Posted: June 6th, 2021

Mr. James is a 62 year old male in a primary care practice

NURS 5315 Advanced Pathophysiology
Case Study #2 – Fall 2023

Mr. James is a 62 year old male in a primary care practice being seen for a health maintenance visit (last visit was over 10 years ago). His only complaint of note is fatigue but generally feels well. He denies any limitations in “doing the things I like to do”, including yard work and fishing. He works full time as a supervisor for a commercial construction company. He is married and has 2 daughters. His oldest daughter is expecting their first grandchild. NURS 5315 Advanced Pathophysiology Case Study.

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He has a history of “recreational” IV drug use when he was in his early 20s while he was in the military. Denies any drug use since that time. He indicates “minimal” alcohol use – generally no more than 2-3 beers or glasses of wine a week. He has no chronic illnesses and does not take any medicines on a regular basis. NURS 5315 Advanced Pathophysiology Case Study.

Physical exam:
Vitals: 38.1-97-18-183/139
Normocephalic. Alert & Oriented x3.
Eyes: PERL. No nystagmus, no icterus.
Neck: Supple, no cervical lymphadenopathy
Cardiovascular: Normal Rate and rhythm. No murmur, gallops. 2+/4+ radial, brachial, dorsalis pedis pulses bilaterally. No jugular venous distension. No edema.
Pulmonary: Lungs are clear. No dyspnea or orthopnea.
Abdomen: Soft and nontender, active bowel sounds. No liver enlargement; abdomen flat. No striae.
Skin: Warm and dry; no rashes. Multiple tattoos on both arms.
Rectal exam: Stool is brown, no rectal masses.

NURS 5315 Advanced Pathophysiology Case Study

Lab results:

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CBC: WBC 9,000; RBC 5.10; Hemoglobin 15.3 g/dL Hematocrit 46%; 90; Platelets 152,000.
Electrolyte Panel: Sodium 136 mEq/L; Potassium 3.7 mEq/L; Creatinine 1.1 mg/dL; BUN 12 mg/dL; Glucose 115mg/dL
Alanine aminotransferase (ALT) 36
Aspartate aminotransferase (AST) 50
Bilirubin (total) 0.9 mg/dL
Hepatitis A IgM negative; IgG positive
Hepatitis B surface antigen negative; surface antibody positive; core antibody negative
Hepatitis C (HCV) antibody reactive (positive), Hepatitis C RNA positive with an undetectable viral load.

Respond to the following questions regarding the Case Study

1. The clinical scenario is most consistent with which type of hepatitis? You may list your answer below using a bullet point format. This does not have to be in a complete sentence. A citation is not required. (10 pts). NURS 5315 Advanced Pathophysiology Case Study.

2. What specific data in the clinical scenario supports your diagnosis? You may list your answers below using bullet point format. This does not have to be in a complete sentence. A citation is not required. (10 pts)

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3. What is the most likely cause of this patient’s diagnosis you noted in Question 1? You may list your answer below using a bullet point format. This does not have to be in a complete sentence. A citation is not required. (10 pts). NURS 5315 Advanced Pathophysiology Case Study.

4.Page Paper Describe key pathophysiologic concepts that relate to the diagnosis in question 1. To answer this question completely, you must answer all of the sub-questions below using complete sentences. Each sub-question may be answered in 1-6 sentences. ***Citations are required for each answer to each question using APA format. You MAY NOT use direct quotes.

a. How does Hepatitis lead to an increased risk of hepatocellular carcinoma?Page Paper Describe how the virus affects the hepatocytes and may lead to cancer. ( 10 pts)

b. How does Hepatitis lead to cirrhosis of the liver?Page Paper Describe the pathologic steps of how cirrhosis develops and how cellular changes can lead to liver failure. ( 10 pts). NURS 5315 Advanced Pathophysiology Case Study.

c. One of the negative sequela of liver failure is increased bleeding. Why do individuals with liver failure experience potentially life threatening bleeding?Page Paper Describe how liver failure leads to coagulopathy. ( 10 pts)

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d. Portal hypertension is also a negative sequela of liver failure.Page Paper Describe how liver failure leads to portal hypertension AND how portal hypertension manifests. (10 pts)

5. Mr. James is concerned that he will transmit the virus to his new granddaughter after she is born.
What is the likelihood of transmitting the virus to his granddaughter? Provide a single sentence that includes your rationale. A citation is not required. (10 pts). NURS 5315 Advanced Pathophysiology Case Study.

APA Format – Best Help Writing My 99 Papers—owl Essay Samples

Information is presented in a scholarly manner (clear, grammatically correct) and reflects synthesis of information from sources. APA format is correctly used for citations and references. Submission follows assignment guidelines; does not exceed page limit. (15 pts). NURS 5315 Advanced Pathophysiology Case Study.

Hepatitis C
Hepatitis C (HCV) antibody reactive (positive), Hepatitis C RNA positive with an undetectable viral load.
IV drug use in his early 20s while in the military
4a. Hepatitis C virus (HCV) infection can lead to hepatocellular carcinoma by causing chronic inflammation and cirrhosis of the liver (Bruix and Sherman, 2011). As the virus persists in hepatocytes, it causes cellular damage and death. Over many years, this process of injury and regeneration increases the risk of mutations that can lead to cancer (El-Serag, 2012).
4b. Chronic HCV infection leads to cirrhosis through a long-term process of hepatic necroinflammation, fibrosis and regeneration (Poynard et al., 1997). As the liver attempts to repair itself from ongoing injury, excessive scar tissue (fibrosis) builds up and disrupts the normal liver architecture and blood flow (Theise, 2000). This scarring process eventually results in cirrhosis.
4c. Liver failure results in coagulopathy due to the liver’s inability to produce clotting factors and proteins that regulate coagulation (Tripodi & Mannucci, 2011). Factors II, VII, IX and X, protein C, protein S and antithrombin are synthesized in the liver and low levels lead to a bleeding diathesis.
4d. Portal hypertension occurs in liver failure as increased resistance to blood flow in the liver leads to elevated pressure in the portal vein (Groszmann & Bosch, 2015). Clinical manifestations include esophageal and gastric varices, ascites and hepatic encephalopathy. Variceal bleeding is a serious complication of portal hypertension.
The likelihood of transmitting the virus to his granddaughter is very low, as HCV is not spread through casual contact like holding or kissing infants.
References:
Bruix, J., & Sherman, M. (2011). Management of hepatocellular carcinoma: an update. Hepatology, 53(3), 1020-1022.
El-Serag, H. B. (2012). Epidemiology of viral hepatitis and hepatocellular carcinoma. Gastroenterology, 142(6), 1264-1273.
Poynard, T., Bedossa, P., & Opolon, P. (1997). Natural history of liver fibrosis progression in patients with chronic hepatitis C. The OBSVIRC, METAVIR, CLINIVIR, and DOSVIRC groups. Lancet, 349(9055), 825-832.
Theise, N. D. (2000). Liver stem cells and the boundaries of regeneration. Seminars in liver disease, 20(01), 83-94.
Tripodi, A., & Mannucci, P. M. (2011). The coagulopathy of chronic liver disease. New England Page Essay – Journal of Medicine, 365(2), 147-156.
Groszmann, R. J., & Bosch, J. (2015). Hemodynamic basis of variceal bleeding. Gastroenterology clinics of North America, 44(1), 1-15.

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