NURS 6501 GASTROINTESTINAL AND HEPATOBILIARY DISORDERS

Sample Answer for NURS 6501 GASTROINTESTINAL AND HEPATOBILIARY DISORDERS Included After Question

NURS 6501 Week 8 Module 5 Assignment: Case Study Analysis 

In this exercise, you will complete a 5-essay type question Knowledge Check to gauge your understanding of this module’s content.   

GASTROINTESTINAL AND HEPATOBILIARY DISORDERS 

Possible topics covered in this Knowledge Check include: 

Ulcers 
Hepatitis markers 
After HP shots 
Gastroesophageal Reflux Disease 
Pancreatitis 
Liver failure—acute and chronic 
Gall bladder disease 
Inflammatory bowel disease 
Diverticulitis 
Jaundice 
Bilirubin 
Gastrointestinal bleed – upper and lower 
Hepatic encephalopathy 
Intra-abdominal infections (e.g., appendicitis) 
Renal blood flow 
Glomerular filtration rate 

Kidney stones 
Infections – urinary tract infections, pyelonephritis 
Acute kidney injury 
Renal failure – acute and chronic 

RESOURCES 

NURS 6501 Week 8 Module 5 Assignment: Case Study Analysis

Be sure to review the Learning Resources before completing this activity.
Click the weekly resources link to access the resources.  

WEEKLY RESOURCES 

BY DAY 7 OF WEEK 5 

Complete the Knowledge Check By Day 7 of Week 5. 

 

 

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A Sample Answer For the Assignment: NURS 6501 GASTROINTESTINAL AND HEPATOBILIARY DISORDERS

Title: NURS 6501 GASTROINTESTINAL AND HEPATOBILIARY DISORDERS

Question 1 

3.8 / 4 pts 

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? 

 

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 

 

Question 2 

3.8 / 4 pts 

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?  

 

Your Answer: 

Peptic ulcers occur when there is a break in the mucous lining of the GI tract, and it comes into contact with hydrochloric acid and pepsin. The epithelial cells of the stomach and duodenum secrete mucus in response to irritation of the epithelial lining due to cholinergic stimulation. Ulcers or breaks in the mucosa of the GI tract occur with H. pylori infection, use of NSAIDs, trauma, infection, and physical or psychological stress (Alsinnari et al., 2022). H. pylori is spread by oral to oral, fecal-oral routes. It damages gastric epithelial cells reducing the effectiveness of gastric mucus. NSAIDs interrupt prostaglandin synthesis, which maintains the mucous barrier of the gastric mucosa. PUD can be chronic, with spontaneous remissions and exacerbations associated with trauma, infection, and physical or psychological stress.  

References 

Alsinnari, Y. M., Alqarni, M. S., Attar, M., Bukhari, Z. M., Almutairi, M., Baabbad, F. M., & Hasosah, M. (2022). Risk factors for recurrence of peptic ulcer disease: A retrospective study in tertiary care referral center. Cureus, 14(2), e22001. https://doi.org/10.7759/cureus.22001 

 

 

Question 3 

3.8 / 4 pts 

Scenario 2: Gastroesophageal Reflux Disease (GERD) 

A 44-year-old morbidly obese female comes to the clinic complaining 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 the symptoms 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, irritable bowel syndrome, osteoarthritis of knees, morbid obesity (BMI 48 kg/m2)  

FH:non contributary    

Medications: Lisinopril 10 mg po qd, Bentyl 10 mg po, ibuprofen 800 mg po q 6 hr prn  

SH: 20 PPY of smoking, ETOH rarely, denies vaping     

Diagnoses: Gastroesophageal reflux disease (GERD).  

 

Question: 

1.     If the client asks what causes GERD how would you explain this as a provider?  

 

Your Answer: 

The patient in the case study has GERD. I would inform her that several factors cause GERD. One of the aspects that I will educate her is that GERD is a condition that develops following the ulceration of the mucosal lining that protects the esophagus. One of the causes of the disorder is Zollinger-Ellison syndrome, which increases the release of gastric acid. Zollinger-Ellison syndrome is characterized by the presence of multiple duodenal or pancreatic tumors that increase gastric acid secretion (Maret-Ouda et al., 2020). 

            The other cause of GERD that the patient should be aware is the prolonged use of NSAIDs. NSAIDs inhibit the synthesis of protective prostaglandins. They also lower the production of bicarbonates and mucus while increasing the secretion of hydrochloric acid. The other factor is smoking. Smoking suppresses the production of prostaglandins, mucus for protection, and weakens the esophageal sphincter. Increased use of irritants such as coffee and alcohol also play a crucial role (Katz et al., 2022). The irritation acts as a source of stress that degrade the protective mucosa and increase the production of destructive gastric acid. 

The other cause is any form of stress. Stressors such as hospitalization and life experiences also act as a source of GERD. Any stressors increase the production of gastric acid. The risk of GERD increases if the patient already has other risk factors for GERD and or peptic ulcer disease. The additional risk factors that should be addressed to prevent GERD include obesity, hiatal hernia, esophageal contractions, prolonged or reduced stomach emptying, and abnormalities of esophageal sphincter (Maret-Ouda et al., 2020). 

References 

Katz, P. O., Dunbar, K. B., Schnoll-Sussman, F. H., Greer, K. B., Yadlapati, R., &Spechler, S. J. (2022). ACG Clinical Guideline for the Diagnosis and Management of Gastroesophageal Reflux Disease. The American Journal of Gastroenterology, 117(1), 27–56. https://doi.org/10.14309/ajg.0000000000001538 

Maret-Ouda, J., Markar, S. R., & Lagergren, J. (2020). Gastroesophageal Reflux Disease: A Review. JAMA, 324(24), 2536–2547. https://doi.org/10.1001/jama.2020.21360Links to an external site. 

 

 

 

Question 4 

3.5 / 4 pts 

Scenario 3: Upper GI Bleed 

A 64-year-old male presents the clinic with complaints of passing 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. 

Question: 

1.     What are the variables here that contribute to an upper GI bleed?  

 

Your Answer: 

The patient in the case study has a potential diagnosis of upper GI bleed. Several variables contribute to the development of the upper GI bleed. One of the variables is peptic ulcer bleeding. Patients with chronic ulcers are increasingly at a risk of developing upper GI bleed. The bleed arises from severe destruction of the protecting mucosal layer by gastric secretions. The other variable is gastritis. The irritation and inflammation of the gastric mucosa increase the risk of its destruction by gastric acid(Graham & Carlberg, 2019). Over time, gastritis causes upper GI bleed due to the destruction of the mucosal barrier in esophagus and stomach. 

            The other variable associated with upper GI bleed is esophagitis. Esophagitis refers to the inflammation of the esophagus. The inflammation occurs from the different irritants to the esophageal mucosa. Chronic inflammation may cause altered mucosa integrity and damage from gastric reflux, hence, the development of upper GI bleed. The other variable is esophageal varices. Esophageal varices are inflamed veins within the esophagus. The varices are highly prone to rupture when exposed to stressors such as straining or irritants(Leebeek& Muslem, 2019). Rupture of the veins cause upper GI bleeding, hence, a potential cause of the client’s problem in this case study. 

            The other variable contributing to upper GI bleed that should be considered in the client is Mallory-Weiss syndrome. Mallory-Weiss syndrome causes tears and bleeding from the stomach or esophageal lining. Cancer of the upper GI also may contribute to upper GI bleed. For example, cancers of the stomach or esophagus may cause rupture of the blood vessels, resulting in the upper GI bleed(Graham & Carlberg, 2019). Consequently, these potential causes should be ruled out through comprehensive diagnostics in the patient’s care. 

References 

Graham, A., & Carlberg, D. J. (2019). Gastrointestinal Emergencies: Evidence-Based Answers to Key Clinical Questions. Springer. 

Leebeek, F. W. G., & Muslem, R. (2019). Bleeding in critical care associated with left ventricular assist devices: Pathophysiology, symptoms, and management. Hematology, 2019(1), 88–96. https://doi.org/10.1182/hematology.2019000067 

 

Question 5 

3.8 / 4 pts 

Scenario 4: Diverticulitis 

A 54-year-old schoolteacher is seeing your today for complaints of passing bright red blood when she had a bowel movement this morning. She stated the first episode occurred last week. The episode today was accompanied by nausea, sweating, and weakness. She states she has had some LLQ pain for several weeks but described it as “coming and going”. She says she has had a fever and abdominal cramps that have worsened this morning. 

Diagnosis is lower GI bleed secondary to diverticulitis. 

Question: 

1.     What can cause diverticulitis in the lower GI tract?  

 

Your Answer: 

The patient in the case study has diverticulitis. Diverticulitis develops when a part of the colon weakens leading to pouches and protrusion in the wall of the colon. Several factors can cause diverticulitis. One of them is aging. The risk of a patient developing diverticulitis increase significantly as one ages. The other cause of obesity. The risks of diverticulitis increase significantly with excessive weight gain. An imbalance between the bacterial flora in the colon has also been attributed to diverticulitis (Peery et al., 2021). For example, an imbalance between Clostridium coccoides and Escherichia have been identified to cause diverticulitis in most of the patients. 

            Diet also plays a role in the development of diverticulitis. Patients with a history of low fiber diet have an elevated risk of developing the disorder as compared to those who take fiber rich diet. Low fiber diet results in too much volume within the colon, hence, increasing the risk of diverticulitis. The other cause is physical inactivity. Physical inactivity affects intestinal microbiome as well as increases the risk of diverticulitis-associated risk factors such as obesity. Genetics also contributes to diverticulitis. Accordingly, people born to families with a history of diverticulitis are increasingly at a risk of developing the disorder. However, the direct link between the exposure and development of diverticulitis is inconclusive. The use of certain medications has also been shown to increase the risk of diverticulitis. For example, NSAIDs and steroids have been shown to increase the risk of diverticulitis due to their effect on gastrointestinal physiology. Lifestyles such as smoking also increases the risk(Peery et al., 2021). This can be seen from the evidence that most of the smokers have a high rate of diverticulitis as compared to non-smokers. 

References 

Peery, A. F., Shaukat, A., & Strate, L. L. (2021). AGA clinical practice update on medical management of colonic diverticulitis: Expert review. Gastroenterology, 160(3), 906-911.e1. https://doi.org/10.1053/j.gastro.2020.09.059 

 

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