Liver Pathology and Patterns of Injury Flashcards

1
Q

Chronic liver injuries lead to _____

A

fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does a liver respond to acute injury?

A

death or regeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Key feature of cirrhosis

A

disruption of hepatocellular architecture by fibrosis w/ associated regions of regenerative hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Stages of cirrhosis

A

normal –> expansion –> septae –> bridging of septae –> cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where does ALT live?

A

liver predominant (cytoplasm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where does GGT live?

A

bile canaliculus of hepatocyte –> indicator of biliary process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where does AST live?

A

muscle, kidney, liver (cytoplasm and mitchondria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where does LDH live?

A

heart, kidney –> not a sign of liver involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Elevated serum enzymes result from ______ post cellular injury

A

cytoplasmic blebbing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

In what cases is AST > ALT?

A

alcohol hepatitis and Wilson’s disease –> mitochondrial involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does GGT increase after injury to the biliary tree?

A

increased synthesis (compensative) and secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is different about the caudate lobe vs other lobes of liver?

A

has independent venous drainage into vena cava –> not dependent on hepatic vein –> safer during times of damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Initial response to outflow blockage (e.g. right side heart failure).

A

hepatomegaly resulting in pain and leakage (ascites) –> congestion (zone 3) –> nutmeg liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Chronic consequence of outflow blockage (e.g. right side heart failure).

A

cardiac type fibrosis (zone 3) in all lobes, atrophy of hepatocytes (low blood, pressure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Consequence of outflow blockage (e.g. hepatic vein ala Budd-Chiari).

A

acute: caudate sparing, hepatomegaly, pain, ascites
chronic: caudate hepatomegaly, atrophy and fibrosis of rest of liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is a complication of caudate lobe enlargement?

A

compression of IVC

17
Q

Consequence of inflow blockage (all vessels).

A

hepatic infarction w/ central necrosis + hyperemic rim –> unpredictable pattern b/c of areas of dual blood supply

18
Q

Consequence of hypotension on liver?

A

diffuse ischemia (zone 3)

19
Q

Consequence of inflow blockage (portal vein).

A

splenomegaly, initially no liver effect –> propagation of a thrombosus can lead to stenosis, obliteration of portal vein AKA portal tract venopathy –> portal hypertension (no pressure increase in sinusoids/cords so no ascites)

20
Q

1 cause of portal hypertension w/o cirrhosis

A

schistosomiasis

21
Q

Blood supply to bile duct

A

hepatic artery

22
Q

Bile duct infarction

A

blockage of hepatic artery can result in infarction of bile duct –> biloma formation in liver b/c of blockage –> infection

23
Q

Features of a hepatitic pattern of injury

A

lymphocytes in portal tracts, apoptotic hepatocytes in parenchyma due to FAS activation by lymphocytes, interface activity, ALT/AST elevation

24
Q

What is hepatitis activity?

A

volume of lymphocytes in chronic hepatitis–> risk of fibrosis

25
Q

Pathophysiology of Acetominophen acute hepatitis

A

metabolic product is toxic (NAPQ1) leads to acute zone 3 damage due to p450 metabolism in dose dependent manner

26
Q

Complication of large dose acetominophen acute injury

A

fulminant hepatic necrosis

27
Q

Steatohepatitis

A

fat in hepatocytes w/evidence of injury (inflammatory cells not necessary, can be due to ROS) –> elevated ALT, AST, GGT

28
Q

Features of steatohepatitis

A

ballooning degeneration, mallory’s hyaline (nonspecific sign), glycogenated hepatocellular nuclei

29
Q

Cholestasis

A

impediment of bile flow –> bile plugs, feathery degeneration due to bile salt buildup–> fibrosis and cirrhosis –> ALT, AST, GGT, ALK, bilirubin all high

30
Q

What does a bile infarct suggest?

A

mechanical blockage