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Nur 4206 The Patient with Digestive Disorders

Nur 4206 The Patient with Digestive Disorders. By Linda Self. GI Changes associated with Aging. Atrophy of the gastric mucosa resulting in hypochlorhydria Decreased peristalsis which results in constipation Calcification of pancreatic vessels occurs with a decrease in lipase production

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Nur 4206 The Patient with Digestive Disorders

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  1. Nur 4206The Patient with Digestive Disorders By Linda Self

  2. GI Changes associated with Aging • Atrophy of the gastric mucosa resulting in hypochlorhydria • Decreased peristalsis which results in constipation • Calcification of pancreatic vessels occurs with a decrease in lipase production • Diminished size of liver with resultant decreased enzyme activity. Decreased enzyme activity depresses drug metabolism which leads to an accumulation of drugs.

  3. Lab Assessment of the GI System • CBC • Clotting factors • Serum electrolytes • Serum enzymes such as AST (aspartate aminotransferase) and ALT (alanine aminotransferase) • Amylase and lipase • Bilirubin—primary pigment in bile which is normally conjugated and excreted by the liver. • NH3—used to rebuild amino aacids or is converted to urea for excretion. Elevations are seen in conditions that cause hepatocellular injury such as cirrhosis. • Tumor markers—CA 19-9 and CEA are evaluated to monitor the success of cancer therapy and to assess for the recurrence of cancer in the GI tract.

  4. Diagnostic Testing • EGD • ERCP (endoscopic retrograde cholangiopancreatography) • Colonoscopy • Gastric analysis—NG, may give Histalog sc. Fifteen minute intervals samples are taken for one hour. Depressed levels of gastric secretion suggest the presence of gastric carcinoma. Increased levels indicate Zollinger-Ellison syndrome and duodenal ulcers.

  5. Candidiasis • Fungal infection resulting from overgrowth of the Candida albicans, a normal flora. • Seen in individuals receiving antibiotics, chemotherapy, steroids, radiation or antirejection medication. • Also common among HIV-infected individuals

  6. Interventions • Anti-infective agents such as abx or antifungals. Tetracycline syrup, chlorhexidine, acyclovir • Analgesics such as lidocaine viscous, benadryl elixir, opioids • Meticulous oral hygiene using soft toothbrush, frequent care, rinsing with H2O2, warm saline, baking soda or a combination • Select soft, bland and nonacidic foods

  7. Malignant Tumors 90% are Squamous cell • Risk factors are increasing age, tobacco use, and alcohol ingestion • Poor dietary habits, poor oral hygiene and infection with HPV increase the likelihood • Common signs and symptoms incude unusual lumps or thickening of the buccal mucosa, sores that do not heal • Seen more commonly in the 6th and 7th decades of life • African Americans have a higher rate of oral cancer

  8. Oral cancers • Basal cells occur primarily on the lip • Do not tend to metastasize but can aggressively involve the skin of the face • Biopsy is the definitive method for diagnosis of oral cancers • An aqueous solution of toluidine blue can be applied to oral lesions to screen for malignancy

  9. Treatment • Surgical excision—local excision, glossectomy, partial mandibulectomy, commando procedure which includes excision of a segment of the mandible in conjunction with a radical neck dissection • Radiation • Chemotherapy • Combination

  10. Role of the Nurse. Helps to: • Maintain patent oral airway through removal of oral secretions • Maintain nutritional status by eating foods that are well tolerated, nutritious and provide adequate calories • Maintain integrity of the oral mucous membrane • Communicates needs to family, friends and personnel • Maintain comfort

  11. Patients with Esophageal Problems Gastroesophageal Reflux Disease • Is the backward flow of gastrointestinal contents into the esophagus • Results in reflex esophagitis • Severity of s/s is not proportional to the extent of reflux • Inflammation and erosions result in substitution of columnar epithelium (Barrett’s epithelium). This tissue is considered premalignant

  12. Factors contributing to decreased lower esophageal sphincter pressure • Fatty foods • Caffeinated beverages • Chocolate • Nicotine • Calcium channel blockers • Nitrates • Peppermint • Alcohol • Anticholinergic drugs • High levels of estrogen and progesterone • NG tube placement

  13. GERD • Affects 35-45% of population • More common in those over 45 years of age • Probably underestimated • Higher in females • More often Caucasians • Severe esophagitis is more prevalent in male Caucasians

  14. Management • Treated by diet, medication, and lifestyle modifications • Diet—restrict spicy and acidic foods; eat small meals, avoid carbonated beverages, avoid eating before bedtime, avoid or reduce fatty foods • Lifestyle changes—elevate HOB, sleep in left lateral decubitus position, smoking cessation, avoidance of alcohol, weight reduction, remain upright for 1-2 hours after eating, avoid heavy lifting, straining and working in a bent-over position

  15. Drug Therapy in GERD • Antacids except in renal failure • Histamine Receptor Antagonists—Zantac, Axid, and Tagamet. Tagamet is shorter-acting and has multiple drug interactions (warfarin, theophylline, phenytoin, nifedipine, erythromycin, others) • Proton Pump Inhibitors—Prilosec, Prevacid, Aciphex. Reserved for severe GERD that is refractory to the Histamine receptor blockers. These agents can decrease gastric acid by 90%. Sometimes have to go to Bid dosing for 4-8 weeks.

  16. Drug Therapy in GERD • Prokinetic drugs such as Reglan which increase gastric emptying. Associated with side effects such as fatigue, anxiety, ataxia, and hallucinations

  17. Surgical Management in GERD Surgery is indicated when other measures have proven to be ineffective Nissen fundoplication • Surgeon wraps and sutures the gastric fundus around the esophagus which anchors the LES area below the diaphragm and reinforces the high pressure area

  18. Hiatal Hernia • Known as diaphragmatic hernia • Classified as sliding or rolling hernias • Sliding hernias are the most common type of hernia and account for 90% of the total number of hiatal hernias. • The hernia generally moves into and out of the thorax • Believed to be caused from weakening in the esophageal hiatus • Congenital weaknesses, trauma, obesity or surgery may be causative

  19. Hiatal Hernia cont. • RollingHernia—the gastroesophageal junction remains in normal location but the fundus rolls through the esophageal hiatus and into the thorax beside the esophagus. Greater risk of volvulus or strangulation in this situation. • Likely caused from improper anchorage of the stomach. • Can be caused by previous esophageal surgeries.

  20. Hiatal Hernias • Incidence increases with age • May occur in up to 60% of persons in the sixth decade of life • More common in women and occur in 20% of adults

  21. Management • Nonsurgical guidelines are similar to those with GERD • Include drug therapy, diet therapy, lifestyle modifications and client education (see section under GERD)

  22. Surgical Management • Nissen fundoplication—wrapping of the fundus a full 360 degrees around the lower esophagus • Primary postoperatively is the prevention of respiratory complications • NG tube management—inserting a large diameter NG tube during surgery prevents the fundoplication wrap from becoming too tight around the esophagus • NG must be properly anchored, cannot risk re-insertion

  23. Surgical Management • Following surgery and after peristalsis is re-established, clear liquids may be given • May have G tube temporarily • Gradually increase diet over next 6 weeks • Frequent, small feedings • May develop gas bloat syndrome (cannot eructate) • Avoid eating high fat foods, chewing gum, drinking with a straw or drinking carbonated beverages

  24. Stomach Disorders • Gastritis—inflammation of the gastric mucosa • Can be erosive or nonerosive • Role of prostaglandins • With progressive disease, stomach lining thins, parietal cell functioning becomes compromised and the patient will develop pernicious anemia • Increased risk of cancer

  25. Gastritis continued • Onset of infection with H.pylori can result in gastritis • Other pathogens implicated are CMV (in HIV patients), staph, strep, E.coli or salmonella • NSAIDS • Ingestion of corrosive substances • radiation

  26. Chronic Gastritis • Type A has autoimmune pathogenesis, genetically linked • Type B is caused by H. pylori. Direct correlation between number of organisms and degree of cellular abnormality. • Can also be caused by alcohol ingestion, radiation therapy and smoking. Other causation may be Crohn’s, graft-versus-host disease and uremia.

  27. Physical Manifestations • Abdominal tenderness • Bloating • Hematemesis • Melena • Can progress to shock

  28. Interventions • Treat symptomatically • Remove causative agents • Treat H. pylori with bismuth, amoxicillin and Flagyl • Treat with H2 receptor antagonists to block gastric secretions • Antacids as buffers • May need B12 • Instruct patient about medications that exacerbate the problem such as steroids, NSAIDS, ASA, erythromycin and chemotherapeutic agents

  29. Diet Therapy • Avoid known foods that cause S/S • Tea, coffee, cola, chocolate, mustard, paprika, cloves, pepper and hot spices may cause discomfort

  30. Management cont. • Surgery--Partial gastrectomy, pyloroplasty, vagotomy or even total gastrectomy may be indicated • Stress reduction

  31. Peptic Ulcer Disease • Peptic ulcer is a mucosal lesion of the stomach or duodenum • Results when gastric mucosal defenses become impaired and no longer protect the epithelium • Gastromucosal prostaglandins increase the barrier against acid • Gastric Ulcers can be caused by reflux of bile into the stomach, by delayed emptying of stomach resulting in backflow of duodenal contents; decreased blood flow also will alter the protective barrier

  32. Peptic Ulcers continued • Duodenal Ulcers—95% develop in the first portion of the duodenum • Characteristic feature of a duodenal ulcer is high gastric acid secretion • Protein rich meals, calcium and vagal excitation stimulate acid secretion • Up to 95% to 100% of clients with duodenal ulcer disease have H.pylori • This pathogen produces substances that damage the gastric mucosa • Urease produced contributes further to the breakdown.

  33. Stress Ulcers • Acute gastric mucosal lesions occurring after an acute medical crisis • Associated with HI, burns, respiratory failure, shock, and sepsis. • Multifocal lesions occur in proximal stomach and duodenum • Begin as focal areas of ischemia and may progress to massive hemorrhage

  34. Complications of ulcers • Hemorrhage in 15-25% of clients • Perforation—severe pain will ensue. Abdomen is tender, rigid, and boardlike and the client will assume the knee-chest position to decrease abdominal wall tension-----is a surgical emergency • Pyloric obstruction—caused by scarring, edema, inflammation or a combination of these

  35. Distinguishing between gastric and duodenal ulcers Gastric ulcers • Usually in those 50 yrs. And older • Equal proportion of males to female • Blood group not defining • May be malnourished • Normal or hyposecretion of stomach acid • Heal and recur • Pain occurs after a meal • Heals and recurs in same area • Atrophic gastritis

  36. Duodenal Ulcers • Occur in those 40-50 yo • Equal male/female ratio • Most often type O blood • Well nourished • Hypersecretion of stomach acid • Occurs 90 min. to 3 hrs. after meal • Eating relieves pain. Melena more common than hematemesis • No gastritis

  37. Diagnostic Testing • EGD • H.pylori testing—by breath test, serologic testing (antibodies revealed). Antibody testing can not be used to determine eradication.

  38. Drug Therapy • Antisecretory drugs such as Prilosec, Prevacid, Aciphex, Nexium • H2 receptor antagonists such as Pepcid, Zantac, Axid, Tagamet • Prostaglandin analogs such as Cytotec. Actually enhances the mucosal resistance • Antacids—buffer and prevent the formation of pepsin.Mylanta and Maalox are examples (aluminum and magnesium hydroxide). Be careful if CHF. Tums is calcium carbonate which actually triggers gastrin release…..rebound secretion. • Antacids may interfere with certain medications such as Dilantin,ketoconazole and tetracycline.

  39. Drug Therapy cont. • Mucosal barrier fortifiers such as carafate. • Creates a protective coat

  40. Diet Therapy • Bland diet may be helpful • Food itself acts as an antacid • Avoid caffeine • Avoid both decaffeinated and caffeinated coffee because coffee causes stimulation of gastrin • Avoid bedtime snacks which increase secretion of acid • Eat small regular meals

  41. Nonsurgical Management • Treat hypovolemia • Recognize s/s of hypovolemia which are …….. • Ready patient for endoscopy • Saline lavage • NG tube placement • Acid suppression • Monitor and document character of stools • Avoid anti-inflammatories • Administer blood products

  42. Surgical Management • Used to: Reduce the acid-secreting ability of the stomach Treat patients who do not respond to medical therapy Treat a surgical emergency that develops as a complication of PUD

  43. Surgical procedures • Gastroenterostomy—permits neutralization of gastric acid by regurgitation of alkaline duodenal contents into the stomach. Also will perform vagotomy to decrease vagal influences • Vagotomy—eliminates the acid-secreting stimulus to gastric cells and decreases the responsiveness of parietal cells. Can be selective, truncal or proximal. • Pyloroplasty—widens the exit of the pylorus

  44. Dumping Syndrome • Is a constellation of vasomotor sysmtoms after eating, especially after a Billroth II • Is a result of rapid emptying of gastric contents into the small intestine, which shifts fluid into the gut, resulting in abdominal distention • Early dumping syndrome occurs within 30 minutes of eating • Vertigo, tachycardia, syncope, pallor, palpitations, sweating and exhibit the need to lie down

  45. Dumping Syndrome cont. • Late dumping syndrome occurs 90 minutes to 3 hours after eating • Caused by a release of an excessive amount of insulin release • Insulin release follows a rapid rise in the blood glucose level that results from the rapid entry of high carbohydrate food into the jejunum • Manifested by dizziness, lightheadedness, palpitations, diaphoresis and confusion

  46. Management of the Dumping Syndrome • Decrease the amount of food taken at one time • Eliminate liquids ingested with meals • Consume high protein, high fat, low carbohydrate diet • Pectin may help reduce severity of s/s(purified carbohydrate obtained from peel of citrus fruits or from apple pulp) • Somatostatin may be used in severe cases (inhibits the secretion of insulin and gastrin)

  47. Complications associated with partial gastrectomy • Deficiency of B12 • Folic acid • Iron • Impaired calcium absorption • Reduced absorption of vitamin D • Result of shortage of intrinsic factor and the now rapid entry of food into the bowel which decreases absorption • Nurse should monitor CBC, assessment of tongue for atrophic glossitis, s/s of anemia

  48. Irritable Bowel Syndrome • Most common digestive disorder seen in clinical practice • Characterized by the presence of diarrhea, constipation, and abdominal pain and bloating • Believed to be due to impairment in the motor or sensory function of the GI tract • Cause unknown • Dx made by careful history, labs and dx procedures which exclude more serious conditions

  49. Irritable Bowel • Food intolerances may be associated with IBS • Dairy products and grains can contribute to bloating, flatulence and distention • Occurs 2:1 more often in women • Education is cornerstone of treatment • Drug therapy includes fiber, tricyclic antidepressants, antidiarrheal agents, laxatives and anticholinergics • Stress management may be helpful

  50. Irritable Bowel • Avoid caffeine, alcohol, beverages that contain sorbitol or fructose.

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