L70 Flashcards
There are 2 ways to define the architecture of the liver. Describe lobule vs acinar.
Lobule - central lobular vein w/ portal tracts outside (hexamer)
Acinus - 3 zones of functional importance, triangles radiating out from central lobular vein
What does the portal tract contain?
Portal triad:
Hepatic artery
Portal vein
Bile duct
What is the limiting plate // interface? What does inflammation here indicate?
Where normal fibrosis in/around the portal tract stops at hepatocytes
Creates the “bounds” of the portal tract
Inflammation crossing plate = ↑risk greater liver fibrosis (-> cirrhosis)
Describe the location of the 3 acinar zones? What is the functional significance of this classification?
Zone 1 = closest to portal triad, LEAST likely for hypoxia
- Damage here indicates chronic hepatitis
Zone 3 = closest to central // hepatic vein, HIGHEST risk hypoxia
- Ischemic region
What is the liver cell plate? What structures are inside?
Separates hepatocytes and sinusoid (blood space)
Stellate cells inside the space of Disse
- Activate cells -> fibrosis (chronic liver injury)
3 ways to biopsy the liver
- Through skin
- Transjugular - best for pts w/ bleeding risk (bleed into IVC)
- OR via laproscopic
Path + lab findings for cholestasis
Bile in hepatocytes/canaliculi - yellowish/brown
Indicates bile stasis in the liver
↑Bili
↑Alk phos **unique
Path + lab finding for apoptosis
Small pink cells, may have inflammation
Look like in holes b/c shrunken
↑AST/ALT
Path + lab finding for necrosis
Loss of hepatocytes, may have inflammation
No staining
↑↑↑ AST/ALT
If you see ↓AST/ALT, bad - indicates no hepatocytes left (all dead)
Path + lab finding for steatosis. Reversible?
= fatty changes
Empty spaces in liver cells = fat in vacuoles
Normal or mild ↑AST/ALT
REVERSIBLE!
4 Path + lab findings for steatohepatitis. Reversible?
= some fat accum + cell damage + inflam + cell breakdown (maybe some fibrosis)
1. Steatosis
2. Mallory bodies = cell trash that can’t be removed
3. Ballooning hepatocytes (degenerating)
4. Inflammation
↑AST/ALT
REVERSIBLE
Path + lab findings for hepatitis
Inflammation (mostly T cells)
↑AST/ALT
What are 2 diseases that cause fatty liver changes?
Alcohol - Alcoholic Fatty Liver Disease
Obesity - Non-Alcoholic Fatty Liver Disease (NAFLD)
In fatty liver disease, what histo change indicates that the damage is irreversible?
Fibrosis / cirrhosis
You might be able to reduce the fat content but the fibrosis is permanent
3 big causes of hepatitis
Viral
Autoimmune
Metabolic/genetic
Why do you biopsy suspected hepatitis? What do you see?
Biopsy for progression - NOT enough for dx alone
See
- Portal inflammation that extends beyond interface
- Hepatocyte damage
- Progressive fibrosis
Do you grade or stage hepatitis?
YEP - chronic hepatitis (why you’d biopsy)
Used to det progression -> therapy decisions
Grade = current inflam, might resolve
Stage = current fibrosis, permanent
Grade 1 vs 4 hepatitis
1: inflam basically contained to portal tract
4: tons inflam everywhere
- See AST/ALT changes at this point
Why is untreated fibrosis such an issue?
Liver can regenerate itself
But fibrosis limits this capacity
Stage 1 vs 2 vs 3 vs 4 fibrosis
1: no fibrosis
2: rare bridging
3: bridging that forms incomplete nodules
4: cirrhosis = fibrosis in nodules
- Nowhere for new liver to go!
How would you treat a pt hepatitis already showing signs of fibrosis?
Steroids!
Which forms of viral hepatitis can be chronic? What is the criteria to call a viral hepatitis chronic?
B & C
6 mos serum +
May/may not be symptomatic -> may never develop fibrosis
Histo for chronic Hep B carrier
Ground glass cells = virus happily living and replicating in hepatocytes
Smudges are virion in the ER
Why are you worried about asymptomatic Hep B carrier?
Progress to HCC
