Liver Pathology 2

Question 1

What does liver regeneration rely on?

Answer 1

Proliferation of surviving cells of the liver in the stromal network.
(Cannot grow new lobes).
Existing lobules can increase in size to make up for lost mass elsewhere.

Question 2

What happens in a focal episode of necrosis AND collapse of the stromal network/framework?

Answer 2

Lobule unable to undergo regeneration to return to normal anatomy.
Stimulates some degree of fibrosis.
Localised distortion of the lobular architecture.
- no restoration of normal anatomy.
- may affect lobular function.
- loss of tissue mass due to loss of cells due to necrosis.
– scattered cells in other lobules can undergo proliferation to restore and replace lost functional mass.

Question 3

What happens if the insults/injuries/necrosis is repeated multiple times e.g. chronic hepatitis?

Answer 3

Multiple insults in multiple lobules.
Regeneration starts to become nodular.
Fibrosis, resulting in distortion of hepatic lobular architecture.
Foci of hepatocyte proliferation to replace hepatic mass, creating nodular regions.
Areas of fibrosis within and around lobules.
Histo - see hepatocytes that form nodular structures, fibrotic tracts which can contain small blood vessels which can offer an alternative route to normal blood flow, causing it to bypass the lobules and affect hepatic function.
Chronic changes w/ abnormal blood and bile flow so reduced hepatic functional capacity.

Question 4

Define…
1. Hepatitis.
2. Cholangitis.
3. Cholangiohepatitis.
4. Cholecystitis.

Answer 4

Inflammation of…
1. liver parenchyma.
2. biliary tree.
3. biliary tree and liver parenchyma.
4. gall bladder.

Question 5

Key features of acute hepatitis.

Answer 5

Caused by some type of insult/injury.
Acute inflammation.
Necrosis.
+/- regenerative changes.

Question 6

Gross features of acute hepatitis.

Answer 6

White, cream, pink, reddened colouration depending on blood pooling.
Mottling.
Can be foci.

Question 7

Causes of acute hepatitis.

Answer 7

Infectious (most common in FA):
- bacteria e.g. salmonella, listeria monocytogenes, campylobacter foetus, fusobacterium necrophorum.
- parasites e.g. liver fluke, ascaris suum, cysticercus tenuicollis.
- protozoa e.g. toxoplasma, neospora.
- viruses e.g. herpesviruses (neonates/fetus), RHD virus.
- fungi.
Toxins/drugs e.g. xylitol, carprofen, trimethoprim-sulphonamide in dogs.

Question 8

Sequelae to acute bacterial hepatitis.

Answer 8

Healing +/- scarring.
Can get persistence of infection and chronic inflammation.
Can get abscessation.
- if abscess impinges on major blood vessel e.g. hepatic vein or CVC:
– can cause a phlebitis, which can lead to a thrombosis (thrombophlebitis), which can lead to release of septic emboli into systemic circulation, to heart, then to the lungs.

Question 9

Key features of chronic hepatitis?

Answer 9

Chronic inflammation.
Fibrosis.
(Necrosis).
(Regenerative changes).

Question 10

Microscopic features of chronic hepatitis.

Answer 10

Fibrotic tracts.
Chronic inflammatory cells (lymphocytes, plasma cells, macrophages, may see neutrophils or eosinophils).
May see nodular pattern of cells due to regenerative changes.

Question 11

Gross features of chronic hepatitis.

Answer 11

Very abnormal morphology / distortion.
Lobes irregular / shrunken.
General bumpy texture to the liver surface.

Question 12

Hepatic fibrosis.

Answer 12

Significance depends on its extent and effect on hepatic function.
Can interfere w/ hepatocyte contact w/ blood in sinusoids by becoming a barrier around hepatocytes.
Fibrosis bridging between portal and central regions can contain vascular channels, allowing blood to bypass hepatocytes, affecting hepatic function.

Question 13

Causes of chronic hepatitis.

Answer 13

Toxins/drugs:
- ragwort toxicity (horses, ruminants).
- copper toxicosis (ruminants, esp. sheep).
- phenytoin, primidone, phenobarbitone, ketoconazole.
Some metabolic diseases:
- e.g. copper-associated hepatitis in dogs.
Idiopathic - esp. in dogs.
Infectious agents:
- e.g. mycobacterial infections, corynebacterium pseudotuberculosis.

Question 14

Key features of cholangitis and cholangiohepatitis.

Answer 14

Acute inflammation
or
chronic inflammation and fibrosis.
Centred on the bile ducts.

Question 15

Microscopic features of cholangitis and cholangiohepatitis.

Answer 15

Acute = Inflammatory cells within and around the bile ducts.
- multilobulated nuclei (neutrophils).
Chronic = Inflammation still focused within and around the bile duct. Mixed inflammatory cells - mainly lymphocytes and plasma cells, some neutrophils. Ring of fibrous tissue too around about the bile duct.
If extending to affect the surrounding hepatocytes = cholangiohepatitis.
Lymphocytic cholangitis seen in cats - intense lymphocytic infiltrate into the portal regions.

Question 16

Gross features of cholangitis.

Answer 16

Enlarged bile duct.
Thickened bile duct wall.
Seen most commonly in chronic liver fluke infection in sheep and cattle.
Cross-sectional creamy round, thick-walled structures (thickened bile ducts)

Question 17

Causes of cholangitis and cholangiohepatitis.

Answer 17

Parasites:
- liver fluke in ruminants.
- hepatic coccidiosis in rabbits.
Bacteria:
- most commonly due to ascending infection.
- predisposed by biliary stasis.
Idiopathic - lymphocytic cholangitis in cats.

Question 18

How can cholecystitis be classified?

Answer 18

Based on type of inflammation.
e.g. acute, chronic.
e.g. neutrophil, lymphoplasmacytic.

Question 19

Causes of cholecystitis.

Answer 19

Parasites - fluke.
Bacteria - often via reflux of intestinal bacteria into the biliary system.