Sale!

Test bank for Pathophysiology 5th Edition by Copstead

$55.00

-21%

👉 A complete Solution Manual & Testbank Solutions

Original Source from Publisher

115 in stock

Test bank for Pathophysiology 5th Edition by Copstead
Test bank for Pathophysiology 5th Edition by Copstead $70.00 $55.00
This item is selling fast!

✅ Format: Digital copy DOC DOCX PDF RTF in a "ZIP file."

☑️ All the chapters are included.

⌛ Time: 30 min to 5 Hours after Payment

😍 Chat Online Available 24/24

Guaranteed Safe Checkout

Test bank for Pathophysiology 5th Edition by Copstead

Test bank for Pathophysiology 5th Edition by Copstead

A clear, comprehensive introduction to disease, Pathophysiology, 5th Edition explores the etiology, pathogenesis, clinical manifestations, and treatment of disorders. Units are organized by body system, and each begins with an illustrated review of anatomy and normal physiology. A discussion then follows on the disease processes and abnormalities that may occur, with a focus on the pathophysiologic concepts involved. Written by leading educators Lee-Ellen Copstead and Jacquelyn Banasik, Pathophysiology simplifies a rigorous subject with practical learning resources and includes coverage of the latest scientific findings and relevant research

 

Front Matter
Dedication
Contributors
Reviewers
Preface
Organization
Features
Ancillaries
Student Learning Resources on Evolve
Study Guide
Instructor Learning Resources on Evolve
Acknowledgments
Interactive Review – Pathophysiology
Unit I Pathophysiologic Processes
Interactive Review – Unit I
Chapter 1 Introduction to Pathophysiology
Key Questions
Framework for Pathophysiology
Etiology
BOX 1-1 ETIOLOGIC CLASSIFICATION OF DISEASES
Pathogenesis
Clinical Manifestations
Stages and Clinical Course
Treatment Implications
KEY POINTS
Concepts of Normality in Health and Disease
Statistical Normality
FIGURE 1-1 Representative example of a normal bell curve for a physiologic variable. Many physiologic variables are normally distributed within the population, so the mean ±2 standard deviations include 95% of the normal values in the sample. Approximately 2.5% of values will be above the normal range and 2.5% will be below it. There may be overlap between the values in a normal sample and those in the population with a disease, making interpretation difficult in some cases.
Reliability, Validity, and Predictive Value
Individual Factors Influencing Normality
Cultural Considerations
Age Differences
Gender Differences
Situational Differences
Time Variations
KEY POINTS
Patterns of Disease in Populations
Concepts of Epidemiology
FIGURE 1-2 Circadian rhythms of several physiologic variables in a human subject depict the effect of light and dark. In an experiment with lights on (open bars at top) for 16 hours and off (black bars at top) for 8 hours, temperature readings and plasma growth hormone, plasma cortisol, and urinary potassium levels exhibit diurnal variation.
Endemic, Pandemic, and Epidemic Diseases
Aggregate Factors
Age
FIGURE 1-3 A, The aggregate focus in disease: influence of crowds upon disease transmission. Crowd gathered at a public market in Russia. B, Crowds gathered to purchase goods at a public market in Guangzhou, China.
Ethnic group
Gender
Socioeconomic factors and lifestyle considerations
FIGURE 1-4 Risk factors for schistosomiasis include the widespread use of irrigation ditches that harbor the intermediate snail host.
Geographic location
FIGURE 1-5
FIGURE 1-6 Healthy aging: elders exercising in an aerobics class (A) and painting (B) illustrate the concept that aging and disease are not synonymous. The artist, a healthy woman in her mid-70s, is also a breast cancer survivor.
Levels of Prevention
Primary prevention
Secondary prevention
Tertiary prevention
KEY POINTS
Summary
Answer Key
Key Points
Additional Resources
References
Chapter 2 Homeostasis and Adaptive Responses to Stressors
Key Questions
Homeostasis and Allostasis
Homeostasis
Allostasis
BOX 2-1 EXAMPLES OF HOMEOSTATIC SYSTEMS
KEY POINTS
Stress as a Concept
The General Adaptation Syndrome and Allostasis
Alarm Stage
FIGURE 2-1 Steps of Selye’s alarm stage of the general adaptation syndrome.
TABLE 2-1 STAGES OF THE GENERAL ADAPTATION SYNDROME
FIGURE 2-2 Neuroendocrine interactions in response to a stressor. Receptors are excited by stressful stimuli and relay the information to the hypothalamus. The hypothalamus signals the adrenal cortex (by way of the anterior pituitary) and the sympathetic pathways (by way of the autonomic nervous system). The stress response is then mediated by the catecholamines (i.e., epinephrine and norepinephrine) and by the glucocorticoids (predominantly cortisol).
Resistance or Adaptation Stage
Exhaustion Stage
Stressors and Risk Factors
KEY POINTS
Neurohormonal Mediators of Stress and Adaptation
Catecholamines: Norepinephrine and Epinephrine
Adrenocortical Steroids: Cortisol and Aldosterone
TABLE 2-2 BRIEF SUMMARY OF EFFECTS OF CATECHOLAMINES ON TISSUES AND ORGANS OF THE BODY
TABLE 2-3 MAJOR EFFECTS OF GLUCOCORTICOIDS IN THE STRESS RESPONSE
Endorphins, Enkephalins, and Immune Cytokines
Sex Hormones: Estrogen, Testosterone, and Dehydroepiandrosterone
Growth Hormone, Prolactin, and Oxytocin
KEY POINTS
Adaptation, Coping, and Illness
Adaptation and Coping
Allostatic Overload and Illness
BOX 2-2 PHYSICAL AND BEHAVIORAL INDICATORS OF HIGH STRESS
Physical Indicators
Behavioral and Emotional Indicators
FIGURE 2-3 Effects of Allostatic Overload on Body Organs and Systems.
KEY POINTS
Summary
Answer Key
Key Points
Additional Resources
References
Unit II Cellular Function
Interactive Review – Unit II
Chapter 3 Cell Structure and Function
Key Questions
FIGURE 3-1 Structure of a typical eukaryotic cell showing intracellular organelles.
Plasma Membrane
Membrane Structure
FIGURE 3-2 Section of the cell membrane showing the lipid bilayer structure and integral membrane proteins.
FIGURE 3-3 Schematic drawing of a typical membrane phospholipid molecule showing the amphipathic nature of the structure.
Lipid Bilayer
FIGURE 3-4 The amphipathic nature of membrane lipids results in bilayer structures that tend to form spheres.
FIGURE 3-5 Chemical structures of the four most common membrane phospholipids.
Membrane Proteins
FIGURE 3-6 Portion of the cell membrane showing orientation of membrane glycoproteins toward the outer surface of the cell.
FIGURE 3-7 Structural orientation of some proteins in the cell membrane. A, Membrane-associated protein with noncovalent attachment to plasma lipids. B, Membrane protein with noncovalent attachment to another membrane protein. C, Transmembrane protein extending through the lipid bilayer. D, Covalently attached peripheral membrane protein.
FIGURE 3-8 Transport proteins may be confined to a particular portion of the cell membrane by tight junctions. Segregation of transport proteins is important for the absorptive functions of the kidney epithelial cells. N, Nucleus.
KEY POINTS
Organization of Cellular Compartments
Cytoskeleton
FIGURE 3-9 Schematic and micrographs of three major types of cytoskeletal proteins. A, Microfilaments shown are composed of actin proteins; B, intermediate filaments are a large group of various types of proteins; C, microtubules (see text).
Nucleus
Endoplasmic Reticulum
FIGURE 3-10 A, Structure of the double-membrane envelope that surrounds the cell nucleus. B, Detail of a nuclear pore.
Golgi Apparatus
FIGURE 3-11 Schematic drawing of the endoplasmic reticulum and its relationship to the Golgi apparatus and nuclear envelope.
Lysosomes and Peroxisomes
Mitochondria
FIGURE 3-12 Electron micrograph (A) and schematic drawing (B) of the mitochondrial structure. The highly convoluted inner membrane provides a large surface area for membrane-bound metabolic enzymes.
KEY POINTS
Cellular Metabolism
Glycolysis
Citric Acid Cycle
FIGURE 3-13 Ten enzymatic steps are required in glycolysis to break glucose into two three-carbon pyruvate molecules. A net gain of two ATP molecules is achieved.
FIGURE 3-14 Space-filling model of acetyl CoA.
FIGURE 3-15 Chemical structures of the compounds of the citric acid cycle (Krebs cycle). In a series of enzymatic reactions, carbon atoms are cleaved to form CO2 and high-energy hydride ions, which are carried by FAD and NAD.
FIGURE 3-16 Representation of the electron transport chain located in the inner mitochondrial membrane. High-energy electrons are passed along the chain until they combine with oxygen to form water. The energy released at each electron transfer is used to pump H+ across the membrane.
Oxidative Phosphorylation
FIGURE 3-17 Inner mitochondrial ATP synthetase captures the potential energy of the H+ gradient in a manner similar to a turbine. The proton gradient drives the synthesis of ATP from adenosine diphosphate (ADP) and inorganic phosphate (Pi). A 360-degree rotation of the rotor requires 12 H+ ions and produces 3 ATP molecules.
KEY POINTS
Functions of the Plasma Membrane
Membrane Transport of Macromolecules
Endocytosis and Exocytosis
Membrane Transport of Small Molecules
FIGURE 3-18 A, Representation of the steps of endocytosis. An invagination of the membrane occurs and pinches off to form a vesicle. Exocytosis progresses in essentially the reverse sequence. B, Electron micrograph showing the steps of endocytosis.
Active Transport Pumps
Sodium-potassium ion pump
FIGURE 3-19 Steps in the process of receptor-mediated endocytosis of cholesterol. Cholesterol is carried in the blood by LDL. The uptake of LDL with its associated cholesterol is mediated by a specific LDL-receptor protein on the cell surface. Once internalized, the cholesterol is removed from the LDL-receptor complex and used by the cell. The LDL receptors are sent back to the cell surface to bind more LDL.
Membrane calcium transporters
FIGURE 3-20 Schematic drawing of the sodium-potassium transport protein, which uses ATP to pump Na+ out of the cell and K+ into the cell against steep electrochemical gradients. This transporter is responsible for maintaining a low intracellular concentration of Na+ and a large Na+ gradient across the membrane. The energy of this Na+ gradient can be harvested by other transporters to actively transport substances.
ABC transporters
Membrane Transport Carriers
Na+-driven carriers
FIGURE 3-21 Two transporters of calcium ions are present in some cell membranes. One uses ATP as the energy source to pump calcium against a gradient (primary active transport). The other captures the potential energy of the sodium gradient to pump calcium out of the cell (secondary active transport).
Passive transport carriers
Membrane Channel Proteins
FIGURE 3-22 The ABC transporters are the largest known family of membrane transport proteins. They are characterized by an ATP-binding domain that causes a substrate pocket to be exposed first on one side of the membrane and then on the other as ATP is bound and hydrolyzed to ADP and Pi.
FIGURE 3-23 In response to insulin binding to its receptor on the cell surface, carrier proteins that transport glucose (Glut-4) are moved to the cell surface where they passively transport glucose into the cell (facilitated diffusion).
KEY POINTS
Cellular Membrane Potentials
Resting Membrane Potential
FIGURE 3-24 Gating of ion channels. A, Voltage-gated channel. B, Ligand-gated channel. C, Mechanically gated channel.
Action Potential
FIGURE 3-25 A relatively large membrane potential results from the separation of a very small number of ions across the plasma membrane.
FIGURE 3-26 Effects of changes in extracellular K+ level on the resting membrane potential. A high level of serum K+ results in a hypopolarization of the membrane. A low serum K+ level results in membrane hyperpolarization. With high serum K+ levels, the resting membrane potential is closer to threshold, making it easier to achieve an action potential. A low serum K+ level moves the resting membrane potential away from threshold, making it more difficult to achieve an action potential.
FIGURE 3-27 The action potential (AP) in excitable cells is propagated along the membrane by the sequential opening of voltage-gated sodium channels in adjacent sections of membrane. A, An action potential is initiated by the opening of sodium channels in a section of membrane. B, The action potential is regenerated in adjacent sections of membrane as more sodium channels open. The initial segment repolarizes as sodium channels close and potassium ions move out of the cell.
KEY POINTS
Intercellular Communication and Growth
Cell Signaling Strategies
FIGURE 3-28 A typical neuronal action potential showing changes in membrane potential and the associated ion conductances. NOTE: mmho is a measure of conductance (amperes per volt), also called millisiemens (mS). The steep upstroke of the action potential is attributed to the sudden influx of Na+ through voltage-gated “fast” sodium ion channels. Voltage-gated K+ channels open more slowly and stay open longer to allow K+ efflux from the cell, which aids in repolarization.
FIGURE 3-29 Three possible states of the voltage-gated sodium channel. In the open state, Na+ is allowed to pass. In the refractory state, the channel is blocked by the inactivation gate and will not open in response to a depolarizing stimulus. In the closed state, the channel will open in response to a membrane depolarization.
FIGURE 3-30 A typical cardiac muscle cell action potential showing the ion fluxes associated with each phase. Note that the repolarization phase is prolonged in comparison to the nerve action potential in Figure 3-28. This occurs because Ca2+ influx offsets the repolarizing effect of K+ efflux and a plateau in the membrane potential is seen. When the Ca2+ channels close, the membrane quickly repolarizes.
Cell Surface Receptor–Mediated Responses
FIGURE 3-31 Methods used for intercellular communication.
FIGURE 3-32 Cell adhesion proteins interact with the extracellular matrix (integrins) and with neighboring cells to maintain cell survival and differentiation.
FIGURE 3-33 Signaling by secreted ligands can occur over variable distances. A, Synaptic signaling over a very small distance between neuron and target cell. B, Paracrine signaling through the extracellular fluid between cells in a tissue. C, Long-range signaling from endocrine cells through the bloodstream to distant targets. D, Localized autocrine signaling in which the secreting cell is also the target cell.
FIGURE 3-34 There are three major types of cell surface receptor proteins. A, Ion channel–linked receptors are also called ligand-gated channels. When the ligand binds, they open to allow specific ions through the membrane. B, Enzyme-linked receptors become activated kinases when a ligand binds to them. Kinases phosphorylate target proteins and change their activity. C, G-protein–linked (coupled) receptors have seven membrane-spanning segments with a ligand-binding pocket on the outside and a G-protein–activating portion on the inside. G-protein–linked receptors activate G-proteins, which in turn influence enzymes that produce second messengers.
FIGURE 3-35 Many growth factor receptors activate protein kinase cascades within the cell. Three common pathways are shown. After binding of ligand, the receptor dimerizes and becomes phosphorylated. A cascade of kinase activations is initiated resulting in a change in target gene transcription. GTP, Guanosine triphosphate; JAK, janus kinase; MAP, mitogen-activated kinase; PI3K, phosphoinositide 3-kinase; RAS, rat sarcoma protein; STAT, signal transducer and activator of transcription.
Intracellular Receptor–Mediated Responses
Regulation of Cellular Growth and Proliferation
FIGURE 3-36 G-protein–coupled signaling. When the ligand binds to the receptor, an intracellular domain is changed into an active configuration that can interact with inactive trimeric G-proteins. The receptor induces the G-protein to release its bound GDP and Pi in exchange for a GTP molecule. When GTP binds to the α subunit of the G-protein, it is activated and diffuses away from the γβ subunits to find its target enzyme (adenylyl cyclase [AC] or phospholipase C). The α GTP stimulates its target enzyme to produce a second messenger, which in turn activates a signaling cascade within the cell. After a time, the α subunit hydrolyzes its GTP to GDP and Pi and becomes inactive. The α subunit is now in the correct conformation to reassociate with the γβ subunits and await another signal from the receptor. A, The Gs pathway increases the production of cyclic adenosine monophosphate (cAMP). B, The Gq pathway increases the production of inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). C, The Gi pathway is inhibitory to the production of cAMP. In some cases the γβ subunit also has functional activity and may regulate ion channels. ER, Endoplasmic reticulum; PKC, protein kinase C.
FIGURE 3-37 Cyclic GMP (cGMP) is an important second messenger. A, It can be synthesized by enzyme-linked receptors that are activated by water-soluble ligands such as atrial natriuretic peptide. B, Nitric oxide is an important signaling molecule that is lipid soluble and can diffuse across the cell membrane. Nitric oxide binds to and stimulates the enzyme guanylyl cyclase to produce cGMP.
FIGURE 3-38 A variety of mechanisms exist to inhibit receptor-mediated signaling cascades. A, Phosphorylation of the receptor by receptor kinases such as G-protein receptor kinases (GRKs) uncouples the enzyme from its intracellular cascade. B, Receptor internalization temporarily reduces the number of receptors displayed at the cell surface. C, Receptor degradation results in a long-term reduction in receptors (down-regulation). D, The cyclic nucleotide second messengers can be degraded by phosphodiesterase enzymes to stop the intracellular cascade. E, Phosphatase enzymes counteract the phosphorylating activities of kinases and inhibit the intracellular cascade.
FIGURE 3-39 Lipid-soluble ligands, such as steroid hormones and gases, can diffuse across the cell membrane and interact with receptors located within the cell cytoplasm or nucleus. Thyroid hormone is not lipid soluble and enters the cell through a carrier to interact with its intracellular receptor. When the ligand binds to its intracellular receptor, it forms a functional gene regulatory protein that affects the rate of transcription of its target genes. The response of the cell to intracellular ligands is generally slow and long lasting.
FIGURE 3-40 Events of the cell cycle. The cycle begins late in G1 when the cell passes a restriction point. The cell then proceeds systematically through the S phase (synthesis), G2, and M phase (mitosis).
FIGURE 3-41 Six stages of mitotic cell division.
FIGURE 3-42 The mechanism of initiation of cellular replication requires appropriate stimulation by extracellular growth factors that bind their complementary receptors on the cell surface. Activation of the receptor stimulates signaling pathways within the cell that increase cyclin proteins. The cyclins bind to cyclin-dependent kinases (Cdks) to form active enzyme complexes. The active cyclin-Cdk enzymes phosphorylate Rb protein (pRb), inducing it to release E2F transcription factors that initiate replication. In the absence of appropriate growth factor signals, the Rb protein functions to inhibit unwanted cell proliferation.
KEY POINTS
Summary
TABLE 3-1 STRUCTURE AND FUNCTION OF MAJOR CELLULAR COMPONENTS
Answer Key
Key Points
Additional Resources
References
Chapter 4 Cell Injury, Aging, and Death
Key Questions
Reversible Cell Injury
Hydropic Swelling
Intracellular Accumulations
FIGURE 4-1 Cellular swelling in kidney tubule epithelial cells. A, Normal kidney tubule with cuboidal cells; B, early ischemic changes showing surface blebs and swelling of cells.
FIGURE 4-2 General mechanisms of intracellular accumulation: (1) abnormal metabolism as in fatty change in the liver, (2) mutations causing alterations in protein folding and transport so that defective proteins accumulate, (3) deficiency of critical enzyme responsible for lysosomal degradation, and (4) an inability to degrade phagocytosed particles such as coal dust.
FIGURE 4-3 Fatty liver showing large intracellular vacuoles of lipid.
FIGURE 4-4 Roles of chaperone proteins in protein refolding and ubiquitin in protein degradation after stress-induced protein damage.
FIGURE 4-5 Accumulations of silicon dust in tissues of the lung.
KEY POINTS
FIGURE 4-6 The adaptive cellular responses of atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia.
Cellular Adaptation
Atrophy
Hypertrophy
Hyperplasia
FIGURE 4-7 A, Hypertrophy of cardiac muscle in the left ventricular chamber. B, Compare with the thickness of the normal left ventricle. This is an example of cellular adaptation to an increased cardiac workload.
Metaplasia
Dysplasia
KEY POINTS
Irreversible Cell Injury
Necrosis
FIGURE 4-8 Comparison of cellular changes in necrosis and apoptosis.
FIGURE 4-9 The four primary types of tissue necrosis. A, Coagulative; B, liquefactive; C, fat; D, caseous.
FIGURE 4-10 Cellular injury as a consequence of intracellular calcium overload.
Apoptosis
FIGURE 4-11 Each cell displays a set of receptors that enable it to respond to extracellular signals that control growth, differentiation, and survival. A, Extracellular signals are provided by the neighboring cells, secreted signaling molecules, and the extracellular matrix. B, Withdrawal of these survival signals induces the cell to initiate apoptosis.
FIGURE 4-12 Induction of apoptosis by Fas ligand. A, Target cell binds to Fas ligand on a signaling cell. B, Active Fas receptors organize and activate caspases. C, The caspases degrade the nucleus and trigger cell death.
KEY POINTS
FIGURE 4-13 Schematic of the events of apoptosis. Numerous triggers can initiate apoptosis through intrinsic cell injury pathways (mitochondrial), such as withdrawal of survival factors, various cell injuries, and protein overload or misfolding; or through extrinsic cell injury pathways (death receptors), such as binding to Fas or tumor necrosis factor receptors. A number of intracellular regulatory proteins may inhibit or promote the activation of caspases, which, when activated begin the process of cellular degradation and apoptotic cell fragmentation. Fragments are internalized by phagocytic cells.
Etiology of Cellular Injury
Ischemia and Hypoxic Injury
FIGURE 4-14 Mechanisms of ischemia-induced cell injury. Cellular damage often occurs through the formation of reactive oxygen radicals.
Nutritional Injury
Infectious and Immunologic Injury
TABLE 4-1 VITAMINS: MAJOR FUNCTIONS AND DEFICIENCY SYNDROMES
TABLE 4-2 SELECTED TRACE ELEMENTS AND DEFICIENCY SYNDROMES
TABLE 4-3 HEALTH EFFECTS OF OUTDOOR AIR POLLUTANTS
Chemical Injury
TABLE 4-4 SELECTED INDOOR AIR POLLUTANTS WITH SIGNIFICANT HEALTH RISKS
Physical and Mechanical Injury
FIGURE 4-15 Types of electromagnetic radiation.
FIGURE 4-16 The mechanism of radiation-induced genetic and cell injury.
KEY POINTS
FIGURE 4-17 Signs and symptoms of acute radiation sickness.
Cellular Aging
FIGURE 4-18 The end caps of the chromosomes are called telomeres. In most body cells, the telomeres progressively shorten with each cell replication until a critical point is reached, at which time the cell becomes dormant or dies.
Cellular Basis of Aging
Physiologic Changes of Aging
KEY POINTS
Somatic Death
TABLE 4-5 OVERVIEW OF THE PHYSIOLOGIC CHANGES OF AGING
KEY POINTS
Summary
Animations/Videos
Answer Key
Case Studies
Key Points
Additional Resources
References
Chapter 5 Genome Structure, Regulation, and Tissue Differentiation
Key Questions
FIGURE 5-1 A nucleotide consists of a sugar (deoxyribose), a phosphate group, and one of the four nucleotide bases. Nucleotides are joined by repeating sugar-phosphate bonds to form long chains, called polymers. A, Adenine; C, cytosine; G, guanine; T, thymine.
Molecular Genetics
Structure of DNA
FIGURE 5-2 The two types of DNA bases are the single-ring pyrimidines and the double-ring purines. Thymine (T) and cytosine (C) are pyrimidines, and adenine (A) and guanine (G) are purines. Base pairing occurs between A and T and between C and G because of hydrogen bonds (dots).
FIGURE 5-3 A schematic and space-filling model of the DNA double helix as proposed by Watson and Crick. The pairing of bases is specific and complementary: Cytosine (C) always pairs with guanine (G), and adenine (A) always pairs with thymine (T).
DNA Replication
FIGURE 5-4 DNA is packaged by wrapping around protein complexes called histones to form beadlike structures called nucleosomes. During cell division, the coiled DNA becomes very condensed into chromosomes that are visible under the light microscope. During interphase and when genes are being transcribed, the DNA is more loosely packaged and not visible.
Genetic Code
FIGURE 5-5 Summary of the major proteins of the DNA replication fork. Helicase unwinds the DNA double helix, whereas helix-destabilizing proteins keep the strands from reuniting. The leading strand (top) can be replicated in a continuous manner, whereas the lagging strand (bottom) must be synthesized in pieces. Okazaki fragments are formed in a “backstitching” direction and then sealed together with DNA ligase.
Transcription
FIGURE 5-6 DNA replication is semiconservative. Each of the new DNA double helices contains one newly synthesized strand and one original strand.
Translation
TABLE 5-1 RNA CODONS FOR THE DIFFERENT AMINO ACIDS AND FOR START AND STOP
BOX 5-1 TYPES OF RNA PRODUCED IN CELLS
KEY POINTS
FIGURE 5-7 A moving RNA polymerase complex unwinds the DNA helix ahead of it while rewinding the DNA behind. One strand of the DNA serves as the template for the formation of mRNA.
Regulation of the Genome
FIGURE 5-8 Schematic drawing of a transfer RNA (tRNA) molecule. Each tRNA binds a specific amino acid, which corresponds with the three-base sequence at the anticodon end.
Transcriptional Controls
FIGURE 5-9 Synthesis of a protein by the ribosomes attached to a mRNA molecule. Ribosomes attach near the start codon and catalyze the formation of the peptide chain. The mRNA strand is read in groups of three nucleotides (codons) until the stop codon is reached and the peptide is released. Several ribosomes may translate a single mRNA into multiple copies of the protein.
FIGURE 5-10 The 20 amino acids that form proteins have different chemical structures that affect their solubility in lipids and water. Nonpolar amino acids tend to locate in the lipid bilayer or in the interior of globular proteins whereas polar and charged amino acids interact well with water.
FIGURE 5-11 Gene activator proteins coordinate the assembly of general transcription factors at the promoter region of the gene to be transcribed. RNA polymerase is unable to bind and begin transcription until the requisite transcription factors are in place.
KEY POINTS
Differentiation of Tissues
Cell Diversification and Cell Memory
Mechanisms of Development
Differentiated Tissues
Epithelial Tissue
FIGURE 5-12 Organization of epidermal skin layers, showing the flattened keratinized outer layer. Epithelial cells are continually produced by stem cells at the basal lamina and then migrate to the surface.
FIGURE 5-13 Various epithelial tissue shapes and layering.
TABLE 5-2 MAJOR CATEGORIES AND LOCATION OF BODY TISSUES
FIGURE 5-14 Schematic drawing of loose connective tissue.
Connective Tissue
FIGURE 5-15 Scanning electron micrograph of fibroblasts in loose connective tissue of a rat cornea. The matrix is composed primarily of collagen fibers (magnification ×440).
FIGURE 5-16 Photomicrograph of a section of compact bone showing circular networks formed by the action of osteoclasts and osteoblasts as they remodel the bone. The osteocytes occupy the lacunae and canals.
FIGURE 5-17 Scanning electron micrograph of red and white blood cells in the lumen of a blood vessel. Red blood cells are smooth and concave, whereas white blood cells are rough and rounded.
Muscle Tissue
FIGURE 5-18 The four classes of muscle cells. A, Skeletal muscle. B, Heart (cardiac) muscle. C, Smooth muscle (bladder). D, Myoepithelial cells in a mammary gland.
FIGURE 5-19 Schematic drawing of a smooth muscle cell when relaxed (A) and contracted (B). Contraction begins with the entry of Ca2+ into the cell through L-type voltage-gated calcium channels. Ca2+ is also released from the sarcoplasmic reticulum. The calcium ions bind to cytoplasmic calmodulin to form a complex that activates myosin light chain kinase (MLCK). The kinase attaches a phosphate to the myosin head area, which stimulates its cycling activity. The myosin binds to actin filaments and tugs on them with each cross-bridge cycle. While the myosin and actin filaments pull closer together and overlap more, the muscle cell shortens. The actin filaments are attached to dense bodies that are analogous in function to the Z-disk protein in cardiac and skeletal muscle. Smooth muscle can maintain long-term actin-myosin cross-bridges that maintain a level of tone.
Nervous Tissue
FIGURE 5-20 Diagram of a typical neuron showing the cell body, axon, and dendrites. Neurons have many shapes and sizes.
KEY POINTS
Summary
Answer Key
Key Points
Additional Resources
References
Chapter 6 Genetic and Developmental Disorders
Key Questions
FIGURE 6-1 Scanning electron micrograph of a chromosome showing the two sister chromatids attached at the centromere. Sister chromatids separate during meiosis with one chromatid being distributed to each daughter cell.
FIGURE 6-2 A standard map of the banding pattern of each of the 23 chromosomes of the human. Somatic cells contain two copies of each chromosome. The centromere region is marked by the line.
FIGURE 6-3 Comparison of meiosis and normal mitotic cell division, showing only one homologous chromosome pair. In meiosis, the homologous chromosomes form a pair and exchange sections of DNA in a process called crossing over. Two nuclear divisions are required in meiosis to form the haploid germ cells.
Principles of Inheritance
DNA Mutation and Repair
FIGURE 6-4 Crossing over during meiotic prophase I results in a reassortment of genes between homologous chromosomes.
FIGURE 6-5 Punnett square shows the distribution of parental genes to their offspring. This example shows the mating of two heterozygous individuals. A, Dominant gene; a, recessive gene.
KEY POINTS
Genetic Disorders
FIGURE 6-6 Steps of DNA repair. In step 1 the damaged section is removed; in steps 2 and 3 the original DNA sequence is restored.
FIGURE 6-7 Schematic illustration of mutations that alter the messenger RNA sequence and the resulting protein amino acid sequence. A, Point mutation alters one amino acid. B, Frameshift mutation alters all downstream amino acids.
Chromosomal Abnormalities
Aberrant Number of Chromosomes
Abnormal Chromosome Structure
FIGURE 6-8 Mechanism of nondisjunction leading to aneuploidy. For simplicity, only one pair of chromosomes is shown.
FIGURE 6-9 Metaphase chromosome showing location of centromere and long and short arms of the chromatids. Gene loci are described by the chromosome number, location on short (p) or long (q) arm, region, and band.
Examples of Autosomal Chromosome Disorders
Trisomy 21 (Down Syndrome)
FIGURE 6-10 Types of chromosomal rearrangement.
Trisomy 18 (Edwards Syndrome) and Trisomy 13 (Patau Syndrome)
Cri du Chat Syndrome
Examples of Sex Chromosome Disorders
Klinefelter Syndrome
FIGURE 6-11 Typical clinical manifestations of trisomy 21 (Down syndrome).
TABLE 6-1 FREQUENCY OF TRISOMY 21 (DOWN SYNDROME) IN RELATION TO MATERNAL AGE
Turner Syndrome
FIGURE 6-12 Typical clinical manifestations of Klinefelter syndrome.
FIGURE 6-13 Typical clinical manifestations of Turner syndrome.
Multiple X Females and Double Y Males
Mendelian Single-Gene Disorders
Autosomal Dominant Disorders
Marfan Syndrome
FIGURE 6-14 A, Common symbols for pedigree analysis. B, Typical family pedigree chart.
Huntington Disease
Autosomal Recessive Disorders
FIGURE 6-15 Typical pattern of inheritance of an autosomal dominant trait (e.g., Marfan syndrome). A, Pedigree chart. B, Punnett square.
TABLE 6-2 AUTOSOMAL DOMINANT DISORDERS
Albinism
FIGURE 6-16 Clinical manifestations of Marfan syndrome. Skeletal deformities such as pectus excavatum and abnormal curvature of the thoracic spine are common findings.
Phenylketonuria
Cystic Fibrosis
Sex-Linked (X-Linked) Disorders
Hemophilia A
Nonmendelian Single-Gene Disorders
FIGURE 6-17 Typical pattern of inheritance of an autosomal recessive trait (e.g., cystic fibrosis, sickle cell anemia). A, Pedigree chart. B,Punnett square.
TABLE 6-3 AUTOSOMAL RECESSIVE DISORDERS
Triplet Repeat Mutations
FIGURE 6-18 Schematic illustration of the cystic fibrosis transmembrane conductance regulator (CFTR) located in an epithelial cell. CFTR is a transmembrane protein that transports chloride from the cytoplasm into the lumen of the bronchiole. Mutations in the CFTR transporter gene are believed to cause the thick secretions typical of cystic fibrosis.
FIGURE 6-19 Typical inheritance pattern for X-linked disorders. The risk of disease varies according to the gender of the offspring.
Mitochondrial Gene Mutations
TABLE 6-4 X-LINKED RECESSIVE DISORDERS
Genomic Imprinting
FIGURE 6-20 Pedigree chart for the transmission of the X-linked disease hemophilia A in the royal families of Europe.
FIGURE 6-21 Angelman and Prader-Willi syndromes are examples of genetic imprinting, where the location of a mutation on the maternal or paternal homologous chromosome produces a different outcome.
Polygenic and Multifactorial Disorders
KEY POINTS
Environmentally Induced Congenital Disorders
Periods of Fetal Vulnerability
Teratogenic Agents
Chemicals and Drugs
TABLE 6-5 CAUSES OF CONGENITAL MALFORMATIONS IN HUMANS
FIGURE 6-22 Vulnerable periods of fetal organ development.
TABLE 6-6 PREGNANCY CATEGORIES FOR MEDICATION ADMINISTRATION
Infectious Agents
FIGURE 6-23 Major clinical findings in the TORCH (toxoplasmosis, others, rubella, cytomegalovirus, herpes) complex of infective congenital disorders.
Radiation
Other Disorders of Infancy
KEY POINTS
Diagnosis, Counseling, and Gene Therapy
Prenatal Diagnosis and Counseling
Genetic Analysis and Therapy
Recombinant DNA Technology
FIGURE 6-24 Fluorescence in situ hybridization assay showing an interphase nucleus. The red probe hybridized to chromosome 21 and the green probe hybridized to chromosome 13. Three copies of chromosome 21 are identified, confirming the diagnosis of trisomy 21.
KEY POINTS
Summary
Answer Key
Key Points
Additional Resources
References
Chapter 7 Neoplasia
Key Questions
Benign Versus Malignant Growth
Characteristics of Benign and Malignant Tumors
Tumor Terminology
FIGURE 7-1 A, Normal Papanicolaou smear from the uterine cervix showing large, flat epithelial cells with small nuclei. B, Typical histologic appearance of anaplastic tumor cells showing variation in cell size and shape, with large, hyperchromic nuclei.
TABLE 7-1 GENERAL CHARACTERISTICS OF BENIGN AND MALIGNANT TUMORS
The Malignant Phenotype
TABLE 7-2 NOMENCLATURE FOR NEOPLASTIC DISEASES
KEY POINTS
Epidemiology and Cancer Risk Factors
Tobacco Use
Nutrition
Fat
Fiber
FIGURE 7-2 United States 2012 estimated new cancer cases (A) and estimated cancer deaths (B) in 10 leading sites by gender. Excludes basal and squamous cell skin cancers and in situ carcinomas except urinary bladder.
TABLE 7-3 SCREENING GUIDELINES FOR THE EARLY DETECTION OF CANCER IN AVERAGE-RISK ASYMPTOMATIC PEOPLE
Alcohol
Antioxidants
KEY POINTS
Genetic Mechanisms of Cancer
FIGURE 7-3 United States age-adjusted cancer death rates for selected sites in men (A) and women (B) from 1930 to 2007.
FIGURE 7-4 Annual cancer deaths attributable to smoking in males and females in the United States.
Proto-Oncogenes
Growth Factors (Mitogens)
TABLE 7-4 EXAMPLES OF GAIN-OF-FUNCTION PROTO-ONCOGENES AND THEIR MECHANISMS OF ACTION
Growth Factor Receptors
Cytoplasmic Signaling Pathways
FIGURE 7-5 Possible effects of proto-oncogene activation on growth signaling pathways. A, Production of growth factors (mitogens). B, Production of growth factor receptors. C, Intracellular pathway disturbances. D, Activation of transcription factors for growth.
FIGURE 7-6 Mechanisms of proto-oncogene activation. A, Retroviral insertion. B, Proto-oncogene mutation. C, Regulatory sequence mutation. D, Proto-oncogene amplification. RT, Reverse transcriptase.
Transcription Factors
From Proto-Oncogene to Oncogene
FIGURE 7-7 Overactivity of proto-oncogenes may be due to normal production of an abnormal protein (mutation in coding sequence) or excessive production of a normal protein (gene amplification or chromosome rearrangement).
Tumor Suppressor Genes
FIGURE 7-8 Both DNA copies (alleles) of the Rb tumor suppression gene must be dysfunctional for occurrence of retinoblastoma. Inheriting a defective Rb gene predisposes an individual to the development of cancer because only a single mutational event is required to inactivate pRb function.
TABLE 7-5 EXAMPLES OF TUMOR SUPPRESSOR GENES
The Rb Gene
FIGURE 7-9 The Rb protein functions to bind transcription factors in the nucleus and keep them from participating in the transcription of cell cycle–related genes. pRb is induced to release its hold on the E2F transcription factors when it is sufficiently phosphorylated by cyclin-dependent kinases (Cdk). Cyclin-dependent kinases are activated by cyclin proteins that accumulate when growth factors bind to receptors and stimulate growth pathways. Other signals, such as transforming growth factor-β (TGF-β), inhibit the activity of cyclin/Cdk through activation of inhibitory proteins such as p16. A loss of pRb function removes the “major brake” on cell division. P, Phosphate group; EGF, epidermal growth factor.
The P53 Gene
BRCA1 and BRCA2
KEY POINTS
Multistep Nature of Carcinogenesis
FIGURE 7-10 Role of P53 (TP53) in maintaining the integrity of the genome. Damage to DNA in cells with functional P53 stalls the cell cycle so that DNA can be repaired. If repair fails, then the cell undergoes apoptosis to prevent the proliferation of DNA-damaged cells. If the P53 is not functional, genetically unstable cells may be allowed to survive and proliferate.
Initiation
FIGURE 7-11 Diagram of the major signaling pathways relevant to human cancer. Overactivity of proto-oncogenes and underactivity of tumor suppressor genes result in enhanced cell proliferation and inhibition of appropriate cell death. More than 100 proto-oncogene products and numerous tumor suppressor gene products have been identified.
FIGURE 7-12 Synergy between oncogenes may be necessary to initiate malignant growth. A, The ras gene only. B, The myc gene only. C, Synergy between ras and myc genes.
FIGURE 7-13 Theoretical steps in the development of cancer include initiation, promotion, and progression.
Promotion
FIGURE 7-14 The development of colorectal cancer illustrates the concept of multistep carcinogenesis. Derangement of several genes is likely to occur in most types of cancer.
BOX 7-1 MAJOR CHEMICAL CARCINOGENS
Direct-Acting Carcinogens
Alkylating Agents
Acylating Agents
Procarcinogens That Require Metabolic Activation
Polycyclic and Heterocyclic Aromatic Hydrocarbons
Aromatic Amines, Amides, Azo Dyes
Natural Plant and Microbial Products
Others
Progression
FIGURE 7-15 Fluorescent images from human ovarian cancer (CH1) cells. A representative karyotype of CH1 cell line shows the balanced t(15;20) chromosomes (arrows). The size of one of the chromosomes 2 (arrowhead) is slightly bigger than normal, which contains a duplication.
KEY POINTS
Metastasis
Patterns of Spread
FIGURE 7-16 Mechanisms of tumor invasion allow tumor cells to escape the site of origin, penetrate the basement membrane, and travel to distant sites. A, Tumor cells decrease cell-to-cell attachments via cadherins that allow detachment and migration toward the basement membrane. B, Enzymes that degrade proteins are released into the area to form a rift. C, The tumor cell migrates away from the site of origin using laminin and fibronectin receptors to pull through the tissue. D, Finally the cell moves through a rift in the matrix.
TABLE 7-6 SELECTED TUMOR MARKERS
Angiogenesis
Grading and Staging of Tumors
KEY POINTS
Effects of Cancer on the Body
FIGURE 7-17 PET scan that detects uptake of radioactively labeled glucose is overlaid onto a CT scan background image. The yellow spots in the abdomen and mediastinum are indicative of multiple metastases of non-Hodgkin lymphoma.
TABLE 7-7 TNM STAGING CRITERIA FOR BREAST CANCER
TABLE 7-8 TNM STAGING CRITERIA FOR COLON CANCER
FIGURE 7-18 General emaciated appearance in cancer cachexia.
BOX 7-2 CANCER’S SEVEN WARNING SIGNS
BOX 7-3 CANCER’S WARNING SIGNS IN CHILDREN
KEY POINTS
Cancer Therapy
Surgery
Radiation Therapy
Drug Therapy
Immunotherapy
Gene and Molecular Therapy
Stem Cell Transplantation
FIGURE 7-19 Cancer cells express abnormal antigens (tumor-associated antigens) on their cell surface that can activate immune cells or be used as targets for monoclonal antibodies. Numerous medications are now available that use monoclonal antibodies to target cellular proteins relevant to several different types of cancer.
KEY POINTS
Summary
Animations/Videos
Answer Key
Case Studies
Key Points
Additional Resources
References
Unit III Defense
Interactive Review – Unit III
Chapter 8 Infectious Processes
Key Questions
Epidemiologic Concepts
Transmission of Infection
FIGURE 8-1 Traditional risks to a population compared to modern risks.
FIGURE 8-2 Chain of transmission of microorganisms from host to victim.
FIGURE 8-3 Breaking the chain of transmission of microorganisms from host to victim.
FIGURE 8-4 A female aedes aegypti mosquito as it breaks the surface of the host.
Role of Host
Host Characteristics
Physical and Mechanical Barriers
TABLE 8-1 OVERVIEW OF HUMAN DEFENSES
FIGURE 8-5 Some of the mechanical and biochemical barriers of the human body.
TABLE 8-2 HOST CHARACTERISTICS INFLUENCING INFECTION
Risk Factors
Nutritional status
Age
Chronic illness and immunosuppression
Role of Immunization
Role of Environment
KEY POINTS
FIGURE 8-6 This depiction of the interactions of host, microbe, and environment provides a framework for understanding infectious processes.
Host-Microbe Relationship
Normal Microbial Flora
TABLE 8-3 CLASSES OF ORGANISMS INFECTIOUS TO HUMANS
Microorganism Characteristics
Virulence
Adherence
Invasion
Toxins and Exotoxins
Bacterial Enzymes
Antiphagocytic Factors
Endospores
Mobility
Antimicrobial Resistance
TABLE 8-4 HISTORICAL PROGRESSION OF STAPHYLOCOCCUS AUREUS RESISTANCE TO ANTIBIOTICS
KEY POINTS
Types of Pathogenic Organisms
Bacteria
BOX 8-1 EXAMPLES OF PRIMARY PATHOGENS ASSOCIATED WITH SPECIFIC INFECTIONS
Burns
Skin Infections
Decubitus and Surgical Wounds
Meninges
Brain Abscess
Paranasal and Middle Ear
Throat
Lungs
Lung Abscess
Pleura
Endocardium
Peritoneum
Biliary Tract
Kidney and Bladder
Urethra
Prostate
Epididymis and Testes
Bone (Osteomyelitis)
Joints
FIGURE 8-7 Examples of pathogenic organisms. A, Prion (infectious protein). B, Viruses (the human immunodeficiency virus [HIV] that causes Aids). C, Bacteria (Streptococcus bacteria that cause strep throat and other infections). D, Fungi (yeast cells that commonly infect the urinary and reproductive tracts). E, Fungi (the mold that causes aspergillosis). F, Protozoa (the flagellated cells that cause traveler’s diarrhea). G, Pathogenic animals (the parasitic worms that cause snail fever).
FIGURE 8-8 Types of microorganisms. A, Bacteria. B, Virus. C, Fungus.
FIGURE 8-9 Spirochetes (e.g., Treponema pallidum): immunohistochemistry of the muscular layer in the small intestine of a newborn with congenital syphilis. Multiple spirochetes are shown in red (both cross-sections and entire treponemes can be noted [×100]).
FIGURE 8-10 Examples of pathogenic bacteria classified according to the part of the human body that they commonly infect.
Viruses
TABLE 8-5 HUMAN DISEASES CAUSED BY SPECIFIC VIRUSES
Fungi
FIGURE 8-11 Scanning electron micrograph of HIV-1–infected T4 lymphocyte. Large numbers of HIV virions are budding from the plasma membrane of the lymphocytes.
Parasites
TABLE 8-6 COMPARISON OF VIRUSES AND OTHER MICROORGANISMS
TABLE 8-7 FUNGAL INFECTIONS
KEY POINTS
FIGURE 8-12 Trypanosoma brucei parasite in a blood smear. Giemsa-stained light photomicrograph.
TABLE 8-8 PARASITIC INFECTIONS
Summary
Animations/Videos
Answer Key
Key Points
Additional Resources
References
Chapter 9 Inflammation and Immunity
Key Questions
Components of the Immune System
Epithelial Barriers
Mononuclear Phagocyte System
FIGURE 9-1 Cells of the mononuclear phagocyte system.
Lymphoid System
Primary Lymphoid Organs
Secondary Lymphoid Organs
Tonsils
FIGURE 9-2 Maturation of human blood cells showing pathways of cell differentiation from the pluripotent stem cell to mature granulocytes, monocytes, lymphocytes, thrombocytes, and erythrocytes. Production begins in embryo blood islands in the yolk sac. As the embryo matures, production shifts to the liver, spleen, and bone marrow. In an adult, nearly all hematopoiesis occurs in the bone marrow. The two major differentiation pathways are the myeloid pathway and the lymphoid pathway. The lymphoid pathway produces lymphocytes, whereas the myeloid pathway produces granulocytes, monocytes, platelets, and red blood cells.
FIGURE 9-3 Principal organs of the lymphoid system.
Spleen
Lymph Nodes and Lymphatics
Peyer Patches
Leukocytes
Neutrophils
FIGURE 9-4 Schematic drawing of a typical lymph node showing afferent and efferent lymph vessels, as well as B-cell and T-cell zones.
TABLE 9-1 LEUKOCYTE PROPORTIONS AND FUNCTIONS
Eosinophils
FIGURE 9-5 Inflammatory cytokines stimulate the release of more immature neutrophils, called bands, from the bone marrow. An increased ratio of bands to mature neutrophils is termed a “shift to the left.” This clinical term evolved from the practice of listing bands to the left of mature cells on the laboratory report sheet. A shift to the left is commonly seen with acute bacterial infections.
Basophils and Mast Cells
FIGURE 9-6 Micrograph of a mast cell showing a large yellow nucleus and numerous packets containing histamine, which are colored red.
FIGURE 9-7 Scanning electron micrograph of a macrophage (red) attaching to and phagocytizing bacteria (yellow).
Monocytes and Macrophages
FIGURE 9-8 Macrophage surface receptors. Macrophages display receptors for a number of extracellular molecules that enhance their function such as cytokines, complement, selectins, integrins, and antibody (Fc). Toll-like receptors recognize patterns of microbial components and trigger intracellular signaling cascades in the macrophage. IFN-γ, Interferon-γ; IL, interleukin; LPS, lipopolysaccharide.
FIGURE 9-9 Macrophages are of central importance in initiating inflammation and recruitment of other leukocytes to areas of need. Macrophages secrete a variety of cytokines that induce inflammation and chemotaxis. Some macrophage cytokines stimulate the growth and differentiation of other white blood cell types.
Dendritic Cells
Lymphocytes
Natural Killer Cells
FIGURE 9-10 Development of dendritic cells from a myelomonocytic progenitor cell and precursor cells in common with monocytes and macrophages.
FIGURE 9-11 Dendritic cell morphology. A, Light micrograph of resting dendritic cells from the bone marrow. B, Scanning electron micrograph of a mature dendritic cell showing extensive projections of the cell membrane.
T Lymphocytes
FIGURE 9-12 Two major classes of T lymphocytes can be differentiated by CD markers on the cell surface. T helper cells have CD4 markers, whereas cytotoxic T cells have CD8 markers. CD4 cells can be further differentiated into TH1, TH2 and TH17, which secrete different cytokines. CD8 cells are cytotoxic T cells.
FIGURE 9-13 Three types of T helper cells, TH1, TH2, and TH17 secrete different cytokines. TH1 cells secrete interleukin-2 and interferon-γ, which stimulate T cells and macrophages. TH2 cells secrete a number of cytokines that affect B cells. TH17 cells secrete a proinflammatory cytokine, IL-17. TH1, TH2, and TH17 cells inhibit the release of cytokines from one another and thus help regulate the immune response. IFN-γ, Interferon-γ; IL, interleukin.
FIGURE 9-14 Scanning electron micrograph of activated T cells (blue) and a tumor cell (red).
B Lymphocytes
Chemical Mediators Of Immune Function
Complement
FIGURE 9-15 Typical B cell showing a number of identical B-cell receptors (BCRs) on the cell surface. Each BCR is capable of binding to two identical antigen epitopes.
FIGURE 9-16 Activation of the complement cascade results in the production of products that perform a variety of functions to augment the immune response. MAC, Membrane attack complex.
FIGURE 9-17 Complement cascade. The cascade is activated by the first complement molecule, C1, which binds an antigen-antibody complex. This event begins a domino effect, with each of the remaining complement proteins performing its part in the attack sequence. The end result is a hole in the membrane of the offending cell and destruction of the cell. Activation of the complement cascade results in the formation of membrane attack complexes that insert in the cell membrane. These porelike structures allow sodium and water influx, which causes the cell to swell and rupture.
Kinins
FIGURE 9-18 Common linkage of the kinin and coagulation systems through the activation of factor XII (Hageman factor). XIIa, Activated factor XII.
Clotting Factors
Cytokines and Chemokines
KEY POINTS
Innate Defenses and Inflammation
TABLE 9-2 SELECTED IMMUNE CYTOKINES AND THEIR FUNCTIONS
Inflammation
FIGURE 9-19 Tissue injury stimulates the release of a number of chemical mediators that promote vasodilation, chemotaxis, and binding of neutrophils and macrophages to area capillaries. These events facilitate the emigration of neutrophils and macrophages into the tissue, where they begin phagocytosis.
Increased Vascular Permeability
TABLE 9-3 MEDIATORS OF ACUTE INFLAMMATION
FIGURE 9-20 Cardinal signs of acute inflammation result mainly from vasodilation and increased vascular permeability.
Emigration of Leukocytes
FIGURE 9-21 Generation of prostaglandins, thromboxane, and leukotrienes from arachidonic acid, and roles in inflammation. HETEs, Hydroeicosatetraenoic acids; HPETEs, hydroperoxyeicosatetraenoic acids.
FIGURE 9-22 Emigration of neutrophils from the bloodstream into tissue is mediated by receptor interactions with the capillary endothelium. With inflammation and injury, endothelial cells begin to express binding molecules on their cell surfaces (selectins). Leukocytes also have selectins, which can bind to endothelial adhesion proteins. The selectin interactions cause the leukocytes to stick and roll. Chemokines on the surface of endothelial cells interact with neutrophils (and macrophages) to increase the binding affinity of integrin receptors on leukocytes. Firm attachment and diapedesis through the capillary wall is facilitated by integrins, which allow the neutrophils to bind to endothelial cells and extracellular matrix and then pull themselves into the tissue. IL, Interleukin; TNF, tumor necrosis factor.
Phagocytosis
FIGURE 9-23 Neutrophils and macrophages have a number of different receptors on their surface that enable them to bind to components of microbes or to opsonins like IgG and complement. Bound microbes are internalized into phagosomes that fuse with lysosomes containing numerous enzymes. Some of these enzymes degrade proteins (proteolytic), and others such as oxidase and inducible nitric oxide synthase (iNOS) produce free radicals that attack molecular bonds. When phagocytes are strongly stimulated or microbes are too large to internalize, the lysosomal enzymes may be activated or released at the cell surface, causing tissue damage and inflammation. ROS, Reactive oxygen species.
Chronic Inflammation
Healing
Inflammatory Exudates
Systemic Manifestations of Inflammation
FIGURE 9-24 The liver is a target for three important cytokines: interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). In response to these cytokines, the liver releases a number of proteins, collectively called acute phase proteins. vWB, von Willebrand factor.
KEY POINTS
Specific Adaptive Immunity
Major Histocompatibility Complex
FIGURE 9-25 Major histocompatibility complex genes are categorized into three main groups known as class I, II, and III. Class I and II genes code for antigen-presenting proteins, whereas class III genes code for a heterogeneous group of proteins, many of which serve immune functions.
FIGURE 9-26 Each individual receives six class I major histocompatibility complex (MHC) genes including pairs of A, B, and C genes. One member of the pair is inherited from each parent. MHC class I genes are expressed in all nucleated cells of the body. Each individual also receives six class II MHC genes, three from each parent. However, class II proteins are composed of 2 polypeptide chains such that an individual may have 10 to 20 different MHC class II protein molecules. Class II MHC proteins are expressed on the surface of specialized antigen-presenting cells like macrophages, dendritic cells, and B cells. The structure of an individual’s MHC proteins is assessed to determine the “tissue type” when matching for tissue transplantation procedures.
Antigen Presentation by MHC
FIGURE 9-27 Nearly all nucleated cells of the body are able to process and display antigen in association with major histocompatibility complex (MHC) class I protein. The antigens come from the intracellular compartment, and a common source of foreign antigen is viral infection. The viral proteins made within the cell’s cytoplasm are processed into peptide fragments in the proteasome and then enter the endoplasmic reticulum (ER) through TAP transporters. There they combine with MHC class I proteins. The MHC class I–antigen complex then shuttles to the cell surface within a vesicle. When the vesicle combines with the plasma membrane, the MHC class I–antigen complex is displayed on the cell surface. CTL, Cytotoxic T lymphocyte; TAP, transporter associated with antigen processing.
MHC Class I Presentation
MHC Class II Presentation
FIGURE 9-28 Schematic (A) and ribbon (B) diagrams of the class I major histocompatibility complex molecule. Note that the peptide-binding cleft is formed from one polypeptide chain that restricts the size of peptide in the pocket to 8 to 11 amino acids.
Mechanisms of Cell-Mediated Immunity
T Helper Cells (CD4+)
FIGURE 9-29 Only specialized cells are able to obtain extracellular antigen for processing and presentation in association with major histocompatibility complex (MHC) class II protein. These cells are primarily dendritic cells, macrophages, and B cells. The antigen is first engulfed into a vesicle called a phagosome, which fuses with a lysosome. Enzymes within the phagosome break the protein into pieces. MHC II molecules are synthesized on the endoplasmic reticulum (ER) and then transported to the phagosome in a vesicle. The binding cleft of the MHC II protein is complexed with a blocking protein to prevent it from retrieving peptide before it reaches the phagosome. The phagosome and vesicle fuse, and the MHC II loses its blocking protein and picks up an antigen peptide. The complex then migrates to the cell surface and combines with the cell membrane. The MHC II–antigen complex is then displayed on the cell surface.
FIGURE 9-30 Schematic (A) and ribbon (B) diagrams of the class II major histocompatibility complex (MHC) molecule. Note that the peptide-binding cleft is formed from 2 separate polypeptide chains, which allows the size of peptide in the pocket to be 10 to 30 amino acids.
FIGURE 9-31 T helper cells can recognize and bind antigen in association with major histocompatibility complex (MHC) class II molecules. The T cell receptor (TCR) on the T helper cell binds to the antigen, and the CD4 protein recognizes the MHC class II protein. Binding is very specific because the TCR must match the antigen fragment precisely. Once binding is achieved, CD3 and ζ proteins associated with the TCR are activated to initiate intracellular enzyme cascades. Major signaling pathways in activated T cells are shown. These ultimately result in activity of transcription factors and changes in gene activity. AP-1, Activation protein-1; DAG, diacylglycerol; IP3, inositol 1,4,5-trisphosphate; NFAT, nuclear factor of activated T cells; NFκB, nuclear factor kappa B; PIP2, phosphatidylinositol 4,5-bisphosphate; PLCγ, phospholipase C-γ.
Cytotoxic T Cells (CD8+)
FIGURE 9-32 Cytotoxic T cells are able to recognize and bind antigen in association with major histocompatibility complex (MHC) class I molecules. The T cell receptor on the cytotoxic T cell binds to the antigen, and the CD8 protein recognizes the MHC I protein. Binding is specific. Binding of a cytotoxic T cell to its target stimulates granules containing perforin and granzymes to migrate to the cell contact site. Perforins then assemble into pores on the target cell, through which the granzymes can enter the target cell cytoplasm. The granzymes interrupt the cellular DNA and trigger apoptosis. FasL, Fas ligand (CD95L); ICAM, intercellular adhesion molecule; LFA, leukocyte function–associated antigen; TCR, T cell receptor.
Mechanisms of Humoral Immunity
Antigen Recognition by B Cells
FIGURE 9-33 Two major classes of genes are responsible for coding for the variable (V) and constant (C) regions of an antibody. Variable genes code for the antibody region that binds to antigen. Constant genes form the stem of the antibody and are the same for any antibody of a given class.
Antibody Structure
Class Switching and Affinity Maturation
FIGURE 9-34 Major signaling pathways in B cells. Cross-linking of two surface B-cell receptors initiates intracellular pathways that subsequently activate several transcription factors leading to altered gene activity. AP-1, Activation protein-1; DAG, diacylglycerol; IP3, inositol 1,4,5-trisphosphate; NFAT, nuclear factor of activated T cells; NFκB, nuclear factor kappa B; PIP2, phosphatidylinositol 4,5-bisphosphate; PLCγ, phospholipase C-γ.
Antibody Functions
FIGURE 9-35 Activation of a B cell requires T helper cell “help.” This help is given through a number of cell-to-cell interactions via receptors, as well as through the secretion of cytokines that stimulate B-cell growth and differentiation.
FIGURE 9-36 In response to nonprotein antigens (T-cell independent), B cells can be activated by complement opsonins on the microbial antigen. The complement-receptor (CR) interaction provides a costimulatory signal to the B-cell receptor–antigen signal.
Passive and Active Immunity
Passive Immunity
FIGURE 9-37 IgA is often combined with a protein called secretory component, which helps bind two IgA molecules together at their Fc ends.
TABLE 9-4 DIAGRAM AND PROPERTIES OF IMMUNOGLOBULIN CLASSES
FIGURE 9-38 Mast cells bind IgE antibody with their Fc receptors (FcεRI) and display the IgE on the cell surface, where they are available to bind antigens.
FIGURE 9-39 Activated B cells undergo class switching from IgM to IgG, IgE, or IgA. Class switching is influenced by the presence of specific cytokines. IFN, Interferon; IL, interleukin; TGF, transforming growth factor.
FIGURE 9-40 Large antigen (Ag)-antibody complexes tend to precipitate out of solution, which makes it easier for phagocytic cells to find and eliminate the antigens.
FIGURE 9-41 Time phases in the immune response. The primary response takes much longer to develop and declines rapidly. On second exposure, a much quicker and greater antibody response is achieved.
Active Immunity
KEY POINTS
PEDIATRIC CONSIDERATIONS: Changes in the Immune System in Infants
Reference
Integrated Function and Regulation of the Immune System
Integrated Response To New Antigen
BOX 9-1 SELECTED VACCINES AVAILABLE FOR IMMUNIZATION IN THE UNITED STATES
GERIATRIC CONSIDERATIONS: Changes in the Immune System
FIGURE 9-42 Diagram showing the integrated function of a number of immune components. Note that the macrophage is at the center of many immune functions, including chemotaxis and inflammation, presentation of antigen to T cells, and phagocytosis of antibody-antigen complexes. BCR, B-cell receptor; MHC, major histocompatibility complex; NK, natural killer; TCR, T cell receptor; WBC, white blood cell.
Regulation of Immune Function
FIGURE 9-43 IgG antibody can bind to antigen to form antigen-antibody (Ag-Ab) complexes that attach to special Fc receptors on the surface of B cells. Binding of the antigen-antibody complexes in this manner inhibits B-cell production of antibody. This process is called negative-feedback regulation. BCR, B-cell receptor.
KEY POINTS
Summary
Animations/Videos
Answer Key
Case Studies
Key Points
Additional Resources
References
Chapter 10 Alterations in Immune Function
Key Questions
Excessive Immune Responses
Autoimmunity
Genetic Factors
Environmental Triggers
TABLE 10-1 MAJOR HISTOCOMPATIBILITY GENES AND AUTOIMMUNE DISEASE
Pharmacotherapies
KEY POINTS
Hypersensitivity
TABLE 10-2 THE FOUR TYPES OF HYPERSENSITIVITY
Type I Hypersensitivity
Etiology
Pathogenesis
FIGURE 10-1 Type I hypersensitivity reaction.
BOX 10-1 POSSIBLE CAUSES OF HUMAN ANAPHYLAXIS
Medications
Biological Agents
Foods
Clinical manifestations
Treatment
Prevention
Pharmacotherapeutic prevention
Type II Hypersensitivity
Etiology and pathogenesis
TABLE 10-3 DISEASE AND AUTOANTIBODIES ASSOCIATED WITH TYPE II HYPERSENSITIVITY
Transfusion Reaction
FIGURE 10-2 Type II hypersensitivity reactions.
TABLE 10-4 MAJOR BLOOD GROUPS
Hemolytic Disease of the Newborn
Myasthenia Gravis
FIGURE 10-3 Type II hypersensitivity reaction in a person with myasthenia gravis. Having limited receptors available for acetylcholine impairs neuromuscular transmission.
Graves Disease and Thyroiditis
Hyperacute Graft Rejection
Type III Hypersensitivity
Etiology
Pathogenesis
TABLE 10-5 DISEASES ASSOCIATED WITH TYPE III HYPERSENSITIVITY
Tissue deposition
FIGURE 10-4 Type III hypersensitivity reaction.
Immune Complex Glomerulonephritis
Etiology
Clinical manifestations and treatment
Systemic Lupus Erythematosus
Etiology
Clinical manifestations
Treatment
Type IV Hypersensitivity
Cutaneous Basophil Hypersensitivity
Contact Hypersensitivity
FIGURE 10-5 Type IV hypersensitivity reaction.
Tuberculin-Type Hypersensitivity
Granulomatous Hypersensitivity
TABLE 10-6 GRANULOMATOUS DISEASE ASSOCIATED WITH TYPE IV HYPERSENSITIVITY
KEY POINTS

 

Free Sample Test bank for Pathophysiology 5th Edition by Copstead

For customer’s satisfaction, we provide free samples for any required Textbook solution or test bank to check and evaluate before making the final purchase..

If you require any further information, let me know. using Live Chat or Contact Us

Test bank for Pathophysiology 5th Edition by Copstead