Presentation on theme: "Nur 4206 The Patient with Digestive Disorders"— Presentation transcript:
1Nur 4206 The Patient with Digestive Disorders By Linda Self
2GI Changes associated with Aging Atrophy of the gastric mucosa resulting in hypochlorhydriaDecreased peristalsis which results in constipationCalcification of pancreatic vessels occurs with a decrease in lipase productionDiminished size of liver with resultant decreased enzyme activity. Decreased enzyme activity depresses drug metabolism which leads to an accumulation of drugs.
3Lab Assessment of the GI System CBCClotting factorsSerum electrolytesSerum enzymes such as AST (aspartate aminotransferase) and ALT (alanine aminotransferase)Amylase and lipaseBilirubin—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.
4Diagnostic Testing EGD ERCP (endoscopic retrograde cholangiopancreatography)ColonoscopyGastric 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.
5CandidiasisFungal 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
6InterventionsAnti-infective agents such as abx or antifungals. Tetracycline syrup, chlorhexidine, acyclovirAnalgesics such as lidocaine viscous, benadryl elixir, opioidsMeticulous oral hygiene using soft toothbrush, frequent care, rinsing with H2O2, warm saline, baking soda or a combinationSelect soft, bland and nonacidic foods
7Malignant Tumors 90% are Squamous cell Risk factors are increasing age, tobacco use, and alcohol ingestionPoor dietary habits, poor oral hygiene and infection with HPV increase the likelihoodCommon signs and symptoms incude unusual lumps or thickening of the buccal mucosa, sores that do not healSeen more commonly in the 6th and 7th decades of lifeAfrican Americans have a higher rate of oral cancer
8Oral cancers Basal cells occur primarily on the lip Do not tend to metastasize but can aggressively involve the skin of the faceBiopsy is the definitive method for diagnosis of oral cancersAn aqueous solution of toluidine blue can be applied to oral lesions to screen for malignancy
9TreatmentSurgical excision—local excision, glossectomy, partial mandibulectomy, commando procedure which includes excision of a segment of the mandible in conjunction with a radical neck dissectionRadiationChemotherapyCombination
10Role of the Nurse. Helps to: Maintain patent oral airway through removal of oral secretionsMaintain nutritional status by eating foods that are well tolerated, nutritious and provide adequate caloriesMaintain integrity of the oral mucous membraneCommunicates needs to family, friends and personnelMaintain comfort
11Patients with Esophageal Problems Gastroesophageal Reflux DiseaseIs the backward flow of gastrointestinal contents into the esophagusResults in reflex esophagitisSeverity of s/s is not proportional to the extent of refluxInflammation and erosions result in substitution of columnar epithelium (Barrett’s epithelium). This tissue is considered premalignant
12Factors contributing to decreased lower esophageal sphincter pressure Fatty foodsCaffeinated beveragesChocolateNicotineCalcium channel blockersNitratesPeppermintAlcoholAnticholinergic drugsHigh levels of estrogen and progesteroneNG tube placement
13GERD Affects 35-45% of population More common in those over 45 years of ageProbably underestimatedHigher in femalesMore often CaucasiansSevere esophagitis is more prevalent in male Caucasians
14Management 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 foodsLifestyle 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
15Drug 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.
16Drug Therapy in GERDProkinetic drugs such as Reglan which increase gastric emptying. Associated with side effects such as fatigue, anxiety, ataxia, and hallucinations
17Surgical Management in GERD Surgery is indicated when other measures have proven to be ineffectiveNissen fundoplicationSurgeon wraps and sutures the gastric fundus around the esophagus which anchors the LES area below the diaphragm and reinforces the high pressure area
18Hiatal Hernia Known as diaphragmatic hernia Classified as sliding or rolling herniasSliding 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 thoraxBelieved to be caused from weakening in the esophageal hiatusCongenital weaknesses, trauma, obesity or surgery may be causative
19Hiatal Hernia cont.Rolling Hernia—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.
20Hiatal Hernias Incidence increases with age May occur in up to 60% of persons in the sixth decade of lifeMore common in women and occur in 20% of adults
21Management Nonsurgical guidelines are similar to those with GERD Include drug therapy, diet therapy, lifestyle modifications and client education(see section under GERD)
22Surgical ManagementNissen fundoplication—wrapping of the fundus a full 360 degrees around the lower esophagusPrimary postoperatively is the prevention of respiratory complicationsNG tube management—inserting a large diameter NG tube during surgery prevents the fundoplication wrap from becoming too tight around the esophagusNG must be properly anchored, cannot risk re-insertion
23Surgical ManagementFollowing surgery and after peristalsis is re-established, clear liquids may be givenMay have G tube temporarilyGradually increase diet over next 6 weeksFrequent, small feedingsMay develop gas bloat syndrome (cannot eructate)Avoid eating high fat foods, chewing gum, drinking with a straw or drinking carbonated beverages
24Stomach Disorders Gastritis—inflammation of the gastric mucosa Can be erosive or nonerosiveRole of prostaglandinsWith progressive disease, stomach lining thins, parietal cell functioning becomes compromised and the patient will develop pernicious anemiaIncreased risk of cancer
25Gastritis continuedOnset of infection with H.pylori can result in gastritisOther pathogens implicated are CMV (in HIV patients), staph, strep, E.coli or salmonellaNSAIDSIngestion of corrosive substancesradiation
26Chronic GastritisType A has autoimmune pathogenesis, genetically linkedType 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.
27Physical Manifestations Abdominal tendernessBloatingHematemesisMelenaCan progress to shock
28Interventions Treat symptomatically Remove causative agents Treat H. pylori with bismuth, amoxicillin and FlagylTreat with H2 receptor antagonists to block gastric secretionsAntacids as buffersMay need B12Instruct patient about medications that exacerbate the problem such as steroids, NSAIDS, ASA, erythromycin and chemotherapeutic agents
29Diet Therapy Avoid known foods that cause S/S Tea, coffee, cola, chocolate, mustard, paprika, cloves, pepper and hot spices may cause discomfort
30Management cont.Surgery--Partial gastrectomy, pyloroplasty, vagotomy or even total gastrectomy may be indicatedStress reduction
31Peptic Ulcer DiseasePeptic ulcer is a mucosal lesion of the stomach or duodenumResults when gastric mucosal defenses become impaired and no longer protect the epitheliumGastromucosal prostaglandins increase the barrier against acidGastric 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
32Peptic Ulcers continued Duodenal Ulcers—95% develop in the first portion of the duodenumCharacteristic feature of a duodenal ulcer is high gastric acid secretionProtein rich meals, calcium and vagal excitation stimulate acid secretionUp to 95% to 100% of clients with duodenal ulcer disease have H.pyloriThis pathogen produces substances that damage the gastric mucosaUrease produced contributes further to the breakdown.
33Stress UlcersAcute gastric mucosal lesions occurring after an acute medical crisisAssociated with HI, burns, respiratory failure, shock, and sepsis.Multifocal lesions occur in proximal stomach and duodenumBegin as focal areas of ischemia and may progress to massive hemorrhage
34Complications of ulcers Hemorrhage in 15-25% of clientsPerforation—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 emergencyPyloric obstruction—caused by scarring, edema, inflammation or a combination of these
35Distinguishing between gastric and duodenal ulcers Gastric ulcersUsually in those 50 yrs. And olderEqual proportion of males to femaleBlood group not definingMay be malnourishedNormal or hyposecretion of stomach acidHeal and recurPain occurs after a mealHeals and recurs in same areaAtrophic gastritis
36Duodenal Ulcers Occur in those 40-50 yo Equal male/female ratio Most often type O bloodWell nourishedHypersecretion of stomach acidOccurs 90 min. to 3 hrs. after mealEating relieves pain. Melena more common than hematemesisNo gastritis
37Diagnostic Testing EGD H.pylori testing—by breath test, serologic testing (antibodies revealed). Antibody testing can not be used to determine eradication.
38Drug TherapyAntisecretory drugs such as Prilosec, Prevacid, Aciphex, NexiumH2 receptor antagonists such as Pepcid, Zantac, Axid, TagametProstaglandin analogs such as Cytotec. Actually enhances the mucosal resistanceAntacids—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.
39Drug Therapy cont. Mucosal barrier fortifiers such as carafate. Creates a protective coat
40Diet Therapy Bland diet may be helpful Food itself acts as an antacid Avoid caffeineAvoid both decaffeinated and caffeinated coffee because coffee causes stimulation of gastrinAvoid bedtime snacks which increase secretion of acidEat small regular meals
41Nonsurgical Management Treat hypovolemiaRecognize s/s of hypovolemia which are ……..Ready patient for endoscopySaline lavageNG tube placementAcid suppressionMonitor and document character of stoolsAvoid anti-inflammatoriesAdminister blood products
42Surgical Management Used to: Reduce the acid-secreting ability of the stomachTreat patients who do not respond to medical therapyTreat a surgical emergency that develops as a complication of PUD
43Surgical proceduresGastroenterostomy—permits neutralization of gastric acid by regurgitation of alkaline duodenal contents into the stomach. Also will perform vagotomy to decrease vagal influencesVagotomy—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
44Dumping SyndromeIs a constellation of vasomotor sysmtoms after eating, especially after a Billroth IIIs a result of rapid emptying of gastric contents into the small intestine, which shifts fluid into the gut, resulting in abdominal distentionEarly dumping syndrome occurs within 30 minutes of eatingVertigo, tachycardia, syncope, pallor, palpitations, sweating and exhibit the need to lie down
45Dumping Syndrome cont.Late dumping syndrome occurs 90 minutes to 3 hours after eatingCaused by a release of an excessive amount of insulin releaseInsulin release follows a rapid rise in the blood glucose level that results from the rapid entry of high carbohydrate food into the jejunumManifested by dizziness, lightheadedness, palpitations, diaphoresis and confusion
46Management of the Dumping Syndrome Decrease the amount of food taken at one timeEliminate liquids ingested with mealsConsume high protein, high fat, low carbohydrate dietPectin 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)
47Complications associated with partial gastrectomy Deficiency of B12Folic acidIronImpaired calcium absorptionReduced absorption of vitamin DResult of shortage of intrinsic factor and the now rapid entry of food into the bowel which decreases absorptionNurse should monitor CBC, assessment of tongue for atrophic glossitis, s/s of anemia
48Irritable Bowel Syndrome Most common digestive disorder seen in clinical practiceCharacterized by the presence of diarrhea, constipation, and abdominal pain and bloatingBelieved to be due to impairment in the motor or sensory function of the GI tractCause unknownDx made by careful history, labs and dx procedures which exclude more serious conditions
49Irritable Bowel Food intolerances may be associated with IBS Dairy products and grains can contribute to bloating, flatulence and distentionOccurs 2:1 more often in womenEducation is cornerstone of treatmentDrug therapy includes fiber, tricyclic antidepressants, antidiarrheal agents, laxatives and anticholinergicsStress management may be helpful
50Irritable BowelAvoid caffeine, alcohol, beverages that contain sorbitol or fructose.
51Colorectal Cancer Familial Autosomal dominant inherited genetic disorder known as familial adenomatous polyposisMore prevalent after age 50Can metastasize by direct invasion or by migrating via the blood or lymphRisk factors include genetics, dietary habits (animal fat, decreased bowel transit time, low fiber diets) and the occurrence of inflammatory bowel disease
52Colorectal cancer Generally are adenocarcinomas Multistep process resulting in a number of molecular changes including loss of tumor suppressor genes and activation of oncogenes that alter colonic mucosa cell division. Proliferation of colonic mucosa forms polyps that can be transformed to malignant tumors. Adenomatous polyps.
53Colorectal CancerTumors predominantly develop in the sigmoid colon or rectumColon tumors can be spread by peritoneal seeding during surgical excisionTumors can cause bowel obstructions20% are diagnosed at time of emergency hospitalization for bowel obstruction75% of all colorectal cancers have no known predisposing causeInflammatory bowel diseases may pose an increased risk for tumor development
54Colorectal CancerManifestations—rectal bleeding, anemia and a change in the character of the stoolLab assessment—CBC, elevated liver enzymes, +fecal occult blood test (Ensure that the patient is not on NSAIDS). Two separate stool samples should be tested on 3 consecutive daysCEA (carcinoembryonic antigen) may be elevated in 70% of people with colorectal cancerColonoscopy, sigmoidoscopy may help reveal polypsLiver scan may locate distant sites of metastasis
55Colorectal CancerGenetic counseling may be appropriate so careful history is very importantClassified by Dukes’ stagingStage A indicates that the tumor has penetrated into the bowel wallStage B- the tumor has penetrated through the bowel wallStage C-bowel wall penetration w/involvement of the lymphStage D-mets
56Colorectal CancerRadiation has not improved outcomes except in regional disease affecting the rectumChemotherapy has proven efficacious, especially in Stages B & C. Drug of choice is 5-FU. Side effects include diarrhea, mucositis and skin effects. Trying other medications such as leukovorin and irinotecan. Studies for use of monoclonal antibodies are under way.
57Colorectal Cancer Surgical Management Three most common surgeries are: Hemicolectomy—excision of the involved area of the colon with reanastomosisColon resection—if healing is thought to be in jeopardy, a colostomy will be createdAbdominoperineal resection—indicated when rectal tumors are present. This approach generally requires a permanent colostomy.
58Colostomy—Nursing Role Apply pouch systemAssess stoma. Should appear pink and moist.Nurse reports any of the following:Signs of ischemia……Unusual bleedingMucocutaneous separationSigns of leakage
59Colostomy Care Teach patients and families: Normal appearance of the stomaSigns and symptoms of complicationsMeasurement of the stomaCare and application of the applianceMeasures to protect the skinDietary measures to control gas and odorResumption of activities
60ColostomyGas producing foods include broccoli, asparagus, cucumbers, brussels sprouts, cabbage, cauliflower, garlic, turnips and beerCrackers, toast and yogurt can help prevent gas
61Intestinal Obstruction--mechanical Mechanical obstruction can be caused from adhesions, tumors, hernias, fecal impactions, strictures, and vascular disordersRegardless of age, adhesions are the most common cause of mechanical obstruction.Adhesions are bands of granulation and scar tissue that develop as a result of inflammation, encircle the intestine and constrict its lumen
62Intestinal Obstruction Paralytic ileus is a nonmechanical obstruction caused by physiologic, neurogenic, or chemical imbalances associated with decreased peristalsis either from trauma or from toxinsNumber of causative factors including MI, hypokalemia, vascular insufficiency, shock, or peritonitis. Any diffuse inflammatory response can cause this problem.
63Intestinal Obstruction—Paralytic Ileus May have vomitingConstant, diffuse discomfortDiarrhea may be present in partial obstructionAbdominal distention will be presentAbdominal rigidityBorborygmi which progresses to a quiet abdomen
64Bowel Obstuction No definitive lab test CT useful Flat-plate and upright films will reveal distention of loops of intestine with fluid and gas in the small intestine and with the absence of gas in the colonPresence of free air in the abdomen indicates perforation
65Paralytic Ileus Care NPO NG tube or nasointestinal tube (cantor, Miller-Abbott) for decompressionEnemas may be helpfulFluid and electrolyte replacement are importantIce chips sparingly, not lemon glycerine swabsClosely monitor I&OOpioids may be withheldMobilize patient if possible
66PeritonitisAcute inflammation of the endothelial lining of the abdominal cavity or peritoneum. Is a life-threatening illness.If peritoneal cavity is contaminated by bacteria, the body produces an inflammatory reaction that walls off a localized area to fight the infection. This reaction involves vascular dilation and increased capillary permeability locally. If this local walling off is not effective, the inflammation spreads and becomes peritonitis
67Peritonitis--pathophysiology Vascular dilation continues,extra blood is brought to the area of inflammationFluid is shifted from the ECF compartment into the peritoneal cavity resulting in “third spacing”.This shifting then will affect circulatory volume.Hypoperfusion of kidneys can resultPeristalsis will slowBowel lumen will become distended with gas and fluidResp. problems can ensue
68Causes of peritonitis Appendicitis PUD Diverticulitis Gangrenous gallbladderBowel obstructionSecondary to CAPDUlcerative colitis
69Presentation of Peritonitis Abdominal pain and tenderness which may be referred to the chest or shoulder—these are the cardinal signsDistended abdomenNausea, vomiting and anorexiaDiminished bowel soundsRebound tendernessHigh feverTachycardiaDehydrationDecreased urinary outputPossible respiratory compromise
70Diagnostics Elevated WBCs with a shift to the left (bands) Possible positive blood culturesAbdominal xray will reveal free air or fluid—and edemaPeritoneal lavage will reveal more than 500 WBCs/mL3 of fluid, greater than 50,000 RBCs/mL or the presence of bacteria on a gram stain
71Interventions for Peritonitis HospitalizedIV fluids and antibioticsDaily weightI&ONG tubeO2Pain medicationsPossible exploratory lap once stabilizedWound healing by secondary intention w/packing and irrigation
72Peritonitis—care continued Upon discharge, teach patientProper handwashingWound care—may require home health nurseReporting fever, unusual drainage or swelling, redness or bleeding from the incision sitePresence of abdominal unlike experienced upon discharge………..
73Chronic Inflammatory Bowel Disease Ulcerative colitisCharacterized by diffuse inflammation of the intestinal mucosaResult is loss of surface epithelium with ulceration and abscess formationUsually begins in rectum and continues gradually and progressively toward the cecumFibrosis and retraction of the bowel resultGenetically linked autoimmune in nature—seen more commonly in European Jews and Ashkenazic Jews
74Complications of ulcerative colitis PerforationToxic megacolonHemorrhageAbscessesIncreased likelihood of cancerobstruction
75Causes tenesmus (uncontrollable straining) DiarrheaLoss of vital nutrientsMay lead to malnutrition
76Diagnosis Elevated ESR Increased WBC r/o ova and parasites Barium enema will be definitiveSigmoidoscopy is most definitive diagnostic procedure
77Treatment Antidiarrheals Salicylate compounds (sulfasalazine) acts by affecting prostaglandinsSteroidsImmunosuppressive drugs-alone not helpful but if used in combination with steroids—positive outcomesDiet—NPO, TPN, low-fiber diet (debatable), avoid lactose containing foodsSurgery—possible proctocolectomy with ileostomy or total colectomy with a continent ileostomyPsychosocial support—support groups
78Crohn’s Disease Regional enteritis Can affect any part of the GI tract from mouth to anusInfectious, genetic and immune etiologies have been proposedDeep fissures and ulcerations develop and extend through all bowel layersDiffuse stricture formations developFistulas can develop
79Diagnosis Weight loss is classic No disease specific tests are availableTesting is similar to that of ulcerative colitisTreatment likewise is similar
80Differential Features of Ulcerative Colitis and Crohn’s disease UC—begins in rectum and progresses toward cecum, etiology is unknown, peaks at ages and 55-65, liquid bloody stools per day, complications include: perforation, hemorrhage, fistula, nutritional deficienciesCrohn’s—occurs in the terminal ileum with patchy involvement through all layers of the bowel, etiology unknown, peaks at ages 15-40, 5-6 soft, loose stools daily (not bloody), frequent fistula development and also with nutritional deficiencies