Cirrhosis (Robbins 5th Ed., p. 834-837) or (6th Ed., p. 852-856)
1. Describe the three microscopic features that are characteristic of cirrhosis.
2. List the major etiologic agents of cirrhosis.
3. Contrast the two gross morphologic variants of cirrhosis, micronodular and macronodular, and understand why such a classification scheme can be clinically misleading.
4. Define the term "cryptogenic cirrhosis."
5. Describe the clinical signs and symptoms of cirrhosis.
Hepatic Failure (Robbins 5th Ed., p. 841-842, particularly Table 18-3, p. 841) or (Robbins 6th Ed., p. 852-853)
1. List the major clinical features of hepatic failure, and describe what their physiologic basis is.
2. Define the terms "hepatic encephalopathy" and "hepatorenal failure."
Alcoholic Liver Disease (Robbins 5th Ed., p. 857-861) or (Robbins 6th Ed., p. 869-873)
1. Describe the pathology of the three forms of alcoholic liver disease: fatty liver, hepatitis, and cirrhosis.
2. Discuss the mechanisms of alcoholic liver damage.
3. Discuss general aspects of susceptibility factors for and the clinical course of the three types of alcoholic liver damage.
Genetic-Metabolic Liver Diseases (Robbins 5th Ed., p. 861-866) or (Robbins 6th Ed., p. 873-876)
1. Compare the difference between the etiologies and pathogenesis of primary hemochromatosis vs. secondary iron overload.
2. List the organs (liver, heart, skin, pancreas, etc.) and cells in which iron deposition occurs in hemochromatosis.
3. Identify the most serious complication of hepatic involvement in hemochromatosis.
4. Describe the pathology of the liver disease associated with alpha1-antitrypsin deficiency.
Hepatic tumors (Robbins 5th Ed., p. 878-883) or (6th Ed., p. 886-891)
1. Know the epidemiology, pathogenesis, pathology, and clinical consequences of the most common liver tumors - benign (cavernous hemangioma, nodular hyperplasia, and adenoma) and malignant (hepatocellular carcinoma and cholangiocarcinoma).
2. Name the risk factors for developing hepatocellular carcinoma or cholangiocarcinoma.
1. (Robbins 5th Ed., p. 834-837, 841-842, 857-861, 878-883) or (Robbins 6th Ed., p. 852-856, 869-876, 886-891)
Images 1 - 6 relate to the case.
Images 7 - 21 are for other objectives.
A 57-year-old white man presented to the emergency room with a history of increasing abdominal girth, increasing somnolence, and vomiting blood. Family members related that he had consumed alcohol for many years, drinking up to 1 liter of liquor per day. Two months prior to admission, increasing abdominal girth was noted, with the need to purchase new pants. The patient had been increasingly somnolent over the past few days, although still imbibing alcohol, and he vomited some blood that day followed by increased confusion. His past medical history was notable for unknown prior abdominal surgical procedures, for which he received blood products. The physical examination showed the patient was a cachectic man who appeared older than his stated age. He had a protuberant abdomen. He had a blood pressure of 90/60, pulse 120, and temperature 36.8oC. He could not sit up to check his blood pressure or pulse. His respiratory rate was 24. He was jaundiced. Small, spider-like tangles of blood vessels were present over the skin of the neck and chest. Palpable breast tissue was present. Auscultation of the chest revealed a few rhonchi. The cardiac examination was unremarkable. The abdomen was protuberant with shifting dullness, and the spleen was palpable. The liver percussed to a span of 10 cm. A few large blood vessels were noted in the periumbilical area. There was bilateral pedal edema to the mid-calves, which was worse on the left side. Neurologically, the patient was somnolent but arousable. He was oriented only to name. On voluntary dorsiflexion of his hands, a flapping motion was noted. Laboratory tests included:
|
Hematocrit |
25% |
Urinalysis: |
pH 7.0; golden brown |
|
WBC |
12,000/µL |
bilirubin - positive (2+) |
|
|
Prothrombin time |
15.8 seconds |
||
|
AST |
190 U/L |
||
|
ALT |
65 U/L |
||
|
ALP |
170 U/L |
||
|
Gamma-glutamyl transferase |
1510 U/L |
||
|
Total bilirubin |
7.4 mg/dl |
||
|
Direct bilirubin |
4.8 mg/dl |
||
|
Total protein |
7.8 g/dl |
||
|
Albumin |
2.8 g/dl |
||
|
Alcohol |
110 mg/dl |
||
|
Amylase |
52 U/L |
||
|
Lipase |
64 U/L |
||
|
HBsAg |
negative |
||
|
Anti-HBc |
total - negative |
||
|
Anti-HCV |
positive |
The patient was treated with intravenous fluids and blood transfusions. Blood cultures were drawn, and an abdominal paracentesis was performed. The fluid obtained was clear and golden yellow. The laboratory reported the fluid had a total protein of 1.7 g/dl and an albumin of 1.0 g/dl, with a white cell count of 180/µl with a differential count of 10% neutrophils, 10% lymphocytes, and 80% monocytes/mesothelial cells. The laboratory also reported that a gram stain of the fluid was negative. Cultures of the fluid were set up. The patient was taken to endoscopy. Endoscopic examination revealed dilated blood vessels in the distal portion of the esophagus, proximal stomach area. There was some adherent blood clot overlying some of these vessels. The vessels were sclerosed by the endoscopist with control of the bleeding. After the procedure, the patient was hemodynamically stable but obtunded, arousable only to deep pain. Lactulose, a nonabsorbable sugar, was administered by enema. After two days, the patient's mental status improved, and he signed out of the hospital against medical advice.
The patient was followed intermittently for several years and eventually had to be readmitted for worsening symptoms, including anorexia and weight loss. A 6.0 cm, homogeneous liver mass was noted on a computerized tomography scan. A serum alpha-fetoprotein level was 2,500 ng/ml. A biopsy of the liver mass was performed. When given the diagnosis, the patient and family refused further treatment and the patient died after several weeks. An autopsy was requested.
At autopsy, there was ascites with 2500 ml of clear, golden-yellow fluid in the peritoneal cavity with small, bilateral, clear, yellow, pleural effusions. Esophageal varices were present. The gold-brown liver was cirrhotic, containing one large and several smaller yellow-green irregular masses of tumor.
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For Comparison: |
Alcoholic fatty liver |
Images 7-8 |
|
Alcoholic hepatitis |
Images 9-10 |
|
|
Alcoholic cirrhosis |
Images 11-13 |
|
|
Hemochromatosis |
Images 14-15 |
|
|
Alpha1-antitrypsin deficiency |
Image 16 |
|
|
Cavernous hemangioma |
Image 17 |
|
|
Focal nodular hyperplasia |
Image 18 |
|
|
Liver cell adenoma |
Image 19 |
|
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Cholangiocarcinoma |
Images 20-21 |