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Y3 Liver and Pancreas pathology > Liver and Biliary System > Flashcards

Liver and Biliary System Flashcards

1
Q

What are the functions of the liver?

A
  • Synthesis: e.g. of enzymes (proteins (e.g. ALT, alanine transferase)
  • Excretion: e.g. bilirubin in bile
  • Catabolic: e.g. processing of nutrients absorbed in the GI tract
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2
Q

Describe the blood supply to the liver

A

75% from the portal vein (25% from the hepatic artery); everything which enters the blood from the GI tract will pass through the liver, including bacteria, parasites and drugs

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3
Q

Name 3 congenital defects that can occur to the liver

A
  • Absence of lobes / supernumerary lobes
  • Intrahepatic congenital cysts - cats
  • Congenital portosystemic vascular shunts - dogs, cats
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4
Q

What is a cysts?

A
  • A structure lined by cuboidal or flattened epithelium
  • Usually a normal structure that has become massively dilated
  • Contain clear serous fluid
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5
Q

Cats with which disease can also have intrahepatic congenital cysts?

A

Polycystic kidney syndrome

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6
Q

An intrahepatic shunt is due to the persistence of?

A

Fetal ductus venosus

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7
Q

Which breeds are predisposed to a intrahepatic congenital shunt

A

Irish wolfhounds

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8
Q

Where does the ductus venosus connect in a foetus?

A

The left umbilical vein and the caudal vena cava

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9
Q

Where does an extrahepatic congenital shunt connect?

A

Direct connection between the portal vein and the caudal vena cava or azygous vein

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10
Q

Which breeds are predisposed to a extrahepatic congenital shunt

A

Small breed dogs (Maltese and Yorkshire terriers) and cats

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11
Q

What are the effects of Congenital portosystemic vascular shunts

A
  • Large amount of blood from portal vein (containing hepatotrophic substances) bypasses the liver
  • Clinically: “failure to thrive”, i.e. small for age / poor growth; ultimately hepatic encephalopathy
  • Not compatible with life in the long term
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12
Q

Describe the gross and histological appearance of a liver with a Congenital portosystemic vascular shunt

A 
Gross finding: small liver
Histology: 
- small hepatocytes
- small / absent portal veins in triads 
- reduplication of arterioles in triads
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13
Q

What are the two forms of liver dislocation?

A

Diaphragmatic hernia

Torsion

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14
Q

Describe Diaphragmatic herniation of the liver and its effects

A
  • May be seen as a traumatic lesion; one on slide is severe
  • Causes increased respiratory effort due to increased pressure/decreased space for inflation of lungs
  • Congenital lesion; if lobar blood supply is affected > necrosis
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15
Q

Describe torsion of the liver and its effects

A
  • Twisting of a lobe on its axis which disrupts the blood supply to the lobe -> necrosis
  • Left lateral lobe is predisposed, but torsion is rare.
  • Haemorrhagic shock > death
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16
Q

What are the possible causes of a ruptured liver?

A
  • Blunt trauma (e.g. road traffic accidents)
  • Alterations in parenchyma (e.g. amyloidosis)
  • Neoplasms (e.g. haemangiosarcoma)
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17
Q

What is the consequence of liver rupture?

A

Haemoperitoneum

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18
Q

Describe the changes following trauma e.g. RTA to the liver

A

Haemorrhage, clot, fibrinolysis; this liver is also yellow with rounded edges > amyloidosis or lipidosis (increased friability and risk of rupture)

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19
Q

What are the effects of amyloid in organs?

A

Causes swelling and makes them friable

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20
Q

Which type of neoplasm could cause liver rupture? How?

A

Haemangiosarcoma

- vascular tumour as it arises from endothelial cells so it often creates blood filled spaces which can rupture

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21
Q

Which animals are most susceptible to liver rupture?

A

Young animals e.g. foals falling to floor during birth

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22
Q

Describe passive hyperaemia in the liver

A

= Congestion from the central vein

- increased pressure within the hepatic vein/venules, compared to the portal vein/venules

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23
Q

What are the 3 causes of acute congestion in the liver?

A
  • Acute cardiovascular failure (i.e. agonal)
  • Anaphylaxis
  • Shock
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24
Q

How does acute congestion appear histologically?

A

Sinusoids surrounding the central vein are dilated by erythrocytes

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25
Q

‘Nutmeg’ liver occurs as a consequence of?

A

Chronic liver congestion

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26
Q

Describe the process of chronic congestions

A

Increased pressure in hepatic vein -> increased pressure in the sinusoids -> thicker capsular surface of the liver and nodular texture

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27
Q

Chronic congestion most commonly occurs secondary to?

A

Congestive heart failure (endocardiosis [dog] or traumatic reticuloperitonitis [cow])

28
Q

Describe the pathophysiology of congestive heart failure and its effects on the liver

A

Increased venous pressure (backwards HF) -> build up of blood in the systemic circulation -> chronic congestion of the liver -> ascites

29
Q

What are the gross findings in a liver with chronic congestion?

A
  • Slightly nodular and rough surface
  • Ascites, fibrin deposition: paler areas
  • Thickened capsule
  • Nodular appearance
  • On the cut surface: very congested and dilated areas of sinusoids with blood pooling
  • Fibrosis around the central vein
30
Q

Describe the histological appearance of a liver with chronic congestion

A
  • Centrolobular necrosis: centrolobular hepatocytes become progressively more hypoxic as they are the furthest away from the blood supply -> necrosis
  • Fibrosis around central vein (repair)
31
Q

What is the pathogenesis of chronic congestion?

A

Congestion > decreased oxygen supply > hypoxia/ anoxia of tissues > necrosis > fibrosis

32
Q

Acquired porto-systemic shunts (extrahepatic) occur due to?

A

Chronic liver disease

33
Q

How does Chronic liver disease cause extrahepatic shunts?

A

Hepatic fibrosis and/or cirrhosis:

  • > development of portal hypertension
  • > dilation of (non-functional) veins between portal vein (or veins which terminate in the portal vein) and caudal vena cava
34
Q

Define teleangiectasis

A

Dilation of functional blood vessels

35
Q

Define Peliosis hepatis

A

Irregular blood-filled cystic spaces in the liver parenchyma

36
Q

Peliosis hepatis occurs due to?

A

Focal necrosis of hepatocytes

37
Q

Why are hepatocytes easily degenerated?

A
  • High metabolic rate

- Prone to alterations in oxygenation of blood

38
Q

What is ‘cloudy swelling’?

A

Hydropic degeneration

  • Non-specific change (e.g. toxins, metabolic insults, hypoxia, cholestasis)
  • Influx of Na+ and water into cytoplasm -> expanded organelles
  • Hepatocytes appear clearer as they are swollen with water
  • Reversible
39
Q

What is atrophy?

A

Reduction in the size of cells

40
Q

What are the causes of atrophy?

A
  • Pressure from other internal organs

- Reduced blood supply e.g. shunt

41
Q

Define steatosis/lipidosis

A

Abnormal accumulation of triglycerides within hepatocytes

42
Q

What are the pathogenic causes of steatosis/lipidosis

A
  • Nutritional: fat or carbohydrate rich diet = obesity
  • Excessive release of fatty acids from adipose tissue; i.e. due to energy demand being greater than supply (starvation, late in pregnancy, early in lactation [dairy cows]
  • Hypoxia: decreased oxidation of FA > accumulation in cells
  • Toxic: impaired synthesis of apoproteins > decreased lipoprotein synthesis > destruction of cellular membranes
43
Q

Describe the gross appearance of a liver with lipidosis

A
  • Enlargement of liver; increase size, rounded edges of lobes
  • Change in colour (pale, yellow)
  • Friable
  • Cut surface: colour change to yellow/orange
44
Q

What clinical scenarios would pre-dispose a horse to hepatic lipidosis?

A
  • Enterocolitis
  • Feed restriction for treatment of colic
  • Obesity
  • Pregnancy
  • Lactation
45
Q

Describe the histological appearance of a liver with lipidosis

A
  • Small droplets of lipid fuse to form bigger vacuoles, which distend the cell and displace the nucleus to the periphery.
  • Vacuoles are white/clear on HE; Fat stain (oil red orange) >orange
46
Q

Hyperlipidaemia occurs with what conditions?

A
  • Diabetes mellitus
  • Pancreatitis
  • Hypothyroidism
  • Hyperadrenocorticism
  • With high dietary fat intake
47
Q

What are ketones?

A

Intermediate or waste products of lipid metabolism -> increased during increased lipolysis

48
Q

Ketosis occurs with which conditions?

A
  • Starvation
  • Diabetes mellitus
  • Pregnancy
  • Lactation
  • Sheep; pregnancy toxaemia “twin lamb disease”
49
Q

How does ketosis occur?

A

Increased demand for gluconeogenesis or glucose, impaired utilisation of glucose -> excessive breakdown of adipose tissue

50
Q

Describe hypoglycaemia and fatty liver syndrome in small dog breeds

A

Puppies; low capacity for gluconeogenesis from muscle protein as small muscle mass; anorexia due to stress (infection, vaccination)

51
Q

How does hepatic lipidosis occur due to hyperadrenocorticism

A

Glucocorticoids lead to:

  • Decreased lipogenesis
  • Increased lipolysis of adipose tissue
  • Increased catabolism of skeletal muscle protein
  • Increased gluconeogenesis in the liver (↑ glycogen stores)
52
Q

Describe the pathogenesis of tension lipidosis

A

Tension > decreased local perfusion > local hypoxia > decreased lipoprotein synthesis and transport from hepatocytes > accumulation of lipid

53
Q

What is glycogen?

A

Rapidly available energy store in cytoplasm of hepatocytes

54
Q

Which conditions cause hepatic glycogen storage?

A
  • Diabetes mellitus
  • Glycogen storage diseases
  • Steroid-induced hepatopathy (dogs)
55
Q

How does diabetes cause glycogen storage?

A

Hyperglycaemia > hepatocytes are highly permeable to glucose > increased glycogen synthesis and storage

56
Q

Describe the histology of a liver with glycogen storage

A
  • Swelling of cell (influx of fluid) “hydropic degeneration”
  • Feathery appearance to cytoplasm
  • PAS positive glycogen – stain for carbohydrates (glycogen)
57
Q

What is amyloid?

A

Pathological proteinaceous substance deposited between cells (in space of Dissé and sinusoids – normally not visible, it lies between the endothelial cells that line the sinusoids and hepatocytes)

58
Q

Which type of amyloid is synthesised within the liver?

A

Serum amyloid A

- Synthesised in hepatocytes (not Ig), derived from SAA (precursor acute phase serum lipoprotein)

59
Q

Describe how a liver with amyloidosis would appear grossly?

A

Pale, enlarged, rounded edges, uneven surface

60
Q

Describe how a liver with amyloidosis would appear histologically?

A

Amyloid in perisinusoidal spaces (space of Dissé) between sinusoidal lining and hepatocyte > compressed hepatocytes
Pale pink extracellular material

61
Q

Name 5 pigments that can be found in the liver

A
  • Bile pigment
  • Lipofuscin
  • Haemosiderin
  • Melanin
  • Iron porphyrin
62
Q

Where is Haemosiderin seen?

A

In Kupffer cells (macrophage cells)

63
Q

What is haemochromatosis?

A

Hepatic Haemosiderin accumulation due to increased iron uptake (sheep, cattle: high levels of iron in pasture and water)

64
Q

What are the pathological findings of haemochromatosis?

A
  • Hepatomegaly
  • Haemosiderin accumulation in hepatocytes, Kupffer cells, lymph nodes, pancreas, spleen
  • Periportal bridging fibrosis and nodular regeneration
65
Q

How does haemochromatosis appear histologically?

A

Disseminated Haemosiderin due to high ferritin and iron (Perl’s Prussian blue stain for iron)

66
Q

What are the two causes of photosensitisation?

A

a) due to defective pigment synthesis

b) due to intoxication e.g. St. John`s wort, buckwheat

Y3 Liver and Pancreas pathology (4 decks)

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