N 246 Health Alterations lll Fall, 2010 Alterations in the GI System Sandra Buckley, RN,MS
A & P of GI system • 30 ft. long from mouth to anus. • Consists of mouth, esophagus, stomach, small intestine, large intestine, rectum, anus. • Associated organs: liver, pancreas, gallbladder. • Organs covered by peritoneum (parietal:lines abdominal cavity, visceral:covers organs), two folds of peritoneum are mesentery (contains blood vessels and lymph glands) and omentum (contains fat and lymph nodes)
Physiology • Innervated by parasympathetic, sympathetic and intrinsic nervous system. • Parasympathetic:excitatory (increased peristalsis). • Sympathetic: inhibitory (decreased peristalsis). • Intrinsic (enteric): coordination of motor and secretory functions-two nerve layers that lie between mucosa, contribute to motor and secretory activities.
Circulation of GI system • Receives approximately 25-30% of cardiac output. Major source from which blood can be diverted during exercise or stress. • Venous blood draining the GI tract organs empties into portal vein, which then perfuses liver. Upper GI- blood from splanchnic artery, small intestine-blood from branches of hepatic and superior mesenteric arteries.Large intestine-superior and inferior mesenteric arteries.
Function/physiology of GI • Each part of system performs different activities. • Ingestion and propulsion of food: mouth, pharynx, esophagus. • Digestion and absorption: mouth, stomach, small intestine. • Elimination: large intestine
Ingestion • Intake of food, impacted by: • appetite-desire to eat, center located in hypothalmus, factors affecting; • (increasing appetite) hypoglycemia, empty stomach, decrease in body temperature, sight, smell, taste of food. • (decreasing appetite) stomach distention, illness (fever),hyperglycemia, nausea, vomiting, drugs, input from higher brain centers. • Hormone Ghrelin; released from stomach mucosa to stimulate appetite. • Hormone Leptin; released and involved in appetite suppression
Factors affecting GI tract • Emotions: stress, anxiety, happiness. May be manifested by anorexia, epigastric and abdominal pain, diarrhea, constipation, gas, decreased satiety and increased consumption (above caloric need). • Physical factors: diet, alcohol, caffeine, cigarette smoking, drugs, fatigue, organic diseases, metabolic factors.
Swallowing (deglutition) • Involve mouth pharynx and esophagus • Mouth-lips and oral (buccal) cavity, roof of cavity is soft palate, contains teeth used in chewing (mastication) and tongue. Taste receptors; sides and tip of tongue (important for speech and pushing food to back of throat). • 3 sets of salivary glands: parotid, submixillary, sublingual-produces saliva (contains salivary enzyme amylase)
Swallowing video • http://www.youtube.com/watch?v=Z7xKYNz9AS0 • http://www.youtube.com/watch?v=uxHUUgLeNzk
Pharynx • Musculomembranous tube; nasopharynx, orophrynx ( when food or water present, stimulates swallowing reflex), laryngeal pharynx • Secretes mucus, aids in swallowing • Epiglottis: lid of fibrocartilage that closes over the larynx during swallowing.
Esophagus • Hollow, muscular tube ~ 10 inches long. • When swallowing: upper esophageal sphincter (cricopharyngeal muscle) relaxes and a peristaltic wave moves the bolus into the esophagus. Muscular layers contract (peristalsis) and propel food to stomach. • Lower esophageal sphincter (LES)- at distal end of esophagus, remains contracted except during swallowing, belching or vomiting. Important barrier that prevents reflux.
Dyspepsia • Refers to host of upper abdominal or epigastric symptoms such as pain, discomfort, fullness, heartburn, regurgitation or “indigestion”. • Etiology: drug intolerance, GI tract dysfunction, pancreatic or biliary tract disease.
Dyspepsia • Functional or nonulcer dyspepcia-most common cause of chronic dyspepsia. 2/3’s of patients have no obvious organic or biochemical cause for symptoms that can be evidenced by endoscopy. • Clinical findings: weight loss, vomiting, dysphagia, melena, anemia.
Reflux esophagitis GERD • Gastroesophageal reflux disease (GERD),not a disease but a syndrome that results in reflux of gastric secretions into esophagus. • Predisposing conditions: LES (incompetent lower esophgeal sphincter), hiatal hernia, decreased gastric emptying. Results in: - irritation – pyrosis (heartburn), -inflammation - esophagitis,hoarseness, -difficulty swallowing – dysphagia.
Gerd-diagnosis • Upper GI x-ray with barium swallow • Esophageal endoscopy • Esophageal manometry • Ph monitoring
Barium swallow • Outlines the esophagus • Contrast is ingested • Gastrografin (water soluble contrast), and barium • Nursing care: educate and support pt.; signed consent, allergy status to meds or contrast, need to drink contrast, assume various positions on table, NPO 8-12 hours before procedure, avoid smoking 12 after midnight. After procedure; take measures to prevent contrast media impaction (fluids, laxatives), stool may be white 72 hours post-test.
PT. education • Lifestyle changes • Dietary changes- alcohol, spices, chocolate, broccoli, salmon, caffeine, smoking, mint, fat. • Medications-antacids(tums, maalox), H2 blockers (tegamet, pepsid), protein pump inhibitors (nexium, Protonix), prokinetic meds (metaclpromide)
Other esophageal disorders • Barrett’s esophagus-precancerous lesion, requires annual tissue biopsy. • Esophagitis-due to chemical irritation (dust, lye, temperature, ETOH abuse). • Achalasia-cardiospasm of lower portion of esophagus muscle. Causes obstruction and accumulation of food and fluid.
Esohageal disorders • Esophageal cancer-rate is high in Asia, low in U.S., but higher incidence in African-Americans and men. Prognosis poor. Clinical manifestations-similar to GERD. • Esophageal strictures-caused by chronic GERD or ingestion of caustic liquids. Intervention-endoscopic dilation.
Dilated tortuous veins in lower portion of esophagus. Complication of liver cirrhosis. Bleeding varices most life-threatening complication of cirrhosis. Factors producing irritation: Alcohol, poorly masticated food,acid regurgitation, increased abdominal pressure (nausea, vomiting, straining, coughing). Esophageal varices
stomach • Function is to store food, mix food with gastric secretions, and empty contents into small intestine. Absorbs only small amount of water, alcohol, electrolytes and certain drugs. • Average length of time food in stomach:3-4 hours • Chief cells secret pepsinogen (antecedent of pepsin-the main enzyme of gastric juice which converts proteins into peptones) • Parietal cells secrete hydrochloric acid, water and intrinsic factor (increases absorption of vitamin B complex)
Gastritis • Results from breakdown in normal gastric mucosal barrier. May be acute or chronic. • Type A-associated with autoimmune disorder, Type B-associated with H. Pylori. • Clinical manifestations similar to GERD, often self-limiting.
Gastritis (continued) • Severe cases may require NPO, IV fluids, NG for lavage. • When atrophy of cells occur, may result in loss of intrinsic factor/decreased RBC’s/anemia. • Tx- education,lifestyle modification, assessment of severity,medication, surgical interventions (gastrectomy,vagotomy or pyloroplasty). • Medications- antacids,Zantac, Tagamet, prilosec, prevacid
Pernicious anemia • Intrinsic factor produced by cells in gastric mucosa • Binds with ingested B12 (degraded by HCL) to form complex that travels to small intestine for absorption. • B12 deficiency: anemia • Atrophic gastritis: common condition in older people, damages cells of stomach, without healthy cells, production of HCL and intrinsic factor is diminished. Vitamin B12 deficiency caused by atrophic gastritis and a lack of intrinsic factor is know as pernicious anemia.
Hiatal Hernia • Herniation (bulging upwards) of a portion of stomach through diaphragmatic opening. • Acid from stomach spills into unprotected esophagus – irritation of mucus lining. • “choking feeling”, lump in throat, food stoppage and regurgitation • More common in older adults and women.
Hiatal Hernia • Diagnositic studies: barium swallow, endoscopy. • Collaborative care: administration of medications (antacids, antisecretory agents), avoidance of lifting and straining, elimination of alcohol and smoking, HOB elevation
Surgical Therapy (hiatal hernia) • Objective to reduce reflux by enhancing integrity of LES. • Procedures: valvuloplasties: also called fundoplication, involves wrapping of fundus of stomach around lower portion of esophagus. Can be preformed laproscopically. Prevents reflux in 90% of patients.
Nursing management Postop care: prevention of respiratory complications, IV therapy, wound care, education. If NG present- maintain patency of tube, dangerous to attempt to replace tube if dislodged due to possibility of perforation of surgical repair.
Upper GI Ulcers • Peptic ulcers- erosion of GI mucosa mostly in Antrum an duodenum • Caused by the digestive action of HCL acid &pepsin. • Acute (superficial) • Chronic (deep, longer healing) • Gastric or duodenal ( by location), but different in etiology and incidence.
Physiology of Peptic ulcer disease • Mucosal defense system may be impaired by: H. pylori, inadequate blood flow, smoking ,NSAIDs
Gastric - superficial, in antrum/body of stomach Common in women and unskilled workers, low socio-eco. Burning, gas pressure left epigastric, to back, high abdominal. Pain 1-2 hrs after food intake. Increased w/ smoking, drugs and alcohol use N/V, weight. loss Duodenal-high end of duodenum. Common in men, associated with psychic stress, 80% of all ulcers Burning, gnawing, mid- epigastric, to back, high abdominal,pain 2-4 hrs after meals, episodic, middle of night. Pain relief with antacids and food intake, N/V. Increased with alcohol, drug use, smoking. Compare gastric vs duodenal
Stress ulcers • Erosive gastritis caused by: • Transient GI ischemia (low blood supply) with shock, severe injury, burns, surgery. • Low blood supply results in imbalance of acid and mucus barrier- causing erosion. • Prevention: prophylactic meds: • antacid, Famotidine (Pepcid)
Complications of chronic ulcer disease. • Hemorrhage, more common with duodenal ulcers • Perforation, most lethal complication, associated with peritonitis. • Gastric outlet obstruction-scaring and atony of pylorus.
Histamine 2 Take any time of day (x2), no food restrictions Zantac, Tagamet (oldest, not for elderly/drug interactions), pepcid (IV, PO) Proton Pump inhibitors Take in AM before meal (30 min.) Usually 1xday Prilosec, Prevacid, Protonex, Aciphex Prilosec not indicated for those on coumadin Systemic Acid Blockers
Surgical interventionsulcer disease • 20% of ulcer pt’s require surgery, but rarely performed now, usually resolved with medications. • Procedures: • gastrectomy (billroth I or II) • vagotomy (cut vagus nerve to decrease gastic acid secretion) • Pyloroplasty(pyloric dilatation)
Nursing interventions of Post-op care • If NG present, maintain patency, nares care, I&O, comfort, educational and emotional support. • Surgical wound monitoring • Observe signs of bowel status: bowel sounds present? r/o obstruction or bleeding) • Pain control (monitor, position change) • Post op teaching: diet, lifestyle risks and changes
Dumping Syndrome • Results from reduced gastric capacity after resection of most of the stomach and pyloric sphincter. • Symptoms occur 15-30 min. after a meal, feelings of weakness, sweating, palpitations, dizziness • Due to large bolus of hypertonic fluid entering intestine and fluid drawn into bowel, causes distention of bowel. • Advise patient to lie down.
Postprandial hypoglycemia • Varian of dumping syndrome • Bolus of concentrated carbohydrate results in hyperglycemia and excessive amounts of insulin, occurs 2 hrs after meals. • Treatment-sugared fluids or candy to relieve hypoglycemia. Then, limit amount of sugar consumed with meal and eat small, frequent meals.
Nutritional therapy related to surgical intervention • Eliminate drinking fluids with meals • Dry foods with low carbohydrate content (avoid high sugar diet) • Small meals • Rest after meals
Heliocobacter pylori bacterium • Promotes peptic ulcer formation • Acquired in childhood and common in adults • Gram-negative bacillus cultured in 1982 • Prevalence of H. Pylori infection in duodenal ulcer patients as high as 95-100%. • Treatment: triple Therapy (amoxicillin, Biaxin,Prilosec)