    • Calcium phosphate (CaHPO4) stones
    • Treatment
    • Emergency issues
    • Acid-base issues
    • Subtype With Lesions Involving Both Distal H+ Ion Secretion and NH3 Availability
    • Pathophysiology
    • Clinical features
    • Treatment
    • INCOMPLETE RENAL TUBULAR ACIDOSIS
    • Distal Renal Tubular Acidosis Caused by Low Net Distal Secretion of H+ Ions
    • Large Intermittent Intake of Alkali in a Normal Subject
    • Patients with True "Incomplete Renal Tubular Acidosis"
    • METABOLIC ACIDOSIS IN PATIENTS WITH RENAL FAILURE
    • ion excretion
    • ion excretion
    • Diet alkali
    • D - INTEGRATIVE PHYSIOLOGY
    • STEADY-STATE ACID-BASE BALANCE IN PATIENTS WITH RENAL TUBULAR ACIDOSIS
    • Generate New Ions by Dissolving the Alkaline Salts in Bone
    • Fewer Organic Anions in the Urine Are Excreted So Dietary Alkali Titrates Some of the Dietary Acid Load
    • NEPHROCALCINOSIS IN PATIENTS WITH DISTAL RENAL TUBULAR ACIDOSIS
    • Mechanisms
    • Raise the medullary interstitial ionized calcium concentration
    • Raise the medullary interstitial concentration of and
    • STIOCHOMETRY OF SLGT1
    • BIOCHEMISTRY OF THE CHOLERA TOXIN
    • DISCUSSION OF CASES
    • Case 4-1: A Man Diagnosed With Type IV Renal Tubular Acidosis
    • What is the basis of the metabolic acidosis?
    • What is the cause of the low rate of excretion of ions?
    • Case 4-2: What Is This Woman's "Basic" Lesion?
    • What is the basis of the metabolic acidosis?
    • What is the cause of the low rate of excretion of ions?
    • 5 - Ketoacidosis
    • Introduction
    • OBJECTIVES
    • Case 5-1: This Man Is Anxious to Know Why He Has Ketoacidosis
    • Questions
    • A - BIOCHEMICAL BACKGROUND
    • METABOLIC PROCESS ANALYSIS
    • PRODUCTION OF KETOACIDS IN THE LIVER
    • Biochemistry of Ketoacid Production
    • Formation of Acetyl-CoA in the Liver
    • The Metabolic Fates of Acetyl-CoA
    • Inhibition of the oxidation of acetyl-CoA in the tricarboxylic acid cycle
    • Inhibition of the conversion of acetyl-CoA to long-chain fatty acids
    • Conversion of Acetyl-CoA to Ketoacids
    • Bypassing Limitation by Availability of ADP on Rate of Hepatic Ketoacid Production
    • REMOVAL OF KETOACIDS
    • Oxidation of Ketoacids in the Brain
    • Removal of Ketoacids by the Kidneys
    • Ketoacid Oxidation in Other Organs
    • Production of Acetone from Acetoacetic Acid
    • Clinical Messages
    • CLINICAL ASPECTS OF KETOACIDOSIS
    • B - DIABETIC KETOACIDOSIS
    • Case 5-2: Hyperglycemia and Acidemia
    • Questions
    • DIAGNOSIS OF DIABETIC KETOACIDOSIS
    • Changes in Body Composition and Laboratory Findings in DKA
    • Hyperglycemia
    • Sodium
    • Plasma Na+ concentration (PNa)
    • Potassium
    • Anchor 388
    • PAnion gap
    • PCO2
    • Ketoacids
    • GFR
    • Natural History
    • Cerebral Edema in Children with DKA
    • Pathophysiology
    • Intracellular fluid issues
    • Extracellular fluid issues
    • An increase in number of effective osmoles in brain cells
    • A fall in the PEffective osm
    • A rapid fall in the PGlucose
    • Gain of EFW
    • Increase ECFV in the brain
    • Clinical implications
    • TREATMENT OF THE PATIENT WITH DIABETIC KETOACIDOSIS
    • Treat a Hemodynamic Emergency if Present
    • Avoid a Large Fall in the PEffective osm
    • Replace the Na+ ion deficit
    • Stop Ketoacids Production
    • Deficit of K+ Ions
    • NaHCO3 Therapy
    • Phosphate Therapy
    • Identify and deal with underlying events that may have precipitated DKA
    • Anticipate and prevent complications that may arise during therapy
    • Case 5-3: Sam Had a Drinking Binge Yesterday
    • Questions
    • C - ALCOHOLIC KETOACIDOSIS
    • BIOCHEMISTRY OF ALCOHOLIC KETOACIDOSIS
    • Steps in Ketoacids Formation From Ethanol
    • REMOVAL OF KETOACIDS IN THE PATIENT WITH ALCOHOLIC KETOACIDOSIS
    • DIAGNOSIS OF ALCOHOLIC KETOACIDOSIS
    • Low EABV
    • PGlucose
    • ß-Hydroxybutyric Acidosis
    • PK
    • Nutritional Deficiencies
    • Acid-Base Disorders
    • Mixed metabolic acidosis and metabolic alkalosis
    • L-Lactic acidosis
    • Respiratory alkalosis
    • TREATMENT OF ALCOHOLIC KETOACIDOSIS
    • Hypoglycemia
    • Low EABV
    • K+ Ion Deficit
    • Thiamin
    • Phosphate
    • Ketoacidosis
    • D - INTEGRATIVE PHYSIOLOGY
    • CONTROL OF KETOGENESIS: A MORE DETAILED ANALYSIS
    • Control by supply of fatty acids to the liver
    • Control by supply of intrahepatic substrates
    • Uncoupled Oxidative Phosphorylation
    • Control by supply of oxygen to the liver
    • REGULATION OF KETOACIDS FORMATION DURING PROLONGED FASTING
    • DISCUSSION OF CASES
    • Case 5-1: A Man Is Anxious to Know Why He Has Ketoacidosis
    • What makes DKA an unlikely diagnosis?
    • What makes alcoholic ketoacidosis an unlikely diagnosis?
    • What makes starvation or hypoglycemic ketoacidosis an unlikely diagnosis?
    • How may the patient's intake of sweetened soft drinks contribute to the development of his ketoacidosis?
    • Is ketoacidosis the only cause of metabolic acidosis in this patient?
    • Case 5-2: Hyperglycemia and Acidemia
    • What are the major threats to Andy's life?
    • Should the physician administer NaHCO3?
    • Case 5-3: Sam Had a Drinking Binge Yesterday
    • What is Sam's acid-base disorder?
    • What are the issues for therapy?
    • 6 - Metabolic Acidosis: Acid Gain Types
    • Introduction
    • OBJECTIVE
    • Case 6-1: Patrick Is in for a Shock
    • Questions
    • Case 6-2: Metabolic Acidosis Associated With Diarrhea
    • Question
    • Case 6-3: Severe Acidemia in a Patient With Chronic Alcoholism
    • Question
    • A - GENERAL CONSIDERATIONS
    • MAJOR THREATS IN THE PATIENT WITH METABOLIC ACIDOSIS
    • BUFFERING OF H+ IONS IN A PATIENT WITH METABOLIC ACIDOSIS
    • ISSUES IN DIAGNOSIS
    • B - SPECIFIC DISORDERS
    • L-LACTIC ACIDOSIS
    • Synopsis of biochemistry of glucose oxidation in skeletal muscles
    • Synopsis of the biochemistry of l-lactic acidosis
    • Increased production of l-lactic acid
    • Decreased removal of l-lactic acid
    • Oxidation of L-lactic acid
    • Gluconeogenesis
    • Classification of l-lactic acidosis
    • Clinical settings with predominantly overproduction of l-lactic acid
    • Inadequate delivery of oxygen
    • Excessive Demand for Oxygen
    • Clinical Settings With Increased Production of L-Lactic Acid in the Absence of Hypoxia
    • Ethanol intoxication
    • Thiamin deficiency and ethanol intoxication
    • Riboflavin deficiency and the use of tricyclic antidepressants
    • Uncoupling of oxidative phosphorylation
    • Clinical settings with predominantly decreased removal of l-lactic acid
    • Antiretroviral Drugs
    • QUESTIONS
    • D-LACTIC ACIDOSIS
    • Pathophysiology
    • Diagnosis and Treatment
    • METABOLIC ACIDOSIS DUE TO TOXIC ALCOHOLS
    • Methanol Intoxication
    • Ethylene Glycol (Antifreeze) Intoxication
    • Therapy of methanol or ethylene glycol intoxication
    • Administration of ethanol
    • Administration of fomepizole (4-methylpyrazole)
    • Propane 1,2-diol (Propylene Glycol)
    • Biochemistry
    • Clinical manifestations
    • Treatment
    • PYROGLUMATIC ACIDOSIS
    • METABOLIC ACIDOSIS CAUSED BY THE INGESTION OF AN ACID
    • C - INTEGRATIVE PHYSIOLOGY
    • ORGANIC ACIDS PRODUCTION IN THE COLON
    • Butyric acid
    • Propionic acid
    • DISCUSSION OF CASES
    • Judging from the time frame for his illness, what is (are) the likely cause(s) of metabolic acidosis?
    • Why did his blood pressure fall so precipitously?
    • Why did he have hyperkalemia?
    • Why did the administration of intravenous calcium cause a rapid recovery?
    • Case 6-2: Metabolic Acidosis Associated With Diarrhea
    • What is the cause of the metabolic acidosis in this patient?
    • Case 6-3: Severe Acidemia in a Patient With Chronic Alcoholism
    • What dangers may be present on admission or arise during therapy?
    • More information
    • What is the cause of the severe L-lactic acidosis in this patient?
    • DISCUSSION OF QUESTIONS
    • 7 - Metabolic Alkalosis
    • Introduction
    • OBJECTIVES
    • Case 7-1: This Man Should Not Have Metabolic Alkalosis
    • Questions
    • Case 7-2: Why Did This Patient Develop Metabolic Alkalosis so Quickly?
    • Question
    • Case 7-3: Milk-Alkali Syndrome, but Without Milk
    • Questions
    • A - PATHOPHYSIOLOGY
    • OVERVIEW
    • Renal Reabsorption of NaHCO3: A More Detailed Analysis
    • Stimuli for the reabsorption of filtered NaHCO3
    • Experiments carried out by Pitts
    • Renal response to a physiologic load of ions
    • QUESTION
    • DEVELOPMENT OF METABOLIC ALKALOSIS
    • Metabolic Alkalosis Caused by Deficits of Cl- Salts
    • Deficit of HCl
    • Gain of ions
    • Balance
    • Drainage period
    • Postdrainage period
    • Deficit of KCl
    • Gain of ions
    • Balance
    • Deficit of NaCl
    • Metabolic Alkalosis Caused by Retention of NaHCO3
    • Primary high mineralocorticoid activity
    • Input and retention of NaHCO3
    • Source of alkali
    • Renal reasons for a markedly reduced rate of excretion of NaHCO3
    • QUESTIONS
    • B - CLINICAL SECTION
    • CLINICAL APPROACH
    • Effect of Alkalemia on Ventilation
    • COMMON CAUSES OF CHRONIC METABOLIC ALKALOSIS
    • Vomiting
    • Diuretics
    • LESS COMMON CAUSES OF CHRONIC METABOLIC ALKALOSIS
    • Conditions With High Mineralocorticoid Activity
    • Metabolic Alkalosis Associated With Milk-Alkali Syndrome
    • Metabolic Alkalosis Associated With a Posthypercapnic State
    • Metabolic Alkalosis Associated With the Intake of Nonreabsorbable Anions
    • Metabolic Alkalosis Associated With Hypomagnesemia
    • THERAPY OF METABOLIC ALKALOSIS
    • Patients With Metabolic Alkalosis Caused by Retention of NaHCO3
    • C - INTEGRATIVE PHYSIOLOGY
    • INTEGRATIVE PHYSIOLOGY OF CALCIUM HOMEOSTASIS
    • INPUT OF CALCIUM FROM THE GASTROINTESTINAL TRACT
    • OUTPUT OF CALCIUM
    • DISCUSSION OF CASES
    • Case 7-1: This Man Should Not Have Metabolic Alkalosis
    • What are the major threats to the patient and how should these dictate the therapy?
    • What is the basis for metabolic alkalosis?
    • Balance data for Na+, K+, and Cl- ions
    • Deficit of HCl
    • Deficit of NaCl
    • Balance for Na+ ions
    • Balance for Cl- ions
    • Balance for K+
    • What is the therapy for metabolic alkalosis in this patient?
    • Case 7-2: Why Did This Patient Develop Metabolic Alkalosis so Quickly?
    • Why did this patient develop metabolic alkalosis on days 3 and 4?
    • CASE 7-3: MILK-ALKALI SYNDROME, BUT WITHOUT MILK
    • What is the basis for the metabolic alkalosis?
    • Deficit of HCl
    • Deficit of NaCl
    • Deficit of KCl
    • Ingestion of alkali
    • What should the initial therapy be?
    • DISCUSSION OF QUESTIONS
    • Loss in the gastric fluid
    • Loss in the Urine
    • 8 - Respiratory Acid-Base Disturbances
    • Introduction
    • OBJECTIVE
    • A - REVIEW OF THE PERTINENT PHYSIOLOGY
    • THE BICARBONATE/CARBONIC ACID BUFFER SYSTEM
    • OVERVIEW OF CO2 HOMEOSTASIS
    • Production of CO2
    • Removal of CO2
    • Control of ventilation
    • PHYSIOLOGY OF CO2 TRANSPORT
    • RENAL RESPONSE TO A CHRONIC CHANGE IN PCO2
    • B - RESPIRATORY ACID-BASE DISORDERS
    • RESPIRATORY ACIDOSIS
    • Permissive Hypercapnia
    • RESPIRATORY ALKALOSIS
    • Salicylate Intoxication
    • Effect of acidemia on the concentration of salicylates in cells
    • Signs and symptoms
    • Acid-base changes
    • Respiratory alkalosis
    • Metabolic acidosis
    • Diagnosis
    • Treatment
    • Two - Salt and Water
    • 9 - Sodium and Water Physiology
    • Introduction
    • OBJECTIVES
    • A - BODY FLUID COMPARTMENTS
    • Case 9-1: A Rise in the PNa After a Seizure
    • Question
    • TOTAL BODY WATER
    • Distribution of Water Across Cell Membranes
    • Defense of Brain Cell Volume
    • Regulatory decrease in brain cell volume
    • Regulatory increase in brain cell volume
    • Distribution of Water in the ECF Compartment
    • Gibbs-Donnan equilibrium
    • B - PHYSIOLOGY OF SODIUM
    • OVERVIEW
    • CONTROL SYSTEM FOR SODIUM BALANCE
    • Normal ECF Volume
    • Control of the Excretion of Sodium Ions
    • Driving force
    • Transport mechanism
    • Proximal convoluted tubule
    • Quantitative analysis
    • Process
    • Control
    • Glomerulotubular balance
    • Neurohumoral effects
    • Disorders involving the PCT
    • Descending thin limb of the loop of Henle
    • Ascending thin limb of the loop of Henle
    • Quantitative analysis
    • Medullary thick ascending limb of the loop of Henle
    • Quantitative analysis
    • Process
    • Control
    • Role of hormones
    • Inhibitors
    • Disorders involving this nephron segment
    • Cortical thick ascending limb of the loop of Henle
    • Quantitative analysis
    • Process
    • Control
    • Reabsorption of Na+ and Cl- ions in the macula densa
    • Early distal convoluted tubule
    • Quantitative analysis
    • Process
    • Control
    • Inhibitors
    • Disorders involving NCC
    • Cortical distal nephron
    • Electrogenic reabsorption of Na+ ions in the CDN
    • Inhibitors
    • Disorders involving the ENaC
    • Electroneutral reabsorption of Na+ ions in the CDN
    • Medullary collecting duct
    • Process
    • Role of hormones
    • Inhibitors
    • C - PHYSIOLOGY OF WATER
    • OVERVIEW
    • CONTROL OF WATER BALANCE
    • Sensor
    • Thirst
    • Vasopressin
    • Excretion of a Large Volume of Dilute Urine
    • 1. Distal delivery of filtrate
    • 2. Reabsorption of Na+ and Cl- ions without water: desalination of luminal fluid
    • Residual water permeability
    • 3. Absence of actions of vasopressin
    • Retain "nondangerous" water load
    • Excretion of Concentrated Urine
    • 1. Conserve water when there is a deficit of water
    • 2. Excrete a large hypertonic load of Na+ and Cl- ions
    • Overview of the renal concentrating process
    • The vasa recta functions as a countercurrent exchanger
    • Insertion of AQP2 when vasopressin acts
    • Generation of a high interstitial osmolality in the outer medulla
    • Regulation of the urine concentrating process in the outer medulla
    • Substrate-driven control
    • Inhibitory control
    • Regulation of the urine concentrating process in the inner medulla
    • Urea and the conservation of water
    • Intrarenal urea recycling: Intrarenal recycling of urea serves a number of important functions. First, this is a critically impo...
    • Process: For simplicity, we shall begin with the absorption of urea in the inner MCD (Fig. 9-21). This absorption requires the p...
    • Quantities: To obtain a quantitative estimate of the amount of urea that is recycled, one needs an estimate of the amount of ure...
    • Avoiding oliguria when the urine is electrolyte poor
    • Lack of AQP1 in the Majority of the Descending Thin Limbs of the Loop of Henle
    • 1. About five-sixths of the GFR is reabsorbed in the PCT
    • 2. During water deprivation, the inhibitory signals that modulate the reabsorption of Na+ and Cl- in the mTAL of the loop of Hen...
    • 3. The rise in the concentrations of Na+ and Cl- ions in the descending thin limb of the loop of Henle in superficial nephrons i...
    • Minimizing the Dangers for the Renal Medulla
    • Preventing the precipitation of calcium salts in the deeper part of the renal medulla
    • Conundrum 1
    • Resolution
    • Conundrum 2
    • Resolution
    • Minimizing the risk of precipitation of calcium salts: role of magnesium
    • Minimizing work in the deep part of the outer medulla
    • Conundrum 3
    • Resolution
    • Conundrum 4
    • Resolution
    • D - INTEGRATIVE PHYSIOLOGY
    • INTEGRATIVE PHYSIOLOGY OF THE RENAL MEDULLA
    • Lack of AQP1 in the Majority of the Descending Thin Limbs of the Loop of Henle
    • Minimizing the Dangers for the Renal Medulla
    • DISCUSSION OF CASE 9-1
    • Case 9-1: A Rise in the PNa After a Seizure
    • What is the basis for the acute rise in the patient's PNa?
    • DISCUSSION OF QUESTIONS
    • 10 - Hyponatremia
    • Introduction
    • OBJECTIVES
    • Case 10-1: This Catastrophe Should Not Have Occurred!
    • Questions
    • Case 10-2: This Is Far From Ecstasy!
    • Questions
    • Case 10-3: Hyponatremia With Brown Spots
    • Questions
    • Case 10-4: Hyponatremia in a Patient on a Thiazide Diuretic
    • Questions
    • A - BACKGROUND
    • REVIEW OF THE PERTINENT PHYSIOLOGY
    • The Plasma Na+ Concentration Reflects the ICF Volume
    • The Content of Na+ Ions Determines the ECF Volume
    • Regulation of Brain Volume
    • Synopsis of Water Physiology
    • Distal delivery of filtrate
    • Residual Water Permeability
    • BASIS OF HYPONATREMIA
    • B - ACUTE HYPONATREMIA
    • CLINICAL APPROACH
    • Deal With Emergencies
    • Caution
    • Calculation of the volume of hypertonic 3% saline
    • DIAGNOSTIC ISSUES
    • SPECIFIC CAUSES
    • Perioperative hyponatremia
    • Hyponatremia caused by retained hypotonic lavage fluid
    • Clinical Settings in Which Acute Hyponatremia Occurs Outside the Hospital
    • Hyponatremia caused by the intake of MDMA
    • Positive balance for water
    • Large water intake
    • Low output of water
    • Negative balance for NaCl
    • Hyponatremia caused by diarrhea in infants and children
    • Exercise-induced hyponatremia (hyponatremia in a marathon runner)
    • QUESTIONS
    • C - CHRONIC HYPONATREMIATABLE
    • OVERVIEW
    • Points to Emphasize
    • CLINICAL APPROACH
    • Identify Emergencies on Admission
    • Anticipate Risks During Therapy
    • Determine Why the Excretion of Water Is Too Low
    • Pseudohyponatremia
    • Hyponatremia Caused by Hyperglycemia
    • Classification
    • Tools to detect a decreased EABV
    • Concentrations of Na+ and Cl- ions in the urine
    • Concentrations of urea and urate in plasma
    • Other laboratory tests
    • SPECIFIC DISORDERS
    • Diuretic-Induced Hyponatremia
    • Beer Potomania
    • Primary Polydipsia
    • "Tea and Toast" Hyponatremia
    • Primary Adrenal Insufficiency
    • Cerebral Salt Wasting
    • Syndrome of Inappropriate Antidiuretic Hormone
    • Subtypes of syndrome of inappropriate antidiuretic hormone
    • Autonomous release of vasopressin
    • Reset osmostat
    • Nonosmotic stimuli (afferent) overload
    • Subtype with absent vasopressin
    • Barostat reset
    • Glucocorticoid Deficiency
    • Hypothyroidism
    • Heart Failure and Liver Cirrhosis
    • TREATMENT OF PATIENTS WITH CHRONIC HYPONATREMIA
    • Hyponatremia Caused by Low EABV/Low Distal Delivery of Filtrate
    • Design of therapy
    • Hyponatremia Caused by SIADH
    • Design of therapy
    • Water restriction
    • Loop diuretics and increasing salt intake
    • Urea
    • Vasopressin receptor antagonists (Vaptans)
    • Hyponatremia in Patients With Heart Failure
    • Hyponatremia in Patients With Liver Cirrhosis
    • QUESTIONS
    • D - DISCUSSION OF CASES
    • Case 10-1: This Catastrophe Should Not Have Occurred!
    • What dangers are there on presentation?
    • What dangers should be anticipated during therapy, and how can they be avoided?
    • Case 10-2: This Is Far From "Ecstasy"!
    • Is this Acute Hyponatremia?
    • Why did she have a seizure if the PNa was 130mmol/l?
    • What role might anorexia nervosa play in this clinical picture?
    • What is your therapy for this patient?
    • Case 10-3: Hyponatremia With Brown Spots
    • What is the most likely basis for the very low EABV?
    • What dangers to the patient are present on presentation?
    • What dangers should be anticipated during therapy, and how can they be avoided?
    • Case 10-4: Hyponatremia in a Patient on a Thiazide Diuretic
    • What is the most likely basis for the chronic hyponatremia in this patient?
    • What dangers should be anticipated during therapy, and how can they be avoided?
    • DISCUSSION OF QUESTIONS
    • QUESTIONS
    • 11 - Hypernatremia
    • Introduction
    • OBJECTIVES
    • Case 11-1: Concentrate on the Danger
    • Questions
    • Case 11-2: What Is "Partial" About Partial Central Diabetes Insipidus?
    • Questions
    • Case 11-3: Where Did the Water Go?
    • Questions
    • A - BACKGROUND
    • SYNOPSIS OF THE PERTINENT PHYSIOLOGY
    • Concentration of Sodium Ions in Plasma
    • Responses to Hypernatremia
    • Thirst
    • Renal response
    • Regulation of Brain Cell Volume
    • PATHOPHYSIOLOGY OF HYPERNATREMIA
    • Hypernatremia Caused by a Deficit of Water
    • Reduced water intake
    • Water loss
    • Nonrenal water loss
    • Sweat
    • Respiratory tract
    • Gastrointestinal tract
    • Renal water loss
    • Shift of water
    • Hypernatremia Caused by Na+ Ion Gain
    • B - CLINICAL APPROACH
    • TOOLS IN THE CLINICAL APPROACH TO THE PATIENT WITH HYPERNATREMIA
    • Tools to Determine the Basis of Hypernatremia
    • Electrolyte-free water balance
    • Tonicity balance
    • QUESTION
    • Tools to Determine the Cause of Hypernatremia
    • STEPS IN THE CLINICAL APPROACH TO THE PATIENT WITH HYPERNATREMIA
    • Identify Emergencies Prior to Therapy
    • Induce a negative balance of Na+ ions
    • Induce a positive balance for water
    • Anticipate and Prevent Dangers That may Arise During Therapy
    • Determine the Appropriate Rate of Fall in the PNa
    • Recognize settings where the development of acute hypernatremia may be advantageous
    • Assess Thirst and the Appropriate Renal Response to Hypernatremia
    • Determine the Cause of Hypernatremia and the Design of Therapy
    • C - SPECIFIC CAUSES OF HYPERNATREMIA
    • DIABETES INSIPIDUS
    • Central diabetes insipidus
    • Circulating vasopressinase
    • Nephrogenic diabetes insipidus
    • Congenital nephrogenic diabetes insipidus
    • Mutations in the V2R gene
    • Mutations in the AQP2 gene
    • Lithium-induced nephrogenic diabetes insipidus
    • Hypokalemia
    • Hypercalcemia
    • Renal concentrating defect
    • QUESTIONS
    • Hypernatremia caused by a shift of water
    • Hypernatremia and polyuria in geriatric patients
    • Low water intake
    • Urea-induced osmotic diuresis
    • Use of a loop diuretic in a patient who has congestive heart failure
    • TREATMENT OF PATIENTS WITH HYPERNATREMIA
    • Acute Hypernatremia
    • Chronic Hypernatremia
    • Intracellular fluid analysis
    • Extracellular fluid analysis
    • Patient 1 has a normal ECF volume (10 L)
    • Patient 2 has an estimated ECF volume of 7 L
    • Therapy for patient 1
    • Therapy for patient 2
    • D - INTEGRATIVE PHYSIOLOGY
    • NEPHROGENIC DIABETES INSIPIDUS IN THE NEWBORN
    • DISCUSSION OF CASES
    • Why did hypernatremia develop?
    • What are the goals for therapy of his hypernatremia?
    • Case 11-2: What Is "Partial" About Partial Central Diabetes Insipidus?
    • What is the basis for the high urine flow rate in this patient?
    • Central DI
    • Primary polydipsia
    • What are the options for therapy?
    • Case 11-3: Where Did the Water Go?
    • What is the basis for the hypernatremia (in quantitative terms): a positive balance for Na+ ions and/or a negative balance for w...
    • A gain of Na+ ions
    • A deficit of water
    • Why does he have such a severe degree of hypernatremia?
    • A shift of water
    • What is the therapy of hypernatremia in this patient?
    • DISCUSSION OF QUESTIONS
    • 12 - Polyuria
    • Introduction
    • OBJECTIVES
    • Case 12-1: Oliguria With a Urine Volume of 4 L per Day
    • Questions
    • Case 12-2: More Than Just Salt and Water Loss
    • Questions
    • A - BACKGROUND
    • SYNOPSIS OF THE PHYSIOLOGY
    • Water Diuresis
    • Distal Delivery of Filtrate
    • Residual Water Permeability
    • Desalination of Luminal Fluid
    • Osmotic Diuresis
    • DEFINITION OF POLYURIA
    • Urine Flow Rate
    • UOsm
    • Osmole excretion rate
    • B - WATER DIURESIS
    • TOOLS USED IN ASSESSMENT OF A PATIENT WITH A WATER DIURESIS
    • CLINICAL APPROACH TO THE PATIENT WITH A WATER DIURESIS
    • Step 1: What Is the UOsm?
    • Step 2: Examine the Renal Response to Vasopressin or dDAVP (See Flow Chart 12-2)
    • Step 3: Establish the Basis for Central DI
    • Step 4: Establish the Basis for Nephrogenic DI
    • ISSUES IN THERAPY
    • UOsm
    • Osmole Excretion Rate
    • Nature of the Urine Osmoles
    • Sources of the Urine Osmoles
    • Source of Urea
    • Source of Glucose
    • C - COSMOTIC DIURESIS
    • TOOLS USED IN THE ASSESSMENT OF A PATIENT WITH AN OSMOTIC DIURESIS
    • CLINICAL APPROACH TO THE PATIENT WITH AN OSMOTIC DIURESIS
    • Step 1: What Is the UOsm?
    • Calculate the osmole excretion rate
    • Step 2: Define the Nature of the Excreted Osmoles
    • Step 3: Identify the Source of the Osmoles in the Urine
    • Postobstructive Diuresis
    • ISSUES IN THERAPY
    • Impact of the Urine Composition on Body Tonicity and ECF Volume
    • Source of Excreted Osmoles
    • QUESTIONS
    • D - DISCUSSION OF CASES
    • CASE 12-1: OLIGURIA WITH A URINE VOLUME OF 4 L PER DAY
    • Does This Patient Have Polyuria?
    • Conventional interpretation
    • Physiology-based interpretation
    • What Dangers Related to Na+ and Water Issues May Develop in This Patient?
    • CASE 12-2: MORE THAN JUST SALT AND WATER LOSS
    • Does This Patient Have an Osmotic Diuresis?
    • What is the Source of Urea? What are the Implications for Therapy?
    • DISCUSSION OF QUESTIONS
    • Three - Potassium
    • 13 - Potassium Physiology
    • Introduction
    • OBJECTIVES
    • Case 13-1: Why Did I Become So Weak?
    • A - PRINCIPLES OF PHYSIOLOGY
    • GENERAL CONCEPTS FOR THE MOVEMENT OF K+ IONS ACROSS CELL MEMBRANES
    • Driving Force for the Shift of K+ Ions across Cell Membranes
    • Pathways for the Movement of K+ Ions across Cell Membranes
    • QUESTION
    • B - SHIFT OF POTASSIUM IONS ACROSS CELL MEMBRANES
    • INCREASING THE NEGATIVE VOLTAGE IN CELLS
    • Raise the Intracellular Concentration of Na+ Ions
    • Electrogenic entry of Na+ ions into cells
    • Clinical implications
    • Electroneutral entry of Na+ into cells
    • Clinical implications
    • Activate Pre-existing Na-K-ATPase
    • Increase in the Number of Na-K-ATPase Units in Cell Membranes
    • Insulin
    • Clinical implications
    • Exercise training
    • Thyroid hormones
    • Clinical implications
    • METABOLIC ACIDOSIS AND SHIFT OF POTASSIUM IONS ACROSS CELL MEMBRANES
    • Clinical Implications
    • HYPERTONICITY AND SHIFT OF POTASSIUM IONS ACROSS CELL MEMBRANES
    • Clinical Implications
    • C - RENAL EXCRETION OF POTASSIUM IONS
    • COMPONENTS OF THE EXCRETION OF K+ IONSIN THE CORTICAL DISTAL NEPHRON
    • Secretion of K+ ions in the Cortical Distal Nephron
    • Generation of a Lumen-Negative Voltage
    • Electrogenic reabsorption of Na+ ions in the CDN
    • Mechanism of action of aldosterone
    • Electroneutral reabsorption of Na+ ions in the CDN
    • Clinical implications
    • Hypokalemia
    • Hyperkalemia
    • K+ Ion Channels
    • ROMK channels
    • Big conductance K+ ion channel (maxi K+ ion channel)
    • WNK Kinases (With No Lysine Kinases)
    • WNK4
    • Effect on NCC
    • Effect on ROMK
    • WNK1
    • Effect on NCC
    • Effect on ROMK
    • The Aldosterone Paradox
    • Flow Rate in the Cortical Distal Nephron
    • INTRARENAL UREA RECYCLING
    • Clinical implications
    • REABSORPTION OF K+ IONS IN THE MEDULLARY COLLECTING DUCT
    • D - INTEGRATIVE PHYSIOLOGY
    • INTEGRATIVE PHYSIOLOGY OF THE RESPONSE TO A DIETARY K+ ION LOAD: A PALEOLITHIC PERSPECTIVE
    • Mechanism to Shift K+ Ions into Liver Cells
    • Control of the Excretion of K+ Ions
    • Integration of the role of WNK kinases and delivery of ions to CDN
    • Conservation of NaCl (Figure 13-14, A)
    • Excretion of a large K+ ion load (Figure 13-14, B)
    • A high rate of electrogenic reabsorption of Na+ ions
    • Open ROMK in the luminal membrane of principal cells
    • Re-establishment of an NaCl-retaining state (Figure 13-14, C)
    • MECHANISM TO INCREASE THE DELIVERY OF NA+ IONS TO THE CDN
    • Reinterpretation of the medullary recycling of K+ ions
    • INTEGRATION OF FLOW RATE IN THE TERMINAL CDN AND ACTIVITY OF K+ ION SECRETION IN THE PATHOPHYSIOLOGY OF HYPERKALEMIA
    • INTEGRATION OF THE RENAL RESPONSE TO DIETARY K+ ION RESTRICTION
    • K+ ION DEPLETION AND HYPERTENSION
    • K+ ION DEPLETION AND THE PATHOPHYSIOLOGY OF CALCIUM KIDNEY STONES
    • DISCUSSION OF CASE 13-1
    • Case 13-1: Why Did I Become So Weak?
    • What is the most likely basis for the repeated episodes of acute hypokalemia?
    • Was an adrenergic effect associated with the acute hypokalemia?
    • Are there any clues in her laboratory results to suggest what the cause of acute hypokalemia might be?
    • DISCUSSION OF QUESTION
    • KATP channel and the release of insulin
    • KATP channel and vasodilatation
    • 14 - Hypokalemia
    • Introduction
    • Objectives
    • Case 14-1: Hypokalemia With Paralysis
    • Questions
    • Case 14-2: Hypokalemia With a Sweet Touch
    • Questions
    • Case 14-3: Hypokalemia in a Newborn
    • Questions
    • A - Synopsis of K+ Ion Physiology
    • Regulation of Distribution of K+ Ions Between the Extracellular Fluid and the Intracellular Fluid Compartments
    • Clinical Implications
    • Regulation of Renal Excretion of K+ Ions
    • Secretion of K+ Ions in the CDN
    • Clinical Implications
    • B - CLINICAL APPROACH
    • TOOLS USED IN THE CLINICAL ASSESSMENT OF THE PATIENT WITH HYPOKALEMIA
    • Assessment of the Rate of Excretion of K+ Ions in the Urine
    • The transtubular K concentration gradient (TTKG)
    • Tools to Establish the Basis for the Inappropriately High Rate of Excretion of K+ Ions
    • Steps in the clinical approach to a patient with hypokalemia
    • Deal with Emergencies
    • Anticipate and Prevent Dangers Due to Therapy
    • Determine if the Major Basis for Hypokalemia is an Acute Shift of K+ Ions Into Cells (Flow Chart 14-2)
    • Clinical Approach to the Patients With Chronic Hypokalemia
    • Subgroup with metabolic acidosis
    • Subgroup with metabolic alkalosis
    • Part C Specific Causes of Hypokalemia
    • C - SPECIFIC CAUSES OF HYPOKALEMIA
    • Hypokalemic Periodic Paralysis
    • Pathophysiology
    • Clinical Picture
    • Diagnosis
    • Differential Diagnosis
    • Therapy
    • Distal Renal Tubular Acidosis
    • Pathophysiology
    • Diagnosis
    • Therapy
    • Glue Sniffing
    • Pathophysiology
    • Diagnosis
    • Therapy
    • Diarrhea
    • Patients With Secretory Diarrhea
    • Pathophysiology
    • Patients With Diarrhea due to Diminished Reabsorption of Na+ and Cl- Ions in the Colon
    • Diagnosis
    • Diuretics
    • Pathophysiology
    • Clinical Picture
    • Therapy
    • Hypomagnesemia
    • Vomiting
    • Pathophysiology
    • Clinical Picture
    • Therapy
    • Bartter Syndrome
    • Pathophysiology
    • Molecular Basis
    • Clinical Picture
    • Therapy
    • Antenatal Bartter Syndrome
    • Gitelman Syndrome
    • Pathophysiology
    • Hypocalciuria
    • Hypomagnesemia
    • Molecular Basis
    • Clinical Picture
    • Diagnosis
    • Therapy
    • Cationic Drugs That Bind to the Ca-SR
    • Pathophysiology
    • Clinical Picture
    • Primary Hyperaldosteronism
    • Pathophysiology
    • Molecular Basis
    • Clinical Picture
    • Diagnosis
    • Differential Diagnosis
    • Therapy
    • Glucocorticoid Remediable Aldosteronism
    • Pathophysiology
    • Molecular Basis
    • Clinical Picture
    • Diagnosis
    • Differential Diagnosis
    • Therapy
    • Adrenocorticotropic Hormone- Producing Tumor or Severe Cushing Syndrome
    • Pathophysiology
    • Clinical Picture
    • Diagnosis
    • Differential Diagnosis
    • Therapy
    • Syndrome of Apparent Mineralocorticoid Excess
    • Pathophysiology
    • Molecular Basis
    • Clinical Picture
    • Diagnosis
    • Differential Diagnosis
    • Therapy
    • Liddle Syndrome
    • Pathophysiology
    • Molecular Basis
    • Clinical Picture
    • Diagnosis
    • Differential Diagnosis
    • Therapy
    • Amphotericin B-Induced Hypokalemia
    • Pathophysiology
    • Clinical Picture
    • Therapy
    • D - THERAPY OF HYPOKALEMIA
    • Medical Emergencies
    • Nonmedical Emergencies
    • Route of Potassium Administration
    • Potassium Preparations
    • Adjuncts to Therapy
    • Risks of Therapy
    • E - DISCUSSION OF CASES
    • Case 14-1: Hypokalemia With Paralysis
    • Is There a Medical Emergency in This Patient
    • What Is the Basis of the Hypokalemia in This Patient
    • What Is the Best Therapy for Acute Hypokalemia in This Patient
    • Case 14-2: Hypokalemia With a Sweet Touch
    • Is There a Medical Emergency in This Patient
    • Is There a Danger to Anticipate During Therapy
    • What Is the Basis of the Hypokalemia in This Patient
    • Case 14-3: Hypokalemia in a Newborn
    • Is There a Medical Emergency in This Patient
    • What Is the Basis of the Hypokalemia in This Patient
    • Why Did the Patient Have Nephrogenic Diabetes Insipidus
    • In What Nephron Segment Might Indomethacin Have Acted to Cause a Marked Decrease in Renal Loss of Na+ Ions
    • 15 - Hyperkalemia
    • Introduction
    • OBJECTIVES
    • Case 15-1: Might This Patient Have Pseudohyperkalemia?
    • Questions
    • Case 15-2: Hyperkalemia in a Patient Treated With Trimethoprim
    • Questions
    • Case 15-3: Chronic Hyperkalemia in a Patient With Type 2 Diabetes Mellitus
    • Questions
    • A - SYNOPSIS OF THE PHYSIOLOGY OF K+ ION HOMEOSTASIS
    • REGULATION OF DISTRIBUTION OF K+ IONS BETWEEN THE EXTRACELLULAR FLUID AND THE INTRACELLULAR FLUID COMPARTMENTS
    • Hormones That Affect the Distribution of K+ Ions Between the ECF and ICF Compartments
    • Catecholamines
    • Clinical implications
    • Insulin
    • Clinical implications
    • Effect of Metabolic Acidosis on the Distribution of K+ Ions Between the ECF and the ICF Compartments
    • Hyperkalemia in Patients With Tissue Catabolism
    • Hypertonicity and Shift of K+ Ions out of Cells
    • Clinical implications
    • REGULATION OF RENAL EXCRETION OF K+ IONS
    • K+ Ion Secretion in the CDN
    • Clinical implications
    • Flow Rate in the Terminal CDN
    • Clinical implications
    • B - STEPS IN THE CLINICAL APPROACH TO THE PATIENT WITH HYPERKALEMIA
    • STEP 1: ADDRESS EMERGENCIES
    • STEP 2: RULE OUT PSEUDOHYPERKALEMIA
    • STEP 3: DETERMINE IF THE CAUSE OF THE HYPERKALEMIA IS AN ACUTE SHIFT OF K+ IONS OUT OF CELLS
    • STEP 4: IS THE RATE OF EXCRETION OF K+ IONS HIGH ENOUGH IN A PATIENT WITH CHRONIC HYPERKALEMIA?
    • STEP 5: DETERMINE THE BASIS FOR THE DEFECT IN RENAL K+ ION EXCRETION (FLOW CHART 15-3)
    • Does the Patient have Advanced Chronic Renal Insufficiency?
    • Is the Patient Taking Drugs that Interfere with the Renal Excretion of K+ Ions?
    • Does the Patient Have a Disorder that Leads to Diminished Reabsorption of Na+ Ions via ENaC in the CDN?
    • Does the Patient Have a Disorder that Increases Electroneutral Reabsorption of Na+ Ions in the DCT?
    • Does the Patient Have a Disorder that Increases Electroneutral Reabsorption of Na+ Ions in the CDN?
    • Is a Low Flow Rate in the Terminal CDN Contributing to Hyperkalemia?
    • C - SPECIFIC CAUSES OF HYPERKALEMIA
    • CHRONIC RENAL INSUFFICIENCY
    • ADDISON'S DISEASE
    • HYPERKALEMIA DUE TO INHERITED DISORDERS OF ALDOSTERONE SYNTHESIS
    • PSEUDOHYPOALDOSTERONISM TYPE I
    • Autosomal Dominant Disorder
    • Autosomal Recessive Form
    • SYNDROME OF HYPORENINEMIC HYPOALDOSTERONISM
    • FAMILIAL HYPERKALEMIA WITH HYPERTENSION
    • HYPERKALEMIC PERIODIC PARALYSIS
    • DRUGS ASSOCIATED WITH HYPERKALEMIA
    • Drugs that Affect Cellular Redistribution of K+ Ions
    • Drugs that Interfere with Renal Excretion of K+ Ions
    • Drugs that inhibit the release of renin: Nonsteroidal antiinflammatory drugs (NSAIDs) and COX-2 inhibitors
    • Drugs that interfere with the renin-angiotensin-aldosterone axis: Direct renin blockers, ACE inhibitors, and ARBs
    • Drugs that inhibit aldosterone synthesis: heparin
    • Aldosterone receptor antagonists: spironolactone and eplerenone
    • Drugs that block ENaC: amiloride, triamterene, trimethoprim, and pentamidine
    • Drugs that increase electroneutral NaCl reabsorption in the DCT: calcineurine inhibitors (cyclosporin, tacrolimus)
    • Drugs that interfere with activation of ENaC via proteolytic cleavage: nafamostat mesylate
    • D - THERAPY OF HYPERKALEMIA
    • EMERGENCY HYPERKALEMIA
    • Antagonize the Cardiac Effects of Hyperkalemia
    • Induce a Shift of K+ Ions Into the ICF
    • Insulin
    • ß2-Adrenergic agonists
    • NaHCO3
    • Remove K+ Ions From the Body
    • NONEMERGENCY HYPERKALEMIA
    • Enhancing the excretion of K+ ions in the urine
    • Enhancing the removal of K+ ions via the gastrointestinal tract
    • Dialysis
    • CASE 15-1: MIGHT THIS PATIENT HAVE PSEUDOHYPERKALEMIA?
    • Why did Hyperkalemia Develop So Soon After He Left the Intensive Care Unit?
    • CASE 15-2: HYPERKALEMIA IN A PATIENT TREATED WITH TRIMETHOPRIM
    • What Is the Cause of Hyperkalemia in This Patient
    • What are the Implications for the Treatment of Hyperkalemia in this Patient?
    • CASE 15-3: CHRONIC HYPERKALEMIA IN A PATIENT WITH TYPE 2 DIABETES MELLITUS
    • What Is the Cause for Hyperkalemia in this Patient?
    • Four - Integrative Physiology
    • 16 - Hyperglycemia
    • Introduction
    • OBJECTIVES
    • A - BACKGROUND
    • Case 16-1: And I Thought Water Was Good for Me!
    • Questions
    • REVIEW OF GLUCOSE METABOLISM
    • QUANTITATIVE ANALYSIS OF GLUCOSE METABOLISM
    • Pool of Glucose in the Body
    • Input of Glucose
    • From the diet
    • From glycogen stores
    • Glycogen in the liver
    • Glycogen in skeletal muscle
    • Conversion of protein to glucose
    • Removal of Glucose
    • Removal of glucose via metabolism
    • Oxidation of glucose
    • Conversion to storage fuels
    • Excretion of glucose in the urine
    • B - RENAL ASPECTS OF HYPERGLYCEMIA
    • GLUCOSE-INDUCED OSMOTIC DIURESIS
    • IMPACT OF HYPERGLYCEMIA ON BODY COMPARTMENT VOLUMES
    • Hyperglycemia and the Shift of Water Across Cell Membranes
    • Quantitative Relationship Between Rise in the PGlucose and the Fall in the PNa
    • The Impact of an Osmotic Diuresis on Body Fluid Composition
    • Sodium Ions
    • Potassium Ions
    • IMPACT OF THE INGESTION OF FRUIT JUICE
    • Na+ and Cl- Ions
    • Water
    • Potassium Ions
    • organic anions
    • C - CLINICAL APPROACH
    • CLASSIFICATION OF HYPERGLYCEMIA
    • PATIENTS WITH HYPERGLYCEMIA AND POLYURIA
    • PATIENTS WITH HYPERGLYCEMIA AND OLIGURIA
    • THERAPY FOR THE PATIENT WITH HYPERGLYCEMIA
    • Fluid Therapy
    • Treat a hemodynamic emergency if present
    • Avoid a large fall in the PEffective osm
    • Replace the deficit of Na+ ions
    • K+ ion therapy
    • Insulin
    • QUESTIONS
    • D - DISCUSSION OF CASES
    • Case 16-1: And I Thought Water Was Good for Me!
    • What is the basis of the polyuria in this patient?
    • In what way might a severe degree of hyperglycemia have "helped" this patient?
    • How can the EABV and the PEffective osm be defended during therapy?
    • EABV
    • PEffective osm
    • Why did her PGlucose fail to fall in the first 100minutes despite the large loss of glucose in the urine?
    • Output
    • Input
    • Why did the PGlucose and the PEffective osm fall in the second 100minutes?
    • Implications for the risk of developing cerebral edema
    • DISCUSSION OF QUESTIONS
    • Index
    • A
    • B
    • C
    • D
    • E
    • F
    • G
    • H
    • I
    • J
    • K
    • L
    • M
    • N
    • O
    • P
    • R
    • S
    • T
    • U
    • V
    • W
    • Z
    • IBC

    Dateiformat: EPUB
    Kopierschutz: Adobe-DRM (Digital Rights Management)

    Systemvoraussetzungen:

    Computer (Windows; MacOS X; Linux): Installieren Sie bereits vor dem Download die kostenlose Software Adobe Digital Editions (siehe E-Book Hilfe).

    Tablet/Smartphone (Android; iOS): Installieren Sie bereits vor dem Download die kostenlose App Adobe Digital Editions (siehe E-Book Hilfe).

    E-Book-Reader: Bookeen, Kobo, Pocketbook, Sony, Tolino u.v.a.m. (nicht Kindle)

    Das Dateiformat EPUB ist sehr gut für Romane und Sachbücher geeignet - also für "fließenden" Text ohne komplexes Layout. Bei E-Readern oder Smartphones passt sich der Zeilen- und Seitenumbruch automatisch den kleinen Displays an. Mit Adobe-DRM wird hier ein "harter" Kopierschutz verwendet. Wenn die notwendigen Voraussetzungen nicht vorliegen, können Sie das E-Book leider nicht öffnen. Daher müssen Sie bereits vor dem Download Ihre Lese-Hardware vorbereiten.

    Weitere Informationen finden Sie in unserer E-Book Hilfe.


    Dateiformat: PDF
    Kopierschutz: Adobe-DRM (Digital Rights Management)

    Systemvoraussetzungen:

    Computer (Windows; MacOS X; Linux): Installieren Sie bereits vor dem Download die kostenlose Software Adobe Digital Editions (siehe E-Book Hilfe).

    Tablet/Smartphone (Android; iOS): Installieren Sie bereits vor dem Download die kostenlose App Adobe Digital Editions (siehe E-Book Hilfe).

    E-Book-Reader: Bookeen, Kobo, Pocketbook, Sony, Tolino u.v.a.m. (nicht Kindle)

    Das Dateiformat PDF zeigt auf jeder Hardware eine Buchseite stets identisch an. Daher ist eine PDF auch für ein komplexes Layout geeignet, wie es bei Lehr- und Fachbüchern verwendet wird (Bilder, Tabellen, Spalten, Fußnoten). Bei kleinen Displays von E-Readern oder Smartphones sind PDF leider eher nervig, weil zu viel Scrollen notwendig ist. Mit Adobe-DRM wird hier ein "harter" Kopierschutz verwendet. Wenn die notwendigen Voraussetzungen nicht vorliegen, können Sie das E-Book leider nicht öffnen. Daher müssen Sie bereits vor dem Download Ihre Lese-Hardware vorbereiten.

    Weitere Informationen finden Sie in unserer E-Book Hilfe.


    Download (sofort verfügbar)

    55,92 €
    inkl. 19% MwSt.
    Download / Einzel-Lizenz
    ePUB mit Adobe DRM
    siehe Systemvoraussetzungen
    PDF mit Adobe DRM
    siehe Systemvoraussetzungen
    Hinweis: Die Auswahl des von Ihnen gewünschten Dateiformats und des Kopierschutzes erfolgt erst im System des E-Book Anbieters
    E-Book bestellen

    Unsere Web-Seiten verwenden Cookies. Mit der Nutzung dieser Web-Seiten erklären Sie sich damit einverstanden. Mehr Informationen finden Sie in unserem Datenschutzhinweis. Ok