NURS 6501 Module 3 Knowledge Check: GI and Hepatobiliary Disorders:

Module 3 Knowledge Check: GI and Hepatobiliary Disorders: A 45-year-old male comes to the clinic with a chief complaint of epigastric abdominal pain that has persisted for 2 weeks. He describes the pain as burning, non-radiating and is worse after meals. He denies nausea, vomiting, weight loss or obvious bleeding. He admits to bloating and frequent belching. PMH: osteoarthritis; seasonal allergies with frequent sinusitis infections Meds: Zyrtec 10mg daily year-round; Ibuprofen 400-600mg prn pain Family Hx: non-contributory Social hx: recently divorced and expressed concern at how expensive it is to support 2 homes. Works as a manager at a local tire and auto company. He has 25 pack/year hx of smoking; drinks 2-3 beers/day; and drinks 5-6 cups of coffee/day. He denies illicit drug use, vaping or unprotected sexual encounters Breath test in office revealed + urease The healthcare provider suspects the client has peptic ulcer disease. What factors may have contributed to the development of PUD? Risk factors include habitual use of NSAIDs; excessive use of alcohol, smoking, physiologic stress. Stress secondary to divorce/financial situation, cigarette smoking, alcohol consumption, use of NSAIDs, excess coffee consumption, +H Pylori test. How do these factors contribute to the formation of peptic ulcers? The chronic use of NSAIDs suppresses mucosal prostaglandin synthesis which results in decreased bicarbonate secretion and mucin (a component of the gut barrier) production and increased secretion of hydrochloric acid. High gastrin level and excessive gastric acid production often seen in Zollinger-Ellison syndrome which can cause gastrinoma. Smoking impairs healing by vasoconstriction. H Pylori causes gastritis and interferes with mucosa. A 36-year-old morbidly obese female comes to the office with a chief complaint of “burning in my chest and a funny taste in my mouth.” The symptoms have been present for years but patient states she had been treating them with antacid tablets which helped until the last 4 or 5 weeks. She never saw a healthcare provider for that. She says the symptoms get worse at night when she is lying down and has had to sleep with 2 pillows. She says she has started coughing at night which has been interfering with her sleep. She denies palpitations, shortness of breath or nausea. PMH: HTN; venous stasis ulcers; IBS; OA of knees; morbid obesity Family hx: non-contributory Meds: Amlodipine 10mg QD; Dicyclomine 20mg QD; Motrin 600mg q6hrs prn Social: 15 pack/year hx of smoking; occasional alcohol use; denies vaping The healthcare provider diagnoses the patient with GERD. The client asks the APRN what causes GERD. What is the APRN’s best response? GERD manifestations result directly from gastric acid reflux into the esophagus. Pyrosis, the classic symptom, is a substernal burning sensation typically described as heartburn. It may be accompanied by regurgitation, particularly in someone who has recently eaten. The lower esophageal sphincter (LES) relaxes due to certain meds (calcium channel blockers), hiatal hernia, and obesity allows stomach contents to enter the lower esophagus causing inflammation and possibly erosion of the esophagus. A 34-year-old construction worker presents to his PCP with a chief complaint of passing foul smelling dark, tarry stools. He stated the first episode occurred last week, but it was only a small amount after he had eaten a dinner of beets and beef. The episode today was accompanied by nausea, sweating, and weakness. He states he has had some mid epigastric pain for several weeks and has been taking OTC antacids. The most likely diagnosis is upper GI bleed which won’t be confirmed until further endoscopic procedures are performed. What factors can contribute to an upper GI bleed? UGI bleeds can be caused by PUD which remains the most common cause. Esophageal bleeding from a Mallory-Weiss tear (caused by repeated vomiting, retching, erosions of the mucosa), gastric carcinomas. A 64-year-old steel worker presents to his PCP with a chief complaint of passing bright red blood when had a BM that morning. He stated the first episode occurred last week, but it was only a small amount after he had eaten a dinner of beets and beef. The episode today was accompanied by nausea, sweating and weakness. He states he has had some LLQ pain for several weeks but described it as “coming and going.” He says he has had a fever and abdominal cramps that have worsened this morning. The likely diagnosis is lower GI bleed secondary to diverticulitis. What can cause diverticulitis in the lower GI tract? Inflammation that forms at weak points in the colon wall, where arteries penetrate the tunica muscularis to nourish the mucosal layer. The colonic mucosa herniates through the smooth muscle layers. Diverticulitis is inflammation of one or more diverticula. Fecal material or undigested food particles may collect in a diverticula causing obstruction. The obstruction can cause vascular compromise. Increased intraluminal pressure or food particles cause erosion of the diverticular wall, resulting in inflammation, localized necrosis and perforation. A 48-year-old man presents to his GI MD for increasing abdominal girth and increasing jaundice. He has a long hx of alcoholic cirrhosis and has multiple admissions for encephalopathy and GI bleeding from esophageal varices. He has been diagnosed with portal HTN and tells the APRN that he was told he had chronic, non-curable cirrhosis. How does cirrhosis cause portal HTN? Portal HTN results from an increase in resistance or blood flow in the portal venous system. In cirrhosis, the most common cause of portal HTN, is the formation of scar tissue and regenerative nodules that lead to an increase in intrahepatic vascular resistance and, consequently, portal pressure. Hepatitis and the resultant inflammation and subsequent scarring also contributes to portal TN. Chronic right sided heart failure can also cause portal HTN due to the increase in preload that the right ventricle cannot pump effectively. A 48-year-old man presents to his GI MD for increasing abdominal girth and increasing jaundice. He has a long hx of alcoholic cirrhosis and has multiple admissions for encephalopathy and GI bleeding from esophageal varices. He has been diagnosed with portal HTN. The increased abd girth has been progressive, and he says it is getting hard to breathe. The APRN reviews his last labs and notes that the total protein is 4.6 gm/dl and albumin is 2.9 g/dl. Upon exam, he has icteric sclera, jaundice, and abd spider angiomas. There is a significant fluid wave when percussed. The APRN tells the patient that he has ascites. Explain how ascites develops as a result of portal HTN. Increased pressure in the portal blood vessels may cause protein-containing (ascitic) fluid to leak from the surface of the liver and intestine and to accumulate within the abdomen. This condition is called ascites. In the underfilling theory, the primary abnormality is inappropriate sequestration of fluid within the splanchic vascular bed due to portal HTN and a subsequent decrease in effective circulation blood volume. This activates the plasma renin, aldosterone, and SNS, resulting in renal sodium and water retention. The overflow theory postulates that increased portal pressure, along with decreased serum albumin, cause capillary hydrostatic pressure to exceed capillary oncotic pressure pushing transudative fluid into the peritoneal cavity. A 45-year-old man with known alcoholic cirrhosis, portal HTN, and ascites is brought into the ED by his family due to increasing confusion. The family states that he had been stumbling for several days but had not fallen. The family also noted that he had been “flapping his hands” as well. Labs revealed: Hgb 9.4 Hct 28 ammonia 159. The APRN informs the family that the patient has developed hepatic encephalopathy. Explain how hepatic encephalopathy develops in patients with cirrhosis of the liver. Hepatic encephalopathy results from a combination of biochemical alterations that affect neurotransmission. The digestion of blood from leaking or ruptured varices adds to the amount of ammonia present in the blood. Ammonia that reaches the brain is metabolized to glutamine, with osmotic disturbances and alterations in cerebral blood flow that interfere with neurotransmitters and cause astrocyte edema and oxidation. The most harmful substances are the end products of protein digestion, especially ammonia that can’t be converted to urea by a diseased liver. The blood that is digested from leaking or ruptured vessels add to the amount of ammonia in the gut. A 65-year-old man with a hx of a-fib presents to his PCP’s office 2 months after suffering a MI. He declined anticoagulation due to fear he would bleed to death. He has had sudden onset, moderately severe diffuse abd pain that began 18 hours ago. He has been vomiting, and has had several episodes of diarrhea, the last of which was bloody. He has a fever of 100.9. CBC reveals WBC of 15,000. What is the most likely mechanism behind his current symptoms? Superior mesenteric artery thrombosis, which causes a sudden decrease or interruption in the primary blood flow to most of the small bowel as well as the ascending colon, which also leads to malperfusion of the involved end organ leading to ischemia and then infarction. Older patients are at risk due to atherosclerosis which leads to thrombus formation. These types of origins usually arise from cardiac arrhythmias, usually a-fib, which leads to pooling of blood in the atria. A 46-year-old white female presents to her PCP’s office with a chief complaint of severe, intermittent RUQ pain for the last 3 days. The pain is described as sharp and has occurred after eating French fries and cheeseburgers and radiates to her right shoulder. She has had a few episodes of vomiting “green stuff.” States had fever and chills last night which precipitated her trip to the office. She aloso had some dark orange urine, but she thought she was dehydrated. Physical exam: slightly obese female with icteric sclera as well as generalized jaundice. Temp 101, pulse 108, resp 18. Abd exam revealed rounded abd with slightly hypoactive BS. + rebound tenderness on palpation of RUQ. No tenderness or rebound in epigastrium or other quadrants. Labs show elevated WBC, elevated serum ALT and AST. Serum bili 2.5. Abd US demonstrated enlarged GB, dilated common bile duct and multiple stones in the bile duct. The APRN diagnoses the patient with acute cholecystitis and refers her to the ED for further treatment. Describe how gallstones are formed and why they caused the symptoms that the patient presented. Gallstones are formed from impaired metabolism of cholesterol, bilirubin, and bile acids. All gallstones contain cholesterol, unconjugated bilirubin, bilirubin calcium salts, fatty acids, calcium carbonates and phophates and mucin glycoproteins. Gallstones form in bile that is supersaturated and can begin the process of cholesterol crystal formation. More crystals aggregate thus enlarging and forming stones. These stones may lie dormant or start to move down the cystic or common bile duct. These stones can cause biliary stasis, bacterial infections, biliary parasites. Explain how the patient became jaundiced. The common bile duct is obstructed, usually by gallstones, a tumor or inflammation. Bilirubin conjugated by the hepatocytes cannot flow through the obstructed common bile duct into the duodenum so it accumulates in the liver and enters the bloodstream, causing hyperbilirubinemia and jaundice. Ruth is a 49-year-old office worker who presents to the clinic with a chief complaint of abd pain x 2 days. The pain has significantly increased over the past 6 hours and is now accompanied by N/V. the pain is described as “sharp and boring” in mid epigastrum radiating to the back. Ruth admits to a long hx of alcohol abuse, and often drinks up to a 1/5 of vodka daily. Physical Exam: Temp 102.2 BP 90/60, Resp 22. Pulse ox 92% RA General: thin, pale white female in obvious pain and leaning forward. Moving around on exam table and unable to sit quietly. CV: tachycardic. RRR without gallops, rubs, clicks or murmurs Resp: decreased BS in both bases with poor inspiratory effort ABD: epigastric guarding with tenderness. No rebound tenderness. Negative Cullen’s and + Turner’s signs observed. Hypoactive BS x 2 upper quads and no bowel sounds in both lower quads. The APRN makes a tentative dx of acute pancreatitis based on hx and physical exam and has the patient transferred to the ER where lab and xrays reveal acute pancreatitis. Explain how pancreatitis develops and the role alcohol played in this patient’s