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• Cover
• Title Page
• Copyright
• Preface
• Contributors
• Reviewers
• Contents
• PART I CELLULAR PHYSIOLOGY
• CHAPTER 1 Medical Physiology: An Overview
• INTRODUCTION
• SCOPE OF PHYSIOLOGY
• The body’s internal environment is tightly regulated to maintain optimal cellular function.
• The neuroendocrine system provides an intricate communication network to tissues and organs.
• Myokines are produced by skeletal muscle.
• The autonomic nervous system regulates the body’s internal organs.
• RECENT DIRECTIONS FOR MEDICAL PHYSIOLOGY
• Telomeres protect chromosomes and enhance organ function and longevity.
• The immune system protects organ function.
• A natural rhythm of organ function is maintained by an internal biological clock.
• Oxygen and HIF take center stage.
• Cellular and organ function is regulated above the level of the gene.
• A paradigm shift is occurring in human physiology.
• CHAPTER 2 Membrane Transport and Cell Signaling
• INTRODUCTION
• BASIS OF PHYSIOLOGIC REGULATION
• Stable internal environment is essential for normal cell function.
• Homeostasis is maintained in the body by coordinated physiologic mechanisms.
• Negative feedback promotes stability, and feedforward control promotes change.
• Positive feedback promotes a change in one direction.
• Energy is required to maintain a steady state and cellular equilibrium.
• CYTOSOL AND THE PLASMA MEMBRANE
• The plasma membrane consists of different types of lipids with dissimilar functions.
• The plasma membrane contains integral proteins, peripheral proteins, and glycoproteins.
• Intracellular fluid composition differs from the extracellular fluid composition.
• SOLUTE TRANSPORT MECHANISMS
• Import of extracellular materials occurs through phagocytosis and endocytosis.
• Export of macromolecules occurs through exocytosis.
• Uncharged solutes cross the plasma membrane by passive diffusion.
• Integral membrane proteins facilitate diffusion of solutes across the plasma membrane.
• Carrier-mediated transport moves ions and organic solutes passively across membranes.
• Active transport systems move solutes against concentration gradients or electrical potential.
• Cells are negatively polarized on the inside compared to the outside.
• Transcellular transport moves solutes across epithelial cell layers.
• WATER MOVEMENT ACROSS THE PLASMA MEMBRANE
• A difference in osmotic pressure moves water across the plasma membrane.
• The osmolality of the extracellular fluid regulates cell volume.
• Oral rehydration therapy is driven by solute transport.
• COMMUNICATION AND SIGNALING MODES
• Cells communicate locally by paracrine and autocrine signaling.
• Nervous system coordinates inputs for rapid and targeted communication.
• Endocrine system provides for slower and more diffuse communication.
• The nervous and endocrine systems provide overlapping control.
• MOLECULAR BASIS OF CELLULAR SIGNALING
• G-protein–coupled receptors transmit signals through trimeric G proteins.
• Ligand-activated ion channels transduce a chemical signal into an electrical signal.
• Tyrosine kinase receptors are enzymes activated by phosphorylation.
• Intracellular hormone receptors directly activate transcription in the cell.
• Second messengers amplify the receptor signal to downstream targets.
• Protein kinase A mediates the signaling effects of cAMP, the predominant second messenger in all cells.
• Soluble and transmembrane guanylyl cyclase produces cGMP.
• Phospholipase C activates the second messengers, diacylglycerol and inositol trisphosphate, which are derived from lipid in the plasma membrane.
• Cells use calcium as a second messenger by keeping resting intracellular calcium levels low.
• Chapter Review Questions
• PART II NEUROMUSCULAR PHYSIOLOGY
• CHAPTER 3 Action Potential, Synaptic Transmission, and Nerve Function
• THE NERVOUS SYSTEM
• Access to the central nervous system is restricted by the blood–brain barrier.
• The primary cell types in the nervous system, neurons and glia, differ in function and morphology.
• Neuronal transport is mediated by cytoskeletal components and occurs to and from the soma.
• RESTING MEMBRANE POTENTIAL
• Neurons regulate the transport of specific ions across neuronal membranes resulting in an electrochemical gradient.
• Ion movement through open channels is driven by the electrochemical potential which can be calculated for a particular ion using the Nernst equation.
• A neuron’s resting membrane potential is influenced by the combined ionic equilibrium potentials and can be calculated with the Chord conductance and Goldman equations.
• ACTION POTENTIALS
• Changes to the permeability of potassium and sodium ions can result in hyperpolarization or depolarization of the membrane.
• Action potentials have different phases depending on the permeability of the sodium and potassium channels.
• Conduction velocity is influenced by myelination and fiber diameter.
• SYNAPTIC TRANSMISSION
• Neurons communicate both by electrical and chemical synapses.
• Upon depolarization of the presynaptic membrane, vesicles mobilize to the membrane, dock, and release neurotransmitters.
• Neurotransmitter actions can be terminated via diffusion, degradation, or cellular uptake.
• NEUROTRANSMISSION
• Neurotransmitters commonly act at ionotropic or metabotropic receptors to produce an effect.
• Classical neurotransmitters are small molecules.
• Neuropeptides often serve a neuromodulatory role.
• Nonclassical neurotransmitters can be synthesized and released “on demand.”
• Chapter Review Questions
• CHAPTER 4 Sensory Physiology
• SENSORY SYSTEMS
• Sensory systems transform physical and chemical signals from the external and internal environments into information in the form of nerve action potentials.
• Sensory transduction changes environmental energy into sensory nerve action potentials.
• Sensory nerve impulse frequency is modulated by the magnitude and duration of the generator potential.
• Sustained sensory receptor stimulation can result in diminished action potential generation over time.
• Perception of sensory information requires encoding and decoding electrical signals sent to the central nervous system.
• SOMATOSENSORY SYSTEM
• Skin receptors provide sensory information from the body surface.
• Thermoreceptors are sensory nerve endings that code for absolute and relative temperatures.
• Nociceptors are free nerve endings that trigger pain sensations in the brain.
• Proprioceptors are sensory receptors that signal movements of the body and limbs.
• VISUAL SYSTEM
• The eyes comprise three layers of specialized tissue.
• Eye structures modify incoming light rays to focus an image on the retina.
• Phototransduction by retinal cells converts light energy into neural electrical–chemical signals.
• Signals from the retina are modified and separated before reaching the thalamus and visual cortex.
• Visual reflexes are partially under central nervous system control.
• AUDITORY SYSTEM
• Sound is an oscillating pressure wave composed of frequencies that are transmitted through different media.
• External ear captures and amplifies sound.
• The middle ear mechanically converts tympanic membrane vibrations to fluid waves in the inner ear.
• Inner ear transduces sound.
• Hearing loss results from a mechanical or a neural problem.
• VESTIBULAR SYSTEM
• Vestibular system comprises the semicircular canals and otolithic organs.
• GUSTATORY AND OLFACTORY SYSTEMS
• Taste buds house the receptor cells for gustatory sensations.
• Gustatory chemoreception distinguishes five primary taste categories.
• Gustatory transduction is mediated by multiple receptors and intracellular mechanisms.
• Olfactory apparatus serves the sense of smell.
• Chapter Review Questions
• CHAPTER 5 Motor System
• INTRODUCTION
• SKELETON AS FRAMEWORK FOR MOVEMENT
• MUSCLE FUNCTION AND BODY MOVEMENT
• NERVOUS SYSTEM COMPONENTS FOR THE CONTROL OF MOVEMENT
• Lower motor neurons are the final common path for motor control.
• Afferent muscle innervation provides feedback for motor control.
• Motor neurons adjust spindle output during muscle contraction.
• SPINAL CORD IN THE CONTROL OF MOVEMENT
• Spinal motor anatomy correlates with function.
• Spinal cord mediates reflex activity.
• Spinal cord reflexes are modified by descending motor pathways.
• SUPRASPINAL INFLUENCES ON MOTOR CONTROL
• Brainstem is the origin of descending tracts that influence posture and movement.
• Terminations of the brainstem motor tracts correlate with their functions.
• Sensory and motor systems work together to control posture.
• Central generator programs help control rhythmic motor behaviors.
• Injuries to the motor cortex or corticospinal tract produce upper motor neuron signs.
• Abnormal posturing results from damage to descending motor tracts.
• CEREBRAL CORTEX ROLE IN MOTOR CONTROL
• Several distinct cortical areas participate in voluntary movement.
• Corticospinal tract is the primary efferent path from the cortex.
• BASAL GANGLIA AND MOTOR CONTROL
• Basal ganglia nuclei are extensively interconnected.
• Functions of the basal ganglia are partially revealed by disease.
• CEREBELLUM IN THE CONTROL OF MOVEMENT
• Structural divisions of the cerebellum correlate with function.
• Intrinsic circuitry of the cerebellum is regulated by Purkinje cells.
• Cerebellar lesions reveal functions of the cerebellum.
• The cerebellum plays a role in several nonmotor cognitive functions.
• Chapter Review Questions
• CHAPTER 6 Autonomic Nervous System
• INTRODUCTION
• ANATOMY OF THE AUTONOMIC NERVOUS SYSTEM
• Autonomic nervous system consists of a two-neuron efferent pathway.
• PSNS and SNS differ in the location of their preganglionic neurons and ganglia.
• NEUROTRANSMITTERS OF THE AUTONOMIC NERVOUS SYSTEM
• All preganglionic axons release acetylcholine.
• Parasympathetic postganglionic neurons release acetylcholine, whereas sympathetic postganglionic neurons primarily release norepinephrine.
• Many autonomic postganglionic fibers contain cotransmitters along with acetylcholine and norepinephrine.
• Some autonomic fibers contain neither acetylcholine nor norepinephrine but instead undergo nonadrenergic noncholinergic transmission.
• THE PARASYMPATHETIC NERVOUS SYSTEM
• PSNS is involved in normal homeostatic functions.
• PSNS effects are mediated by cholinergic receptors.
• SYMPATHETIC NERVOUS SYSTEM
• SNS effects are mediated mostly by adrenergic receptors.
• AUTONOMIC INTEGRATION
• Presynaptic inhibition can modulate functioning of the ANS.
• The input from the PSNS and SNS to the eye is an example of autonomic integration.
• Vasculature receives input only from the SNS, which contributes to the maintenance of appropriate blood pressure.
• Epinephrine can produce both vasoconstriction and vasodilation.
• Receptors and pathways of the autonomic nervous system provide targets for therapeutics.
• Chapter Review Questions
• CHAPTER 7 Integrative Functions of the Central Nervous System
• INTRODUCTION
• HYPOTHALAMUS
• Hypothalamus consists of distinct nuclei that interface between the endocrine, autonomic, and limbic systems.
• Hypothalamus regulates energy balance by integrating metabolism and eating behavior.
• Sexual drive and sexual behavior are controlled by the hypothalamus.
• Hypothalamus contains the “master biological clock” that controls rhythms and cycles.
• Reticular formation governs the level of consciousness and regulates arousal and the sleep–wake pattern.
• Ascending reticular activating system modulates consciousness and arousal.
• BRAIN ELECTRICAL ACTIVITY
• EEG waves have characteristic patterns corresponding to state of arousal.
• Sleep stages are defined by the EEG.
• Abnormal brain waves indicate a seizure disorder.
• FUNCTIONAL COMPONENTS OF THE FOREBRAIN
• Cerebral cortex comprises three functional areas: sensory, motor, and association areas.
• Cortical and subcortical structures are part of the architectural design of the limbic system.
• Limbic system malfunction leads to psychiatric disorders.
• HIGHER COGNITIVE SKILLS
• Cerebral cortex and the limbic system provide the architectural components for learning and memory systems.
• Long-term and short-term memory comprise the brain’s memory system.
• Language and speech are coordinated in specific areas within the association cortex.
• Chapter Review Questions
• CHAPTER 8 Skeletal and Smooth Muscle
• SKELETAL MUSCLE
• Protein filaments provide the architecture and contractile machinery of skeletal muscle.
• Sarcomeres are the structural and functional unit of actin:myosin–linked muscle contraction.
• EXCITATION–CONTRACTION COUPLING IN SKELETAL MUSCLE
• Electrochemical events at a neuromuscular junction link nerve action potentials to the skeletal muscle action potentials that trigger contraction.
• Neuromuscular transmission can be altered by toxins, drugs, and trauma.
• Muscle action potentials release calcium from the sarcoplasmic reticulum to activate the cross-bridge cycle.
• Intracellular calcium concentration is the key variable in switching muscle between relaxation and contraction.
• The cyclic interaction of actin and myosin is the molecular engine driving muscle contraction.
• Cellular structure of skeletal muscle transforms cross-bridge cycling into mechanical motion.
• THE NEUROMUSCULAR MOTOR UNIT AND MECHANICS OF SKELETAL MUSCLE CONTRACTION
• Contraction of large muscle groups is modified by temporal and spatial summation of single muscle unit contractions.
• Skeletal muscle is a composite of smaller functional neuromuscular units that allow graded partial activation of the whole muscle.
• Skeletal muscle metabolism, environment, and motor neuron type create slow, low-fatigue and fast, high-fatigue muscle units.
• Metabolic differences among muscle fibers affect their ability to sustain contraction.
• LOADING CONDITIONS AND MUSCLE MECHANICS
• Isometric muscle contraction occurs when muscle contracts against a load that is too heavy to move.
• Isotonic contractions in muscle results when the force it generates is greater than the load on which it acts.
• The mechanics of muscle contraction are altered by its initial passive stretch and its afterload.
• Loading conditions affect the extent of skeletal muscle shortening.
• Skeletal attachments create lever systems that modify muscle action.
• MUSCLE PLASTICITY, EPIGENETICS, AND ENDOCRINE MUSCLE
• SMOOTH MUSCLE
• Smooth muscle cells lack the ultrastructural organization of skeletal muscle fibers.
• Mechanical activity in smooth muscle is adapted for its specialized physiologic roles.
• Altering internal dimensions of hollow organs is a major physiological role of smooth muscle.
• Multiple smooth muscle contractile patterns are created from neural, humoral, chemical, and physical stimuli.
• ACTIVATION–CONTRACTION COUPLING IN SMOOTH MUSCLE
• Calcium required to contract smooth muscle is obtained from extra- and intracellular sources.
• Primary phosphorylation of myosin is necessary to activate the smooth muscle cross-bridge cycle.
• The latch state is a unique cross-bridge mechanism that reduces the energy cost of continual smooth muscle contraction.
• A large number of chemical and physical stimuli can actively contract or relax smooth muscle by direct or receptor-mediated mechanisms.
• Smooth muscle can be relaxed actively by several stimuli.
• Chapter Review Questions
• PART III BLOOD AND IMMUNOLOGY
• CHAPTER 9 Blood Composition and Function
• INTRODUCTION
• BLOOD FUNCTIONS
• Blood provides the ability to transport vital components to the body.
• An effective system in the blood limits bleeding after an injury.
• The blood helps the body maintain homeostasis.
• The blood plays a major role in immunity.
• WHOLE BLOOD
• Blood is a specialized connective tissue.
• SOLUBLE COMPONENTS OF BLOOD AND THEIR TESTS
• Plasma becomes serum after the removal of clotting factors.
• Analyzing blood samples reveals a patient’s health status.
• Plasma contains ions, carbohydrates, lipid, and proteins.
• Blood lipid profile helps determine a patient’s cardiovascular disease risk.
• Basic and complete metabolic panels are indicators of metabolic health.
• Abnormal serum protein patterns in electrophoresis reveal health problems.
• Immunologic assays detect and measure serum antigens and antibodies.
• FORMED ELEMENTS OF BLOOD AND COMMON DIAGNOSTIC TESTS
• Blood is a viscous liquid.
• Hematocrit is the percent volume of red blood cells per volume of whole blood.
• Complete blood counts determine the number and type of cells in the blood.
• Blood smears detect blood parasites and other hematologic disorders.
• RED BLOOD CELLS
• Erythrocytes consist mainly of hemoglobin, a unique pigment containing heme groups in which oxygen binds to iron atoms.
• Changes in erythrocyte morphology provide insights into specific blood disorders.
• Red blood cell components are recycled.
• Iron profile evaluates iron stores of the body.
• Understanding the blood group system is necessary to transfuse red blood cells.
• WHITE BLOOD CELLS
• Leukocytes contain five diverse cell types and constitute part of the immune system.
• Neutrophils defend against bacterial and fungal infection through phagocytosis.
• Eosinophils are inflammatory cells that defend against parasitic infections.
• Basophils release histamine, causing the inflammation of allergic and antigen reactions.
• Monocytes migrate from the blood stream and become macrophages.
• Lymphocytes contain three cell types that participate in the immune system.
• PLATELET FORMATION
• BLOOD CELL FORMATION
• Hematopoiesis takes place in bone marrow and lymphatic tissue.
• Mature blood cells originate from a multipotent stem cell.
• Erythropoiesis is regulated by the renal hormone erythropoietin.
• BLOOD CLOTTING
• In hemostasis step 1, the vascular phase begins.
• In hemostasis step 2, platelet plug forms.
• In hemostasis step 3, thrombin catalyzes the conversion of fibrinogen into fibrin to form a stable clot.
• In hemostasis step 4, plasmin mediates fibrinolysis.
• Chapter Review Questions
• CHAPTER 10 Immunology, Organ Interaction, and Homeostasis
• INTRODUCTION
• IMMUNE SYSTEM COMPONENTS
• The defense system consists of layered specificity and sophistication.
• Thymus and bone marrow are linked to the adaptive immune system.
• IMMUNE SYSTEM ACTIVATION
• Large complex molecules and proteins are the best activators of the immune response.
• The immune system is highly selective and is activated with severe injury and necrosis.
• Complementary processes are involved in the activation of innate and adaptive immunity.
• IMMUNE DETECTION SYSTEM
• The immune system exhibits tolerance by preventing a response against specific antigens.
• IMMUNE SYSTEM DEFENSES
• Physical barriers are the immune system’s first line of defense.
• Innate immunity is the second line of defense.
• Adaptive immunity is the third line of defense.
• CELL-MEDIATED AND HUMORAL RESPONSES
• Cell-mediated response involves activation of T cells and release of cytokines.
• Humoral immunity is mediated by secreting antibodies that protects the extracellular space.
• ACUTE AND CHRONIC INFLAMMATION
• Acute inflammation is a short-term process and is characterized by five cardinal signs.
• Acute inflammation is a three-step process involving vasodilation and cell migration from blood to tissue.
• Inflammatory mediators develop and maintain the inflammatory response.
• The profile of the inflammatory cytokines provides a biomarker for the severity of inflammation.
• Acute inflammation is a stereotypic, highly complex process that self-terminates.
• CHRONIC INFLAMMATION
• Chronic inflammation is both a symptom and the underlying cause of a disease.
• ANTI-INFLAMMATORY DRUGS
• Some treatments are available to help manage the inflammation.
• ORGAN TRANSPLANTATION AND IMMUNOLOGY
• Histocompatibility is the most important criterion for a match in organ donation.
• IMMUNOLOGIC DISORDERS
• Immunological dysfunction leads to tissue and organ damage.
• Immune cells may become carcinogenic, leading to hematologic malignancies.
• Tumor antigens can identify tumor cells and serve as potential candidates for cancer immunotherapy.
• NEUROENDOIMMUNOLOGY
• Immune system is down-regulated by neuronal and hormonal stress signals.
• Chapter Review Questions
• PART IV CARDIOVASCULAR PHYSIOLOGY
• CHAPTER 11 Overview of the Cardiovascular System and Hemodynamics
• INTRODUCTION
• FUNCTIONAL ORGANIZATION OF THE CARDIOVASCULAR SYSTEM
• The outputs of the right and left heart are interdependent because they are connected in series.
• Parallel arrangement of organ circulations permits independent control of blood flow in individual organs.
• Vascular smooth muscle actively controls the diameter of arteries and veins.
• HEMODYNAMICS: THE PHYSICS OF BLOOD CONTAINMENT AND MOVEMENT
• Blood vessel volume is a function of vessel flexibility and the pressure difference across the vessel wall.
• Blood vessels must overcome wall stress to contract.
• Dynamics are the hemodynamic principles that govern the movement of blood in the cardiovascular system.
• Relationships between pressure, fluid flow, and resistance are quantified by the Poiseuille law.
• The series and parallel arrangement of blood vessels within an organ affects vascular resistance in the organ.
• High blood flow velocity decreases lateral pressure while increasing shear stress on the arterial wall.
• High blood flow velocity can create turbulent flow in arteries.
• RHEOLOGY
• Axial streaming of cells reduces viscosity of blood in small vessels.
• DISTRIBUTION OF PRESSURE, FLOW, VELOCITY, AND BLOOD VOLUME
• Chapter Review Questions
• CHAPTER 12 Electrical Activity of the Heart
• INTRODUCTION
• ELECTROPHYSIOLOGY OF CARDIAC MUSCLE
• All cardiac cells are coupled electrically and mechanically.
• Action potential forms in the heart are markedly different than those in skeletal muscle.
• Selective modulation of conductances for sodium, potassium, and calcium create the myocardial action potential.
• Voltage-gated sodium channels initiate phase 0 of the fast response.
• The refractory period in cardiac muscle is prolonged by opening of slow, voltage-gated Ca2+ channels.
• Repolarization of cardiac muscle cells involves activation of late K+ channels.
• The sinoatrial node initiates and maintains the rhythm of electrical activation in the heart.
• Unique repeating changes of ion conductances create automaticity and rhythmicity in cardiac nodal tissue.
• Action potential conduction velocity through the myocardium is proportional to the amplitude and phase 0 upstroke of the cardiac action potential.
• THE PATHOPHYSIOLOGY OF ABNORMAL GENERATION OF CARDIAC ACTION POTENTIALS
• Partial depolarization and shortened refractory periods can lead to abnormal pacemaker sites in the myocardium.
• THE ELECTROCARDIOGRAM
• The normal ECG depicts cyclic, time-varying electrical activity and conduction in the atria and ventricles.
• Moment-to-moment orientation and magnitude of net dipoles in the heart determine the formation of the ECG.
• Clinical ECG evaluation is standardized by using a common, specific, 12-lead system.
• Six standardized limb leads create an image of electrical activity in the heart in the frontal plane.
• Imaging cardiac electrical activity in the horizontal plane uses six standardized chest leads.
• Information about the orientation of the heart, ventricular size, and conduction pathways can be obtained by determining a mean frontal QRS vector.
• Mean QRS axis analysis helps detect underlying pathological conditions in the heart.
• The ECG can detect abnormalities in cardiac activation and conduction.
• Disorders in plasma electrolytes and myocardial ischemia can be revealed by ECG recordings.
• The ECG is a critical tool for detecting myocardial ischemia and infarction.
• Chapter Review Questions
• CHAPTER 13 Mechanics of the Cardiac Pump
• EXCITATION–CONTRACTION COUPLING IN CARDIAC MUSCLE
• Contractile force in myocardial fibers can be altered by mechanisms that can change their intracellular calcium concentration.
• The ability to modify force generation in myocardium at the cellular level is largely independent of afterload and preload on cardiac muscle.
• THE CARDIAC CYCLE
• Ventricular systole is divided into isovolumetric contraction, rapid ejection, and reduced ejection phases.
• Ventricular diastole is divided into isovolumetric relaxation, rapid filling, and reduced filling phases.
• Changes in venous pressure waveforms can reveal abnormalities in heart valves.
• DETERMINANTS OF MYOCARDIAL PERFORMANCE
• Net cardiac muscle performance arises from interactions between preload, afterload, and the inotropic state.
• Effects of preload and afterload on cardiac contraction are enhanced or depressed by changes in cardiac inotropic state.
• Variables associated with contractile performance of the heart in situ are analogous representations of afterload, preload, and muscle shortening.
• Aortic pressure and wall stress are major determinants of afterload on the heart in situ.
• Pressure–volume loops are a means of illustrating the effects of loading conditions and inotropic state on cardiac performance.
• Stroke volume is positively related to the level of the inotropic state of the heart.
• Stroke volume is increased by an increase in preload or a decrease in afterload.
• DETERMINANTS OF MYOCARDIAL OXYGEN DEMAND AND CLINICAL EVALUATION OF CARDIAC PERFORMANCE
• Increased afterload increases myocardial oxygen demand more than does increased preload, shortening, or inotropic state.
• Ejection fraction and hemodynamic evaluations are used as simple clinical indices of myocardial performance.
• CARDIAC OUTPUT
• Cardiac output is maintained over a large range of heart rates through a reciprocal interaction between heart rate and stroke volume.
• Changes in heart rate occur through the reciprocal activation of parasympathetic and sympathetic nerves to the heart.
• Multiple techniques are used to measure cardiac output.
• IMAGING TECHNIQUES FOR MEASURING CARDIAC STRUCTURES, VOLUMES, BLOOD FLOW, AND CARDIAC OUTPUT
• Chapter Review Questions
• CHAPTER 14 Interactions between the Heart and the Systemic Circulation
• INTRODUCTION
• COMPONENTS OF ARTERIAL PRESSURE
• Mean arterial pressure is determined by cardiac output and systemic vascular resistance, whereas arterial pulse pressure is a function of stroke volume and arterial compliance.
• Interactions among stroke volume, heart rate, and systemic vascular resistance differentially alter different components of arterial pressure.
• CLINICAL MEASUREMENT OF ARTERIAL PRESSURE
• Sphygmomanometry is a noninvasive measurement of blood pressure in humans.
• THE CONCEPT OF PERIPHERAL AND CENTRAL BLOOD VOLUME
• Large compliance in the veins allows them to accommodate high volumes with little change in pressure.
• The concept of central blood volume is useful for evaluating the effects of changes in blood volume on cardiac output.
• Central venous pressure is a reflection of central blood volume.
• Cardiac output is altered by changes in central blood volume.
• INTERCONNECTIONS BETWEEN VASCULAR AND CARDIAC FUNCTION
• Compliant arteries reduce cardiac work.
• Increasing venous filling pressure increases cardiac output, but increasing cardiac output decreases venous filling pressure.
• Two interrelationships between venous pressure and cardiac output are used to predict how cardiac output and central venous pressure change in response to altered states in the cardiovascular system.
• Chapter Review Questions
• CHAPTER 15 Regulation of Organ Blood Flow and Capillary Transport
• LOCAL REGULATION OF ORGAN BLOOD FLOW
• The sympathetic nervous system creates tonic, partial vasoconstriction to arteries and veins in most systemic organs.
• In response to changes in arterial pressure, most organs can control their blood flow through local autoregulation.
• Myogenic regulation causes arterioles to actively contract or relax in response to changes in intravascular pressure.
• Organ blood flow is increased by increased tissue metabolism through local, nonneurogenic mechanisms.
• Reactive hyperemia is an oversupply of blood flow to a tissue following periods of sustained low or zero tissue flow.
• Vascular smooth muscle tone is modified by vasoactive molecules released from endothelial cells.
• Endothelium-derived NO mediates numerous beneficial cardiovascular effects, but its production is impaired in all forms of cardiovascular disease.
• Vascular endothelium releases the powerful vasoconstrictor, endothelin, in pathological conditions.
• THE MICROCIRCULATION AND CAPILLARY DYNAMICS
• Control of total peripheral vascular resistance is predominantly at the level of the arterial microvasculature.
• Exchange of water and materials between blood and tissues occurs across capillaries.
• Passage of molecules occurs between and through capillary endothelial cells.
• Venules collect blood from capillaries and act as a blood reservoir.
• SOLUTE EXCHANGE BETWEEN THE CARDIOVASCULAR SYSTEM AND TISSUES
• Transport across capillaries is enhanced by increasing their collective surface area and reducing diffusion distances from capillaries to cells.
• Transport of a solute across capillaries is enhanced by increasing the capillary permeability and concentration gradient for the solute across the capillaries.
• Increases in vascular permeability, surface area, or blood flow enhance the diffusion of small molecules between the capillaries and tissues.
• CAPILLARY WATER TRANSPORT
• The relative contributions of capillary hydrostatic and oncotic forces determine the net direction of fluid exchange across the capillaries.
• Effects of capillary oncotic and hydrostatic pressure on fluid flux are modified by these pressures in the interstitium.
• The Starling-Landis equation quantifies fluid flow across the capillaries.
• Capillary hydrostatic pressure is altered by changes in precapillary and postcapillary resistance as well as arteriolar and venule blood pressure.
• THE LYMPHATIC SYSTEM
• Lymphatic vessels mechanically collect fluid and proteins from tissue fluid between cells.
• Edema is a condition of excess fluid accumulation in the interstitial space that impairs diffusional transport across the capillaries.
• Chapter Review Questions
• CHAPTER 16 Special Vascular Physiology of Individual Organs
• INTRODUCTION
• THE CORONARY CIRCULATION
• Coronary blood flow occurs primarily during diastole because of inhibition of flow from cardiac contraction during systole.
• Coronary blood flow is closely linked to cardiac oxygen demand.
• Direct and indirect actions of sympathetic nerves dilate coronary arteries.
• Autoregulation of coronary blood flow has different limits in the endocardium versus the epicardium.
• THE CEREBRAL CIRCULATION
• Brain blood flow remains essentially constant over a large range of arterial blood pressures.
• Brain microvessels are uniquely sensitive to vasodilation by CO2 and H+.
• Cerebral vessels are insensitive to hormones and sympathetic nerve activity.
• The cerebral vasculature adapts to chronic high blood pressure.
• Cerebral edema impairs blood flow to the brain.
• THE CIRCULATION OF THE SMALL INTESTINE
• Autoregulation efficiency in the small intestine is modulated by intestinal oxygen consumption.
• High blood flow is required in the intestinal mucosal for absorption of nutrients.
• Low capillary pressure in intestinal villi facilitates water absorption.
• Sympathetic nerve activity greatly decreases intestinal blood flow and venous volume.
• THE HEPATIC CIRCULATION
• The hepatic circulation is perfused by a mixed supply of venous and arterial blood from the portal vein and hepatic arteries.
• Regulation of hepatic arterial and portal venous blood flow requires an interactive control system.
• SKELETAL MUSCLE CIRCULATION
• Skeletal muscle blood flow can be altered significantly by sympathetic neural and local metabolic factors.
• Muscle blood flow is markedly altered by numerous local vasoactive agents.
• THE CUTANEOUS CIRCULATION
• Adjustment of cutaneous blood flow is used for temperature regulation.
• FETAL AND PLACENTAL CIRCULATIONS
• Placental exchange of oxygen and carbon dioxide is limited.
• Absence of lung ventilation in the fetus necessitates a bypass arrangement around the fetal pulmonary circulation.
• Transition from fetal to neonatal life requires complex changes in the structure of the fetal circulation after birth.
• Chapter Review Questions
• CHAPTER 17 Neurohumoral Control Mechanisms in Cardiovascular Function
• INTRODUCTION
• AUTONOMIC NEURAL CONTROL OF THE CARDIOVASCULAR SYSTEM
• Neurogenic control of the heart involves reciprocal activation of parasympathetic and sympathetic nerves.
• The baroreceptor reflex buffers changes in mean arterial pressure by altering cardiac output and total peripheral vascular resistance.
• The baroreceptor reflex also activates hormonal systems affecting blood pressure.
• Baroreceptor activation is site, pressure, and time dependent.
• Cardiopulmonary baroreceptors sense central blood volume.
• Chemoreceptors for PCO2, pH, and PO2 affect mean arterial pressure.
• Pain and myocardial ischemia initiate cardiovascular reflexes.
• Higher-order CNS processes can alter blood pressure and cardiac output.
• HORMONAL CONTROL OF THE CARDIOVASCULAR SYSTEM
• Circulating epinephrine exerts different cardiovascular effects compared to those caused by activation of sympathetic nerves.
• The renin–angiotensin–aldosterone system supports blood pressure and blood volume.
• The RAAS is activated by pathophysiological states.
• Arginine vasopressin primarily regulates blood volume.
• Stretch-activated release of atrial natriuretic peptide counteracts volume overload.
• Renal hypoxia stimulates red blood cell production.
• Different short- and long-term mechanisms are used in blood pressure control.
• CIRCULATORY SHOCK
• Shock is divided into three stages of increasing severity.
• Progressive shock causes a vicious cycle of cardiac and brain deterioration.
• Malfunctions involving the heart, brain, vascular system, or blood volume can cause shock.
• Clinical classification systems for shock provide a different perspective on the principal characteristics of different forms of shock.
• Chapter Review Questions
• PART V RESPIRATORY PHYSIOLOGY
• CHAPTER 18 Ventilation and the Mechanics of Breathing
• INTRODUCTION
• LUNG STRUCTURAL AND FUNCTIONAL RELATIONSHIPS
• The airway tree divides repeatedly to increase the lung’s surface area for gas exchange.
• Vascular and airway trees merge to form a blood–gas interface for gas diffusion.
• PULMONARY PRESSURES AND AIRFLOW DURING BREATHING
• The diaphragm is the main muscle of breathing to expand the thoracic cavity.
• A difference in partial pressure causes O2 and CO2 to diffuse across the alveoli/capillary membrane.
• A change in pleural pressure is critical for lung inflation and deflation.
• Transpulmonary and transairway pressures prevent lung and airway collapse.
• Changes in alveolar pressure moves air in and out of the lungs.
• SPIROMETRY AND LUNG VOLUMES
• Spirometry measures specific lung volumes.
• Forced vital capacity is one of the most important test in assessing overall lung function.
• Residual lung volume cannot be measured directly by spirometry.
• MINUTE VENTILATION VERSUS ALVEOLAR VENTILATION
• Not all of the inspired air reaches the alveoli and becomes wasted air.
• Alveolar ventilation is the amount of fresh air that participates in alveolar gas exchange.
• Alveolar ventilation is determined by measuring the patient’s volume of expired carbon dioxide.
• ELASTIC PROPERTIES OF LUNG AND CHEST WALL
• Elastic recoil of the lungs directly affects inflation and deflation.
• Lung compliance measures distensibility.
• Elastic recoil of the chest wall affects lung expansion.
• Differences in regional lung compliance cause uneven ventilation.
• Alveolar surface tension affects lung compliance.
• Surfactant lowers surface tension and stabilizes alveoli at low lung volumes.
• Alveolar type II cells produce pulmonary surfactant.
• Alveoli are interconnected, which promotes alveolar stability.
• AIRWAY RESISTANCE AND THE WORK OF BREATHING
• The major sites of airway resistance for decreasing airflow are the bronchi.
• At low lung volumes, airways become compressed causing a mark increase in airway resistance.
• Airway patency is affected by changes in smooth muscle tone.
• Deep-sea diving alters airway resistance.
• Forced expiration compresses airways and increases airway resistance.
• Lung compliance affects where the equal pressure point is established in airways.
• Inspiratory muscles inflate the lungs and overcome airway resistance.
• Chapter Review Questions
• CHAPTER 19 Gas Transfer and Transport
• GAS DIFFUSION AND UPTAKE
• Oxygen and carbon dioxide move across the alveolar–capillary membrane by diffusion.
• Pulmonary capillary blood flow is the major determinant in transferring oxygen from the alveoli to the blood.
• DIFFUSING CAPACITY
• Diffusing capacity measures oxygen uptake across the alveolar–capillary membrane.
• Blood hematocrit and pulmonary capillary blood volume affect lung diffusing capacity (DL) for oxygen.
• GAS TRANSPORT BY THE BLOOD
• Most of the oxygen in the blood is transported by hemoglobin.
• Oxyhemoglobin–equilibrium curve illustrates the effect that plasma PO2 has on the loading and unloading of oxygen from hemoglobin.
• Blood pH, body temperature, and arterial PCO2 significantly alter the P50.
• Carbon monoxide has a greater binding affinity for hemoglobin than that of oxygen.
• Most of the carbon dioxide in the blood is transported as bicarbonate.
• RESPIRATORY CAUSES OF HYPOXEMIA
• The difference between alveolar–arterial oxygen tension is due to venous admixture.
• Regional hypoventilation is the major cause of hypoxemia.
• Chapter Review Questions
• CHAPTER 20 Pulmonary Circulation and Matching Ventilation/Perfusion
• FUNCTIONAL ORGANIZATION
• Pulmonary vessels and airways branch together in parallel.
• Pulmonary circulation has numerous secondary functions.
• Conducting airways have their own separate circulation.
• PULMONARY HEMODYNAMIC
• Pulmonary vascular resistance falls with increased cardiac output.
• Pulmonary vascular resistance increases at high and low lung volumes.
• Low oxygen tension in the lung causes pulmonary vasoconstriction.
• FLUID EXCHANGE IN THE PULMONARY CAPILLARIES
• Surface tension causes a fluid flux out of the pulmonary capillaries.
• Pulmonary edema is caused by excess fluid accumulation in lung alveoli and interstitial space.
• BLOOD FLOW DISTRIBUTION IN THE LUNGS
• Gravity causes lungs to be underperfused at the apex and overperfused at the base.
• Regional ventilation and blood flow are not matched at the base of the lungs and apex.
• SHUNTS AND VENOUS ADMIXTURE
• Venous admixture is caused by a shunt and a low ventilation/perfusion ratio.
• Chapter Review Questions
• CHAPTER 21 Control of Breathing
• INTRODUCTION
• INVOLUNTARY AND VOLUNTARY CONTROL OF BREATHING
• Minute ventilation is linked to metabolic demands and to blood gases.
• The respiratory centers are located in the pons and medulla.
• Inspiratory activity is switched off to initiate expiration.
• Expiration can be either involuntary or voluntary.
• PULMONARY NEURAL REFLEXES MODIFY BREATHING
• Mechanoreceptors mediate reflexes that protect the lung.
• Pulmonary irritant receptors respond to inhaled irritants.
• Pulmonary J receptors provide feedback about fluid volume adjacent to the alveoli and pulmonary capillaries.
• Proprioceptors provide feedback regarding the body’s position and movement.
• Central and peripheral chemoreceptors affect the rate and depth of breathing.
• Cerebrospinal fluid has a weak buffering system and is sensitive to changes in pH.
• Changes in cerebrospinal pH stimulate the respiratory centers in the medulla.
• The ventilatory response to hypoxia is inversely related to the arterial blood oxygen saturation.
• PHYSIOLOGIC RESPONSES TO ALTERED OXYGEN AND CARBON DIOXIDE
• VENTILATORY RESPONSES TO ALTERED ENVIRONMENTS
• Ventilatory response to acidosis is initiated and sustained by stimulating the peripheral chemoreceptors.
• Arterial PCO2, pH, or PaO2 are not involved in stimulating exercise-induced hyperpnea.
• CONTROL OF BREATHING DURING SLEEP
• Sleep changes the breathing frequency and inspiratory flow rate.
• Sleep blunts the respiratory sensitivity to carbon dioxide.
• Arousal mechanisms protect the sleeper.
• Upper airway tone may be compromised during REM sleep.
• CONTROL OF BREATHING IN UNUSUAL ENVIRONMENTS
• Ventilatory response to chronic hypoxia differs from acute hypoxia.
• The ventilatory response to chronic hypoxia occurs in two stages.
• Acclimatization to altitude leads to a sustained increase in ventilation.
• Cardiovascular changes that accompany acclimatization improve oxygen delivery to the tissues.
• Hypoxia-induced pulmonary hypertension leads to altered lung function.
• Breath-holding overrides basic breathing reflexes.
• The diving reflex allows divers to stay under water over an extended period of time.
• Chapter Review Questions
• PART VI RENAL PHYSIOLOGY AND BODY FLUIDS
• CHAPTER 22 Kidney Function
• INTRODUCTION
• OVERVIEW OF RENAL FUNCTION
• Kidneys are innervated by the sympathetic nervous system.
• Kidneys perform a wide range of key functions.
• THE NEPHRON: THE FUNCTIONAL UNIT OF THE KIDNEY
• The renal tubules are divided into segments with unique transport and structural properties.
• The juxtaglomerular apparatus is the functional site of renin production.
• The nephron architecture gives rise to two distinct regions in the kidney.
• Urine formation results from three basic processes.
• RENAL BLOOD FLOW
• Optimal renal blood flow is maintained by autoregulation.
• Renal blood flow is altered by several neurohumoral factors.
• GLOMERULAR FILTRATION
• The glomerular filtration barrier is thicker than the systemic capillaries but more permeable.
• The GFR is determined by the combined effects of glomerular capillary hydrostatic pressure, capillary oncotic pressure, and renal blood flow.
• Changes in afferent and efferent arteriolar resistance affect GFR by altering both glomerular capillary hydrostatic pressure and renal blood flow.
• Hydrostatic and oncotic pressures in the Bowman capsule alter glomerular filtration primarily in renal pathological states.
• The ultrafiltration coefficient depends on the properties of the glomerular filtration barrier.
• Proteinuria is the hallmark of a glomerular disorder.
• RENAL CLEARANCE AND KIDNEY FUNCTION
• GFR can be calculated by calculating the renal clearance of inulin.
• Plasma creatinine clearance is used clinically to estimate GFR.
• Plasma creatinine concentration is inversely related to GFR.
• Renal blood flow can be determined from para-aminohippurate clearance.
• Renal clearance can be used to calculate net tubular reabsorption or secretion.
• BASIC PRINCIPLES OF RENAL TUBULAR TRANSPORT
• The proximal tubule is the primary reclamation unit for essential plasma solutes that are filtered by the glomerulus.
• Tubular reabsorption involves diffusion and active transport.
• Urea reabsorption is dependent on the reabsorption of water in the proximal tubule.
• The Na+/K+-ATPase pump is essential for tubular reabsorption of sodium and other solutes.
• Sodium transport in the renal tubule is load dependent as part of the glomerulotubular balance mechanism for sodium excretion.
• Reabsorption of glucose by the proximal tubule is transport limited.
• Transport of NaCl, urea, and water in the loop of Henle is determined by unique transport properties and peritubular environments in different segments of the loop.
• Active sodium reabsorption in the thick ascending limb of the loop of Henle, without reabsorption of water, further reduces the osmolarity of the tubular fluid.
• Solute reabsorption processes in the distal nephron are quantitatively small but can be altered by drugs and hormonal control mechanisms.
• Sodium and chloride enter the distal convoluted tubule cells at the apical membrane through a Na–Cl cotransporter and are actively reabsorbed across the basolateral membrane.
• Aldosterone stimulates Na+ reabsorption in the collecting duct.
• TUBULE SECRETION
• PAH is secreted exclusively by the proximal tubules and provides insight into proximal secretory processes.
• Proximal tubule secretion eliminates many toxins and drugs from the blood.
• The cortical collecting duct is the primary site for potassium secretion.
• URINARY CONCENTRATION MECHANISMS AND WATER CONSERVATION BY THE KIDNEY
• The kidney’s ability to concentrate urine osmotically is an important adaptive mechanism for survival.
• Antidiuretic hormone produces urine that is osmotically concentrated.
• Creation of the vertical peritubular osmotic gradient by countercurrent multiplication in the loops of Henle is the underlying driver for the urine concentrating ability of the kidney.
• The countercurrent multiplication mechanism in juxtamedullary nephrons requires urea.
• Countercurrent exchange and the vasa recta maintain the vertical osmotic gradient in the renal medullary interstitium.
• Urine hyperosmolarity requires the loops of Henle, vasa recta, and collecting ducts to function as an integrated system.
• Low plasma ADH levels lead to dilute urine.
• MICTURITION
• The urinary tract provides the pathway for transporting, storing, and eliminating urine.
• Urinary incontinence is loss of bladder control.
• Chapter Review Questions
• CHAPTER 23 Regulation of Fluid and Electrolyte Balance
• INTRODUCTION
• FLUID COMPARTMENTS OF THE BODY
• Fluid compartment volumes are measured by indicator–dilution methods.
• The ICF and ECF have different solute composition but similar osmolalities.
• Changes in intracellular volume and osmolality occur through changes in volume and osmolality in the extracellular fluid.
• Diagrammatic methods can be used to demonstrate changes in the volume and osmolality of the ICF and fastECF in response to volume and osmolal perturbations.
• WATER BALANCE
• Homeostatic fluid balance is dependent on water intake and water loss.
• ADH control of water balance is critical in regulating extracellular fluid osmolality.
• Excess water intake and blood loss have opposite effects on plasma ADH levels.
• Plasma osmolality and blood volume work in concert to regulate ADH release.
• FLUID–ELECTROLYTE DISTURBANCES AND RENAL FUNCTION
• Water intake is governed by the thirst center in the hypothalamus.
• SODIUM BALANCE
• Kidneys conserve sodium and limit sodium excretion to a small percentage of the initial sodium-filtered load.
• Glomerulotubular balance prevents major changes in Na+ excretion.
• Elevated renal capillary hydrostatic pressure increases Na+ excretion.
• Extracellular Na+ is regulated by the renin–angiotensin–aldosterone system and atrial natriuretic peptide.
• Stimulation of the renal sympathetic nerves inhibits Na+ excretion.
• Diuretics promote Na+ excretion by the kidney.
• Sodium balance is maintained by the kidney adjusting renal excretion of sodium to match sodium intake.
• Modifying sodium excretion to match changes in sodium intake is triggered in the body by the effect of sodium on plasma volume.
• POTASSIUM BALANCE
• Distribution of potassium between the intracellular and extracellular fluid is sensitive to blood chemistry, hormones, drugs, and pathological conditions.
• Abnormal renal K+ excretion is the major cause of potassium imbalance.
• Changes in renal potassium excretion parallel changes in dietary potassium intake.
• Sodium deprivation does not lead to potassium loss by the kidneys.
• RENAL HANDLING OF CALCIUM
• RENAL HANDLING OF MAGNESIUM
• RENAL HANDLING OF PHOSPHATE
• Chronic renal disease often leads to an elevate plasma phosphate.
• Chapter Review Questions
• CHAPTER 24 Acid–Base Homeostasis
• INTRODUCTION
• BASIC PRINCIPLES OF ACID–BASE CHEMISTRY
• Acids dissociate to release hydrogen ions in solution.
• pH is inversely related to hydrogen ion concentration.
• Buffers protect the stability of the blood pH.
• METABOLIC PRODUCTION OF ACIDS IN THE BODY
• Cellular oxidation provides a constant source of carbon dioxide and H+.
• Incomplete metabolism of carbohydrates and fats are a major source of acid production.
• Dietary proteins from meat and vegetables produce a net acid gain that threatens acid–base balance.
• THE BODY’S INTEGRATED BUFFERING SYSTEMS
• Phosphate, protein, and bicarbonate are the body’s main chemical buffers.
• The bicarbonate–carbon dioxide system is a key physiologic buffer.
• A negative feedback system protects the blood pH from a surge of endogenous acids.
• Lungs regulate blood pH by exhaling CO2 to change arterial PCO2.
• Kidneys maintain the body’s acid–base homeostasis by reclaiming filtered bicarbonate, generating new bicarbonate, and excreting excess acids or bases.
• Urinary ammonia is the major source of excess acid secreted.
• Kidneys regulate blood pH first by reabsorbing filtered bicarbonate.
• Blood electrolytes, blood gases, aldosterone, and carbonic anhydrase activity affect renal acid secretion.
• REGULATION OF INTRACELLULAR pH
• Cellular pH is maintained by extruding hydrogen ions.
• PHYSIOLOGIC DISTURBANCES OF ACID–BASE BALANCE
• Respiratory acidosis and alkalosis are caused by altered levels of PaCO2.
• Respiratory acidosis and alkalosis are buffered primarily within cells.
• Lungs and kidneys compensate for respiratory acidosis and alkalosis.
• Metabolic acidosis is the result of an abnormally low pH in tissue and blood due to an increase in nonvolatile acids.
• Metabolic acidosis is buffered by cellular fluid, bone, lungs, and kidneys.
• Plasma anion gap is used to determine the etiology of metabolic acidosis.
• Metabolic alkalosis is due primarily to the abnormally high loss of nonvolatile acids.
• Metabolic alkalosis is buffered primarily by lungs and kidneys.
• pH–bicarbonate diagrams can be used clinically to determine the cause of acid–base disorders.
• Chapter Review Questions
• PART VII GASTROINTESTINAL PHYSIOLOGY
• CHAPTER 25 Gastrointestinal Motility
• INTRODUCTION
• ORGANIZATION OF THE DIGESTIVE SYSTEM
• Gastrointestinal tract wall contains smooth muscle for motility.
• Circular and longitudinal muscle layers of the intestine differ in both structure and function.
• Sphincters prevent reflux between specialized compartments of the GI tract.
• Enteric nervous system controls activity along the GI tract.
• GASTROINTESTINAL MOTILITY
• Peristalsis and propulsion are the major types of GI motility.
• Peristalsis occurs during and shortly after a meal.
• Peristalsis is a polysynaptic neural reflex.
• SWALLOWING AND ESOPHAGEAL MOTILITY
• Swallowing involves voluntary and involuntary muscular contractions.
• ESOPHAGEAL MOTILITY
• Motility disorders constitute a major cause for gut pathophysiological conditions.
• GASTRIC MOTILITY
• Gastric motility impacts stomach filling.
• Gastric contents impacts motility and emptying.
• Vomiting is a forceful discharge of the stomach contents.
• SMALL INTESTINAL MOTILITY
• Gastric contents entering the upper GI tract stimulate the enteric nervous system.
• Leaky gut syndrome is a digestive disorder that alters the lining of the gut.
• LARGE INTESTINAL MOTILITY
• Power propulsion is unique to the large intestine.
• Ascending colon receives intestinal contents from the terminal ileum.
• Motility of the transverse colon is uniquely designed for storage and removal of water from the feces.
• Power propulsion in the descending colon is responsible for mass movements of feces into the sigmoid colon and rectum.
• Rectosigmoid, anal canal, and pelvic floor musculature preserve fecal continence.
• Anal canal is innervated by somatosensory nerves.
• Control of defecation involves the central and enteric nervous systems.
• Motility disorders are multifactorial and difficult to detect.
• INTESTINAL SMOOTH MUSCLE
• Smooth muscles of the GI track contract spontaneously in the absence of neural or endocrine influence.
• GI and esophageal smooth muscles behave as a functional electrical syncytium due to the close proximity of adjacent muscle fibers.
• Electrical activity in GI muscles consists of slow waves and action potentials.
• Electrical slow waves of the gastric and intestinal track are generated by the interstitial cells of Cajal.
• Each slow wave of the stomach, small intestine, and colon are determined by ENS.
• GUT MOTILITY AND DIGESTIVE FUNCTION
• Neural integrative centers control the moment-to-moment motor activity of the gut.
• Parasympathetic neurons innervate the gut from the medulla oblongata and sacral spinal cord.
• Dorsal vagal complex in the medulla controls the upper GI tract.
• Vagovagal reflex controls contractions of GI muscle layers in response to food stimuli.
• Sympathetic stimulation to the gut inhibits gastrointestinal function.
• Mixed splanchnic nerves innervate the gut and carry sensory information from and efferent sympathetic signals to the GI tract.
• ENTERIC MOTOR NEURONS
• Excitatory musculomotor neurons activate smooth muscle contraction in the gut.
• Inhibitory junction potentials diminish gut smooth muscle excitability.
• Inhibitory neurotransmitters block phasic contractions in the gut.
• Strength of gut smooth muscle contraction is directly related to the activation of the inhibitory neurons.
• Motor behavior of the antral pump consists of leading and trailing contractile components triggered by gastric action potentials.
• Action potentials in the antral pump are modulated by musculomotor neurons in the gastric ENS.
• Motor behavior of the gastric reservoir differs from the gastric antrum.
• Motor patterns in the stomach and small intestine reflect the presence and absence of intraluminal nutrients.
• MMC acts as “housekeeper” for the small intestine.
• Chapter Review Questions
• CHAPTER 26 Gastrointestinal Secretory Functions
• GASTROINTESTINAL SECRETION
• SALIVARY SECRETION
• The salivon is the functional unit of the salivary gland.
• The intercalated ducts contain secretory granules that synthesize proteins.
• Saliva electrolyte composition is dependent on the rate of secretion.
• Saliva contains two major proteins that serve as lubricant and aids in the digestion of starches.
• Saliva is the medium that baths the oral taste receptors in which aroma and taste compounds are released.
• Saliva performs immunologic functions by lysing bacteria and killing HIV-infected leukocytes.
• Acidic food is a potent stimulus of salivary secretion.
• Saliva secretion is under autonomic control.
• Hormones affect saliva secretion.
• Esophageal secretion acts as a lubricant and a protective barrier.
• GASTRIC SECRETION
• Mucous gel layer protects the gastric epithelium.
• Parietal cells of the oxyntic glands secrete hydrochloric acid.
• Gastric secretion occurs in three phases.
• Acid production in the stomach parallels rates of gastric secretion.
• Pepsin is the main gastric enzyme in protein digestion.
• Gastric secretion is under neural and hormonal control.
• Gastric hormones inhibit acid secretion.
• PANCREATIC SECRETION
• Pancreatic secretion occurs in three phases.
• Pancreatic acinar cells are the functional unit of the exocrine pancreas.
• Pancreatic secretions are rich in bicarbonate ions.
• Pancreatic enzyme secretion is under neural and hormonal control.
• BILIARY SECRETION
• Two main functions of bile acids are to emulsify fat and excrete cholesterol.
• Cholesterol is an essential lipid for cellular function and its homeostasis is tightly regulated.
• Bile secretion is under neural and hormonal control.
• Bile acids are secreted into bile by two transport systems, an ATP-dependent system and a voltage-dependent system.
• Bile acids are potentially toxic to cells, and their concentrations are tightly regulated.
• Gallbladder bile differs from hepatic bile.
• Bile salts are recycled between the small intestine and the liver.
• Bilirubin is the major component of bile pigments.
• Gallstones form when cholesterol becomes supersaturated.
• INTESTINAL SECRETION
• Intestinal secretions provide lubrication and protective functions.
• Intestinal fluid hypersecretion is stimulated by toxins and other luminal stimuli.
• Dietary fiber enhances gastrointestinal function.
• Chapter Review Questions
• CHAPTER 27 Gastrointestinal Digestion and Absorption of Nutrients
• INTRODUCTION
• THE GASTROINTESTINAL SYSTEM
• Mechanical and enzymatic digestion starts in the mouth.
• Salivary amylase initiates digestion of carbohydrates.
• Salivary lipase digests triglycerides.
• GASTRIC DIGESTION AND ABSORPTION
• Gastric enzymes include pepsin, gastric amylase, and gastric lipase.
• Gastric epithelium absorbs certain non-nutrient molecules.
• THE SMALL INTESTINE
• Dietary fiber is beneficial for gut motility and digestion.
• Carbohydrates are the main source of energy for the body.
• DIGESTION AND ABSORPTION: CARBOHYDRATES
• Pancreatic α-amylase digests carbohydrates in the duodenum.
• Enterocytes hydrolyze disaccharides and absorb monosaccharides.
• Disaccharide deficiency impairs carbohydrate absorption.
• DIGESTION AND ABSORPTION: LIPIDS
• Emulsification is the first step in fat digestion.
• Lipases are water-soluble enzymes that digest fats into monoglycerides and free fatty acids.
• Phospholipase A2 and carboxyl ester hydrolase enhance lipolytic activity.
• Enterocytes absorb lipids and secrete chylomicrons and very low density lipoproteins.
• Altered lipase and bile secretion lead to dysfunction of lipid digestion and absorption.
• DIGESTION AND ABSORPTION: PROTEINS
• Nondietary proteins have endogenous sources.
• Protein digestion occurs in the stomach and the small intestine.
• Specific transporters are used by the intestinal enterocytes to absorb digested proteins.
• Genetic disorders lead to impaired protein absorption.
• Nucleoproteins are digested in the small intestine.
• ABSORPTION: VITAMINS
• Vitamins are essential for metabolic function.
• ABSORPTION: ELECTROLYTES AND MINERALS
• Minerals are required for physiologic function.
• ABSORPTION: WATER
• Water is absorbed in the gut by osmosis.
• LIVER FUNCTION
• Liver function is essential for maintaining the body’s homeostatic and metabolic activity.
• Liver’s arrangement of lobule hepatocytes enhances rapid exchange of metabolites.
• Hepatic portal vein is the main blood supply to the liver.
• Hepatic portal vein contains nutrients, minerals, and toxins extracted from the gut’s digestion.
• Liver serves as a blood reservoir and a source of lymph.
• Liver regeneration is a unique phenomenon that helps to maintain optimal homeostasis for the body.
• LIVER: CARBOHYDRATE METABOLISM
• Liver plays a central role in regulating carbohydrate metabolism.
• Liver kinases are involved in monosaccharide metabolism.
• Fasting triggers glycogenolysis in the liver.
• LIVER: LIPID METABOLISM
• Lipoproteins function as transport carriers for blood lipids.
• Liver produces ketone bodies during gluconeogenesis.
• Liver is involved in maintaining blood cholesterol levels.
• LIVER: PROTEIN METABOLISM
• Ammonia is converted to urea by the liver.
• LIVER: NUTRIENT STORAGE
• Liver takes up, stores, and releases fat-soluble vitamins.
• Liver plays a key role in the transport, storage, and metabolism of iron.
• LIVER: DRUG METABOLISM
• Drug elimination by the liver occurs in three phases.
• Liver enzymes involved in drug metabolism are affected by multiple factors.
• Liver clears the blood clotting factors from the circulatory system.
• LIVER: ENDOCRINE FUNCTION
• Liver activates and degrades hormones.
• LIVER: IMMUNE FUNCTION
• Liver architecture contributes to its role in immunity.
• Liver cells are involved in innate immunity.
• Chapter Review Questions
• PART VIII TEMPERATURE REGULATION AND EXERCISE PHYSIOLOGY
• CHAPTER 28 Regulation of Body Temperature
• INTRODUCTION
• BODY TEMPERATURE AND HEAT TRANSFER
• Core temperature mirrors central blood temperature.
• Skin, the largest organ in the body, plays a major role in heat exchange and thermoregulation.
• Peripheral thermoreceptors in the skin code absolute and relative temperatures.
• THERMOREGULATION: HEAT PRODUCTION AND HEAT LOSS
• METABOLIC RATE AND HEAT PRODUCTION AT REST
• Metabolic rate is the amount of energy expended under standard conditions.
• Skeletal muscle is the main source of heat during external work.
• Sweating is the primary means of heat loss in humans.
• Heat exchange with the environment is proportional to the body’s surface area.
• Heat storage is a balance between net heat production and net heat loss.
• HEAT DISSIPATION
• Large amounts of body heat can be dissipated through sweat evaporation.
• Increased vasodilation of the skin augments heat loss.
• THERMOREGULATORY CONTROL
• Temperature is perceived through thermal sensation.
• Thermal defense mechanisms operate through changes in heat production and heat loss.
• Hypothalamus integrates thermal information from the core and the skin.
• The set point is the body’s internal “thermostat.”
• Biologic rhythms and altered physiologic states can change the thermoregulatory set point.
• Skin temperature alters cutaneous blood flow and sweat gland responses.
• Sweat gland “fatigue” alters thermoregulation and can cause overheating.
• THERMOREGULATORY RESPONSES DURING EXERCISE
• Core temperature rises during exercise, triggering heat loss responses.
• Exercise in hot environments can impair cardiac filling.
• HEAT ACCLIMATIZATION
• Changes in basal metabolism, heart rate, cutaneous blood flow, and sweat rate occur with heat acclimation.
• Heat acclimatization modifies fluid and electrolyte balance.
• PHYSIOLOGICAL RESPONSES TO COLD
• Arteriole vasoconstriction reroutes blood away from the skin to conserve heat.
• Shivering is a heat-producing mechanism in response to hypothermia.
• Cold acclimatization is an important characteristic in thermal regulation and maintaining homeostasis.
• CLINICAL ASPECTS OF THERMOREGULATION
• Fever is one of the body’s immunologic responses to a bacterial or viral infection.
• Tolerance to heat and cold is dependent on factors affecting thermoregulatory responses.
• Heat stress can lead to pathophysiologic disorders.
• Drop in core temperature results in hypothermia.
• Chapter Review Questions
• CHAPTER 29 Exercise Physiology
• INTRODUCTION
• OXYGEN UPTAKE AND EXERCISE
• Maximal oxygen uptake quantitates the energy expenditure during dynamic exercise.
• CARDIOVASCULAR RESPONSES TO EXERCISE
• Blood flow is preferentially directed to the working skeletal muscle during exercise.
• Cardiovascular responses differ with acute and chronic exercise.
• Exercise increases levels of “good” cholesterol and reduces the “bad” cholesterol.
• Exercise prevents cardiovascular diseases and reduces mortality.
• Cardiovascular response to pregnancy is similar to chronic exercise.
• RESPIRATORY RESPONSES TO EXERCISE
• Ventilation is matched to meet the metabolic demands during a wide range of exercise conditions.
• Training has minimal effects on improving lung function.
• EXERCISE-INDUCED CHANGES IN SKELETAL MUSCLE DYNAMICS AND BONE METABOLISM
• ADP accumulation, not lactic acid production, is the major cause of muscle fatigue.
• Endurance training enhances muscle oxidative capacity.
• Isometric contraction stimulates muscle hypertrophy.
• Exercise plays a key role in calcium homeostasis.
• Skeletal muscle secretes a spectrum of cytokines and proteins called myokines in response to exercise.
• Exercise is the best medicine for the brain.
• OBESITY, AGING, AND IMMUNE RESPONSES TO EXERCISE
• In obese patients, chronic exercise preferentially increases caloric expenditures over increased appetite.
• Exercise has a major impact on regulating blood glucose in diabetic patients.
• Exercise affects aging more profoundly than longevity.
• Exercise has modest effect on immune function.
• Chapter Review Questions
• PART IX ENDOCRINE PHYSIOLOGY
• CHAPTER 30 Endocrine Control Mechanisms
• INTRODUCTION
• GENERAL ENDOCRINE CONCEPTS
• Hormones are chemical messengers released by a cell that regulate many biological functions.
• Hormones initiate a cell response by binding to specific receptors.
• Hormone regulation occurs through feedback control.
• Signal amplification is part of the overall mechanism of hormone action.
• Hormones can have multiple, and share some, actions with other hormones.
• Many hormones are secreted in a defined rhythmic pattern.
• CHEMICAL NATURE OF HORMONES
• Amine-derived hormones consist of one or two modified amino acids.
• Polypeptide-derived hormones are diverse in size and complexity.
• Steroid hormones are derived from cholesterol.
• MEASUREMENT OF CIRCULATING HORMONES
• Hormones can circulate either free or bound to carrier proteins.
• Peripheral tissues transform, degrade, and excrete hormones.
• MECHANISMS OF HORMONE ACTION
• Biologic response is partly determined by hormone–receptor binding kinetics.
• Dose–response curves determine changes in responsiveness and sensitivity.
• Chapter Review Questions
• CHAPTER 31 Hypothalamus and the Pituitary Gland
• STRUCTURE OF THE HYPOTHALAMIC–PITUITARY AXIS
• Hypothalamic neurons terminate in the posterior lobe to secrete posterior pituitary hormones.
• Distinct cell types within the anterior pituitary lobe synthesize six different hormones.
• Releasing hormones can stimulate or inhibit the synthesis and secretion of an anterior pituitary hormone.
• POSTERIOR PITUITARY HORMONES
• Arginine vasopressin increases the reabsorption of water by the kidneys.
• Oxytocin stimulates the contraction of smooth muscle in the mammary glands and uterus.
• ANTERIOR PITUITARY HORMONES
• ACTH regulates the function of the adrenal cortex.
• ACTH is synthesized by the enzymatic cleavage of proopiomelanocortin.
• TSH regulates thyroid gland function.
• TSH synthesis is stimulated by continuous hypothalamic TRH secretion.
• LH and FSH regulate sexual development and reproductive function.
• Prolactin regulates milk secretion from the mammary gland.
• Target tissue hormones feedback to inhibit anterior pituitary hormone synthesis and release.
• HYPOTHALAMIC–PITUITARY REGULATION OF GROWTH
• GHRH and somatostatin regulate GH synthesis and secretion by somatotrophs.
• GH stimulates production of insulin-like growth factor 1 (IGF-1) and IGF binding protein by the liver.
• GH and IGF-1 both inhibit GH secretion by somatotrophs.
• Growth hormone release is pulsatile and changes with age.
• IGF-1 mediates most of the growth promoting effects of GH.
• GH acts on liver, muscle, and adipose tissue to regulate metabolism in these tissues.
• GH deficiency impairs growth in children and alters body composition in adults.
• GH excess results in gigantism in children and acromegaly in adults.
• Thyroid hormone, sex hormones, and glucocorticoids also influence growth.
• Chapter Review Questions
• CHAPTER 32 Thyroid Gland
• THYROID HORMONE SYNTHESIS, SECRETION, AND METABOLISM
• Thyroid hormones are made by iodinating and storing thyroglobulin in the follicular lumen.
• Follicular cells phagocytose and hydrolyze thyroglobulin to secrete thyroid hormones.
• Deiodination in peripheral tissues activate and inactivate thyroid hormones.
• Thyroid hormones are degraded by enzymatic modification.
• The hypothalamus and pituitary regulate thyroid hormone production by the thyroid gland.
• TSH stimulates thyroid hormone release and follicular cell growth.
• Dietary iodide is essential for the synthesis of thyroid hormones.
• THYROID HORMONE EFFECTS ON THE BODY
• Triiodothyronine (T3) binds a nuclear receptor to regulate gene transcription.
• Thyroid hormones are crucial for brain maturation during fetal development.
• Body growth and development require thyroid hormone.
• Thyroid hormones are a major determinant of basal metabolic rate.
• Carbohydrate, fat, and protein metabolism are regulated by thyroid hormone.
• ABNORMALITIES OF THYROID FUNCTION IN ADULTS
• Hyperthyroidism increases energy expenditure and causes weight loss.
• Hypothyroidism decreases metabolism and causes weight gain.
• Resistance to thyroid hormone impairs thyroid hormone action.
• Significant decreases in T3 and T4 occur in severe illness.
• Chapter Review Questions
• CHAPTER 33 Adrenal Gland
• ADRENAL STEROID HORMONE SYNTHESIS, SECRETION, AND METABOLISM
• The adrenal cortex comprises three zones that produce and secrete distinct hormones.
• Adrenal cortical cells synthesize cholesterol and take it up from the blood, for steroidogenesis.
• Cortisol and androgens are synthesized in the zona fasciculata and zona reticularis.
• Aldosterone is the result of steroidogenesis in the zona glomerulosa.
• Binding proteins increase the half-life of steroids in the circulation.
• Adrenal steroids are degraded and eliminated from the body in the urine.
• Adrenal steroid hormone synthesis and secretion are controlled by the anterior pituitary.
• ACTH regulates cholesterol uptake and steroidogenic enzyme expression in adrenal cortical cells.
• GLUCOCORTICOID EFFECTS ON THE BODY
• Glucose homeostasis during fasting is regulated by glucocorticoid action on multiple tissues.
• Anti-inflammatory and immunosuppressive effects of glucocorticoids modulate the response to injury.
• Glucocorticoids are essential for normal function of the CNS.
• Glucocorticoids support blood pressure and electrolyte homeostasis.
• Glucocorticoids can have mineralocorticoid actions, but only in disease or with pharmacologic therapy.
• ADRENAL CATECHOLAMINES
• Adrenal medulla is a modified sympathetic ganglion.
• Catecholamines defend against hypoglycemia.
• Pheochromocytomas produce excessive amounts of catecholamines.
• Chapter Review Questions
• CHAPTER 34 Endocrine Pancreas
• INTRODUCTION
• ISLETS OF LANGERHANS
• Cells of the islets of Langerhans display a highly organized arrangement.
• Cell, vascular, and neural connections likely contribute to islet cell functionality.
• MECHANISMS OF ISLET HORMONE SYNTHESIS AND SECRETION
• Glucose is a major physiological factor regulating insulin synthesis and secretion.
• Hypoglycemia stimulates glucagon secretion.
• Hyperglycemia and glucagon stimulate somatostatin secretion.
• Pancreatic polypeptide secretion and action are regulated by several factors.
• Amylin functions to mitigate the influx of glucose into the circulation.
• INSULIN AND GLUCAGON ACTION
• Insulin receptor signaling is complex and controls several biological responses.
• Insulin stimulates the transport, storage, and metabolism of glucose.
• Insulin has important lipogenic and antilipolytic effects.
• Insulin enhances the synthesis and suppresses the degradation of proteins.
• Glucagon primarily exerts its metabolic actions, via cAMP signaling, in the liver.
• Glucagon promotes hepatic glucose production, coupled with ammonia disposal.
• Glucagon promotes the oxidation of fats and ketogenesis in the liver.
• Insulin/glucagon ratio determines metabolic status.
• DIABETES MELLITUS
• Autoimmune disorder underlies type 1 diabetes.
• Insulin resistance is an underlying aspect of prediabetes, type 2 diabetes, and gestational diabetes.
• Obesity is closely linked to insulin resistance.
• Lifestyle changes and multiple classes of drugs provide therapeutic intervention.
• Diabetes mellitus leads to organ dysfunction and tissue damage.
• Chapter Review Questions
• CHAPTER 35 Endocrine Regulations of Calcium, Phosphate, and Bone Homeostasis
• INTRODUCTION
• OVERVIEW OF CALCIUM AND PHOSPHATE IN THE BODY
• Calcium and phosphate are major constituents of bone and key cellular functions.
• Distributions of calcium and phosphorus differ in bone and cells.
• Calcium and phosphorus exist in the plasma in several forms.
• Calcium and phosphorous regulation involves the GI tract, kidneys, and bone.
• CALCIUM AND PHOSPHATE METABOLISM
• Calcium and phosphate are absorbed primarily by the small intestine.
• Kidneys play an important role in plasma calcium and phosphate regulation.
• Calcium and phosphate in bone are in continuous flux.
• Osteoblasts, osteocytes, and osteoclasts constitute the major cell types in bone.
• Bone formation starts with neonatal development and continues throughout life.
• PLASMA CALCIUM AND PHOSPHATE REGULATION
• Plasma-free calcium can be rapidly buffered by nonhormonal mechanisms.
• Long-term regulation of plasma calcium and phosphate is under the control of parathyroid hormone, calcitonin, and 1,25-dihydroxycholecalciferol.
• Plasma calcium and phosphate PTH is regulated by PTH, CT, and 1,25-(OH)2D.
• BONE DYSFUNCTION
• Osteoporosis leads to decreased bone density and increased risk of fracture.
• Osteomalacia and rickets are disorders of defective bone mineralization.
• Paget disease is a chronic disorder leading to enlarged and deformed bones.
• Osteogenesis imperfecta is a genetic disorder characterized by brittle bones.
• Chapter Review Questions
• PART X REPRODUCTIVE PHYSIOLOGY
• CHAPTER 36 Male Reproductive System
• INTRODUCTION
• THE ENDOCRINE GLANDS OF THE MALE REPRODUCTIVE SYSTEM
• TESTICULAR FUNCTION AND REGULATION
• Hypothalamic GnRH regulates both LF and FSH secretion.
• LH and FSH regulate testosterone secretion and sperm production.
• Low-frequency GnRH pulses lead to FSH release, whereas high-frequency GnRH pulses stimulate LH release.
• Steroids and polypeptides from the testis inhibit both LH and FSH secretion.
• Testis is the site of sperm and seminal fluid formation.
• Sertoli cells aid in the development of sperm cells through spermatogenesis.
• Luteinizing hormone stimulates Leydig cells to produce testosterone.
• Duct system functions in sperm maturation, storage, and transport sites.
• Erection and ejaculation are under neural control.
• SPERMATOGENESIS
• Spermatogenesis, the transformation of male germ cells into spermatozoa, occurs in three phases.
• Spermatogenesis is sensitive to injury and environmental stress.
• Spermatogonia undergo several rounds of mitotic division prior to entering the meiotic phase.
• Formation of a mature spermatozoon requires extensive cell remodeling.
• Testosterone is essential for sperm production and maturation.
• ENDOCRINE FUNCTION OF THE TESTIS
• Testosterone is the major steroid produced by the Leydig cells in the testis.
• cAMP regulates luteinizing hormone that, in turn, regulates the number of Leydig cells.
• ANDROGEN ACTION AND MALE DEVELOPMENT
• Testosterone is not stored, but circulated and metabolized by peripheral tissue.
• Androgens target both reproductive and nonreproductive tissues.
• Androgens are responsible for secondary sex characteristics and masculinity.
• Androgen is involved in sexual differentiation of the brain.
• MALE REPRODUCTIVE DISORDERS
• Hypogonadism leads to a decrease in spermatogenesis, and masculine growth and development.
• Most male reproductive disorders are due to hypogonadism or hypergonadism.
• Disorders of sexual differentiation is a reproductive paradox that results from insensitivity to androgens.
• Chapter Review Questions
• CHAPTER 37 Female Reproductive System
• FEMALE REPRODUCTIVE ORGANS
• PUBERTY
• Physical signs of female puberty include thelarche, pubarche, and a growth spurt.
• An increase in pulsatile gonadotropin release stimulates gonadarche at the start of puberty.
• The timing of puberty is influenced by genetic and environmental factors.
• Defects in hypothalamic–pituitary function can alter the timing of pubertal onset.
• HORMONAL REGULATION OF THE FEMALE REPRODUCTIVE SYSTEM
• Pulsatile GnRH release is essential in regulating LH and FSH secretion.
• LH and FSH promote hormone synthesis by the ovary.
• Positive and negative ovarian feedback modulates gonadotropin secretion.
• OVARIAN STEROID SYNTHESIS
• Theca cells synthesize androgens and progesterone.
• Granulosa cells synthesize estradiol from theca cell androgens.
• Following ovulation, progesterone is the primary steroid product of the corpus luteum.
• Ovarian steroids circulate in association with binding proteins in the blood and are degraded in the liver.
• OVARIAN CYCLE
• Oogonia produce an oocyte, which is arrested in meiosis.
• Primary follicles develop independently of gonadotropins.
• LH and FSH stimulate development of the mature graafian follicle.
• A dominant follicle develops by maintaining the ability to respond to FSH.
• Dominant follicle estradiol release triggers the midcycle LH surge, leading to maturation of the oocyte and ovulation.
• Corpus luteum forms from the postovulatory follicle.
• MENSTRUAL CYCLE
• The dominant follicle matures and ovarian steroidogenesis increases during the follicular phase.
• Increased estradiol production stimulates the midcycle LH surge, inducing ovulation.
• Luteal phase progesterone and estrogen are produced by the corpus luteum.
• Estradiol and progesterone prepare the uterus for pregnancy.
• Estradiol and progesterone prepare the ductal system to support fertilization and signal ovulation.
• Menses occurs in the absence of fertilization.
• Menopause is the cessation of ovarian function and reproductive cycles.
• FEMALE REPRODUCTIVE SYSTEM DISORDERS
• Chapter Review Questions
• CHAPTER 38 Fertilization, Pregnancy, and Fetal Development
• FERTILIZATION, IMPLANTATION, AND PLACENTA DEVELOPMENT
• Cilia and smooth muscle in the female genital tract transport the gametes toward each other.
• Fertilization begins with the sperm binding to the zona pellucida, initiating the acrosomal reaction.
• Following implantation of the blastocyst in the uterine wall the placenta forms.
• The maternal and fetal circulations exchange oxygen, nutrients, and waste via the placenta.
• The placenta makes hCG, hPL, and other peptide hormones to support pregnancy.
• The maternal–placental–fetal unit produces progesterone and estrogen during pregnancy.
• MATERNAL ADAPTATION DURING AND FOLLOWING PREGNANCY
• Cardiac output and blood volume increase during pregnancy.
• Progesterone and the enlarging uterus alter pulmonary function.
• Increased renal blood flow results in decreased plasma creatinine, blood nitrogen, and osmolality.
• Endocrine function and maternal metabolism change to support fetal growth.
• The mammary gland develops to provide nutrition for the newborn.
• Placental and fetal factors signal the start of parturition.
• During the puerperium, the mother’s body returns to the prepregnancy state.
• FETAL DEVELOPMENT AND GROWTH
• Sex chromosomes dictate the development of the fetal gonads.
• Hormones from the fetal testes regulate differentiation of the internal and external genitalia.
• Disorders of sex development occur when chromosomes, gonads, or development of reproductive anatomy is atypical.
• The fetal endocrine system develops early to regulate fetal homeostasis.
• Insulin-like growth factors and insulin are required for fetal growth.
• CONTRACEPTION
• Behavioral and mechanical approaches can prevent contact of egg and sperm.
• Hormonal methods utilize progesterone and estrogen to prevent ovulation and implantation.
• Emergency contraception can be utilized following intercourse to prevent pregnancy.
• Chapter Review Questions
• PART XI AGING
• CHAPTER 39 Physiology of Aging and Organ Function
• INTRODUCTION
• AGING DEFINED
• The body’s ability to adapt to change declines with advancing age.
• Insight into successful aging came initially from adult development studies.
• Everyone wants to live longer, but no one wants to get old.
• SCIENCE OF AGING
• Epigenetics is the new science behind healthy aging.
• DNA is the master molecule of the cell.
• Epigenetics is the science studying regulatory mechanisms of organ functions that are above the level of the gene.
• Aging starts at the cellular level.
• PHYSIOLOGICAL CHANGES AND AGING
• Age-related changes in the neurological system impact the activities of the body’s organ systems.
• Cardiovascular function changes with advancing age.
• Cardioprotective and compensatory mechanisms are altered with aging.
• AGING AND RESPIRATORY CHANGES
• The chest cavity becomes weaker in older individuals.
• Lung parenchyma loses its elasticity with age.
• Environmental insult alters the lung’s immune system.
• AGING AND MUSCULOSKELETAL CHANGES
• Musculoskeletal degeneration that occurs with advancing age is caused by many factors.
• AGING AND GASTROINTESTINAL CHANGES
• Older individuals have common digestive disorders.
• Stomach function is altered with age.
• Age has little effect on intestinal function.
• Constipation is a common problem for older individuals.
• AGING AND THE ENDOCRINE SYSTEM
• AGING AND THE SENSORY SYSTEM
• Eye structure changes can affect vision with advancing age.
• The senses of smell, taste, and touch change with age.
• With advancing age, sensitivity to touch and pain decline.
• AGING AND THE URINARY SYSTEM
• Bladder function is altered with advancing age.
• Prostate growth is a normal part of aging.
• CONCLUSION
• Chapter Review Questions
• Appendix A: Common Abbreviations in Physiology
• Appendix B: Normal Blood, Plasma, or Serum Values
• Glossary
• Index