Liver and Biliary System Flashcards

(66 cards)

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
'Nutmeg' liver occurs as a consequence of?
Chronic liver congestion
26
Describe the process of chronic congestions
Increased pressure in hepatic vein -> increased pressure in the sinusoids -> thicker capsular surface of the liver and nodular texture
27
Chronic congestion most commonly occurs secondary to?
Congestive heart failure (endocardiosis [dog] or traumatic reticuloperitonitis [cow])
28
Describe the pathophysiology of congestive heart failure and its effects on the liver
Increased venous pressure (backwards HF) -> build up of blood in the systemic circulation -> chronic congestion of the liver -> ascites
29
What are the gross findings in a liver with chronic congestion?
- 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
Describe the histological appearance of a liver with chronic congestion
- 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
What is the pathogenesis of chronic congestion?
Congestion > decreased oxygen supply > hypoxia/ anoxia of tissues > necrosis > fibrosis
32
Acquired porto-systemic shunts (extrahepatic) occur due to?
Chronic liver disease
33
How does Chronic liver disease cause extrahepatic shunts?
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
Define teleangiectasis
Dilation of functional blood vessels
35
Define Peliosis hepatis
Irregular blood-filled cystic spaces in the liver parenchyma
36
Peliosis hepatis occurs due to?
Focal necrosis of hepatocytes
37
Why are hepatocytes easily degenerated?
- High metabolic rate | - Prone to alterations in oxygenation of blood
38
What is 'cloudy swelling'?
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
What is atrophy?
Reduction in the size of cells
40
What are the causes of atrophy?
- Pressure from other internal organs | - Reduced blood supply e.g. shunt
41
Define steatosis/lipidosis
Abnormal accumulation of triglycerides within hepatocytes
42
What are the pathogenic causes of steatosis/lipidosis
- 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
Describe the gross appearance of a liver with lipidosis
- Enlargement of liver; increase size, rounded edges of lobes - Change in colour (pale, yellow) - Friable - Cut surface: colour change to yellow/orange
44
What clinical scenarios would pre-dispose a horse to hepatic lipidosis?
- Enterocolitis - Feed restriction for treatment of colic - Obesity - Pregnancy - Lactation
45
Describe the histological appearance of a liver with lipidosis
- 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
Hyperlipidaemia occurs with what conditions?
- Diabetes mellitus - Pancreatitis - Hypothyroidism - Hyperadrenocorticism - With high dietary fat intake
47
What are ketones?
Intermediate or waste products of lipid metabolism -> increased during increased lipolysis
48
Ketosis occurs with which conditions?
- Starvation - Diabetes mellitus - Pregnancy - Lactation - Sheep; pregnancy toxaemia “twin lamb disease”
49
How does ketosis occur?
Increased demand for gluconeogenesis or glucose, impaired utilisation of glucose -> excessive breakdown of adipose tissue
50
Describe hypoglycaemia and fatty liver syndrome in small dog breeds
Puppies; low capacity for gluconeogenesis from muscle protein as small muscle mass; anorexia due to stress (infection, vaccination)
51
How does hepatic lipidosis occur due to hyperadrenocorticism
Glucocorticoids lead to: - Decreased lipogenesis - Increased lipolysis of adipose tissue - Increased catabolism of skeletal muscle protein - Increased gluconeogenesis in the liver (↑ glycogen stores)
52
Describe the pathogenesis of tension lipidosis
Tension > decreased local perfusion > local hypoxia > decreased lipoprotein synthesis and transport from hepatocytes > accumulation of lipid
53
What is glycogen?
Rapidly available energy store in cytoplasm of hepatocytes
54
Which conditions cause hepatic glycogen storage?
- Diabetes mellitus - Glycogen storage diseases - Steroid-induced hepatopathy (dogs)
55
How does diabetes cause glycogen storage?
Hyperglycaemia > hepatocytes are highly permeable to glucose > increased glycogen synthesis and storage
56
Describe the histology of a liver with glycogen storage
- Swelling of cell (influx of fluid) “hydropic degeneration” - Feathery appearance to cytoplasm - PAS positive glycogen – stain for carbohydrates (glycogen)
57
What is amyloid?
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
Which type of amyloid is synthesised within the liver?
Serum amyloid A | - Synthesised in hepatocytes (not Ig), derived from SAA (precursor acute phase serum lipoprotein)
59
Describe how a liver with amyloidosis would appear grossly?
Pale, enlarged, rounded edges, uneven surface
60
Describe how a liver with amyloidosis would appear histologically?
Amyloid in perisinusoidal spaces (space of Dissé) between sinusoidal lining and hepatocyte > compressed hepatocytes Pale pink extracellular material
61
Name 5 pigments that can be found in the liver
- Bile pigment - Lipofuscin - Haemosiderin - Melanin - Iron porphyrin
62
Where is Haemosiderin seen?
In Kupffer cells (macrophage cells)
63
What is haemochromatosis?
Hepatic Haemosiderin accumulation due to increased iron uptake (sheep, cattle: high levels of iron in pasture and water)
64
What are the pathological findings of haemochromatosis?
- Hepatomegaly - Haemosiderin accumulation in hepatocytes, Kupffer cells, lymph nodes, pancreas, spleen - Periportal bridging fibrosis and nodular regeneration
65
How does haemochromatosis appear histologically?
Disseminated Haemosiderin due to high ferritin and iron (Perl’s Prussian blue stain for iron)
66
What are the two causes of photosensitisation?
a) due to defective pigment synthesis | b) due to intoxication e.g. St. John`s wort, buckwheat