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NURS 6501 Knowledge Check: Gastrointestinal and Hepatobiliary Disorders

NURS 6501 Knowledge Check: Gastrointestinal and Hepatobiliary Disorders

  • 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 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:
    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

    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 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:
    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]
  • Question 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:

    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:
    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:

    Bleeding within the GI tract itself is not a disease, but rather a symptom of a disease. This bleeding may be divided into upper and lower GI bleeding The gastrointestinal (GI) tract begins in the mouth and works its way down the esophagus, through the stomach, small and large intestines, and rectum, before terminating at the anus. Bleeding anywhere along this pathway may be acute or chronic and can be due to a host of factors.                                                                                                                                                                                          Bleeds from the upper GI tract are significant causes of morbidity and mortality and are much more common than lower GI bleeds. Important to note that mortality associated with upper GI bleeds is often because of comorbidities rather than the actual bleeding itself.

    signs of upper GI bleed include Melena or dark, tarry stool that is almost black in color, pale skin, Nausea, vomiting blood, shortness of breath, sweating, alterations of consciousness, and epigastric and diffuse abdominal pain.

    The major causes of upper GI bleeding include: peptic ulcer bleeding,  erosive esophagitis and erosive gastritis, esophageal inflammation due to acid reflux, esophageal varicies, or abnormally dilated vessels; typically seen in patients with portal hypertension and chronic liver disease and these patients are at an increased risk for hemorrhage. also, Mallory-Weiss syndrome (caused by violent coughing or vomiting; results in a tear of mucous membrane most commonly were stomach and esophagus meet).                                                                    Patients in shock due to trauma, sepsis, or organ failure can also have upper GI bleeds as a result of erosions occurring in the presence of decreased blood flow and altered acidity of the gastric lumen, and cancer.

    Common risk factors for upper GI bleeding include:  prior upper GI bleeding, anticoagulant use, high-dose nonsteroidal anti-inflammatory drug use, and older age.

    The most common conditions associated with lower GI bleeding include diverticulitis, infections, polyps, inflammatory bowel disease, hemorrhoids, anal fissures, and cancer.

    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:

    Diverticula are small, bulging pouches that can form in the lining of your digestive system. They are found most often in the lower part of the large intestine (colon).                                   Diverticula are common, especially after age 40, and seldom cause problems. The presence of diverticula is known as diverticulosis. When one or more of the pouches become inflamed, and in some cases infected, that condition is known as diverticulitis.

    Diverticulitis can cause severe abdominal pain, fever, nausea, and a marked change in your bowel habits. Mild diverticulitis can be treated with rest, changes in your diet, and antibiotics.

    The signs and symptoms of diverticulitis include pain, which may be constant and persist for several days.  The lower left side of the abdomen is the usual site of the pain. Sometimes, however, the right side of the abdomen is more painful, especially in people of Asian descent.                                                                                                                                                         Other symptoms include nausea and vomiting, Fever, Abdominal tenderness, Constipation, or diarrhea.

    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]

In this exercise, you will complete a 10- to 20-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

Photo Credit: Getty Images

Complete the Knowledge Check By Day 7 of Week 5

To complete this Knowledge Check:

Module 3 Knowledge Check

 

What’s Coming Up in Module 4?

Photo Credit: [BrianAJackson]/[iStock / Getty Images Plus]/Getty Images

In Module 4, you will analyze processes related to endocrine disorders. To do this, you will analyze alterations in the relevant systems and the resultant disease processes. You will also consider patient characteristics, including racial and ethnic variables, that may impact physiological functioning and altered physiology.

Week 6 Knowledge Check: Endocrine Disorders

In the Week 6 Knowledge Check, you will demonstrate your understanding of the topics covered during Module 4. This Knowledge

NURS 6501 Knowledge Check Gastrointestinal and Hepatobiliary Disorders

NURS 6501 Knowledge Check Gastrointestinal and Hepatobiliary Disorders

Check will be composed of a series of questions related to specific scenarios provided. It is highly recommended that you review the Learning Resources in their entirety prior to taking the Knowledge Check, since the resources cover the topics addressed. Plan your time accordingly.

Also, during this week you will take your Midterm Exam. Please make sure to finalize and complete your Knowledge Check prior to completing your exam.

Next Module

To go to the next Module:

Module 4

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

Week 5: Concepts of Gastrointestinal and Hepatobiliary Disorders

Patients of gastrointestinal and hepatobiliary disorders often face life-altering changes, including changes to diet, new treatment regimens, and more. For some disorders, treatments can include surgery.

Gastrointestinal conditions, such as ulcers, diverticulitis, and pancreatitis, often cause varying levels of pain and discomfort. Hepatobiliary conditions can also bring significant changes to patient routines and well-being.

This week, you examine fundamental concepts of gastrointestinal and hepatobiliary disorders. You explore common disorders in these categories, and you apply the key terms and concepts that help communicate the pathophysiological nature of these issues to patients.

Learning Objectives

Students will:

  • Analyze concepts and principles of pathophysiology across the life span

Learning Resources

Required Readings (click to expand/reduce)

 

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

 

Document: NURS 6501 Midterm Exam Review (PDF document) 

 

Note: Use this document to help you as you review for your Midterm Exam in Week 6.

 

Required Media (click to expand/reduce)

 

Module 3 Overview with Dr. Tara Harris 

Dr. Tara Harris reviews the structure of Module 3 as well as the expectations for the module. Consider how you will manage your time as you review your media and Learning Resources throughout the module to prepare for your Knowledge Check. (2m)

Concepts of Gastrointestinal and Hepatobiliary Disorders – Week 5 (15m)

Liver Function Tests

MedCram. (2013, April 14). Liver function tests LFTs explained clearly by MedCram.com [Video file]. Retrieved from https://www.youtube.com/watch?v=bFdTgty0T0I

Note: The approximate length of the media program is 11 minutes.

 

Liver Diseases

MedCram. (2019, May 15). Diagnosis of key liver diseases: Hepatitis A, B C vs. alcoholic vs. ischemic (AST vs ALT labs) [Video file]. Retrieved from https://www.youtube.com/watch?v=ZZRHA2JvCGA 

Note: The approximate length of the media program is 13 minutes.

 

Liver Pathophysiology

MedCram. (2013, April 9). Liver explained clearly: Pathophysiology, LFTs, hepatic diseases  [Video file]. Retrieved from https://www.youtube.com/watch?v=BTGkB8nOu7g

Note: The approximate length of the media program is 14 minutes.

 

Online Media from Pathophysiology: The Biologic Basis for Disease in Adults and Children

In addition to this week’s media, it is highly recommended that you access and view the resources included with the course text, Pathophysiology: The Biologic Basis for Disease in Adults and Children. Focus on the videos and animations in Chapters 41 and 42 that relate to the hepatobiliary system. Refer to the Learning Resources in Week 1 for registration instructions. If you have already registered, you may access the resources at https://evolve.elsevier.com/

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