NUR 660 Week 12 Discussion 1: Case Study Discussion – Gastrointestinal Disorders
NUR 660 Week 12 Discussion 1: Case Study Discussion – Gastrointestinal Disorders
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?
