Upper Gastrointestinal Tract and Accessory Digestive Structures PDF

26.2 Upper Gastrointestinal Tract and Associated Accessory Digestive Structures The upper gastrointestinal tract consists of the oral cavity (where salivary glands release their secretions), the pharynx, esophagus, stomach, and duodenum. It is where the initial mechanical and chemical processing of...

26.2 Upper Gastrointestinal Tract and Associated Accessory Digestive Structures The upper gastrointestinal tract consists of the oral cavity (where salivary glands release their secretions), the pharynx, esophagus, stomach, and duodenum. It is where the initial mechanical and chemical processing of ingested material takes place. 26.2a Overview LEARNING OBJECTIVE 13. Describe the components of the upper gastrointestinal tract and associated accessory digestive structures. An overview of the upper GI tract organs and accessory structures helps integrate their general structures with their digestive activities and functions (see figure 26.1): Oral cavity and salivary glands. Mechanical digestion (mastication) begins in the oral cavity. Saliva is secreted from the salivary glands in response to food being present within the oral cavity. It is mixed with the ingested materials to form a globular, wet mass called a bolus. One component of saliva is salivary amylase, an enzyme that initiates the chemical digestion of starch (amylose). Pharynx (far′ingks). The bolus is moved into the pharynx during swallowing. Mucus secreted in saliva and in the superior part of the pharynx provides lubrication to facilitate swallowing. Esophagus. The bolus is transported from the pharynx through the esophagus into the stomach. Mucus secretion by the esophagus lubricates the passage of the bolus. Stomach. The bolus is mixed with gastric secretions as the muscularis in the stomach wall contracts. These secretions are released into the stomach lumen by epithelial cells of the stomach mucosa and include acid (hydrochloric acid [HCl]), digestive enzymes, and mucin. The mixing continues as an acidic “purée” called chyme is formed. Note that the first part of the small intestine is the duodenum. It is also included in the upper GI tract; however, it will be described with the rest of the small intestine in section 26.3b. WHAT DID YOU LEARN? 10 What structures are considered part of the upper GI tract? How is the ingested material referred to as it moves through each of the structures of the upper GI tract? 26.2b Oral Cavity and Salivary Glands LEARNING OBJECTIVES 14. Identify and describe the anatomic structures of the oral cavity. 15. Explain how the release of saliva is regulated. 16. Describe the process of mastication. 17. Explain the growth and development of the teeth. The Oral Cavity The oral cavity, or mouth, is the entrance to the GI tract ( figure 26.4). Food is ingested into the oral cavity, where it undergoes the initial processes of mechanical and chemical digestion. Page 1034 Figure 26.4 Oral Cavity. Ingested food and drink enter the GI tract through the oral cavity and move into the pharynx. (a) An anterior view shows the structures of the oral cavity. (b) A sagittal section shows the structures of both the oral cavity and the pharynx. APR Module 12: Digestive: Dissection: Oral Cavity and Pharynx: Oral cavity proper Gross Anatomy The oral cavity has two distinct spatial regions: (a) the vestibule (or buccal cavity), which is the space between the gums, lips, and cheeks; and (b) the oral cavity proper, which lies central to the teeth. The oral cavity is bounded laterally by the cheeks and anteriorly by the teeth and lips, and it leads posteriorly into the oropharynx. The cheeks are covered externally by the integument and contain the buccinator muscles (see figure 11.5). These muscles compress the cheeks against the teeth to hold solid materials in place during mastication (chewing). The cheeks terminate at the fleshy lips (or labia) that are formed primarily by the orbicularis oris muscle (see section 11.3a). Lips have a reddish hue because of their abundant supply of superficial blood vessels and the reduced amount of keratin within their outer skin. The internal surfaces of both the superior and inferior lips each are attached to the gingivae (gums) by a thin mucosa fold in the midline, called the labial frenulum (lā′bē-ăl; labium = lip, fren′ū-lŭm; frenum = bridle). You can feel the labial frenulum associated with the upper lips by firmly pressing your tongue into the midline of the vestibule. The palate (pal′ăt) forms the superior boundary, or “roof,” of the oral cavity and acts as a barrier to separate it from the nasal cavity. The anterior two-thirds of the palate is hard and bony (called the hard palate), whereas the posterior one-third is soft and muscular (called the soft palate). You can feel the distinction between the hard palate and soft palate by moving your tongue along the roof of your mouth. The hard palate is formed by fusion of the two palatine processes of the maxillae and the horizontal plates of the two palatine bones (see section 8.2b). Failure of these bones to fuse results in a cleft palate, which is associated with swallowing issues. (See Clinical View 8.1: “Cleft Lip and Palate.”) Prominent transverse palatine folds, or friction ridges, on the anterior hard palate assist the tongue in manipulating ingested materials prior to swallowing. Extending inferiorly from the posterior part of the soft palate is a cone-shaped medial projection called the uvula (ū′vū-lă). When you swallow, the soft palate and the uvula elevate to close off the posterior entrance into the nasopharynx and prevent ingested materials from entering the nasal region (see section 26.2c). The fauces (faw′sēz) represent the opening (or “doorway”) between the oral cavity and the oropharynx. The fauces are bounded by paired muscular folds or arches: the anterior palatoglossal (păl′a-tō-glos′ăl; glossa = tongue) arch and the posterior palatopharyngeal (păl′a- tō-fa-rin′jē-ăl; pharynx = throat) arch. The name of each of these folds reflects its proximity to the tongue and pharynx, respectively. The palatine tonsils are housed between the arches. These tonsils are clusters of lymphoid tissue (see section 21.4c) that protect us by monitoring ingested food and drink for potentially harmful agents (see section 22.2a). The inferior surface, or floor, of the oral cavity houses the tongue. The tongue is formed primarily from skeletal muscle. Both extrinsic and intrinsic muscles move the tongue (see section 11.3c). Numerous small projections called papillae (pă-pil′ē; sing., papilla; papula = pimple) cover the superior (dorsal) surface of the tongue and are involved in the sense of taste (see section 16.3b). The posteroinferior region of the tongue also contains clusters of lymphoid tissue called the lingual tonsils (see section 21.4c). The inferior surface of the tongue attaches to the floor of the oral cavity by a thin vertical mucous membrane, the lingual frenulum. The tongue manipulates and mixes ingested materials during chewing and helps compress the partially digested materials against the palate to assist in mechanical digestion. The tongue also performs important functions in both swallowing and speech production (as well as when infants are breastfeeding). The teeth and gums are described in detail at the end of this section. Histology The epithelial lining of the oral cavity is a stratified squamous epithelium that protects against the abrasive activities associated with chewing. The nonkeratinized type of epithelium lines most of the oral cavity; the keratinized type lines the lips, portions of the tongue, and a small region of the hard palate. Salivary Glands Salivary glands, which produce saliva, are located both within the oral cavity (intrinsic salivary glands) and outside the oral cavity (extrinsic salivary glands). Intrinsic salivary glands are unicellular exocrine glands (see section 5.1d) that continuously release relatively small amounts of secretions independent of the presence of food. Only the secretions from the intrinsic salivary glands contain lingual lipase, an enzyme that begins the digestion of triglycerides (after the bolus enters the stomach, as described later). Most saliva, however, is produced from multicellular exocrine glands outside the oral cavity called extrinsic salivary glands. Gross Anatomy Three pairs of multicellular salivary glands are located external to the oral cavity: the parotid, submandibular, and sublingual glands ( figure 26.5a). Figure 26.5 Salivary Glands. Saliva is produced primarily by three paired extrinsic salivary glands. (a) The relative locations of the parotid, submandibular, and sublingual salivary glands are shown in a side view. (b) Serous and mucous alveoli are shown in a diagrammatic representation of salivary gland histology. (c) Both mucous and serous cells may be seen in a micrograph of the submandibular salivary gland. (c) Al Telser/McGraw-Hill Education APR Module 12: Digestive: Dissection: Salivary glands: Submandibular gland The parotid (pă-rot′id; para = beside, ot = ear) salivary glands are the largest salivary glands. Each parotid gland is located anterior and inferior to the ear, partially overlying the masseter muscle. The parotid salivary glands produce a portion (about 25–30%) of the saliva, which is transported through the parotid duct to the oral cavity. The parotid duct extends from the gland, across the external surface of the masseter muscle, before penetrating the buccinator muscle and opening into the vestibule of the oral cavity near the second upper molar. Mumps is an infection of the parotid glands by a virus (see section 22.1) called myxovirus. Children are protected against mumps when immunized with the MMR (measles, mumps, and rubella) vaccine. Page 1035 The submandibular salivary glands are both inferior to the floor of the oral cavity and medial to the body of the mandible, as their name suggests. The submandibular salivary glands produce most of the saliva (about 60–70%). A submandibular duct opens from each gland through a papilla in the floor of the oral cavity on either side of the lingual frenulum. The sublingual salivary glands are inferior to the tongue, and medial and anterior to the submandibular salivary glands. Each sublingual salivary gland extends multiple tiny sublingual ducts that open onto the inferior surface of the oral cavity, posterior to the submandibular duct papilla. These small glands contribute only a limited amount (about 3– 5%) of the total saliva. Histology Two types of secretory cells are housed within the large, paired salivary glands and collectively produce the components of saliva: mucous cells and serous cells ( figure 26.5b, c). Mucous cells secrete mucin, which forms mucus upon hydration, whereas serous cells secrete a watery fluid containing electrolytes and salivary amylase. The proportion of mucous cells to serous cells varies among the three types of salivary glands. The parotid glands primarily produce serous secretions, whereas the submandibular and sublingual glands produce both mucus and serous secretions. Saliva The volume of saliva (sa-li′va) secreted daily ranges between 1 and 1.5 liters. (Imagine that volume of saliva in a liter drink container!) Most saliva is produced during mealtime, but smaller amounts are produced continuously to ensure that the oral cavity mucous membrane remains moist. Saliva is composed of 99.5% water and a mixture of solutes. Saliva is formed as water and electrolytes are filtered from plasma within blood capillaries, then through cells (acini) of a salivary gland. Other components are added by cells of the salivary glands, including salivary amylase, mucin, and lysozyme. The functions of saliva include the following: Moistens ingested food as it is formed into a bolus (bō′lŭs; bolos = lump), a globular, wet mass of partially digested material that is more easily swallowed Initiates the chemical breakdown of starch (a polymer of glucose molecules; see section 2.7c) in the oral cavity because of the salivary amylase it contains Acts as a watery medium into which food molecules are dissolved so taste receptors may be stimulated (see section 16.3b) Cleanses the oral cavity structures Helps inhibit bacterial growth in the oral cavity because it contains antibacterial substances, including lysozyme and IgA antibodies (IgA is formed by plasma cells in the lamina propria and transported across the epithelial cells [see section 22.8c]) Page 1036 Regulation of Salivary Secretions The salivary nuclei within the pons (see section 13.5b) regulate salivation. A basal level of salivation in response to parasympathetic stimulation ensures that the oral cavity remains moist (see section 15.3a). Input to the salivary nuclei is received from chemoreceptors or baroreceptors in the upper GI tract. These receptors detect various types of stimuli, including the introduction of substances into the oral cavity, especially those that are acidic, such as a lemon; and arrival of foods into the stomach lumen, especially foods that are spicy or acidic. If one eats spoiled food, bacterial toxins within the stomach stimulate receptors that initiate sensory nerve signals to the salivary nuclei. Input is also received by the salivary nuclei from the higher brain centers in response to the thought, smell, or sight of food. Stimulation of the salivary nuclei by either sensory receptors or higher brain centers results in increased nerve signals relayed along parasympathetic neurons within both the facial nerve (CN VII), which innervates the submandibular and sublingual salivary glands, and the glossopharyngeal nerve (CN IX), which innervates the parotid salivary glands, and additional saliva is released. Sympathetic stimulation, which occurs during exercise or when an individual is excited or anxious (see section 15.4c), results in a more viscous saliva by decreasing the water content of saliva. (This occurs because sympathetic stimulation constricts blood vessels of the salivary gland, which decreases the fluid added to saliva.) WHAT DO YOU THINK? 2 Research suggests that a dry mouth (inadequate production of saliva) is correlated with an increase in both bad breath (halitosis) and dental problems, such as cavities. What are the possible reasons for this correlation? Mechanical Digestion: Mastication Mechanical digestion in the oral cavity is called mastication (mas′ti-kā′shŭn; mastico = to chew) or chewing. It requires the coordinated activities of teeth, skeletal muscles in lips, tongue, cheeks, and jaws that are controlled by nuclei within the medulla oblongata and pons, collectively called the mastication center. The primary function in chewing the food is to mechanically reduce its bulk into smaller particles to facilitate swallowing. Chemical digestion and absorption are affected very little by chewing, except that the surface area of the food is increased, which facilitates exposure to and action by digestive enzymes. Mastication also promotes salivation to help soften and moisten the food to form a bolus. Note that medications composed of small, nonpolar molecules, which are described in section 2.3c (e.g., nitroglycerin, to treat angina pectoris) may be absorbed directly into the blood from the mouth. When these medications are placed under the tongue, they pass through the oral cavity epithelium by simple diffusion (see into the blood. section 4.3a) and are absorbed Teeth The teeth are collectively known as the dentition (den-tish′ŭn; dentition = teething). A tooth has an exposed crown, a constricted neck, and one or more roots that anchor it to the jaw ( figure 26.6a). The roots of the teeth fit tightly into dental alveoli, which are sockets within the alveolar processes of both the maxillae and the mandible. Collectively, the roots, the dental alveoli, and the periodontal membranes that bind the roots to the alveolar processes form a gomphosis joint (see section 9.2a). Figure 26.6 Teeth. Ingested food is chewed by the teeth in the oral cavity. (a) Anatomy of a molar. (b, c) Comparison of the average dentition of deciduous and permanent teeth, including the approximate age at eruption for each tooth. APR Module 12: Digestive: Dissection: Teeth: Mandibular teeth Page 1037 Dentin (den′tin; dens = tooth) forms the primary mass of a tooth. Dentin is comparable to bone but harder. On the external surface of the dentin, a tough, durable layer of enamel forms the crown of the tooth. Enamel is the hardest substance in the body and is primarily composed of calcium phosphate crystals. The center of the tooth is a pulp cavity that contains pulp, which is a soft gelatinous tissue containing nerves and blood and lymph vessels. A root canal is continuous with the pulp cavity and opens into the connective tissue surrounding the root through an opening called the apical foramen. Blood vessels and nerves housed in the pulp pass through the apical foramen. Each root of a tooth is ensheathed within hardened material called cementum (se-men′tŭm). Dental caries (tooth decay or tooth cavities) are damage to the dentin, tooth enamel, or cementum. Dental caries are promoted by bacteria within the mouth, which metabolize (break down) ingested carbohydrate to form acidic products that damage the teeth. Deciduous and Permanent Teeth Two sets of teeth develop and erupt during a normal lifetime ( figure 26.6b, c). In an infant, 20 deciduous (dē-sid′ū-ŭs; deciduus = falling off) teeth, also called milk teeth, erupt between 6 months and 30 months after birth. These teeth are eventually lost and replaced by 32 permanent teeth. As figure 26.6b shows, the more anteriorly placed permanent teeth tend to appear first, followed by the posteriorly placed teeth. (The major exception to this rule is the first molars, which appear at about age 6 and sometimes are referred to as the 6year molars.) The last teeth to erupt are the third molars, often called wisdom teeth, in the late teens or early 20s. The jaw often lacks space to accommodate these final molars, and they may either emerge only partially or grow at an angle and become impacted (wedged against another structure). Impacted teeth cannot erupt properly because of the angle of their growth. Pressure or pain caused by impacted teeth may require removal of the impacted tooth (or teeth) by surgical extraction. The most anteriorly placed permanent teeth are called incisors (in-sī′zōr; incido = to cut into). They are shaped like a chisel and have a single root. They are designed for slicing or cutting into food. Immediately posterolateral to the incisors are the canines (kā′nīn; canis = dog), or cuspids, which have a single pointed tip for puncturing and tearing food. Premolars (or bicuspids) are located posterolateral to the canines and anterior to the molars. They have flat crowns with prominent ridges called cusps that are used to crush and grind ingested materials. Premolars may have one or two roots. The molars are the thickest and most posteriorly placed teeth. They have large, broad, flat crowns with distinctive cusps and three or more roots. Molars are also adapted for grinding and crushing ingested materials. If the oral cavity is divided into quadrants, each quadrant contains the following number of permanent teeth: two incisors, one canine, two premolars, and three molars (see figure 8.6). The gingivae (jin′ji-vă, -vē) are the gums. They are composed of dense irregular connective tissue, with an overlying nonkeratinized stratified squamous epithelium that covers the alveolar processes of the upper and lower jaws and surrounds the neck of the teeth. Gingivitis is inflammation of the gingivae—the gums appear red and swollen, and they may bleed. It is important to have gingivitis treated because it can lead to dental disease and tooth loss. WHAT DID YOU LEARN? 11 What are the roles of the tongue, teeth, and salivary glands in forming a bolus? 26.2c Pharynx and Esophagus LEARNING OBJECTIVE 18. Describe the anatomy of the pharynx and esophagus and their complementary activities in the process of swallowing. The pharynx and the esophagus connect the oral cavity to the stomach ( figure 26.7a). Figure 26.7 The Oropharynx, Laryngopharynx, and Esophagus. (a) The oropharynx and laryngopharynx are the parts of the pharynx that connect the mouth to the esophagus. The esophagus is a normally collapsed, muscular tube that extends inferiorly from the pharynx to the stomach and functions in the passage of food and drink. (b) A photomicrograph of a transverse section through the esophagus identifies the tunics in its wall. The esophagus is shown here in its normal collapsed position. (b) Alfred Pasieka/Science Source APR Module 12: Digestive: Dissection: Esophagus: Anterior: Esophagus Page 1038 INTEGRATE CLINICAL VIEW 26.2 Reflux Esophagitis and Gastroesophageal Reflux Disease (GERD) Reflux esophagitis is an inflammation of the esophagus caused by backflow (or reflux) of acidic stomach contents into the esophagus. Because the pain is felt posterior to the sternum and may be so intense that it is mistaken for a heart attack, this condition is commonly known as heartburn. Unlike the stomach epithelium, the esophageal epithelium is poorly protected against acidic contents and easily becomes inflamed and irritated. Reflux esophagitis is seen most frequently in overweight individuals, smokers, those who have eaten a very large meal (especially just before bedtime), and people with hiatal hernias (hī-ā΄tăl her΄nē-ă; rupture), in which a portion of the stomach protrudes through the diaphragm into the thoracic cavity. Eating spicy foods, or ingesting too much caffeine, may exacerbate the symptoms in people affected by reflux esophagitis. Preventive treatment includes lifestyle changes such as losing weight, quitting smoking, limiting meal size, and not lying down until 2 hours after eating. Sleeping with the head of the bed elevated 4 to 6 inches, so that the body lies at an angle rather than flat, also may alleviate symptoms. Chronic reflux esophagitis may lead to gastroesophageal reflux disease (GERD). Frequent gastric reflux erodes the esophageal tissue in this condition, so over a period of time, scar tissue builds up in the esophagus, leading to narrowing of the esophageal lumen. In more advanced cases, the esophageal epithelium may change from stratified squamous to columnar epithelium, a condition known as Barrett esophagus. The secretions of columnar epithelium may provide protection from the erosive gastric secretions. Unfortunately, this metaplasia increases the risk of cancerous growths. GERD may be treated with a series of medications. Proton pump inhibitors (e.g., omeprazole [Prilosec], esomeprazole [Nexium]) and histamine (H2) blockers (e.g., famotidine [Pepcid]) limit acid secretion in the stomach, whereas antacids help neutralize stomach acid. Gastrolab/Science Source Gross Anatomy of the Pharynx The pharynx was described in detail in section 23.2c. It is a funnel-shaped, muscular passageway with distensible (stretchable) lateral walls that serves as the passageway for both air and food. Three skeletal muscle pairs called the superior, middle, and inferior pharyngeal constrictors form the wall of the pharynx (see section 11.3c). The oropharynx and laryngopharynx are lined with nonkeratinized stratified squamous epithelium that provides protection against abrasion associated with swallowing ingested materials. Gross Anatomy of the Esophagus The esophagus (ĕ-sof′ă-gŭs) is a normally collapsed, tubular passageway. It is about 25 centimeters (10 inches) long in an adult and begins at approximately the level of the cricoid cartilage of the larynx (see figure 23.5), with most of its length within the thoracic cavity. This tube is directly anterior to the vertebral bodies and posterior to the trachea (see figure 23.8a, b), until it passes through an opening in the diaphragm called the esophageal hiatus (hī-ā′tŭs; to yawn). Only the last 1.5 centimeters (slightly more than 1/2 inch) of the esophagus is located within the abdominal cavity, where its inferior end connects to the stomach. The superior esophageal sphincter (or pharyngoesophageal sphincter) is a contracted ring of circular skeletal muscle at the superior end of the esophagus. It is the area where the esophagus and the pharynx meet. This sphincter is closed during inhalation of air, so air does not enter the esophagus and instead enters the larynx and trachea. The inferior esophageal sphincter (gastroesophageal, or cardiac, sphincter) is a contracted ring of circular smooth muscle at the inferior end of the esophagus. This sphincter is not strong enough alone to prevent materials from refluxing back into the esophagus; instead, the muscles of the diaphragm at the esophageal opening contract to help prevent materials from regurgitating from the stomach into the esophagus (see Clinical View 26.2: “Reflux Esophagitis and Gastroesophageal Reflux Disease [GERD]”). Histology of the Esophagus The mucosa of the esophagus is lined with a nonkeratinized stratified squamous epithelium ( figure 26.7b). It protects this region from abrasion as food is swallowed. The esophagus submucosa is thick and composed of abundant elastic fibers that permit distension during swallowing (and recoil after the bolus has passed through). It also houses numerous mucous glands that provide thick, lubricating mucus for the epithelium. The ducts of these glands project through the mucosa and open into the lumen. The muscularis of the esophagus is unique in that it contains a blend of both skeletal and smooth muscle. The two layers of muscle in the superior one-third of the esophageal muscularis are skeletal, rather than smooth, to ensure that the swallowed material moves rapidly out of the pharynx and into the esophagus before the next respiratory cycle begins. (Remember that smooth muscle contracts more slowly than does skeletal muscle; see section 10.10c.) Skeletal muscle and smooth muscle cells intermingle in the middle onethird of the esophageal muscularis, and only smooth muscle is found within the wall of the inferior one-third of this muscularis. This transition marks the beginning of a continuous smooth muscle muscularis that extends throughout the stomach and the small and large intestines to the anus. The outermost layer of the esophagus is an adventitia. Motility: The Swallowing Process Swallowing, also called deglutition (dē-glū-tish′ŭn), is the process of moving ingested materials from the oral cavity to the stomach. Swallowing has three phases: the voluntary phase, the pharyngeal phase, and the esophageal phase ( figure 26.8). Page 1039 Figure 26.8 Phases of Swallowing. Swallowing occurs as a result of coordinated muscular activities that force the bolus from the oral cavity into the stomach. The process is organized into three phases: (1) voluntary phase, (2) pharyngeal phase, and (3) esophageal phase. The voluntary phase occurs after ingestion. It is controlled by the cerebral cortex (primarily the temporal lobes and motor cortex of the frontal lobe). Ingested materials and saliva mix in the oral cavity. Chewing forms a bolus that is mixed and manipulated by the tongue and then pushed superiorly against the hard palate. Transverse palatine folds in the hard palate help direct the bolus posteriorly toward the oropharynx. The arrival of the bolus at the entryway to the oropharynx (fauces) initiates the swallowing reflex of the pharyngeal phase. The pharyngeal phase is involuntary. Tactile sensory receptors around the fauces are stimulated by the bolus and initiate nerve signals along sensory neurons to the swallowing center (or deglutition center) in the medulla oblongata (see section 13.5c). Nerve signals are then relayed along motor neurons to effectors to cause the following response: Entry of the bolus into the oropharynx Elevation of the soft palate and uvula to block the passageway between the oropharynx and nasopharynx Elevation of the larynx by the extrinsic muscles (see section 23.2d) move the larynx anteriorly and superiorly, resulting in the epiglottis covering the laryngeal inlet; this prevents ingested material from entering the trachea In addition, nerve signals are relayed to the respiratory center within the medulla oblongata to assure that a breath is not taken during swallowing. During this time, the bolus passes quickly and involuntarily through the pharynx to the esophagus—about 1 second elapses in this phase. Sequential contraction of the pharyngeal constrictors decreases the diameter of the pharynx, beginning at its superior end and moving toward its inferior end. This creates a pressure difference, forcing swallowed material from the pharynx into the esophagus. The esophageal phase is also involuntary. It is the time during which the bolus passes through the esophagus and into the stomach—about 5 to 8 seconds. The presence of the bolus within the lumen of the esophagus stimulates sequential waves of muscular contraction that assist in propelling the bolus toward the stomach. Higher pressure occurs in the superior region of the esophagus relative to the inferior region. The superior and inferior esophageal sphincters are normally closed at rest. When the bolus is swallowed, these sphincters relax to allow it to pass through the esophagus. The inferior esophageal sphincter contracts after passage of the bolus, helping to prevent reflux of materials and fluids from the stomach into the esophagus. INTEGRATE CLINICAL VIEW 26.3 Achalasia Achalasia (ak-ă-lā΄zē΄ă) is failure of the smooth muscle of a sphincter to relax (preventing passage of material). The term typically refers to esophageal achalasia when not specified. Esophageal achalasia (also called achalasia cardiae, cardiospasm, or esophageal aperistalsis) is failure of the lower esophageal sphincter to relax and smooth muscle within the wall of the esophagus to contract (resulting in decreased peristalsis). Impaired ability to swallow (dysphagia), which becomes progressively worse, and regurgitation characterize esophageal achalasia. Treatments include calcium channel blockers, botulinum toxin (Botox), and surgery (Heller myotomy, which is a lengthwise cut along the esophagus). Page 1040 WHAT DID YOU LEARN? 12 How do the tunics of the esophagus differ from the “default” tunic pattern in both the mucosa and muscularis? 13 How is the bolus moved from the oral cavity into the stomach, as described in the three phases of swallowing? 26.2d Stomach LEARNING OBJECTIVES 19. Identify and describe the gross anatomy and histology of the stomach. 20. Explain the two general functional activities of the stomach. 21. Describe the phases that regulate motility and secretion in the stomach. The stomach (stŭm′ŭk) is a holding sac in the superior left quadrant of the abdomen immediately inferior to the diaphragm (see figure 26.1). Under normal conditions, between 3 and 4 liters of food, drink, and saliva enter the stomach daily and generally spend between 2 and 6 hours there, depending upon the amount and composition of the ingested material. It mixes the ingested food with secretions released from the stomach wall and mechanically digests the contents into a semifluid mass called chyme. Chemical digestion of both protein and fat begins in the stomach, but absorption from it is limited to small, nonpolar molecules (see section 2.7b) that are in contact with the mucosa of the stomach. Both alcohol and aspirin are examples of substances that are absorbed in the stomach. One significant function of the stomach is to serve as a “holding bag” for controlled release of partially digested materials into the small intestine, where most chemical digestion and absorption occur. One of the most vital functions performed by the stomach is the release of intrinsic factor (a substance required for the absorption of vitamin B12, which occurs within the small intestine). Gross Anatomy of the Stomach The stomach is a muscular, J-shaped organ ( figure 26.9). It has both a larger, convex inferolateral surface called the greater curvature and a smaller, concave superomedial surface called the lesser curvature. This organ is composed of four regions: The cardia (kar′dē-ă) is a small, narrow, superior entryway into the stomach lumen from the esophagus. The internal opening where the cardia meets the esophagus is called the cardiac orifice, which is the location of the inferior esophageal sphincter (also known as the cardiac sphincter; see section 26.2c). The fundus (fŭn′dŭs; bottom) is the dome-shaped region lateral and superior to the esophageal connection with the stomach. Its superior surface contacts the inferior surface of the thoracic diaphragm. The fundus has both weaker muscular contractions and a higher pH in its lumen area than other regions of the stomach. The body is the largest region of the stomach; it is inferior to the cardiac orifice and the fundus and extends to the pylorus. The pylorus (pī-lōr′ŭs; pylorus = gatekeeper) is the narrow, funnel-shaped terminal region of the stomach. Its opening into the duodenum of the small intestine is called the pyloric orifice. Surrounding this pyloric orifice is a thick ring of circular smooth muscle called the pyloric sphincter. The pyloric sphincter regulates the movement of material from the stomach into the small intestine. Figure 26.9 Gross Anatomy of the Stomach. The stomach is a muscular sac where mechanical and some chemical digestion of the bolus occur. (a) The major regions of the stomach are the cardia, the fundus, the body, and the pylorus. Three layers of smooth muscle make up the muscularis tunic. (b) A photomicrograph of the abrupt transition from stratified squamous epithelium in the esophagus to simple columnar in the stomach. (c) A cadaver photo shows an anterior, open section of the stomach, revealing the gastric folds and the cardiac orifice (opening of stomach connected to esophagus). (b) Victor P. Eroschenko; (c) Christine Eckel/McGraw-Hill Education APR Module 12: Digestive: Animations: Stomach INTEGRATE CLINICAL VIEW 26.4 Gastric Bypass Gastric bypass is a treatment used in extremely obese individuals to assist in weight loss. It is a surgical procedure that involves sectioning off a small part of the stomach (so the individual eats smaller portions) and attaching it to a lower part of the small intestine (so fewer nutrients are absorbed). Several changes are noted following surgery, including a decrease in appetite and altered response to hormones, including insulin. One of the most surprising changes is that the surgery can induce type 2 diabetes into remission—often within a few days of the surgery. The International Diabetes Foundation now endorses gastric bypass surgery for treatment of type 2 diabetes (see Clinical View 17.8: “Conditions Resulting in Abnormal Blood Glucose Levels”). Alila Medical Media/Shutterstock The internal stomach lining is composed of numerous gastric folds, or rugae (rū′jē; ruga = wrinkle). These gastric folds are seen only when it is empty. They allow the stomach to expand greatly when it fills with food and drink and then return to its normal J shape when it empties. In addition, the stomach is able to accommodate varying quantities of food due to the stress-relax response exhibited by the smooth muscle within the stomach wall. (Recall from section 10.10d that the stress-relaxation response is a characteristic response of smooth muscle to a prolonged stretch. The smooth muscle initially contracts, but after a period of time it relaxes.) Two serous membranes structures are associated with the stomach: the greater omentum and the lesser omentum, which were described in section 26.1e. The greater omentum extends inferiorly from the greater curvature of the stomach, forming the fatty apron that covers the anterior surface of abdominal organs. The lesser omentum extends superiorly from the lesser curvature of the stomach and duodenum to attach these structures to the liver. Histology The mucosa of the stomach is only 1.5 millimeters at its thickest region (about the thickness of a nickel). This inner lining has three significant features ( figure 26.10): The stomach mucosa is composed of a simple columnar epithelium supported by lamina propria. The transition from stratified squamous in the esophagus to simple columnar epithelium in the stomach is abrupt ( figure 26.9b). The simple columnar epithelial cells are replaced often (usually within a week) because of the harsh acidic environment of the stomach contents. The lining is indented by numerous depressions called gastric pits. Several gastric glands extend deep into the mucosa from the base of each gastric pit. The muscularis mucosae partially surrounds the gastric glands and helps expel gastric gland secretions when it contracts. Figure 26.10 Histology of the Stomach Wall. (a) The stomach wall contains invaginations within the mucosa called gastric pits that lead into gastric glands. (b) A photomicrograph shows the cells lining the gastric pit and gastric glands. (c) A diagrammatic section of a gastric gland shows its structure and the distribution of different secretory cells. (b) Al Telser/McGraw-Hill Education APR Module 12: Digestive: Histology: Stomach: LM Medium magnification: Gastric pit Page 1041 The muscularis of the stomach varies from the general GI tract pattern in that it is composed of three smooth muscle layers instead of two: an inner oblique layer, a middle circular layer, and an outer longitudinal layer. The presence of a third (oblique) layer of smooth muscle assists the continued churning and blending of the swallowed bolus to help mechanically digest the food. The muscularis becomes increasingly thicker (and stronger) as it progresses from the body to the pylorus. The outermost layer of the stomach is a serosa because the stomach is intraperitoneal (see section 26.1e). It produces serous fluid that lubricates the external surface of the stomach to decrease friction associated with stomach motility. WHAT DO YOU THINK? 3 The stomach secretes highly acidic gastric juices that facilitate the breakdown of food. What prevents the gastric juices from eating away at the stomach itself? Gastric Secretions Five types of secretory cells of the gastric epithelium are integral contributors to the process of digestion ( figure 26.10c). Four of these cell types produce the approximately 3 liters per day of gastric juice that are released into the stomach lumen. The fifth type of cell (Gcell) secretes a hormone into the blood. Surface Mucous Cells Surface mucous cells line the stomach lumen and extend into the gastric pits. They continuously secrete an alkaline mucin onto the gastric surface. Mucin becomes hydrated, producing a 1- to 3-millimeter mucus layer that coats the epithelial lining. This mucus layer, along with a high rate of cell turnover in the mucosa, helps to prevent ulceration of the stomach lining upon exposure to both the high acidity of the gastric fluid and gastric enzymes. Mucous Neck Cells Mucous neck cells are located immediately deep to the base of the gastric pit and are interspersed among the parietal cells (discussed next). Mucous neck cells release a less alkaline mucin that differs structurally and functionally from the alkaline mucin released by the surface mucous cells. The mucus produced by both types of mucous cells has lubricating properties to protect the stomach lining from abrasion or mechanical injury. Chief Cells Chief cells (also called zymogenic cells, or peptic cells) are the most numerous secretory cells within the gastric glands, hence the name “chief” cells. These cells produce and secrete packets of zymogen granules, which primarily contain pepsinogen. Pepsinogen is the inactive precursor of the proteolytic enzyme pepsin. Pepsin must be produced in this inactive form to prevent the destruction of chief cell proteins. Pepsinogen is activated into pepsin following its release into the stomach. It is activated by both the low pH and active pepsin molecules already present within the stomach. Pepsin chemically digests denatured proteins in the stomach into smaller peptide fragments (oligopeptides) (see section 26.4b). Page 1043 Chief cells also produce the enzyme gastric lipase. Gastric lipase is one of the acidic lipases that has a limited role in fat digestion (digests about 10–15% of the ingested fat) (see section 26.4c). Parietal Cells Parietal cells (also called oxyntic cells) are responsible for the addition of two substances into the lumen of the stomach: Intrinsic factor. The production and release of intrinsic factor (a glycoprotein) is the only essential function performed by the stomach. Intrinsic factor is required for absorption of vitamin B12 in the ileum (the final portion of the small intestine), as described in section 26.4e. B12 is necessary for production of normal erythrocytes. A critical decrease or absence of B12 results in pernicious anemia (see “Anemia”). Clinical View 18.2: Hydrochloric acid (HCl). HCl is not formed within the parietal cell; it would destroy the cell. Instead, the parietal cell forms H+ and releases both H+ and Cl– into the stomach lumen. The details of this process are described in figure 26.11. HCl is responsible for the low pH of between 1.5 and 2.5 within the stomach. Figure 26.11 Formation of HCl from Parietal Cells. H+ and HCO3– are produced within parietal cells of the stomach. The net movement is H+ into the stomach lumen and HCO3– into the blood. Additionally, Cl− is transferred from the blood into the stomach lumen, where it combines with H+ to form hydrochloric acid (HCl). APR Module 12: Digestive: Animations: HCl production The low pH created by HCl facilitates the digestive processes of the stomach. The processes include: Food breakdown. The relatively tough plant cell walls and animal connective tissue are made easier to digest. Protein denaturation. Proteins unfold and denature (see chemical digestion by the proteolytic enzyme pepsin. section 2.8b), thus facilitating Pepsin activation. Pepsinogen (released from chief cells) is converted into pepsin (the active proteolytic enzyme). Enhanced enzymatic activity. HCl creates the optimal pH environment for enzymatic activity of both pepsin and the acidic lipases (lingual lipase, released from intrinsic salivary glands and gastric lipase, released from the stomach). The very low pH within the stomach also protects us from infectious agents (see section 22.1). Most bacteria, bacterial toxins, and other microbes that enter the stomach cannot survive in the harsh acidic stomach environment (see section 22.3a). G-Cells G-cells are a type of enteroendocrine (en′ter-ō-en′dō-krin; enteron = gut, intestine) cell that are hormone-producing cells in the gastric glands of the stomach. G-cells secrete the hormone gastrin into the blood. Gastrin stimulates stomach motility and stomach secretions. Other enteroendocrine cells produce different hormones, such as somatostatin, a peptide hormone that modulates the function of nearby enteroendocrine and exocrine cells (see table 26.1). The five primary types of secretory cells of the stomach and their products are integrated in figure 26.12. Figure 26.12 Gastric Secretions. Secretory cells and their products are identified. Secretions enter the lumen of the stomach, except the hormone gastrin, which enters the blood. Motility in the Stomach Smooth muscle activity in the stomach wall has two primary functions: (a) mixing the bolus with gastric juice to form chyme and (b) emptying chyme from the stomach into the small intestine ( figure 26.13). Figure 26.13 Motility in the Stomach: Gastric Mixing and Gastric Emptying. (a) Gastric mixing occurs in the stomach as the bolus is combined with gastric secretions to form chyme. (b) Gastric emptying occurs when a small volume of chyme is then forced from the stomach into the duodenum through the partially open pyloric sphincter, and then the sphincter closes and retropulsion occurs. Gastric mixing is a form of mechanical digestion that changes the semidigested bolus into chyme (kīm; chymos = juice). Chyme has the consistency of a pastelike soup. Contractions of the stomach’s thick muscularis layer churn and mix the bolus with the gastric secretions, leading to a reduction in the size of swallowed particles. INTEGRATE LEARNING STRATEGY 26.3 To distinguish the products formed from parietal cells and chief cells, remember: Chief cells are both “peppy” (produce pepsinogen) and “lippy” (produce gastric lipase). Parietal cells are like “parental” cells because they are protective. These cells release (a) intrinsic factor to protect from pernicious anemia and (b) H+ and Cl- that create a low pH environment within the stomach that protects us from most ingested pathogens (which cannot survive in the hostile acidic environment of the stomach). Page 1044 Gastric emptying is the movement of acidic chyme from the stomach through the pyloric sphincter into the duodenum of the small intestine. This movement is facilitated by the progressive thickening of the muscularis layer in the pyloric region. As a wave of peristaltic muscular contraction moves through the pylorus toward the pyloric sphincter, a pressure gradient is established that drives the chyme toward the duodenum. The interaction here is unique: The peristaltic wave establishes a greater pressure on the contents in the pylorus than the pressure exerted by the pyloric sphincter to stay closed and prevent movement. Consequently, a few milliliters (about 3 milliliters) of chyme are emptied into the duodenum. After the peristaltic wave has moved past the pyloric sphincter, the pressure of the sphincter is once again greater than the pressure on the contents, and the pyloric sphincter closes. As this sphincter closes, stomach contents are squeezed back toward the stomach body. This reverse flow event is called retropulsion. Retropulsion not only results in the prevention of further chyme moving into the small intestine but also contributes to additional mixing of the stomach contents to further reduce the size of food particles. Regulation of the Digestive Processes in the Stomach The stomach is essentially a holding bag for partially digested food until the food is moved into the small intestine, where its digestion will be completed. Both the stomach’s motility and the release of its secretions are highly regulated so that ingested material is “pulverized” into chyme, which can then be effectively processed within the small intestine. Pacemaker cells (interstitial cells of Cajal) are specialized cells located within the GI tract wall. In the stomach wall, these cells are located within the longitudinal layer of smooth muscle, and initiate the smooth muscle contraction. These cells spontaneously depolarize less than four times per minute and establish its basic muscular contraction rhythm. Electrical signals spread via gap junctions (see section 4.6d) between the smooth muscle cells in the muscularis layer of the stomach. These muscular contractions by the stomach wall are regulated by both nervous reflexes and hormones, which alter the force but not rate of contraction, which is constant. Secretory activity of gastric glands is also altered. How these occur is organized into three phases: cephalic phase, gastric phase, and intestinal phase. The cephalic and gastric phases involve the events before and during a meal, whereas the intestinal phase involves the events that occur after a meal, as the ingested materials are being digested. See figure 26.14 as you read through this section. Figure 26.14 Regulation of Digestive Processes in the Stomach. Both muscular contractions of the stomach wall and secretions released by the gastric glands of the stomach are regulated by nervous reflexes and hormones. These processes are organized into three phases: cephalic phase, gastric phase, and intestinal phase. APR Module 12: Digestive: Animations: Gastric secretion Watch Video: Hormones and gastric secretion Page 1045 Cephalic Phase The cephalic phase primarily involves the cephalic reflex, which is a nervous system reflex initiated by the thought, smell, sight, or taste of food ( figure 26.14a). Nerve signals from the higher regions of the brain are sent to the hypothalamus, which then relays signals to the medulla oblongata. The medulla oblongata increases parasympathetic stimulation of the stomach via the vagus nerve (vagal stimulation), causing both an increase in contractile force in the gastric wall (increases motility) and secretory activity of the gastric glands. Sometimes you become aware of these processes when your stomach “growls.” Gastric Phase The gastric phase involves processes that begin after the bolus reaches the stomach ( figure 26.14b). This phase is regulated by both the nervous system via the gastric reflex and the endocrine system through the release of gastrin. The gastric reflex is a nervous system reflex initiated as food enters the stomach. Baroreceptors in the wall of the stomach detect increased distension in its wall, and chemoreceptors detect both the presence of protein and an increase in pH of stomach contents. (Higher pH indicates presence of protein because proteins buffer H+ and increase pH; see section 25.5d.) Nerve signals are relayed along sensory neurons to the medulla oblongata, resulting in nerve signals relayed along motor neurons to the stomach to cause the same effects as described in the cephalic reflex—an increase in both stomach motility and secretory activity of gastric cells. The presence of food (especially protein) in the stomach also causes release of gastrin from enteroendocrine cells. Gastrin enters the blood and circulates back to the stomach to further stimulate the contractile activity of muscle in the stomach wall and to primarily increase release of HCl from parietal cells. Gastrin also stimulates contraction of the pyloric sphincter to slow stomach emptying, thereby allowing sufficient time for completion of digestive activities associated with the stomach before the chyme is moved into the small intestine. Page 1046 Intestinal Phase The intestinal phase involves the processes following the chyme reaching the small intestine, a phase that is also regulated by both the nervous system and the endocrine system (see figure 26.14c). The intestinal phase involves both the intestinal reflex and the release of two significant hormones from the duodenum: cholecystokinin (CCK) and secretin. The intestinal reflex is a nervous system reflex that opposes the other two reflexes (cephalic reflex and gastric reflex). It protects the small intestine from being overloaded with chyme. The intestinal reflex is initiated with entry of acidic chyme into the duodenum, which causes a decrease in nerve signals relayed to the medulla oblongata. Consequently, vagal stimulation to the stomach is decreased, which lessens both motility and secretory activity of the stomach. Chyme entering the small intestine also causes release of cholecystokinin and secretin. Cholecystokinin (CCK) (ko′lē-sis-to-kī′nin; chole = bile, cyst = sac, kinin = to move) is a hormone released by the enteroendocrine cells of the duodenum (see section 26.3b), primarily in response to fatty chyme within the small intestine. CCK causes a decrease in stomach motility. Secretin (se-krē′tin) is a hormone released by the enteroendocrine cells of the duodenum, primarily in response to the presence of acidic chyme in the small intestine. Secretin causes a decrease in secretory activity of the stomach. Both cholecystokinin and secretin inhibit the release of gastrin. This slows down the emptying of the stomach, thus allowing the small intestine to continue its digestive processes before additional chyme is added. Both hormones also influence the digestive processes in the lower GI tract and are discussed in more detail in section 26.3c. In addition, the details for gastrin, secretin, and CCK hormones are included in directly follows table R.8: “Regulating the Digestive System,” which chapter 17 (Endocrine System). Note that researchers initially believed an additional hormone released from the small intestine called gastric inhibitory peptide regulated stomach activity. However, this hormone is now thought to primarily regulate the release of insulin in response to increased glucose concentration in the contents of the small intestine. To better reflect its role, it has been renamed glucose-dependent insulinotropic peptide (GIP) (see table 26.1). INTEGRATE CLINICAL VIEW 26.5 Peptic Ulcers Watch Video: Ulcers Normally, a balance exists in the stomach between the acidic gastric juices and the protective, regenerative nature of the mucosa lining. When this balance is thrown off, the stage is set for the development of a peptic ulcer— a chronic, solitary erosion of a portion of the lining of either the stomach or the duodenum. Annually, over 4 million people in the United States are diagnosed with an ulcer. Javier Domingo/Phototake Gastric ulcers are peptic ulcers that occur in the stomach, whereas duodenal ulcers are peptic ulcers that occur in the superior part of the duodenum, the first segment of the small intestine. Duodenal ulcers are common because the first part of the duodenum receives the acidic chyme from the stomach but has yet to receive the alkaline bile and pancreatic juice that may neutralize chyme’s acidic content. Symptoms of an ulcer include a gnawing, burning pain in the epigastric region (see figure 1.10), which may be worse after eating a meal; nausea; vomiting; and extreme belching. Bleeding also may occur, and the partially digested blood results in dark, tarlike stools. If left untreated, an ulcer may erode through the organ wall and cause perforation, which is a medical emergency. Irritation of the gastric mucosa (gastritis) has been linked to many cases of peptic ulcer. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen and aspirin, are a common cause of gastritis, and these drugs impair healing of the gastric lining. Previously, the cause of ulcers was attributed to high production of HCl and low production of the protective mucus, which was exacerbated by stress, smoking, alcohol, coffee, and spicy food. However, numerous research studies have determined that the major influence in peptic ulcer formation is an acid-resistant bacterium called Helicobacter pylori, which is present in over 70% of gastric ulcer cases and over 90% of duodenal ulcer cases. H. pylori residing within the stomach produces enzymes that break down the components in the gastric mucus, lessening its protective effects. As leukocytes enter the stomach to destroy the bacteria, they also destroy the mucous neck cells, which produce mucin ( figure 26.12). The decreased ability to produce mucus both irritates the stomach, causing possible erosion of the layers of the stomach wall, and allows for a favorable environment for continued proliferation of H. pylori. This sets up a positive feedback cycle that can lead to perforation of the stomach wall. A similar process occurs within the duodenum. Categories of medications prescribed in the treatment of ulcers include antibiotics taken for 2 weeks to eradicate H. pylori and medications used in the treatment for gastric reflux, including proton-pump inhibitors, a histamine (H2) blocker, and antacids. Page 1047 INTEGRATE CLINICAL VIEW 26.6 Vomiting Vomiting is the rapid expulsion of gastric contents through the oral cavity. Prior to vomiting, heart rate and sweating increase, nausea is felt, and a noticeable increase in saliva production occurs. The vomiting reflex is a complicated act that is controlled by the vomiting center in the medulla oblongata (see section 13.5c). This brainstem region responds to head injury, motion sickness, infection, toxicity (e.g., alcohol, drugs, bacterial toxins), or food irritation in the stomach and intestines. Vomiting is initiated following a deep inspiration and the closure of both nasal cavities by the soft palate and the larynx (laryngeal inlet) by the epiglottis. Skeletal muscle contraction (abdominal muscles and diaphragm) increase pressure within the stomach and thus supply the primary force for expulsion of digestive tract contents. As the pressure increases in the stomach, the acidic gastric contents are forced into and through the esophagus and out of the oral cavity. Care must be taken that vomit is not aspirated into the respiratory tract, a risk for a semiconscious or unconscious individual. Thus, it is critical that individuals undergoing surgical procedures have an empty stomach and small intestine because general anesthesia has an associated risk of inducing nausea and vomiting. Additionally, vomiting causes increased formation of HCl; this results in increased HCO3− in the blood, raising blood pH. Extensive vomiting can lead to metabolic alkalosis (see Clinical View 25.6: “How Does Vomiting or Diarrhea Alter Blood H+ Concentration?”). WHAT DID YOU LEARN? 14 List the secretory cell types in the stomach, their products, and the function of the products. 15 Which neural reflex is initiated by food in the stomach, and what does it control?