Clinical Topics Conference:Chapter 3, Repair, Regeneration, & Fibrosis

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  1. Alcoholic liver disease, cirrhosis
  2. Post-necrotic liver cirrhosis, hepatitis C
  3. Myocardial infarction, acute, with rupture and cardiac tamponade
Case 1: Alcoholic liver disease, cirrhosis

Clinical vignette

The patient was a 59 year old male, who had abused alcohol for almost 35 years. He presented with ascites, jaundice, and slight mental confusion. He had recently entered an alcohol abuse program. Liver transplantation was done emergently, but the surgical pathology examination of the resected liver revealed hepatocellular carcinoma. The patient expired 2 weeks after transplantation, despite beginning chemotherapy for what ultimately proved to be metastatic hepatocellular carcinoma. (RIP #7)

Discussion topics

  1. Describe the pathogenic events, in sequence, that ultimately lead to the destruction of this man's liver parenchyma, the ensuing fibrosis, ascites, and jaundice. To paraphrase, how did the process of regeneration, repair and fibrosis lead to this man's presenting clinical symptoms?

  2. Describe the pattern of fibrosis expected in the liver.

  3. Do you think the process of repair had anything to do with the ultimate development of hepatocellular carcinoma?

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    Case 2: Post-necrotic liver cirrhosis, hepatitis C

    Clinical vignette

    The patient was a 42-year-old woman who was admitted for the first time 2 1/2 months prior to death complaining of jaundice, dark-colored urine and light-colored stools of four weeks' duration. Physical examination revealed a blood pressure of 150/40, icterus (jaundice) of sclerae and skin, palpable liver and spleen, ankle edema and ascites. Liver function tests were indicative of severe hepatocellular damage. Past medical history was positive for transfusion, given for severe hemorrhage during childbirth. Serological studies were positive for antibodies to Hepatitis C virus. She was put on a the list for liver transplantation, and a liver was being sought. However, she was readmitted three weeks before death, jaundiced, confused and disoriented.

    Laboratory examinations showed a greatly prolonged prothrombin time; direct serum bilirubin, 2 mg/dl (normal 0 to 0.3 mg/dl%); total serum bilirubin, 5 mg/dl (normal is 0.2 to 0.8 mg/dl); total serum cholesterol, 160 mg/dl (normal is 180 to 270 mg/dl). Clinical diagnoses were: chronic liver disease, massive hepatic necrosis and hepatic coma. The patient was not considered a good risk for liver transplantation.

    During the hospital course the patient became more lethargic, disoriented, confused and finally unconscious. Clinically, the terminal event was related to the aspiration of gastric contents into the bronchi.

    Discussion topics

    1. What is hepatitis C, where did this patient acquire it, and why did it lead to hepatic failure?

    2. The pathologic term for the gross appearance of a liver from such a case is post-necrotic cirrhosis. The nodules were large. Describe why the liver would have this appearance.

    3. Why was the patient's cholesterol lower than normal? Why were her bleeding times prolonged?

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    Case 3: Myocardial infarction, acute, with rupture and cardiac tamponade

    Clinical vignette

    The patient was a 58-year-old male who entered KUMC 4 days before death with progressively severe anterior chest pain of 48 hour's duration. He had a past medical history of systemic hypertension for 4 years. The admission electrocardiogram indicated acute posterior and septal myocardial infarction with atrial fibrillation. Subsequent electrocardiograms showed extension of the infarction. In the last 3 days it was necessary to give vasopressor drugs continuously to keep the patient's blood pressure above shock level. His total white blood count on the second day of illness was 14,000 per cc, with 87% polymorphonuclear leukocytes. On day 4, the cardiac monitor showed electro-mechanical dissociation. A code blue was called. The patient was found to have pulsus paradoxicus. Despite resuscitative efforts, including a pericardiocentensis that yielded 50cc of blood, the patient expired.

    Discussion topics

    1. In this patient, what effect may the persistent lowered blood pressure have had on myocardial oxygenation?

    2. Why should conduction abnormalities have been anticipated in this patient?

    3. What is pulsus paradoxicus? Describe its pathophysiology.

    4. When in the course of myocardial infarction is left ventricular rupture likely to occur ? Describe the probable histologic appearance of the myocardium at the time of rupture.

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