Hepatobiliary_Images Flashcards

1
Q

What pathology is seen here?

Specifically, what is the cell that the cursor is on (brighter pink than others)?

A

The cell w/ the cursor is an acidophilic body, or apoptotic cell (generated usually by CD8 cytotoxic cells).

There are a few lymphocytes surrounding the apopototic body.

The rest of the slide is filled w/ hepatocyte ballooning, which is characteristic of acute hepatitis.

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

What pathology is seen here?

A

Left: Acidophilic Apoptotic body surrounded by lymphocytes (likely CD8+).

Right: confirm that above is correct by CD3+ immune peroxidase stain, which is a T-cell marker.

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

What are the grey cells in between the hepatocytes that the cursor is pointing to in the bottom-rightish?

A

Grayish cells = Ceroid-laden macrophages, or Kupffer cells, which are filled w/ hepatocyte debris.

The bright red/pink cells that can also be seen are acidophilic Apoptotic bodies.

Finally, there is also an increased # of lymphocytes in between the hepatocytes.

This slide depicts lobular disarray of Acute Viral Hepatitis.

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

Describe the pathology seen in these 2 slides.

A

Feathery degeneration w/ intracellular cholestasis

Path: Cholestasis

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

Describe path seen

A

Degeneration & Intracellular Accumulation of Lipofuscin

Lipofuscin is a breakdown product of lysosomal material, reflecting cell activity, and is referred to as ‘wear and tear’ pigment.

It is more prominent in the pericentral hepatocytes (zone 3), also tends not to be in periportal hepatocytes.

Path: Acute Hepatitis

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

Describe path seen

A

Iron & Copper

Hereditary Hemochromatosis hepatocellular iron granules outlining canaliculi.

Path = Wilson disease showing copper depositionin Zone 1 hepatocytes
(Acute Hepatitis)

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

Describe path seen

A

Microvesicular steatosis

Central nucleus w/ multiple small, clear lipid droplets.

Seen in: Acute Fatty Liver of Pregnancy & Valproic Acid Toxicity

Mixed in Alcoholic Fatty Liver Disease

(Acute Hepatitis)

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

Describe path seen.

A

Macrovesicular Steatosis

One large lipid droplet, peripheral nucleus

Seen in: Obesity, Diabetics, & Hepatitis C

Mixed in Alcoholic Fatty Liver Disease

(Acute Hepatitis)

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

Describe path seen here.

A

Mallory Denk Bodies

Seen in: Acute Steatohepatitis (fatty liver)

Liver cells w/ ballooned cytoplasm, Mallory material (condensed intermediate filaments), surrounded by inflammatory cells

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

Describe path seen in 2 images

A

Glycogenosis type IV

Cytoplasmic inclusions, intensely stained with PAS (left) have been digested by pectinase (right).

PAS before and after pectinase

(Acute Hepatitis)

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

Describe path seen

A

Tay Sachs disease

Pale-staining Kupffer cells filled w/ granulofibrillar material

(Acute Hepatitis)

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

Describe path seen here.

A

So called, “Naked” acidophilic bodies – w/out surrounding lymphocytic infiltrate

(Acute Hepatitis)

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

Describe path seen here

A

Ischemic Coagulative Necrosis following hepatic artery occlusion post-transplant

Right - hepatocyte features are completely lost, leaving only indistinct eosinophilic remnants of the hepatocyte cords, occasional pyknotic hepatocyte nuclei, and partial preservation of some sinusoidal cells such as macrophages.

Left - there are more viable liver cells.

(Acute Hepatitis)

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

Describe path seen here.

A

Lytic Oncotic Necrosis due to osmotic swelling & rupture

Oncotic hepatocellular death in alcoholic hepatitis.

Severely ballooned hepatocytes have lost their sharply defined cell borders, and have undergone cell death.

In the centre of the field a residual Mallory–Denk body (*) and brown discoloration of cholestasis is also present.

(Acute Hepatitis)

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

Describe the distribution of cell death seen here

A

Centrilobular cell death

Paracetamol (acetaminophen) toxicity. Confluent coagulative necrosis involving the perivenular and mid-zones

This can be due to any of the following:

  • ischemic injury
  • drug and toxic reactions
  • eclampsia

(Acute Hepatitis)

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

Describe the distribution of cell death seen here.

A

Focal or Spotty Necrosis

17
Q

Describe the distribution of cell death seen here.

A

Bridging Necrosis

Acute hepatitis with bridging necrosis. Curving bridges are formed as a result of confluent necrosis linking central and portal zones. (H&E)

Bridging necrosis can be: Portal to portal, portal to central, or central to central

(Acute Hepatitis)

18
Q

Describe the distribution of cell death seen here.

A

Entire Lobules (submassive necrosis)

(Acute Hepatitis)

19
Q

Describe the distribution of cell death seen here.

A

Most of liver (massive necrosis)

34-year-old pregnant woman with preeclampsia; hemolysis, elevated liver enzymes, low platelets; and fulminant hepatic failure.

(Acute Hepatitis)

20
Q

Describe inflammation seen here

A

Neutrophils
• Lobular: Toxic (steatohepatitis) or ischemic hepatocyte necrosis
• Portal: Bile duct obstruction

(Acute Hepatitis)

21
Q

Describe the inflammation seen here.

A

Lymphocytes:
• Destruction of antigen-expressing liver cells by cytotoxic lymphocytes
• Limited to the portal tracts
• Interface hepatitis
• Suffuse the entire parenchyma

(Acute Hepatitis)

22
Q

Describe the inflammation seen here.

A

Scavenger macrophages
• Kupffer cells and circulating monocytes
• Ceroid engulfed apoptotic cell fragments

Granulomas
• Foreign bodies, organisms, drugs

(Acute Hepatitis)

23
Q

Describe pathology seen here

A

Regeneration:
seen in all but the most fulminant hepatic diseases

Hepatocellular proliferation:
• Mitoses
• Thickening of the hepatocyte cords
• Disorganization of the parenchymal structure.

Hyperchromatic liver cells with frequent two-cell layer thick trabecules and increased mitotic activity and biinuclaeated hepatocytes.

(Acute Hepatitis)

24
Q

Describe path seen here

A

Fibrosis

Response to inflammation or direct toxic insult to the liver.

“Point of no return” irreversible liver damage
• Debated if fibrosis or even cirrhosis
• Change of hep blood flow & perfusion of hepatocytes
Initial stage:
• portal tracts
• terminal hepatic vein
• within the space of Disse

Portal fibrosis in mildly active hepatitic C infection.

Cental vein fibrosis in a steatohelatitis

This example of dense zone 3 perisinusoidal fibrosis illustrates the characteristic “chickenwire” network of fibrosis often seen in steatohepatitis.

(Acute Hepatitis)

25
Q

Describe path seen here

A

Fibrosis

Bridging fibrosis in chronic hepatitis (viral C-type)

Cirrhosis in chronic hepatitis (viral C type)

Biliary cirrhosis with jigsaw puzzle-like haphazard shaped regenerative nodules.

26
Q

Describe path seen here.

A

Classic acute hepatitis.

Hepatocyte swelling and lymphocytic infiltrates are seen in the lobule (spotty or lytic necrosis).

27
Q

Describe path seen here.

A

Interface Hepatitits

(Acute Hepatitis)

28
Q

Describe path seen here

A

Massive necrosis, ductular reaction

(Acute Hepatitis)

29
Q

Describe path seen here.

A

Few specific features may indicate viral type:
• HBV = ground glass hepatocytes
• cytoplasm packed with HBsAg, finely granular eosinophilic cytoplasm

Dx = HCV
• lymphoid aggregates within portal tracts
• hepatocyte macrovesicular steatosis

(Acute Hepatitis)

30
Q

Describe path seen here.

A

Fulminant Hepatic Failure

2 to 3 weeks from onset to hepatic encephalopathy
• Subfulminant failure (up to 3 months)

Causes (US):
• Fulminant viral hepatitis ~12%
• almost all due to HAV or HBV.• Rarely reactivation of chronic hepatitis B or acute herpesvirus infection

  • Drug and chemical toxicity ~52%,
  • Acetaminophen (in suicidal doses), isoniazid, antidepressants (MAO inhibitors), halothane, methyldopa.
  • Mycotoxin – Amanita phalloides
  • 18% unknown
31
Q

Describe pathology seen here

A

Autoimmune Hepatitis

Plasma cells more prominent

32
Q

Inflammation seen here w/ predominantly plasma cells.

Likely diagnosis?

A

Autoimmune Hepatitis

(w/ pan-lobular infiltrate)

33
Q

Diagnosis?

A

Alcoholic Hepatitis

Above = Hepatocyte swelling & necrosis

Below = Mallory bodies

34
Q

Describe pathology seen in each image.

A

This is Wilson’s Disease

Left: Liver disease, Chronic Hepatitis

  • Periportal Mallory Hyaline in hepatocytes
  • Bile Canaliculi deposits (cholestasis – brown)

Right: Micronodular Cirrhosis

  • May be rapid, even in childhood
  • Eventually macronodular
35
Q

What is this? What is it seen in?

A

Kayser-Fleischer Ring

Seen in Wilson’s Disease

36
Q

Is this Early or Late Fibrosis?

A

Early Fibrosis

(b/c limited to portal tract area — would be Stage 1)

37
Q

Is this Fibrosis early (acute) or late (chronic)?

A

Later, more chronic Hepatitis

Shows a relatively well-developed bridge btwn central vein & portal tract

38
Q

Is this Fibrosis from acute or chronic hepatitis?

A

Chronic Hepatitis, shows well-developed bridges which indicate complete or near-complete Cirrhosis

39
Q
A