SFP: general principles/lab eval of the liver Flashcards

1
Q

In normal conditions, what kinds of inflammatory cells do we see in the liver?

A

None

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2
Q

When we do an LFT, what are we testing for? Why?

A

AST and/or ALT. These are liver enzymes that are found in serum where there has been damage or death to hepatocytes. We also test for proteins, as hepatocytes make a huge amount of these (ex-albumin).

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3
Q

What is the major job of hepatocytes?

A

Protein synthesis; makes albumin, fibrinogen, prothrombin, etc.

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4
Q

Lobular inflammation is an indication of what kind of hepatitis?

A

Acute

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5
Q

Portal inflammation is an indication of what kind of hepatitis?

A

Chronic

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6
Q

What do hepatocytes look like upon being damaged?

A

They’ll start with ballooning/looking swollen. They may also begin to look foamy, have fatty changes, and necrosis.

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7
Q

What is centrilobular necrosis?

A

Necrosis in zone 3, around the central vein. This is often seen in ischemia and possible as a result of drugs like Tylenol.

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8
Q

What is piecemeal necrosis?

A

Portal tract is eaten away, and inflammatory cells begin to spill out into the rest of the liver lobule.

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9
Q

What is bridging necrosis?

A

Necrosis that connects two major structures, like central veins and portal tracts.

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10
Q

What is massive necrosis?

A

The hepatocytes alone are being killed; portal structures are still intact.

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11
Q

What is the histology of cirrhosis?

A

Loss of central vein, massive bridging and fibrosis around the lobule. This wipes out the vascular organization of the liver, blocking the blood from getting from the portal system back to the systemic system.

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12
Q

What is cholestasis?

A

Accumulation of bile due to damage of bile duct structures.

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13
Q

What is seen on histology in cholestasis?

A

Bile backing up, proliferation of bile ducts, apoptosis, Kupffer cells.

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14
Q

What enzymes can we measure to indicate damage to biliary cells?

A

ALP and GGT.

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15
Q

What are the functions of the biliary tract in terms of elimination?

A

Elimination of bilirubin, cholesterol and xenobiotics.

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16
Q

What is bilirubin?

A

A product from the breakdown of RBCs that is transported to the liver for excretion.

17
Q

What does the liver do to bilirubin?

A

Conjugates it to glucuronides and excretes it to bile canaliculus as bile.

18
Q

What happens to bile/bilirubin in the small intestine?

A

The bilirubin is deconjugated to stercobilinogen that can be reabsorbed and excreted in the urine as urobilinogen.

19
Q

What are typical causes of unconjugated hyperbilirubinemia?

A

Excess production of bilirubin, reduced hepatic uptake of bilirubin, or impaired bilirubin conjugation.

20
Q

What lab values demonstrate excess bilirubin production?

A

Increased total bilirubin, increased indirect bilirubin, slight increase in direct bilirubin, and increased urobilinogen.

21
Q

What lab values demonstrate impaired conjugation of bilirubin?

A

Increased total bilirubin that is mostly due to increased indirect bilirubin and decreased urobilinogen.

22
Q

What does UDP-glucuronyl transferase do?

A

Conjugate bilirubin; may be deficient in premature infants.

23
Q

What is type 1 Crigler-Najjar syndrome?

A

No UDP-glucuronyl activity; it is usually fatal. Will show with markedly increased total bilirubin and indirect bilirubin. No direct bilirubin or urobilinogen.

24
Q

What is type 2 Crigler-Najjar syndrome?

A

A partial defect in UDP-glucuronyl activity that results in increased total and indirect bilirubin.

25
Q

What is Gilbert’s syndrome?

A

A benign inherited disorder with reduced UDP-glucuronyl transferase activity. Increased total and indirect bilirubin with decreased direct bilirubin and urobilinogen.

26
Q

What is direct hyperbilirubinemia?

A

Direct hyperbilirubinemia refers to elevated levels of direct (conjugated) bilirubin in the blood.

27
Q

What are common causes of direct hyperbilirubinemia?

A

Biliary obstruction, pancreatic cancers, biliary atresia.

28
Q

What are lab values for direct hyperbilirubinemia?

A

Increased total bilirubin with direct and indirect being equal, and urobilinogen absent.

29
Q

What is Dubin-Johnson syndrome?

A

Defect in transport protein for hepatocellular bile excretion across the canalicular membrane. Results in black pigment in the liver.

30
Q

What are the three presentations of hepatic failure?

A

Chronic progressive disorder, ultrastructural lesions, and massive hepatocellular destruction.

31
Q

What is hepatic encephalopathy?

A

Metabolic disorder of the CNS and neuromuscular system resulting from liver failure. It can be subtle or can result in coma. It is reversed with a new liver!

32
Q

What is hepatorenal syndrome?

A

Renal failure resulting from liver failure; reversed with a new liver!

33
Q

What is the pathogenesis of cirrhosis?

A

Deposition of types 1 and 3 collagens in all portions of the lobule and associated inflammation.

34
Q

What are complications of cirrhosis?

A

Portal HTN/ascites and hepatic failure.