Guyton and Hall Textbook of Medical Physiology

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Note to Instructors
Guyton and Hall Textbook of Medical Physiology
Copyright
Dedication
Preface
Unit I: Introduction to Physiology: The Cell and General Physiology
Chapter 1: Functional Organization of the Human Body and Control of the “Internal Environment”
Human Physiology
CELLS ARE THE LIVING UNITS OF THE BODY
Microorganisms Living in the Body Outnumber Human Cells
EXTRACELLULAR FLUID—THE “INTERNAL ENVIRONMENT”
Differences in Extracellular and Intracellular Fluids
HOMEOSTASIS—MAINTENANCE OF A NEARLY CONSTANT INTERNAL ENVIRONMENT
Homeostatic Compensations in Diseases
EXTRACELLULAR FLUID TRANSPORT AND MIXING SYSTEM—THE BLOOD CIRCULATORY SYSTEM
ORIGIN OF NUTRIENTS IN THE EXTRACELLULAR FLUID
Respiratory System
Gastrointestinal Tract
Liver and Other Organs That Perform Primarily Metabolic Functions
Musculoskeletal System
REMOVAL OF METABOLIC END PRODUCTS
Removal of Carbon Dioxide by the Lungs
Kidneys
Gastrointestinal Tract
Liver
REGULATION OF BODY FUNCTIONS
Nervous System
Hormone Systems
PROTECTION OF THE BODY
Immune System
Integumentary System
REPRODUCTION
CONTROL SYSTEMS OF THE BODY
EXAMPLES OF CONTROL MECHANISMS
Regulation of Oxygen and Carbon Dioxide Concentrationsin the Extracellular Fluid
Regulation of Arterial Blood Pressure
Normal Ranges and Physical Characteristics of Important Extracellular Fluid Constituents
CHARACTERISTICS OF CONTROL SYSTEMS
Negative Feedback Nature of Most Control Systems
Gain of a Control System
Positive Feedback May Cause Vicious Cycles and Death
Positive Feedback Can Sometimes Be Useful
More Complex Types of Control Systems—Feed-Forwardand Adaptive Control
PHYSIOLOGICAL VARIABILITY
SUMMARY—AUTOMATICITY OF THE BODY
Bibliography
Chapter 2: The Cell and Its Functions
ORGANIZATION OF THE CELL
Water
Ions
Proteins
Lipids
Carbohydrates
CELL STRUCTURE
MEMBRANOUS STRUCTURES OF THE CELL
Cell Membrane
The Cell Membrane Lipid Barrier Impedes Penetrationby Water-Soluble Substances
Integral and Peripheral Cell Membrane Proteins
Membrane Carbohydrates—The Cell “Glycocalyx”
CYTOPLASM AND ITS ORGANELLES
Endoplasmic Reticulum
Ribosomes and the Rough (Granular) Endoplasmic Reticulum
Smooth (Agranular) Endoplasmic Reticulum
Golgi Apparatus
Lysosomes
Peroxisomes
Secretory Vesicles
Mitochondria
Cell Cytoskeleton—Filament and Tubular Structures
Nucleus
Nuclear Membrane
Nucleoli and Formation of Ribosomes
COMPARISON OF THE ANIMAL CELL WITH PRECELLULAR FORMS OF LIFE
FUNCTIONAL SYSTEMS OF THE CELL
ENDOCYTOSIS—INGESTION BY THE CELL
Pinocytosis
Phagocytosis
LYSOSOMES DIGEST PINOCYTOTIC AND PHAGOCYTIC FOREIGN SUBSTANCES INSIDE THE CELL
Lysosomes and Regression of Tissues and Autolysis of Damaged Cells
Autophagy and Recycling of Cell Organelles
SYNTHESIS OF CELLULAR STRUCTURES BY ENDOPLASMIC RETICULUM AND GOLGI APPARATUS
Endoplasmic Reticulum Functions
Proteins Synthesis by the Rough Endoplasmic Reticulum
Lipid Synthesis by the Smooth Endoplasmic Reticulum
Other Functions of the Endoplasmic Reticulum
Golgi Apparatus Functions
Synthetic Functions of the Golgi Apparatus
Processing of Endoplasmic Secretions by the Golgi Apparatus—Formation of Vesicles
Types of Vesicles Formed by the Golgi Apparatus—Secretory Vesicles and Lysosomes
Use of Intracellular Vesicles to Replenish CellularMembranes
THE MITOCHONDRIA EXTRACT ENERGY FROM NUTRIENTS
Functional Characteristics of Adenosine Triphosphate
Chemical Processes in the Formation of ATP—Role of the Mitochondria
Uses of ATP for Cellular Function
LOCOMOTION OF CELLS
AMEBOID MOVEMENT
Mechanism of Ameboid Locomotion
Types of Cells That Exhibit Ameboid Locomotion
Control of Ameboid Locomotion—Chemotaxis
CILIA AND CILIARY MOVEMENTS
Mechanism of Ciliary Movement
Nonmotile Primary Cilia Serve as Cell Sensory “Antennae”
Bibliography
Chapter 3: Genetic Control of Protein Synthesis, Cell Function, and Cell Reproduction
CELL NUCLEUS GENES CONTROL PROTEIN SYNTHESIS
Building Blocks of DNA
Nucleotides
Nucleotides Are Organized to Form Two Strands of DNA Loosely Bound to Each Other
GENETIC CODE
TRANSCRIPTION—TRANSFER OF CELL NUCLEUS DNA CODE TO CYTOPLASM RNA CODE
RNA IS SYNTHESIZED IN THE NUCLEUS FROM A DNA TEMPLATE
Building Blocks of RNA
Formation of RNA Nucleotides
“Activation” of RNA Nucleotides
RNA CHAIN ASSEMBLY FROM ACTIVATED NUCLEOTIDES USING THE DNA STRAND AS A TEMPLATE
There Are Several Different Types of RNA
MESSENGER RNA—THE CODONS
RNA Codons for the Different Amino Acids
TRANSFER RNA—THE ANTICODONS
RIBOSOMAL RNA
Formation of Ribosomes in the Nucleolus
miRNA AND SMALL INTERFERING RNA
TRANSLATION—FORMATION OF PROTEINS ON THE RIBOSOMES
Polyribosomes
Many Ribosomes Attach to the Endoplasmic Reticulum
Chemical Steps in Protein Synthesis
Peptide Linkage—Combination of Amino Acids
SYNTHESIS OF OTHER SUBSTANCES IN THE CELL
CONTROL OF GENE FUNCTION AND BIOCHEMICAL ACTIVITY IN CELLS
GENETIC REGULATION
The Promoter Controls Gene Expression
Other Mechanisms for Control of Transcription by the Promoter
CONTROL OF INTRACELLULAR FUNCTION BY ENZYME REGULATION
Enzyme Inhibition
Enzyme Activation
Summary
THE DNA–GENETIC SYSTEM CONTROLS CELL REPRODUCTION
Life Cycle of the Cell
Cell Reproduction Begins with Replication of DNA
DNA Replication
DNA Repair, DNA “Proofreading,” and “Mutation”
CHROMOSOMES AND THEIR REPLICATION
CELL MITOSIS
Mitotic Apparatus: Function of the Centrioles
Prophase
Prometaphase
Metaphase
Anaphase
Telophase
CONTROL OF CELL GROWTH AND CELL REPRODUCTION
Telomeres Prevent the Degradation of Chromosomes
Regulation of Cell Size
CELL DIFFERENTIATION
APOPTOSIS—PROGRAMMED CELL DEATH
CANCER
Invasive Characteristic of the Cancer Cell
Why Do Cancer Cells Kill?
Bibliography
Unit II: Membrane Physiology, Nerve, and Muscle
Chapter 4: Transport of Substances Through Cell Membranes
THE CELL MEMBRANE IS A LIPID BILAYER WITH CELL MEMBRANE TRANSPORT PROTEINS
“Diffusion” Versus “Active Transport”
DIFFUSION
DIFFUSION THROUGH THE CELL MEMBRANE
Diffusion of Lipid-Soluble Substances Through the Lipid Bilayer
Diffusion of Water and Other Lipid-Insoluble Molecules Through Protein Channels
DIFFUSION THROUGH PROTEIN PORES AND CHANNELS—SELECTIVE PERMEABILITY AND “GATING” OF CHANNELS
Selective Permeability of Protein Channels
Gating of Protein Channels
Open-State Versus Closed-State of Gated Channels
Patch Clamp Method for Recording Ion Current Flow Through Single Channels
FACILITATED DIFFUSION REQUIRESMEMBRANE CARRIER PROTEINS
FACTORS THAT AFFECT NET RATE OF DIFFUSION
Net Diffusion Rate Is Proportional to the Concentration Difference Across a Membrane
Membrane Electrical Potential and Diffusion ofIons—The “Nernst Potential”
Effect of a Pressure Difference Across the Membrane
OSMOSIS ACROSS SELECTIVELY PERMEABLE MEMBRANES—“NETDIFFUSION” OF WATER
Osmotic Pressure
Importance of Number of Osmotic Particles (Molar Concentration) in Determining Osmotic Pressure
Osmolality—The Osmole
Relationship of Osmolality to Osmotic Pressure
The Term Osmolarity
ACTIVE TRANSPORT OF SUBSTANCES THROUGH MEMBRANES
Primary Active Transport and Secondary Active Transport
PRIMARY ACTIVE TRANSPORT
Sodium-Potassium Pump Transports Sodium Ions Out of Cells and Potassium Ions into Cells
The Na+-K+ Pump Is Important for Controlling Cell Volume
Electrogenic Nature of the Na+-K+ Pump
Primary Active Transport of Calcium Ions
Primary Active Transport of Hydrogen Ions
Energetics of Primary Active Transport
SECONDARY ACTIVE TRANSPORT—CO-TRANSPORT AND COUNTER-TRANSPORT
Co-Transport of Glucose and Amino Acids Along with Sodium Ions
Sodium Counter-Transport of Calcium and Hydrogen Ions
ACTIVE TRANSPORT THROUGH CELLULAR SHEETS
Bibliography
Chapter 5: Membrane Potentials and Action Potentials
Basic Physics of Membrane Potentials
Membrane Potentials Caused by Ion Concentration Differences Across a Selectively Permeable Membrane
The Nernst Equation Describes the Relationship of Diffusion Potential to the Ion Concentration Difference Across a Membrane
The Goldman Equation Is Used to Calculate the Diffusion Potential When the Membrane Is Permeable to Several Different Ions
Measuring the Membrane Potential
Resting Membrane Potential of Neurons
Active Transport of Sodium and Potassium Ions Through the Membrane—the Sodium-­Potassium (Na+-K+) Pump
Leakage of Potassium Through the Nerve Cell Membrane
Origin of the Normal Resting Membrane Potential
Contribution of the Potassium Diffusion Potential
Contribution of Sodium Diffusion Through the Nerve Membrane
Contribution of the Na+­K+ Pump
Neuron Action Potential
Resting Stage
Depolarization Stage
Repolarization Stage
Voltage­Gated Sodium and Potassium Channels
Activation and Inactivation of the Voltage­Gated Sodium Channel
Activation of the Sodium Channel
Inactivation of the Sodium Channel
Voltage-Gated Potassium Channel and Its Activation
SUMMARY OF EVENTS THAT CAUSE THE ACTION POTENTIAL
Initiation of the Action Potential
A Positive­Feedback Cycle Opens the Sodium Channels
Initiation of the Action Potential Occurs Only After the Threshold Potential is Reached
Propagation of the Action Potential
Direction of Propagation
All-or-Nothing Principle
RE-ESTABLISHING SODIUM AND POTASSIUM IONIC GRADIENTS AFTER ACTION POTENTIALS ARE COMPLETED—IMPORTANCE OF ENERGY METABOLISM
Plateau in Some Action Potentials
Rhythmicity of Some Excitable Tissues—Repetitive Discharge
Re-Excitation Process Necessary for Spontaneous Rhythmicity
Special Characteristics of Signal Transmission in Nerve Trunks
Myelinated and Unmyelinated Nerve Fibers
Saltatory Conduction in Myelinated Fibers from Node to Node
Velocity of Conduction in Nerve Fibers
Excitation—The Process of Eliciting the Action Potential
Threshold for Excitation and Acute Local Potentials
REFRACTORY PERIOD AFTER AN ACTION POTENTIAL, DURING WHICH A NEW STIMULUS CANNOT BE ELICITED
Bibliography
Chapter 6: Contraction of Skeletal Muscle
PHYSIOLOGICAL ANATOMY OF SKELETAL MUSCLE
The Sarcolemma Is a Thin Membrane Enclosing a Skeletal Muscle Fiber
Myofibrils Are Composed of Actin and Myosin Filaments
Titin Filamentous Molecules Keep the Myosin and Actin Filaments in Place
Sarcoplasm Is the Intracellular Fluid Between Myofibrils
Sarcoplasmic Reticulum Is a Specialized Endoplasmic Reticulum of Skeletal Muscle
GENERAL MECHANISM OF MUSCLE CONTRACTION
MOLECULAR MECHANISM OF MUSCLE CONTRACTION
Muscle Contraction Occurs by a Sliding Filament Mechanism
Molecular Characteristics of the Contractile Filaments
Myosin Filaments Are Composed of Multiple Myosin Molecules
Adenosine Triphosphatase Activity of the Myosin Head
Actin Filaments Are Composed of Actin, Tropomyosin, and Troponin
Tropomyosin Molecules
Troponin and Its Role in Muscle Contraction
Interaction of One Myosin Filament, Two Actin Filaments, and Calcium Ions to Cause Contraction
Inhibition of the Actin Filament by the Troponin-Tropomyosin Complex
Activation of the Actin Filament by Calcium Ions
Interaction of the Activated Actin Filament and the Myosin Cross-Bridges—The Walk-Along Theory of Contraction
ATP Is the Energy Source for Contraction—Chemical Events in the Motion of the Myosin Heads
Amount of Actin and Myosin Filament Overlap Determines Tension Developed by the Contracting Muscle
Effect of Muscle Length on Force of Contraction in the Whole Intact Muscle
ENERGETICS OF MUSCLE CONTRACTION
Work Output During Muscle Contraction
Three Sources of Energy for Muscle Contraction
CHARACTERISTICS OF WHOLE MUSCLE CONTRACTION
Isometric Contractions Do Not Shorten Muscle, Whereas Isotonic Contractions Shorten Muscle at a Constant Tension
Characteristics of Isometric Twitches Recorded from Different Muscles
Fast Versus Slow Muscle Fibers
Slow Fibers (Type 1, Red Muscle)
Fast Fibers (Type II, White Muscle)
MECHANICS OF SKELETAL MUSCLECONTRACTION
Motor Unit—All the Muscle Fibers Innervated by a Single Nerve Fiber
Muscle Contractions of Different Force—Force Summation
Multiple Fiber Summation
Frequency Summation and Tetanization
Maximum Strength of Contraction
Changes in Muscle Strength at the Onset of Contraction—the Staircase Effect (Treppe)
Skeletal Muscle Tone
Muscle Fatigue
REMODELING OF MUSCLE TO MATCH FUNCTION
Muscle Hypertrophy and Muscle Atrophy
Adjustment of Muscle Length
Hyperplasia of Muscle Fibers
Muscle Denervation Causes Rapid Atrophy
Bibliography
Chapter 7: Excitation of Skeletal Muscle: Neuromuscular Transmission and Excitation-Contraction Coupling
Neuromuscular Junction and Transmission of Impulses from Nerve Endings to Skeletal Muscle Fibers
PHYSIOLOGIC ANATOMY OF THE NEUROMUSCULAR JUNCTION—THE MOTOR END PLATE
SECRETION OF ACETYLCHOLINE BY THE NERVE TERMINALS
Acetylcholine Opens Ion Channels on Postsynaptic Membranes
Destruction of the Released Acetylcholine by Acetylcholinesterase
End Plate Potential and Excitation of the Skeletal Muscle Fiber
Safety Factor for Transmission at the Neuromuscular Junction—Fatigue of the Junction
Muscle Action Potential
Action Potentials Spread to the Interior of the Muscle Fiber by Way of Transverse Tubules
Excitation-Contraction Coupling
Transverse Tubule–Sarcoplasmic Reticulum System
Release of Calcium Ions by the Sarcoplasmic Reticulum
Calcium Pump Removes Calcium Ions from the Myofibrillar Fluid After Contraction Occurs
Excitatory Pulse of Calcium Ions
Bibliography
Chapter 8: Excitation and Contraction of Smooth Muscle
Contraction of Smooth Muscle
Types of Smooth Muscle
Multi-Unit Smooth Muscle
Unitary Smooth Muscle
Contractile Mechanism in Smooth Muscle
Chemical Basis for Smooth Muscle Contraction
Physical Basis for Smooth Muscle Contraction
Comparison of Smooth Muscle Contraction and Skeletal Muscle Contraction
Slow Cycling of the Myosin Cross-Bridges
Low Energy Requirement to Sustain Smooth Muscle Contraction
Slowness of Onset of Contraction and Relaxation of the Total Smooth Muscle Tissue
Maximum Force of Contraction Is Often Greater in Smooth Muscle Than in Skeletal Muscle
Latch Mechanism Facilitates Prolonged Holding of Contractions of Smooth Muscle
Stress-Relaxation of Smooth Muscle
Regulation of Contraction by Calcium Ions
Calcium Ions Combine with Calmodulin to Cause Activation of Myosin Kinase and Phosphorylation of the Myosin Head
Source of Calcium Ions That Cause Contraction
Role of the Smooth Muscle Sarcoplasmic Reticulum
Smooth Muscle Contraction Is Dependent on Extracellular Calcium Ion Concentration
A Calcium Pump Is Required to Cause Smooth Muscle Relaxation
Myosin Phosphatase Is Important in Cessation of Contraction
Possible Mechanism for Regulating the Latch Phenomenon
Nervous and Hormonal Control of Smooth Muscle Contraction
Neuromuscular Junctions of Smooth Muscle
Physiologic Anatomy of Smooth Muscle Neuromuscular Junctions
Excitatory and Inhibitory Transmitter Substances Secretedat the Smooth Muscle Neuromuscular Junction
Membrane Potentials and Action Potentials in Smooth Muscle
Membrane Potentials in Smooth Muscle
Action Potentials in Unitary Smooth Muscle
Spike Potentials
Action Potentials with Plateaus
Calcium Channels Are Important in Generating the Smooth Muscle Action Potential
Slow Wave Potentials in Unitary Smooth Muscle Can Lead to Spontaneous Generation of Action Potentials
Excitation of Visceral Smooth Muscle by Muscle Stretch
DEPOLARIZATION OF MULTI-UNIT SMOOTH MUSCLE WITHOUT ACTION POTENTIALS
Local Tissue Factors and Hormones Can Cause Smooth Muscle Contraction Without Action Potentials
Smooth Muscle Contraction in Response to Local Tissue Chemical Factors
Effects of Hormones on Smooth Muscle Contraction
Mechanisms of Smooth Muscle Excitation or Inhibition by Hormones or Local Tissue Factors
Bibliography
Unit III: The Heart
Chapter 9: Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves
Physiology of Cardiac Muscle
Cardiac Muscle Anatomy
Left Ventricular Rotation (Twist) Aids Left Ventricular Ejection and Relaxation
Cardiac Muscle Is a Syncytium
ACTION POTENTIALS IN CARDIAC MUSCLE
What Causes the Long Action Potential and Plateau in Cardiac Muscle
Phases of Cardiac Muscle Action Potential
Phase 0 (Depolarization): Fast Sodium Channels Open
Phase 1 (Initial Repolarization): Fast Sodium Channels Close
Phase 2 (Plateau): Calcium Channels Open and Fast Potassium Channels Close
Phase 3 (Rapid Repolarization): Calcium Channels Close and Slow Potassium Channels Open
Phase 4 (Resting Membrane Potential)
Velocity of Signal Conduction in Cardiac Muscle
Refractory Period of Cardiac Muscle
EXCITATION-CONTRACTION COUPLING—FUNCTION OF CALCIUM IONS AND THE TRANSVERSE TUBULES
Duration of Contraction
Cardiac Cycle
Diastole and Systole
Increasing Heart Rate Decreases Duration of Cardiac Cycle
Relationship of the Electrocardiogram to the Cardiac Cycle
The Atria Function as Primer Pumps for the Ventricles
FUNCTION OF THE VENTRICLES AS PUMPS
The Ventricles Fill with Blood During Diastole
Outflow of Blood from the Ventricles During Systole
Period of Isovolumic (Isometric) Contraction
Period of Ejection
Period of Isovolumic (Isometric) Relaxation
End-Diastolic Volume, End-Systolic Volume, and Stroke Volume Output
THE HEART VALVES PREVENT BACKFLOW OF BLOOD DURING SYSTOLE
Atrioventricular Valves
Function of the Papillary Muscles
Aortic and Pulmonary Artery Valves
AORTIC PRESSURE CURVE
GRAPHIC ANALYSIS OF VENTRICULAR PUMPING
Volume-Pressure Diagram During the Cardiac Cycle; Cardiac Work Output
Phase I: Period of Filling
Phase II: Period of Isovolumic Contraction
Phase III: Period of Ejection
Phase IV: Period of Isovolumic Relaxation
Concepts of Preload and Afterload
Regulation of Heart Pumping
INTRINSIC REGULATION OF HEART PUMPING—THE FRANK-STARLING MECHANISM
What Is the Explanation of the Frank Starling Mechanism?
Ventricular Function Curves
Control of the Heart by the Sympathetic and Parasympathetic Nerves
Mechanisms of Excitation of the Heart by the Sympathetic Nerves
Parasympathetic (Vagal) Stimulation Reduces Heart Rate and Strength of Contraction
Effect of Sympathetic or Parasympathetic Stimulationon the Cardiac Function Curve
EFFECT OF POTASSIUM AND CALCIUMIONS ON HEART FUNCTION
Effect of Potassium Ions
Effect of Calcium Ions
EFFECT OF TEMPERATURE ON HEART FUNCTION
INCREASING THE ARTERIAL PRESSURE LOAD (UP TO A LIMIT) DOES NOT DECREASE CARDIAC OUTPUT
Bibliography
Chapter 10: Rhythmical Excitation of the Heart
Specialized Excitatory and Conductive System of the Heart
Sinus (Sinoatrial) Node
AUTOMATIC ELECTRICAL RHYTHMICITYOF THE SINUS FIBERS
Mechanism of Sinus Nodal Rhythmicity
Leakiness of Sinus Nodal Fibers to Sodium and Calcium Causes Self-Excitation
INTERNODAL AND INTERATRIAL PATHWAYS TRANSMIT CARDIAC IMPULSES THROUGH THE ATRIA
THE ATRIOVENTRICULAR NODE DELAYS IMPULSE CONDUCTION FROM THE ATRIA TO THE VENTRICLES
Cause of the Slow Conduction
RAPID TRANSMISSION OF THE CARDIAC IMPULSE IN THE VENTRICULAR PURKINJE SYSTEM
The A-V Bundle Is Normally a One-Way Conduction Path
Distribution of the Purkinje Fibers in the Ventricles—Left and Right Bundle Branches
TRANSMISSION OF THE CARDIAC IMPULSE IN THE VENTRICULAR MUSCLE
SUMMARY OF THE SPREAD OF THE CARDIAC IMPULSE THROUGH THE HEART
CONTROL OF EXCITATION ANDCONDUCTIONIN THE HEART
The Sinus Node is the Normal Pacemaker of the Heart
Abnormal Pacemakers—Ectopic Pacemaker
ROLE OF THE PURKINJE SYSTEM IN CAUSING SYNCHRONOUS CONTRACTION OF THE VENTRICULAR MUSCLE
SYMPATHETIC AND PARASYMPATHETIC NERVES CONTROL HEART RHYTHMICITY AND IMPULSE CONDUCTION BY THE CARDIAC NERVES
Parasympathetic (Vagal) Stimulation Slows the Cardiac Rhythm and Conduction
Mechanism of the Vagal Effects
Sympathetic Stimulation Increases the Cardiac Rhythm and Conduction
Mechanism of the Sympathetic Effect
Bibliography
Chapter 11: Fundamentals of Electrocardiography
Waveforms of the Normal Electrocardiogram
CARDIAC DEPOLARIZATION WAVES VERSUS REPOLARIZATION WAVES
Relation of the Monophasic Action Potential of Ventricular Muscle to the QRS and T Waves in the Standard Electrocardiogram
RELATIONSHIP OF ATRIAL AND VENTRICULAR CONTRACTION TO THE WAVES OF THE ELECTROCARDIOGRAM
ELECTROCARDIOGRAPHIC CALIBRATION AND DISPLAY
Normal Voltages in the Electrocardiogram
P-Q or P-R Interval
Q-T Interval
Heart Rate as Determined from the Electrocardiogram
FLOW OF CURRENT AROUND THE HEART DURING THE CARDIAC CYCLE
Recording Electrical Potentials from a Partially Depolarized Mass of Syncytial Cardiac Muscle
Flow of Electrical Currents in the Chest Around the Heart
Electrocardiographic Leads
Three Standard Bipolar Limb Leads
Lead I
Lead II
Lead III
Einthoven’s Triangle
Einthoven’s Law
Normal Electrocardiograms Recorded from the Three Standard Bipolar Limb Leads
Precordial Leads
Augmented Limb Leads
Bibliography
Chapter 12: Electrocardiographic Interpretation of Cardiac Muscle and Coronary Blood Flow Abnormalities: Vectorial Analysis
VECTORIAL ANALYSIS OF ELECTROCARDIOGRAMS
VECTORS CAN REPRESENT ELECTRICAL POTENTIALS
Resultant Vector in the Heart at Any Given Instant
THE DIRECTION OF A VECTOR IS DENOTED IN TERMS OF DEGREES
AXIS FOR EACH STANDARD BIPOLAR LEAD AND EACH UNIPOLAR LIMB LEAD
VECTORIAL ANALYSIS OF POTENTIALS RECORDED IN DIFFERENT LEADS
Vectorial Analysis of Potentials in the Three Standard Bipolar Limb Leads
VECTORIAL ANALYSIS OF THE NORMAL ELECTROCARDIOGRAM
VECTORS THAT OCCUR AT SUCCESSIVE INTERVALS DURING DEPOLARIZATION OF THE VENTRICLES—THE QRS COMPLEX
ELECTROCARDIOGRAM DURING VENTRICULAR REPOLARIZATION—THE T WAVE
ATRIAL DEPOLARIZATION—THE P WAVE
Repolarization of the Atria—the Atrial T Wave
MEAN ELECTRICAL AXIS OFTHE VENTRICULAR QRS AND ITS SIGNIFICANCE
DETERMINING THE ELECTRICAL AXIS FROM STANDARD LEAD ELECTRO CARDIOGRAMS
ABNORMAL VENTRICULAR CONDITIONS THAT CAUSE AXIS DEVIATION
Change in the Position of the Heart in the Chest
Hypertrophy of One Ventricle
Vectorial Analysis of Left Axis Deviation Resulting from Hypertrophy of the Left Ventricle
Vectorial Analysis of Right Axis Deviation Resulting from Hypertrophy of the Right Ventricle
Bundle Branch Block Causes Axis Deviation
Vectorial Analysis of Left Axis Deviation in Left Bundle Branch Block
Vectorial Analysis of Right Axis Deviation in Right Bundle Branch Block
CONDITIONS THAT CAUSE ABNORMAL VOLTAGES OF THE QRS COMPLEX
INCREASED VOLTAGE IN THE STANDARD BIPOLAR LIMB LEADS
DECREASED VOLTAGE OF THE ELECTROCARDIOGRAM
Decreased Voltage Caused by Cardiac Myopathies
Decreased Voltage Caused by Conditions Surrounding the Heart
PROLONGED AND BIZARRE PATTERNS OF THE QRS COMPLEX
CARDIAC HYPERTROPHY OR DILATION PROLONG THE QRS COMPLEX
PURKINJE SYSTEM BLOCK PROLONGS THE QRS COMPLEX
CONDITIONS THAT CAUSE BIZARRE QRS COMPLEXES
CURRENT OF INJURY
EFFECT OF CURRENT OF INJURY ON THE QRS COMPLEX
THE J POINT IS THE ZERO REFERENCE POTENTIAL FOR ANALYZING CURRENT OF INJURY
Use of the J Point in Plotting Axis of Injury Potential
CORONARY ISCHEMIA AS A CAUSE OF INJURY POTENTIAL
Acute Anterior Wall Infarction
Posterior Wall Infarction
Infarction in Other Parts of the Heart
ECG Progression During and After Acute Coronary Thrombosis
Q Waves on an ECG Represent Old Myocardial Infarction
Current of Injury in Angina Pectoris
ABNORMALITIES IN THE T WAVE
EFFECT OF SLOW CONDUCTION OF THE DEPOLARIZATION WAVE ON THE CHARACTERISTICS OF THE T WAVE
SHORTENED DEPOLARIZATION IN PORTIONS OF THE VENTRICULAR MUSCLE CAN CAUSE T-WAVE ABNORMALITIES
Effect of Digitalis on the T Wave
Bibliography
Chapter 13: Cardiac Arrhythmias and Their Electrocardiographic Interpretation
Abnormal Sinus Rhythms
Tachycardia
Bradycardia
Bradycardia in Athletes
Vagal Stimulation Causes Bradycardia
Sinus Arrhythmia
Heart Block Within the Intracardiac Conduction Pathways
Sinoatrial Block
Atrioventricular Block
Incomplete Atrioventricular Block
First-Degree Block—Prolonged P-R Interval
Second-Degree Block
Complete A-V Block (Third-Degree Block)
Stokes-Adams Syndrome—Ventricular Escape
INCOMPLETE INTRAVENTRICULAR BLOCK—ELECTRICAL ALTERNANS
Premature Contractions
Causes of Premature Contractions
Premature Atrial Contractions
Pulse Deficit
A-V NODAL OR A-V BUNDLE PREMATURE CONTRACTIONS
PREMATURE VENTRICULAR CONTRACTIONS
Vector Analysis of the Origin of an Ectopic Premature Ventricular Contraction
Disorders of Cardiac Repolarization—the Long QT Syndromes
Paroxysmal Tachycardia
Paroxysmal Atrial Tachycardia
A-V Nodal Paroxysmal Tachycardia
Ventricular Tachycardia
Ventricular Fibrillation
PHENOMENON OF RE-ENTRY—CIRCUS MOVEMENTS AS THE BASIS FOR VENTRICULAR FIBRILLATION
CHAIN REACTION MECHANISM OF FIBRILLATION
Fibrillation Caused by 60-Cycle Alternating Current
ELECTROCARDIOGRAM IN VENTRICULAR FIBRILLATION
VENTRICULAR DEFIBRILLATION
HAND PUMPING OF THE HEART (CARDIOPULMONARY RESUSCITATION) AS AN AID TO DEFIBRILLATION
Atrial Fibrillation
Impaired Pumping of the Atria During Atrial Fibrillation
ELECTROCARDIOGRAM IN ATRIAL FIBRILLATION
IRREGULARITY OF VENTRICULAR RHYTHM DURING ATRIAL FIBRILLATION
ELECTROSHOCK TREATMENT OF ATRIAL FIBRILLATION
Atrial Flutter
Cardiac Arrest
Bibliography
Unit IV: The Circulation
Chapter 14: Overview of the Circulation: Pressure, Flow, and Resistance
Physical Characteristics of the Circulation
Functional Parts of the Circulation
Volumes of Blood in the Different Parts of the Circulation
Cross-Sectional Areas and Velocities of Blood Flow
Pressures in the Various Portions of the Circulation
Basic Principles of Circulatory Function
Interrelationships of Pressure, Flow, and Resistance
Blood Flow
Laminar Flow of Blood in Vessels
Parabolic Velocity Profile During Laminar Flow
Turbulent Flow of Blood Under Some Conditions
Blood Pressure
Standard Units of Pressure
Resistance to Blood Flow
Units of Resistance
Expression of Resistance in CGS Units
Total Peripheral Vascular Resistance and Total Pulmonary Vascular Resistance
Conductance of Blood in a Vessel Is the Reciprocal of Resistance
Small Changes in Vessel Diameter Markedly Change Its Conductance
Poiseuille’s Law
Importance of the Vessel Diameter Fourth Power Law in Determining Arteriolar Resistance
Resistance to Blood Flow in Series and Parallel Vascular Circuits
Effect of Blood Hematocrit and Blood Viscosity on Vascular Resistance and Blood Flow
Hematocrit—the Proportion of Blood That Is Red Blood Cells
Increasing Hematocrit Markedly Increases Blood Viscosity
Effects of Pressure on Vascular Resistance and Tissue Blood Flow
Autoregulation Attenuates the Effect of Arterial Pressure on Tissue Blood Flow
Pressure-Flow Relationship in Passive Vascular Beds
Vascular Wall Tension
Vascular Shear Stress
Bibliography
Chapter 15: Vascular Distensibility and Functions of the Arterial and Venous Systems
Vascular Distensibility
Units of Vascular Distensibility
The Veins Are Much More Distensible Than the Arteries
VASCULAR COMPLIANCE (OR VASCULAR CAPACITANCE)
VOLUME-PRESSURE CURVES OF THE ARTERIAL AND VENOUS CIRCULATIONS
Effect of Sympathetic Stimulation or Sympathetic Inhibition on the Volume-Pressure Relationships of the Arterial and Venous Systems
Delayed Compliance (Stress-Relaxation) of Vessels
Arterial Pressure Pulsations
Abnormal Pressure Pulse Contours
TRANSMISSION OF PRESSURE PULSES TO THE PERIPHERAL ARTERIES
Pressure Pulses Are Damped in the Smaller Arteries, Arterioles, and Capillaries
CLINICAL METHODS FOR MEASURINGSYSTOLIC AND DIASTOLIC PRESSURES
Auscultatory Method
Automated Oscillometric Method
Normal Arterial Pressures as Measured by the Auscultatory and Oscillatory Methods
Mean Arterial Pressure
Veins and Their Functions
VENOUS PRESSURES—RIGHT ATRIAL PRESSURE (CENTRAL VENOUS PRESSURE) AND PERIPHERAL VENOUS PRESSURES
Venous Resistance and Peripheral Venous Pressure
Effect of High Right Atrial Pressure on Peripheral Venous Pressure
Effect of Intra-abdominal Pressure on Venous Pressures of the Leg
Effect of Gravitational Pressure on Venous Pressure
Effect of the Gravitational Factor on Arterial and Other Pressures
Venous Valves and the Venous Pump: Their Effects on Venous Pressure
Venous Valve Incompetence Causes Varicose Veins
BLOOD RESERVOIR FUNCTION OF THE VEINS
SPECIFIC BLOOD RESERVOIRS
THE SPLEEN IS A RESERVOIR FOR RED BLOOD CELLS
Bibliography
Chapter 16: The Microcirculation and Lymphatic System: Capillary Fluid Exchange, Interstitial Fluid, and Lymph Flow
Structure of the Microcirculation and Capillary System
Structure of the Capillary Wall
Pores in the Capillary Membrane
Special Types of Pores in Capillaries of Certain Organs
Flow of Blood in the Capillaries—Vasomotion
Regulation of Vasomotion
Average Function of the Capillary System
EXCHANGE OF WATER, NUTRIENTS, AND OTHER SUBSTANCES BETWEEN THE BLOOD AND INTERSTITIAL FLUID
Diffusion Through the Capillary Membrane Is the Most Important Means of Transferring Substances Between Plasma and Interstitial Fluid
Lipid-Soluble Substances Diffuse Directly Through the Cell Membranes of the Capillary Endothelium
Water-Soluble, Non–Lipid-Soluble Substances Diffuse Through Intercellular Pores in the Capillary Membrane
Effect of Molecular Size on Passage Through the Pores
Diffusion Through the Capillary Membrane Is Proportional to the Concentration Difference Between the Two Sides of the Membrane
Interstitium and Interstitial Fluid
Gel in the Interstitium
Free Fluid in the Interstitium
Fluid Filtration Across Capillaries
Hydrostatic and Colloid Osmotic Forces Determine Fluid Movement Through the Capillary Membrane
Capillary Hydrostatic Pressure
INTERSTITIAL FLUID HYDROSTATIC PRESSURE
Interstitial Fluid Pressures in Tightly Encased Tissues
Summary: Interstitial Fluid Pressure in Loose Subcutaneous Tissue Usually Subatmospheric
Pumping by the Lymphatic System—Basic Cause of the Negative Interstitial Fluid Pressure
Plasma Colloid Osmotic Pressure
Plasma Proteins Cause Colloid Osmotic Pressure
Normal Values for Plasma Colloid Osmotic Pressure
INTERSTITIAL FLUID COLLOID OSMOTIC PRESSURE
FLUID VOLUME EXCHANGE THROUGH THE CAPILLARY MEMBRANE
Analysis of the Forces Causing Filtration at the Arterial End of the Capillary
Analysis of Reabsorption at the Venous End of the Capillary
STARLING EQUILIBRIUM FOR CAPILLARY EXCHANGE
CAPILLARY FILTRATION COEFFICIENT
Effect of Abnormal Imbalance of Forces at the Capillary Membrane
Lymphatic System
Lymph Channels of the Body
Terminal Lymphatic Capillaries and Their Permeability
Formation of Lymph
Rate of Lymph Flow
Effect of Interstitial Fluid Pressure on Lymph Flow
Lymphatic Pump Increases Lymph Flow. Valves exist in all lymph channels. Figure 16-­9 shows typical valves for collecting lympha...
Pumping Caused by External Intermittent Compression of the Lymphatics. In addition to the pumping caused by intrinsic intermitte...
Lymphatic Capillary Pump. The terminal lymphatic capillary is also capable of pumping lymph, in addition to the pumping by the l...
Summary of Factors That Determine Lymph Flow. From the previous discussion, one can see that the two primary factors that determ...
Lymphatic System Plays a Key Role in Controlling Interstitial Fluid Protein Concentration, Volume, and Pressure
Significance of Negative Interstitial Fluid Pressure for Holding Body Tissues Together
Bibliography
Chapter 17: Local and Humoral Control of Tissue Blood Flow
Local Control of Blood Flow in Response to Tissue Needs
Variations in Blood Flow in Different Tissues and Organs
Importance of Blood Flow Control by the Local Tissues
Mechanisms of Blood Flow Control
Acute Control of Local Blood Flow
Increases in Tissue Metabolism Increase Tissue Blood Flow
Reduced Oxygen Availability Increases Tissue Blood Flow
Vasodilator Theory for Acute Local Blood Flow Regulation—Possible Special Role of Adenosine
Oxygen Demand Theory for Local Blood Flow Control
Possible Role of Other Nutrients Besides Oxygen in Control of Local Blood Flow
Special Examples of Acute Metabolic Control of Local Blood Flow
Reactive Hyperemia Occurs After Tissue Blood Supply Is Blocked for a Short Time
Active Hyperemia Occurs When Tissue Metabolic Rate Increases
Autoregulation of Blood Flow During Changes in Arterial Pressure—Metabolic and Myogenic Mechanisms
Special Mechanisms for Acute Blood Flow Control in Specific Tissues
Control of Tissue Blood Flow: Endothelium Derived Relaxing or Constricting Factors
Nitric Oxide Is a Vasodilator Released from Healthy Endothelial Cells
Endothelin Is a Powerful Vasoconstrictor Released From Damaged Endothelium
Long Term Blood Flow Regulation
Blood Flow Regulation by Changes in Tissue Vascularity
Role of Oxygen in Long-Term Regulation
Importance of Vascular Growth Factors in Formation of New Blood Vessels
Vascularity Determined by Maximum Blood Flow Need, Not by Average Need
Blood Flow Regulation by Development of Collateral Circulation
Vascular Remodeling in Response to Chronic Changes in Blood Flow or Blood Pressure
Humoral Control of the Circulation
Vasoconstrictors
Norepinephrine and Epinephrine
Angiotensin II
Vasopressin
Vasodilators
Bradykinin
Histamine
Most Vasodilators or Vasoconstrictors Have Little Effecton Long-Term Blood Flow Unless They Alter the Metabolic Rate of the Tissues
Bibliography
Chapter 18: Nervous Regulation of the Circulation and Rapid Control of Arterial Pressure
Nervous Regulation of the Circulation
Autonomic Nervous System
Sympathetic Nervous System
Sympathetic Innervation of the Blood Vessels
Sympathetic Stimulation Increases Heart Rate and Contractility
Parasympathetic Stimulation Decreases Heart Rate and Contractility
Sympathetic Vasoconstrictor System and Its Control by the Central Nervous System
Vasomotor Center in the Brain and Its Control of the Vasoconstrictor System
Continuous Partial Constriction of Blood Vessels by Sympathetic Vasoconstrictor Tone
Control of Heart Activity by the Vasomotor Center
Control of the Vasomotor Center by Higher Nervous Centers
Norepinephrine Is the Sympathetic Vasoconstrictor Neurotransmitter
Adrenal Medullae and Their Relationship to the Sympathetic Vasoconstrictor System
Role of the Nervous System in Rapid Control of Arterial Pressure
Nervous Control of Arterial Pressure Is Rapid
INCREASES IN ARTERIAL PRESSURE DURING MUSCLE EXERCISE AND OTHER STRESSES
Reflex Mechanisms for Maintaining Normal Arterial Pressure
Baroreceptor Arterial Pressure Control System—Baroreceptor Reflexes
Physiologic Anatomy of the Baroreceptors and Their Innervation
Response of the Baroreceptors to Changes in Arterial Pressure
Circulatory Reflex Initiated by the Baroreceptors
Baroreceptors Attenuate Blood Pressure Changes During Changes in Body Posture
Pressure Buffer Function of the Baroreceptor Control System
Are the Baroreceptors Important in Long-Term Regulation of Arterial Pressure?
Control of Arterial Pressure by the Carotid and Aortic Chemoreceptors—Effect of Low Oxygen on Arterial Pressure
Atrial and Pulmonary Artery Reflexes Regulate Arterial Pressure
Atrial Reflexes That Activate the Kidneys—The Volume Reflex
Increased Atrial Pressure Raises Heart Rate—Bainbridge Reflex
DECREASED BLOOD FLOW TO BRAIN VASOMOTOR CENTER ELICITS INCREASED BLOOD PRESSURE—CNS ISCHEMIC RESPONSE
Importance of CNS Ischemic Response as a Regulator of Arterial Pressure
Cushing Reaction to Increased Pressure Around the Brain
SPECIAL FEATURES OF NERVOUS CONTROL OF ARTERIAL PRESSURE
ROLE OF THE SKELETAL NERVES AND SKELETAL MUSCLES IN INCREASING CARDIAC OUTPUT AND ARTERIAL PRESSURE
Abdominal Compression Reflex Increases Cardiac Output and Arterial Pressure
Skeletal Muscle Contraction Increases Cardiac Output and Arterial Pressure During Exercise
RESPIRATORY WAVES IN THE ARTERIAL PRESSURE
Arterial Pressure Vasomotor Waves—Oscillation of Pressure Reflex Control Systems
Oscillation of Baroreceptor and Chemoreceptor Reflexes
Oscillation of CNS Ischemic Response
Bibliography
Chapter 19: Role of the Kidneys in Long-Term Control of Arterial Pressure and in Hypertension: The Integrated System for Arterial Pressure Regulation
Renal–Body Fluid System for Arterial Pressure Control
QUANTITATION OF PRESSURE DIURESIS AS A BASIS FOR ARTERIAL PRESSURE CONTROL
Experiment Demonstrating the Renal–Body Fluid System for Arterial Pressure Control
Renal–Body Fluid Mechanism Provides Nearly Infinite Feedback Gain for Long-term Arterial Pressure Control
Two Key Determinants of Long-Term Arterial Pressure
Chronic Renal Output Curve Much Steeper Than the Acute Curve
Failure of Increased Total Peripheral Resistance to Elevate Long-Term Level of Arterial Pressure if Fluid Intake and Renal Function Do Not Change
Increased Fluid Volume Can Elevate Arterial Pressure by Increasing Cardiac Output or Total Peripheral Resistance
Importance of Salt (NaCl) in the Renal–Body Fluid Schema for Arterial Pressure Regulation
CHRONIC HYPERTENSION (HIGH BLOOD PRESSURE) CAUSED BY IMPAIRED RENAL FUNCTION
Experimental Volume-Loading Hypertension Caused by Reduced Kidney Mass and Increased Salt Intake
Sequential Changes in Circulatory Function During Development of Volume-Loading Hypertension
Volume-Loading Hypertension in Patients Who Have No Kidneys but Are Being Maintained With an Artificial Kidney
Hypertension Caused by Excess Aldosterone
Role of the Renin­Angiotensin System in Arterial Pressure Control
COMPONENTS OF THE RENIN-ANGIOTENSIN SYSTEM
Rapidity and Intensity of the Vasoconstrictor Pressure Response to the Renin-­Angiotensin System
Angiotensin II Causes Renal Retention of Salt and Water—An Important Means for Long­Term Control of Arterial Pressure
Mechanisms of the Direct Renal Effects of Angiotensin II to Cause Renal Retention of Salt and Water
Angiotensin II Increases Kidney Salt and Water Retention by Stimulating Aldosterone
Role of the Renin­Angiotensin System in Maintaining a Normal Arterial Pressure Despite Large Variations in Salt Intake
HYPERTENSION CAUSED BY RENIN-SECRETING TUMOR OR RENAL ISCHEMIA
One­Kidney Goldblatt Hypertension
Two­Kidney Goldblatt Hypertension
Hypertension Caused by Diseased Kidneys That Secrete Renin Chronically
Primary (Essential) Hypertension
Graphic Analysis of Arterial Pressure Control in Essential Hypertension
Treatment of Essential Hypertension
Summary of Integrated Multifaceted Systems for Arterial Pressure Regulation
Arterial Pressure Control Mechanisms That Act Within Seconds or Minutes
Arterial Pressure Control Mechanisms That Act After Many Minutes
Long­Term Mechanisms for Arterial Pressure Regulation
Bibliography
Chapter 20: Cardiac Output, Venous Return, and Their Regulation
Normal Values for Cardiac Output at Rest and During Activity
Effect of Age on Cardiac Output
Control of Cardiac Output by Venous Return—Frank-Starling Mechanism of the Heart
Cardiac Output Is the Sum of All Tissue Blood Flows—Tissue Metabolism Regulates Most Local Blood Flow
Cardiac Output Varies Inversely With Total Peripheral Resistance When Arterial Pressure Is Unchanged
Limits for the Cardiac Output
Factors That Cause a Hypereffective Heart
Nervous Excitation Can Increase Heart Pumping
Heart Hypertrophy Can Increase Pumping Effectiveness
Factors That Cause a Hypoeffective Heart
Nervous System Regulation of Cardiac Output
Importance of Nervous System For Maintaining Arterial Pressure When Peripheral Blood Vessels Are Dilated and Venous Return and Cardiac Output Increase
Effect of Nervous System to Increase Arterial Pressure During Exercise
CARDIAC OUTPUT CURVES USED IN QUANTITATIVE ANALYSIS OF CARDIAC OUTPUT REGULATION
Effect of External Pressure Outside the Heart on Cardiac Output Curves
Combinations of Different Patterns of Cardiac Output Curves
VENOUS RETURN CURVES
Normal Venous Return Curve
Plateau in Venous Return Curve at Negative Atrial Pressures Caused by Collapse of the Large Veins
Mean Circulatory Filling Pressure, Mean Systemic Filling Pressure—Effects on Venous Return
Increased Blood Volume Raises Mean Circulatory Filling Pressure
Sympathetic Nervous Stimulation Increases Mean Circulatory Filling Pressure
Mean Systemic Filling Pressure and Relationship to Mean Circulatory Filling Pressure
Effect on Venous Return Curve of Changes in Mean Systemic Filling Pressure
When Pressure Gradient for Venous Return Is Zero There Is No Venous Return
Resistance to Venous Return
Effect of Resistance to Venous Return on the Venous Return Curve
Combinations of Venous Return Curve Patterns
ANALYSIS OF CARDIAC OUTPUT AND RIGHT ATRIAL PRESSURE BY SIMULTANEOUS CARDIAC OUTPUT AND VENOUS RETURN CURVES
Effect of Increased Blood Volume on Cardiac Output
Compensatory Effects Initiated in Response to Increased Blood Volume
Effect of Sympathetic Stimulation on Cardiac Output
Effect of Sympathetic Inhibition on Cardiac Output
Effect of Opening a Large Arteriovenous Fistula
Other Analyses of Cardiac Output Regulation
Methods For Measuring Cardiac Output
Pulsatile Output of the Heart Measured by Electromagnetic or Ultrasonic Flowmeter
Measurement of Cardiac Output Using the Oxygen Fick Principle
Indicator Dilution Method
Echocardiography
Thoracic Electrical Bioimpedance Method
Bibliography
Chapter 21: Muscle Blood Flow and Cardiac Output During Exercise; the Coronary Circulation and Ischemic Heart Disease
Blood Flow Regulation in Skeletal Muscle at Rest and During Exercise
Skeletal Muscle Blood Flow Rate
Blood Flow During Muscle Contractions
Increased Blood Flow in Muscle Capillaries During Exercise. During rest, some muscle capillaries have little or no flowing blood...
Control of Skeletal Muscle Blood Flow
Decreased Oxygen in Muscle Greatly Enhances Flow
Nervous Control of Muscle Blood Flow
CIRCULATORY READJUSTMENTS DURING EXERCISE
Effects of Sympathetic Activation
Sympathetic Stimulation May Increase Arterial Pressure During Exercise
Why Is Increased Arterial Pressure During Exercise Important?
Importance of Increased Cardiac Output During Exercise
Graphic Analysis of Changes in Cardiac Output During Heavy Exercise
Coronary Circulation
PHYSIOLOGIC ANATOMY OF THE CORONARY BLOOD SUPPLY
NORMAL CORONARY BLOOD FLOWAVERAGES 5% OF CARDIAC OUTPUT
Cardiac Muscle Compression Causes Phasic Changes in Coronary Blood Flow During Systole and Diastole
Epicardial Versus Subendocardial Coronary Blood Flow—Effect of Intramyocardial Pressure
CONTROL OF CORONARY BLOOD FLOW
Local Muscle Metabolism Is the Primary Controller of Coronary Flow
Oxygen Demand Is a Major Factor in Local Coronary Blood Flow Regulation
Nervous Control of Coronary Blood Flow
Direct Effects of Nervous Stimuli on Coronary Vasculature
SPECIAL FEATURES OF CARDIAC MUSCLE METABOLISM
ISCHEMIC HEART DISEASE
Atherosclerosis Is a Major Cause of Ischemic Heart Disease
Acute Coronary Artery Occlusion
Lifesaving Value of Collateral Circulation in the Heart
Myocardial Infarction
Subendocardial Infarction
CAUSES OF DEATH AFTER ACUTE CORONARY OCCLUSION
Decreased Cardiac Output—Systolic Stretch and Cardiac Shock
Damming of Blood in the Body’s Venous System
Fibrillation of the Ventricles After Myocardial Infarction
Rupture of Infarcted Area
STAGES OF RECOVERY FROM ACUTE MYOCARDIAL INFARCTION
Replacement of Dead Muscle by Scar Tissue
Value of Rest in Treating Myocardial Infarction
HEART FUNCTION AFTER RECOVERY FROM MYOCARDIAL INFARCTION
PAIN IN CORONARY HEART DISEASE
Angina Pectoris (Cardiac Pain)
Drug Treatment
SURGICAL TREATMENT OF CORONARYARTERY DISEASE
Aortic-Coronary Bypass Surgery
Coronary Angioplasty
Bibliography
Chapter 22: Cardiac Failure
CIRCULATORY DYNAMICS IN CARDIAC FAILURE
ACUTE EFFECTS OF MODERATE CARDIAC FAILURE
Compensation for Acute Cardiac Failure by Sympathetic Nervous Reflexes
CHRONIC STAGE OF FAILURE—FLUID RETENTION AND COMPENSATED CARDIAC OUTPUT
Renal Retention of Fluid and Increase inBlood Volume Occur for Hours to Days
Moderate Fluid Retention in Cardiac Failure Can Be Beneficial
Detrimental Effects of Excess Fluid Retention in Severe Cardiac Failure
Recovery of the Heart After Myocardial Infarction
Cardiac Output Curve After Partial Recovery
SUMMARY OF CHANGES AFTER ACUTE CARDIAC FAILURE—COMPENSATED HEART FAILURE
Compensated Heart Failure
DYNAMICS OF SEVERE CARDIAC FAILURE—DECOMPENSATED HEART FAILURE
Graphic Analysis of Decompensated Heart Failure
Treatment of Decompensation
Mechanism of Action of Cardiotonic Drugs
UNILATERAL LEFT HEART FAILURE
LOW-OUTPUT CARDIAC FAILURE—CARDIOGENIC SHOCK
Vicious Cycle of Cardiac Deterioration in Cardiogenic Shock
Physiology of Cardiogenic Shock Treatment
EDEMA IN PATIENTS WITH CARDIAC FAILURE
Acute Cardiac Failure Does Not Cause Immediate Peripheral Edema
LONG-TERM FLUID RETENTION BY THE KIDNEYS CAUSES PERIPHERAL EDEMA IN PERSISTING HEART FAILURE
Role of Natriuretic Peptides in Delaying Onset of Cardiac Decompensation
Acute Pulmonary Edema in Late-Stage Heart Failure—Another Lethal Vicious Cycle
CARDIAC RESERVE
Diagnosis of Low Cardiac Reserve—Exercise Test
QUANTITATIVE GRAPHIC ANALYSIS OF CARDIAC FAILURE
Graphic Analysis of Acute Heart Failure and Chronic Compensation
Acute Heart Attack Reduces Cardiac Output Curve
Sympathetic Reflexes Raise Cardiac Output and Venous Return Curves
Compensation During the Next Few Days Further Increases Cardiac Output and Venous Return Curves
Graphic Analysis of Decompensated Cardiac Failure
Treatment of Decompensated Heart Disease With Digitalis
HEART FAILURE WITH DIASTOLIC DYSFUNCTION AND NORMAL EJECTION FRACTION
HIGH-OUTPUT CARDIAC FAILURE
Arteriovenous Fistula Increases Venous Return
Beriberi Weakens the Heart, Causes Fluid Retention by the Kidneys, and Increases Venous Return
Bibliography
Chapter 23: Heart Valves and Heart Sounds; Valvular and Congenital Heart Defects
HEART SOUNDS
NORMAL HEART SOUNDS
The First Heart Sound Is Associated With Closure of A-V
The Second Heart Sound Is Associated With Closure of the Aortic and Pulmonary Valves
Duration and Pitch of First and Second Heart Sounds
The Third Heart Sound Occurs at the Beginning of the Middle Third of Diastole
Atrial Contraction—Fourth Heart Sound
Chest Surface Areas for Auscultation of Normal Heart Sounds
Phonocardiogram
VALVULAR LESIONS
Rheumatic Valvular Lesions
Aging and Aortic Valve Stenosis
Heart Murmurs Caused by Valvular Lesions
Systolic Murmur of Aortic Stenosis
Diastolic Murmur of Aortic Regurgitation
Systolic Murmur of Mitral Regurgitation
Diastolic Murmur of Mitral Stenosis
Phonocardiograms of Valvular Murmurs
ABNORMAL CIRCULATORY DYNAMICS IN VALVULAR HEART DISEASE
CIRCULATORY DYNAMICS IN AORTIC STENOSIS AND AORTIC REGURGITATION
Hypertrophy of Left Ventricle
Increase in Blood Volume
Aortic Valvular Lesions May Be Associated With Inadequate Coronary Blood Flow
Eventual Failure of Left Ventricle and Development of Pulmonary Edema
DYNAMICS OF MITRAL STENOSIS AND MITRAL REGURGITATION
Pulmonary Edema in Mitral Valvular Disease
Enlarged Left Atrium and Atrial Fibrillation
Compensation in Early Mitral Valvular Disease
CIRCULATORY DYNAMICS DURING EXERCISE IN PATIENTS WITH VALVULAR LESIONS
ABNORMAL CIRCULATORY DYNAMICS IN CONGENITAL HEART DEFECTS
PATENT DUCTUS ARTERIOSUS—A LEFT-TO-RIGHT SHUNT
Closure of Ductus Arteriosus After Birth
Dynamics of the Circulation With a Persistent Patent Ductus
Recirculation Through the Lungs
Diminished Cardiac and Respiratory Reserve
Heart Sounds: Machinery Murmur
Surgical Treatment
TETRALOGY OF FALLOT—A RIGHT-TO-LEFT SHUNT
Abnormal Circulatory Dynamics
Surgical Treatment
CAUSES OF CONGENITAL ANOMALIES
USE OF EXTRACORPOREAL CIRCULATION DURING CARDIAC SURGERY
HYPERTROPHY OF THE HEART IN VALVULAR AND CONGENITAL HEART DISEASE
Detrimental Effects of Late Stages of Cardiac Hypertrophy
Bibliography
Chapter 24: Circulatory Shock and Its Treatment
Physiological Causes of Shock
Circulatory Shock Caused by Decreased Cardiac Output
CIRCULATORY SHOCK WITHOUT DIMINISHED CARDIAC OUTPUT
WHAT HAPPENS TO THE ARTERIAL PRESSURE IN CIRCULATORY SHOCK?
TISSUE DETERIORATION IS THE END RESULT OF CIRCULATORY SHOCK
Stages of Shock
Shock Caused by Hypovolemia—Hemorrhagic Shock
Relationship of Bleeding Volume to Cardiac Output and Arterial Pressure
Sympathetic Reflex Compensations in Shock—Their Special Value to Maintain Arterial Pressure
Greater Effect of Sympathetic Nervous Reflexes in Maintaining Arterial Pressure Than in Maintaining Cardiac Output
Protection of Coronary and Cerebral Blood Flow by the Reflexes
PROGRESSIVE AND NONPROGRESSIVE HEMORRHAGIC SHOCK
Nonprogressive Shock—Compensated Shock
Progressive Shock—Caused by Vicious Cycle of Cardiovascular Deterioration
Cardiac Depression
Vasomotor Failure
Blockage of Very Small Vessels by Sludged Blood
Increased Capillary Permeability
Release of Toxins by Ischemic Tissue
Cardiac Depression Caused by Endotoxin
Generalized Cellular Deterioration
Patchy Areas of Tissue Necrosis Caused by Patchy Blood Flows in Different Organs
Acidosis in Shock
Positive Feedback Deterioration of Tissues in Shock and Vicious Cycle of Progressive Shock
Irreversible Shock
Depletion of Cellular High-Energy Phosphate Reserves in Irreversible Shock
HYPOVOLEMIC SHOCK CAUSED BY PLASMA LOSS
HYPOVOLEMIC SHOCK CAUSED BY TRAUMA
Neurogenic Shock—Increased Vascular Capacity
Causes of Neurogenic Shock
Anaphylactic Shock and Histamine Shock
Septic Shock
Special Features of Septic Shock
Physiology of Treatment in Shock
Replacement Therapy
Blood and Plasma Transfusion
Dextran Solution as a Plasma Substitute
TREATMENT OF NEUROGENIC AND ANAPHYLACTIC SHOCK WITH SYMPATHOMIMETIC DRUGS
Other Therapy
Treatment by the Head-Down Position
Oxygen Therapy
Treatment With Glucocorticoids
Circulatory Arrest
Effect of Circulatory Arrest on the Brain
Bibliography
Unit V: The Body Fluids and Kidneys
Chapter 25: Regulation of Body Fluid Compartments: Extracellular and Intracellular Fluids; Edema
Fluid Intake and Output Are Balanced During Steady-State Conditions
Daily Intake of Water
Daily Loss of Body Water
Insensible Water Loss
Fluid Loss in Sweat
Water Loss in Feces
Water Loss by the Kidneys
Body Fluid Compartments
Intracellular Fluid Compartment
Extracellular Fluid Compartment
Blood Volume
Hematocrit (Packed Red Blood Cell Volume)
Constituents of Extracellular and Intracellular Fluids
Similar Ionic Composition of Plasma and Interstitial Fluid
Intracellular Fluid Constituents
Measurement of Body Fluid Compartment Volumes—Indicator-Dilution Principle
Determination of Volumes of Specific Body Fluid Compartments
Measurement of Total Body Water
Measurement of Extracellular Fluid Volume
Calculation of Intracellular Volume
Measurement of Plasma Volume
Calculation of Interstitial Fluid Volume
Measurement of Blood Volume
Fluid Exchange and Osmotic Equilibrium Between Intracellular and Extracellular Fluid
BASIC PRINCIPLES OF OSMOSIS AND OSMOTIC PRESSURE
Osmolality and Osmolarity
Calculation of the Osmolarity and Osmotic Pressure of a Solution
Osmolarity of Body Fluids
Corrected Osmolar Activity of Body Fluids
Osmotic Equilibrium Between Intracellular and Extracellular Fluids
Isotonic, Hypotonic, and Hypertonic Fluids
Isosmotic, Hyperosmotic, and Hypo-Osmotic Fluids
Osmotic Equilibrium Between Intracellular and Extracellular Fluids Is Rapidly Attained
Volume and Osmolality of Extracellular and Intracellular Fluids in Abnormal States
Effect of Adding Saline Solution to the Extracellular Fluid
Calculation of Fluid Shifts and Osmolarities After Infusion of Hypertonic Saline Solution
Glucose and Other Solutions Administered For Nutritive Purposes
Clinical Abnormalities of Fluid Volume Regulation: Hyponatremia and Hypernatremia
Causes of Hyponatremia: Excess Water or Loss of Sodium
Hyponatremia Causes Cell Edema
Causes of Hypernatremia: Water Loss or Excess Sodium
Hypernatremia Causes Cell Shrinkage
Edema: Excess Fluid in the Tissues
Intracellular Edema
Extracellular Edema
Factors That Can Increase Capillary Filtration
Lymphedema—Failure of Lymph Vessels to Return Fluid and Protein to the Blood
Summary of Causes of Extracellular Edema
Edema Caused by Heart Failure
Edema Caused by Decreased Kidney Excretion of Salt and Water
Edema Caused by Decreased Plasma Proteins
Increased Lymph Flow as a Safety Factor Against Edema
Washdown of Interstitial Fluid Protein as a Safety Factor Against Edema
SAFETY FACTORS THAT NORMALLY PREVENT EDEMA
Safety Factor Caused by Low Compliance of the Interstitium in the Negative Pressure Range
Importance of Interstitial Gel in Preventing Fluid Accumulation in the Interstitium
Importance of Proteoglycan Filaments as a Spacer for Cells and in Preventing Rapid Flow of Fluid in Tissues
Increased Lymph Flow as a Safety Factor Against Edema
Washdown of Interstitial Fluid Protein as a Safety Factor Against Edema
SUMMARY OF SAFETY FACTORS THAT PREVENT EDEMA
Fluids in Potential Spaces of the Body
Fluid Is Exchanged Between Capillaries and Potential Spaces
Lymphatic Vessels Drain Protein From the Potential Spaces
Edema Fluid in the Potential Spaces Is Called Effusion
Bibliography
Chapter 26: The Urinary System: Functional Anatomy and Urine Formation by the Kidneys
Multiple Functions of the Kidneys
Excretion of Metabolic Waste Products, Foreign Chemicals, Drugs, and Hormone Metabolites
Regulation of Water and Electrolyte Balances
Regulation of Arterial Pressure
Regulation of Acid–Base Balance
Regulation of Erythrocyte Production
Regulation of 1,25-Dihydroxyvitamin D3 Production
Glucose Synthesis
PHYSIOLOGIC ANATOMY OF THE KIDNEYS
General Organization of the Kidneys and Urinary Tract
Renal Blood Supply
THE NEPHRON IS THE FUNCTIONAL UNIT OF THE KIDNEY
Regional Differences in Nephron Structure: Cortical and Juxtamedullary Nephrons
Micturition
PHYSIOLOGIC ANATOMY OF THE BLADDER
Innervation of the Bladder
URINE TRANSPORT FROM THE KIDNEYS THROUGH THE URETERS AND INTO THE BLADDER
Pain Sensation in the Ureters and the Ureterorenal Reflex
Micturition Reflex
Facilitation or Inhibition of Micturition by the Brain
Urine Formation Results from Glomerular Filtration, Tubular Reabsorption, and Tubular Secretion
FILTRATION, REABSORPTION, AND SECRETION OF DIFFERENT SUBSTANCES
Why Are Large Amounts of Solutes Filtered and Then Reabsorbed by the Kidneys?
Bibliography
Chapter 27: Glomerular Filtration, Renal Blood Flow, and Their Control
Glomerular Filtration—The First Step in Urine Formation
COMPOSITION OF THE GLOMERULAR FILTRATE
GLOMERULAR FILTRATION RATE IS ABOUT 20% OF RENAL PLASMA FLOW
Glomerular Capillary Membrane
Filterability of Solutes Inversely Related to Their Size
Negatively Charged Large Molecules Are Filtered Less Easily Than Positively Charged Molecules of Equal Molecular Size
Minimal-Change Nephropathy and Increased Glomerular Permeability to Plasma Proteins
Determinants of the Glomerular Filtration Rate
INCREASED GLOMERULAR CAPILLARY FILTRATION COEFFICIENT INCREASES GLOMERULAR FILTRATE RATE
INCREASED BOWMAN’S CAPSULE HYDROSTATIC PRESSURE DECREASES GLOMERULAR FILTRATION RATE
INCREASED GLOMERULAR CAPILLARY COLLOID OSMOTIC PRESSURE DECREASES GLOMERULAR FILTRATION RATE
INCREASED GLOMERULAR CAPILLARY HYDROSTATIC PRESSURE INCREASES GLOMERULAR FILTRATION RATE
Renal Blood Flow
RENAL BLOOD FLOW AND OXYGEN CONSUMPTION
Determinants of Renal Blood Flow
BLOOD FLOW IN VASA RECTA OF RENAL MEDULLA IS LOW COMPARED WITH RENAL CORTEX FLOW
Physiological Control of Glomerular Filtration and Renal Blood Flow
STRONG SYMPATHETIC NERVOUS SYSTEM ACTIVATION DECREASES GLOMERULAR FILTRATION RATE
HORMONAL AND AUTACOID CONTROL OF RENAL CIRCULATION
Norepinephrine, Epinephrine, and Endothelin Constrict Renal Blood Vessels and Decrease Glomerular Filtration Rate
Angiotensin II Preferentially Constricts Efferent Arterioles in Most Physiological Conditions
Endothelial Derived Nitric Oxide Decreases Renal Vascular Resistance and Increases Glomerular Filtration Rate
Prostaglandins and Bradykinin Decrease Renal Vascular Resistance and Tend to Increase Glomerular Filtration Rate
Autoregulation of Glomerular Filtration Rate and Renal Blood Flow
Importance of Glomerular Filtration Rate Autoregulation in Preventing Extreme Changes in Renal Excretion
TUBULOGLOMERULAR FEEDBACK AND AUTOREGULATION OF GLOMERULAR FILTRATION RATE
Decreased Macula Densa Sodium Chloride Causes Dilation of Afferent Arterioles and Increased Renin Release
MYOGENIC AUTOREGULATION OF RENAL BLOOD FLOW AND GLOMERULAR FILTRATION RATE
Bibliography
Chapter 28: Renal Tubular Reabsorption and Secretion
Tubular Reabsorption is Quantitatively Large and Highly Selective
Tubular Reabsorption Includes Passive and Active Mechanisms
Active Transport
Solutes Can Be Transported Through Epithelial Cells or Between Cells
Primary Active Transport Through the Tubular Membrane Linked to Hydrolysis of Adenosine Triphosphatase
Secondary Active Reabsorption Through the Tubular Membrane
Secondary Active Secretion Into the Tubules
Pinocytosis Is an Active Transport Mechanism for Reabsorption of Proteins
Transport Maximum for Substances That Are Actively Reabsorbed
Transport Maximums for Actively Secreted Substances
Substances That Are Actively Transported but Do Not Exhibit a Transport Maximum
PASSIVE WATER REABSORPTION BY OSMOSIS COUPLED MAINLY TO SODIUM REABSORPTION
REABSORPTION OF CHLORIDE, UREA, AND OTHER SOLUTES BY PASSIVE DIFFUSION
Reabsorption and Secretion Along Different Parts of the Nephron
Proximal Tubular Reabsorption
Proximal Tubules Have High Capacity for Active and Passive Reabsorption
Concentrations of Solutes Along Proximal Tubules
Secretion of Organic Acids and Bases by Proximal Tubules
SOLUTE AND WATER TRANSPORT IN LOOPS OF HENLE
Distal Tubules
LATE DISTAL TUBULES AND CORTICAL COLLECTING TUBULES
Principal Cells Reabsorb Sodium and Secrete Potassium
Intercalated Cells Can Secrete or Reabsorb Hydrogen, Bicarbonate, and Potassium Ions
Medullary Collecting Ducts
SUMMARY OF CONCENTRATIONS OF DIFFERENT SOLUTES IN DIFFERENT TUBULAR SEGMENTS
Tubular Fluid/Plasma Inulin Concentration Ratio Can Be Used to Assess Water Reabsorption by Renal Tubules
Regulation of Tubular Reabsorption
GLOMERULOTUBULAR BALANCE—REABSORPTION RATE INCREASES IN RESPONSE TO INCREASED TUBULAR LOAD
PERITUBULAR CAPILLARY AND RENAL INTERSTITIAL FLUID PHYSICAL FORCES
Normal Values for Physical Forces and Reabsorption Rate
Regulation of Peritubular Capillary Physical Forces
Renal Interstitial Hydrostatic and Colloid Osmotic Pressures
EFFECT OF ARTERIAL PRESSURE ON URINE OUTPUT—PRESSURE NATRIURESIS AND PRESSURE DIURESIS
HORMONAL CONTROL OF TUBULAR REABSORPTION
Aldosterone Stimulates Renal Sodium Reabsorption and Potassium Secretion
Angiotensin II Increases Sodium and Water Reabsorption
Antidiuretic Hormone Increases Water Reabsorption
Atrial Natriuretic Peptide Decreases Sodium and Water Reabsorption
Parathyroid Hormone Increases Calcium Reabsorption
SYMPATHETIC NERVOUS SYSTEM ACTIVATION INCREASES SODIUM REABSORPTION
Use of Clearance Methods to Quantify Kidney Function
INULIN CLEARANCE CAN BE USED TO ESTIMATE GLOMERULAR FILTRATION RATE
CREATININE CLEARANCE AND PLASMA CREATININE CONCENTRATION CAN BE USED TO ESTIMATE GLOMERULAR FILTRATION RATE
PARA-AMINOHIPPURIC ACID CLEARANCE CAN BE USED TO ESTIMATE RENAL PLASMA FLOW
FILTRATION FRACTION IS CALCULATED FROM GFR DIVIDED BY RPF
CALCULATION OF TUBULAR REABSORPTION OR SECRETION FROM RENAL CLEARANCES
Bibliography
Chapter 29: Urine Concentration and Dilution; Regulation of Extracellular Fluid Osmolarity and Sodium Concentration
Kidneys Excrete Excess Water by Forming Dilute Urine
ANTIDIURETIC HORMONE CONTROLS URINE CONCENTRATION
RENAL MECHANISMS FOR EXCRETING DILUTE URINE
Tubular Fluid Remains Isosmotic in Proximal Tubules
Tubular Fluid Is Diluted in the Ascending Loop of Henle
Tubular Fluid in Distal and Collecting Tubules Is Further Diluted in Absence of ADH
Kidneys Conserve Water by Excreting Concentrated Urine
EXCRETING CONCENTRATED URINE REQUIRES HIGH ADH LEVELS AND HYPEROSMOTIC RENAL MEDULLA
Countercurrent Multiplier Mechanism Produces Hyperosmotic Renal Medullary Interstitium
Loop of Henle Characteristics That Cause Solutes to be Trapped in the Renal Medulla
Steps Involved in Causing Hyperosmotic Renal Medullary Interstitium
ROLE OF DISTAL TUBULE AND COLLECTING DUCTS IN EXCRETING CONCENTRATED URINE
UREA CONTRIBUTES TO HYPEROSMOTIC RENAL MEDULLARY INTERSTITIUM AND FORMATION OF CONCENTRATED URINE
Recirculation of Urea from Collecting Duct to Loop of Henle Contributes to Hyperosmotic Renal Medulla
COUNTERCURRENT EXCHANGE IN VASA RECTA PRESERVES HYPEROSMOLARITY OF RENAL MEDULLA
Increased Medullary Blood Flow Reduces Urine-Concentrating Ability
SUMMARY OF URINE-CONCENTRATING MECHANISM AND CHANGES IN OSMOLARITY IN DIFFERENT TUBULAR SEGMENTS
Proximal Tubule
Descending Loop of Henle
Thin Ascending Loop of Henle
Thick Ascending Loop of Henle
Early Distal Tubule
Late Distal Tubule and Cortical Collecting Tubules
Inner Medullary Collecting Ducts
Control of Extracellular Fluid Osmolarity and Sodium Concentration
Estimating Plasma Osmolarity From Plasma Sodium Concentration
Osmoreceptor­ADH Feedback System
ADH SYNTHESIS IN SUPRAOPTIC AND PARAVENTRICULAR NUCLEI OF HYPOTHALAMUS AND ADH RELEASE FROM POSTERIOR PITUITARY
STIMULATION OF ADH RELEASE BY DECREASED ARTERIAL PRESSURE AND/OR DECREASED BLOOD VOLUME
Quantitative Importance of Osmolarity and Cardiovascular Reflexes in Stimulating ADH Secretion
Other Stimuli for ADH Secretion
Importance of Thirst in Controlling Extracellular Fluid Osmolarity and Sodium Concentration
CENTRAL NERVOUS SYSTEM CENTERS FOR THIRST
Stimuli for Thirst
THRESHOLD FOR OSMOLAR STIMULUS OF DRINKING
INTEGRATED RESPONSES OF OSMORECEPTOR-ADH AND THIRST MECHANISMS
Bibliography
Chapter 30: Renal Regulation of Potassium, Calcium, Phosphate, and Magnesium; Integration of Renal Mechanisms for Control of Blood Volume and Extracellular Fluid Volume
Regulation of Extracellular Fluid Potassium Concentration and Potassium Excretion
REGULATION OF INTERNAL POTASSIUM DISTRIBUTION
Insulin Stimulates Potassium Uptake Into Cells
Aldosterone Increases Potassium Uptake Into Cells
β-Adrenergic Stimulation Increases Cellular Uptake of Potassium
Acid–Base Abnormalities Can Cause Changes in Potassium Distribution
Cell Lysis Causes Increased Extracellular Potassium Concentration
Strenuous Exercise Can Cause Hyperkalemia by Releasing Potassium From Skeletal Muscle
Increased Extracellular Fluid Osmolarity Causes Redistribution of Potassium From Cells to Extracellular Fluid
OVERVIEW OF RENAL POTASSIUM EXCRETION
Variable Potassium Secretion in Distal and Collecting Tubules Mediates Most Daily Changes in Potassium Excretion
PRINCIPAL CELLS OF LATE DISTAL AND CORTICAL COLLECTING TUBULES SECRETE POTASSIUM
Control of Potassium Secretion by Principal Cells
Intercalated Cells Can Reabsorb or Secrete Potassium
SUMMARY OF MAJOR FACTORS THAT REGULATE POTASSIUM SECRETION
Increased Extracellular Fluid Potassium Concentration Stimulates Potassium Secretion
Aldosterone Stimulates Potassium Secretion
Increased Extracellular Potassium Ion Concentration Stimulates Aldosterone Secretion
Blockade of Aldosterone Feedback System Greatly Impairs Potassium Regulation
Increased Distal Tubular Flow Rate Stimulates Potassium Secretion
Acute Acidosis Decreases Potassium Secretion
Regulation of Renal Calcium Excretion and Extracellular Calcium Ion Concentration
CONTROL OF CALCIUM EXCRETION BY THE KIDNEYS
Proximal Tubular Calcium Reabsorption
Loop of Henle and Distal Tubule Calcium Reabsorption
Regulation of Tubular Calcium Reabsorption
Regulation of Renal Phosphate Excretion
Regulation of Renal Magnesium Excretion and Extracellular Magnesium Ion Concentration
Integration of Renal Mechanisms for Control of Extracellular Fluid
SODIUM INTAKE AND EXCRETION ARE BALANCED UNDER STEADY-STATE CONDITIONS
SODIUM EXCRETION IS CONTROLLED BY ALTERING GLOMERULAR FILTRATION OR TUBULAR SODIUM REABSORPTION RATES
Importance of Pressure Natriuresis and Pressure Diuresis in Maintaining Body Sodium and Fluid Balance
Pressure Natriuresis and Diuresis: Key Components of A Renal–Body Fluid Feedback for Regulating Body Fluid Volumes and Arterial Pressure
EFFECTIVENESS OF BLOOD VOLUME AND EXTRACELLULAR FLUID VOLUME REGULATION
Distribution of Extracellular Fluid Between Interstitial Spaces and Vascular System
Nervous and Hormonal Factors Increase Effectiveness of Renal–Body Fluid Feedback Control
SYMPATHETIC NERVOUS SYSTEM CONTROL OF RENAL EXCRETION: ARTERIAL BARORECEPTOR AND LOW-PRESSURE STRETCH RECEPTOR REFLEXES
ROLE OF ANGIOTENSIN II IN CONTROLLING RENAL EXCRETION
Importance of Changes in Angiotensin II in Regulating Sodium Balance and Altering Pressure Natriuresis
ROLE OF ALDOSTERONE IN CONTROLLING RENAL EXCRETION
ROLE OF ANTIDIURETIC HORMONE IN CONTROLLING RENAL WATER EXCRETION
ROLE OF ATRIAL NATRIURETIC PEPTIDE IN CONTROLLING RENAL EXCRETION
Integrated Responses to Changes in Sodium Intake
High Sodium Intake Suppresses Antinatriuretic Systemsand Activates Natriuretic Systems
Conditions That Cause Large Increases in Blood Volume and Extracellular Fluid Volume
INCREASED BLOOD VOLUME AND EXTRACELLULAR FLUID VOLUME CAUSED BY HEART DISEASES
INCREASED BLOOD VOLUME CAUSED BY INCREASED VASCULAR CAPACITY
Conditions That Cause Large Increases in Extracellular Fluid Volume With Normal or Reduced Blood Volume
NEPHROTIC SYNDROME—LOSS OF PLASMA PROTEINS IN URINE AND SODIUM RETENTION BY THE KIDNEYS
LIVER CIRRHOSIS—DECREASED SYNTHESIS OF PLASMA PROTEINS BY THE LIVER AND SODIUM RETENTION BY THE KIDNEYS
Bibliography
Chapter 31: Acid–Base Regulation
Hydrogen Ion Concentration is Precisely Regulated
Acids and Bases—Definitions and Meanings
Strong and Weak Acids and Bases
Normal H+ Concentration and pH of Body Fluids and Changes That Occur in Acidosis and Alkalosis
Defending Against Changes in H+ Concentration: Buffers, Lungs, and Kidneys
Buffering of H+ in the Body Fluids
Bicarbonate Buffer System
Phosphate Buffer System
Proteins are Important Intracellular Buffers
Respiratory Regulation of Acid–­Base Balance
PULMONARY EXPIRATION OF CO2 BALANCES METABOLIC FORMATION OF CO2
INCREASING ALVEOLAR VENTILATION DECREASES EXTRACELLULAR FLUID H+ CONCENTRATION AND RAISES pH
INCREASED H+ CONCENTRATION STIMULATES ALVEOLAR VENTILATION
Feedback Control of H+ Concentration by the Respiratory System
Efficiency of Respiratory Control of H+ Concentration
Buffering Power of the Respiratory System
Impairment of Lung Function Can Cause Respiratory Acidosis
Renal Control of Acid–Base Balance
Secretion of H+ and Reabsorption of HCO3− by the Renal Tubules
H+ SECRETED BY SECONDARY ACTIVE TRANSPORT IN EARLY TUBULAR SEGMENTS
FILTERED HCO3− IS REABSORBED BY INTERACTION WITH H+ IN THE TUBULES
HCO3− Is Titrated Against H+ in the Tubules
PRIMARY ACTIVE SECRETION OF H+ IN THE INTERCALATED CELLS OF LATE DISTAL AND COLLECTING TUBULES
Combination of Excess H+ with Phosphate and Ammonia Buffers In the Tubule Generates “New” HCO3−
PHOSPHATE BUFFER SYSTEM CARRIES EXCESS H+ INTO THE URINE AND GENERATES NEW HCO3−
EXCRETION OF EXCESS H+ AND GENERATION OF NEW HCO3− BY AMMONIA BUFFER SYSTEM
Chronic Acidosis Increases NH4+ Excretion
Quantifying Renal Acid–Base Excretion
Regulation of Renal Tubular H+ Secretion
Renal Correction of Acidosis—Increased Excretion of H+ and Addition of HCO3− to the Extracellular Fluid
ACIDOSIS DECREASES HCO3−/H+ RATIO IN RENAL TUBULAR FLUID
Renal Correction of Alkalosis—Decreased Tubular Secretion of H+ and Increased Excretion of HCO3−
ALKALOSIS INCREASES HCO3−/H+ RATIO IN RENAL TUBULAR FLUID
Bibliography
Chapter 32: Diuretics and Kidney Diseases
DIURETICS AND THEIR MECHANISMS OF ACTION
Osmotic Diuretics Decrease Water Reabsorption by Increasing Osmotic Pressure of Tubular Fluid
Loop Diuretics Decrease Sodium-Chloride-Potassium Reabsorption in the Thick Ascending Loop of Henle
Thiazide Diuretics Inhibit Sodium-Chloride Reabsorption in the Early Distal Tubule
Carbonic Anhydrase Inhibitors Block Sodium Bicarbonate Reabsorption
Mineralocorticoid Receptor Antagonists Decrease Sodium Reabsorption From and Potassium Secretion Into the Collecting Tubules
Sodium Channel Blockers Decrease Sodium Reabsorption in the Collecting Tubules
KIDNEY DISEASES
ACUTE KIDNEY INJURY
PRERENAL ACUTE KIDNEY INJURY CAUSED BY DECREASED BLOOD FLOW TO THE KIDNEY
INTRARENAL ACUTE KIDNEY INJURY CAUSED BY ABNORMALITIES IN THE KIDNEY
Acute Kidney Injury Caused by Glomerulonephritis
Tubular Necrosis as a Cause of Acute Kidney Injury
Acute Tubular Necrosis Caused by Severe Renal Ischemia
Acute Tubular Necrosis Caused by Toxins or Medications
POSTRENAL ACUTE KIDNEY INJURY CAUSED BY ABNORMALITIES OF THE LOWER URINARY TRACT
PHYSIOLOGICAL EFFECTS OF ACUTE KIDNEY INJURY
CHRONIC KIDNEY DISEASE IS OFTEN ASSOCIATED WITH IRREVERSIBLE LOSS OF FUNCTIONAL NEPHRONS
VICIOUS CYCLE OF CHRONIC KIDNEY DISEASE LEADING TO END-STAGE RENAL DISEASE
INJURY TO RENAL BLOOD VESSELS AS A CAUSE OF CHRONIC KIDNEY DISEASE
INJURY TO THE GLOMERULI AS A CAUSE OF CHRONIC KIDNEY DISEASE—GLOMERULONEPHRITIS
INJURY TO THE RENAL INTERSTITIUM AS A CAUSE OF CHRONIC KIDNEY DISEASE—INTERSTITIAL NEPHRITIS
NEPHROTIC SYNDROME—EXCRETION OF PROTEIN IN THE URINE
NEPHRON FUNCTION IN CHRONIC KIDNEY DISEASE
Loss of Functional Nephrons Requires Surviving Nephrons to Excrete More Water and Solutes
Isosthenuria—Inability of the Kidney to Concentrate or Dilute the Urine
Bibliography
Unit VI: Blood Cells, Immunity, and Blood Coagulation
Chapter 33: Red Blood Cells, Anemia, and Polycythemia
Red Blood Cells (Erythrocytes)
Shape and Size of Red Blood Cells
Concentration of Red Blood Cells in the Blood
Quantity of Hemoglobin in the Cells
PRODUCTION OF RED BLOOD CELLS
Areas of the Body That Produce Red Blood Cells
Genesis of Blood Cells
Multipotential Hematopoietic Stem Cells, Growth Inducers, and Differentiation Inducers
Stages of Differentiation of Red Blood Cells
Erythropoietin Regulates Red Blood Cell Production
Tissue Oxygenation—Essential Regulator of Red Blood Cell Production
Hypoxia Increases Formation of Erythropoietin Which Stimulates Red Blood Cell Production
Erythropoietin Is Formed Mainly in the Kidneys
Erythropoietin Stimulates Production of Proerythroblasts From Hematopoietic Stem Cells
Maturation of Red Blood Cells Requires Vitamin B12 (Cyanocobalamin) and Folic Acid
Maturation Failure Anemia Caused by Poor Absorption of Vitamin B12 From the Gastrointestinal Tract—Pernicious Anemia
Maturation Failure Anemia Caused by Folic Acid (Pteroylglutamic Acid) Deficiency
HEMOGLOBIN FORMATION
Hemoglobin Combines Reversibly With Oxygen
IRON METABOLISM
Transport and Storage of Iron
Daily Loss of Iron
Absorption of Iron From the Intestinal Tract
Regulation of Total Body Iron by Controlling Absorption Rate
LIFE SPAN OF RED BLOOD CELLS IS ABOUT 120 DAYS
Destruction of Hemoglobin by Macrophages
Anemias
Blood Loss Anemia
Aplastic Anemia Due to Bone Marrow Dysfunction
Megaloblastic Anemia
Hemolytic Anemia
EFFECTS OF ANEMIA ON CIRCULATORY SYSTEM FUNCTION
Polycythemia
Secondary Polycythemia
Polycythemia Vera (Erythremia)
EFFECT OF POLYCYTHEMIA ON FUNCTION OF THE CIRCULATORY SYSTEM
Bibliography
Chapter 34: Resistance of the Body to Infection: I. Leukocytes, Granulocytes, the Monocyte-Macrophage System, and Inflammation
Leukocytes (White Blood Cells)
GENERAL CHARACTERISTICS OF LEUKOCYTES
Types of White Blood Cells
Concentrations of Different White Blood Cells in Blood
GENESIS OF WHITE BLOOD CELLS
LIFE SPAN OF WHITE BLOOD CELLS
Neutrophils and Macrophages Defend Against Infections
White Blood Cells Enter the Tissue Spaces by Diapedesis
White Blood Cells Move Through Tissue Spaces by Ameboid Motion
White Blood Cells Are Attracted to Inflamed Tissue Areas by Chemotaxis
Phagocytosis
Phagocytosis by Neutrophils
Phagocytosis by Macrophages
Once Phagocytized, Most Particles Are Digested by Intracellular Enzymes
Neutrophils and Macrophages Can Kill Bacteria
Monocyte-Macrophage Cell System (Reticuloendothelial System)
Tissue Macrophages in Skin and Subcutaneous Tissues (Histiocytes)
Macrophages in Lymph Nodes
Alveolar Macrophages in Lungs
Macrophages (Kupffer Cells) in Liver Sinusoids
Macrophages of Spleen and Bone Marrow
INFLAMMATION: ROLE OF NEUTROPHILS AND MACROPHAGES
Inflammation
Walling-Off Effect of Inflammation
Macrophage and Neutrophil Responses During Inflammation
Tissue Macrophages Provide First Line of Defense Against Infection
Neutrophil Invasion of the Inflamed Area Is a Second Line of Defense
Acute Increase in the Number of Neutrophils in Blood—Neutrophilia
Second Macrophage Invasion Into the Inflamed Tissue Is a Third Line of Defense
Increased Production of Granulocytes and Monocytes by Bone Marrow Is a Fourth Line of Defense
Feedback Control of Macrophage and Neutrophil Responses
Formation of Pus
Eosinophils
Basophils
Leukopenia
Leukemias
Effects of Leukemia on the Body
Bibliography
Chapter 35: Resistance of the Body to Infection: II. Immunity and Allergy
Acquired (Adaptive) Immunity
BASIC TYPES OF ACQUIRED IMMUNITY—HUMORAL AND CELL-MEDIATED
BOTH TYPES OF ACQUIRED IMMUNITY ARE INITIATED BY ANTIGENS
LYMPHOCYTES ARE RESPONSIBLE FOR ACQUIRED IMMUNITY
T and B Lymphocytes Promote Cell­Mediated and Humoral Immunity
PREPROCESSING OF T AND BLYMPHOCYTES
Thymus Gland Preprocesses T Lymphocytes
Liver and Bone Marrow Preprocess B Lymphocytes
T LYMPHOCYTES AND B-LYMPHOCYTEANTIBODIES REACT AGAINST SPECIFICANTIGENS—ROLE OF LYMPHOCYTECLONES
Millions of Specific Types of Lymphocytes Are Stored in Lymphoid Tissue
ORIGIN OF THE MANY CLONES OF LYMPHOCYTES
MECHANISM FOR ACTIVATING LYMPHOCYTE CLONES
Role of Macrophages in the Activation Process
Role of T Cells in Activation of B Lymphocytes. Most antigens activate both T lymphocytes and B lymphocytes at the same time. So...
Specific Attributes of The B­Lymphocyte System—Humoral Immunity and Antibodies
Antibody Formation by Plasma Cells
Formation of Memory Cells Enhances Antibody Response to Subsequent Antigen Exposure
Generation of Lifelong Immunity by Plasma Cells
Nature of Antibodies
Specificity of Antibodies
Five General Classes of Antibodies
Mechanisms of Action of Antibodies
Direct Action of Antibodies on Invading Agents
COMPLEMENT SYSTEM FOR ANTIBODY ACTION
Classical Pathway
Special Attributes of T­Lymphocyte System—Activated T Cells and Cell­Mediated Immunity
Release of Activated T Cells From Lymphoid Tissue and Formation of Memory Cells
Antigen­Presenting Cells, Major Histocompatibility Complex Proteins, and Antigen Receptors on T Lymphocytes
Different Types of T Cells and Their Functions
T­Helper Cells Are the Most Numerous T Cells
Specific Regulatory Functions of Lymphokines
Stimulation of Growth and Proliferation of Cytotoxic T Cells and Regulatory T Cells
Stimulation of B­Cell Growth and Differentiation to Form Plasma Cells and Antibodies
Activation of the Macrophage System
Feedback Stimulatory Effect on T­Helper Cells
Cytotoxic T Cells Are Killer Cells
Regulatory T Cells
TOLERANCE OF ACQUIRED IMMUNITY SYSTEM TO THE BODY’S OWN TISSUES—ROLE OF PREPROCESSING IN THYMUS AND BONE MARROW
Most Tolerance Results From Clone Selection During Preprocessing
Failure of the Tolerance Mechanism Causes Autoimmune Diseases
IMMUNIZATION BY INJECTION OF ANTIGENS
Passive Immunity
Allergy and Hypersensitivity
ALLERGY CAUSED BY ACTIVATED T CELLS: DELAYED-REACTION ALLERGY
ATOPIC ALLERGIES ASSOCIATED WITH EXCESS IgE ANTIBODIES
Anaphylaxis—Widespread Allergic Reaction
Urticaria—Localized Anaphylactoid Reactions
Hay Fever
Asthma
Bibliography
Chapter 36: Blood Types; Transfusion; and Tissue and Organ Transplantation
Antigenicity Causes Immune Reactions of Blood
Multiplicity of Antigens in the Blood Cells
O­A­B Blood Types
A and B Antigens—Agglutinogens
Major O-A-B Blood Types
Genetic Determination of the Agglutinogens
Relative Frequencies of Different Blood Types
Agglutinins
Titer of Agglutinins at Different Ages
Origin of Agglutinins in Plasma
AGGLUTINATION PROCESS IN TRANSFUSION REACTIONS
Acute Hemolysis Occurs in Some Transfusion Reactions
Blood Typing
Rh Blood Types
Rh Antigens—Rh-Positive and Rh-Negative
Rh Immune Response
Formation of Anti-Rh Agglutinins
Characteristics of Rh Transfusion Reactions
Erythroblastosis Fetalis (Hemolytic Disease of the Newborn)
Incidence of Erythroblastosis Fetalis
Effect of Mother’s Antibodies on the Fetus
Clinical Picture of Erythroblastosis
Treatment of Neonates With Erythroblastosis Fetalis
Prevention of Erythroblastosis Fetalis
Transfusion Reactions Resulting From Mismatched Blood Types
Acute Kidney Failure After Transfusion Reactions
Transplantation of Tissues and Organs
Autografts, Isografts, Allografts, and Xenografts
Transplantation of Cellular Tissues
ATTEMPTS TO OVERCOME IMMUNE REACTIONS IN TRANSPLANTED TISSUE
Tissue Typing—Human Leukocyte Antigen Complex of Antigens
Prevention of Graft Rejection by Suppressing the Immune System
Bibliography
Chapter 37: Hemostasis and Blood Coagulation
HEMOSTASIS EVENTS
VASCULAR CONSTRICTION
FORMATION OF THE PLATELET PLUG
Physical and Chemical Characteristics
Mechanism of Platelet Plug Formation
Importance of Platelet Mechanism for Closing Vascular Holes
BLOOD COAGULATION IN THE RUPTURED VESSEL
FIBROUS ORGANIZATION OR DISSOLUTION OF BLOOD CLOTS
MECHANISM OF BLOOD COAGULATION
GENERAL MECHANISM
CONVERSION OF PROTHROMBIN TO THROMBIN
Prothrombin and Thrombin
CONVERSION OF FIBRINOGEN TO FIBRIN—FORMATION OF THE CLOT
Fibrinogen Formed in the Liver Essential for Clot Formation
Action of Thrombin on Fibrinogen to Form Fibrin
Blood Clot
Clot Retraction and Expression of Serum
POSITIVE FEEDBACK OF CLOT FORMATION
INITIATION OF COAGULATION: FORMATION OF PROTHROMBIN ACTIVATOR
Extrinsic Pathway for Initiating Clotting
Intrinsic Pathway for Initiating Clotting
Role of Calcium Ions in the Intrinsic and Extrinsic Pathways
Interaction Between Extrinsic and Intrinsic Pathways—Summary of Blood-­Clotting Initiation
Intravascular Anticoagulants Prevent Blood Clotting in the Normal Vascular System
Endothelial Surface Factors
Antithrombin Action of Fibrin and Antithrombin III
Heparin
PLASMIN CAUSES LYSIS OF BLOOD CLOTS
Activation of Plasminogen to Form Plasmin, Then Clot Lysis
CONDITIONS THAT CAUSE EXCESSIVE BLEEDING IN HUMANS
DECREASED PROTHROMBIN, FACTOR VII, FACTOR IX, AND FACTOR X CAUSED BY VITAMIN K DEFICIENCY
HEMOPHILIA
THROMBOCYTOPENIA
THROMBOEMBOLIC CONDITIONS
Thrombi and Emboli
Causes of Thromboembolic Conditions
Use of Tissue Plasminogen Activator in Treating Intravascular Clots
FEMORAL VENOUS THROMBOSIS AND MASSIVE PULMONARY EMBOLISM
DISSEMINATED INTRAVASCULAR COAGULATION
ANTICOAGULANTS FOR CLINICAL USE
COUMARINS AS ANTICOAGULANTS
HEPARIN—INTRAVENOUS ANTICOAGULANT
PREVENTION OF BLOOD COAGULATION OUTSIDE THE BODY
BLOOD COAGULATION TESTS
BLEEDING TIME
CLOTTING TIME
PROTHROMBIN TIME AND INTERNATIONAL NORMALIZED RATIO
Bibliography
Unit VII: Respiration
Chapter 38: Pulmonary Ventilation
MECHANICS OF PULMONARY VENTILATION
MUSCLES THAT CAUSE LUNG EXPANSION AND CONTRACTION
PRESSURES THAT CAUSE MOVEMENT OF AIR IN AND OUT OF THE LUNGS
Pleural Pressure and Its Changes During Respiration
Alveolar Pressure—Air Pressure Inside the Lung Alveoli
Transpulmonary Pressure—Difference between Alveolar and Pleural Pressures
Compliance of the Lungs
Compliance Diagram of the Lungs
Surfactant, Surface Tension, and Collapse of the Alveoli
Principle of Surface Tension
Surfactant and Its Effect on Surface Tension
EFFECT OF THE THORACIC CAGE ON LUNG EXPANSIBILITY
Compliance of Thorax and Lungs Together
PULMONARY VOLUMES AND CAPACITIES
RECORDING CHANGES IN PULMONARY VOLUME—SPIROMETRY
Pulmonary Volumes
Pulmonary Capacities
ABBREVIATIONS AND SYMBOLS USED IN PULMONARY FUNCTION STUDIES
DETERMINATION OF FUNCTIONAL RESIDUAL CAPACITY, RESIDUAL VOLUME, AND TOTAL LUNG CAPACITY—HELIUM DILUTION METHOD
MINUTE RESPIRATORY VOLUME EQUALS RESPIRATORY RATE TIMES TIDAL VOLUME
ALVEOLAR VENTILATION
DEAD SPACE AND ITS EFFECT ON ALVEOLAR VENTILATION
RATE OF ALVEOLAR VENTILATION
Bibliography
Chapter 39: Pulmonary Circulation, Pulmonary Edema, and Pleural Fluid
PHYSIOLOGICAL ANATOMY OF THE PULMONARY CIRCULATORY SYSTEM
Pulmonary Vessels
Bronchial Vessels
Lymphatics
PRESSURES IN THE PULMONARY SYSTEM
Pressures in the Right Ventricle
Pressures in the Pulmonary Artery
Pulmonary Capillary Pressure
Left Atrial and Pulmonary Venous Pressures
BLOOD VOLUME OF THE LUNGS
Lungs Serve as a Blood Reservoir
Cardiac Pathology May Shift Blood From Systemic Circulation to Pulmonary Circulation
BLOOD FLOW THROUGH THE LUNGS AND ITS DISTRIBUTION
Decreased Alveolar Oxygen Reduces Local Alveolar Blood Flow and Regulates Pulmonary Blood Flow Distribution
EFFECT OF HYDROSTATIC PRESSURE GRADIENTS IN THE LUNGS ON REGIONAL PULMONARY BLOOD FLOW
Zones 1, 2, and 3 of Pulmonary Blood Flow
Zone 1 Blood Flow Occurs Only Under Abnormal Conditions
Exercise Increases Blood Flow Through All Parts of the Lungs
Increased Cardiac Output During Heavy Exercise Is Normally Accommodated by the Pulmonary Circulation Without Large Increases in Pulmonary Artery Pressure
Function of Pulmonary Circulation When Left Atrial Pressure Rises as a Result of Left-Sided Heart Failure
PULMONARY CAPILLARY DYNAMICS
Pulmonary Capillary Pressure
Length of Time Blood Stays in the Pulmonary Capillaries
Capillary Exchange of Fluid in the Lungs and Pulmonary Interstitial Fluid Dynamics
Interrelationships Between Interstitial Fluid Pressure and Other Pressures in the Lung
Negative Pulmonary Interstitial Pressure and Mechanism for Keeping Alveoli Dry
FLUID IN THE PLEURAL CAVITY
Negative Pressure in Pleural Fluid
Pleural Effusion—Collection of Large Amounts of Free Fluid in the Pleural Space
Bibliography
Chapter 40: Principles of Gas Exchange; Diffusion of Oxygen and Carbon Dioxide Through the Respiratory Membrane
Compositions of Alveolar Air and Atmospheric Air are Different
Air Is Humidified in the Respiratory Passages
Alveolar Air Is Slowly Renewed by Atmospheric Air
Slow Replacement of Alveolar Air Helps Stabilize Respiratory Control
Oxygen Concentration and Partial Pressure in Alveoli
CO2 Concentration and Partial Pressure in Alveoli
DIFFUSION OF GASES THROUGH THE RESPIRATORY MEMBRANE
Respiratory Unit
Respiratory Membrane
Factors Affecting Rate of Gas Diffusion Through the Respiratory Membrane
Diffusing Capacity of the Respiratory Membrane
Diffusing Capacity for Oxygen
Increased Oxygen Diffusing Capacity During Exercise
Diffusing Capacity for Carbon Dioxide
Bibliography
Chapter 41: Transport of Oxygen and Carbon Dioxide in Blood and Tissue Fluids
TRANSPORT OF OXYGEN FROM THE LUNGS TO THE BODY TISSUES
DIFFUSION OF OXYGEN FROM THE ALVEOLI TO THE PULMONARY CAPILLARY BLOOD
Uptake of Oxygen by the Pulmonary Blood During Exercise
TRANSPORT OF OXYGEN IN ARTERIAL BLOOD
DIFFUSION OF OXYGEN FROM THE PERIPHERAL CAPILLARIES INTO THE TISSUE FLUID
Increasing Blood Flow Raises Interstitial Fluid Po2
Increasing Tissue Metabolism Decreases Interstitial Fluid Po2
DIFFUSION OF OXYGEN FROM PERIPHERAL CAPILLARIES TO TISSUE CELLS
DIFFUSION OF CO2 FROM PERIPHERAL TISSUE CELLS INTO CAPILLARIES AND FROM PULMONARY CAPILLARIES INTO ALVEOLI
Effect of Tissue Metabolism and Tissue Blood Flow Rate on Interstitial Pco2
ROLE OF HEMOGLOBIN IN OXYGEN TRANSPORT
Reversible Combination of O2 With Hemoglobin
Oxygen-Hemoglobin Dissociation Curve
Maximum Amount of Oxygen That Can Combine With the Hemoglobin of the Blood
Amount of Oxygen Released From Hemoglobin When Systemic Arterial Blood Flows Through Tissues
Transport of Oxygen Is Markedly Increased During Strenuous Exercise
Utilization Coefficient
Hemoglobin “Buffers” Tissue Po2
Hemoglobin Helps Maintain Nearly Constant Po2 in the Tissues
When Atmospheric Oxygen Concentration Changes Markedly, the Buffer Effect of Hemoglobin Still Maintains Almost Constant Tissue Po2
Factors That Shift the Oxygen-Hemoglobin Dissociation Curve—Their Importance for Oxygen Transport
Increased Delivery of Oxygen to Tissues When CO2 and H+ Shift the Oxygen-Hemoglobin Dissociation Curve—the Bohr Effect
Effect of BPG to Cause Rightward Shift of the Oxygen-Hemoglobin Dissociation Curve
Rightward Shift of the Oxygen-Hemoglobin Dissociation Curve During Exercise
Metabolic Use of Oxygen by Cells
Effect of Intracellular Po2 on Oxygen Usage Rate
Effect of Diffusion Distance From the Capillary to the Cell on Oxygen Usage
Effect of Blood Flow on Metabolic Use of Oxygen
Transport of CO2 in Blood
CHEMICAL FORMS IN WHICH CO2 IS TRANSPORTED
Transport of CO2 in a Dissolved State
Transport of CO2 in the Form of Bicarbonate Ion
Carbonic Anhydrase Catalyzes the Reaction of CO2 With Water in Red Blood Cells
Dissociation of Carbonic Acid Into Bicarbonate and Hydrogen Ions
Transport of CO2 in Combination With Hemoglobin and Plasma Proteins—Carbaminohemoglobin
Carbon Dioxide Dissociation Curve
When Oxygen Binds With Hemoglobin, CO2 Is Released (the Haldane Effect) to Increase CO2 Transport
Respiratory Exchange Ratio
Bibliography
Chapter 42: Regulation of Respiration
Respiratory Center
DORSAL RESPIRATORY GROUP OF NEURONS CONTROLS INSPIRATION AND RESPIRATORY RHYTHM
Rhythmical Inspiratory Discharges From the Dorsal Respiratory Group
Inspiratory “Ramp” Signal
PNEUMOTAXIC CENTER LIMITS DURATION OF INSPIRATION AND INCREASES RESPIRATORY RATE
VENTRAL RESPIRATORY GROUP OF NEURONS—FUNCTIONS IN BOTH INSPIRATION AND EXPIRATION
LUNG INFLATION SIGNALS LIMIT INSPIRATION—THE HERING-BREUER INFLATION REFLEX
CONTROL OF OVERALL RESPIRATORY CENTER ACTIVITY
Chemical Control of Respiration
Direct Control of Respiratory Center Activity by Co2 and H+
Chemosensitive Area of the Respiratory Center Beneath the Medulla’s Ventral Surface
Excitation of the Chemosensitive Neurons by H+ Is Likely the Primary Stimulus
CO2 Indirectly Stimulates the Chemosensitive Neurons
Attenuated Stimulatory Effect of CO2 After the First 1 to 2 Days
Quantitative Effects of Blood Pco2 and H+ Concentration on Alveolar Ventilation
Changes in O2 Have Little Direct Effect on Control of the Respiratory Center
Peripheral Chemoreceptor System—Role of Oxygen in Respiratory Control
Decreased Arterial Oxygen Stimulates the Chemoreceptors
Basic Mechanism of Stimulation of the Chemoreceptors by O2 Deficiency. The exact means whereby low Po2 excites the nerve endings...
Increased CO2 and H+ Concentration Stimulates the Chemoreceptors. An increase in CO2 or H+ concentration also excites the chemor...
Effect of Low Arterial Po2 to Stimulate Alveolar Ventilation When Arterial CO2 and H+ Concentrations Remain Normal
Chronic Breathing of Low O2 Stimulates Respiration Even More—The Phenomenon of “Acclimatization”
Composite Effects of Pco2, pH, and Po2 on Alveolar Ventilation
Regulation of Respiration During Exercise
Interrelationship Between Chemical and Nervous Factors in Controlling Respiration During Exercise
Neurogenic Control of Ventilation During Exercise May Be Partly a Learned Response
Bibliography
Chapter 43: Respiratory Insufficiency—Pathophysiology, Diagnosis, Oxygen Therapy
Useful Methods for Studying Respiratory Abnormalities
Study of Blood Gases and Blood ph
Determination of Blood pH
Determination of Blood CO2
Determination of Blood Po2
MEASUREMENT OF MAXIMUM EXPIRATORY FLOW
Abnormalities of the Maximum Expiratory Flow-Volume Curve
FORCED EXPIRATORY VITAL CAPACITY AND FORCED EXPIRATORY VOLUME
PATHOPHYSIOLOGY OF SPECIFIC PULMONARY ABNORMALITIES
Chronic Pulmonary Emphysema
PNEUMONIA—LUNG INFLAMMATION AND FLUID IN ALVEOLI
Atelectasis—Collapse of the Alveoli
Airway Obstruction Causes Lung Collapse
Lack of “Surfactant” as a Cause of Lung Collapse
ASTHMA—SPASMODIC CONTRACTION OF SMOOTH MUSCLES IN BRONCHIOLES
Tuberculosis
Hypoxia and Oxygen Therapy
Inadequate Tissue Capability to Use Oxygen
Effects of Hypoxia on the Body
OXYGEN THERAPY IN DIFFERENT TYPES OF HYPOXIA
Cyanosis
Hypercapnia—Excess Carbon Dioxide in the Body Fluids
Dyspnea
Artificial Respiration
Resuscitator
Tank Respirator (the “Iron Lung”)
Effect of the Resuscitator and the Tank Respirator on Venous Return
Bibliography
Unit VIII: Aviation, Space, and Deep-Sea Diving Physiology
Chapter 44: Aviation, High Altitude, and Space Physiology
EFFECTS OF LOW OXYGEN PRESSURE ON THE BODY
Barometric Pressures at Different Altitudes
Alveolar Po2 at Different Elevations
Carbon Dioxide and Water Vapor Decrease the Alveolar Oxygen
Alveolar Po2 at Different Altitudes
Saturation of Hemoglobin With Oxygen at Different Altitudes
EFFECT OF BREATHING PURE OXYGEN ON ALVEOLAR Po2 AT DIFFERENT ALTITUDES
The “Ceiling” When Breathing Air and When Breathing Oxygen in an Unpressurized Airplane
ACUTE EFFECTS OF HYPOXIA
Acclimatization to Low Po2
Increased Pulmonary Ventilation—Role of Arterial Chemoreceptors
Increase in Red Blood Cells and Hemoglobin Concentration During Acclimatization
Increased Diffusing Capacity After Acclimatization
Peripheral Circulatory System Changes During Acclimatization—Increased Tissue Capillarity
Cellular Acclimatization
HYPOXIA-INDUCIBLE FACTORS—A“MASTER SWITCH” FOR THE BODY’S RESPONSE TO HYPOXIA
NATURAL ACCLIMATIZATION OF NATIVE PEOPLE LIVING AT HIGH ALTITUDES
REDUCED WORK CAPACITY AT HIGH ALTITUDES AND POSITIVE EFFECT OF ACCLIMATIZATION
ACUTE MOUNTAIN SICKNESS AND HIGH-ALTITUDE PULMONARY EDEMA
CHRONIC MOUNTAIN SICKNESS
Bibliography
Chapter 45: Physiology of Deep Sea Diving and Other Hyperbaric Conditions
Relationship of Pressure to Sea Depth
Effect of Sea Depth on the Volume of Gases—Boyle’s Law
Effect of High Partial Pressures of Individual Gases on the Body
NITROGEN NARCOSIS AT HIGH NITROGEN PRESSURES
Oxygen Toxicity at High Pressures
Effect of Very High Po2 on Blood Oxygen Transport
Effect of High Alveolar Po2 on Tissue Po2
Acute Oxygen Poisoning
Excessive Intracellular Oxidation as a Cause of Nervous System Oxygen Toxicity—Oxidizing Free Radicals
Chronic Oxygen Poisoning Causes Pulmonary Disability
Carbon Dioxide Toxicity at Great Depths in the Sea
Decompression of the Diver After Excess Exposure to High Pressure
Volume of Nitrogen Dissolved in the Body Fluids at Different Depths
Decompression Sickness (Also Known as Bends, Compressed Air Sickness, Caisson Disease, Diver’s Paralysis, Dysbarism)
Symptoms of Decompression Sickness (“Bends”)
Nitrogen Elimination From the Body; Decompression Tables
Tank Decompression and Treatment of Decompression Sickness
Self­Contained Underwater Breathing Apparatus (Scuba) Diving
Bibliography
Unit IX: The Nervous System: A. General Principles and Sensory Physiology
Chapter 46: Organization of the Nervous System, Basic Functions of Synapses, and Neurotransmitters
GENERAL DESIGN OF THE NERVOUS SYSTEM
Central Nervous System Neuron: The Basic Functional Unit
SENSORY PART OF THE NERVOUS SYSTEM—SENSORY RECEPTORS
MOTOR PART OF THE NERVOUS SYSTEM—EFFECTORS
PROCESSING OF INFORMATION—INTEGRATIVE FUNCTION OF THE NERVOUS SYSTEM
ROLE OF SYNAPSES IN PROCESSING INFORMATION
STORAGE OF INFORMATION—MEMORY
Major Levels of Central Nervous System Function
Spinal Cord Level
Lower Brain or Subcortical Level
Higher Brain or Cortical Level
Comparison of the Nervous System to A Computer
Central Nervous System Synapses
TYPES OF SYNAPSES—CHEMICAL AND ELECTRICAL
“One­Way” Conduction at Chemical Synapses
PHYSIOLOGIC ANATOMY OF THE SYNAPSE
Presynaptic Terminals
Transmitter Release From Presynaptic Terminals—Role of Calcium Ions
Transmitter Actions on Postsynaptic Neurons—Function of Receptor Proteins
Ion Channels
“Second Messenger” System in the Postsynaptic Neuron
Excitatory or Inhibitory Receptors in the Postsynaptic Membrane
Excitation
Inhibition
CHEMICAL SUBSTANCES THAT FUNCTION AS SYNAPTIC TRANSMITTERS
Small­Molecule, Rapidly Acting Transmitters
Recycling of Small­Molecule Types of Vesicles
Characteristics of Some Important Small­Molecule Transmitters
Neuropeptides
Neuropeptide and Small­Molecule Transmitters May Coexist in the Same Neurons
ELECTRICAL EVENTS DURING NEURONAL EXCITATION
Resting Membrane Potential of the Neuronal Soma
Concentration Differences of Ions Across the Neuronal Somal Membrane
Uniform Distribution of Electrical Potential Inside the Neuronal Soma
Effect of Synaptic Excitation on the Postsynaptic Membrane—Excitatory Postsynaptic Potential
Generation of Action Potentials in the Initial Segment of the Axon Leaving the Neuron—Threshold for Excitation
Electrical Events During Neuronal Inhibition
Effect of Inhibitory Synapses on the Postsynaptic Membrane—Inhibitory Postsynaptic Potential
Presynaptic Inhibition
Time Course of Postsynaptic Potentials
“Spatial Summation” in Neurons—Threshold for Firing
“Temporal Summation” Caused by Successive Discharges of a Presynaptic Terminal
Simultaneous Summation of Inhibitory and Excitatory Postsynaptic Potentials
Facilitation of Neurons
Special Functions of Dendrites for Exciting Neurons
Large Spatial Field of Excitation of Dendrites
Most Dendrites Cannot Transmit Action Potentials—But They Can Transmit Signals Within the Same Neuron by Electrotonic Conduction
Decrement of Electrotonic Conduction in the Dendrites—Greater Excitatory (or Inhibitory) Effect by Synapses Located Near the Soma
Summation of Excitation and Inhibition in Dendrites
Excitation State of the Neuron and Rate of Firing
“Excitatory State” Is the Summated Degree of Excitatory Drive to the Neuron
SPECIAL CHARACTERISTICS OF SYNAPTIC TRANSMISSION
Fatigue of Synaptic Transmission
Effect of Acidosis or Alkalosis on Synaptic Transmission
Effect of Hypoxia on Synaptic Transmission
Effect of Drugs on Synaptic Transmission
Synaptic Delay
Bibliography
Chapter 47: Sensory Receptors, Neuronal Circuits for Processing Information
Types of Sensory Receptors and the Stimuli they Detect
Differential Sensitivity of Receptors
Modality of Sensation—The “Labeled Line” Principle
TRANSDUCTION OF SENSORY STIMULI INTO NERVE IMPULSES
Local Electrical Currents at Nerve Endings—Receptor Potentials
Mechanisms of Receptor Potentials
Maximum Receptor Potential Amplitude
Relation of the Receptor Potential to Action Potentials
Receptor Potential of the Pacinian Corpuscle—an Example of Receptor Function
Relation Between Stimulus Intensity and the Receptor Potential
Adaptation of Receptors
Mechanisms by Which Receptors Adapt
Slowly Adapting Receptors Detect Continuous Stimulus Strength—the “Tonic” Receptors
Rapidly Adapting Receptors Detect Change in Stimulus Strength—the “Rate Receptors,” “Movement Receptors,” or “Phasic Receptors.”
Predictive Function of the Rate Receptors
Signal Intensity Transmission in Nerve Tracts—Spatial and Temporal Summation
Spatial Summation
Temporal Summation
Transmission and Processing of Signals in Neuronal Pools
Relaying of Signals Through Neuronal Pools
Organization of Neurons for Relaying Signals
Threshold and Subthreshold Stimuli—Excitation or Facilitation
Inhibition of a Neuronal Pool
Divergence of Signals Passing Through Neuronal Pools
Convergence of Signals
Neuronal Circuit With Both Excitatory and Inhibitory Output Signals
PROLONGATION OF A SIGNAL BY A NEURONAL POOL—AFTERDISCHARGE
Synaptic Afterdischarge
Reverberatory (Oscillatory) Circuit as a Cause of Signal Prolongation
Signal Prolongation Characteristics of a Reverberatory Circuit
Continuous Signal Output From Some Neuronal Circuits
Continuous Discharge Caused by Intrinsic Neuronal Excitability
Continuous Signals Emitted From Reverberating Circuits as a Means for Transmitting Information
Rhythmical Signal Output
Instability and Stability of Neuronal Circuits
INHIBITORY CIRCUITS AS A MECHANISM FOR STABILIZING NERVOUS SYSTEM FUNCTION
SYNAPTIC FATIGUE AS A MEANS OF STABILIZING THE NERVOUS SYSTEM
Automatic Short­Term Adjustment of Pathway Sensitivity by the Fatigue Mechanism
Long-Term Changes in Synaptic Sensitivity Caused by Automatic Downregulation or Upregulation of Synaptic Receptors
Bibliography
Chapter 48: Somatic Sensations: I. General Organization, Tactile and Position Senses
Classification of Somatic Senses
Other Classifications of Somatic Sensations
Detection and Transmission of Tactile Sensations
Interrelations Among the Tactile Sensations of Touch, Pressure, and Vibration
Tactile Receptors
Transmission of Tactile Signals in Peripheral Nerve Fibers
Detection of Vibration
Detection of Tickle and Itch by Mechanoreceptive Free Nerve Endings
Sensory Pathways for Transmitting Somatic Signals Into the Central Nervous System
TRANSMISSION IN THE DORSAL COLUMN–MEDIAL LEMNISCAL SYSTEM
Anatomy of the Dorsal Column–Medial Lemniscal System
Spatial Orientation of the Nerve Fibers in the Dorsal Column–Medial Lemniscal System
SOMATOSENSORY CORTEX
Somatosensory Areas I and II
Spatial Orientation of Signals From Different Parts of the Body in Somatosensory Area I
Layers of the Somatosensory Cortex and Their Function
The Sensory Cortex Is Organized in Vertical Columns of Neurons; Each Column Detects a Different Sensory Spoton the Body With a Specific Sensory Modality
Functions of Somatosensory Area I
SOMATOSENSORY ASSOCIATION AREAS
Amorphosynthesis Effect of Removing the Somatosensory Association Area
Characteristics of Dorsal Column–Medial Lemniscal Signal Transmission and Analysis
Basic Neuronal Circuit in the Dorsal Column–Medial Lemniscal System
Two­Point Discrimination
Effect of Lateral Inhibition to Increase the Degree of Contrast in the Perceived Spatial Pattern
Transmission of Rapidly Changing and Repetitive Sensations
Vibratory Sensation
Position Senses
Position Sensory Receptors
Processing of Position Sense Information in the Dorsal Column–Medial Lemniscal Pathway
Transmission of Sensory Signals in the Anterolateral Pathway
CHARACTERISTICS OF TRANSMISSION IN THE ANTEROLATERAL PATHWAY
Bibliography
Chapter 49: Somatic Sensations: II. Pain, Headache, and Thermal Sensations
Fast Pain and Slow Pain and Their Qualities
PAIN RECEPTORS AND THEIR STIMULATION
Pain Receptors Are Free Nerve Endings
Mechanical, Thermal, and Chemical Stimuli Excite Pain Receptors
Nonadapting Nature of Pain Receptors
Rate of Tissue Damage as a Stimulus for Pain
Special Importance of Chemical Pain Stimuli During Tissue Damage
Tissue Ischemia as a Cause of Pain
Muscle Spasm as a Cause of Pain
Dual Pathways for Transmission of Pain Signals Into the Central Nervous System
PERIPHERAL PAIN FIBERS—“FAST” AND “SLOW” FIBERS
DUAL PAIN PATHWAYS IN THE CORD AND BRAIN STEM—THE NEOSPINOTHALAMIC TRACT AND THE PALEOSPINOTHALAMIC TRACT
Neospinothalamic Tract for Fast Pain
Termination of the Neospinothalamic Tract in the Brain Stem and Thalamus
The Nervous System Can Localize Fast Pain in the Body
Glutamate, the Probable Neurotransmitter of the Type Aδ Fast Pain Fibers
Paleospinothalamic Pathway for Transmitting Slow­Chronic Pain
Substance P, the Probable Slow­Chronic Neurotransmitter of Type C Nerve Endings
Projection of Paleospinothalamic Pathway (Slow­Chronic Pain Signals) Into the Brain Stem and Thalamus
Poor Capability of the Nervous System to Localize Precisely the Source of Pain Transmitted in the Slow­Chronic Pathway
Function of the Reticular Formation, Thalamus, and Cerebral Cortex in the Appreciation of Pain
Special Capability of Pain Signals to Arouse Overall Brain Excitability
Surgical Interruption of Pain Pathways
Pain Suppression (Analgesia) System in the Brain and Spinal Cord
The Brain’s Opiate System—Endorphins and Enkephalins
Referred Pain
Mechanism of Referred Pain
Visceral Pain
“PARIETAL PAIN” CAUSED BY VISCERAL DISEASE
LOCALIZATION OF VISCERAL PAIN—“VISCERAL” AND “PARIETAL” PAIN TRANSMISSION PATHWAYS
Localization of Referred Pain Transmitted via Visceral Pathways
Parietal Pathway for Transmission of Abdominal and Thoracic Pain
Thermal Sensations
Thermal Receptors and Their Excitation
Stimulation of Thermal Receptors—Sensations of Cold, Cool, Indifferent, Warm, and Hot
Stimulatory Effects of Rising and Falling Temperature—Adaptation of Thermal Receptors
MECHANISM OF STIMULATION OF THERMAL RECEPTORS
Spatial Summation of Thermal Sensations
TRANSMISSION OF THERMAL SIGNALS IN THE NERVOUS SYSTEM
Bibliography
Unit X: The Nervous System: B. The Special Senses
Chapter 50: The Eye: I. Optics of Vision
Physical Principles of Optics
Optics of the Eye
Consideration of All Refractive Surfaces of the Eye as a Single Lens—The “Reduced” Eye
Formation of an Image on the Retina
Mechanism of “accommodation”
Accommodation Is Controlled by Parasympathetic Nerves
Presbyopia—Loss of Accommodation by the Lens
Pupillary Diameter
“Depth of Focus” of the Lens System Increases With Decreasing Pupillary Diameter
Visual Acuity
Clinical Method for Stating Visual Acuity
DETERMINATION OF DISTANCE OF AN OBJECT FROM THE EYE—”DEPTH PERCEPTION”
Determination of Distance by Sizes of Retinal Images of Known Objects
Determination of Distance by Moving Parallax
Determination of Distance by Stereopsis—Binocular Vision
Fluid System of the Eye—Intraocular Fluid
FORMATION OF AQUEOUS HUMOR BY THE CILIARY BODY
OUTFLOW OF AQUEOUS HUMOR FROM THE EYE
Intraocular Pressure
Measuring Intraocular Pressure by Tonometry
Bibliography
Chapter 51: The Eye: II. Receptor and Neural Function of the Retina
Anatomy and Function of the Structural Elements of the Retina
The Retina Is Composed of Ten Layers or Boundaries
Foveal Region of the Retina and Its Importance in Acute Vision
Rods and Cones Are Essential Components of Photoreceptors
Pigment Layer of the Retina
Photochemistry of Vision
Rhodopsin­Retinal Visual Cycle and Excitation of the Rods
Rhodopsin and Its Decomposition by Light Energy
Re­Formation of Rhodopsin
Role of Vitamin A for Formation of Rhodopsin
Excitation of the Rod When Rhodopsin Is Activated by Light
The Rod Receptor Hyperpolarizes in Response to Light
Duration of the Receptor Potential, and Logarithmic Relation of the Receptor Potential to Light Intensity
Mechanism Whereby Rhodopsin Decomposition Decreases Membrane Sodium Conductance—The Excitation “Cascade"
Photochemistry of Color Vision by the Cones
AUTOMATIC REGULATION OF RETINAL SENSITIVITY—LIGHT AND DARK ADAPTATION
Value of Light and Dark Adaptation in Vision
Color Vision
Spectral Sensitivities of the Three Types of Cones
Interpretation of Color in the Nervous System
Perception of White Light
Neural Function of the Retina
The Visual Pathway From the Cones to the Ganglion Cells Functions Differently From the Rod Pathway
Neurotransmitters Released by Retinal Neurons
Transmission of Most Signals Occurs in the Retinal Neurons by Electrotonic Conduction, Not by Action Potentials
Lateral Inhibition to Enhance Visual Contrast—Function of the Horizontal Cells
Depolarizing and Hyperpolarizing Bipolar Cells
Amacrine Cells and Their Functions
GANGLION CELLS AND OPTIC NERVE FIBERS
Retinal Ganglion Cells and Their Respective Fields
W, X, and Y Cells
P and M Cells
Excitation of the Ganglion Cells
Spontaneous, Continuous Action Potentials in the Ganglion Cells
Transmission of Changes in Light Intensity—The On-Off Response
Transmission of Signals Depicting Contrasts in the Visual Scene—The Role of Lateral Inhibition
Transmission of Color Signals by the Ganglion Cells
Bibliography
Chapter 52: The Eye: III. Central Neurophysiology of Vision
Visual Pathways
FUNCTION OF THE DORSAL LATERAL GENICULATE NUCLEUS OF THE THALAMUS
Organization and Function of the Visual Cortex
Primary Visual Cortex
Secondary Visual Areas of the Cortex
The Primary Visual Cortex has six Major Layers
Vertical Neuronal Columns in the Visual Cortex
“Color Blobs” in the Visual Cortex
Interaction of Visual Signals From the Two Separate Eyes
Two Major Pathways for Analysis of Visual Information: (1) The Fast “Position” and “Motion” Pathway and (2) the Accurate Color Pathway
Analysis of Contrasts in Visual Images
Visual Cortex Also Detects Orientation of Lines and Borders—“Simple” Cells
NEURONAL PATTERNS OF STIMULATION DURING ANALYSIS OF VISUAL IMAGES
Analysis of Contrasts in Visual Images
Visual Cortex Also Detects Orientation of Lines and Borders—“Simple” Cells
“Complex” Cells Detect Line Orientation When a Line Is Displaced Laterally or Vertically in the Visual Field
Detection of Lines of Specific Lengths, Angles, or Other Shapes
DETECTION OF COLOR
Eye Movements and Their Control
Muscular Control of Eye Movements
Neural Pathways for Control of Eye Movements
Fixation Movements of the Eyes
Mechanism of Involuntary Locking Fixation—Role of the Superior Colliculi
Saccadic Movement of the Eyes—A Mechanism of Successive Fixation Points
Saccadic Movements During Reading
Fixation on Moving Objects—“Pursuit Movement”
Superior Colliculi Are Mainly Responsible for Turning the Eyes and Head Toward a Visual Disturbance
“FUSION” OF THE VISUAL IMAGES FROM THE TWO EYES
Neural Mechanism of Stereopsis for Judging Distances of Visual Objects
AUTONOMIC CONTROL OF ACCOMMODATION AND PUPILLARY APERTURE
Autonomic Nerves to the Eyes
CONTROL OF ACCOMMODATION (FOCUSING THE EYES)
Control of Pupillary Diameter
Pupillary Light Reflex
Bibliography
Chapter 53: The Sense of Hearing
TYMPANIC MEMBRANE AND THE OSSICULAR SYSTEM
CONDUCTION OF SOUND FROM THE TYMPANIC MEMBRANE TO THE COCHLEA
“Impedance Matching” by the Ossicular System
Attenuation of Sound by Contraction of the Tensor Tympani and Stapedius Muscles
TRANSMISSION OF SOUND THROUGH BONE
COCHLEA
FUNCTIONAL ANATOMY OF THE COCHLEA
Basilar Membrane and Resonance in the Cochlea
TRANSMISSION OF SOUND WAVES IN THE COCHLEA—“TRAVELING WAVE”
Vibration Patterns of the Basilar Membrane for Different Sound Frequencies
Vibration Amplitude Pattern of the Basilar Membrane
FUNCTION OF THE ORGAN OF CORTI
Excitation of the Hair Cells
Auditory Signals Are Transmitted Mainly by the Inner Hair Cells
Hair Cell Receptor Potentials and Excitation of Auditory Nerve Fibers
DETERMINATION OF SOUND FREQUENCY—THE “PLACE” PRINCIPLE
DETERMINATION OF LOUDNESS
Detection of Changes in Loudness—The Power Law
Decibel Unit
Threshold for Hearing Sound at Different Frequencies
Frequency Range of Hearing
CENTRAL AUDITORY MECHANISMS
AUDITORY NERVOUS PATHWAYS
FUNCTION OF THE CEREBRAL CORTEX IN HEARING
Sound Frequency Perception in the Primary Auditory Cortex
Discrimination of Sound “Patterns” by the Auditory Cortex
DETERMINATION OF THE DIRECTION FROM WHICH SOUND COMES
Neural Mechanisms for Detecting Sound Direction
Bibliography
Chapter 54: The Chemical Senses—Taste and Smell
Sense of Taste
Primary Taste Sensations
Sour Taste
Salty Taste
Sweet Taste
Bitter Taste
Umami Taste
Threshold for Taste
Taste Blindness
Taste Buds and Their Function
Location of the Taste Buds
Specificity of Taste Buds for a Primary Taste Stimulus
Mechanism of Stimulation of Taste Buds
Receptor Potential
Generation of Nerve Impulses by the Taste Bud
TRANSMISSION OF TASTE SIGNALS INTO THE CENTRAL NERVOUS SYSTEM
Taste Reflexes Are Integrated in the Brain Stem
Rapid Adaptation of Taste
TASTE PREFERENCE AND CONTROL OF THE DIET
Sense of Smell
Olfactory Membrane
Olfactory Cells Are the Receptor Cells for Smell Sensation
Stimulation of the Olfactory Cells
Mechanism of Excitation of the Olfactory Cells
Membrane Potentials and Action Potentials in Olfactory Cells
Rapid Adaptation of Olfactory Sensations
Search for the Primary Sensations of Smell
Affective Nature of Smell
Threshold for Smell
Gradations of Smell Intensities
TRANSMISSION OF SMELL SIGNALS INTO THE CENTRAL NERVOUS SYSTEM
Transmission of Olfactory Signals Into the Olfactory Bulb
Primitive and Newer Olfactory Pathways Into the Central Nervous System
The Primitive Olfactory System—The Medial Olfactory Area
The Less Old Olfactory System—The Lateral Olfactory Area
The Newer Pathway
Summary
Centrifugal Control of Activity in the Olfactory Bulb by the Central Nervous System
Bibliography
Unit XI: The Nervous System: C. Motor and Integrative Neurophysiology
Chapter 55: Spinal Cord Motor Functions; the Cord Reflexes
Organization of the Spinal Cord for Motor Functions
Anterior Motor Neurons
Alpha Motor Neurons
Gamma Motor Neurons
Interneurons
Muscle Sensory Receptors—Muscle Spindles and Golgi Tendon Organs—and Their Roles in Muscle Control
Receptor Function of the Muscle Spindle
Structure and Motor Innervation of the Muscle Spindle
Sensory Innervation of the Muscle Spindle
Primary Ending
Secondary Ending
Division of the Intrafusal Fibers Into Nuclear Bag and Nuclear Chain Fibers—Dynamic and Static Responses of the Muscle Spindle
The Primary and the Secondary Endings Both Respond to the Length of the Receptor—“Static” Response
The Primary Ending (but Not the Secondary Ending) Responds to Rate of Change of Receptor Length—“Dynamic” Response
Control of Intensity of the Static and Dynamic Responses by the Gamma Motor Nerves
Continuous Discharge of the Muscle Spindles Under Normal Conditions
Muscle Stretch Reflex
Neuronal Circuitry of the Stretch Reflex
Dynamic Stretch Reflex and Static Stretch Reflexes
“Damping” Function of the Dynamic and Static Stretch Reflexes in Smoothing Muscle Contraction
ROLE OF THE MUSCLE SPINDLE IN VOLUNTARY MOTOR ACTIVITY
Brain Areas for Control of the Gamma Motor System
The Muscle Spindle System Stabilizes Body Position During Tense Action
Golgi Tendon Reflex
Golgi Tendon Organ Helps Control Muscle Tension
Transmission of Impulses From the Tendon Organ Into the Central Nervous System
The Tendon Reflex Prevents Excessive Tension on the Muscle
Possible Role of the Tendon Reflex to Equalize Contractile Force Among the Muscle Fibers
Function of the Muscle Spindles and Golgi Tendon Organs in Motor Control by Higher Levels of the Brain
Flexor Reflex and the Withdrawal Reflexes
Neuronal Mechanism of the Flexor Reflex
Pattern of Withdrawal During Flexor Reflex
Crossed Extensor Reflex
Neuronal Mechanism of the Crossed Extensor Reflex
Reciprocal Inhibition and Reciprocal Innervation
REFLEXES OF POSTURE AND LOCOMOTION
Postural and Locomotive Reflexes of the Cord
Positive Supportive Reaction
Cord “Righting” Reflexes
Stepping and Walking Movements
Rhythmical Stepping Movements of a Single Limb
Reciprocal Stepping of Opposite Limbs
Diagonal Stepping of All Four Limbs—“Mark Time” Reflex
Bibliography
Chapter 56: Cortical and Brain Stem Control of Motor Function
Motor Cortex and Corticospinal Tract
Primary Motor Cortex
Premotor Area
Supplementary Motor Area
SOME SPECIALIZED AREAS OF MOTOR CONTROL FOUND IN THE HUMAN MOTOR CORTEX
Broca’s Area (Motor Speech Area)
“Voluntary” Eye Movement Field
Head Rotation Area
Area for Hand Skills
TRANSMISSION OF SIGNALS FROM THE MOTOR CORTEX TO THE MUSCLES
Corticospinal (Pyramidal) Tract
THE RED NUCLEUS SERVES AS AN ALTERNATIVE PATHWAY FOR TRANSMITTING CORTICAL SIGNALS TO THE SPINAL CORD
The Corticorubrospinal System Is an Accessory Pathway for Transmitting Relatively Discrete Signals From the Motor Cortex to the Spinal Cord
EXCITATION OF THE SPINAL CORD MOTOR CONTROL AREAS BY THE PRIMARY MOTOR CORTEX AND RED NUCLEUS
Neurons in the Motor Cortex Are Arranged in Vertical Columns
Each Column of Neurons Functions as an Integrative Processing System
Dynamic and Static Signals Are Transmitted by the Pyramidal Neurons
Somatosensory Feedback to the Motor Cortex Helps Control Precision of Muscle Contraction
Stimulation of the Spinal Motor Neurons
Patterns of Movement Elicited by Spinal Cord Centers
Control of Motor Functions by the Brain Stem
SUPPORT OF THE BODY AGAINST GRAVITY—ROLES OF THE RETICULAR AND VESTIBULAR NUCLEI
Excitatory­Inhibitory Antagonism Between Pontine and Medullary Reticular Nuclei
Pontine Reticular System Transmits Excitatory Signals
Medullary Reticular System Transmit Inhibitory Signals
Role of the Vestibular Nuclei to Excite the Antigravity Muscles
The Decerebrate Animal Develops Spastic Rigidity
VESTIBULAR SENSATIONS AND MAINTENANCE OF EQUILIBRIUM
Vestibular Apparatus
“Maculae”—Sensory Organs of the Utricle and Saccule for Detecting Orientation of the Head With Respect to Gravity
Directional Sensitivity of the Hair Cells—Kinocilium
Semicircular Ducts
Function of the Utricle and Saccule in the Maintenance of Static Equilibrium
Detection of Linear Acceleration by the Utricle and Saccule Maculae
Detection of Head Rotation by the Semicircular Ducts
“Predictive” Function of the Semicircular Duct System in the Maintenance of Equilibrium
Bibliography
Chapter 57: Cerebellum and Basal Ganglia Contributions to Overall Motor Control
The Cerebellum and its Motor Functions
FUNCTIONAL UNIT OF THE CEREBELLAR CORTEX—THE PURKINJE AND DEEP NUCLEAR CELLS
Neuronal Circuit of the Functional Unit
Purkinje Cells and Deep Nuclear Cells Fire Continuously Under Normal Resting Conditions
Balance Between Excitation and Inhibition at the Deep Cerebellar Nuclei
Basket Cells and Stellate Cells Cause Lateral Inhibition of Purkinje Cells in the Cerebellum
Turn­On/Turn-Off and Turn­Off/Turn­On Output Signals From the Cerebellum
The Purkinje Cells “Learn” to Correct Motor Errors—Role of the Climbing Fibers
FUNCTION OF THE CEREBELLUM IN OVERALL MOTOR CONTROL
The Vestibulocerebellum Functions in Association With the Brain Stem and Spinal Cord to Control Equilibrium and Postural Movements
Spinocerebellum—Feedback Control of Distal Limb Movements via the Intermediate Cerebellar Cortex and the Interposed Nucleus
Function of the Cerebellum to Prevent Overshoot and to “Damp” Movements
Cerebellar Control of Ballistic Movements
Cerebrocerebellum—Function of the Large Lateral Zone of the Cerebellar Hemisphere to Plan, Sequence, and Time Complex Movements
Planning of Sequential Movements
Timing Function for Sequential Movements
Extramotor Predictive Functions of the Cerebrocerebellum
The Basal Ganglia and Their Motor Functions
NEURONAL CIRCUITRY OF THE BASAL GANGLIA
FUNCTION OF THE BASAL GANGLIA IN EXECUTING PATTERNS OF MOTOR ACTIVITY—THE PUTAMEN CIRCUIT
Neural Pathways of the Putamen Circuit
Abnormal Function in the Putamen Circuit: Athetosis, Hemiballismus, and Chorea
ROLE OF THE BASAL GANGLIA FOR COGNITIVE CONTROL OF MOTOR PATTERN SEQUENCES—THE CAUDATE CIRCUIT
FUNCTION OF THE BASAL GANGLIA TO CHANGE THE TIMING AND TO SCALE THE INTENSITY OF MOVEMENTS
FUNCTIONS OF SPECIFIC NEUROTRANSMITTER SUBSTANCES IN THE BASAL GANGLIAL SYSTEM
Integration of the Many Parts of the Total Motor Control System
Spinal Level
Hindbrain Level
Motor Cortex Level
Associated Functions of the Cerebellum
Associated Functions of the Basal Ganglia
What drives us to action
Bibliography
Chapter 58: Cerebral Cortex, Intellectual Functions of the Brain, Learning, and Memory
Physiologic Anatomy of the Cerebral Cortex
ANATOMICAL AND FUNCTIONAL RELATIONS OF THE CEREBRAL CORTEX TO THE THALAMUS AND OTHER LOWER CENTERS
Functions of Specific Cortical Areas
Association Areas
Parieto­Occipitotemporal Association Area
Analysis of the Spatial Coordinates of the Body
Wernicke’s Area Is Important for Language Comprehension
The Angular Gyrus Area Is Needed for Initial Processing of Visual Language (Reading)
Area for Naming Objects
Prefrontal Association Area
Broca’s Area Provides the Neural Circuitry for Word Formation. Broca’s area, shown in Figure 58-­5, is located partly in the pos...
Limbic Association Area
Area for Recognition of Faces
COMPREHENSIVE INTERPRETATIVE FUNCTION OF THE POSTERIOR SUPERIOR TEMPORAL LOBE—”WERNICKE’S AREA” (A GENERAL INTERPRETATIVE AREA)
Angular Gyrus—Interpretation of Visual Information
Concept of the Dominant Hemisphere
Role of Language in the Function of Wernicke’s Area and in Intellectual Functions
FUNCTIONS OF THE PARIETO-OCCIPITOTEMPORAL CORTEX IN THE NONDOMINANT HEMISPHERE
HIGHER INTELLECTUAL (“EXECUTIVE”) FUNCTIONS OF THE PREFRONTAL ASSOCIATION AREAS
Decreased Aggressiveness and Inappropriate Social Responses
Inability to Progress Toward Goals or to Carry Through Sequential Thoughts
Elaboration of Thought, Prognostication, and Performance of Higher Intellectual Functions by the Prefrontal Areas—Concept of a “Working Memory"
THE CORPUS CALLOSUM AND ANTERIOR COMMISSURE TRANSFER THOUGHTS, MEMORIES, TRAINING, AND OTHER INFORMATION BETWEEN THE TWO CEREBRAL HEMISPHERES
Thoughts, Consciousness, and Memory
MEMORY—ROLES OF SYNAPTIC FACILITATION AND SYNAPTIC INHIBITION
Positive and Negative Memory—“Sensitization” or “Habituation” of Synaptic Transmission
Classification of Memories
Short­Term Memory
Intermediate Long­Term Memory
Memory Based on Chemical Changes in Presynaptic Terminals or Postsynaptic Neuronal Membranes
Molecular Mechanism of Intermediate Memory
Mechanism for Habituation
Mechanism for Facilitation
Long­Term Memory
Structural Changes Occur in Synapses During Development of Long­Term Memory
Number of Neurons and Their Connectivities Often Change Significantly During Learning
Consolidation of Memory
Rehearsal Enhances the Transference of Short­Term Memory Into Long­Term Memory
New Memories Are Codified During Consolidation
Role of the Hippocampus and Other Brain Regions in Memory
Anterograde Amnesia—Inability to Create New Declarative Long-Term Memories After Hippocampal Lesions
Retrograde Amnesia—Inability to Recall Memories From the Past After Hippocampal or Thalmic Lesions
Hippocampi Are Not Important in Reflexive Learning
Bibliography
Chapter 59: The Limbic System and the Hypothalamus—Behavioral and Motivational Mechanisms of the Brain
Activating—Driving Systems Of The Brain
Control Of Cerebral Activity By Continuous Excitatory Signals From The Brain Stem
Reticular Excitatory Area of the Brain Stem—a Driver of Brain Activity
Excitation of the Reticular Excitatory Area by Peripheral Sensory Signals
Increased Activity of the Excitatory Area Causedby Feedback Signals Returning From the Cerebral Cortex
The Thalamus Is a Distribution Center That Controls Activity in Specific Regions of the Cortex
A Reticular Inhibitory Area Is Located in the Lower Brain Stem
NEUROHORMONAL CONTROL OF BRAIN ACTIVITY
Neurohormonal Systems in the Human Brain
Other Neurotransmitters and Neurohormonal Substances Secreted in the Brain
Limbic System
FUNCTIONAL ANATOMY OF THE LIMBIC SYSTEM—KEY POSITION OF THE HYPOTHALAMUS
The Hypothalamus, a Major Control Headquarters for the Limbic System
VEGETATIVE AND ENDOCRINE CONTROL FUNCTIONS OF THE HYPOTHALAMUS
Cardiovascular Regulation
Body Temperature Regulation
Body Water Regulation
Regulation of Uterine Contractility and Milk Ejection from the Breasts
Gastrointestinal and Feeding Regulation
Hypothalamic Control of Endocrine Hormone Secretion by the Anterior Pituitary Gland
Hypothalamic Control of Circadian Rhythms—The Suprachiasmatic Nucleus
Summary
Behavioral Functions of the Hypothalamus and Associated Limbic Structures
Effects Caused by Stimulation of the Hypothalamus
Effects Caused by Hypothalamic Lesions
“REWARD” AND “PUNISHMENT” FUNCTION OF THE LIMBIC SYSTEM
Reward Centers
Punishment Centers
Association of Rage With Punishment Centers
Placidity and Tameness
IMPORTANCE OF REWARD OR PUNISHMENT ON BEHAVIOR
Effect of Tranquilizers on the Reward or Punishment Centers
Importance of Reward or Punishment in Learning and Memory—Habituation Versus Reinforcement
SPECIFIC FUNCTIONS OF OTHER PARTS OF THE LIMBIC SYSTEM
Functions Of The Hippocampus
Role of the Hippocampus in Learning
Anterograde Amnesia After Bilateral Removal of the Hippocampi
Theoretical Function of the Hippocampus in Learning
Bibliography
Chapter 60: States of Brain Activity—Sleep, Brain Waves, Epilepsy, Psychoses, and Dementia
Sleep
TWO TYPES OF SLEEP—SLOW-WAVE SLEEP AND RAPID EYE MOVEMENT SLEEP
REM (Paradoxical, Desynchronized) Sleep
Slow­Wave Sleep
Basic Theories of Sleep
Sleep Is Caused by an Active Inhibitory Process
Neuronal Centers, Neurohumoral Substances, and Mechanisms That Can Cause Sleep—Possible Role for Serotonin
Lesions in Sleep­Promoting Centers Can Cause Intense Wakefulness
Other Possible Transmitter Substances Related to Sleep
Possible Cause of REM Sleep
Cycle Between Sleep and Wakefulness
SLEEP HAS IMPORTANT PHYSIOLOGICAL FUNCTIONS
Bibliography
Chapter 61: The Autonomic Nervous System and the Adrenal Medulla
General Organization of the Autonomic Nervous System
BASIC CHARACTERISTICS OFS YMPATHETIC AND PARASYMPATHETIC FUNCTION
Cholinergic and Adrenergic Fibers—Secretion of Acetylcholine or Norepinephrine
Mechanisms of Transmitter Secretion and Removal at Postganglionic Endings
Secretion of Acetylcholine and Norepinephrine by Postganglionic Nerve Endings
Synthesis of Acetylcholine, Its Destruction After Secretion, and Its Duration of Action
Synthesis of Norepinephrine, Its Removal, and Its Duration of Action
Receptors on the Effector Organs
Excitation or Inhibition of the Effector Cell by Changing Its Membrane Permeability
Receptor Action by Altering Intracellular “Second Messenger” Enzymes
Two Principal Types of Acetylcholine Receptors—Muscarinic and Nicotinic Receptors
Alpha and Beta Adrenergic Receptors
Function of the Adrenal Medullae
The Adrenal Medullae Support Sympathetic Nervous System Functions. Epinephrine and norepinephrine are almost always released by ...
Tone Caused by Basal Secretion of Epinephrine and Norepinephrine by the Adrenal Medullae. The normal resting rate of secretion b...
Effect of Loss of Sympathetic or Parasympathetic Tone After Denervation. Immediately after a sympathetic or parasympathetic nerv...
EXCITATORY AND INHIBITORY ACTIONS OF SYMPATHETIC AND PARASYMPATHETIC STIMULATION
FUNCTION OF THE ADRENAL MEDULLAE
The Adrenal Medullae Support Sympathetic Nervous System Functions
RELATION OF STIMULUS RATE TO SYMPATHETIC AND PARASYMPATHETIC EFFECTS
SYMPATHETIC AND PARASYMPATHETIC “TONE”
Tone Caused by Basal Secretion of Epinephrine and Norepinephrine by the Adrenal Medullae
Effect of Loss of Sympathetic or Parasympathetic Tone After Denervation
Selective Stimulation of Target Organs by Sympathetic and Parasympathetic Systems or “Mass Discharge”
The Sympathetic System Sometimes Responds by Mass Discharge
The Parasympathetic System Usually Causes Specific Localized Responses
“ALARM” OR “STRESS” RESPONSE OF THE SYMPATHETIC NERVOUS SYSTEM
MEDULLARY, PONTINE, AND MESENCEPHALIC CONTROL OF THE AUTONOMIC NERVOUS SYSTEM
Control of Brain Stem Autonomic Centers by Higher Areas
Bibliography
Chapter 62: Cerebral Blood Flow, Cerebrospinal Fluid, and Brain Metabolism
Cerebral Blood Flow
Regulation of Cerebral Blood Flow
Excesses of CO2 or H+ Concentration Increase Cerebral Blood Flow
Importance of Cerebral Blood Flow Control by CO2 and H+
Oxygen Deficiency as a Regulator of Cerebral Blood Flow
Cerebral Microcirculation
Cerebrospinal Fluid System
CUSHIONING FUNCTION OF THE CEREBROSPINAL FLUID
FORMATION, FLOW, AND ABSORPTION OF CEREBROSPINAL FLUID
Secretion by the Choroid Plexus
Absorption of Cerebrospinal Fluid Through the Arachnoidal Villi
Perivascular Spaces and Cerebrospinal Fluid
Lymphatic Function of the Perivascular Spaces
Brain Metabolism
Total Brain Metabolic Rate and Metabolic Rate of Neurons
Special Requirement of the Brain for Oxygen—Lack of Significant Anaerobic Metabolism
Under Normal Conditions, Most Brain Energy Is Supplied by Glucose
Bibliography
Unit XII: Gastrointestinal Physiology
Chapter 63: General Principles of Gastrointestinal Function—Motility, Nervous Control, and Blood Circulation
GENERAL PRINCIPLES OF GASTROINTESTINAL MOTILITY
Physiologic Anatomy of the Gastrointestinal Wall
Gastrointestinal Smooth Muscle Functions as a Syncytium
Electrical Activity of Gastrointestinal Smooth Muscle
“Slow Waves” Caused by Undulating Changes in Resting Membrane Potential
Spike Potentials
Changes in Voltage of the Resting Membrane Potential
Entry of Calcium Ions Causes Smooth Muscle Contraction
Tonic Contraction of Some Gastrointestinal Smooth Muscle
Neural Control of Gastrointestinal Function—Enteric Nervous System
DIFFERENCES BETWEEN THE MYENTERIC AND SUBMUCOSAL PLEXUSES
TYPES OF NEUROTRANSMITTERS SECRETED BY ENTERIC NEURONS
Autonomic Control of the Gastrointestinal Tract
Parasympathetic Stimulation Increases Activity of the Enteric Nervous System
Sympathetic Stimulation Usually Inhibits Gastrointestinal Tract Activity
Afferent Sensory Nerve Fibers From the Gut
Gastrointestinal Reflexes
Hormonal Control of Gastrointestinal Motility
Functional Movements in the Gastrointestinal Tract
PROPULSIVE MOVEMENTS—PERISTALSIS
Function of the Myenteric Plexus in Peristalsis
Peristaltic Waves Move Toward the Anus With Downstream Receptive Relaxation—“Law of the Gut”
SEGMENTATION CONTRACTIONS—MIXING MOVEMENTS
Gastrointestinal Blood Flow—Splanchnic Circulation
ANATOMY OF THE GASTROINTESTINAL BLOOD SUPPLY
EFFECT OF GUT ACTIVITY AND METABOLIC FACTORS ON GASTROINTESTINAL BLOOD FLOW
Mechanisms of Increased Blood Flow During Gastrointestinal Activity
“Countercurrent” Blood Flow in the Villi
NERVOUS CONTROL OF GASTROINTESTINAL BLOOD FLOW
Importance of Nervous Depression of Gastrointestinal Blood Flow When Other Parts of the Body Need Extra Blood Flow
Bibliography
Chapter 64: Propulsion and Mixing of Food in the Alimentary Tract
Ingestion of Food
Mastication (Chewing)
Swallowing (Deglutition)
Voluntary Stage of Swallowing
Involuntary Pharyngeal Stage of Swallowing
Nervous Initiation of the Pharyngeal Stage of Swallowing
The Pharyngeal Stage of Swallowing Momentarily Interrupts Respiration
The Esophageal Stage of Swallowing Involves Two Types of Peristalsis
Receptive Relaxation of the Stomach
Function of the Lower Esophageal Sphincter (Gastroesophageal Sphincter)
Prevention of Esophageal Reflux by Valvelike Closure of the Distal End of the Esophagus
Motor Functions of the Stomach
Storage Function of the Stomach
FOOD MIXING AND PROPULSION IN THE STOMACH—BASIC ELECTRICAL RHYTHM OF THE STOMACH WALL
Chyme
Hunger Contractions
Stomach Emptying
Intense Antral Peristaltic Contractions During Stomach Emptying—“Pyloric Pump”
Role of the Pylorus in Controlling Stomach Emptying
Regulation of Stomach Emptying
Gastric Factors That Promote Emptying
Effect of Gastric Food Volume on Rate of Emptying
The Hormone Gastrin Promotes Stomach Emptying
Powerful Duodenal Factors That Inhibit Stomach Emptying
Duodenum Enterogastric Nervous Reflexes Inhibit Stomach Emptying
Hormonal Feedback From the Duodenum Inhibits Gastric Emptying—Role of Fats and the Hormone Cholecystokinin
Summary of the Control of Stomach Emptying
Movements of the Small Intestine
MIXING CONTRACTIONS (SEGMENTATION CONTRACTIONS)
Propulsive Movements
Peristalsis in the Small Intestine
Control of Peristalsis by Nervous and Hormonal Signals
Propulsive Effect of the Segmentation Movements
Powerful, Rapid Peristalsis—“Peristaltic Rush”
THE ILEOCECAL VALVE PREVENTS BACKFLOW FROM THE COLON TO THE SMALL INTESTINE
Feedback Control of the Ileocecal Sphincter by Reflexes From the Cecum
Movements of the Colon
Mixing Movements—“Haustrations”
Propulsive Movements—“Mass Movements”
Initiation of Mass Movements by Gastrocolic and Duodenocolic Reflexes
Defecation
Defecation Reflexes
Other Autonomic Reflexes That Affect Bowel Activity
Bibliography
Chapter 65: Secretory Functions of the Alimentary Tract
GENERAL PRINCIPLES OF ALIMENTARY TRACT SECRETION
TYPES OF ALIMENTARY TRACT GLANDS
Basic Mechanisms of Stimulation of the Alimentary Tract Glands
Contact of Food With Gut Epithelium Activates the Enteric Nervous System and Stimulates Secretion
Autonomic Stimulation of Secretion
Parasympathetic Stimulation Increases Alimentary Tract Glandular Secretion Rate
Sympathetic Stimulation Has a Dual Effect on Alimentary Tract Glandular Secretion Rate
Regulation of Glandular Secretion by Hormones
Basic Mechanism of Secretion by Glandular Cells
Secretion of Organic Substances
Water and Electrolyte Secretion
Secretion of Saliva
Saliva Contains a Serous Secretion and a Mucus Secretion
Secretion of Ions in Saliva
NERVOUS REGULATION OF SALIVARY SECRETION
Gastric Secretion
Secretions From the Gastric (Oxyntic) Glands
Basic Mechanism of Hydrochloric Acid Secretion
The Basic Factors That Stimulate Gastric Secretion Are Acetylcholine, Gastrin, and Histamine
Secretion and Activation of Pepsinogen
Secretion of Intrinsic Factor by Parietal Cells
PYLORIC GLANDS SECRETE MUCUS AND GASTRIN
Surface Mucous Cells
Stimulation of Gastric Acid Secretion
Parietal Cells of the Oxyntic Glands Are the Only Cells That Secrete Hydrochloric Acid
Stimulation of Acid Secretion by Gastrin
Regulation of Pepsinogen Secretion
Pancreatic Secretion
Pancreatic Digestive Enzymes
Secretion of Trypsin Inhibit or Prevents Digestion of the Pancreas
Secretion of Bicarbonate Ions
Regulation of Pancreatic Secretion
Basic Stimuli That Cause Pancreatic Secretion
Multiplicative Effects of Different Stimuli
Phases of Pancreatic Secretion
Cephalic and Gastric Phases
Intestinal Phase
Secretin Stimulates Copious Secretion of Bicarbonate Ions, Which Neutralizes Acidic Stomach Chyme
Cholecystokinin Contributes to Control of Digestive Enzyme Secretion by the Pancreas
Bile Secretion by the Liver
PHYSIOLOGIC ANATOMY OF BILIARY SECRETION
The Gallbladder Stores and Concentrates Bile
Composition of Bile
Cholecystokinin Stimulates Gallbladder Emptying
FUNCTION OF BILE SALTS IN FAT DIGESTION AND ABSORPTION
Secretions of the Small Intestine
Secretion of Mucus by Brunner's Glands in the Duodenum
SECRETION OF INTESTINAL DIGESTIVEJUICES BY THE CRYPTS OF LIEBERKÜHN
Mechanism of Secretion of the Watery Fluid
Digestive Enzymes in the Small Intestinal Secretion
REGULATION OF SMALL INTESTINE SECRETION—LOCAL STIMULI
Secretion of Mucus by The Large Intestine
Mucus Secretion
Diarrhea Caused by Excess Secretion of Water and Electrolytes in Response to Irritation
Bibliography
Chapter 66: Digestion and Absorption in the Gastrointestinal Tract
DIGESTION OF VARIOUS FOODS BY HYDROLYSIS
Hydrolysis of Carbohydrates
Hydrolysis of Fats
Hydrolysis of Proteins
Digestion of Carbohydrates
Carbohydrate Foods of the Diet
Digestion of Carbohydrates Begins in the Mouth and Stomach
Digestion of Carbohydrates in the Small Intestine
Digestion by Pancreatic Amylase
Hydrolysis of Disaccharides and Small Glucose Polymers Into Monosaccharides by Intestinal Epithelial Enzymes
Digestion of Proteins
Proteins of the Diet
Digestion of Proteins in the Stomach
Most Protein Digestion Results From Actions of Pancreatic Proteolytic Enzymes
Digestion of Peptides by Peptidases in the Enterocytes That Line the Small Intestinal Villi
Digestion of Fats
Fats of the Diet
Digestion of Fats Occurs Mainly in the Small Intestine
The First Step in Fat Digestion Is Emulsification by Bile Acids and Lecithin
Triglycerides Are Digested by Pancreatic Lipase
End Products of Fat Digestion Are Free Fatty Acids
Bile Salts Form Micelles That Accelerate Fat Digestion
Digestion of Cholesterol Esters and Phospholipids
Basic Principles of Gastrointestinal Absorption
Anatomical Basis of Absorption
Folds of Kerckring, Villi, and Microvilli Increase the Mucosal Absorptive Area by Nearly 1000-Fold
Absorption in the Small Intestine
Isosmotic Absorption of Water
Absorption of Ions
Sodium Is Actively Transported Through the Intestinal Membrane
Osmosis of the Water
Aldosterone Greatly Enhances Sodium Absorption
Absorption of Chloride Ions in the Small Intestine
Absorption of Bicarbonate Ions in the Duodenum and Jejunum
Secretion of Bicarbonate and Absorption of Chloride Ions in the Ileum and Large Intestine
Active Absorption of Calcium, Iron, Potassium, Magnesium, and Phosphate
Absorption of Nutrients
Carbohydrates Are Mainly Absorbed as Monosaccharides
Glucose Is Transported by a Sodium Co­Transport Mechanism
Absorption of Other Monosaccharides
Absorption of Proteins as Dipeptides, Tripeptides, or Amino Acids
Absorption of Fats
Direct Absorption of Fatty Acids Into the Portal Blood
Absorption in the Large Intestine: Formation of Feces
Absorption and Secretion of Electrolytes and Water
Maximum Absorption Capacity of the Large Intestine
Composition of the Feces
Bibliography
Chapter 67: Physiology of Gastrointestinal Disorders
Bibliography
Unit XIII: Metabolism and Temperature Regulation
Chapter 68: Metabolism of Carbohydrates and Formation of Adenosine Triphosphate
Bibliography
Chapter 69: Lipid Metabolism
Basic Chemical Structure of Triglycerides (Neutral Fat)
TRANSPORT OF LIPIDS IN THE BODY FLUIDS
Transport of Triglycerides and Other Lipids From the Gastrointestinal Tract by Lymph—the Chylomicrons
REMOVAL OF THE CHYLOMICRONS FROM THE BLOOD
Chylomicron Triglycerides Are Hydrolyzed by Lipoprotein Lipase, and Fat Is Stored in Adipose Tissue
Bibliography
Chapter 70: Protein Metabolism
Bibliography
Chapter 71: The Liver
Bibliography
Chapter 72: Dietary Balances; Regulation of Feeding; Obesity and Starvation; Vitamins and Minerals
ENERGY INTAKE AND OUTPUT BALANCED UNDER STEADY­STATE CONDITIONS
REGULATION OF FOOD INTAKE AND ENERGY STORAGE
NEURAL CENTERS REGULATE FOOD INTAKE
The Hypothalamus Contains Hunger and Satiety Centers
Neurons and Neurotransmitters in the Hypothalamus That Stimulate or Inhibit Feeding
Neural Centers That Influence the Mechanical Process of Feeding
FACTORS THAT REGULATE QUANTITY OF FOOD INTAKE
Short­Term Regulation of Food Intake
Gastrointestinal Filling Inhibits Feeding
Gastrointestinal Hormonal Factors Suppress Feeding
Ghrelin, a Gastrointestinal Hormone, Increases Feeding
Oral Receptors Meter Food Intake
Intermediate­ and Long­Term Regulation of Food Intake
Effect of Blood Concentrations of Glucose, Amino Acids, and Lipids on Hunger and Feeding
Temperature Regulation and Food Intake
Feedback Signals From Adipose Tissue Regulate Food Intake
Summary of Long-Term Regulation
Importance of Having Both Long­ and Short­Term Regulatory Systems for Feeding
Bibliography
Chapter 73: Energetics and Metabolic Rate
Bibliography
Chapter 74: Body Temperature Regulation and Fever
Normal Body Temperatures
Body Core Temperature and Skin Temperature
Normal Core Temperature
Body Temperature is Controlled by Balancing Heat Production and Heat Loss
Heat Production
Heat Loss
Insulator System of the Body
Blood Flow to the Skin From the Body Core Provides Heat Transfer
Control of Heat Conduction to the Skin by the Sympathetic Nervous System
Basic Physics of Heat Loss From the Skin Surface
Radiation Causes Heat Loss in the Form of Infrared Rays
Conductive Heat Loss Occurs by Direct Contact With an Object
Convective Heat Loss Results From Air Movement
Cooling Effect of Wind
Conduction and Convection of Heat From a Person Suspended in Water
Evaporation
Evaporation is a Necessary Cooling Mechanism at Very High Air Temperatures
Clothing Reduces Conductive and Convective Heat Loss
Sweating and Its Regulation by the Autonomic Nervous System
Mechanism of Sweat Secretion
Acclimatization of the Sweating Mechanism to Heat—The Role of Aldosterone
Regulation of Body Temperature—Role of the Hypothalamus
ROLE OF THE ANTERIOR HYPOTHALAMIC-PREOPTIC AREA IN THERMOSTATIC DETECTION OF TEMPERATURE
DETECTION OF TEMPERATURE BY RECEPTORS IN THE SKIN AND DEEP BODY TISSUES
POSTERIOR HYPOTHALAMUS INTEGRATES CENTRAL AND PERIPHERAL TEMPERATURE SENSORY SIGNALS
NEURONAL EFFECTOR MECHANISMS THAT DECREASE OR INCREASE BODY TEMPERATURE
Temperature­Decreasing Mechanisms When the Body Is Too Hot
Temperature­Increasing Mechanisms When the Body Is Too Cold
Hypothalamic Stimulation of Shivering
Sympathetic “Chemical” Excitation of Heat Production
Increased Thyroxine Output as a Long­Term Cause of Increased Heat Production
“SET POINT” FOR TEMPERATURE CONTROL
Feedback Gain for Body Temperature Control
Skin Temperature Can Slightly Alter the Set Point for Core Temperature Control
BEHAVIORAL CONTROL OF BODY TEMPERATURE
ABNORMALITIES OF BODY TEMPERATURE REGULATION
Fever
Resetting the Hypothalamic Temperature­Regulating Center in Febrile Diseases—Effect of Pyrogens
Mechanism of Action of Pyrogens in Causing Fever—Role of Cytokines
Fever Caused by Brain Lesions
Bibliography
Unit XIV: Endocrinology and Reproduction
Chapter 75: Introduction to Endocrinology
Coordination of Body Functions by Chemical Messengers
Chemical Structure and Synthesis of Hormones
Polypeptide and Protein Hormones Are Stored in Secretory Vesicles Until Needed
Steroid Hormones Are Usually Synthesized From Cholesterol and Are Not Stored
Amine Hormones Are Derived From Tyrosine
HORMONE SECRETION, TRANSPORT, AND CLEARANCE FROM THE BLOOD
Hormone Secretion After a Stimulus and Duration of Action of Different Hormones
Concentrations of Hormones in the Circulating Blood and Hormonal Secretion Rates
Feedback Control of Hormone Secretion
Negative Feedback Prevents Overactivity of Hormone Systems
Surges of Hormones Can Occur With Positive Feedback
Cyclical Variations Occur in Hormone Release
TRANSPORT OF HORMONES IN THE BLOOD
“Clearance” of Hormones From the Blood
MECHANISMS OF ACTION OF HORMONES
Hormone Receptors and their Activation
The Number and Sensitivity of Hormone Receptors Are Regulated
INTRACELLULAR SIGNALING AFTER HORMONE RECEPTOR ACTIVATION
Ion Channel–Linked Receptors
G Protein–Linked Hormone Receptors
Enzyme-­Linked Hormone Receptors
Intracellular Hormone Receptors and Activation of Genes
SECOND MESSENGER MECHANISMS FOR MEDIATING INTRACELLULAR HORMONAL FUNCTIONS
Adenylyl Cyclase–cAMP Second Messenger System
Cell Membrane Phospholipid Second Messenger System
Calcium-­Calmodulin Second Messenger System
Hormones that Act Mainly on the Genetic Machinery of the Cell
Steroid Hormones Increase Protein Synthesis
Thyroid Hormones Increase Gene Transcription in the Cell Nucleus
Bibliography
Chapter 76: Pituitary Hormones and Their Control by the Hypothalamus
PITUITARY GLAND AND ITS RELATION TO THE HYPOTHALAMUS
ANTERIOR AND POSTERIOR LOBES OF THE PITUITARY GLAND
Posterior Pituitary Hormones Are Synthesized by Cell Bodies in the Hypothalamus
Hypothalamus Controls Pituitary Secretion
HYPOTHALAMIC-HYPOPHYSIAL PORTAL BLOOD VESSELS OF THE ANTERIOR PITUITARY GLAND
Hypothalamic Releasing and Inhibitory Hormones Are Secreted Into the Median Eminence
Hypothalamic Releasing and Inhibitory Hormones Control Anterior Pituitary Secretion
Specific Areas in the Hypothalamus Control Secretion of Specific Hypothalamic Releasing and Inhibitory Hormones
Physiological Functions of Growth Hormone
GROWTH HORMONE PROMOTES GROWTH OF MANY BODY TISSUES
GROWTH HORMONE HAS SEVERAL METABOLIC EFFECTS
Growth Hormone Promotes Protein Deposition in Tissues
Enhancement of Amino Acid Transport Through the Cell Membranes
Enhancement of RNA Translation to Cause Protein Synthesis by the Ribosomes
Increased Nuclear Transcription of DNA to Form RNA
Decreased Catabolism of Protein and Amino Acids
Summary
Growth Hormone Enhances Fat Utilization for Energy
“Ketogenic” Effect of Excessive Growth Hormone
Growth Hormone Decreases Carbohydrate Utilization
Necessity of Insulin and Carbohydrate for the Growth­Promoting Action of Growth Hormone
GROWTH HORMONE STIMULATES CARTILAGE AND BONE GROWTH
GROWTH HORMONE EXERTS MUCH OF ITS EFFECT THROUGH INSULIN-LIKE GROWTH FACTORS (SOMATOMEDINS)
Short Duration of Action of Growth Hormone but Prolonged Action of IGF-1
REGULATION OF GROWTH HORMONE SECRETION
Hypothalamic Growth Hormone–Releasing Hormone Stimulates, and Somatostatin Inhibits Growth Hormone Secretion
Posterior Pituitary Gland and its Relation to the Hypothalamus
PHYSIOLOGICAL FUNCTIONS OF ANTIDIURETIC HORMONE
Regulation of Antidiuretic Hormone Production
Increased Extracellular Fluid Osmolarity Stimulates ADH Secretion
Low Blood Volume and Low Blood Pressure Stimulate ADH Secretion—Vasoconstrictor Effects of ADH
Physiological Functions of Oxytocin
Oxytocin Causes Contraction of the Pregnant Uterus
Oxytocin Aids in Milk Ejection by the Breasts
Bibliography
Chapter 77: Thyroid Metabolic Hormones
Synthesis and Secretion of the Thyroid Metabolic Hormones
PHYSIOLOGIC ANATOMY OF THE THYROID GLAND
IODINE IS REQUIRED FOR THYROXINE FORMATION
Fate of Ingested Iodides
IODIDE PUMP—THE SODIUM-IODIDE SYMPORTER (IODIDE TRAPPING)
Thyroglobulin and Formation of Thyroxine and Triiodothyronine
Formation and Secretion of Thyroglobulin by the Thyroid Cells
Oxidation of the Iodide Ion
Iodination of Tyrosine and Thyroid Hormone Formation—“Organification” of Thyroglobulin
Storage of Thyroglobulin
RELEASE OF THYROXINE AND TRIIODOTHYRONINE FROM THE THYROID GLAND
Daily Rate of Secretion of Thyroxine and Triiodothyronine
Transport of Thyroxine and Triiodothyronine to Tissues
Thyroxine and Triiodothyronine Are Bound to Plasma Proteins
Thyroxine and Triiodothyronine Are Released Slowly to Tissue Cells
Thyroid Hormones Have Slow Onset and Long Duration of Action
PHYSIOLOGICAL FUNCTIONS OF THE THYROID HORMONES
Thyroid Hormones Increase Transcription of Many Genes
Most of the Thyroxine Secreted by the Thyroid Is Converted to Triiodothyronine
Thyroid Hormones Activate Nuclear Receptors
THYROID HORMONES INCREASE CELLULAR METABOLIC ACTIVITY
Thyroid Hormones Increase the Number and Activity of Mitochondria
Thyroid Hormones Increase Active Transport of Ions Through Cell Membranes
Effects of Thyroid Hormone on Specific Body Functions
Stimulation of Carbohydrate Metabolism
Stimulation of Fat Metabolism
Effect on Plasma and Liver Fats
Increased Requirement for Vitamins
Increased Basal Metabolic Rate
Decreased Body Weight
Increased Blood Flow and Cardiac Output
Increased Heart Rate
Increased Heart Strength
Normal Arterial Pressure
Increased Respiration
Increased Gastrointestinal Motility
Excitatory Effects on the Central Nervous System
Effect on the Function of the Muscles
Muscle Tremor
Effect on Sleep
Effect on Other Endocrine Glands
Effect of Thyroid Hormone on Sexual Function
Regulation of Thyroid Hormone Secretion
TSH (FROM THE ANTERIOR PITUITARY GLAND) INCREASES THYROID SECRETION
Cyclic Adenosine Monophosphate Mediates the Stimulatory Effect of TSH
ANTERIOR PITUITARY SECRETION OF TSH IS REGULATED BY THYROTROPIN-RELEASING HORMONE FROM THE HYPOTHALAMUS
Effects of Cold and Other Neurogenic Stimuli on TRH and TSH Secretion
FEEDBACK EFFECT OF THYROID HORMONE TO DECREASE ANTERIOR PITUITARY SECRETION OF TSH
Bibliography
Chapter 78: Adrenocortical Hormones
Corticosteroids: Mineralocorticoids, Glucocorticoids, and Androgens
SYNTHESIS AND SECRETION OF ADRENOCORTICAL HORMONES
The Adrenal Cortex has Three Distinct Layers
FUNCTIONS OF MINERALOCORTICOIDS—ALDOSTERONE
Mineralocorticoid Deficiency Causes Severe Renal Sodium Chloride Wasting and Hyperkalemia
Aldosterone Is the Major Mineralocorticoid Secreted by the Adrenals
Renal and Circulatory Effects of Aldosterone
Aldosterone Increases Renal Tubular Reabsorption of Sodium and Secretion of Potassium
Excess Aldosterone Increases Extracellular Fluid Volume and Arterial Pressure But Has Only a Small Effect on Plasma Sodium Concentration; Aldosterone Deficiency Causes Hyponatremia
Excess Aldosterone Causes Hypokalemia and Muscle Weakness; Aldosterone Deficiency Causes Hyperkalemia and Cardiac Toxicity
Excess Aldosterone Increases Tubular Hydrogen Ion Secretion and Causes Alkalosis
ALDOSTERONE STIMULATES SODIUM AND POTASSIUM TRANSPORT IN SWEAT GLANDS, SALIVARY GLANDS, AND INTESTINAL EPITHELIAL CELLS
CELLULAR MECHANISM OF ALDOSTERONE ACTION
POSSIBLE NONGENOMIC ACTIONS OF ALDOSTERONE AND OTHER STEROID HORMONES
REGULATION OF ALDOSTERONE SECRETION
Functions of Glucocorticoids
Effects of Cortisol on Carbohydrate Metabolism
Stimulation of Gluconeogenesis
Decreased Glucose Utilization by Cells
Elevated Blood Glucose Concentration and “Adrenal Diabetes”
Effects of Cortisol on Protein Metabolism
Reduction in Cellular Protein
Cortisol Increases Liver and Plasma Proteins
Increased Blood Amino Acids, Diminished Transport of Amino Acids Into Extrahepatic Cells, and Enhanced Transport Into Hepatic Cells
Effects of Cortisol on Fat Metabolism
Mobilization of Fatty Acids
Excess Cortisol Causes Obesity
CORTISOL IS IMPORTANT IN RESISTING STRESS AND INFLAMMATION
Anti­inflammatory Effects of High Levels of Cortisol
Cortisol Prevents the Development of Inflammation by Stabilizing Lysosomes and by Other Effects
Cortisol Causes Resolution of Inflammation
Regulation of Cortisol Secretion by Adrenocorticotropic Hormone from the Pituitary Gland
ACTH Stimulates Cortisol Secretion
Chemistry of ACTH
ACTH Secretion Is Controlled by Corticotropin­Releasing Factor From the Hypothalamus
ACTH Activates Adrenocortical Cells to Produce Steroids by Increasing cAMP
Physiological Stress Increases ACTH and Adrenocortical Secretion
Inhibitory Effect of Cortisol on the Hypothalamus and Anterior Pituitary to Decrease ACTH Secretion.
Summary of the Cortisol Control System
Synthesis and Secretion of ACTH in Association With Melanocyte­Stimulating Hormone, Lipotropin, and Endorphin
Bibliography
Chapter 79: Insulin, Glucagon, and Diabetes Mellitus
Insulin and its Metabolic Effects
INSULIN IS A HORMONE ASSOCIATED WITH ENERGY ABUNDANCE
INSULIN CHEMISTRY AND SYNTHESIS
ACTIVATION OF TARGET CELL RECEPTORS BY INSULIN AND THE RESULTING CELLULAR EFFECTS
EFFECT OF INSULIN ON CARBOHYDRATE METABOLISM
Insulin Promotes Muscle Glucose Uptake and Metabolism
Storage of Glycogen in Muscle
Quantitative Effect of Insulin to Facilitate Glucose Transport Through the Muscle Cell Membrane
Insulin Promotes Liver Uptake, Storage, and Use of Glucose
Glucose Is Released From the Liver Between Meals
Insulin Promotes Conversion of Excess Glucose Into Fatty Acids and Inhibits Gluconeogenesis in the Liver
Lack of Effect of Insulin on Glucose Uptake and Usage by the Brain
Effect of Insulin on Carbohydrate Metabolism in Other Cells
Effect of Insulin on Fat Metabolism
Insulin Promotes Fat Synthesis and Storage
Role of Insulin in Storage of Fat in the Adipose Cells
Insulin Deficiency Increases Use of Fat for Energy
Insulin Deficiency Causes Lipolysis of Storage Fat and Release of Free Fatty Acids
Insulin Deficiency Increases Plasma Cholesterol and Phospholipid Concentrations
Excess Usage of Fats During Insulin Deficiency Causes Ketosis and Acidosis
Effect of Insulin on Protein Metabolism and Growth
Insulin Promotes Protein Synthesis and Storage
Insulin Deficiency Causes Protein Depletion and Increased Plasma Amino Acids
Insulin and Growth Hormone Interact Synergistically to Promote Growth
Mechanisms of Insulin Secretion
Control of Insulin Secretion
Increased Blood Glucose Stimulates Insulin Secretion
Feedback Relation Between Blood Glucose Concentration and the Insulin Secretion Rate
THE ROLE OF INSULIN (AND OTHER HORMONES) IN “SWITCHING” BETWEEN CARBOHYDRATE AND LIPID METABOLISM
Glucagon and its Functions
Effects on Glucose Metabolism
Glucagon Causes Glycogenolysis and Increased Blood Glucose Concentration
Glucagon Increases Gluconeogenesis
Other Effects of Glucagon
Regulation of Glucagon Secretion
Increased Blood Glucose Inhibits Glucagon Secretion
Increased Blood Amino Acids Stimulate Secretion of Glucagon
Exercise Stimulates Secretion of Glucagon
Summary of Blood Glucose Regulation
Importance of Blood Glucose Regulation
Bibliography
Chapter 80: Parathyroid Hormone, Calcitonin, Calcium and Phosphate Metabolism, Vitamin D, Bone, and Teeth
Overview of Calcium and Phosphate Regulation in Extracellular Fluid and Plasma
CALCIUM IN THE PLASMA AND INTERSTITIAL FLUID
INORGANIC PHOSPHATE IN THE EXTRACELLULAR FLUIDS
NONBONE PHYSIOLOGICAL EFFECTS OF ALTERED CALCIUM AND PHOSPHATE CONCENTRATIONS IN THE BODY FLUIDS
Hypocalcemia Causes Nervous System Excitement and Tetany
Hypercalcemia Depresses Nervous System and Muscle Activity
Absorption and Excretion of Calcium and Phosphate
Intestinal Absorption and Fecal Excretion of Calcium and Phosphate
Renal Excretion of Calcium and Phosphate
Bone and its Relationship to Extracellular Calcium and Phosphate
Organic Matrix of Bone
Bone Salts
Tensile and Compressional Strength of Bone
Precipitation and Absorption of Calcium and Phosphate in Bone—Equilibrium With the Extracellular Fluids
Hydroxyapatite Does Not Precipitate in Extracellular Fluid Despite Supersaturation of Calcium and Phosphate Ions
Mechanism of Bone Calcification
Precipitation of Calcium in Nonosseous Tissues Under Abnormal Conditions
CALCIUM EXCHANGE BETWEEN BONE AND EXTRACELLULAR FLUID
Deposition and Resorption of Bone—Remodeling of Bone
Deposition of Bone by the Osteoblasts
Resorption of Bone—Function of the Osteoclasts
Bone Deposition and Resorption Are Normally in Equilibrium
Value of Continual Bone Remodeling
Control of the Rate of Bone Deposition by Bone “Stress”
Vitamin D
Cholecalciferol (Vitamin D3) Is Formed in the Skin
Cholecalciferol Is Converted to 25­Hydroxycholecalciferol in the Liver
Formation of 1,25­Dihydroxycholecalciferol in the Kidneys and Its Control by Parathyroid Hormone
Calcium Ion Concentration Controls the Formation of 1,25­Dihydroxycholecalciferol
Actions of Vitamin D
“Hormonal” Effect of Vitamin D to Promote Intestinal Calcium Absorption
Vitamin D Promotes Phosphate Absorption by the Intestines
Vitamin D Decreases Renal Calcium and Phosphate Excretion
Effect of Vitamin D on Bone and Its Relation to Parathyroid Hormone Activity
Parathyroid Hormone
PARATHYROID HORMONE EFFECTS ON EXTRACELLULAR FLUID CALCIUM AND PHOSPHATE CONCENTRATIONS
Parathyroid Hormone Mobilizes Calcium and Phosphate From Bone
Rapid Phase of Calcium and Phosphate Mobilization From Bone—Osteolysis
Slow Phase of Bone Resorption and Calcium Phosphate Release—Activation of the Osteoclasts
Parathyroid Hormone Decreases Calcium Excretion and Increases Phosphate Excretion by the Kidneys
Parathyroid Hormone Increases Intestinal Absorption of Calcium and Phosphate
Cyclic Adenosine Monophosphate Mediates the Effects of Parathyroid Hormone
CONTROL OF PARATHYROID SECRETION BY CALCIUM ION CONCENTRATION
SUMMARY OF EFFECTS OF PARATHYROID HORMONE
Calcitonin
Increased Plasma Calcium Concentration Stimulates Calcitonin Secretion
Calcitonin Decreases Plasma Calcium Concentration
Calcitonin Has a Weak Effect on Plasma Calcium Concentration in Adult Humans
Summary of Control of Calcium ion Concentration
Buffer Function of the Exchangeable Calcium in Bones—The First Line of Defense
Hormonal Control of Calcium Ion Concentration—The Second Line of Defense
Physiology of the Teeth
FUNCTION OF THE DIFFERENT PARTS OF THE TEETH
Enamel
Dentin
Cementum
Pulp
Dentition
Formation of the Teeth
Eruption of Teeth
Development of the Permanent Teeth
Metabolic Factors Influence Development of the Teeth
Mineral Exchange in Teeth
Bibliography
Chapter 81: Reproductive and Hormonal Functions of the Male (and Function of the Pineal Gland)
Spermatogenesis
Steps of Spermatogenesis
Meiosis
Sex Chromosomes
Formation of Sperm
Hormonal Factors That Stimulate Spermatogenesis
Maturation of Sperm in the Epididymis
Storage of Sperm in the Testes
Physiology of the Mature Sperm
Function of the Seminal Vesicles
Function of the Prostate Gland
Semen
“Capacitation” of Spermatozoa Is Required for Fertilization of the Ovum
Acrosome Enzymes, the “Acrosome Reaction,” and Penetration of the Ovum
Why Does Only One Sperm Enter the Oocyte?
Male Sexual Act
Neuronal Stimulus for Performance of the Male Sexual Act
Psychic Element of Male Sexual Stimulation
Integration of the Male Sexual Act in the Spinal Cord
Stages of the Male Sexual Act
Penile Erection—Role of the Parasympathetic Nerves
Lubrication Is a Parasympathetic Function
Emission and Ejaculation Are Functions of the Sympathetic Nerves
TESTOSTERONE AND OTHER MALE SEX HORMONES
Secretion, Metabolism, and Chemistry of the Male Sex Hormones
Secretion of Testosterone by the Interstitial Cells of Leydig in the Testes
Functions of Testosterone
Functions of Testosterone During Fetal Development
Effect of Testosterone to Cause Descent of the Testes
Effect of Testosterone on Development of Adult Primary and Secondary Sexual Characteristics
Effect on the Distribution of Body Hair
Male Pattern Baldness
Effect on the Voice
Testosterone Increases Thickness of the Skin and Can Contribute to Development of Acne
Testosterone Increases Protein Formation and Muscle Development
Testosterone Increases Bone Matrix and Causes Calcium Retention
Testosterone Increases the Basal Metabolic Rate
Testosterone Increases Red Blood Cells
Effect on Electrolyte and Water Balance
BASIC INTRACELLULAR MECHANISM OF ACTION OF TESTOSTERONE
CONTROL OF MALE SEXUAL FUNCTIONS BY HORMONES FROM THE HYPOTHALAMUS AND ANTERIOR PITUITARY GLAND
Gonadotropin­Releasing Hormone Increases Secretion of Luteinizing Hormone and Follicle­Stimulating Hormone
Gonadotropic Hormones: Luteinizing Hormone and Follicle­Stimulating Hormone
Regulation of Testosterone Production by Luteinizing Hormone
Inhibition of Anterior Pituitary Secretion of Luteinizing and Follicle­Stimulating Hormones by Testosterone—Negative Feedback Control of Testosterone Secretion
Regulation of Spermatogenesis by Follicle­Stimulating Hormone and Testosterone
Role of Inhibin in Negative Feedback Control of Seminiferous Tubule Activity
Human Chorionic Gonadotropin Secreted by the Placenta During Pregnancy Stimulates Testosterone Secretion by the Fetal Testes
Puberty and Regulation of Its Onset
Bibliography
Chapter 82: Female Physiology Before Pregnancy and Female Hormones
Physiologic Anatomy of the Female Sexual Organs
Oogenesis and Follicular Development in the Ovaries
Female Hormonal System
Monthly Ovarian Cycle and Function of Gonadotropic Hormones
GONADOTROPIC HORMONES AND THEIR EFFECTS ON THE OVARIES
OVARIAN FOLLICLE GROWTH—THEF OLLICULAR PHASE OF THE OVARIAN CYCLE
Development of Antral and Vesicular Follicles
Only One Follicle Fully Matures Each Month, and the Remainder Undergo Atresia
Ovulation
A Surge of Luteinizing Hormone Is Necessary for Ovulation
Initiation of Ovulation
CORPUS LUTEUM—THE LUTEAL PHASE OF THE OVARIAN CYCLE
Luteinizing Function of Luteinizing Hormone
Secretion by the Corpus Luteum: An Additional Function of Luteinizing Hormone
Involution of the Corpus Luteum and Onset of the Next Ovarian Cycle
Summary
Functions of Ovarian Hormones—Estradiol and Progesterone
Chemistry of the Sex Hormones
Estrogens
Progestins
Synthesis of the Estrogens and Progestins
Estrogens and Progesterone Are Transported in the Blood Bound to Plasma Proteins
Functions of the Liver in Estrogen Degradation
Fate of Progesterone
FUNCTIONS OF THE ESTROGENS—THEIR EFFECTS ON THE PRIMARY AND SECONDARY FEMALE SEX CHARACTERISTICS
Effect of Estrogens on the Uterus and External Female Sex Organs
Effect of Estrogens on the Fallopian Tubes
Effect of Estrogens on the Breasts
Effect of Estrogens on the Skeleton
Osteoporosis of the Bones Caused by Estrogen Deficiency in Old Age
Estrogens Slightly Increase Protein Deposition
Estrogens Increase Body Metabolism and Fat Deposition
Estrogens Have Little Effect on Hair Distribution
Effect of Estrogens on the Skin
Effect of Estrogens on Electrolyte Balance
Functions of Progesterone
Progesterone Promotes Secretory Changes in the Uterus
Progesterone Promotes Secretion by the Fallopian Tubes
Progesterone Promotes Development of the Breasts
MONTHLY ENDOMETRIAL CYCLE AND MENSTRUATION
Proliferative Phase (Estrogen Phase) of the Endometrial Cycle Occurs Before Ovulation
Secretory Phase (Progestational Phase) of the Endometrial Cycle Occurs After Ovulation
Menstruation
Leukorrhea During Menstruation
Regulation of Female Monthly Rhythm—Interplay Between Ovarian and Hypothalamic­Pituitary Hormones
THE HYPOTHALAMUS SECRETES GNRH, WHICH STIMULATES THE ANTERIOR PITUITARY GLAND TO SECRETE LH AND FSH
Intermittent, Pulsatile Secretion of GnRH by the Hypothalamus Stimulates Pulsatile Release of LH From the Anterior Pituitary Gland
Hypothalamic Centers for Release of Gonadotropin­Releasing Hormone
NEGATIVE FEEDBACK EFFECTS OF ESTROGEN AND PROGESTERONE TO DECREASE LH AND FSH SECRETION
Inhibin From the Corpus Luteum Inhibits FSH and LH Secretion
POSITIVE FEEDBACK EFFECT OF ESTROGEN BEFORE OVULATION—THE PREOVULATORY LUTEINIZING HORMONE SURGE
FEEDBACK OSCILLATION OF THE HYPOTHALAMIC-PITUITARY-OVARIAN SYSTEM
Anovulatory Cycles—Sexual Cycles at Puberty
Puberty and Menarche
Menopause
Female Sexual Act
Stimulation of the Female Sexual Act
Female Erection and Lubrication
Female Orgasm
Bibliography
Chapter 83: Pregnancy and Lactation
Maturation and Fertilization of the Ovum
Entry of the Ovum Into the Fallopian Tube (Uterine Tube)
Fertilization of the Ovum
WHAT DETERMINES THE SEX OF THE FETUS THAT IS CREATED?
TRANSPORT OF THE FERTILIZED OVUM IN THE FALLOPIAN TUBE
IMPLANTATION OF THE BLASTOCYST IN THE UTERUS
Early Nutrition of the Embryo
Anatomy and Function of the Placenta
PLACENTAL PERMEABILITY AND MEMBRANE DIFFUSION CONDUCTANCE
Diffusion of Oxygen Through the Placental Membrane
Diffusion of Carbon Dioxide Through the Placental Membrane
Diffusion of Foodstuffs Through the Placental Membrane
Excretion of Waste Products Through the Placental Membrane
Hormonal Factors in Pregnancy
HUMAN CHORIONIC GONADOTROPIN CAUSES PERSISTENCE OF THE CORPUS LUTEUM AND PREVENTS MENSTRUATION
Function of Human Chorionic Gonadotropin
Human Chorionic Gonadotropin Stimulates the Male Fetal Testes to Produce Testosterone
SECRETION OF ESTROGENS BY THE PLACENTA
Function of Estrogen in Pregnancy
SECRETION OF PROGESTERONE BY THE PLACENTA
HUMAN CHORIONIC SOMATOMAMMOTROPIN
Parturition
Increased Uterine Excitability Near Term
Hormonal Factors That Increase Uterine Contractility
Increased Ratio of Estrogens to Progesterone
Oxytocin Causes Contraction of the Uterus
Effect of Fetal Hormones on the Uterus
Mechanical Factors That Increase Uterine Contractility
Stretch or Irritation of the Cervix
ONSET OF LABOR—A POSITIVE FEEDBACK MECHANISM FOR ITS INITIATION
ABDOMINAL MUSCLE CONTRACTIONS DURING LABOR
Lactation
Development of the Breasts
Estrogens Stimulate Growth of the Ductal System of the Breasts
Progesterone Is Required for Full Development of the Lobule­Alveolar System
Prolactin Promotes Lactation
The Hypothalamus Secretes Prolactin Inhibitory Hormone
Suppression of the Female Ovarian Cycles in Nursing Mothers for Many Months After Delivery
EJECTION (OR “LET-DOWN”) PROCESS IN MILK SECRETION—FUNCTION OF OXYTOCIN
Inhibition of Milk Ejection
MILK COMPOSITION AND THE METABOLIC DRAIN ON THE MOTHER CAUSED BY LACTATION
Antibodies and Other Anti­infectious Agents in Milk
Bibliography
Chapter 84: Fetal and Neonatal Physiology
Bibliography
Unit XV: Sports Physiology
Chapter 85: Sports Physiology
Bibliography
Normal Values for Selected Common Laboratory Measurements