Reply Posts

Please reply to these two peer’s posts. Each reply must use at least one scholarly peer-reviewed reference other than your textbook. Add doi #if available

Thinking about your population-specific NP track and anticipated practice area: (Advance Psychiatric Nurse Practitioner)

  • Identify and explain two “pearls of wisdom” or “key concepts/ideas” you learned from reading your peers’ responses.
  • Describe a patient you might encounter in your future practice where you could apply the information learned in your peer’s post.

Please refer to the Grading Rubric for details on how this activity will be graded.

Please adhere to these instructions above

Re: Team B

by Elizabeth Hess

Team B: Peptic Ulcer and Peritonitis

Week 12 Discussion Team B Worksheet

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, so she was admitted. Six hours later, Ms. X.’s blood pressure began to drop, and her pulse was rapid but thready. Exploratory abdominal surgery revealed a perforated gastric ulcer and peritonitis.

1. Describe the process by which an ulcer develops. Are ulcers limited to the stomach or can they occur elsewhere in the GI system? If so, where?

The formation of an ulcer results from a breakdown in the mucosal lining of the gastrointestinal tract (Hubert & VanMeter, 2018). This mucosa layer is vital as it offers protection from ingested acids or from the production of hydrochloric acid. When this lining is disturbed, acid penetrates deep layers of the cavity wall, which causes an erosive cavity. This erosion or ulcer, continues to enlarge and can affect surrounding blood vessels which results in bleeding. 

Ulcers can present in different areas of the GI tract, most notably the stomach and duodenum (Prabhu & Shivani, 2014). Duodenal ulcers form in the duodenum of the small intestine and are a result of mucosa layer distribution (Quinones & Woolf, 2021). Gastric ulcers are located in the stomach and are also related to the disturbance of mucosa lining. 

2. Suggest several possible factors contributing to ulcer formation. What questions would you want to as Ms. X. to determine her risk for gastric ulcers?

According to Quinones and Woolf (2021), the primary cause of both gastric and duodenal ulcers is a “history of recurrent or heavy NSAID use and a diagnosis of H. pylori”. They continue to add that “malignancy, vascular insufficiency, and history of chemotherapy,” are also contributors to ulcer formation (Quinones & Woolf, 2021). Multifactorial etiologies may be present or exacerbate an ulcer. An inadequate blood supply to the gut and excessive steroid use are other causes (Hubert & VanMeter, 2018). 

Ms. X presents with a gastric ulcer. Further investigation is needed into the cause of the ulcer such as medication history and use (NSAIDS, ASA, steroids, chemotherapy), recent or past diagnosis of H. pylori, alcohol use, caffeine intake, tobacco use, and recent stressors. Age is also a factor as they have a decrease in vascular flow (Hubert & VanMeter, 2018). This in combination with the above risk factors would increase Ms X’s risk for ulcer development.

3. Explain why peptic ulcer may not be diagnosed in an early stage of development. In other words, why were there not any initial significant findings?

Quinones and Woolf (2021) share that 70% of individuals with peptic ulcers, which include gastric and duodenal formation, are asymptomatic. Ulcers take time to develop and are insidious in nature. Symptoms are typically not reported until significant erosion has occurred (Hubert & VanMeter, 2018). After initial cavity development, continued damage produced by acids leads to worse damage which leads to manifestations. Once damage is significant, the first symptom is usually dyspepsia (Prabhu & Shivani, 2014) followed by nausea, vomiting, weight loss, anemia, and active bleeding (Hubert & VanMeter, 2018). 

4. During her admission, Ms. X. continued to decompensate, and developed bacterial peritonitis. Describe the process of perforation of an ulcer and how this can lead to complications, including bacterial peritonitis.

A gastric or duodenal perforation is a serious complication of peptic ulcers and is often a medical emergency. Perforation occurs when the ulcer completely erodes through the intestinal or gastric wall (Hubert & VanMeter, 2018). This results in leakage of gastrointestinal (GI) content into the peritoneum which activates the inflammatory response cascade. This leads to further inflammation and irritation to the peritoneal space. Translocation of bacteria occurs as they move from the GI tract to the peritoneum which causes bacterial peritonitis. According to Prabhu and Shivani (2014) duodenal ulcers are more likely to perforate than gastric ulcers, yet both pose great danger to the patient. Bacterial peritonitis may progress to septic shock if interventions are delayed.

5. Explain why Ms. X. showed signs of shock. Which type of shock would you expect?

“Sepsis is a leading cause of death in patients” with an ulcer perforation (Boyd-Carson et al., 2020). Ms X presented with a perforated gastric ulcer which resulted in bacterial peritonitis. Without immediate intervention she progressed to septic shock as evidenced by her hypotension and tachycardia. Sepsis is a clinical syndrome of life threatening organ dysfunction” caused by an infection (Maggio, 2020). Septic shock results when there is depletion of tissue perfusion which results in multiorgan failure (Maggio, 2020). Ms X may also be presenting in hypovolemic shock from the significant loss of fluid from vomiting as well as the fluid shift seen with peritonitis (Hubert & VanMeter, 2018). It’s not unlikely for there to be a combination of shock states occurring in her case.

6. Ms. X. was given antibiotics, intravenous fluids, and intravenous alimentation (total parenteral nutrition). Explain how each of these treatments functions to return Ms. X. to a more homeostatic state.

Ms X was in a low perfusion state with uncontrolled infection and fluid loss. Interventions are aimed at removing the infection and optimizing nutrition and hydration status to promote healing. The source of the ulcer (H. pylori) and the organism causing the bacterial peritonitis will need to be determined for targeted antibiotic use. By eliminating the harmful organism, one can restore homeostasis. Due to the significant fluid loss, Ms X will require IV hydration. This will replete the volume lost from the vascular space due to the shift in fluid between the peritoneum and the interstitial space and from vomiting. According to Maggio (2020), IV hydration is the first step in restoring perfusion and is a critical step in maintaining homeostasis in septic shock. Total parenteral nutrition (TPN) will likely be needed as the stomach begins to heal. Allowing food or liquid intake into the perforated gastric cavity would only lead to continued damage, inflammation, and translocation of bacteria. TPN is recommended to deliver needed proteins, fats, and minerals to promote healing of the perforation and restore homeostasis (Tarasconi et al., 2020).


Boyd-Carson, H., Doleman, B., Cromwell, D., Lockwood, S., Williams, J. P., Tierney, G. M., Lund, J. N., & Anderson, I. D. (2020). Delay in Source Control in Perforated Peptic Ulcer Leads to 6% Increased Risk of Death Per Hour: A Nationwide Cohort Study. World Journal of Surgery44(3), 869–875.

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

Maggio, P. (2020). Critical care medicine: sepsis and septic shock. Merck Manual, Professional Version.

Prabhu, V. & Shivani, A. (2014). An overview of history, pathogenesis and treatment of perforated peptic ulcer disease with evaluation of prognostic scoring in adults. Annals of medical and health sciences research4(1), 22–29.

Quinones, G. & Woolf, A. (2021). Duodenal ulcer. StatPearls [Internet]

Tarasconi, A., Coccolini, F., Walter, B., Matteo, T., Ansaloni, L., Picetti, E., Molfino, S., Shelat, V., Cimbanassi, S., Weber, D., Abu-Zidan, F., Campanile, F., Di SAverio, S., Baiocchi, G., Casella, C., Kelly, M., Kirkpatrick, A., Leppaneimi, A., Moorse, E., Peitzman, A., Frage, G., Ceresoli, M., Maier, R., Wani, I., Pattonieri, V., Perrone, G., Velmahos, G., Sugrue, M., Sartelli, M., Kluger, Y., & Catena, F. (2020). Perforated and bleeding peptic ulcer: WSWS guidelines. World Journal of Emergency Surgery, 15(3).

Re: Team C: Hepatitis C and Cirrhosis

by Megan Stark

You are caring for J.B., age 35, who has had chronic hepatitis B for nine years. The origin of his acute infection was never ascertained. He is not married, lives alone, and sometimes has trouble managing his disease.

Describe the pathophysiology of acute hepatitis B infection. How is this different from chronic hepatitis B infection?

Acute Hepatitis B is a result of a double-stranded DNA virus which contains two core antigens and one surface antigen, each of which stimulate the production of antibodies (Hubert & VanMeter, 2018). There are two different stages of HBV: the acute and chronic stage. When the body is infected with the virus, primarily from blood transmission, the acute stage develops in which the incubation period runs over a course of 6-8 weeks, but typically 12 weeks; the first serum antigen to appear is the surface antigen HBsAG (Mehta & Reddivari, 2021). Hubert and VanMeter (2018) describe how when HBV is transmitted, a cell-mediated immune response occurs in which T lymphocytes recognize the HBV antigen and stimulate the production of antibodies. This process causes an immune response in liver cells, reducing its capability and causing liver necrosis (Hubert & VanMeter, 2018).

In the acute stage of HBV, the virus produces large amounts of antigens HBsAg and HBeAg. As these levels of antigens fall, the first form of antibody detected is the IgM anti-HBc antibody (to core antigen); this is required to make a diagnosis of active, acute HBV (Mehta & Reddivari, 2021). Then, IgG anti-HBs antibodies are formed and last in the body for several of years (Hubert & VanMeter, 2018).

Acute HBV differs from chronic HBV in that with acute HBC, antigen levels rise for an average of 8 weeks and then fall, followed by elevated antibody levels (Hubert & VanMeter, 2018). However, in chronic HBV, antigen levels remain elevated for prolonged time > 6months to several years or even for life (Hubert & VanMeter, 2018; Mehta & Reddivari, 2021). While acute HBV can resolve, chronic HBV often leads to cirrhosis and cancer.

If J.B. had known about his exposure at the time, could any treatment measures have been undertaken at the time?

According to Hubert and VanMeter (2018), there are no active forms of treatment to get rid of the HBV virus completely, however, individuals with chronic HBV may receive interferon alpha and lamivudine which help decrease the viral load and reduce replication, thus, reducing further damage to the hepatocytes and liver itself.

Describe two signs of the preicteric stage and three signs of the icteric stage of acute hepatitis B infection. In which of the stages could J.B. transmit the virus? Be sure to include discussion of the mode of transmission.

Pre-icteric Stage:

Elevated AST & ALT as hepatocytes are negatively affected and inflamed from initial infection (Liang, 2009; Hubert & VanMeter, 2018).

Fatigue from decreased ability to perform gluconeogenesis (Hubert & VanMeter, 2018).

Anorexia & nausea from impaired ability to secrete bile to aid in digestion (Huebrt & VanMeter, 2018).

Icteric Stage:

Stools are light in color from decreased bilirubin excretion (Hubert & VanMeter, 2018)

Prolonged blood clotting times (from decreased production of clotting factors (Hubert & VanMeter, 2018).

Jaundice – yellow sclera

Enlarged liver (from inflammation)

Although transmissible in any stage, J.B would most likely transmit the virus during the pre-icteric stage which is the acute onset in which serum markers may not yet be fully present. It could be transmitted via blood or stool through oral-fecal route and by bodily fluids, including those from sexual intercourse (Hubert & VanMeter, 2018). Healthcare workers are at increased risk of getting the virus, therefore, proper hygiene practices must be followed (Hubert & VanMeter, 2018).

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

Serum markers that remain high are HBsAG and HBeAG (Hubert & VanMeter, 2018).

Explain how cirrhosis develops from chronic hepatitis B. Why is the early stage of cirrhosis relatively asymptomatic?

In chronic hepatitis, serum antigen levels remain elevated for many of years leading to the progressive inflammation and then fibrosis of the liver tissue and hepatocytes themselves (Liang, 2009). As fibrosis occurs, it alters the proper flow of blood through the liver, reducing its supply, and causing necrosis (Hubert & VanMeter, 2018). The cirrhosis associated with chronic HBV is called postnecrotic cirrhosis and occurs as the lobes of the liver fail to function due to the chronic inflammation, irritation and necrosis of the hepatocytes. This leads to impaired blood supply and blockage of tissue, bile ducts and function (Hubert & VanMeter, 2018).

J.B.’s cirrhosis is now well advanced. He has developed ascites, edema in the legs and feet, and esophageal varices. His appetite is poor, he is fatigued, and he has frequent respiratory and skin infections. Jaundice is noticeable. He has been admitted with hematemesis and shock resulting from ruptured esophageal varices.

Explain why each of the following events occur: (1) excessive bleeding from trauma, (2) increased serum ammonia levels, and (3) hand-flapping tremors and confusion.

Excessive bleeding from trauma – the liver is responsible for the production of clotting factors, and when the hepatocytes are damaged as in the case of cirrhosis, the liver is unable to produce those clotting factors (Hubert & VanMeter, 2018). Therefore, when an individual begins to bleed from trauma, they will continue to bleed due to a lack of synthesis of factors responsible for the clotting of blood. Additionally, bile is secreted and aids in digestion of fat-soluble vitamins such as Vit K, which aids in coaguability. When the liver is damaged, decreased secretion of bile results, therefore, fat soluble vitamins are not absorbed as they should be (Hubert & VanMeter, 2018).

Increased serum ammonia levels – ammonia a result of protein breakdown by the liver. When ammonia is formed, the liver is responsible for converting it to urea, which is then excreted in the urine. When hepatocytes are damaged, the liver is unable to convert ammonia into urea, therefore levels of ammonia are elevated and causes ammonia induced encephalopathy (Hubert & VanMeter, 2018).

Hand flapping tremors and confusion results from hepatic induced encephalopathy, which is caused by increased ammonia levels in the body. Therefore, the hand flapping and tremors results from increased protein metabolism which forms ammonia, but when liver cells are damaged, this ammonia cannot be excreted. Therefore, high intake of protein may induce these symptoms as ammonia can cross the BBB (Hubert & VanMeter, 2018).  


Liang T. J. (2009). Hepatitis B: the virus and disease. Hepatology (Baltimore, Md.)49(5 Suppl), S13–S21.

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

 Mehta &  Reddivari.(2021). Hepatitis. StatPearls Publishing.

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