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GI Week 4 > Lecture 33: Liver Pathology I > Flashcards

Lecture 33: Liver Pathology I Flashcards

1
Q

What is the difference between acute and chronic injury?

A 
Acute = death or recovery
Chronicity = fibrosis
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2
Q

What are the compartments of injury to the liver?

A
  1. Hepatocytes
  2. vessels, endothelial cells
  3. biliary system
    • ducts
    • canaliculus
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3
Q

Can the recovery of acute injuries lead to fibrosis?

A

No (for the purposes of GI)

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4
Q

What is the capacity of regeneration of liver?

A

Huge regenerative capacity
Re-entry from G0 into S phase
Reticulin framework is important serving as a scaffold for mitotic hepatocytes to replace dead hepatocytes
-collagen in this framework are used for signaling which imparts polarity to cells as well as helping control mitotic state

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5
Q

What does acute injury look like?

A

Loss of hepatocytes and mitoses
On the right side are examples of mitoses!!
APOPTOSIS (look below for another slide!)

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6
Q

What does chronic injury look like?

A

Cirrhosis and nodular surface

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7
Q

What is cirrhosis?

A

Disruption of hepatocellular architecture by fibrosis (shown by blue arrows) which is collagen I
With associated regenerative nodules of hepatocytes

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8
Q

What is the gold standard for diagnosis of cirrhosis?

A

Liver biopsy

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9
Q

Why do we care about fibrosis?

A
  1. Fibrosis impedes and disrupts the synthetic and cleaning function of the liver
    2 .fibrosis increases the resistance of the liver leading to portal hypertension
    Pressure = Flow x Resistance
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10
Q

What are the stages of cirrhosis?

A
  1. Expansion
  2. Septae
  3. Bridging
  4. Cirrhosis
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11
Q

How do transaminases get elevated?

A

Because hepatocytes in the liver die

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12
Q

What are the types of injuries to hepatocytes that lead to elevated transaminases?

A
  1. Apoptosis/Councilman body
    • shrunken, dead cell
  2. Necrosis
    • confluent death e.g. ischemia
  3. Ballooning degeneration
    • swelling
  4. Cholestasis
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13
Q

What is LFT?

A

Liver Function Tests that measure Liver associated enzymes

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14
Q

What does the elevation of ALT mean?

A

Something’s wrong with the liver

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15
Q

What does the elevation of GGT mean?

A

Bile duct injury

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16
Q

What does the elevation of AST mean?

A

It could be produced by

i. liver
ii. muscle
iii. kidney
iv. heart
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17
Q

What does elevated LDH mean?

A

Somethings wrong with
i. heart
ii. kidney
Should never be solely attributed to a primary liver problem

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18
Q

How do you get elevated aminotransferases?

A

Elevated serum enzymes results from cytoplasmic blebbing post cellular injury

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19
Q

Where do you find AST?

A

Mitochondria

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20
Q

Where do you find ALT?

A

Cytoplasm

21
Q

Where do you get GGT?

A

Bile canaliculus
GGT gets SYNTHESIZED (whereas the other ones don’t get synthesized)
When bile gets fucked, hepatocytes are induced to form GGT

22
Q

What are the patterns of injury and liver associated enzymes?

A
  1. vascular
  2. hepatitis
  3. Infiltrative
  4. Cholestatic
23
Q

What are the types of vascular injuries to the liver?

A
  1. outflow
  2. inflow
    • arteries
    • portal vein
24
Q

What is the inflow into the liver?

A
  1. portal vein

2. hepatic artery

25
Q

What is the outflow out of the liver?

A

Hepatic veins  inferior vena cava  right heart

There are three hepatic veins (L, R and middle)

26
Q

What if you block the vena cava?

A

Right heart blockage means that liver is going to get enlarged (initially)

27
Q

What are the gross and histological features of an acute venous outflow blockage of liver?

A
  1. gross = nutmeg liver

2. histologically = congested liver

28
Q

What is the significance of a nutmeg liver?

A

A gross feature that implies congestion or venous OUTFLOW blockage

29
Q

OVER TIME, if you have venous obstruction, what happens?

A

Cardiac type fibrosis
Fibrosis will be along the lines of force and increased pressure
INITIALLY you see a nutmeg liver

30
Q

What is Budd-chiari?

A

A clinical picture caused by occlusion of only ONE of the hepatic veins
Presents with triad of abdominal pain, ascites and hepatomegaly

31
Q

What is the Budd-chiari triad?

A
  1. Abdominal pain
  2. Ascites
  3. Hepatomegaly (of the compensating part of liver)
32
Q

What are the manifestations of CHRONIC budd-chiari?

A

Cardiac lobe HYPERTROPHY (while other lobes atrophy)
Because this is where other two hepatic veins
Are still patent
So hypertrophies to compensate for the atrophy
Of the other lobes
Can you get coagulative necrosis in the liver?
Yes
You can get hyperemia and coagulative necrosis

33
Q

How else can you get infarction besides blockage?

A

HYPOtension

34
Q

What is zone 3?

A

The portion of the liver that is last to receive blood (most likely to become ischemic)
The lines of pressure/force from cardiac fibrosis will be along Zone 3 because that is where pressure is most in venous output blockage!!

35
Q

What is portal tract venopathy?

A

Obliteration of portal vein due to fibrosis and irregular remodeling

36
Q

What is the most common cause of portal vein obstruction?

A

Schistosomiasis

37
Q

What happens when you block the hepatic artery?

A

Infarction of the bile duct

This is because the bile duct ONLY gets blood from the hepatic artery

38
Q

What is a biloma?

A

All the contents of liver/gall bladder leak out because hepatic artery is blocked/ischemia to bile duct

39
Q

What are example of hepatitis injury?

A

Hep C

Acetaminophen (DILI)

40
Q

What is hepatitis?

A

Injury directed at the HEPATOCYTES

41
Q

In a hepatitis pattern, what are the enzyme levels?

A

Elevated ALT and AST

Same level of ALK, GGT and bilirubin

42
Q

What are the infiltrative patterns of injury in the liver?

A
  1. Steatosis
  2. Amyloid
    Defined by the fact that they are PARAhepatocellular
43
Q

What is the significance of steatosis and amyloid accumulation in the liver?

A

These are examples of INFILTRATIVE injuries to the liver

Do NOT directly damage the hepatocytes, rather just grow around it

44
Q

What is steatohepatitis?

A

Evidence of hepatocellular injury

45
Q

What is steatosis of the liver?

A

Fat but without hepatocellular injury

46
Q

What are Mallory’s hyaline?

A

Ubiquinated intermediate fibers

Not diagnostic, but associated with alcohol fatty liver

47
Q

What is cholestasis?

A

When a bile plug leads to hepatocyte apoptosis (enlarged hepatocytes)
This leads to elevated GGT

48
Q

What are the types of inflow blockage?

A
  1. Portal vein thrombosis

2. hepatic artery thrombosis

GI Week 4 (12 decks)

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