Nursing Care Management 116 PDF

College of Nursing COLEGIO DE SAN ANTONIO DE PADUA Ramon M. Durano Foundation Compound Guinsay, Danao City **Nursing Care Management 116:** **Care of Clients with Problems in Gastro-Intestinal, Metabolism & Endocrine, Perception & Coordination, Acute and Chronic** **MODULE...

College of Nursing COLEGIO DE SAN ANTONIO DE PADUA Ramon M. Durano Foundation Compound Guinsay, Danao City **Nursing Care Management 116:** **Care of Clients with Problems in Gastro-Intestinal, Metabolism & Endocrine, Perception & Coordination, Acute and Chronic** **MODULE 1** This course deals with the application of concepts, principles and techniques of nursing care management of sick clients across life span in varied settings, with alterations/problems in Nutrition and Gastrointestinal, Metabolism and Endocrine, Perception and Coordination (Acute and Chronic). The students are expected to utilize the nursing process inthe management of individuals, families and community in varied settings. Students are likewise expected to observe core values and nursing standards in the care of clients. Prepared by: **NURSE FAITH I. MANINGO** College of Nursing/Midwifery COLEGIO DE SAN ANTONIO DE PADUA Ramon M. Durano Foundation Compound Guinsay, Danao City **Nursing Care Management 116:** **Care of Clients with Problems in Gastro-Intestinal, Metabolism & Endocrine, Perception & Coordination, Acute and Chronic** **Nursing Care of Clients with Problems of Ingestion, Digestion, Absorption, and Elimination** Abnormalities of the gastrointestinal (GI) tract are numerous and represent every type of major pathology that can affect other organ systems, including bleeding, perforation, obstruction, inflammation, and cancer. Congenital, inflammatory, infectious, traumatic, and neoplastic lesions have been encountered in every portion and at every site along the length of the GI tract. As with all other organ systems, the GI tract is subject to circulatory disturbances, faulty nervous system control, and aging. Apart from the many organic diseases to which the GI tract is susceptible, many extrinsic factors can interfere with its normal function and produce symptoms. Stress and anxiety, for example, often find their chief expression in indigestion, anorexia, or motor disturbances of the intestines, sometimes producing constipation or diarrhea. In addition to the state of mental health, physical factors such as fatigue and an inadequate or abruptly changed dietary intake can markedly affect the GI tract. When assessing and instructing the patient, the nurse should consider the variety of mental and physical factors that affect the function of the GI tract. ***Learning Outcomes: After reading this chapter, the student should be able to:*** 1. Describe the structures and functions of the organs of the gastrointestinal tract. 2. Differentiate the processes of ingestion, digestion, absorption, and elimination. 3. Link the age-related changes of the gastrointestinal system to the differences in assessment findings. 4. Select significant subjective and objective assessment data related to the gastrointestinal system that should be obtained from a patient. 5. Describe the purpose, significance of results, and nursing responsibilities related to diagnostic studies of the gastrointestinal system. 6. Describe the etiology, clinical manifestations, complications, collaborative care, and nursing management of oral and stomach cancer, gastrointestinal bleeding and colorectal cancer. 7. Explain the types, pathophysiology, clinical manifestations, complications, and collaborative care (including surgical therapy and nursing management) of gastroesophageal reflux disease (GERD) and hiatal hernia, esophageal cancer, diverticula, achalasia, and esophageal strictures. 8. Differentiate between acute and chronic gastritis, mechanical and nonmechanical bowel obstructions, including the etiology, pathophysiology, collaborative care, and nursing management. 9. Compare and contrast gastric and duodenal ulcers, inflammatory bowel diseases of ulcerative colitis and Crohn's disease, including pathophysiology, clinical manifestations, complications, collaborative care, and nursing management. 10. Describe the collaborative care and nursing management of acute appendicitis, peritonitis, and gastroenteritis. ***CHAPTER I: STRUCTURES AND FUNCTIONS OF GASTROINTESTINAL SYSTEM*** The gastrointestinal (GI) system (also called the digestive system) consists of the GI tract and its associated organs and glands. Included in the GI tract are the mouth, esophagus, stomach, small intestine, large intestine, rectum, and anus. The associated organs are the liver, pancreas, and gallbladder (Fig. 39-1). The GI tract extends approximately 30 ft (9 m) from the mouth to the anus. It is composed of four common layers. From the inside to the outside, these layers are (1) mucosa, (2) submucosa, (3) muscle, and (4) serosa. The muscular coat consists of two layers: the circular (inner) layer and the longitudinal (outer) layer. The GI tract is innervated by the parasympathetic and sympathetic branches of the autonomic nervous system. The parasympathetic (cholinergic) system is mainly excitatory, and the sympathetic (adrenergic) system is mainly inhibitory. For example, peristalsis is increased by parasympathetic stimulation and decreased by sympathetic stimulation. Sensory information is relayed via both sympathetic and parasympathetic afferent fibers. The GI tract has its own nervous system: the enteric (or intrinsic) nervous system. The enteric nervous system is composed of two nerve layers that lie between the mucosa and the muscle layers. These neurons have receptors for pressure and movement. The GI tract and accessory organs receive approximately 25% to 30% of the cardiac output at rest and 35% or more after eating. Circulation in the GI system is unique in that venousblood draining the GI tract organs empties into the portal vein, which then perfused the liver. The vascular supply to the GI tract includes the celiac artery, superior mesenteric artery (SMA), and the inferior mesenteric artery (IMA). The stomach and duodenum receive their blood supply from the celiac axis. The distal small intestine to mid larger intestine receives its blood supply from branches of the hepatic and SMAs. The distal large intestine through the anus receives its blood supply from the IMA. Because such a large percentage of the cardiac output perfused these organs, the GI tract is a major source from which blood flow can be diverted during exercise, stress, or injury. The abdominal organs are almost completely covered by the peritoneum. The two layers of the peritoneum are the parietal layer, which lines the abdominal cavity wall, and the visceral layer, which covers the abdominal organs. The peritoneal cavity is the potential space between the parietal and visceral layers. The two folds of the peritoneum are the mesentery and the omentum. The mesentery attaches the small intestine and part of the large intestine to the posterior abdominal wall and contains blood and lymph vessels. The omentum hangs like an apron from the stomach to the intestines and contains fat and lymph nodes. The main function of the GI system is to supply nutrients to body cells. This is accomplished through the processes of (1) ingestion (taking in food), (2) digestion (breaking down food), and (3) absorption (transferring food products into circulation). Elimination is the process of excreting the waste products of digestion. Ingestion is the intake of food. A person's appetite or desire to ingest food influences how much food is eaten. An appetite center is located in the hypothalamus. It is directly or indirectly stimulated by hypoglycemia, an empty stomach, decrease in body temperature, and input from higher brain centers. The hormone ghrelin released from the stomach mucosa plays a role in appetite stimulation. Another hormone, leptin, is involved in appetite suppression. The sight, smell, and taste of food frequently stimulate appetite. Appetite may be inhibited by stomach distention, illness (especially accompanied by fever), hyperglycemia, nausea and vomiting, and certain drugs (e.g., amphetamines). Deglutition (swallowing) is the mechanical component of ingestion. The organs involved in the deglutition of food are the mouth, pharynx, and esophagus.Digestion is the physical and chemical breakdown of food into absorbable substances. Digestion in the GI tract is facilitated by the timely movement of food through the GI tract and the secretion of specific enzymes. These enzymes break down foodstuffs to particles of appropriate size for absorption (Table 39-1). In the stomach the digestion of proteins begins with the release of pepsinogen from chief cells. The stomach's acidic environment results in the conversion of pepsinogen to its active form, pepsin. Pepsin begins the breakdown of proteins. There is minimal digestion of starches and fats. The food is mixed with gastric secretions, which are under neural and hormonal control (Tables 39-2 and 39-3). The stomach also serves as a reservoir for food, which is slowly released into the small intestine. The length of time that food remains in the stomach depends on the composition of the food, but average meals remain from 3 to 4 hours. In the small intestine, carbohydrates are broken down to monosaccharides, fats to glycerol and fatty acids, and proteins to amino acids. The physical presence and chemical nature of chyme (food mixed with gastric secretions) stimulate motility and secretion. Secretions involved in digestion include enzymes from the pancreas, bile from the liver (see Table 39-1), and enzymes from the small intestine. Enzymes on the brush border of the microvilli complete the digestion process. These enzymes break down disaccharides to monosaccharides and peptides to amino acids for absorption. Both secretion and motility are under neural and hormonal control. When food enters the stomach and small intestine, hormones are released into the bloodstream (see Table 39-3). These hormones play important roles in the control of HCl acid secretion, production and release of digestive enzymes, and motility.         ***CHAPTER II: NURSING MANAGEMENT -- UPPER GASTROINTESTINAL PROBLEMS*** - **NAUSEA AND VOMITING** Nausea and vomiting are the most common manifestations ofgastrointestinal (GI) diseases. Although nausea and vomitingcan occur independently, they are usually closely related andtreated as one problem. **Nausea** is a feeling of discomfort inthe epigastrium with a conscious desire to vomit. **Vomiting** isthe forceful ejection of partially digested food and secretions*(emesis)* from the upper GI tract.Vomiting is a complex act that requires the coordinatedactivities of several structures: closure of the glottis, deepinspiration with contraction of the diaphragm in the inspiratory position, closure of the pylorus, relaxation of the stomachand lower esophageal sphincter (LES), and contraction of theabdominal muscles with increasing intraabdominal pressure.These simultaneous activities force the stomach contents upthrough the esophagus, into the pharynx, and out the mouth. *Etiology and Pathophysiology* Nausea and vomiting occur in a wide variety of GI disordersand in conditions that are unrelated to GI disease. Theseinclude pregnancy; infection; central nervous system (CNS)disorders (e.g., meningitis, tumor); cardiovascular problems(e.g., myocardial infarction, heart failure); metabolic disorders(e.g., diabetes mellitus, Addison's disease, renal failure); postoperativelyafter general anesthesia; side effects of drugs (e.g., chemotherapy,opioids, digitalis); psychologic factors (e.g., stress,fear); and conditions in which the GI tract becomes overlyirritated, excited, or distended.A vomiting center in the brainstem coordinates the multiplecomponents involved in vomiting. This center receives inputfrom various stimuli. Neural impulses reach the vomiting centervia afferent pathways through branches of the autonomicnervous system. Receptors for these afferent fibers are locatedin the GI tract, kidneys, heart, and uterus. When stimulated,these receptors relay information to the vomiting center, whichthen initiates the vomiting reflex (Fig. 42-1). *Collaborative Care* The goals of collaborative care are to determine and treat theunderlying cause of the nausea and vomiting and to providesymptomatic relief. Assess the patient for precipitating factors and describe the contents of the emesis. Women are more likelyto suffer from nausea and vomiting associated with surgicalprocedures and motion sickness. It is important to differentiate among vomiting, regurgitation,and projectile vomiting. *Regurgitation* is an effortlessprocess in which partially digested food slowly comes up fromthe stomach. Retching or vomiting rarely occurs before it. *Projectilevomiting* is a forceful expulsion of stomach contentswithout nausea and is characteristic of CNS (brain and spinalcord) tumors.Emesis containing partially digested food several hours aftera meal is indicative of gastric outlet obstruction or delayedgastric emptying. The presence of fecal odor and bile after prolongedvomiting suggests intestinal obstruction below the levelof the pylorus. Bile in the emesis may suggest obstruction belowthe ampulla of Vater. The color of the emesis aids in identifyingthe presence and source of bleeding. Vomitus with a "coffeeground" appearance is related to gastric bleeding, where bloodchanges to dark brown as a result of its interaction with HClacid. Bright red blood indicates active bleeding. This could bedue to a **Mallory-Weiss tear** (disruption of the mucosal liningnear the esophagogastric junction), esophageal varices, gastricor duodenal ulcer, or neoplasm. A Mallory-Weiss tear is mostoften related to severe retching and vomiting. *GERONTOLOGIC CONSIDERATIONS* The older adult experiencing nausea and vomiting requirescareful assessment and monitoring, particularly during periodsof fluid loss and subsequent rehydration therapy. Older patientsare more likely to have cardiac or renal insufficiency that placesthem at greater risk for life-threatening fluid and electrolyteimbalances. Excessive replacement of fluid and electrolytes may result in adverse consequences for the person who has heartfailure or renal disease. The older adult with a decreased levelof consciousness may be at high risk for aspiration of vomitus.Close monitoring of the patient's physical status and level ofconsciousness during episodes of vomiting is important.Older adults are particularly susceptible to the CNS sideeffects of antiemetic drugs, since these drugs may produce confusionand increase their risk for falls. Dosages should bereduced and efficacy closely evaluated. Institute safety precautionsfor these patients (e.g., removing rugs that may causeslipping). - **ORAL INFLAMMATION AND INFECTIONS** Oral inflammation and infections may be due to specific mouthdiseases or secondary to systemic disorders such as leukemia orvitamin deficiency. Oral inflammation and infections canseverely impair oral ingestion. Common inflammations andinfections of the oral cavity are presented in Table 42-3. Thepatient who is immunosuppressed (e.g., receiving chemotherapyfor cancer) or using corticosteroid inhalant treatment forasthma is at risk for oral infections (e.g.,candidiasis). Oral infections may predispose the patient to infections inother body organs. For example, the oral cavity is a potentialreservoir for respiratory pathogens. In addition, oral pathogenshave been associated with diabetes and heart disease.Regular and good oral and dental hygiene reduces oral infectionsand inflammation. Management of these conditionsfocuses on identification of the cause, elimination of infection,provision of comfort measures, and maintenance of nutritionalintake. - **ORAL CANCER** There are two types of oral cancer: *oral cavity cancer,* whichstarts in the mouth, and *oropharyngeal cancer,* which developsin the part of the throat just behind the mouth (called theoropharynx).*Head and neck squamous cell carcinoma* (HNSCC) isa term used for cancers of the oral cavity, pharynx, and larynx,which account for 90% of malignant oral tumors.Most oral malignant lesions occur on the lower lip. Othercommon sites are the lateral border and undersurface of thetongue, the labial commissure, and the buccal mucosa. Carcinomaof the lip has the most favorable prognosis of any of theoral tumors because lip lesions are usually diagnosed earlier.Although the definitive cause of oral cancer is unknown, it hasa number of predisposing factors (Table 42-4). The risk of developingoral cancer is related to the duration of tobacco use. Ahistory of frequent alcohol consumption is reported by 75% to80% of patients who develop oral cancer. More than 30% ofpatients with cancer of the lip have outdoor occupations, indicatingthat prolonged exposure to sunlight is a risk factor. Irritationfrom the pipe stem resting on the lip is a factor in pipesmokers. Human papillomavirus (HPV) contributes to 25% of oral cancer cases. HPV-associated oropharyngeal cancer isassociated with multiple sexual partners, especially multipleoral sex partners. *Nursing Diagnoses* Nursing diagnoses for the patient with oral cancer may include,but are not limited to, the following: Imbalanced nutrition: less than body requirements *relatedto* oral pain, difficulty chewing and swallowing, surgicalresection, and radiation treatment Chronic pain *related to* the tumor, surgery, or radiation Anxiety *related to* diagnosis of cancer, uncertain future,potential for disfiguring surgery, potential for recurrence,and prognosis Ineffective health maintenance *related to* lack of knowledgeof disease process and therapeutic regimen andunavailability of a support system *Planning* The overall goals are that the patient with carcinoma of the oralcavity will (1) have a patent airway, (2) be able to communicate,(3) have adequate nutritional intake to promote wound healing,and (4) have relief of pain and discomfort. *Nursing Implementation* You have a significant role in early detection and treatment oforal cancer. Identify patients at risk (see Table 42-4) and provideinformation regarding predisposing factors. Inform the patient who smokes about smoking cessation programs available in thecommunity. Warn adolescents and teenagers about the dangerof using snuff or chewing tobacco.Because early detection of oral cancer is important, teach thepatient to report unexplained pain or soreness of the mouth,unusual bleeding, dysphagia, sore throat, voice changes, orswelling or lump in the neck. Refer any individual with anulcerative lesion that does not heal within 2 to 3 weeks to ahealth care provider. *Evaluation* The expected outcomes are that the patient with oral cancer will Have no respiratory complications Be able to communicate Maintain an adequate nutritional intake to promotewound healing Experience minimal pain and discomfort with eating,drinking, and talking - **ESOPHAGEAL DISORDERS** - *GASTROESOPHAGEAL REFLUX DISEASE* ***Gastroesophageal reflux disease (GERD)***is a chronic symptomof mucosal damage caused by reflux of stomach acid into thelower esophagus. GERD is not a disease but a syndrome. GERDis the most common upper GI problem. ***Etiology and Pathophysiology*** GERD has no one single cause (Fig. 42-2). GERD results whenthe defenses of the esophagus are overwhelmed by the reflux ofacidic gastric contents into the esophagus. Gastric HCl acid andpepsin secretions that reflux cause esophageal irritation andinflammation *(esophagitis).* If the refluxate contains intestinalproteolytic enzymes (e.g., trypsin) and bile, this further irritatesthe esophageal mucosa. The degree of inflammation dependson the amount and composition of the gastric reflux and on theesophagus's mucosal defense mechanisms.One of the primary etiologic factors in GERD is an incompetentLES. Under normal conditions, the LES acts as an antirefluxbarrier. An incompetent LES lets gastric contents movefrom the stomach to the esophagus when the patient is supineor has an increase in intraabdominal pressure.Decreased LES pressure can be due to certain foods (e.g.,caffeine, chocolate, peppermint) and drugs (e.g., anticholinergics).Obesity is a risk factor for GERD, although the specificmechanism remains to be determined.In an obese person theintraabdominal pressure is increased, which can exacerbateGERD. Cigarette and cigar smoking can also contribute toGERD. A common cause of GERD is a hiatal hernia, which isdiscussed in the next section.Heartburn *(pyrosis)* is the most common clinicalmanifestation.Heartburn is a burning, tight sensation felt intermittentlybeneath the lower sternum and spreading upward to the throator jaw. Heartburn may occur after ingestion of food or drugsthat decrease the LES pressure or directly irritate the esophagealmucosa (Table 42-7). A health care provider should evaluateheartburn that occurs more than twice a week, is rated as severe,occurs at night and wakes a person from sleep, or is associatedwith dysphagia. Older adults who complain of recent onset ofheartburn should receive medical evaluation.Patients may also complain of dyspepsia. *Dyspepsia* ispain or discomfort centered in the upper abdomen (mainlyin or around the midline as opposed to the right or lefthypochondrium).Regurgitation is a fairly common manifestation of GERD. Itis often described as hot, bitter, or sour liquid coming into thethroat or mouth. Hypersalivation (water brash) may also bereported.An individual with GERD may also report respiratory symptoms,including wheezing, coughing, and dyspnea. Nocturnaldiscomfort and coughing can awaken the patient, resulting indisturbed sleep patterns. Otolaryngologic symptoms includehoarseness, sore throat, a *globus sensation* (sense of a lump inthe throat), and choking.GERD-related chest pain can mimic angina and is describedas burning; squeezing; or radiating to the back, neck, jaw, orarms. Complaints of chest pain are more common in olderadults with GERD. Unlike angina, GERD-related chest pain isrelieved with antacids. ***Complications*** Complications of GERD aredue to the direct local effects ofgastric acid on the esophageal mucosa. ***Esophagitis***(inflammationof the esophagus) is a common complication of GERD.Esophagitis with esophageal ulcerations is shown in Fig. 42-3.Repeated esophagitis may lead to scar tissue formation, stricture,and ultimately dysphagia.Another complication of chronic GERD is ***Barrett's esophagus***(esophageal metaplasia). (*Metaplasia* is the reversiblechange from one type of cell to another type and is generallycaused by some sort of abnormal stimulus.) In Barrett's esophagusthe flat epithelial cells in the distal esophagus change tocolumnar epithelial cells. These cell changes are thought to bedue primarily to GERD. However, people with no history ofreflux symptoms can develop Barrett's esophagus.Barrett's esophagus is considered a precancerous lesion thatincreases the patient's risk for esophageal adenocarcinoma. Surgical therapy (*antireflux*surgery) isreserved for patients with complications of reflux, includingesophagitis, intolerance of medications, stricture, Barrett'smetaplasia, and persistence of severe symptoms. Most surgicalprocedures are performed laparoscopically. The goal of surgicalinterventions is to reduce reflux by enhancing the integrity ofthe LES. In these procedures the fundus of the stomach iswrapped around the lower portion of the esophagus to reinforceand repair the defective barrier. Laparoscopically performedNissen and Toupetfundoplications are common antireflux surgeries(Fig. 42-4). ***Nursing Management*** Nursing care for the patient with acute symptoms of GERDconsists of encouraging the patient to follow the necessaryregimen. The head of the bed is elevated to approximately 30degrees. This can be done using pillows or with 4- to 6-in blocksunder the bed. For 2 to 3 hours after a meal the patient shouldnot be supine. Teach the patient to avoid food and activities that cause reflux (e.g., late-night eating). Instruct patients to contact their health care provider if symptoms persist. The patient on a PPI needs to take medication before the first meal of the day. Instruct the patient about possible medication side effects. Tell the patient on a prescription H2-receptor agent to take the medication as prescribed and not to stop without checking with his or her health care provider. Postoperative care focuses on prevention of respiratory complications, maintenance of fluid and electrolyte balance, and prevention of infection. If an open high abdominal incision is used, respiratory complications can occur. Respiratory assessment includes respiratory rate and rhythm, pulse rate and rhythm, and signs of pneumothorax (e.g., dyspnea, chest pain, cyanosis). - HIATAL HERNIA Hiatal hernia is herniation of a portion of the stomach into the esophagus through an opening, or hiatus, in the diaphragm. It is also referred to as diaphragmatic hernia and esophageal hernia. It is the most common abnormality found on x-ray examination of the upper GI tract. Hiatal hernias are common in older adults and occur more often in women than in men.Hiatal hernias are classified into the following two types (Fig. 42-5): 1. Sliding: The junction of the stomach and the esophagus is above the diaphragm, and a part of the stomach slides through the hiatal opening in the diaphragm. This occurs when the patient is supine, and the hernia usually goes back into the abdominal cavity when the patient is standing upright. This is the most common type of hiatal hernia. 2. Paraesophageal, or rolling: The esophagogastric junction remains in the normal position, but the fundus and the greater curvature of the stomach roll up through the diaphragm, forming a pocket alongside the esophagus. Acute paraesophageal hernia is a medical emergency. *Etiology and Pathophysiology* Many factors contribute to the development of hiatal hernia. Structural changes, such as weakening of the muscles in the diaphragm around the esophagogastric opening, occur with aging. Factors that increase intraabdominal pressure, including obesity, pregnancy, ascites, tumors, intense physical exertion, and heavy lifting on a continual basis, may also predispose patients to development of a hiatal hernia. Clinical Manifestations and Complications Some individuals with hiatal hernia are asymptomatic. When present, signs and symptoms of hiatal hernia are similar to those described for GERD. Complications that may occur with hiatal hernia include GERD, esophagitis, hemorrhage from erosion, stenosis (narrowing of the esophagus), ulcerations of the herniated portion of the stomach, strangulation of the hernia, and regurgitation with tracheal aspiration. *Diagnostic Studies* An esophagram (barium swallow) may show the protrusion of gastric mucosa through the esophageal hiatus. Endoscopic visualization of the lower esophagus provides information on the degree of mucosal inflammation or other abnormalities. Other tests are listed in Table 42-8. *Nursing and Collaborative Management* Conservative therapy of hiatal hernia is similar to that described for GERD. Teach the patient to reduce intraabdominal pressure by eliminating constricting garments and avoiding lifting and straining. Surgical approaches to hiatal hernias can include reduction of the herniated stomach into the abdomen, herniotomy (excision of the hernia sac), herniorrhaphy (closure of the hiatal defect), an antireflux procedure, and gastropexy (attachment of the stomach subdiaphragmatically to prevent reherniation). The goals are to reduce the hernia, provide an acceptable LES pressure, and prevent movement of the gastroesophageal junction. Antireflux surgeries for hiatal hernia are laparoscopically performed Nissen and Toupet techniques (see Fig. 42-4). A thoracic or an open abdominal approach may be done, depending on the patient. - ESOPHAGEAL CANCER Esophageal cancer (malignant neoplasm of the esophagus) is not common. However, the rates are increasing. The majority of esophageal cancers are adenocarcinomas, with the remainder being squamous cell tumors. Adenocarcinomas arise from the glands lining the esophagus and resemble cancers of the stomach and small intestine. The incidence of esophageal cancer increases with age, with those between 70 and 84 at greatest risk. There is a higher incidence of esophageal cancer in non-Hispanic white men and Alaska Natives compared with other ethnic groups. The incidence of esophageal cancer is higher in men than in women. *Etiology and Pathophysiology* The cause of esophageal cancer is unknown. Several important risk factors include Barrett's metaplasia, smoking, excessive alcohol intake, and obesity. For example, current smoking or a history of smoking are associated with a 2-fold higher risk of esophageal cancer. Patients with injury to the esophageal mucosa (e.g., from occupational exposure) are at greater risk. Achalasia, a condition in which there is delayed emptying of the lower esophagus, is associated with squamous cell cancer. Most esophageal tumors are located in the middle and lower portions of the esophagus. The malignant tumor usually appears as an ulcerated lesion and has often advanced by the time the patient experiences symptoms. The tumor may penetrate the muscular layer and even extend outside the wall of the esophagus. Obstruction of the esophagus occurs in the later stages. *Clinical Manifestations and Complications* The onset of symptoms is usually late relative to tumor growth. The majority of patients have advanced disease at diagnosis. Progressive dysphagia is the most common symptom and may be described as a substernal feeling as if food is not passing. Initially the dysphagia occurs only with meat, then with soft foods, and eventually with liquids. Pain develops late. It is described as occurring in the substernal, epigastric, or back areas and usually increases with swallowing. The pain may radiate to the neck, jaw, ears, and shoulders. If the tumor is in the upper third of the esophagus, symptoms such as sore throat, choking, and hoarseness may occur. Weight loss is fairly common. When esophageal stenosis (narrowing) is severe, regurgitation of blood-flecked esophageal contents is common. *Nursing Assessment* Ask the patient about a history of GERD, hiatal hernia, achalasia, Barrett's esophagus, and tobacco and alcohol use. Assess the patient for progressive dysphagia and odynophagia (burning, squeezing pain while swallowing). Ask about the type of substances (e.g., meats, soft foods, liquids) that cause dysphagia. Also assess the patient for pain (substernal, epigastric, or back areas), choking, heartburn, hoarseness, cough, anorexia, weight loss, and regurgitation. N*Nursing Diagnoses* Chronic pain related to the compression of tumor on surrounding tissues, esophageal stenosis Imbalanced nutrition: less than body requirements related to dysphagia, odynophagia, weakness, chemotherapy, and radiation therapy Ineffective health maintenance related to lack of knowledge of disease process and treatment, lack of a support system, and chronic debilitating disease Anxiety and grieving related to diagnosis of cancer, uncertain future, and poor prognosis *Planning* The overall goals are that the patient with esophageal cancer will (1) have relief of symptoms, including pain and dysphagia; (2) achieve optimal nutritional intake; (3) understand the prognosis of the disease; and (4) experience a quality of life appropriate to disease progression. *Nursing Implementation* Counsel the patient with GERD, Barrett's esophagus, or hiatal hernia about the importance of regular follow-up evaluation. Health counseling should focus on elimination of smoking and excessive alcohol intake, as well as other risk factors for GERD (see Table 42-7). Maintenance of good oral hygiene and dietary habits (e.g., intake of fresh fruits and vegetables) is important. Encourage patients to seek medical attention for any esophageal problems, especially dysphagia. - ***DISORDERS OF THE STOMACH AND UPPER SMALL INTESTINE*** - GASTRITIS Gastritis, an inflammation of the gastric mucosa, is one of the most common problems affecting the stomach. Gastritis may be acute or chronic and diffuse or localized. *Etiology and Pathophysiology* Gastritis occurs as the result of a breakdown in the normal gastric mucosal barrier. This mucosal barrier normally protects the stomach tissue from the corrosive action of HCl acid and pepsin. When the barrier is broken, HCl acid and pepsin can diffuse back into the mucosa. This back diffusion results in tissue edema, disruption of capillary walls with loss of plasma into the gastric lumen, and possible hemorrhage. *Nursing and Collaborative Management* *ACUTE GASTRITIS* Eliminating the cause and preventing or avoiding it in the future are generally all that is needed to treat acute gastritis. The plan of care is supportive and similar to that described for nausea and vomiting. If vomiting accompanies acute gastritis, rest, NPO status, and IV fluids may be prescribed. Dehydration can occur rapidly in acute gastritis with vomiting. Antiemetics are given for nausea and vomiting. In severe cases of acute gastritis, an NG tube may be used (1) to monitor for bleeding, (2) to lavage the precipitating agent from the stomach, or (3) to keep the stomach empty and free of noxious stimuli. Clear liquids are resumed when symptoms have subsided, with gradual reintroduction of solids. If hemorrhage is considered likely, frequently check vital signs and test the vomitus for blood. All of the management strategies discussed in the section on upper GI bleeding apply to the patient with severe gastritis. *CHRONIC GASTRITIS* The treatment of chronic gastritis focuses on evaluating and eliminating the specific cause (e.g., cessation of alcohol intake, abstinence from drugs, H. pylori eradication). Currently, antibiotic combinations are used to eradicate H. pylori. The patient undergoing treatment for chronic gastritis may have to adapt to lifestyle changes and strictly adhere to a drug regimen. Some patients find a nonirritating diet consisting of six small feedings a day helpful. Smoking is contraindicated in all forms of gastritis. - PEPTIC ULCER DISEASE Peptic ulcer disease (PUD) is a condition characterized by erosion of the GI mucosa resulting from the digestive action of HCl acid and pepsin. Any portion of the GI tract that comes into contact with gastric secretions is susceptible to ulcer development, including the lower esophagus, stomach, duodenum, and margin of a gastrojejunal anastomosis after surgical procedures. *Types* Peptic ulcers can be classified as acute or chronic, depending on the degree and duration of mucosal involvement, and gastric or duodenal, according to the location. The acute ulcer (Fig. 42-9) is associated with superficial erosion and minimal inflammation. It is of short duration and resolves quickly when the cause is identified and removed. A chronic ulcer is one of long duration, eroding through the muscular wall with the formation of fibrous tissue. It is present continuously for many months or intermittently throughout the person's lifetime. Chronic ulcers are more common than acute erosions. Gastric and duodenal ulcers, although defined as PUD, are different in their etiology and incidence (Table 42-14). Generally, the treatment of all types of ulcers is similar. *Etiology and Pathophysiology* Peptic ulcers develop only in an acid environment. However, an excess of HCl acid may not be necessary for ulcer development. Pepsinogen, the precursor of pepsin, is activated to pepsin in the presence of HCl acid and a pH of 2 to 3. When the stomach acid level is neutralized by food or antacids or acid secretion is blocked by drugs, the pH is increased to 3.5 or more. At a pH of 3.5 or more, pepsin has little or no proteolytic activity. The pathophysiology of ulcer development is outlined in Fig. 42-11. *Clinical Manifestations* The discomfort generally associated with gastric ulcers is located high in the epigastrium and occurs about 1 to 2 hours after meals. The pain is described as "burning" or "gaseous." If the ulcer has eroded through the gastric mucosa, food tends to aggravate rather than alleviate the pain. For some patients, the earliest symptoms are due to a serious complication such as perforation. The symptoms of duodenal ulcers occur when gastric acid comes in contact with the ulcers. With meal ingestion, food is present to help buffer the acid. Symptoms of duodenal ulcers occur generally 2 to 5 hours after a meal. The pain is described as "burning" or "cramplike." It is most often located in the midepigastric region beneath the xiphoid process. Duodenal ulcers can also produce back pain. Antacids alone or in combination with an H2-receptor blocker, as well as food, neutralize the acid to provide relief. A characteristic of duodenal ulcer is its tendency to occur continuously for a few weeks or months and then disappear for a time, only to recur some months later. Not all patients with gastric or duodenal ulcers experience pain or discomfort. Silent peptic ulcers are more likely to occur in older adults and those taking NSAIDs. The presence or absence of symptoms is not directly related to the size of the ulcer or the degree of healing. *Complications* The three major complications of chronic PUD are hemorrhage, perforation, and gastric outlet obstruction. All are considered emergency situations and may require surgical intervention. Hemorrhage is the most common complication of PUD. Duodenal ulcers account for a greater percentage of upper GI bleeding episodes than gastric ulcers. Perforation is considered the most lethal complication of PUD. Perforation is commonly seen in large penetrating duodenal ulcers (Fig. 42-13). Even though duodenal ulcers are more prevalent and perforate more often, mortality rates associated with perforation of gastric ulcers are higher. The patient with gastric ulcers is older and often has concurrent medical problems, which accounts for the higher mortality rate. *Nursing Management* Nursing assessment Subjective and objective data to obtain from a patient with PUD are presented in Table 42-16. Nursing Diagnoses Acute pain related to increased gastric secretions Ineffective self--health management related to lack of knowledge of long-term management of PUD Nausea related to acute exacerbation of disease process *Planning* The overall goals are that the patient with PUD will (1) adhere to the prescribed therapeutic regimen, (2) experience a reduction in or absence of discomfort, (3) exhibit no signs of GI complications, (4) have complete healing of the peptic ulcer, and (5) make appropriate lifestyle changes to prevent recurrence. Nursing *Implementation* You have an important role in identifying patients at risk for PUD. Early detection and effective treatment of ulcers are important aspects of reducing morbidity risks associated with PUD. Patients who are taking ulcerogenic drugs (e.g., aspirin, NSAIDs) are at risk for PUD. Encourage patients to take these drugs with food. Teach patients to report symptoms related to gastric irritation, including epigastric pain, to their health care provider. During the acute exacerbation of an ulcer, the patient often complains of increased pain and nausea and vomiting, and some may have evidence of bleeding. Initially many patients attempt to cope with the symptoms at home before seeking medical assistance. During this acute phase the patient may be NPO for a few days, have an NG tube inserted and connected to intermittent suction, and have IV fluid replacement. Explain to the patient and the caregiver the reasons for these therapies so they understand that the advantages far outweigh any temporary discomfort. Regular mouth care alleviates the dry mouth. Cleansing and lubrication of the nares facilitate breathing and decrease soreness. Analysis of gastric contents may include pH testing and analysis for blood, bile, or other substances. When the stomach is empty of gastric secretions, the ulcer pain diminishes and ulcer healing begins. *Collaborative Care Surgical Therapy for Peptic Ulcer Disease* With the use of antisecretory and antibiotic agents, surgery for PUD is uncommon. Surgery is performed on patients with complications that are unresponsive to medical management or concerns about stomach cancer. Surgical procedures include partial gastrectomy, vagotomy, and pyloroplasty. Partial gastrectomy with removal of the distal two thirds of the stomach and anastomosis of the gastric stump to the duodenum is called a gastroduodenostomy or Billroth I operation. Partial gastrectomy with removal of the distal two thirds of the stomach and anastomosis of the gastric stumpto the jejunum is called a gastrojejunostomy or Billroth II operation. Vagotomy is the severing of the vagus nerve, either totally (truncal) or selectively (highly selective vagotomy). These procedures are done to decrease gastric acid secretion. Pyloroplasty consists of surgical enlargement of the pyloric sphincter to facilitate the easy passage of contents from the stomach. It is commonly done after vagotomy or to enlarge an opening that has been constricted from scar tissue. *Postoperative Complications.* As with all surgeries, acute postoperative bleeding at the surgical site can occur. Monitoring of patients is similar to that described under acute upper GI bleeding. The most common long-term postoperative complications from PUD surgery are (1) dumping syndrome, (2) postprandial hypoglycemia, and (3) bile reflux gastritis. *Dumping Syndrome.* Dumping syndrome is the direct result of surgical removal of a large portion of the stomach and the pyloric sphincter. Approximately 20% of patients experience dumping syndrome after PUD surgery. Normally, gastric chyme enters the small intestine in small amounts. However, after surgery the stomach no longer has control over the amount of gastric chyme entering the small intestine. Consequently, a large bolus of hypertonic fluid enters the intestine and results in fluid being drawn into the bowel lumen. This creates a decrease in plasma volume along with distention of the bowel lumen and rapid intestinal transit. The onset of symptoms occurs within 15 to 30 minutes after eating. The patient usually describes feelings of generalized weakness, sweating, palpitations, and dizziness. These symptoms are due to the sudden decrease in plasma volume. The patient complains of abdominal cramps, borborygmi (audible abdominal sounds produced by hyperactive intestinal peristalsis), and the urge to defecate. These manifestations usually last less than 1 hour after eating. *Postprandial Hypoglycemia*. Postprandial hypoglycemia is considered a variant of dumping syndrome because it is the result of uncontrolled gastric emptying of a bolus of fluid high in carbohydrate into the small intestine. The bolus of concentrated carbohydrate results in hyperglycemia and the release of excessive amounts of insulin into the circulation. This results in reflex hypoglycemia. Symptoms are similar to those of any hypoglycemic reaction and include sweating, weakness, mental confusion, palpitations, tachycardia, and anxiety. Symptoms generally occur 2 hours after eating. *Bile Reflux Gastritis.* Gastric surgery that involves the pylorus, with either reconstruction or removal, can result in reflux of bile into the stomach. Prolonged contact with bile causes damage to the gastric mucosa, chronic gastritis, and recurrence of PUD. The symptoms associated with reflux alkaline gastritis are continuous epigastric distress that increases after meals. Vomiting relieves the distress, but only temporarily. The administration of cholestyramine (Questran), either before or with meals, has been used successfully to treat this problem. Cholestyramine binds with the bile salts that are the source of gastric irritation. - STOMACH CANCER Stomach (gastric) cancer is an adenocarcinoma of the stomach wall (Fig. 42-15). Asian Americans and Pacific Islanders, Hispanics, and African Americans have higher rates of stomach cancer than non-Hispanic whites. Stomach cancer is more prevalent in men of the lower socioeconomic class, primarily those living in urban areas. The incidence of stomach cancer increases with age, with the majority being diagnosed between 65 and 80. At the time of diagnosis, only 10% to 20% of patients have disease confined to the stomach, and more than 50% have advancedmetastatic disease. The 5-year survival rate is 80% in patients with early stages (confined to the stomach) and less than 30% in those with advanced disease. *Etiology and Pathophysiology* Many factors have been implicated in the development of stomach cancer, yet no single causative agent has been identified. Stomach cancer probably begins with a nonspecific mucosal injury as a result of infection (H. pylori), autoimmunerelated inflammation, repeated exposure to irritants such as bile, antiinflammatory agents, and tobacco use. Stomach cancer has been associated with diets containing smoked foods, salted fish and meat, and pickled vegetables. Whole grains and fresh fruits and vegetables are associated with reduced rates of stomach cancer. Infection with H. pylori, especially at an early age, is a risk factor for stomach cancer. It is possible that H. pylori and resulting cell changes can induce a sequence of transitions from dysplasia to cancer. Individuals with lymphoma of the stomach (mucosa-associated lymphoid tissue \[MALT\]) are at higher risk of stomach cancer. Other predisposing factors include atrophic gastritis, pernicious anemia, adenomatous polyps, hyperplastic polyps, and achlorhydria. Smoking and obesity both increase the risk of stomach cancer. Although first-degree relatives of patients with stomach cancer are at increased risk, only 8% to 10% of stomach cancers have an inherited familial component. Stomach cancer spreads by direct extension and typically infiltrates rapidly to the surrounding tissue and liver. Seeding of tumor cells into the peritoneal cavity occurs late in the course of the disease. *Clinical Manifestations* Stomach cancers often spread to adjacent organs before any distressing symptoms occur. The clinical manifestations can include unexplained weight loss, early satiety, indigestion, abdominal discomfort or pain, and signs and symptoms of anemia. The patient may report early satiety, or a sense of being full sooner than usual. Anemia, which is common, is caused by chronic blood loss as the lesion erodes through the mucosa or as a result of pernicious anemia (caused by loss of intrinsic factor). The person appears pale and weak and complains of fatigue, weakness, dizziness, and, in extreme cases, shortness of breath. The stool may be positive for occult blood. Supraclavicular lymph nodes that are hard and enlarged suggest metastasis via the thoracic duct. The presence of ascites is a poor prognostic sign. - UPPER GASTROINTESTINAL BLEEDING Although the most serious loss of blood from the upper GI tract is characterized by a sudden onset, insidious occult bleeding can also be a major problem. The severity of bleeding depends on whether the origin is venous, capillary, or arterial. (Types of upper GI bleeding are presented in Table 42-20.) Bleeding from an arterial source is profuse, and the blood is bright red, indicating it has not been in contact with gastric HCl acid secretion. In contrast, "coffee-ground" vomitus indicates that the blood has been in the stomach for some time. A massive upper GI hemorrhage is a loss of more than 1500 mL of blood or 25% of intravascular blood volume. Melena (black, tarry stools) indicates slow bleeding from an upper GI source. The longer the passage of blood through the intestines, the darker the stool color because of the breakdown of hemoglobin and the release of iron. Discovering the cause of the bleeding is not always easy. A variety of areas in the GI tract may be involved. Table 42-21 lists the common causes of upper GI bleeding. *Esophageal Origin.* Bleeding from the esophagus is most likely due to chronic esophagitis, Mallory-Weiss tear, or esophageal varices. Chronic esophagitis can be caused by GERD, the ingestion of drugs irritating to the mucosa, alcohol, and cigarette smoking. Esophageal varices most often occur secondary to cirrhosis of the liver. *Stomach and Duodenal Origin.* Bleeding peptic ulcers account for 40% of the cases of upper GI bleeding. Drugs (either prescription or OTC) are a major cause of upper GI bleeding. Approximately 25% of people on chronic NSAIDs (e.g., ibuprofen) develop endoscopically determined ulcer disease; of these, 2% to 4% will bleed. Aspirin, NSAIDs, and corticosteroids can cause irritation and disruption of the gastroduodenal mucosa. Even low-dose aspirin is associated with risk for GI bleeding. Many OTC preparations contain aspirin. A careful history of all commonly used drugs is necessary whenever upper GI bleeding is suspected. *Stress-related mucosal disease (SRMD)*, also called physiologic stress ulcers, occurs in patients who have had severe burns or trauma or major surgery. In SRMD, there is either diffuse superficial mucosal injury or discrete deeper ulcers in the fundus and body portions of the stomach. Patients with coagulopathy and those who experience respiratory failure resulting in mechanical ventilation for more than 48 hours are at highest risk. Subjective and objective data that should be obtained from the patient or caregiver are presented in Table 42-23. Nursing diagnoses for the patient with upper GI bleeding include, but are not limited to, the following: Decreased cardiac output related to loss of blood Deficient fluid volume related to acute loss of blood and gastric secretions Ineffective peripheral tissue perfusion related to loss of circulatory volume Anxiety related to upper GI bleeding, hospitalization, uncertain outcome, source of bleeding *PLANNING* The overall goals are that the patient with upper GI bleeding will (1) have no further GI bleeding, (2) have the cause of the bleeding identified and treated, (3) experience a return to a normal hemodynamic state, and (4) experience minimal or no symptoms of pain or anxiety. ***CHAPTER III: NURSING MANAGEMENT -- LOWER GASTROINTESTINAL PROBLEMS*** - ACUTE ABDOMINAL PAIN Etiology and Pathophysiology Acute abdominal pain is pain of recent onset. It may signal a life-threatening problem and therefore requires immediate attention. Causes include damage to organs in the abdomen and pelvis, which leads to inflammation, infection, obstruction, bleeding, and perforation (Fig. 43-1). The most common causes of acute abdominal pain are listed in Table 43-9. Perforation of the GI tract also results in irritation of the peritoneum (serous membrane lining the abdominal cavity) and peritonitis. Hypovolemic shock occurs from bleeding or when obstruction and peritonitis cause large amounts of fluid to move from the vascular space into the abdomen (third spacing). *NURSING ASSESSMENT* For the patient complaining of acute abdominal pain, take vital signs immediately and again at frequent intervals. Increased pulse and decreasing blood pressure indicate impending shock. An elevated temperature suggests an inflammatory or infectious process. Intake and output measurement provides essential information about the adequacy of vascular volume. Altered mental status indicates poor cerebral perfusion. Skin color and temperature and peripheral pulse strength provide information about skin perfusion. Inspect the abdomen for distention, masses, abnormal pulsation, symmetry, hernias, rashes, scars, and pigmentation changes. Auscultate bowel sounds. Bowel sounds that are diminished or absent in a quadrant may indicate a bowel obstruction, acute peritonitis, or paralytic ileus. Palpation should be gentle. Determine pain from peritoneal irritation by asking the person to cough, palpating the abdomen gently, or gently shaking the bed. Ask the patient about the onset, location, intensity, duration, frequency, and character of pain. Note whether the pain has spread or moved to new sites (quadrants) and what makes the pain worse or better. Is the pain associated with other symptoms, such as nausea, vomiting, changes in bowel and bladder habits, or vaginal discharge in women? Assessment of vomiting includes the amount, color, consistency, and odor of the emesis. Also ask about usual and changes in bowel patterns and habits. Nursing diagnoses for the patient with acute abdominal pain include, but are not limited to, the following: Acute pain related to inflammation of the peritoneum and abdominal distention Risk for deficient fluid volume related to collection of fluid in peritoneal cavity secondary to inflammation or infection Anxiety related to pain and uncertainty of cause or outcome of condition *PLANNING* The overall goals are that the patient with acute abdominal pain will have (1) relief of abdominal pain, (2) resolution of inflammation, (3) freedom from complications (especially hypovolemic shock), and (4) normal nutritional status. *NURSING IMPLEMENTATION* General care for the patient with acute abdominal pain involves management of fluid and electrolyte imbalances, pain, and anxiety. Assess the quality and intensity of pain at regular intervals, and provide medication and other comfort measures. Maintain a calm environment and provide information to help allay anxiety. A nasogastric (NG) tube may be used to decrease vomiting and relieve discomfort from gastric distention. Conduct ongoing assessments of vital signs, intake and output, and level of consciousness, which are key indicators of hypovolemic shock. - CHRONIC ABDOMINAL PAIN Chronic abdominal pain may originate from abdominal structures or may be referred from a site with the same or a similar nerve supply. The pain is often described as dull, aching, or diffuse. Common causes of chronic abdominal pain include irritable bowel syndrome (IBS), peptic ulcer disease, chronic pancreatitis, hepatitis, pelvic inflammatory disease, and vascular insufficiency. (Some of these disorders are discussed in this chapter). Diagnosis of the cause of chronic abdominal pain begins with a thorough history and description of specific pain characteristics, including severity, location, frequency, duration, and onset. The assessment also includes factors that increase or decrease the pain, such as meals, defecation, and activities. - IRRITABLE BOWEL SYNDROME Irritable bowel syndrome (IBS) is a common, chronic functional disorder, meaning that no organic cause is currently known. Symptoms of IBS, including abdominal pain or discomfort and alterations in bowel patterns, are intermittent and may occur for years. Patients often report a history of GI infections and food intolerances. However, the role of food allergies in IBS is unclear. Psychologic stressors (e.g., depression, anxiety, sexual abuse, posttraumatic stress disorder) are associated with development and exacerbation of IBS. IBS is more frequently diagnosed in women than in men. In addition to abdominal pain and diarrhea or constipation, patients commonly experience abdominal distention, excessive flatulence, bloating, urgency, and sensation of incomplete evacuation. Non-GI symptoms may include fatigue and sleep disturbances. There are no specific physical findings with IBS. The key to accurate diagnosis is a thorough history and physical examination. Ask patients to describe symptoms, past health history (including psychosocial factors such as stress and anxiety), family history, and drug and diet history. Determine if and how IBS symptoms interfere with school, work, or recreational activities. Diagnostic tests are selectively used to rule out other disorders such as colorectal cancer, IBD, endometriosis, and malabsorption disorders (lactose intolerance, celiac disease). Symptom-based criteria for IBS have been standardized and are referred to as the Rome criteria III. Treatment is directed at psychologic and dietary factors and drugs to regulate stool output. Patients are more likely to improve with treatment if they have a trusting relationship with their health care provider. Encourage the patient to verbalize concerns. Since treatment is often focused on symptoms, patients may benefit from keeping a diary of symptoms, diet, and episodes of stress to help identify factors that seem to trigger the IBS symptoms. If tolerated, encourage the patient to have a dietary fiber intake of at least 20 g/day (see Table 43-6) or to use a stool bulking agent. Increases in dietary fiber should be started gradually to avoid bloating and abdominal discomfort from gas. Advise the patient whose primary symptoms are abdominal distention and flatulence to avoid common gas-producing foods such as broccoli and cabbage. Yogurt may be better tolerated than milk products. Probiotics may be used because alterations in intestinal bacteria are believed to exacerbate the condition. - *ABDOMINAL TRAUMA* Etiology and Pathophysiology Injuries to the abdominal area usually are a result of blunt trauma or penetrating injuries. Common injuries of the abdomen include lacerated liver, ruptured spleen, mesenteric artery tears, diaphragm rupture, urinary bladder rupture, great vessel tears, renal or pancreas injury, and stomach or intestine rupture. Blunt trauma commonly occurs with motor vehicle accidents, beatings, and falls and may not be obvious because it does not leave an open wound. Both compression injuries (e.g., direct blow to the abdomen) and shearing injuries (e.g., rapid deceleration in a motor vehicle crash allowing some tissue to move forward while other tissues are held stationary) occur with blunt trauma. Penetrating injuries occur when a gunshot or stabbing produces an obvious, open wound into the abdomen. When solid organs (liver, spleen) are injured, bleeding can be profuse, resulting in hypovolemic shock. When contents from hollow organs (e.g., bladder, stomach, intestines) spill into the peritoneal cavity, the patient is at risk for peritonitis. In addition, abdominal compartment syndrome can develop. Abdominal compartment syndrome is excessively high pressure in the abdomen (abdominal hypertension). Anything that increases the volume in the abdominal cavity---including edematous organs, bleeding, and third spacing caused by obstruction and inflammation---increases abdominal pressure. High abdominal pressure restricts ventilation, potentially leading to respiratory failure. The high pressure also decreases cardiac output, venous return, and arterial perfusion of organs. Decreased perfusion to the kidneys can lead to renal failure. *NURSING AND COLLABORATIVE MANAGEMENT* Emergency management of abdominal trauma focuses on establishing a patent airway and adequate breathing, fluid replacement, and prevention of hypovolemic shock (see Table 43-11). IV lines are inserted, and volume expanders or blood is given if the patient is hypotensive. An NG tube is inserted to decompress the stomach and prevent aspiration. Frequent ongoing assessment is necessary to monitor fluid status, detect deterioration in condition, and determine the necessity for surgery. An impaled object should never be removed until skilled care is available. Removal may cause further injury and bleeding. - INFLAMMATORY DISORDERS - APPENDICITIS Appendicitis is inflammation of the appendix, a narrow blind tube that extends from the inferior part of the cecum (Fig. 43-2). It is most common in individuals 10 to 30 years of age. It is the most common cause of acute abdominal pain. A common cause of appendicitis is obstruction of the lumen by a fecalith (accumulated feces) (see Fig. 43-2). Obstruction results in distention; venous engorgement; and the accumulation of mucus and bacteria, which can lead to gangrene, perforation, and peritonitis. Diagnosis can be difficult because many patients do not have classic symptoms. Typically, appendicitis begins with periumbilical pain, followed by anorexia, nausea, and vomiting. The pain is persistent and continuous, eventually shifting to the right lower quadrant and localizing at McBurney's point (halfway between the umbilicus and the right iliac crest). Further assessment reveals localized tenderness, rebound tenderness, and muscle guarding. Coughing, sneezing, and deep inhalation magnify the pain. The patient usually prefers to lie still, often with the right leg flexed. Low-grade fever may or may not be present. The older adult may report less severe pain, slight fever, and discomfort in the right iliac fossa. *NURSING MANAGEMENT* Encourage the patient with abdominal pain to see a health care provider and to avoid self-treatment. Laxatives and enemas are especially dangerous because the resulting increased peristalsis may cause perforation of the appendix. To ensure that the stomach is empty in case surgery is needed, keep patients on nothing-by-mouth (NPO) status until they can be seen by a health care provider. Postoperative nursing management for the patient who has an appendectomy is similar to postoperative care of the patient after laparotomy. Ambulation begins the day of surgery or the first postoperative day. The diet is advanced as tolerated. The patient is usually discharged on the first or second postoperative day and resumes normal activities 2 to 3 weeks after surgery. - PERITONITIS Peritonitis results from a localized or generalized inflammatory process of the peritoneum. Causes of peritonitis are listed in Table 43-12. Primary peritonitis occurs when blood-borne organisms enter the peritoneal cavity. For example, the ascites that occurs with cirrhosis of the liver provides an excellent liquid environment for bacteria to flourish. Organisms can also enter the peritoneum during peritoneal dialysis. Secondary peritonitis is much more common. It occurs when abdominal organs perforate or rupture and release their contents (bile, enzymes, and bacteria) into the peritoneal cavity. Common causes include a ruptured appendix, perforated gastric or duodenal ulcer, severely inflamed gallbladder, and trauma from gunshot or knife wounds. Intestinal contents and bacteria irritate the normally sterile peritoneum and produce an initial chemical peritonitis, which is followed a few hours later by a bacterial peritonitis. The resulting inflammatory response leads to massive fluid shifts (peritoneal edema) and adhesions as the body attempts to wall off the infection. *Clinical Manifestations* Abdominal pain is the most common symptom of peritonitis. A universal sign of peritonitis is tenderness over the involved area. Rebound tenderness, muscular rigidity, and spasm are other signs of irritation of the peritoneum. Patients may lie still and take only shallow breaths because movement causes pain. Abdominal distention, fever, tachycardia, tachypnea, nausea, vomiting, and altered bowel habits may also be present. These manifestations vary depending on the severity and acuteness of the underlying condition. Complications of peritonitis include hypovolemic shock, sepsis, intraabdominal abscess formation, paralytic ileus, and acute respiratory distress syndrome. If treatment is delayed, peritonitis can be fatal. - GASTROENTERITIS Gastroenteritis is an inflammation of the mucosa of the stomach and small intestine. Acute gastroenteritis is defined as sudden diarrhea accompanied by nausea, vomiting, and abdominal cramping. Viruses are the most common cause of gastroenteritis. Other causes are presented in Table 43-1. Most cases of gastroenteritis are self-limiting. However, older adults and chronically ill patients may be unable to consume sufficient fluids orally to compensate for fluid loss. If dehydration occurs, IV fluid replacement may be necessary. As soon as tolerated, oral fluids containing glucose and electrolytes (e.g., Pedialyte) should be given. Nursing management of the patient with gastroenteritis is the same as for the patient with acute diarrhea. - INFLAMMATORY BOWEL DISEASE Inflammatory bowel disease (IBD) is a chronic inflammation of the GI tract. It is characterized by periods of remission interspersed with periods of exacerbation. The exact cause is unknown, and there is no cure. IBD is classified as either Crohn's disease or ulcerative colitis based on clinical manifestations (Table 43-14). As the name suggests, ulcerative colitis isusually limited to the colon. Crohn's disease can involve any segment of the GI tract from the mouth to the anus. The most commonly used surgical procedure for ulcerative colitis is a total proctocolectomy with ileal pouch/anal anastomosis (IPAA). In this procedure a diverting ileostomy is performed, and an ileal pouch is created and anastomosed directly to the anus (Fig. 43-4).  - INTESTINAL OBSTRUCTION Intestinal obstruction occurs when intestinal contents cannot pass through the GI tract. The obstruction may occur in the small intestine or colon and can be partial or complete, simple or strangulated. A partial obstruction usually resolves with conservative treatment, whereas a complete obstruction usually requires surgery. A simple obstruction has an intact blood supply, and a strangulated one does not. *TYPES OF INTESTINAL OBSTRUCTION* The causes of intestinal obstruction can be classified as mechanical or nonmechanical. Mechanical obstruction is a detectable occlusion of the intestinal lumen. Most intestinal obstructions occur in the small intestine. Surgical adhesion is the most common cause of small bowel obstructions and can occur within days of surgery or several years later (Fig. 43-5). Other causes of intestinal obstruction are hernia, strictures from Crohn's disease, and intussusception following bariatric abdominal surgery. The most common cause of colon obstruction is cancer, followed by diverticular disease. Nonmechanical obstruction may result from a neuromuscular or vascular disorder. Paralytic (adynamic) ileus (lack of intestinal peristalsis and bowel sounds) is the most common form of nonmechanical obstruction. It occurs to some degree after any abdominal surgery. It can be difficult to know whether postoperative obstruction is due to paralytic ileus or adhesions. One clue is that bowel sounds usually return before postoperative adhesions develop. Other causes of paralytic ileus include peritonitis, inflammatory responses (e.g., acute pancreatitis, acute appendicitis), electrolyte abnormalities (especially hypokalemia), and thoracic or lumbar spinal fractures. Pseudo-obstruction is a mechanical obstruction of the intestine without demonstration of obstruction by radiologic methods. Collagen vascular diseases and neurologic and endocrine disorders may cause pseudo-obstruction, but many times the cause is unknown. Vascular obstructions are rare and are the result of an interference with the blood supply to a portion of the intestines. The most common causes are emboli and atherosclerosis of the mesenteric arteries. Emboli may originate from thrombi in patients who have chronic atrial fibrillation, diseased heart valves, and prosthetic valves. Venous thrombosis may be seen in conditions of low blood flow, such as heart failure and shock. - COLORECTAL CANCER Colorectal cancer (CRC) is the third most common form of cancer and responsible for 9% of cancer deaths. CRC is more common in men than in women. Risk factors for CRC include a diet high in red or processed meat, obesity, physical inactivity, alcohol, long-term smoking, and low intake of fruits and vegetables. Genetic conditions such as FAP and a personal history of IBD place an individual at risk for CRC. About one third of cases of CRC occur in patients with a family history of CRC. Hereditary diseases (e.g., FAP) account for about 5% to 10% of CRC cases. Hereditary nonpolyposis colorectal cancer (HNPCC) syndrome (also called Lynch syndrome) is the most common form of hereditary CRC. Physical exercise and a diet with large amounts of fruits, vegetables, and grains may decrease the risk of CRC. Long-term use of NSAIDs (e.g., aspirin) is associated with reduced CRC risk. (See Table 43-21 for a list of risk factors.) Adenocarcinoma is the most common type of CRC. Typically, it begins as adenomatous polyps. Approximately 85% of CRCs arise from adenomatous polyps (see Fig. 43-6). *Nursing diagnoses* Diarrhea or constipation related to altered bowel elimination patterns Fear and anxiety related to diagnosis of CRC, surgical or therapeutic interventions, and possible terminal illness Ineffective coping related to diagnosis of cancer and side effects of treatment *PLANNING* The overall goals are that the patient with CRC will have (1) normal bowel elimination patterns, (2) quality of life appropriate to disease progression, (3) relief of pain, and (4) feelings of comfort and well-being. OSTOMY SURGERY An ostomy is a surgical procedure that allows intestinal contents to pass from the bowel through an opening in the skin on the abdomen. The opening is called a stoma. The stoma is created when the intestine is brought through the abdominal wall and sutured to the skin. The intestinal contents then empty through the hole on the surface of the abdomen rather than being eliminated through the anus. An ostomy is used when the normal elimination route is no longer possible. For example, if the person has CRC, the diseased portion is removed together with a certain margin of healthy tissue. Most stage I to III tumors of the colon can be resected, leaving enough healthy tissue to immediately anastomose the two remaining ends of healthy bowel, and no ostomy is necessary. If the tumor involves the rectum and is large enough to necessitate the removal of the anal sphincters, the anus is sutured shut and a permanent ostomy is created. Patients at high risk for CRC, such as those with FAP, and patients with ulcerative colitis may have a total colectomy. Ostomies are described according to location and type (Fig. 43-9).  - DIVERTICULOSIS AND DIVERTICULITIS Diverticula are saccular dilations or outpouchings of the mucosa that develop in the colon (Fig. 43-12). Multiple noninflamed diverticula are present in diverticulosis. Diverticulitis is inflammation of the diverticula, resulting in perforation into the peritoneum. Clinically, diverticular disease covers a spectrum from asymptomatic, uncomplicated diverticulosis to diverticulitis with complications such as perforation, abscess, fistula, and bleeding. Diverticula are common, especially in older adults, but most people never develop diverticulitis. Diverticula may occur anywhere in the GI tract but are most commonly found in the left (descending, sigmoid) colon. The etiology of diverticulosis of the sigmoid colon is thought to be associated with high luminal pressures from a deficiency in dietary fiber intake. The disease is more prevalent in Western, industrialized populations that consume diets low in fiber and high in refined carbohydrates. Diverticula are uncommon in vegetarians. Inadequate dietary fiber slows transit time, and more water is absorbed from the stool, making it more difficult to pass through the lumen. Decreased stool size raises intraluminal pressure, thus promoting diverticula formation.Diverticular disease can be asymptomatic and is typically discovered during routine sigmoidoscopy or colonoscopy.Diagnosis of diverticulitis is based on the history and physical examination (Table 43-30). - HERNIAS A hernia is a protrusion of the viscus (internal organ such as the intestine) through an abnormal opening or a weakened area in the wall of the cavity in which it is normally contained. A hernia may occur in any part of the body, but it usually occurs within the abdominal cavity (Fig. 43-14). Hernias that easily return to the abdominal cavity are called reducible. The hernia can be reduced manually or may reduce spontaneously when the person lies down. If the hernia cannot be placed back into the abdominal cavity, it is known as irreducible or incarcerated. In this situation the intestinal flow may be obstructed. When the hernia is irreducible and the intestinal flow and blood supply are obstructed, the hernia is strangulated. The result is an acute intestinal obstruction. The inguinal hernia is the most common type of hernia and occurs at the point of weakness in the abdominal wall where the spermatic cord (in men) or the round ligament (in women) emerges (see Fig. 43-14, C). Inguinal hernias are more common in men. A femoral hernia occurs when there is a protrusion through the femoral ring into the femoral canal. It appears as a bulge below the inguinal ligament. It easily becomes strangulated. It occurs more often in women (see Fig. 43-14, B). The umbilical hernia occurs when the rectus muscle is weak (as with obesity) or the umbilical opening fails to close after birth (see Fig. 43-14, A). Ventral or incisional hernias are due to weakness of the abdominal wall at the site of a previous incision. They occur most commonly in patients who are obese, have had multiple surgical procedures in the same area, or have had inadequate wound healing because of poor nutrition or infection. Diagnosis is based on history and physical examination findings. Laparoscopic surgery is the treatment of choice for hernias. The surgical repair of a hernia, known as a herniorrhaphy, is usually an outpatient procedure. Reinforcement of the weakened area with wire, fascia, or mesh is known as a hernioplasty. Strangulated hernias are treated immediately with resection of the involved area or a temporary colostomy so that necrosis and gangrene do not occur. After a hernia repair, the patient may have difficulty voiding. Measure intake and output and observe for a distended bladder. Scrotal edema is a painful complication after an inguinal hernia repair. A scrotal support with application of an ice bag may help relieve pain and edema. Encourage deep breathing, but not coughing. Teach patients to splint the incision and keep their mouths open when coughing or sneezing are unavoidable. The patient may be restricted from heavy lifting for 6 to 8 weeks. - MALABSORPTION SYNDROME Malabsorption results from impaired absorption of fats, carbohydrates, proteins, minerals, and vitamins. The stomach, small intestine, liver, and pancreas regulate normal digestion and absorption. Digestive enzymes ordinarily break down nutrients so that absorption can take place. If this process is interrupted at any point, malabsorption may occur. Several problems can cause malabsorption (Table 43-31). Lactose intolerance is the most common malabsorption disorder, followed by IBD, celiac disease, tropical sprue, and cystic fibrosis. The most common signs of malabsorption are weight loss, diarrhea, and steatorrhea (bulky, foul-smelling, yellow-gray, greasy stools with putty-like consistency) (Table 43-32). Steatorrhea does not occur with lactose intolerance. Tests used to determine the cause of malabsorption include qualitative examination of stool for fat (e.g., Sudan III stain), a 72-hour stool collection for quantitative measurement of fecal fat, serologic testing for celiac disease, and fecal elastase testing to determine if there is pancreatic insufficiency. - CELIAC DISEASE Celiac disease is an autoimmune disease characterized by damage to the small intestinal mucosa from the ingestion of wheat, barley, and rye in genetically susceptible individuals. It is a relatively common disease that occurs at all ages and has a wide variety of symptoms. Celiac sprue and gluten-sensitive enteropathy are other names for celiac disease. Celiac disease is not the same disease as tropical sprue, a chronic disorder acquired in tropical areas that is characterized by progressive disruption of jejunal and ileal tissue, resulting in nutritional difficulties. Tropical sprue is treated with folic acid and tetracycline. Three factors necessary for developing celiac disease are genetic predisposition, gluten ingestion, and an immune-mediated response. Classic manifestations of celiac disease include foul-smelling diarrhea, steatorrhea, flatulence, abdominal distention, and malnutrition. Some people have no obvious GI symptoms and may instead have atypical signs and symptoms such as decreased bone density and osteoporosis, dental enamel hypoplasia, iron and folate deficiencies, peripheral neuropathy, and reproductive problems. A pruritic, vesicular skin lesion, called dermatitis herpetiformis, is sometimes present and occurs as a rash on the buttocks, scalp, face, elbows, and knees. Celiac disease is also associated with other autoimmune diseases, particularly rheumatoid arthritis, type 1 diabetes mellitus, and thyroid disease. The link between celiac disease and reproductive problems is less clear. Protein, fat, and carbohydrate absorption is affected. Weight loss, muscle wasting, and other signs of malnutrition may be present. Abnormal serum folate, iron, and cobalamin levels can occur. Iron-deficiency anemia is one of the most common manifestations of celiac disease. Patients may exhibit lactose intolerance and need to refrain from lactose-containing products until the disease is under control. Inadequate calcium intake and vitamin D absorption can lead to decreased bone density and osteoporosis. - LACTASE DEFICIENCY Lactase deficiency is a condition in which the lactase enzyme is deficient or absent. Lactase is the enzyme that breaks down lactose into two simple sugars: glucose and galactose. Primary lactase insufficiency is most commonly a result of genetic factors. Certain ethnic or racial groups, especially those with Asian or African ancestry, develop low lactase levels in childhood. Less common causes include low lactase levels resulting from premature birth and congenital lactase deficiency, a rare genetic disorder. Lactose malabsorption can also occur when conditions leading to bacterial overgrowth promote lactose fermentation in the small bowel, and when intestinal mucosal damage interferes with absorption. The latter occurs with IBD and celiac disease. The symptoms of lactose intolerance include bloating, flatulence, cramping abdominal pain, and diarrhea. Symptoms generally occur within 30 minutes to several hours after drinking a glass of milk or ingesting a milk product. The diarrhea of lactose intolerance results from fluid secretion into the small intestine, responding to the osmotic action of undigested lactose. Many lactose-intolerant persons are aware of their milk intolerance and avoid milk and milk products. Lactose intolerance is diagnosed with a lactose tolerance test, a lactose hydrogen breath test, or genetic testing. Treatment consists of eliminating lactose from the diet by avoiding milk and milk products and/or replacing lactase with commercially available preparations. Milk and ice cream contain more lactose than cheese. Live culture yogurt is an alternative source of calcium, but the patient needs to be sure that milk products have not been added to the yogurt. - SHORT BOWEL SYNDROME Short bowel syndrome (SBS) is a condition in which the small intestine does not have adequate surface area to absorb enough nutrients. Thus the person is unable to meet energy, fluid, electrolyte, and nutritional needs on a standard diet. Causes of SBS include diseases that damage the intestinal mucosa, surgical removal of too much small intestine (primarily in patients with Crohn's disease), and congenital defects. Without adequate surface area, lifetime parenteral nutrition is necessary for survival. The predominant manifestations of SBS are diarrhea and steatorrhea (unabsorbed fat in the stool). Signs of malnutrition as well as vitamin and mineral deficiencies include weight loss, cobalamin and zinc deficiency, and hypocalcemia. The patient may develop lactase deficiency and bacterial overgrowth. Oxalate kidney stones may form because of increased colonic absorption of oxalate. The overall goals of treatment are that the patient with SBS will have fluid and electrolyte balance, normal nutritional status, and control of diarrhea. In the period immediately following massive bowel resection, patients receive parenteral nutrition to replace fluid, electrolyte, and nutrient losses and to rest the bowel. An antisecretory agent (histamine \[H2\]-blocker or proton pump inhibitor) may be given to decrease gastric acid secretion. A diet high in carbohydrate and low in fat supplemented with soluble fiber, pectin, and the amino acid glutamine is often recommended. The patient with SBS is encouraged to eat at least six meals per day to increase the time of contact between food and the intestine. - GASTROINTESTINAL STROMAL TUMORS Gastrointestinal stromal tumors (GISTs) are a rare form of cancer that originates in cells found in the wall of the GI tract. These cells, known as interstitial cells of Cajal, help control the movement of food and liquid through the stomach and intestines. About 55% of GISTs are found in the stomach; 35% are found in the small intestine; 5% are found in the rectum; and the rest are found in the esophagus, colon, or peritoneum.53 GISTs are most frequently diagnosed in people between the ages of 50 and 70. Most GISTs are caused by genetic mutations. Patients initially undergo surgery to remove the tumor, but the GIST has often metastasized by the time of diagnosis or commonly recurs. - ANORECTAL PROBLEMS - HEMORRHOIDS Hemorrhoids are dilated hemorrhoidal veins. They may be internal (occurring above the internal sphincter) or external (occurring outside the external sphincter) (Figs. 43-15 and 43-16). Symptoms include rectal bleeding, pruritus, prolapse, and pain. In affected persons, hemorrhoids appear periodically, depending on the amount of anorectal pressure. Hemorrhoids develop as a result of increased anal pressure and weakened connective tissue that normally supports the hemorrhoidal veins. When supporting tissues in the anal canal weaken, usually as a result of straining at defecation, venules become dilated. In addition, blood flow through the veins of the hemorrhoidal plexus is impaired. An intravascular clot in the venule results in a thrombosed external hemorrhoid. Hemorrhoids are the most common reason for bleeding with defecation. The amount of blood lost at one time may be small, but over time it may lead to iron-deficiency anemia. Hemorrhoids may be precipitated by many factors, including pregnancy, prolonged constipation, straining in an effort to defecate, heavy lifting, prolonged standing and sitting, and portal hypertension (as found in cirrhosis). Conservative nursing management for the patient with hemorrhoids includes teaching measures to prevent constipation, avoid prolonged standing or sitting, and properly use OTC drugs for hemorrhoidal symptoms. Teach the patient to seek medical care for severe symptoms of hemorrhoids (e.g., excessive pain and bleeding, prolapsed hemorrhoids). Sitz baths (15 to 20 minutes) two or three times each day for 7 to 10 days may help reduce discomfort and swelling associated with hemorrhoids. Postoperatively, topical nitroglycerin preparations may be used to decrease pain and subsequent opioid use. Sitz baths are started 1 or 2 days after surgery. A warm sitz bath provides comfort and keeps the anal area clean. A sponge ring in the sitz bath helps relieve pressure on the area. Initially, the patient should not be left alone because of the possibility of weakness or fainting. - ANAL FISSURE An anal fissure is a skin ulcer or a crack in the lining of the anal wall that is caused by trauma, local infection, or inflammation (Fig. 43-17). Fissures are considered either primary or secondary based on their etiology. Primary fissures usually occur as a result of local trauma, such as vaginal delivery. High pressure in the internal anal sphincter can result in ischemia, which can lead to fissuring. Secondary fissures are due to a variety of conditions, including IBD, prior anal surgery, and infection (syphilis; tuberculosis; gonorrhea; or infection with Chlamydia, herpes simplex virus, or HIV). Anal tissue ulcerates because of ischemia caused by a combination of high resting anal sphincter tone and poor blood supply to the area. The ischemic tissue may ulcerate spontaneously or when traumatized by factors such as hard stools that would not normally cause tissue breakdown. If ischemia is not corrected, the anal fissures will not be able to heal. The major symptoms are anal pain and bleeding. Pain is especially severe during and after defecation and has been described as "passing broken glass." Bleeding is bright red and usually slight. Constipation results because of fear of pain associated with bowel movements. - ANORECTAL ABSCESS An anorectal abscess is a collection of perianal pus (see Fig. 43-17). The abscess is the result of obstruction of the anal glands, leading to infection and subsequent abscess formation. Abscess formation can occur secondary to anal fissures, trauma, or IBD. The most common causative organisms are Escherichia coli, staphylococci, and streptococci. Clinical manifestations include local severe pain and swelling, foul-smelling drainage, tenderness, and elevated temperature. Sepsis can occur as a complication. Anorectal abscesses are diagnosed by rectal examination. Surgical therapy consists of drainage of abscesses. If packing is used, it should be impregnated with petroleum jelly, and the area should be allowed to heal by granulation. The packing is changed every day, and moist, hot compresses are applied to the area. Care must be taken to avoid soiling the dressing during urination or defecation. A low-fiber diet is given. The patient may leave the hospital with the wound still open. Teach the patient about wound care and the importance of sitz baths, thorough cleaning after bowel movements, and follow-up visits to a health care provider. - ANAL FISTULA An anal fistula is an abnormal tunnel leading from the anus or rectum. It may extend to the outside of the skin, vagina, or buttocks and often precedes an abscess. Anal fistulas are a complication of Crohn's disease and may resolve when drug treatment (i.e., with infliximab) achieves remission of the disease. About 50% of anal fistulas are due to anorectal abscess. Feces may enter the fistula and cause an infection. There may be persistent, blood-stained, purulent discharge or stool leakage from the fistula. The patient may need to wear a pad to avoid staining clothes. Surgical therapy involves a fistulotomy or a fistulectomy. In a fistulotomy the fistula is opened, and healthy tissue is allowed to granulate. A fistulectomy is an excision of the entire fistulous tract. Gauze packing is inserted, and the wound is allowed to heal by granulation. Care is the same as that given after a hemorrhoidectomy. In patients with complex fistulas, fibrin glue may be injected to seal the fistula. - ANAL CANCER Anal cancer is uncommon in the general population, but the incidence is increasing. Human papillomavirus (HPV) is associated with about 80% of the cases of anal cancer. Risk factors include having many sexual partners, genital warts (which are caused by HPV), smoking, receptive anal sex, and HIV infection. The average age at diagnosis is 60. Anal cancer is more common in African Americans than in whites. Most frequently the initial symptom is rectal bleeding. Other symptoms include rectal pain and sensation of a rectal mass. Some patients have no symptoms, which leads to delayed diagnosis and treatment. It is especially important to screen high-risk individuals. A swab of the anal mucosa can be obtained during a digital rectal examination. Identification of cell changes (e.g., dysplasia, neoplasia) can be determined. High-resolution anoscopy allows for visualization of the mucosa and biopsy. An endo-anal (endorectal) ultrasound may also be done. **MODULE 1 LEARNING ACTIVITIES**  Research the following, encode your research output using legal size, Times New Roman, 12, 1. The use of drugs in the treatment of nausea and vomiting 2. **Scientific evidence** that ginger may be effective for nausea and vomiting of pregnancy when used at recommended doses for short periods. **LEARNINGACTIVITY 1:**Labeling Exercise(1 POINT PER ITEM) *The Digestive System: Write the name of each numbered part on the corresponding line of the answer sheet.*  *Accessory Organs of Digestion: Write the name of each numbered part on the corresponding line of the answer sheet.*  **LEARNING ACTIVITY 2:**Matching Exercise(1 POINT PER ITEM) *Match the following terms and write the appropriate letter to the left of each number:* \_\_\_\_\_ 1. polysialia a. pertaining to the lip \_\_\_\_\_ 2. gingiva b. gum \_\_\_\_\_ 3. agnathia c. absence of the jaw \_\_\_\_\_ 4. hypoglossal d. excess secretion of saliva \_\_\_\_\_ 5. labial e. sublingual \_\_\_\_\_ 6. choledochal a. jaundice \_\_\_\_\_ 7. lithiasis b. pertaining to the common bile duct \_\_\_\_\_ 8. cholangiectasis c. crushing of a biliary calculus \_\_\_\_\_ 9. icterus d. condition of having stones \_\_\_\_\_ 10. cholelithotripsy e. dilation of a bile duct \_\_\_\_\_ 11. gastropathy a. narrowing of the pylorus \_\_\_\_\_ 12. pylorostenosis b. substance that induces vomiting \_\_\_\_\_ 13. gastrocele c. hernia of the stomach \_\_\_\_\_ 14. pylorospasm d. any disease of the stomach \_\_\_\_\_ 15. emetic e. sudden contraction of the pylorus \_\_\_\_\_ 16. cecopexy a. stoppage of bile flow \_\_\_\_\_ 17. proctocele b. hernia of the rectum \_\_\_\_\_ 18. cholestasis c. surgical fixation of the cecum \_\_\_\_\_ 19. proctorrhaphy d. surgical puncture of the colon \_\_\_\_\_ 20. colocentesis e. surgical repair of the rectum *SUPPLEMENTARY TERMS* \_\_\_\_\_ 21. cachexia a. malnutrition and wasting \_\_\_\_\_ 22. caries b. chewing \_\_\_\_\_ 23. deglutition c. tooth decay \_\_\_\_\_ 24. gavage d. swallowing \_\_\_\_\_ 25. mastication e. feeding through a tube \_\_\_\_\_ 26. bolus a. inability to eat \_\_\_\_\_ 27. cardia b. partially digested food \_\_\_\_\_ 28. peritoneum c. part of the stomach near the esophagus \_\_\_\_\_ 29. aphagia d. a mass, as of food \_\_\_\_\_ 30. chyme e. serous membrane in the abdomen **LEARNING ACTIVITY 3:**Fill in the blanks(1 POINT PER ITEM) 31\. The palatine tonsils are located on either side of the \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. 32\. Stomatosis is any disease condition of the \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. 33\. Dentin is the main substance of the \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. 34\. Glossorrhaphy is suture of the \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. 35\. From its name you might guess that the buccinator muscle is in the \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. 36\. An enterovirus is a virus that infects the \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. 37\. A wave of contractions in an organ wall, such as the contractions that move material through the digestive tract, is called \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. 38\. The blind pouch at the beginning of the colon is the \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. 39\. The anticoagulant heparin is found throughout the body, but it is named for its presence in the \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. 40\. The substance cholesterol is named for its chemical composition (sterol) and for its presence in \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. 41\. The organ that produces bile is the \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. 42\. The organ that stores bile is the \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. **LEARNING ACTIVITY 4:**True-False(1 POINT PER ITEM) *Examine each of the following statements. If the statement is true, write T in the first blank. If the statement is false, write F in the first blank and correct the statement by replacing the underlined word in the second blank.* 43\. The epigastrium is the region of the abdomen [above] the stomach. \_\_\_\_\_ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 44\. The first portion of the small intestine is the [jejunum.] \_\_\_\_\_ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 45\. The cystic duct carries bile to and from the [gallbladder.] \_\_\_\_\_ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 46\. Cirrhosis is a disease of the [esophagus.] \_\_\_\_\_ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 47\. The appendix is attached to the [ileum.] \_\_\_\_\_ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 48\. The common hepatic duct and the cystic duct merge to form the [common bile duct.] \_\_\_\_\_ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 49\. Enteropathy is any disease of the [intestine.] \_\_\_\_\_ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 50\. The hepatic portal system carries blood to the [spleen.] \_\_\_\_\_ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **LEARNING ACTIVITY 5:**Write the meaning of each of the following abbreviations: (1 POINT PER ITEM) 51\. IBD \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 52\. TPN \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 53\. HAV \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 54\. GI \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 55\. HCl \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 56\. ERCP \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 57\. PEG (tube) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 58\. GERD \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 59\. ERCP \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_60. NG \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_  MULTIPLE CHOICE: Select the best answer for each question. Answer provided at the end of this module. 1\. Reflux of food into the esophagus from the stomach is prevented by contraction of the: a\. ampulla of Vater. b. cardiac sphincter. c. ileocecal valve. d. pyloric sphincter. 2\. The digestion of starches begins in the mouth with the secretion of the enzyme: a\. lipase. b. pepsin. c. ptyalin. d. trypsin. 3\. The stomach, which derives its acidity from hydrochloric acid, has a pH of approximately: a\. 1.0. b. 3.5. c. 5.0. d. 7.5. 4\. Intrinsic factor is a gastric secretion necessary for the intestinal absorption of the vitamin that prevents pernicious anemia, that is: a\. vitamin B1. b. vitamin B12. c. vitamin C. d. vitamin K. 5\. A hormonal regulatory substance that inhibits stomach contraction and gastric secretions is: a\. acetylcholine. b. gastrin. c. norepinephrine. d. secretin. 6\. An enzyme, secreted by the gallbladder, that is responsible for fat emulsification is: a\. amylase. b. bile. c. maltase. d. steapsin. 7\. During the initial assessment of a patient complaining of increased stomach acid related to stress, the nurse knows that the physician will want to consider the influence of the neuroregulator: a\. gastrin. b. cholecystokinin. c. norepinephrine. d. secretin. 8\. Pancreatic secretions into the duodenum: a\. are stimulated by hormones released in the presence of chyme as it passes through the duodenum. b\. have an alkaline effect on intestinal contents. c\. increase the pH of the food contents. d\. accomplish all of the above. 9\. Bile, which emulsifies fat, enters the duodenum through the: a\. cystic duct. b. common bile duct. c. common hepatic duct. d. pancreatic duct. 10\. Secretin is a gastrointestinal hormone that: a\. causes the gallbladder to contract. b\. influences contraction of the esophageal and pyloric sphincters. c\. regulates the secretion of gastric acid. d\. stimulates the production of bicarbonate in pancreatic juice. 11\. The major carbohydrate that tissues use for fuel is: a\. fructose. b. galactose. c. glucose. d. sucrose. 12\. It usually takes how long for food to enter the colon? a\. 2 to 3 hours after a meal is eaten c. 6 to 7 hours after a meal is eaten b\. 4 to 5 hours after a meal is eaten d. 8 to 9 hours after a meal is eaten 13\. During a nursing assessment, the nurse knows that the most common symptom of patients with gastrointestinal dysfunction is: a\. diffuse pain. b. dyspepsia. c. constipation. d. abdominal bloating. 14\. When completing a nutritional assessment of a patient who is admitted for a gastrointestinal disorder, the nurse notes a recent history of dietary intake. This is based on the knowledge that a portion of digested waste products can remain in the rectum for how many days after a meal is digested? a\. 1 day b. 2 days c. 3 days d. 4 days 15\. Obstruction of the gastrointestinal tract leads to: a\. increased force of intestinal contraction. b\. distention above the point of obstruction. c\. pain and a sense of bloating. d\. all of the above. 16\. A nurse who is investigating a patient's statement about duodenal pain should assess the: a\. epigastric area and consider possible radiation of pain to the right subscapular region. b\. hypogastrium in the right or left lower quadrant. c\. left lower quadrant. d\. periumbilical area, followed by the right lower quadrant. 17\. Abdominal pain associated with indigestion is usually: a\. described as crampy or burning. b\. in the left lower quadrant. c\. less severe after an intake of fatty foods. d\. relieved by the intake of coarse