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P&T Block 3 Pulm & GI > L70 > Flashcards

L70 Flashcards

1
Q

There are 2 ways to define the architecture of the liver. Describe lobule vs acinar.

A

Lobule - central lobular vein w/ portal tracts outside (hexamer)
Acinus - 3 zones of functional importance, triangles radiating out from central lobular vein

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2
Q

What does the portal tract contain?

A

Portal triad:
Hepatic artery
Portal vein
Bile duct

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3
Q

What is the limiting plate // interface? What does inflammation here indicate?

A

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)

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4
Q

Describe the location of the 3 acinar zones? What is the functional significance of this classification?

A

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

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5
Q

What is the liver cell plate? What structures are inside?

A

Separates hepatocytes and sinusoid (blood space)
Stellate cells inside the space of Disse
- Activate cells -> fibrosis (chronic liver injury)

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6
Q

3 ways to biopsy the liver

A
  1. Through skin
  2. Transjugular - best for pts w/ bleeding risk (bleed into IVC)
  3. OR via laproscopic
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7
Q

Path + lab findings for cholestasis

A

Bile in hepatocytes/canaliculi - yellowish/brown
Indicates bile stasis in the liver
↑Bili
↑Alk phos **unique

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8
Q

Path + lab finding for apoptosis

A

Small pink cells, may have inflammation
Look like in holes b/c shrunken
↑AST/ALT

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9
Q

Path + lab finding for necrosis

A

Loss of hepatocytes, may have inflammation
No staining
↑↑↑ AST/ALT
If you see ↓AST/ALT, bad - indicates no hepatocytes left (all dead)

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10
Q

Path + lab finding for steatosis. Reversible?

A

= fatty changes
Empty spaces in liver cells = fat in vacuoles
Normal or mild ↑AST/ALT
REVERSIBLE!

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11
Q

4 Path + lab findings for steatohepatitis. Reversible?

A

= 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

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12
Q

Path + lab findings for hepatitis

A

Inflammation (mostly T cells)

↑AST/ALT

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13
Q

What are 2 diseases that cause fatty liver changes?

A

Alcohol - Alcoholic Fatty Liver Disease

Obesity - Non-Alcoholic Fatty Liver Disease (NAFLD)

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14
Q

In fatty liver disease, what histo change indicates that the damage is irreversible?

A

Fibrosis / cirrhosis

You might be able to reduce the fat content but the fibrosis is permanent

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15
Q

3 big causes of hepatitis

A

Viral
Autoimmune
Metabolic/genetic

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16
Q

Why do you biopsy suspected hepatitis? What do you see?

A

Biopsy for progression - NOT enough for dx alone
See
- Portal inflammation that extends beyond interface
- Hepatocyte damage
- Progressive fibrosis

17
Q

Do you grade or stage hepatitis?

A

YEP - chronic hepatitis (why you’d biopsy)
Used to det progression -> therapy decisions
Grade = current inflam, might resolve
Stage = current fibrosis, permanent

18
Q

Grade 1 vs 4 hepatitis

A

1: inflam basically contained to portal tract
4: tons inflam everywhere
- See AST/ALT changes at this point

19
Q

Why is untreated fibrosis such an issue?

A

Liver can regenerate itself

But fibrosis limits this capacity

20
Q

Stage 1 vs 2 vs 3 vs 4 fibrosis

A

1: no fibrosis
2: rare bridging
3: bridging that forms incomplete nodules
4: cirrhosis = fibrosis in nodules
- Nowhere for new liver to go!

21
Q

How would you treat a pt hepatitis already showing signs of fibrosis?

A

Steroids!

22
Q

Which forms of viral hepatitis can be chronic? What is the criteria to call a viral hepatitis chronic?

A

B & C
6 mos serum +
May/may not be symptomatic -> may never develop fibrosis

23
Q

Histo for chronic Hep B carrier

A

Ground glass cells = virus happily living and replicating in hepatocytes
Smudges are virion in the ER

24
Q

Why are you worried about asymptomatic Hep B carrier?

A

Progress to HCC

25
Q

What causes liver damage in viral hepatitis?

A

Immune response to the virus in the liver cells
Repair -> fibrosis
NOT the virus itself

26
Q

Describe autoimmune chronic hepatitis

  • Male vs female
  • Young vs old
  • IgG or IgM
  • Lab findings
  • Treat
A 
Female 3:1
Bimodal: young - post-menopause
IgG
Titers of auto-Abs (ANA)
Responds to STEROIDS
27
Q

Histo of autoimmune chronic hepatitis

A

Plasma cells
Interface hepatitis
- Fibrosis at presentation indicates subclinical hepatitis (duh its been brewing for a while)
Regenerative nodules (recovery from injury)
Multi-nucleated giant cell hepatocytes (replicating so fast don’t full divide)

28
Q

What genetic cause of chronic hepatitis would also present with brown skin color and swollen joints?

A

Hereditary hemochromatosis
C282Y mutation
No neg FB -> iron absorption signal always on
+ We don’t readily excrete iron (esp men)
Excrete via GI lumen shedding or periods

29
Q

Which hepatocytes are effected first by hereditary hemochromatosis?

A

Periportal - zone 1

Will eventually effect all

30
Q

Treat hereditary hemochromatosis

A

PHLEBOTOMY until use excess iron in making new RBCs

31
Q

What genetic cause of chronic hepatitis is common in young people possible with cornea and basal ganglia involvement?

A

Wilson Disease

Can’t excrete copper from hepatocyte into bile

32
Q

Lab findings to dx Wilson’s disease

A

↓serum ceruloplasmin
↑urine Cu
↑hepatic Cu - must burn liver sample and weigh after Cu removal

33
Q

What does A1AT def effect the liver?

A

A1AT is made in the liver!
Abnormal protein retained in hepatocytes -> chronic hepatitis
*Globules in hepatocytes on histo
Otherwise -> panacinar emphysema

34
Q

What is the protease inhibitor phenotyping results for normal vs A1AT def pts?

A

PiZZ = homo A1AT def
PiMZ
PiMM = homo normal

P&T Block 3 Pulm & GI (31 decks)

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