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  #1  
Old 06-25-2011
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Liver Abdominal CT Scan Diagnosis!

A 55-year-old man sees his primary care physician with a complaint of increasing abdominal girth. After a history and physical exam, his physician orders a CT scan of the abdomen. An image from the study is shown in the figure. What is the patientís most likely diagnosis?

Abdominal CT Scan Diagnosis!-ctscan.jpg
click image to enlarge

Answer Choices Correct answer Your answer
A. Cirrhosis of the liver
B. Hodgkin disease
C. Liver cancer
D. Pancreatic cancer
E. Portal vein thrombosis
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  #2  
Old 06-25-2011
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not sure but im with cirrhosis...because of it s smaller size nad shape...is the spleen enlarged too? i thin it is ...correct me if i m wrong please
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Old 06-25-2011
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this is portal vein thrombosis
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  #4  
Old 06-25-2011
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A or C ???
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  #5  
Old 06-25-2011
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I am with cirrhosis as well, because the liver size is small and I can not see any mass as well. Correct me if I am wrong, thanks.

Last edited by Patan; 06-25-2011 at 05:29 PM.
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Old 06-25-2011
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i choose A . liver is enlarged and homogeneous . maybe maybe not!
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Old 06-25-2011
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i think it's portal v. thrombosis but maybe not
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Old 06-26-2011
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its surely DVT, with ascities
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Old 06-26-2011
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liver cancer
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Old 06-26-2011
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i'm leaning towards E
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Old 06-26-2011
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I am also unsure about this, I choose E as well
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Old 06-26-2011
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I'm going with Cirrhosis

But can anyone answering E tell us Why ?
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Old 06-26-2011
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Quote:
Originally Posted by Abdulhakeem View Post
I'm going with Cirrhosis

But can anyone answering E tell us Why ?
Because you see a different density in the area where the portal vein should be, but I am not sure if thrombosis is seen as hypodensity or hyperdensity in the CT scan.
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Old 06-26-2011
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Here is a link to images of portal vein thrombosis CTs
http://liveratlas.org/case/129/

Here are two examples of cirrhosis (alcoholic and primary biliary)
http://liveratlas.org/case/166/
http://liveratlas.org/case/169/
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Old 06-26-2011
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m voting for E). portal vein thrombosis
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  #16  
Old 06-26-2011
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C - liver cancer
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  #17  
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Option A (Cirrhosis of the liver) is correct. Splenomegaly, an irregular lobulated liver, and enlargement of collateral vessels beneath the anterior abdominal wall are seen, indicating cirrhosis of the liver.

Option B (Hodgkin disease) is incorrect. Splenomegaly, hepatomegaly, and possibly portal hypertension could occur in Hodgkin disease. There is no lymphadenopathy present. There is an irregular lobulated liver, splenomegaly, and enlargement of collateral vessels beneath the anterior abdominal wall (arrows) as a result of portal hypertension. This is the pathology seen in cirrhosis of the liver.

Option C (Liver cancer) is incorrect. There is no obvious liver mass. Splenomegaly, an irregular lobulated liver, and enlargement of collateral vessels beneath the anterior abdominal wall are seen, indicating cirrhosis of the liver.

Option D (Pancreatic cancer) is incorrect. The pancreas is not seen in the CT image. There is splenomegaly and enlargement of collateral vessels beneath the anterior abdominal wall (arrows) as a result of portal hypertension.

Option E (Portal vein thrombosis) is incorrect. Portal hypertension would occur but not splenomegaly or irregular lobulation of the liver. The incidence of portal vein thrombosis is also much lower than cirrhosis of the liver.

High-yield Hit 1
43 Cirrhosis of the Liver and Its Complications
Miguel R. Arguedas
Michael B. Fallon
Cirrhosis is the irreversible end result of the fibrous scarring and hepatocellular regeneration that constitute the major responses of the liver to a variety of long-standing inflammatory, toxic, metabolic, and congestive insults. In cirrhosis, the normal hepatic lobular architecture is replaced by interconnecting bands of fibrous tissue surrounding nodules derived from foci of regenerating hepatocytes.
Regenerative nodules may be small (<3 mm; micronodular cirrhosis), a typical feature of alcoholic cirrhosis, or large (>3 mm; macronodular cirrhosis). The latter, also termed postnecrotic cirrhosis, is more commonly seen as a sequela to chronic active hepatitis. The pathologic features of cirrhosis determine its natural history and clinical manifestations. Thus fibrous scarring and disruption of the hepatic architecture distort the vascular bed and contribute to portal hypertension and intrahepatic shunting. Normal hepatocyte function is disturbed by the resulting inadequacy of blood flow and ongoing direct toxic, inflammatory, and/or metabolic damage to hepatocytes.
Clinical and Laboratory Features
Clinical features of cirrhosis are attributable to hepatocellular dysfunction and portal hypertension (Table 43-1). Hepatocellular dysfunction leads to impaired protein synthesis (hypoalbuminemia and prolongation of prothrombin time); hyperbilirubinemia, which may result in jaundice; low blood urea nitrogen levels; and elevated ammonia levels. Portal hypertension is responsible for the formation of gastroesophageal varices, ascites, and hypersplenism (thrombocytopenia and leukopenia).
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