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GI Path Lab 3: Part II
The Liver Sequence


Reading Assignments (Robbins: Pathologic Basis of Disease, 8th Ed.)
835 - 836 Morphology of hepatic injury
857 - 861 Morphology of fatty liver, including non-alcoholic fatty liver disease
870 - 873 Circulatory disorders through hepatic vein thrombosis
843 - 856 Morphology of acute viral hepatitis and chronic hepatitides
850 - 853 Submassive to massive necrosis
867 - 869 Primary biliary cirrhosis and primary sclerosing cholangitis
837 - 838 Cirrhosis (introduction)
857 - 860 Alcoholic liver disease. Skip the clinical stuff and get it from the Medicine book.
861 - 864 Hemochromatosis and Wilsonís disease as cirrhoses
875 - 882 Tumors of the liver

Areas of Concentration

  • Injuries to the liver, including those that induce hepatocyte damage, lipid accumulation, and retention of bile constituents

  • Acute liver disease

  • Chronic liver diseases

  • The complications of chronic liver diseases


Upon completion of this exercise, you should be able to:

  1. Recognize a fatty liver histologically and understand the general concepts of its etiology.

  2. Identify the gross and histologic changes induced by low arterial flow and deficient venous drainage.

  3. Recognize the chaos induced in the liver by hepatitis viruses.

  4. Diagnose cirrhosis both grossly and microscopically.

  5. Recognize the many causes of cirrhosis.

  6. Know the complications of cirrhosis.



ACUTE LIVER DISEASE

Slide 32 [WebScope] [ImageScope]

Acute Ischemic Liver Disease (Central Hemorrhagic Necrosis)

On low power examination of this section, viable-looking liver cells are found in a predictable location, namely, around the portal tracts. In contrast, there are hemorrhagic areas around the central veins. Some of these areas contain only blood; others contain ghosts of hepatocyte cords in addition to the blood, while still others contain mainly necrotic hepatocytes and little blood. This is the essence of a zonal injury that has caused confluent necrosis, in this case, confluent central necrosis with blood, or central hemorrhagic necrosis.

  1. What insults, other than ischemia, most commonly lead to confluent central necrosis?

  2. What mechanism might account for the pooling of such large quantities of blood in the necrotic areas?



Slide 3 [WebScope] [ImageScope]

Fatty Liver

This is an example of a cellular alteration, sometimes, but not always, an injury, but generally reversible. Normal hepatocytes contain lipid, but not in large clumps that are seen in routine light microscopy. Fatty livers of mild degree are very common. Fatty livers of severe degree indicate a profound metabolic imbalance.

  1. How does a hepatocyte become filled with so much lipid?

  2. What is the best source of information that might offer a hint of the cause of a fatty liver?



Slide 94 [WebScope] [ImageScope]

Cholestasis

The dominant change is the presence of brown or brownish-green pigment that is mainly found between liver cells. On occasions, the brown pigment forms long and even branched structures. This appearance indicates that the material is within the bile canaliculi between hepatocytes. Remember, bile canaliculi are tubes or channels for bile flow which are formed by specialized parts of cell membranes of adjacent liver cells. Cholestasis is defined simply as interference with bile flow. Cholestasis is a common accompaniment of many liver diseases. Therefore, it is more like a sign or symptom of liver disease, rather than a disease by itself.

  1. What is the pigmented constituent of bile that is present in the dilated canaliculi?

  2. Are there any other constituents of bile that you can see in this slide? To answer this question, you must know what are the constituents of bile.

  3. This liver has no scars, virtually no inflammation, hardly any liver cell necrosis, except for a few cells in the most intensely bile-loaded areas. What changes would you expect to see in the following serum chemical parameters?

    Bilirubin? Any specific fraction that is most abnormal?

    Alkaline phosphatase?

    Aminotransferase?



Slide 93 [WebScope] [ImageScope]

Acute Viral Hepatitis

Most of the liver cells are pale and rounded, creating disorganized cords. Scattered about are necrotic liver cells with dark red cytoplasm and either no nucleus or fragments of a nucleus. Scattered about also are slightly granular, pale yellow-brown phagocytes similar to those in the central zones in Slide 32, which contain necrotic liver cell debris. In some places, it appears as if whole clusters of hepatocytes have disappeared. The portal tracts contain inflammatory cells, mostly lymphocytes, and scattered lymphocytes are present within the sinusoids. This is a characteristic picture of the peak phase of an active, intense hepatitis, such as might be caused by one of the hepatitis viruses. Occasionally, drugs or poisons can cause a similar process.

  1. What would usually be expected to happen to this liver if this were viral hepatitis?

  2. Do you see any significant degree of cholestasis similar to that in Slide 94?

  3. What would you expect the serum liver chemistries to be, based on what you see on this slide?

    Bilirubin?

    Alkaline phosphatase?

    Aminotransferases?

  4. What would you expect the serum parameters of liver function to be?

    The albumin?

    The clotting factors?

  5. If this were caused by the hepatitis B virus, what would you expect the circulating B markers to be at this time:

    B surface antigen?

    B core antigen?

    B core antibody?

    B surface antibody?

  6. If this were caused by the hepatitis A virus, would you expect to see antibody to the virus at this time?



The answers to the path lab questions will be posted approximately 48-72 hours after the lab sessions. These are abbreviated answers, not a full discussion of the topics. You can find them in the M2 CTools site resources. In the folder for each sequence the will be a folder called 'Path Lab Resources'


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