Cirrhosis Information and Courses from MediaLab, Inc.
These are the MediaLab courses that cover Cirrhosis and links to relevant pages within the course.
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| Clinical Significance Liver damage or an obstructed bile duct allows conjugated bilirubin to enter the circulation and ultimately to appear in the urine. Patients with clinical jaundice due to hepatitis or cirrhosis will have bilirubinuria. If the jaundice is due to red cell destruction, there is an increase in unconjugated bilirubin which the kidneys cannot excrete. | View Page |
| Clinical Significance Urinary urobilinogen may be increased in the presence of a hemolytic process such as hemolytic anemia. It may also be increased with infectious hepatitis, or with cirrhosis. Comparing the urinary bilirubin result with the urobilinogen result may assist in distinguishing between red cell hemolysis, hepatic disease, and biliary obstruction. Urobilinogen is increased in hemolytic disease and urine bilirubin is negative. Urobilinogen is increased in hepatic disease, and urine bilirubin may be positive or negative. Urobilinogen is low with biliary obstruction, and urine bilirubin is positive. Reagent strips methods however, cannot distinguish normal urobilinogen from absent urobilinogen, as might be seen in complete biliary obstruction. | View Page |
| Urobilinogen is excreted in the urine in increased amounts in: (Choose ALL of the correct answers) | View Page |
| Increases in blood ammonia levels would be expected in which of the following conditions: | View Page |
| Elevation in conjugated bilirubin is most likely to be found in which of the following conditions: | View Page |
| Which of the following conditions will not produce a characteristic protein electrophoresis pattern: | View Page |
| Match these autoimmune diseases with their corresponding serological markers: | View Page |
| General Clinical Considerations Hereditary hemochromatosis (HH) is frequently discovered only during management of associated illness or routine health evaluations. It has been estimated that only a small percentage of all affected persons are actually diagnosed. Individuals with HH may be symptomatic for several years prior to diagnosis and may have consulted multiple health care providers.Under-diagnosis of HH is thought to occur due to:• Lack of specificity of early signs and symptoms• Asymptomatic status of some patients until damage to organs and tissues has occurred• Confusion with liver disease due to other causes• Insufficient awareness and knowledge of HHEarly identification of persons with HH is essential to prevent serious and irreversible complications associated with severe iron overload. A classic triad of skin hyperpigmentation (bronzing), type 2 diabetes, and hepatic cirrhosis has long been recognized as evidence of advanced iron overload. However, persons with HH may present with a much wider variety of signs and symptoms, particularly if they are seen before significant iron accumulation has occurred. Age of presentation and disease severity are highly variable. A diagnosis of HH is based on laboratory evidence of iron overload, genetic mutations associated with HH, and presence of clinical signs and symptoms consistent with HH.(10) | View Page |
| Prognosis and Mortality The major determinant of prognosis in cases of hereditary hemochromatosis (HH) is the degree of organ damage from iron overload at the point of diagnosis. The presence of liver cirrhosis reduces life expectancy. Damage that has occurred to tissues and organs is irreversible, but further damage can be halted with treatment. When there is no evidence of cirrhosis at time of diagnosis, life expectancy may be equal to that of persons without HH. With proper management of HH through treatment, affected individuals have good long-term outcomes. Hepatocellular carcinoma associated with cirrhosis, hepatic failure, and cardiac failure are the most common causes of death in persons with HH. Compared to the normal population, liver cancer is many times more prevalent as a cause of death in persons with HH. Cardiomyopathy, diabetes, and cirrhosis are all more common causes of death among persons with HH than among normal persons. The earlier HH is detected, before the onset of severe organ damage, the lower the risk of mortality. | View Page |
| Rationale for Treatment Treatment for hereditary hemochromatosis (HH) is typically indicated for iron overload in symptomatic patients. The goal of therapy is to reduce stored iron which may result in reversal or resolution of some symptoms and improve prognosis. Causes of death in patients with HH include serious medical conditions such as hepatocellular carcimoma, cirrhosis, cardiomyopathy, and diabetes. Ideally, treatment should begin before these conditions develop. The earlier HH is detected, before the onset of severe organ damage, the lower the risk of mortality. | View Page |
| Which of the following is NOT a cause of death in patients with hereditary hemochromatosis (HH)? | View Page |
| Increase Marrow Iron Stores Markely increased stainable iron is present in this biopsy. Iron stores may be increased in sideroblastic anemia, chronic infections, hemochromatosis, hemosiderosis due to numerous blood transfusions, chronic hepatitis, cirrhosis, and uremia. | View Page |
| Serious adverse outcomes from HBV infection About 10% of adults who are infected with hepatitis B go on to chronic hepatitis, which lasts for years.Chronic hepatitis B eventually can cause scarring of the liver (known as cirrhosis), liver failure, and, more rarely, liver cancer.While these complications are uncommon, they serve to emphasize the need for proper techniques to prevent transmission of HBV. | View Page |
| HCV disease Like HBV disease, HCV disease results in damage to the liver. About 75% of individuals who are infected with HCV go on to develop chronic hepatitis C. Patients with chronic hepatitis C may eventually develop scarring of the liver (known as cirrhosis) and liver failure. | View Page |
| The peripheral blood picture is consistent with each of the following conditions except: | View Page |
| The cells marked by blue arrows in the photograph are associated with all of the following conditions except: | View Page |
| Case History A 54 year-old man was brought to the clinic by his sister who was emphatic that her brother was "not taking care of himself."The patient had a previous gastrectomy and splenectomy. He also had a diagnosis of alcoholism, malnutrition, and hepatic cirrhosis. The following five pages discuss a variety of erythrocyte changes that have occurred as a result of his various conditions. | View Page |
| Pseudomacrocytes Another type of macrocyte can be seen in this image. Notice it appears larger than the lymphocyte but in contrast to the macrocytes (megalocytes) seen in megaloblastic anemias (vitamin B12 or folic acid deficiency), these macrocytes have an area of central pallor. These macrocytes are sometimes referred to as "pseudomacrocytes," since their size is the result of exaggerated flattening and thus the presence of central pallor. When this type of macrocyte is present on a blood slide, the MCV will most likely be within normal range. Pseudomacrocytes can be seen in peripheral blood smears from patients with cirrhosis of the liver, obstructive jaundice, post splenectomy and conditions that affect the red cell membrane. | View Page |
| More Acanthocytes Acanthocytes can also be seen in this slide. Alcoholic cirrhosis is the most common source of acanthocytes seen in blood smears in the laboratory (10-50%). Other sources are lipid disorders and a small number following splenectomy.
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