NURS 6501 Knowledge Check: Gastrointestinal and Hepatobiliary Disorders
Walden University NURS 6501 Knowledge Check: Gastrointestinal And Hepatobiliary Disorders-Step-By-Step Guide
This guide will demonstrate how to complete the Walden University NURS 6501 Knowledge Check: Gastrointestinal And Hepatobiliary Disorders assignment based on general principles of academic writing. Here, we will show you the A, B, Cs of completing an academic paper, irrespective of the instructions. After guiding you through what to do, the guide will leave one or two sample essays at the end to highlight the various sections discussed below.
How to Research and Prepare for NURS 6501 Knowledge Check: Gastrointestinal And Hepatobiliary Disorders
Whether one passes or fails an academic assignment such as the Walden University NURS 6501 Knowledge Check: Gastrointestinal And Hepatobiliary Disorders depends on the preparation done beforehand. The first thing to do once you receive an assignment is to quickly skim through the requirements. Once that is done, start going through the instructions one by one to clearly understand what the instructor wants. The most important thing here is to understand the required format—whether it is APA, MLA, Chicago, etc.
After understanding the requirements of the paper, the next phase is to gather relevant materials. The first place to start the research process is the weekly resources. Go through the resources provided in the instructions to determine which ones fit the assignment. After reviewing the provided resources, use the university library to search for additional resources. After gathering sufficient and necessary resources, you are now ready to start drafting your paper.
How to Write the Introduction for NURS 6501 Knowledge Check: Gastrointestinal And Hepatobiliary Disorders
The introduction for the Walden University NURS 6501 Knowledge Check: Gastrointestinal And Hepatobiliary Disorders is where you tell the instructor what your paper will encompass. In three to four statements, highlight the important points that will form the basis of your paper. Here, you can include statistics to show the importance of the topic you will be discussing. At the end of the introduction, write a clear purpose statement outlining what exactly will be contained in the paper. This statement will start with “The purpose of this paper…” and then proceed to outline the various sections of the instructions.
How to Write the Body for NURS 6501 Knowledge Check: Gastrointestinal And Hepatobiliary Disorders
After the introduction, move into the main part of the NURS 6501 Knowledge Check: Gastrointestinal And Hepatobiliary Disorders assignment, which is the body. Given that the paper you will be writing is not experimental, the way you organize the headings and subheadings of your paper is critically important. In some cases, you might have to use more subheadings to properly organize the assignment. The organization will depend on the rubric provided. Carefully examine the rubric, as it will contain all the detailed requirements of the assignment. Sometimes, the rubric will have information that the normal instructions lack.
Another important factor to consider at this point is how to do citations. In-text citations are fundamental as they support the arguments and points you make in the paper. At this point, the resources gathered at the beginning will come in handy. Integrating the ideas of the authors with your own will ensure that you produce a comprehensive paper. Also, follow the given citation format. In most cases, APA 7 is the preferred format for nursing assignments.
How to Write the Conclusion for NURS 6501 Knowledge Check: Gastrointestinal And Hepatobiliary Disorders
After completing the main sections, write the conclusion of your paper. The conclusion is a summary of the main points you made in your paper. However, you need to rewrite the points and not simply copy and paste them. By restating the points from each subheading, you will provide a nuanced overview of the assignment to the reader.
How to Format the References List for NURS 6501 Knowledge Check: Gastrointestinal And Hepatobiliary Disorders
The very last part of your paper involves listing the sources used in your paper. These sources should be listed in alphabetical order and double-spaced. Additionally, use a hanging indent for each source that appears in this list. Lastly, only the sources cited within the body of the paper should appear here.
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Sample Answer for 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).
Also Read:
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Question:
- If the client asks what causes GERD how would you explain this as a provider?
Your Answer:
The patient in the case study has GERD. I would inform her that several factors cause GERD. One of the aspects that I will educate her is that GERD is a condition that develops following the ulceration of the mucosal lining that protects the esophagus. One of the causes of the disorder is Zollinger-Ellison syndrome, which increases the release of gastric acid. Zollinger-Ellison syndrome is characterized by the presence of multiple duodenal or pancreatic tumors that increase gastric acid secretion (Maret-Ouda et al., 2020).
The other cause of GERD that the patient should be aware is the prolonged use of NSAIDs. NSAIDs inhibit the synthesis of protective prostaglandins. They also lower the production of bicarbonates and mucus while increasing the secretion of hydrochloric acid. The other factor is smoking. Smoking suppresses the production of prostaglandins, mucus for protection, and weakens the esophageal sphincter. Increased use of irritants such as coffee and alcohol also play a crucial role (Katz et al., 2022). The irritation acts as a source of stress that degrade the protective mucosa and increase the production of destructive gastric acid.
The other cause is any form of stress. Stressors such as hospitalization and life experiences also act as a source of GERD. Any stressors increase the production of gastric acid. The risk of GERD increases if the patient already has other risk factors for GERD and or peptic ulcer disease. The additional risk factors that should be addressed to prevent GERD include obesity, hiatal hernia, esophageal contractions, prolonged or reduced stomach emptying, and abnormalities of esophageal sphincter (Maret-Ouda et al., 2020).
References
Katz, P. O., Dunbar, K. B., Schnoll-Sussman, F. H., Greer, K. B., Yadlapati, R., &Spechler, S. J. (2022). ACG Clinical Guideline for the Diagnosis and Management of Gastroesophageal Reflux Disease. The American Journal of Gastroenterology, 117(1), 27–56. https://doi.org/10.14309/ajg.0000000000001538
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.2020.21360Links to an external site.
Sample Answer 2 for NURS 6501 Knowledge Check: Gastrointestinal And Hepatobiliary Disorders
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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
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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.
Musculoskeletal, metabolic, and multisystem health dysfunctions represent one of the most challenging health conditions that may have a complex challenge to the affected patient (Beefcroft & Hough, 2016). Symptoms of these conditions may range in severity. Musculoskeletal complications can affect the muscle, bone, tendons and joints. A major symptom that patients encounter is pain. Conditions may range from the ones that are sudden and short-lived to the ones that are lifelong and are associated with disability as well as ongoing pain. Among the notable changes that a patient with this condition may experience include persistent pain as well as mobility limitations. In this, the patients who may suffer from the long-term condition may experience severe pain that may be related to the wearing out of the tendons. For some patients with complex conditions, they may experience joint deformity that may be a long term condition, and it may be relatively challenging to treat it. When these abnormal changes occur, the involved patient may find it hard to handle some of the changes in weight, thus affecting some parts of the body (Black, 2016). Although musculoskeletal conditions may arise in many forms as well as a result of different factors, there are many ways that the situation may represent itself. The identification of specific symptoms of the disorder plays an essential role in the development of an approach to assist in the management of the stated condition.
Questions:
1. Explain what contributed to the development from this patient’s history of PUD?
Selected Answer: PUD is defined as an ulcer in the mucosal lining of the lower esophagus, stomach, or duodenum. This patient has a number of risk factors for developing peptic ulcer disease. Patient’s age of 65, daily use of NSAIDs for osteoarthritis pain, high stress due to an impending divorce, working, and managing two homes are all factors. The patient smokes and consumes alcohol on a daily basis. Coffee consumption could also be a factor in PUD. Her positive urease breath test also indicates the presence of H. pylori infection.
Ibuprofen suppresses mucosal prostaglandin synthesis, resulting in decreased bicarbonate secretion and mucin production. Mucin is a component of the gut barrier, and bicarbonate acts as a buffer against HCl. As a result, HCl secretion is increased. Because both NSAIDS and H. Pylori disrupt the integrity of the mucosa, their interaction can contribute to the pathogenesis of peptic ulcers. Submucosal areas are exposed to gastric secretions and autodigestion, resulting in 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
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
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] -
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?
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: 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
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: 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:
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- 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
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
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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
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
Note: The approximate length of the media program is 11 minutes.
Liver Diseases
Note: The approximate length of the media program is 13 minutes.
Liver Pathophysiology
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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User | |
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Course | NURS-6501N-32-Advanced Pathophysiology-2021-Summer-QTR-Term-wks-1-thru-11-(05/31/2021-08/15/2021)-PT27 |
Test | Module 5 Knowledge Check |
Started | 7/12/21 6:50 PM |
Submitted | 7/14/21 10:17 AM |
Due Date | 7/19/21 1:59 AM |
Status | Completed |
Attempt Score | 20 out of 20 points |
Time Elapsed | 39 hours, 27 minutes |
Results Displayed | All Answers, Submitted Answers, Correct Answers, Feedback, Incorrectly Answered Questions |
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Question 1
Damage to an upper motor neuron will cause muscle ________________________
Selected Answer: spasticity
Answers: spasticity
flaccidity
tremor
paralysis
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Question 2
Neurons need insulin in order to take in glucose.
Selected Answer: False
Answers: True
False
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Question 3
Stimulation of the parasympathetic nervous system would cause:
Selected Answer: Contraction of bladder detrusor muscle, bradycardia, and increased salivation
Answers: Increased diameter of pupils, dry mouth, and increased plasma free fatty acids
Contraction of bladder detrusor muscle, bradycardia, and increased salivation
Decreased diameter of pupils, dry mouth, and decreased plasma free fatty acids
Relaxation of bladder detrusor muscle, tachycardia, and increased salivation
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Question 4
Inflammation of the eyelid is best described as:
Selected Answer: Blepharitis
Answers: Keratitis
Blepharitis
Chalazion
Entropion
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Question 5
Neurons with cell bodies in the substantia nigra use _______________ as a neurotransmitter.
Selected Answer: dopamine
Answers: norepinephrine
epinephrine
dopamine
serotonin
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Question 6
Muscle protein that stores oxygen is called:
Selected Answer: Myoglobin
Answers: Epiphysis
Myoglobin
Hyaluronate
Diaphysis
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Question 7
Brain system that includes the amygdala, hippocampus, and thalamus is called:
Selected Answer: Limbic
Answers: Axon
Dendrite
Limbic
Myelin
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Question 8
Damage to the cerebellum will cause what symptoms?
Selected Answer: intention tremor and ataxic gait
Answers: resting tremor and ataxic gait
resting tremor and shuffling gait
intention tremor and ataxic gait
intention tremor and shuffling gait
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Question 9
Visual, sensory, or motor symptoms that may last up to an hour prior to the onset of a headache is called:
Selected Answer: Migraine aura
Answers: Headache phase
Migraine aura
Premonitory phase
Recovery phase
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Question 10
Involuntary slow, twisting, writhing movement is called:
Selected Answer: Athetosis
Answers: Athetosis
Apraxia
Aphasia
Agnosia
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Question 11
Which substances inhibit bone re absorption?
Selected Answer: Osteoprotegerin (OPG) and estrogen
Answers: Osteoprotegerin (OPG) and estrogen
Prostaglandin E2 (PGE2) and tumor necrosis factor-a (TNF-a)
Osteoprotegerin (OPG) and t umor necrosis factor-a (TNF-a)
Prostaglandin E2 (PGE2) and estrogen
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Question 12
A neuron extension that carries impulses toward the cell body is called:
Selected Answer: Dendrite
Answers: Axon
Dendrite
Limbic
Myelin
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Question 13
Which of the following conditions are have an autoimmune cause?
Selected Answer: Lichen planus and lupus erythematosus
Answers: Lichen planus and lupus erythematosus
Erysipelas and impetigo
Tinea pedis and candidiasis
Erysipelas and candidiasis
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Question 14
Impaired recognition of tactile, visual, or auditory stimuli is called:
Selected Answer: Agnosia
Answers: Athetosis
Apraxia
Aphasia
Agnosia
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Question 15
Which of the following conditions are have a bacterial cause?
Selected Answer: Erysipelas and impetigo
Answers: Lichen planus and lupus erythematosus
Erysipelas and impetigo
Tinea pedis and candidiasis
Erysipelas and candidiasis
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Question 16
Immune defenses against bacteria and viruses are increased by:
Selected Answer: fever
Answers: platelets
fever
chills
inflammation
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Question 17
Changes in the pupils are useful to evaluate the function of what area of the brain?
Selected Answer: brainstem
Answers: grey matter
corticol
brainstem
white matter
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Question 18
What brain structure is responsible for the thermoregulation and heat production in the body?
Selected Answer: hypothalamus
Answers: hypothalamus
thalamus
cerebellum
pons
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Question 19
Inability to perform purposeful or skilled motor actions is called:
Selected Answer: Apraxia
Answers: Athetosis
Apraxia
Aphasia
Agnosia
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Question 20
During what stage of sleep is growth hormone released?
Selected Answer: slow-wave
Answers: Stage N1
REM sleep
slow-wave
Stage N2
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:
- 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
- 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:
- 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:
- 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.
Sample Answer for NURS 6501 Knowledge Check: Gastrointestinal And Hepatobiliary Disorders
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:
- What are the variables here that contribute to an upper GI bleed?
Your Answer:
The patient in the case study has a potential diagnosis of upper GI bleed. Several variables contribute to the development of the upper GI bleed. One of the variables is peptic ulcer bleeding. Patients with chronic ulcers are increasingly at a risk of developing upper GI bleed. The bleed arises from severe destruction of the protecting mucosal layer by gastric secretions. The other variable is gastritis. The irritation and inflammation of the gastric mucosa increase the risk of its destruction by gastric acid(Graham & Carlberg, 2019). Over time, gastritis causes upper GI bleed due to the destruction of the mucosal barrier in esophagus and stomach.
The other variable associated with upper GI bleed is esophagitis. Esophagitis refers to the inflammation of the esophagus. The inflammation occurs from the different irritants to the esophageal mucosa. Chronic inflammation may cause altered mucosa integrity and damage from gastric reflux, hence, the development of upper GI bleed. The other variable is esophageal varices. Esophageal varices are inflamed veins within the esophagus. The varices are highly prone to rupture when exposed to stressors such as straining or irritants(Leebeek& Muslem, 2019). Rupture of the veins cause upper GI bleeding, hence, a potential cause of the client’s problem in this case study.
The other variable contributing to upper GI bleed that should be considered in the client is Mallory-Weiss syndrome. Mallory-Weiss syndrome causes tears and bleeding from the stomach or esophageal lining. Cancer of the upper GI also may contribute to upper GI bleed. For example, cancers of the stomach or esophagus may cause rupture of the blood vessels, resulting in the upper GI bleed(Graham & Carlberg, 2019). Consequently, these potential causes should be ruled out through comprehensive diagnostics in the patient’s care.
References
Graham, A., & Carlberg, D. J. (2019). Gastrointestinal Emergencies: Evidence-Based Answers to Key Clinical Questions. Springer.
Leebeek, F. W. G., & Muslem, R. (2019). Bleeding in critical care associated with left ventricular assist devices: Pathophysiology, symptoms, and management. Hematology, 2019(1), 88–96. https://doi.org/10.1182/hematology.2019000067