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NURS 6501 Knowledge Check: Gastrointestinal and Hepatobiliary Disorders

NURS 6501 Knowledge Check: Gastrointestinal and Hepatobiliary Disorders

The case study concerns DC, a 46-year-old woman with RUQ pain that has lasted 24 hours. The onset of the RUQ pain was roughly 1 hour after having a large family dinner. She reports having nausea and one episode of vomiting. The purpose of this paper is to discuss the patient’s diagnosis and recommend an appropriate medication therapy.

Diagnosis

The likely diagnosis for this patient is Acute Cholecystitis. Gallaher and Charles (2022) define Acute cholecystitis as an acute inflammatory disorder of the gallbladder, usually resulting from gallstone obstruction at the cystic duct. The classic clinical presentation of acute cholecystitis includes acute right upper quadrant (RUQ) pain, fever, and nausea associated with eating (Bridges et al., 2018). Physical exam findings include RUQ tenderness. Diagnostic findings in acute cholecystitis include elevated white blood cell count (WBC), Liver enzymes, and bilirubin levels. The patient has RUQ pain, nausea, and vomiting after eating. She also has an elevated WBC count and Direct and indirect serum bilirubin levels.

Appropriate drug therapy

The recommended drug therapy for DC will comprise analgesics, antiemetics, and IV antibiotics. Ketorolac IV 30 mg STAT dose, followed by 10 mg OO QID, will be recommended to relieve RUQ pain (Mou et al., 2019). The antiemetic of choice will be IV Promethazine 12.5 mg QID to manage nausea and vomiting. IV antibiotics will include Levofloxacin 500 mg IV once daily and Flagyl, 1 g IV loading dose followed by 500 mg IV QID (Markotic et al., 2020).

Conclusion

Cholecystitis mainly develops as a complication of gallstone disease but can occur without gallstones. The patient has positive symptoms of Acute Cholecystitis, including RUQ pain, nausea, vomiting, and elevated WBC and bilirubin. Treatment will include antibiotics, antiemetics, and analgesics.

.

References

Bridges, F., Gibbs, J., Melamed, J., Cussatti, E., & White, S. (2018). Clinically diagnosed cholecystitis: a case series. Journal of surgical case reports2018(2), rjy031. https://doi.org/10.1093/jscr/rjy031

Gallaher, J. R., & Charles, A. (2022). Acute cholecystitis: a review. Jama327(10), 965-975. doi:10.1001/jama.2022.2350

Markotic, F., Grgic, S., Poropat, G., Fox, A., Nikolova, D., Vukojevic, K., Jakobsen, J. C., & Gluud, C. (2020). Antibiotics for adults with acute cholecystitis or acute cholangitis or both. The Cochrane Database of Systematic Reviews2020(6), CD013646. https://doi.org/10.1002/14651858.CD013646

Mou, D., Tesfasilassie, T., Hirji, S., & Ashley, S. W. (2019). Advances in the management of acute cholecystitis. Annals of gastroenterological surgery3(3), 247–253. https://doi.org/10.1002/ags3.12240

Question 1

4 out of 4 points

Correct

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 osteoarthri

NURS 6501 Knowledge Check Gastrointestinal and Hepatobiliary Disorders
NURS 6501 Knowledge Check Gastrointestinal and Hepatobiliary Disorders

tis,

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:

Peptic Ulcer is the break in the mucosa lining  gastric and duodenal mucosadue to excessive secretion of gastric acid..Usually affect the stomach and the lower duodenum and it affect the muscularis layer of the gastric epithelia. The contributory factors are the frequent use of Nonsteriodial anti-inflammatory d medications, smoking, drinking alcohol.Stress can cause PUD.

Correct Answer:

Correct 

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

    Correct

    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

    NURS 6501 Knowledge Check Gastrointestinal and Hepatobiliary Disorders
    NURS 6501 Knowledge Check Gastrointestinal and Hepatobiliary Disorders

    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:

    This is in two part, which is decreased mucosal  protection and  increased acid production. The causative factor most likely is the H.pyloris that destroy the mucosal lining, causing inflammatory process  that increased  gastric acid production that erode  the liniing ,The increasesd  acid create open sore that bleed.

    Correct Answer:

    Correct 

    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]
  • NURS 6501 Knowledge Check: Gastrointestinal and Hepatobiliary DisordersQuestion 3

    4 out of 4 points

    Correct

    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? 

    Selected Answer:

    Gastroesophageal reflux disease is the backflow of acid from stomach to the esophagus causing irriation of the mucousa lining.

    The  symotoms are heartburn,reguritation,and pain with swallowing. The lower end of the oesphaus there is a circular ring of muscle  called  the  spinicter that prevent the backflow of food and acid from escaping into the oesphagus, as a  result of  the relaxaton  of sphinicter  muscle from pressure from the  stomach.  There are riak factor for GERD. Hiatus hernia,obesity, pregnancy,lifestyle factors, like smoking,alchol  consumption, excessive intake of nonsteriodal antinflammatory drugs , Certains  steps can be taken to relief the sysptoms. The GERD  can be manged  with theses steps,Loose weight, stop smoking, Decrease alcohol intake,decrease meal size, avoid eating late. Avoid lieing down 2hours to 3hours after eating,

    Correct Answer:

    Correct 

    GERD manifestations result directly from gastric acid reflux into the esophagus. Pyrosis, the classic symptom, is a substernal burning sensation typically described as heartburn. It may be accompanied by regurgitation, particularly in someone who has recently eaten. The lower esophageal sphincter (LES) relaxes due to certain medications (calcium channel blockers), hiatal hernia, and obesity allows stomach contents to enter the lower esophagus causing inflammation and possibly erosion of the esophagus.

    Response Feedback: [None Given]
  • Question 4

    4 out of 4 points

    Correct

    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? 

    Selected Answer:

    The major causes of upper GIB include esophageal varices, gastritis, peptic ulcers.The variaiable to upper GIBleed is the history of the patient about epigastric pain several weeks, passing of dark tarry stool , Now presenting with signs of shock from bleeding.

    Correct Answer:

    Correct 

    UGI bleeds can be caused by Peptic ulcer disease (PUD) which remains the most common cause of UGIB. Esophageal bleeding from a Mallory-Weiss tear (caused by repeated vomiting, retching, erosions of the mucosa), gastric carcinomas.

    Response Feedback: [None Given]
  • Question 5

    4 out of 4 points

    Correct

    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? 

    Selected Answer:

    Diverticulosis  occur in the large intestine,caused by lack of fiber in the diet that cause constipation,this exert pressure on the  wall of the colon and cause pouch  known as the diverticula , This pouch are formed in weak area of the colon. Diverticulitis occur when the pouch is inflammed and  infected due to erosion of the wall . This can also result in lower GI bleed.

    Correct Answer:

    Correct 

    Diverticulitis is defined as an inflammation of one or more diverticula. Fecal material or undigested food particles may collect in a diverticula causing obstruction. The obstruction can cause vascular compromise. Increased intraluminal pressure or food particles cause erosion of the diverticular wall, resulting in inflammation, localized necrosis, and perforation.

    Response Feedback: [None Given]

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? 

I would explain to the client that GERD is caused by excessive relaxation of the lower esophageal sphincter (LES). This allows reflux of gastric contents into the esophagus and exposes the esophageal mucosa to acidic gastric contents. Nighttime reflux usually causes prolonged exposure of the esophagus to acid since the supine position reduces peristalsis and the benefit of gravity (Maret-Ouda et al., 2020). The refluxed gastric contents are then returned to the stomach through a combination of gravity, saliva, and peristalsis. However, the inflamed esophagus cannot remove the refluxed material as quickly as a healthy one. Thus, the length of exposure to gastric acid increases with each reflux episode (Maret-Ouda et al., 2020). Consequently, increased blood flow and erosion occur in the esophagus in response to the chronic inflammation.

4 points   

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? 

The patient’s variables contributing to the upper GI bleed (UGIB) include sex, advanced age, history of upper GI bleeding, use of high-dose NSAID, and anticoagulant use. Wilkins et al. (2020) explain that UGIB is twice more common in males than females, and its prevalence increases with age. Persons aged 60 years and older have the highest risk. The common medical causes of UGIB include esophagitis, peptic ulcer bleeding, gastritis, variceal bleeding, and gastric cancer. The patient has a history of mild epigastric pain, which points to gastritis. His gender,  advanced age, and possible gastritis can be attributed to the upper GI bleed (Wilkins et al., 2020).4 points   

 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? 

Diverticulitis is inflammation of a diverticulum with or without infection. It can occur when there is a micro or macro perforation in a diverticulum, which causes the release of intestinal bacteria that triggers inflammation (Barbaro et al., 2022). If bacteria get trapped in a diverticulum, the blood supply to that diverticulum is reduced. Bacteria invade the diverticulum, causing diverticulitis, which then can perforate and progress to a local abscess.

 References

Barbaro, M. R., Cremon, C., Fuschi, D., Marasco, G., Palombo, M., Stanghellini, V., & Barbara, G. (2022). Pathophysiology of diverticular disease: from diverticula formation to symptom generation. International Journal of Molecular Sciences23(12), 6698. https://doi.org/10.3390/ijms23126698

Kavitt, R. T., Lipowska, A. M., Anyane-Yeboa, A., & Gralnek, I. M. (2019). Diagnosis and treatment of peptic ulcer disease. The American journal of medicine132(4), 447-456. https://doi.org/10.1016/j.amjmed.2018.12.009

Maret-Ouda, J., Markar, S. R., & Lagergren, J. (2020). Gastroesophageal reflux disease: a review. Jama324(24), 2536-2547. https://doi.org/10.1001/jama.2020.21360

McEvoy, L., Carr, D. F., & Pirmohamed, M. (2021). Pharmacogenomics of NSAID-induced upper gastrointestinal toxicity. Frontiers in pharmacology, 1302. https://doi.org/10.3389/fphar.2021.68416

Wilkins, T., Wheeler, B., & Carpenter, M. (2020). Upper Gastrointestinal Bleeding in Adults: Evaluation and Management. American family physician101(5), 294–300.