Pathology of the GI Tract- Liver and Gallbladder (1) Flashcards

1
Q

What are two causes of conjugated hyperbilirubinemia?

A
  1. deficiency of canalicular membrane transporters (Dubin-Johnson syndrome or Rotor syndrome) 2. impaired bile flow from duct obstruction or autoimmune cholangiopathies
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2
Q

what tests assess the hepatocyte integrity?

A

AST, ALT, and LDH

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3
Q

what tests assess the biliary excretory function?

A

serum bilirubin, serum bile salts, alk phos, GGT

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4
Q

what tests assess the true functions of the liver?

A

albumin, coagulation factos (PT/PTT/INR), ammonia

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5
Q

which test is particularly sensitive for liver disease?

A

GGT

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6
Q

elevated ALP can suggest what?

A

either liver or bone disease

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7
Q

what is the pattern of liver function tests seen in a person with obstructive liver disease?

A

elevated ALP and bilirubin

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8
Q

injured or dysfunctional hepatocytes in a variety of disorders may demonstrate several potentially reversible morphologic changes. These include?

A

steatosis, cholestasis, ballooning (ballooning may form Mallory hyaline)

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9
Q

what is the pattern of cell death seen in acute toxic or ischemic injuries or in severe viral or autoimmune hepatitis?

A

coagulative necrosis

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10
Q

what is the principal cell type involved in scar deposition in the liver?

A

hepatic stellate cell

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11
Q

regeneration of the liver occurs by two major mechanisms, what are they?

A

proliferation of remaining hepatocytes and repopulation from progenitor cells

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12
Q

what are the stimuli for stellate cell activation?

A

inflammatory cytokines (TNF-alpha), altered interactions with ECM, and toxins and ROS

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13
Q

in chronic liver disease, surviving hepatocytes replicate in an effort to restore the parenchyma, forming what?

A

regenerative nodules- predominant feature in most cirrhotic livers

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14
Q

what defines hepatic failure?

A

80-90% of functional capacity must be lost

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15
Q

what defines acute liver failure?

A

an acute liver illness associated with encephalopathy and coagulopathy that occurs within 26 weeks of the initial liver injury in the absence of pre-existing liver disease

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16
Q

50% of ALF in the US is due to what?

A

acetaminophen

17
Q

acute liver failure is usually associated with what?

A

massive hepatic necrosis

18
Q

what are two cases that may result in acute liver failure with widespread dysfunction of liver cells?

A

diffuse microvesicular steatosis or idiosyncratic reactions to toxins

19
Q

what are the clinical features of acute hepatic failure?

A

nausea, vomiting, icterus and jaundice, itching, and elevated liver enzymes; life threatening coagulation abnormalities; hepatic encephalopathy (asterixis)

20
Q

what is chronic liver failure most often associated with?

A

cirrhosis

21
Q

what are the leading causes of chronic liver failure worldwide?

A

chronic hepatitis B, chronic hepatitis C, nonalcoholic fatty liver disease, and alcoholic liver disease

22
Q

what are the non-specific early symptoms of chronic liver failure?

A

anorexia, weight loss, and weakness

23
Q

what are the specific features of chronic liver failure?

A

palmar erythema, spider angiomata, hypogonadism, and gynecomastia (symptoms of acute liver failure+ portal hypertension)

24
Q

what are the major prehepatic conditions that lead to portal hypertension?

A

obstructive thrombosis, narrowing of the portal vein, or massive splenomegaly with increased splenic vein blood flow

25
Q

what is the main posthepatic causes of portal hypertension?

A

severe right sided heart failure, constrictive pericarditis, and hepatic vein outflow obstruction

26
Q

what is the dominant intrahepatic cause of portal hypertension?

A

cirrhosis

27
Q

what is ascites?

A

the accumulation of fluid in the peritoneal cavity

28
Q

what are the principal sites of shunts that form in cases of chronic portal hypertension?

A

veins around and within the rectum, esophagogastric junction, the retroperitoneum, and the falciform ligament of the liver

29
Q

what are the four major consequences of portal hypertension?

A

hepatic encephalopathy, ascites, the formation of portosystemic venous shunts, and congestive splenomegaly