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KNOWLEDGE CHECK GASTROINTESTINAL AND HEPATOBILIARY DISORDERS NURS 6501
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- Question 1
4 out of 4 points
| Scenario 1: Peptic Ulcer A 65-year-old female comes to the clinic with a complaint of abdominal pain in the epigastric area. The pain has been persistent for two weeks. The pain described as burning, non-radiating and worse after meals. Denies N&V, weight loss or obvious bleeding. She admits to frequent belching with bloating. PMH: seasonal allergies with Chronic Sinusitis, positive for osteoarthritis, Meds: Claritin 10 mg po daily, ibuprofen 400-600 mg po prn pain Family Hx-non contributary Social history: Separated recently pending divorce; stressful situation with trying to manage two homes. Works as a Legal Assistant at a local law firm. She has 35 PPY of smoking, drinks 1-2 glasses of wine a day, and 6-7 cups of coffee per day. She denies illicit drug use, vaping or unprotected sexual encounters. Breath test in the office revealed + urease. The healthcare provider suspects the client has peptic ulcer disease. Questions: 1. Explain what contributed to the development from this patient’s history of PUD? | ||||
| Selected Answer: PUD is ulceration in the mucosal lining of the lower esophagus, stomach, and or duodenum. This patient has several risk factors contributing to the development of peptic ulcer disease. including, Patient’s age of 65, Daily use of NSAIDs for osteoarthritis pain, High stress due to a pending divorce, working, and managing 2 homes. The patient smokes and drinks Alcohol daily. Coffee consumption may be another causative factor for PUD. Also, her positive breath test for urease indicates the presence of H. pylori infection. Chronic use of ibuprofen suppresses mucosal prostaglandin synthesis which in turn results in decreased bicarbonate secretion and mucin production. The bicarbonate is a buffer against HCl, and mucin is a component of the gut barrier. Subsequently, the secretion of HCl is increased. The interaction of NSAIDS and H. Pylori can contribute to the pathogenesis of peptic ulcers as both disrupt the integrity of the mucosa. This exposes submucosal areas to gastric secretions and autodigestion, causing erosion and ulceration Correct Answer: Stress secondary to divorce and financial situation, cigarette smoking, alcohol consumption, use of NSAIDS, excess coffee consumption, +H Pylori test Response Feedback: [None Given] |
- Question 2
4 out of 4 points
| Scenario 1: Peptic Ulcer A 65-year-old female comes to the clinic with a complaint of abdominal pain in the epigastric area. The pain has been persistent for two weeks. The pain described as burning, non-radiating and worse after meals. Denies N&V, weight loss or obvious bleeding. She admits to frequent belching with bloating. PMH: seasonal allergies with Chronic Sinusitis, positive for osteoarthritis, Meds: Claritin 10 mg po daily, ibuprofen 400-600 mg po prn pain Family Hx-non contributary Social history: Separated recently pending divorce; stressful situation with trying to manage two homes. Works as a Legal Assistant at a local law firm. She has 35 PPY of smoking, drinks 1-2 glasses of wine a day, and 6-7 cups of coffee per day. She denies illicit drug use, vaping or unprotected sexual encounters. Breath test in the office revealed + urease. The healthcare provider suspects the client has peptic ulcer disease. Question: 1. What is the pathophysiology of PUD/ formation of peptic ulcers? | ||||
| Selected Answer: The two major types of peptic ulcers are duodenal ulcers and gastric ulcers. Both are predominately caused by H. pylori and NSAID usage. The pathophysiology of both is similar, however, in duodenal ulcers, acid and pepsin concentrations in the duodenum penetrate the mucosal barrier and lead to ulceration. In the case of gastric ulcers, duodenal reflux of bile precipitates ulcer formation by limiting the mucosa’s ability to secrete a protective layer of mucus. The pyloric sphincter may fail to respond properly allowing reflux of bile and pancreatic enzymes to damage the gastric mucosa. The damaged mucosal barrier permits hydrogen ions to diffuse into the mucosa. Here they disrupt permeability and cellular structure. A vicious cycle is then established as the damaged mucosa liberates histamine. This stimulates the increase of acid and pepsinogen production, blood flow, and capillary permeability. The disrupted mucosa becomes edematous and loses plasma proteins. The destruction of small vessels causes bleeding. Thus, the pathophysiology of the various peptic ulcer formation has similar beginnings and can diverge from there to follow a couple of different pathways. Initially: 1. Causative factors: H. pylori, bile salts, NSAIDS, alcohol, ischemia 2. Damaged mucosal barrier 3. Decreased function of mucosal cells, decreased quality of mucus, loss of tight junctions between cells 4. Back-diffusion of acid into gastric mucosa which leads to A. Conversion of pepsinogen to pepsin. This leads to further mucosal erosion, destruction of blood vessels, and bleeding. Resulting in ulceration. B. Formation and liberation of histamine. This leads to local vasodilation and results in increased capillary permeability, loss of plasma proteins, mucosal edema, and loss of plasma into the gastric lumen. This formation and liberation of histamine also increase acid secretion leading to both ulceration and muscle spasms. it should be also be noted that H. pylori which thrive in the presence of increased acidity also leads to mucosal injury, and thereby, ulceration. High-risk for PUD include alcoholics, patients on extensive NSAIDs, and those with chronic renal failure. PUD has been strongly linked to infection with Helicobacter pylori. This bacterium is responsible for the destruction of protective mechanisms in the stomach and duodenum leading to damage by stomach acid that would otherwise not be a problem. These ulcers are found more commonly in the duodenum than in the stomach, although both locations present equal incidences of bleeding. Correct Answer: Chronic use of NSAIDS causes suppresses of mucosal prostaglandin and direct irritative topical effect. High gastrin level and excessive gastric acid production often seen in Zollinger-Ellison syndrome which can caused by gastrinoma. Smoking impairs healing by vasoconstriction. H Pylori causes gastritis and interferes with mucosa Response Feedback: [None Given] |
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