Understanding Pathophysiology 4th Edition Huether Test Bank

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This easy-to-read textbook provides you with the basic concepts of pathophysiology and the processes of specific diseases with the most accurate, up-to-date information on the treatments, manifestations, and mechanisms of disease. “Understanding Pathophysiology, 4th Edition” offers complete coverage in clear and concise detail with extensive full-color illustrations to make learning pathophysiology easy.

 

Table of Content:

  1. Part One: Basic Concepts of Pathophysiology
  2. Part Two: Body Systems and Diseases
  3. Features To Promote Learning
  4. Art Program
  5. Teaching/Learning Package
  6. For Students
  7. For Instructors
  8. Acknowledgments
  9. Introduction to Pathophysiology
  10. Part One Basic Concepts of Pathophysiology
  11. Unit 1 The Cell
  12. Chapter 1 Cellular Biology
  13. Electronic Resources
  14. Companion CD
  15. Website
  16. Prokaryotes and Eukaryotes
  17. Cellular Functions
  18. Structure and Function of Cellular Components
  19. Nucleus
  20. Cytoplasmic Organelles
  21. Quick Check 1-1
  22. Plasma Membranes
  23. Figure 1-1 Typical Components of a Eukaryotic Cell.
  24. Membrane composition
  25. Lipids
  26. Proteins
  27. Figure 1-2 The Nucleus. The nucleus is composed of a double membrane, called a nuclear envelope, that encloses the fluid-filled interior, called nucleoplasm. The chromosomes are suspended in the nucleoplasm (here shown much larger than real size to show the tightly packed DNA strands). Swelling at one or more points of the chromosome, shown in A, occurs at a nucleolus where genes are being copied into RNA. The nuclear envelope is studded with pores. B, The pores are visible as dimples in this freeze etch of a nuclear envelope. C, Histone-folding DNA in chromosomes. B from Raven PH, Johnson GB: Biology, St Louis, 1992, Mosby.
  28. Table 1-1 Principal Cytoplasmic Organelles
  29. Table 1-2 Plasma Membrane Functions
  30. Figure 1-3 Amphipathic Molecule. In cellular membranes, amphipathic phospholipid molecules are organized in a bimolecular layer. The hydrophilic regions of the molecules are located at the membrane surfaces, and the hydrophobic regions are oriented toward the center of the membrane.
  31. Figure 1-4 Functions of Plasma Membrane Proteins. The plasma membrane proteins illustrated here show a variety of functions performed by the different types of plasma membranes. From Raven PH, Johnson GB: Understanding biology, ed 3, Dubuque, Iowa, 1995, Brown.
  32. Carbohydrates
  33. Fluid mosaic model
  34. Figure 1-5 Fluid Mosaic Model. Schematic, three-dimensional view of the fluid mosaic model of membrane structure. The lipid bilayer provides the basic structure and serves as a relatively impermeable barrier to most water-soluble molecules. Modified from Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  35. Cellular Receptors
  36. Figure 1-6 Cellular Receptors. A, Plasma membrane receptor for a ligand (here, a hormone molecule) on the surface of an integral protein. A neurotransmitter can exert its effect on a postsynaptic cell by means of two fundamentally different types of receptor proteins: B, channel-linked receptors, and C, non–channel-linked receptors. Channel-linked receptors are also known as ligand-gated channels.
  37. Cell-to-Cell Adhesions
  38. Extracellular Matrix
  39. Figure 1-7 Extracellular Matrix. Tissues are not just cells but also extracellular space. The extracellular space is an intricate network of macromolecules called the extracellular matrix (ECM). The macromolecules that constitute the ECM are secreted locally (by mostly fibroblasts) and assembled into a meshwork in close association with the surface of the cell that produced them. Two main classes of macromolecules include proteoglycans, which are bound to polysaccharide chains called glycosaminoglycans, and fibrous proteins (e.g., collagen, elastin, fibronectin, and laminin), which have structural and adhesive properties. Together the proteogylcan molecules form a gel-like ground substance in which the fibrous proteins are embedded. The gel permits rapid diffusion of nutrients, metabolites, and hormones between the blood and the tissue cells. Matrix proteins modulate cell-matrix interactions including normal tissue remodeling (which can become abnormal, for example, with chronic inflammation). Disruptions of this balance results in serious diseases such as arthritis, tumor growth, and others. Modified from Kumar V, Abbas A, Fausto N: Robbins and Cotran pathologic basis of disease, ed 7, Philadelphia, 2005, Saunders.
  40. Specialized Cell Junctions
  41. Figure 1-8 Junctional Complex. A, Schematic drawing of a belt desmosome between epithelial cells. This junction, also called the zonula adherens, encircles each of the interacting cells. The spot desmosomes and hemidesmosomes, like the belt desmosomes, are adhering junctions. This tight junction is an impermeable junction that holds cells together but seals them in such a way that molecules cannot leak between them. The gap junction, as a communicating junction, mediates the passage of small molecules from one interacting cell to the other. B, Electron micrograph of desmosomes. From Raven PH, Johnson GB: Biology, St Louis, 1992, Mosby.
  42. Cellular Communication and Signal Transduction
  43. Figure 1-9 Cellular Communication. Three primary ways in which cells communicate with one another.
  44. Figure 1-10 Primary Modes of Chemical Signaling. Five forms of signaling mediated by secreted molecules. Hormones, paracrines, autocrines, neurotransmitters, and neurohormones are all intracellular messengers that accomplish communication between cells. Not all neurotransmitters act in the strictly synaptic mode shown; some act in a paracrine mode as local chemical mediators that influence multiple target cells in the area.
  45. Table 1-3 Classes of Plasma Membrane Receptors
  46. Figure 1-11 Schematic of a Signal Transduction Pathway. Like a telephone receiver that converts an electrical signal into a sound signal, a cell converts an extracellular signal, A, into an intracellular signal, B. C, An extracellular chemical messenger (ligand) bonds to a receptor protein located on the plasma membrane where it is transduced into an intracellular signal. This process initiates a signaling cascade that relays the signal into the cell interior, amplifying and distributing it en route. Steps in the cascade can be modulated by other events in the cell.
  47. Cellular Metabolism
  48. Role of Adenosine Triphosphate
  49. Food and Production of Cellular Energy
  50. Figure 1-12 Three Phases of Catabolism: From Breakdown of Food to Elimination of Waste Products. These reactions produce adenosine triphosphate (ATP), which is used to power other processes in the cell.
  51. Oxidative Phosphorylation
  52. Figure 1-13 Glycolysis. Each of the numbered reactions is catalyzed by a different enzyme. At step 4, a six-carbon sugar is broken down to give two three-carbon sugars, so that the number of molecules at every step after this is doubled. Reactions 5 and 6 are responsible for the net synthesis of adenosine triphosphate (ATP) and reduced nicotinamide adenine dinucleotide (NADH) molecules.
  53. Figure 1-14 What Happens to Pyruvate, the Product of Glycolysis? In the presence of oxygen, pyruvate is oxidized to acetyl CoA and enters the citric acid cycle. In the absence of oxygen, pyruvate instead is reduced, accepting the electrons extracted during glycolysis and carried by reduced nicotinamide adenine dinucleotide (NADH). When pyruvate is reduced directly, as it is in muscles, the product is lactic acid. When carbon dioxide (CO2) is first removed from pyruvate and the remainder is reduced, as it is in yeasts, the resulting product is ethanol.
  54. Membrane Transport: Cellular Intake and Output
  55. Movement of Water and Solutes
  56. Passive transport: diffusion, filtration, and osmosis
  57. Diffusion
  58. Figure 1-15 Passive Diffusion of Solute Molecules Across the Plasma Membrane. Oxygen (O2), nitrogen (N2), water (H2O), urea, glycerol, and carbon dioxide (CO2) can diffuse readily down the concentration gradient. Macromolecules are too large to diffuse through pores in the plasma membrane. Ions may be repelled if the pores contain substances with identical charges. If the pores are lined with cations, for example, other cations will have difficulty diffusing because the positive charges will repel one another. Diffusion can still occur, but it occurs more slowly. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  59. Filtration: hydrostatic pressure
  60. Osmosis
  61. Quick Check 1-2
  62. Mediated and active transport
  63. Mediated transport
  64. Figure 1-16 Conformational-change Model of Mediated Transport (Facilitated Diffusion). The transporter protein has two states, “ping” and “pong.” In the ping state, sites for molecules of a specific solute are exposed on the outside of the bilayer. In the pong state, the sites are exposed to the inner side of the bilayer.
  65. Figure 1-17 Channel Mode of Mediated Transport (Facilitated Diffusion). A channel protein forms a water-filled pore across the bilayer through which specific ions can diffuse.
  66. Figure 1-18 Mediated Transport. Illustration shows simultaneous movement of a single solute molecule in one direction (uniport), of two different solute molecules in one direction (symport), and of two different solute molecules in opposite directions (antiport).
  67. Figure 1-19 Active Transport and the Sodium-Potassium Pump. Three sodium (Na+) ions bind to sodium-binding sites on the carrier’s inner face. At the same time, an energy-containing adenosine triphosphate (ATP) molecule produced by the cell’s mitochondria binds to the carrier. The ATP breaks apart, transferring its stored energy to the carrier. The carrier then changes shape, releases the three Na+ ions to the outside of the cell, and attracts two potassium (K+) ions to its potassium-binding sites. The carrier then returns to its original shape, releasing the two K+ ions and the remnant of the ATP molecule to the inside of the cell. The carrier is now ready for another pumping cycle. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  68. Active transport of Na+ and K+
  69. Table 1-4 Major Transport Systems in Mammalian Cells
  70. Transport by Vesicle Formation
  71. Endocytosis and exocytosis
  72. Figure 1-20 Endocytosis and Exocytosis. A, Endocytosis and fusion with lysosome and exocytosis. B, Electron micrograph of exocytosis. B from Raven PH, Johnson GB: Biology, ed 5, New York, 1999, McGraw-Hill.
  73. Receptor-mediated endocytosis
  74. Caveolae
  75. Figure 1-21 Ligand Internalization by Means of Receptor-Mediated Endocytosis. A, The ligand attaches to its surface receptor (through the bristle coat or clathrin coat) and, through receptor-mediated endocytosis, enters the cell. The ingested material fuses with a lysosome and is processed by hydrolytic lysosomal enzymes. Processed molecules can then be transferred to other cellular components. B, Electron micrograph of a coated pit showing different sizes of filaments of the cytoskeleton (× 82,000). B from Erlandsen SL, Magney JE: Color atlas of histology, St Louis, 1992, Mosby.
  76. Movement of Electrical Impulses: Membrane Potentials
  77. Figure 1-22 Sodium-Potassium Pump and Propagation of an Action Potential. A, Concentration difference of sodium (Na+) and potassium (K+) intracellularly and extracellularly. The direction of active transport by the sodium-potassium pump is also shown. B, The top diagram represents the polarized state of a neuronal membrane when at rest. The lower diagrams represent changes in sodium and potassium membrane permeabilities with depolarization and repolarization. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  78. Quick Check 1-3
  79. Cellular Reproduction: The Cell Cycle
  80. Phases of Mitosis and Cytokinesis
  81. Figure 1-23 Interphase and the Phases of Mitosis. A, The G1/S checkpoint is to “check” for cell size, nutrients, growth factors, and DNA damage. The G0 is the resting state. The G2/M checkpoint checks for cell size and DNA replication. B, The orderly progression through the phases of the cell cycle is regulated by cyclins (so called because levels rise and fall) and cyclin-dependent protein kinases (CdKs) and their inhibitors. When cyclins are complexed with CdKs, it triggers cell cycle events.
  82. Rates of Cellular Division
  83. Growth Factors
  84. Table 1-5 Examples of Growth Factors and Their Actions
  85. Tissues
  86. Figure 1-24 How Growth Factors Stimulate Cell Proliferation. A, Resting cell. With the absence of growth factors, the retinoblastoma (Rb) protein is not phosphorylated; thus, it holds the gene regulatory proteins in an inactive state. The gene regulatory proteins are required to stimulate the transcription of genes needed for cell proliferation. B, Proliferating cell. Growth factors bind to the cell surface receptors and activate intracellular signaling pathways leading to activation of intracellular proteins. These intracellular proteins phosphorylate and thereby inactivate the Rb protein. The gene regulatory proteins are now free to activate the transcription of genes, leading to cell proliferation.
  87. Tissue Formation
  88. Types of Tissues
  89. Quick Check 1-4
  90. Box 1-1 Characteristics of Epithelial Tissues
  91. Box 1-2 Connective Tissues
  92. Box 1-3 Muscle Tissues
  93. Did You Understand?
  94. Cellular Functions
  95. Structure and Function of Cellular Components
  96. Cell-to-Cell Adhesions
  97. Cellular Communication and Signal Transduction
  98. Cellular Metabolism
  99. Membrane Transport: Cellular Intake and Output
  100. Cellular Reproduction: The Cell Cycle
  101. Tissues
  102. Key Terms
  103. References
  104. Chapter 2 Genes and Genetic Diseases
  105. Electronic Resources
  106. Companion CD
  107. Website
  108. DNA, RNA, and Proteins: Heredity at the Molecular Level
  109. Definitions
  110. Composition and structure of DNA
  111. Figure 2-1 Watson-Crick Model of the DNA Molecule. The DNA structure illustrated here is based on that published by James Watson (photograph, left) and Francis Crick (photograph, right) in 1953. Note that each side of the DNA molecule consists of alternating sugar and phosphate groups. Each sugar group is united to the sugar group opposite it by a pair of nitrogenous bases (adenine-thymine or cytosine-guanine). The sequence of these pairs constitutes a genetic code that determines the structure and function of a cell. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  112. DNA as the genetic code
  113. Replication of DNA
  114. Mutation
  115. Figure 2-2 Replication of DNA. The two chains of the double helix separate, and each chain serves as the template for a new complementary chain. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, 2007, St Louis, Mosby.
  116. Figure 2-3 Different Kinds of Mutations. C, Cytosine; A, adenine; T, thymine; G, guanine.
  117. From Genes to Proteins
  118. Transcription
  119. Gene splicing
  120. Translation
  121. Figure 2-4 General Scheme of Ribonucleic Acid (RNA) Transcription. (See text for explanation.) From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, 2007, St Louis, Mosby.
  122. Chromosomes
  123. Chromosome Aberrations and Associated Diseases
  124. Figure 2-5 Protein Synthesis. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, 2007, St Louis, Mosby.
  125. Figure 2-6 From Molecular Parts to the Whole Cell.
  126. Polyploidy
  127. Figure 2-7 Phases of Meiosis. From Jorde LB et al, Medical genetics, ed 3, updated, St Louis, 2006, Mosby.
  128. Figure 2-8 Karyotype of Chromosomes. A, G-banded metaphase of a normal cell showing the bands of all normal chromosomes. B, G-banded karyotype of a normal female cell showing the banding patterns of the various chromosomes. Identical patterns characterize homologous chromosomes. The chromosomes are arranged from largest to smallest in size. From Damjanov I, Linder J: Anderson’s pathology, ed 10, vol 1, St Louis, 1996, Mosby.
  129. Aneuploidy
  130. Figure 2-9 Structure of Chromosomes. A, Human chromosomes 2, 5, and 13. Each is replicated and consists of two chromatids. Chromosome 2 is a metacentric chromosome because the centromere is close to the middle; chromosome 5 is submetacentric because the centromere is set off from the middle; chromosome 13 is acrocentric because the centromere is at or very near the end. B, During mitosis, the centromere divides and the chromosomes move to opposite poles of the cell. At the time of centromere division, the chromatids are designated as chromosomes.
  131. Figure 2-10 Nondisjunction. Causes aneuploidy when chromosomes or sister chromatids fail to divide properly. From Jorde LB et al: Medical genetics, ed 3, updated, St Louis, 2006, Mosby.
  132. Autosomal aneuploidy
  133. Sex chromosome aneuploidy
  134. Figure 2-11 Child with Down Syndrome. Courtesy Drs. A. Olney and M. MacDonald, University of Nebraska Medical Center, Omaha.
  135. Abnormalities of chromosome structure
  136. Figure 2-12 Down Syndrome Increases with Maternal Age. Rate is per 1000 live births related to maternal age.
  137. Table 2-1 Characteristics of Various Chromosome Disorders
  138. Deletions
  139. Duplications
  140. Inversions
  141. Figure 2-13 Turner Syndrome. A sex chromosome is missing, and the person’s chromosomes are 45,X. Characteristic signs are short stature, female genitalia, webbed neck, shieldlike chest with underdeveloped breasts and widely spaced nipples, and imperfectly developed ovaries. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, 2007, St Louis, Mosby.
  142. Figure 2-14 Klinefelter Syndrome. This young man exhibits many characteristics of Klinefelter syndrome: small testes, some development of the breasts, sparse body hair, and long limbs. This syndrome results from the presence of two or more X chromosomes with one Y chromosome (genotypes XXY or XXXY, for example). From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, 2007, St Louis, Mosby.
  143. Figure 2-15 Abnormalities of Chromosome Structure. A, Deletion occurs when a chromosome segment is lost. B, Normal crossing over. C, The generation of duplication and deletion through unequal crossing over.
  144. Translocations
  145. Fragile sites
  146. Figure 2-16 Normal and Abnormal Chromosome Translocation. A, Normal chromosomes and reciprocal translocation. B, Pairing at meiosis. C, Consequences of translocation in gametes; unbalanced gametes result in zygotes that are partially trisomic and partially monosomic and consequently develop abnormally.
  147. Quick Check 2-1
  148. Elements of Formal Genetics
  149. Phenotype and Genotype
  150. Dominance and Recessiveness
  151. Transmission of Genetic Diseases
  152. Autosomal Dominant Inheritance
  153. Characteristics of pedigrees
  154. Figure 2-17 Symbols Commonly Used in Pedigrees. From Jorde LB et al: Medical genetics, ed 3, updated, St Louis, 2006, Mosby.
  155. Recurrence risks
  156. Figure 2-18 Punnett square and autosomal dominant traits. A, Punnett square for the mating of two individuals with an autosomal dominant gene. Here both parents are affected by the trait. B, Punnett square for the mating of a normal individual with a carrier for an autosomal dominant gene.
  157. Figure 2-19 Pedigree for Achondroplasia. Pedigree showing the transmission of an autosomal dominant disease.
  158. Delayed age of onset
  159. Penetrance and expressivity
  160. Figure 2-20 Pedigree for Retinoblastoma Showing Incomplete Penetrance. Female with marked arrow in line II must be heterozygous, but she does not express the trait.
  161. Epigenetics and genomic imprinting
  162. Figure 2-21 Neurofibromatosis. Tumors. The most common is sessile or pedunculated. Early tumors are soft, dome-shaped papules or nodules that have a distinctive violaceous hue. Most are benign. From Habif et al: Skin disease: diagnosis and treatment, ed 2, St Louis, 2005, Mosby.
  163. Autosomal Recessive Inheritance
  164. Characteristics of pedigrees
  165. Recurrence risks
  166. Figure 2-22 Epigenetic Modifications. Because DNA is a long molecule, it needs packaging to fit in the tiny nucleus. Packaging involves coiling of the DNA in a “left-handed” spiral around spools, made of four pairs of proteins individually known as histones and collectively as the histone octamer. The entire spool is called a nucleosome (also see Figure 1-2). Nucleosomes are organized into chromatin, the repeating building blocks of a chromosome. Histone modifications are correlated with methylation, are reversible, and occur at multiple sites. Methylation occurs at the 5 position of cytosine and provides a “footprint” or signature as a unique epigenetic alteration (red). When genes are expressed, chromatin is open or active; however, when chromatin is condensed because of methylation and histone modification, genes are inactivated.
  167. Figure 2-23 Pedigree for Cystic Fibrosis. The double bar denotes a consanguineous mating. Because cystic fibrosis is relatively common in European populations, most cases do not involve consanguinity.
  168. Figure 2-24 Punnett Square for the Mating of Heterozygous Carriers Typical of Most Cases of Recessive Disease.
  169. Consanguinity
  170. X-Linked Inheritance
  171. X inactivation
  172. Figure 2-25 The X Inactivation Process. The maternal (m) and paternal (p) X chromosomes are both active in the zygote and in early embryonic cells. X inactivation then takes place, resulting in cells having either an active paternal X or an active maternal X. Females are thus X chromosome mosaics, as shown in the tissue sample at the bottom of the page. From Jorde LB et al: Medical genetics, ed 3, updated, St Louis, 2006, Mosby.
  173. Sex determination
  174. Figure 2-26 Distal Short Arms of the X and Y Chromosomes Exchange Material During Meiosis in the Male. The region of the Y chromosome in which this crossover occurs is called the pseudoautosomal region. The SRY gene, which triggers the process leading to male gonadal differentiation, is located just outside the pseudoautosomal region. Occasionally, the crossover occurs on the centrometric side of the SRY gene, causing it to lie on an X chromosome instead of a Y chromosome. An offspring receiving this X chromosome will be an XX male, and an offspring receiving the Y chromosome will be an XY female.
  175. Quick Check 2-2
  176. Characteristics of pedigrees
  177. Recurrence risks
  178. Sex-limited and sex-influenced traits
  179. Figure 2-27 Punnett Square and X-linked Recessive Traits. A, Punnett square for the mating of a normal male (XHY) and a female carrier of an X-linked recessive gene (XHXh). B, Punnett square for the mating of a normal female (XHXH) with a male affected by an X-linked recessive disease (XhY). C, Punnett square for the mating of a female who carries an X-linked recessive gene (XHXh) with a male who is affected with the disease caused by the gene (XhY).
  180. Evaluation of Pedigrees
  181. Linkage Analysis and Gene Mapping
  182. Classical Pedigree Analysis
  183. Figure 2-28 Genetic Results of Crossing Over. A, No crossing over. B, Crossing over with recombination. C, Double crossing over, resulting in no recombination.
  184. Complete Human Gene Map: Prospects and Benefits
  185. Figure 2-29 Example of Diseases: A Gene Map. PKU, phenylketonuria; ALD, adrenoleukodystrophy; ADA, adenosine deaminase.
  186. Health Alert Gene Therapy
  187. Table 2-2 Some Important Genetic Diseases That Have Been Mapped to Specific Chromosome Locations and Cloned
  188. Multifactorial Inheritance
  189. Figure 2-30 Multifactorial Inheritance. Analysis of mode of inheritance for grain color in wheat. The trait is controlled by three independently assorted gene loci.
  190. Figure 2-31 Threshold of Liability for Pyloric Stenosis in Males and Females.
  191. Box 2-1 Criteria Used to Define Multifactorial Diseases
  192. Quick Check 2-3
  193. Did You Understand?
  194. DNA, RNA, and Proteins: Heredity at the Molecular Level
  195. Chromosomes
  196. Elements of Formal Genetics
  197. Transmission of Genetic Diseases
  198. Linkage Analysis and Gene Mapping
  199. Multifactorial Inheritance
  200. Key Terms
  201. References
  202. Chapter 3 Altered Cellular and Tissue Biology
  203. Electronic Resources
  204. Companion CD
  205. Website
  206. Cellular Adaptation
  207. Atrophy
  208. Figure 3-1 Adaptive and Dysplastic Alterations in Simple Cuboidal Epithelial Cells.
  209. Hypertrophy
  210. Figure 3-2 Hypertrophy of Cardiac Muscle in Response to Valve Disease. A, Transverse slices of a normal heart and a heart with hypertrophy of the left ventricle (L, normal thickness of left ventricular wall; T, thickened wall from heart in which severe narrowing of aortic valve caused resistance to systolic ventricular emptying). B, Histology of cardiac muscle from the normal heart. C, Histology of cardiac muscle from a hypertrophied heart. From Stevens A, Lowe J: Pathology: illustrated review in color, ed 2, Edinburgh, 2000, Mosby.
  211. Hyperplasia
  212. Dysplasia: Not a True Adaptive Change
  213. Figure 3-3 Hyperplasia of the Prostate with Secondary Thickening of the Obstructed Urinary Bladder. The enlarged prostate is seen protruding into the lumen of the bladder, which appears trabeculated. These “trabeculae” result from hypertrophy and hyperplasia of smooth muscle cells that occurs in response to increased intravesical pressure caused by urinary obstruction. From Damjanov I: Pathology for the health professions, ed 3, St Louis, 2006, Saunders.
  214. Metaplasia
  215. Figure 3-4 Reversible Changes in Cells Lining the Bronchi.
  216. Cellular Injury
  217. Table 3-1 Types of Progressive Cell Injury and Responses
  218. Figure 3-5 Cellular Injury and Responses. Depiction of the relationship among normal, adapted (hypertrophied), and reversibly injured cells and cell death of myocardial cells.
  219. General Mechanisms of Cell Injury
  220. Hypoxic Injury
  221. Table 3-2 Common Themes in Cell Injury and Cell Death
  222. Figure 3-6 Hypoxic Injury Induced by Ischemia. Purple boxes involve reversible cell injury, light blue boxes involve irreversible cell death, and green boxes are clinical manifestations.
  223. Figure 3-7 Reperfusion Injury. Without oxygen, or anoxia, the cells display hypoxic injury and become swollen. With reoxygenation, reperfusion injury increases because of the formation of reactive oxygen radicals that can cause cell necrosis. Redrawn from Damjanov I: Pathology for the health professions, ed 3, St Louis, 2006, Saunders.
  224. Health Alert Natural Antioxidants
  225. Quick Check 3-1
  226. Free Radicals and Reactive Oxygen Species Injury
  227. Figure 3-8 Generation of Reactive Oxygen Species and Antioxidant Mechanisms in Biologic Systems. Mitochondria have four sites of entry for electrons coming into the electron transport system: one for reduced nicotinamide adenine dinucleotide (NADH) and three for the reduced form of flavin adenine dinucleotide (FADH2). These pathways meet at the small, lipophilic molecule, ubiquinone (coenzyme Q), at the beginning of the common electron transport pathway. Ubiquinone transfers electrons in the inner membrane, ultimately enabling their interaction with oxygen (O2) and hydrogen (H2) to yield water (H2O). In so doing, the transport allows free energy change and the synthesis of one mole of adenosine triphosphate (ATP). With the transport of electrons, free radicals are generated within the mitochondria. Reactive oxygen species ( O2⋅−, H2O2, OH⋅, and nitric oxide [NO]) act as physiologic modulators of some mitochondrial functions but may also cause cell damage. O2 is converted to superoxide ( O2⋅−) by oxidative enzymes in the mitochondria, endoplasmic reticulum (ER), plasma membrane, peroxisomes, and cytosol. O2 is converted to H2O2 by superoxide dismutase (SOD) and further to OH⋅ by the Cu/Fe Fenton reaction. Superoxide catalyzes the reduction of Fe++ to Fe+++, thus increasing OH⋅ formation by the Fenton reaction. H2O2 is also derived from oxidases in peroxisomes. The three reactive oxygen species (H2O2, OH⋅, and O2⋅−), cause free radical damage to lipids (peroxidation of the membrane), proteins (ion pump damage), and DNA (impaired protein synthesis). The major antioxidant enzymes include SOD, catalase, and glutathione peroxidase. Data from Dröge W: Physiol Rev 82:47–95, 2002; Buetler TM, Krauskopf A, Ruegg UT: News Physiol Sci 19:120–123, 2004.
  228. Table 3-3 Biologically Relevant Free Radicals
  229. Mechanisms of Chemical Injury
  230. Box 3-1 Diseases and Disorders Linked to Oxygen-Derived Free Radicals
  231. Table 3-4 Methods Contributing to Inactivation or Termination of Free Radicals
  232. Chemical agents
  233. Figure 3-9 Chemical Injury of Liver Cells Induced by Carbon Tetrachloride (CCl4) Poisoning. Light blue boxes are mechanisms unique to chemical injury, purple boxes involve hypoxic injury, and green boxes are clinical manifestations.
  234. Lead
  235. Table 3-5 Common Sources of Lead Exposure
  236. Carbon monoxide
  237. Ethanol
  238. Figure 3-10 Major Pathway of Metabolism of Alcohol in the Liver through ADH.
  239. Figure 3-11 Fetal Alcohol Syndrome. When alcohol enters the fetal blood, the potential result can cause tragic congenital abnormalities, such as microcephaly (“small head”), low birth weight, and cardiovascular defects, as well as developmental disabilities, such as physical and mental retardation, and even death. Note the small head, thinned upper lip, small eye openings (palpebral fissures), epicanthal folds, and receded upper jaw (retrognathia) typical of fetal alcohol syndrome. From Fortinash KM, Holoday Worret PA: Psychiatric mental health nursing, ed 3, St Louis, 2004, Mosby.
  240. Table 3-6 Major Sources of Mercury Exposure and Health Effects
  241. Mercury
  242. Figure 3-12 Alcoholic Hepatitis. Chicken-wire fibrosis extending between hepatocytes (Mallory trichrome stain.) From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  243. Social or street drugs
  244. Table 3-7 Social or Street Drugs and Their Effects
  245. Quick Check 3-2
  246. Unintentional and Intentional Injuries
  247. Blunt-force injuries
  248. Contusion
  249. Abrasion
  250. Figure 3-13 Patterned Abrasion Caused by a Piece of Rebar. Note the tissue tags at the inferior margins indicating a downward direction to the blow that caused this injury.
  251. Laceration
  252. Figure 3-14 Avulsed Laceration in Motor Vehicle Accident Victim. The victim was the driver, and this injury most likely was caused by the brake pedal.
  253. Fractures
  254. Sharp-force injuries
  255. Incised wounds
  256. Stab wounds
  257. Figure 3-15 Self-inflicted Incised Wound of the Neck with Multiple Hesitation Marks.
  258. Figure 3-16 Stab Wound with Associated Hilt Mark. Note the sharp margin away from the hilt mark with the blunt margin toward it. This wound was caused by a single-edge knife.
  259. Puncture wounds
  260. Chopping wounds
  261. Gunshot wounds
  262. Entrance wounds
  263. Figure 3-17 Contact Range Gunshot Wound of the Chest with a Muzzle Abrasion.
  264. Figure 3-18 Intermediate Range Gunshot Wound with Stippling and Tattooing.
  265. Exit wounds
  266. Figure 3-19 Indeterminate Range Entrance Wound with Eccentric Collar of Abrasion Resulting from the Bullet Striking the Skin at an Angle.
  267. Wounding potential of firearms
  268. Asphyxial injuries
  269. Suffocation
  270. Strangulation
  271. Chemical asphyxiants
  272. Drowning
  273. Quick Check 3-3
  274. Infectious Injury
  275. Immunologic and Inflammatory Injury
  276. Table 3-8 Mechanisms of Cellular Injury
  277. Manifestations of Cellular Injury
  278. Water
  279. Figure 3-20 The Process of Oncosis (formerly referred to as “Hydropic Degeneration”). ATP, Adenosine triphosphate.
  280. Lipids and Carbohydrates
  281. Glycogen
  282. Proteins
  283. Figure 3-21 Fatty Liver. The liver appears yellow. From Damjanov I, Linder J: Pathology: a color atlas, St Louis, 2000, Mosby.
  284. Pigments
  285. Melanin
  286. Hemoproteins
  287. Figure 3-22 Hemosiderin Accumulation Is Noted as the Color Changes in a “Black Eye.”
  288. Calcium
  289. Figure 3-23 Free Cytosolic Calcium: A Destructive Agent. Normally, calcium is removed from the cytosol by adenosine triphosphate (ATP)-dependent calcium pumps. In normal cells, calcium is bound to buffering proteins, such as calbindin or paralbumin, and is contained in the endoplasmic reticulum and the mitochondria. If there is abnormal permeability of calcium-ion channels, direct damage to membranes, or depletion of ATP (i.e., hypoxic injury), calcium increases in the cytosol. If the free calcium cannot be buffered or pumped out of cells, uncontrolled enzyme activation takes place, causing further damage. Uncontrolled entry of calcium into the cytosol is an important final common pathway in many causes of cell death.
  290. Urate
  291. Systemic Manifestations
  292. Figure 3-24 Aortic Valve Calcification. A, This calcified aortic valve is an example of dystrophic calcification. B, This algorithm shows the dystrophic mechanism of calcification. A from Damjanov I: Pathology for the health professions, ed 3, St Louis, 2006, Saunders.
  293. Cellular Death
  294. Necrosis
  295. Table 3-9 Systemic Manifestations of Cellular Injury
  296. Figure 3-25 Stages of Necrosis.
  297. Figure 3-26 Coagulative Necrosis of Myocardium of Posterior Wall of Left Ventricle of Heart. A large, anemic (white) infarct is readily apparent; note also the necrosis of papillary muscle. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  298. Figure 3-27 Liquefactive Necrosis of the Brain. The area of infarction is softened as a result of liquefaction necrosis. From Damjanov I: Pathology for the health professions, ed 3, St Louis, 2006, Saunders.
  299. Figure 3-28 Granuloma with Central Caseous Necrosis Typical of Pulmonary Tuberculosis. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  300. Figure 3-29 Fat Necrosis of Pancreas. Interlobular adipocytes are necrotic; acute inflammatory cells surround these. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  301. Figure 3-30 Gangrene, a Complication of Necrosis. In certain circumstances, necrotic tissue will be invaded by putrefactive organisms that are both saccharolytic and proteolytic. Foul-smelling gases are produced, and the tissue becomes green or black as a result of breakdown of hemoglobin. Obstruction of the blood supply to the bowel almost inevitably is followed by gangrene.
  302. Apoptosis
  303. Figure 3-31 Necrosis and Apoptosis in Liver Cells. Necrosis is caused by exogenous injury whereby cells are swollen and have nuclear changes in ruptured cell membrane. Apoptosis is single cell death. It is genetically programmed (suicide genes) and depends on energy. Apoptotic bodies contain part of the nucleus and cytoplasmic organelles, which are ultimately taken up by macrophages or adjacent cells. RER, Rough endoplasmic reticulum. Redrawn from Damjanov I: Pathology for the health professions, ed 3, St Louis, 2006, Saunders.
  304. Quick Check 3-4
  305. Aging & Altered Cellular and Tissue Biology
  306. Figure 3-32 Microinsults. Redrawn from Johnson HA, editor: Is aging physiological or pathological? Relations between normal aging and a disease, New York, 1985, Raven.
  307. Normal Life Span
  308. Life Expectancy and Gender Differences
  309. Theories and Mechanisms of Aging
  310. Table 3-10 Theories of Aging
  311. Genetic and environmental lifestyle factors
  312. Alterations of cellular control mechanisms
  313. Degenerative extracellular changes
  314. Cellular Aging
  315. Tissue and Systemic Aging
  316. Frailty
  317. Somatic Death
  318. Quick Check 3-5
  319. Did You Understand?
  320. Cellular Adaptation
  321. Cellular Injury
  322. Manifestations of Cellular Injury
  323. Cellular Death
  324. AGING & Altered Cellular and Tissue Biology
  325. Somatic Death
  326. Key Terms
  327. References
  328. Chapter 4 Fluids and Electrolytes, Acids and Bases
  329. Electronic Resources
  330. Companion CD
  331. Website http://evolve.elsevier.com/Huether/
  332. Distribution of Body Fluids
  333. Maturation and the Distribution of Body Fluids
  334. Table 4-1 Total Body Water (%) in Relation to Body Weight
  335. Table 4-2 Distribution of Body Water
  336. Table 4-3 Normal Water Gains and Losses (70-kg Man)
  337. Pediatrics & Distribution of Body Fluids
  338. Newborn Infants
  339. Children and Adolescents
  340. Aging & Distribution of Body Fluids
  341. Water Movement Between Plasma and Interstitial Fluid
  342. Water Movement Between ICF and ECF
  343. Alterations in Water Movement
  344. Edema
  345. Figure 4-1 Fluid Movement Between Plasma and Interstitial Space. The movement of fluid between the vascular, interstitial spaces, and the lymphatics is the result of net filtration of fluid across the semipermeable capillary membrane. Capillary hydrostatic pressure is the primary force for fluid movement out of the arteriolar end of the capillary and into the interstitial space. At the venous end, capillary oncotic pressure (from plasma proteins) attracts water back into the vascular space. Interstitial hydrostatic pressure promotes the movement of fluid and proteins in to the lymphatics. Osmotic pressure accounts for the movement of fluid between the interstitial space and the intracellular space. Normally intracellular and extracellular fluid osmotic pressures are equal (280 to 294mOsm) and water is equally distributed between the interstitial and intracellular compartments.
  346. Pathophysiology
  347. Figure 4-2 Examples of Changes in Osmotic Equilibrium Between ECF and ICF. A, Normal ECF and ICF volumes. Intracellular and extracellular fluid osmotic pressures are equal and water is equally distributed between the compartments. B, Extracellular fluid volume excess or sodium deficit. ECF volume excess or sodium deficit decreases the ECF osmotic pressure and water is attracted to the ICF space (see C). C, Fluid movement from the ECF to ICF to reestablish osmotic equilibrium. The intracellular osmotic pressure attracts water from the ECF causing an increase in ICF water volume with a balancing of osmotic forces between the ECF and ICF. The consequence is an increase in ICF volume and cell swelling. D, Extracellular fluid volume deficit or sodium excess. ECF volume deficit increases the ECF osmotic pressure and intracellular water is attracted to the ECF space (see E). E, Fluid movement from the ICF to the ECF to reestablish osmotic equilibrium. Water from the intracellular space has moved to the extracellular space until the osmotic forces are equal. The consequence is a decrease in ICF water volume and cell size. ICF, Intracellular fluid; ECF, extracellular fluid.
  348. Clinical Manifestations
  349. Quick Check 4-1
  350. Figure 4-3 Mechanisms of Edema Formation. Na+, sodium; H2O, water.
  351. Sodium, Chloride, and Water Balance
  352. Water Balance
  353. Sodium and Chloride Balance
  354. Figure 4-4 The Antidiuretic Hormone (ADH) System.
  355. Table 4-4 Representative Distribution of Electrolytes in Body Compartments
  356. Figure 4-5 The Renin-Angiotensin-Aldosterone System. (1) Renal juxtaglomerular cells sense decrease in blood pressure and release renin; (2) Renin activates angiotensinogen to angiotensin I; (3) Angiotensin I is converted to angiotensin II via angiotensin-converting enzyme (ACE) in the lung; (4) Angiotensin II promotes vasoconstriction and stimulates aldosterone secretion from the adrenal cortex resulting in renal sodium and water retention and an increase in blood pressure. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  357. Figure 4-6 The Atrial Natriuretic Hormone (ANH) System. Na+, sodium; GFR, glomerular filtration rate. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 5, St Louis, 2003, Mosby.
  358. Quick Check 4-2
  359. Alterations in Sodium, Chloride, and Water Balance
  360. Isotonic Alterations
  361. Table 4-5 Water and Solute Imbalances
  362. Hypertonic Alterations
  363. Hypernatremia
  364. Pathophysiology
  365. Health Alert Breastfeeding and Hypernatremia
  366. Clinical Manifestations
  367. Table 4-6 Causes and Consequences of Hypertonic Imbalances
  368. Water Deficit
  369. Pathophysiology
  370. Clinical Manifestations
  371. Hyperchloremia
  372. Hypotonic Alterations
  373. Hyponatremia
  374. Pathophysiology
  375. Table 4-7 Causes and Consequences of Hypotonic Imbalances
  376. Clinical Manifestations
  377. Water excess
  378. Pathophysiology
  379. Clinical Manifestations
  380. Hypochloremia
  381. Quick Check 4-3
  382. Alterations in Potassium and Other Electrolytes
  383. Potassium
  384. Hypokalemia
  385. Pathophysiology
  386. Clinical Manifestations
  387. Figure 4-7 Electrocardiogram Changes with Potassium Imbalance.
  388. Hyperkalemia
  389. Pathophysiology
  390. Table 4-8 Clinical Manifestations of Potassium Alterations
  391. Clinical Manifestations
  392. Quick Check 4-4
  393. Other Electrolytes
  394. Acid-Base Balance
  395. Hydrogen Ion and pH
  396. Table 4-9 Alterations in Other Body Electrolytes
  397. Buffer Systems
  398. Table 4-10 pH of Body Fluids
  399. Table 4-11 Buffer Systems
  400. Carbonic acid–bicarbonate buffering
  401. Protein buffering
  402. Renal buffering
  403. Figure 4-8 Integration of pH Control Mechanisms. Elevated carbon dioxide (CO2) levels result in increased formation of carbonic acid (H2CO3) in red blood cells. The resulting increase in hydrogen ions (H+), coupled with elevated CO2 levels, results in HHbCO2 and an increase in respiratory rate and secretion of H+ by the kidneys, thus helping to regulate the pH of body fluids. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  404. Acid-Base Imbalances
  405. Metabolic acidosis
  406. Figure 4-9 Davenport Diagram: Classic Working Diagram for Studying Primary Uncompensated Acid-Base Imbalance. The point ⊗ represents a normal pH value (7.4) and normal values for partial pressure of carbon dioxide (PaCO2 = 40mm Hg) and bicarbonate ( HCO3−=24mEq/L). Note that as the PaCO2 increases toward 60mm Hg (A), the pH decreases (respiratory acidosis), and that as it decreases toward 20mm Hg (B), the pH increases (respiratory alkalosis). Metabolic acidosis develops as the concentration of HCO3− decreases (C), and metabolic alkalosis develops as the concentration of HCO3− increases (D).
  407. Table 4-12 Causes of Metabolic Acidosis
  408. Metabolic alkalosis
  409. Figure 4-10 Metabolic Acidosis. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  410. Box 4-1 Anion Gap
  411. Respiratory acidosis
  412. Figure 4-11 Metabolic Alkalosis. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  413. Figure 4-12 Respiratory Acidosis. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  414. Respiratory alkalosis
  415. Quick Check 4-5
  416. Figure 4-13 Respiratory Alkalosis. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  417. Did You Understand?
  418. Distribution of Body Fluids
  419. Alterations in Water Movement
  420. Sodium, Chloride, and Water Balance
  421. Alterations in Sodium, Chloride, and Water Balance
  422. Alterations in Potassium and Other Electrolytes
  423. Acid-Base Balance
  424. Key Terms
  425. References
  426. Unit 2 Mechanisms of Self-Defense
  427. Chapter 5 Innate Defenses: Inflammation
  428. Electronic Resources
  429. Companion CD
  430. Website http://evolve.elsevier.com/Huether/
  431. Human Defense Mechanisms
  432. Table 5-1 Overview of Human Defenses
  433. First Line of Defense: Physical, Mechanical, and Biochemical Barriers
  434. Physical and Mechanical Barriers
  435. Biochemical Barriers
  436. Second Line of Defense: Inflammation
  437. Figure 5-1 The Sequence of Events in the Process of Inflammation. See the text for details.
  438. Figure 5-2 Acute Inflammatory Response.Inflammation is usually initiated by cellular injury and may be complicated by infection. Mast cell degranulation, the activation of three plasma systems, and the release of subcellular components from the damaged cells occur as a consequence. These systems are interdependent, so that induction of one (e.g., mast cell degranulation) can result in the induction of the other two. The result is the development of the characteristic microscopic and clinical hallmarks of inflammation. The figure numbers refer to additional figures in which more detailed information may be found on that portion of the response.
  439. The Mast Cell
  440. Figure 5-3 Degranulation (left) and Synthesis (right) of Biologic Mediators by Mast Cells during Inflammation. Mast cells are filled with darkly staining granules that contain a large number of biologically active substances. Among these are histamine, which is a major initiator of vascular changes, and a variety of chemotactic factors. These substances are released immediately after stimulation of mast cells. Other substances are synthesized in response to mast cell stimulation. These include lipid-based molecules that originate from plasma membrane phospholipids as a result of the action of phospholipase A2. These include platelet-activating factor and a variety of prostaglandins and leukotrienes.
  441. Mast Cell Degranulation
  442. Figure 5-4 Effects of Histamine through H1 and H2 Receptors. The effects depend on (1) density and affinity of H1 or H2 receptors on the target cell and (2) the identity of the target cell. GTP, Guanosine triphosphate; cGMP, cyclic guanosine monophosphate; ATP, adenosine triphosphate; cAMP, cyclic adenosine monophosphate.
  443. Mast Cell Synthesis of Mediators
  444. Quick Check 5-1
  445. Plasma Protein Systems
  446. Figure 5-5 Plasma Protein Systems in Inflammation: Complement, Clotting, and Kinin Systems. See the text for more detailed information. In this scheme some systems are activated by multiple pathways that come together (at C3 for the complement system and factor X for the clotting system). Some of the components of the pathways are activated by being split into two active components (C3 and C5 of the complement system and fibrinogen of the clotting system). The larger of the components usually activates the next component of the pathway (as do C3b and C5b of the complement system). Hageman factor participated in both the clotting and kinin pathways (i.e., activated factor XII [XIIa] helps activate factor X and prekallikrein). Many of the components of each pathway have potent biologic activities (in red colored boxes). Many other components of each pathway are not shown in this drawing but play very important roles in activation of the pathway. FP, Fibrinopeptides.
  447. Complement System
  448. Clotting System
  449. Kinin System
  450. Control and Interaction of Plasma Protein Systems
  451. Cellular Components of Inflammation
  452. Neutrophils
  453. Monocytes and Macrophages
  454. Figure 5-6 Activation of a Macrophage by Cytokines. Some cytokines produced by lymphocytes can react with surface receptors on macrophages and greatly increase their ability to kill bacteria. A, Electron micrograph of a peripheral blood monocyte. B, Electron micrograph of an activated tissue macrophage showing increases in cytoplasmic volume, plasma membrane, and numbers of lysosomal granules. Additionally, activation includes increases in glucose metabolism, phagocytic activity, and bacterial killing. (A, From Abbas AK, Lichtman AH: Cellular and molecular immunology, ed 5, Philadelphia, 2003, Saunders; B, from Bloom W, Fawcett DW: A textbook of histology, ed 11, Philadelphia, 1986, Saunders.)
  455. Eosinophils
  456. Natural Killer (NK) Cells
  457. Platelets
  458. Phagocytosis
  459. Figure 5-7 Process of Phagocytosis. Phagocytosis is a multistep process that involves diffusion of chemotactic factors from a site of injury. Many additional factors affect the blood vessels and increase adhesion molecules on endothelial cells and neutrophils, resulting in adherence of the neutrophils to the vessel wall (pavementing), retraction of endothelial cells (vascular permeability), and movement of the neutrophils through the opened intercellular junctions (diapedesis) and into the tissue. The cells move up the gradient toward the highest concentration of chemotactic factors (chemotaxis). At the site of injury, neutrophils begin phagocytosis of contaminating bacteria. The actual process of phagocytosis involves several steps (see enlargement): (1) adherence to the bacteria, which is increased by opsonins such as antibody (Ab) and complement component C3b; (2) engulfment of the bacteria by extensions of the neutrophil’s membrane (pseudopods); (3) formation of a phagosome containing the bacterium surrounded by the neutrophil’s plasma membrane; (4) fusion of lysosomes with the vacuole to form a phagolysosome and the production of toxic oxygen molecules (H2O2, hydrogen peroxide; O2−, superoxide); and (5) killing and breakdown of the bacterium.
  460. Figure 5-8 Steps in Phagocytosis. This scanning electron micrograph shows the progressive steps in phagocytosis of red blood cells by a macrophage. A, The macrophage (M) attaches to the red blood cells (R). B, An extension of the macrophage membrane (P; pseudopod) starts to enclose the red cell. C, The red blood cells are almost totally engulfed by the macrophage. (Modified from King DW, Fenoglio CM, Lefkowitch JH: General pathology: principles and dynamics, Philadelphia, 1983, Lea & Febiger.)
  461. Quick Check 5-2
  462. Cellular Products
  463. Figure 5-9 Selected Cytokines that Mediate Inflammation and the Acquired Immune Response. See the text for a more detailed description. IL, Interleukin; IFN, interferon; TNF, tumor necrosis factor; TGF, transforming growth factor; CSFs, colony stimulating factors.
  464. Cytokines
  465. Interleukins
  466. Interferons
  467. Other cytokines
  468. Figure 5-10 The Action of Interferon.
  469. Chemokines
  470. Quick Check 5-3
  471. Health Alert Fat Is “Inflammatory”
  472. Local Manifestations of Acute Inflammation
  473. Systemic Manifestations of Acute Inflammation
  474. Fever
  475. Leukocytosis
  476. Plasma Protein Synthesis
  477. Table 5-2 Acute-Phase Reactants: Proteins That Are Increased or Decreased in the Blood During Inflammation
  478. Chronic Inflammation
  479. Figure 5-11 The Chronic Inflammatory Response. Inflammation usually becomes chronic because of the persistence of an infection, an antigen, or a foreign body in the wound. Chronic inflammation is characterized by the persistence of many of the processes of acute inflammation. In addition, large amounts of neutrophil degranulation and death, the activation of lymphocytes, and the concurrent activation of fibroblasts result in the release of mediators that induce the infiltration of more lymphocytes and monocytes/macrophages and the beginning of wound healing and tissue repair. For more detailed information on each portion of the response, see the figures referred to in this illustration.
  480. Figure 5-12 Tuberculous Granuloma. Granulomas frequently form around areas of infection with the organism that causes tuberculosis. The granulomas consist of a central area of amorphous caseous (cheeselike) necrosis that is surrounded by a zone of activated macrophages, in which multinucleate macrophages (Langerhans giant cells) are present. There are outer layers of lymphocytes and fibroblasts. A wall of fibrin is laid down around the granulomas, and the contents eventually breakdown and liquefy. (From Stevens A, Lowe J: Pathology, ed 2, Edinburgh, 2000, Mosby.)
  481. Quick Check 5-4
  482. Resolution and Repair
  483. Figure 5-13 Wound Repair by Primary or Secondary Intention.A to D, Healing by primary intention. E to I, Healing by secondary intention. Please see the text for more details.
  484. Reconstructive Phase
  485. Maturation Phase
  486. Dysfunctional Wound Healing
  487. Dysfunction during the inflammatory response
  488. Dysfunction during the reconstructive phase
  489. Impaired collagen synthesis
  490. Figure 5-14 Keloid (scar) Formation. Scar and keloid caused by excessive synthesis of collagen at a suture site. (From Damjanov I, Linder J: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.)
  491. Impaired epithelialization
  492. Wound disruption
  493. Impaired contraction
  494. Quick Check 5-5
  495. Pediatrics & Factors Affecting Mechanisms of Self-Defense in the Newborn Child
  496. Aging & Factors Affecting Mechanisms of Self-Defense in the Elderly
  497. Did You Understand?
  498. Human Defense Mechanisms
  499. First Line of Defense: Physical, Mechanical, and Biochemical Barriers
  500. Second Line of Defense: Inflammation
  501. The Mast Cell
  502. Plasma Protein Systems
  503. Cellular Components of Inflammation
  504. Cellular Products
  505. Local Manifestations of Acute Inflammation
  506. Systemic Manifestations of Acute Inflammation
  507. Chronic Inflammation
  508. Resolution and Repair
  509. PEDIATRICS & Factors Affecting Mechanisms of Self-Defense in the Newborn Child
  510. AGING & Factors Affecting Mechanisms of Self-Defense in the Elderly
  511. Key Terms
  512. References
  513. Chapter 6 Adaptive Immunity
  514. Electronic Resources
  515. Companion CD
  516. Website http://evolve.elsevier.com/Huether/
  517. General Characteristics of Adaptive Immunity
  518. Table 6-1 Clinical Use of Antigen or Antibody
  519. Humoral and Cell-Mediated Immunity
  520. Active and Passive Immunity
  521. Figure 6-1 Overview of the Immune Response. The immune response can be separated into two phases: the generation of clonal diversity and clonal selection. During the generation of clonal diversity, lymphoid stem cells from the bone marrow migrate to the central lymphoid organs (the thymus or regions of the bone marrow) where they undergo a series of cellular divisions and differentiation stages resulting in either immunocompetent T cells from the thymus or immunocompetent B cells from the bone marrow. These cells have never encountered foreign antigen. The immunocompetent cells enter the circulation and migrate to the secondary lymphoid organs (e.g., spleen and lymph nodes), where they take up residence in B and T cell–rich areas (more detail in Figure 6-14). The clonal selection phase is initiated by exposure to foreign antigen. The antigen is usually processed by antigen-presenting cells (APCs) for presentation to helper T cells (Th cells) (more detail in Figures 6-16 and 6-17). The intercellular cooperation among APCs, Th cells, and immunocompetent T and B cells results in a second stage of cellular proliferation and differentiation (more detail in Figures 6-19 and 6-20). Because antigen has “selected” those T and B cells with compatible antigen receptors, only a small population of T and B cells undergo this process at one time. The end result is an active cellular immunity or humoral immunity or both. Cellular immunity is mediated by a population of “effector” T cells that can kill targets (cytotoxic T cells) or regulate the immune response (regulatory T cells), as well as a population of memory T cells that can respond more quickly to a second challenge with the same antigen. Humoral immunity is mediated by a population of soluble proteins (antibodies) produced by plasma cells and by a population of memory B cells that can produce more antibody rapidly to a second challenge with the same antigen.
  522. Quick Check 6-1
  523. Antigens and Immunogens
  524. Figure 6-2 Lymphoid System. Immature lymphocytes migrate through central (primary) lymphoid tissues: the bone marrow (central lymphoid tissue for B lymphocytes) and the thymus (central lymphoid tissue for T lymphocytes). Mature lymphocytes later reside in the T and B lymphocyte–rich areas of the peripheral (secondary) lymphoid tissues.
  525. Figure 6-3 Scanning Electron Micrograph of Lymphocytes and Macrophages. The lymphocytes are small and spherical; the macrophages are larger and more irregular in shape. From Raven PH, Johnson GB: Biology, ed 5, New York, 1999, McGraw-Hill.
  526. Figure 6-4 Antigenic Determinants (Epitopes). Generic examples of epitopes on protein (A) and polysaccharide (B) molecules are shown. In A, an antigenic protein may have multiple different epitopes (epitopes 1 and 2) that react with different antibodies. Each sphere represents an amino acid with the red spheres representing epitope 1 and the yellow spheres representing epitope 2. Individual epitopes may consist of 8 or 9 amino acids. In B, a polysaccharide is constructed of a backbone with branched side chains. Each sphere represents an individual carbohydrate with the red spheres representing the carbohydrates that form the epitope. In this example, two identical epitopes are shown that would bind two identical antibodies.
  527. Humoral Immune Response
  528. Antibodies
  529. Classes of immunoglobulins
  530. Figure 6-5 Structure of Different Immunoglobulins. Secretory IgA, IgD, IgE, IgG, and IgM. The black circles attached to each molecule represent carbohydrate residues.
  531. Table 6-2 Properties of Immunoglobulins
  532. Molecular structure
  533. Figure 6-6 Molecular Structure of an Antibody. A, The typical antibody molecule consists of four chains—two identical light (L) and two identical heavy (H)—held together by intrachain and interchain disulfide linkages. The primary interchain disulfides between heavy chains occur in the hinge region (Hi) and provide flexibility in some classes of antibody. Each heavy chain and light chain is divided into regions that have relatively constant amino acid sequences (green areas) and regions with a variable amino acid sequence (VH, VL). Within the VH and VL regions are three highly variable complementary-determining regions (CDR1, CDR2, CDR3). B, Fragmentation of IgG by limited digestion with the enzyme papain has identified three important portions of the molecule: an Fc and two identical Fab fragments. Both Fab fragments could bind antigen. C, In this molecular model of a typical antibody molecule, the light chains are represented by strands of red spheres (each represents an individual amino acid), and heavy chains are represented by strands of blue spheres. Note that the heavy chain contains sites where carbohydrates are bound. As the chains fold and interact, the six CDRs within a Fab region are placed in close proximity to form the antigen-binding site. C from Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  534. Antigen binding
  535. Function of antibodies
  536. Figure 6-7 Antigen-Antibody Binding. The specificity of an antibody binding with an antigen is determined by the shape and chemistry of the six complementary-determining regions (CDRs) in the combining site on the variable region of the antibody. This figure indicates two different antibodies (Fab portions of antibody 1 and antibody 2), which have different sets of CDRs and, therefore, different specificities. As indicated, the antigenic determinant that reacts well with antibody 1 is unable to react with antibody 2 because of differences in the antibody- combining site. Fab, Antigen-binding fragment.
  537. Direct effects
  538. Indirect effects
  539. IgE
  540. Figure 6-8 Direct and Indirect Functions of Antibody. Activities of antibodies can be direct (through the action of antibody alone) or indirect (requiring activation of other components of inflammation, usually through the Fc region). Direct means they include neutralization of viruses or bacterial toxins before they bind to receptors on the surface of the host’s cells. Indirect means they include activation of the classical complement pathway through C1 resulting in formation of the membrane-attack complex (MAC) or by increased phagocytosis of bacteria opsonized with antibody and complement components bound to appropriate surface receptors (FcR and C3bR) on the phagocyte.
  541. B cell antigen receptor
  542. Figure 6-9 Immunologic Mechanisms That Activate the Inflammatory Response. Immunologic factors may activate inflammation through three mechanisms: (1) IgE can bind to the surface of a mast cell and, after binding antigen, induce the cell’s degranulation (see Figure 6-9); (2) antigen and antibody can activate the complement system, releasing anaphylatoxins and chemotactic factors, especially C5a that result in mast cell degranulation and neutrophil chemotaxis; and (3) antigen may also react with T lymphocytes, resulting in the production of lymphokines that may contribute to the development of either acute or chronic inflammation.
  543. Secretory immune system
  544. Figure 6-10 IgE-Mediated Destruction of a Parasite. (1) Soluble antigens from a parasitic infection cause production of IgE antibody by B cells. (2) Secreted IgE binds to IgE-specific receptors on the mast cell. (3) Additional soluble parasite antigen cross-links the IgE on the mast cell surface, (4) leading to mast cell degranulation and release of many proinflammatory products, including eosinophil chemotactic factor of anaphylaxis (ECF-A). (5) ECF-A attracts eosinophils from the circulation. (6) The eosinophil attaches to the surface of the parasite and releases potent lysosomal enzymes that damage microorganisms.
  545. Monoclonal antibodies
  546. Quick Check 6-2
  547. Cell-Mediated Immune Response
  548. Figure 6-11 Secretory Immune System. Lymphocytes from the mucosal-associated (secretory) lymphoid tissues circulate throughout the body in a pattern separate from other lymphocytes. For example, lymphocytes from the gut-associated lymphoid tissue circulate through the regional lymph nodes, the thoracic duct, and the blood and return to other mucosal-associated lymphoid tissues rather than to lymphoid tissue of the systemic immune system.
  549. T Cell Recognition of a Target Cell
  550. T cell receptor complex
  551. Antigen presentation molecules
  552. Figure 6-12 Antigen-Presenting Molecules. Two sets of molecules are primarily responsible for antigen presentation: MHC class I and MHC class II. The MHC molecules are encoded from the major histocompatibility complex on chromosome 6. This complex also contains genes for several other molecules that participate in the innate or immune responses, including some complement proteins and cytokines, which are referred to as MHC class III molecules. This region contains information for the α chains of three principal class I molecules, called HLA-A, HLA-B, and HLA-C. These will be discussed in more detail in Chapter 7. Each of the MHC class I α chains complex with β2 microglobulin, which is encoded by a gene on chromosome 15. The MHC class I molecules present small peptide antigens (8 or 9 amino acids in length) in a pocket formed by the α1 and α2 domains of the α chain. The conformation of the molecule is stabilized by β2 microglobulin as well as by intrachain disulfide bonds (-S-S-). The α and β chains of class II molecules are also encoded in the MHC region. The principal class II molecules are HLA-DR, HLA-DP, and HLA-DQ. The MHC class II molecules present peptide antigens in a pocket formed by the α1 domain of the α chain and β1 domain of the β chain. Both MHC class I and II molecules are anchored to the plasma membrane by hydrophobic regions on the ends of the α and β chains.
  553. CD molecules
  554. T Lymphocyte Function
  555. Killing abnormal cells
  556. Cytotoxic T lymphocytes
  557. Figure 6-13 Cellular Killing Mechanisms. Several cells have the capacity to kill abnormal (e.g., virally infected, cancerous) target cells. (1) Cytotoxic T (Tc) cells recognized endogenous antigen presented by MHC class I molecules. The Tc cell mobilizes multiple killing mechanisms that induce apoptosis of the target cell. (2) Natural killer (NK) cells identify and kill target cells through receptors that recognize abnormal surface changes. NK cells specifically kill targets that do not express surface MHC class I molecules. (3) Several cells, including macrophages and NK cells, can kill by antibody-dependent cellular cytotoxicity (ADCC). IgG antibodies bind to foreign antigen on the target cell, and cells involved in ADCC bind IgG through Fc receptors (FcR) and initiate killing. The insert is a scanning electron microscopic view of Tc cells (L) attacking a much larger tumor cell (Tu). Insert from Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  558. Other cells that kill abnormal cells
  559. T cells that activate macrophages
  560. Regulatory T lymphocytes
  561. Quick Check 6-3
  562. Generation of Clonal Diversity
  563. Table 6-3 Generation of Clonal Diversity vs. Clonal Selection
  564. B Lymphocytes
  565. T Lymphocytes
  566. Induction of the Immune Response
  567. Figure 6-14 Secondary Lymphoid Tissues: Sites of B Cell and T Cell Differentiation. A, A lymph node is organized into an outer cortex (C) and an inner medulla (M).B, The lymph node contains areas that are rich in immunocompetent B cells (stained green) and T cells (stained red). C, In response to antigen, B cells undergo proliferation resulting in the formation of germinal centers (GC). From Kumar V, Abbas A, Fausto N: Robbins and Cotran pathologic basis of disease, ed 7, Philadelphia, 2005, Saunders.
  568. Primary and Secondary Immune Responses
  569. Figure 6-15 Primary and Secondary Immune Responses. The initial administration of antigen induces a primary response during which IgM is initially produced, followed by IgG. Another administration of the antigen induces the secondary response in which IgM is transiently produced and larger amounts of IgG are produced over a longer period of time.
  570. Cellular Interactions in the Immune Response
  571. Antigen processing and presentation
  572. Helper T lymphocytes
  573. Figure 6-16 Antigen Processing. Antigen processing and presentation are required for initiation of most immune responses. Foreign antigen may be either endogenous (cytoplasmic protein) or exogenous (e.g., bacterium). Endogenous antigenic peptides are transported into the endoplasmic reticulum (1) where the MHC molecules are being assembled. In the ER, antigenic peptides bind to the α chains of the MHC class I molecule (2), and the complex is transported to the cell surface (3). The α and β chains of the MHC class II molecules are also being assembled in the endoplasmic reticulum (4), but the antigen-binding site is blocked by a small molecule (invariant chain) to prevent interactions with endogenous antigenic peptides. The MHC class II–invariant chain complex is transported to phagolysosomes (5) where exogenous antigenic fragments have been produced as a result of phagocytosis (6). In the phagolysosomes, the invariant chain is digested and replaced by exogenous antigenic peptides (7), after which the MHC class II–antigen complex is inserted into the cell membrane (8).
  574. Superantigens
  575. Figure 6-17 Development of Th1 and Th2 Cells. Antigen presenting cells (APC) present antigen to a precursor Th cells. (1) An antigen signal is produced by the interaction of the T cell receptor (TCR) and CD4 with antigen presented by MHC class II molecules. (2) Cytokines (particularly IL-1) produced by the APC provide a second signal. (3) In response to these signals, the precursor Th cells begin producing the cytokine IL-2, which binds with the same cell to accelerate differentiation and proliferation. Commitment to a Th1 or Th2 phenotype results from the effects of other cytokines. (4) IL-12 and IFN-γ favor differentiation into the Th1 cell phenotype, whereas (5) IL-4 favors differentiation into the Th2 cell phenotype. (6) The Th1 cell produces cytokines that assist in the differentiation of cytotoxic T (Tc) cells (e.g., TNF-β, IL-2), whereas (7) the Th2 cell produces cytokines that favor B cell differentiation (e.g., IL-4, IL-5, IL-6). (8) Th1 and Th2 cells affect each other through the production of inhibitory cytokines: IFN-γ will inhibit development of Th2 cells, and IL-4 will inhibit the development of Th1 cells.
  576. T cell clonal selection: The cellular immune response
  577. B cell clonal selection: The humoral immune response
  578. Figure 6-18 Superantigens. The T cell receptor (TCR) and major histocompatibility complex (MHC) class II molecule are normally held together by processed antigen. Superantigens, such as some bacterial exotoxins, bind directly to the variable region of the TCR-β chain and the MHC class II molecule. Each superantigen activates sets of V-β chains independently of the antigen specificity of the TCR.
  579. Figure 6-19 Tc-Cell Clonal Selection. The immunocompetent Tc cell can react with antigen but cannot yet “kill” target cells. During clonal selection, this cell reacts with antigen presented by MHC class I molecules on the surface of a virally infected or cancerous “abnormal” cell. (1) The antigen–MHC class I complex is recognized simultaneously by the T cell receptor (TCR), which binds to antigen, and CD8, which binds to the MHC class I molecule. (2) A separate signal is provided by cytokines, particularly IL-2 from Th1 cells. (3) In response to these signals, the Tc cell develops into an “effector” Tc cell with the ability to kill abnormal cells.
  580. Figure 6-20 B Cell Clonal Selection. Immunocompetent B cells undergo proliferation and differentiation into antibody-secreting plasma cells. Multiple signals are necessary (1). The B cell itself can directly bind soluble antigen through the B cell receptor (BCR) and act as an antigen processing cell. Antigen is internalized, processed (2), and presented (3) to the TCR on a Th2 cell by MHC class II molecules (4). A cytokine signal is provided by the Th2 cell cytokines (e.g., IL-4) that react with the B cell (5). The B cell differentiates into plasma cells that secrete antibody (6).
  581. Memory cells
  582. Figure 6-21 Activation of a B Cell by a T Cell-Independent Antigen. Molecules containing repeating identical antigenic determinants may interact simultaneously with several receptors on the surface of the B cell and induce the proliferation and production of immunoglobulins. Because Th2 cells do not participate, class switch does not occur and the resultant antibody response is IgM.
  583. Quick Check 6-4
  584. Pediatrics & Immune Function
  585. Transport of IgG Across the Syncytiotrophoblast. The human placenta is covered with a specialized multinucleate cell, the syncytiotrophoblast. Transport of maternal IgG across the syncytiotrophoblast and into the fetal circulation is an active process. Maternal IgG binds to Fc receptors on the surface of the syncytiotrophoblast and is internalized by the process of endocytosis. Receptors on the syncytiotrophoblast are specific for the Fc portion of IgG and do not bind other classes of immunoglobulins. Interaction of IgG with Fc receptors protects the antibody from lysosomal digestion during transport of the vacuole across the cell (i.e., transcytosis). On the fetal side of the syncytiotrophoblast, IgG is released by exocytosis (see Chapter 1).
  586. Antibody Levels in Umbilical Cord Blood and in Neonatal Circulation. Early in gestation, maternal IgG begins active transport across the placenta and enters the fetal circulation. At birth, the fetal circulation may contain nearly adult levels of IgG, which is almost exclusively from the maternal source. The fetal immune system has the capacity to produce IgM and small amounts of IgA before birth (not shown). After delivery, maternal IgG is rapidly destroyed and neonatal IgG production increases
  587. Aging & Immune Function
  588. Did You Understand?
  589. General Characteristics of the Immune Response
  590. Antigens and Immunogens
  591. Humoral Immune Response
  592. Cell-Mediated Immune Response
  593. Generation of Clonal Diversity
  594. Induction of the Immune Response
  595. PEDIATRICS & Immune Function
  596. AGING & Immune Function
  597. Key Terms
  598. References
  599. Chapter 7 Hypersensitivities, Infection, and Immune Deficiencies
  600. Electronic Resources
  601. Companion CD
  602. Website http://evolve.elsevier.com/Huether/
  603. Hypersensitivity: Allergy, Autoimmunity, and Alloimmunity
  604. Table 7-1 Relative Incidence and Examples of Hypersensitivity Diseases*
  605. Mechanisms of Hypersensitivity
  606. Type I: IgE-mediated hypersensitivity reactions
  607. Mechanisms of IgE-mediated hypersensitivity
  608. Table 7-2 Examples of Autoimmune Disorders
  609. Clinical Manifestations
  610. Table 7-3 Immunologic Mechanisms of Tissue Destruction
  611. Evaluation and Treatment
  612. Type II: Tissue-specific hypersensitivity reactions
  613. Figure 7-1 Mechanism of Type I, IgE-Mediated Reactions. First exposure to an allergen stimulates B lymphocytes to mature into plasma cells that produce IgE. The IgE is adsorbed to the surface of the mast cell by binding with IgE-specific Fc receptors. When an adequate amount of IgE is bound the mast cell is “sensitized.” During a second exposure, the allergen cross-links the surface-bound IgE and causes degranulation of the mast cell. The initial phase is characterized by vasodilation, vascular leakage, and smooth muscle spasm or glandular secretions, usually within 5 to 30 minutes after exposure to antigen. The late phase occurs 2 to 8 hours later without additional exposure to antigen and results from infiltration of tissues with inflammatory cells, including eosinophils, neutrophils, and basophils. (See Chapter 5 for more details on the role of mast cells in inflammation.)
  614. Figure 7-2 Type I Hypersensitivity Reactions. Symptoms of type I allergic reactions are indicated.
  615. Table 7-4 Causes of Clinical Allergic Reactions
  616. Type III: Immune complex–mediated hypersensitivity reactions
  617. Mechanisms of type III hypersensitivity
  618. Figure 7-3 Type I Hypersensitivity Reactions. Photographs show diffuse allergic-like (A) eye (angioedema) and (B) skin (allergic urticaria) reactions. The skin lesions have raised edges and develop within minutes or hours, with resolution occurring after about 12 hours. From Male D et al: Immunology, ed 7, St Louis, 2006, Mosby.
  619. Immune complex disease
  620. Figure 7-4 Mechanisms of Type II, Tissue-Specific Reactions. Antibody binds to antigens on the cell surface and destroys or prevents the cell from functioning by A, complement-mediated lysis (an erythrocyte target is illustrated here); B, phagocytosis by macrophages in the tissue; C, neutrophil-mediated destruction; D, antibody-dependent cell-mediated cytotoxicity (ADCC); or E, modulation or blocking the normal function of receptors by antireceptor antibody. C1, Complement component C1; C3b, complement fragment produced from C3, which acts as an opsonin.
  621. Figure 7-5 Mechanism of Type III, Immune-Complex-Mediated Reactions.(1) Immune complexes form in the blood from circulating antigen and antibody and (2) are deposited in certain target tissues. (3) The complexes activate complement through C1 and generate fragments that are chemotactic for neutrophils. (4) The neutrophils attach to the IgG and C3b in the immune complexes and (5) release a variety of degradative enzymes that destroy the healthy tissues.
  622. Type IV: Cell-mediated hypersensitivity reactions
  623. Figure 7-6 Mechanism of Type IV Cell-Mediated Reactions. Antigens from target cells stimulate T cells to differentiate into T cytotoxic cells, which have direct cytotoxic activity, and T helper cells, which produce cytokines (especially interferon-γ) that activate macrophages. The macrophages can attach to targets and release enzymes and reactive oxygen species that induce apoptosis of the target.
  624. Figure 7-7 Development of Allergic Contact Dermatitis.A, The development of allergy to poison ivy. The first (primary) contact with allergen sensitizes (produces reactive T cells) the individual but does not produce a rash (dermatitis). Secondary contact activates a type IV cell-mediated reaction that causes dermatitis. B, Contact dermatitis caused by a delayed hypersensitivity reaction leading to vesicles and scaling at the sites of contact. From Damjanov I, Linder J: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  625. Quick Check 7-1
  626. Antigenic Targets of Hypersensitivity Reactions
  627. Allergy
  628. Allergens
  629. Allergic disease: bee sting allergy
  630. Autoimmunity
  631. Breakdown of tolerance
  632. Autoimmune disease: systemic lupus erythematosus
  633. Health Alert Autoimmune Diseases Affect Women More Than Men
  634. Alloimmunity
  635. Alloantigens
  636. Alloimmune disease: transfusion reactions
  637. ABO system
  638. Rh system
  639. Figure 7-8 ABO Blood Types. The relationship of antigens and antibodies associated with the ABO blood groups. The surfaces of erythrocytes of individuals with blood group A have the A antigenic carbohydrate. The blood of these individuals has IgM antibodies against the B antigen. In individuals with blood group B, the red blood cells have the B antigenic carbohydrate, and the blood contains IgM antibodies against the A antigen. In individuals of the blood group AB, the same cells have both the A and B antigens. These individuals do not have antibody to either A or B antigens. The erythrocytes of blood group O individuals have neither antigen, but their blood contains both antibodies to A and B.
  640. Alloimmune disease: transplant rejection
  641. Major histocompatibility complex
  642. Figure 7-9 Human Leukocyte Antigens (HLA). The major histocompatibility complex (MHC) is located on chromosome 6 and contains genes that code for class I antigens, class II antigens, and class III proteins (i.e., complement proteins and cytokines). From Mudge-Grout C: Immunologic disorders, St Louis, 1992, Mosby.
  643. Transplantation
  644. Figure 7-10 Inheritance of HLA. HLA alleles are inherited in a codominant fashion; both maternal and paternal antigens are expressed. Specific HLA alleles are commonly given numbers to indicate different antigens. In this example, the mother has linked genes for HLA-A3 and HLA-B12 on one chromosome 6 and genes for HLA-A10 and HLA-B5 on the second chromosome 6. The father has HLA-A28 and HLA-B7 on one chromosome and HLA-A1 and HLA-B35 on the second chromosome. The children from this pairing may have one of four possible combinations of maternal and paternal HLA.
  645. Rejection
  646. Quick Check 7-2
  647. Infection
  648. Microorganisms and Humans: A Dynamic Relationship
  649. Box 7-1 The Many Relationships Between Humans and Microorganisms
  650. Table 7-5 Normal Indigenous Flora of the Human Body
  651. Figure 7-11 The Spread of Infection. Redrawn from Mims CA et al: Medical microbiology, St Louis, 1993, Mosby.
  652. Classes of Infectious Microorganisms
  653. Pathogenic Defense Mechanisms
  654. Table 7-6 Classes of Human Infectious Microorganisms
  655. Infection and Injury
  656. Bacterial disease
  657. Table 7-7 Summary of Some Mechanisms of Tissue Damage and the Microorganisms That Cause Them
  658. Table 7-8 Examples of Mechanisms Used by Pathogens to Resist the Immune System
  659. Figure 7-12 Types of Gram-Positive and Gram-Negative Bacteria.
  660. Health Alert Antibiotic-Resistant Microorganisms Have Become the Primary Cause of Skin and Soft-Tissue Infections
  661. Viral disease
  662. Viral replication
  663. Figure 7-13 General Structure of Bacteria.A, The structure of the bacterial cell wall determines its staining characteristics with gram stain. A gram-positive bacterium has a thick layer of peptidoglycan (left). A gram-negative bacterium has a thick peptidoglycan layer and an outer membrane (right). B, Example of a gram-positive (darkly stained microorganisms, arrow) group A Streptococcus. This microorganism consists of cocci that frequently form chains. C, Example of a gram-negative (pink microorganisms, arrow) Neisseria meningitides in cerebrospinal fluid. Neisseria form complexes of two cocci (diplococci). From Murray PR et al: Medical microbiology, ed 4, St Louis, 2002, Mosby.
  664. Figure 7-14 Stages of Viral Infection of a Host Cell. The virion (1) becomes attached to the cell’s plasma membrane by absorption; (2) releases enzymes that weaken the membrane and allow it to penetrate the cell; (3) uncoats itself; (4) replicates; and (5) matures and escapes from the cell by budding from the plasma membrane. The infection then can spread to other host cells.
  665. Cellular effects of viruses
  666. Table 7-9 List of DNA and RNA Viruses of Human Importance
  667. Fungal disease
  668. Figure 7-15 Types of Fungi. From Mims CA et al: Medical microbiology, ed 3, London, 2004, Mosby.
  669. Table 7-10 Common Pathologic Fungi
  670. Clinical Manifestations of Infection
  671. Fever
  672. Figure 7-16 Progression of Measles. The pathogenesis of measles is representative of most viral infections in unimmunized individuals. The virus enters through the oropharynx, from where it infects the regional lymph nodes. After 5 to 7 days, virus enters the blood (viremia) and spreads to the body surfaces (respiratory, gastrointestinal, and urinary tracts, and the skin). The measles virus replicates in these tissues, leading to upper respiratory tract symptoms, with the appearance of red spots with bluish-white specks (Koplik spots) in the oral mucosa and later to an extensive rash involving most parts of the skin. At or near the onset of overt symptoms, the infected individual is shedding virus and is highly infectious to others. Antibodies against the measles virus are primarily responsible for resolving the infection. They are produced within 10 to 11 days but are immediately absorbed by viral particles in the blood so that free antibody is not measurable until about 2 weeks after the initial infection.
  673. Countermeasures Against Pathogenic Defenses
  674. Vaccines
  675. Figure 7-17 The Effect of Vaccination on the Incidence of Polio Worldwide,1980–2004.The number of global cases of polio has progressively decreased as the extent of immunization (coverage) has increased. The coverage is the percent of the world’s population that has been reported to the World Health Organization (WHO) by 192 member countries as being immunized. From World Health Organization: WHO vaccine-preventable diseases: monitoring system, 2005 global summary, Geneva, Switzerland, 2006; additional information is available at www.who.int/vaccines-documents.)
  676. Antimicrobials
  677. Table 7-11 Immunization Schedule: Range of Ages for Routine Immunizations
  678. Recent pathogenic adaptations
  679. Table 7-12 Chemicals or Antimicrobials Identified That Prevent Growth of or Destroy Microorganisms
  680. Quick Check 7-3
  681. Deficiencies in Immunity
  682. Initial Clinical Presentation
  683. Primary (Congenital) Immune Deficiencies
  684. B lymphocyte deficiencies
  685. T lymphocyte deficiencies
  686. Table 7-13 Examples of Primary Immune Deficiencies
  687. Combined deficiencies
  688. Figure 7-18 Facial Anomalies Associated With DiGeorge Syndrome. Note the wide-set eyes, low-set ears, and shortened structure of the upper lip. From Male D, et al: Immunology, ed 7, St Louis, 2006, Mosby.
  689. Complement deficiencies
  690. Phagocytic deficiencies
  691. Secondary (Acquired) Immune Deficiencies
  692. Acquired immunodeficiency syndrome (AIDS)
  693. Epidemiology
  694. Figure 7-19 Estimated Incidence of AIDS and Deaths Among Adults and Adolescents With AIDS in the United States (1985–2004). The incidence of AIDS and deaths related to AIDS rose almost linearly until about 1994. The introduction of effective antiviral treatments in the mid-1990s slowed the progression of the disease from HIV infection to AIDS and has maintained the number of AIDS-related deaths at about 17,000 per year. From Centers for Disease Control website, 2005; available at www.cdc.gov/hiv/topics/surveillance/resources/slides/index.htm.
  695. Pathogenesis
  696. Health Alert Risk of HIV Transmission Associated With Sexual Practices
  697. High Risk (in descending order of risk)
  698. Some Risk (in descending order of risk)
  699. Some Risk (depending on situation, intactness of mucous membranes, etc.)
  700. No Risk
  701. Unresolved Issues
  702. Clinical Manifestations
  703. Figure 7-20 Proportion of AIDS Cases Among Adults and Adolescents, by Exposure Category and Year of Diagnosis, in the United States (1985–2004). Worldwide, AIDS is primarily spread by heterosexual transmission. In the United States, the predominant route was by male-to-male sexual contact. The trend, however, is toward increasing heterosexual transmission. Transmission by injected drug use has remained relatively stable, as has the number of cases where both male-to-male sexual activity and injected drug use risk factors occur in the same individual. Redrawn from Centers for Disease Control website, 2005; available at www.cdc.gov/hiv/topics/surveillance/resources/slides/index.htm.
  704. Figure 7-21 Life Cycle and Possible Sites of Therapeutic Intervention of Human Immunodeficiency Virus (HIV). The HIV virion consists of a core of two identical strands of viral RNA encoated in a protein structure with viral proteins gp41 and gp120 on its surface (envelope). HIV infection begins when a virion binds to CD4 and chemokine coreceptors on a susceptible cell and follows the process described here. The provirus may remain latent in the cell’s DNA until it is activated (e.g., by cytokines). The HIV life cycle is susceptible to blockage at several sites (see the text for further information), including entrance inhibitors, reverse transcriptase inhibitors, integrase inhibitors, and protease inhibitors. Modified from Kumar V, Abbas A, Fausto N: Robbins and Cotran pathologic basis of disease, ed 7, Philadelphia, 2005, Saunders.
  705. Figure 7-22 Summary of Human Immunodeficiency Virus (HIV) Infection on the Immune System. Redrawn from Morse SA, Ballard RC, Holmes KK, et al, editors: Atlas of sexually transmitted diseases and AIDS, ed 3, Edinburgh, 2003, Mosby.
  706. Box 7-2 AIDS-Defining Opportunistic Infections and Neoplasms Found in Individuals With HIV Infection
  707. Infections
  708. Protozoal and Helminthic Infections
  709. Fungal Infections
  710. Bacterial Infections
  711. Viral Infections
  712. Neoplasms
  713. Treatment and Prevention
  714. Figure 7-23 Typical Progression From HIV Infection to AIDS in Untreated Persons.A, Clinical progression begins within weeks after infection; the person may experience symptoms of acute HIV syndrome. During this early period, the virus progressively infects T cells and other cells and spreads to the lymphoid organs, with a sharp decrease in circulating CD4+ T cells. During a period of clinical latency, the virus replicates and T cell destruction continues, although the person is generally asymptomatic. The individual may develop HIV-related disease (constitutional symptoms)—a variety of symptoms of acute viral infection that do not involve opportunistic infections or malignancies. When the number of CD4+ cells is critically suppressed, the individual becomes susceptible to a variety of opportunistic infections and cancers with a diagnosis of AIDS. The length of time for progression from HIV infection to AIDS may vary considerably from person to person. B, Laboratory tests are changing throughout infection. Antibody and Tc cell (cytotoxic T lymphocytes [CTLs]) levels change during the progression to AIDS. During the initial phase, antibodies against HIV-1 are not yet detectable (window period), but viral products, including proteins and RNA, and infectious virus, may be detectable in the blood a few weeks after infection. Most antibodies against HIV are not detectable in the early phase. During the latent phase of infection, antibody levels against p24 and other viral proteins, as well as HIV-specific CTLs, increase, then remain constant until the development of AIDS. A redrawn from Fauci AS, Lane HC: Human immunodeficiency virus disease: AIDS and related conditions. In Fauci AS et al, editors: Harrison’s principles of internal medicine, ed 14, New York, 1997, McGraw-Hill. B from Kumar V, Abbas A, Fausto N: Robbins and Cotran pathologic basis of disease, ed 7, Philadelphia, 2005, Saunders.
  715. Evaluation and Care of Those With Immune Deficiency
  716. Figure 7-24 Distribution of Tissues That Can Be Infected by HIV. Infection is closely linked to the presence of CD4 receptors or chemokine coreceptors on host tissue, particularly T cells and macrophages. Modified from Weber JN, Weiss RA: HIV infection: the cellular picture, in the science of AIDS: readings from Scientific American, New York, 1989, Freeman.
  717. Replacement Therapies for Immune Deficiencies
  718. Figure 7-25 Clinical Symptoms of AIDS.A, Severe weight loss and anorexia. B, Kaposi sarcoma lesions. C, Perianal lesions of herpes simplex infection. D, Deterioration of vision from cytomegalovirus retinitis leading to areas of infection, which can lead to blindness. A and D from Taylor PK: Diagnostic picture tests in sexually transmitted diseases, London, 1995, Mosby; B and C from Morse SA, Ballard RC, Holmes KK, et al, editors: Atlas of sexually transmitted diseases and AIDS, ed 3, Edinburgh, 2003, Mosby.
  719. Quick Check 7-4
  720. Table 7-14 Laboratory Evaluation of Immunodeficiencies
  721. Did You Understand?
  722. Hypersensitivity: Allergy, Autoimmunity, and Alloimmunity
  723. Infection
  724. Deficiencies in Immunity
  725. Key Terms
  726. References
  727. Chapter 8 Stress and Disease
  728. Electronic Resources
  729. Companion CD
  730. Website http://evolve.elsevier.com/Huether/
  731. Concepts of Stress
  732. Table 8-1 Examples of Stress-Related Diseases and Conditions
  733. General Adaptation Syndrome
  734. Figure 8-1 The Alarm Reaction. The alarm reaction includes increased secretion of glucocorticoids (cortisol) by the adrenal cortex and increased secretion of epinephrine and small amounts of norepinephrine from the adrenal medulla. The response to the release of cortisol and sympathetic nerve activation is summarized in Figure 8-2. ACTH, Adrenocorticotropic hormone. (From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.)
  735. Figure 8-2 The Stress Response.
  736. Psychologic Mediators and Specificity
  737. Quick Check 8-1
  738. The Stress Response
  739. Neuroendocrine Regulation
  740. Catecholamines
  741. Cortisol
  742. Table 8-2 Physiologic Effects of the Catecholamines*
  743. Cortisol and the immune system
  744. Table 8-3 Physiologic Effects of Cortisol
  745. Figure 8-3 Effect of Corticotropin-Releasing Hormone (CRH)—Mast Cell—Histamine Axis, Cortisol, and Catecholamines on the Th1/Th2 Balance—Cellular and Humoral Immunity. Humoral immunity provides protection against multicellular parasites, extracellular bacteria, some viruses, soluble toxins, and allergens. Cellular immunity provides protection against intracellular bacteria, fungi, protozoa, and several viruses. Type 1 cytokines or proinflammatory cytokines include IL-12, interferon-gamma (IFN-γ), and tumor necrosis factor-alpha (TNF-α). Type 2 cytokines or anti-inflammatory cytokines include IL-10 and IL-4. Solid lines (black) represent stimulation, whereas dashed lines (blue) represent inhibition (i.e., Th1 and Th2 are mutually inhibitory, IL-12 and IFN-γ inhibit Th2, and vice versa; IL-4 and IL-10 inhibit Th1 responses). Stress and CRH modulate inflammatory/immune and allergic responses by stimulating cortisol (glucocorticoid), catecholamines, and peripheral (immune) CRH secretion and by changing the production of regulatory cytokines and histamines. CRH (peripheral, immune), corticotropin-releasing hormone; NE, norepinephrine; Th, helper T cell; IL, interleukin; Tc, cytotoxic T cell; NK, natural killer cell; ↓, decreased (inhibited); ↑, increased (stimulation). (Redrawn from Elenkov IJ, Chrousos GP: Stress hormones, Th1/Th2 patterns, pro/anti-inflammatory cytokines and susceptibility to disease, Trends Endocrinol Metab 10[9]:359–368, 1999.)
  746. Other hormones
  747. Endorphins
  748. Growth hormone
  749. Prolactin
  750. Oxytocin
  751. Sex steroids
  752. Psychoneuroimmunologic Regulation
  753. Health Alert Chronic Stress, NPY, and Atherosclerosis
  754. Role of the Immune System
  755. Figure 8-4 Nervous System/Endocrine System/Immune System Interactions. Interconnections or pathways of communication among the immune, nervous, and endocrine systems.
  756. Stress, Personality, Coping, and Illness
  757. Health Alert Partner’s Survival and Spouse’s Hospitalizations and/or Death
  758. Aging & The Stress-Age Syndrome
  759. Figure 8-5 Health Outcome Determination in Stressful Life Situations Is Moderated by Numerous Factors. Whether a life-challenged individual experiences distress or illness depends on the subject’s appraisal of the event and the coping strategies used during the stressful period. Models A and B reflect possible outcomes in stressed healthy and symptomatic individuals. Model C illustrates the dynamic clinical setting in which the diagnosis of a serious illness and subsequent medical interventions may be perceived as stressful challenges and have potentially detrimental influences on physical outcome.
  760. Quick Check 8-3
  761. Did You Understand?
  762. Concepts of Stress
  763. The Stress Response
  764. Stress, Personality, Coping, and Illness
  765. AGING & Stress-Age Syndrome
  766. Key Terms
  767. References
  768. Unit 3 Cellular Proliferation: Cancer
  769. Chapter 9 Biology of Cancer and Tumor Spread
  770. Electronic Resources
  771. Companion CD
  772. Website http://evolve.elsevier.com/Huether/
  773. Cancer Characteristics and Terminology
  774. Tumor Classification and Nomenclature
  775. Table 9-1 Benign vs. Malignant Tumors
  776. Figure 9-1 Progression of Dysplasia to Neoplasm. A sequence of cellular and tissue changes progressing from dysplasia to in situ neoplasia and then to invasive neoplasia is seen often in the development of cancer. In this diagram, as in real life, distinguishing between dysplasia and in situ neoplasia is difficult. Loss of normal tissue architecture signifies development of neoplasia. The in situ neoplasms are most commonly found in the squamous epithelium of the uterine cervix, the epidermis of sun-exposed skin, and colonic and gastric mucosa after long-standing inflammation. The altered cell turnover during inflammation probably allows local environmental factors to cause genetic abnormalities leading to neoplasia. Modified from Stevens A, Lowe J: Pathology: illustrated review in color, ed 2, Edinburgh, 2000, Mosby.
  777. Figure 9-2 Loss of Cellular and Tissue Differentiation During the Development of Cancer.A, Normal colonic epithelium. B, Benign neoplasm of colon. C, Well-differentiated malignant neoplasm of colon. D, Poorly differentiated malignant neoplasm of colon. E, Anaplastic malignant neoplasm of colon. F, Benign neoplasm of smooth muscle. The cells of a benign neoplasm (B) resemble those of the normal epithelium (A) in that they are columnar and have an orderly arrangement. Loss of some degree of differentiation is evident in that the neoplastic cells do not show much mucin vacuolation. The cells of the benign neoplasm of smooth muscle (F) closely resemble normal muscle cells. Cells of the well-differentiated malignant neoplasm (C) have a haphazard arrangement, and although gland lumina (G) are formed, they are architecturally abnormal and irregular. Nuclei vary in shape and size. Cells in the poorly differentiated malignant neoplasm (D) have an even more haphazard arrangement, with poor formation of gland lumina (G). Nuclei show greater variation in shape and size compared with the well-differentiated malignant neoplasm (C). Cells in anaplastic malignant neoplasms (E) bear no relation to the normal epithelium, with no attempt at gland formation. Tremendous variation is found in the size of cells and nuclei, with intense staining (nuclear hyperchromatism) of the latter. Not knowing the site of origin would make it impossible to tell what sort of tumor this was by microscopic appearance alone. Well-differentiated tumors often resemble their cell of origin, as shown in the example of a benign tumor of smooth muscle (F). From Stevens A, Lowe J: Pathology: iIlustrated review in color, ed 2, Edinburgh, 2000, Mosby.
  778. Table 9-2 Examples of Tumor Nomenclature
  779. Box 9-1 Diagnosis and Clinical Staging of Cancer
  780. Diagnosis
  781. Clinical Staging
  782. Stages of Cancer Spread
  783. Cell Differentiation
  784. Figure 9-3 Tumor Staging by the TNM System. Example of staging for breast cancer. (See the figure for explanation of the abbreviations.)
  785. Tumor Markers
  786. Figure 9-4 Normal and Anaplastic Skeletal Muscle Cells.A, Normal skeletal muscle cells. B, Anaplastic tumor of the skeletal muscle (rhabdomyosarcoma). Note the marked cellular and nuclear pleomorphism (cellular and nuclear variation in size and shape) hyperchromatic nuclei, and giant tumor cells. The prominent cell in the center field has an abnormal tripolar spindle. Often the tissue of origin of an anaplastic tumor can only be established by the use of molecular markers such as immunohistochemical stains and chromosome analysis. A from Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby; B from Kumar V, Abbas AK, Fausto N: Pathologic basis of disease, ed 7, Philadelphia, 2005, Saunders, courtesy Dr. Trace Worrell, Department of Pathology, University of Texas Southwestern Medical School.
  787. Table 9-3 Examples of Tumor Markers
  788. Figure 9-5 Example of Differentiation. There often is a block in differentiation in cancer. Differentiation occurs several times in the lifetime of a granulocyte, with each step further limiting the cell’s potential. Eventually, the cell terminally differentiates and can no longer divide, and the mature cell dies.
  789. Quick Check 9-1
  790. The Genetic Basis of Cancer
  791. Cancer Is Caused by Mutations in Genes
  792. Clonal selection
  793. Figure 9-6 Cancer Incidence Increases Markedly With Age. The graph depicts the number of cases of colon cancer diagnosed in women in England and Wales in 1 year. The incidence of cancer increases dramatically with advancing age. This type of data suggests that accumulation of genetic mutations over time increases the risk of developing cancer. The slope of the curve suggests that five to seven mutations must occur before a full-blown cancer develops. Modified from Alberts B et al: Molecular biology of the cell, ed 4, New York, 2002, Garland.
  794. Types of Gene Mutations in Cancer
  795. Alteration of progrowth and antigrowth signals
  796. Figure 9-7 Sequential Acquisition of Genetic Changes. Progression from benign to malignant colon cancer is accompanied by an accumulation of mutations. One of the earliest mutations in colon cancer is loss of the tumor suppressor gene APC. Additional mutations, often in the oncogene ras, and loss of the tumor suppressors DCC and p53 occur as the lesion progresses from a benign polyp to an invasive carcinoma. APC, adenomatosis polyposis coli; DCC, deleted in colon cancer. Modified from Kumar V, Cotran RS, Robbins SL: Basic pathology, ed 6, Philadelphia, 1997, Saunders.
  797. Figure 9-8 Six Hallmarks of Cancer. Most cancers acquire mutations in six distinct areas of cell control during their development. All cancers must acquire the same six hallmark mutations, but their means of doing so varies mechanistically and chronologically. The order in which these capabilities are acquired is variable across different cancers. In some tumors, a particular mutation may confer several capabilities simultaneously, decreasing the number of intermediate mutational steps required for full development. Loss of the p53 tumor-suppressor gene may facilitate angiogenesis and resistance to apoptosis. In other tumors, by comparison, a collaboration of two or more distinct genetic changes may be needed to acquire a given trait. Modified from Hanahan D, Weinbert, RA: The hallmarks of cancer. Cell 100(1):57, 2000.
  798. Figure 9-9 Model for Action of ras Genes. When a normal cell is stimulated through a growth factor receptor, inactive (GDP-bound) ras is activated to a GTP-bound state. Activated ras sends growth signals to the nucleus through cytoplasmic kinases. The mutant ras protein is permanently activated because of its inability to hydrolyze GTP, leading to continual stimulation of the cell without any external trigger. GDP, Guanosine diphosphate; GTP, guanosine triphosphate; GAP, GTPase activating protein. From Kumar V, Cotran RS, Robbins SL: Basic pathology, ed 7, Philadelphia, 2003, Saunders.
  799. Angiogenesis
  800. Figure 9-10 Tumor-Induced Angiogenesis. Malignant tumors, especially those in metastatic sites, induce formation of blood vessels, which serve as routes for the transport of nutrients into the tumor. The approved drug bevacizumab blocks VEGF. VEGF, Vascular endothelial growth factor. From Damjanov I: Pathology for the health professions, ed 3, St Louis, 2006, Saunders.
  801. Telomeres and immortality
  802. Figure 9-11 Control of Replication: Telomeres. Normal cells cannot divide indefinitely. The ends of their chromosomes are capped by telomeres. In the absence of the telomerase enzyme, telomeres get shorter with each division until the cells finally stop dividing. In cancer cells, telomerase is switched on, producing an enzyme that rebuilds the telomeres. Thus, the cancer cell can divide indefinitely.
  803. Oncogenes and Tumor-Suppressor Genes: Accelerators and Brakes
  804. Mutations that create oncogenes
  805. Point mutations
  806. Table 9-4 Types of Cancer Genes
  807. Box 9-2 Types of Genetic Lesions in Cancers
  808. Chromosome translocations
  809. Figure 9-12 Chromosome Translocations Are Oncogenic in Two Ways. Chromosome translocations can lead to inappropriate activation of an oncogene by fusing the transcriptional control elements of one gene, for example, the immunoglobulin (Ig) heavy chain promoter to the coding sequence for an oncogene, in this example, the c-myc oncogene. This leads to high-level expression of c-myc in B lymphocytes as they make immunoglobulins (antibodies). This type of translocation is found in B cell lymphomas. Chromosome translocations also can fuse two genes right in the middle, leading to synthesis of novel chimeric proteins. The fusion often creates a protein that either has new cancer-promoting properties or has lost the ability to regulate a protein kinase. A novel activated protein tyrosine kinase is created in chronic myeloid leukemia.
  810. Chromosome amplification
  811. Tumor suppressor genes
  812. Figure 9-13 N-myc Gene Amplification in Neuroblastoma. The N-myc gene is detected in human neuroblastoma cells using a technique called FISH (fluorescent in situ hybridization). A, A single pair of N-myc genes is detected in normal cells and in low-grade neuroblastoma. B, Multiple, amplified copies of the N-myc gene are detected in some cases of neuroblastoma. Amplification of N-myc is strongly associated with a poor prognosis in childhood neuroblastoma. Courtesy Arthur R. Brothman, PhD, University of Utah School of Medicine.
  813. Table 9-5 Familial Cancer Syndromes Caused by Tumor-Suppressor Gene Function Loss
  814. Loss of heterozygosity
  815. Figure 9-14 Two Distinct Hits Are Required to Inactivate a Tumor Suppressor Gene. Tumor suppressor genes are often inactivated by a mutation (first hit) followed by complete loss of an entire region of chromosome encompassing the remaining normal allele (second hit, also known as loss of heterozygosity). LOH, Loss of heterozygosity.
  816. Quick Check 9-2
  817. Gene silencing
  818. Guardians of the Genome
  819. Figure 9-15 Silencing of Tumor Suppressor Genes.A, Paternal allele methylated and inactivated. In this example, the first copy of a gene is turned off by gene silencing without mutation. B, Mutation of maternal allele results in no functional protein production. In this example, the remaining normal gene can be inactivated by mutation.
  820. Genetics and Cancer-Prone Families
  821. Figure 9-16 Germline Mutation. Inherited mutations are carried in the DNA of reproductive cells. When reproductive cells containing mutations combine to produce offspring, the mutation will be present in all of the offspring’s body cells. Modified from Lea DN, Jenkins JF, Francomano CA: Genetics in clinical practice, Boston, 1998, Bartlett.
  822. Figure 9-17 A Familial Colon Cancer Pedigree. Darkened symbols represent individuals diagnosed with cancer. From Jorde LB et al: Medical genetics, ed 3, updated, St Louis, 2006, Mosby.
  823. Quick Check 9-3
  824. Infection, Immunity, Inflammation, and Cancer
  825. Viral Causes of Cancer
  826. Table 9-6 Human Viruses Associated With Cancer
  827. Bacterial Cause of Cancer
  828. Immunity and Cancer
  829. An Active Immune Response Causes Cancer
  830. Figure 9-18 The intimate association of inflammation and cancer. Cancers attract inflammatory cells by a number of methods. Cancer cell hypoxia and death releases factors that activate stromal and tumor-infiltrating macrophages. The activated Ras protein in many cancer cells also drives secretion of cytokines such as interleukin 8 (IL-8) that then stimulates inflammatory cells to secrete growth factors and pro-angiogenic factors. Redrawn from Karin M: Inflammation and cancer: the long reach of Ras. Nature Med 11(1):20–21, 2005.
  831. Quick Check 9-4
  832. Cancer Progression and Metastasis
  833. Figure 9-19 Multistep Nature of Metastasis. From Fidler IT: The pathogenesis of cancer metastasis: the “seed and soil” hypothesis revisited. Nat Rev Ca 3:453–458, 2003.
  834. Patterns of Spread
  835. Figure 9-20 Main Sites of Blood-Borne Metastasis.A, Sites of hematogenous metastasis. B, Metastasis in bone. C, Metastasis in brain. D, Metastasis in liver. E, Metastasis in adrenals. F, Metastasis in lung. Blood-borne tumor metastasis leads to growth of secondary tumors in several main sites. The macroscopic appearances of bone metastasis are shown in B, where lesions are seen in vertebrae. Numerous metastases from a neoplasm of the stomach are seen in the brain in C. The liver is the most common site for metastases from tumors in the gastrointestinal tract, as seen in D, which arose from a colonic neoplasm. In E, metastatic tumor has replaced both adrenal glands, as is commonly seen with spread from lung and breast tumors. The lung, F, is the most common site for blood-borne metastases from tumors outside the spinal tract, particularly mesenchymal tumors. From Stevens A, Lowe J: Pathology: illustrated review in color, ed 2, Edinburgh, 2000, Mosby.
  836. Figure 9-21 Metastatic Nonsmall Cell Lung Cancer (NSCLC). This 54-year-old woman had a NSCLC resected from the left upper lobe. Five years later, these studies were obtained. The positron emission tomography (PET) scan using 18fluoro-deoxyglucose shows metastatic lesions in the brain, right shoulder, mediastinal and cervical lymph nodes, as well as the liver, left pelvis, and proximal femur. (Left) PET whole body image. (Right) Representative coronal image from the whole body FDG-PET/CT fused image of the same patient. The fused image consists of the CT image with the metabolic information superimposed in color. The pattern of spread is most likely from the primary tumor to the large mediastinal lymph nodes, followed by lymphatic spread to cervical nodes. Blood-borne spread produced the bone, brain, and liver metastases. Normally, only the heart, brain, and bladder show strong signal in PET scan. Images courtesy John Hoffman, MD, Huntsman Cancer Institute.
  837. Table 9-7 Common Sites of Metastasis
  838. Distant Metastasis
  839. Quick Check 9-5
  840. Did You Understand?
  841. Cancer Characteristics and Terminology
  842. The Genetic Basis of Cancer
  843. Infection, Immunity, Inflammation, and Cancer
  844. Cancer Progression and Metastasis
  845. Key Terms
  846. References
  847. Chapter 10 Cancer Epidemiology, Manifestations, and Treatment
  848. Electronic Resources
  849. Companion CD
  850. Website http://evolve.elsevier.com/Huether/
  851. Gene-Environment Interaction and Risk Factors
  852. Figure 10-1 Estimated Numbers of New Cancer Cases (Incidence) and Deaths (Mortality) in 2002. Data shown in thousands for developing and developed countries by cancer site and sex. From Parkin DM et al: CA Cancer J Clin 55:74–108, 2005. © American Cancer Society.
  853. Table 10-1 Estimated New Cancer Cases and Deaths by Gender, United States, 2007*
  854. Tobacco Use
  855. Ionizing Radiation
  856. Radiation-induced cancer
  857. Carcinogenesis: genomic instability
  858. Bystander effects
  859. Figure 10-2 Models of the Responses of Clonogenic Cells to Ionizing Radiation. Mutations or chromosomal aberrations are shown as filled circles and apparently normal cells as open circles. A, If a cell faithfully repairs DNA damage, then its clonal descendents will appear normal. B, If a cell is directly mutated by radiation, then all its descendents will express the same mutation. C, Radiation-induced genomic instability is characterized by nonclonal effects in descendant cells. From Lorimore SA, Coates PJ, Wright EG: Radiation-induced genomic instability and bystander effects: inter-related nontargeted effects of exposure to ionizing radiation. Oncogene 22[45]:7058–7069, 2003.
  860. Gap junction function
  861. Ultraviolet Radiation
  862. Electromagnetic Fields
  863. Diet and Endogenous Hormones
  864. Obesity
  865. Biologic mechanisms
  866. Table 10-2 Relationship of Dietary Factors With Risk of Major Cancers*
  867. Figure 10-3 Energy Balance, Lipid Metabolism, and Insulin Sensitivity and Tumor Development. In obesity, increased release from adipose tissue of free fatty acids (FFA), tumor necrosis factor alpha (TNF-α) and resistin, and reduced release of adiponectin lead to insulin resistance and compensatory chronic hyperinsulinemia. Increased insulin levels ultimately lead to decreased liver synthesis and blood levels of insulin-like growth factor-binding protein 1 (IGFBP1) and, theoretically, also decrease IGFBP1 synthesis locally in other tissues. Increased fasting levels of insulin in plasma are also correlated with decreased levels of IGFBP2 in the blood leading to increased levels of bioavailable IGF-1. Insulin and IGF-1 signal through the insulin receptors (IRs) and IGF-1 receptor (IGF1R) to stimulate cellular proliferation and inhibit apoptosis in many tissue types. These effects could promote tumor development. Adapted from Calle EE, Kaaks R: Overweight, obesity and cancer: epidemiological evidence and proposed mechanisms. Nat Rev Cancer 4(8):579–591, 2004.
  868. Endogenous hormones
  869. Alcohol Consumption
  870. Health Alert Possible Components of a Cancer-Prevention Diet
  871. Increase
  872. Decrease
  873. Sexual and Reproductive Behavior
  874. Physical Activity
  875. Occupational Hazards as Carcinogens
  876. Air Pollution
  877. Clinical Manifestations of Cancer
  878. Pain
  879. Figure 10-4 Theoretical Framework for Cytokine-Induced Cancer Symptoms. Solid blue lines proinflammatory cytokines and chemokines (IL-1, TNF-α, IL-6, IFN) are released by immune cells. They exert their effect on peripheral nerves and the brain. Neurotransmitter responses by the brain are affected. The hypothalamic-pituitary-adrenal axis is activated with increased release of corticosteroids, which provide feedback (dotted red lines) to decrease cytokine production. Adapted from Cleeland CS et al: Actytokine-immunologic model of cancer symptoms, Cancer 97(11):2919–2925, 2003.
  880. Fatigue
  881. Cachexia
  882. Figure 10-5 Cachexia. This severe form of malnutrition results in wasting and extensive loss of adipose tissue. From Kamal A, Brockelhurst JC: Color atlas of geriatric medicine, ed 2, St Louis, 1991, Mosby.
  883. Anemia
  884. Leukopenia and Thrombocytopenia
  885. Infection
  886. Paraneoplastic Syndromes
  887. Table 10-3 Factors Predisposing Individuals With Cancer to Infection
  888. Quick Check 10-1
  889. Table 10-4 Paraneoplastic Syndromes
  890. Cancer Treatment
  891. Chemotherapy
  892. Table 10-5 Examples of Treatment of Site-Specific Cancers
  893. Figure 10-6 Chemotherapy and Resistant Cells. A cell resistant to single-agent chemotherapy can develop from the pool of fast-growing tumor cells. Combination therapy helps prevent the development of resistant cells. From Stevens A, Lowe J: Pathology: illustrated review in color, ed 2, Edinburgh, 2000, Mosby.
  894. Table 10-6 Examples of Chemotherapeutic Drugs
  895. Radiation
  896. Table 10-7 Mechanisms of Action of Common Chemotherapeutic Drugs
  897. Surgery
  898. Hormonal Therapy
  899. Table 10-8 Common Hormonal Agents and Types of Tumors
  900. Immunotherapy
  901. Health Alert l-Glutamine
  902. Side Effects of Cancer Treatment
  903. Gastrointestinal Tract
  904. Bone Marrow
  905. Hair and Skin
  906. Reproductive Tract
  907. Quick Check 10-2
  908. Did You Understand?
  909. Gene-Environment Interaction
  910. Clinical Manifestations of Cancer
  911. Cancer Treatment
  912. Side Effects of Cancer Treatment
  913. Key Terms
  914. References
  915. Chapter 11 Cancer in Children
  916. Electronic Resources
  917. Companion CD
  918. Website http://evolve.elsevier.com/Huether/
  919. Incidence and Types of Childhood Cancer
  920. Table 11-1 Childhood Age-Adjusted Invasive Cancer Incidence Rates by Primary Site and Age, United States*
  921. Table 11-2 Childhood Age-Adjusted Cancer Incidence Rates for Children 0–19 Years of Age by Primary Site and Race and Ethnicity, United States*
  922. Etiology
  923. Genetic Factors
  924. Table 11-3 Congenital Factors Associated With Childhood Cancer
  925. Environmental Factors
  926. Table 11-4 Selected Oncogenes and Tumor-Suppressor Genes Associated With Childhood Cancer
  927. Prenatal exposure
  928. Childhood exposure
  929. Prognosis
  930. Health Alert Late Effects of Childhood Cancer
  931. Quick Check 11-1
  932. Did You Understand?
  933. Incidence and Types of Childhood Cancers
  934. Etiology
  935. Prognosis
  936. Key Terms
  937. References
  938. Part Two Body Systems and Disease
  939. Unit 4 The Neurologic System
  940. Chapter 12 Structure and Function of the Neurologic System
  941. Electronic Resources
  942. Companion CD
  943. Website http://evolve.elsevier.com/Huether/
  944. Overview and Organization of the Nervous System
  945. Cells of the Nervous System
  946. The Neuron
  947. Health Alert Neuroimaging Techniques
  948. Figure 12-1 Neuron With Composite Parts.A, Multipolar neuron: neuron with multiple extensions from the cell body. B, Scanning electron micrograph. Modified from Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  949. Figure 12-2 Neuronal Transmission and Synaptic Cleft. Electrical impulse travels along axon of first neuron to synapse. Chemical transmitter is secreted into synaptic space to depolarize membrane (dendrite or cell body) of next neuron in pathway. Cell A represents unipolar cell; cell B represents multipolar cell.
  950. Neuroglia and Schwann Cells
  951. Nerve Injury and Regeneration
  952. Figure 12-3 Types of Neuroglial Cells.A, Fibrous astrocyte; B, oligodendrocytes; C, microglia cells; D, ependymal cells. Modified from Chipps E, Clanin N, Campbell V: Neurologic disorders, St Louis, 1992, Mosby.
  953. Table 12-1 Support Cells of the Nervous System
  954. Figure 12-4 Repair of a Peripheral Nerve Fiber. When cut, a damaged motor axon can regrow to its distal connection only if the Schwann cells remain intact (to form a guiding tunnel) and if scar tissue does not block its way.
  955. Quick Check 12-1
  956. The Nerve Impulse
  957. Synapses
  958. Neurotransmitters
  959. Quick Check 12-2
  960. The Central Nervous System
  961. The Brain
  962. Table 12-2 Substances That Are Neurotransmitters or Neuromodulators
  963. Table 12-3 Divisions of the Central Nervous System
  964. Figure 12-5 Reticular Activating System. System consists of nuclei in the brain stem reticular formation plus fibers that conduct to the nuclei from below and fibers that conduct from the nuclei to widespread areas of the cerebral cortex. Functioning of the reticular activating system is essential for consciousness.
  965. Forebrain
  966. Telencephalon
  967. Figure 12-6 The Cerebral Hemispheres.A, Left hemisphere of cerebrum, lateral view. B, Functional areas of the cerebral cortex, midsagittal view. C, Functional areas of the cerebral cortex, lateral view.
  968. Figure 12-7 Primary Somatic Sensory (A) and Motor (B) Areas of the Cortex. The body parts illustrated here show which parts of the body are “mapped” to specific areas of each cortical area. The exaggerated face indicates that more cortical area is devoted to processing information to and from the many receptors and motor units of the face than for the leg or arm, for example. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  969. Figure 12-8 Examples of Somatic Motor and Sensory Pathways.A, Motor: The pyramidal pathway illustrated by the lateral corticospinal tract and the extrapyramidal pathways illustrated by the rubrospinal and reticulospinal tracts. B, Sensory: pathways of the medial lemniscal system that conducts information about discriminating touch and kinesthesis and the spinothalamic pathway that conducts information about pain and temperature. Modified from Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  970. Health Alert Surgery for Parkinson Disease
  971. Box 12-1 Functions of the Hypothalamus
  972. Diencephalon
  973. Midbrain
  974. Hindbrain
  975. Metencephalon
  976. Myelencephalon
  977. Quick Check 12-3
  978. The Spinal Cord
  979. Figure 12-9 Spinal Cord Within Vertebral Canal and Exiting Spinal Nerves.A, Posterior view of brain stem and spinal cord in situ with spinal nerves and plexus. B, Lateral view of brain stem and spinal cord. C, Enlargement of caudal area showing termination of spinal cord (conus medullaris) and group of nerve fibers constituting the cauda equina. Redrawn from Rudy EB, editor: Advanced neurological and neurosurgical nursing, St Louis, 1984, Mosby.
  980. Motor Pathways
  981. Sensory Pathways
  982. Figure 12-10 Coverings of the Spinal Cord. The dura mater is shown in natural color. Note how it extends to cover the spinal nerve roots and nerves. The arachnoid is highlighted in blue and the pia mater in pink. Modified from Thibodeau GA, Patton KT: Structure and function of the human body, ed 12, St Louis, 2004, Mosby.
  983. Figure 12-11 Major Tracts of the Spinal Cord. The major ascending (sensory) tracts, shown only on the left here, are highlighted in blue. The major descending (motor) tracts, shown only on the right, are highlighted in red. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  984. Protective Structures of the Central Nervous System
  985. Cranium
  986. Figure 12-12 Cross Section of Spinal Cord Showing Simple Reflex Arc. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  987. Figure 12-13 Neuromuscular Junction. This figure shows how the distal end of a motor neuron fiber forms a synapse, or “chemical junction,” with an adjacent muscle fiber. Neurotransmitters (specifically, acetylcholine) are released from the neuron’s synaptic vesicles and diffuse across the synaptic cleft. There they stimulate receptors in the motor end-plate region of the sarcolemma. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 5, St Louis, 2003, Mosby.
  988. Meninges
  989. Figure 12-14 Meninges of the Brain. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  990. Cerebrospinal fluid and the ventricular system
  991. Table 12-4 Composition of Cerebrospinal Fluid
  992. Vertebral column
  993. Figure 12-15 Vertebral Column.A, Right lateral view. B, Anterior view. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  994. Figure 12-16 Vertebra and Intervertebral Disk. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 5, St Louis, 2003, Mosby.
  995. Quick Check 12-4
  996. Blood Supply of the Central Nervous System
  997. Blood supply to the brain
  998. Figure 12-17 Major Arteries of the Head and Neck. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  999. Figure 12-18 Arteries at the Base of the Brain. The arteries that compose the circle of Willis are the two anterior cerebral arteries, joined to each other by the anterior communicating artery and two short segments of the internal carotids, off of which the posterior communicating arteries connect to the posterior cerebral arteries. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 5, St Louis, 2003, Mosby.
  1000. Table 12-5 Arterial Systems Supplying the Brain
  1001. Figure 12-19 Areas of the Brain Affected by Occlusion of the Anterior, Middle, and Posterior Cerebral Artery Branches.A, Inferior view. B, Lateral view.
  1002. Blood-brain barrier
  1003. Blood supply to the spinal cord
  1004. Figure 12-20 Large Veins of the Head. Deep veins and dural sinuses are projected on the skull. Note connections (emissary veins) between the superficial and deep veins. From Thibodeau GA, Patton KT: Anatomy & Physiology, ed 6, St Louis, 2007, Mosby.
  1005. Figure 12-21 Arteries of the Spinal Cord.A, Arteries of cervical cord exposed from the rear. B, Arteries of spinal cord diagrammatically shown in horizontal section. Redrawn from Rudy EB, editor: Advanced neurological and neurosurgical nursing, St Louis, 1984, Mosby.
  1006. The Peripheral Nervous System
  1007. Quick Check 12-5
  1008. The Autonomic Nervous System
  1009. Anatomy of the Sympathetic Nervous System
  1010. Figure 12-22 Cranial and Peripheral Nerves.A, Ventral surface of the brain showing attachment of the cranial nerves. B, Peripheral nerve trunk and coverings. C, Scanning electron micrograph of a freeze-fractured preparation of peripheral nerve. A and C from Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1011. Table 12-6 The Cranial Nerves
  1012. Figure 12-23 Locations of Neurotransmitters and Receptors of the Autonomic Nervous System. In all pathways, preganglionic fibers are cholinergic, secreting acetylcholine (Ach), which stimulates nicotinic receptors in the postganglionic neuron. Most sympathetic postganglionic fibers are adrenergic, A, secreting norepinephrine (NE), thus stimulating α- or β-adrenergic receptors. A few sympathetic postganglionic fibers are cholinergic, stimulating muscarinic receptors in effector cells, B. All parasympathetic postganglionic fibers are cholinergic, C, stimulating muscarinic receptors in effector cells. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1013. Figure 12-24 Sympathetic Division of the Autonomic Nervous System.CiG, Ciliary ganglion; SpG, sphenopalatine ganglion; SCG, superior cervical ganglion; OG, otic ganglion; SG, submandibular ganglion; CG, celiac ganglion; SMG, superior mesenteric ganglion; IMG, inferior mesenteric ganglion; PP, pelvic plexus. Redrawn from Rudy EB, editor: Advanced neurological and neurosurgical nursing, St Louis, 1984, Mosby.
  1014. Anatomy of the Parasympathetic Nervous System
  1015. Figure 12-25 Parasympathetic Division of the Autonomic Nervous System.CiG, Ciliary ganglion; SpG, sphenopalatine ganglion; OG, otic ganglion; SG, submandibular ganglion; VN, vagus nerve; PP, pelvic plexus; PN, pelvic nerve. Redrawn from Rudy EB, editor: Advanced neurological and neurosurgical nursing, St Louis, 1984, Mosby.
  1016. Neurotransmitters and Neuroreceptors
  1017. Figure 12-26 The Autonomic Nervous System and the Type of Neurotransmitters Secreted by Preganglionic and Postganglionic Fibers. Note that all preganglionic fibers are cholinergic (Ach). A somatic nerve is used for comparison.
  1018. Functions of the Autonomic Nervous System
  1019. Quick Check 12-6
  1020. Table 12-7 Actions of Autonomic Nervous System Neuroreceptors
  1021. Figure 12-27 Some Important Functions of the Sympathetic Nervous System.A, Regulation of vasomotor tone. B, Regulation of strenuous muscular exercise (“fight or flight” response). (See also Chapter 8 and Figure 8-1 for more detail on the stress response.)
  1022. Aging & The Nervous System
  1023. Structural Changes With Aging
  1024. Cellular Changes With Aging
  1025. Cerebrovascular Changes With Aging
  1026. Functional Changes With Aging
  1027. Did You Understand?
  1028. Overview and Organization of the Nervous System
  1029. Cells of the Nervous System
  1030. The Nerve Impulse
  1031. The Central Nervous System
  1032. The Peripheral Nervous System
  1033. The Autonomic Nervous System
  1034. AGING & the Nervous System
  1035. Key Terms
  1036. References
  1037. Chapter 13 Pain, Temperature, Sleep, and Sensory Function
  1038. Electronic Resources
  1039. Companion CD
  1040. Website http://evolve.elsevier.com/Huether/
  1041. Pain
  1042. The Experience of Pain
  1043. Neuroanatomy of Pain
  1044. Figure 13-1 Transmission of Pain Sensations. The Aδ and C fibers synapse in the laminae of the dorsal horn cross over to the contralateral spinothalamic tract then ascend to synapse in the midbrain through the neospinothalamic and paleospinothalamic tracts. Impulses are then conducted to the sensory cortex.
  1045. Table 13-1 Stimuli that Activate Nociceptors (Pain Receptors)
  1046. Theories of Pain
  1047. Figure 13-2 Gate Control Theory of Pain. Schematic diagram of the gate control theory of pain mechanism. Large fiber non-nociceptor impulses (i.e., mechanical and thermal) activate inhibitory interneuron in spinal cord dorsal horn and decrease pain transmission (close pain gate). Small fiber impulses block the inhibitory interneuron and promote pain transmission (open pain gate).
  1048. Neuromodulation of pain
  1049. Figure 13-3 Descending Pathway and Endorphin Response. Endorphin receptors are located close to known pain receptors in the periphery and ascending and descending pain pathways.
  1050. Common Clinical Descriptions of Pain
  1051. Box 13-1 Categories of Pain
  1052. Figure 13-4 Sites of Referred Pain.A, Front. B, Back.
  1053. Table 13-2 Common Chronic Pain Conditions
  1054. Pain threshold and pain tolerance
  1055. Quick Check 13-1
  1056. Temperature Regulation
  1057. Table 13-3 Comparison of Acute and Chronic Pain
  1058. Table 13-4 Pain Perception in Infants, Children, and Elderly Persons
  1059. Hypothalamic Control of Temperature
  1060. Table 13-5 Mechanisms of Heat Production and Loss
  1061. Mechanisms of heat production and loss
  1062. Mechanisms of heat conservation
  1063. Temperature Regulation in Infants and Elderly Persons
  1064. Pathogenesis of Fever
  1065. Figure 13-5 Production of Fever. When monocytes/macrophages are activated, they secrete endogenous pyrogenic cytokines such as interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor (TNF) and interferon (IF) which reach the hypothalamic temperature-regulating center. These cytokines promote the synthesis and secretion of prostaglandin E2 (PGE2) in the anterior hypothalamus. PGE2 increases the thermostatic set point, and the autonomic nervous system is stimulated, resulting in shivering, muscle contraction, and peripheral vasoconstriction. Adapted from Lewis SM, Heitkemper MM, Dirksen SR: Medical-surgical nursing: assessment and management of clinical problems, ed 5, St Louis, 2000, Mosby.
  1066. Benefits of Fever
  1067. Box 13-2 Effects of Fever at the Extremes of Age
  1068. Elderly Persons
  1069. Children
  1070. Disorders of Temperature Regulation
  1071. Hyperthermia
  1072. Hypothermia
  1073. Trauma and temperature
  1074. Quick Check 13-2
  1075. Box 13-3 Defining Characteristics of Hypothermia
  1076. Accidental Hypothermia*
  1077. Therapeutic Hypothermia†‡
  1078. Sleep
  1079. Sleep Disorders
  1080. Box 13-4 Sleep Characteristics of Infants and Elderly Persons
  1081. Infants
  1082. Elderly Persons
  1083. Common dyssomnias
  1084. Insomnia
  1085. Sleep disordered breathing
  1086. Disorders of the sleep-wake schedule
  1087. Common parasomnias
  1088. Box 13-5 Restless Leg Syndrome (RLS)
  1089. Quick Check 13-3
  1090. The Special Senses
  1091. Vision
  1092. The eye and its external structures
  1093. Figure 13-6 Internal Anatomy of the Eye. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1094. Visual dysfunction
  1095. Alterations in ocular movements
  1096. Figure 13-7 Extrinsic Muscles of the Right Eye. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1097. Figure 13-8 Lacrimal Apparatus. Fluid produced by lacrimal glands (tears) streams across the eye surface, enters the canals, and then passes through the nasolacrimal duct to enter the nose. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1098. Alterations in visual acuity
  1099. Table 13-6 Changes in the Eye Caused by Aging
  1100. Table 13-7 Causes of Visual Acuity Changes
  1101. Alterations in accommodation
  1102. Alterations in refraction
  1103. Alterations in color vision
  1104. Neurologic disorders causing visual dysfunction
  1105. Figure 13-9 Alterations in Refraction.A, Myopic eye. Parallel rays of light are brought to a focus in front of the retina. B, Hyperopic eye. Parallel rays of light come to a focus behind the retina in the unaccommodative eye. C, Simple myopic astigmatism. The vertical bundle of rays is focused on the retina; the horizontal rays are focused in front of the retina. From Stein HA, Slatt BJ, Stein RM: The ophthalmic assistant: fundamentals and clinical practice, ed 5, St Louis, 1998, Mosby.
  1106. External eye structure disorders
  1107. Hearing
  1108. The normal ear
  1109. Figure 13-10 Visual Pathways and Defects. Modified from Thompson JM et al: Mosby’s clinical nursing, ed 5, St Louis, 2002, Mosby.
  1110. Figure 13-11 The Ear. External, middle, and inner ears. (Anatomic structures are not drawn to scale.) From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1111. Figure 13-12 The Inner Ear.A, The bony labyrinth (orange) is the hard outer wall of the entire inner ear and includes the semicircular canals, vestibule, and cochlea. Within the bony labyrinth is the membranous labyrinth (purple), which is surrounded by perilymph and filled with endolymph. Each ampulla in the vestibule contains a crista ampullaris that detects changes in head position and sends sensory impulses through the vestibular nerve to the brain. B, The inset shows a section of the membranous cochlea. Hair cells in the organ of Corti detect sound and send the information through the cochlear nerve. The vestibular and cochlear nerves join to form the eighth cranial nerve. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1112. Auditory dysfunction
  1113. Aging & Changes in Hearing
  1114. Conductive hearing loss
  1115. Sensorineural hearing loss
  1116. Mixed and functional hearing loss
  1117. Meniere disease
  1118. Ear infections
  1119. Otitis externa
  1120. Otitis media
  1121. Olfaction and Taste
  1122. Figure 13-13 Olfaction. Midsagittal section of the nasal area shows the location of major olfactory sensory structures. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1123. Aging & Changes in Olfaction and Taste
  1124. Olfactory and taste dysfunctions
  1125. Quick Check 13-4
  1126. Somatosensory Function
  1127. Touch
  1128. Proprioception
  1129. Quick Check 13-5
  1130. Did You Understand?
  1131. Pain
  1132. Temperature Regulation
  1133. Sleep
  1134. The Special Senses
  1135. Somatosensory Function
  1136. Key Terms
  1137. References
  1138. Chapter 14 Concepts of Neurologic Dysfunction
  1139. Electronic Resources
  1140. Companion CD
  1141. Website at http://evolve.elsevier.com/Huether/
  1142. Alterations in Cognitive Networks
  1143. Alterations in Arousal
  1144. Pathophysiology
  1145. Clinical Manifestations and Evaluation
  1146. Table 14-1 Clinical Manifestations of Metabolic and Structural Causes of Comas
  1147. Level of consciousness
  1148. Pattern of breathing
  1149. Table 14-2 Differential Characteristics of States Causing Coma
  1150. Table 14-3 Levels of Altered Consciousness
  1151. Pupillary changes
  1152. Figure 14-1 Abnormal Respiratory Patterns With Corresponding Level of Central Nervous System Activity. From Urden LD, Davie JK, Lough ME: Thelan’s critical care nursing: diagnosis and management, ed 5, St Louis, 2006, Mosby.
  1153. Table 14-4 Patterns of Breathing
  1154. Oculomotor responses
  1155. Motor responses
  1156. Figure 14-2 Pupils at Different Levels of Consciousness.
  1157. Vomiting
  1158. Quick Check 14-1
  1159. Figure 14-3 Test for Oculocephalic Reflex Response (Doll’s Eyes Phenomenon).A, Normal response—eyes turn together to side opposite from turn of head. B, Abnormal response—eyes do not turn in conjugate manner. C, Absent response—eyes do not turn as head position changes. From Rudy EB: Advanced neurological and neurosurgical nursing, St Louis, 1984, Mosby.
  1160. Outcomes
  1161. Figure 14-4 Test for Oculovestibular Reflex (Caloric Ice Water Test).A, Normal response—conjugate eye movements. B, Abnormal response—dysconjugate or asymmetric eye movements. C, Absent response—no eye movements.
  1162. Figure 14-5 Pathologic Reflexes.A, Grasp reflex. B, Snout reflex. C, Palmomental reflex. D, Suck reflex.
  1163. Table 14-5 Abnormal Motor Responses With Decreased Responsiveness
  1164. Figure 14-6 Decorticate and Decerebrate Responses. A, Decorticate response. Flexion of arms, wrists, and fingers with adduction in upper extremities; extension, internal rotation, and plantar flexion in lower extremities. B, Decerebrate response. All four extremities in rigid extension, with hyperpronation of forearms and plantar extension of feet. C, Decorticate response on right side of body and decerebrate response on left side of body. From Rudy EB: Advanced neurological and neurosurgical nursing, St Louis, 1984, Mosby.
  1165. Box 14-1 Criteria for Brain Death
  1166. Seizures
  1167. Pathophysiology
  1168. Conditions associated with seizure disorders
  1169. Table 14-6 Causes of Recurrent Seizures in Different Age-Groups
  1170. Types of seizure disorders
  1171. Table 14-7 International Classification of Epileptic Seizures
  1172. Table 14-8 Terminology Applied to a Seizure Disorder
  1173. Health Alert Epilepsy Surgery Stands the Test of Time
  1174. Clinical Manifestations
  1175. Evaluation and Treatment
  1176. Quick Check 14-2
  1177. Cognitive Disorders
  1178. Pathophysiology
  1179. Table 14-9 Clinical Manifestations of Cognitive Network Deficits
  1180. Clinical Manifestations
  1181. Evaluation and Treatment
  1182. Figure 14-7 Development of Dysphasia. Portion of the left cerebral hemisphere considered most important in the development of dysphasia.
  1183. Data Processing Deficits
  1184. Agnosia
  1185. Dysphasia
  1186. Acute confusional states
  1187. Table 14-10 Major Types of Dysphagia
  1188. Quick Check 14-3
  1189. Pathophysiology
  1190. Clinical Manifestations
  1191. Evaluation and Treatment
  1192. Dementia
  1193. Pathophysiology
  1194. Table 14-11 Examples of Language Disturbances
  1195. Table 14-12 Differences Between Organic and Functional Confusion
  1196. Health Alert Exercising the Body Can Benefit the Mind
  1197. Clinical Manifestations
  1198. Evaluation and Treatment
  1199. Table 14-13 Clinical Manifestations of Dementia
  1200. Alzheimer disease
  1201. Figure 14-8 Common Pathologic Findings in Alzheimer Disease. From Beare PG, Myers JL: Principles and practice of adult health nursing, ed 3, St Louis, 1998, Mosby.
  1202. Pathophysiology
  1203. Figure 14-9 Pathologic Changes in Alzheimer Disease.A, A neuritic (mature) plaque with central amyloid core (white arrow) next to a neurofibrillary tangle (white arrow). Alzheimer disease (B) compared with age-matched and sex-matched control (C): reduced size, narrow gyri, and wide sulci, notably in frontal and temporal lobes. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  1204. Clinical Manifestations
  1205. Evaluation and Treatment
  1206. Pick disease
  1207. Alterations in Cerebral Homeostasis
  1208. Cerebral Hemodynamics
  1209. Increased Intracranial Pressure
  1210. Figure 14-10 Clinical Correlates of Compensated and Uncompensated Phases of Intracranial Hypertension. From Beare PG, Myers JL: Principles and practice of adult health nursing, ed 3, St Louis, 1998, Mosby.
  1211. Figure 14-11 Herniation.A, Normal relationship of intracranial structures. B, Shift of intracranial structures. C, Downward herniation of the cerebellar tonsils into the foramen magnum.
  1212. Cerebral Edema
  1213. Box 14-2 Herniation Syndrome
  1214. Supratentorial Herniation
  1215. Infratentorial Herniation
  1216. Figure 14-12 Brain Edema. Intercellular lakes of high protein content fluid. (Hematoxylin-eosin stain; ×90.) From Kissane JM, editor: Anderson’s pathology, ed 9, St Louis, 1993, Mosby.
  1217. Hydrocephalus
  1218. Table 14-14 Types of Hydrocephalus
  1219. Pathophysiology
  1220. Clinical Manifestations
  1221. Evaluation and Treatment
  1222. Quick Check 14-4
  1223. Alterations in Motor Function
  1224. Alterations in Muscle Tone
  1225. Hypotonia
  1226. Table 14-15 Alterations in Muscle Tone
  1227. Hypertonia
  1228. Figure 14-13 A Paroxysm of Left-Sided Hemifacial Spasm. From Perkin GD: Mosby’s color atlas and text of neurology, ed 2, London, 2002, Mosby.
  1229. Figure 14-14 Dystonic Posturing of the Hand and Foot. From Perkin GD: Mosby’s color atlas and text of neurology, ed 2, London, 2002, Mosby.
  1230. Alterations in Movement
  1231. Figure 14-15 Spasmodic Torticollis. A characteristic head posture. From Perkin GD: Mosby’s color atlas and text of neurology, ed 2, London, 2002, Mosby.
  1232. Figure 14-16 Pseudohypertrophy of the Calf Muscles. From Perkin GD: Mosby’s color atlas and text of neurology, ed 2, London, 2002, Mosby.
  1233. Paresis/paralysis
  1234. Upper motor neuron syndromes
  1235. Table 14-16 Upper and Lower Motor Neuron Syndromes
  1236. Figure 14-17 Disturbances in Motor Function. Disturbances in motor function are classified pathologically along upper and lower motor neuron structures. It should be noted that the same pathologic condition occurs at more than one site in an upper motor neuron (above right). A few pathologic conditions involve both upper and lower motor neuron structures, as in amyotrophic lateral sclerosis, for example. Other lesion sites include myoneural junction and primary muscle, making it possible to classify conditions as neuromuscular and muscular, respectively.
  1237. Lower motor neuron syndromes
  1238. Amyotrophies
  1239. Figure 14-18 Structures Making up Upper Motor Neuron, or Pyramidal, System. Pyramidal system fibers are shown to originate primarily in cells in precentral gyrus of motor cortex; to converge at internal capsule; to descend to form central third of cerebral peduncle; to descend further through pons, where small fibers are given off to cranial nerve motor nuclei along the way; to form pyramids at medulla, where most of the fibers decussate; and then to continue to descend in lateral column of white matter of spinal cord. A few fibers descend without crossing at medulla level (see Figure 12-8).
  1240. Figure 14-19 Structures Making up Lower Motor Neuron, Including Motor (Efferent) and Sensory (Afferent) Elements.(Top) Anterior horn cell (in anterior gray column of spinal cord and its axon), terminating in motor end plate as it innervates extrafusal muscle fibers in quadriceps muscle. (Detailed enlargement) Sensory and motor elements of gamma loop system. Gamma efferent fibers shown innervating polar, or end, region of muscle spindle (sensory receptor of skeletal muscle). Contraction of muscle spindle fibers stretches central portion of spindle and causes afferent spindle fiber to transmit impulse centrally to cord. Muscle spindle afferent fibers in turn synapse on anterior horn cell and are transmitted by way of gamma efferent fibers to skeletal (extrafusal) muscle, causing it to contract. Muscle spindle discharge is interrupted by active contraction of extrafusal muscle fibers.
  1241. Hyperkinesia
  1242. Table 14-17 Types of Hyperkinesia
  1243. Huntington disease
  1244. Pathophysiology
  1245. Clinical Manifestations
  1246. Evaluation and Treatment
  1247. Hypokinesia
  1248. Akinesia and bradykinesia
  1249. Loss of associated neuron syndromes
  1250. Parkinson disease
  1251. Figure 14-20 Nigrostriatal Disorders Produce the Parkinson Syndrome. Coronal section of the brain shows the basal ganglia. Pathways controlling normal and abnormal motor function are depicted in a portion of the basal ganglia (caudate nucleus), A; they are shown enlarged in B. Dopaminergic synaptic activity is mediated by dopamine. Cholinergic synaptic activity is mediated by acetylcholine. A balance between the two kinds of activity produces normal motor function. A relative excess of cholinergic activity produces akinesia and rigidity. A relative excess of dopaminergic activity produces involuntary movements. Neurons in the caudate nucleus contain gamma-aminobutyric acid (GABA) and possibly control dopaminergic neurons in the substantia nigra through a feedback pathway. A from Cutler WP: Degenerative and hereditary diseases, ed 7, Washington, DC, 1983, Scientific American Medicine.
  1252. Pathophysiology
  1253. Clinical Manifestations
  1254. Figure 14-21 Stooped Posture of Parkinson Disease. From Perkin DG: Mosby’s color atlas and text of neurology, ed 2, London, 2002, Mosby.
  1255. Evaluation and Treatment
  1256. Alterations in Complex Motor Performance
  1257. Disorders of posture (stance)
  1258. Disorders of gait
  1259. Disorders of expression
  1260. Extrapyramidal Motor Syndromes
  1261. Basal ganglia motor syndromes
  1262. Table 14-18 Dyspraxias and Apraxias
  1263. Figure 14-22 Pathways Disrupted in Dyspraxias. Formulation of the idea of the motor act is thought to originate in the region of the supramarginal gyrus in the inferior left parietal lobe. This area is connected via associational pathways to the left premotor cortex. The left premotor cortex is connected through the corpus callosum to the right premotor and motor areas. An injury that interrupts the pathways between the left supramarginal gyrus and the premotor region produces a dyspraxia that involves the entire body. An injury that disrupts the callosal pathways produces a dyspraxia of the left side of the body only.
  1264. Quick Check 14-5
  1265. Cerebellar motor syndromes
  1266. Table 14-19 Pyramidal vs. Extrapyramidal Motor Syndrome
  1267. Did You Understand?
  1268. Alterations in Cognitive Networks
  1269. Alterations in Cerebral Homeostasis
  1270. Alterations in Motor Function
  1271. Key Terms
  1272. References
  1273. Chapter 15 Alterations of Neurologic Function
  1274. Electronic Resources
  1275. Companion CD
  1276. Website http://evolve.elsevier.com/Huether/
  1277. Central Nervous System Disorders
  1278. Trauma
  1279. Brain trauma
  1280. Table 15-1 Severity of Trauma Related to Trauma State Induced and Onset and Persistence of Clinical Manifestations
  1281. Table 15-2 Categories of Diffuse Brain Injury
  1282. Cause
  1283. Pathophysiology
  1284. Focal brain injury
  1285. Table 15-3 Causes of Brain Injuries
  1286. Figure 15-1 Coup and Contrecoup Head Injury After Blunt Trauma.1, Coup injury: impact against object; a, site of impact and direct trauma to brain; b, shearing of subdural veins; c, trauma to base of brain. 2, Contrecoup injury: impact within skull; a, site of impact from brain hitting opposite side of skull; b, shearing forces through brain. These injuries occur in one continuous motion—the head strikes the wall (coup) and then rebounds (contrecoup). Modified from Rudy EB: Advanced neurological and neurosurgical nursing, St Louis, 1984, Mosby.
  1287. Figure 15-2 Acute Subdural Hematoma (Dura Removed). Leptomeninges are intact. From Damjanov I, Linder J: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  1288. Figure 15-3 Hematomas. Recent hematomas, resulting from trauma, in frontal lobes. From Kissane JM, editor: Anderson’s pathology, ed 9, St Louis, 1993, Mosby.
  1289. Diffuse brain injury
  1290. Clinical Manifestations, Evaluation, and Treatment
  1291. Focal brain injury
  1292. Diffuse brain injury
  1293. Quick Check 15-1
  1294. Spinal cord trauma
  1295. Pathophysiology
  1296. Figure 15-4 Hyperextension Injuries of the Spine. Hyperextension injuries of the spine can result in fracture or nonfracture injuries with spinal cord damage.
  1297. Figure 15-5 Flexion Injury of the Spine. Hyperflexion produces translation (subluxation) of vertebrae that compromises the central canal and compresses spinal cord parenchyma or vascular structures.
  1298. Figure 15-6 Axial Compression Injuries of the Spine. In axial compression injuries of the spine, the spinal cord is contused directly by retropulsion of bone or disk material into the spinal canal.
  1299. Figure 15-7 Flexion-Rotation Injuries of the Spine.
  1300. Clinical Manifestations
  1301. Table 15-4 Mechanisms of Vertebral Injury Involving Bone, Ligaments, and Joints
  1302. Table 15-5 Spinal Cord Injuries
  1303. Table 15-6 Clinical Manifestations of Spinal Cord Injury
  1304. Figure 15-8 Autonomic Hyperreflexia.A, Normal response pathway. B, Autonomic dysreflexia pathway. SA, sinoatrial. Modified from Rudy EB: Advanced neurological and neurosurgical nursing, St Louis, 1984, Mosby.
  1305. Evaluation and Treatment
  1306. Degenerative Disorders of the Spine
  1307. Degenerative joint disease (DJD)
  1308. Degenerative disk disease
  1309. Spondylolysis
  1310. Spondylolisthesis
  1311. Spinal stenosis
  1312. Low back pain
  1313. Pathogenesis
  1314. Evaluation and Treatment
  1315. Figure 15-9 Herniated Nucleus Pulposus. Modified from Thompson JM et al: Mosby’s clinical nursing, ed 5, St Louis, 2002, Mosby.
  1316. Health Alert Percutaneous Vertebroplasty
  1317. Herniated intervertebral disk
  1318. Pathophysiology
  1319. Clinical Manifestations
  1320. Figure 15-10 Clinical Features of a Herniated Nucleus Pulposus.
  1321. Evaluation and Treatment
  1322. Cerebrovascular Disorders
  1323. Cerebrovascular accidents (stroke syndromes)
  1324. Thrombotic stroke
  1325. Health Alert Two New Warning Signs Found for Impending Stroke
  1326. Embolic stroke
  1327. Hemorrhagic stroke
  1328. Lacunar stroke
  1329. Pathophysiology
  1330. Cerebral infarction
  1331. Cerebral hemorrhage
  1332. Clinical Manifestations
  1333. Evaluation and Treatment
  1334. Intracranial aneurysm
  1335. Pathophysiology
  1336. Figure 15-11 Types of Aneurysms.
  1337. Clinical Manifestations
  1338. Evaluation and Treatment
  1339. Vascular malformation
  1340. Figure 15-12 Ophthalamic Artery Aneurysm.A, With endovascular coil; B, in situ. From Perkin GD: Mosby’s color atlas and text of neurology, London, 1998, Mosby-Wolfe.
  1341. Pathophysiology
  1342. Clinical Manifestations
  1343. Evaluation and Treatment
  1344. Subarachnoid hemorrhage
  1345. Pathophysiology
  1346. Clinical Manifestations
  1347. Table 15-7 Subarachnoid Hemorrhage Classification Scale
  1348. Evaluation and Treatment
  1349. Quick Check 15-2
  1350. Infection and Inflammation of the Central Nervous System
  1351. Meningitis
  1352. Pathophysiology
  1353. Clinical Manifestations
  1354. Evaluation and Treatment
  1355. Health Alert Meningococcal Vaccine and Guillain-Barré Syndrome
  1356. Abscess
  1357. Pathophysiology
  1358. Figure 15-13 Brain Abscess. Early brain abscess appearing as a poorly demarcated area (arrow) of cerebritis at the gray-white junction. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  1359. Clinical Manifestations
  1360. Health Alert West Nile Virus
  1361. Evaluation and Treatment
  1362. Encephalitis
  1363. Pathophysiology
  1364. Table 15-8 Classification and Characteristics of Viruses Causing Encephalitis
  1365. Clinical Manifestations
  1366. Evaluation and Treatment
  1367. Neurologic complications of AIDS
  1368. Human immunodeficiency-associated cognitive dysfunction (HIV encephalopathy)
  1369. HIV myelopathy
  1370. HIV neuropathy
  1371. Aseptic viral meningitis
  1372. Opportunistic infections
  1373. CNS neoplasms
  1374. Other CNS complications
  1375. Degenerative Diseases
  1376. Multiple sclerosis
  1377. Pathophysiology
  1378. Figure 15-14 Chronic Multiple Sclerosis. Demyelination plaque at gray-white junction and adjacent partially remyelinated shadow plaque (arrows). From Damjanov I, Linder J: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  1379. Clinical Manifestations
  1380. Health Alert Neural Stem Cells Protect and Restore Brain Functions
  1381. Evaluation and Treatment
  1382. Amyotrophic lateral sclerosis
  1383. Pathophysiology
  1384. Clinical Manifestations
  1385. Evaluation and Treatment
  1386. Quick Check 15-3
  1387. Peripheral Nervous System and Neuromuscular Junction Disorders
  1388. Peripheral Nervous System Disorders
  1389. Table 15-9 Peripheral Nervous System Disorders
  1390. Neuromuscular Junction Disorders
  1391. Myasthenia gravis
  1392. Pathophysiology
  1393. Clinical Manifestations
  1394. Evaluation and Treatment
  1395. Quick Check 15-4
  1396. Myopathies
  1397. Tumors of the Central Nervous System
  1398. Cranial Tumors
  1399. Figure 15-15 Origin of Clinical Manifestations Associated with an Intracranial Neoplasm.
  1400. Primary intracerebral tumors
  1401. Astrocytoma
  1402. Oligodendroglioma
  1403. Table 15-10 Brain and Spinal Cord Tumors
  1404. Table 15-11 Classification Systems for Astrocytomas
  1405. Ependymoma
  1406. Figure 15-16 Large Septal Ependymoma. This tumor represents the severity of tissue compression that occurs with a large brain tumor. The area in the upper-right part of the picture represents a secondary hydrocephalus that has further compressed brain tissue. Courtesy Dr. JE Olivera-Rabiela, Mexico City, Mexico. From Rosai J: Ackerman’s surgical pathology, ed 7, St Louis, 1989, Mosby.
  1407. Primary extracerebral tumors
  1408. Meningioma
  1409. Nerve sheath tumors
  1410. Metastatic carcinoma
  1411. Spinal Cord Tumors
  1412. Pathophysiology
  1413. Clinical Manifestations
  1414. Evaluation and Treatment
  1415. Quick Check 15-5
  1416. Did You Understand?
  1417. Central Nervous System Disorders
  1418. Peripheral Nervous System and Neuromuscular Junction Disorders
  1419. Tumors of the Central Nervous System
  1420. Key Terms
  1421. References
  1422. Chapter 16 Alterations of Neurologic Function in Children
  1423. Electronic Resources
  1424. Companion CD
  1425. Website http://evolve.elsevier.com/Huether/
  1426. Normal Growth and Development of the Nervous System
  1427. Figure 16-1 Cranial Sutures and Fontanelles in Infancy. Fibrous union of suture lines and interlocking of serrated edges (occurs by 6 months; solid union requires approximately 12 years).
  1428. Table 16-1 Reflexes of Infancy
  1429. Structural Malformations
  1430. Defects of Neural Tube Closure
  1431. Clinical Manifestations
  1432. Figure 16-2 Disorders Associated With Specific Stages of Embryonic Development.
  1433. Figure 16-3 Normal Spine, Meningocele, and Myelomeningocele. Diagram showing section through normal spine (A), meningocele (B), and myelomeningocele (C).
  1434. Table 16-2 Functional Alterations in Myelodysplasia Related to Level of Lesion
  1435. Malformations of the Axial Skeleton
  1436. Spina bifida occulta
  1437. Figure 16-4 Normal Brain and Arnold-Chiari II Malformation. Diagram showing normal brain (A) and brain with Arnold-Chiari II malformation (B).
  1438. Cranial deformities
  1439. Figure 16-5 Normal and Abnormal Head Configurations.Normal skull: Bones separated by membranous seams until sutures gradually close. Microcephaly and craniostenosis: Microcephaly is head circumference more than 2 standard deviations below the mean for age, gender, race, and gestation and reflects a small brain; craniosynostosis is premature closure of sutures. Scaphocephaly or dolichocephaly (frequency 56%): Premature closure of sagittal suture, resulting in restricted lateral growth. Brachycephaly: Premature closure of coronal suture, resulting in excessive lateral growth. Oxycephaly or acrocephaly (frequency 5.8% to 12%): Premature closure of all coronal and sagittal sutures resulting in accelerated upward growth and small head circumference. Plagiocephaly (frequency 13%): Unilateral premature closure of coronal suture, resulting in asymmetric growth. From Hockenberry MJ: Wong’s nursing care of infants and children, ed 7, St Louis, 2003, Mosby.
  1440. Table 16-3 Causes of Microcephaly
  1441. Quick Check 16-1
  1442. Encephalopathies
  1443. Static Encephalopathies
  1444. Inherited Metabolic Disorders of the Central Nervous System
  1445. Defects in amino acid metabolism
  1446. Phenylketonuria
  1447. Table 16-4 Inherited Metabolic Disorders of the Central Nervous System
  1448. Figure 16-6 Metabolic Error and Consequences in Phenylketonuria. From Hockenberry MJ: Wong’s nursing care of infants and children, ed 8, St Louis, 2007, Mosby.
  1449. Defects in lipid metabolism
  1450. Quick Check 16-2
  1451. Seizure Disorders
  1452. Epilepsy
  1453. Acute Encephalopathies
  1454. Reye syndrome
  1455. Intoxications of the central nervous system
  1456. Table 16-5 Major Types of Seizure Disorders Found in Children
  1457. Table 16-6 Commonly Ingested Poisons
  1458. Health Alert Iron and Cognitive Function
  1459. Figure 16-7 Systemic Effects of Increased Lead Absorption in Children.
  1460. Meningitis
  1461. Bacterial meningitis
  1462. Viral meningitis
  1463. Human Immunodeficiency Virus and Central Nervous System Involvement
  1464. Tumors
  1465. Brain Tumors
  1466. Table 16-7 Brain Tumors in Children
  1467. Figure 16-8 Location of Brain Tumors in Children.
  1468. Table 16-8 Treatment Strategies for Childhood Brain Tumors
  1469. Box 16-1 Clinical Manifestations of Brain Tumors
  1470. Headache
  1471. Vomiting
  1472. Neuromuscular Changes
  1473. Behavioral Changes
  1474. Cranial Nerve Neuropathy
  1475. Vital Sign Disturbances
  1476. Other Signs
  1477. Embryonal Tumors
  1478. Neuroblastoma
  1479. Retinoblastoma
  1480. Figure 16-9 Retinoblastoma. The tumor occupies a large portion of the inside of the eye bulbus. From Damjanov I: Pathology for the health professions, ed 3, St Louis, 2006, Saunders. Courtesy Dr. Walter Richardson and Dr. Jamsheed Khan, Kansas City, Kansas.
  1481. Figure 16-10 The Two-Mutation Model of Retinoblastoma Development. In inherited retinoblastoma, the first mutation is transmitted through the germline of an affected parent. The second mutation occurs somatically in a retinal cell, leading to development of the tumor. In sporadic retinoblastoma, development of a tumor requires two somatic mutations.
  1482. Quick Check 16-3
  1483. Did You Understand?
  1484. Normal Growth and Development of the Nervous System
  1485. Structural Malformations
  1486. Encephalopathies
  1487. Human Immunodeficiency Virus and Central Nervous System Involvement
  1488. Tumors
  1489. Key Terms
  1490. References
  1491. Unit 5 The Endocrine System
  1492. Chapter 17 Mechanisms of Hormonal Regulation
  1493. Electronic Resources
  1494. Companion CD
  1495. Website http://evolve.elsevier.com/Huether/
  1496. Mechanisms of Hormonal Regulation
  1497. Regulation of Hormone Release
  1498. Figure 17-1 Principal Endocrine Glands. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1499. Table 17-1 Structural Categories of Hormones
  1500. Hormone Transport
  1501. Figure 17-2 Feedback Loops.A, Endocrine feedback loops involving the hypothalamus-pituitary gland and end organs, in this example, the thyroid gland (endocrine regulation). B, General model for control and negative feedback to hypothalamic–pituitary target organ systems. Negative-feedback regulation is possible at three levels: target organ (ultrashort feedback), anterior pituitary (short feedback), and hypothalamus (long feedback). TRH, Thyroid releasing hormone; TSH, thyroid stimulating hormone; T3, triiodothyronine; T4, tetraiodothyronine.
  1502. Table 17-2 Binding Proteins, Their Hormones, and Variables That Affect Their Circulating Levels
  1503. Mechanisms of Hormone Action
  1504. Figure 17-3 Regulation of Target Cell Sensitivity.A, Low hormone level and up-regulation, or an increase in number of receptors. B, High hormone level and down-regulation, or a decrease in number of receptors. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1505. Hormone receptors
  1506. First and second messengers
  1507. Figure 17-4 Hormone Binding at Target Cell.
  1508. Table 17-3 Types of Hormones, Their Receptors, and Their Mechanisms of Action
  1509. Steroid (lipid-soluble) hormone receptors
  1510. Figure 17-5 Example of First- and Second-Messenger Mechanisms. A nonsteroid hormone (first messenger) binds to a fixed receptor in the plasma membrane of the target cell (1). The hormone-receptor complex activates the G protein (2). The activated G protein (G) reacts with guanosine triphosphate (GTP), which in turn activates the membrane-bound enzyme adenylyl cyclase (3). Adenylyl cyclase catalyzes the conversion of adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP) (second messenger) (4). cAMP activates protein kinase A (5). Protein kinases activate specific intracellular enzymes (6). These activated enzymes then influence specific cellular reactions, thus producing the target cell’s response to the hormone (7). From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1511. Quick Check 17-1
  1512. Structure and Function of the Endocrine Glands
  1513. Hypothalamic-Pituitary System
  1514. Figure 17-6 Lipid-Soluble Hormone Signaling Process. Free hormones either (1) attach to a receptor on the plasma membrane, and or readily diffuse across the cell membrane and (2) attach to a receptor in the cytosol, or (3) attach to a receptor molecule in the nucleus. DNA, Deoxyribonucleic acid.
  1515. Table 17-4 Hypothalamic Hormones
  1516. The anterior pituitary
  1517. Figure 17-7 Location and Structure of the Pituitary Gland (Hypophysis). The pituitary gland is located within the sella turcica of the skull’s sphenoid bone and is connected to the hypothalamus by a stalklike infundibulum. The pituitary stalk passes through a gap in the portion of the dura mater that covers the pituitary (the pituitary diaphragm). The inset shows that the pituitary is divided into an anterior portion, the adenohypophysis, and a posterior portion, the neurohypophysis. The adenohypophysis is further subdivided into the pars anterior and pars intermedia. The pars intermedia is almost absent in the adult pituitary. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1518. The posterior pituitary
  1519. Antidiuretic hormone
  1520. Figure 17-8 Hypophysial Portal System. Neurons in the hypothalamus secrete releasing hormones into veins that carry the releasing hormones directly to the vessels of the adenohypophysis, thus bypassing the normal circulatory route. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1521. Oxytocin
  1522. Quick Check 17-2
  1523. Thyroid and Parathyroid Glands
  1524. Thyroid gland
  1525. Synthesis of thyroid hormone
  1526. Figure 17-9 Anterior Pituitary Hormones and Their Target Hormones.LH, Luteinizing hormone; ICSH, interstitial cell–stimulating hormone (male); FSH, follicle-stimulating hormone (female). Modified from Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1527. Regulation of thyroid hormone secretion
  1528. Table 17-5 Hormones of the Anterior Pituitary and Their Functions
  1529. Parathyroid glands
  1530. Health Alert Recombinant PTH (rPTH)
  1531. Figure 17-10 Relationship of the Hypothalamus and Neurohypophysis. Neurosecretory cells have their cell bodies in the hypothalamus and their axon terminals in the neurohypophysis. Thus, hormones synthesized in the hypothalamus are actually released from the neurohypophysis. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1532. Quick Check 17-3
  1533. Endocrine Pancreas
  1534. Figure 17-11 Thyroid and Parathyroid Glands. Note their location in relation to each other and to the larynx and trachea. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1535. Figure 17-12 Thyroid Follicle Cells.
  1536. Insulin
  1537. Table 17-6 Thyroid Gland Hormones and Their Regulation and Functions
  1538. Amylin
  1539. Glucagon
  1540. Somatostatin
  1541. Figure 17-13 The Pancreas.A, Pancreas dissected to show main and accessory ducts. The main duct may join the common bile duct, as shown here, to enter the duodenum by a single opening at the major duodenal papilla, or the two ducts may have separate openings. The accessory pancreatic duct is usually present and has a separate opening into the duodenum. B, Exocrine glandular cells (around small pancreatic ducts) and endocrine glandular cells of the pancreatic islets (adjacent to blood capillaries). Exocrine pancreatic cells secrete pancreatic juice, alpha endocrine cells secrete glucagon, and beta cells secrete insulin. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1542. Gastrin and pancreatic polypeptide
  1543. Adrenal Glands
  1544. Figure 17-14 Insulin Action on Cells. Binding of insulin to its receptor causes autophosphorylation of the receptor, which then itself acts as a tyrosine kinase that phosphorylates insulin receptor substrate 1 (IRS-1). Numerous target enzymes, such as protein kinase B and MAP kinase, are activated, and these enzymes have a multitude of effects on cell function. The glucose transporter, GLUT4, is recruited to the plasma membrane, where it facilitates glucose entry into the cell. The transport of amino acids, potassium, magnesium, and phosphate into the cell is also facilitated. The synthesis of various enzymes is induced or suppressed, and signal molecules that modulate gene expression regulate cell growth. mRNA, Messenger ribonucleic acid; IREs, insulin responsive elements. From Berne RM, Levy MN: Principles of physiology, ed 3, St Louis, 2000, Mosby.
  1545. Table 17-7 Insulin Actions
  1546. Figure 17-15 Structure of the Adrenal Gland Showing Cell Layers (Zonae) of the Cortex. Zona glomerulosa secretes aldosterone. Zona fasciculata secretes abundant amounts of glucocorticoids, chiefly cortisol. Zona reticularis secretes minute amounts of sex hormones and glucocorticoids. A portion of the medulla is visible at the lower right in the photomicrograph (×35) and at the bottom of the drawing. A from Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby; B from Kierszenbaum A: Histology and cell biology, St Louis, 2002, Elsevier.
  1547. Adrenal cortex
  1548. Glucocorticoids
  1549. Functions of the glucocorticoids
  1550. Box 17-1 Major Functions of Glucocorticoids
  1551. Metabolic
  1552. Inflammatory and Immune
  1553. Other
  1554. Cortisol
  1555. Figure 17-16 Feedback Control of Glucocorticoid Synthesis and Secretion.
  1556. Mineralocorticoids: aldosterone
  1557. Figure 17-17 The Feedback Mechanisms Regulating Aldosterone Secretion. cAMP, Cyclic adenosine monophosphate; ACTH, adrenocorticotropic hormone.
  1558. Adrenal estrogens and androgens
  1559. Adrenal medulla
  1560. Figure 17-18 Synthesis of Catecholamines.
  1561. Box 17-2 Methods of Hormone Measurement
  1562. Radioimmunoassay (RIA)
  1563. Enzyme-Linked Immunosorbent Assay (Elisa)
  1564. Bioassay
  1565. Quick Check 17-4
  1566. Neuroendocrine Response to Stressors
  1567. Aging & Its Effects on Specific Endocrine Glands
  1568. General Endocrine Changes With Aging
  1569. Pancreas
  1570. Thyroid
  1571. Adrenal
  1572. Gonads
  1573. Pituitary
  1574. Did You Understand?
  1575. Mechanisms of Hormonal Regulation
  1576. Structure and Function of the Endocrine Glands
  1577. AGING & Its Effects on Specific Endocrine Glands
  1578. Key Terms
  1579. References
  1580. Chapter 18 Alterations of Hormonal Regulation
  1581. Website http://evolve.elsevier.com/Huether/
  1582. Mechanisms of Hormonal Alterations
  1583. Figure 18-1 Hormone Delivery to Cells. Phases at which pathogenic mechanisms may develop in delivering appropriate amounts of hormone to the cells.
  1584. Alterations of the Hypothalamic-Pituitary System
  1585. Diseases of the Posterior Pituitary
  1586. Syndrome of inappropriate antidiuretic hormone secretion
  1587. Figure 18-2 Loss of Hypothalamic Hormones.GnRH, Gonadotropin-releasing hormone; TRH, thyrotropin-releasing hormone; CRH, corticotropin-releasing hormone; PIF, prolactin inhibitory factor (probably dopamine); GHRH, growth hormone releasing hormone; FSH, follicle-stimulating hormone; LH, luteinizing hormone; TSH, thyroid-stimulating hormone; ACTH, adrenocorticotropic hormone.
  1588. Pathophysiology
  1589. Clinical Manifestations
  1590. Evaluation and Treatment
  1591. Diabetes insipidus
  1592. Pathophysiology
  1593. Clinical Manifestations
  1594. Evaluation and Treatment
  1595. Diseases of the Anterior Pituitary
  1596. Hypopituitarism
  1597. Pathophysiology
  1598. Clinical Manifestations
  1599. Figure 18-3 Hypopituitary Dwarfism. A 4-year-old boy whose height is 25 inches. Girl is also 4 years old and has a normal height of 39 inches. Boy (dwarf) has a normal face, as well as head, trunk, and limbs of approximately normal proportions. From Brashear HR, Raney RB: Handbook of orthopaedic surgery, ed 10, St Louis, 1986, Mosby.
  1600. Evaluation and Treatment
  1601. Hyperpituitarism: primary adenoma
  1602. Pathophysiology
  1603. Clinical Manifestations
  1604. Evaluation and Treatment
  1605. Quick Check 18-1
  1606. Hypersecretion of growth hormone: acromegaly
  1607. Pathophysiology
  1608. Figure 18-4 Giantism. A pituitary giant and dwarf contrasted with normal-size men. Excessive secretion of growth hormone by the anterior lobe of the pituitary gland during the early years of life produces giants of this type, whereas deficient secretion of this substance produces well-formed dwarfs. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1609. Clinical Manifestations
  1610. Figure 18-5 Acromegaly. Chronologic sequence of photographs showing slow development of acromegaly. From Belchetz P, Hammond P: Mosby’s color atlas and text of diabetes and endocrinology, Edinburgh, 2003, Mosby.
  1611. Evaluation and Treatment
  1612. Prolactinoma
  1613. Pathophysiology
  1614. Clinical Manifestations
  1615. Evaluation and Treatment
  1616. Alterations of Thyroid Function
  1617. Hyperthyroidism
  1618. Thyrotoxicosis
  1619. Clinical Manifestations
  1620. Figure 18-6 Evaluation of Hyperthyroidism. Radioactive iodine is used in the differential diagnosis of hyperthyroidism.
  1621. Evaluation and Treatment
  1622. Hyperthyroid conditions
  1623. Graves disease
  1624. Table 18-1 Systemic Effects of Hyperthyroidism
  1625. Figure 18-7 Graves Disease. Note large and protruding eyeballs. From Belchetz P, Hammond P: Mosby’s color atlas and text of diabetes and endocrinology, Edinburgh, 2003, Mosby.
  1626. Hyperthyroidism resulting from nodular thyroid disease
  1627. Thyrotoxic crisis
  1628. Hypothyroidism
  1629. Health Alert Subclinical Hypothyroidism
  1630. Pathophysiology
  1631. Clinical Manifestations
  1632. Table 18-2 Systemic Manifestations of Hypothyroidism
  1633. Figure 18-8 Myxedema. Note edema around eyes and facial puffiness. From Thibodeau GA, Patton KT: Anatomy & physiology, St Louis, 1987, Mosby.
  1634. Evaluation and Treatment
  1635. Hypothyroid conditions
  1636. Primary hypothyroidism
  1637. Myxedema coma
  1638. Congenital hypothyroidism
  1639. Thyroid Carcinoma
  1640. Figure 18-9 An Adult Cretin. Note the characteristic facial features, dwarfism (44 inches), absent axillary and scant pubic hair, poorly developed breasts, potbelly, and small umbilical hernia. From Schneeberg NG: Essentials of clinical endocrinology, St Louis, 1970, Mosby.
  1641. Quick Check 18-2
  1642. Alterations of Parathyroid Function
  1643. Hyperparathyroidism
  1644. Pathophysiology
  1645. Clinical Manifestations
  1646. Evaluation and Treatment
  1647. Hypoparathyroidism
  1648. Pathophysiology
  1649. Clinical Manifestations
  1650. Evaluation and Treatment
  1651. Quick Check 18-3
  1652. Dysfunction of the Endocrine Pancreas: Diabetes Mellitus
  1653. Table 18-3 Classification and Characteristics of Diabetes Mellitus
  1654. Box 18-1 Diagnostic Criteria for Diabetes Mellitus
  1655. Types of Diabetes Mellitus
  1656. Type 1 diabetes mellitus
  1657. Pathophysiology
  1658. Hyperglycemia and other symptoms
  1659. Clinical Manifestations
  1660. Evaluation and Treatment
  1661. Type 2 diabetes mellitus
  1662. Table 18-4 Epidemiology and Etiology of Diabetes Mellitus
  1663. Box 18-2 Specific Environmental Factors Linked to Type 1 Diabetes
  1664. Drugs and Chemicals
  1665. Nutritional Intake
  1666. Viruses
  1667. Table 18-5 Clinical Manifestations and Mechanisms for Type 1 Diabetes Mellitus
  1668. Health Alert The Metabolic Syndrome/Insulin Resistance Syndrome/Syndrome X
  1669. Pathophysiology
  1670. Clinical Manifestations
  1671. Table 18-6 Clinical Manifestations and Mechanisms for Type 2 Diabetes Mellitus
  1672. Evaluation and Treatment
  1673. Gestational diabetes
  1674. Acute Complications of Diabetes Mellitus
  1675. Chronic Complications of Diabetes Mellitus
  1676. Hyperglycemia and nonenzymatic glycosylation
  1677. Figure 18-10 Diabetic Ketoacidosis. Contributing causes of metabolic acidosis that result from ketosis and consequences of hyperglycemia.
  1678. Hyperglycemia and the polyol pathway
  1679. Table 18-7 Common Acute Complications of Diabetes Mellitus
  1680. Protein kinase C
  1681. Diabetic neuropathies
  1682. Microvascular disease
  1683. Visual changes
  1684. Diabetic nephropathy
  1685. Macrovascular disease
  1686. Figure 18-11 Diabetes Mellitus and Atherosclerosis. Diabetes with its associated hyperglycemia, relative hypoinsulinemia, oxidative stress, and proinflammatory state contributes to atherogenesis by causing arterial endothelial dysfunction (impaired vasodilation and adhesion of inflammatory cells), dyslipidemia, and smooth muscle proliferation.LDL, Low-density liprotein. Data from Charo IF, Ransohoff RM: The many roles of chemokines and chemokine receptors in inflammation, N Engl J Med 354[6]:610–621, 2006; Heinecke JW: Lipoprotein oxidation in cardiovascular disease: chief culprit or innocent bystander? J Exp Med 203[4]:813–816, 2006; Kaperonis EA et al: Inflammation and atherosclerosis, Eur J Vasc Endovasc Surg 31[4]:386–393, 2006; Tedgui A, Mallat Z: Cytokines in atherosclerosis: pathogenic and regulatory pathways, Physiol Rev 86(2):515–581, 2006.
  1687. Coronary artery disease
  1688. Stroke
  1689. Peripheral vascular disease
  1690. Infection
  1691. Quick Check 18–4
  1692. Alterations of Adrenal Function
  1693. Disorders of the Adrenal Cortex
  1694. Hypercortical function (Cushing syndrome, Cushing disease)
  1695. Pathophysiology
  1696. Clinical Manifestations
  1697. Figure 18-12 Symptoms of Cushing Disease.
  1698. Figure 18-13 Cushing Syndrome.A, Patient before onset of Cushing syndrome. B, Patient four months later. Moon facies is clearly demonstrated. From Zitelli BJ, Davis HW: Atlas of pediatric physical diagnosis, ed 3, London, 1997, Gower.
  1699. Evaluation and Treatment
  1700. Congenital adrenal hyperplasia
  1701. Hyperaldosteronism
  1702. Pathophysiology
  1703. Clinical Manifestations
  1704. Evaluation and Treatment
  1705. Hypersecretion of adrenal androgens and estrogens
  1706. Hypocortical functioning
  1707. Figure 18-14 Virilization. Virilization of a young girl by an androgen-secreting tumor of the adrenal cortex. Masculine features include lack of breast development, increased muscle bulk, and hirsutism (excessive hair). From Thibodeau GA, Patton KT: Anatomy & physiology, St Louis, 1987, Mosby.
  1708. Pathophysiology
  1709. Idiopathic Addison disease
  1710. Secondary hypocortisolism
  1711. Clinical Manifestations
  1712. Evaluation and Treatment
  1713. Table 18-8 Clinical Manifestations and Pathophysiologic Mechanisms of Addison Disease
  1714. Disorders of the Adrenal Medulla
  1715. Tumor of the adrenal medulla
  1716. Pathophysiology
  1717. Clinical Manifestations
  1718. Evaluation and Treatment
  1719. Quick Check 18-5
  1720. Did You Understand?
  1721. Mechanisms of Hormonal Alterations
  1722. Alterations of the Hypothalamic-Pituitary System
  1723. Alterations of Thyroid Function
  1724. Alterations of Parathyroid Function
  1725. Dysfunction of the Endocrine Pancreas: Diabetes Mellitus
  1726. Alterations of Adrenal Function
  1727. Key Terms
  1728. References
  1729. Unit 6 The Hematologic System
  1730. Chapter 19 Structure and Function of the Hematologic System
  1731. Electronic Resources
  1732. Companion CD
  1733. Website
  1734. Components of the Hematologic System
  1735. Composition of Blood
  1736. Plasma and plasma proteins
  1737. Figure 19-1 Composition of Whole Blood. Approximate values for the components of blood in a normal adult. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1738. Cellular components of the blood
  1739. Table 19-1 Organic and Inorganic Components of Arterial Plasma
  1740. Erythrocytes
  1741. Table 19-2 Cellular Components of the Blood
  1742. Leukocytes
  1743. Granulocytes
  1744. Figure 19-2 Blood Cells. Leukocytes are spherical and have irregular surfaces with numerous extending pili. Leukocytes are the cotton candy–like cells in yellow. Erythrocytes are flattened spheres with a depressed center. Copyright by Dennis Kunkel Microscopy, Inc.
  1745. Figure 19-3 Leukocytes. An example of leukocytes in human blood smear. A, Neutrophil. B, Eosinophil. C, Basophil with obscured nucleus. D, Typical monocyte showing vacuolated cytoplasm and cerebriform nucleus. E, Lymphocyte. A, C, D, and E from Rodak, BF: Hematology: clinical principles and applications, ed 2, Philadelphia, 2002, Saunders; B from Carr JC, Rodak BF: Clinical hematology atlas, Philadelphia, 1999, Saunders.
  1746. Agranulocytes
  1747. Platelets
  1748. Quick Check 19-1
  1749. Lymphoid Organs
  1750. Figure 19-4 Scanning Electron Micrograph of Moderately Active Platelet. From Bick RL: Hematology: clinical and laboratory practice, St Louis, 1993, Mosby.
  1751. Spleen
  1752. Figure 19-5 Red Cells in the Spleen. Scanning electron micrograph of spleen, demonstrating erythrocytes (numbered 1–6) squeezing through the fenestrated wall in transit from the splenic cord to the sinus. The view shows the endothelial lining of the sinus wall, to which platelets (P) adhere, along with “hairy” white cells, probably macrophages. The arrow shows a protrusion on a red blood cell (×5000). From Weiss L: A scanning electron microscope study of the spleen, Blood 1974;43;665; reprinted with permission.
  1753. Lymph nodes
  1754. Figure 19-6 Cross Section of Lymph Node. Several afferent valved lymphatics bring lymph to node. A single efferent lymphatic leaves the node at the hilus. Note that the artery and vein also enter and leave at the hilus. Arrows show direction of lymph flow. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  1755. The Mononuclear Phagocyte System
  1756. Table 19-3 Mononuclear Phagocyte System (Formerly Called the Reticuloendothelial System)
  1757. Quick Check 19-2
  1758. Development of Blood Cells
  1759. Hematopoiesis
  1760. Bone marrow
  1761. Cellular differentiation
  1762. Figure 19-7 Differentiation of Hematopoietic Cells.SCF, Stem cell factor; FTL-3L, fms-like tyrosine kinase 3 ligand; GM-CSF, granulocyte-macrophage colony-stimulating factor; M-CSF, macrophage colony-stimulating factor; G-CSF, granulocyte colony-stimulating factor; CFU, colony-forming unit; Eo, eosinophil; G, granulocyte; M, macrophage; BFU, burst-forming unit; IL, interleukin; E, erythrocyte; Mega, megakaryocyte; Baso, basophil. (Mast cells are discussed in Chapter 5.)
  1763. Figure 19-8 Hematopoiesis. Hematopoiesis from the stem cell pool; activity mainly in the bone marrow and in the peripheral blood.
  1764. Figure 19-9 Erythrocyte Differentiation. Erythrocyte differentiation from large, nucleated stem cell to small, nonnucleated erythrocyte.
  1765. Quick Check 19-3
  1766. Development of Erythrocytes
  1767. Erythropoiesis
  1768. Figure 19-10 Role of Erythropoietin in Regulation of Erythropoiesis. Decreased arterial oxygen levels stimulate production of erythropoietin, which in turn stimulates red cell production and expansion of the erythron. The increase in red cells frequently corrects the problem of low oxygen levels (hypoxia). This restoration to normal oxygen levels alerts the kidney to stop producing erythropoietin (negative feedback). Further erythrocyte production is not needed. RBCs, Red blood cells; PO2, partial pressure of oxygen in the blood.
  1769. Hemoglobin synthesis
  1770. Figure 19-11 Molecular Structure of Hemoglobin. Molecule is spherical tetramer weighing approximately 64,500 daltons. It contains a pair of α-polypeptide chains and a pair of β-polypeptide chains and several heme groups.
  1771. Nutritional requirements for erythropoiesis
  1772. Figure 19-12 Hemoglobin (Hb) Binding to Nitric Oxide. In the lungs, hemoglobin (Hb) binds to nitric oxide (NO) as S-nitrosothiol (SNO). In tissue, this SNO is released, and free, circulating NO is bound to a different site for exhalation. Fe, Iron; N, nitrogen.
  1773. Table 19-4 Nutritional Requirements for Erythropoiesis
  1774. Iron cycle
  1775. Normal destruction of senescent erythrocytes
  1776. Figure 19-13 Iron Cycle. Iron (Fe) released from gastrointestinal epithelial cells circulates in the bloodstream associated with its plasma carrier, transferrin. It is delivered to erythroblasts in bone marrow, where most of it is incorporated into hemoglobin. Mature erythrocytes circulate for approximately 120 days, after which they become senescent and are removed by mononuclear phagocyte system (MPS). Macrophages of MPS (mostly in spleen) break down ingested erythrocytes and return iron to the bloodstream directly or after storing it as ferritin or hemosiderin.
  1777. Quick Check 19-4
  1778. Development of Leukocytes
  1779. Figure 19-14 Metabolism of Bilirubin Released by Heme Breakdown.MPS, Mononuclear phagocyte system.
  1780. Development of Platelets
  1781. Mechanisms of Hemostasis
  1782. Figure 19-15 Three Hemostatic Compartments.
  1783. Function of Platelets and Blood Vessels
  1784. Table 19-5 Types of Bleeding: Sources, Vessel Size, and Sealing Requirements
  1785. Figure 19-16 Platelet Degranulation.A, Plug formation and clot dissolution. B, After simple endothelial denudation, platelets adhere to the subendothelium in a monolayer fashion. C, Platelet-fibrin thrombus formation. D, Higher magnification of the thrombus shows a mixture of red cells and platelets incorporated into the fibrin meshwork. B to D from Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  1786. Function of Clotting Factors
  1787. Figure 19-17 Blood Clotting Mechanism.A, The clotting mechanism involves release of platelet factors at the injury site, formation of thrombin, and trapping of red blood cells (RBCs) in fibrin to form a clot. B, An electron micrograph showing entrapped RBCs in a fibrin clot. A from Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby; B copyright by Dennis Kunkel Microscopy, Inc.
  1788. Health Alert Sticky Platelets, Genetic Variations, and Cardiovascular Complications
  1789. Health Alert Changes in the Management of Abnormalities in the Hemostatic System
  1790. Retraction and Lysis of Blood Clots
  1791. Figure 19-18 The Fibrinolytic System. The central reaction is the conversion of plasminogen to the enzyme plasmin. Activity of plasminogen is achieved by the extrinsic pathway (blue) initiated by the release of tissue-type plasminogen activator t-PAI (also called T-PA) released from the endothelial cells and by the intrinsic pathway (gold) from factor XIIa and urokinase. Plasmin splits fibrin in the clot into fibrin degradation products.
  1792. Table 19-6 Common Blood Tests for Hematologic Disorders
  1793. Quick Check 19-5
  1794. Pediatrics & Hematologic Value Changes
  1795. Aging & Hematologic Value Changes
  1796. Table 19-7 Hematologic Values from Birth to Adulthood
  1797. Did You Understand?
  1798. Components of the Hematologic System
  1799. Development of Blood Cells
  1800. Mechanisms of Hemostasis
  1801. PEDIATRICS & Hematologic Value Changes
  1802. AGING & Hematologic Value Changes
  1803. Key Terms
  1804. References
  1805. Chapter 20 Alterations of Hematologic Function
  1806. Electronic Resources
  1807. Companion CD
  1808. Website http://evolve.elsevier.com/Huether/
  1809. Alterations of Erythrocyte Function
  1810. Classification of Anemias
  1811. Clinical Manifestations
  1812. Table 20-1 Morphologic Classification of Anemias
  1813. Figure 20-1 Progression and Manifestations of Anemia.SV, Stroke volume; DPG, 2,3-diphosphoglycerate.
  1814. Macrocytic-Normochromic Anemias
  1815. Table 20-2 Laboratory Tests for Various Anemias
  1816. Pernicious anemia
  1817. Pathophysiology
  1818. Clinical Manifestations
  1819. Evaluation and Treatment
  1820. Folate deficiency anemias
  1821. Figure 20-2 Appearance of Red Blood Cells in Various Disorders.A, Normal blood smear. B, Hypochromic-microcytic anemia (iron deficiency). C, Macrocytic anemia (pernicious anemia). D, Macrocytic anemia in pregnancy. E, Hereditary elliptocytosis. F, Myelofibrosis (teardrop). G, Hemolytic anemia associated with prosthetic heart valve. H, Microangiopathic anemia. I, Stomatocytes. J, Spherocytes (hereditary spherocytosis). K, Sideroblastic anemia; note the double population of red blood cells. L, Sickle cell anemia. M, Target cells (after splenectomy). N, Basophil stippling in case of unexplained anemia. O, Howell-Jolly bodies (after splenectomy). From Wintrobe MM et al: Clinical hematology, ed 8, Philadelphia, 1981, Lea & Febiger.
  1822. Microcytic-Hypochromic Anemias
  1823. Iron deficiency anemia
  1824. Pathophysiology
  1825. Clinical Manifestations
  1826. Figure 20-3 Pallor and Iron Deficiency. Pallor of the skin, mucous membranes, and palmar creases in an individual with hemoglobin of 9g/dl. Palmar creases become as pale as the surrounding skin when the hemoglobin level approaches 7g/dl. From Hoffbrand AV, Pettit JE: Sandoz atlas of clinical hematology, London, 1988, Gower Medical.
  1827. Figure 20-4 Koilonychia. The nails are concave, ridged, and brittle. From Hoffbrand AV, Pettit JE: Sandoz atlas of clinical hematology, London, 1988, Gower Medical.
  1828. Figure 20-5 Glossitis. Tongue of individual with iron deficiency anemia has bald, fissured appearance caused by loss of papillae and flattening. From Hoffbrand AV, Pettit JE: Sandoz atlas of clinical hematology, London, 1988, Gower Medical.
  1829. Evaluation and Treatment
  1830. Sideroblastic anemia
  1831. Pathophysiology
  1832. Clinical Manifestations
  1833. Evaluation and Treatment
  1834. Normocytic-Normochromic Anemias
  1835. Quick Check 20-1
  1836. Myeloproliferative Red Cell Disorders
  1837. Polycythemia Vera
  1838. Pathophysiology
  1839. Table 20-3 Normocytic-Normochromic Anemias
  1840. Clinical Manifestations
  1841. Table 20-4 Disorders Classified as Polycythemia
  1842. Evaluation and Treatment
  1843. Alterations of Leukocyte Function
  1844. Quantitative Alterations of Leukocytes
  1845. Granulocyte and monocyte alterations
  1846. Table 20-5 Other Conditions Associated With Neutrophils, Eosinophils, Basophils, Monocytes, and Lymphocytes
  1847. Lymphocyte alterations
  1848. Infectious mononucleosis
  1849. Clinical Manifestations
  1850. Evaluation and Treatment
  1851. Quick Check 20-2
  1852. Qualitative Alterations of Leukocytes
  1853. Leukemias
  1854. Figure 20-6 Cell-Specific Leukemias. Differentiation pathways of blood-forming cells and reported sites of blockage resulting in cell-specific leukemias. Ig, Immunoglobulin.
  1855. Pathophysiology
  1856. Table 20-6 Estimated New Cases and Deaths from Leukemia in the United States—2007
  1857. Figure 20-7 Philadelphia Chromosome. Schema of the Philadelphia (Ph) translocation (+) seen in chronic myelocytic leukemia. The Ph1 chromosome results from an exchange of materials between chromosomes 9 and 22—that is, t(9;22)(q34;q11). Because chromosome 22 gives up much more of its long arm than that translocated to it from chromosome 9, chromosome 22 becomes much abbreviated and is known as Ph1. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  1858. Acute leukemias
  1859. Clinical Manifestations
  1860. Table 20-7 Clinical Manifestations and Related Pathophysiology in Leukemia
  1861. Evaluation And Treatment
  1862. Table 20-8 Some Examples of Human CSFs
  1863. Morphologic Effects of Growth Factor. Marrow aspirate from a patient receiving granulocyte colony-stimulating factor (G-CSF) showing an early neutrophil response. There is a marked shift toward immaturity in the neutrophils with the majority at the promyelocyte and early myelocyte stages of maturation. (Wright-Giemsa stain.) Courtesy Laura Schmitz, MD, Hennepin County Medical Center, Minn. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  1864. Chronic leukemias
  1865. Pathophysiology and Clinical Manifestations
  1866. Evaluation and Treatment
  1867. Quick Check 20-3
  1868. Alterations of Lymphoid Function
  1869. Lymphadenopathy
  1870. Figure 20-8 Lymphadenopathy. Individual with lymphocyte leukemia with extreme but symmetric lymphadenopathy. Courtesy Dr. AR Kagan, Los Angeles. From del Regato JA, Spjut HJ, Cox JD: Cancer: diagnosis, treatment, and prognosis, ed 6, St Louis, 1985, Mosby.
  1871. Malignant Lymphomas
  1872. Hodgkin lymphoma
  1873. Pathophysiology
  1874. Figure 20-9 Lymph Nodes.A, Lymphocytes and histiocytes of Hodgkin lymphoma, nodular type. Large nodules with small, round lymphocytes, histiocytes, and scattered lymphocyte and histiocyte cells. B, Diagnostic Reed-Sternberg cell. A large multinucleated or multilobed cell with inclusion body-like nucleoli surrounded by a halo of clear nucleoplasm. From Damjanov I, Linder J, editors, Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  1875. Clinical Manifestations
  1876. Table 20-9 Subtypes of Classical Hodgkin Lymphoma
  1877. Figure 20-10 Hodgkin Lymphoma and Enlarged Cervical Lymph Node. Typical enlarged cervical lymph node in the neck of a 35-year-old woman with Hodgkin lymphoma. From del Regato JA, Spjut HJ, Cox JD: Cancer: diagnosis, treatment, and prognosis, ed 6, St Louis, 1985, Mosby.
  1878. Figure 20-11 Common and Uncommon Involved Lymph Node Sites for Hodgkin Lymphoma.
  1879. Table 20-10 Modified Cotswold Staging Classification System
  1880. Evaluation and Treatment
  1881. Non-Hodgkin lymphomas
  1882. Pathophysiology
  1883. Clinical Manifestations
  1884. Table 20-11 Clinical Differences Between Non-Hodgkin Lymphoma and Hodgkin Lymphoma
  1885. Evaluation and Treatment
  1886. Burkitt lymphoma
  1887. Pathophysiology
  1888. Clinical Manifestations
  1889. Figure 20-12 Burkitt Lymphoma. Burkitt lymphoma involving the jaw in young African boy. Courtesy Dr. JNP Davies, Albany, NY. From del Regato JA, Spjut HJ, Cox JD: Cancer: diagnosis, treatment, and prognosis, ed 6, St Louis, 1985, Mosby.
  1890. Evaluation and Treatment
  1891. Multiple myeloma
  1892. Pathophysiology
  1893. Figure 20-13 Multiple Myeloma, Bone Marrow Aspirate. Normal marrow cells are largely replaced by plasma cells, including atypical forms with multiple nuclei, and cytoplasmic droplets containing immunoglobulin. From Kumar V, Abbas AK, Fausto N: Robbins and Cotran pathologic basis of disease, ed 7, Philadelphia, 2005, Saunders.
  1894. Clinical Manifestations
  1895. Figure 20-14 Multiple (Plasma Cell) Myeloma.A, Roentgenogram of femur showing extensive bone destruction caused by tumor. Note absence of reactive bone formation. B, Gross specimen from same individual; myelomatous sections appear as dark granular sections. From Kissane JM, editor: Anderson’s pathology, ed 9, St Louis, 1990, Mosby.
  1896. Evaluation and Treatment
  1897. Figure 20-15 M Protein Detection. Serum protein (SP) electrophoresis is used to screen for M proteins (M) in multiple myeloma. In normal serum the proteins separate into several regions between albumin (Alb) and a broad band in the gamma (γ) region, where most antibodies (γ-globulins) are found. Serum from an individual with multiple myeloma contains a sharp M protein (M) band. Using specific antibodies the location of specific types of heavy (G, A, M) and light (κ, λ) chains can be determined. In this example, normal serum contains a broad band with polyclonal IgG molecules that contain κ and λ light chains. The M protein is monoclonal and contains only one heavy chain and one light chain. The M protein in this example is an IgG that contains κ light chain. Courtesy Dr. David Sacks, Department of Pathology, Brigham and Women’s Hospital, Boston, MA. Modified from Kumar V, Abbas A, Fausto N: Robbins and Cotran pathologic basis of disease, ed 7, Philadelphia, 2005, Saunders.
  1898. Quick Check 20-4
  1899. Lymphoblastic lymphoma
  1900. Pathophysiology
  1901. Clinical Manifestations
  1902. Evaluation and Treatment
  1903. Alterations of Splenic Function
  1904. Pathophysiology
  1905. Clinical Manifestations
  1906. Box 20-1 Diseases Related to Classification of Splenomegaly
  1907. Inflammation or Infection
  1908. Congestive
  1909. Infiltrative
  1910. Tumors or Cysts
  1911. Evaluation and Treatment
  1912. Quick Check 20-5
  1913. Alterations of Platelets and Coagulation
  1914. Disorders of Platelet Function
  1915. Thrombocytopenia
  1916. Pathophysiology
  1917. Heparin-induced thrombocytopenia
  1918. Clinical Manifestations
  1919. Evaluation and Treatment
  1920. Idiopathic (immune) thrombocytopenia purpura
  1921. Clinical Manifestations
  1922. Evaluation and Treatment
  1923. Thrombotic thrombocytopenia purpura
  1924. Clinical Manifestations
  1925. Evaluation and Treatment
  1926. Thrombocythemia
  1927. Pathophysiology
  1928. Clinical Manifestations
  1929. Evaluation and Treatment
  1930. Alterations of Platelet Function
  1931. Health Alert Dark Chocolate, Wine, and Platelet-Inhibitory Functions
  1932. Disorders of Coagulation
  1933. Impaired hemostasis
  1934. Vitamin K deficiency
  1935. Liver disease
  1936. Consumptive thrombohemorrhagic disorders
  1937. Disseminated intravascular coagulation
  1938. Pathophysiology
  1939. Figure 20-16 Pathophysiology of Disseminated Intravascular Coagulation (DIC). DIC is initiated by exposure of tissue factor (TF) after vessel damage, on tumor cells, or on the surface of endothelial cells or monocytes after exposure to cytokines, some of which may be produced by cytokines. TF reacts with and activates factor VII to produce a TF-VIIa complex, which can directly activate clotting factors IX and X. Activated factor IX (IXa) can interact with factors VIIIa and X to activate factor X to Xa. Factor Xa complexes with factor Va and prothrombin (PT) to form the prothrombinase complex that produces thrombin, which in turn activates fibrinogen to fibrin. Fibrin polymerizes to form clots. In DIC, natural regulators of the clotting system (tissue factor pathway inhibitor [TFPI], antithrombin-III [AT-III], and protein C [Prot C]) are decreased resulting in increased thrombin formation. Clots are normally broken down by plasmin, which is produced from plasminogen and degrades fibrin into fibrin degradation products (FDPs). In DIC, fibrinolysis is prevented by high levels of plasminogen-activator inhibitor type 1 (PAI-1), which inhibits the production of plasmin. The summation of these changes is greatly increased deposition of fibrin clots in the vessels and thrombosis.
  1940. Box 20-2 Acute Disseminated Intravascular Coagulation (DIC)
  1941. Clinical Manifestations
  1942. Box 20-3 Clinical Manifestations Associated With DIC
  1943. Integumentary System
  1944. Central Nervous System
  1945. Gastrointestinal System
  1946. Pulmonary System
  1947. Renal System
  1948. Evaluation and Treatment
  1949. Thromboembolic disorders
  1950. Figure 20-17 Thrombus arising in valve pocket at upper end of superficial femoral vein. Postmortem clot on the right is shown for comparison. From McLachlin J, Paterson JC: Some basic observations on venous thrombosis and pulmonary embolism, Surg Gynecol Obstet 93(1):1–8, 1951.
  1951. Hereditary hypercoagulability and thrombosis
  1952. Acquired hypercoagulability and thrombosis
  1953. Quick Check 20-6
  1954. Did You Understand?
  1955. Alterations of Erythrocyte Function
  1956. Myeloproliferative Red Cell Disorders
  1957. Alterations of Leukocyte Function
  1958. Alterations of Lymphoid Function
  1959. Alterations of Splenic Function
  1960. Alterations of Platelets and Coagulation
  1961. Key Terms
  1962. References
  1963. Chapter 21 Alterations of Hematologic Function in Children
  1964. Electronic Resources
  1965. Companion CD
  1966. Website http://evolve.elsevier.com/Huether/
  1967. Disorders of Erythrocytes
  1968. Acquired Disorders
  1969. Iron deficiency anemia
  1970. Table 21-1 Anemias of Childhood
  1971. Pathophysiology
  1972. Clinical Manifestations
  1973. Evaluation and Treatment
  1974. Hemolytic disease of the newborn
  1975. Pathophysiology
  1976. Figure 21-1 Hemolytic Disease of the Newborn (HDN).A, Before or during delivery, Rh-positive erythrocytes from the fetus enter the blood of an Rh-negative woman through a tear in the placenta. B, The mother is sensitized to the Rh antigen and produces Rh antibodies. Because this usually happens after delivery, there is no effect on the fetus in the first pregnancy. C, During a subsequent pregnancy with an Rh-positive fetus, Rh-positive erythrocytes cross the placenta, enter the maternal circulation, and stimulate the mother to produce antibodies against the Rh antigen. The Rh antibodies from the mother cross the placenta, using agglutination and hemolysis of fetal erythrocytes, and HDN develops. Modified from Seeley RR, Stephens TD, Tate P: Anatomy and physiology, ed 3, St Louis, 1995, Mosby.
  1977. Clinical Manifestations
  1978. Evaluation and Treatment
  1979. Inherited Disorders
  1980. Sickle cell disease
  1981. Figure 21-2 Sickle Cell Hemoglobin.A, Sickle cell hemoglobin is produced by a recessive allele of the gene encoding the beta chain of the protein hemoglobin. It represents a single amino acid change from glutamic acid to valine at the sixth position of the chain. In the folded beta-chain molecule, the sixth position contacts the alpha chain and the amino acid change causes the hemoglobins to aggregate into long chains, altering the shape of the cell. B, Characteristic shape of sickled red blood cell (or cells). A from Raven PH, Johnson GB: Biology, ed 3, Boston, 1993, Times Mirror Higher Education Group. B from Miale JB: Laboratory medicine: hematology, ed 6, St Louis, 1982, Mosby; courtesy Dr. M. Bessis.
  1982. Table 21-2 Inheritance of Sickle Cell Disease
  1983. Pathophysiology
  1984. Figure 21-3 Sickling of Erythrocytes.
  1985. Clinical Manifestations
  1986. Figure 21-4 Differences between Effects of A, Normal, and B, Sickled RBCs on Blood Circulation and Selected Consequences in a Child. C, Tissue effects of sickle cell anemia.CVA, Cerebrovascular accident; RBC, red blood cell; GI, gastrointestinal. A and B adapted from Hockenberry MJ et al, editors: Wong’s nursing care of infants and children, ed 8, St Louis, 2007, Mosby.
  1987. Evaluation and Treatment
  1988. Health Alert Hydroxyurea Treatment for Severe Sickle Cell Disease
  1989. Thalassemias
  1990. Pathophysiology
  1991. Clinical Manifestations
  1992. Figure 21-5 A Young Girl with Beta-Thalassemia Demonstrating Mild Frontal Bossing (prominent) of the Right Forehead and Mild Maxillary Prominence. From Hockenberry MJ et al, editors: Wong’s nursing care of infants and children, ed 8, St Louis, 2007, Mosby.
  1993. Figure 21-6 A Child with Beta-Thalassemia Major Who Has Severe Splenomegaly. From Jorde LB et al: Medical genetics, ed 3, updated, St Louis, 2006, Mosby.
  1994. Evaluation and Treatment
  1995. Quick Check 21-1
  1996. Disorders of Coagulation and Platelets
  1997. Inherited Hemorrhagic Disease
  1998. Hemophilias
  1999. Pathophysiology
  2000. Table 21-3 Coagulation Factors and Associated Disorders
  2001. Table 21-4 The Hemophilias
  2002. Clinical Manifestations
  2003. Evaluation and Treatment
  2004. Table 21-5 Laboratory Tests of Coagulation
  2005. Antibody-Mediated Hemorrhagic Disease
  2006. Idiopathic thrombocytopenic purpura
  2007. Pathophysiology
  2008. Clinical Manifestations
  2009. Evaluation and Treatment
  2010. Quick Check 21-2
  2011. Neoplastic Disorders
  2012. Leukemia and Lymphoma
  2013. Leukemia
  2014. Table 21-6 Major Classifications of Leukemia
  2015. Pathogenesis
  2016. Clinical Manifestations
  2017. Evaluation and Treatment
  2018. Lymphomas
  2019. Figure 21-7 Monoblasts from Acute Monoblastic Leukemia. Monoblasts in a marrow smear from a patient with acute monoblastic leukemia. The monoblasts are larger than myeloblasts and usually have abundant cytoplasm, often with delicate scattered azurophilic granules (an element that stains well with blue aniline dyes). From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  2020. Health Alert Monoclonal Antibody Therapy to Treat Chronic Myeloid Leukemia
  2021. Non-Hodgkin lymphoma
  2022. Figure 21-8 Lymphomas.A, Large cell lymphoma. The tumor contains prominent areas of sclerosis. B, Burkitt lymphoma. A starry sky pattern is seen at low magnification. From Damjanov I, Linder J: Pathology: a color atlas, St Louis, 2000, Mosby.
  2023. Pathogenesis
  2024. Clinical Manifestations
  2025. Evaluation and Treatment
  2026. Hodgkin lymphoma
  2027. Figure 21-9 Diagnostic Reed-Sternberg Cell. A large multinucleated or multilobated cell with inclusion body-like nucleoli surrounded by a halo of clear nucleoplasm. From Damjanov I, Linder J: Pathology: a color atlas, St Louis, 2000, Mosby.
  2028. Figure 21-10 Main Areas of Lymphadenopathy and Organ Involvement in Hodgkin Lymphoma. From Hockenberry MJ et al, editors: Wong’s nursing care of infants and children, ed 8, St Louis, 2007, Mosby.
  2029. Quick Check 21-3
  2030. Did You Understand?
  2031. Disorders of Erythrocytes
  2032. Disorders of Coagulation and Platelets
  2033. Neoplastic Disorders
  2034. Key Terms
  2035. References
  2036. Unit 7 The Cardiovascular and Lymphatic Systems
  2037. Chapter 22 Structure and Function of the Cardiovascular and Lymphatic Systems
  2038. Electronic Resources
  2039. Companion CD
  2040. Website http://evolve.elsevier.com/Huether/
  2041. The Circulatory System
  2042. The Heart
  2043. Figure 22-1 Diagram Showing Serially Connected Pulmonary and Systemic Circulatory Systems and How to Trace the Flow of Blood. Right heart chambers propel unoxygenated blood through the pulmonary circulation, and the left heart propels oxygenated blood through the systemic circulation. From Thibodeau GA, Patton KT: Anatomy & Physiology, ed 6, St Louis, 2007, Mosby.
  2044. Structures That Direct Circulation Through the Heart
  2045. The heart wall
  2046. Figure 22-2 Wall of the Heart. This section of the heart wall shows the fibrous pericardium, the parietal and visceral layers of the serous pericardium (with the pericardial space between them), the myocardium, and the endocardium. Note the fatty connective tissue between the visceral layer of the serous pericardium (epicardium) and the myocardium. Note also that the endocardium covers beamlike projections of myocardial muscle tissue called trabeculae. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 5, St Louis, 2003, Mosby.
  2047. Chambers of the heart
  2048. Figure 22-3 Structures That Direct Blood Flow Through the Heart. Arrows indicate path of blood flow through chambers, valves, and major vessels.
  2049. Fibrous skeleton of the heart
  2050. Valves of the heart
  2051. Figure 22-4 Structure of the Heart Valves.A, The heart valves in this drawing are depicted as viewed from above (looking down into the heart). Note that the semilunar (SL) valves are closed and the atrioventricular (AV) valves are open, as when the atria are contracting. B is similar to A except that the semilunar valves are open and the atrioventricular valves are closed, as when the ventricles are contracting. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2052. Figure 22-5 Blood Flow Through the Heart During a Single Cardiac Cycle.A, During diastole, blood flows into atria, atrioventricular valves are pushed open, and blood begins to fill ventricles. Atrial systole squeezes any blood remaining in atria out into ventricles. B, During ventricular systole, ventricles contract, pushing blood out through semilunar valves into pulmonary artery (right ventricle) and aorta (left ventricle). Modified from Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2053. The great vessels
  2054. Blood flow during the cardiac cycle
  2055. Normal intracardiac pressures
  2056. Quick Check 22-1
  2057. Figure 22-6 Composite Chart of heart function. This chart is a composite of several diagrams of heart function (cardiac pumping cycle, blood pressure, blood flow, volume, heart sounds, venous pulse, and electrocardiogram [ECG]), all adjusted to the same timescale.
  2058. Figure 22-7 The Phases of the Cardiac Cycle.1, Atrial systole. 2, Isovolumetric ventricular contraction. Ventricular volume remains constant as pressure increases rapidly. 3, Ejection. 4, Isovolumetric ventricular relaxation. Both sets of valves are closed, and the ventricles are relaxing. 5, Passive ventricular filling. The atrioventricular (AV) valves are forced open, and the blood rushes into the relaxing ventricles. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2059. Table 22-1 Normal Intracardiac Pressures
  2060. Structures That Support Cardiac Metabolism: The Coronary Vessels
  2061. Coronary arteries
  2062. Collateral arteries
  2063. Figure 22-8 Coronary Circulation.A, Arteries. B, Veins. Both A and B are anterior views of the heart. Vessels near the anterior surface are more darkly colored than vessels of the posterior surface seen through the heart. C, View of the anterior (sternocostal) surface. A and B modified from Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby; C from Seeley RR, Stephens TD, Tate P: Anatomy and physiology, ed 3, St Louis, 1995, Mosby.
  2064. Box 22-1 Main Branches of the Coronary Arteries
  2065. Coronary capillaries
  2066. Coronary veins and lymphatic vessels
  2067. Structures That Control Heart Action
  2068. The conduction system
  2069. Figure 22-9 Autonomic innervation of cardiovascular system. − = Inhibition; + = activation.
  2070. Figure 22-10 Conduction System of Heart. Specialized cardiac muscle cells in the wall of the heart rapidly conduct an electrical impulse throughout the myocardium. The signal is initiated by the sinoatrial (SA) node (pacemaker) and spreads to the rest of the atrial myocardium and to the atrioventricular (AV) node. The AV node then initiates a signal that is conducted through the ventricular myocardium by way of the atrioventricular bundle (of His) and Purkinje fibers. Modified from Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2071. Quick Check 22-2
  2072. Propagation of cardiac action potentials
  2073. Table 22-2 Intercellular and Extracellular Ion Concentrations in the Myocardium
  2074. The normal electrocardiogram
  2075. Automaticity
  2076. Rhythmicity
  2077. Figure 22-11 Electrocardiogram (ECG) and Cardiac Electrical Activity.A, Normal ECG. Depolarization and repolarization. B, ECG intervals among P, QRS, and T waves. C, Schematic representation of ECG and its relationship to cardiac electrical activity.RA, Right atrium; LA, left atrium; AV, atrioventricular; RV, right ventricle; LV, left ventricle; RBB, right bundle branch; LBB, left bundle branch. A and B from Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2078. Quick Check 22-3
  2079. Cardiac innervation
  2080. Sympathetic and parasympathetic nerves
  2081. Myocardial cells
  2082. Figure 22-12 Sarcomere.A, Electron photomicrograph of sarcomere. B, Schematic of location and interaction of actin and myosin. Modified from Thibodeau GA, Patton KT: Anatomy & physiology, ed 3, St Louis, 1996, Mosby.
  2083. Actin, myosin, and the troponin-tropomyosin complex
  2084. Myocardial metabolism
  2085. Figure 22-13 Structure of Myosin.A, Each myosin molecule is a coil of two chains wrapped around one another. At the end of each chain is a globular region, much like a golf club, called the head. B, Myosin molecules usually are combined into filaments, which are stalks of myosin from which the heads protrude. C, Actin microfilament. From Raven PH, Johnson GB: Understanding biology, ed 3, Dubuque, 1995, Brown.
  2086. Myocardial contraction and relaxation
  2087. Figure 22-14 Myofilaments and Mechanisms of Muscle Contraction.A, Thin and thick myofilaments. In resting muscle, calcium ions are stored in the sarcoplasmic reticulum. When an action potential reaches the muscle cell, the T tubules carry the action potential deep into the sarcoplasm. The action potential causes the sarcoplasmic reticulum to release the store of calcium ions. B, In resting muscle the myosin binding sites are covered by troponin and tropomyosin. The calcium ions released into the sarcoplasm as a result of action potential bind to the troponin. C, This binding causes the tropomyosin and troponin to move out of the way of the myosin binding sites, leaving the myosin heads free to bind to the actin microfilament. ATP, Adenosine triphosphate. From Raven PH, Johnson GB: Understanding biology, ed 3, Dubuque, 1995, Brown.
  2088. Calcium and excitation-contraction coupling
  2089. Figure 22-15 Cross-Bridge Theory of Muscle Contraction.A, Each myosin cross-bridge in the thick filament moves into a resting position after an adenosine triphosphate (ATP) molecule binds and transfers its energy. B, Calcium ions released from the sarcoplasmic reticulum bind to troponin in the thin filament, allowing tropomyosin to shift from its position blocking the active sites of actin molecules. C, Each myosin cross-bridge then binds to an active site on a thin filament, displacing the remnants of ATP hydrolysis—adenosine diphosphate (ADP) and inorganic phosphate (Pi). D, The release of stored energy from step A provides the force needed for each cross-bridge to move back to its original position, pulling actin along with it. Each cross-bridge will remain bound to actin until another ATP molecule binds to it and pulls it back into its resting position, A. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2090. Myocardial relaxation
  2091. Quick Check 22-4
  2092. Factors Affecting Cardiac Performance
  2093. Preload
  2094. Table 22-3 Cardiovascular Function in Elderly Persons
  2095. Figure 22-16 Frank-Starling Law of the Heart. Relationship between length and tension in heart. End-diastolic volume determines end-diastolic length of ventricular muscle fibers and is proportional to tension generated during systole, as well as to cardiac output, stroke volume, and stroke work. A change in myocardial contractility causes the heart to perform on a different length-tension curve. A, Increased contractility, B, Normal contractility. C, Heart failure or decreased contractility. (See text for further explanation.)
  2096. Afterload
  2097. Figure 22-17 Factors Affecting Cardiac Performance. Cardiac output, which is the amount of blood (in liters) ejected by the heart per minute, depends on heart rate (beats per minute) and stroke volume (milliliters of blood ejected during ventricular systole).
  2098. Myocardial contractility
  2099. Heart rate
  2100. Cardiovascular control centers in the brain
  2101. Neural reflexes
  2102. Figure 22-18 Heart Rate and Intravenous Infusions. Intravenous infusions of blood or electrolyte solutions tend to increase heart rate through the Bainbridge reflex and to decrease heart rate through the baroreceptor reflex. The actual change in heart rate induced by such infusions is the result of these two opposing effects. From Berne RM, Levy MN: Cardiovascular physiology, ed 8, St Louis, 2001, Mosby.
  2103. Atrial receptors
  2104. Hormones and biochemicals
  2105. Quick Check 22-5
  2106. The Systemic Circulation
  2107. Structure of Blood Vessels
  2108. Arterial vessels
  2109. Endothelium
  2110. Veins
  2111. Figure 22-19 Circulatory System.A, Principal arteries of body. B, Principal veins of body. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2112. Figure 22-20 Schematic Drawings and Micrograph of Artery and Vein.A, Shown are the comparative thickness of three layers: outer layer (tunica adventitia), muscle layer (tunica media), and lining of endothelium (tunica intima). Note that muscle and outer coats are much thinner in veins than in arteries and that veins have valves. B, Micrograph (× 250) of a cross section of tissue containing both an artery (left) and a vein (right). Note the thickness of the smooth muscle (tunica media) in the artery compared with the vein. C, Micrograph showing both an artery and vein. The tunica media is much thicker in the artery. A modified from Thompson JM et al: Mosby’s clinical nursing, ed 5, St Louis, 2002, Mosby; B from Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby; C, Copyright Ed Reschke.
  2113. Factors Affecting Blood Flow
  2114. Pressure and resistance
  2115. Figure 22-21 Capillary Wall.A, Capillaries have a wall composed of only a single layer of flattened cells, whereas the walls of the larger vessels also have smooth muscle. B, Capillary with red blood cells in single file (× 500). A from Thibodeau GA, Patton KT: Anatomy & physiology, ed 5, St Louis, 2003, Mosby; B, Copyright Ed Reschke.
  2116. Figure 22-22 Capillary Network. Blood enters network as arterial blood and exits as venous blood.
  2117. Figure 22-23 Endothelium. Practically imperceptible, the endothelial cells arrange themselves as a fine lining that has numerous life-support functions (see Table 22-4).
  2118. Table 22-4 Functions of the Endothelium
  2119. Figure 22-24 Valves of Vein. Pooled blood is moved toward heart as valves are forced open by pressure from volume of blood downstream. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 5, St Louis, 2003, Mosby.
  2120. Figure 22-25 Muscle Pump.
  2121. Figure 22-26 Lumen Diameter, Blood Flow, and Resistance.A, Effect of lumen diameter on flow through vessel. d, Diameter. B, Blood flows with great speed in the large arteries. However, branching of arterial vessels increases the total cross-sectional area of the arterioles and capillaries, reducing the flow rate. When capillaries merge into venules and venules merge into veins, the total cross-sectional area decreases, causing the flow rate to increase. B from Thibodeau GA, Patton KT: Anatomy & physiology, ed 5, St Louis, 2003, Mosby.
  2122. Figure 22-27 Schematic Diagram of the Parallel and Series Arrangement of the Vessels Composing the Circulatory System.A, Resistance in blood vessels arranged in series or parallel. R, Resistance in an individual vessel. B, The capillary beds are represented by thin lines connecting the arterioles (right) and the veins (left). The crescent-shaped thickenings proximal to the capillary beds represent the arterioles (resistance vessels). B modified from Berne RM, Levy MN: Cardiovascular physiology, ed 8, St Louis, 2001, Mosby.
  2123. Neural control of total peripheral resistance
  2124. Velocity
  2125. Figure 22-28 Baroreceptors and Chemoreceptor Reflex Control of Blood Pressure.A, Baroreceptor reflexes. Baroreceptors located in the carotid sinuses and aortic arch detect changes in blood pressure. Action potentials are conducted to the cardioregulatory and vasomotor centers. The heart rate can be decreased by the parasympathetic system; the heart rate and stroke volume can be increased by the sympathetic system. The sympathetic system also can constrict or dilate blood vessels. B, Chemoreceptor reflexes. Chemoreceptors located in the medulla oblongata and in the carotid and aortic bodies detect changes in blood oxygen, carbon dioxide, or pH. Action potentials are conducted to the medulla oblongata. In response, the vasomotor center can cause vasoconstriction or dilation of blood vessels by the sympathetic system, and the cardioregulatory center can cause changes in the pumping activity of the heart through the parasympathetic and sympathetic systems. From Seeley RR, Stephens TD, Tate P: Anatomy and physiology, ed 3, St Louis, 1995, Mosby.
  2126. Laminar versus turbulent flow
  2127. Figure 22-29 Laminar and Turbulent Blood Flow.A, Laminar flow. Fluid flows in long, smooth-walled tubes as if it is composed of a large number of concentric layers. B, Turbulent flow. Turbulent flow is caused by numerous small currents flowing crosswise or oblique to the long axis of the vessel, resulting in flowing whorls and eddy currents. From Seeley RR, Stephens TD, Tate P: Anatomy and physiology, ed 3, St Louis, 1995, Mosby.
  2128. Vascular compliance
  2129. Quick Check 22-6
  2130. Regulation of Blood Pressure
  2131. Arterial pressure
  2132. Baroreceptors
  2133. Arterial chemoreceptors
  2134. Antidiuretic hormone, renin-angiotensin system, natriuretic peptides, adrenomedullin, and insulin
  2135. Figure 22-30 Factors Regulating Blood Pressure.
  2136. Table 22-5 Factors That Affect Mean Arterial Pressure and Capillary Flow
  2137. Health Alert Aldosterone and Injury
  2138. Figure 22-31 Three Mechanisms That Influence Total Plasma Volume. The antidiuretic hormone (ADH) mechanism and renin-angiotensin and aldosterone mechanisms tend to increase water retention and thus increase total plasma volume. The natriuretic peptides antagonize these mechanisms by promoting water loss and sodium loss, thus promoting a decrease in total plasma volume. NPs, Natriuretic peptides; ACE, angiotensin converting enzyme. Modified from Thibodeau GA, Patton KT: Anatomy & physiology, ed 5, St Louis, 2003, Mosby.
  2139. Health Alert Angiotensin II
  2140. Figure 22-32 Angiotensins and the Organs Affected.A, The shaded blue area is the classic pathway of biosynthesis that generates the renin and angiotensin I. Angiotensinogen is synthesized in the liver and is released into the blood where it is cleaved to form angiotensin I by renin secreted by cells in the kidneys. Angiotensin converting enzyme (ACE) in the lung catalyzes the formation of angiotensin II from angiotensin I and destroys the potent vasodilator, bradykinin. Further cleavage generates the angiotensins III and IV. The reddish shading shows the organs affected by angiotensin II, including brain, heart, adrenals, kidney, and the kidney’s efferent arterioles. The dashed arrow (left) shows the inhibition of renin by angiotensin II. B, Summary of angiotensin II effects on blood vessel structure and function leading to atherosclerosis. Adapted from Goodfriend TL et al: N Engl J Med 334:2649–2654, 1996.
  2141. Figure 22-33 Angiotensins and Their Receptors, AT1 and AT2. Blocking the angiotensin-converting enzyme (ACE) with ACE inhibitors decreases the amount of angiotensin II. Blocking the receptor AT1 with drugs (AT1 antagonists) blocks the attachment of angiotensin II to the cell preventing the cellular effects and decreasing the vascular, cardiac, and renal effects.
  2142. Venous pressure
  2143. Regulation of the Coronary Circulation
  2144. Box 22-2 Vascular Protection and Injury Properties of Insulin
  2145. Protection
  2146. Injury
  2147. Autoregulation
  2148. Autonomic regulation
  2149. Quick Check 22-7
  2150. The Lymphatic System
  2151. Figure 22-34 Role of the Lymphatic System in Fluid Balance. Fluid from plasma flowing through the capillaries moves into interstitial spaces. Although much of this interstitial fluid is either absorbed by tissue cells or reabsorbed by capillaries, some of the fluid tends to accumulate in the interstitial spaces. As this fluid builds up, it tends to drain into lymphatic vessels that eventually return the fluid to the venous blood. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2152. Figure 22-35 Principle Organs of the Lymphatic System. The inset shows the areas drained by the right lymphatic duct (green) and the thoracic duct (blue). From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2153. Figure 22-36 Lymphatic Capillaries.A, Schematic representation of lymphatic capillaries. B, Anatomic components of microcirculation.
  2154. Quick Check 22-8
  2155. Did You Understand?
  2156. The Circulatory System
  2157. The Heart
  2158. The Systemic Circulation
  2159. The Lymphatic System
  2160. Key Terms
  2161. References
  2162. Chapter 23 Alterations of Cardiovascular Function
  2163. Electronic Resources
  2164. Companion CD
  2165. Website http://evolve.elsevier.com/Huether/
  2166. Diseases of the Arteries and Veins
  2167. Diseases of the Veins
  2168. Varicose veins and chronic venous insufficiency
  2169. Thrombus formation in veins
  2170. Figure 23-1 Venous Stasis Ulcer. From Rosai J: Ackerman’s surgical pathology, ed 7, vol 2, St Louis, 1989, Mosby.
  2171. Figure 23-2 Multiple Venous Thrombi. From Rosai J: Ackerman’s surgical pathology, ed 7, vol 2, St Louis, 1989, Mosby.
  2172. Superior vena cava syndrome
  2173. Quick Check 23-1
  2174. Hypertension
  2175. Table 23-1 Classification of Blood Pressure for Adults Age 18 Years or Older
  2176. Factors associated with primary hypertension
  2177. Health Alert Genes and the Risk for Hypertension
  2178. Risk Factors Primary Hypertension
  2179. Pathophysiology
  2180. Primary hypertension
  2181. Figure 23-3 Factors that Cause a Shift in the Pressure-Natriuresis Relationship. Numerous factors have been implicated in the pathogenesis of sodium retention in individuals with hypertension. These factors cause less renal excretion of salt than would normally occur with increased blood pressure. This is called a shift in the pressure-natriuresis relationship and is believed to be a central process in the pathogenesis of primary hypertension. SNS, Sympathetic nervous system; RAA, renin-angiotensin-aldosterone.
  2182. Health Alert Obesity and Hypertension
  2183. Secondary hypertension
  2184. Isolated systolic hypertension
  2185. Figure 23-4 Pathophysiology of Hypertension. Numerous genetic vulnerabilities have been linked to hypertension and these, in combination with environmental risks, cause neurohumoral dysfunction (sympathetic nervous system [SNS], renin-angiotensin-aldosterone [RAA] system, adducin, and natriuretic hormones) and promote inflammation and insulin resistance. Insulin resistance and neurohumoral dysfunction contribute to sustained systemic vasoconstriction and increased peripheral resistance. Inflammation contributes to renal dysfunction, which, in combination with the neurohumoral alterations, results in renal salt and water retention and increased blood volume. Increased peripheral resistance and increased blood volume are two primary causes of sustained hypertension.
  2186. Complicated hypertension
  2187. Clinical Manifestations
  2188. Table 23-2 Pathologic Effects of Sustained, Complicated Primary Hypertension
  2189. Evaluation and Treatment
  2190. Orthostatic (Postural) Hypotension
  2191. Figure 23-5 Summary of Treatment Recommendations for Hypertension.BP, Blood pressure; ACE, angiotensin-converting enzyme; ARB, angiotensin-receptor blocker; CCB, calcium channel blocker. Data from Chobanian AV et al: The JNC 7 Report, JAMA 289(19):2560–2572, 2003.
  2192. Quick Check 23-2
  2193. Aneurysm
  2194. Figure 23-6 Aneurysms.A, Abdominal aortic atherosclerotic aneurysm. B, In a long-axis view of the left ventricle there is a large, thin-walled apical aneurysm that does not contain thrombus. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  2195. Figure 23-7 Longitudinal Sections Showing Types of Aneurysms. The fusiform circumferential and fusiform saccular aneurysms are true aneurysms, caused by weakening of the vessel wall. False and saccular aneurysms involve a break in the vessel wall, usually caused by trauma.
  2196. Figure 23-8 Dissecting Aneurysm of Thoracic Aorta. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  2197. Thrombus Formation
  2198. Embolism
  2199. Table 23-3 Types of Emboli
  2200. Quick Check 23-3
  2201. Peripheral Vascular Disease
  2202. Thromboangiitis obliterans (Buerger disease)
  2203. Raynaud phenomenon and disease
  2204. Quick Check 23-4
  2205. Arteriosclerosis
  2206. Atherosclerosis
  2207. Figure 23-9 Arteriosclerosis.A, Cross section of a normal artery and an artery altered by disease. B, A small artery in the myocardium is occluded by a mass of blue-staining platelets, yellow-staining red cells, and cholesterol bodies. B from Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  2208. Pathophysiology
  2209. Figure 23-10 Endothelium Regulation of Vasomotion (Constriction and Dilation) and Platelet Aggregation. With injury, the endothelium loses its normal ability to decrease clot formation (antithrombotic) and maintain vasodilation. Injury results in platelet aggregation with increases in thromboxane A2 (which aspirin inhibits) and the release of serotonin and endothelin causing vasoconstriction, a decrease in blood flow, and ischemia. Sympathetic nerve activation causes vasoconstriction with the release of epinephrine. Endothelin is a potent amino acid peptide. The endothelium also converts angiotensin I into angiotensin II by the membrane-bound angiotensin-converting enzyme (ACE). Angiotensin II plays an important role in the pathophysiology of hypertension, atherosclerosis, myocardial infarction, and left heart failure (congestive heart failure) (see text under the heading for each). Modified from Stern S, editor: Silent myocardial ischemia, St Louis, 1998, Mosby.
  2210. Figure 23-11 Factors That Cause Endothelium-Dependent Vasodilation. Several pharmacologic and physiologic factors stimulate the release of nitric oxide synthase (NOS) that results in the release of nitric oxide (NO). These factors include norepinephrine, acetylcholine, bradykinin, substance P, angiotensin II, thrombin, vasopressin, ATP, 5-HT, and ADP. In addition, the continuous normal production of NO can be increased by physiologic events including shear stress (on the vessel walls) and movement of platelets. Nitric oxide leads to relaxation of the smooth muscle cells resulting in vasodilation. Prostacyclin (PGI2) also causes relaxation of the smooth muscle cells and inhibits platelet aggregation downstream. Modified from Stern S, editor: Silent myocardial ischemia, St Louis, 1998, Mosby.
  2211. Clinical Manifestations
  2212. Figure 23-12 Low-density Lipoprotein Oxidation. Low-density lipoprotein (LDL) enters the arterial intima through an intact endothelium. In hypercholesterolemia, the influx of LDL exceeds the eliminating capacity and an extracellular pool of LDL is formed. This is enhanced by association of LDL with the extracellular matrix. Intimal LDL is oxidized through the actin of free oxygen radicals formed by enzymatic or nonenzymatic reactions. This generates proinflammatory lipids that induce endothelial expression of the adhesion molecule, vascular cell adhesion molecule-1 activate complement and stimulate chemokine secretion. All of these factors cause adhesion and entry of mononuclear leukocytes, particularly monocytes and T lymphocytes. Monocytes differentiate into macrophages. Macrophages up-regulate and internalize oxidized LDL and transform into foam cells. Macrophage uptake of oxidized LDL also leads to presentation of fragments of it to antigen-specific T cells. This induces an autoimmune reaction that leads to production of proinflammatory cytokines. Such cytokines include interferon-γ, tumor necrosis factor-α, and interleukin-1, which act on endothelial cells to stimulate expression of adhesion molecules and procoagulant activity; on macrophages to activate proteases, endocytosis, nitric oxide (NO), and cytokines; and on smooth muscle cells (SMCs) to include NO production and inhibit growth, collagen, and actin expression. LDL, low-density lipoprotein. Modified from Crawford MH, DiMarco JP, editors: Cardiology, London, 2001, Mosby.
  2213. Evaluation and Treatment
  2214. Figure 23-13 Progression of Atherosclerosis. A, Damaged endothelium. B, Diagram of fatty streak and lipid core formation (see Figure 23-5 for a diagram of oxidized low-density lipoprotein [LDL]). C, Diagram of fibrous plaque. Raised plaques are visible: some are yellow; others are white. D, Diagram of complicated lesion; thrombus is red; collagen is blue. Plaque is complicated by red thrombus deposition.
  2215. Peripheral Artery Disease
  2216. Coronary Artery Disease, Myocardial Ischemia, and Acute Coronary Syndromes
  2217. Figure 23-14 Atherosclerosis.A, Concentric coronary plaque. The lumen is central. There are multiple, new small blood vessels within the plaque, the late result of disruption. B, Cell types in fibrolipid plaque. The plaque cap (brownish color) contains numerous elongated, smooth muscle cells; some contain lipid. Macrophages are clustered on the edge of the core. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  2218. Development of coronary artery disease
  2219. Health Alert The Basics on Fats
  2220. Table 23-4 Criteria for Dyslipidemia
  2221. Dyslipidemia
  2222. Hypertension
  2223. Cigarette smoking
  2224. Diabetes mellitus
  2225. Obesity/sedentary lifestyle
  2226. Nontraditional risk factors
  2227. Markers of inflammation and thrombosis
  2228. Hyperhomocysteinemia
  2229. Infection
  2230. Health Alert Inflammatory Markers for Cardiovascular Risk
  2231. Figure 23-15 Cycle of Ischemic Events.
  2232. Myocardial ischemia
  2233. Pathophysiology
  2234. Clinical Manifestations
  2235. Figure 23-16 Angiogram of Coronary Arteries.A, Baseline. B, Transient total occlusion of left anterior descending branch of the left coronary artery after mental stress. C, After nitrates and nifedipine, artery reopened to same diameter as baseline. Modified from Stern S, editor: Silent myocardial ischemia, St Louis, 1998, Mosby.
  2236. Health Alert Women and Coronary Artery Disease
  2237. Figure 23-17 The Ischemic Cost of Aggravation. Linkages among daily mental and emotional stimuli, brain activity, and coronary and myocardial physiology. Modified from Papodemetrion V et al: Am Heart J 132:1299, 1996.
  2238. Evaluation and Treatment
  2239. Figure 23-18 Pathophysiologic Model of the Effects of Acute Stress as a Trigger of Cardiac Clinical Events. Acting via the central and autonomic nervous systems, stress can produce a cascade of physiologic responses that may lead to myocardial ischemia, especially in patients with coronary artery disease; potentially fatal dysrhythmia; plaque rupture; or coronary thrombosis. VF, Ventricular fibrillation; VT, ventricular tachycardia; MI, myocardial infarction; LV, left ventricular. From Krantz DS et al: Mental stress as a trigger of myocardial ischemia and infarction. In Deedwania PC, Tofler GH, editors: Triggers and timing of cardiac events, ed 2, London, 1996, Saunders.
  2240. Figure 23-19 Electrocardiogram (ECG) and Ischemia.A, Normal ECG. B, Electrocardiographic alterations associated with ischemia.
  2241. Quick Check 23-5
  2242. Acute coronary syndromes
  2243. Figure 23-20 Pathophysiology of Acute Coronary Syndromes. The atherosclerotic process can lead to stable plaque formation and stable angina or can result in unstable plaques that are prone to rupture and thrombus. Thrombus formation on a ruptured plaque that disperses in less than 20 minutes leads to transient ischemia and unstable angina. If the vessel obstruction is sustained, myocardial infarction with inflammation and necrosis of the myocardium results. In addition, myocardial infarction is associated with other structural and functional changes, including myocyte stunning and hibernation and myocardial remodeling.
  2244. Figure 23-21 Pathogenesis of Unstable Plaques and Thrombus Formation.
  2245. Figure 23-22 Plaque Disruption and Myocardial Infarction.A, Plaque disruption. The cap of the lipid-rich plaque has become torn with the formation of a thrombus, mostly inside the plaque. B, Myocardial infarction. This infarct is 6 days old. The center is yellow and necrotic with a hemorrhagic red rim. The responsible artery occlusion is probably in the right coronary artery. The infarct is on the posterior wall. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  2246. Unstable angina
  2247. Myocardial infarction
  2248. Pathophysiology
  2249. Cellular injury
  2250. Cellular death
  2251. Structural and functional changes
  2252. Figure 23-23 Myocardial Infarction.A, Local infarct confined to one region. B, Massive large infarct caused by occlusion of three coronary arteries. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  2253. Repair
  2254. Clinical Manifestations
  2255. Complications
  2256. Figure 23-24 Three Interacting Factors Related to Sudden Cardiac Death. The three factors are ischemia, left ventricular dysfunction, and electrical instability.
  2257. Evaluation and Treatment
  2258. Table 23-5 Complications With Myocardial Infarctions
  2259. Figure 23-25 Electrocardiographic Alterations Associated With the Three Zones of Myocardial Infarction.
  2260. Quick Check 23-6
  2261. Disorders of the Heart Wall
  2262. Disorders of the Pericardium
  2263. Acute pericarditis
  2264. Figure 23-26 Acute Pericarditis. Note shaggy coat of fibers covering the surface of heart. From Damjanov I, Linder J: Pathology: a color atlas, St Louis, 2000, Mosby.
  2265. Pericardial effusion
  2266. Figure 23-27 Exudate of Blood in the Pericardial Sac from Rupture of Aneurysm. From Damjanov I, Linder J: Pathology: a color atlas, St Louis, 2000, Mosby.
  2267. Constrictive pericarditis
  2268. Figure 23-28 Constrictive Pericarditis. The fibrotic pericardium encases the heart in a rigid shell. From Damjanov I, Linder J: Pathology: a color atlas, St Louis, 2000, Mosby.
  2269. Disorders of the Myocardium: The Cardiomyopathies
  2270. Quick Check 23-7
  2271. Figure 23-29 Diagram Showing Major Distinguishing Pathophysiologic Features of the Three Types of Cardiomyopathy.A, The normal heart. B, In the dilated type of cardiomyopathy, the heart has a globular shape and the largest circumference of the left ventricle is not at its base but midway between apex and base. C, In the hypertrophic type, the wall of the left ventricle is greatly thickened; the left ventricular cavity is small, but the left atrium may be dilated because of poor diastolic relaxation of the ventricle. D, In the restrictive (constrictive) type, the left ventricular cavity is of normal size, but, again, the left atrium is dilated because of the reduced diastolic compliance of the ventricle. From Kissane JM, editor: Anderson’s pathology, ed 9, St Louis, 1990, Mosby.
  2272. Disorders of the Endocardium
  2273. Valvular dysfunction
  2274. Stenosis
  2275. Aortic stenosis
  2276. Table 23-6 Pathophysiologic Effects of the Cardiomyopathies
  2277. Mitral stenosis
  2278. Regurgitation
  2279. Aortic regurgitation
  2280. Table 23-7 Clinical Manifestations of Valvular Stenosis and Regurgitation
  2281. Figure 23-30 Valvular Stenosis and Regurgitation.A, Normal position of the valve leaflets, or cusps, when the valve is open and closed. B, Open position of a stenosed valve (left) and open position of a closed regurgitant valve (right). C, Hemodynamic effect of mitral stenosis. The stenosed valve is unable to open sufficiently during left atrial systole, inhibiting left ventricular filling. D, Hemodynamic effect of mitral regurgitation. The mitral valve does not close completely during left ventricular systole, permitting blood to reenter the left atrium.
  2282. Figure 23-31 Mitral Stenosis With Classic “Fish Mouth” Orifice. From Stevens A, Lowe J: Pathology, ed 2, London, 2000, Mosby.
  2283. Mitral regurgitation
  2284. Tricuspid regurgitation
  2285. Mitral valve prolapse syndrome
  2286. Figure 23-32 Mitral Valve Prolapse.A, Normal mitral valve (lower right) and prolapsed mitral valve (left). Prolapse permits the valve leaflets to billow back into the atrium during left ventricular systole. The billowing causes the leaflets to part slightly, permitting regurgitation into the atrium. B, Looking down into the mitral valve, the ballooning of the leaflets is visible. B from Stevens A, Lowe J: Pathology, ed 2, Edinburgh, 2000, Mosby.
  2287. Acute rheumatic fever and rheumatic heart disease
  2288. Pathophysiology
  2289. Figure 23-33 Pathogenesis and Structural Alterations of Acute Rheumatic Heart Disease. Beginning usually with a sore throat, rheumatic fever can develop only as a sequel to pharyngeal infection by group A β-hemolytic streptococcus. Suspected as a hypersensitivity reaction, it is proposed that antibodies directed against the M proteins of certain strains of streptococci cross-react with tissue glycoproteins in the heart, joints, and other tissues. The exact nature of cross-reacting antigens has been difficult to define, but it appears that the streptococcal infection causes an autoimmune response against self-antigens. Inflammatory lesions are found in various sites; the most distinctive within the heart are called Aschoff bodies. The chronic sequelae result from progressive fibrosis because of healing of the inflammatory lesions and the changes induced by valvular deformities. From Damjanov I: Pathology for the health professions, ed 3, St. Louis, 2006, Saunders.
  2290. Figure 23-34 Mitral Stenosis with Vegitations. Mitral stenosis and clumps of vegetation (V) containing platelets and fibrin as shown in this micrograph. Mitral leaflets are thickened and fused. From Stevens A, Lowe J: Pathology, Edinburgh, 2000, Mosby.
  2291. Clinical Manifestations
  2292. Carditis
  2293. Polyarthritis
  2294. Table 23-8 Jones Criteria (Updated) Used for Diagnosis of Initial Attack of Rheumatic Fever
  2295. Chorea
  2296. Erythema marginatum
  2297. Evaluation and Treatment
  2298. Quick Check 23-8
  2299. Infective endocarditis
  2300. Risk Factors Infective Endocarditis
  2301. Pathophysiology
  2302. Figure 23-35 Pathogenesis of Infective Endocarditis.
  2303. Clinical Manifestations
  2304. Figure 23-36 Bacterial Endocarditis of Mitral Valve. The valve is covered with large, irregular vegetations (arrow). From Damjanov I, Linder J: Pathology: a color atlas, St Louis, 2000, Mosby.
  2305. Evaluation and Treatment
  2306. Cardiac Complications in Acquired Immunodeficiency Syndrome (AIDS)
  2307. Quick Check 23-9
  2308. Manifestations of Heart Disease
  2309. Dysrhythmias
  2310. Table 23-9 Disorders of Impulse Formation
  2311. Table 23-10 Disorders of Impulse Conduction
  2312. Heart Failure
  2313. Left heart failure (congestive heart failure)
  2314. Box 23-1 Inflammation, Immunity, and Humoral Factors in the Pathogenesis of Congestive Heart Failure
  2315. Figure 23-37 Pathophysiology of Ventricular Remodeling. Myocardial dysfunction activates the renin-angiotensin-aldosterone and sympathetic nervous systems releasing neurohormones (angiotensin II, aldosterone, catecholamines, and cytokines). These neurohormones contribute to ventricular remodeling. Redrawn from Carelock J, Clark AP: Heart failure: pathophysiologic mechanisms, Am J Nurs 101[12]:27, 2001.
  2316. Figure 23-38 The Effect of Elevated Preload on Myocardial Oxygen Supply and Demand.LVEDV, Left ventricular end-diastolic volume.
  2317. Figure 23-39 The Role of Increased Afterload in the Pathogenesis of Heart Failure.
  2318. Figure 23-40 The Vicious Cycle of Systolic Heart Failure. Although the initial insult may be one of primary decreased contractility (e.g., myocardial infarction), increased preload (e.g., renal failure), or increased afterload (e.g., hypertension), all three factors play a role in the progression of left heart failure (LHF). LVEDV, Left ventricular end-diastolic volume.
  2319. Health Alert Brain Natriuretic Peptide (BNP) and Heart Failure
  2320. Right heart failure
  2321. Figure 23-41 Right Heart FailureRV, Right ventricular; RA, right atrial; JVD, jugular venous distension.
  2322. High-output failure
  2323. Quick Check 23-10
  2324. Shock
  2325. Figure 23-42 High-Output Failure.SVR, Systemic vascular resistance.
  2326. Impairment of Cellular Metabolism
  2327. Impairment of oxygen use
  2328. Figure 23-43 Impaired Cellular Metabolism in Shock.ATP, Adenosine triphosphate.
  2329. Impairment of glucose use
  2330. Types of Shock
  2331. Cardiogenic shock
  2332. Hypovolemic shock
  2333. Figure 23-44 Cardiogenic Shock. Shock becomes life threatening when compensatory mechanisms (in blue) cause increased myocardial oxygen requirements. Renal and hypothalamic adaptive responses (i.e., renin-angiotensin-aldosterone and antidiuretic hormone [ADH]) maintain or increase blood volume. The adrenal gland releases catecholamines (e.g., mostly epinephrine, some norepinephrine), causing vasoconstriction and increases in contractility and heart rate. These adaptive mechanisms, however, increase myocardial demands for oxygen and nutrients. These demands further strain the heart, which can no longer pump an adequate volume, resulting in shock and impaired metabolism. SVR, Systemic vascular resistance.
  2334. Neurogenic shock
  2335. Figure 23-45 Hypovolemic Shock. This type of shock becomes life threatening when compensatory mechanisms (in purple) are overwhelmed by continued loss of intravascular volume. ADH, Antidiuretic hormone; SVR, systemic vascular resistance.
  2336. Anaphylactic shock
  2337. Figure 23-46 Neurogenic Shock.SVR, Systemic vascular resistance.
  2338. Figure 23-47 Anaphylactic Shock.IgE, Immunoglobulin E; SVR, systemic vascular resistance.
  2339. Quick Check 23-11
  2340. Septic shock
  2341. Table 23-11 Causes and Definitions of Septic Shock
  2342. Figure 23-48 Septic Shock Cascade.
  2343. Health Alert The Role of Nitric Oxide in Severe Sepsis
  2344. Risk Factors Inflammatory and Anti-inflammatory Mediators Contributing to Septic Shock
  2345. The Interleukins
  2346. Tumor Necrosis Factor
  2347. Platelet-Activating Factor
  2348. Myocardial Depressant Factor
  2349. Clinical Manifestations of Shock
  2350. Treatment for Shock
  2351. Quick Check 23-12
  2352. Multiple Organ Dysfunction Syndrome
  2353. Risk Factors Development of Multiple Organ Dysfunction Syndrome
  2354. Pathophysiology
  2355. Figure 23-49 Pathogenesis of Multiple Organ Dysfunction Syndrome.
  2356. Clinical Manifestations
  2357. Table 23-12 Cells of Inflammation and Multiple Organ Dysfunction
  2358. Evaluation and Treatment
  2359. Health Alert Nutritional Support to Prevent and Treat MODS
  2360. Quick Check 23-13
  2361. Did You Understand?
  2362. Diseases of the Arteries and Veins
  2363. Disorders of the Heart Wall
  2364. Manifestations of Heart Disease
  2365. Shock
  2366. Key Terms
  2367. References
  2368. Chapter 24 Alterations of Cardiovascular Function in Children
  2369. Electronic Resources
  2370. Companion CD
  2371. Website
  2372. Congenital Heart Disease
  2373. Table 24-1 Maternal Conditions and Environmental Exposures and the Associated Congenital Heart Defects
  2374. Table 24-2 Congenital Heart Disease in Selected Fetal Chromosomal Aberrations
  2375. Obstructive Defects
  2376. Coarctation of the aorta
  2377. Pathophysiology
  2378. Clinical Manifestations
  2379. Evaluation and Treatment
  2380. Figure 24-1 Shunting of Blood in Congenital Heart Disease.A, Normal. B, Acyanotic defect. C, Cyanotic defect. ASD, Atrial septal defect; VSD, ventricular septal defect; RA, right atrium; LA, left atrium; RV, right ventricle; LV, left ventricle. From Wong DL: Whaley & Wong’s essentials of pediatric nursing, ed 4, St Louis, 1993, Mosby.
  2381. Figure 24-2 Comparison of Acyanotic-Cyanotic and Hemodynamic Classification Systems of Congenital Heart Disease. From Hockenberry MJ et al: Wong’s nursing care of infants and children, ed 8, St Louis, 2007, Mosby.
  2382. Figure 24-3 Coarctation of the Aorta (COA) (Postductal). From James SR, Ashwill JW: Nursing care of children: principles and practice, ed 3, St Louis, 2007, Saunders.
  2383. Aortic stenosis
  2384. Pathophysiology
  2385. Figure 24-4 Aortic Stenosis (AS). From James SR, Ashwill JW: Nursing care of children: principles and practice, ed 3, St Louis, 2007, Saunders.
  2386. Clinical Manifestations
  2387. Evaluation and Treatment
  2388. Valvular aortic stenosis
  2389. Subvalvular aortic stenosis
  2390. Pulmonic stenosis
  2391. Pathophysiology
  2392. Clinical Manifestations
  2393. Evaluation and Treatment
  2394. Figure 24-5 Pulmonic Stenosis (PS).A, The pulmonary valve narrows at the entrance of the pulmonary artery. B, Balloon angioplasty is used to dilate the valve. A catheter is inserted across the stenotic pulmonic valve into the pulmonary artery, and a balloon at the end of the catheter is inflated while across the narrowed valve opening. A from James SR, Ashwill JW: Nursing care of children: principles and practice, ed 3, St Louis, 2007, Saunders. B redrawn from Hockenberry MJ et al: Wong’s nursing care of infants and children, ed 8, St Louis, 2007, Mosby.
  2395. Defects With Increased Pulmonary Blood Flow
  2396. Patent ductus arteriosus
  2397. Pathophysiology
  2398. Clinical Manifestations
  2399. Figure 24-6 Patent Ductus Arteriosus (PDA). From James SR, Ashwill JW: Nursing care of children: principles and practice, ed 3, St Louis, 2007, Saunders.
  2400. Evaluation and Treatment
  2401. Atrial septal defect
  2402. Pathophysiology
  2403. Clinical Manifestations
  2404. Evaluation and Treatment
  2405. Ventricular septal defect
  2406. Pathophysiology
  2407. Clinical Manifestations
  2408. Evaluation and Treatment
  2409. Atrioventricular canal defect
  2410. Pathophysiology
  2411. Clinical Manifestations
  2412. Evaluation and Treatment
  2413. Figure 24-7 Atrioventricular Canal (AVC) Defect. From James SR, Ashwill JW: Nursing care of children: principles and practice, ed 3, St Louis, 2007, Saunders.
  2414. Defects With Decreased Pulmonary Blood Flow
  2415. Tetralogy of fallot
  2416. Pathophysiology
  2417. Clinical Manifestations
  2418. Figure 24-8 Tetralogy of Fallot (TOF). From James SR, Ashwill JW: Nursing care of children: principles and practice, ed 3, St Louis, 2007, Saunders.
  2419. Evaluation and Treatment
  2420. Tricuspid atresia
  2421. Pathophysiology
  2422. Figure 24-9 Tricuspid Atresia. From James SR, Ashwill JW: Nursing care of children: principles and practice, ed 3, St Louis, 2007, Saunders.
  2423. Clinical Manifestations
  2424. Evaluation and Treatment
  2425. Mixing Defects
  2426. Transposition of the great arteries or transposition of the great vessels
  2427. Pathophysiology
  2428. Clinical Manifestations
  2429. Figure 24-10 Hemodynamics in Transposition of the Great Vessels (TGV).A, Complete transposition of the great vessels with an intact interventricular septum. The aorta arises from the right ventricle and the pulmonary artery from the left. B, Oxygen saturation in the two parallel circuits. RA, Right atrium; RV, right ventricle; Ao, aorta; ASD, atrial septal defect; VSD, ventricular septal defect; PDA, patent ductus arteriosus; LA, left atrium; LV, left ventricle; PA, pulmonary artery. A redrawn from Hockenberry MJ et al: Wong’s nursing care of infants and children, ed 8, St Louis, 2007, Mosby.
  2430. Evaluation and Treatment
  2431. Total anomalous pulmonary venous connection
  2432. Pathophysiology
  2433. Figure 24-11 Total Anomalous Pulmonary Venous Connection (TAPVC). Redrawn from Hockenberry MJ et al: Wong’s nursing care of infants and children, ed 8, St Louis, 2007, Mosby.
  2434. Clinical Manifestations
  2435. Evaluation and Treatment
  2436. Truncus arteriosus
  2437. Pathophysiology
  2438. Clinical Manifestations
  2439. Evaluation and Treatment
  2440. Figure 24-12 Truncus Arteriosus (TA). From James SR, Ashwill JW: Nursing care of children: principles and practice, ed 3, St Louis, 2007, Saunders.
  2441. Hypoplastic left heart syndrome
  2442. Pathophysiology
  2443. Clinical Manifestations
  2444. Evaluation and Treatment
  2445. Figure 24-13 Hypoplastic Left Heart Syndrome (HLHS). Redrawn from Hockenberry MJ et al: Wong’s nursing care of infants and children, ed 8, St Louis, 2007, Mosby.
  2446. Quick Check 24-1
  2447. Health Alert Endocarditis Risk
  2448. Congestive Heart Failure
  2449. Table 24-3 Causes of Congestive Heart Failure Resulting From Congenital Heart Disease
  2450. Box 24-1 Clinical Manifestations of Congestive Heart Failure
  2451. Impaired Myocardial Function
  2452. Pulmonary Congestion
  2453. Acquired Cardiovascular Disorders
  2454. Kawasaki Disease
  2455. Pathophysiology
  2456. Clinical Manifestations
  2457. Evaluation and Treatment
  2458. Box 24-2 Diagnostic Criteria for Kawasaki Disease
  2459. Systemic Hypertension
  2460. Table 24-4 Diagnosing Hypertension in Children (Selected Ages)
  2461. Pathophysiology
  2462. Box 24-3 Conditions Associated With Secondary Hypertension in Children
  2463. Renal Disorders
  2464. Cardiovascular Disease
  2465. Metabolic and Endocrine Diseases
  2466. Neurologic Disorders
  2467. Miscellaneous Causes
  2468. Clinical Manifestations
  2469. Health Alert U.S. Childhood Obesity and Its Association With Cardiovascular Disease
  2470. Evaluation and Treatment
  2471. Table 24-5 Most Common Causes of Chronic Sustained Hypertension
  2472. Table 24-6 Routine and Special Laboratory Tests for Hypertension
  2473. Quick Check 24-2
  2474. Did You Understand?
  2475. Congenital Heart Disease
  2476. Acquired Cardiovascular Disorders in Children
  2477. Key Terms
  2478. References
  2479. Unit 8 The Pulmonary System
  2480. Chapter 25 Structure and Function of the Pulmonary System
  2481. Electronic Resources
  2482. Companion CD
  2483. Website http://evolve.elsevier.com/Huether/
  2484. Structures of the Pulmonary System
  2485. Conducting Airways
  2486. Figure 25-1 Structures of the Pulmonary System. The enlargement in the circle depicts the acinus, where oxygen and carbon dioxide are exchanged. From Thibodeau GA, Patton, KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2487. Table 25-1 Pulmonary Defense Mechanisms
  2488. Figure 25-2 Structures of the Upper Airway. Redrawn from Thompson JM et al: Mosby’s clinical nursing, ed 5, St Louis, 2002, Mosby.
  2489. Gas-Exchange Airways
  2490. Figure 25-3 Structures of the Lower Airway. Redrawn from Thompson JM et al: Mosby’s clinical nursing, ed 5, St Louis, 2002, Mosby.
  2491. Quick Check 25-1
  2492. Pulmonary and Bronchial Circulation
  2493. Figure 25-4 Changes in the Bronchial Wall With Progressive Branching. From Wilson SF, Thompson JM: Respiratory disorders, St Louis, 1990, Mosby.
  2494. Figure 25-5 Alveoli. Bronchioles subdivide to form tiny tubes called alveolar ducts, which end in clusters of alveoli called alveolar sacs. From Thibodeau GA, Patton, KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2495. Figure 25-6 Section Through the Alveolar Septum (Gas-Exchange Membrane). Inset shows a magnified view of the respiratory membrane composed of the alveolar wall (fluid coating, epithelial cells, basement membrane), interstitial fluid, and wall of a pulmonary capillary (basement membrane, endothelial cells). The gases CO2 (carbon dioxide) and O2 (oxygen) diffuse across the respiratory membrane.
  2496. Chest Wall and Pleura
  2497. Figure 25-7 Thoracic (Chest) Cavity and Related Structures. The thoracic (chest) cavity is divided into three subdivisions (left and right pleural divisions and mediastinum) by a partition formed by a serous membrane called the pleura. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 3, St Louis, 1996, Mosby.
  2498. Function of the Pulmonary System
  2499. Ventilation
  2500. Figure 25-8 Functional Components of the Respiratory System. The central nervous system responds to neurochemical stimulation of ventilation and sends signals to the chest wall musculature. The response of the respiratory system to these impulses is influenced by several factors that impact the mechanisms of breathing and, therefore, affect the adequacy of ventilation. Gas transport between the alveoli and pulmonary capillary blood depends on a variety of physical and chemical activities. Finally, the control of the pulmonary circulation plays a role in the appropriate distribution of blood flow.
  2501. Quick Check 25-2
  2502. Neurochemical Control of Ventilation
  2503. Lung receptors
  2504. Figure 25-9 Spirogram. During normal, quiet respirations, the atmosphere and lungs exchange about 500ml of air (VT). With a forcible inspiration, about 3300ml more air can be inhaled (IRV). After a normal inspiration and normal expiration, approximately 1000ml more air can be forcibly expired (ERV). Vital capacity (VC) is the amount of air that can be forcibly expired after a maximal inspiration and indicates, therefore, the largest amount of air that can enter and leave the lungs during respiration. Residual volume (RV) is the air that remains trapped in the alveoli. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 5, St Louis, 2003, Mosby.
  2505. Chemoreceptors
  2506. Figure 25-10 Neurochemical Respiratory Control System.
  2507. Health Alert Changes in the Chemical Control of Breathing During Sleep
  2508. Quick Check 25-3
  2509. Mechanics of Breathing
  2510. Major and accessory muscles
  2511. Alveolar surface tension
  2512. Figure 25-11 Muscles of Ventilation.A, Anterior view. B, Posterior view. Modified from Thompson JM et al: Mosby’s clinical nursing, ed 5, St Louis, 2002, Mosby.
  2513. Elastic properties of the lung and chest wall
  2514. Figure 25-12 Interaction of Forces During Inspiration and Expiration.A, Outward recoil of the chest wall equals inward recoil of the lungs at the end of expiration. B, During inspiration, contraction of respiratory muscles, assisted by chest wall recoil, overcomes the tendency of lungs to recoil. C, At the end of inspiration, respiratory muscle contraction maintains lung expansion. D, During expiration, respiratory muscles relax, allowing elastic recoil of the lungs to deflate the lungs.
  2515. Airway resistance
  2516. Work of breathing
  2517. Quick Check 25-4
  2518. Figure 25-13 Relationship Between Number of Gas Molecules and Pressure Exerted by the Gas in an Enclosed Space.A, Theoretically, 10 molecules of the same gas exert a total pressure of 10 within the space.B, If the number of molecules is increased to 20, total pressure is 20. C, If there are different gases in the space, each gas exerts a partial pressure: here the partial pressure of nitrogen (N2) is 20, that of oxygen (O2) is 6, and total pressure is 26.
  2519. Gas Transport
  2520. Measurement of gas pressure
  2521. Table 25-2 Common Pulmonary Abbreviations
  2522. Distribution of ventilation and perfusion
  2523. Figure 25-14 Pulmonary Blood Flow and Gravity. The greatest volume of pulmonary blood flow normally will occur in the gravity-dependent areas of the lung. Body position has a significant effect on the distribution of pulmonary blood flow.
  2524. Oxygen transport
  2525. Diffusion across the alveolocapillary membrane
  2526. Figure 25-15 Gravity and Alveolar Pressure. Effects of gravity and alveolar pressure on pulmonary blood flow in the three lung zones. In zone I, alveolar pressure (PA) is greater than arterial and venous pressure, and no blood flow occurs. In zone II, arterial pressure (Pa) exceeds alveolar pressure, but alveolar pressure exceeds venous pressure (PV). Blood flow occurs in this zone, but alveolar pressure compresses the venules (venous ends of the capillaries). In zone III, both arterial and venous pressures are greater than alveolar pressure and blood flow fluctuates depending on the difference between arterial and venous pressure.
  2527. Determinants of arterial oxygenation
  2528. Oxyhemoglobin association and dissociation
  2529. Figure 25-16 Partial Pressure of Respiratory Gases in Normal Respiration. The numbers shown are average values near sea level. The values of PO2, PCO2, and PN2 fluctuate from breath to breath. Modified from Thompson JM et al: Mosby’s clinical nursing, ed 5, St Louis, 2002, Mosby.
  2530. Carbon dioxide transport
  2531. Figure 25-17 Oxyhemoglobin Dissociation Curve. The horizontal or flat segment of the curve at the top of the graph is the arterial or association portion, or that part of the curve where oxygen is bound to hemoglobin and occurs in the lungs. This portion of the curve is flat because partial pressure changes of oxygen between 60 and 100mm Hg do not significantly alter the percentage saturation of hemoglobin with oxygen and allow adequate hemoglobin saturation at a variety of altitudes. If the relationship between SaO2 and PaO2 were linear (in a downward sloping straight line) instead of flat between 60 and 100mm Hg, there would be inadequate saturation of hemoglobin with oxygen. The steep part of the oxyhemoglobin dissociation curve represents the rapid dissociation of oxygen from hemoglobin that occurs in the tissues. During this phase there is rapid diffusion of oxygen from the blood into tissue cells. The P50 is the PaO2 at which hemoglobin is 50% saturated, normally 26.6mm Hg. A lower than normal P50 represents increased affinity of hemoglobin for O2; a high P50 is seen with decreased affinity. Note that variation from the normal is associated with decreased (low P50) or increased (high P50) availability of O2 to tissues (dotted lines). The shaded area shows the entire oxyhemoglobin dissociation curve under the same circumstances. 2,3-DPG, 2,3-Diphosphoglycerate. From Lane EE, Walker JF: Clinical arterial blood gas analysis, St Louis, 1987, Mosby.
  2532. Quick Check 25-5
  2533. Control of the Pulmonary Circulation
  2534. Quick Check 25-6
  2535. Aging & The Pulmonary System
  2536. Elasticity/Chest Wall
  2537. Gas Exchange
  2538. Exercise
  2539. Changes in Lung Volumes With Aging. With aging, note particularly the dense vital capacity and the increase in residual volume. See also McClaran SR et al: Longitudinal effects of aging on lung function at rest and exercise in healthy active fit elderly adults, J Appl Physiol 78(5):1957–1968, 1995; Hardie JA et al: Reference values for arterial blood gases in the elderly, Chest 125(6):2053–2060, 2004; Zeleznik J: Normative aging of the respiratory system, Clin Geriatr Med 19(1):1–18, 2003; Meyer KC: The role of immunity in susceptibility to respiratory infection in the aging lung, Respir Physiol 128(1):23–31, 2001.
  2540. Did You Understand?
  2541. Structures of the Pulmonary System
  2542. Function of the Pulmonary System
  2543. AGING & the Pulmonary System
  2544. Key Terms
  2545. References
  2546. Chapter 26 Alterations of Pulmonary Function
  2547. Electronic Resources
  2548. Companion CD
  2549. Website http://evolve.elsevier.com/Huether/
  2550. Clinical Manifestations of Pulmonary Alterations
  2551. Signs and Symptoms of Pulmonary Disease
  2552. Dyspnea
  2553. Abnormal breathing patterns
  2554. Hypoventilation/hyperventilation
  2555. Cyanosis
  2556. Clubbing
  2557. Cough
  2558. Figure 26-1 Clubbing of Fingers Caused by Chronic Hypoxemia. Modified from Seidel HM et al: Mosby’s guide to physical examination, ed 5, St Louis, 2003, Mosby.
  2559. Hemoptysis
  2560. Abnormal sputum
  2561. Pain
  2562. Conditions Caused by Pulmonary Disease or Injury
  2563. Hypercapnia
  2564. Hypoxemia
  2565. Figure 26-2 Ventilation-Perfusion ( V./Q.) Abnormalities.
  2566. Quick Check 26-1
  2567. Acute respiratory failure
  2568. Pulmonary edema
  2569. Figure 26-3 Pathogenesis of Pulmonary Edema.
  2570. Aspiration
  2571. Atelectasis
  2572. Figure 26-4 Pores of Kohn.A, Absorption atelectasis caused by lack of collateral ventilation through pores of Kohn. B, Restoration of collateral ventilation during deep breathing.
  2573. Bronchiectasis
  2574. Bronchiolitis
  2575. Pleural abnormalities
  2576. Pneumothorax
  2577. Figure 26-5 Pneumothorax. Air in the pleural space causes the lung to collapse around the hilus and may push mediastinal contents (heart and great vessels) toward the other lung.
  2578. Pleural effusion
  2579. Table 26-1 Mechanism of Pleural Effusion
  2580. Empyema
  2581. Chest wall restriction
  2582. Flail chest
  2583. Figure 26-6 Flail Chest. Normal respiration: A, inspiration; B, expiration. Paradoxical motion: C, inspiration, area of lung underlying unstable chest wall sucks in on inspiration; D, expiration, unstable area balloons out. Note movement of mediastinum toward opposite lung during inspiration.
  2584. Quick Check 26-2
  2585. Pulmonary Disorders
  2586. Restrictive Lung Diseases
  2587. Pulmonary fibrosis
  2588. Inhalation disorders
  2589. Exposure to toxic gases
  2590. Pneumoconiosis
  2591. Allergic alveolitis
  2592. Acute respiratory distress syndrome
  2593. Pathophysiology
  2594. Figure 26-7 Proposed Mechanisms for the Pathogenesis of Acute Respiratory Distress Syndrome (ARDS). IL-1-β, Interleukin-1-β; TNF, tumor necrosis factor; ROS, reactive oxygen species; TGF-β, transforming growth factor-β; PDGF, platelet derived growth factor. From Soubani AO, Pieroni R: Acute respiratory distress syndrome: a clinical update, South Med J 92[5]:452, 1999.
  2595. Clinical Manifestations
  2596. Evaluation and Treatment
  2597. Quick Check 26-3
  2598. Obstructive Lung Diseases
  2599. Asthma
  2600. Pathophysiology
  2601. Figure 26-8 Airway Obstruction Caused by Emphysema, Chronic Bronchitis, and Asthma.A, The normal lung. B, Emphysema: enlargement and destruction of alveolar walls with loss of elasticity and trapping of air; (left) panlobular emphysema showing abnormal weakening and enlargement of all air spaces distal to the terminal bronchioles (normal alveoli shown for comparison only); (right) centrilobular emphysema showing abnormal weakening and enlargement of the respiratory bronchioles in the proximal portion of the acinus. C, Chronic bronchitis: inflammation and thickening of mucous membrane with accumulation of mucus and pus leading to obstruction; characterized by cough.D, Bronchial asthma: thick mucus, mucosal edema, and smooth muscle spasm causing obstruction of small airways; breathing becomes labored, and expiration is difficult. Modified from Des Jardins T, Burton GG: Clinical manifestations and assessment of respiratory disease, ed 5, St Louis, 2006, Mosby.
  2602. Clinical Manifestations
  2603. Figure 26-9 Pathophysiology of Asthma. Allergen or irritant exposure results in a cascade of inflammatory events leading to acute and chronic airway dysfunction.
  2604. Evaluation and Treatment
  2605. Chronic obstructive pulmonary disease
  2606. Health Alert Monoclonal Antibodies to IgE for Treatment of Asthma
  2607. Chronic bronchitis
  2608. Pathophysiology
  2609. Clinical Manifestations
  2610. Evaluation and Treatment
  2611. Table 26-2 Clinical Manifestations of Chronic Obstructive Lung Disease
  2612. Figure 26-10 Pathogenesis of Chronic Bronchitis and Emphysema (Chronic Obstructive Pulmonary Disease [COPD]).
  2613. Health Alert Nutrition and Chronic Obstructive Pulmonary Disease
  2614. Figure 26-11 Mechanisms of Air Trapping in COPD. Mucus plugs and narrowed airways cause air trapping and hyperinflation on expiration. During inspiration, the airways are pulled open allowing gas to flow past the obstruction. During expiration, decreased elastic recoil of the bronchial walls results in collapse of the airways and prevents normal expiratory airflow.
  2615. Emphysema
  2616. Pathophysiology
  2617. Clinical Manifestations
  2618. Evaluation and Treatment
  2619. Figure 26-12 Types of Emphysema.A, Centriacinar emphysema. B, Panacinar emphysema. Micrographs from Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  2620. Quick Check 26-4
  2621. Respiratory Tract Infections
  2622. Pneumonia
  2623. Pathophysiology
  2624. Pneumococcal pneumonia
  2625. Viral pneumonia
  2626. Health Alert Avian Influenza
  2627. Clinical Manifestations
  2628. Figure 26-13 Pathophysiologic Course of Pneumococcal Pneumonia.
  2629. Evaluation and Treatment
  2630. Tuberculosis
  2631. Health Alert Multidrug Resistant Tuberculosis in HIV Infection
  2632. Pathophysiology
  2633. Clinical Manifestations
  2634. Evaluation and Treatment
  2635. Acute bronchitis
  2636. Abscess formation and cavitation
  2637. Quick Check 26-5
  2638. Pulmonary Vascular Disease
  2639. Pulmonary embolism
  2640. Pathophysiology
  2641. Clinical Manifestations
  2642. Figure 26-14 Pathogenesis of Massive Pulmonary Embolism Caused by a Thrombus (Pulmonary Thromboembolism).
  2643. Evaluation and Treatment
  2644. Pulmonary hypertension
  2645. Pathophysiology
  2646. Clinical Manifestations
  2647. Figure 26-15 Pathogenesis of Pulmonary Hypertension and Cor Pulmonale.
  2648. Evaluation and Treatment
  2649. Cor pulmonale
  2650. Pathophysiology
  2651. Clinical Manifestations
  2652. Evaluation and Treatment
  2653. Quick Check 26-6
  2654. Respiratory Tract Malignancies
  2655. Lip cancer
  2656. Pathophysiology
  2657. Clinical Manifestations
  2658. Figure 26-16 Lip Cancer. Carcinoma of lower lip with central ulceration and raised, rolled borders. From del Regato JA, Spjut HJ, Cox JD: Ackerman and del Regato’s cancer, ed 2, St Louis, 1985, Mosby.
  2659. Evaluation and Treatment
  2660. Laryngeal cancer
  2661. Pathophysiology
  2662. Clinical Manifestations
  2663. Box 26-1 Staging of Lip Cancer
  2664. Stage I
  2665. Stage II
  2666. Stage III
  2667. Stage IV
  2668. Figure 26-17 Laryngeal Cancer.A, Mirror view of carcinoma of the right false cord partially hiding the true cord. B, Lateral view. Redrawn from del Regato JA, Spjut HJ, Cox JD: Ackerman and del Regato’s cancer, ed 2, St Louis, 1985, Mosby.
  2669. Evaluation and Treatment
  2670. Lung cancer
  2671. Types of lung cancer
  2672. Non–small cell lung cancer
  2673. Table 26-3 Characteristics of Lung Cancers
  2674. Figure 26-18 Lung Cancer.A, Squamous cell carcinoma. This hilar tumor originates from the main bronchus. B, Peripheral adenocarcinoma. The tumor shows prominent black pigmentation, suggestive of having evolved in an anthracotic scar. C, Small cell carcinoma. The tumor forms confluent nodules. On cross section, the nodules have an encephaloid appearance. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  2675. Small cell lung cancer
  2676. Pathophysiology
  2677. Clinical Manifestations
  2678. Evaluation AND Treatment
  2679. Health Alert Genetic and Immunologic Breakthroughs in Lung Cancer Treatment
  2680. Quick Check 26-7
  2681. Did You Understand?
  2682. Clinical Manifestations of Pulmonary Alterations
  2683. Pulmonary Disorders
  2684. Key Terms
  2685. References
  2686. Chapter 27 Alterations of Pulmonary Function in Children
  2687. Electronic Resources
  2688. Companion CD
  2689. Website http://evolve.elsevier.com/Huether/
  2690. Pulmonary Disorders
  2691. Disorders of the Upper Airways
  2692. Croup
  2693. Pathophysiology
  2694. Clinical Manifestations
  2695. Evaluation and Treatment
  2696. Table 27-1 Comparison of Upper Airway Infections
  2697. Figure 27-1 Upper Airway Obstruction With Croup.
  2698. Acute epiglottitis
  2699. Figure 27-2 Listening Can Help Locate the Site of Airway Obstruction. A loud, gasping snore suggests enlarged tonsils or adenoids. In inspiratory stridor, the airway is compromised at the level of the supraglottic larynx, vocal cords, subglottic region, or upper trachea. Expiratory stridor results from a narrowing or collapse in the trachea or bronchi. Airway noise during both inspiration and expiration often represents a fixed obstruction of the vocal cords or subglottic space. Hoarseness or a weak cry is a by-product of obstruction at the vocal cords. If a cough is croupy, suspect constriction below the vocal cords Redrawn from Eavey RD: Contemp Ped 3(6):79, 1986; original illustration by Paul Singh-Roy.
  2700. Figure 27-3 The Larynx and Subglottic Trachea.A, Normal. B, Narrowing and obstruction from edema caused by croup. From Hockenberry MJ et al: Wong’s nursing care of infants and children, ed 8, St Louis, 2007, Mosby.
  2701. Figure 27-4 Areas of Chest Muscle Retraction.
  2702. Clinical Manifestations
  2703. Evaluation and Treatment
  2704. Aspiration of foreign bodies
  2705. Obstructive sleep apnea
  2706. Pathophysiology
  2707. Clinical Manifestations
  2708. Evaluation and Treatment
  2709. Quick Check 27-1
  2710. Disorders of the Lower Airways
  2711. Respiratory distress syndrome of the newborn
  2712. Risk Factors Respiratory Distress Syndrome of the Newborn
  2713. Pathophysiology
  2714. Clinical Manifestations
  2715. Evaluation and Treatment
  2716. Figure 27-5 Pathogenesis of Respiratory Distress Syndrome (RDS) of the Newborn.
  2717. Bronchopulmonary dysplasia
  2718. Risk Factors Bronchopulmonary Dysplasia (BPD)
  2719. Pathophysiology
  2720. Clinical Manifestations
  2721. Evaluation and Treatment
  2722. Quick Check 27-2
  2723. Respiratory infections
  2724. Bronchiolitis
  2725. Pathophysiology
  2726. Figure 27-6 Pathophysiology of Bronchopulmonary Dysplasia (BPD).
  2727. Clinical Manifestations
  2728. Evaluation and Treatment
  2729. Pneumonia
  2730. Table 27-2 Common Types of Pneumonia in Children
  2731. Evaluation and Treatment
  2732. Quick Check 27-3
  2733. Aspiration pneumonitis
  2734. Bronchiolitis obliterans
  2735. Asthma
  2736. Health Alert Asthma Genes and Tailored Therapies
  2737. Pathophysiology
  2738. Clinical Manifestations
  2739. Figure 27-7 Asthmatic Responses.A, In the early asthmatic response, inhaled antigen (1) binds to preformed IgE on mast cells. Mast cells degranulate (2) and release mediators such as histamine, leukotrienes, prostaglandin D2, platelet activating factor, and others. Acute inflammation opens intercellular tight junctions, allowing allergen to penetrate and activate submucosal mast cells. Secreted mediators (3) induce active bronchospasm, edema, and mucus secretion. Inflammatory responses are set in motion by chemotactic factors and up-regulation of adhesion molecules (not shown). At the same time, as shown on the left, antigen may be received by dendritic cells and later present it, either in regional lymph nodes to naïve (Tho) T-lymphocytes or locally to memory Th2 cells in the airway mucosa (see B). B, In the late asthmatic response, there are areas of epithelial damage caused at least in part by toxicity of eosinophil products (major basic protein, eosinophilic cationic protein, eosinophil-derived neurotoxin, and eosinophil peroxidase). Many inflammatory cells are recruited by chemokines and up-regulation of vascular cell adhesion molecules. Local T-lymphocytes display a predominant Th2 cytokine profile. They produce IL-4 and IL-13, which promote switching of B cells to favor IgE production, and IL-3, IL-5, and granulocyte-macrophage colony-stimulating factor, which encourage eosinophil differentiation and survival.
  2740. Evaluation and Treatment
  2741. Quick Check 27-4
  2742. Acute respiratory distress syndrome
  2743. Pathophysiology
  2744. Clinical Manifestations
  2745. Evaluation and Treatment
  2746. Cystic fibrosis
  2747. Pathophysiology
  2748. Figure 27-8 Pathology of the Lung in End-Stage Cystic Fibrosis. Key features are widespread mucus impaction of airways and bronchiectasis (especially from upper lobe [U]), with hemorrhagic pneumonia in the lower lobe (L). Small cysts (C) are present at the apex of the lung. From Kleinerman J, Vauthy P: Pathology of the lung in cystic fibrosis, Atlanta, 1976, Cystic Fibrosis Foundation.
  2749. Figure 27-9 Pathogenesis of Cystic Fibrosis Lung Disease.CFTR, Cystic fibrosis transmembrane conductance regulator.
  2750. Clinical Manifestations
  2751. Health Alert Newborn Screening for Cystic Fibrosis
  2752. Evaluation and Treatment
  2753. Health Alert A Cure for Cystic Fibrosis?
  2754. Sudden Infant Death Syndrome
  2755. Risk Factors Sudden Infant Death Syndrome (SIDS)
  2756. Quick Check 27-5
  2757. Did You Understand?
  2758. Pulmonary Disorders in Children
  2759. Sudden Infant Death Syndrome (SIDS)
  2760. Key Terms
  2761. References
  2762. Further Reading
  2763. Unit 9 The Renal and Urologic Systems
  2764. Chapter 28 Structure and Function of the Renal and Urologic Systems
  2765. Electronic Resources
  2766. Companion CD
  2767. Website http://evolve.elsevier.com/Huether/
  2768. Structures of the Renal System
  2769. Structures of the Kidney
  2770. Nephron
  2771. Figure 28-1 Organs of the Urinary System. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2772. Figure 28-2 Kidney Structure. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2773. Figure 28-3 Components of Nephron. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2774. Blood vessels of the kidney
  2775. Figure 28-4 Epithelial Cells of the Various Segments of Nephron Tubules. The brush border and high number of mitochondria in cells of the proximal tubule promote reabsorption of 50% of the glomerular filtrate. Intercalated cells (blue type) secrete either H+ (resorb) HCO3− or HCO3− and reabsorb K+. Principal cells (magenta type) reabsorb Na+ and water and secrete K+.
  2776. Quick Check 28-1
  2777. Urinary Structures
  2778. Ureters
  2779. Bladder and urethra
  2780. Figure 28-5 The Nephron Unit With Its Blood Vessels. Blood flows through nephron vessels as follows: interlobular artery, afferent arteriole, glomerulus, efferent arteriole, peritubular capillaries (around the tubules), venules, interlobular vein. The vasa recta capillaries distribute along the long loops of Henle of the juxtamedullary nephrons. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2781. Figure 28-6 Anatomy of the Glomerulus and Juxtaglomerular Apparatus.A, Longitudinal cross section of glomerulus and juxtaglomerular apparatus. B, Horizontal cross section of glomerulus. C, Enlargement of glomerular capillary filtration membrane.
  2782. Figure 28-7 Structure of the Urinary Bladder. Frontal view of a dissected urinary bladder (male) in a fully distended position. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2783. Renal Blood Flow
  2784. Autoregulation of Intrarenal Blood Flow
  2785. Figure 28-8 Renal Autoregulation. Blood flow and glomerular filtration rate are stabilized in the face of changes in perfusion pressure. From Levy MN, editors: Berne & Levy Principles of physiology, ed 4, Philadelphia, 2006, Mosby.
  2786. Neural Regulation of Renal Blood Flow
  2787. Hormonal Regulation of Renal Blood Flow
  2788. Figure 28-9 Cooperative Roles of Antidiuretic Hormone (ADH) and Aldosterone in Regulating Urine and Plasma Volume. The drop in blood pressure that accompanies loss of fluid from the internal environment triggers the hypothalamus to rapidly release ADH from the posterior pituitary gland. ADH increases water reabsorption by the kidney by increasing water permeability of the distal tubules and collecting ducts. The drop in blood pressure is also detected by each nephron’s juxtaglomerular apparatus, which responds by secreting renin. Renin triggers the formation of angiotensin II, which stimulates release of aldosterone from the adrenal cortex. Aldosterone then slowly boosts water reabsorption by the kidneys by increasing reabsorption of Na+. Because angiotensin II also stimulates secretion of ADH, it serves as an additional link between the ADH and aldosterone mechanisms. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  2789. Quick Check 28-2
  2790. Kidney Function
  2791. Nephron Function
  2792. Glomerular filtration
  2793. Figure 28-10 Major Functions of Nephron Segments.ADH, Antidiuretic hormone. Modified from Hockenberry MJ et al: Wong’s nursing care of infants and children, ed 8, St Louis, 2007, Mosby.
  2794. Figure 28-11 Glomerular Filtration Pressures.
  2795. Table 28-1 Glomerular Filtration Pressures
  2796. Filtration rate
  2797. Tubular transport
  2798. Proximal tubule
  2799. Glomerulotubular balance
  2800. Loop of Henle and distal tubule
  2801. Box 28-1 Substances Transported by Renal Tubules
  2802. Figure 28-12 Countercurrent Mechanism for Concentrating and Diluting Urine. (note: Numbers on illustration represent milliosmoles [mOsm].)
  2803. Acidification of urine
  2804. Figure 28-13 Acidification of Urine by Tubule Excretion of Ammonia (NH3).A, Acidification of urine and conservation of base by distal renal tubule excretion of H+. B, An amino acid (glutamine) moves into tubule cell and forms ammonia (NH3) which is secreted into the urine. To combine with H+ to form ammonia (NH4+) and an ammonium salt (NH4Cl). From Thibodeau, GA, Patton KT: Anatomy & physiology, ed 4, St Louis, 1999, Mosby.
  2805. Urine
  2806. Health Alert Cranberry Juice and Urinary Tract Infection
  2807. Hormones and Nephron Function
  2808. Antidiuretic hormone
  2809. Aldosterone
  2810. Atrial natriuretic peptide
  2811. Table 28-2 Action of Diuretics
  2812. Diuretics as a factor in urine flow
  2813. Renal Hormones
  2814. Urodilatin
  2815. Vitamin D
  2816. Erythropoietin
  2817. Quick Check 28-3
  2818. The Concept of Clearance
  2819. Clearance and glomerular filtration rate
  2820. Plasma creatinine concentration
  2821. Blood urea nitrogen
  2822. Table 28-3 Normal Renal Function Tests
  2823. Table 28-4 Bladder Function Tests
  2824. Pediatrics & Renal Function
  2825. Quick Check 28-4
  2826. Aging & Renal Function
  2827. Did You Understand?
  2828. Structures of the Renal System
  2829. Renal Blood Flow
  2830. Kidney Function
  2831. PEDIATRICS & Renal Function
  2832. AGING & Renal Function
  2833. Key Terms
  2834. References
  2835. Chapter 29 Alterations of Renal and Urinary Tract Function
  2836. Electronic Resources
  2837. Companion CD
  2838. Website http://evolve.elsevier.com/Huether/
  2839. Urinary Tract Obstruction
  2840. Upper Urinary Tract Obstruction
  2841. Figure 29-1 Major Sites of Urinary Tract Obstruction.
  2842. Figure 29-2 Hydronephrosis. Hydronephrosis with renal stones in renal pelvis and calyces. From Kissane JM, editor: Anderson’s pathology, ed 9, St Louis, 1990, Mosby.
  2843. Kidney stones
  2844. Pathophysiology
  2845. Clinical Manifestations
  2846. Evaluation and Treatment
  2847. Lower Urinary Tract Obstruction
  2848. Table 29-1 Types of Incontinence
  2849. Table 29-2 Neurogenic Bladder
  2850. Neurogenic bladder
  2851. Overactive bladder syndrome
  2852. Obstructions to urine flow
  2853. Evaluation and Treatment
  2854. Figure 29-3 Neurogenic Detrusor Overactivity With Vesico-Sphincter. The arrow indicates narrowing of the striated sphincter consistent with electromyographic activity (line 6) noted on the urodynamic tracing. Note the characteristic poor flow pattern (line 1) with elevated voiding pressures (lines 4 and 5) indicating obstruction. Line 1, Urine flow rate; line 2, urine volume; line 3, abdominal pressure (Pabd); line 4, intravesicular (inside bladder) pressure (Pues); line 5, detrusor muscle pressure (Pdet); line 6, bladder electromyelogram (EMG).
  2855. Tumors
  2856. Renal tumors
  2857. Pathogenesis
  2858. Clinical Manifestations
  2859. Figure 29-4 Renal Cell Carcinoma. Renal cell carcinomas usually are spheroidal masses composed of yellow tissue mottled with hemorrhage, necrosis, and fibrosis. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  2860. Evaluation and Treatment
  2861. Bladder tumors
  2862. Table 29-3 Staging of Renal Cell Carcinoma
  2863. Pathogenesis
  2864. Clinical Manifestations
  2865. Evaluation and Treatment
  2866. Table 29-4 Staging of Bladder Carcinoma (TNM* System)
  2867. Quick Check 29-1
  2868. Urinary Tract Infection
  2869. Causes of Urinary Tract Infection
  2870. Types of Urinary Tract Infection
  2871. Acute cystitis
  2872. Pathophysiology
  2873. Clinical Manifestations
  2874. Evaluation and Treatment
  2875. Health Alert Urinary Tract Infection and Antibiotic Resistance
  2876. Painful bladder syndrome/interstitial cystitis
  2877. Acute pyelonephritis
  2878. Pathophysiology
  2879. Table 29-5 Common Causes of Pyelonephritis
  2880. Clinical Manifestations
  2881. Evaluation and Treatment
  2882. Figure 29-5 Pyelonephritis.Right: Small, shrunken, irregularly scarred kidney of an individual with chronic pyelonephritis. Left: Kidney is of normal size but also shows scarring on the upper pole. From Damjanov I: Pathology for the health professions, ed 3, St Louis, 2006, Saunders.
  2883. Chronic pyelonephritis
  2884. Pathophysiology
  2885. Clinical Manifestations
  2886. Evaluation and Treatment
  2887. Quick Check 29-2
  2888. Glomerular Disorders
  2889. Glomerulonephritis
  2890. Types of glomerulonephritis
  2891. Table 29-6 Types of Glomerular Lesions
  2892. Table 29-7 Features of the Common Types of Glomerulonephritis
  2893. Acute glomerulonephritis
  2894. Rapidly progressive glomerulonephritis
  2895. Chronic glomerulonephritis
  2896. Pathophysiology
  2897. Figure 29-6 Chronic Glomerulonephritis. The kidneys appear small, are uniformly shrunken, and have a finely granular external surface From Damjanov I: Pathology for the health professions, ed 3, St Louis, 2006, Saunders.
  2898. Clinical Manifestations
  2899. Evaluation and Treatment
  2900. Table 29-8 Immunologic Pathogenesis of Glomerulonephritis
  2901. Nephrotic Syndrome
  2902. Pathophysiology
  2903. Clinical Manifestations
  2904. Evaluation and Treatment
  2905. Table 29-9 Clinical Manifestations of Nephrotic Syndrome
  2906. Quick Check 29-3
  2907. Renal Failure
  2908. Types of Renal Failure
  2909. Acute renal failure
  2910. Table 29-10 Classification of Acute Renal Failure
  2911. Pathophysiology
  2912. Clinical Manifestations
  2913. Figure 29-7 Mechanisms of Oliguria in Acute Renal Failure.GFR, Glomerular filtration rate.
  2914. Evaluation and Treatment
  2915. Table 29-11 Differentiation of Acute Oliguric Renal Failure
  2916. Chronic renal failure
  2917. Stages of chronic renal failure
  2918. Pathophysiology
  2919. Clinical Manifestations
  2920. Creatinine and urea clearance
  2921. Table 29-12 Systemic Effects of Uremia
  2922. Table 29-13 Stages of Chronic Kidney Disease
  2923. Table 29-14 Factors Representing Progression of Chronic Renal Failure
  2924. Fluid and electrolyte balance
  2925. Figure 29-8 Mechanisms Related to the Progression of Chronic Renal Failure.
  2926. Musculoskeletal system
  2927. Protein, carbohydrate, and fat metabolism
  2928. Cardiovascular system
  2929. Pulmonary system
  2930. Hematologic system
  2931. Immune system
  2932. Neurologic system
  2933. Gastrointestinal system
  2934. Endocrine and reproductive systems
  2935. Integumentary system
  2936. Evaluation and Treatment
  2937. Quick Check 29-4
  2938. Did You Understand?
  2939. Urinary Tract Obstruction
  2940. Urinary Tract Infection
  2941. Glomerular Disorders
  2942. Renal Failure
  2943. Key Terms
  2944. References
  2945. Chapter 30 Alterations of Renal and Urinary Tract Function in Children
  2946. Electronic Resources
  2947. Companion CD
  2948. Website http://evolve.elsevier.com/Huether/
  2949. Structural Abnormalities
  2950. Hypospadias
  2951. Figure 30-1 Hypospadias. Courtesy H. Gil Rushton, MD, Children’s National Medical Center, Washington, DC; from Hockenberry MJ, Wilson D: Wong’s nursing care of infants and children, ed 8, St Louis, 2007, Mosby.
  2952. Figure 30-2 Hypospadias with Significant Chordee. From Shirkey HC, editor: Pediatric therapy, ed 6, St Louis, 1980, Mosby.
  2953. Epispadias and Exstrophy of the Bladder
  2954. Figure 30-3 Exstrophy of Bladder. Courtesy H. Gil Rushton, MD, Children’s National Medical Center, Washington, DC; from Hockenberry MJ, Wilson D: Wong’s nursing care of infants and children, ed 8, St Louis, 2007, Mosby.
  2955. Bladder Outlet Obstruction
  2956. Ureteropelvic Junction Obstruction
  2957. Hypoplastic/Dysplastic Kidneys
  2958. Polycystic Kidneys
  2959. Renal Agenesis
  2960. Quick Check 30-1
  2961. Glomerular Disorders
  2962. Glomerulonephritis
  2963. Poststreptococcal glomerulonephritis
  2964. Box 30-1 Primary Glomerulonephritis in Children
  2965. Cause
  2966. Immunologic Mechanism
  2967. Glomerular Histopathology
  2968. Manifestations of Glomerulonephritis
  2969. Immunoglobulin A Nephropathy
  2970. Nephrotic Syndrome
  2971. Pathophysiology
  2972. Clinical Manifestations
  2973. Evaluation and Treatment
  2974. Hemolytic Uremic Syndrome
  2975. Pathophysiology
  2976. Clinical Manifestations
  2977. Evaluation and Treatment
  2978. Other Renal Disorders
  2979. Bladder Disorders
  2980. Urinary Tract Infections
  2981. Figure 30-4 Normal and Abnormal Configuration of the Ureterovesical Junction. Shown from left to right, progressive lateral displacement of the ureteral orifices and shortening of the intramural tunnels. (Top) Endoscopic appearance. (Bottom) Sagittal view through the intramural ureter. From Behrman R et al, editors: Nelson textbook of pediatrics, ed 16, Philadelphia, 2000, Saunders.
  2982. Health Alert Childhood Urinary Tract Infections
  2983. Vesicoureteral Reflux
  2984. Pathophysiology
  2985. Clinical Manifestations
  2986. Figure 30-5 Grades of Visicoureteral Reflux.
  2987. Evaluation and Treatment
  2988. Quick Check 30-2
  2989. Nephroblastoma
  2990. Pathogenesis
  2991. Clinical Manifestations
  2992. Evaluation and Treatment
  2993. Enuresis
  2994. Table 30-1 Staging of Nephroblastoma Tumor*
  2995. Types of Enuresis
  2996. Pathogenesis
  2997. Table 30-2 Classification of Incontinence
  2998. Quick Check 30-3
  2999. Did You Understand?
  3000. Structural Abnormalities
  3001. Glomerular Disorders
  3002. Obstructive Disorders
  3003. Nephroblastoma
  3004. Enuresis
  3005. Key Terms
  3006. References
  3007. Unit 10 The Reproductive Systems
  3008. Chapter 31 Structure and Function of the Reproductive Systems
  3009. Electronic Resources
  3010. Companion CD
  3011. Website http://evolve.elsevier.com/Huether/
  3012. Development of the Reproductive Systems
  3013. Sexual Differentiation in Utero
  3014. Figure 31-1 Internal Genitalia Development. Embryonic and fetal development of the internal genitalia.
  3015. Puberty
  3016. Figure 31-2 External Genitalia Development. Embryonic and fetal development of the external genitalia.
  3017. Figure 31-3 Hormonal Stimulation of the Gonads. The hypothalamic-pituitary-gonadal axis.
  3018. Quick Check 31-1
  3019. The Female Reproductive System
  3020. External Genitalia
  3021. Figure 31-4 External Female Genitalia.
  3022. Internal Genitalia
  3023. Vagina
  3024. Figure 31-5 Internal Female Genitalia and Other Pelvic Organs. From Seidel HM et al: Mosby’s guide to physical examination, ed 6, St Louis, 2006, Mosby.
  3025. Uterus
  3026. Figure 31-6 Uterine Positions.
  3027. Figure 31-7 Cross Section of Uterus, Fallopian Tube, and Ovary. From Seidel HM et al: Mosby’s guide to physical examination, ed 6, St Louis, 2006, Mosby.
  3028. Quick Check 31-2
  3029. Fallopian tubes
  3030. Ovaries
  3031. Figure 31-8 Cross Section of Ovary During Reproductive Years. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3032. Female Sex Hormones
  3033. Estrogens
  3034. Figure 31-9 Development of an Ovarian Follicle. Schematic representation (not to scale) of the structure of the ovary, showing the various stages in the development of the follicle and its successor structure, the corpus luteum. Adapted from Berne RM, Levy MN, editors: Physiology, ed 5, St Louis, 2003, Mosby.
  3035. Progesterone
  3036. Androgens
  3037. Table 31-1 Complementary and Opposing Effects of Estrogen and Progesterone
  3038. Quick Check 31-3
  3039. Menstrual Cycle
  3040. Phases of the menstrual cycle
  3041. Figure 31-10 The Menstrual Cycle. From Lowdermilk DL, Perry SE, Bobak IM: Maternity and women’s health care, ed 8, St Louis, 2004, Mosby.
  3042. Hormonal controls
  3043. Table 31-2 Hormonal Feedback Mechanism in the Menstrual Cycle
  3044. Figure 31-11 Estrogen, Progesterone, Gonadotropin, and Inhibin Fluctuations Over the Menstrual Cycle. Inhibin rises slowly but steadily throughout the follicular phase, peaking at midcycle and again during the midluteal phase. The midcycle peak coincides with surges of luteinizing hormone (LH) and follicle-stimulating hormone (FSH).
  3045. Ovarian cycle
  3046. Uterine phases
  3047. Vaginal response
  3048. Body temperature
  3049. Quick Check 31-4
  3050. The Male Reproductive System
  3051. External Genitalia
  3052. Testes
  3053. Figure 31-12 Structure of the Male Reproductive Organs. From Seidel HM et al: Mosby’s guide to physical examination, ed 6, St Louis, 2006, Mosby.
  3054. Epididymis
  3055. Figure 31-13 Descent of a Testis. The testes descend from the abdominal cavity to the scrotum during the last 3 months of fetal development.
  3056. Scrotum
  3057. Penis
  3058. Figure 31-14 The Testes. External and sagittal views showing interior anatomy. Redrawn from Seidel HM et al: Mosby’s guide to physical examination, ed 5, St Louis, 2003, Mosby.
  3059. Figure 31-15 Cross Section of the Penis. From Thompson JM et al, editors: Mosby’s clinical nursing, ed 5, St Louis, 2002, Mosby.
  3060. Internal Genitalia
  3061. Figure 31-16 Anatomy of the Prostate Gland and Seminal Vesicles. From Seidel HM et al: Mosby’s guide to physical examination, ed 6, St Louis, 2006, Mosby.
  3062. Health Alert Lycopene and Prostate Cancer
  3063. Spermatogenesis
  3064. Figure 31-17 Seminiferous Tubule. Section shows process of meiosis and sperm cell formation. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3065. Figure 31-18 Mature Sperm Cell (Spermatozoon). Anatomy of mature sperm cell.
  3066. Male Sex Hormones
  3067. Quick Check 31-5
  3068. Structure and Function of the Breast
  3069. Female Breast
  3070. Figure 31-19 The Female Breast. From Seidel HM et al: Mosby’s guide to physical examination, ed 6, St Louis, 2006, Mosby.
  3071. Figure 31-20 Lymphatic Drainage of the Female Breast. From Seidel HM et al: Mosby’s guide to physical examination, ed 6, St Louis, 2006, Mosby.
  3072. Male Breast
  3073. AGING & Reproductive Function
  3074. Aging and the Female Reproductive System
  3075. Figure 31-21 The Perimenopausal Transition. Mean circulating hormone levels. From Speroff L et al: Clinical gynecologic endocrinology and infertility, ed 7, Baltimore, 2005, Lippincott.
  3076. Aging and the Male Reproductive System
  3077. Quick Check 31-6
  3078. Did You Understand?
  3079. Development of the Reproductive Systems
  3080. The Female Reproductive System
  3081. The Male Reproductive System
  3082. Structure and Function of the Breast
  3083. Key Terms
  3084. References
  3085. Chapter 32 Alterations of the Reproductive Systems, Including Sexually Transmitted Infections
  3086. Electronic Resources
  3087. Companion CD
  3088. Website http://evolve.elsevier.com/Huether/
  3089. Alterations of Sexual Maturation
  3090. Delayed Puberty
  3091. Box 32-1 Causes of Delayed Puberty
  3092. Hypergonadotropic Hypogonadism (Increased Follicle-Stimulating Hormone [FSH] and Luteinizing Hormone [LH])
  3093. Hypogonadotropic Hypogonadism (Decreased LH, Depressed FSH)
  3094. Eugonadism
  3095. Precocious Puberty
  3096. Box 32-2 The Three Forms of Precocious Puberty
  3097. Isosexual Precocious Puberty
  3098. Heterosexual Precocious Puberty
  3099. Incomplete Precocious Puberty
  3100. Quick Check 32-1
  3101. Disorders of the Female Reproductive System
  3102. Hormonal and Menstrual Alterations
  3103. Dysmenorrhea
  3104. Pathophysiology
  3105. Clinical Manifestations
  3106. Evaluation and Treatment
  3107. Primary amenorrhea
  3108. Pathophysiology
  3109. Clinical Manifestations
  3110. Evaluation and Treatment
  3111. Secondary amenorrhea
  3112. Figure 32-1 Causes of Secondary Amenorrhea.
  3113. Pathophysiology
  3114. Clinical Manifestations
  3115. Evaluation and Treatment
  3116. Abnormal uterine bleeding
  3117. Pathophysiology
  3118. Table 32-1 Definitions of Abnormal Menstrual Bleeding
  3119. Table 32-2 Common Causes of Abnormal (Vaginal/Genital) Bleeding in Descending Order of Frequency
  3120. Clinical Manifestations
  3121. Evaluation and Treatment
  3122. Polycystic ovary syndrome
  3123. Pathophysiology
  3124. Figure 32-2 Polycystic Ovary. Both ovaries shown are enlarged with multiple cysts. From Symonds EM, Macpherson, MBA: Diagnosis in color: obstetrics and gynecology, London, 1997, Mosby.
  3125. Clinical Manifestations
  3126. Figure 32-3 Insulin Resistance and Hyperinsulinemia in PCOS. See text for explanation. SHBG, Sex hormone-binding globulin; LH, luteinizing hormone; FSH, follicle-stimulating hormone.
  3127. Evaluation and Treatment
  3128. Premenstrual syndrome
  3129. Pathophysiology
  3130. Clinical Manifestations
  3131. Box 32-3 Clinical Manifestations of Polycystic Ovary Syndrome (PCOS)
  3132. Presenting Signs and Symptoms (Percentage of Women Affected)
  3133. Hormonal Disturbances
  3134. Possible Late Sequelae
  3135. Other
  3136. Box 32-4 General Criteria for Premenstrual Dysphoric Disorder
  3137. Evaluation and Treatment
  3138. Quick Check 32-2
  3139. Infection and Inflammation
  3140. Figure 32-4 Pelvic Inflammatory Disease.A, Drawing depicting involvement of both ovaries and fallopian tubes. B, Total abdominal hysterectomy and bilateral salpingo-oophorectomy specimen showing unilateral pyosalpinx. A from Seidel HM et al: Mosby’s guide to physical examination, ed 6, St Louis, 2006, Mosby; B from Morse SA, Ballard RC, Holmes KK, Moreland AA: Atlas of sexually transmitted diseases and AIDS, ed 3, Edinburgh, 2003, Mosby.
  3141. Pelvic inflammatory disease
  3142. Pathophysiology
  3143. Figure 32-5 Salpingitis.A, Note the swollen fallopian tubes. B, Bilateral, retort-shaped, swollen sealed tubes and adhesions of ovaries are typical of salpingitis. A from Seidel HM et al: Mosby’s guide to physical examination, ed 6, St Louis, 2006, Mosby; B from Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  3144. Clinical Manifestations
  3145. Evaluation and Treatment
  3146. Vaginitis
  3147. Cervicitis
  3148. Vulvitis
  3149. Bartholinitis
  3150. Figure 32-6 Inflammation of Bartholin Glands. From Gardner HL, Kaufman RH: Benign diseases of the vulva and vagina, St Louis, 1969, Mosby.
  3151. Pelvic Relaxation Disorders
  3152. Figure 32-7 Vaginal Prolapse.A, Anatomic positioning involving cystocele. B, Large cystocele. C, Anatomic positioning involving rectocele. D, Rectocele associated with ulceration of vaginal wall. A and C from Seidel HM et al: Mosby’s guide to physical examination, ed 4, St Louis, 1999, Mosby; B and D from Symonds EM, Macpherson MBA: Color atlas of obstetrics and gynecology, London, 1994, Mosby.
  3153. Table 32-3 Cystocele, Urethrocele, and Rectocele
  3154. Figure 32-8 Degrees of Uterine Prolapse.A, Normal positioning of uterus. B, First-degree prolapse: descent within the vagina. C, Second-degree prolapse: the cervix protrudes through the introitus. D, Third-degree prolapse: the vagina is completely everted.
  3155. Health Alert Dietary Interventions and Lifestyle Changes for Pelvic Prolapse
  3156. Benign Growths and Proliferative Conditions
  3157. Benign ovarian cysts
  3158. Figure 32-9 Depiction of Ovarian Cyst.
  3159. Quick Check 32-3
  3160. Endometrial polyps
  3161. Leiomyomas
  3162. Figure 32-10 Endometrial Polyp. Polyp is protruding through the cervical os. From Symonds EM, Macpherson MBA: Color atlas of obstetrics and gynecology, London, 1994, Mosby.
  3163. Pathophysiology
  3164. Clinical Manifestations
  3165. Figure 32-11 Leiomyomas. Depiction of uterine section showing whorl-like appearance and locations of leiomyomas, also called uterine fibroids.
  3166. Evaluation and Treatment
  3167. Adenomyosis
  3168. Endometriosis
  3169. Pathophysiology
  3170. Clinical Manifestations
  3171. Box 32-5 Theories of Endometriosis
  3172. Figure 32-12 Pelvic Sites of Endometrial Implantation. Endometrial cells may enter the pelvic cavity during retrograde menstruation.
  3173. Evaluation and Treatment
  3174. Cancer
  3175. Cervical cancer
  3176. Health Alert Vaccine Offers Promise of Cervical Cancer Prevention
  3177. Pathogenesis
  3178. Clinical Manifestations
  3179. Evaluation and Treatment
  3180. Table 32-4 Clinical Staging for Cancer of the Cervix
  3181. Vaginal cancer
  3182. Figure 32-13 Cervical Intraepithelial Neoplasia (CIN).A, Diagram of cervical endothelium showing progressive degrees of CIN. B, Normal multiparous cervix. C, CIN stage 1. Note the white appearance of part of the anterior lip of the cervix associated with neoplastic changes. A from Herbst AL et al: Comprehensive gynecology, ed 2, St Louis, 1992, Mosby; B and C from Symonds EM, Macpherson MBA: Color atlas of obstetrics and gynecology, London, 1994, Mosby.
  3183. Table 32-5 Recommended Treatment Based on Clinical Staging for Cancer of the Cervix
  3184. Vulvar cancer
  3185. Endometrial cancer
  3186. Figure 32-14 Endometrial Cancer. Tumor fills the endometrial cavity. Obvious myometrial invasion is shown. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis. 1996, Mosby.
  3187. Risk Factors Endometrial Cancer
  3188. Ovarian cancer
  3189. Figure 32-15 Ovarian Tumors. Bilateral multicystic ovarian tumors. From Symonds EM, Macpherson MBA: Color atlas of obstetrics and gynecology, London, 1994, Mosby.
  3190. Risk Factors Ovarian Cancer
  3191. Pathogenesis
  3192. Clinical Manifestations
  3193. Evaluation and Treatment
  3194. Figure 32-16 Metastasis of Ovarian Cancer. Pattern of spread for epithelial cancer of the ovary.
  3195. Table 32-6 FIGO* Staging of Carcinoma of the Ovary
  3196. Health Alert Recovery After Cancer Treatment
  3197. Table 32-7 Possible Effects of Chronic Disease on Sexual Functioning in Women
  3198. Sexual Dysfunction
  3199. Impaired Fertility
  3200. Quick Check 32-4
  3201. Disorders of the Male Reproductive System
  3202. Disorders of the Urethra
  3203. Urethritis
  3204. Urethral strictures
  3205. Disorders of the Penis
  3206. Phimosis and paraphimosis
  3207. Figure 32-17 Phimosis and Paraphimosis.A, Phimosis: the foreskin has a narrow opening that is not large enough to permit retraction over the glans. B, Lesions on the prepuce secondary to infection cause swelling, and retraction of foreskin may be impossible. Circumcision is usually required. C, Paraphimosis: the foreskin is retracted over the glans but cannot be reduced to its normal position. Here it has formed a constricting band around the penis. D, Ulcer on the retracted prepuce with edema. A and C from Monahan FD et al: Phipps’ Medical-surgical nursing: health and illness perspectives, ed 8, St Louis, 2007, Mosby; B from Taylor PK: Diagnostic picture tests in sexually transmitted diseases, St Louis, 1995, Mosby; D from Morse SA, Ballard RC, Holmes KK, Moreland AA: Atlas of sexually transmitted diseases and AIDS, ed 3, Edinburgh, 2003, Mosby.
  3208. Peyronie disease
  3209. Figure 32-18 Peyronie Disease. This person complained of pain and deviation of his penis to one side on erection. From Taylor PK: Diagnostic picture tests in sexually transmitted diseases, London, 1995, Mosby.
  3210. Priapism
  3211. Balanitis
  3212. Figure 32-19 Priapism. From Lloyd-Davies RW et al: Color atlas of urology, ed 2, London, 1994, Wolfe Medical.
  3213. Figure 32-20 Balanitis. From Taylor PK: Diagnostic picture tests in sexually transmitted diseases, London, 1995, Mosby.
  3214. Penile cancer
  3215. Box 32-6 Tumor, Node, Metastasis (TNM)* Staging for Penile Cancer
  3216. Quick Check 32-5
  3217. Disorders of the Scrotum, Testis, and Epididymis
  3218. Disorders of the scrotum
  3219. Figure 32-21 Depiction of a Varicocele. Dilation of veins within the spermatic cord. From Seidel HM et al: Mosby’s guide to physical examination, ed 6, St Louis, 2006, Mosby.
  3220. Cryptorchidism
  3221. Figure 32-22 Depiction of a Hydrocele. Accumulation of clear fluid between the visceral (inner) and parietal (outer) layers of the tunica vaginalis.
  3222. Figure 32-23 Spermatocele. Retention cyst of the head of the epididymis or of an aberrant tubule or tubules of the rete testis. The spermatocele lies outside the tunica vaginalis; therefore, on palpation it can be readily distinguished and separated from the testis. From Lloyd-Davies RW et al: Color atlas of urology, ed 2, London, 1994, Wolfe Medical.
  3223. Torsion of the testis
  3224. Figure 32-24 Torsion of the Testis. The testes appear dark red and partially necrotic owing to hemorrhagic infarction. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  3225. Orchitis
  3226. Figure 32-25 Depiction of Orchitis. From Seidel HM et al: Mosby’s guide to physical examination, ed 6, St Louis, 2006, Mosby.
  3227. Cancer of the testis
  3228. Pathophysiology
  3229. Figure 32-26 Testicular Tumor. From 400 Self-assessment picture tests in clinical medicine, London, 1984, Wolfe Medical.
  3230. Risk Factors Cancer of the Testis
  3231. Clinical Manifestations
  3232. Evaluation and Treatment
  3233. Impairment of sperm production and quality
  3234. Epididymitis
  3235. Figure 32-27 Epididymitis Secondary to Gonorrhea or Nongonococcal Urethritis. This infection spread to the testes, and rupture through the scrotal wall is threatened. From Taylor PK: Diagnostic picture tests in sexually transmitted disease, London, 1995, Mosby.
  3236. Pathophysiology
  3237. Clinical Manifestations
  3238. Evaluation and Treatment
  3239. Quick Check 32-6
  3240. Disorders of the Prostate Gland
  3241. Benign prostatic hyperplasia
  3242. Figure 32-28 Benign Prostatic Hyperplasia (BPH).A, Condition becomes a problem as prostatic tissue compresses the urethra. B, Gross appearance of BPH showing transition zone resulting from bulging nodules of varying size. B from Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  3243. Prostatitis
  3244. Bacterial prostatitis
  3245. Nonbacterial prostatitis
  3246. Cancer of the prostate
  3247. Figure 32-29 Selected World Population Age-Standardized (to the World Population) Incidence Rates of Prostate Cancer. ASR, Age-standardized rate. Data from Ferlay J et al: GLOBOCAN 2000: cancer incidence, mortality, and prevalence worldwide, Lyon, 2001, International Agency for Research on Cancer.
  3248. Dietary factors
  3249. Health Alert Nutritional and Chemopreventive Agents for Risk Reduction of Prostate Cancer
  3250. Hormones
  3251. Vasectomy
  3252. Chronic inflammation
  3253. Familial factors
  3254. Pathogenesis
  3255. Box 32-7 Determining the Grade of Prostate Cancer With the Gleason Score
  3256. Figure 32-30 Testosterone and Conversion to Dihydrotestosterone (DHT).
  3257. Clinical Manifestations
  3258. Figure 32-31 Carcinoma of Prostate.A, Schematic of carcinoma of the prostate. B, Carcinoma of the prostate extending into the rectum and urinary bladder. B from Damjanov I, Linder J, editors: Pathology: a color atlas, St Louis, 2000, Mosby.
  3259. Figure 32-32 Distribution of Hematogenous Metastases in Prostate Cancer. Study of 556 individuals with metastatic prostate cancer. Adapted from Budendorf L et al: Metastatic patterns of prostate cancer: an autopsy study of 1,589 patients, Hum Pathol 31:578, 2000.
  3260. Evaluation and Treatment
  3261. Sexual Dysfunction
  3262. Pathophysiology
  3263. Clinical manifestations and treatment
  3264. Quick Check 32-7
  3265. Disorders of the Breast
  3266. Disorders of the Female Breast
  3267. Galactorrhea
  3268. Pathophysiology
  3269. Clinical Manifestations
  3270. Evaluation and Treatment
  3271. Benign breast conditions
  3272. Nonproliferative breast lesions
  3273. Box 32-8 Classification of Breast Biopsy Tissue According to Risk for Breast Cancer
  3274. No Increased Risk
  3275. Slightly Increased Risk (One and One-Half to Two Times)
  3276. Moderately Increased Risk (Three to Five Times)
  3277. Proliferative breast lesions without atypia
  3278. Table 32-8 Examples of Benign Breast Disorders
  3279. Proliferative breast lesions with atypia
  3280. Breast cancer
  3281. Figure 32-33 Age-Specific Incidence Rates of Breast Cancer Among Women. Data from Ferlay J et al: GLOBOCAN 2000: cancer incidence, mortality, and prevalence worldwide, Lyon, 2001, International Agency for Research on Cancer.
  3282. Reproductive factors
  3283. Table 32-9 Factors Associated With Increased Risk of Breast Cancer*
  3284. Hormonal factors
  3285. Figure 32-34 Local Biosynthesis of Estrogens. Three main enzyme complexes (yellow) involved in estrogen formation in breast tissue, including aromatase, sulfatase, and 17β-estradiol hydroxysteroid dehydrogenase (HSD). Thus, despite low levels of circulating estrogens in postmenopausal women with breast cancer, the tissue levels are several-fold higher than these in plasma, suggesting tumor accumulation of these estrogens. Data suggest that most abundant is sulfatase in both premenopausal and postmenopausal women with breast cancer. Numerous agents can block the aromatase action, exploration of progesterone, and various progestins to inhibit sulfatase and 17β-HSD or stimulate sulfotransferase (i.e., breast cancer cells cannot inactivate estrogens because they lack sulfotransferase) may provide new possibilities for treatment. LOH, Loss of heterozygosity (see Chapter 9). Adapted from Russo J, Russo I: Molecular basis of breast cancer: prevention and treatment, Germany, 2004, Springer.
  3286. Figure 32-35 Formation, Metabolism, and DNA Adducts of Estrogen. Catechol estrogens are the major metabolites of E1 and E2. If these metabolites are oxidized to the electrophilic (CE-Q), they may react with DNA. The carcinogenic 4-OHE1 (E2) are oxidized to E1 (E2-3,4-Q), which reacts with DNA to form depurinating adducts. These adducts are complexes that form when a chemical (e.g., estrogen metabolites) binds to DNA and damages DNA. These adducts generate the damaged sites—known as apurinic sites—that may lead to misrepair and cancer-initiating pathways. Activating enzymes and depurinating adducts are in purple.
  3287. Box 32-9 Estrogen Carcinogenesis
  3288. Standard Theory
  3289. Updated Theory
  3290. Environmental factors
  3291. Radiation
  3292. Diet
  3293. Environmental Chemicals
  3294. Physical Activity
  3295. Familial factors
  3296. Pathogenesis
  3297. Table 32-10 Types of Breast Carcinomas and Major Distinguishing Features
  3298. Figure 32-36 Control of Breast Cell Growth. Two levels of control of breast cell growth: (1) paracrine signaling by estrogen (E-receptor) and progesterone (P-receptor) steroids and (2) autocrine signaling by locally secreted growth factors, such as transforming growth factor (TGF-α and -β) and others, including insulin-like growth factor (IGF), epidermal growth factor (EGF), and platelet-derived growth factor (PGF). mRNA, Messenger ribonucleic acid.
  3299. Clinical Manifestations
  3300. Evaluation and Treatment
  3301. Figure 32-37 Retraction of Nipple Caused by Carcinoma. From del Regato JA, Spjut HJ, Cox JD: Ackerman and del Regato’s cancer: diagnosis, treatment, and prognosis, ed 6, St Louis, 1985, Mosby.
  3302. Quick Check 32-8
  3303. Table 32-11 Clinical Manifestations of Breast Cancer
  3304. Disorders of the Male Breast
  3305. Gynecomastia
  3306. Pathophysiology
  3307. Evaluation and Treatment
  3308. Table 32-12 Staging of Breast Cancer
  3309. Carcinoma
  3310. Sexually Transmitted Infections
  3311. Table 32-13 Estimated New Cases of STIs Each Year
  3312. Table 32-14 Currently Recognized Sexually Transmitted Infections
  3313. Health Alert Anti-Infective Treatment for Victims of Sexual Assault
  3314. Table 32-15 Major Sexually Transmitted Infections
  3315. Did You Understand?
  3316. Alterations of Sexual Maturation
  3317. Disorders of the Female Reproductive System
  3318. Disorders of the Male Reproductive System
  3319. Disorders of the Breast
  3320. Sexually Transmitted Infections
  3321. Key Terms
  3322. References
  3323. Unit 11 The Digestive System
  3324. Chapter 33 Structure and Function of the Digestive System
  3325. Electronic Resources
  3326. Companion CD
  3327. Website http://evolve.elsevier.com/Huether/
  3328. The Gastrointestinal Tract
  3329. Mouth and Esophagus
  3330. Figure 33-1 Structure and Function of the Digestive System. Digestion begins in the mouth with chewing, which breaks down food mechanically and mixes it with saliva. Swallowing propels chewed food through the esophagus to the stomach, where acids and stomach motility liquefy it further. Next the liquefied food enters the small intestine, where secretions of the intestinal walls, liver, gallbladder, and pancreas digest it into absorbable nutrients. Nutrients are absorbed through intestinal walls, and unabsorbed wastes enter the large intestine (colon), where fluids are removed. Solid wastes then enter the rectum and leave the body through the anus. From Thibodeau GA, Patton KT:Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3331. Salivation
  3332. Swallowing
  3333. Figure 33-2 Wall of the Gastrointestinal Tract. The wall of the gastrointestinal tract is made up of four layers with a network of nerves between the layers. This generalized diagram shows a segment of the gastrointestinal tract. Note that the serosa is continuous with a fold of serous membrane called amesentery. Note also that digestive glands may empty their products into the lumen of the gastrointestinal tract by way of ducts. From Thibodeau GA, Patton KT:Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3334. Figure 33-3 Salivary Glands. From Thibodeau GA, Patton KT:Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3335. Figure 33-4 Salivary Electrolyte Concentrations and Flow Rate. Changes in concentration of sodium (Na+), potassium (K+), chloride (Cl−), and bicarbonate () HCO3−increases in flow rate of saliva.Green line, sodium;orange line, bicarbonate;red line, chloride;blue line, potassium. At low rates of salivary flow (i.e., between meals), sodium, chloride, and bicarbonate are reabsorbed in the collecting ducts of the salivary glands, and the saliva contains fewer of these electrolytes (i.e., is more hypotonic). At higher flow rates (i.e., stimulated by food), reabsorption decreases and saliva is hypertonic. By this mechanism, sodium, chloride, and bicarbonate are recycled until they are released to help with digestion and absorption.
  3336. Figure 33-5 Stomach. A portion of the anterior wall has been cut away to reveal the muscle layers of the stomach wall. Note that the mucosa lining the stomach forms folds calledrugae. The dotted lines distinguish the fundus, body, and antrum of the stomach. Modified from Thibodeau GA, Patton KT:Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3337. Quick Check 33-1
  3338. Stomach
  3339. Table 33-1 Selected Hormones and Neurotransmitters of the Digestive System
  3340. Gastric motility
  3341. Gastric secretion
  3342. Acid
  3343. Figure 33-6 Gastric Pits and Gastric Glands. Gastric pits are depressions in the epithelial lining of the stomach. At the bottom of each pit is one or more tubulargastric glands. Chief cells produce the enzymes of gastric juice (such as pepsinogen), parietal cells produce stomach acid, and G cells produce the hormone gastrin. From Thibodeau GA, Patton KT:Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3344. Figure 33-7 Relationship Between Secretory Rate and Electrolyte Composition of the Gastric Juice. Sodium (Na+) concentration is lower in the gastric juice than in the plasma, whereas hydrogen (H+), potassium (K+), and chloride (Cl−) concentrations are higher.Red line, chloride;orange line, hydrogen;green line, sodium;blue line, potassium.
  3345. Figure 33-8 Hydrochloric Acid Secretion by Parietal Cell.
  3346. Pepsin
  3347. Mucus
  3348. Phases of gastric secretion
  3349. Quick Check 33-2
  3350. Small Intestine
  3351. Figure 33-9 The Small Intestine.
  3352. Intestinal digestion and absorption
  3353. Box 33-1 Dietary Fat
  3354. Saturated Fatty Acids (Palmitic Acid [C16H32O2])
  3355. Unsaturated Fatty Acids
  3356. Monounsaturated Fatty Acids (Oleic Acid [C18H34O2])
  3357. Polyunsaturated Fatty Acids (Linoleic Acid [C18H32O2])
  3358. Intestinal motility
  3359. Figure 33-10 Digestion and Absorption of Foodstuffs.
  3360. Figure 33-11 Sites of Absorption of Major Nutrients.
  3361. Box 33-2 Major Nutrients Absorbed in the Small Intestine
  3362. Water and Electrolytes
  3363. Carbohydrates
  3364. Proteins
  3365. Fats
  3366. Minerals
  3367. Vitamins
  3368. Quick Check 33-3
  3369. Large Intestine
  3370. Figure 33-12 Division of the Large Intestine. From Thibodeau GA, Patton KT:Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3371. Figure 33-13 The Major Blood Vessels and Organs Supplied with Blood in the Splanchnic Circulation. Numbers in parentheses reflect approximate blood flow values (ml/minute) for each major vessel in an 80-kg normal, resting, adult human subject. Arrows indicate the direction of blood flow. Modified from Johnson LR:Gastrointestinal pathophysiology, St Louis, 2001, Mosby.
  3372. Health Alert Diet and Colon Cancer Prevention
  3373. Quick Check 33-4
  3374. Intestinal Bacteria
  3375. Splanchnic Blood Flow
  3376. Accessory Organs of Digestion
  3377. Liver
  3378. Figure 33-14 Location of the Liver, Gallbladder, and Exocrine Pancreas, Which Are the Accessory Organs of Digestion.
  3379. Figure 33-15 Gross Structure of the Liver.A, Anterior view. B, Inferior view. From Thibodeau GA, Patton KT:Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3380. Quick Check 33-5
  3381. Secretion of bile
  3382. Figure 33-16 Hepatic Portal Circulation. In this unusual circulatory route, a vein is located between two capillary beds. The hepatic portal vein collects blood from capillaries in visceral structures located in the abdomen and empties into the liver. Hepatic veins return blood to the inferior vena cava. (Organs are not drawn to scale.) From Thibodeau GA, Patton KT:Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3383. Figure 33-17 Diagrammatic Representation of a Liver Lobule. A central vein is located in the center of the lobule with plates of hepatic cells disposed radially. Branches of the portal vein and hepatic artery are located on the periphery of the lobule and blood from both perfuse the sinusoids. Peripherally located bile ducts drain the bile canaliculi that run between the hepatocytes. Modified from Thibodeau GA, Patton KT:Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3384. Metabolism of bilirubin
  3385. Figure 33-18 The Enterohepatic Circulation of Bile Salts.
  3386. Vascular and hematologic functions
  3387. Metabolism of nutrients
  3388. Fats
  3389. Proteins
  3390. Figure 33-19 Bilirubin Metabolism.
  3391. Carbohydrates
  3392. Metabolic detoxification
  3393. Table 33-2 Importance of Proteins in the Body
  3394. Storage of minerals and vitamins
  3395. Gallbladder
  3396. Exocrine Pancreas
  3397. Table 33-3 Selected Tests of Liver Function
  3398. Figure 33-20 Associated Structures of the Gallbladder, Pancreas, and Pancreatic Acinar Cells and Duct. Main illustration from Thibodeau GA, Patton KT:Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3399. Table 33-4 Selected Laboratory Tests of Pancreatic Function
  3400. Aging & The Gastrointestinal System
  3401. Oral Cavity and Esophagus
  3402. Stomach and Intestines
  3403. Liver
  3404. Pancreas and Gallbladder
  3405. Quick Check 33-6
  3406. Did You Understand?
  3407. The Gastrointestinal Tract
  3408. Accessory Organs of Digestion
  3409. Key Terms
  3410. References
  3411. Chapter 34 Alterations of Digestive Function
  3412. Electronic Resources
  3413. Companion CD
  3414. Website http://evolve.elsevier.com/Huether/
  3415. Disorders of the Gastrointestinal Tract
  3416. Clinical Manifestations of Gastrointestinal Dysfunction
  3417. Anorexia
  3418. Vomiting
  3419. Constipation
  3420. Pathophysiology
  3421. Clinical Manifestations
  3422. Evaluation and Treatment
  3423. Diarrhea
  3424. Pathophysiology
  3425. Clinical Manifestations
  3426. Evaluation and Treatment
  3427. Abdominal pain
  3428. Gastrointestinal bleeding
  3429. Table 34-1 Presentations of Gastrointestinal Bleeding
  3430. Quick Check 34-1
  3431. Disorders of Motility
  3432. Dysphagia
  3433. Pathophysiology
  3434. Clinical Manifestations
  3435. Evaluation and Treatment
  3436. Figure 34-1 Pathophysiology of Gastrointestinal (GI) Bleeding.
  3437. Gastroesophageal reflux
  3438. Figure 34-2 Achalasia. Increased LES muscle tone and loss of peristaltic function prevent food from entering the stomach, causing esophageal distention.LES, Lower esophageal sphincter.
  3439. Pathophysiology
  3440. Clinical Manifestations
  3441. Evaluation and Treatment
  3442. Hiatal hernia
  3443. Pathophysiology
  3444. Figure 34-3 Types of Hiatal Hernia.A, Sliding hiatal hernia. B, Paraesophageal hiatal hernia.
  3445. Clinical Manifestations
  3446. Evaluation and Treatment
  3447. Pyloric obstruction
  3448. Pathophysiology
  3449. Clinical Manifestations
  3450. Evaluation and Treatment
  3451. Intestinal obstruction
  3452. Pathophysiology
  3453. Table 34-2 Common Causes of Intestinal Obstruction
  3454. Table 34-3 Large and Small Bowel Obstruction
  3455. Table 34-4 Classifications of Intestinal Obstruction
  3456. Clinical Manifestations
  3457. Evaluation and Treatment
  3458. Figure 34-4 Intestinal Obstructions.A, Hernia. B, Intussusception. C, Volvulus. D, Constriction adhesions. A, B, and C from Damjanov I:Pathology for the health professions, ed 3, Philadelphia, 2006, Saunders. D from Monahan FD et al:Phipps’ medical-surgical nursing: concepts and clinical practice, ed 8, St Louis, 2007, Mosby.
  3459. Figure 34-5 Pathophysiology of Intestinal Obstruction.
  3460. Quick Check 34-2
  3461. Gastritis
  3462. Figure 34-6 Lesions Caused by Peptic Ulcer Disease.
  3463. Peptic Ulcer Disease
  3464. Risk Factors Peptic Ulcer
  3465. Duodenal ulcers
  3466. Pathophysiology
  3467. Clinical Manifestations
  3468. Evaluation and Treatment
  3469. Gastric ulcers
  3470. Pathophysiology
  3471. Clinical Manifestations
  3472. Figure 34-7 Duodenal Ulcer. A, A deep ulceration in the duodenal wall extending as a crater through the entire mucosa and into the muscle layers. B, Sequence of ulcerations from normal mucosa to duodenal ulcer. C, Bilateral (kissing) duodenal ulcers in a person using nonsteroidal anti-inflammatory drugs (NSAIDs). C courtesy David Bjorkman, MD, University of Utah School of Medicine, Department of Gastroenterology.
  3473. Table 34-5 Characteristics of Gastric and Duodenal Ulcers
  3474. Stress ulcers
  3475. Surgical treatment of ulcer
  3476. Quick Check 34-3
  3477. Postgastrectomy syndromes
  3478. Figure 34-8 Pathophysiology of Gastric Ulcer Formation.NSAIDs, nonsteroidal antiinflammatory drugs.
  3479. Malabsorption Syndromes
  3480. Pancreatic insufficiency
  3481. Lactase deficiency
  3482. Bile salt deficiency
  3483. Inflammatory Bowel Disease
  3484. Ulcerative colitis
  3485. Pathophysiology
  3486. Clinical Manifestations
  3487. Evaluation and Treatment
  3488. Crohn disease
  3489. Pathophysiology
  3490. Clinical Manifestations
  3491. Table 34-6 Features of Ulcerative Colitis and Crohn Disease
  3492. Evaluation and Treatment
  3493. Diverticular disease of the colon
  3494. Pathophysiology
  3495. Figure 34-9 Diverticular Disease. In diverticular disease, the outpouches(arrows) of mucosa seen in the sigmoid colon appear as slitlike openings from the mucosal surface of the opened bowel. Modified from Stevens A, Lowe, J:Pathology, ed 2, Edinburgh, 2000, Mosby.
  3496. Clinical Manifestations
  3497. Evaluation and Treatment
  3498. Appendicitis
  3499. Pathophysiology
  3500. Clinical Manifestations
  3501. Evaluation and Treatment
  3502. Irritable Bowel Syndrome
  3503. Pathophysiology
  3504. Clinical Manifestations
  3505. Evaluation and Treatment
  3506. Vascular Insufficiency
  3507. Box 34-1 Rome III—Diagnostic Criteria for Irritable Bowel Syndrome
  3508. Disorders of Nutrition
  3509. Obesity
  3510. Pathophysiology
  3511. Box 34-2 Examples of Adipocytokines and Hormones From Adipose Tissue
  3512. Adipocytokines
  3513. Other Hormones
  3514. Clinical Manifestations
  3515. Figure 34-10 Leptin Theory of Obesity. The hypothalamus controls appetite, fat cell mass, and energy expenditure by responding to circulating levels of leptin and other hormones. Regulation of normal body weight is presented in the green boxes. Changes occurring with obesity are presented in the orange boxes, and changes occurring with starvation or weight loss are presented in the yellow boxes.
  3516. Evaluation And Treatment
  3517. Anorexia nervosa and bulimia nervosa
  3518. Health Alert Refeeding Syndrome
  3519. Malnutrition and starvation
  3520. Quick Check 34-4
  3521. Disorders of the Accessory Organs of Digestion
  3522. Clinical Manifestations of Liver Disorders
  3523. Portal hypertension
  3524. Pathophysiology
  3525. Figure 34-11 Varices Related to Portal Hypertension. Portal vein, its major tributaries, and the most important shunts (collateral veins) between the portal and caval systems. From Mohahan FD et al:Phipps’ medical-surgical nursing: concepts and clinical practice, ed 8, St Louis, 2007, Mosby.
  3526. Clinical Manifestations
  3527. Evaluation and Treatment
  3528. Ascites
  3529. Pathophysiology
  3530. Clinical Manifestations
  3531. Evaluation and Treatment
  3532. Hepatic encephalopathy
  3533. Figure 34-12 Mechanisms of Ascites Caused by Cirrhosis.
  3534. Figure 34-13 Massive Ascites in an Individual With Cirrhosis. Distended abdomen, dilated upper abdominal veins, and inverted umbilicus are classic manifestations. From Prior JA, Silberstein JS, Stang JM:Physical diagnosis: the history and examination of the patient, ed 6, St Louis, 1981, Mosby.
  3535. Pathophysiology
  3536. Clinical Manifestations
  3537. Evaluation and Treatment
  3538. Jaundice
  3539. Pathophysiology
  3540. Figure 34-14 Mechanisms of Jaundice.
  3541. Clinical Manifestations
  3542. Table 34-7 Three Common Types of Jaundice
  3543. Evaluation and Treatment
  3544. Hepatorenal syndrome
  3545. Pathophysiology
  3546. Clinical Manifestations
  3547. Evaluation and Treatment
  3548. Quick Check 34-5
  3549. Disorders of the Liver
  3550. Viral hepatitis
  3551. Table 34-8 Characteristics of Viral Hepatitis
  3552. Pathophysiology
  3553. Clinical Manifestations
  3554. Evaluation and Treatment
  3555. Health Alert Hepatitis
  3556. Fulminant hepatitis
  3557. Cirrhosis
  3558. Table 34-9 Cirrhosis of the Liver
  3559. Alcoholic liver disease
  3560. Pathophysiology
  3561. Figure 34-15 Clinical Manifestations of Cirrhosis.ADH, Antidiuretic hormone;AST, aspartate transaminase;ALT, alanine transaminase.
  3562. Clinical Manifestations
  3563. Evaluation and Treatment
  3564. Biliary cirrhosis
  3565. Quick Check 34-6
  3566. Disorders of the Gallbladder
  3567. Cholelithiasis
  3568. Pathophysiology
  3569. Figure 34-16 Resected Gallbladder Containing Mixed Gallstones. From Kissane JM, editor:Anderson’s pathology, ed 9, St Louis, 1990, Mosby.
  3570. Clinical Manifestations
  3571. Evaluation and Treatment
  3572. Cholecystitis
  3573. Disorders of the Pancreas
  3574. Acute pancreatitis
  3575. Pathophysiology
  3576. Clinical Manifestations
  3577. Evaluation and Treatment
  3578. Chronic pancreatitis
  3579. Cancer of the Digestive System
  3580. Cancer of the Gastrointestinal Tract
  3581. Cancer of the esophagus
  3582. Pathogenesis
  3583. Risk Factors Esophageal Cancer
  3584. Clinical Manifestations
  3585. Evaluation and Treatment
  3586. Table 34-10 Cancer of the Gut, Liver, and Pancreas
  3587. Cancer of the stomach
  3588. Pathogenesis
  3589. Clinical Manifestations
  3590. Evaluation and Treatment
  3591. Figure 34-17 Typical Sites of Stomach Cancer. From del Regato JA, Spjut HJ, Cox JD:Cancer: diagnosis, treatment, and prognosis, ed 2, St Louis, 1985, Mosby.
  3592. Quick Check 34-7
  3593. Cancer of the colon and rectum
  3594. Pathogenesis
  3595. Risk Factors Cancer of the Colon and Rectum
  3596. Figure 34-18 Neoplastic Polyps.A, Tubular adenomata(A) are rounded lesions 0.5 to 2cm in size that are generally red and sit on a stalk(S) of normal mucosa that has been dragged up by traction of the polyp in the bowel lumen. B, Villous adenomata are velvety lesions about 0.6cm thick that occupy a broad area of mucosa generally 1 to 5cm in diameter. From Stevens A, Lowe J:Pathology, ed 2, Edinburgh, 2000, Mosby.
  3597. Figure 34-19 Signs and Symptoms of Colorectal Cancer by Location of Primary Lesion. Clinical manifestations are listed in order of frequency for each region (lymphatics of colon also shown).
  3598. Clinical Manifestations
  3599. Table 34-11 Conditions Commonly Confused With Colorectal Cancer
  3600. Evaluation and Treatment
  3601. Figure 34-20 Development of Cancer of the Colon From Adenomatous Polyps. The tumor becomes invasive if it penetrates the muscularis mucosae and enters the submucosal layer. From del Regato JA, Spjut HJ, Cox JD:Cancer: diagnosis, treatment, and prognosis, ed 2, St Louis, 1985, Mosby.
  3602. Box 34-3 Screening for Colorectal Cancer
  3603. Cancer of the Accessory Organs of Digestion
  3604. Cancer of the liver
  3605. Risk Factors Primary Liver Cancer
  3606. Pathogenesis
  3607. Clinical Manifestations
  3608. Evaluation and Treatment
  3609. Cancer of the gallbladder
  3610. Pathogenesis
  3611. Clinical Manifestations
  3612. Evaluation and Treatment
  3613. Cancer of the pancreas
  3614. Pathogenesis
  3615. Clinical Manifestations
  3616. Evaluation and Treatment
  3617. Quick Check 34-8
  3618. Did You Understand?
  3619. Disorders of the Gastrointestinal Tract
  3620. Disorders of the Accessory Organs of Digestion
  3621. Cancer of the Digestive System
  3622. Key Terms
  3623. References
  3624. Chapter 35 Alterations of Digestive Function in Children
  3625. Electronic Resources
  3626. Companion CD
  3627. Website http://evolve.elsevier.com/Huether/
  3628. Disorders of the Gastrointestinal Tract
  3629. Congenital Impairment of Motility
  3630. Cleft lip and cleft palate
  3631. Pathophysiology
  3632. Cleft lip
  3633. Figure 35-1 Variations in Clefts of the Lip and Palate.A, Notch in vermilion border. B, Unilateral cleft lip and palate. C, Bilateral cleft lip and cleft palate. D, Cleft palate.
  3634. Cleft palate
  3635. Clinical Manifestations
  3636. Evaluation and Treatment
  3637. Esophageal malformations
  3638. Pathophysiology
  3639. Clinical Manifestations
  3640. Figure 35-2 Five Types of Esophageal Atresia and Tracheoesophageal Fistulas.A, Simple esophageal atresia. Proximal esophagus and distal esophagus end in blind pouches, and there is no tracheal communication. Nothing enters the stomach; regurgitated food and fluid may enter the lungs. B, Proximal and distal esophageal segments end in blind pouches, and a fistula connects the proximal esophagus to the trachea. Nothing enters the stomach; food and fluid enter the lungs. C, Proximal esophagus ends in a blind pouch, and a fistula connects the trachea to the distal esophagus. Air enters the stomach; regurgitated gastric secretions enter the lungs through the fistula. D, Fistula connects both proximal and distal esophageal segments to the trachea. Air, food, and fluid enter the stomach and the lungs. E, Simple tracheoesophageal fistula between otherwise normal esophagus and trachea. Air, food, and fluid enter the stomach and the lungs. Between 85% and 90% of esophageal anomalies are type C; 6% to 8% are type A; 3% to 5% are type E; and fewer than 1% are type B or D.
  3641. Evaluation and Treatment
  3642. Pyloric stenosis
  3643. Pathophysiology
  3644. Clinical Manifestations
  3645. Evaluation and Treatment
  3646. Intestinal malrotation
  3647. Pathophysiology
  3648. Clinical Manifestations
  3649. Evaluation and Treatment
  3650. Quick Check 35-1
  3651. Meconium ileus
  3652. Pathophysiology
  3653. Clinical Manifestations
  3654. Evaluation and Treatment
  3655. Distal intestinal obstruction syndrome
  3656. Obstructions of the duodenum, jejunum, and ileum
  3657. Meckel diverticulum
  3658. Congenital aganglionic megacolon
  3659. Pathophysiology
  3660. Clinical Manifestations
  3661. Figure 35-3 Congenital Aganglionic Megacolon (Hirschsprung Disease).
  3662. Evaluation and Treatment
  3663. Anorectal malformations
  3664. Acquired Impairment of Motility
  3665. Intussusception
  3666. Pathophysiology
  3667. Clinical Manifestations
  3668. Figure 35-4 Anorectal Stenosis and Imperforate Anus.
  3669. Figure 35-5 Ileocolic Intussusception.
  3670. Evaluation and Treatment
  3671. Gastroesophageal reflux
  3672. Pathophysiology
  3673. Clinical Manifestations
  3674. Evaluation and Treatment
  3675. Quick Check 35-2
  3676. Impairment of Digestion, Absorption, and Nutrition
  3677. Cystic fibrosis
  3678. Pathophysiology
  3679. Clinical Manifestations
  3680. Evaluation and Treatment
  3681. Gluten-sensitive enteropathy
  3682. Table 35-1 Pathophysiology, Clinical Manifestations, and Complications of Cystic Fibrosis
  3683. Pathophysiology
  3684. Figure 35-6 Pathophysiology of Gluten-Sensitive Enteropathy.
  3685. Clinical Manifestations
  3686. Evaluation and Treatment
  3687. Protein energy malnutrition
  3688. Pathophysiology
  3689. Clinical Manifestations
  3690. Evaluation and Treatment
  3691. Failure to thrive
  3692. Pathophysiology
  3693. Clinical Manifestations
  3694. Evaluation and Treatment
  3695. Necrotizing enterocolitis
  3696. Pathophysiology
  3697. Clinical Manifestations
  3698. Evaluation and Treatment
  3699. Quick Check 35-3
  3700. Diarrhea
  3701. Acute diarrhea
  3702. Health Alert Rotavirus Vaccine
  3703. Chronic diarrhea
  3704. Chronic nonspecific diarrhea
  3705. Primary lactose intolerance
  3706. Disorders of the Liver
  3707. Disorders of Biliary Metabolism and Transport
  3708. Neonatal jaundice
  3709. Pathophysiology
  3710. Clinical Manifestations
  3711. Evaluation and Treatment
  3712. Biliary atresia
  3713. Inflammatory Disorders
  3714. Hepatitis
  3715. Hepatitis A (HAV)
  3716. Health Alert Hepatitis Vaccines for Children
  3717. Hepatitis B Vaccine Guidelines
  3718. Hepatitis B (HBV)
  3719. Hepatitis C (HCV)
  3720. Chronic hepatitis
  3721. Cirrhosis
  3722. Portal Hypertension
  3723. Types of portal hypertension
  3724. Extrahepatic portal hypertension
  3725. Intrahepatic portal hypertension
  3726. Course of the disease
  3727. Clinical Manifestations
  3728. Evaluation and Treatment
  3729. Metabolic Disorders
  3730. Quick Check 35-4
  3731. Table 35-2 Galactosemia, Fructosemia, and Wilson Disease
  3732. Did You Understand?
  3733. Disorders of the Gastrointestinal Tract
  3734. Disorders of the Liver
  3735. Key Terms
  3736. References
  3737. Unit 12 The Musculoskeletal and Integumentary Systems
  3738. Chapter 36 Structure and Function of the Musculoskeletal System
  3739. Electronic Resources
  3740. Companion CD
  3741. Website http://evolve.elsevier.com/Huether/
  3742. Structure and Function of Bones
  3743. Elements of Bone Tissue
  3744. Table 36-1 Structural Elements of Bone
  3745. Bone cells
  3746. Osteoblast
  3747. Osteoclast
  3748. Figure 36-1 Bone Cells.A, Osteoblasts are responsible for the production of collagenous and noncollagenous proteins that compose osteoid. Active osteoblasts are lined up on the osteoid. Note the eccentrically located nuclei. B, Scanning electron micrograph showing an osteocyte within a lacuna. The cell is surrounded by collagen fibers and mineralized bone. C, Osteoclasts actively resorb mineralized tissue. The scalloped surface in which the multinucleated osteoclasts rest is termed Howship lacuna. A and C from Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby; B from Erlandsen S, Magney J: Color atlas of histology, St Louis, 1992, Mosby.
  3749. Table 36-2 Effects of Selected Cytokines (Growth Factors) on Skeletal Tissues
  3750. Osteocyte
  3751. Bone matrix
  3752. Collagen fibers
  3753. Proteoglycans
  3754. Glycoproteins
  3755. Bone minerals
  3756. Types of Bone Tissue
  3757. Table 36-3 Sequence of Calcium and Phosphate Compound Formation and Crystallization
  3758. Figure 36-2 Cross Section of Bone. Longitudinal section of long bone (tibia) showing spongy (cancellous) and compact bone. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3759. Characteristics of Bone
  3760. Maintenance of Bone Integrity
  3761. Remodeling
  3762. Figure 36-3 Structure of Compact and Cancellous Bone.A, Longitudinal section of a long bone showing both cancellous and compact bone. B, A magnified view of compact bone. C, Section of a flat bone. Outer layers of compact bone surround cancellous bone. Fine structure of compact and cancellous bone is shown to the right. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3763. Figure 36-4 Anterior View of Skeleton. Axial skeleton in blue; appendicular skeleton in tan. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3764. Repair
  3765. Quick Check 36-1
  3766. Structure and Function of Joints
  3767. Figure 36-5 Bone Remodeling. In the remodeling sequence, bone sections are removed by bone-resorbing cells (osteoclasts) and replaced with a new section laid down by bone-forming cells (osteoblasts). The cells work in response to signals generated in that environment. Only the multinucleated osteoclastic cells mediate the first phase of remodeling. They are activated, scoop out bone (A), and resorb it; then the work of the osteoblasts begins (B). They form new bone that replaces bone removed by the resorption process (C). The sequence takes 4 to 5 months. D, Micrograph of active bone remodeling seen in the settings of primary or secondary hyperparathyroidism. Note the active osteoblasts surmounted on red-stained osteoid. Marrow fibrosis is present. D from Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  3768. Fibrous Joints
  3769. Cartilaginous Joints
  3770. Joint (articular) capsule
  3771. Figure 36-6 Main Tissues of a Joint. Micrographs from Gartner LP, Hiatt JL: Color textbook of histology, ed 3, Philadelphia, 2007, Saunders.
  3772. Synovial membrane
  3773. Joint (synovial) cavity
  3774. Synovial fluid
  3775. Articular cartilage
  3776. Figure 36-7 Types of Joints. Cartilaginous (amphiarthrodial) joints, which are slightly movable, include (A) a synchondrosis that attaches ribs to costal cartilage, (B) a symphysis that connects vertebrae, and (C) the symphysis that connects the two pubic bones. Fibrous (synarthrodial) joints, which are immovable, include (D) the syndesmosis between the tibia and fibula and (E) sutures that connect the skull bones and the gomphosis (not shown), which holds teeth in their sockets. The synovial joints include (F) the spheroid type at the shoulder, (G) the hinge type at the elbow, and (H) the gliding joints of the hand.
  3777. Synovial Joints
  3778. Structure of synovial joints
  3779. Movement of synovial joints
  3780. Quick Check 36-2
  3781. Structure and Function of Skeletal Muscles
  3782. Whole Muscle
  3783. Figure 36-8 Knee Joint (Synovial Joint).A, Frontal view. B, Lateral view.
  3784. Figure 36-9 Movements of Synovial (Diarthrodial) Joints.
  3785. Motor unit
  3786. Figure 36-10 Body Movements Made Possible by Synovial (Diarthrodial) Joints.
  3787. Sensory receptors
  3788. Muscle fibers
  3789. Figure 36-11 Skeletal Muscles of Body.A, Anterior view. B, Posterior view.
  3790. Figure 36-12 Cross Section of Skeletal Muscle Showing Muscle Fibers and Their Coverings. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3791. Figure 36-13 Motor Units of a Muscle. Each motor unit consists of a motor neuron and all the muscle fibers (cells) supplied by the neuron and its axon branches.
  3792. Figure 36-14 Myofibrils. Myofibrils of a skeletal muscle fiber (cells) and overall organization of skeletal muscle. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3793. Table 36-4 Characteristics of Muscle Fibers
  3794. Myofibrils
  3795. Muscle proteins
  3796. Nonprotein constituents of muscle
  3797. Components of Muscle Function
  3798. Figure 36-15 Muscle Fibers.A, Lines and bands in striated muscle. B, Relationships of bands, actin, myosin, and lines in relaxed and contracted muscle fibers. A modified from Thompson JM et al: Mosby’s clinical nursing, ed 5, St Louis, 2002, Mosby.
  3799. Muscle contraction at the molecular level
  3800. Table 36-5 Contractile Proteins of Skeletal Muscle Fibrils
  3801. Muscle metabolism
  3802. Table 36-6 Energy Sources for Muscular Activity
  3803. Health Alert Soft Tissue Repair
  3804. Muscle mechanics
  3805. Types of muscle contraction
  3806. Movement of muscle groups
  3807. AGING & The Musculoskeletal System
  3808. Aging of Bones
  3809. Aging of Joints
  3810. Figure 36-16 Isotonic and Isometric Contraction.A, In isotonic contraction, the muscle shortens, producing movement. B, In isometric contraction, the muscle pulls forcefully against a load but does not shorten. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 6, St Louis, 2007, Mosby.
  3811. Aging of Muscles
  3812. Quick Check 36-3
  3813. Did You Understand?
  3814. Structure and Function of Bones
  3815. Structure and Function of Joints
  3816. Structure and Function of Skeletal Muscles
  3817. AGING & the Musculoskeletal System
  3818. Key Terms
  3819. References
  3820. Chapter 37 Alterations of Musculoskeletal Function
  3821. Electronic Resources
  3822. Companion CD
  3823. Website http://evolve.elsevier.com/Huether/
  3824. Musculoskeletal Injuries
  3825. Skeletal Trauma
  3826. Fractures
  3827. Classification of fractures
  3828. Figure 37-1 Examples of Types of Bone Fractures.A, Oblique: fracture at oblique angle across both cortices. Cause: Direct or indirect energy, with angulation and some compression. B, Occult: Fracture that is hidden or not readily discernible. Cause: Minor force or energy. C, Open: Skin broken over fracture; possible soft tissue trauma. Cause: Moderate to severe energy that is continuous and exceeds tissue tolerances. D, Pathologic: transverse, oblique, or spiral fracture of bone weakened by tumor pressure or presence. Cause: Minor energy or force, which may be direct or indirect. E, Comminuted: Fracture with two or more pieces or segments. Cause: Direct or indirect moderate to severe force. F, Spiral: Fracture that curves around cortices and may become displaced by twist. Cause: Direct or indirect twisting energy or force with distal part held or unable to move. G, Transverse: horizontal break through bone. Cause: Direct or indirect energy toward bone. H, Greenstick: Break in only one cortex of bone. Cause: Minor direct or indirect energy. I, Impacted: Fracture with one end wedged into opposite end of inside fractured fragment. Cause: Compressive axial energy or force directly to distal fragment. Redrawn from Mourad L: Musculoskeletal system. In Thompson JM et al, editors: Mosby’s clinical nursing, ed 7, St Louis, 2002, Mosby.
  3829. Table 37-1 Types of Fractures
  3830. Pathophysiology
  3831. Figure 37-2 Bone Healing (Schematic Representation).A, Bleeding at broken ends of the bone with subsequent hematoma formation. B, Organization of hematoma into fibrous network. C, Invasion of osteoblasts, lengthening of collagen strands, and deposition of calcium. D, Callus formation; new bone is built up as osteoclasts destroy dead bone. E, Remodeling is accomplished as excess callus is reabsorbed and trabecular bone is laid down. From Monahan FD et al: Phipps’ Medical-surgical nursing: health and illness perspectives, ed 8, St Louis, 2007, Mosby.
  3832. Clinical Manifestations
  3833. Figure 37-3 Exuberant Callus Formation Following Fracture. From Rosai J: Ackerman’s surgical pathology, ed 8, St Louis, 1996, Mosby.
  3834. Evaluation and Treatment
  3835. Dislocation and subluxation
  3836. Pathophysiology
  3837. Clinical Manifestations
  3838. Evaluation and Treatment
  3839. Support Structures
  3840. Sprains and strains of tendons and ligaments
  3841. Pathophysiology
  3842. Clinical Manifestations
  3843. Evaluation and Treatment
  3844. Tendonitis, epicondylitis, and bursitis
  3845. Figure 37-4 Tendionitis and Epicondylitis.A, Medial or lateral epicondyles of humerus, site of epicondylitis. B, Achilles tendon, site of commonly occurring tendonitis.
  3846. Pathophysiology
  3847. Clinical Manifestations
  3848. Figure 37-5 Olecranon Bursitis. A case of olecranon bursitis in a patient with rheumatoid arthritis. A rheumatoid nodule is also shown. From Klippel JH, Deippe PA, editors: Rheumatology, ed 2, London, 1998, Mosby.
  3849. Evaluation and Treatment
  3850. Muscle strains
  3851. Table 37-2 Muscle Strain
  3852. Myoglobinuria
  3853. Figure 37-6 Pathogenesis of Compartment Syndrome and Crush Syndrome Caused by Prolonged Muscle Compression.ECF, Extracellular fluid.
  3854. Pathophysiology
  3855. Clinical Manifestations
  3856. Figure 37-7 The Muscle Compartments of the Lower Leg. From Mohahan FD et al: Phipps’ Medical-surgical nursing: health and illness perspectives, ed 8, St Louis, 2007, Mosby.
  3857. Evaluation and Treatment
  3858. Quick Check 37-1
  3859. Disorders of Bones
  3860. Metabolic Bone Diseases
  3861. Osteoporosis
  3862. Figure 37-8 Vertebral Body. Osteoporotic vertebral body (right) shortened by compression fractures compared with a normal vertebral body. Note that the osteoporotic vertebra has a characteristic loss of horizontal trabeculae and thickened vertical trabeculae. From, Kumar V et al: Robbins and Cotran pathologic basis of disease, ed 7, Philadelphia, 2005, Saunders.
  3863. Figure 37-9 Osteoporosis in Cortical and Trabecular Bone.
  3864. Health Alert Osteoporosis in Men
  3865. Health Alert Osteoporosis Facts and Figures at a Glance
  3866. Table 37-3 T-score and World Health Organization Diagnosis of Bone Density
  3867. Risk Factors Osteoporosis
  3868. Genetic
  3869. Anthropometric
  3870. Hormonal and Metabolic
  3871. Dietary
  3872. Lifestyle
  3873. Concurrent
  3874. Illness and Trauma
  3875. Liver Disease
  3876. Drugs
  3877. Figure 37-10 OPG/RANKL/RANK System. RANKL, receptor activator of nuclear factor κβ ligand, a cytokine and part of the tumor necrosis factor (TNF) family, expression and OPG, a glycoprotein receptor antagonist, are modulated by various cytokines, hormones, drugs, and mechanical strains (see inserts). In bone, RANKL is expressed by both stromal cells and osteoblasts. RANKL stimulates the receptor RANK on osteoclast precursor cells and mature osteoclasts and activates intracellular signaling pathways to promote osteoclast differentiation and activation, as well as cytoskeletal reorganization and survival (PKB/Akt pathway) that increases resorption and bone loss. OPG, secreted by stromal cells and osteoblasts, acts as a “decoy” receptor and blocks RANKL binding to and activating RANK. BMP, Bone morphogenic protein; IL, interleukin; TGF-β, transforming growth factor beta; TNF-α, tumor necrosis factor alpha; PTH, parathyroid hormone. Adapted from Hofbauer LC, Schoppet M: JAMA 292(4):490–495, 2004.
  3878. Pathophysiology
  3879. Figure 37-11 Mechanism of Loss of Trabecular Bone in Women and Trabecular Thinning in Men. Bone thinning predominates in men because of reduced bone formation. Loss of connectivity and complete trabeculae predominates in women.
  3880. Figure 37-12 Bone Loss in Men and Women. Absolute amount of bone resorbed on the inner bone surface and formed on the outer bone surface is more in men than women during aging.
  3881. Health Alert Vitamin D and Fracture Risk
  3882. Clinical Manifestations
  3883. Figure 37-13 Kyphosis. This elderly woman’s condition was caused by a combination of spinal osteoporotic vertebral collapse and chronic degenerative changes in the vertebral column. From Kamal A, Brocklehurst JC: Color atlas of geriatric medicine, ed 2, St Louis, 1992, Mosby.
  3884. Evaluation and Treatment
  3885. Box 37-1 Biochemical Markers of Bone Turnover
  3886. Health Alert Newer Treatments for Osteoporosis: Strontium and Teriparatide
  3887. Osteomalacia
  3888. Pathophysiology
  3889. Clinical Manifestations
  3890. Evaluation and Treatment
  3891. Paget disease
  3892. Pathophysiology
  3893. Clinical Manifestations
  3894. Evaluation and Treatment
  3895. Infectious Bone Disease: Osteomyelitis
  3896. Figure 37-14 Osteomyelitis Showing Sequestration and Involucrum.
  3897. Pathophysiology
  3898. Clinical Manifestations
  3899. Figure 37-15 Resected Femur in a Patient With Draining Osteomyelitis. The drainage tract in the subperiosteal shell of viable new bone (involucrum) reveals the inner native necrotic cortex (sequestrum). From Kumar V et al: Robbins and Cotran pathologic basis of disease, ed 7, Philadelphia, 2005, Saunders.
  3900. Evaluation and Treatment
  3901. Quick Check 37-2
  3902. Disorders of Joints
  3903. Osteoarthritis
  3904. Types of osteoarthritis
  3905. Figure 37-16 Osteoarthritis (OA).A, Cartilage and degeneration of the hip joint from osteoarthritis. B, Heberden nodes and Bouchard nodes. C, Severe osteoarthritis with small islands of residual articular cartilage next to exposed subchondral bone. 1, Eburnated articular surface. 2, Subchondral cyst. 3, Residual articular cartilage. C from Kumar V, et al: Robbins and Cotran pathologic basis of disease, ed 7, Philadelphia, 2005, Saunders.
  3906. Pathophysiology
  3907. Clinical Manifestations
  3908. Risk Factors Osteoarthritis
  3909. Evaluation and Treatment
  3910. Figure 37-17 Typical Varus Deformity of Knee Osteoarthritis. From Doherty M: Color atlas and text of osteoarthritis, London, 1994, Wolfe.
  3911. Health Alert Body Weight and Osteoarthritis
  3912. Classic Inflammatory Joint Disease
  3913. Rheumatoid arthritis
  3914. Figure 37-18 Rheumatoid Arthritis of the Hand. Note swelling from chronic synovitis of metacarpophalangeal joints, marked ulnar drift, subcutaneous nodules, and subluxation of metacarpophalangeal joints with extension of proximal interphalangeal joints and flexion of distal joints. Note also deformed position of thumb. Hand has wasted appearance. Redrawn from Mourad LA: Orthopedic disorders, St Louis, 1991, Mosby.
  3915. Pathophysiology
  3916. Figure 37-19 Synovitis. Inflamed synovium showing typical arrangements of macrophages (red) and fibroblastic cells.
  3917. Figure 37-20 Emerging Model of Pathogenesis of Rheumatoid Arthritis. Rheumatoid arthritis is an autoimmune disease of a genetically susceptible host triggered by an unknown antigenic agent. Chronic autoimmune reaction with activation of CD4+ helper T cells and possibly other lymphocytes and the local release of inflammatory cytokines and mediators that eventually destroys the joint. T cells stimulate cells in the joint to produce cytokines that are key mediators of synovial damage. Apparently, immune complex deposition also plays a role. Tumor necrosis factor (TNF) and interleukin-1 (IL-1), as well as some other cytokines, stimulate synovial cells to proliferate and produce other mediators of inflammation, such as prostaglandins (PGE2) matrix metalloproteinases, and enzymes that all contribute to destruction of cartilage. Activated T cells and synovial fibroblasts also produce receptor activator of nuclear factor κβ ligand (RANKL), which activates the osteoclasts and promotes bone destruction. Pannus is a mass of synovium and synovial stroma with inflammatory cells, granulation tissue, and fibroblasts that grows over the articular surface and causes its destruction.
  3918. Clinical Manifestations
  3919. Evaluation and Treatment
  3920. Health Alert New Rheumatoid Arthritis Treatments
  3921. Ankylosing spondylitis
  3922. Pathophysiology
  3923. Clinical Manifestations
  3924. Evaluation and Treatment
  3925. Figure 37-21 Ankylosing Spondylitis. Characteristic posture and primary pathologic sites of inflammation and resulting damage. Redrawn from Mourad LA: Orthopedic disorders, St Louis, 1991, Mosby.
  3926. Gout
  3927. Table 37-4 Mean Urate Concentrations by Age and Gender
  3928. Pathophysiology
  3929. Figure 37-22 Uric Acid Synthesis and Elimination. Uric acid is derived from purines ingested or synthesized from ingested foods, as well as being recycled after cell breakdown. Uric acid is then eliminated through the kidneys and gastrointestinal tract. Redrawn from Klippel JH, Dieppe PA, editors: Rheumatology, ed 2, St Louis, 1998, Mosby.
  3930. Clinical Manifestations
  3931. Figure 37-23 Pathogenesis of Acute Gouty Arthritis.A, Depending on the urate crystal coating, a variety of cells may be stimulated to produce a wide range of inflammatory mediators. IgG, Immunoglobulin G; Apo E, apolipoprotein E; PGE2, prostaglandin E2; LTB4, leukotriene B4; IL, interleukin. B, Sequence of events in the production of inflammatory response to urate crystals. C, Gouty tophus on right foot. C from Dieppe PA et al: Arthritis and rheumatism in practice, London, 1991, Gower.
  3932. Figure 37-24 Theoretic Pathophysiologic Model of Fibromyalgia.
  3933. Treatment
  3934. Quick Check 37-3
  3935. Disorders of Skeletal Muscle
  3936. Secondary Muscular Dysfunction
  3937. Contractures
  3938. Stress-induced muscle tension
  3939. Disuse atrophy
  3940. Fibromyalgia
  3941. Table 37-5 Comparison of Fibromyalgia and Myofascial Pain Syndromes
  3942. Pathophysiology
  3943. Clinical Manifestations
  3944. Figure 37-25 Location of Specific Tender Points for Diagnostic Classification of Fibromyalgia. Redrawn from Freundlich B, Leventhal L: The fibromyalgia syndrome. In Schumacher HR Jr, Klippel JH, Koopman WJ, editors: Primer on the rheumatic diseases, ed 11, Atlanta, 1997, Arthritis Foundation.
  3945. Evaluation and Treatment
  3946. Muscle Membrane Abnormalities
  3947. Myotonia
  3948. Box 37-2 Educating and Providing Reassurance for Individuals With Fibromyalgia
  3949. Periodic paralysis
  3950. Metabolic Muscle Diseases
  3951. Endocrine disorders
  3952. Diseases of energy metabolism
  3953. McArdle disease
  3954. Acid maltase deficiency
  3955. Myoadenylate deaminase deficiency
  3956. Lipid deficiencies
  3957. Inflammatory Muscle Diseases: Myositis
  3958. Viral, bacterial, and parasitic myositis
  3959. Polymyositis, dermatomyositis, and inclusion-body myositis
  3960. Pathophysiology
  3961. Clinical Manifestations
  3962. Evaluation and Treatment
  3963. Figure 37-26 Dermatomyositis. Heliotrope (violaceous) discoloration around the eyes and periorbital edema. From Habif TP: Clinical dermatology, ed 3, St Louis, 1996, Mosby.
  3964. Toxic Myopathies
  3965. Quick Check 37-4
  3966. Musculoskeletal Tumors
  3967. Bone Tumors
  3968. Figure 37-27 Derivation of Bone Tumors.
  3969. Epidemiology
  3970. Patterns of bone destruction
  3971. Evaluation
  3972. Table 37-6 Patterns of Bone Destruction Caused by Bone Tumors
  3973. Types
  3974. Osteogenic tumors: osteosarcoma
  3975. Table 37-7 Surgical Staging System for Bone Tumors
  3976. Figure 37-28 Osteosarcoma.A, Common locations of osteosarcoma. B, Femur has a large mass involving the metaphysis of the bone; the tumor has destroyed the cortex, forming a soft tissue component. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  3977. Chondrogenic tumors: chondrosarcoma
  3978. Collagenic tumors: fibrosarcoma
  3979. Myelogenic tumors
  3980. Giant cell tumor
  3981. Muscle Tumors
  3982. Rhabdomyoma
  3983. Rhabdomyosarcoma
  3984. Other tumors
  3985. Quick Check 37-5
  3986. Did You Understand?
  3987. Musculoskeletal Injuries
  3988. Disorders of Bones
  3989. Disorders of Joints
  3990. Disorders of Skeletal Muscle
  3991. Musculoskeletal Tumors
  3992. Key Terms
  3993. References
  3994. Chapter 38 Alterations of Musculoskeletal Function in Children
  3995. Electronic Resources
  3996. Companion CD
  3997. Website http://evolve.elsevier.com/Huether/
  3998. Congenital Defects
  3999. Clubfoot
  4000. Developmental Dysplasia of the Hip
  4001. Table 38-1 Terms Used to Describe Foot Abnormalities
  4002. Figure 38-1 Infant with Bilateral Congenital Talipes Equinovarus. From Brashear HR, Raney RB: Shand’s handbook of orthopedic surgery, ed 9, St Louis, 1978, Mosby.
  4003. Figure 38-2 Idiopathic Clubfoot. Idiopathic clubfoot displaying forefoot adduction (toward midline of body), supination (upturning), and hindfoot equinus (pointed downward). Note skin creases along arch and back of heel.
  4004. Osteogenesis Imperfecta
  4005. Figure 38-3 Surgically Treated Bilateral Hip Dislocation. Postoperative x-ray of 5-year-old child after femoral, acetabular, and joint surgery bilaterally. The plates will be removed once the child heals. The extent of surgery necessitated staged (i.e., one side at a time) intervention.
  4006. Bone Infection
  4007. Osteomyelitis
  4008. Figure 38-4 Osteogenesis Imperfecta Treated With Osteotomies and Telescoping Medullary Rods.A, Severe deformity of both femurs. B, Same individual after multiple osteotomies with telescoping medullary rod fixation. C, Same individual 4 years later demonstrating growth of femurs, no recurrence of deformity, and elongation of rods. (Plaster casts are in place for immobilization of tibial osteotomies.) From Crenshaw AH, editor: Campbell’s operative orthopaedics, ed 8, vol 3, St Louis, 1992, Mosby.
  4009. Septic Arthritis
  4010. Box 38-1 Causative Microorganisms of Osteomyelitis According to Age
  4011. Newborns
  4012. Infants
  4013. Older Children
  4014. Adolescents and Adults
  4015. Juvenile Rheumatoid Arthritis
  4016. Figure 38-5 Pathogenesis of Acute Osteomyelitis Differs With Age.A, In infants younger than 1 year the epiphysis is nourished by arteries penetrating through the physis, allowing development of the condition within the epiphysis. B, In children up to 15 years of age, the infection is restricted to below the physis because of interruption of the vessels.
  4017. Figure 38-6 The Routes of Infection to the Joint.1, The hematogenous route. 2, Dissemination from osteomyelitis. 3, Spread from an adjacent soft tissue infection. 4, Diagnostic or therapeutic measures. 5, Penetrating damage by puncture or cutting.
  4018. Table 38-2 Characteristics of Juvenile Arthritis Related to Mode of Onset
  4019. Quick Check 38-1
  4020. Osteochondroses
  4021. Legg-Calvé-Perthes Disease
  4022. Pathophysiology
  4023. Figure 38-7 Stages of Legg-Calvé-Perthes Disease, a Form of Osteochondrosis.
  4024. Clinical Manifestations
  4025. Evaluation and Treatment
  4026. Osgood-Schlatter Disease
  4027. Figure 38-8 Pelvis of a 7-Year-Old Boy With Legg-Calvé-Perthes Disease. The femoral head is flat and extruded from the edge of the joint. This hip is at risk for early arthritis if left to revascularize and heal in this position.
  4028. Figure 38-9 Surgical Replacement of Femoral Head of a 7-Year-Old Boy With Legg-Calvé-Perthes Disease. As the Perthes heals, the ball has taken on a round shape that matches the socket well.
  4029. Scoliosis
  4030. Figure 38-10 Rotation and Curvature of Scoliosis. Scoliosis screening involves viewing the individual from behind, which discloses scapular asymmetry caused by not only curvature but also true rotation of the spine.
  4031. Muscular Dystrophy
  4032. Figure 38-11 Duchenne Muscular Dystrophy.A, Patient with late-stage Duchenne muscular dystrophy showing severe muscle loss. B, Transverse section of gastrocnemius muscle from a normal boy. C, Transverse section of gastrocnemius muscle from a boy with Duchenne muscular dystrophy. Normal muscle fiber is replaced with fat and connective tissue. From Jorde LB et al: Medical genetics, ed 3, updated, St Louis, 2006, Mosby.
  4033. Duchenne Muscular Dystrophy
  4034. Pathophysiology
  4035. Clinical Manifestations
  4036. Table 38-3 Major Muscular Dystrophy Syndromes
  4037. Evaluation and Treatment
  4038. Quick Check 38-2
  4039. Musculoskeletal Tumors
  4040. Benign Bone Tumors
  4041. Osteochondroma
  4042. Nonossifying fibroma
  4043. Malignant Bone Tumors
  4044. Osteosarcoma
  4045. Pathophysiology
  4046. Clinical Manifestations
  4047. Evaluation and Treatment
  4048. Ewing sarcoma
  4049. Pathophysiology
  4050. Clinical Manifestations
  4051. Evaluation and Treatment
  4052. Figure 38-12 Ewing Sarcoma.A, Most common anatomic sites. B, Closeup view of Ewing sarcoma of the distal end of the tibia. Tumor extends into the soft tissue. From Damjanov I, Linder J, editors: Anderson’s pathology, ed 10, St Louis, 1996, Mosby.
  4053. Figure 38-13 Ewing Sarcoma of the Distal Radius. Radiograph of an 8-year-old boy showing a permeative lesion of the distal radius. Note the loss of bone cortex on the ulnar border suggesting an aggressive process. Bone biopsy revealed Ewing sarcoma.
  4054. Quick Check 38-3
  4055. Nonaccidental Trauma
  4056. Fractures in Nonaccidental Trauma
  4057. Evaluation
  4058. Treatment
  4059. Did You Understand?
  4060. Congenital Defects
  4061. Bone Infection
  4062. Juvenile Rheumatoid Arthritis
  4063. Osteochondroses
  4064. Scoliosis
  4065. Muscular Dystrophy
  4066. Musculoskeletal Tumors
  4067. Nonaccidental Trauma
  4068. Key Terms
  4069. References
  4070. Chapter 39 Structure, Function, and Disorders of the Integument
  4071. Electronic Resources
  4072. Companion CD
  4073. Website http://evolve.elsevier.com/Huether/
  4074. Structure and Function of the Skin
  4075. Layers of the Skin
  4076. Health Alert Tissue Adhesives for Closure of Skin Lacerations
  4077. Figure 39-1 Structure of the Skin. From Thibodeau GA, Patton KT: Anatomy & physiology, ed 5, St Louis, 2003, Mosby.
  4078. Dermal appendages
  4079. Table 39-1 Layers of the Skin
  4080. Figure 39-2 Structures of the Nail. Redrawn from Thompson JM et al: Mosby’s clinical nursing, ed 5, St Louis, 2002, Mosby.
  4081. Blood supply and innervation
  4082. Quick Check 39-1
  4083. Clinical Manifestations of Skin Dysfunction
  4084. Lesions
  4085. Pressure ulcers
  4086. Risk Factors Pressure Ulcer
  4087. Figure 39-3 Progression of Decubitus Ulcer. Sustained pressure over a bony prominence compresses the tissue and reduces blood flow resulting in progressive ischemia and necrosis of tissue.
  4088. Table 39-2 Primary and Secondary Skin Lesions
  4089. Table 39-3 Clinical Manifestations of Select Skin Lesions
  4090. Keloids
  4091. Pruritus
  4092. Figure 39-4 Keloid Formation. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4093. Quick Check 39-2
  4094. Aging & Changes in Skin Integrity
  4095. Disorders of the Skin
  4096. Inflammatory Disorders
  4097. Allergic contact dermatitis
  4098. Irritant contact dermatitis
  4099. Figure 39-5 Poison Ivy.A, Poison ivy on knee. B, Poison ivy dermatitis. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4100. Atopic dermatitis
  4101. Stasis dermatitis
  4102. Seborrheic dermatitis
  4103. Figure 39-6 Stasis Ulcer. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4104. Papulosquamous Disorders
  4105. Psoriasis
  4106. Figure 39-7 Seborrheic Dermatitis. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4107. Figure 39-8 Psoriasis. Typical oval plaque with well-defined borders and silvery scale. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4108. Figure 39-9 Guttate Psoriasis Following Streptococcal Infection. Numerous uniformly small lesions may abruptly occur following streptococcal pharyngitis. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4109. Health Alert Biologic Treatment for Psoriasis
  4110. Pityriasis rosea
  4111. Figure 39-10 Pityriasis Rosea Herald Patch. A collarette pattern has formed around the margins. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4112. Lichen planus
  4113. Figure 39-11 Hypertrophic Lichen Planus on Arms. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4114. Quick Check 39-3
  4115. Acne vulgaris
  4116. Acne rosacea
  4117. Figure 39-12 Granulomatous Rosacea. Pustules and erythema occur on the forehead, cheeks, and nose. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4118. Lupus erythematosus
  4119. Discoid lupus erythematosus
  4120. Figure 39-13 Subacute Cutaneous Lupus (Discoid Lupus Erythematosus). Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4121. Vesiculobullous Disorders
  4122. Pemphigus
  4123. Figure 39-14 Bullous Pemphigoid. Generalized eruption with blisters arising from an edematous, erythematous annular base. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4124. Erythema multiforme
  4125. Quick Check 39-4
  4126. Infections
  4127. Bacterial infections
  4128. Folliculitis
  4129. Furuncles and carbuncles
  4130. Figure 39-15 Furuncle of the Forearm. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4131. Cellulitis
  4132. Erysipelas
  4133. Impetigo
  4134. Viral infections
  4135. Herpes simplex virus
  4136. Figure 39-16 Herpes Simplex Labialis. Typical presentation with tense vesicles appearing on the lips and extending onto the skin. From Habif TP: Clinical dermatology: a color guide to diagnosis and therapy, ed 4, St Louis, 2004, Mosby.
  4137. Herpes zoster and varicella
  4138. Warts
  4139. Figure 39-17 Herpes Zoster. Diffuse involvement of a dermatome. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4140. Figure 39-18 Verruca Vulgaris. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4141. Fungal infections
  4142. Tinea infections
  4143. Figure 39-19 Tinea Pedis. Inflammation has extended from the web area onto the dorsum of the foot. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4144. Candidiasis
  4145. Table 39-4 Common Sites of Tinea Infections
  4146. Vascular Disorders
  4147. Cutaneous vasculitis
  4148. Table 39-5 Sites of Candidiasis Infection
  4149. Urticaria
  4150. Scleroderma
  4151. Figure 39-20 Scleroderma (Acrosclerosis). Note inflammation and shiny skin. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4152. Quick Check 39-5
  4153. Insect Bites
  4154. Mosquitoes, flies, and bees
  4155. Benign Tumors
  4156. Seborrheic keratosis
  4157. Keratoacanthoma
  4158. Figure 39-21 Seborrheic Keratosis. Typical lesion that is broad, flat, and comparatively smooth surfaced. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4159. Actinic keratosis
  4160. Nevi (moles)
  4161. Quick Check 39-6
  4162. Cancer
  4163. Box 39-1 Important Trends for Skin Cancer
  4164. Incidence
  4165. Mortality
  4166. Risk Factors
  4167. Warning Signals
  4168. Prevention and Early Detection
  4169. Treatment
  4170. Survival
  4171. Basal cell carcinoma
  4172. Squamous cell carcinoma
  4173. Figure 39-22 Basal Cell Carcinoma. Center has ulcerated. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4174. Malignant melanoma
  4175. Figure 39-23 Squamous Cell Carcinoma. The sun-exposed ear is a common site for squamous cell carcinoma. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4176. Table 39-6 Classification of Nevi
  4177. Figure 39-24 Lentigo Malignant Melanoma. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4178. Kaposi sarcoma
  4179. Figure 39-25 Kaposi Sarcoma. The purple lesion commonly seen on the skin. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4180. Quick Check 39-7
  4181. Burns
  4182. Table 39-7 Depth of Burn Injury
  4183. Burn wound depth
  4184. Figure 39-26 Superficial Partial-Thickness Injury. Scald injury following débridement of overlying blister and nonadherent epithelium. Courtesy Intermountain Burn Center, University of Utah.
  4185. Figure 39-27 Axillary Burn Scar Contracture. Note the blanching of the anterior axillary fold and small ulceration from a deep partial thickness burn, both indicating the diminished range of motion. Courtesy Intermountain Burn Center, University of Utah.
  4186. Figure 39-28 Deep Partial-Thickness Wound. Note pale appearance and minimal exudate. Courtesy Intermountain Burn Center, University of Utah.
  4187. Figure 39-29 Full-Thickness Thermal Injury. The wound is dry and insensate. Courtesy Intermountain Burn Center, University of Utah.
  4188. Figure 39-30 Estimation of Burn Injury: Rule of Nines. A commonly used assessment tool with estimates of the percentages (in multiples of 9) of the total body surface area burned. A, Adults (anterior view). B, Adults (posterior view).
  4189. Box 39-2 Burn Unit Referral Criteria
  4190. Pathophysiology and Clinical Manifestations
  4191. Figure 39-31 Immediate Cellular and Immunologic Alterations of Burn Shock.
  4192. Evaporative water loss
  4193. Box 39-3 Maintenance Fluid Replacements After Major Burn Injury*
  4194. Cardiovascular response to burn
  4195. Cellular response to burn injury
  4196. Metabolic response to burn injury
  4197. Immunologic response to burn injury
  4198. Evaluation and Treatment
  4199. Figure 39-32 Hypertrophic Scarring. Deep partial-thickness thermal injury can result in extensive hypertrophic scarring. Courtesy Intermountain Burn Center, University of Utah.
  4200. Figure 39-33 Application of Cultured Epithelial Autografts. The thin sheets of keratinocytes are attached to gauze backing to allow application onto the clean, excised thigh. Courtesy Intermountain Burn Center, University of Utah.
  4201. Frostbite
  4202. Disorders of the Hair
  4203. Alopecia
  4204. Male-pattern alopecia (androgenic alopecia)
  4205. Female-pattern alopecia
  4206. Alopecia areata
  4207. Hirsutism
  4208. Disorders of the Nail
  4209. Paronychia
  4210. Onychomycosis
  4211. Quick Check 39-8
  4212. Did You Understand?
  4213. Structure and Function of the Skin
  4214. Disorders of the Skin
  4215. Disorders of the Hair
  4216. Disorders of the Nail
  4217. Key Terms
  4218. References
  4219. Chapter 40 Alterations of the Integument in Children
  4220. Electronic Resources
  4221. Companion CD
  4222. Website http://evolve.elsevier.com/Huether/
  4223. Dermatitis
  4224. Atopic Dermatitis
  4225. Figure 40-1 Atopic Dermatitis. Characteristic lesions with crusting from irritation and scratching over knees and around ankles. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4226. Diaper Dermatitis
  4227. Acne Vulgaris
  4228. Figure 40-2 Diaper Dermatitis.A, Diaper dermatitis with erosions. B, Diaper dermatitis with Candida albicans secondary infection. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4229. Figure 40-3 Cystic Acne. Multiple pustules (erythematous papules and pustules) are present, and several have become confluent. Note areas of scarring. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4230. Quick Check 40-1
  4231. Infections of the Skin
  4232. Bacterial Infections
  4233. Impetigo contagiosum
  4234. Box 40-1 Impetigo
  4235. Vesicular Impetigo
  4236. Bullous Impetigo
  4237. Figure 40-4 Impetigo and Herpes Simplex Virus (HSV) of Upper Lip. Note weeping and crusting lesions. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4238. Staphylococcal scalded-skin syndrome
  4239. Figure 40-5 Staphylococcal Scalded-Skin Syndrome (SSSS). The skin lesions, showing desquamation and wrinkling of the skin margins, appeared 1 day after drainage of a staphylococcal abscess. From Levine G, Norden C: N Engl J Med 287:1339, 1972.
  4240. Fungal Infections
  4241. Tinea capitis
  4242. Tinea corporis
  4243. Figure 40-6 Tinea Capitis. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4244. Thrush
  4245. Viral Infections
  4246. Molluscum contagiosum
  4247. Figure 40-7 Molluscum Contagiosum. Waxy pink globules with umbilicated centers. From Habif TP: Clinical dermatology: a color guide to diagnosis and therapy, ed 4, St Louis, 2004, Mosby.
  4248. Rubella (German or 3-day measles)
  4249. Health Alert MMR and Varicella Vaccines
  4250. Figure 40-8 Rubella (3-Day Measles). Typical distribution of full-blown maculopapular rash with tendency to coalesce.
  4251. Table 40-1 Differential Presentation of Viral Diseases Producing Rashes
  4252. Rubeola (red measles)
  4253. Roseola (exanthema subitum)
  4254. Chickenpox, herpes zoster, and smallpox
  4255. Chickenpox
  4256. Figure 40-9 Chickenpox. Pattern of generalized, polymorphous eruption.
  4257. Herpes zoster
  4258. Smallpox
  4259. Quick Check 40-2
  4260. Insect Bites and Parasites
  4261. Scabies
  4262. Figure 40-10 Scabies.A, Scabies mite, as seen clinically when removed from its burrow. B, Characteristic scabies bites. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4263. Pediculosis (Lice Infestation)
  4264. Fleas
  4265. Ticks
  4266. Figure 40-11 Flea Bites. Fleabite producing an urticarial wheal with central puncture.
  4267. Bedbugs
  4268. Hemangiomas and Vascular Malformations
  4269. Hemangiomas
  4270. Vascular Malformations
  4271. Figure 40-12 Capillary Hemangioma. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4272. Figure 40-13 Cavernous Hemangioma. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4273. Figure 40-14 Port-Wine Hemangioma. Port-wine hemangioma in a child. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4274. Other Skin Disorders
  4275. Miliaria
  4276. Figure 40-15 Miliaria Rubra. Note discrete erythematous papules or papulovesicles. Courtesy Department of Dermatology, School of Medicine, University of Utah.
  4277. Erythema Toxicum Neonatorum
  4278. Quick Check 40-3
  4279. Did You Understand?
  4280. Dermatitis
  4281. Acne Vulgaris
  4282. Infections of the Skin
  4283. Insect Bites and Parasites
  4284. Vascular Disorders
  4285. Other Skin Disorders
  4286. Key Terms
  4287. References
  4288. Back Matter
  4289. Appendix: Most Common Laboratory Values
  4290. Glossary

 

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