NURS 6501 GASTROINTESTINAL AND HEPATOBILIARY DISORDERS

Scenario 1: Peptic Ulcer

A 65-year-old female from the NURS 6501 GASTROINTESTINAL AND HEPATOBILIARY DISORDERS assignment, 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?
Your Answer:
Peptic ulcer disease (PUD) occurs following impairment of the mucosal defenses, which
leaves them incapable of protecting the epithelium from the effects of acid and pepsin. 
The development of PUD is associated primarily with bacterial infection with H. pylori and
NSAIDs.  NSAIDs like diclofenac and ibuprofen break down the stomach mucosal barrier
and disrupt the mucosal protection mediated systemically by cyclooxygenase (COX)
inhibition (Kuna et al., 2019).  The patient’s PUD may have been contributed by H.pylori
infection, owing to the positive urease breath test, which reveals the presence of
Helicobacter pylori bacteria.  Besides, the PUD may have been caused by taking a high
dose of ibuprofen 400-600 mg for pain relief.  Ibuprofen causes reduced endogenous
prostaglandins, resulting in local gastric mucosal injury.

In addition, lifestyle factors like tobacco smoking and excessive alcohol and caffeine
consumption are associated with PUD.  Caffeine stimulates the production of
hydrochloric acid.  Smoking accelerates gastric emptying and decreases pancreatic
bicarbonate production (Kuna et al., 2019).  Besides, ethanol irritates gastric mucosal and
nonspecific gastritis.  The patient’s history of tobacco smoking, heavy caffeine intake, and
daily alcohol intake may have led to the development of PUD.

References

 Kuna, L., Jakab, J., Smolic, R., Raguz-Lucic, N., Vcev, A., & Smolic, M. (2019). Peptic ulcer
disease: a brief review of conventional therapy and herbal treatment options. Journal of
clinical medicine, 8(2), 179. doi: 10.3390/jcm8020179


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