Feb 23, 2024 KNOWLEDGE CHECK GASTROINTESTINAL AND HEPATOBILIARY DISORDERS NURS 6501
KNOWLEDGE CHECK GASTROINTESTINAL AND HEPATOBILIARY DISORDERS NURS 6501
KNOWLEDGE CHECK GASTROINTESTINAL AND HEPATOBILIARY DISORDERS NURS 6501
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?
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Your Answer:
Diverticulitis is a condition characterized by inflammation or infection of the diverticula, which are small pouches that can form in the lining of the lower gastrointestinal (GI) tract. These pouches, called diverticula, typically develop in weakened areas of the colon wall.
The exact cause of diverticulitis is not fully understood, but several factors can contribute to its development. These include:
1. Diverticulosis: Diverticulosis is the presence of multiple diverticula in the colon. It is a common condition, particularly in older individuals. When the diverticula become inflamed or infected, it leads to diverticulitis.
2. Obstruction: Fecal matter or undigested food particles can get trapped in the diverticula, causing obstruction and promoting the development of diverticulitis. The trapped material can create an environment conducive to bacterial overgrowth and infection.
3. Microperforation: Sometimes, the diverticula can develop small perforations or micro-tears in their walls. This can allow bacteria present in the colon to enter the surrounding tissues, leading to inflammation and infection.
4. Decreased blood supply: If the blood vessels that supply the diverticula become compromised, it can result in reduced blood flow to the area. The lack of adequate blood supply can weaken the diverticular walls, making them more susceptible to inflammation and infection.
Other factors that may increase the risk of developing diverticulitis include a diet low in fiber, obesity, sedentary lifestyle, smoking, and certain medications.
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Question 1
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. 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? Selected Answer: The two major types of peptic ulcers are duodenal ulcers and gastric ulcers. Both are predominately caused by H. pylori and NSAID usage. The pathophysiology of both is similar, however, in duodenal ulcers, acid and pepsin concentrations in the duodenum penetrate the mucosal barrier and lead to ulceration. In the case of gastric ulcers, duodenal reflux of bile precipitates ulcer formation by limiting the mucosa’s ability to secrete a protective layer of mucus. The pyloric sphincter may fail to respond properly allowing reflux of bile and pancreatic enzymes to damage the gastric mucosa. The damaged mucosal barrier permits hydrogen ions to diffuse into the mucosa. Here they disrupt permeability and cellular structure. A vicious cycle is then established as the damaged mucosa liberates histamine. This stimulates the increase of acid and pepsinogen production, blood flow, and capillary permeability. The disrupted mucosa becomes edematous and loses plasma proteins. The destruction of small vessels causes bleeding. Thus, the pathophysiology of the various peptic ulcer formation has similar beginnings and can diverge from there to follow a couple of different pathways. Initially: 1. Causative factors: H. pylori, bile salts, NSAIDS, alcohol, ischemia 2. Damaged mucosal barrier 3. Decreased function of mucosal cells, decreased quality of mucus, loss of tight junctions between cells 4. Back-diffusion of acid into gastric mucosa which leads to A. Conversion of pepsinogen to pepsin. This leads to further mucosal erosion, destruction of blood vessels, and bleeding. Resulting in ulceration. B. Formation and liberation of histamine. This leads to local vasodilation and results in increased capillary permeability, loss of plasma proteins, mucosal edema, and loss of plasma into the gastric lumen. This formation and liberation of histamine also increase acid secretion leading to both ulceration and muscle spasms. it should be also be noted that H. pylori which thrive in the presence of increased acidity also leads to mucosal injury, and thereby, ulceration. High-risk for PUD include alcoholics, patients on extensive NSAIDs, and those with chronic renal failure. PUD has been strongly linked to infection with Helicobacter pylori. This bacterium is responsible for the destruction of protective mechanisms in the stomach and duodenum leading to damage by stomach acid that would otherwise not be a problem. These ulcers are found more commonly in the duodenum than in the stomach, although both locations present equal incidences of bleeding. Correct Answer: 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]
QUESTION 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.T
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?
The patient’s PUD can be attributed to NSAID use, stress, and excessive caffeine intake. NSAIDs like ibuprofen break down the mucosal barrier and interrupt the mucosal protection mediated systemically by cyclooxygenase (COX) inhibition. NSAIDs cause reduced endogenous prostaglandins, causing local gastric mucosal injury (McEvoy, et al., 2021). Caffeine contributes to gastroduodenal ulceration by altering gastric secretion through stimulation of hydrochloric acid production. This results in localized damage to mucosa and interferes with the healing process. Individuals under extreme physiologic stress experience mucosal erosions and superficial hemorrhages that can cause minimal-to-severe gastrointestinal blood loss (Kavitt et al., 2019). Stress results in elevated levels of hydrochloric acid, resulting in erosive gastritis and subsequent ulcerations.
QUESTION 2
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?
Peptic ulcers usually develop following a break in the mucosal barrier often caused by H. pylori infection resulting in hydrochloric acid injuring the epithelium. Peptic ulcers can then result from back-diffusion of acid or dysfunction of the pyloric sphincter (Kavitt et al., 2019). Without normal functioning of the pyloric sphincter, the bile refluxes into the stomach. This breaks the integrity of the mucosal barrier resulting in hydrogen ion back-diffusion, which causes mucosal inflammation. Toxic agents and bile then destroy the gastric mucosa membrane (Kavitt et al., 2019). Besides, gastric emptying is often delayed in individuals with gastric ulceration. This results in regurgitation of duodenal contents, which worsens the gastric mucosal injury.
QUESTION 3
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.
QUESTION 4
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
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 Sciences, 23(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 medicine, 132(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. Jama, 324(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 physician, 101(5), 294–300.
Question 1
The contributing factors to the patient’s development of PUD comprise smoking, excessive alcohol consumption, stress and the persistent use of NSAIDS medications. The disease develops due to chronic wounds around and beyond the stomach’s muscular mucosa lining (Sadiq et al., 2020). Underlying factors triggering such occurrences constitute alcohol and smoking, producing acids that erode the lining. The two have the greatest possibility of increasing the production of hydrochloric acid, destroying the mucosa lining and creating wounds around the duodenum and the stomach walls (Sadiq et al., 2020). Different medications alongside chronic stress also heighten the risk of PUD for the patient. The factors explain the underlying reasons for the health outcome.
Question 2
Scenario 1: Peptic Ulcer
What is the pathophysiology of PUD formation of peptic ulcer?
PUD formation into a peptic ulcer results from an imbalance between the destructive and the mucosal protective aspects of the gastric lining in the stomach. Most of the time, PUD is characterized by the development of mucosal wounds due to a high difference in the aggressive and mucosal aspects (Malik et al., 2018). H-pylori infections enhance the problem by creating an imbalance that perforates the ulcers in the peritoneal activity. The outcome interferes with gastric activity, causing severe discomfort and pain (Malik et al., 2018). Such elements illustrate the pathophysiology of PUD formation with a peptic ulcer.
Flag question 3
Scenario 2: Gastroesophageal Reflux Disease (GERD)
If the client asks what causes GERD, how will you explain this as a provider?
The client needs to understand that GERD is caused by the continuous regurgitation of contents in the gastric area into the esophagus. Most of the time, the condition develops due to delayed emptying of the gastric contents, impairments on the lower levels of the esophageal sphincter (LES) and reduced acid clearance from the esophagus (Clarrett & Hachem, 2018). The three factors, together with unhealthy eating habits accompanying sleep time, influence the development of GERD. The development of GERD is directly influenced by other factors that constitute morbid obesity, causing an excessive body mass index (Clarrett & Hachem, 2018). The foul taste in the mouth is also a common symptom,
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