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CVSOH 4 > Liver > Flashcards

Liver Flashcards

1
Q

What is the normal colour of the liver?

A

Typically a reddish-brown, but may be brown in animals, such as cattle, sheep and pigs, that have been bled out

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2
Q

Why might a liver be yellow-brownish in colour?

A

Accumulation of fats in the liver can cause it to have a yellowish-brown appearance

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3
Q

Why might a liver be greenish/yellow?

A

Post-mortem changes can cause areas of pallor or darkening or greenish-yellow discolouration, especially adjacent to the gall bladder

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4
Q

What is the weight of the liver dependent on?

A

The weight of the liver as a proportion of body wieght can vary depending on factors includin the species (higher in carnoviores comapred to herbivores), nutritional status (hepatic storage of glycogen and fat) and age (liver weight decreases with age).

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5
Q

What is the percentage of body weight of the liver?

A

Dog = 3-4%

Horse = 1-1.5%

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6
Q

What blood vessels deliver blood to the liver?

A

Portal vein – provides 70-80% of the blood inflow

Hepatic artery

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7
Q

From which organs does the blood in the portal vein come from?

A

Collects blood from the spleen, pancreas, stomach and intestines

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8
Q

From what blood vessel does the hepatic artery originate from?

A

From the ceoliac artery, which arises from the aorta

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9
Q

What blood vessels drain blood from the liver?

A

Hepatic vein to the caudal vena cava

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10
Q

After blood enters the liver from the portal vein and hepatic artery, what structures for sit flow through before arriving in the hepatic veins?

A

Portal vein and hepatic artery > hepatic sinusoids > across hepatic lobule > central vein > interlobualr veins > hepatic veins

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11
Q

Within the functional unit, the hepatic acinus, what are the 3 zones?

A

Zone 1 – periportal region. The area that recievs the blood frm the portal vein and hepatic artery first

Zone 2 – midzonal region. Receives blood next

Zone 3 – centtilobular region. Recives the blood last before it drains into the central vein

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12
Q

What are the metabolic differences between the 3 zones of the hepatic acinus?

A

Zone 1 – periportal will receive blood with the highest oxygen and nutrient content

Zone 3 – centrilobualr will receive blood with lower oxygen and nutrient content. Hepatocytes in zone 3 also have higher levels of metabolic enzymes. These factors make this zone the most sensitive to injury by toxic compounds

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13
Q

Name 3 circulatory disorders affecting the liver.

A
  • Congenital portosystemic shunts
  • Post-hepatic conditions affecting outflow of blood from the liver
  • Intra-hepatic or pre-hepatic conditions associated with abnormal portal vein inflow
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14
Q

How can portosystemic shunts be classified?

A

Whether the anomlous blood vessel is within the liver or not

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15
Q

How does an intra-hepatic portosystemic shunt form?

A

Large blood vessel connects the portal vein directly to the hepatic vein, which is a lower resistance path than through the lobule and smaller sinusoides, so a significant portion of blood flow is through this shunt and bypasses the functional part of the liver

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16
Q

How does an extrahepatic portosystemic shunt form?

A

Large blood vessel connect the portal vein/tributaries of the portal vein, bypassing the liver and through extra-hepatic anomalous vein to connect to the systemic circulation (caudal vena cava or hepatic vein).

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17
Q

Distinguish which breeds are affected by which type of portosystemic shunt.

A

Extrahepatic – small (wEe) dog breeds

Intra-hepatic – large (bIg) dog breeds

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18
Q

Distinguish intra and extrahepatic CPSS.

A

Intrahepatic CPSS – left or right portal vein branch to hepatic vein or directly with caudal vena cava

Extra-hepatic CPSS – left or right gastric vein or splenic vein to the caudal vena cava or azygous vein

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19
Q

What are the functional consequences of congenital portosystemic shunts?

A
  • Reduced hepatic perfusion
  • Small liver due to underperfusion – microhepatica
  • Poor growth due to less liver and so less functional capacity
  • Hepatic encephalopathy, as the liver is unable to detoxify waste products and these build up and affect the central nervous system
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20
Q

Will congenital portosystemic shunts result in increased blood pressure in the portal venous system – portal hypertension?

A

No – offer a lower resistance route

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21
Q

How does heart disease affect outflow from the liver?

A

Especially right sided CHF, which will increase pressure in the caudal vena cava which can be referred back through the hepatic vein to the liver and impair outflow of blood from the liver

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22
Q

How does hepatic vein/vena cava obstruction affect outflow from the liver?

A

Luminal obstruction (thrombus), vessle wall thickening (neoplasia, inflammation), external compression (by a mass, such as an abscess or tumour)

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23
Q

What are the consequences of impairment of post-hepatic outflow?

A
  • Hepatic passive venous congestion – dilation of the sinusoids and central vein and becoming packed full of the blood, can extend to portal vein
  • Hepatomegaly – blood pools and congest in the liver may make it appear larger so there is some degree of hepatomegaly
  • Chronic passive congestion may develop an enhanced lobular or reticular pattern on the sectioned surface of the liver (nutmeg liver). Reddening due to congestion and the yellowish colour caused by accumulation of fat, create enhanced lobular pattern
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24
Q

Could post-hepatic conditions causing passive congestion of the liver cause an increased blood pressure in the portal venous system (portal hypertension)?

A

Yes

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25
Q

Name 3 intra-hepatic and pre-hepatic conditions associated with abnormal portal vein inflow.

A
  • Advanced chronic liver disease with fibrosis
  • Portal vein obstruction – thrombosis, inflammation, abscess, neoplasia
  • Portal vein hypoplasia – portal vein is smaller than normal
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26
Q

Could intra-hepatic conditions, such as diffuse liver fibrosis or pre-hepatic conditions, such as portal vein hypoplasia, be a cause of portal hypertension?

A

Yes

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27
Q

What are the potential causes of portal hypertension?

A
  • Post-hepatic conditions affecting outflow of blood from the liver
  • Intra-hepatic or pre-hepatic conditions associated with abnormal portal vein inflow
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28
Q

What are the potential consequences of portal hypertension?

A
  • Ascites
  • Acquired portosystemic shunts – intra-hepatic and re-hepatic causes of portal hypertension (not by passive hepatic congestion, such as heart failure). Allow portal blood to flow directly to the systemic venous system bypassing the liver
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29
Q

What are the possible responses to hepatic injury?

A
  • Hepatocellular vacuolation
  • Necrosis
  • Hepatocellular regeneration
  • Inflammation
  • End stage liver (cirrhosis)
  • Hyperplastic and neoplastic changes
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30
Q

What are the possible hepatocellular vacuolar changes?

A
  • Vacuoles may contain lipid (fatty change), water (hydropic change) and glycogen
  • Potential gross changes – enlargement, altered colour change (pallor or yellow-brown), or altered consistency (greasy if lipid accumulation, increased fragility)
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31
Q

Why do cats’ livers appear more brown than dogs’ livers?

A

Cats can store more fat in their livers so can end up naturally appearing more brown than dogs

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32
Q

What are the 2 mechanisms of lipid accumulation in the liver?

A

There is excess delivery of free fatty acids to hepatocytes, causing negative energy balance and metabolic/endocrine disease

Reduced hepatocellular capacity to metabolise fats often due to hepatocellular injury – hypoxia, toxins, dietary deficiencies lipotropes for lipid metabolism

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33
Q

What are the causes of water accumulation/hydropic change in the liver?

A

Various toxins
Metabolic insults
Hypoxia

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34
Q

What are the causes of glycogen accumulation?

A

Associated with hyperadrenocorticism or corticosteroid administration – ‘steroid induced hepatopathy’

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35
Q

What is a property of the liver on PME if there is significant fat present?

A

It can cause the liver to be bouyant in water

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36
Q

What does a focal/random pattern of necrosis suggest of the cause?

A

Scattered, randomonly distributed foci of necrosis. Typical of some infectious agents, such as bacteria, viruses, protozoa, migrating parasites. May be of little functional significance to the liver

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37
Q

What is the appearance of focal/random necrosis?

A

Area of necrosis in hepatocytes and there is variable amounts of erythrocytes in necrosis. So typical gross appearance is one or more white/grey or reddish foci (if lots of blood associated with them).

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38
Q

What does a zonal pattern of necrosis suggest of the cause?

A

Zone 3/certrilobular/periacinar most commonly affected as it is more prone to hypoxia as it receives blood last and also the hepatocytes in zone 3 contain a lot of metabolic enzymes and so may activate toxins

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39
Q

What are some typical causes of zonal necrosis?

A
  • Hypoxia/ischaemia
  • Exposure to some toxins
  • Some severe viral infections, such as canine adenovirus 1
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40
Q

Describe the appearance of zonal necrosis.

A

Multiple areas of necrosis, paler pink, surrounding central veins. In some areas, these join, known as bridging necrosis. This results in a gross pattern of mottled appearance, with colour intensity perhaps dictated by amount of haemorrhage. Microscopy needed to identify necrotic areas. Pattern sometimes called enhanced lobular pattern/enhanced reticular pattern.

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41
Q

What are the causes of massive necrosis?

A
  • Severe toxic injury
  • Vitamin E/selenium deficiency in pigs/hepatosis dietetica
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42
Q

Describe the appearance of massive necrosis.

A

Red appearance due to red blood cell snow filling the spaces left by the necrotic hepatocytes. There is a fine rim of surviving hepatocytes along the edge of the lobules but most have died and been replaced with blood

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43
Q

You submit a liver biopsy in formalin for histopathology. The pathology report report indicates a vacuolar hepatopathy. What type of material could be present in the vacuoles?

A

Lipid, water or glycogen – intracellular accumulation of lipid, water or glycogen can all create cytoplasmic vacuolation. Sometimes some features of the vacuolated hepatocytes may allow the pathologist to suggest the most likely material.

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44
Q

A 6 month old frenhc bulldog has severe jaundice and rasied liver enzymes. Severe centrilobular necrosis is rpeorted on a liver biopsy submitted for histopathology. Of the aetiologies, which should you include as the potential cause of the hepatic necrosis?

A

Recent hepatotoxin ingestion and severe hypoxia

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45
Q

What are the vague clinical signs of liver disease?

A

Inappetence
Lethargy
Weight loss
Vomiting
Diarrhoea
Polyuria/polydipsia

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46
Q

What are the specific clinical signs of liver disease?

A
  • Jaundice/icterus) - hyperbilirubinaemia – normal is 10-1 umol/L, 10-35umol/L high but not appear yellow, so significantly high to appear yellow
  • Ascites
  • Hepatic encephalopathy
  • Coagulopathy
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47
Q

Summarise the cycle of bilirubin.

A

Bilirubin from senescent RBC, macrophages break down these in liver, spleen and bone marrow. Bilirubin bound to albumin and uptaken into liver cells. Stored in gall bladder and excreted when gall bladder contracts and is released when eating

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48
Q

Distinguish pre-hepatic, hepatic and post-hepatic jaundice.

A
  • Pre-hepatic for a process prior to the liver, such as increased breakdown of RBC, so patients would be anaemic
  • Hepatic would be inherent liver disease, as we can’t convert these
  • Post hepatic is something wrong with the pancreas or gall bladder
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49
Q

Why do effusions in liver disease occur?

A

From either increased hydrostatic pressure or low albumin

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50
Q

What is hepatic encephalopathy?

A

Toxins that accumulate in bloodstream such as ammonia due to liver disease affects rain function. With extreme hepatic dysfunction or portosystemic shunting

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51
Q

What are the clinical signs of hepatic encephalopathy?

A

Obtunded
Lethargic
More vague forebrain signs seizures
Comas or death in more severe cases
High ammonia in the blood or other evidence of liver disease

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52
Q

What is the hepatic link to coagulopathy?

A

Liver dysfunction may mean not enough clotting factors

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53
Q

What is hepatocutaneous syndrome?

A

Hyperkeratotic footpads, skin biopsy specific diagnostic. Ultrasound looks like Swiss cheese

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54
Q

Describe the severity-time graph for differentials of liver disease.

A
  • Vascular, trauma, toxin = 2-6 hours
  • Inflammatory (infectious/sterile) = acute over hours to a few days – main challenge is owners not noticing clinical signs in first stages so appears more acute than actually is
  • Metabolic quiet insidious, but progressively worsen with wax and wane, more chronic in terms of months, owners may not notice
  • Neoplastic often chronic, can be acute, as insidious part at the beginning is progressive,
  • Degenerative months to years, vague clinical signs reported over months and years
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55
Q

What is done next after a differential list for liver disease is made?

A

Use hepatic enzyme elevations to determine whether predominantly hepatocellular or cholestatic

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56
Q

Which are the hepatocellular enzymes in dogs and cats?

A

ALT and AST in cats and dogs (and/or GGT)

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57
Q

Which are the cholestatic enzymes in dogs and cats?

A

ALP and/or GGT (> ALT and/or AST) with/without other features of cholestasis – hypercholesterolaemia with/without hyperbilirubinaemia with/without overt jaundice

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58
Q

How do liver enzymes differ between cats and dogs?

A

Be aware of limitations, especially in cats, as short half-life. Dog half life is 3-4 days and cats is 4-6 hours, so can miss window of opportunity for cats – may have normal blood ranges on cats with liver disease.

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59
Q

What are some acute toxic causes of hepatobiliary disease with hepatocellular patterns?

A
  • Drugs – antimicrobials like TMPS and doxycycline, immunosuppressants like azathioprine, anti-thyroidals like methimazole
  • Toxins like blue-green algae, aflatoxins
  • Amantia species (mushrooms)
  • Xylitol
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60
Q

What are some chronic toxic causes of hepatobiliary disease with hepatocellular patterns?

A

Chronic, low-level exposure, such as phenobarbitone (seizure medication, can give accumulative toxic injury if wrong dose over time)

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61
Q

What are some acute traumatic causes of hepatobiliary disease with hepatocellular patterns?

A

Blunt trauma – hepatic contusions

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62
Q

What are some acute inflammatory causes of hepatobiliary disease with hepatocellular patterns?

A

Infections – neutrophilic cholangitis (cats)/cholangiohepatitis (dogs), leptospirosis (dogs), CAV-1 in unvaccinated dogs

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63
Q

What are some chronic inflammatory causes of hepatobiliary disease with hepatocellular patterns?

A

Sterile – lymphocytic cholangitis (cats), chronic hepatitis (dogs)

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64
Q

What are some metabolic and neoplastic causes of hepatobiliary disease with hepatocellular patterns?

A

Metabolic - reactive hepatopathies

Neoplastic - hepatocellular adeno/carcinoma, lymphoma – metastasise to liver

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65
Q

What are some acute toxic causes of hepatobiliary disease with cholestatic patterns?

A

Drugs/toxins – some can cause an idiosyncratic cholestatic pattern

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66
Q

What are some chronic toxic causes of hepatobiliary disease with cholestatic patterns?

A

Chronic, low-level exposure, such as phenobarbitone

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67
Q

What are some acute traumatic causes of hepatobiliary disease with cholestatic patterns?

A

Biliary rupture – typically secondary to underlying disease, such as trauma

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68
Q

What are some acute inflammatory causes of hepatobiliary disease with cholestatic patterns?

A
  • Infections – neutrophilic cholangitis (cats)/cholangiohepatitis (dogs, cholecystitis, FIP (cats), toxoplasma
  • Sterile – acute pancreatitis, not hepatobiliary but critical differential
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69
Q

What are some chronic inflammatory causes of hepatobiliary disease with cholestatic patterns?

A

Sterile – lymphocytic cholangitis (cats), chronic hepatitis (dogs), chronic pancreatitis

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70
Q

What are some acute metabolic causes of hepatobiliary disease with cholestatic patterns?

A

Hepatic lipidosis, gall bladder mucocele, obstructive choleliths

71
Q

What are some chronic metabolic causes of hepatobiliary disease with cholestatic patterns?

A

Vacuolar hepatopathies, including steroid/metabolic, gall bladder mucocele

72
Q

What are some neoplastic causes of hepatobiliary disease with cholestatic patterns?

A

Hepatocellular adeno/carcinoma – sometimes just cause isolated ALP elevation, primarily biliary neoplasia

73
Q

What are the other possible origins of ALP not specific to liver disease?

A

As well as cholestatic, there are steroid (dogs) and bone isoenzymes, so in growing cats and dogs. Commonly induced by some drugs (steroid in dogs, phenobarbitone)

73
Q

What are the other possible origins of GGT not specific to liver disease?

A

Cholestatic and steroid induction in dogs, can be induced by some drugs (steroid in dogs, phenobarbitone)

74
Q

What are the other possible origins of AST not specific to liver disease?

A

Found in muscle, concurrent creatine kinase will help evaluate for myopathy

75
Q

What are the other possible origins of ALT not specific to liver disease?

A

Found in muscle – needs to be very severe myopathy to increase ALT

76
Q

What are some possible conditions causing secondary liver disease?

A
  • Liver as an immune organ – any systemic inflammatory disease
  • Drugs causing enzyme induction (glucocorticoids, phenobarbitone)
  • Metabolic diseases causing vacuolar hepatic change (hyperadrenocorticism, diabetes mellitus) or a toxic hepatopathy (hyperthyroidism)
  • Hepatic hypoxaemia, anaemia, hypovolaemia, heart failure
77
Q

What may magnitude of enzyme elevation indicate about liver disease?

A
  • May be low with end stage liver disease or in cats
  • Often low-moderate with secondary/reactive – can be markedly increased with steroid induction
  • Can be anything (low-high) with primary liver disease
  • May fluctuate – re-assess if not sure of significance and animal clinically well
78
Q

What is the evidence of multisystemic disease with liver disease?

A
  • Renal – leptospirosis, toxins
  • Lymphadenomegaly, multiple organs – lymphoma
  • Ocular – canine adenovirus 1 (CAV-1)
79
Q

What does structural hepatic disease suggest on ultrasound?

A

Structural hepatic disease indicates hepatic pathology is present, regardless of enzyme elevations (such as nodular regeneration)

80
Q
A
81
Q

Is the size of the gall bladder on ultrasound significant?

A

Size of gall bladder never significant, only when ducts are dilated indicates back pressure and obstruction

82
Q

What is sludge on the gall bladder?

A

Normal in dogs and much less normal in cats. Majority of cats with sludge probably have biliary disease. Biliary mucocele looks like kiwi in cross section (border terriers prone to), mucus overproduction in wall of gall bladder and produces very solid gall bladder, can get bigger over time and cause pressure necrosis and may rupture.

83
Q

What is the problem with colour ultrasound imaging the bile ducts?

A

Vessels are coloured, bile ducts are non-coloured. Previous obstruction – bile ducts may never go back to normal, so may not be an active problem

84
Q

Why are cats with liver disease hard to diagnose?

A
  • Every cat with hyperthyroidism has increased liver enzymes
  • Short enzyme half-lives
  • Commonly have non-specific signs
  • Commonly have multiple comorbidities
  • Older cats, elevated hepatic enzymes, normal function
85
Q

What are the functions of the liver?

A
  • Protein metabolism
  • Carbohydrate metabolism – synthesis, storage and release of glucose
  • Lipid metabolism
  • Excretion of bile – no gall bladder so continuous flow
  • Detoxification – biotransformation of endogenous and exogenous compounds
  • Mononuclear – phagocyte system
  • Miscellaneous – storage of vitamins
86
Q

How does the liver do protein metabolism?

A
  • Protein synthesis, including factors involved in coagulation
  • Gluconeogenesis from amino acids
  • Eliminating ammonia the major toxic byproduct of amino acid catabolism
87
Q

When are hepatic functions impaired in horses?

A

Most hepatic functions not impaired until greater than 80% of the hepatic mass is lost

88
Q

What are the common clinical signs of hepatic insufficiency in horses?

A

Depression
Anorexia
Colic
Hepatic encephalopathy
Weight loss
Icterus

89
Q

What are the less common clinical signs of hepatic insufficiency in horses?

A

Photosensitization
Diarrhoea
Bilateral laryngeal paralysis
Bleeding
Ascites
Dependent oedema

90
Q

What is stage 1 hepatic encephalopathy in horses?

A

Probably missed in most equine patients. Subtle impairment of intellect

91
Q

What is stage 2 hepatic encephalopathy in horses?

A

Motor function, intellectual ability and consciousness impaired:

Depression
Head pressing
Circling
Ataxia
Aimless walking
Yawning

92
Q

What is stage 3 hepatic encephalopathy in horses?

A

Aggressive
Periods of stupor
Recumbent
Coma

93
Q

What is the cause of hepatic encephalopathy in horses?

A

Insufficient hepatocellular function, irrespective of the cause of the liver disease

94
Q

What is the pathogenesis of hepatic encephalopathy in horses?

A
  • Accumulation of toxins in the blood (including ammonia)
  • Augmented activity of inhibitory neurotransmitters
95
Q

How is hepatic encephalopathy diagnosed in horses?

A
  • Presence of neurologic signs of cerebral dysfunction
  • With physical examination and laboratory findings compatible with liver disease
96
Q

What are the disease states resulting in hyperbilirubinaemia in horses?

A
  • Increased production of bilirubin – haemolysis, intracorporeal haemorrhage
  • Impaired uptake and conjugation of bilirubin – liver disease, anorexia, prematurity
  • Impaired excretion of bilirubin into biliary tract = regurgitation icterus
97
Q

Why might there be impaired excretion into the biliary tract in horses?

A
  • Blockage of bile with cholangitis, hepatitis, cholelithisasis, neoplasia, fibrosis
  • If congested bilirubin more than 30% greater than normal, indicative cholestasis
98
Q

What is hepatogenic photosensitisation in horses?

A
  • Abnormally heightened reactivity of the skin to UV
  • Increased blood concentration of a photodynamic agent phylloerythrin if hepatogenic
  • UV + phylloerythrin = free radicals = cell membrane damage and necrosis
99
Q

Distinguish conjugated and unconjugated bilirubin in horses.

A

Conjugated (direct) + unconjugated (indirect) = total bilirubin

Increase in unconjugated bilirubin seen in hepatic disease – usually acute hepatocellular. But also anorexia, haemolysis, others

100
Q

How is bile acid concentration indicative of disease in horses?

A
  • Enterohepatic circulation normally removes greater than 90% bile acids
  • Blood concentration increases with liver disease
  • Quantitation is an excellent screen of liver failure
101
Q

How is protein synthesis tested in horses?

A
  • Hypoalbuminaemia – non-specific
  • Evaluation of haemostasis – non-specific
  • Liver removes ammonia from circulation, converts to urea – increase in ammonia, decrease in BUN, not specific
102
Q

Why are increased liver enzymes indicative of disease in horses?

A
  • Hepatocellular necrosis results in the release of enzymes
  • So increased serum activity may be indicative of active hepatic disease
103
Q

What is the indication of increased SDH, ARG and GLDH in horses?

A
  • Liver specific and not inducible
  • Specific for hepatocellular disease but not type of disease
  • All usually better for acute disease
  • SDH would be the best test but doesn’t survive in a tube
104
Q

What is the indication of increased ALT in horses?

A
  • Also found in other tissues
  • So low specificity
105
Q

What is the indication of increased GGT in horses?

A
  • Specific for hepatic disease in horses
  • The most sensitive indicator of hepatic disease
  • Hepatocellular damage
  • Continues to rise for 1-2 weeks after liver improving
  • May not increase in chronic disease
  • Higher in young foals
106
Q

What are the first line lab tests investigating liver disease in horses?

A
  • GGT – damage
  • Bile acids – function
107
Q

How is the liver biopsied in horses?

A
  • Ultrasound guided
  • Check they can clot first
  • But usually low risk
  • Not if hepatic lipidosis
108
Q

What is the treatment for hepatic insufficiency in horses?

A
  • Therapy for hepatic insufficiency largely supportive
  • Maintain until enough liver regenerates to provide adequate function
  • If severe hepatic fibrosis, adequate regeneration often not possible
  • Care with sedation – low dose xylazine
  • Correct fluid deficit, acid-base, electrolyte imbalances – IV fluids spiked appropriately. If anorexic, spike fluids to be 5% glucose
109
Q

How can hepatic insufficiency in horses be managed with diet?

A
  • High carbohydrate, low in (good quality) protein
  • Multiple small feeds as impaired gluconeogenesis
110
Q

How can absorption and production of toxins by enteric bacteria be reduced?

A

Reduce absorption – paraffin/magnesium sulphate by nasogastric tube

Reduce production – neomycin, metronidazole, lactulose

111
Q

What may chronic hepatic disease in horses show?

A

Hyperglobulinaemia
Hypoalbuminaemia
Fibrosis

112
Q

What is theiler’s disease in horses?

A
  • ‘Serum associated hepatitis’
  • Usually received an equine origin antiserum 4-10 weeks before
  • Supportive treatment
113
Q

Describe bacterial hepatitis in horses.

A
  • Primary is rare
  • Secondary more common – after cholelithisasis, intestinal obstruction, anterior enteritis
  • Liver biopsy for histology and culture
  • Supportive therapy
  • Appropriate antibiotics 4-6 weeks
114
Q

How is acute lipidosis treated in horses?

A
  • Secondary to hyperlipidaemia
  • Supportive
  • Treat hyperlipidaemia
115
Q

What are the causes of chronic meagolocytic hepatopathy in horses?

A
  • Ingestion of pyrrolizidine alkaloid containing plants
  • Ragwort
  • Cumulative toxicity
116
Q

What is the pathogenesis of chronic megalocytic hepatopathy in horses?

A
  • Toxin stops cell division – hepatocytes enlarge ‘megalocytes’
  • When megalocytes die, get fibrosis
  • Extensive fibrosis results in the liver shrinking > failure
117
Q

What are the clinical signs of chronic megalocytic hepatopathy?

A
  • Clinical signs 4 weeks – 12 months after ingestion
  • Abrupt onset of H.E. and photosensitisation late in disease
  • Earlier, anorexia, weight loss, icterus
118
Q

What is the prognosis of chronic megalocytic hepatopathy?

A

Generally poor prognosis as fibrosis limits regeneration

119
Q

What are the clinical signs of cholelithiasis in horses?

A

Icterus
Colic
Pyrexia
Weight loss
Often intermittent signs
Conjugated bilirubin more than 30% increased often
Many have dilated bile ducts on ultrasound

120
Q

How is cholelithiasis in horses treated?

A
  • May have underlying bacterial cause so long term antibiotics (culture biopsy)
  • Surgery
121
Q

What is non-septic hepatitis in horses?

A
  • Lymphoplasmacytic
  • Inflammatory infiltrate without infection
122
Q

How is non-septic hepatitis in horses treated?

A
  • Corticosteroids, azathioprine
  • Monitor with biopsies
123
Q

You see a horse which has been losing weight and has some sunburn on his white patches. There is a tight budget. What test(s) do you take?

A

GGT and bile acids

124
Q

Increased serum activity of GGT but bile acids are borderline OK. What next?

A

Liver panel, clotting and biopsy

125
Q

Non-infectious hepatitis. What next?

A

Treat horse and test other horses there

126
Q

Describe normal abdominal palpation of the liver.

A

Normal to not feel liver on palpation, should be very tucked up in costal arch

127
Q

How might cholestatic and hepatocellular hepatopathy be presented?

A

ALT and ALP both raised

128
Q

What is the normal cut off point for bile acids on biochemistry?

A

30-35 cut off for normal). Can do bile acid stimulation test but with bile acids that are so persistently high, no point in doing this test.

129
Q

What are the characteristics of chronic hepatitis?

A

Small liver so such as vascular compromise, such as portosystemic shunts, or if losing liver cells over time due to fibrosis and scarring from chronic hepatitis.

130
Q

What do characteristics of abdominal effusion analysis indicate?

A
  • Transudate – hypoalbuminaemia
  • Modified transudate – portal hypertension
  • Bile – biliary rupture
131
Q

What are 2 other specific infectious disease tests that can be used in chronic hepatopathy cases?

A

Leptospirosis – serology, PCR

Feline Infectious Peritonitis – PCR, immunocyto/histochemistry, can sample admonial fluids to diagnose, will often have liver changes

132
Q

When is hepatic sampling required?

A
  • Required for definitive diagnosis of many diseases – neoplasia cannot be diagnosed on appearance alone. Never put an animal to sleep based on imaging of the liver, always sample
  • Rarely used in the acute or toxic setting
133
Q

What are the indications for hepatic sampling?

A
  • Persistent/progressive enzyme elevations – exclude extra-hepatic causes first
  • Structural parenchymal pathology
  • Monitoring response to therapy
  • Breed screening – Bedlington terriers prone to copper storage in the liver
134
Q

Describe liver cytology as a way of hepatic sampling.

A

Normal gauge needle but longer to get FNA from liver – works well in small number of cases, such as round cell tumours, hepatic lipidosis. Does not perform well in sterile inflammatory disease as you can’t see architecture of the liver and does not perform well for hepatic masses/primary tumours of the liver as these are often not discernible on cytology.

135
Q

Describe liver histology as a way of hepatic sampling.

A

Percutaneous (‘tru-cut’) biopsy needles to take a core of the liver, biopsy on both sides as you can have different disease processes on different lobes/sides.

136
Q

Describe cholecystocentesis as a way of hepatic sampling.

A

Bile cytology (EDTA), culture (plain). Sample of bile, empty gallbladder as much as possible as this will leak if left full after this

137
Q

Describe laparoscopy as a method liver sampling.

A

Larger and can access more, minimally invasive, more expensive, specialist equipment

138
Q

Describe laparotomy as a method liver sampling.

A

More likely to be done if being taken to surgery and likely to be sampling multiple organs

139
Q

What can be done before liver sampling?

A

Check platelets, PT, aPTT first with/without pre-treat with vitamin K

140
Q

What are the possible complications of liver sampling?

A
  • Haemorrhage
  • Ascites
  • Bile peritonitis
  • Clinical deterioration
  • Unnecessary sample
  • Non-diagnostic sample
141
Q

When can’t hepatic sample be cultured?

A

If fixed in formalin

142
Q

What are the 3 most common feline liver diseases in the UK?

A

Neutrophilic cholangitis
Lymphocytic cholangitis
Hepatic lipidosis

143
Q

Why might cats be jaundiced?

A
  • FIP is a common and important cause of jaundice in cats
  • Septic cats can become jaundiced
144
Q

Which multisystemic diseases can the liver be involved with?

A

Lymphoma
Toxoplasma
FIP

145
Q

Describe neutrophilic cholangitis.

A
  • Ascending bacterial biliary infection
  • Acute disease
  • Often sick/pyrexic
  • Diagnosis - bile cytology/culture
  • Chronic/mixed cholangitis possible
  • May accompany pancreatitis and/or inflammatory enteropathies ‘triaditis’
146
Q

Describe lymphocytic cholangitis.

A
  • Immune-mediated biliary disease
  • Chronic disease
  • May have hepatomegaly, abdominal effusion, jaundice and hyperglobulinaemia (FIP differential diagnosis)
  • Diagnose with a liver biopsy
  • Chronic/mixed cholangitis possible
  • May accompany pancreatitis and/or inflammatory enteropathies ‘triaditis’
147
Q

Describe hepatic lipidosis.

A
  • Triglyceride deposition within hepatocytes, due to fat mobilisation in times of starvation
  • Look for underlying disease
  • Often sick with significant hepatic dysfunction - coagulopathy, encephalopathy
  • Diagnosis - liver FNA
148
Q

How do cats with liver disease appear on bloods and on imaging?

A

Hepatocellular on bloods and then cholestatic on imaging

149
Q

When is cholecystocentesis not done?

A

Don’t do this if gallbladder wall is very thickened, makes this very risky of leaking

150
Q

When is surgery indicated in liver disease?

A
  • Abdominal free fluid – if bile peritonitis, if haemoabdomen secondary to hepatic pathology
  • Hepatic mass lesion
  • As a diagnostic/therapeutic procedure, where minimally invasive sampling is contraindicated
  • Gall bladder compromise
  • Symptomatic gall bladder mucocele
  • Obstructive biliary disease – exemption is pancreatitis
151
Q

How is dietary modification used to address liver disease?

A
  • To avoid exacerbating hepatic dysfunction
  • With/without copper restriction
152
Q

What are the complications of liver disease management?

A
  • Hepatic encephalopathy
  • Portal hypertension
153
Q

List the ways of managing liver disease?

A
  • Anti-inflammatory/immunosuppressive therapies
  • Specific – copper chelation, treatment of infectious agents, neoplastic disease
  • Hepatoprotective therapies – antioxidants, choleretics
  • Various supportive – fluids, nutrition, anti-emetics
154
Q

What is the characteristic of congenital shunting?

A

1 abnormal vessel not multiple

155
Q

What are the clinical problems in congenital portosystemic shunt patients?

A
  • Hepatic encephalopathy
  • Inappetence
  • Gastrointestinal signs
  • Urolithiasis – ammonium biurate. High excretion of ammonia and concentrated in ammonia and crystals form and crystals aggregate to form stones
  • Urinary tract infections
  • Coagulopathies/gastrointestinal haemorrhage
156
Q

How can congenital portosystemic shunts be medically managed?

A
  • Normalise macroscopic vascular anatomy to prevent further shunting
  • Requires period of pre-operative medical stabilisation
157
Q

How can congenital portosystemic shunts be surgically managed?

A
  • As a precursor to intended surgical management
  • As a long-term option where surgery is declined/not possible
158
Q

What dietary modification can be used for hepatic encephalopathy?

A
  • Transition to plant based protein diets > produce fewer aromatic amino acids > less likely to get encephalopathy
  • Protein modification to minimise encephalopathy
  • Vegetable based protein vs. protein restriction
  • With/without cottage cheese as this doesn’t produce aromatic amino acids and helps with palatability
159
Q

How can lactulose be used to medically manage hepatic encepahlopathy?

A

Human laxative that can work in cats and dogs but not used as a laxative in animals, smaller dose but laxative traps ammonia in colon in ionised form to prevent going into the blood

160
Q

How is hepatic encephalopathy crisis managed?

A
  • Ensure euhydrated, normokalaemic – IV fluids
  • Dietary/protein modification/GI haemorrhage – if owner gives a very high protein meal with PSS, such as a steak, they can become comatose quickly
  • Lactulose retention enema
  • Check blood glucose
  • Anti-epileptic therapy – Levetiracetam vs. phenobarbitone
  • Mannitol? Controls cerebral oedema
161
Q

What are the medical considerations in portosystemic shunt patients?

A
  • Inappetence – palatability considerations vs. medical management
  • Gastrointestinal signs – avoid fluid deficit
  • Urolithiasis – may dissolve post-op/may need intervention/surgery
  • Urinary tract infections – indication for antibiotics
  • Check coagulation times (PT/aPTT)
  • Gastric ulceration/haemorrhage especially in intrahepatic shunts
162
Q

What is done when you suspect leptospirosis?

A
  • Amoxicillin-clavulanate/penicillins – IV/pending results
  • Doxycycline – 2 weeks oral to clear carrier state
163
Q

What is done when you suspect hepatic abscesses?

A

Surgery + antibiotics - amoxicillin-clavulanate, then guided by culture/sensitivity

164
Q

What is done if you suspect toxoplasmosis?

A
  • Clindamycin
  • Protozoa – but some antimicrobials have efficacy
165
Q

What are choleretics?

A
  • Ursodeoxycholic acid (UDCA)
  • Hydrophilic, ‘beneficial’ bile acid
  • Synthetically derived
166
Q

What is the mechanism of choleretics?

A
  • Alters bile composition
  • Stimulates bile flow
  • Modulates inflammatory response in liver
  • Modifies apoptosis
167
Q

When are choleretics indicated and contraindicated?

A

Indicated if cholestatic disease

Not safe in rabbits

168
Q

What are some antioxidants that can be used in liver disease management?

A
  • N-Acetyl-Cystine (IV option)
  • Milk thistle extracts/isolates. Naturally occurring antioxidant
  • S-Adenosyl-L-methionine (SAMe) – naturally occurring antioxidant
  • Vitamin E
  • Vitamin C?
169
Q

When might steroids be used in liver disease?

A
  • Anti-inflammatory vs. immunosuppressive
  • Chronic hepatitis (some cases), lymphocytic cholangitis
170
Q

When might immunosuppressants used in liver disease and how?

A
  • Diseases benefitting from immunosuppression – lymphocytic cholangitis, chronic hepatitis
  • Start with steroids
  • May need adjuncts
171
Q

What are the complications of liver disease?

A
  • Hepatic encephalopathy
  • Portal hypertension
  • Coagulopathies
  • Hypoglycaemia
172
Q

What are the consequences of portal hypertension?

A
  • Secondary shunting
  • Splanchnic bed oedema > impairs GI perfusion and health, GI haemorrhage
  • Ascites
173
Q

How is portal hypertension managed?

A
  • Treat cause of portal hypertension (if possible)
  • Spironolactone with/without Na+ restriction
  • Avoid GI toxic drugs

CVSOH 4 (13 decks)

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