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Applications Animal Health > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

what are 3 broad causal mechanisms that you should consider in cases of jaundice?

A
  1. Inc # RBC broken down
  2. Generalised liver Dx affecting functional parenchyma
  3. Cholestasis
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2
Q

Which domestic animal species develop hepatogenous photosensitisation?

A

Herbivores that eat green stuff –> chlorophyll!

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3
Q

How does grass become a photodynamic agent that contributes to hepatogenous photosensitisation??

A

Chlorophyll in plants made into phylloerythrin by gut flora (natural photodynamic agent) –> usually made soluble in liver and secreted

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4
Q

Which liver disease contributes to hepatogenous photosentitisation?

A

Cholestasis (days) –> phylloerythrin back spills out of erythrocytes into sinusoids –> circulation –> sunlight activates –> free radicals generated –> tissue ulceration

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5
Q

What are symptoms of hepatic encephalopathy?

A

head pressing
ataxia
ptyalism
generalised behavioural changes

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6
Q

What functional changes in the liver contribute to hepatic encephalopathy?

A

Reduced liver functional mass (E.g. by repeat toxicity)

PSS

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7
Q

Which compound in the blood primarily causes hepatic encephalopathy?

A

Ammonia

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8
Q

In which types of liver disease can hypoalbuminaemia develop and why?

A

Liver produces albumin. Dramatically reduced parenchyma (e.g. cirrhosis/ liver failure)

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9
Q

Why is hypoalbuminaemia usually chronic?

A

T1/2 albumin very long

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10
Q

Describe the symptoms of hypoalbuminaemia

A 
Decreased oncotic pressure in blood stream 
Transudate oedema (ascites)
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11
Q

What are various hepatic causes of ascites?

A

Hypoalbuminaemia
Chronic liver fluke
Portal vein hypertension
Inc hepatic lymph formation due to inc pressure in hepatic sinusoids (Right heart failure, scarring, tumor, amyloid in perisinusoidal spaces)

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12
Q

What are various causes of portal vein hypertension?

A

Compression of portal vein

Enlarged GIT

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13
Q

Define polyuria

A

Inc urination

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14
Q

Define polydipsia

A

Inc drinking

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15
Q

Define acholic

A

White fresh faeces!

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16
Q

In what circumstances might an animal have acholic faeces

A

Loss of conjugated bilirubin into bile due to major extra-hepatic bile duct obstruction

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17
Q

Why does hepatic Dx potentially predispose haemorrhage?

A

clotting factors are produced in the liver?

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18
Q

Describe portosystemic shunting PSSSSSSSSS

A

Diversion of blood from portal vein (bypassing liver) to tributaries of portal vein (e.g caudal vena cava/ splenic vein etc)

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19
Q

What happens to liver subsequent of PSS?

A

Microhepatica due to hypoplasia

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20
Q

Why does liver become hypoplastic subsequent of PSS?

A

Deprivation of trophic factors

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21
Q

What could cause liver rupture?

A

severe congestions, hepatic lipidosis etc. anything causing extreme tension on hepatic capsule

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22
Q

What is a common cause of cranial liver displacement?

A

Diaphragmatic hernias

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23
Q

What is a common cause of caudal displacement of the liver?

A

Hepatomegaly, space-occupying masses in the thorax

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24
Q

Which clinical signs in a dog might make you suspect liver disfunction?

A 
Ascites 
Neurologic signs 
Jaundice 
PU & PD
Stool changes
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25
Q

which conditions predispose livers to diffuse hepatic atrophy?

A
  1. Nutritional (catabolism)
  2. PSS
  3. Impaired mitotic division (low trophic factors)
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26
Q

Which conditions cause local hepatic atrophy?

A

Local compression

Local obstruction of bile drainage

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27
Q

Why can sublethal injury to hepatocytes lead to hydropic degeneration?

A

Loss of control of fluid and ionic movements across membranes –> influx Na+ & water

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28
Q

Define steroid hepatopathy

A

glycogen accumulation

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29
Q

Which conditions stimulate steroid hepatopathy?

A

Hyperadrenocorticism

e. g. from pituitary tumour in adrenal cortex
e. g. iatrogenic –> excessive admin corticosteroids

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30
Q

Define hepatic lipidosis

A

Excessive accumulation of triglycerides in hepatocyte cytoplasm

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31
Q

What is a cause of hepatic lipidosis?

A

Any process that overloads or impairs lipid metabolism of hepatocytes
e.g. diabetes/ high energy diet/ starvation/ sublethal injury to hepatocytes/ preg tox/ ketosis/ endocrine disorders/ equine hyperlipaemia

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32
Q

What gross anatomical changes of the liver are seen in early hepatic lipidosis?

A

Zonal pattern in early stages (Zone 3 rappoport’s acinus)

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33
Q

What gross anatomical changes of the liver are seen in moderate/severe hepatic lipidosis?

A

Megahepatica, rounded borders, diffuse cream yellow colour, soft, friable, greasy cut surface

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34
Q

What is amyloid?

A

An extracellular glycoprotein –> amorphous/ pink/ homogenous

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35
Q

In what circumstances does hepatic amyloidosis develop in domestic animals?

A

Active inflammation or tissue damage in the body, meaning that there is inc hepatic synthesis and release of SAA

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36
Q

Which pigment might result in a yellow or green liver?

A

Bilirubin accumulation (jaundice/ cholestasis)

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37
Q

Which pigment might result in a spotted black liver?

A

melanin

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38
Q

Which pigment might result in a diffusely black liver?

A

“lipofuscin like pigment” from ingestion of random plants, or black pigment from fasciola hepatica waste

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39
Q

What are some causes of multifocal hepatic necrosis?

A

viral/ bacterial/ protozoal infections –> multifocal pattern due to haematogenous origin

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40
Q

Define embolic

A

Originating from blood

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41
Q

What contributes to zonal necrosis of the liver?

A

Necrosis of acinar areas of hepatocytes

Due to toxins or hypoxia (mainly) :)

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42
Q

Define telangiectasis

A

Dilation of local areas of capillaries leading to gross appearance as red/ purple bumps on skin

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43
Q

Define massive necrosis

A

Necrosis of an entire acini, not necessarily the whole liver

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44
Q

What insults result in massive necrosis?

A

Very severe toxic or hypoxic insult

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45
Q

In what circumstances do hepatic fibrosis develop?

A

Scarring following liver surviving episode of hepatocellular necrosis

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46
Q

Which cells in the liver can proliferate and grow up to become hepatocytes?

A

hepatocytes, oval cells, ductal cells

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47
Q

Which cells produce collagen in the liver?

A

stellate cells

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48
Q

Define cirrhosis

A

End stage liver marked by degeneration of hepatocytes, inflammation and fibrous thickening of tissue.

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49
Q

How can liver cirrhosis affect circulation?

A

Can lead to portal hypertension due to increased resistance into the sinusoids

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50
Q

What gross features are indicative of cirrhosis

A

involvement of the entire liver, diffuse fibrosis, regenerative hyper plastic parenchymal nodules, permanent distortion of liver architecture, development of new vascular anastomoses

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51
Q

What 3 general disorders can result from portal hypertension?

A
  1. Congestion of viscera normally drained by portal vein
  2. Ascites
  3. Acquired portosystemic shunting
52
Q

What causes acquired portosystemic shunting?

A

Anything reducing portal venous inflow and diversion of portal venous blood away from liver. Usually multiple vessels

53
Q

How can congenital and portosystemic shunting be distinguished?

A 
Congenital= one anamolous vessel & due to DEC portal venous inflow/ INC arterial inflow 
Acquired= Generally multi anomalous vessels & due to portal hypertension
54
Q

Describe the differences in the location of portosystemic shunts in small and large breed dogs

A

Small –> outside liver but inside abdomen

Large –> inside liver (usually remnant of foetal vessel)

55
Q

Which disorders are likely to contribute to focal hepatitis?

A

Hardware dx –> pyogenic abscess
Ruminal acidosis –> infection of ulcers that enter blood and travel to liver
Bacteria crawling up bile duct to liver!

56
Q

A drop in circulating blood glucose elicits what response?

A

gluconeogenesis

57
Q

Which stain is used to assess hepatocellular glycogen storage disease histologically?

A

PAS (Acid schiff)

58
Q

Oriental breed cats have an inherited form of which systemic liver disfunction?

A

Amyloidosis

Progressive accumulation of Amyloid A which leads to hepatomegaly

59
Q

Blood in liver sinusoids would suggest which disfunction? (at whole body level)

A

Right-sided congestive heart failure

60
Q

Why do atrophic/ cirrhotic/ PSS livers demonstrate increased bile acids??

A

Their reduced functional mass means that they don’t have enough efficient live hepatocytes to reabsorb the high percentage of bile acids

61
Q

What are causes of hydronic degeneration of hepatocytes?

A

Sublethal injury that damages cell membranes causing uncontrolled movement of fluid & ions across cell membranes.

e.g. sublethal hypoxia, sublethal toxaemia, prolonged cholestasis

62
Q

Define steroid hepatopathy

A

Glycogen accumulation in hepatocytes

63
Q

Define bridging fibrosis

A

Fibrotic pattern joining one structure to another e.g. portal area to central vein

64
Q

Why is portal hypertension a consequence of cirrhosis?

A

Increase pressure in the portal vein is due to increased resistance to portal venous blood flow into sinusoids

65
Q

What are 3 consequences of portal hypertension?

A
  1. Congestion of viscera normally drained by portal vein
  2. Ascites
  3. Acquired portosystemic shunting
66
Q

Define “hepatitis”

A

inflammation of the hepatic parenchyma

67
Q

What pattern of hepatitis is most likely to progress to cirrhosis?

A

Severe DIFFUSE hepatitis

68
Q

Which conditions commonly lead to hepatic abscess formation in cattle?

A
  1. direct foreign body implantation e.g. hardware disease
  2. direct extension from adjacent suppurative lesions e.g. hardware
  3. Ascending infx up bile duct
  4. Haematogenous infx
69
Q

What are potential consequences of hepatic abscessation?

A
  1. Production –> weight loss/ decreased milk production/ liver condemnation
  2. Health –> Perforated liver (+/- peritonitis), Eroded hepatic veins (thrombus + inflammation), systemic spread (death from toxaemia)
70
Q

Describe the aetiopathogenesis of Black’s disease

A

Liver damage due to low O2 conc –> Clostridial spores germinate –> proliferation + toxin release –> necrosis –> toxins become systemic –> widespread vascular injury –> death + rapid carcass putrefaction

71
Q

What is the causative agent of Black’s disease?

A

Clostridium novyi Type B

72
Q

What is bacillary haemoglobinuria?

A

Similar pathogenesis to Black’s disease but gross lesions are usually a single large focal necrotic centre. Clinical signs include jaundice/ anaemia due to exotoxins causing hepatic necrosis & intravascular haemolysis

73
Q

The gross appearance of multifocal hepatitis suggests which agents of disease? (bing bing bing bing bing)

A

Multifocal hepatic necrosis due to

  1. Bacteraemia
  2. Systemic protozoal infection
  3. Some viraemias
  4. Systemic fungal infection
  5. Migrating parasites
74
Q

What is a useful microscopic tool suggesting multifocal hepatitis is due to parasite migration?

A

Linear/ squiggly tunnels containing haemorrhage/ necrotic debris/ fibrin wherever liver capsule is breached

75
Q

Name a few parasites that commonly migrate through the liver?

A 
Liver fluke (cattles/sheeps)
Round worm (piggies)
Tapeworm (sheep)
76
Q

What is a viral cause of zonal hepatitis (Note, don’t think this is the same as zonal necrosis?! [Which is from toxaemia/ hypoxia])

A

Canine adenovirus-1

77
Q

What are 3 characteristic features of chronic hepatitis in doggies?

A
  1. Deposition collagen in perisinusoidal space
  2. Periportal hepatitis
  3. Frequent progression to cirrhosis
78
Q

Which dog breed are predisposed to a form of chronic hepatitis?

A

Doberman’s –> immune-mediated pathogenesis

79
Q

What are two mechanisms by which certain dog breeds can develop copper storage disorders?

A
  1. Primary copper storage disease –> usually breed related

2. Secondary –> copper accumulation due to cholestasis

80
Q

Why exactly does copper storage in the liver cause pathogenesis?

A

Copper has a 2+ valency, causes free radical generation & the per oxidation of cell membranes, fuck!

81
Q

Define cholangitis

A

inflammation of bile ducts

82
Q

Define cholecystitis

A

Inflammation of gall bladder

83
Q

Define Cholangiohepatitis

A

Inflammation on bile ducts in portal areas (usually spreads to involve whole liver parenchyma)

84
Q

Which liver lobe is more susceptible to parasitic insults?

A

Left –> closer route for entry!

85
Q

How do the gross lesions of chronic fascioliasis present in cattle?

A

Bile duct fibrosis, severe duct mucosal erosion & ulceration

86
Q

How do the gross lesions of chronic fascioliasis present in sheep?

A

Dilation of thin walled vessels & catarrhal inflammation

87
Q

How do bacteria reach the biliary tree?

A

Migrate from duodenum up bile duct

88
Q

Outline the aetiology of facial eczema in ruminants?

A

Sporadesmin fungal mycotoxin origin

89
Q

Outline the pathogenesis and typical lesions of facial eczema in ruminants

A

Sporadesmin ingested –> carried from GIT to liver via portal vein –> liver can’t modify so tries to excrete through biliary system –> concentrates in bile and becomes increasingly toxic –> burns biliary epithelium –> obstructive jaundice & photosensitisation

90
Q

How will acute and chronic lesions in the liver differ in an animal presenting with hepatogenous photosensitisation from sporadesmin poisoning?

A 
Acute= swollen & jaundiced liver 
Chronic= Fibrotic, atrophic left lobe, fibrous thickening of bile duct walls
91
Q

How common are gall stones in domestic animals?

A

Uncommon- don’t have diet high in cholesterol!

92
Q

Are gall stones in domestic animals usually of clinical concern?

A

Rarely- usually soft

93
Q

Why is the liver most affected by toxins?!

A
  1. First pass metabolism, receives most afferent blood from portal vein
  2. May naturally concentrate toxins e.g. Cu/ Sporadesmin
  3. Hepatic biotransformation (metabolises stuff)
94
Q

What is the major purpose of hepatic biotransformation in the liver?

A

Make incoming fat soluble molecules into water soluble so can be excreted from hepatocytes & eliminated in poo/ urine

95
Q

What happens during phase 1 hepatic biotransformation?

A

Oxidation in SER

96
Q

What can be two adverse consequences of phase 1 hepatic oxidative biotransformation?

A

Generation of toxic metabolites or free radicals

97
Q

What happens during phase 2 hepatic biotransformation?

A

Conjugation, usually with reduced glutathione to increase water solubility

98
Q

What role does glutathione play in liver metabolism?

A

Anti-oxidant activity to mop up free radicals!

99
Q

What is the difference between primary and secondary poisoning?

A 
Primary= animal ate poison 
Secondary= animal eats other animal who had previously ingested toxin
100
Q

What is a predictable hepatotoxin?

A

A toxin that in a sufficient dose, will cause predictably cause hepatic injury in virtually all susceptible animals

101
Q

What is an example of a predictable hepatotoxin?

A

Paracetamol in catties

102
Q

What is an idiosyncratic hepatotoxin?

A

toxin that causes hepatic injury in a minority of exposed animals

103
Q

What factors influence the response of an individual animal to exposure of a hepatotoxin?

A

age/ gender/ diet/ nutritional status/ endocrine function/ genetics/ previous drug exposure

104
Q

In what circumstances are large domestic animals likely to consume fatal doses of hepatotoxins?

A

E.g. Ruminants with limited food supply
Naive eating habits
high stocking density –> starvation

105
Q

what clinical signs might you expect in an animal with acute hepatotoxitiy?

A

few… it’ll be dead asap

106
Q

What is the most common lesion seen in animals that have died from an acute hapatotoxic insult?

A

Zone 3 zonal hepatitis or massive necrosis

107
Q

Why are periacinar hepatocytes so vulnerable to toxic injury?

A

Highest activity of Mixed function oxidase (MFO) enzymes

Damaged by the products of biotransformation

108
Q

What are the main gross anatomical changes you might find in a liver that has been exposed to long term hepatotoxins?

A

Cirrhosis (hyperplastic nodules & fibrosis)

109
Q

What are some common toxins that cause chronic hepatotoxicity in domestic animals

A

Aflatoxins

Pyrrolizidine alkaloids

110
Q

What are some common toxins that cause acute hepatotoxicity?

A

Amatoxins

Blue green algae

111
Q

Why are kitties particularly prone to paracetamol poisoning?

A

They are less effective at conjugating metabolites (phase 2) therefore generate more toxic intermediates. What is metabolised via Phase 1 produces toxic metabolites. Glutathionine levels in catties are insufficient to mop up free radicals

112
Q

What are some common species of plants that contain pyrrolizidine alkaloids?

A

Paterson’s curse

113
Q

Why is acute pyrrolizidine poisoning far less common than chronic poisoning?

A

For acute onset of signs, requires large volume of toxic plant species (e.g. paterson’s curse) to be ingested

114
Q

What clinical signs might you observe in an animal with chronic pyrrolizidine poisoning?

A

Variable - depend on individual animal. Jaundice, photosensitisation, hepatic encephalopathy

115
Q

What is the most diagnostically useful microscopic lesion that can be used to diagnose chronic pyrrolizidine alkaloid poisoning?

A

Hepatic megalocytes and karymegaly

116
Q

What are Alfatoxins?

A

Toxins produced by fungi

117
Q

How do aflatoxin cause injury to the liver?

A

Toxins are biotransformed by MFO enzymes into toxic metabolites –> can bind to DNA/RNA and inhibit mitosis and protein synthesis

118
Q

Which animals are most susceptible to aflatoxins?

A

Birds > pigs > calves > horses > dogs

119
Q

Which domestic animals is most often affected by ACUTE aflatoxicosis?

A

Garbage eating dogs!!

120
Q

How does lantana cause jaundice?

A

Gall bladder paralysis

Canaliculi disruption

121
Q

Outline the aetiopathogenesis of chronic copper poisoning in sheep

A

Dietary copper intake –> Cu usually excreted in bile –> cholestasis = Cu accumulation in hepatocytes –> Cu valency (++) forms reactive oxygen species –> peroxidation of lipid membranes

122
Q

How do sheep die of copper poisoning?

A

Cooper concentrates in hepatocytes –> apoptosis –> Cu accumulation in adjacent cells –> increase plasma conc –> acute intravascular haemolysis –> hypoxic damage –> further copper release –> death

123
Q

Which tumours are more common in the liver, metastatic tumours or primary hepatobiliary tumours?

A

Metastatic tumours –> due to liver’s central location in body, huge afferent blood flow from GIT, storage function etc.

124
Q

Which tumours commonly metastasise to the liver?

A

Carcinomas
Sarcomas
Haemangiosarcomas
Malignant haematopoietic cells

125
Q

What are the most common primary tumours of the liver?

A 
Hepatocullular adenoma (benign tumour of hepatocytes) 
Hepatocellular carcinoma (malignant tumour of hepatocytes)
126
Q

What is the difference between primary and secondary photosensitisation?

A 
Primary= Direct deposits e.g. from ingested substance 
Secondary= photodynamic compounds deposited due to liver DAMAGE
127
Q

Why do cats die of paracetamol poisoning?

A

RBC are exposed to the free radicals (oxidising agents) from toxin metabolites –> Heinz inclusion bodies on RBC –> cells lyse –> PCR drops

Applications Animal Health (9 decks)

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