Lower Gastrointestinal Tract and Associated Accessory Digestive Organs PDF

26.3 Lower Gastrointestinal Tract and Associated Accessory Digestive Organs The lower gastrointestinal (GI) tract is composed of the small and large intestine. The lower GI tract continues the processes of digestion and functions in the absorption of nutrients. Material that cannot be digested and a...

26.3 Lower Gastrointestinal Tract and Associated Accessory Digestive Organs The lower gastrointestinal (GI) tract is composed of the small and large intestine. The lower GI tract continues the processes of digestion and functions in the absorption of nutrients. Material that cannot be digested and absorbed is then eliminated. 26.3a Overview LEARNING OBJECTIVE 22. Describe the components of the lower gastrointestinal tract and the associated accessory digestive organs. A superficial view of the lower GI tract organs and accessory digestive organs helps to integrate their general structure with their digestive activities and functions ( figure 26.15): Small intestine. The small intestine is divided into three continuous regions (duodenum, jejunum, and ileum). Recall from section 26.2a that the duodenum is considered part of the upper GI tract, but it is described in this section on the lower GI tract organs. The small intestine receives acidic chyme from the stomach that is then mixed with accessory digestive organ secretions. Most chemical digestion of macromolecules and absorption of nutrients, water, and electrolytes occur within the small intestine. Accessory digestive organs. The accessory digestive organs associated with the lower GI tract include the liver, gallbladder, and pancreas. Their collective secretions include bile and pancreatic juice. Bile is produced by the liver and then stored, concentrated, and released by the gallbladder. Pancreatic juice contains numerous digestive enzymes and is produced and released by the pancreas. Accessory digestive organ secretions—both bile and pancreatic juice—contain HCO3− (a weak base), which neutralizes acidic chyme entering the duodenum. Large intestine. The large intestine primarily absorbs water, electrolytes, and vitamins (including vitamins B and K produced by bacteria within the large intestine). The digestive process is completed as the semifluid mass of partly digested food is converted to feces and then eliminated through the anus. Figure 26.15 Gross Anatomy of the Lower GI Tract Organs and Associated Accessory Digestive Organs. The three regions of the small intestine—duodenum, jejunum, and ileum—are continuous and framed within the abdominal cavity by the large intestine. Accessory digestive organs within the abdominal cavity release secretions into the duodenum. WHAT DID YOU LEARN? 16 What organs are considered part of the lower GI tract? 26.3b Small Intestine LEARNING OBJECTIVES 23. Identify and describe the anatomy of the small intestine. 24. List the glands found in the small intestine and their secretions. 25. Explain motility within the small intestine. The small intestine, also called the small bowel, is a long tube that extends between the stomach and the large intestine. Generally, about 9 to 10 liters of ingested food, water, and digestive system secretions enter the small intestine daily. Ingested nutrients typically spend at least 12 hours in the small intestine. The small intestine finishes chemical digestion and is responsible for absorbing almost all of the nutrients and a large percentage of the water, electrolytes, and vitamins. Page 1048 INTEGRATE CLINICAL VIEW 26.7 Inflammatory Bowel Disease and Irritable Bowel Syndrome The term inflammatory bowel disease (IBD) applies to two autoimmune disorders, Crohn disease and ulcerative colitis. In both of these disorders, selective regions of the intestine become inflamed. Crohn disease is a condition of young adults characterized by inflammation of the inner lining of the GI tract. Although any region of the Gl tract may be involved, the distal ileum is the most frequently and severely affected site. Inflammation involves the entire thickness of the intestinal wall, extending from the mucosa to the serosa. For reasons that are not clear, lengthy regions of the intestine having no trace of injury or inflammation may be followed abruptly by several inches of markedly diseased intestine. Symptoms include intermittent and relapsing episodes of abdominal cramping and pain, severe diarrhea, fatigue, weight loss, and malnutrition. The age distribution and symptoms of ulcerative colitis are similar to those of Crohn disease, but ulcerative colitis involves only the large intestine. The rectum and descending colon are the first to show signs of inflammation and are generally the most severely affected. Also, in ulcerative colitis the inflammation is confined to the mucosa, instead of the full thickness of the intestinal wall. Finally, unlike Crohn disease, ulcerative colitis is associated with a significantly increased risk of colon cancer. Crohn disease and ulcerative colitis are distinctly different from a much more common disorder called irritable bowel syndrome (IBS). IBS is characterized by abnormal function of the colon with symptoms of crampy abdominal pain, bloating, constipation, and diarrhea. It occurs in about one in every five people in the United States, and is more common in women than men. Irritable bowel syndrome may be diagnosed if a medical evaluation has ruled out Crohn disease and ulcerative colitis. Although neither a cause nor a cure for IBS is known, most people can control their symptoms by reducing stress, changing their diet, and using certain medications. Recently, fecal transplants are being studied as a means to treat Crohn disease, ulcerative colitis, and IBS (see Clinical View 26.13: “Fecal Transplant”). Gross Anatomy of the Small Intestine The small intestine is a coiled, thin-walled tube about 1 inch in diameter and approximately 6 meters (20 feet) in length in the unembalmed cadaver. (It is much shorter in a living individual due to smooth muscle tone; see section 10.10c.) It extends from the pylorus of the stomach to the cecum of the large intestine; thus, it occupies a significant portion of the abdominal cavity. The small intestine consists of three specific segments: the duodenum, jejunum, and ileum. The duodenum (dū-ō-dē′nŭm, dū-od′ĕ-nŭm; breadth of 12 fingers) forms the first segment of the small intestine. It is approximately 25 centimeters (10 inches) long and originates at the pyloric sphincter, which regulates movement of chyme from the stomach into the small intestine (see figure 26.9). The duodenum is arched into a C shape around the head of the pancreas and becomes continuous with the jejunum at the duodenojejunal flexure (flek′sher; fleksura = bend) ( figure 26.15). Most of the duodenum is retroperitoneal, although the very initial portion is intraperitoneal. The most significant function of the duodenum is to serve as an “anatomic blender” that allows for efficient chemical digestion. The duodenum receives (a) acidic chyme from the stomach and (b) the secretions from the abdominal accessory digestive organs. These secretions include bile from the liver and gallbladder and pancreatic juice from the pancreas. Thus, it is within the lumen of the duodenum where all of these substances are mixed, and where digestive enzymes (with many released from the pancreas) have contact with ingested molecules and chemical digestion primarily occurs. The jejunum (jĕ-jū′nŭm; jejunus = empty) is the middle region of the small intestine ( figure 26.15). Extending approximately 2.5 meters (7.5 feet), it makes up about two-fifths of the small intestine’s total length. The jejunum is the primary region within the small intestine for nutrient absorption (i.e., where the chemically digested contents that are received from the duodenum are moved from the small intestine lumen into either the blood or the lymph; see figure 26.2b). The ileum (il′ē-ŭm; eiles = twisted) is the last region of the small intestine. At about 3.6 meters (10.8 feet) in length, the ileum forms approximately three-fifths of the small intestine. Its distal end terminates at the ileocecal (il′ē-ō-sē′kăl) valve, a sphincter that controls the entry of materials from the small intestine into the large intestine. Absorption of digested materials continues in the ileum along with the absorption of bile salts (see section 26.4c) and vitamin B12 (see section 26.4e). Both the jejunum and the ileum are intraperitoneal organs and are suspended within the abdomen by the mesentery proper (see figure 26.3). Small Intestine Structures That Increase Surface Area Absorption of substances from within the small intestine into the blood or the lymph requires vast amounts of surface area of the epithelial lining (see figure 26.2b). Three structures increase this surface area: circular folds, villi, and microvilli. Circular folds (also called plicae circulares) are macroscopic structures that are easily seen by the naked eye: They are projections formed by both the mucosal and submucosal tunics of the small intestine ( figure 26.16). Circular folds also act as “speed bumps” to slow down the movement of chyme and ensure that it remains within the small intestine for maximal nutrient absorption. Circular folds are more numerous in the duodenum and jejunum and least numerous in the ileum. Villi and microvilli are both microscopic structures described in the histology section. Figure 26.16 Histology of the Small Intestine. (a) The wall of the small intestine is formed by four tunics: mucosa, submucosa, muscularis, and serosa. (b) Circular folds are inward projections of both the mucosa and submucosa, whereas villi are fingerlike projections of only the epithelium and lamina propria of the mucosa. Both circular folds and villi increase the surface area of the small intestine. (c) The epithelial cells covering the surface of each villus have microvilli to further increase the surface area. The lamina propria within each villus houses both blood capillaries and lacteals (lymphatic capillaries) where substances are absorbed. APR Module 12: Digestive: Histology: Small Intestine WHAT DO YOU THINK? 4 Why are the circular folds much more numerous in the duodenum and least numerous in the ileum? How does the abundance of circular folds relate to the main functions of the duodenum? Histology of the Small Intestine Villi are microscopic structures of the small intestine mucosa. A villus (vil′ŭs; pl., vil′ī) is a small, fingerlike projection of the simple columnar epithelium and lamina propria of the mucosa. They, like circular folds, increase the surface area of the epithelial lining through which nutrients are absorbed. Villi are larger and most numerous in the jejunum, where much of the absorption takes place. The epithelium and lamina propria of each villus appears analogous to a glove (epithelium) covering a finger (lamina propria). Each villus contains an arteriole, a rich blood capillary network, and a venule. Most nutrients are absorbed into these blood capillaries. A lacteal is a type of lymphatic capillary also within the villus (described in section 21.1a). A lacteal is responsible for absorbing lipids and lipid-soluble vitamins that are too large to be absorbed by the blood capillaries (see sections 26.4c, e). Microvilli (mī-krō-vil′ī; micros = small) are microscopic extensions of the plasma membrane of the simple columnar epithelial cells lining the small intestine (and average about 1 μm high) (see section 4.6c). Microvilli further increase the surface area of the small intestine. Individual microvilli are not clearly visible in light micrographs of the small intestine; instead, they appear as a fuzzy edge of the simple columnar cells called the brush border. Embedded within this brush border are various enzymes that complete the chemical digestion of most nutrients immediately before absorption (see section 26.4). Collectively, these are called brush border enzymes. Located in close proximity and also embedded within the plasma membrane are the required proteins for membrane transport of digested molecules. Histologic images of both villi and microvilli are shown in figure 26.17. Between the intestinal villi are invaginations of the mucosa called intestinal glands (also known as intestinal crypts or crypts of Lieberkühn), which secrete intestinal juice. These glands extend to the base of the mucosa and slightly resemble the anatomy of the gastric glands of the stomach ( figure 26.16c). Figure 26.17 Intestinal Villi and Microvilli. Photomicrographs show (a) the internal structure of villi projecting into the intestinal lumen and (b) microvilli epithelium’s apical surface. (a) Al Telser/McGraw-Hill Education; (b) Dr. Lee Peachey Watch Video: Absorption of Nutrients in the Small Intestine Small Intestine Secretions Four types of secretory cells of the intestinal epithelium contribute to the process of digestion ( figure 26.16c). Three of these cell types produce intestinal juice. The fourth type of cell secretes hormones into the blood. Goblet cells within the simple columnar epithelium produce mucin that when hydrated form mucus, which lubricates and protects the intestinal lining. These cells increase in number from the duodenum to the ileum, because more lubrication is needed as digested materials (and water) are absorbed and undigested materials (and less water) remain in the lumen. The enteroendocrine cells release hormones such as CCK and secretin into the blood. We have already discussed the stomach-associated functions of these hormones (see section 26.2d). Several other functions are described in summarized in section 26.3c and table 26.1. Paneth cells are located only in the base of the intestinal crypts. These cells assist with the functioning of the innate immune system (see section 22.3) by secreting lysozyme, as well as some other antimicrobial agents, to help protect against potentially harmful substances (e.g., virus) that are within the small intestine. Another type of gland housed within the submucosal layer and found only in the proximal duodenum is called a duodenal submucosal gland (or Brunner gland) (not shown in figure 26.16). This gland produces a viscous, alkaline mucus secretion that protects the duodenum from the acidic chyme entering the duodenum from the stomach. Page 1050 Motility of the Small Intestine Smooth muscle activity of the muscularis within the small intestine wall has three primary functions: (a) mixing chyme with accessory gland secretions, (b) moving the chyme continually against the brush border, and (c) propelling the contents through the small intestine toward the large intestine. All these functions facilitate chemical digestion and absorption, employing the processes of segmentation and peristalsis. When chyme first enters the small intestine, segmentation is more prevalent than peristalsis. Segmentation mixes chyme with secretions from the accessory digestive organs through a “backward-and-forward” motion (see figure 26.2c). Peristalsis then propels material within the GI lumen by alternating contraction of the circular and longitudinal muscle layers in small regions. The rhythm of muscular contractions is more frequent in the duodenum than in the ileum; thus, the net movement of intestinal contents is toward the large intestine. Regulation of Small Intestine Motility During the Intestinal Phase The small intestine is the primary portion of the GI tract for both (a) the disassembly of complex molecules into a smaller, simpler form (chemical digestion) and (b) absorption of these smaller, simpler molecules (and the absorption of most of the water, electrolytes, and vitamins). Thus, for optimal chemical digestion and absorption, it is essential that small intestine motility is highly regulated. The regulation of motility of the small intestinal occurs during the intestinal phase, a phase first described in the section “Regulation of the Digestive Processes of the Stomach” (see section 26.2d). This phase can be split into an early intestinal phase and a late intestinal phase. Early Intestinal Phase and Segmentation Segmentation is more prevalent early in the intestinal phase (when chyme is entering from the stomach into the small intestine). The function of segmentation is to thoroughly mix the chyme, accessory digestive organ secretions, and intestinal juice released from the small intestine. Recall that segmentation is the “back-and-forth” motion of a few centimeters for mixing contents. Imagine these events as placing the ingredients for a cake mix into an elongated balloon, then using your hands on the outside of the balloon to squeeze the contents back and forth until they are mixed. The muscular contractions are initiated by pacemaker cells (interstitial cells of Cajal), which are located between the smooth muscle layers of the muscularis within the small intestine wall (as they are in the stomach wall). Electrical signals spread through the smooth muscle cells in the muscularis layer of the stomach via gap junctions to allow the single-unit smooth muscle (see section 10.10e) to contract. This establishes the basic rhythm of muscular contraction of the small intestine to cause segmentation. The specific rate the pacemaker cells spontaneously depolarize is more frequent than the rate within the stomach (which is less than four times per minute), but it differs depending upon the segment of the small intestine. The rhythm is the most frequent in the duodenum (about 12–14 times per minute) and declines along the length of the small intestine to the ileum (about 8–9 times per minute). The significance of the difference is that because contractions occur more frequently in the proximal portion of the small intestine, there is a slow net movement of chyme from the duodenum to the ileum—allowing time for optimal digestion and absorption. Note that while the frequency is typically unchanging, the intensity (force) of the contractions can be altered by both short reflexes involving the enteric nervous system and long reflexes involving the autonomic nervous system (see section 26.1d). Late Intestinal Phase and Peristalsis Peristalsis is more prevalent (and segmentation decreases) late in the intestinal phase after most substances have been digested and absorbed. The function of peristalsis is to move the remaining undigested material, sloughed-off epithelial cells, and bacteria toward the ileum for their movement into the large intestine. Recall that peristalsis is a directional movement. Imagine these events like placing your hands on an elongated balloon and squeezing from one end to the other—to empty the contents from the balloon. The peristaltic muscular contractions are initiated by motilin hormone, which is released from the duodenum in progressively greater amounts late in the intestinal phase. Peristalsis is first initiated in the proximal portion of the duodenum. A peristaltic wave of muscle contraction squeezes on the contents and moves approximately 2 feet before the wave of contraction wanes and ceases. Another peristaltic wave is then initiated a small distance (distally) from the original point of initiation. This peristaltic wave travels about 2 feet before waning and ceasing. This pattern repeats itself down the length of the small intestine, moving the contents within the lumen toward the ileum. These successive waves of contractions are called a migrating motility complex, which requires about 2 hours from duodenum to ileum. The migrating motility complex repeats until all of the content is moved into the large intestine. Note that these events are also regulated by the enteric nervous system and long reflexes involving the autonomic nervous system (see section 26.1d). Moving Chyme from the Small Intestine into the Large Intestine The ileocecal valve, which is located between the ileum and the cecum (the first part of the large intestine) is typically contracted and closed, preventing movement of chyme from the small intestine into the large intestine. Regulatory processes including the gastroileal reflex, which is initiated during the gastric phase, function to open this valve. The gastroileal (gas′trō-il′ē-ăl) reflex (which is thought to have both short reflexes and long reflexes that involve the medulla oblongata) is initiated by food entering the stomach. As part of this reflex, the ileum contracts, the ileocecal valve relaxes, and the cecum (the first part of the large intestine) relaxes. Thus, contents within the GI tract are moved from the ileum through the open ileocecal valve into the cecum. Then, the ileocecal valve contracts to prevent backflow from the cecum into the ileum. During the intestinal phase, the release of CCK causes relaxation of the ileocecal valve. Page 1051 WHAT DID YOU LEARN? 17 What are the three anatomic structures that increase the surface area of the small intestine? Describe each. 18 Which type of motility is primarily responsible for mixing the chyme and accessory gland secretions within the small intestine—segmentation or peristalsis? Which for propulsion? Explain each. 26.3c Accessory Digestive Organs and Ducts LEARNING OBJECTIVES 26. List the accessory digestive organs associated with releasing secretions into the duodenum, and describe the ducts that deliver these secretions. 27. Identify and describe the liver, and explain how both blood and bile flow through the liver. 28. Identify and describe the pancreas, and explain its general function in digestion. 29. Explain the regulation of the accessory digestive glands associated with the small intestine. Three accessory digestive organs release secretions into the duodenum: the liver, the gallbladder, and the pancreas. Here we examine the ducts from each organ to the duodenum, the anatomy and histology of each organ, and their products conveyed to the small intestine that contribute to the digestion of the chyme arriving from the stomach. Accessory Digestive Organ Ducts A series of ducts deliver secretions from the accessory digestive organs to the duodenum of the small intestine ( figure 26.18). These ducts include the biliary apparatus from the liver and gallbladder, and the pancreatic ducts from the pancreas. Figure 26.18 Biliary Apparatus and Pancreatic Ducts. Various ducts merge to transport bile and pancreatic juice from accessory digestive organs to the duodenum. The biliary (bil′ē-ăr-ē) apparatus is a network of thin ducts that include the right and left hepatic ducts, which drain the right and left lobes of the liver, respectively. The right and left hepatic ducts merge to form a single common hepatic duct. The union of the cystic duct from the gallbladder and the common hepatic duct forms the common bile duct, which extends to the hepatopancreatic ampulla (described shortly). The pancreatic ducts include both the main pancreatic duct and the accessory pancreatic duct. The main pancreatic duct transports the majority of the pancreatic juice. It joins with the common bile duct to form the hepatopancreatic ampulla. The accessory pancreatic duct is a smaller duct whereby limited amounts of pancreatic juice may also enter the duodenum. This duct penetrates the duodenal wall, forming the minor duodenal papilla. The hepatopancreatic ampulla (or ampulla of vater) is a swelling either adjacent to or within the posterior duodenal wall, which penetrates through the duodenal wall forming a small projection called the major duodenal papilla. The hepatopancreatic ampulla receives bile from the common bile duct (coming from the liver and gallbadder) and pancreatic juice from the main pancreatic duct. The release of these accessory gland secretions (bile and pancreatic juice) is regulated by the hepatopancreatic sphincter that is located within the ampulla. This sphincter is normally closed, preventing accessory digestive gland secretions from entering the duodenum. Relaxation and opening of this sphincter permits the flow of these secretions into the duodenum (a process stimulated by the cholecystokinin [CCK] hormone). Page 1052 Liver The liver is an accessory digestive organ located in the right upper quadrant of the abdomen, immediately inferior to the diaphragm (see (described in figure 26.1). It has numerous functions section 27.6), but its main function in digestion is the production of bile. Gross Anatomy of the Liver The liver is the largest internal organ, weighing 1 to 2 kilograms (2 to 4 pounds), and it constitutes approximately 2% of an adult’s body weight. The liver is covered by a connective tissue capsule except at the porta hepatis (described shortly). Covering the connective tissue capsule is a layer of visceral peritoneum, except for a small region on its diaphragmatic surface called the bare area ( figure 26.19). Figure 26.19 Gross Anatomy of the Liver. (a) Anterior and (b) posteroinferior views show the four lobes of the liver. APR Module 12: Digestive: Animations: Liver The liver is composed of four partially separated lobes and is supported by two ligaments. The major lobes are the right lobe and the left lobe. The right lobe is separated from the smaller left lobe by the falciform ligament, a peritoneal fold that secures the liver to the internal surface of the anterior abdominal wall, as discussed in section 26.1e. In the inferior free edge of the falciform ligament lies the round ligament of the liver (ligamentum teres), which represents the remnant of the fetal umbilical vein (see section 20.12a). Within the right lobe are the caudate (kaw′dāt; cauda = tail) lobe and the quadrate (kwah′drāt; quadrates = square) lobe. The caudate lobe is adjacent to the inferior vena cava, and the quadrate lobe is adjacent to the gallbladder. Along the inferior surface of the liver are several structures that collectively resemble the letter H. The gallbladder and the round ligament of the liver form the vertical superior parts of the H; the inferior vena cava and the ligamentum venosum form the vertical inferior parts. (Recall from section 20.12 that the ligamentum venosum is a remnant of the ductus venosus in the embryo. This vessel, which allows blood to bypass the liver, shunted blood from the umbilical vein to the inferior vena cava.) Finally, the porta (pōr′tă; gate); hepatis (hep′ă-tis; hepatikos = liver), the horizontal crossbar of the H, is the site at which blood and lymph vessels, bile ducts, and nerves (not shown) extend from the liver. In particular, the hepatic portal vein and branches of the hepatic artery proper enter at the porta hepatis. Histology The liver’s connective tissue capsule branches throughout the organ and forms septa (walls) that partition the liver into thousands of microscopic polyhedral hepatic lobules, which are the structural and functional units of the liver ( figure 26.20). Within hepatic lobules are liver cells called hepatocytes (hep′ă-tō-sīt). At the periphery of each lobule are several portal triads, composed of a bile ductule, and microscopic branches of both the hepatic portal vein and the hepatic artery. At the center of each lobule is a central vein that drains the blood flow from the lobule. Central veins collect the blood and merge throughout the liver to form left and right hepatic veins that eventually empty into the inferior vena cava. Figure 26.20 Histology of the Liver. (a) The functional units of the liver are called hepatic lobules. (b) A central vein projects through the center of a hepatic lobule, and several portal triads are positioned at its periphery. (c) A photomicrograph depicts a liver lobule and portal triad. (d) Diagram of the hepatic portal system. (c) Victor P. Eroschenko; (c [inset]) Al Telser/McGraw-Hill Education APR Module 12: Digestive: Histology: Liver: LM Low Magnification: Portal Triad In cross section, a hepatic lobule looks like a side view of a bicycle wheel. The central vein is like the hub of the wheel. At the circumference of the wheel (where the tire would be) are the portal triads that are usually equidistant apart. Cords of hepatocytes make up the numerous spokes of the wheel, and they are bordered by hepatic sinusoids, which transport blood (see section 20.1c). Blood Flow in Liver Lobules The cells of the liver receive blood from two sources; one is oxygenated and the other is deoxygenated (see section 20.10d). The hepatic artery is a branch of the celiac trunk that extends off of the descending abdominal aorta and transports oxygenated blood to the liver (see figure 20.24). The hepatic portal vein is part of the hepatic portal system and transports deoxygenated and nutrient-rich blood from the capillary beds of the GI tract, spleen, and pancreas (see figure 20.25). The hepatic portal vein delivers approximately 75% of the blood volume to the liver (the hepatic artery brings the other 25%). The hepatic artery and hepatic portal vein branch extensively into smaller vessels until microscopic branches form components of the portal triad. The oxygenated blood from the hepatic artery branch (within the portal triad) and the deoxygenated blood of the hepatic portal vein branch (within the portal triad) both enter a sinusoid where the blood is “processed.” (Recall from section 20.1c that sinusoids are thin-walled capillaries with large gaps between these cells, which make the sinusoids significantly more permeable than other capillaries.) Blood then drains into the central vein of the lobule. Central veins collect the blood from each lobule and merge throughout the liver to ultimately form left and right hepatic veins that empty into the inferior vena cava ( figure 26.20). Page 1053 INTEGRATE CONCEPT CONNECTION The hepatic portal system is a venous network that drains the digestive organs and shunts the blood to the liver (see section 20.10d). The blood exits the liver through hepatic veins that merge with the inferior vena cava. The GI tract absorbs digested nutrients. These nutrients must be transported to and processed within the liver. The liver also detoxifies any potentially harmful agents that have been absorbed into the GI blood vessels. It is much more efficient and potentially protective to transport blood containing these substances first to the liver via the hepatic portal system for processing, before this blood is distributed throughout the body. Page 1054 Several significant events occur as blood is transported through hepatic sinusoids: Nutrients are absorbed from the sinusoids and enter the hepatocytes. Oxygen is delivered to hepatocytes for aerobic cellular respiration (see section 3.4). Stellate cells (or Kupffer cells), which are macrophages that line the liver sinusoid, engage in phagocytosis of potentially harmful substances (e.g., microbes). (Stellate cells are fixed macrophages of the immune system; see section 22.2a.) Bile: Its Formation and Flow in Liver Lobules Bile is a yellowish-green, alkaline fluid containing mostly water, bicarbonate ions (HCO3–), bile salts, bile pigments (e.g., bilirubin), cholesterol, lecithin (a phospholipid), and mucin. Hepatocytes of the liver produce bile at a rate of 0.5 to 1 liter per day. Bile is released from hepatocytes into bile canaliculi ( figure 26.20b). These small channels transport bile to bile ductules of portal triads. (Observe that bile flow, which is away from the central vein to the portal triad, is in the opposite direction of blood flow, which moves from the portal triad to the central vein.) Bile within the bile ductules flows into progressively larger bile ducts until reaching either the right or left hepatic duct (see figure 26.18). The ducts of the biliary apparatus transport the bile to the duodenum. Bile has several functions, including: Neutralizing acidic chyme within the small intestine through bicarbonate ions (HCO3–) Emulsification of lipids by bile salts and lecithin (which is a type of mechanical digestion; see section 26.4c) Elimination of bilirubin, a waste product of erythrocyte destruction (see section 18.3b) Note that bile does not contain digestive enzymes for the chemical breakdown of nutrients within the GI tract. Instead, components of bile (e.g., bile salts) are dividing the larger aggregates of lipid into smaller aggregates of lipid by mechanical digestion (like ice cubes broken into ice chips). This allows for more effective chemical digestion by pancreatic lipase (see section 26.4c). Watch Video: Digestion, Absorption: Emulsification with Bile Gallbladder Attached to the inferior surface of the liver ( figure 26.19), the gallbladder (or cholecyst) is a saclike organ that stores, concentrates, and releases bile that the liver produces. The gallbladder has three tunics: an inner mucosa, a middle muscularis, and an external serosa. The mucosa is thrown into folds that permit distension of the wall as the gallbladder fills with bile. The gallbladder drains bile into the cystic (sis′tik; cysto = bladder) duct, which connects to the common bile duct (see figure 26.18). At the neck of the gallbladder, a sphincter valve controls the flow of bile into and out of the gallbladder. Bile enters the gallbladder when the hepatopancreatic sphincter associated with the hepatopancreatic ampulla is closed. It backs up through both the common bile duct and the cystic duct into the gallbladder. The gallbladder can hold approximately 40 to 60 milliliters of concentrated bile. Concentrated bile is transported from the gallbladder through the cystic duct and then the common bile duct through the hepatopancreatic ampulla into the duodenum. INTEGRATE CLINICAL VIEW 26.8 Cirrhosis of the Liver Liver cirrhosis (sir-rō΄sis; kirrhos = yellow) results when hepatocytes have been destroyed and are replaced by fibrous scar tissue. This scar tissue, which results from collagen synthesis by stellate cells in the liver, often surrounds isolated nodules of regenerating hepatocytes. The fibrous scar tissue also compresses (a) the blood vessels within the liver, resulting in hepatic portal hypertension (high blood pressure in the hepatic portal venous system), and (b) bile ducts in the liver, which impedes bile flow. Liver cirrhosis is caused by injury to the hepatocytes, as may result from chronic alcoholism, liver diseases, or certain drugs or toxins. Most frequently, viral infections from either hepatitis B or hepatitis C produce chronic hepatitis. Other disorders that result in liver cirrhosis include some inherited diseases, chronic biliary obstruction, and biliary cirrhosis. Early stages of liver cirrhosis may be asymptomatic. However, once liver function begins to falter, the individual complains of fatigue, weight loss, and nausea and may have pain in the right upper quadrant. During an exam, a doctor may palpate an abnormally small and hard liver. To confirm the diagnosis, a liver biopsy is done to obtain a small portion of liver tissue through a needle passed into the liver; the cells are then examined microscopically. The fibrosis and scarring of liver cirrhosis are irreversible. However, further scarring may be slowed or prevented by treating the cause of the cirrhosis (e.g., alcoholism, hepatitis). Advanced liver cirrhosis may have a variety of complications: Jaundice (yellowing of the skin and sclerae of the eyes) occurs when the liver’s ability to eliminate bilirubin (a component of bile) is impaired (see section 18.3b). Edema (e-dē΄m˘a), the accumulation of fluid in body tissues, is evident due to reduced formation and release of albumin (which results in a decrease in colloid osmotic pressure; see section 20.3). Ascites (˘a-sī΄tēz; fluid accumulation in the abdomen) may also develop because of decreased albumin production. Intense itching occurs when bile products are deposited in the skin. Toxins in the blood and brain accumulate because the liver cannot effectively process them. Hepatic portal hypertension may lead to dilated veins of the inferior esophagus (esophageal varices). End-stage liver cirrhosis may be treated only with a liver transplant. Otherwise, death results either from progressive liver failure or from the complications. This gross specimen depicts a type of nodular cirrhosis of the liver. Yoav Levy/Medical Images Page 1055 INTEGRATE CLINICAL VIEW 26.9 Gallstones Concentration of bile within the gallbladder may lead to the eventual formation of gallstones. Gallstones occur twice as frequently in women as in men and are more prevalent in developed countries. Obesity, advanced age, female sex hormones, Caucasian ethnicity, and lack of physical activity are all risk factors for developing gallstones. The term cholelithiasis (kō΄lē-li-thī΄ă-sis; chol = bile, lithos = stone, iasis = condition) refers to the presence of gallstones in the gallbladder. If the gallstones leave the gallbladder and enter the biliary apparatus, the term choledocholethiasis is used. Gallstones are typically formed from condensations of either cholesterol or calcium and bile salts. These stones may vary from the tiniest grains to almost golf-ball-sized. The majority of gallstones are asymptomatic until a gallstone becomes lodged in the neck of the cystic duct, causing the gallbladder to become inflamed (cholecystitis) and dilated. The most common symptom is severe pain (called biliary colic). This pain may be perceived in the right hypochondriac region (see figure 1.10), between the scapulae, or in the area of the right posterior deltoid region (see section 16.2c). Nausea and vomiting may occur, along with indigestion and bloating. Symptoms are typically worse after eating a fatty meal. Treatment consists of surgical removal of the gallbladder, called cholecystectomy (kō΄lē-sis-tek΄tō-mē; kystis = bladder, ektome = excision). Following surgery, the liver continues to produce bile, even in the absence of the gallbladder, but concentrating bile (which is a function of the gallbladder) no longer occurs. A photograph of gallstones in a gallbladder. Clinical Photography, Central Manchester University Hospitals NHS Foundation Trust, UK/Science Source WHAT DO YOU THINK? 5 If your gallbladder were surgically removed, how would this affect your digestion of fatty meals? What diet alterations might you have to make after this surgery? Pancreas The pancreas has both endocrine and exocrine functions. Endocrine cells produce and secrete hormones such as insulin and glucagon (see section 17.10b). Exocrine cells produce pancreatic juice to assist with chemical digestion. Disorders that affect either (a) the pancreatic ducts that lead from the pancreas into the duodenum (e.g., cystic fibrosis; see Clinical View 26.17: “Cystic Fibrosis and the Pancreas”) or (b) the pancreas (e.g., pancreatic cancer; see Clinical View 26.10: “Pancreatic Cancer”) have serious and potentially fatal effects on the ability to digest and absorb nutrients. Gross Anatomy of the Pancreas The pancreas is approximately 5 to 6 inches in length and about 1 inch thick. It is a retroperitoneal organ that extends horizontally from the duodenum toward the left side of the abdominal cavity, where it has contact with the spleen. The pancreas exhibits a wide head adjacent to the curvature of the duodenum; a central, elongated body projecting toward the left lateral abdominal wall; and a tail that tapers as it approaches the spleen ( figure 26.21). Figure 26.21 Anatomy of the Pancreas. The (a) diagram and (b) photo show the components of the pancreas in relationship to the duodenum. (b) Christine Eckel/McGraw-Hill Education APR Module 12: Digestive: Dissection: Biliary Ducts: Anterior: Pancreas Histology The pancreas contains modified simple cuboidal epithelial cells called acinar (as′i-năr) cells that are arranged in saclike acini (sing., acinus = grape) ( figure 26.22). These cells are organized into large clusters termed lobules. Acinar cells produce and release digestive enzymes. Small ducts lead from each acinus into larger ducts that empty into either the main pancreatic duct or the accessory pancreatic duct, which lead to the duodenum (as described). The simple cuboidal epithelial cells lining the pancreatic ducts have the important function of secreting alkaline fluid containing bicarbonate ion (HCO3–). This weak base functions to neutralize acidic chyme entering the small intestine. Figure 26.22 Histology of the Pancreas. Photomicrograph of the histology of pancreatic acini and pancreatic islets, with diagram of pancreatic acinus. Carolina Biological Supply Company/Phototake Pancreatic Secretions Together, secretions of acinar cells and cells that line the pancreatic ducts form pancreatic juice. Pancreatic juice (approximately 1 to 1.5 liters per day) is an alkaline fluid containing mostly water, HCO3–, and a versatile mixture of digestive enzymes, which are described in detail in section 26.4. These enzymes include the following: Pancreatic amylase to digest starch Pancreatic lipase for the digestion of triglycerides Inactive proteases (trypsinogen, chymotrypsinogen, and procarboxypeptidase) that, when activated, digest protein Nucleases for the digestion of nucleic acids (DNA and RNA) Regulation of Accessory Digestive Structures Several of the same processes that regulate stomach motility and secretions described in sections 26.2d and 26.3b also control the release of secretions from the accessory digestive organs. Recall that regulation of the stomach is organized into three phases: cephalic phase, gastric phase, and intestinal phase. The increase in vagal stimulation in the cephalic phase and gastric phase, in addition to stimulating stomach motility and secretion, also activates the pancreas to release pancreatic juice. Recall that in the intestinal phase, both cholecystokinin (CCK) and secretin are released. Cholecystokinin is a hormone released from the small intestine primarily in response to free fatty acids in chyme. The functions of CCK include: Stimulating smooth muscle within the gallbladder wall to strongly contract, causing the release of concentrated bile (this primary function of stimulating the gallbladder, also called the cholecyst, is how the name cholecystokinin is derived) Stimulating the pancreas to release enzyme-rich pancreatic juice Relaxing the smooth muscle within the hepatopancreatic ampulla, allowing entry of bile and pancreatic juice into the small intestine Secretin is released from the small intestine primarily in response to an increase in chyme acidity. Secretin primarily causes the release of an alkaline solution that contains HCO3– from both the liver and ducts of the pancreas. Upon entering the small intestine, this alkaline fluid helps neutralize the acidic chyme. (Recall from section 26.2d that CCK and secretin also inhibit stomach motility and release of gastric secretions.) Hormones that regulate digestion are summarized in table 26.1. Page 1056 WHAT DID YOU LEARN? 19 Diagram the ducts of the accessory digestive organs that release their secretions into the duodenum. 20 Does the liver produce digestive enzymes? If not, what substance does it produce that assists in digestion? 21 What are the primary functions of pancreatic juice? 26.3d Large Intestine LEARNING OBJECTIVES 30. Identify and describe the three major regions of the large intestine and four segments of the colon of the large intestine. 31. Explain the distinguishing histologic features of the large intestine. 32. Describe the bacterial action that takes place in the large intestine. The large intestine, also called the large bowel, is a relatively wide tube that is significantly shorter than the small intestine. It is called the “large” intestine because its diameter is greater than that of the small intestine. Approximately 2 liters of digested material passes from the small intestine to the large intestine daily. Most nutrients (including water, electrolytes, and vitamins) have been absorbed within the small intestine. The large intestine absorbs water (about 1.8 liters per day, for an adult). The large intestine also absorbs some electrolytes (primarily sodium [Na+] and chloride [Cl–] ions) from the remaining digested material that enters it from the small intestine (as well as vitamins B and K, which are synthesized by bacteria within the large intestine). It is estimated that only 200 milliliters of the water entering the colon daily is lost in feces (see figure 25.4). Thus, the watery chyme that first enters the large intestine, including all of the undigested materials as well as the waste products secreted by the accessory digestive organs (e.g., bilirubin by the liver), solidifies and is compacted into feces, or fecal material. The large intestine then stores this fecal material until it is eliminated through defecation. Page 1057 INTEGRATE CLINICAL VIEW 26.10 Pancreatic Cancer The pancreas is both an endocrine gland (producing the hormones insulin and glucagon that are released into the blood; see section 17.10) and an exocrine gland (producing digestive enzymes that are released into ducts that empty into the duodenum). Pancreatic cancer is cancer of pancreatic cells, most commonly originating in exocrine cells of the pancreas (in approximately 95% of cases). Risk factors for pancreatic cancer include smoking (which doubles your risk), obesity, diabetes, and advanced age. The prognosis for pancreatic cancer, like most other types of cancers, is more favorable with early detection—before the cancer has metastazied to the lymph nodes. Unfortunately, early detection of pancreatic cancer is difficult due to (a) the lack of a screening test for pancreatic cancer and (b) the fact that symptoms and signs tend to be nonspecific to the pancreas (e.g., abdominal pain, loss of appetite, weight loss). Consequently, pancreatic cancer is often detected in advanced stages of the disease when complete surgical removal of the tumor is no longer possible. It is for this reason (its late detection) that pancreatic cancer is often fatal. Gross Anatomy of the Large Intestine The large intestine has a diameter of 6.5 centimeters (2.5 inches) and an approximate length of 1.5 meters (5 feet) from its origin at the ileocecal junction to its termination at the anus ( figure 26.23). Three major regions constitute the large intestine: the cecum, the colon, and the rectum. Figure 26.23 Gross Anatomy of the Large Intestine. (a) Anterior view of the large intestine that forms the distal end of the GI tract. (b) Details of the anal canal. APR Module 12: Digestive: Dissection: Abdominal Cavity: Anterior: Transverse colon Cecum The cecum (sē′kŭm; caecus = blind) is a blind sac. It is the first portion of the large intestine and located in the right lower abdominal quadrant. This pouch extends inferiorly from the ileocecal valve. Chyme enters the cecum from the ileum. Projecting inferiorly from the posteromedial region of the cecum is the vermiform (ver′mi-fōrm; vermis = worm) appendix (ă-pen′diks; appendage), a thin, fingerlike sac lined by lymphocyte-filled lymphoid nodules (see section 21.4d). Both the cecum and the vermiform appendix are intraperitoneal organs. Research studies indicate that the appendix may serve as a reservoir of bacteria that are beneficial to the function of the colon. Colon At the level of the ileocecal valve, the second region of the large intestine, the colon, begins and forms an inverted U-shaped arch. The colon is partitioned into four segments: the ascending colon, transverse colon, descending colon, and sigmoid colon. The ascending colon originates at the ileocecal valve and extends superiorly from the superior edge of the cecum along the right lateral border of the abdominal cavity. The ascending colon is retroperitoneal, since its posterior wall directly adheres to the posterior abdominal wall, and only its anterior surface is covered with peritoneum. As it approaches the inferior surface of the liver, the ascending colon makes a 90-degree turn toward the left side and anterior region of the abdominal cavity. This bend in the colon is called the right colic (kol′ik) flexure, or the hepatic flexure. Page 1058 INTEGRATE CLINICAL VIEW 26.11 Appendicitis Inflammation of the appendix is called appendicitis (ă-pen-di-sī΄tis). Most cases of appendicitis occur because fecal matter obstructs the appendix, although sometimes an appendix becomes inflamed without any obstruction. As the tissue becomes inflamed, the appendix swells, the blood supply is compromised, and bacteria may proliferate in the wall. Untreated, the appendix may burst and release its contents into the peritoneum, causing a massive and potentially deadly infection called peritonitis (see Clinical View 26.1: “Peritonitis”). During the early stages of acute appendicitis, the smooth muscle wall contracts and goes into spasms. Because this smooth muscle is innervated by the autonomic nervous system, pain is referred to the T10 dermatome around the umbilicus (see section 16.2c). As the inflammation worsens and the parietal peritoneum becomes inflamed as well, the pain becomes sharp and localized to the right lower quadrant of the abdomen. Individuals with appendicitis typically experience nausea or vomiting, abdominal tenderness in the inferior right quadrant, a low fever, and an elevated leukocyte count. An inflamed appendix is surgically removed in a procedure called an appendectomy. Inflamed appendix. UIG/Phototake The transverse colon originates at the right colic flexure and curves slightly anteriorly as it projects horizontally to the left across the anterior region of the abdominal cavity. The transverse colon is intraperitoneal. As the transverse colon approaches the spleen in the left upper quadrant of the abdomen, it makes a 90-degree turn inferiorly and posteriorly. The resulting bend in the colon is called the left colic flexure, or the splenic flexure. The descending colon is retroperitoneal and located along the left side of the abdominal cavity and slightly posterior. It originates at the left colic flexure and descends vertically to the sigmoid colon. The sigmoid (sig′moyd; resembling letter S) colon originates at the sigmoid flexure and turns inferomedially into the pelvic cavity. The sigmoid colon, like the transverse colon, is intraperitoneal. The sigmoid colon terminates at the rectum. Recall from section 26.1e that a type of mesentery, called the mesocolon, attaches each section of the colon to the posterior abdominal wall, with the mesocolon of each region specifically named (e.g., ascending mesocolon, transverse mesocolon). Rectum The rectum (rek′tŭm; rectus = straight) is the third major region of the large intestine. It is a retroperitoneal structure that extends from the sigmoid colon. The rectum is a muscular tube that readily expands to store accumulated fecal material prior to defecation. Three thick transverse folds of the rectum, called rectal valves, ensure that fecal material is retained during the passing of gas. The anal canal makes up the terminal few centimeters of the large intestine. The anal canal is lined by a stratified squamous epithelium, and it passes through an opening in the levator ani muscles of the pelvic floor (see section 11.7) and terminates at the anus. The internal lining of the anal canal contains relatively thin longitudinal ridges, called anal columns, between which are small depressions termed anal sinuses. As fecal material passes through the anal canal during defecation, pressure exerted on the anal sinuses causes their cells to release mucin to form mucus. The extra mucus lubricates the anal canal during defecation. At the base of the anal canal are the involuntary smooth muscle internal anal sphincter and voluntary skeletal muscle external anal sphincter, which close off the opening to the anal canal. The muscles composing these sphincters relax and allow the sphincter to open during defecation. Specialized Structures of the Large Intestine Several features are unique to the large intestine, including teniae coli, haustra, and epiploic appendages. Teniae (tē′nē-ē; ribbons, band) coli (kō′lī) are thin, distinct, longitudinal bundles of smooth muscle. The teniae coli act like elastic in a waistband—they help bunch up the large intestine into many sacs, collectively called haustra (haw′stră; sing., haustrum; haustus = to drink up). Hanging off the external surface of the haustra are lobules of fat called omental appendices, or epiploic (e-pi-plō′ik; membrane-covered) appendages. Histology of the Large Intestine The mucosa of the large intestine is lined by a simple columnar epithelium with numerous goblet cells ( figure 26.24). Unlike the small intestine, the large intestine mucosa is smooth and lacks intestinal villi, yet it resembles the small intestine in that it has epithelial cells and numerous intestinal glands (or crypts) that extend inward toward the muscularis mucosae. The glands’ mucous cells secrete mucin into the lumen to lubricate the undigested material and facilitate its passage through the large intestine. Many lymphoid nodules and immune cells occupy the lamina propria of the large intestine (see section 21.4d). Figure 26.24 Histology of the Large Intestine. (a) The luminal wall of the large intestine is composed of four tunics: mucosa, submucosa, muscularis, and serosa. (b) A photomicrograph shows the histology of the mucosa and submucosa of the large intestine wall. (b) ©Al Telser/McGraw-Hill Education The muscularis of the cecum and colon has two layers of smooth muscle, but the outer longitudinal layer is discontinuous and does not completely surround the colon and cecum. Instead, these longitudinal smooth muscle fibers form the teniae coli, just described. Bacterial Action in the Large Intestine Numerous normal bacterial flora inhabit the large intestine; these microorganisms are called the intestinal microbiota (or gut microbiota). The intestinal microbiota are responsible for the chemical breakdown of complex carbohydrates, proteins, and lipids that remain in the chyme after it has passed through the small intestine. Bacterial actions produce gases (carbon dioxide, hydrogen, hydrogen sulfide, and methane) from digestion of carbohydrates, and indoles and skatoles from digestion of protein. Some of these substances account for the odor of feces. Additionally, bacteria of the intestinal microbiota produce B vitamins and vitamin K, which are then absorbed from the large intestine into the blood. (Note that these vitamins are also absorbed in the small intestine from the foods that we eat.) Feces is the final product formed and then eliminated from the GI tract. Feces (fē′cēz; faex = dregs) are composed of water, salts, epithelial cells (sloughed from GI lining), bacteria, and undigested material (see Clinical View 26.13: “Fecal Transplant”). Note that the study of the composition of our intestinal microbiome (which consists of a trillion microbial cells and their genetic composition) is part of the worldwide research efforts of the Human Microbiome Project (HMP). Research studies have correlated the composition of the intestinal microbiota with diseases of the GI tract (e.g., ulcerative colitis, Crohn disease), as well as diseases not associated with the GI tract (e.g., obesity, atherosclerosis, psychiatric disorders) (see Clinical View 1.2: “The Human Microbiome: Another Human Organ?”). Page 1059 INTEGRATE CLINICAL VIEW 26.12 Colorectal Cancer The term colorectal cancer refers to a malignant growth anywhere along the large intestine (colon or rectum). The majority of colorectal cancers appear in the distal descending colon, sigmoid colon, and rectum, which are the segments of the large intestine that have the longest contact with fecal matter before it is expelled from the body. Most colorectal cancers arise from polyps (pol΄ip), which are outgrowths from the colon mucosa. Note, however, that colon polyps are very common, and most of them never become cancerous. Low-fiber diets have also been implicated in increasing the risk of colon cancer, because decreased dietary fiber leads to decreased stool bulk and longer time for stools to remain in the large intestine. Theoretically, this condition exposes the large intestine mucosa to toxins in the stools for longer periods of time. Other traditional risk factors include a family history of colorectal cancer, personal history of ulcerative colitis, and increased age (most patients are over the age of 40). African Americans are disproportionately affected, with greater numbers of cases and higher rates of deaths compared to other ethnicities. A recent American Cancer Society study showed an increase in the number of individuals in their 20s and 30s who are being diagnosed with the disease. The reasons for this rise are unclear but may be an increase in obesity rates or a change in the large intestine intestinal microbiota (due to dietary trend changes). Initially, most patients are asymptomatic. Later, they may notice rectal bleeding (often evidenced as blood in the stool or on the toilet paper) and a persistent change in bowel habits (typically constipation or diarrhea). Eventually, the person may experience abdominal pain, fatigue, unexplained weight loss, and anemia. The cancerous growth must be removed surgically, and sometimes radiation or chemotherapy is used as well. Colorectal cancers that are limited to the mucosa have a 5-year survival rate, but the prognosis is poor for cancers that have spread into deeper colon wall tunics or to the lymph nodes. The key to an increased survival rate for colorectal cancer is early detection. If caught early, colorectal cancer is very treatable. An individual should see his or her doctor if rectal bleeding or any persistent change in bowel habits is experienced. Screening tests recommended by age 50 (or earlier, for those who have symptoms or a family history of colorectal cancer) include a fecal occult (ō-kŭlt΄, ok΄ŭlt) blood test, sigmoidoscopy (sig΄moy-dos΄kŏ-pē; skopeo = to view), and colonoscopy (kō-lon-os΄ kŏ-pē). Polyps in the large intestine may lead to colorectal cancer. Page 1060 INTEGRATE CONCEPT CONNECTION Recall that heme is broken down into bilirubin and absorbed from the blood in the liver (see section 18.3b). Bilirubin is then released as a component of bile into the small intestine. It is either reabsorbed back into the blood and eliminated as urobilin in the urine, or it continues through the GI tract into the large intestine, where bacteria convert it to stercobilin. Stercobilin is a brown pigment that contributes to the normal color of feces. INTEGRATE CLINICAL VIEW 26.13 Fecal Transplant A fecal transplant (or fecal microbiota transplant or bacteriotherapy) involves a relatively low-cost, low-risk procedure of collecting the fecal matter of a stool from a healthy donor (stool contains normal microbiota), combining it with a solution (e.g., saline solution), straining it, and then placing it in the colon of a patient (e.g., through an enema or a colonoscopy). Fecal transplants are done to treat recurrent Clostridium difficile (C. difficile) colitis, which is an often debilitating pathogenic bacterial infection that sometimes results in fatal diarrhea (in an estimated 4–14% of cases). C. difficile colitis is usually the result of a previous antibiotic treatment that decreased or eliminated the normal microbiota within the colon. Fecal transplants are considered investigational by the Federal Drug Administration (FDA), and only qualified physicians with an Investigational New Drug (IND) application are permitted by the Federal Drug Administration (FDA) to perform fecal transplants for treating recurrent C. difficile infections. An important step is screening donors to determine if they are at risk for carrying multi-drug-resistant organisms (MDROs). Research studies are investigating the use of fecal transplants in treating intestinal disorders (e.g., Crohn disease, ulcerative colitis, irritable bowel syndrome; see Clinical View 26.7: “Inflammatory Bowel Disease and Irritable Bowel Syndrome”). Results have shown that fecal transplant may be an effective treatment, and research continues into the types of conditions that might benefit from this treatment. INTEGRATE CLINICAL VIEW 26.14 Diverticulosis and Diverticulitis Diverticulosis (dī΄ver-tik΄yū-lō΄sis) is the presence of diverticula (small “bulges”) in the intestinal lining. These are formed typically when the colon tightens and narrows in response to low amounts of fiber or bulk in the colon. Diverticulitis is inflammation of diverticula. Diverticulitis may be lifethreatening if the diverticula rupture and fecal matter leaks into the abdominal cavity. An external view and endoscopic view of the sigmoid colon show diverticula. Gastrolab/SPL/Science Source Motility and Regulation of the Large Intestine Several types of movements are noted in the large intestine: Peristalsis of the large intestine is usually weak and sluggish, but otherwise it resembles the peristalsis that occurs in the wall of the small intestine. Haustral churning occurs after a relaxed haustrum fills with digested or fecal material until its distension stimulates reflex contractions in the muscularis. These contractions increase churning and move the material to more distal haustra. Mass movements are powerful, peristaltic-like contractions involving the teniae coli, which propel fecal material toward the rectum. A wave of contraction begins in the middle of the transverse colon, forcing a large amount of fecal matter into the descending colon, sigmoid colon, and rectum. Generally, mass movements occur two or three times a day, often during or immediately after a meal. Two major reflexes of the nervous system are associated with motility in the large intestine: The gastrocolic (gas′trō-kol′ik) reflex is initiated by stomach distension to cause a mass movement (motility in the large intestine, just described). The defecation reflex is the involuntary component in the elimination of feces from the GI tract by the process of defecation (def-ĕ-kā′shŭn; defaeco = to remove the dregs) ( figure 26.25). Filling of the rectum initiates the urge to defecate. This stimulus results in transmission of nerve signals from the receptors along sensory neurons to the spinal cord. In response, increased nerve signals are relayed along parasympathetic motor neurons (see section 15.3), which causes both the sigmoid colon and rectum to contract and the internal (involuntary) anal sphincter to relax. (The defecation reflex is an example of a monosynaptic reflex; see section 14.6c.) Page 1061 Figure 26.25 Defecation. The defecation reflex involves sensory perception of stretch in the rectum that initiates a spinal reflex, stimulating muscles in the sigmoid colon and rectum to contract and the internal anal sphincter to relax. Conscious regulation of defecation requires the relaxation of the external anal sphincter and the Valsalva maneuver. Watch Video: Reflexes in the Colon INTEGRATE CLINICAL VIEW 26.15 Constipation and Diarrhea Constipation is typically a temporary, impaired ability to defecate and generally results in compacted feces that are difficult to eliminate. Constipation may result from a combination of factors, including a diet low in fiber (insufficient bulk), dehydration, lack of exercise, and improper bowel habits (not defecating when the urge arises, allowing additional water to be absorbed from the feces). Constipation is also a common side effect of general anesthesia. Part of postoperative care is to verify that GI motility has returned to normal by determining that the patient has had a bowel movement. Additionally, long-term use of opiate medications (e.g., oxycontin) causes constipation. This is because the large intestine contains opioid receptors and when opiates bind to them, GI motility decreases and water absorption from the feces is greater. Constipation increases the risk of both hemorrhoids (hem΄o΄roydz; rhoia = flow), which are dilated and inflamed veins around the rectum and anus, and anal fissures, which are oval-shaped tears of the anus that often bleed. In contrast, diarrhea may result as a consequence of disruption in normal mechanisms to absorb intestinal water, or excessive amounts of osmotically active solutes that keep water in the intestinal lumen and prevent its reabsorption. One example of such an osmotically active solute is sorbitol, a sugar substitute often found in sugar-free ice cream, diet sodas, cough syrups, and sugar-free gum. Sorbitol is considered a nonstimulant laxative because it draws water into the large intestine and stimulates bowel movements. Loperamide (i.e., Immodium AD) is an antidiarrheal drug that essentially works by binding to the opiate receptors and thereby decreasing GI motility and limiting diarrhea symptoms. Voluntary elimination of feces from the body typically is learned sometime after age 3 years. The conscious decision (initiated by the cerebral cortex) to defecate involves both the Valsalva maneuver (see section 23.2d) and relaxation of the external anal sphincter. WHAT DID YOU LEARN? 22 What is the pathway of chyme from its entry into the large intestine until feces is eliminated? 23 What are the general functions of intestinal microbiota within the large intestine? 24 Which substances are typically absorbed by the large intestine?