NURS 6051: Module 3 Knowledge Check

NURS 6051: Module 3 Knowledge Check

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

Cite each of the short essay answers with at least one resource.

QUESTION 1

1. 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?

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QUESTION 2

1. 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?

 

QUESTION 3

1. 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?

QUESTION 4

1. 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?

QUESTION 5

1. 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?

Course Resources include the following:

McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.
• Chapter 38: Structure and Function of the Renal and Urological Systems including Summary Review
• Chapter 39: Alteration of Renal and Urinary Function (stop at Fluids and electrolytes); Summary Review
• Chapter 41: Structure and Function of the Digestive System (stop at Tests of digestive function); Summary Review
• Chapter 42: Alterations of Digestive Function (stop at Cancer of the digestive track); Summary Review

Osna, N. A., Donohue, T. M., Jr., & Kharbanda, K. K. (2017). Alcoholic liver disease: Pathogenesis and current management. Alcohol Research: Current Reviews, 38(2), 7–21

 

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Answers: NURS 6051: Module 3 Knowledge Check

Scenario 1: Peptic Ulcer

Q1

Based on the case study, it is clear that the patient’s PUD had been caused by NSAID, ibuprofen usage, H. Pylori infection, and stress (Dunlapas et al.,2019) a result of separation and imminent divorce, as well as the burden of attempting to maintain two homes.

Q2

There is no known pathophysiology of PUD however, it is thought to be produced by an imbalance of aggressive and defensive forces in the mucosal area of the stomach and duodenum. These aggressive factors may include increased acid secretion, enhanced pepsin activity, and bacterial growth (Shell,2021). Mucus and bicarbonate production, on the other hand, are defensive factors. PUD is most commonly caused by helicobacter pylori, a bacterium found in the stomach and duodenum. Smoking, persistent gastritis, and recent use of antibiotics or other medicines, such as NSAIDs, all increase H. Pylori risk. This ailment is distinguished by chronic non-ulcerative stomach pains that get more severe after eating and then radiate to the left side of the abdomen, perhaps accompanied by nausea, vomiting, and diarrhea.

Scenario 2: Gastroesophageal Reflux Disease (GERD)

Q3

GERD is a condition in which stomach contents reflux into the esophagus. This could arise when the lower esophageal sphincter (LES), relaxes or weakens (Lin & Fang, 2019). This permits stomach acid and contents to creep back up into the esophagus, causing irritation to the throat and mouth lining. Smoking, obesity, chronic stress, and the use of certain medications, such as calcium channel blockers, antidepressants, NSAIDs, histamine, and glucocorticoids, can all contribute to GERD. This condition produces pyrosis, which worsens when lying down. In the management of GERD, lifestyle changes such as losing weight and avoiding alcohol, as well as medications such as proton pump inhibitors or surgery, are strongly encouraged. Treatment techniques varies depending on the severity of GERD.

Scenario 3: Upper GIT bleeding

Q4

Upper GIT bleeding is linked to peptic ulcers, esophageal varices, and Mallory-Weiss tears (Abougergi,2018). The most common cause of upper GI bleeding is ulcers, which can be caused by Helicobacter pylori infection, radiation treatment, or chronic gastritis induced by food sensitivities or intolerances. Obesity, liver cirrhosis, and trauma can all cause esophageal varices. Mallory-Weiss tears are caused by pregnancy or eating disorders.

Scenario 4: Diverticulitis

Q5

Diverticulitis occurs when one or more diverticula become inflamed. A high-refined-carbohydrate, low-fiber diet, sedentary lifestyle, obesity, and smoking all predispose to this syndrome (Strate et al.,2019). Medical disorders such as Crohn’s disease and ulcerative colitis can also cause it. While the pathogenesis is not clear, it is thought to be caused by a blockage produced by fecal waste or undigested food particles that accumulate in the diverticulum. Diverticulum distension is caused by mucus production and intestinal bacterial overgrowth. As a result, there is vascular dysfunction and subsequent microperforation. In contrast, increased intraluminal pressure and inspissated food particles may encourage diverticular wall erosion, resulting in inflammation, fecal necrosis, and perforation.

 

References

Abougergi, M. S. (2018). Epidemiology of upper gastrointestinal hemorrhage in the USA: is the bleeding slowing down?. Digestive Diseases and Sciences, 63(5), 1091-1093.

Dunlap, J. J., & Patterson, S. (2019). Peptic ulcer disease. Gastroenterology Nursing, 42(5), 451-454. doi: 10.1097/SGA.0000000000000478

Lin, S., Li, H., & Fang, X. (2019). Esophageal motor dysfunctions in gastroesophageal reflux disease and therapeutic perspectives. Journal of neurogastroenterology and motility, 25(4), 499. https://doi.org/10.5056%2Fjnm19081

Shell, E. J. (2021). Pathophysiology of peptic ulcer disease. Physician Assistant Clinics, 6(4), 603-611. https://doi.org/10.1016/j.cpha.2021.05.005

Strate, L. L., & Morris, A. M. (2019). Epidemiology, pathophysiology, and treatment of diverticulitis. Gastroenterology, 156(5), 1282-1298. https://doi.org/10.1053/j.gastro.2018.12.033