GI Case Study

Re: Week 10 Discussion 1: GI Case Study


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Week 10 Discussion: Case Study D: Chron’s Disease

Mr. P.T. is a 19-year-old who has Chron’s disease that has been affecting the ileum and part of the jejunum for the past five years. Several extended family members of Mr. P.T. have a history of Chron’s disease. The purpose of this discussion is to describe the pathophysiology of Chron’s disease, describe the common signs of an exacerbation, and to explain how nutritional deficits may occur with Chron’s disease.

  1. Describe the pathophysiology of Chron disease.

Chron disease is a gastrointestinal tract disorder that affects any area of the digestive tract. It most commonly occurs in the small intestine in the terminal ileum and occasionally in the ascending colon. Skip lesions, or inflammation that occurs in segments separated by normal tissue, are present in Chron’s disease. In the first stages inflammation occurs in the mucosal layer along with development of shallow ulcers. These ulcers then combine to form fissures that are separated by thickened nodules that give the wall of the digestive tract a cobblestone effect. The inflammation and fibrosis may be transmural, or affecting all layers of the wall, which leads to a thickened wall. These changes leave a narrow lumen that may become obstructed. Chronic inflammation and granulomas may be found in the wall and lymph nodes. These changes that occur damage the wall and impairs the ability of the small intestine so that they are unable to process and absorb food. The inflammation that occurs increases the mobility of the intestine which does not allow for adequate time for digestion and absorption. Decreased digestion and absorption may lead to hypoproteinemia, malnutrition, nutritional deficiencies, and fatty stools or steatorrhea. Complications that commonly occur are adhesions between two loops of the intestine, penetrating ulcers through the intestinal wall causing abscesses, fissures, and fistulas. The fistulas that occur are seen in the loops of the intestine, the intestine, the bladder, the intestine, and the skin (VanMeter & Hubert).

  1. Describe the common signs of an exacerbation.

Symptoms of Chron’s disease vary from patient to patient (VanMeter & Hubert, 2018). In a person with Chron’s disease, such as Mr. P.T., who is having an exacerbation, typical presenting symptoms include right lower quadrant abdominal pain, flatulence, bloating, diarrhea, fatty stools, stools with mucus and blood, fever, weight loss, and anemia. In a severe case, perianal abscesses, perianal inflammation and nodules, and fistulas can be present. If the small bowel is involved in this condition, diarrhea, malabsorption, weight loss, abdominal pain, anorexia, and frequent urinary tract infections and abnormal vaginal discharge due to fistulas may be present. There are also symptoms that can occur outside of the gastrointestinal tract including inflammation in the eye, eye redness and blurred vision, painful sores in the mouth, gallstones, and arthritis (Ranasinghe & Hsu, 2017). Malabsorption and malnutrition may occur causing anorexia, weight loss, anemia, and fatigue. Children who are suffering from Chron disease experience delayed growth and sexual maturation. This is due to the lack of protein and vitamins, such as the fat soluble vitamins A and D. Due to the presenting symptoms and burden of this chronic illness, psychological conditions may arise (VanMeter & Hubert, 2018).

  1. Explain how nutritional deficits may occur with Chron disease.

Malnutrition is common in people with Chron’s disease due to reduced oral intake, malabsorption, and nutrient losses through the gut. Voluntary food restrictions, satiety, decreases pleasure related to eating, changes in mood, and medical advice that aim to reduce symptoms are factors that can lead to malnutrition. Dietary restrictions include a reduction in dairy and some fruits and vegetables, appetite sensation decrease, satiety, and inadequate food intake contribute to nutritional deficiencies seen in the population with Chron’s disease. The most common deficiencies are in micronutrients, such as iron, copper, selenium, magnesium, zinc, vitamins, and antioxidants. The top contributors to malnutrition are malabsorption and the symptoms that are experienced (Cioffi et al. 2020). Inflammation and damage in the digestive tract are to blame for malabsorption. Symptoms, such as abdominal pain and diarrhea are examples of symptoms that cause malnutrition (VanMeter & Hubert, 2018).

Mr. P.T. is one of the estimated 3 million Americans that suffers from an inflammatory bowel disease in the form of Chron’s disease (CDC, 2020). As an APRN, understanding the pathophysiology, the presenting symptoms, and the nutritional deficiencies is important in order to treat this population and create better health outcomes.


CDC. (2020, August 11). Inflammatory bowel disease prevalence (IBD) in the United States.

Cioffi, I., Imperatore, N., Di Vincenzo, O., Pagano, M. C., Santarpia, L., Pellegrini, L., … & Pasanisi, F. (2020). Evaluation of nutritional adequacy in adult patients with Crohn’s disease: a cross-sectional study. European Journal of Nutrition, 1-12.

Ranasinghe, I. R., & Hsu, R. (2017). Crohn disease.

VanMeter, K.C., & Hubert, R.J. (2018). Gould’s pathophysiology for the health professions. (6th ed.). Elsevier Saunders

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In reply to Michelle Valdez

Re: Re: Week 10 Discussion 1: GI Case Study

by Sarah Bishop – Tuesday, 3 November 2020, 4:14 PM

Thank you for your post on Crohn’s disease. The problems that Crohn’s disease leads to are an impaired ability of the damaged intestines to absorb food and interference with digestion which leads to hypoproteinemia, avitaminonis, malnutrition, and steatorrhea (Hubert & VanMeter, 2018). If the ulcers penetrate the intestinal walls, abscesses will form, as well as fistulas as the walls of the intestines erode (Hubert & VanMeter, 2018). The most common symptom of Crohn’s disease is chronic diarrhea, but as you pointed out, symptoms may vary (Lichenstein, 2017). Also common is abdominal pain, localized in the right quadrant, and fatigue, which may arise from inflammation, anemia, and malnutrition (Lichenstein, 2017). To diagnose Crohn’s, patient history, laboratory data, pathology findings, and endoscopic and radiographic tests are all used. The presence of chronic intestinal inflammation solidifies the diagnosis (Lichenstein, 2017). NSAIDS and cigarette smoking can exacerbate Crohn’s disease and should be avoided. Management of stress, depression, and anxiety should be.a part of the comprehensive care of a Crohn’s patient. Corticosteroids can be used to alleviate symptoms short-term, but is not recommended for long-term use (Lichenstein, 2017). Therapeutic treatments are based on the disease location, disease severity, complications, and future disease prognosis (Lichenstein, 2017). Therapeutic interventions are on a continuum to treat the acute phase of the disease, to induce remission, and then maintain remission. The patient needs to be monitored closely during initial therapy in order to evaluate response to treatment. For patients at low risk of progression, treatment of symptoms with anti-diarrheals and dietary manipulation is acceptable. For mild to moderate disease, sulfasalazine and budenoside have been shown to be effective at treating symptoms and inducing remission (Lichenstein, 2017).


Hubert, R. & VanMeter, K. (2018) Gould’s Pathophysiology for the Health Professions. 6th ed.


Lichenstein, G., Loftus, E., Isaacs, K., Regueiro, M., Gerson, L., & Sands, B. (2017) ACG clinical guideline: Management of Crohn’s disease in adults. The American Journal of Gastroenterology, 113. 481-517. doi:10.1038/ajg.2018.27

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Re: Re: Re: Week 10 Discussion 1: GI Case Study

by Johana Hurst – Tuesday, 3 November 2020, 4:54 PM


Week 10 Discussion

Case Study: Gastroenteritis

The purpose of this discussion is to describe the physiological changes that occur in an infant diagnosed with gastroenteritis caused by a food borne illness. This discussion will cover signs and symptoms of dehydration, management of dehydration in the child and a set of arterial blood gases that can be expected from a child with severe dehydration resulting from manifestations of gastroenteritis illness.

  1. Briefly describe how S. aureus in the custard could cause vomiting and


  1. aureus bacteria in the child’s custard can cause illness such as vomiting and diarrhea. People carry S. aureus bacteria on their hands and if food handlers do not properly wash their hands before touching food, then the food can become contaminated with staph and the bacteria can multiple and produce toxins that make people sick (Centers for Disease Control and Prevention, 2018). Endotoxins from the bacteria could have made Baby K. sick due to unsanitary practices from food handlers or from inadequate refrigeration of the custard.
  2. Describe the fluid and electrolyte imbalances that can be expected in Baby K.

The loss of fluid from diarrhea and vomiting is associated with extreme volume depletion or hypovolemia that can result in dehydration and loss of many electrolytes. Electrolyte imbalances seen in Baby K. would include sodium, potassium and bicarbonate. Hyponatremia is the most common electrolyte abnormality encountered in children under 5 with severe dehydration due to acute gastroenteritis (Emmett & Palmer, 2020). When there is significant water and sodium loss from the body, due to vomiting, the relative concentrations of sodium in the fluid compartments of the body change. If the fluid and sodium deficit is not corrected then the low concentration of sodium ions in the intravascular fluid will lower the osmotic pressure within the vascular and interstitial fluids causing the fluid to move from low pressure in the extracellular fluid to an area of high osmotic pressure into cells causing a fluid imbalance (Gould, VanMeter & Hubert, 2018). Hypokalemia and bicarbonate losses result from increased diarrhea. Low serum bicarbonate in hypovolemia can cause acid-base imbalances resulting in metabolic acidosis. In children with gastroenteritis, the acidosis is due to the loss of bicarbonate in the stool (Somers, 2020).

  1. What arterial blood gas levels would you expect to find in this child with


Duodenal secretions contain large quantities of bicarbonate ions. Metabolic acidosis can occur when bicarbonate ions are lost in the stool from diarrhea and lack of fluid and glucose absorption (Hubert & VanMeter, 2018). Dehydration and decreased blood volume can lead to decreased excretion of acids by the kidneys. This increased amount of acids in the blood then bind with bicarbonate buffer and result even more of a serum bicarbonate deficit and decreased serum pH causing metabolic acidosis (Hubert & VanMeter, 2018).

Decompensated Metabolic Acidosis

pH: 7.31 (7.35-7.45)

PCO2: 30 (35-45)

HCO3: 14 (22-26)

  1. Describe the signs of dehydration that can be expected in a child.

Some of the signs of dehydration expected in a child depend on the degree of hypovolemia. In mild hypovolemia, clinical signs are minimal and can include a reduction in urine output. Moderate hypovolemia can result in tachycardia, decreased in blood pressure, decreased skin turgor, dry mucous membranes, irritability, decreased peripheral perfusion as evidenced by a delay in capillary refill, deep respirations, and decreased urine output. In babies, a decrease in number of wet diapers, sunken fontanels and decreased tearing are signs of moderate dehydration (Sombers, 2020). In severe dehydration, in which there is a >10 percent of volume loss, children will exhibit in a near shock presentation with hypotension, decreased peripheral perfusion with a capillary refill >3 seconds, cool and mottled extremities, lethargy, and deep increased respirations (Sombers, 2020; Hubert & VanMeter, 2018).

  1. Explain the process and factors involved by which a young child can quickly

develop vascular collapse if vomiting and diarrhea are severe.

Children are at increased risk for severe hypovolemia and vascular collapse compared with adults because they have higher insensible losses due to a greater surface area-to-volume ratio and lack sufficient fluid reserves and ability to conserve fluids quickly. Infants also require an increased need for fluid/water due to their higher metabolic rate (Hubert & VanMeter, 2018).  When the vascular compartment is quickly depleted in children, it can profoundly affect their heart, brain, and kidneys.

  1. Explain why water alone would not be adequate treatment for Baby K.

In the treatment of Baby K, fluid repletion with water alone may not be adequate treatment if there are major electrolyte imbalances resulting from ongoing vomiting and diarrhea. For example, when hypovolemia is associated with alterations in serum sodium, attention must be paid to correction of the serum sodium concentration. Careful correction is needed to avoid excessive shifts of water between fluid compartments (Hubert & VanMeter, 2018). To adequately treat dehydration and volume depletion, electrolytes as well as fluid must be replaced.


Center for Disease Control and Prevention (2018). Staphylococcal (Staph) Food Poisoning. Retrieved from:

Emmett, M. & Palmer, B. F. (2020) Acid-base and electrolyte abnormalities with diarrhea. UpToDate. Retrieved on November 2, 2020, from

Hubert, R. J. & VanMeter, K. C., (2018) Gould’s pathophysiology for the health professions. St. Louis, MO: Elsevier Saunders.

Sobers, M. J., (2020). Clinical assessment and diagnosis of hypovolemia dehydration in children. UpToDate. Retrieved on November 2, 2020, from children?search=signs%20of%20dehydration%20in%20children&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H3



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In reply to Michelle Valdez

Re: Re: Week 10 Discussion 1: GI Case Study

by Jonathan Beauchamp – Wednesday, 4 November 2020, 1:26 PM

Week 10: Reply 1

Great post on Crohn’s disease. This disease has a conglomeration of symptoms, many of which mimic other gastrointestinal disorders so accurate and expedient diagnostics are extremely important. This is especially important when attempting to differentiate between fibrosis and inflammation, as these will call for different treatment therapies (Coelho et al, 2017). Diagnostic imaging is used with some success in the past but still did not have the refinement to tell the difference between the two conditions. Contrast-enhanced ultrasound and sonoelastography, an ultrasound method used to estimate soft-tissue’s elasticity versus stiffness. Once accurately diagnosed, the appropriate intervention can be implemented.
Surgery is an intervention used in the treatment of Crohn’s disease. To health effectively from surgery calories, nutrition, is required. As you pointed out many people who suffer from Crohn’s disease suffer from malnutrition. Brennan et al (2018) discuss in their article this very issue and propose that preoperative nutrition be administered to reduce the risk of post-operative complications. They found that post-operative complications dropped from 61% in people with impaired nutrition to 20% in people who received preoperative nutrition.

Brennan, G. T., Ha, I., Hogan, C., Nguyen, E., Jamal, M. M., Bechtold, M. L., & Nguyen, D. L. (2018). Does preoperative enteral or parenteral nutrition reduce postoperative complications in Crohn’s disease patients: a meta-analysis. European journal of gastroenterology & hepatology, 30(9), 997–1002.

Coelho, R., Ribeiro, H., & Maconi, G. (2017). Bowel Thickening in Crohn’s Disease: Fibrosis or Inflammation? Diagnostic Ultrasound Imaging Tools. Inflammatory bowel diseases, 23(1), 23–34.

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Re: Week 10 Discussion 1: GI Case Study

by Jason Carriveau – Monday, 2 November 2020, 9:10 AM

Case Study D: Crohn’s Disease

Case Study Overview

Mr. P.T., age 19, has had Crohn disease, affecting the ileum and part of the jejunum, for 5 years and has had numerous exacerbations. Several members of his extended family have a history of Crohn disease.

Purpose Statement

            The purpose of this forum post is to answer three questions related to the case study above on Crohn disease. I will discuss the pathophysiology, explain possible factors that exacerbate the condition, and describe the common signs of these exacerbations. Answers to these questions will be cited using evidence-based and peer reviewed research.

  1. Describe the pathophysiology of Crohn disease.

Regional ileitis or regional enteritis otherwise known as Crohn disease (CD) is an autoimmune disease that frequently causes inflammation in the small intestine, predominantly in the terminal ilium and occasionally the ascending colon (Evans, 2015; VanMeter & Hubert, 2018). Like most autoimmune diseases the specific etiology of the condition is not fully known. What is known is that there is a distinctive distribution of inflammation that are called skip lesions that separates normal tissue from affected tissues. This progressive inflammation causes a breakdown of the protective mucosal layer, leading to ulcerations. As the disease progresses the inflammation causes physical changes to the tissues within the small intestines including fissures, nodules, fibrosis, granulomas, fistulas and abscesses. The speed of intestinal motility is increased, and malabsorption of nutrition is also prevalent which can lead to malnutrition, hypoproteinemia, avitaminosis, and steatorrhea in some instances (VanMeter & Hubert, 2018).

  1. Suggest several possible exacerbating factors for Crohn disease.

This chronic inflammatory condition has a multitude of acute and chronic complications that require effective and timely management (Tun and colleagues, 2018). One exacerbating factor that precipitates medical intervention is poor sleep quality. A study by Sofia and colleagues (2020) found a strong correlation between poor sleep quality and CD patients with a high risk for exacerbation and hospitalization. Food choices are also a potential exacerbating factor for CD. While the data is inconclusive of specific foods that may cause an acute inflammatory response, there are certain foods that do cause inflammation within the digestive system including milk, simple carbohydrates, and animal protein and need to be eaten with caution (Cope, 2015). It is suggested that individuals with CD start a food diary to pinpoint the specific foods that may exacerbate their condition and slowly ween them from their diet (Cope, 2015). Still another study by Schoultz and colleagues suggests a weak to moderate link between psychological stress and exacerbations of inflammatory bowel diseases (IBD) such as CD. While the overall results of this study were inconclusive, it is suggested that psychological interventions should be addressed as it may help reduce exacerbations (Schoultz et al., 2020).

  1. Describe the common signs of an exacerbation.

Common signs of exacerbation which may or may not be present depending on the acuteness of the exacerbation include peri-umbilical pain with tenderness and guarding upon palpation, hyperactive bowel sounds due to increased motility, fever with increased pulse and respirations, nausea, vomiting, and diarrhea (Evans et al., 2015).


            Crohn disease can be a debilitating ailment for those who live with it. Like many other autoimmune diseases with no definitive cure, people can develop mental health changes such as anxiety and depression due to the inability to cope with the disease long-term. It is important for the advanced practice registered nurse to educate the patient on the disease process as well as provide information on how CD can be exacerbated and strategies that the individual can use to manage it effectively.


Cope, G. (2015). Overview of dietary choices for ulcerative colitis and Crohn’s disease. Gastrointestinal Nursing13(1), 35–41.

Evans, M. M. (2015). Severe Crohn’s Disease: A case study describing standards of care. MEDSURG Nursing, 1–12.

Schoultz, M., Beattie, M., Gorely, T., & Leung, J. (2020). Assessment of causal link between psychological factors and symptom exacerbation in inflammatory bowel disease: a systematic review utilising Bradford Hill criteria and meta-analysis of prospective cohort studies. Systematic Reviews9(1), 1–18.

Sofia, M. A., Lipowska, A. M., Zmeter, N., Perez, E., Kavitt, R., & Rubin, D. T. (2020). Poor sleep quality in Crohn’s Disease is associated with disease activity and risk for hospitalization or surgery. Inflammatory Bowel Diseases26(8), 1251–1259.

Tun, G. S. Z., Cripps, S., & Lobo, A. J. (2018). Crohn’s disease: management in adults, children and young people – concise guidance. Clinical Medicine18(3), 231–236.

VanMeter, K.C., & Hubert, R.J. (2018). Gould’s pathophysiology for the health professions. (6th ed.). Elsevier Saunders.


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Re: Week 10 Discussion 1: GI Case Study

by Leah Loconte – Monday, 2 November 2020, 4:56 PM

Case Study D: Crohn’s Disease

Mr. P.T. is 19 years old and suffers from Crohn’s disease. Crohn’s affects the ileum and part of the jejunum. Mr P.T has been dealing with Crohn’s for 5 years and has had numerous exacerbations. Several members of his extended family have a history as well. The purpose of this post will be to discuss the pathophysiology of Crohn’s disease, exacerbating factors, and signs and symptoms of an exacerbation that could be seen in Mr. P.T.

  1. Describe the pathophysiology of Crohn disease.

    Crohn’s disease is a a common disorder that can affect any area of the digestive tract. Inflammation occurs in a pattern called “skip lesions” (VanMeter & Hubert, 2018). Inflammation starts in the mucosal layer of the digestive tract which then forms fissures or nodules which forms what is known as a cobblestone appearance (VanMeter & Hubert 2018). As the inflammation progressively becomes worse it affects all the layers of the digestive tract which can cause the tract to become completely obstructed. Lesions can occur all the way from the mouth to the anus (Veauthier & Hornecker, 2018). Over time a decrease of digestion and absorption occur which affects the patients overall nutritional status. Complications like loops of bowel, fistulas and fissures can occur in drastic cases of Crohns (VanMeter & Hubert, 2018). Sobczak (2019) reports that Crohn’s is more common in women.

    2. Suggest several possible exacerbating factors for Crohn disease.

    Crohn’s disease is still being studied and unfortunately there are is not one reason that causes it. Crohn’s affects over 3 million Americans worldwide (Crohn’s Foundation). The causes have been narrowed down to genetics, environmental factors, and changes in the microorganisms of the gut (Torres et al., 2017). In relation to genetics, 10-25% of people with irritable bowel disease have a family member with the disease, and over 200 genes have been identified in relation to IBD (Feuerstein, & Cheifetz, 2017). The environmental factors and changes in the microorganisms of the gut include gastrointestinal infections, antibiotics, and nonsteroidal anti-inflammatory drugs have all been shown to be exacerbating factors in patients with Crohn’s (Feuerstein, & Cheifetz, 2017).

    3. Describe the common signs of an exacerbation.

    Signs and symptoms that are common and would occur in Mr. P.T if he was experiencing an exacerbation would be cramping and diarrhea (VanMeter & Hubert, 2018). Other less common symptoms can include rectal bleeding, fever, weight loss and fatigue (Veauthier & Hornecker, 2018). The stool during exacerbations can be soft and not formed, melena can occur as well (VanMeter & Hubert, 2018). Pain and tenderness occur in the abdomen and often in the right lower quadrant and around the belly button (VanMeter & Hubert, 2018).


    Causes of Crohn’s Disease. (n.d.). Retrieved from

    Feuerstein, J. D., & Cheifetz, A. S. (2017). Crohn disease: epidemiology, diagnosis, and management. Mayo Clinic Proceedings, 92(7), 1088+.

    Sobczak, L. L. R. N. C. (2019). Crohn’s disease. Magill’s Medical Guide (Online Edition).

    Torres, J., Mehandru, S., Colombel, J. F., & Peyrin-Biroulet, L. (2017). Crohn’s disease. Lancet (London, England), 389(10080), 1741–1755.

    Veauthier, B., & Hornecker, J. R. (2018). Crohn’s Disease: Diagnosis and Management. American family physician, 98(11), 661–669.

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In reply to Leah Loconte

Re: Re: Week 10 Discussion 1: GI Case Study

by Suzette Dore – Tuesday, 3 November 2020, 4:06 PM

Hi Leah,

The purpose of this reply to respond to your discussion regarding Crohn’s disease.  Crohn’s disease is a common type of inflammatory bowel disease (IBD) and is characterized by inflammation of the mucosal layer that may involve any portion of gastrointestinal tract from the mouth to anus (Peppercorn & Kane, 2019).  The cardinal symptoms of Crohn’s Disease are abdominal pain, diarrhea, with or without bleeding, fatigue, and weight loss. (Peppercorn & Kane, 2019).  According to Qui et al., (2020) people who have Crohn’s disease experience periods of remission and relapse.  Crohn’s disease can be mild, moderate, to severe and treatment depends on severity and personal choice.

Treatment is controversial for Crohn’s disease as the benefits of some medications do not outweigh the adverse effects.  Budesonide is used as the first line treatment management of mild Crohn’s disease of the ileum and proximal colon to induce remission (Regueiro & Hashash, 2020).  Treatment of moderate to severe Crohn’s disease is typically aminosalicylates, however, aminosalicylates are associated with the possibility of developing rare but serious adverse events such as interstitial nephritis, pleuritis, myopericarditis and pancreatitis exists (East et al., 2019).  In children, to maintain remission immunosuppressants such as thiopurines, methotrexate and/ or biologics adalimumab, infliximab are generally used (Dabritz et al., 2017).  According to Lin & Cheifetz, (2018) there are complementary and alternative medicine (CAM) options that include herbal and dietary supplements, probiotics, traditional Chinese medicines, and a variety of mind-body techniques to treat Crohn’s.  Probiotics are among the most popular CAM therapies (Lin & Cheifetz, 2018).  Additional CAM therapies include Curcumin (Tumeric), which has anti-inflammatory and antioxidative properties on human lymphocytes and gut epithelial cell lines, cannabis, fish oil, acupuncture and moxibustion, cognitive physical mind-body therapies, and exercise (Lin & Cheifetz, 2018).

To conclude, Crohn’s disease is a chronic inflammatory bowel disease.  Many treatment options are available to achieve remission and prevent debilitating relapses.  The benefits should outweigh the consequences.  The APRN should establish a trusting provider-patient relationship to provide effective education, treatment options, and management of Crohn’s disease.


Däbritz, J., Gerner, P., Enninger, A., Claßen, M., & Radke, M. (2017). Inflammatory Bowel Disease in Childhood and Adolescence: Diagnosis and Treatment. Deutsches Aerzteblatt International114(19), 331–338.

East, J. E., Boyapati, R. K., Torres, J., Parker, C. E., MacDonald, J. K., Chande, N., & Feagan, B. G. (2019). Controversies in Inflammatory Bowel Disease: Exploring Clinical Dilemmas Using Cochrane Reviews. Inflammatory Bowel Diseases25(1/3/1900), 472–478.

Lin, S. C., & Cheifetz, A. S. (2018). The Use of Complementary and Alternative Medicine in Patients With Inflammatory Bowel Disease. Gastroenterology & hepatology14(7), 415–425.

Peppercorn, M., & Kane, S. (2019, November 13). Clinical manifestations, diagnosis, and prognosis of Crohn disease in adults. Retrieved November 3, 2020, from diagnosis&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H2536922438

Regueiro, M., & Hashash, J. (2020, October 12). Overview of the medical management of mild (low risk) Crohn’s disease in adults. Retrieved November 3, 2020, from diagnosis&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2#H2555882547

Qiu, T., Li, H., Sun, T., Men, P., Cui, X., Liu, C., & Zhai, S. (2020). Thalidomide as a treatment for inflammatory bowel disease in children and adolescents: A systematic review. Journal of Clinical Pharmacy & Therapeutics45(5), 1134–1142.

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Re: Week 10 Discussion 1: GI Case Study

by Sarah Bishop – Monday, 2 November 2020, 6:21 PM

Case Study A: Gastroenteritis

Baby K., age 14 months, has vomiting and diarrhea and is crying continuously because of what appears to be severe abdominal pain. The suspected cause is gastroenteritis attributable to Staphylococcus aureus from milk custard that had not been properly stored.

Gastoenteritis is the inflammation of the stomach and intestines as a result of infection, but sometimes as a result of food reactions (Hubert & VanMeter, 2018). The inflammation of the gastric mucosa and intestines causes vomiting and diarrhea and impaired absorption. Also present is fever, malaise, nausea, and abdominal cramps (Hubert & VanMeter, 2018). Transmission is through contaminated food and water. Often, there are outbreaks from a food and water-borne microorganisms (Hubert & VanMeter, 2018).

Briefly describe how S. aureus in the custard could cause vomiting and diarrhea

Staphylococcus aureus is an enterotoxin that is found in custards, salad dressings, and cold meats when inadequately cooked or refrigerated (Hubert & VanMeter, 2018). S. aureus is a major foodborne pathogen and causes staphylococcus food poisoning when enterotoxins are in ingested food (Carfora, 2015). When the microorganism adheres to the mucosa and secretes the enterotoxins, gastroenteritis develops, leading to the inflammation that causes vomiting and diarrhea (Hubert & VanMeter, 2018).

Describe the signs of dehydration that can be expected in a child.

Dehydration secondary to gastroenteritis is a major cause of morbidity and mortality (Hoxha, 2015). Children quickly develop dehydration and commonly present to the emergency department following gastroenteritis (Hoxha, 2015). A systemic review identified the best signs for assessment of dehydration were prolonged capillary refill time, abnormal skin turgor, and abnormal respiratory pattern (Hoxha, 2015). Clinical features of dehydration include thirst, decreased skin turgor, dry mucous membranes, sunken eyes, and oliguria (Anigilaje, 2018).

Explain the process and factors involved by which a young child can quickly develop vascular collapse if vomiting and diarrhea are severe.

Solute loss in vomiting and diarrhea occurs in an isosmotic fluid that has sodium and potassium concentrations that are less than that of plasma, and loss of these fluids does not directly lower plasma sodium unless water is retained (Anigilaje, 2018). The water retention then leads to an excess of water in relation to sodium in a hyponatremic state. There is a fluid shift from the extracellular fluid to the intracellular fluid due to the loss of extracellular fluid, which leads to vascular collapse. In vascular collapse, urgent circulatory support is required (Anigilaje, 2018).

Anigilaje, E. (2018) Management of diarrhoeal dehydration in childhood: A review for clinicians in developing countries. Frontiers in Pediatrics, 6 (28). Doi:10.3389/fped.2018.00028

Carora, V., Caprioli, A., Marri, N., Sagrafoli, D., Boselli, C., Giacinti, G., Giangolini, G., Sorbara, L., Dottarelli, S., Battisti, A., & Amatiste, S. (2015). Enterotoxin genes, enterotoxin production, and methicillin resistance in Staphylococcus aureas isolated from milk and dairy products in Central Italy. International Dairy Journal, 42. 12-15.

Hubert, R. & VanMeter, K. (2018) Gould’s Pathophysiology for the Health Professions. 6th ed.

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Re: Re: Week 10 Discussion 1: GI Case Study

by Michelle Valdez – Tuesday, 3 November 2020, 4:32 AM


Great information on gastroenteritis. This inflammatory process can be caused by many microorganisms that are transferred through fecally contaminated food and water. A virulent agent or an immunocompromised individual poses a risk for serious illnesses, but most infections remain mild and self-limiting. Many times, these food and water borne illnesses are part of an outbreak with a large number of cases, sometimes including entire communities. Sanitation and food and water safety teaching are an important part of preventing gastroenteritis. Epidemics may occur seasonally, such as rotavirus. The rotavirus infection causes vomiting and watery diarrhea, and on occasion, ulceration and bleeding. The winter months are most common for viral gastroenteritis outbreaks and they are common in day care centers and institutions (VanMeter & Hubert, 2018).

Viral gastroenteritis, such as rotaviruses and noroviruses are the leading cause of gastroenteritis worldwide. Children are most commonly affected and make up 40% of hospital admissions for diarrhea and 200,000 deaths worldwide. Two vaccines were developed in 2006 and were administered in 95 countries in April 2018. There was a 49-89% decrease in rotavirus associated hospitalizations and a 17-55% decline in all gastroenteritis associated hospitalizations among children within two years of the vaccination being administrated. Norovirus is the leading cause of foodborne disease and outbreak of gastroenteritis worldwide. To prevent noroviruses, hand hygiene, limiting contact with confirmed cases of norovirus, and disinfection of contaminated environments are necessary measures. There is no current vaccine for norovirus, but they are in clinical trials. Treatment options for gastroenteritis include treatment of the symptoms, including replacement of fluid and electrolytes (Banyai et al., 2018).

Great post! I look forward to hearing more from you in the future.


Bányai, K., Estes, M. K., Martella, V., & Parashar, U. D. (2018). Viral gastroenteritis. The Lancet, 392(10142), 175-186.

VanMeter, K.C., & Hubert, R.J. (2018). Gould’s pathophysiology for the health professions. (6th ed.). Elsevier Saunders

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In reply to Sarah Bishop

Re: Re: Week 10 Discussion 1: GI Case Study

by Jason Carriveau – Tuesday, 3 November 2020, 5:21 AM

Hi Sarah,
Thank you for your informative post on gastroenteritis in a pediatric patient. The purpose of this response post is to add new information to what you have already provided. As a nurse it is important to have comprehensive knowledge of the body’s anatomy and pathophysiological processes in order to critically think about clinical presentation and differential diagnoses for presenting condition.
In your case study a 14-month old baby has signs and symptoms indicative of gastroenteritis from a Staphylococcus aureus infection as a result of eating milk custard. While this scenario provides one way in which an infant can develop gastroenteritis from a one microorganism, there are a number of organisms that can cause gastroenteritis. A study by Arnold and colleagues (2016) found that water quality played a major role in the development of gastroenteritis among U.S. children swimming in recreational water. The data showed that children aged 0 to 4 and 5 to 10 years were at the highest risk of illness due to poor water quality. The specific microorganisms in this case were enterococcus, campylobacter, salmonella, cryptosporidium, and giardia (Arnold et al., 2016). Rotavirus infection can also cause a form of viral gastroenteritis and is a concern for younger children as well (VanMeter & Hubert, 2018).
While it is important to treat the symptoms, it is also very important to discover whether or not the cause is from a bacteria or virus in order to provide the most effective treatment protocol and decide on the use of antibiotics. Having a complete medical history, clinical exam, and differential diagnoses are important for best serving this patient.


Arnold, B. F., Wade, T. J., Benjamin-Chung, J., Schiff, K. C., Griffith, J. F., Dufour, A. P., Weisberg, S. B., & Colford Jr., J. M. (2016). Acute Gastroenteritis and Recreational Water: Highest Burden Among Young US Children. American Journal of Public Health, 106(9), 1690–1697.

Hubert, R. & VanMeter, K. (2018) Gould’s Pathophysiology for the Health Professions. 6th ed.

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Re: Re: Week 10 Discussion 1: GI Case Study

by Leah Loconte – Tuesday, 3 November 2020, 12:36 PM


Thank you for your case study this week.

When I first think of gastroenteritis I instantly think of vomiting and diarrhea and a patient being miserable with these symptoms. It never occurred to be that a baby age 14 months like baby K could suffer from gastroenteritis as well. I assumed we would call it something different, or it would be due to something other than food. Your case study opened my eyes.

Gastroenteritis as described by VanMeter & Hubert (2018) is when the stomach and intestines go through and inflammatory process due to food or drugs. As I mentioned above signs and symptoms of gastroenteritis are vomiting due to the inflammation of the gastric mucosa, and diarrhea due to increased motility, increased secretions, and impaired absorption (VanMeter & Hubert 2018). After reading your case study I was specifically interested in how we treat children who have a great surface area than adults and dehydrate faster than adults when it comes to gastroenteritis. In the US, 473,832 hospitalizations are related to gastroenteritis every year (Freedman et al., 2020). The success in treating pediatric patients that present with gastroenteritis like baby K and are dehydrated comes from administering Zofran and encouraging the use of oral rehydration. Freedman et al. (2020) contrasted the use of administering Zofran to children presenting to the emergency room with dehydration secondary to gastroenteritis with IV hydration and the results were drastically better when Zofran was used as well. It also gave the oral rehydration an option and decreased inpatient admissions allowing families to go home and treat symptoms. The children in the study were ages 6 months to 18 years of age, so as an FNP it is important to remember to treat all the symptoms of gastroenteritis and look at the picture. As an FNP if I can prevent a patient from being admitted to the hospital that is a top goal.

Thank you for sharing your case study, this really helped me better understand our pediatric population!


Stephen B. Freedman, Sarah Williamson-Urquhart, Anna Heath, Petros Pechlivanoglou, Gareth Hopkin, Serge Gouin, Amy C. Plint, Andrew Dixon, Darcy Beer, Gary Joubert, Christopher McCabe, Yaron Finkelstein, Terry P. Klassen, & on behalf of the KidsCAN-Pediatric Emergency Research Canada (PERC) Innovative Pediatric Clinical Trials DOSE-AGE Study Group. (2020). Multi-dose Oral Ondansetron for Pediatric Gastroenteritis: study Protocol for the multi-DOSE oral ondansetron for pediatric Acute GastroEnteritis (DOSE-AGE) pragmatic randomized controlled trial. Trials, 21(1), 1–13.

VanMeter, K.C., & Hubert, R.J. (2018). Gould’s pathophysiology for the health professions. (6th ed.). St. Louis, MO: Elsevier Saunders. ISBN 9780323414425

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Re: Week 10 Discussion 1: GI Case Study

by Suzette Dore – Monday, 2 November 2020, 8:08 PM

Chapter 17 Case Study A: Gastroenteritis

The purpose of this discussion to provide a summary of, Case Study A: Gastroenteritis, and answer three questions from the case study. In summary, fourteen-month-old Baby K. has been vomiting, diarrhea, and constantly crying.  It appears he may have severe abdominal pain and the suspected cause is gastroenteritis attributed to Staphylococcus aureus from ingesting improperly stored curdled milk.

Briefly describe how S. aureus in the custard could cause vomiting and diarrhea.

Staphylococcus aureus is one of the most important food-borne pathogens globally with milk being an important source of staphylococcal food poisoning (Dai et al., 2019).  Milk is suitable medium for bacterial growth and serve as a source of bacterial contamination (Berhe et al., 2020).  The pathogenicity of S. aureus is enhanced by enterotoxins that are resistant to denaturing conditions such as low pH, low temperature, heating, and digestion by proteolytic enzymes which allows them to remain intact in food or milk, contributing to the high prevalence of staphylococcal food poisoning.  According to Switaj et al., (2015) early onset of vomiting and diarrhea results from ingestion of preformed toxins, most often S. aureus.  S. aureus in the custard can cause vomiting and diarrhea due to an inflammatory response after the invasion of the pathogen in the stomach and intestines.  Inflammation of the gastric mucosa initiated by S. aureus causes vomiting and inflammation of the intestine’s triggering increased motility, impaired absorption, and sometimes increased secretions (Hubert & VanMeter, 2018).

Describe the sings of dehydration that can be expected in a child.

Signs of dehydration that can be expected in a child are increased irritability, lethargy or a change in normal behavior, sunken eyes or dark circles under the eyes, dry mouth and lips, low blood pressure, high heart rate, weak peripheral pulses, reduced elasticity of skin, capillary refill time of more than 2 seconds, urine output less than 1 ml per hour in children or 2 ml per hour in infants, loss of skin color or mottled skin, and/or cooler than usual extremities (Rosengarten, 2019).

Explain why water alone would not be adequate treatment for Baby K.

According to Rosengarten (2019) Children are more likely to experience dehydration than adults because a greater proportion of bodyweight in children is composed of water than in adults.  Electrolytes are lost in both vomiting and diarrhea resulting in acid-base imbalances that may lead to metabolic alkalosis or, with severe vomiting, metabolic acidosis (Hubert & VanMeter, 2018).  Sodium is lost in addition to gastric secretions that are high in chloride ion from vomiting, while diarrhea leads to potassium ion losses (Hubert & VanMeter, 2018).  Water would not be adequate treatment for Baby K because it will not replace the electrolytes that were lost.


Berhe, G., Wasihun, A. G., Kassaye, E., & Gebreselasie, K. (2020). Milk-borne bacterial health hazards in milk produced for commercial purpose in Tigray, northern Ethiopia. BMC Public Health20(1), 894.

Dai, J., Wu, S., Huang, J., Wu, Q., Zhang, F., Zhang, J., Wang, J., Ding, Y., Zhang, S., Yang, X., Lei, T., Xue, L., & Wu, H. (2019). Prevalence and Characterization of Staphylococcus aureus Isolated From Pasteurized Milk in China. Frontiers in microbiology10, 641.

Hubert, J., & VanMeter, K. (2018). ​Goulds Pathophysiology for the Health Professions​ (6th ed.). St. Louis, MO: Elsevier.

Rosengarten, L. (2019). How to manage the care of the dehydrated child. British Journal of Nursing28(21), 1366–1368.

Switaj, T. L., Winter, K. J., & Christensen, S. R. (2015). Diagnosis and Management of Foodborne Illness. American Family Physician92(5), 358–365.

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Re: Week 10 Discussion 1: GI Case Study

by Sandy Leger – Tuesday, 3 November 2020, 7:07 PM

Case Study B. Ulcer and Peritonitis

Ms. X age 76 has been admitted to the emergency department with severe generalized abdominal pain and vomiting. No significant findings were immediately evident to indicate a cause. Six hours later, Ms. X.’s blood pressure began to drop and her pulse was rapid and thread. Exploratory abdominal surgery revealed a perforated gastric ulcer and peritonitis.

1. Describe the process by which an ulcer develops

The development of peptics ulcers begins with a breakdown of the mucosal barrier, which results from an imbalance between the mucosal defense system and forces that are potentially damaging to it (VanMeter & Hubert, 2018). Once acid or pepsin penetrates the mucosal barrier, the tissues are expose to continued damaged because acid diffuses into the gastric wall. Ulcers may erode more deeply into the muscularis and penetrate into the wall (VanMeter & Hubert, 2018). Peptic ulcers can appear in the stomach, duodenum or esophagus. Peptic ulcers occur when peptic acids erode the lining of these organs. A peptic ulcer extends more in-depth into the lining, and it also causes an inflammatory reaction (Deby, 2018).

2. Suggest several possible factors contributing to ulcer formation

Several possible factors may contribute to ulcer formation. The bacteria Helicobacter pylori is a factor but not all persons with H. Pylori infection develop ulcers. H. Pylori are known to secrete cytotoxins and the enzymes protease, phospholipase and urease which all cause damage to mucosal defense (VanMeter & Hubert, 2018). Some other possible factors include increase gastrin secretion, increase vagal stimulation, rapid gastric emptying, increase alcohol, caffeine or certain food, increase glucocorticoid secretion, cigarette smoking and altered eating patterns (VanMeter & Hubert, 2018).

3. Explain why peptic ulcer may not be diagnosed in an early stage of development

Peptic ulcer may not be diagnosed in an early stage of development because the stomach pain may go away. The severe symptoms appear less often. Some individuals with peptic ulcers don’t have any symptoms (Mayoclinic, 2020).

4. Describe the process of perforation of an ulcer and the development of bacterial peritonitis.

Perforation is when the ulcer erodes completely through the wall allowing chime to enter the peritoneal cavity. This process result in chemical peritonitis inflammation of the peritoneal membranes and other structures in the abdomen cavity (VanMeter & Hubert, 2018). This inflammation causes increases permeability of their intestinal wall passage of the bacteria and their toxins in to the peritoneal cavity and bacterial peritonitis (VanMeter & Hubert, 2018).

5. Explain why Ms. X. showed signs of shock. Following surgery, Ms. X. had no bowel sounds and her abdomen was distended.

Ms. X showed signs of shock due to inadequate blood supply by the damage of the mucosal barrier which interferes with the rapid regeneration of the epithelium and the production of sufficient mucus as well as reducing the secretion of the alkaline bicarbonate ions in the protective mucus and reducing secretion of protective prostaglandins (VanMeter & Hubert, 2018).

6. Describe how paralytic ileus could have developed. Ms. X. was given antibiotics, intravenous fluids and intravenous alimentation (total parenteral nutrition).

Paralytic ileus may have developed due to persist inflammation and nerve conduction is impaired and peristalsis decreased leading to obstruction of the intestines (VanMeter & Hubert, 2018).


Deby, F. (2018, November 28). Causes, symptoms and treatment for a Peptic Ulcers.

MayoClinic, 2020. Peptic Ulcer.

VanMeter, K.C., & Hubert, R.J. (2018). Gould’s pathophysiology for the health professions. (6th ed.). Elsevier Saunders

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Re: Re: Week 10 Discussion 1: GI Case Study

by Michelle Valdez – Wednesday, 4 November 2020, 3:09 AM


An estimated 25 million people in the United States suffer from peptic ulcers in their lifetime and 500,000 to 850,000 people suffer from ulcers in a year. One million ulcer associated hospitalizations occur annually and 6,500 deaths are due to peptic ulcers yearly (VanMeter & Hubert, 2018). Peptic ulceration is more common in men than women and lifestyle factors play a role in the formation of these ulcers, making the prevalence in developed countries higher. Many times, genetic factors are involved in duodenal ulcer formation and people with blood type O have an increased risk. Gastric ulcers are common in older individuals with scar tissue and in those who regularly take ulcerogenic anti-inflammatory medications such as aspirins and NSAIDs. An ulcer is developed as mucus penetrating, small, round hollow with surrounding inflammation that may erode deeply into the muscularis and may perforate the wall. This causes bleeding and may lead to hemorrhage and chronic blood loss and blood in the stool. Iron deficiency anemia are indicative of a peptic ulcer. A person with an ulcer presents with epigastric burning or aching pain after meals and at night and the pain resolves with food or with an antacid. Other symptoms that can be present are heartburn, nausea, vomiting, and weight loss. Weight gain may occur in people whose pain is resolved with food intake. An edoscopy, barium x-ray, or biopsy are diagnostic tools. Ulcers are treated with a combination of medications including antimicrobial drugs and acid secretion reducing medications (VanMeter & Hubert, 2018).

As you stated, a paralytic ileus can develop from the persistent inflammation and obstruction of the intestines. A paralytic ileus occurs when there is a decrease or stoppage of flow of intestinal contents. Many times, a patient will suffer from abdominal distention and bloating, pain, nausea, vomiting, inability to pass gas, and inability to tolerate food intake. Bowel rest, intravenous fluid therapy, and NG decompression may be indicated to lower the risk for complications and improve outcomes, but time is needed to heal. Studies have observed the effect of chewing gum to stimulate the cephalocaudal reflex which promotes peristalsis and inhibits inflammation to treat paralytic ileus and this has shown promising outcomes. Most who suffer from this condition will recover and bowel function will return to normal (Beach & De Jesus, 2020).

Great post!


Beach, E. C., & De Jesus, O. (2020). Ileus. StatPearls [Internet].

VanMeter, K.C., & Hubert, R.J. (2018). Gould’s pathophysiology for the health professions. (6th ed.). Elsevier Saunders

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In reply to Sandy Leger

Re: Re: Week 10 Discussion 1: GI Case Study

by Jason Carriveau – Wednesday, 4 November 2020, 10:32 AM

Hi Sandy,

Thank you for your informative post on gastric ulcers and peritonitis in a 76-year-old patient. The purpose of this response post is to add new information to what you have already provided. As a nurse it is critical that we have comprehensive knowledge of the body’s anatomy and pathophysiological processes to critically think about clinical presentations and differential diagnoses for the presenting conditions of our patients.

As your case study presented, the patient was admitted to the emergency department with abdominal pain and vomiting. The diagnosis was deemed to be a perforated gastric ulcer and peritonitis. The perforation of the ulcer was likely the cause of the peritonitis in this case; however, another common cause of peritonitis is from peritoneal dialysis (VanMeter & Hubert, 2018). Peritoneal dialysis is when the peritoneal cavity of the abdomen is used as a semipermeable membrane for the exchange of wastes and electrolytes (VanMeter & Hubert, 2018).

While peritoneal dialysis has made considerable advancements over the last few decades, the risk of peritonitis while decreased is still prevalent at 0.5 episodes per year, or once per year. This is compared to 6 cases per year in the 1960’s (Salzer, 2018). While these are good numbers, the other numbers are that 5% of peritonitis cases end in death, with 16% having peritonitis as a cofactor (Salzer, 2018). In both the case study and peritoneal dialysis, the presentation is the same, but the cause is different and may be a differential diagnosis in patients with kidney failure utilizing peritoneal dialysis. The APRN needs to be aware of these causes and know the presentation of peritonitis to manage the disease quickly and effectively.


Salzer WL. (2018). Peritoneal dialysis-related peritonitis: challenges and solutions. International Journal of Nephrology and Renovascular Diseaseume 11, 173–186.

VanMeter, K.C., & Hubert, R.J. (2018). Gould’s pathophysiology for the health professions. (6th ed.). Elsevier Saunders.


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Re: Re: Week 10 Discussion 1: GI Case Study

by Leah Loconte – Wednesday, 4 November 2020, 12:52 PM


Thank you for your case study on ulcer and peritonitis.

Peptic ulcers are sores that develop in the lining of the stomach, esophagus, and small intestine (George, 2018). These sores form due to stomach acid causing erosion in the tissue. Peptic ulcers are more common in women than men and happen in well developed countries (VanMeter & Hubert, 2018). Many peptic ulcers are due to the bacteria H. Pylori (VanMeter & Hubert, 2018).

As an advanced practitioner it will be very important to be able to determine all different types of gastrointestinal issues that patients present with. Peptic ulcers cause signs and symptoms like epigastric burning and aching pain especially after eating (VanMeter & Hubert, 2018). 5000,000 cases of new ulcers are diagnosed every year in the US (George, 2018). At one time ulcers were thought to be due to stress, spicy foods, and alcohol and the medical treatment was a bland diet and rest, but since then we have learned so much. In a study conducted by George (2018) he reviewed the risk factors of peptic ulcers that most affect people. 76% of the cases were in people over the age of 50, 52.5% of peoples cases were aggravated by food, and 30% of cases included h. pylori. Other risk factors that were common in the study included O blood group, spicy and hot foods, use of NSAIDS, consumption of food at irregular intervals, coffee intake, stress, and taking medications regularly (George, 2018). Understanding all of these risk factors when someone presents with the signs and symptoms of an ulcer can help me as an FNP diagnose an ulcer rather than putting someone through lots of testing. Treating the cause and educating patients on their diet choices will prevent further ulcers and slow symptoms.

As you mentioned in your post sometimes ulcers may not be diagnosed in the early stages because pain may go away and then patients do not bring it to a medical professionals attention. As an FNP if I can educate my patients on ulcer signs and symptoms and what can cause ulcers especially excess NSAID use and alcohol use then that will be an important teaching moment.

Thank you for sharing your case study!


George, F. (2018). Risk Factors of Peptic Ulcer- A Case Control Study. International Journal of Nursing Education, 10(1), 66–71.

VanMeter, K.C., & Hubert, R.J. (2018). Gould’s pathophysiology for the health professions. (6th ed.). St. Louis, MO: Elsevier Saunders. ISBN 9780323414425

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Re: Re: Week 10 Discussion 1: GI Case Study

by Sarah Bishop – Wednesday, 4 November 2020, 5:27 PM

Thank you for your post on ulcers and peritonitis. When peptic ulcers develop, the mucosal barrier breaks down, which results in an imbalance between the mucosal defense system and forces that are potentially damaging to it (Hubert & VanMeter, 2018). Impaired mucosal defenses is a common condition in gastric ulcer development and increased acid secretion is common in duodenal ulcer development (Hubert & VanMeter, 2018). Helicobacter pylori is found in almost everyone with peptic ulcer disease; when this bacteria is eracticated, the ulcer will rapidly heal. This bacteria secretes cytotoxins and enzymes that release ammonia, which damaged the mucosal defenses (Hubert & VanMeter, 2018). Other causes of damage to the mucosal barrier are inadequate blood supply, medications, and ulcerogenic substances such as, aspirin, NSAIDs, and alcohol. Severe stress is linked to ulcer development due to restricted mucosal blood flow and glucocorticoid effects (Hubert & VanMeter, 2018). Symptoms of ulcers include epigastric burning or aching pain is common with ulcers two to three hours after food, which is usually relieved by taking in food or antacids (Hubert & VanMeter, 2018). Endoscopic therapy is more effective than pharmacotherapy alone in regard to initial homeostasis and rebleeding (Satoh, 2016). AFter endoscopic therarpy, medication with antacid agents is recommended for hemorrhagic ulcers. PPI therapy and H.Pylori eradication treatment, which consists of amoxicillin and clarithromycin, are strongly recommended treatments for ulcers (Satoh, 2016).

The Japanese Society of Gastoenterology (2016) Evidence-based clinical practice guidelines for peptic ulcer disease 2015. Journal of Gastroenterology, 51. 177–194. DOI 10.1007/s00535-016-1166-4


VanMeter, K.C., & Hubert, R.J. (2018). Gould’s pathophysiology for the health professions. (6th ed.). Elsevier Saunders

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Re: Week 10 Discussion 1: GI Case Study

by Jonathan Beauchamp – Tuesday, 3 November 2020, 9:05 PM

Case study C: Hepatitis B and Cirrhosis

Hepatitis virus B is a virus that affects the functioning of the liver. Hubert & VanMeter (2018) report that Hepatitis can be either idiopathic, occurring spontaneously, or arising from disease process from infection and/or injury. It is a blood-born pathogen, and to date there is no viral cure for the Hepatitis B virus (Razavi et at, 2018). It is estimated that 3.9% of the world’s population has chronic hepatitis virus infection, the translates to roughly 291,992,000 infections worldwide, and approximately 25% of them will develop cirrhosis or hepatocellular cancer (Inoue & Tanaka, 2016). The World Health Assembly plans to irradicate Hepatitis B, HBV, by 2030. With a relatively long incubation period, roughly 1- 3 months, unknowingly transmitting the virus has high potential.
1. Pathophysiology
Humans are the only hosts for HBV. It is a partially double-stranded DNA virus. This allows for easier attachment to host cell’s DNA because of less nucleotides to bind. It travels to the liver by systemic circulation where it binds to the hepatocytes, the only cells the virus can replicate in. It is this mutation of the hepatocytes that triggers the cell-mediated immune response to destroy the mutant cells causing liver destruction through inflammation and necrosis (Inoue & Tanaka, 2018). Liver destruction also occurs through direct action on the hepatocytes by the virus itself. After 80- 90% of the liver has been destroyed, a cirrhotic condition is present (Hubert & VanMeter, 2018).
Cirrhosis is condition in which the liver has wide spread scaring and loss of lobular organization. This scaring and lack of organization is accompanied by impaired vascularity, so many of the regenerated hepatocytes will not be functional due to lack of blood flow (Hubert & VanMeter, 2018).
2. Treatments for exposure
While the goal of the vaccine is to create immunity within the potential host producing an antibody response to the hepatitis B surface antigen. When exposure happens in a non-vaccinated person, some studies have identified the administration of immunoglobulin within 12 hours of exposure to the virus, but they also recommend receiving the hepatitis B vaccine at the same time (Das et al, 2019), although Lok (2019) says that treatment for an initial acute HBV exposure is mostly supportive because the rate of liver damage is less than 1% in this scenario.
4. Serum markers
During an acute exposure to the HBV, hepatitis B surface antigen, HBsAg, is present in serological studies. This usually occurs 1- 10 weeks after exposure, but if this marker persists to be present after 6 months it indicates chronic infection (Song & Kim, 2016). Along with the presence of HBsAg, HBeAg will be present and is indicative of infectious.

Das, S., Ramakrishnan, K., Behera, S. K., Ganesapandian, M., Xavier, A. S., & Selvarajan, S. (2019). Hepatitis B Vaccine and Immunoglobulin: Key Concepts. Journal of clinical and translational hepatology, 7(2), 165–171.

Hubert, R. J., & VanMeter, K. (2018). Gould’s pathophysiology for the health professions (6th ed.). St. Louis, MO. Elsevier.
Inoue, T., & Tanaka, Y. (2016). Hepatitis B virus and its sexually transmitted infection – an update. Microbial cell (Graz, Austria), 3(9), 420–437.

Lok, A. (2019). Hepatitis B virus: Overview of management. Retrieved from:

Razavi-Shearer, D., Gamkrelidze, I., Nguyen, M. H., Chen, D.-S., Damme, P. V., Abbas, Z., … Razavi, H. (2018). Global prevalence, treatment, and prevention of hepatitis B virus infection in 2016: a modelling study. The Lancet Gastroenterology & Hepatology, 3(6), 383–403.

Song, J. E., & Kim, D. Y. (2016). Diagnosis of hepatitis B. Annals of translational medicine, 4(18), 338.

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In reply to Jonathan Beauchamp

Re: Re: Week 10 Discussion 1: GI Case Study

by Suzette Dore – Wednesday, 4 November 2020, 8:20 PM

Hi Jonathan,

The purpose of this response is to discuss your Hepatitis B and Cirrhosis case study.  I learned that Hep B effects the liver and chronic hepatitis B virus (HBV) infection is the main etiology of hepatocellular carcinoma (HCC) (Wang et al., 2020).  Furthermore, compensated and decompensated liver cirrhosis appears after the progression of chronic HBV and leads to severe complications such as ascites, gastrointestinal-varix bleeding, and hepatic encephalopathy (Zhao et al., 2020).  Untreated patients with decompensated liver cirrhosis typically have a poor prognosis, however, long-term prognosis can be improved with increased levels of symptomatic and supportive therapies, and adhering to prescribed antiviral drugs (Zhao et al., 2020).  The recommended first-line options for the treatment of HBV-caused cirrhosis are entecavir or tenofovir (Shi et al., 2020).  HBV directly affects the liver and can develop into long term serious health problems. Therefore, treatment is key to improving morbidity and mortality.

As you stated, HBV is a blood-born pathogen and there are several risk factors for contracting HBV.  Risk factors for HBV infection include intravenous drug users, blood transfusions, healthcare workers, engaging in unprotected sex with an HBV infected person, people on hemodialysis, as they have a higher prevalence than the general population, and infants are at risk for acquiring HBV from infected women during childbirth (Devinney et al., 2020; Winston et al., 2020; Tufon et al., 2020).  It’s important to consider those who are at high risk of contracting HBV infection to screen and begin treatment as soon as possible to decrease complications.

To conclude, Hepatitis B and Cirrhosis are interconnected.  Although there is no cure for HBV antiviral treatment is available to prevent or delay the onset of cirrhosis and HCC.  As the APRN, family planning education is important regarding promotion of the Hep B vaccine, in addition to, testing for the hepatitis B surface antigen, if indicated, disease education, risk prevention, and exploring treatment options for those who are infected to prevent severe complications and promote health.


Devinney, K., Lazaroff, J., Rosen, J. B., Zimmerman, C. M., & Zucker, J. R. (2020). Use of Capture–Recapture Analysis to Assess Reporting Completeness of Births to Hepatitis B–Positive Women in New York City, 2013-2014. Public Health Reports135(3), 322–328.

Shi, K., Liu, Y., Wang, X., Li, Y., Zhang, Q., Hu, Y., Ran, C., Huang, Y., Hou, J., & Wang, X. (2020). Adjuvant Fuzheng Huayu Capsule Reduces the Incidence of Hepatocellular Carcinoma in Patients with Hepatitis B-Caused Cirrhosis. Evidence-Based Complementary & Alternative Medicine (ECAM), 1–9.

Tufon, K. A., Meriki, H. D., Kwenti, T. E., Tony, N. J., Malika, E., Bolimo, A. F., Kouanou, Y. S., Nkuo-Akenji, T., & Anong, D. N. (2019). HBV Transmission Risk Assessment in Healthcare Workers, Household and Sexual Contacts of HBV Infected Patients in the Southwest Region of Cameroon. Oman Medical Journal34(4), 313–321.

Wang, M., Li, C., Liang, L., Xing, H., Sun, L., Quan, B., Wu, H., Xu, X., Wu, M., Pawlik, T. M., Lau, W. Y., Shen, F., & Yang, T. (2020). Early and Late Recurrence of Hepatitis B Virus‐Associated Hepatocellular Carcinoma. Oncologist25(10), e1541–e1551.

Winston, A., Wurcel, A. G., Gordon, C., & Goyal, N. (2020). Viral hepatitis in patients on hemodialysis. Seminars in Dialysis33(3), 254–262.

Zhao, H., Wang, Q., Luo, C., Liu, L., & Xie, W. (2020). Recompensation of Decompensated Hepatitis B Cirrhosis: Current Status and Challenges. BioMed Research International, 1–7.

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Re: Week 10 Discussion 1: GI Case Study

by Jocelyn Martinez-Johnson – Tuesday, 3 November 2020, 10:37 PM

Case Study B: Ulcer and Peritonitis 

Summary and Purpose Statement

The case is about a female patient admitted to a health facility’s emergency department with severe abdominal pain and vomiting. No immediate significant findings indicated the cause. After some hours, the patient’s blood pressure was low, and the pulse became rapid. It was later established through an exploratory abdominal surgery that the patient was suffering from peritonitis and perforated gastric ulcer. The case explains how cancer develops, the possible factors of exposure, reasons for lack of early detection, the symptoms, and treatment.

The Process by Which the Ulcer Develops

A peptic ulcer is an ulcer that develops, especially in the proximal duodenum. The ulcers appear as tiny and circular cavities with regular margins that pass through the submucosa. After pepsin infiltrates the mucosal barriers, the tissues are laid bare to further injury since acid fans out into the gastric wall (Gilmore, 2013). Ulcers might eat away the tissues more deeply and may eventually puncture the wall.

Possible Factors Contributing to Ulcer Formation

The possible factors that contribute to ulcers are an inadequate supply of blood, excess secretion of glucocorticoid, and acid-pepsin. Insufficient blood supply may be caused by stress, smoking, anemia, age-related circulatory impairment, and scar tissues. Lack of enough blood supply hampers the regeneration of epithelium and inhibits mucus production (Malfertheiner & Ditschuneit, 2012). Besides, it reduces the amount of bicarb ions that help in protecting the body against acidity.

Reasons Why Peptic Ulcer May Not Be Diagnosed in an Early Stage of Development

Aches after meals and at night is a common symptom of most types of ulcers. The cyclic pain is relieved through the ingestion of anti-acids and the consumption of food. People experiencing such symptoms may think they are having heartburn and will not think about it until later when they experience weight loss or vomiting (VanMeter, 2013). One of the initial symptoms of peptic ulcers is iron-deficiency anemia or blood in the stool. This cannot be promptly diagnosed because they are similar to heartburn. In most cases, the patient is hesitant to go for lab tests until the later stages of peptic ulcers.

Description of the Process of Perforation of an Ulcer and the Development of Bacterial Peritonitis

Peritonitis is an inflammation of the peritoneal membranes that may result from chemical irritation or directly from bacterial invasion of the sterile peritoneal cavity (VanMeter & Hubert, 2018). Perforation is a complex effect of an ulcer that takes place when there is an erosion of the ulcer through the wall. The complete erosion through the wall allows the entry of chyme into the peritoneal cavity. The process leads to inflammation of membranes and other abdominal cavities (VanMeter, 2013). The inflammation allows leakage of bacteria into the peritoneal cavity leading to the development of bacterial peritonitis.

Reasons Why Ms. X. Showed Signs of Shock, Had No Bowel Sounds, and The Abdomen Was Distended


The patient was in shock because of the peritoneal membrane infection that shifted to the intestinal blood vessels, leading to hypovolemic shock. The shock occurs because the fluids and proteins are not recycled into the blood (Lancaster-Smith, 2012). Therefore, they do not add any value to the regulation of body fluids. Also, vomiting leads to loss of fluids, which is evident through low blood pressure, reduced skin turgor, dry buccal mucosa and agitation.

Description of How Paralytic Ileus Might Have Developed
When inflammation continues, it impairs different functions of nerves and reduces peristalsis. This leads to the obstruction of the intestines or paralytic ileus. The patient was given antibiotics to reduce the secretion of acids. Intravenous fluids are used to regulate dehydration and to replace electrolytes (Gilmore, 2013). After the surgery and the loss of fluids, the patient needs to feed. However, given that the ulcer is in the digestive system, the consumption of solid foods may lead to further damage to her weak digestive system. Therefore, the patient needs to feed on fluids to avoid any damage to the digestive system.


Gilmore, D. (2013). Medical Transcription Projects. Boston: Cengage Learning.
Lancaster-Smith, M. (2012). Ulcer and Non-Ulcer Dyspepsias Practical Clinical Medicine.

Berlin: Springer Science & Business Media. Malfertheiner, P., & Ditschuneit, H. (2012). Helicobacter pylori, Gastritis and Peptic Ulcer. Berlin: Springer Science & Business Media.

VanMeter, K. (2013). Gould’s Pathophysiology for the Health Professions Pathophysiology for the Health Professions. Edinburgh: Elsevier Health Sciences.

VanMeter, K.C., & Hubert, R.J. (2018). Gould’s pathophysiology for the health professions. (6th ed.). St. Louis, MO: Elsevier Saunders. ISBN 9780323414425

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Re: Week 10 Discussion 1: GI Case Study

by Laura Richard – Wednesday, 4 November 2020, 1:43 PM

Gastroenteritis Case Study

Gastroenteritis is the inflammatory process of the stomach and the intestines often caused by infection or allergic reactions to foods or drugs (Szajewska et al., 2019). Infections that cause gastroenteritis are often contracted through fecally contaminated food or water and include microorganisms such as E-Coli, Staph aureus, Salmonella, and C-diff (VanMeter & Hubert, 2018). The most common symptoms of gastroenteritis include nausea, abdominal cramping, fever, and malaise (VanMeter & Hubert, 2018). The inflammation of the stomach and intestines cause the hallmark signs of gastroenteritis, vomiting and diarrhea (VanMeter & Hubert, 2018). Gastroenteritis is often mild and self-limiting however in cases where an individual is immunocompromised, or the microorganism is especially aggressive treatment may be necessary (Szajewska et al., 2019). Supportive treatment may include rehydration therapy, monitoring electrolytes, and antidiarrheal medications (Bruzzese, Giannattasio, & Guarino, 2018). For more aggressive agents or those with poor immune systems, a course of antibiotic therapy may be necessary (Bruzzese, Giannattasio, & Guarino, 2018).

  1. Briefly describe how S. aureus in the custard could cause vomiting and diarrhea.

Custard that is not properly cooked or refrigerated can develop staph aureus (VanMeter & Hubert, 2018). This type of microorganism excretes an enterotoxin that damages the intestinal epithelium causing the body to initiate an inflammation response (Szajewska et al., 2019). The inflammation response in the gastric mucosa of the stomach stimulates vomiting (Szajewska et al., 2019). The inflammation response in the intestines causes impaired absorption and increased mobility and secretions causing diarrhea (Szajewska et al., 2019).

  1. Describe the fluid and electrolyte imbalances that can be expected in Baby K.

Baby K will likely be dehydrated due to the fluid loss from the nausea and vomiting. Infants are more prone to dehydration due to greater metabolic needs and are unable to retain and conserve fluids as efficiently as adults with more developed kidneys (Bruzzese, Giannattasio, & Guarino, 2018). The electrolyte imbalances that can be expected include hypo or hypernatremia, hypokalemia, hypophosphatemia, and hypochloremia all caused by electrolyte and fluid losses due to the nausea and vomiting (VanMeter & Hubert, 2018).

  1. What arterial blood gas levels would you expect to find in this child with gastroenteritis?

I expect this child to be in a state of metabolic acidosis due to the loss of bicarbonate ions due to diarrhea and excessive intestinal secretions (VanMeter & Hubert, 2018). This means they will have a pH value below 7.4 (Florez et al., 2018). Their HCO3 or, bicarbonate ions, will be decreased (Florez et al., 2018). They may have a low PCO2 due to respiratory compensation (Florez et al., 2018).


Bruzzese, E., Giannattasio, A., & Guarino, A. (2018). Antibiotic treatment of acute gastroenteritis in children. F1000Research7, 193-198.

Florez, I. D., Veroniki, A.-A., Al Khalifah, R., Yepes-Nuñez, J. J., Sierra, J. M., Vernooij, R. W. M., Acosta-Reyes, J., Granados, C. M., Pérez-Gaxiola, G., Cuello-Garcia, C., Zea, A. M., Zhang, Y., Foroutan, N., Guyatt, G. H., & Thabane, L. (2018). Comparative effectiveness and safety of interventions for acute diarrhea and gastroenteritis in children: A systematic review and network meta-analysis. PLoS ONE13(12), 1–22.

Szajewska, H., Kołodziej, M., Gieruszczak, B. D., Skórka, A., Ruszczyński, M., & Shamir, R. (2019). Systematic review with meta‐analysis: Lactobacillus rhamnosus GG for treating acute gastroenteritis in children – a 2019 update. Alimentary Pharmacology & Therapeutics49(11), 1376–1384

VanMeter, K.C., & Hubert, R.J. (2018). Gould’s pathophysiology for the health professions. (6th ed.). Elsevier Saunders.

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Re: Week 10 Discussion 1: GI Case Study

by Leonora Urbano – Wednesday, 4 November 2020, 5:34 PM

Case Study C: Hepatitis B and Cirrhosis

J.B., age 35, has had chronic hepatitis B for 9 years. The origin of his acute infection was never ascertained.

Hepatitis B infection (HBV) is a body fluid-transmitted viral infection that primarily attacks the liver. When infected at infancy or childhood, chronic hepatitis is likely to occur in 95% of cases while 5% when infection occurs at adulthood. The hepatitis B virus can survive outside the body for at least 7 days. The average incubation period 75 days but can vary from 30 to 180 days. Viral detection is possible within the first 30-60 days and can persist progressing to chronic hepatitis B, chronic liver disease or cirrhosis (CLD), and/or liver cancer. While there is no treatment for hepatitis B infection, prevention by vaccination is 98-100% effective (World Health Organization, 2020).

Describe the pathophysiology of acute hepatitis B infection.

The course of HBV infection is variable. 65% is subclinical (barely detected viral load), 25% symptomatic but spontaneously resolves, and 10% progress to chronic infection (more than 6 months virus and antigens persistence in the blood. The pathophysiology of HBV infection can be summarized as mainly immune-mediated and in some circumstances, HBV can be directly cytotoxic to liver tissue. HBsAg present on cell membranes promote T cells-induced cellular lysis of HBV-infected cells but not that effective in hepatocytes (Feitelson, 2018). Tripathi & Mousa (2020) suggest that majority of HBV DNA is cleared from the hepatic system before T cell infiltration, which means that the immune response is more effective early in the early stage of infection.

Describe two signs of the preicteric stage and three signs of the icteric stage of acute hepatitis B infection.

The preicteric stage precedes the icteric stage by a few days to 4 weeks. It is usually asymptomatic. However, in 10-20% of cases, it can present as a brief episode of serum sickness-like syndrome consisting of low-grade fever; red skin rash which can be maculo-papular, petechial or nodular; and arthralgia. The mechanism by which this syndrome occurs is thought to be due to the circulating immune complexes composed of hepatitis B surface antigen and deposition of HBV containing complexes in the synovial tissues (Hsu et al., 2016; Kappus & Sterling, 2013).

In the icteric phase, the signs include jaundice with yellowing of the sclera; dark-colored urine and pale-colored stools; and right upper quadrant tenderness with liver enlargement  (Mehta & Reddivari, 2020). In the icteric phase, the liver is compromised and is unable to metabolize bilirubin from the breakdown of old red blood cells properly. This results to increased levels of both conjugated (soluble) and un-conjugated (non-soluble) bilirubin. Unconjugated bilirubin cannot be acted upon by colonic bacteria resulting to decreased production of urobilinogen and stercobilin (gives the feces its distinct color if liver is normal), thereby the pale-colored stools. The remaining bilirubin is re-circulated in the compromised hepatic system and into the systemic, peripheral (resulting to yellowing of the sclerae and skin), and renal circulation with urinary bilirubin excretion resulting to the dark colored urine (Joseph & Samant, 2020).  The right upper quadrant tenderness is due to the inflammation of the liver membrane.

What serum markers remain high when chronic hepatitis B is present?

Chronic hepatitis comes as chronic HBV infection or as chronic inactive carrier form. In chronic HBV infection, the HBsAg and anti-HBc IgG is positive plus the alanine transaminase (ALT) is elevated. In chronic inactive HBV carrier state, the HBsAg and anti-HBc IgG is positive but the ALT is normal (Tripathi & Mousa, 2020; Gonzalez, 2017).

Explain why each of the following events occur:

(1) excessive bleeding from trauma – Most of the blood clotting factors are synthesized by hepatocytes (liver cells). Inn cirrhosis, hepatocytes are replaced by scar tissue. As such, production of clotting factors is greatly reduced resulting to excessive bleeding from trauma (Heinz & Braspenning, 2015).

(2) increased serum ammonia levels – the liver is the main filtering system for ammonia and other nitrogen by products from the breakdown of amino acids from food intake. In cirrhosis, this filtering system is compromised. Therefore, ammonia is not removed resulting to increased ammonia levels (Griffin & Bradshaw, 2019). Additionally,

(3) hand-flapping tremors and confusion – the high ammonia levels in the brain resulting from the failure of the liver to filter ammonia results to brain inflammation, impaired blood circulation in the brain and compromised neurotransmitter systems. This can manifest as a range of altered consciousness from confusion to coma and hand-flapping or asterixis (Lee & Huang, 2019; Agarwal & Baid, 2016). Additionally, when circulating blood containing toxins from the gastrointestinal tract passes through, the liver breaks these toxins down into non-toxic substances. In cirrhosis, this function is compromised. Toxins are recirculated, reaches the brain causing increased brain stress, poor concentration and confusion (infohep, 2017).


Agarwal, R., & Baid, R. (2016). Asterixis. Journal of Postgraduate Medicine62(2), 115.

Feitelson, M. A. (2018). Pathogenesis of Hepatitis B Virus Associated Chronic Liver Disease. IntechOpen.

Gonzalez, S. A. (2017). Hepatitis B Virus—Infectious Disease and Antimicrobial Agents. Infectious Disease & Antimicrobial Agents.

Griffin, J. W. D., & Bradshaw, P. C. (2019). Effects of a high protein diet and liver disease in an in silico model of human ammonia metabolism. Theoretical Biology and Medical Modelling16(1), 1–14.

Heinz, S., & Braspenning, J. (2015). Measurement of blood coagulation factor synthesis in cultures of human hepatocytes. Methods in Molecular Biology (Clifton, N.J.)1250, 309–316.

Hsu, C.-S., Lang, H.-C., Huang, K.-Y., Lin, H. H., & Chen, C.-L. (2016). Association of rheumatoid arthritis and hepatitis B infection: A Nationwide nested case-control study from 1999 to 2009 in Taiwan. Medicine95(18).

infohep. (2017). Hepatitis B – Disease course and symptoms.

Joseph, A., & Samant, H. (2020). Jaundice. In StatPearls [Internet]. StatPearls Publishing.

Kappus, M. R., & Sterling, R. K. (2013). Extrahepatic manifestations of acute hepatitis B virus infection. Gastroenterology & Hepatology9(2), 123.

Lee, E. J. S., & Huang, J. C. (2019). Ammonia. IntechOpen.

Mehta, P., & Reddivari, A. K. R. (2020). Hepatitis. In StatPearls [Internet]. StatPearls Publishing.

Tripathi, N., & Mousa, O. (2020). Hepatitis B.

World Health Organization. (2020, July 27). Hepatitis B.


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Re: Week 10 Discussion 1: GI Case Study

by Lynne Barry – Wednesday, 4 November 2020, 7:26 PM

Case Study D: Crohn’s Disease

Mr. P.T. is a 19-year-old suffering from Crohn’s disease that affects both his ileum and jejunum. He has a strong family history of Crohn’s disease and has experiences several exacerbations throughout the past 5 years. The purpose of this case study is to discuss the pathophysiology of the disease, the common signs of exacerbation and to explain how nutritional deficits can occur with Crohn’s disease.

  1. Describe the pathophysiology of Crohn’s disease. 

Crohn’s disease is one of the diseases referred to as an inflammatory bowel disease. The disease has cycles of remission and relapsing and can range from mild to severe (Ranasinghe et al., 2020). Crohn’s disease can affect all parts of the digestive tract; however, it most commonly affects the terminal ileum and ascending colon of the small intestine. Inflammation causes lesions that are separated by areas of normal tissues. These are referred to as skip lesions. Inflammation starts in the mucosal layer with the development of ulcers and as the disease progresses, fibrosis occurs and both fibrosis and the inflammation begin to affect all layers of the intestine wall. The lumen is narrowed as a result of the changes and can be completely obstructed. This damage results in impaired digestion and absorption, therefore, the intestine having difficulty processing and absorbing food (VanMeter and Hubert, 2018).

2. Describe the common signs of an exacerbation.

Signs of a Crohn’s disease exacerbation will vary based on the gastrointestinal area that is affected by the disease. Other factors that impact symptoms of reoccurrence includes severity of the disease for example if fistula’s or strictures are present and also the characteristics of the inflammation (McDowell et al., 2020. Chronic diarrhea greater than 4 weeks, abdominal pain, weight loss and blood and/or mucous in stool are common signs and symptoms related to Crohn’s disease and a Crohn’s exacerbation (Ha and Khalil, 2015).

3. Explain how nutritional deficits may occur with Crohn’s disease. 

A loss of appetite is often seen in patients suffering from inflammatory bowel diseases. Decreased appetite and impaired absorption can quickly lead to nutrient deficiencies in those living with Crohn’s disease. Vitamins A, B, D and K as well as iron and zinc are often low in patients with Crohn’s disease (Jayawardena and Dudeja, 2020). Malnutrition is considered a severe complication of Crohn’s disease including sarcopenia which can lead to more severe complications such as cardiovascular disease (Scaldaferri et al., 2017). Crohn’s disease also causes severe issues within the pediatric population including delayed linear growth (Kim, 2016).

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