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Elimination (Bowel)Pathophysiology Case Study & Integration Concept MapCase Study 1Mr. Sander is 67 years old with a long history of knee osteoarthritis for which he self-medicates regularly with over-the-counter (OTC) naproxen. He is in the clinic today complaining of a swallowing difficulty that has progressively worsened over the past several months. He has otherwise been healthy and has not seen a doctor in many years. He denies significant past medical history. A review of systems is negative except for arthritic symptoms and swallowing difficulty. He denies noticing blood in his stool or vomiting blood. He denies history of gastroesophageal reflux disease (GERD) or ulcer. He does not drink alcohol, although he drank heavily many years ago. He does not smoke. The dysphagia is described as “food gets stuck in my throat and I can’t get it down.” The feeling occurs only after he has ingested solid food; liquids are not a problem. There is burning chest pain associated with meals. He is scheduled for an upper GI endoscopy. What is the likely cause of the dysphagia? The most likely cause of his dysphagia is due to an obstruction in the LES, most likely from a hiatal hernia (sliding).Hiatal hernia is the most common cause of LES.What are the usual signs and symptoms of GERD? The usual signs and symptoms of GERD are pyrosis (burning), chest pain, dysphagia, use of NSAIDs (in this case Naproxen), & Hx/o ETOH abuse.Other signs & symptoms of GERD not relating to the case are H. pylori, regurgitation, smoking, & chemical exposure, food (e.g spicy food), obesity, stroke, & spinal cord injury. Case Study 2A.D., a 48-year-old business executive, is brought to the emergency room by a co-worker. At work, he started vomiting a large amount of coffee-ground appearing material and requested to go to the hospital. A.D. has a 9-year history of PUD and was hospitalized with upper GI bleeding 4 years ago. At that time, specimens obtained with fiberoptic endoscopy were positive for H. pylori and he was treated with original triple therapy. His ulcer disease has been controlled with medications since that time, but recently he has been under much more stress than usual because of company merger negotiations. He started smoking again after having quit for 7 years, and he has also been drinking more alcohol in the last 3 months when he meets with other business executives. His work demands have caused a major disruption of his life, and he has not taken his medications routinely or eaten or slept well. He has a chronic intermittent headache, but he has been careful not to use aspirin, taking ibuprofen instead, for relief of the headache. He reports that he has had increasingly dark stools for the past week and developed severe nausea before he started vomiting this morning. He says he has no real pain, only mild upper abdominal discomfort and nausea.Your initial assessment reveals the following vital signs: blood pressure 102/62 mm Hg, heart rate 98 beats/min, respiratory rate 24 breaths/min, and temperature 98.0° F (36.7° C); capillary refill at 4 sec; skin cool and slightly moist, no distention of jugular veins, clear lung sounds, and a soft abdomen with hyperactive bowel sounds.1. Explain the pathophysiology of peptic ulcer disease. PUD begins with an infection by H. pylori produces ammonium that breaks down gastric mucosal lining. In time, each lining of the stomach, the mucosa, muscularis, submucosa, tunica, then eventually the serosa is broken down. The back flow of bile acids, NSAIDs, aspirin, & ETOH from the duodenum back into the stomach increases the breakdown of gastric mucosal lining by stripping away its surface and causes degeneration of epithelial cell membranes then causes hydrochloric acid to leak out of the stomach.2. What are the risk factors for duodenal ulcers? Which of these did F.H. have? H. pylori, smoking NSAIDs, stress, ETOH, caffeine & genetics.A.D. has stress, ETOH, smoking, takes Ibuprofen, & has a Hx/o H. pylori infection.3. What is the pathophysiology of H. pylori? H. pylori makes ammonium that is more acidic then the gastric defenses causing a breakdown in the mucosal epithelial layer. 4. What are lifestyle changes that you would recommend for F.H.? Lifestyle changes that would be recommended fro F.H. are to reduce stress, quit smoking & drinking, stop taking Ibuprofen and take non-NSAID medications (other then aspirin also), eat a healthy meal & a lot of rest, & take medications routinely to treat PUD as prescribed.5. Draw a concept map depicting development of peptic ulcer disease. (25 points)Peptic Ulcer Disease (PUD)2286000100330StressH00StressH3771900100330Chronic exposure to substances00Chronic exposure to substances114300120015H. pylori infectionH00H. pylori infectionH11430015367000-11430015367000125730092710002628900105410003314700927100038862009271000-6858009271000 102870043180RecurrentH00RecurrentH1828800108585Release of glucocorticoids00Release of glucocorticoids137160010858500354330097155IbuprofenH00IbuprofenH445770097155 ETOHH00 ETOHH11430059055Acidic conditions allow for H. pylori to growH00Acidic conditions allow for H. pylori to growH2628900349250016002003492500125730034925003086100254000354330024130SmokingH00SmokingH3657600895350080010050165Excess acid production00Excess acid production6858006477000331470067310Removal of gastric mucus layer & degeneration of epithelial cell membranes00Removal of gastric mucus layer & degeneration of epithelial cell membranes26289001536700011430093345H. pylori produces NH4+ from urea H+ H00H. pylori produces NH4+ from urea H+ H-1143002794000205740081280006858002032000685800134620Spread of HCl into gastric epithelial wall00Spread of HCl into gastric epithelial wall228600158750H. pylori produces NH4+ from urea H+ H00H. pylori produces NH4+ from urea H+ H26289002032000182880024130000445770090170Poor ulcer healing00Poor ulcer healing8001009017000365760081280001943100172720Peptic ulcer disease00Peptic ulcer disease Causes Diagnostic tests Clinical Manifestations0100330H. pyloriNSAIDsStressSmokinggenetics00H. pyloriNSAIDsStressSmokinggenetics1828800100330Barium SwallowEGD PillcamTesting x H. pyloriUrea breath testIgG00Barium SwallowEGD PillcamTesting x H. pyloriUrea breath testIgG4343400100330Epigastric burning pain00Epigastric burning pain80010061595ComplicationsPreforationHemorrhageObstructionShock (late)00ComplicationsPreforationHemorrhageObstructionShock (late)TreatmentSmoking cessationAvoid NSAIDs & AspirinReduce stressAvoid irritating foods (caffeinated drinks, ETOH) Triple therapy (if H. pylori test is positive)H2 blockers, PPI inhibitors, antibioticsCase Study 3J.S. is a 56-year-old general contractor who is admitted to your telemetry unit directly from his internist’s office with a diagnosis of chest pain. On report, you are informed that he has an intermittent 2-month history of chest tightness with substernal burning that radiates through to the mid-back intermittently, in a stabbing fashion. Symptoms occur after a large meal; with heavy lifting at the construction site; and in the middle of the night when he awakens from sleep with coughing, shortness of breath (SOB), and a foul, bitter taste in his mouth. Recently he has developed nausea, without emesis, worse in the morning or after skipping meals. He complains of “heartburn” 3 or 4 times a day. He takes a couple Rolaids or Tums. He keeps a bottle at home, at the office, and in his truck. Vital signs (VS) at his physician’s office were 130/80 lying, 120/72 standing, 100, 20, 98.6F, Sao2 92% on room air. What are some common causes of “chest pain”? Some common causes of “chest pain” are heartburn, esophageal distension, powerful contractions, esophageal spasms, infectious esophagitis, & dyspnea. What tests will be done to help determine the source of the problem? Barium swallow & EGD, CXR, ABGsA barium swallow confirms a large sliding esophageal hiatal hernia. J.S. asks, “What is a hiatal hernia, and what do you mean it’s sliding?” How would you explain this to him? Sliding hiatal hernia is a type of hernia that protrudes above the weak area of the diaphragm at the junction of the esophagus & stomach. What symptoms did J.S. display that are indicative of an esophageal hiatal hernia? Symptoms displayed by J.S. are chest pain & tightness, substernal burning (location of hiatal hernia), SOB & coughing (due to diaphragm obstruction when lying down at night), nausea (due to slow stomach empyting), & foul, bitter taste (due to acid reflux). 5. J.S. would rather try more conservative medical treatment before having surgery. What measures can he try to minimize his pain? List at least five. Measures to try first are PPIs, H2 blockers, antacids, sleeping elevated, eating earlier, change in diet to reduce acid reflux (e.g. no spicy or oily food), eat smaller more frequent meals, and decrease lifting load at work.Case Study 4While you are working as a nurse on a GI/GU floor, you receive a call from your affiliate outpatient clinic notifying you of a direct admission, ETA (estimated time of arrival) 60 minutes. She gives you the following information: A.G. is an 87-year-old woman with a 3-day history of intermittent abdominal pain, abdominal bloating, and N/V. A.G. moved from Italy to join her grandson and his family only 2 months ago and she speaks very little English. All information was obtained through her grandson.PMH: colectomy for colon CA 6 years ago, hernia repair 2 years ago. No hx of CAD, DM,or pulmonary disease. She takes only ibuprofen occasionally for mild arthritis. Allergies include sulfa drugs and meperidine. A.G.’s tentative diagnosis is small bowel obstruction (SBO). A.G. is being admitted to your floor for diagnostic work-up. Her VS are stable, she has an IV of D5 1?2 NS with 20 mEq KCl at 100 mL/h, and 3 L O2 per NC.Based on the nurse’s report, what signs of bowel obstruction did A.G. present? What is the possible cause of A.G. bowel obstruction? Signs of bowel obstruction presented are intermittent abdominal pain, abdominal bloating, & N/V.Possible cause of A.G.’s bowel obstruction could be due to her history of a colectomy & hernia repair that can cause a loss of propulsive ability by the bowel. Are there other S/S that you should observe for while A.G. is in your care? Other S/S that should be observed are hyperkalemia, distention/ascites (fluid retention), hyperactive bowel sounds in the upper quadrant (proximal to obstruction), electrolyte depletion. VS should be continued to be monitored for fever (possible septicemia), Increased in BP & HR (impedance in venous return). How would the description of A.G.’s pain differ if she has a small versus large bowel obstruction and mechanical vs functional obstruction?Although there is very little description of A.G.’s pain, due to pt’s complaints pt is experiencing SBO. SBO would experience vomiting, dehydration, & electrolyte depletion; distal to SBO would experience constipation. LBO would have gas distention & electrolyte lost but less severe than SBO.Mechanical obstruction differ from function in that mechanical is due to blockage (from adhesions, tumor, hernia, inflammation, or stricture) that prevents normal GI flow. Functional obstruction is due to obstruction that prevents GI tract from normal propulsive ability due to post-op abdominal surgery. A.G. most likely has functional obstruction due to Hx/o colectomy & a hernia repair.Case Study 5M.B., a 26-year-old cosmetologist, is admitted to the hospital with an acute exacerbation of ulcerative colitis. She has an 8-year history of the bowel disease and has been taking 40 mg of prednisone (Deltasone) daily for the past year to control exacerbations of her symptoms. This is her third hospitalization for an exacerbation this year. Her life has become gradually dominated by her disease and the need to plan access to a bathroom everywhere she goes. She reports that she has been having 16 to 18 bloody diarrhea stools a day, abdominal pain, and nausea and vomiting that has become progressively worse the past 4 days. Her admission vital signs are as follows: blood pressure 100/72 mm Hg, heart rate 92 beats/min, respiratory rate 22 breaths/min, and temperature 101° F (38.3° C). She is 5 ft 2 in tall and weighs 92 lb (41.8 kg).1.What symptoms distinguish Crohn’s disease from ulcerative colitis? Symptoms that distinguish Crohn’s from UC is, Crohn’s rarely has bloody diarrhea, rectal bleeding, tenesmus, experiences fever all the time not just during an attack, weight loss, & chronic, colicky pain only in the RLQ region.What is the pathophysiology of ulcerative colitis?Unknown etiology ? triggers inflammation in the crypts of Lieberkuhn ?leukocytes invade sight of inflammation ?abscesses in the crypts formed close together ?abscess combined and coalesced? large ulcers formed in the epithelium ? decreased bowel absorption of H2O & Na+ ?attempts to repair damaged tissue ? development of fragile & highly vascularized granulation tissue3. What blood tests should be ordered based on M.B. signs and symptoms?CBCs, basic metabolic panel (for electrolyte levels), & serum protein levels.4. What are the complications of inflammatory bowel disease?5.Draw a concept map depicting inflammatory bowel disease. (25 points)center141605Inflammatory Bowel Disease (IBD)00Inflammatory Bowel Disease (IBD)297180081280001714500108585Autoimmune disease/other unknown etiology00Autoimmune disease/other unknown etiology29718004826000160020074930Inflammation occurs at base of crypts of Lieberkuhun & damages epithelium00Inflammation occurs at base of crypts of Lieberkuhun & damages epithelium29718004191000160020069215Leukocytes migrate to site of inflammation causing abscesses to form00Leukocytes migrate to site of inflammation causing abscesses to form29718003619500194310062865Accumulation of abscess grows close together & coalesces00Accumulation of abscess grows close together & coalesces29718002984500182880057150Purulent pus drain out from abscesses destroying mucosal layer00Purulent pus drain out from abscesses destroying mucosal layer46863008445500400050084455004343400-3175004000500-31750029718002413000217170050800Repair of damaged tissue & growth of fragile & highly vascularized tissue00Repair of damaged tissue & growth of fragile & highly vascularized tissue4572000192405Decreased bowel function00Decreased bowel function-229870017145000228600159385Clinical ManifestationRectal BleedingAbdominal pain00Clinical ManifestationRectal BleedingAbdominal pain217170045085Large areas of ulcerations results00Large areas of ulcerations results34290007239000018669000194310018669000 2628900126365Clinical ManifestationDiarrhea (? reabsorption of Na+ & H2O)00Clinical ManifestationDiarrhea (? reabsorption of Na+ & H2O)13716001206500171450038735Ulcerative colitis00Ulcerative colitis914400183515DiagnosisCBCs, electrolyte & protein levelStool cultureSigmoidoscopy, Colonoscopy w/Bx, PillcamBarium enema w/contrast00DiagnosisCBCs, electrolyte & protein levelStool cultureSigmoidoscopy, Colonoscopy w/Bx, PillcamBarium enema w/contrast3086100183515TreatmentSteroidal medicationsAnti-inflammatory medsImmune system suppressorsHealthy dietStress/anxiety managementColectomy w/colostomy00TreatmentSteroidal medicationsAnti-inflammatory medsImmune system suppressorsHealthy dietStress/anxiety managementColectomy w/colostomy30861005397500center-228600Inflammatory Bowel Disease (IBD)00Inflammatory Bowel Disease (IBD)240030053975Crohn’s Disease00Crohn’s Disease3086100-5715001257300102235Enlarged lymph nodes/inflammation in the lymphatic system00Enlarged lymph nodes/inflammation in the lymphatic system3086100162560002057400189230Flow of GI tract gets blocked00Flow of GI tract gets blocked3086100129540001828800156210Obstruction causes inflammation, mucosal ulceration (skipping lesions), fissures, abscess, & sometimes granulomas00Obstruction causes inflammation, mucosal ulceration (skipping lesions), fissures, abscess, & sometimes granulomas434340096520004572000965200030861003619500205740062865Peyer’s patches in the small intestine inflame, eventually becoming fibrous 00Peyer’s patches in the small intestine inflame, eventually becoming fibrous 308610054610002286000144145Fibrosis causes intestinal stenosis 00Fibrosis causes intestinal stenosis 46863005715000411480057150004914900313055004686300313055001943100198755Inflammation of the serous membrane causes bowel loops to stick to other (normal/diseased) bowel loops 00Inflammation of the serous membrane causes bowel loops to stick to other (normal/diseased) bowel loops 42291001587500422910043180002057400184785Affected bowel parts (all layers) become more fibrotic & stenosis causing strictures 00Affected bowel parts (all layers) become more fibrotic & stenosis causing strictures 400050012446000 28575006413500388620029210TreatmentAnti-inflammatory medicationsSteroidal medicationsMetronidazoleAzathioprine, 6-mercaptourine, methotrexateBiological therapiesAnti-tumor necrosis factors (infliximab, adalimumab, & certolizumab00TreatmentAnti-inflammatory medicationsSteroidal medicationsMetronidazoleAzathioprine, 6-mercaptourine, methotrexateBiological therapiesAnti-tumor necrosis factors (infliximab, adalimumab, & certolizumab194310029210Clinical ManifestationsRLQ painFeverWeight lossSevere malabsorptionDiarrheaN/VLater signs: dehydration, anemia, & electrolyte imbalance00Clinical ManifestationsRLQ painFeverWeight lossSevere malabsorptionDiarrheaN/VLater signs: dehydration, anemia, & electrolyte imbalance114300205740DiagnosisCBCsElectrolyte levelsProtein levelsStool cultureSigmoidoscopy, Colonoscopy w/Bx, Barium enema w/contrast00DiagnosisCBCsElectrolyte levelsProtein levelsStool cultureSigmoidoscopy, Colonoscopy w/Bx, Barium enema w/contrast ................
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