xv Table of Contents Acute Effects of moderate cardiac Failure 258 Neurogenic Shock-Increased Vascular Chronic Stage of Failure-Fluid Retention Capacity Helps to compensate cardiac output 259 Anaphylactic shock and Histamine Summary of the Changes That Occur After Shock 285 Acute Cardiac Failure-"Compensated Septic Shock Heart Failure 26 Physiology of Treatment in Shock Dynamics of Severe Cardiac Failure. Replacement Therapy Decompensated Heart Failure 202 Treatment of Shock with Sympathomimetic Unilateral Left Heart Failure Drugs-Sometimes Useful, Sometimes Low-Output Cardiac Failure Cardiogenic Shock 262 Other Therapy Edema in patients with cardiac Failure Circulatory Arrest Cardiac Reserve Effect of Circulatory Arrest on the Brain Quantitative Graphical Method for Analysis of cardiac Failure UNIT V CHAPTER 2 3 The Body Fluids and Kidneys Heart Valves and Heart Sounds Dynamics of Valvular and Congenital A PTER 2 Heart Defects 269 The Body Fluid Compartments: Heart Sounds Extracellular and intracellular fluids ormal Heart Sounds Interstitial fluid and edema Valvular Lesions Abnormal Circulatory Dynamics in Fluid Intake and Output Are Balanced Valvular heart Disease During Steady-State Conditions Dynamics of the Circulation in Aortic Daily Intake of Water Stenosis and Aortic Regurgitation 272 Daily Loss of Body Water Dynamics of Mitral Stenosis and Mitral body Fluid Compartments Regurgitation 273 Intracellular Fluid Compartment Circulatory Dynamics During Exercise in Extracellular Fluid Compartment Patients with Valvular Lesions 273 Blood volume Abnormal Circulatory Dynamics in Constituents of Extracellular and Intracellular Fluids Congenital Heart Defects 293 Patent Ductus Arteriosus-A Left-to-Right lonic Composition of Plasma and Interstitial Fluid Is Simila Tetralogy of Fallot-A Right-to-Left Shunt Important Constituents of the Intracellular Causes of Congenital Anomalies 276 Use of Extracorporeal Circulation Measurement of fluid volumes in the During Cardiac Surgery Different Body Fluid Compartments- Hypertrophy of the Heart in Valvular The Indicator-Dilution Principle and Congenital Heart Disease Determination of Volumes of specific Body Fluid Compartments Regulation of Fluid Exchange and CHAPTER 2 4 Osmotic Equilibrium Between Circulatory Shock and Physiology of Intracellular and Extracellular Fluid Its Treatment Basic Principles of Osmosis and 278 Osmotic pressure Physiologic Causes of shock 278 Osmotic Equilibrium Is Maintained Circulatory Shock Caused by Decreased Between Intracellular and ardiac output Extracellular Fluids Circulatory Shock That Occurs Without Volume and osmolality of Extracellular Diminished Cardiac Output and Intracellular Fluids in Abnorma hat Happens to the Arterial Pressure in States Circulatory Shock? Effect of Adding saline Solution to the Tissue Deterioration is the End result of Extracellular Fluid Circulatory Shock, Whatever the Cause 279 Glucose and other Solutions Stages of Shock Administered for Nutritive Purposes Shock Caused by Hypovolemia- Clinical Abnormalities of Fluid volume Hemorrhagic Shock Regulation: Hyponatremia and Relationship of bleeding volume to Cardiac Output and Arterial Pressure Causes of Hyponatremia: Excess Water or Progressive and Nonprogressive Loss of sodium Hemorrhagic Shock Causes of Hypernatremia: Water Loss ol Irreversible shock Excess sodium hypovolemic Shock Caused by Plasma Edema: Excess Fluid in the Tissues Intracellular Edem 302 Hypovolemic Shock Caused by Trauma 285 Extracellular edema
xviii Table of Contents Acute Effects of Moderate Cardiac Failure 258 Chronic Stage of Failure—Fluid Retention Helps to Compensate Cardiac Output 259 Summary of the Changes That Occur After Acute Cardiac Failure—“Compensated Heart Failure” 260 Dynamics of Severe Cardiac Failure— Decompensated Heart Failure 260 Unilateral Left Heart Failure 262 Low-Output Cardiac Failure— Cardiogenic Shock 262 Edema in Patients with Cardiac Failure 263 Cardiac Reserve 264 Quantitative Graphical Method for Analysis of Cardiac Failure 265 CHAPTER 23 Heart Valves and Heart Sounds; Dynamics of Valvular and Congenital Heart Defects 269 Heart Sounds 269 Normal Heart Sounds 269 Valvular Lesions 271 Abnormal Circulatory Dynamics in Valvular Heart Disease 272 Dynamics of the Circulation in Aortic Stenosis and Aortic Regurgitation 272 Dynamics of Mitral Stenosis and Mitral Regurgitation 273 Circulatory Dynamics During Exercise in Patients with Valvular Lesions 273 Abnormal Circulatory Dynamics in Congenital Heart Defects 274 Patent Ductus Arteriosus—A Left-to-Right Shunt 274 Tetralogy of Fallot—A Right-to-Left Shunt 274 Causes of Congenital Anomalies 276 Use of Extracorporeal Circulation During Cardiac Surgery 276 Hypertrophy of the Heart in Valvular and Congenital Heart Disease 276 CHAPTER 24 Circulatory Shock and Physiology of Its Treatment 278 Physiologic Causes of Shock 278 Circulatory Shock Caused by Decreased Cardiac Output 278 Circulatory Shock That Occurs Without Diminished Cardiac Output 278 What Happens to the Arterial Pressure in Circulatory Shock? 279 Tissue Deterioration Is the End Result of Circulatory Shock, Whatever the Cause 279 Stages of Shock 279 Shock Caused by Hypovolemia— Hemorrhagic Shock 279 Relationship of Bleeding Volume to Cardiac Output and Arterial Pressure 279 Progressive and Nonprogressive Hemorrhagic Shock 280 Irreversible Shock 284 Hypovolemic Shock Caused by Plasma Loss 284 Hypovolemic Shock Caused by Trauma 285 Neurogenic Shock—Increased Vascular Capacity 285 Anaphylactic Shock and Histamine Shock 285 Septic Shock 286 Physiology of Treatment in Shock 286 Replacement Therapy 286 Treatment of Shock with Sympathomimetic Drugs—Sometimes Useful, Sometimes Not 287 Other Therapy 287 Circulatory Arrest 287 Effect of Circulatory Arrest on the Brain 287 UNIT V The Body Fluids and Kidneys CHAPTER 25 The Body Fluid Compartments: Extracellular and Intracellular Fluids; Interstitial Fluid and Edema 291 Fluid Intake and Output Are Balanced During Steady-State Conditions 291 Daily Intake of Water 291 Daily Loss of Body Water 291 Body Fluid Compartments 292 Intracellular Fluid Compartment 293 Extracellular Fluid Compartment 293 Blood Volume 293 Constituents of Extracellular and Intracellular Fluids 293 Ionic Composition of Plasma and Interstitial Fluid Is Similar 293 Important Constituents of the Intracellular Fluid 295 Measurement of Fluid Volumes in the Different Body Fluid Compartments— The Indicator-Dilution Principle 295 Determination of Volumes of Specific Body Fluid Compartments 295 Regulation of Fluid Exchange and Osmotic Equilibrium Between Intracellular and Extracellular Fluid 296 Basic Principles of Osmosis and Osmotic Pressure 296 Osmotic Equilibrium Is Maintained Between Intracellular and Extracellular Fluids 298 Volume and Osmolality of Extracellular and Intracellular Fluids in Abnormal States 299 Effect of Adding Saline Solution to the Extracellular Fluid 299 Glucose and Other Solutions Administered for Nutritive Purposes 301 Clinical Abnormalities of Fluid Volume Regulation: Hyponatremia and Hypernatremia 301 Causes of Hyponatremia: Excess Water or Loss of Sodium 301 Causes of Hypernatremia: Water Loss or Excess Sodium 302 Edema: Excess Fluid in the Tissues 302 Intracellular Edema 302 Extracellular Edema 302
Summary of Causes of Extracellular Edema 303 mportance of gFr Autoregulation in Safety Factors That Normally Prevent Preventing Extreme Changes in Renal Edema Excretion 323 Fluids in the“ Potential Spaces”of Role of tubuloglomerular Feedback in the body Autoregulation of GFR 323 Myogenic Autoregulation of Renal Blood Flow and GFR Other Factors That Increase renal blood Urine Formation by the kidneys Flow and GFR: High Protein Intake and L. Glomerular Filtration Renal blood Increased blood glucose 325 Flow and Their Control Multiple Functions of the Kidneys in Homeostasis 307 CHA PTER 2 7 Physiologic Anatomy of the Kidneys 308 Urine Formation by the Kidneys: General Organization of the Kidneys and Urinary Tract 308 I. Tubular Processing of the Renal Blood Supply 309 Glomerular Filtrate The Nephron Is the Functional Unit of the Reabsorption and secretion by the Kidney 3I0 Renal Tubules Micturition 31l Tubular Reabsorption Is Selective and Physiologic Anatomy and Nervous Quantitatively Large 327 Connections of the bladder 311 Tubular Reabsorption Includes Transport of Urine from the Kidney Passive and active mechanisms Through the Ureters and into Active Transport the Bladder Passive Water Reabsorption by Osmosis Innervation of the bladder 312 Is Coupled Mainly to sodium Filling of the Bladder and Bladder Wall Tone; the Cystometrogram 312 Reabsorption of chloride, Urea, and Other Micturition Reflex Solutes by Passive Diffusion Facilitation or inhibition of micturition Reabsorption and Secretion Along the brain 313 Different Parts of the Nephron 333 Abnormalities of micturition Proximal Tubular Reabsorption 333 Urine Formation results from olute and Water Transport in the Loop Glomerular Filtration Tubular of henle Reabsorption, and Tubular Secretion 314 Distal Tubule Filtration, Reabsorption, and Secretion of Late Distal Tubule and Cortical Collecting Different Substances 315 Tubule Glomerular Filtration-The First Step in Medullary Collecting Duct 337 Urine Formation 316 Summary of Concentrations of Different Composition of the Glomerular Filtrate Solutes in the different tubular GFR Is About 20 Per Cent of the renal Plasma Flow 316 Regulation of Tubular Reabsorption 38 Glomerular Capillary Membrane 316 Glomerulotubular Balance-The Ability Determinants of the gfr 317 of the Tubules to Increase Reabsorption Increased glomerular capillary Filtration Rate in Response to Increased Tubular Coefficient Increases GFr 38 339 Increased Bowman's Capsule Hydrostatic Peritubular Capillary and Renal Interstitial Pressure Decreases gFr 38 Fluid Physical Forces Increased Glomerular Capillary Colloid Effect of Arterial Pressure on urine Osmotic Pressure Decreases Fr 38 Output-The Pressure-Natriuresis and Increased Glomerular Capillary Hydrostatic ressure- Diuresis mechanisms 341 Pressure Increases GFr Hormonal Control of Tubular Reabsorption 342 Renal Blood Flow Sympathetic Nervous System Activation Renal Blood Flow and Oxygen creases Sodium Reabsorption 343 Consumption Use of Clearance Methods to Quantify Determinants of renal blood Flow 320 Kidney Function 343 Blood flow in the vasa recta of the renal Inulin Clearance can Be Used to estimate Medulla Is Very Low Compared with Flow GFR 344 in the renal cortex 321 Creatine Clearance and Plasma Creatinine hysiologic Control of Glomerular learance can be used to estimate Filtration and Renal Blood Flow 321 GFR 344 Sympathetic Nervous System Activation PAH Clearance Can Be Used to Estimate Decreases GFR 321 Renal Plasma flow 345 Hormonal and autacoid Control of ren Filtration Fraction is Calculated from GFr Circulation 322 Divided by Renal Plasma Flow Autoregulation of GFR and Renal Calculation of Tubular Reabsorption ol Blood Flow Secretion from renal clearance
Table of Contents xix Summary of Causes of Extracellular Edema 303 Safety Factors That Normally Prevent Edema 304 Fluids in the “Potential Spaces” of the Body 305 CHAPTER 26 Urine Formation by the Kidneys: I. Glomerular Filtration, Renal Blood Flow, and Their Control 307 Multiple Functions of the Kidneys in Homeostasis 307 Physiologic Anatomy of the Kidneys 308 General Organization of the Kidneys and Urinary Tract 308 Renal Blood Supply 309 The Nephron Is the Functional Unit of the Kidney 310 Micturition 311 Physiologic Anatomy and Nervous Connections of the Bladder 311 Transport of Urine from the Kidney Through the Ureters and into the Bladder 312 Innervation of the Bladder 312 Filling of the Bladder and Bladder Wall Tone; the Cystometrogram 312 Micturition Reflex 313 Facilitation or Inhibition of Micturition by the Brain 313 Abnormalities of Micturition 313 Urine Formation Results from Glomerular Filtration, Tubular Reabsorption, and Tubular Secretion 314 Filtration, Reabsorption, and Secretion of Different Substances 315 Glomerular Filtration—The First Step in Urine Formation 316 Composition of the Glomerular Filtrate 316 GFR Is About 20 Per Cent of the Renal Plasma Flow 316 Glomerular Capillary Membrane 316 Determinants of the GFR 317 Increased Glomerular Capillary Filtration Coefficient Increases GFR 318 Increased Bowman’s Capsule Hydrostatic Pressure Decreases GFR 318 Increased Glomerular Capillary Colloid Osmotic Pressure Decreases GFR 318 Increased Glomerular Capillary Hydrostatic Pressure Increases GFR 319 Renal Blood Flow 320 Renal Blood Flow and Oxygen Consumption 320 Determinants of Renal Blood Flow 320 Blood Flow in the Vasa Recta of the Renal Medulla Is Very Low Compared with Flow in the Renal Cortex 321 Physiologic Control of Glomerular Filtration and Renal Blood Flow 321 Sympathetic Nervous System Activation Decreases GFR 321 Hormonal and Autacoid Control of Renal Circulation 322 Autoregulation of GFR and Renal Blood Flow 323 Importance of GFR Autoregulation in Preventing Extreme Changes in Renal Excretion 323 Role of Tubuloglomerular Feedback in Autoregulation of GFR 323 Myogenic Autoregulation of Renal Blood Flow and GFR 325 Other Factors That Increase Renal Blood Flow and GFR: High Protein Intake and Increased Blood Glucose 325 CHAPTER 27 Urine Formation by the Kidneys: II. Tubular Processing of the Glomerular Filtrate 327 Reabsorption and Secretion by the Renal Tubules 327 Tubular Reabsorption Is Selective and Quantitatively Large 327 Tubular Reabsorption Includes Passive and Active Mechanisms 328 Active Transport 328 Passive Water Reabsorption by Osmosis Is Coupled Mainly to Sodium Reabsorption 332 Reabsorption of Chloride, Urea, and Other Solutes by Passive Diffusion 332 Reabsorption and Secretion Along Different Parts of the Nephron 333 Proximal Tubular Reabsorption 333 Solute and Water Transport in the Loop of Henle 334 Distal Tubule 336 Late Distal Tubule and Cortical Collecting Tubule 336 Medullary Collecting Duct 337 Summary of Concentrations of Different Solutes in the Different Tubular Segments 338 Regulation of Tubular Reabsorption 339 Glomerulotubular Balance—The Ability of the Tubules to Increase Reabsorption Rate in Response to Increased Tubular Load 339 Peritubular Capillary and Renal Interstitial Fluid Physical Forces 339 Effect of Arterial Pressure on Urine Output—The Pressure-Natriuresis and Pressure-Diuresis Mechanisms 341 Hormonal Control of Tubular Reabsorption 342 Sympathetic Nervous System Activation Increases Sodium Reabsorption 343 Use of Clearance Methods to Quantify Kidney Function 343 Inulin Clearance Can Be Used to Estimate GFR 344 Creatine Clearance and Plasma Creatinine Clearance Can Be Used to Estimate GFR 344 PAH Clearance Can Be Used to Estimate Renal Plasma Flow 345 Filtration Fraction Is Calculated from GFR Divided by Renal Plasma Flow 346 Calculation of Tubular Reabsorption or Secretion from Renal Clearance 346
ChaPter 8 ChAPTer 2 9 Regulation of extracellular fluid Renal regulation of potassium, Osmolarity and sodium Calcium, Phosphate, and Magnesium; Concentration 348 Integration of Renal Mechanisms for The Kidneys Excrete Excess Water by Forming a Dilute Urine 34 Control of Blood Volume and Extracellular fluid volume Antidiuretic Hormone controls urine Concentration 348 Regulation of Potassium Excretion Renal Mechanisms for Excreting a and Potassium Concentration in Dilute Urine 349 Extracellular Fluid The Kidneys Conserve Water by Requlation of Internal Potassium Excreting a Concentrated Urine Distribution Obligatory Urine Volume 350 Overview of renal Potassium Excretion Requirements for Excreting a Concentrated Potassium Secretion by Principal Cells of Urine-High ADH Levels and Hyperosmotic Late Distal and Cortical Collecting 350 Tubules 367 Countercurrent Mechanism Produces a Summary of Factors That Regulate Hy perosmotic Renal Medullary Interstitium 35/ Potassium Secretion: Plasma Potassium Role of Distal Tubule and Collecting Ducts Concentration Aldosterone, Tubular Flow Excreting a Concentrated Urine 352 Rate, and Hydrogen lon Concentration 368 Urea Contributes to Hyperosmotic Renal Control of renal calcium Excretion Medullary Interstitium and to a and Extracellular Calcium Ion Concentrated Urine 353 371 Countercurrent Exchange in the Vasa Recta Control of Calcium Excretion by the Preserves Hy perosmolarity of the 372 Renal medulla 354 Regulation of Renal Phosphate Excretion 372 Summary of Urine Concentrating Mechanism Control of Renal Magnesium Excretion and Changes in Osmolarity in Different and Extracellular Magnesium lon Segments of the Tubules Concentration Quantifying Renal Urine Concentration Integration of Renal Mechanisms for and Dillution:“ Free water" and osm。lar Control of extracellular Fluid 373 Cleara 357 Sodium Excretion Is Precisely Matched to Disorders of Urinary Concentrating Intake Under Steady-State Conditions 373 Ability Sodium Excretion Is Controlled by Altering Control of Extracellular Fluid Osmolarity 358 Glomerular Filtration or tubular sodium and Sodium concentration Reabsorption Rates 374 Estimating Plasma Osmolarity from Plasma Importance of Pressure Natriuresis and Sodium Concentration Pressure Diuresis in Maintaining Body OsmoreceptorADH Feedback System 358 Sodium and Fluid Balance 374 ADH Synthesis in Supraoptic and Pressure Natriuresis and Diuresis Are Key Paraventricular Nuclei of the Components of a Renal-Body Fluid Hy pothalamus and ADH Release from Feedback for Regulating Body Fluid the Posterior Pituitary 359 Volumes and Arterial Pressure 375 Cardiovascular Reflex stimulation of adh Precision of blood volume and Extracellular Release by Decreased Arterial Pressure Fluid Volume Regulation 376 and/or Decreased blood volume 360 Distribution of Extracellular Fluid Quantitative Importance of Cardiovascular Between the Interstitial Spaces and Reflexes and osmolarity in Stimulating Vascular System 376 ADH Secretion 360 Nervous and hormonal Factors Increase Other Stimuli for ADh Secretion 360 the Effectiveness of Renal-Body Fluid Role of Thirst in Controlling Extracellular Feedback Control Fluid Osmolarity and Sodium Sympathetic Nervous System Control of Concentration Renal Excretion: Arterial Baroreceptor and Central Nervous System Centers for Thirst 361 Low-Pressure Stretch Receptor Reflexes 377 Stimuli for Thirst Role of Angiotensin ll In Controlling Renal Threshold for Osmolar Stimulus of Drinking 362 377 Integrated Responses of Osmoreceptor-ADH Role of Aldosterone in Controlling Renal and Thirst Mechanisms in Controlling Excretion 378 Extracellular Fluid Osmolarity and Sodium Role of ADh in Controlling Renal Water Concentration 362 Excretion 379 Role of Angiotensin ll and Aldosterone Role of Atrial Natriuretic Peptide in in Controlling Extracellular Fluid Controlling Renal Excretion 378 Osmolarity and Sodium Concentrati 362 Integrated Responses to Changes in Salt-Appetite Mechanism for Sodium intake 380 Controlling Extracellular Fluid Conditions That Cause Large Increases Sodium Concentration and volume in Blood volume and Extracellular Fluid volume 380
xx Table of Contents CHAPTER 28 Regulation of Extracellular Fluid Osmolarity and Sodium Concentration 348 The Kidneys Excrete Excess Water by Forming a Dilute Urine 348 Antidiuretic Hormone Controls Urine Concentration 348 Renal Mechanisms for Excreting a Dilute Urine 349 The Kidneys Conserve Water by Excreting a Concentrated Urine 350 Obligatory Urine Volume 350 Requirements for Excreting a Concentrated Urine—High ADH Levels and Hyperosmotic Renal Medulla 350 Countercurrent Mechanism Produces a Hyperosmotic Renal Medullary Interstitium 351 Role of Distal Tubule and Collecting Ducts in Excreting a Concentrated Urine 352 Urea Contributes to Hyperosmotic Renal Medullary Interstitium and to a Concentrated Urine 353 Countercurrent Exchange in the Vasa Recta Preserves Hyperosmolarity of the Renal Medulla 354 Summary of Urine Concentrating Mechanism and Changes in Osmolarity in Different Segments of the Tubules 355 Quantifying Renal Urine Concentration and Dilution: “Free Water” and Osmolar Clearances 357 Disorders of Urinary Concentrating Ability 357 Control of Extracellular Fluid Osmolarity and Sodium Concentration 358 Estimating Plasma Osmolarity from Plasma Sodium Concentration 358 Osmoreceptor-ADH Feedback System 358 ADH Synthesis in Supraoptic and Paraventricular Nuclei of the Hypothalamus and ADH Release from the Posterior Pituitary 359 Cardiovascular Reflex Stimulation of ADH Release by Decreased Arterial Pressure and/or Decreased Blood Volume 360 Quantitative Importance of Cardiovascular Reflexes and Osmolarity in Stimulating ADH Secretion 360 Other Stimuli for ADH Secretion 360 Role of Thirst in Controlling Extracellular Fluid Osmolarity and Sodium Concentration 361 Central Nervous System Centers for Thirst 361 Stimuli for Thirst 361 Threshold for Osmolar Stimulus of Drinking 362 Integrated Responses of Osmoreceptor-ADH and Thirst Mechanisms in Controlling Extracellular Fluid Osmolarity and Sodium Concentration 362 Role of Angiotensin II and Aldosterone in Controlling Extracellular Fluid Osmolarity and Sodium Concentration 362 Salt-Appetite Mechanism for Controlling Extracellular Fluid Sodium Concentration and Volume 363 CHAPTER 29 Renal Regulation of Potassium, Calcium, Phosphate, and Magnesium; Integration of Renal Mechanisms for Control of Blood Volume and Extracellular Fluid Volume 365 Regulation of Potassium Excretion and Potassium Concentration in Extracellular Fluid 365 Regulation of Internal Potassium Distribution 366 Overview of Renal Potassium Excretion 367 Potassium Secretion by Principal Cells of Late Distal and Cortical Collecting Tubules 367 Summary of Factors That Regulate Potassium Secretion: Plasma Potassium Concentration, Aldosterone, Tubular Flow Rate, and Hydrogen Ion Concentration 368 Control of Renal Calcium Excretion and Extracellular Calcium Ion Concentration 371 Control of Calcium Excretion by the Kidneys 372 Regulation of Renal Phosphate Excretion 372 Control of Renal Magnesium Excretion and Extracellular Magnesium Ion Concentration 373 Integration of Renal Mechanisms for Control of Extracellular Fluid 373 Sodium Excretion Is Precisely Matched to Intake Under Steady-State Conditions 373 Sodium Excretion Is Controlled by Altering Glomerular Filtration or Tubular Sodium Reabsorption Rates 374 Importance of Pressure Natriuresis and Pressure Diuresis in Maintaining Body Sodium and Fluid Balance 374 Pressure Natriuresis and Diuresis Are Key Components of a Renal-Body Fluid Feedback for Regulating Body Fluid Volumes and Arterial Pressure 375 Precision of Blood Volume and Extracellular Fluid Volume Regulation 376 Distribution of Extracellular Fluid Between the Interstitial Spaces and Vascular System 376 Nervous and Hormonal Factors Increase the Effectiveness of Renal-Body Fluid Feedback Control 377 Sympathetic Nervous System Control of Renal Excretion: Arterial Baroreceptor and Low-Pressure Stretch Receptor Reflexes 377 Role of Angiotensin II In Controlling Renal Excretion 377 Role of Aldosterone in Controlling Renal Excretion 378 Role of ADH in Controlling Renal Water Excretion 379 Role of Atrial Natriuretic Peptide in Controlling Renal Excretion 378 Integrated Responses to Changes in Sodium Intake 380 Conditions That Cause Large Increases in Blood Volume and Extracellular Fluid Volume 380
Table of c ncreased Blood volume and Extracellular Renal Correction of Acidosis--Increased Fluid Volume Caused by Heart Diseases 380 xcretion of Hydrogen lons and Increased Blood Volume Caused by Addition of bicarbonate lons to the ncreased capacity of circulatio 380 Extracellular Fluid Conditions That Cause Large Increases Acidosis Decreases the Ratio of HcO3 /H in in Extracellular fluid volume but with Renal Tubular Fluid Normal blood volume 38l Renal Correction of alkalosis-Decreased tic Syndrome-Loss of Plas Tubular Secretion of Hydrogen lons Proteins in Urine and Sodium Retention and Increased Excretion of y the Kidneys 38l Bicarbonate lons Liver Cirrhosis-Decreased Synthesis of Alkalosis Increases the Ratio of HCO3/H lasma Proteins by the Liver and in renal tubular Fluid 396 Sodium Retention by the Kidneys 38l clinical Causes of acid-Base disorders 397 Respiratory Acidosis Is Caused by ecreased ventilation and Increased p CHAPTER 3 0 Respiratory Alkalosis Results from Increased Ventilation and Decreased pco 397 Regulation of Acid-Base Balance 383 Metabolic Acidosis Results from Decreased Hydrogen lon Concentration I Extracellular Fluid Bicarbonate Precisely Regulated Concentration Acids and Bases-Their Definitions Treatment of acidosis or alkalosis and Meanings 383 Clinical Measurements and Analysis of Defenses Against Changes in Hydroge Acid- Base Disorders 398 lonc。 ncentratio。n: Buffers, lungs, Complex Acid-Base Disorders and Use of and Kidneys the Acid-Base Nomogram for Diagnosis 399 Buffering of Hydrogen lons in the body Use of Anion Gap to Diagnose Acid-Base Fluids 385 Bicarbonate Buffer System Quantitative Dynamics of the Bicarbonate Buffer System CHAPTER 3 1 Phosphate Buffer System Kidney Diseases and Diuretics 402 Proteins: Important Intracellular Diuretics and Their Mechanisms of Buffers Action Respiratory Regulation of Acid-Base Osmotic Diuretics Decrease water Reabsorption by Increasing Osmotic Pulmonary Expiration of CO2 Balances Pressure of tubular Fluid Metabolic formation of co 388 Loop"Diuretics Decrease Active Increasing Alveolar Ventilation Decreases odium-Chloride-Potassium Reabsorption Extracellular Fluid Hydrogen lon in the Thick Ascending Loop of Henle Concentration and Raises pH 388 Thiazide Diuretics Inhibit Sodium-Chloride Increased Hydrogen lon Concentration Reabsorption in the Early Distal Tubule 404 Stimulates Alveolar ventilation 389 Carbonic Anhydrase Inhibitors Block Renal Control of acid-Base balance 390 odium-Bicarbonate Reabsorption in the Secretion of Hydrogen lons and Proximal tubules 404 Reabsorption of Bicarbonate lons Competitive Inhibitors of Aldosterone by the Renal Tubules 390 Decrease Sodium Reabsorption from and Hydrogen lons Are Secreted by Secondary Potassium secretion into the cortical Active Transport in the Early Tubular Collecting Tubule 404 Segments 391 Diuretics That Block Sodium Channels Filtered Bicarbonate lons Are reabsorbed in the Collecting Tubules Decrease by Interaction with Hydrogen lons in the Sodium Reabsorption 39l Kidney Diseases Primary Active Secretion of Hydrogen lons in Acute Renal Failure the Intercalated Cells of Late Distal and Prerenal Acute Renal Failure Caused by Collecting Tubules Decreased Blood Flow to the Kidney Combination of Excess Hydrogen lons Intrarenal Acute Renal Failure Caused by with Phosphate and Ammonia Buffers Abnormalities within the Kidney in the Tubule-A Mechanism for Postrenal Acute Renal Failure Caused by Generating New"Bicarbonate lons Abnormalities of the Lower Urinary Phosphate Buffer System Carries Excess Hydrogen lons into the Urine and Physiologic Effects of Acute Renal Failure 406 Generates New Bicarbonate 393 Chronic Renal failure: an irreversible Excretion of Excess Hydroge s and Decrease in the number of Functional Generation of New Bicarbonate by the irons Ammonia Buffer System 393 Vicious Circle of chronic Renal Failure Quantifying Renal Acid-Base Excretion Leading to End-stage Renal Disease Regulation of Renal Tubular Hydrogen lon Injury to the Renal Vasculature as a Cause Secretion of chronic renal Failure 408
Table of Contents xxi Increased Blood Volume and Extracellular Fluid Volume Caused by Heart Diseases 380 Increased Blood Volume Caused by Increased Capacity of Circulation 380 Conditions That Cause Large Increases in Extracellular Fluid Volume but with Normal Blood Volume 381 Nephrotic Syndrome—Loss of Plasma Proteins in Urine and Sodium Retention by the Kidneys 381 Liver Cirrhosis—Decreased Synthesis of Plasma Proteins by the Liver and Sodium Retention by the Kidneys 381 CHAPTER 30 Regulation of Acid-Base Balance 383 Hydrogen Ion Concentration Is Precisely Regulated 383 Acids and Bases—Their Definitions and Meanings 383 Defenses Against Changes in Hydrogen Ion Concentration: Buffers, Lungs, and Kidneys 384 Buffering of Hydrogen Ions in the Body Fluids 385 Bicarbonate Buffer System 385 Quantitative Dynamics of the Bicarbonate Buffer System 385 Phosphate Buffer System 387 Proteins: Important Intracellular Buffers 387 Respiratory Regulation of Acid-Base Balance 388 Pulmonary Expiration of CO2 Balances Metabolic Formation of CO2 388 Increasing Alveolar Ventilation Decreases Extracellular Fluid Hydrogen Ion Concentration and Raises pH 388 Increased Hydrogen Ion Concentration Stimulates Alveolar Ventilation 389 Renal Control of Acid-Base Balance 390 Secretion of Hydrogen Ions and Reabsorption of Bicarbonate Ions by the Renal Tubules 390 Hydrogen Ions Are Secreted by Secondary Active Transport in the Early Tubular Segments 391 Filtered Bicarbonate Ions Are Reabsorbed by Interaction with Hydrogen Ions in the Tubules 391 Primary Active Secretion of Hydrogen Ions in the Intercalated Cells of Late Distal and Collecting Tubules 392 Combination of Excess Hydrogen Ions with Phosphate and Ammonia Buffers in the Tubule—A Mechanism for Generating “New” Bicarbonate Ions 392 Phosphate Buffer System Carries Excess Hydrogen Ions into the Urine and Generates New Bicarbonate 393 Excretion of Excess Hydrogen Ions and Generation of New Bicarbonate by the Ammonia Buffer System 393 Quantifying Renal Acid-Base Excretion 394 Regulation of Renal Tubular Hydrogen Ion Secretion 395 Renal Correction of Acidosis—Increased Excretion of Hydrogen Ions and Addition of Bicarbonate Ions to the Extracellular Fluid 396 Acidosis Decreases the Ratio of HCO3 - /H+ in Renal Tubular Fluid 396 Renal Correction of Alkalosis—Decreased Tubular Secretion of Hydrogen Ions and Increased Excretion of Bicarbonate Ions 396 Alkalosis Increases the Ratio of HCO3 - /H+ in Renal Tubular Fluid 396 Clinical Causes of Acid-Base Disorders 397 Respiratory Acidosis Is Caused by Decreased Ventilation and Increased PCO2 397 Respiratory Alkalosis Results from Increased Ventilation and Decreased PCO2 397 Metabolic Acidosis Results from Decreased Extracellular Fluid Bicarbonate Concentration 397 Treatment of Acidosis or Alkalosis 398 Clinical Measurements and Analysis of Acid-Base Disorders 398 Complex Acid-Base Disorders and Use of the Acid-Base Nomogram for Diagnosis 399 Use of Anion Gap to Diagnose Acid-Base Disorders 400 CHAPTER 31 Kidney Diseases and Diuretics 402 Diuretics and Their Mechanisms of Action 402 Osmotic Diuretics Decrease Water Reabsorption by Increasing Osmotic Pressure of Tubular Fluid 402 “Loop” Diuretics Decrease Active Sodium-Chloride-Potassium Reabsorption in the Thick Ascending Loop of Henle 403 Thiazide Diuretics Inhibit Sodium-Chloride Reabsorption in the Early Distal Tubule 404 Carbonic Anhydrase Inhibitors Block Sodium-Bicarbonate Reabsorption in the Proximal Tubules 404 Competitive Inhibitors of Aldosterone Decrease Sodium Reabsorption from and Potassium Secretion into the Cortical Collecting Tubule 404 Diuretics That Block Sodium Channels in the Collecting Tubules Decrease Sodium Reabsorption 404 Kidney Diseases 404 Acute Renal Failure 404 Prerenal Acute Renal Failure Caused by Decreased Blood Flow to the Kidney 405 Intrarenal Acute Renal Failure Caused by Abnormalities within the Kidney 405 Postrenal Acute Renal Failure Caused by Abnormalities of the Lower Urinary Tract 406 Physiologic Effects of Acute Renal Failure 406 Chronic Renal Failure: An Irreversible Decrease in the Number of Functional Nephrons 406 Vicious Circle of Chronic Renal Failure Leading to End-Stage Renal Disease 407 Injury to the Renal Vasculature as a Cause of Chronic Renal Failure 408
xrl Table of Contents Injury to the Glomeruli as a Cause of CHAPTER 3 4 hronic Renal Failure- Resistance of the body to Infection: ll Glomerulonephritis Injury to the Renal Interstitium as a Immunity and Allergy 439 Cause of chronic renal Failure- Innate Immunity Pyelonephritis Acquired(Adaptive)Immunity Nephrotic Syndrome-Excretion of Protein Basic Ty pes of Acquired Immunity in the Urine because of increased Both Types of Acquired Immunity Are Glomerular Permeability Initiated by Antigens 440 Nephron Function in Chronic Renal Failure 409 Lymphocytes Are Responsible for Effects of Renal Failure on the body 440 411 Preprocessing of the T and B lymphocytes 440 Hy pertension and Kidney Disease 412 T Lymphocytes and B-Lymphocyte Specific Tubular Disorders 413 Antibodies React Highly Specificall Treatment of Renal Failure by Dialysis Against Specific Antigens-Role of with an Artificial Kidney 414 ymphocyte Clones 442 Origin of the Many Clones of Lymphocytes 442 ttributes U NI T unity and th Blood Cells, Immunity, and Blood Special Attributes of the T-Lymphocyte Clotting System-Activated T Cells and Cell- Mediated Immunity Several Types of T Cells and their Different CHAPTER 3 2 Functions Red Blood cells. Anemia and Tolerance of the Acquired Immunity System to One's Own Tissues -Role Polycythemia 419 of Preprocessing in the Thymus and Red Blood Cells(Erythrocytes) 419 Bone marrow Production of red Blood cells 420 Immunization by Injection of Antigens Formation of Hemoglobin Passive Immunit 449 Iron Metabolism 425 Allergy and Hypersensitivity Life Span and Destruction of Red Blood Allergy Caused by Activated T Cells Cells 426 Delayed-Reaction Allergy Allergies in the"Allergic"Person, Who Has Effects of anemia on function of the Excess igE Antibodies Circulatory Syste Polycythemia CHAPTER 3 5 Effect of Polycythemia on Function of the Circulatory System Blood Types; Transfusion; Tissue and Organ Transplantation CHAPTER 3 3 Antigenicity Causes Immune Reactions f Blood Resistance of the body to Infection: L. o-A-B Blood Types Leukocytes, Granulocytes, the A and B Antigens-Agglutinogens 45l Monocyte-Macrophage System, and Agglutinins 452 Inflammation Agglutination Process In Transfusion Reactions 452 Leukocytes (White Blood Cells 429 Blood Ty ping 453 General Characteristics of Leukocytes 429 Rh Blood Types Genesis of the white blood cells Rh Immune Response 453 Life Span of the white blood cells Transfusion Reactions Resulting from Neutrophils and Macrophages Defend Mismatched Blood Types Against Infections Transplantation of Tissues and or gocytosis geoctsans 453 Attempts to Overcome Immune Reaction oocyte Macrophage Cell system in Transplanted Tissue 455 (Reticuloendothelial System) Inflammation: Role of Neutrophils and Macr。 phages 43 CHAPTER 36 nflammation Hemostasis and Blood coagulat Macrophage and Neutrophil Responses Events in Hemostasis During Inflammation 434 Vascular Constriction Eosinophils Formation of the Platelet Plug Basophils Blood Coagulation in the Ruptured Leuk。 penia The Leukemias Fibrous Organization or Dissolution of the Effects of Leukemia on the body Blood Clot
xxii Table of Contents Injury to the Glomeruli as a Cause of Chronic Renal Failure— Glomerulonephritis 408 Injury to the Renal Interstitium as a Cause of Chronic Renal Failure— Pyelonephritis 409 Nephrotic Syndrome—Excretion of Protein in the Urine Because of Increased Glomerular Permeability 409 Nephron Function in Chronic Renal Failure 409 Effects of Renal Failure on the Body Fluids—Uremia 411 Hypertension and Kidney Disease 412 Specific Tubular Disorders 413 Treatment of Renal Failure by Dialysis with an Artificial Kidney 414 UNIT VI Blood Cells, Immunity, and Blood Clotting CHAPTER 32 Red Blood Cells, Anemia, and Polycythemia 419 Red Blood Cells (Erythrocytes) 419 Production of Red Blood Cells 420 Formation of Hemoglobin 424 Iron Metabolism 425 Life Span and Destruction of Red Blood Cells 426 Anemias 426 Effects of Anemia on Function of the Circulatory System 427 Polycythemia 427 Effect of Polycythemia on Function of the Circulatory System 428 CHAPTER 33 Resistance of the Body to Infection: I. Leukocytes, Granulocytes, the Monocyte-Macrophage System, and Inflammation 429 Leukocytes (White Blood Cells) 429 General Characteristics of Leukocytes 429 Genesis of the White Blood Cells 430 Life Span of the White Blood Cells 431 Neutrophils and Macrophages Defend Against Infections 431 Phagocytosis 431 Monocyte-Macrophage Cell System (Reticuloendothelial System) 432 Inflammation: Role of Neutrophils and Macrophages 434 Inflammation 434 Macrophage and Neutrophil Responses During Inflammation 434 Eosinophils 436 Basophils 436 Leukopenia 436 The Leukemias 437 Effects of Leukemia on the Body 437 CHAPTER 34 Resistance of the Body to Infection: II. Immunity and Allergy 439 Innate Immunity 439 Acquired (Adaptive) Immunity 439 Basic Types of Acquired Immunity 440 Both Types of Acquired Immunity Are Initiated by Antigens 440 Lymphocytes Are Responsible for Acquired Immunity 440 Preprocessing of the T and B Lymphocytes 440 T Lymphocytes and B-Lymphocyte Antibodies React Highly Specifically Against Specific Antigens—Role of Lymphocyte Clones 442 Origin of the Many Clones of Lymphocytes 442 Specific Attributes of the B-Lymphocyte System—Humoral Immunity and the Antibodies 443 Special Attributes of the T-Lymphocyte System–Activated T Cells and CellMediated Immunity 446 Several Types of T Cells and Their Different Functions 446 Tolerance of the Acquired Immunity System to One’s Own Tissues—Role of Preprocessing in the Thymus and Bone Marrow 448 Immunization by Injection of Antigens 448 Passive Immunity 449 Allergy and Hypersensitivity 449 Allergy Caused by Activated T Cells: Delayed-Reaction Allergy 449 Allergies in the “Allergic” Person, Who Has Excess IgE Antibodies 449 CHAPTER 35 Blood Types; Transfusion; Tissue and Organ Transplantation 451 Antigenicity Causes Immune Reactions of Blood 451 O-A-B Blood Types 451 A and B Antigens—Agglutinogens 451 Agglutinins 452 Agglutination Process In Transfusion Reactions 452 Blood Typing 453 Rh Blood Types 453 Rh Immune Response 453 Transfusion Reactions Resulting from Mismatched Blood Types 454 Transplantation of Tissues and Organs 455 Attempts to Overcome Immune Reactions in Transplanted Tissue 455 CHAPTER 36 Hemostasis and Blood Coagulation 457 Events in Hemostasis 457 Vascular Constriction 457 Formation of the Platelet Plug 457 Blood Coagulation in the Ruptured Vessel 458 Fibrous Organization or Dissolution of the Blood Clot 458