NURS 6501 Knowledge Check Gastrointestinal and Hepatobiliary Disorders

Sample Answer for NURS 6501 Knowledge Check Gastrointestinal and Hepatobiliary Disorders Included After Question

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

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

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.

A Sample Answer For the Assignment: NURS 6501 Knowledge Check Gastrointestinal and Hepatobiliary Disorders

Title: NURS 6501 Knowledge Check Gastrointestinal and Hepatobiliary Disorders

	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

Click here to ORDER an A++ paper from our Verified MASTERS and DOCTORATE WRITERS: NURS 6501 Knowledge Check Gastrointestinal and Hepatobiliary Disorders

	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 3

4 out of 4 points

	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: GERD is caused by frequent acid reflux; the reflux of acid and pepsin or bile salts from the stomach to the esophagus. This, in turn, causes esophagitis, or inflammation and irritation of the esophagus. To break it down even more, when you swallow, a circular band of muscle around the bottom of your esophagus (lower esophageal sphincter or LES) relaxes to allow food and liquid to flow into your stomach. Then the sphincter closes again. If the sphincter relaxes abnormally or weakens, stomach acid can flow back up into your esophagus. This constant backwash of acid irritates the lining of your esophagus, often causing it to become inflamed.                                                                                                                                                  I would then explain to the patient the risk factors that increase a person’s susceptibility to developing GERD, as well as factors that can aggravate acid reflux as follows: Conditions that can increase your risk of GERD include Obesity, Bulging of the top of the stomach up into the diaphragm (hiatal hernia), Drugs or chemicals that relax the lower esophageal sphincter, (such as anti-cholinergic, nitrates, calcium channel blockers, nicotine), Pregnancy, and Connective tissue disorders, such as scleroderma, Delayed stomach emptying. Factors that can aggravate acid reflux include Smoking, Eating large meals, eating late at night, Eating certain foods (triggers) such as fatty or fried foods, drinking certain beverages, such as alcohol or coffee, and Taking certain medications, such as NSAIDs or aspirins. Correct Answer: 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]

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:

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. 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. Different medications alongside chronic stress also heighten the risk of PUD for the patient. The factors explain the underlying reasons for the health outcome.

A Sample Answer 2 For the Assignment: NURS 6501 Knowledge Check Gastrointestinal and Hepatobiliary Disorders

Title: NURS 6501 Knowledge Check Gastrointestinal and Hepatobiliary Disorders

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:

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. 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. Such elements illustrate the pathophysiology of PUD formation with a peptic ulcer.

A Sample Answer 3 For the Assignment: NURS 6501 Knowledge Check Gastrointestinal and Hepatobiliary Disorders

Title: NURS 6501 Knowledge Check Gastrointestinal and Hepatobiliary Disorders

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 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.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. The foul taste in the mouth is also a common symptom, signaling problems in acid control in the patient’s gastric region. The insights guide the patient’s understanding of the causative factors of GERD.