NUR 660 Week 12 Discussion 1 Case Study Discussion Team C: Hepatitis B and Cirrhosis

March 8, 2022
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NUR 660 Week 12 Discussion 1 Case Study Discussion Team C: Hepatitis B and Cirrhosis

NUR 660 Week 12 Discussion 1 Case Study Discussion Team C: Hepatitis B and Cirrhosis

Describe the pathophysiology of acute hepatitis B infection. How is this different from chronic hepatitis B infection?
Hepatitis is a group of different viruses that attack the liver cells called hepatocytes. In hepatitis B, the cells become damaged through a cell-mediated immune response to the virus. The antigens of this virus include HBcAg, HBeAg, and HBsAg. Recognizing these antigens in the blood is important for diagnosis and further monitoring the course of Hepatitis B. If these antigens continually stay in the blood, especially HBsAg, then the individual is at a higher risk of chronic hepatitis B. If the antigens rise and then fall, it is most likely acute (Hubert & VanMeter, 2018, p. 461).
If J.B. had known about his exposure at the time, could any treatment measures have been undertaken at the time?
There is no direct treatment that can fully destroy the virus even in the early stages. However, immune therapy (Gamma globulin) can be given to boost the patient’s immune system and help fight the disease. This treatment works best if given immediately, within 7-14 days of exposure.
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.
Acute hepatitis has three stages: preicteric, icteric, and posticteric. The first stage, preicteric, is subtle may only show signs of elevated AST/ALT (liver enzymes), fever, and muscle aches (Hubert & VanMeter, 2018, p. 462). When the inflammation of the liver persists, the bile duct becomes blocked and leads to a backup of waste including bilirubin. The following phase, the icteric stage, is marked by jaundice due to the increase in bilirubin. Three common signs of the icteric stage include light colored stools, dark urine, and itchy skin (Hubert & VanMeter, 2018, p. 462). J.B. can transmit the virus from the preinteric stage even if asymptomatic. It can be transmitted through blood and other body fluids. Examples of transmission include birth, sex, drug use through a needle, sharing toothbrushes & razors, various medical equipment, or hemodialysis (CDC, 2020).
What serum markers remain high when chronic hepatitis B is present?
HBsAg is a hallmark serum marker of hepatitis. If this antigen consistently remains in the blood after six months, it implies chronic hepatitis B. The presence of anti-HBc is also another marker of chronic infection (Hubert & VanMeter, 2018, p. 462)..
Explain how cirrhosis develops from chronic hepatitis B. Why is the early stage of cirrhosis relatively asymptomatic?
In chronic hepatitis B, the hepatocytes are constantly being inflamed leading to necrosis. As these cells die, fibrous scar tissue forms on the liver leading to obstruction and decreased blood supply causing permanent damage and cirrhosis. The early stages are often asymptomatic and may only have vague mild signs of fatigue, anorexia, weight loss, and diarrhea (Hubert & VanMeter, 2018, p. 458).
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.
As the liver becomes cirrhotic, its function severely decreases. It cannot produce enough clotting factors or absorb and store iron and vitamin B12 leading to anemia and increased bleeding. Ammonia is a waste product of protein and is metabolized by the liver to be further excreted by the kidneys in urine. When the cirrhotic liver cannot remove the waste, ammonia builds up in the blood causing hepatic encephalopathy leading to muscle twitching and confusion (Eberhardt & Topka, 2017).
Resources:
Centers for Disease Control and Prevention (CDC). (2020, July 28). Hepatitis B Questions and Answers for Health Professionals. https://www.cdc.gov/hepatitis/hbv/hbvfaq.htm
Eberhardt, O., & Topka, H. (2017). Myoclonic Disorders. Brain sciences, 7(8), 103. https://doi.org/10.3390/brainsci7080103
Hubert, R. J., & VanMeter, K. C. (2018). Pathophysiology Online for Gould’s Pathophysiology for the Health Professions(6th ed.). Elsevier
Team C: Hepatitis B and Cirrhosis
Week 12 Discussion Team C Worksheet
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?
• If J.B. had known about his exposure at the time, could any treatment measures have been undertaken at the time?
• 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.
• What serum markers remain high when chronic hepatitis B is present?
• Explain how cirrhosis develops from chronic hepatitis B. Why is the early stage of cirrhosis relatively asymptomatic?
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.
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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.
1. Describe the pathophysiology of acute hepatitis B infection. How is this different from chronic hepatitis B infection?
Hepatitis is inflammation to the liver and can be caused from a few different factors. Acute Hepatitis B is a result of contact with infectious body fluids that target hepatocytes. The liver cells are damaged in two ways either by direct action of the virus or by cell-mediated immune responses of the virus, such as in Hepatitis B (Hubert, R. J., & VanMeter, K. C., 2018).
2. If J.B. had known about his exposure at the time, could any treatment measures have been undertaken at the time?
According to Hubert, R. J., & VanMeter, K. C., (2018), there is no current treatment for Hepatitis at this time. There is a Gamma globulin that can be given early on in the course of the virus.
3. 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.
1. malaise
2. anorexia
1. stools become clay colored
2. jaundice occurs
3. urine darkens
When looking at the stages and which stage can J.B. transmit the virus would be the preicteric stage. These are marked with nonspecific symptoms that can be easily masked with other diseases or illnesses that also cause anorexia and malaise. Transmissions of Hepatitis B can occur through childbirth, hemodialysis, sexual activity, tattooing, or even body piercing exposes an individual for transmission (Hubert, R. J., & VanMeter, K. C., 2018)
4. What serum markers remain high when chronic hepatitis B is present?
HBsAg anti-HBs, HBcAb IgM, HBcAb IgG, HBeAg, and HBeAb (Hubert, R. J., & VanMeter, K. C., 2018)
5. Explain how cirrhosis develops from chronic hepatitis B. Why is the early stage of cirrhosis relatively asymptomatic?
Cirrhosis develops when there is progressive destruction of liver tissue that eventually will lead to liver failure. With this there is extensive damage to diffuse fibrosus and loss of lobar organization. (Hubert, R. J., & VanMeter, K. C., 2018). The early stages of cirrhosis is usually silent because when liver function starts to decline, your body will feel sluggish; you will feel tired and lose your appetite. Typically, we do not recognize these early symptoms as issues with our liver. When symptoms such as jaundice become apparent, the disorder will have already reached an advanced stage (Otsuka Pharmaceutical Co., n.d.).
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.

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6. Explain why each of the following events occur:
(1) excessive bleeding from trauma— The gastric veins have several points of channels that join with the gastric veins. With this increase of pressure of blood then it extends into esophageal veins. This creates large, distended and distorted veins and can be easily torn from something as simple as food passing though. (2) increased serum ammonia levels— With this there is a metabolic dysfunction in which the body is unable to remove ammonia from protein metabolism. There is too much crossing the blood-brain barrier. (Hubert, R. J., & VanMeter, K. C., 2018). (3) hand-flapping tremors and confusion— But when the liver is impaired for any reason, it may not remove toxins efficiently. Consequently, they can build up in the blood and enter the brain, where they disrupt brain function (Healthline, 2018).
Healthline. (2018). Asterixis: Causes, treatment, relation to the liver, and more. https://www.healthline.com/health/asterixis
Hubert, R. J., & VanMeter, K. C. (2018). Gould’s Pathophysiology for the Health Professions (6th ed.). Elsevier.
Otsuka Pharmaceutical Co. (n.d.). Early detection of “silent” liver cirrhosis | otsuka pharmaceutical co., ltd. Otsuka Pharmaceutical Co., Ltd.. https://www.otsuka.co.jp/en/health-and-illness/liver-cirrhosis-nutritional-therapy/early-detection/
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NUR 660 Week 12 Discussion 1 Case Study Discussion Team B: Peptic 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, 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?
Ulcers tend to start with a defect in the mucosa that extends to the muscularis mucosa (Malik et al., 2021). Once the mucosal layer is damaged, the inner walls are susceptible to acidity (Malik et al., 2021). Acid or pepsin penetrates the mucosal barrier, and the tissues are exposed to continued damage because the acid diffuses into the gastric wall (VanMeter & Hubert, 2018 p.451). “Further, the ability of the mucosal cells to secrete bicarbonate is compromised” (Malik et al., 2021). Ulcers may erode more deeply into the muscularis and eventually perforate the wall (VanMeter & Hubert, 2018 p.451). Ulcers are not limited to the stomach can appear in the esophagus. Peptic ulcers are most common in the proximal do denim, otherwise known as duodenal ulcers. It can also be found in the antrum of the stomach, aka as gastric ulcers or lower esophagus (VanMeter & Hubert, 2018 p.451).
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?
Some possible factors contributing to ulcer formation could be an H. pylori infection, the use of NSAIDs, and other medications (Malik et al., 2021). Clinicians and healthcare providers should ask what kind of medications Ms. X is taking and how often she takes them. They should also ask about her diet and any pertinent past medical history she may have related to abdominal pain/stomach issues such as epigastric abdominal pain, bloating, abdominal fullness, recent or recurring nausea and vomiting during or after meals, recent weight loss/weight gain, hematemesis (vomiting blood), and melena (dark tarry stool with or without visible blood) (Malik et al. 2021).
3. Explain why peptic ulcers may not be diagnosed in an early stage of development. In other words, why were there not any significant initial findings?
Signs and symptoms of ulcers may vary depending on the ulcer’s location in the patient’s age (Malik et al., 2021). Gastric and duodenal ulcers can differentiate from the timing of the symptoms concerning meals (Malik et al., 2021). Epigastric burning or achy pain comes with ulcers, usually 2 to 3 hours after meals and at night. Nocturnal pain is common with duodenal ulcers (VanMeter & Hubert, 2018 p.453). “Those with gastric outlet obstruction commonly report a history of abdomen bloating and or fullness” (Malik et al., 2021). Some patients may associate this irritation or the stomach upset with spicy food intake or with medication taken on an empty stomach and not necessarily concerning an ulcer. Some patients may also encourage waking because frequent food intake relieves the discomfort between meals that they experience (VanMeter & Hubert, 2018 p.453).
4. During her admission, Ms. X. continued to decompensate and developed bacterial peritonitis. Describe the perforation of an ulcer and how this can lead to complications, including bacterial peritonitis.
Peritonitis is inflammation of the peritoneal membranes that may result from a chemical irritation or a bacterial infection of the sterile peritoneal cavity. The ulcer that forms in the stomach can perforate the stomach wall, allowing gastric juices to spill into the peritoneal cavity. Gastric juices contain acid bile, chyme, and other foreign objects such as undigested food, which irritate the peritoneal membranes (VanMeter & Hubert, 2018 p.483). This information increases the permeability of the intestinal wall, permitting enteric bacteria to enter the peritoneal cavity (VanMeter & Hubert, 2018 p.483). “Necrosis or perforation of the intestinal wall allows for infection directly by enteric organisms” (VanMeter & Hubert, 2018 p.483). This intern leads to infection within the cavity. This can also delay peristalsis in the area, decreasing the risk of spreading toxins and bacteria. However, if the original cause of the problem is not removed, that information or infection will likely continue to apply (VanMeter & Hubert, 2018 p.483).
5. Explain why Ms. X. showed signs of shock. Which type of shock would you expect?

M. X is likely experiencing hypovolemic or cardiogenic shock. She is most likely experiencing hypovolemic shock as she losing fluid through her gastric system via the perforated ulcer. Some signs and symptoms of hypovolemic shock are cold or clammy skin, pale skin, rapid, shallow breathing, rapid heart rate, little or no urine output, confusion, weakness, weak pulse, blue lips and fingernails, lightheadedness, and loss of consciousness (Nall, 2018). The patient presented with abdominal pain, a rapid but thready pulse, and normal blood pressure. Abdominal pain or pressure can be a sign of internal bleeding along with a quick but thready pulse.
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.
Antibiotics were given to treat the infection. Intravenous fluids were given to bolster her cardiac system and replace some fluid loss during the hypovolemic shock. There is also a high likelihood that if her hemoglobin or low enough, it should be supplemented with a unit or two of packed red blood cells. Total parental nutrition is given because chances are she will not be able to eat for a considerable amount of time in her digestive tract, including her intestines need time to heal and recover. During this time, her intestines will not digest food normally and will most likely be put on a diet of clear liquids or strict NPO, depending on the amount of damage. There is also a high chance that she might need a colostomy of some sort later date, depending on the healing process and where the ulcer occurred. In addition, she might need more corrective surgery, which could include additional bowel resections or complete removal of specific intestine depending on the amount of damage done in the impact of the infection on the intestines. Whether not she is on antibiotics depends on the first couple of hours post-discovery of the perforation to determine whether the intestines will become necrotic or need to be removed. After partial total removal of necrotic tissue, they might resume her back onto clear liquids or introduce a feeding tube or some sort she would need to heal. All these interventions would return her to a more hemodynamic state; however, depending on the ulcer, how long it was perforated, how long she was in shock, how much necrotic tissue there is in the intestines, how many surgeries needed to be performed, and how she responds to antibiotics will determine whether or not she will be able to live a whole and healthy life after.
References
Malik TF, Gnanapandithan K, Singh K. Peptic Ulcer Disease. [Updated 2021 July 29]. In:StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534792/
Nall, R. M. (2018, September 17). Hypovolemic Shock. Healthline. Retrieved November 15, 2021, from https://www.healthline.com/health/hypovolemic-shock#symptoms
VanMeter, K. C., & Hubert, R. J. (2018). GouGould’sthophysiology for the health professions. (6th ed.). Elsevier Saunders.
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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.
• 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?
• Suggest several possible factors contributing to ulcer formation. What questions would you want to as Ms. X. to determine her risk for gastric ulcers?
• 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?
• 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.
• Explain why Ms. X. showed signs of shock. Which type of shock would you expect?
• 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.
Posting to the Discussion Forum
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