Liver Pathology 1

Question 1

1. What is the normal colour of the liver?
2. Colour changes due to other circumstances?

Answer 1

1. Reddish-brown.
2. May be brown in animals, e.g. cattle, sheep, pigs, that have been bled out. Accumulation of fats in liver can cause it to have a yellowish-brown appearance.
   Post-mortem changes can cause areas of pallor or darkening or greenish-yellow discolouration, esp. adjacent to gall bladder. These changes may only affect the liver surface.

Question 2

What feature of the pig’s liver allows it to be distinguished from livers of other spp.?

Answer 2

The “Moroccan leather” appearance, or reticular pattern, is caused by prominent amounts of interlobular connective tissue and is normal in the pig.

Question 3

What factors affect the weight of a liver as a proportion to body weight?

Answer 3

Spp. (higher is carnivores, lower in herbivores), nutritional status (e.g. hepatic storage of glycogen and fat), age (liver weight decreases w/ age).

Question 4

What blood vessels deliver blood to the liver?

Answer 4

Portal vein (70-80%), hepatic artery.

Question 5

1. From which organs does the blood in the portal vein come from?
2. From what blood vessel does the hepatic artery originate from?
3. What blood vessels drain blood from the liver?
4. What structures does blood flow through after entering the portal vein and hepatic artery and before arriving at the hepatic veins?

Answer 5

1. Spleen, pancreas, stomach and intestines.
2. Coeliac artery which arises from the aorta.
3. Hepatic veins to caudal vena cava.
4. Hepatic sinusoids, across the hepatic lobule, into central vein, to interlobular veins.

Question 6

Hepatic acinus.

Answer 6

Triangular region bounded by central and 2 adjacent portal tracts.
3 zones:
- 1 = periportal region – receives blood from portal vein and hepatic artery first (w/ highest O2 and nutrient content).
- 2 = midzonal region – receives blood next.
- 3 = centrilobular region – receives blood last (lower O2 and nutrient content) (also has higher levels of metabolic enzymes so most sensitive to injury by toxic compounds) before it drains into central vein .

Question 7

Congenital portosystemic shunt (CPSS).

Answer 7

Anomalous venous connection between portal v system and systemic v system (e.g. caudal vena cava or azygous vein).
Allows some of the blood that would normally be travelling through the liver to by-pass the liver

Question 8

Classification of CPSS?

Answer 8

Intra-hepatic - anomalous v w/in the liver (larger breed dogs predisposed).
Extra-hepatic - anomalous v outside of the liver (smaller breed dogs predisposed).

High proportions can be shunted due to lower pressure through the anomalous v and therefore making it the path of least resistance.

Question 9

Intra-hepatic CPSS.

Answer 9

Originate from the left or the right portal vein branch.
Terminate either directly into the hepatic v or directly into the caudal vena cava.

Question 10

Extra-hepatic CPSS.

Answer 10

Most of them will originate from the left or the right gastric v or splenic v.
Terminate at the caudal vena cava or azygous v.

Question 11

CPSS functional consequences.

Answer 11

Reduced hepatic perfusion.
- will not develop to its normal size so the liver will be smaller (microhepatica).
Lower hepatic functional capacity:
- affects growth of animal.
Inability to detoxify waste products sufficiently, causing them to build up and stimulate CNS – hepatic encephalopathy.

Question 12

What is the most common post-hepatic condition affecting the outflow of blood from the liver?

Answer 12

Heart disease - esp. R sided CHF.
– Increases pressure in caudal vena cava which increases pressure in the hepatic v and in the liver, impairing blood flow from the liver.

Question 13

Other causes of post-hepatic conditions affecting outflow of blood from the liver.

Answer 13

Obstruction of the hepatic veins or caudal vena cava.
- Luminal obstruction e.g. thrombus.
- Vessel wall thickening e.g. inflammation, neoplasia.
- External compression e.g. by a mass, such as an abscess or tumour.

Question 14

Consequences of impairment of post-hepatic flow.

Answer 14

Hepatic passive venous congestion.
- Histo – dilation of the sinusoids, central vein and portal vein.
Hepatomegaly - as engorged with blood.
Chronic - Enhanced lobular (or reticular) pattern on the sectioned surface of the liver.
– Due to reddening and fat accumulation.
- Colour change on cut surface of the liver, mottling of darker and lighter brown due to congestion and hypoxia due to sluggish flow.
– Nutmeg liver.

Question 15

Intra-hepatic and pre-hepatic conditions associated w/ abnormal portal vein flow.

Answer 15

Advanced chronic liver disease w/ fibrosis.
- increased resistance to blood flow into and through liver.
Portal vein obstruction e.g. thrombosis, inflammation/abscesses, neoplasia.
Portal vein hypoplasia.
- congenital.
- portal vein does not develop to its normal size and is therefore smaller than normal.
- variable extent and severity.
– if sufficient to cause hypoperfusion of the liver, then can result in reduced liver development so smaller liver.
- most commonly identified in dogs (small breeds e.g. Yorkshire terrier, Maltese terrier).
- may not have clinical signs until few years old.
- some remain asymptomatic.

Question 16

Potential causes of portal hypertension?

Answer 16

Ascites - increased portal pressure can disturb fluid balance and lead to effusion in peritoneal cavity.
Acquired portosystemic shunt (APSS) - seen w/ intra-hepatic and pre-hepatic causes of portal hypertension. Not usually caused by passive hepatic congestion e.g. heart failure.

Question 17

Pathogenesis of APSS.

Answer 17

Multiple, small, tortuous vessels open up from portal system and extend to systemic system.
This allows blood to shunt from the portal system to the systemic system, allowing blood to by-pass the liver.
Many possible routes.

Question 18

Potential liver responses to injury.

Answer 18

Hepatocellular vacuolation (common).
Necrosis.
Hepatocellular regeneration.
Inflammation.
End stage liver (cirrhosis).
Hyperplastic and neoplastic changes.

Question 19

Hepatocellular vacuolation / hepatocellular vacuolar change / ‘vacuolar hepatopathy’.

Answer 19

Hepatocytes have air spaces in their cytoplasm.
Varying degrees of swelling of the cells.
Caused by accumulation of product of a substance which has been washed out during tissue sample processing for histo.
- Lipid (fatty change).
- Water (hydropic change).
- Glycogen
Gross changes:
- engorgement of the liver.
- altered colour – pallor, yellow-brown.
- altered consistency – greasy (if lipid accumulation), increased fragility.

Question 20

Why might lipid accumulation occur?

Answer 20

Hepatocyte capacity to process and release lipid is exceeded.
- FFAs to the liver include dietary source and products of fat reserve breakdown.
- Excess delivery of FFAs to hepatocytes.
– limited enzymes to process these at the liver.
–> high fat diet.
–> negative energy balance so breaking down lots of fat reserve, overwhelming the liver e.g. late pregnancy, peak lactation, anorexia.
–> Metabolic or endocrine disease e.g. DM, equine hyperlipidaemia.
- Reduced hepatocellular capacity to metabolise fats e.g. problem in lipoprotein release – build up of lipoproteins and triglycerides –> excess lipid accumulation.
– caused by hepatocellular injury most commonly e.g. hypoxia, toxins, dietary deficiencies in substances (lipotropes) required for lipid metabolism

Question 21

Why might water accumulation occur in the liver (hydropic change)?

Answer 21

Insult or injury caused by various toxins, metabolic insults, hypoxia.

Question 22

Why might glycogen accumulate in the liver?

Answer 22

Associated with hyperadrenocorticism or corticosteroid administration.
- “steroid-induced hepatopathy”.

Question 23

3 main patterns of necrosis in the liver.

Answer 23

Focal (random).
Zonal.
Massive.

Question 24

Focal (random) necrosis.

Answer 24

Scattered, randomly distributed foci necrosis.
May be 1 or multiple.
Variable erythrocytes in the area microscopically.
Grossly:
- 1 or more reddish, white or grey foci w/ blood associated, randomly distributed in parenchyma on capsular surface or sectioned surface.
Typical of various infectious agents e.g. bacteria, viruses, protozoa, migrating parasites (may also produce tracts w/in liver.
May be of little functional significance to the liver as liver has such huge reserve of tissue,

Question 25

Zonal necrosis.

Answer 25

Zones w/in the acinus.
- 1 = periportal zone.
- 2 = midzonal region.
- 3 = centrilobular zone (peri-acinar zone).
– more prone to hypoxic injury as receives the blood last.
– hepatocytes contain lots of metabolic enzymes which activate toxins which will make them most susceptible to toxic insults.
Typical causes = hypoxia/ischaemia (severe anaemia or R sided HF/other circulatory failure), toxins, severe viral infections e.g. canine adenovirus.
Microscopically = multiple areas of paler pink regions, each located around the central veins, some areas join together (bridging necrosis).
Grossly = mottled on cut surface, darker and lighter regions corresponding to normal liver and necrotic liver - intensity determined by level of haemorrhage. Referred to as enhanced lobular pattern or enhance reticular pattern.

Question 26

Massive necrosis.

Answer 26

Least common pattern.
Affecting all or majority of the hepatocytes w/in lobules.
Microscopically = most hepatocytes gone (death) and area filled w/ RBCs. Fine rim of surviving hepatocytes along edges of lobules.
Grossly = dark red cut surface.
Causes include - severe toxic injury, vitamin E / Selenium deficiency in pigs (hepatosis dietetica).