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Flashcards in GI 3 Deck (49):

Jaundice results from the retention of ______ and an abnormality in the processing of ________.

retention of bile, abnormal processing of bilirubin


What are the four general stages of bilirubin metabolism?

1. Production (heme degradation)
2. Uptake by liver
3. Conjugation
4. Transport to the duodenum through the bile ducts.


What are the three types of jaundice?

1. Hemolytic
2. Hepatocellular
3. Obstructive


Describe hemolytic jaundice.

Hemolytic anemia with excessive production of unconjugated bilirubin (excessive heme breakdown)


Describe hepatocellular jaundice.

When there is a problem in the liver:
1. Messed up liver uptake.
2. Messed up conjugation of bilirubin
3. Messed up. transport to the duodenum.


Crigler-Najjar and Gilbert are characterized by a problem with bilirubin _______.



Hepatitis, generalized liver cell injury, and some drugs can affect the liver's ability to ________ bilirubin.



Dubin-Johnson syndrome is characterized by defective ________ of conjugated bilirubin.



What is cholestasis?

Arrested bile flow.


What are two causes of cholestasis?

1. Intrinsic liver disease (intrahepatic cholestasis)
2. Bile duct obstruction (extrahepatic cholestasis)


What is the "hallmark" of cholestasis?

Brownish pigment within dilated canaliculi and hepatocytes and bile duct proliferation.


Name two clinical findings that would suggest cholestasis.

1. Jaundice and pruritus (itchiness) due to deposition of bile acids in skin.
2. Elevated serum alkaline phosphatase.


Cirrhosis is the end stage of ________ _______ disease.

chronic liver disease


Define liver cirrhosis and list its 3 main characteristics

End stage of chronic liver disease characterized by:
1. Bridging fibrous septa around multiple adjacent lobules.
2. Parenchymal nodules (fibrous bands surrounding several hepatocytes).
3. Disruption of the normal architecture of the entire liver


Name 5 causes of cirrhosis.

1. Alcoholic liver disease
3. Chronic hepatitis
4. Biliary disease
5. Metabolic diseases like hemochromatosis, a-1-alphatrypsin deficiency, glycogen storage diseases.


List the four pathogenic stages of cirrhosis.

1. Hepatocyte death
2. Regeneration
3. ECM deposition and fibrosis
4. Vascular reorganization


Answer these questions regarding cirrhosis:
1. How does collagen contribute to the disease?
2. Why is vascular reorganization a bad thing?
3. What role do hepatic stellate cells play?

1. Collagens Type 1 and 3 are deposited in the space of Disse (where only thin strtands of Type 4 normally are), resulting in the loss of capillary fenestration and impaired exchange of solutes.
2. The fibrotic capillaries promote revascularization, which shunts blood away from the hepatocytes - eliminating the point of having a liver.
3. Hepatic stellate cells proliferate and turn into highly fibrogenic MYOFIBROBLASTS.


What do the hepatocytes that are able to survive in the case of cirrhosis end up doing?

They proliferate as spherical nodules within the confines of the fibrous septa to create a fibrotic, nodular liver with poor blood flow and impaired function.


Are Kupffer cells also involved in the fibrogenic pathogenesis of cirrhosis?



Name the clinical features of liver cirrhosis and three complications from it that can cause death.

1. Weight loss or anorexia
2. Weakness --> debilitation

Death results from liver failure, complications related to portal hypertension, development of hepatocellular carcinoma.


Name three major complications resulting from portal hypertension.

1. Esophogeal varices and hemorrhage.
2. Ascites from decreased liver function (no albumin).
3. Splenomegaly


Portal hypertension in women may result in hypogonadism, potentially causing _______, ________, and ________.

oligomenorrhea, amenorrhea, or sterility


Portal system collateral veins are located in the __________ of the lower esophagus and upper stomach and communicate with the portal and the _______ coronary vein.

located in the submucosa of the lower esophagus and upper stomach and communicate with the portal and the gastric coronary vein


Can dilation of the submucosal esophogeal/gastric veins due to portal hypertension protrude into the GI lumen?



How can portal hypertension affect the spleen?

The portal vein and splenic vein are connected, so a backup in the portal vein shunts blood to the spleen --> enlargement - splenomegaly.


What is pancytopenia? Name a disease that can cause it.

It is when there are decreased numbers of red, white cells, and platelets in the blood. Hypersplenism from portal hypertension can cause it.


Describe the gross morphological changes of splenomegaly.

Firm, enlarged, cut surface is deep red, no apparent white pulp.


By what four physiologic mechanisms can fluid accumulate in the peritoneal cavity (ascites)?

1. Decreased plasma oncotic pressure due to liver dysfunction.
2. Portal hypertension increases hydrostatic pressure of mesenteric arteries.
3. Sinusoidal hypertension in the liver --> lymph "weeps" into the abdomen.
4. Hyperaldosteronism --> renal retention of Na+ and H2O.


What is caput medusae? What causes it?

It is the appearance of distended and engorged paraumbilical veins, which are seen radiating from the umbilicus across the abdomen to join systemic veins.. It is caused by recanalization of the umbilical vein by liver failure/portal hypertension.


The hepatotropic viruses are named from A to ___.



What is viral hepatitis?

An infection of the hepatocytes that produces necrosis and inflammation of the liver.


Describe five morphological changes characteristic of acute viral hepatitis.

1. Scattered necrosis of single hepatocytes or clusters of cells.
2. Ballooning degeneration of infected cells.
3. COUNCILMAN BODIES (apoptotic hepatocytes that are small and deeply eosinophilic).
4. Intralobular and portal tract infiltration of lymphocytes and macrophages.
5. Kupffer cell hyperplasia and hypertrophy.


Chronic hepatitis is a complication of hepatitis types ___ and ___, and a number of ______ and ______ disorders.

B and C and a number of metabolic and immune disorders.


Can chronic hepatitis range from mild portal inflammation with little hepatocyte necrosis to a widespread, necrotizing and fibrosing condition that ends in cirrhosis?



Name four morphological changes associated with chronic hepatitis.

1. Periportal necrosis with focal destruction of the limiting plate (the hepatocytes near the portal triad) - "moth-eaten"
2. Intralobular and portal tract inflammation.
3. Bridging necrosis (formation of connective tissue septa between adjacent portal tracts)
4. Ground-glass hepatocytes (have large granular cytoplasm with HBsAg).


What are the three morphologic and clinical entities of alcoholic liver disease?

1. Fatty change (accumulation of fat in hepatocytes, steatosis).
2. Hepatitis - necrosis of hepatocytes in the central zone, cytoplasmic hyaline inclusions in hepatocytes (Mallory Bodies/alcoholic hyaline), collagen deposition around central vein).
3. Cirrhosis - fibrosis, vascular remodeling.


What is hepatocellular carcinoma? How common are they?

Malignant primary tumor derived from hepatocytes which appears as a soft, hemorrhagic mass in the liver. One of the most common worldwide tumors but uncommon in the U.S.


Which viruses are associated with hepatocellular carcinoma?

Hep B and C


Which virus type is known to ingetrate its genome into hepatocytes in cases of hepatocellular carcinoma?

Hep B


Aside from Hep B and C infection, name three other risk factors for hepatocellular carcinoma development.

1. Hemochromatosis
2. a-1-antitrypsin deficiency
3. Aflatoxin B1 (product of fungi in poorly stored grains - environmental agent, seen in developing countries).


Describe the morphological changes involved in hepatocellular carcinoma.

Variable. Most HCCs exhibit a ‘trabecular pattern’ with the tumor cells arranged in trabeculae or plate that resemble the normal liver. Others can have a glandular pattern. They like to invade vascular channels.


Can hepatocellular carcinoma produce paraneoplastic syndrome? What is the tumor marker for hepatocellular carcinoma?

Yeah paraneoplastic syndrome often. Alpha-fetoprotein is the marker - detectable in blood.


What is the prognosis for hepatocellular carcinoma?

Very poor.


What is cholelithiasis?

Gallstones within the gall bladder lumen or extrahepatic biliary tree.


What are gallstones made of?

Cholesterol primarily, esp. in the west, calcium, bilirubinate.


Gallstones form partly from excess ________ that precipitates as solid crystals.



What causes cholecystitis? Compare acute cholecystitis to chronic cholecystitis.

Stones/obstruction cause it.

Acute: Gallbladder wall is thickened and edematous, mucosa is deep red or purple. Infiltration of neutrophils in the epithelium.

Chronic: Wall is thickened and firm, wall may be ulcerated. Inflammation seen in ALL layers of the walls.


What cells infiltrate the liver in the case of chronic viral hepatitis? What cell type are you least likely to see?

1. Lymphocytes
2. Plasma cells
3. Macrophages



What are Mallory bodies and in which disease are they seen?

Accumulation of intermediate filaments in hepatocytes. Seen in alcoholic hepatitis.