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MODULE 16 - Alimentary Tract Disease > PATHOLOGY - Hepatobiliary Disease > Flashcards

PATHOLOGY - Hepatobiliary Disease Flashcards

1
Q

What are the three zones of the hepatic lobules?

A

Periportal zone
Midzonal zone
Centrilobular zone

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2
Q

Which zone of the hepatic lobules is most vunerable to injury?

A

Centrilobular

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3
Q

What is the portal triad?

A

The portal triad consists of a branch of the hepatic artery, branch of the hepatic portal vein, lymphatic vessel and a bile ductile located at the corners of the hepatic lobules

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4
Q

Describe the direction of blood flow through the hepatic lobules

A

Blood flows through the hepatic artery and hepatic portal vein through the hepatic sinusoids to the central venule within the hepatic lobules where the blood is drained

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5
Q

What are the functions of the liver?

A

Bilirubin metabolism
Bile acid metabolism
Lipid metabolism
Carbohydrate metabolism
Xenobiotic metabolism

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6
Q

What is the biliary system?

A

The biliary system is a branched system which transports bile from each hepatocyte into the bile ducts which come together to form the common bile duct which empties bile into the duodenum

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7
Q

How does the anatomy of the biliary system differ between dogs and cats?

A

In cats, the common bile duct combines with the pancreatic duct before entering the duodenum, forming the pancreaticobiliary duct, whereas the pancreatic duct and common bile duct are seperate in dogs

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8
Q

What are the functions of bile?

A

Emusifies fats to allow for absorption of fats and fat soluble vitamins
Excretes bilirubin and excess cholesterol
Neutralises gastric acid

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9
Q

What is primary hepatopathy?

A

Primary hepatopathy refers to liver disease which originates in the liver

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10
Q

What is secondary hepatopathy?

A

Secondary hepatopathy refers to systemic disease which has secondary effects on the liver

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11
Q

What are some of the potential causes of secondary hepatopathy?

A

Hypoxia
Hypotension
Endocrine disease
Drugs
Metastatic neoplasia
Right sided congestive heart failure
Pericardial effusion

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12
Q

What are the potential clinical signs of liver disease?

Remember these can be variable and non-specific to liver disease

A

Anorexia
Weight loss
Lethargy
Vomiting
Diarrhoea
Polyuria, polydipsia (PUPD)
Jaundice
Ascites
Alteration in liver size
Clinical signs of a coagulopathy
Clinical signs of hepatocutaneous syndrome
Clinical signs of hepatic encephalopathy

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13
Q

What is hepatocutaneous syndrome?

Remember this is very rare

A

Hepatocutaneous syndrome is a disease characterised by degeneration of the skin cells as a consequence of nutritional imbalances resulting from metabolic abnormalities resulting from severe liver dysfunction

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14
Q

What are some useful history questions to ask when investigating liver disease?

A
  1. Are the clinical signs acute or chronic?
  2. Try to determine if it is a primary or secondary hepatopathy?
  3. Any exposure to toxins?
  4. Which medications is the animal currently on?
  5. Vaccination status?
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15
Q

What are some of the most common causes of acute liver disease?

A

Hepatotoxic drugs
Toxins
Infectious disease
Idiopathic
Metabolic disease

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16
Q

List some examples of hepatotoxic drugs which can cause acute liver disease

A

NSAIDS
Paracetamol
Azathioprine
Trimethroprim-sulphonamide antibiotics
Antiepileptic drugs
Lomustine
Methimazole/carbimazole

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17
Q

List some examples of toxic agents which can cause acute liver disease

A

Xylitol
Mycotoxins
Aflatoxins
Amantia mushrooms
Microcystin (found in blue green algae)

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18
Q

List some infectious causes of acute liver disease

A

Leptospirosis
Canine adenovirus 1 (CAV-1)
Bacterial hepatitis
Bacterial cholangitis/cholangiohepatitis

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19
Q

Give a metabolic causes of acute liver disease

A

Hepatic lipidosis

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20
Q

What are some of the most common causes of chronic liver disease in dogs?

A

Chronic hepatitis
Neoplasia
Congenital portosystemic shunts
Portal vein hypoplasia
Copper-associated hepatitis

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21
Q

What are some of the most common causes of chronic liver disease in cats?

A

Chronic cholangitis (usually lymphocytic)
Infectious disease (FIP and toxoplasmosis)
Neoplasia
Congenital portosystemic shunts
Hepatic amyloidosis

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22
Q

Which diagnostic tests can be done to investigate hepatobiliary disease?

A

Biochemistry
Bile acid stimulation test
Coagulation times
Haematology
Urinalysis
Diagnostic imaging
Liver biopsy/fine needle aspirate (FNA)

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23
Q

Which liver enzymes are markers of liver damage?

A

Alanine aminotransferase (ALT)
Aspartate aminotransferase (AST)

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24
Q

Where is alanine aminotransferase (ALT) located?

A

Alanine aminotransferase (ALT) is located in the hepatic cytosol

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25
Q

Where is aspartate aminotransferase (AST) found?

A

Aspartate aminotransferase (AST) is found in the hepatic cytosol and mitochondria, as well as in skeletal and cardiac muscle

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26
Q

Why is AST less specific for liver damage than alanine aminotransferase ALT?

A

AST is less specific for liver damage than ALT as it is found in other tissues such as the skeletal and cardiac muscle so can increase in response to skeletal and cardiac muscle damage, not just liver damage. However, it is important to note that ALT is less sensitive than AST

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27
Q

(T/F) In the presence of liver damage, AST is usually higher than ALT

A

FALSE. In the presence of liver damage, ALT is usually higher than AST. So, if AST is higher than ALT, this can indicate disease of the cardiac and/or skeletal muscle and warrants further investiagtion using creatine kinase (CK) and cardiac troponin levels

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28
Q

Which liver enzymes are markers of cholestasis (abnormal bile flow)?

A

Alkaline phosphatase (ALP)
Gamma glutamyl transferase (GGT)

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29
Q

Where is alkaline phosphatase (ALP) located?

A

Alkaline phosphatase (ALP) is membrane bound to the surface of the bile caniliculi, however, ALP does have isoforms within the bone and there is a steroid-induced ALP isoform

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30
Q

Where is gamma glutamyl transferase (GGT) located?

A

Gamma glutamyl transferase (GGT) is membrane bound to the surface of bile canaliculi

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31
Q

Why is ALP less specific for cholestasis than alanine aminotransferase GGT?

A

ALP is less specific for cholestasis than GGT as there are ALP isoforms elsewhere is the body which can be increased by other disease processes. However, it is important to not that GGT is less sensitive than ALP (i.e. it can be at normal levels even when there is cholestasis)

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32
Q

How can end stage liver cirrhosis affect liver enzymes?

A

In end stage liver cirrhosis, the liver becomes less functional as the damage progresses and fibrotic tissue replaces the hepatocytes, causing ALT and AST levels to either decrease or remain normal as even through the liver is severely damaged there are so few functioning hepatocytes to release these enzymes

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33
Q

What are the main limitations of of liver enzymes for investigating hepatobiliary disease?

A

Liver enzymes do not assess liver function and thus they provide no information on the degree of liver dysfunction, prognosis or if there is primary or secondary hepatopathy

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34
Q

Which parameters are markers of liver function?

A

Bilirubin
Glucose
Urea
Albumin
Cholesterol
Bile acids
Ammonia
Coagulation factors

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35
Q

Which parameters of liver function are not in a standard biochemistry profile?

A

Bile acids
Ammonia
Coagulation factors

Remember for coagulation factors you will have to do PT and aPTT

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36
Q

How is bilirubin produced and excreted?

A

Bilirubin is a byproduct of haem breakdown due to haemolysis. When unconjugated bilirubin is released into the bloodstream it binds to albumin which is transported to the liver where it is conjugated and excreted into the bile

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37
Q

What is jaundice?

A

Jaundice is the yellow staining of the tissues due to excessive bilirubin in the bloodstream

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38
Q

Where in the body can jaundice be seen?

A

Mucous membranes
Sclera
Skin
Gingiva

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39
Q

What are the three classifications of jaundice?

A

Pre-hepatic jaundice
Hepatic jaundice
Post-hepatic jaundice

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40
Q

What causes pre-hepatic jaundice?

A

Pre-hepatic jaundice is caused by haemolysis

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41
Q

What is a key indicator of pre-hepatic jaundice?

A

A decreased packed cell volume (PCV) is a key sign of pre-hepatic jaundice

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42
Q

What causes hepatic jaundice?

A

Hepatic jaundice is caused by abnormal uptake of bilirubin into the hepatocytes, abnormal conjugation of bilirubin, or abnormal excretion of bilirubin by the hepatocytes

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43
Q

What are key indicators of hepatic jaundice?

A

To determine if a patient has hepatic jaundice, you have to rule out pre- and post-hepatic jaundice and to get a definitive diagnosis a liver biopsy should be performed

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44
Q

What causes post-hepatic jaundice?

A

Post-hepatic jaundice is caused by impaired excretion of bilirubin in the bile

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45
Q

What are key indicators of post-hepatic jaundice?

A

ALP and GGT being higher than ALT and AST
Hypercholesteraemia
Biliary abnormalities on ultrasound
Increased biomarkers of pancreatitis

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46
Q

Why are increased biomarkers of pancreatitis a potential sign of post-hepatic jaundice?

A

Increased biomarkers of pancreatitis is a potential sign of post-hepatic jaundice as pancreatitis is a common cause of biliary disease

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47
Q

Why are serum glucose, urea, albumin and cholesterol levels indicators of liver dysfunction?

A

Glucose, urea, abumin and cholesterol are all produced within the liver and thus can decrease in response to liver dysfunction

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48
Q

What is the most specific marker of liver dysfunction?

A

Bile acids

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49
Q

Describe normal physiological function of bile acids

A

Bile acids are synthesised from cholesterol in the hepatocytes and are secreted into the bile and stored in the gallbladder. In response to the ingestion of fats, cholecystokinin (CCK) triggers contraction of the gallbladder to secrete bile into the common bile duct and into the duodenum to emulsify fats for absorption. Bile acids are absorbed back into the bloodstream within the ileum and transported via the portal vein back to the hepatocytes via enterohepatic circulation

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50
Q

What is indicated by increased serum bile acids?

A

Liver dysfunction
Impaired enteroheptic circulation

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51
Q

Which test should you do to assess the level of serum bile acids?

A

Bile acid stimulation test

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52
Q

How do you carry out a bile acid stimulation test?

A

Starve your patient for 12 hours and take a pre-prandial blood sample. Following this sample, feed your patient and take a post-prandial blood sample two hours after feeding

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53
Q

What is the reference range for pre-prandial serum bile acid levels?

A

0 - 10 μmol/L

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54
Q

What is the reference range for post-prandial serum bile acid levels?

A

0 - 20 μmol/L

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55
Q

What level of serum bile acids indicates hepatic dysfunction?

A

Serum bile acids over 40 μmol/L indicates hepatic dysfunction

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56
Q

Which dog breed has abnormally high serum bile acids even with no disease processes?

A

Bichon Frisé

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57
Q

Why should you not do bile acid stimulation tests in jaundiced patients?

A

It is pointless to do bile acid stimulation tests in jaundiced patients as serum bile acids will increase prior to the patient becoming jaundiced

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58
Q

Describe normal physiological excretion of ammonia

A

Ammonia (NH3) is a waste product produced by dietary protein breakdown by bacteria in the intestines. Ammonia (NH3) is transported via the hepatic portal vein to the liver where it is converted to urea via the urea cycle. The majority of urea is transported to the kidneys where it is excreted into the urine, and the rest of the urea is transported to the colon where it is converted to ammonium (NH4) which is excreted in the faeces

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59
Q

What is indicated by hyperammonaemia?

A

Hepatic dysfunction
Abnormal portal blood flow
Abnormal urea cycle

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60
Q

Why are coagulation times indicators of liver dysfunction?

A

The liver produces all coagulation factors except for factor VII and von willebrands factors, and activates all vitamin K dependent coagulation factors (II, VII, IX and X) as the liver stores fat soluble vitamins (i.e. vitamin K). So, if there is liver dysfunction, this can be indicated by prolonged coagulation times

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61
Q

What are potential indicators of hepatobiliary disease on haematology?

A

Mild anaemia

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62
Q

What are potential indicators of hepatobiliary disease on urinalysis?

A

Low urine specific gravity (USG) if polydipsic
Bilirubinuria
Ammonium urate crystals

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63
Q

What can radiography be used to evaluate when investigating hepatobiliary disease?

A

Radiography can be used to evaluate liver size, shape, position and opacity

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64
Q

What can ultrasound be used to evaluate when investigating hepatobiliary disease?

A

Hepatic parenchyma, branches of the portal vein and hepatic vein
Gallbladder
Biliary ducts
Identification and sampling of nodules, masses and abdominal effusions

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65
Q

What should you always do prior to doing a liver fine needle aspirate (FNA) or biopsy?

A

You should always check the coagulation times prior to doing a liver fine needle aspirate (FNA) or biopsy as there is a high risk of haemorrhage. If the coagulation times are prolonged, administer plasma and vitamin K

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66
Q

What are the advantages of liver fine needle aspirate (FNA)?

A

Minimally invasive procedure
Little equipment required
Only requires sedation
Can take bile samples

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67
Q

What are the disadvantages of liver fine needle aspirate (FNA)?

A

Limited accuracy of cytology
Does not evaluate hepatic architecture
Risk of haemorrhage
Risk of gallbladder rupture with bile sampling

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68
Q

Which biopsy needle can be used for a liver biopsy?

A

Tru-cut needle

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69
Q

What are the advantages of a tru-cut liver biopsy?

A

Allows for assessment of hepatic architecture
Does not require a laparotomy

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70
Q

What are the disadvantages of a tru-cut liver biopsy?

A

Required general anaesthetic
Specialist equipment is required
Less accurate than surgical biopsy
Risk of haemorrhage

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71
Q

What is a surgical liver biopsy?

A

A surgical liver biopsy is a wedge biopsy of the liver carried out either laparoscopically or via a laparotomy

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72
Q

What are the advantages of a surgical liver biopsy?

A

Allows for assessment of hepatic architecture
Allows for better diagnostic samples
Allows for sampling of multiple liver lobes
Allows for bile aspirate samples
Can visualise any haemorrhage

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73
Q

What are the disadvantages of a surgical liver biopsy?

A

Requires general anaesthetic
More invasive procedure
Risk of haemorrhage

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74
Q

What are the two classfications of congenital portosystemic shunts?

A

Extrahepatic shunts
Intrahepatic shunts

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75
Q

What are the two main forms of congenital extrahepatic shunts?

A

Porto-caval shunt
Porto-azygos shunt

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76
Q

What is a porto-caval shunt?

A

A porto-caval shunt is the shunting of blood from the hepatic portal vein to the caudal vena cava

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77
Q

What is a porto-azygos shunt?

A

A porto-azygos shunt is the shunting of blood from the hepatic portal vein to the azygos vein

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78
Q

Which signalement is more prone to congenital extrahepatic shunts?

A

Small breed dogs

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79
Q

What is the most common form of a congenital intrahepatic shunt?

A

Patent ductus venosus

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80
Q

Which signalement is more prone to congenital intrahepatic shunts?

A

Large breed dogs

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81
Q

Which dog breeds can inherit congenital shunts?

A

Maltese
Yorkshire Terrier
Irish Wolfhound

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82
Q

What are the clinical signs of congenital shunts?

A

Failure to thrive
Microhepatica
Hepatic encephalopathy
Polyuria, polydipsia (PUPD)
Vomiting
Diarrhoea
Copper irises (in cats)

Remember this is congenital so the animals will be young

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83
Q

Why can patients with congenital shunts present with polyuria, polydipsia (PUPD)?

A

Patients with congenital portosystemic shunts can present with polyuria and polydipsia (PUPD) due to the development of ammonium urate crystals

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84
Q

What is the best form of diagnostic imaging to diagnose congenital postosystemic shunts?

A

Ultrasound (will require referral level experience)
CT angiogram

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85
Q

How do you treat congenital portosystemic shunts?

A

Medical management of clinical signs, including hepatic encephalopathy
Referral surgery
Long term medical management if surgery not feasible

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86
Q

Which form of shunt is most commonly seen in acquired shunts?

A

Portosystemic shunts

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87
Q

Describe the pathogenesis of acquired shunts

A

Acquired vascular shunts result from chronic liver disease which results in portal vein fibrosis and portal hypertension resulting in the development of compensatory tortuous shunting vessels

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88
Q

How do you treat acquired portosystemic shunts?

A

Long term medical management of clinical signs, including hepatic encephalopathy

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89
Q

Which pathogen causes canine infectious hepatitis?

A

Canine adenovirus 1 (CAV-1)

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90
Q

(T/F) Canine adenovirus 1 (CAV-1) is an RNA virus

A

FALSE. Canine adenovirus 1 (CAV-1) is a DNA virus

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91
Q

Which tissues does canine adenovirus 1 (CAV-1) have tropism for?

A

Endothelium
Mesothelium
Hepatocytes

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92
Q

What are the clinical signs of canine infectious hepatitis?

A

Pyrexia
Abdominal pain
Vomiting
Meleana

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93
Q

What are the clinical signs of peracute canine infectious hepatitis?

A

Sudden death with no clinical signs

This is a rare form of canine infectious hepatitis

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94
Q

What is one of the key clinical signs of chronic canine infectious hepatitis?

A

Coreneal opacity (‘blue eye’) due to corneal oedema

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95
Q

What are the gross pathological features of canine infectious hepatitis?

A

Petechiation and ecchymoses of the organ serosal and mucosal surfaces
Enlarged, friable, necrotic liver
Fibrin on the liver surface
Thickening of the gallbladder
Small quantities of blood tinged ascites

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96
Q

What causes the fibrin present on the liver in canine infectious hepatitis?

A

Canine adenovirus 1 (CAV-1) has tissue tropism for mesothelial cells which make up the peritoneum, resulting in peritonitis and fibrin deposition

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97
Q

What is a key gross pathological feature of canine adenovirus 1 (CAV-1) infection?

A

Thickening of the gall bladder is a key gross pathological feature of canine adenovirus-1 (CAV-1) infection

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98
Q

What is the histological appearance of canine infectious hepatitis?

A

Hepatocellular necrosis
Hepatocellular and endothelial intranuclear inclusion bodies

99
Q

How does hepatocellular necrosis appear on histology?

A

Eosinophilic, disorganised hepatocytes

100
Q

Which bacteria cause leptospirosis?

A

Leptospira

101
Q

Which signalement are at increased risk of leptospirosis infection?

A

Unvaccinated patients
Patients living in areas with a high rodent population

102
Q

How is leptospirosis transmitted?

A

Leptospirosis is transmitted through contact with infected urine (often via ingestion of stagnant water)

103
Q

(T/F) Leptospirosis is a zoonotic disease

A

TRUE.

104
Q

Which conditons can be caused by leptospirosis?

A

Acute hepatopathy and/or acute renal injury

105
Q

What are the potential iochemistry changes that can be seen on biochemistry with a leptospirosis infection?

A

Increased liver enzymes
Hyperbilirubinaemia
Hypoglycaemia
Hyperalbuminaemia
Azotaemia

106
Q

How do you diagnose leptospirosis?

A

Take a blood sample when the patient presents and do a macroscopic agglutination test (MAT). This will take several days to give you a result so you will have to begin treatment prior to diagnosis. Repeat the test 7 to 14 days later to assess if there has been an increase in antibody levels againts leptospira to confirm your diagnosis

107
Q

How do you treat leptospirosis?

A

Supportive care
Antibiotics

Remember to barrier nurse as this is a zoonotic disease

108
Q

Which antibiotics should you use to treat leptospirosis?

A

Doxycycline

109
Q

What are the potential underlying aetiologies for chronic hepatitis?

A

Idiopathic (most common)
Infectious
Toxic
Copper-associated

110
Q

What is the proposed cause of idiopathic chronic hepatitis?

A

Autoimmune disease as in chronic hepatitis, the dominating inflammatory cells are T-lymphocytes which infiltrate and cause hepatocellular necrosis and loss which overtime will cause parenchymal collapse and fibrosis

111
Q

How can copper act as a secondary cause of chronic hepatitis?

A

When there is chronic hepatitis, hepatocytes can aggregate copper resulting in an abnormal accumulation of copper in the hepatocytes and seconday copper induced hepatitis

112
Q

Which dog breeds are prone to chronic hepatitis?

A

English Springer Spaniels
Cocker Spaniels
Dobermans
Labradors

113
Q

What are the clinical signs of chronic hepatitis?

A

The clinical signs of chronic hepatitis are very non specific such as lethargy, decreased appetite, vomiting, diarrhoea, weight loss, icterus etc

114
Q

What changes will be seen on biochemistry for chronic hepatitis?

A

Increased liver enzymes
Decreased albumin and urea
Increased PT and aPTT (in some cases)
Increased white blood cell count (in some cases)

115
Q

What is the histological appearance of chronic hepatitis?

A

Hepatocellular necrosis in regions of inflammation
Fibrosis
Secondary copper accumulation within hepatocytes

116
Q

How do you treat chronic hepatitis?

A

Immunosuppressive therapy

117
Q

Which dog breeds are predisposed to copper-associated hepatopathy?

A

Bedlington Terrier
West Highland White Terrier
Skye Terrier
Dalmation
Labrador
Dobermann

118
Q

Which dog breed has an autosomal recessive mutation resulting in copper-associated hepatopathy?

A

Bedlington Terriers have an autosomal recessive mutation of the COMMD1 gene resulting in exon two deletion. This gene has an important role in the biliary excretion of copper, with a mutation in this gene resulting in an abnormal accumulation of copper within the hepatocytes resulting in primary copper-associated hepatopathy

119
Q

What are the clinical signs of copper-associated hepatopathy?

A

Lethargy
Decreased appetite
Vomiting
Diarrhoea
Weight loss
Icterus
Haemolysis (only in Bedlington Terriers)

120
Q

How can you diagnose copper-associated hepatopathy?

A

Increased liver enzymes on biochemistry
Submit a fresh liver biopsy for copper evaluation
Histopathology to determine presence of copper in hepatocytes

121
Q

What is the normal reference range for copper levels in a fresh liver biopsy?

A

200 - 400 μg/g

122
Q

What level of copper in a fresh liver biopsy is indicative of primary copper-associated hepatopathy?

A

Over 2000 μg/g

123
Q

What level of copper in a fresh liver biopsy is indicative of secondary copper-associated hepatopathy?

A

Betwee 400 - 2000 μg/g

124
Q

Which specific stain should be used to determine the presence of copper in hepatocytes on histology?

A

Rhodanine stain

125
Q

What is the histological appearance of copper-associated hepatopathy?

A

Centrilobular hepatitis with macrophages with abundant intracytoplasmic copper
Hepatocellular necrosis
Fibrosis
Intrahepatic cholestasis

126
Q

How do you treat copper-associated hepatopathy?

A

Penicillamine
Low copper diet with added zinc (can use prescription hepatic diet)

127
Q

What is the mechanism of action of penicillamine when treating copper-associated hepatopathy?

A

Penicillamine is a chelating agent whihc binds to copper and transports it to the kidneys for excretion

128
Q

Which second line drug can be used if a patient is not responsive to penicillamine?

A

Trientine

129
Q

What are the benefits of dietary zinc when managing copper-associated liver disease?

A

Zinc helps to prevent absorption of copper by the small intestine into the bloodstream where it would usually travel to the liver

130
Q

What are vacuolar hepatopathies?

A

Vacuolar hepatopathies are characterised by intraplasmocytic accumulations of glycogen and fluid within the hepatocytes resulting in hepatocellular swelling and vacuolation on histology

131
Q

What are the possible causes of vacuolar hepatopathies?

A

Exogenous steroids
Endogenous steroids
Diabetes mellitus
Neoplasia

132
Q

What are the two classifications of steroid-induced hepatopathy?

A

Iatrogenic steroid-induced hepatopathy
Endogenous steroid-indiced hepatopathy

133
Q

What causes iatrogenic steroid-induced hepatopathy?

A

Iatrogenic steroid-induced hepatopathy is caused by the sustained administration of corticosteroids

134
Q

What causes endogenous steroid-induced hepatopathy?

A

Endogenous steroid-induced hepatopathy is caused by hyperadrenocorticism (cushing’s disease) which increases the circulating levels of glucocorticoids

135
Q

What changes will be seen on biochemistry for steroid-induced hepatopathy?

A

Increased liver enzymes however normal liver function will be maintained

136
Q

What is the histological appearance of steroid-induced hepatopathy?

A

Intracytoplasmic accumulation of glycogen and fluid within the hepatocytes resulting in hepatocellular swelling and vacuolation

137
Q

Why does steroid-induced hepatopathy cause glycogen accumulation within the hepatocytes?

A

Steroids induce hyperglycaemia, causing increased glycogen production and storage within the liver

138
Q

What is hepatic lipidosis?

A

Hepatic lipidosis is the excessive accumulation of triglycerides (fat) within the hepatocytes

139
Q

Describe the pathophysiology of hepatic lipidosis

A

Hepatic lipodosis occurs when there is an imbalance between the mobilisation of fat to the liver, usually caused by anorexia, and the liver’s ability to metabolise the fat, resulting in excessive accumulation of triglycerides within the hepatocytes, which can result in intrehepatic cholestasis and hepatic dysfunction

140
Q

Which signalement is at increased risk of hepatic lipidosis?

A

Middle age, overweight cats with a recent history of anorexia

141
Q

How do you diagnose hepatic lipidosis?

A

Biochemistry
Ultrasound
Fine needle aspirate (FNA)

142
Q

What is a key sign of hepatic lipidosis on biochemistry?

A

Increased ALP with a normal GGT

143
Q

How does hepatic lipidosis appear on ultrasound?

A

The hepatic parenchyma will appear homogenous and hyperechoic with hepatomegaly

144
Q

How do you manage hepatic lipidosis?

A

Treat the underlying disease
Enteral nutritional support (place a tube)
Monitor for refeeding syndrome
Supportive care

145
Q

What kind of diet should you feed a patient with hepatic lipidosis?

A

High protein diet

146
Q

What is triaditis?

A

Triaditis is the concurrent inflammation of the biliary system, small intestine and the pancreas

147
Q

What is the primary cause of triaditis?

A

The primary cause of triaditis is intestinal inflammation resulting in dysbiosis and reflux of bacteria and enteric content into the pancreaticobiliary duct

148
Q

Which species is triaditis seen in?

A

Cats (this is due to cats having a slightly different anatomy compared to dogs where dogs have a seperate pancreatic duct whereas the cats pancreatic duct combines with the common bile duct, forming the pancreaticobiliary duct)

149
Q

What are the clinical signs of triaditis?

A

Anorexia
Weight loss
Vomiting
Icterus
Hepatomegaly
Thickened intestines
Pancreatic masses
Abdominal pain
Abdominal effusion
Pyrexia
Hypothermia
Tachypnoea
Dyspnoea
Shock

150
Q

How does triaditis appear on biochemistry?

A

Increased liver enzymes
Increased pancreatic specific lipase
Decreased cobalamin
Decreased folate
Hypoalbuminaemia

151
Q

What are some of the common causes of biliary disease?

A

Pancreatitis
Cholecystitis
Cholelithiasis
Gallbladder mucocoeles
Neoplasia

152
Q

What is cholecystitis?

A

Cholecystitis is inflammation of the gallbladder

153
Q

What is cholelithiasis?

A

Cholelithiasis is a term used to describe gallstones (when bile hardens into stone-like material)

|Cholelithiasis is often an incidental finding with no clinical significance

154
Q

Which species are more prone to cholelithiasis?

A

Dogs

155
Q

What are some of the potential clinical signs of biliary disease?

A

Jaundice
Pale white faeces (very rare)

156
Q

What changes can be seen on biochemistry for biliary disease?

A

ALP and GGT more increased than ALT and AST
Increased cholesterol
Increased bilirubin

157
Q

What is the most useful form of diagnostic imaging for biliary disease?

A

Abdominal ultrasound

158
Q

What is suppurative cholangitis/cholangiohepatitis?

A

Suppurative cholangitis/cholangiohepatitis is the neutrophil driven inflammation of the bile ducts, gall bladder, and surrounding liver tissue

159
Q

Which pathogen most commonly causes suppurative cholangitis/cholangiohepatitis?

A

Ascending E.coli infection from the intestines into the pancreaticobiliary duct (can cause triaditis)

160
Q

Which species is most commonly affected by suppurative cholangitis/cholangiohepatitis?

A

Cats

161
Q

What are the clinical signs of suppurative cholangitis/cholangiohepatitis?

A

Pyrexia
Icterus
Lethargy
± Vomiting

|Usually presents acutely

162
Q

How do you treat suppurative cholangitis/cholangiohepatitis?

A

6 to 8 weeks of antibiotics

163
Q

What is lymphocytic cholangitis/cholangiohepatitis?

A

Lymphocytic cholangitis/cholangiohepatitis is the lymphocyte driven inflammation of the bile ducts, gall bladder, and surrounding liver tissue

164
Q

What is the cause of lymphocytic cholangitis/cholangiohepatitis?

A

The cause of lymphocytic cholangitis/cholangiohepatitis is unknown however assumed to be autoimmune

165
Q

Which signalement is prone to lymphocytic cholangitis/cholangiohepatitis?

A

Cats over 4 years old

166
Q

What are the clinical signs of lymphocytic cholangitis/cholangiohepatitis?

A

Generally cats with lymphocytic cholangitis/cholangiohepatitis present with a chornic history or vague illness but will be systemically well

167
Q

What is the histological appearance of lymphocytic cholangitis/cholangiohepatitis?

A

Dense aggregates of lymphocytes
Fibrosis

168
Q

Which disease can be hard to differentiate from lymphocytic cholangitis/cholangiohepatitis?

A

Lymphoma

169
Q

What can be done to differentiate between lymphocytic cholangitis/cholangiohepatitis and lymphoma?

A

PCR for antigen receptor rearrangements (PARR)

170
Q

How do you treat lymphocytic cholangitis/cholangiohepatitis?

A

Immunosuppressive therapy

171
Q

What is a gallbladder mucocoele?

Only seen in dogs

A

A gallbladder mucocoele is a distension of the gallbladder with accumulated mucoid secretions which may progress to semi-solid materials

172
Q

Which dog breeds are prone to gallbladder mucocoeles?

A

Border Terriers
Shetland Sheep Dogs

173
Q

What are the potential consequences of a gallbladder mucocoele?

A

Extrahepatic biliary obstruction
Gallbladder rupture and bile peritonitis

174
Q

How do you treat a gallbladder mucocoele?

A

Surgical cholecystectomy

175
Q

(T/F) Primary hepatobiliaryst neoplasia is very common

A

FALSE. Primary hepatobiliary neoplasia is uncommon

176
Q

List examples of primary hepatobiliary neoplasia

A

Hepatocellular adenoma
Hepatocellular adenocarcinoma
Hepatic lymphoma
Hepatic haemangiosarcoma (HSA)
Biliary adenoma
Biliary adenocarcinoma

177
Q

List examples of secondary/metastatic hepatobiliary neoplasia

A

Lymphoma
Leukaemia
Haemangiosarcoma (HSA)
Histiocytic sarcoma

178
Q

What is hepatobiliary nodular hyperplasia?

A

Hepatic nodular hyperplasia is a benign hyperplastic condition seen in older dogs

179
Q

What changes will be seen on biochemistry for hepatobiliary nodular hyperplasia?

A

Increased ALP
± Increased ALT

180
Q

How do you diagnose hepatobiliary nodular hyperplasia?

A

You diagnose hepatobiliary nodular hyperplasia using a liver biopsy

181
Q

How do you treat hepatobiliary nodular hyperplasia?

A

No treatment is required for hepatobiliary nodular hyperplasia as it is a normal change in ageing dogs

182
Q

What is the general approach to managing acute hepatopathies?

A
  1. Treat the underlying cause of disease if known, however the majority of these cases are idiopathic or cannot be diagnosed
  2. Supportive treatment
  3. Clinical any clinical consequences of hepatic disease
183
Q

What is the general approach to managing chronic hepatopathies?

A
  1. Treat the underlying cause of disease if known, however the majority of these cases are idiopathic or cannot be diagnosed
  2. Any specific treatment should be done based on a liver biopsy results if possible
  3. Supportive treatment
  4. Clinical any clinical consequences of hepatic disease
184
Q

What supportive treatment should you provide when managing hepatic disease?

A

Intravenous fluid therapy if clinically dehydrated
Antiemetics
Antioxidants

185
Q

What are the physiological roles of antioxidants in the liver?

A

Within the liver, glutathione is synthesised from cysteine, glutamate and glycine. Glutathione is an antioxidant and free radical scavenger which is involved in the protective defence mechanisms of the liver as there is evidence that free radicals and oxidative stress are involved in the pathogenesis of hepatic disease

186
Q

Which antioxidants can be used when managing hepatic disease?

A

S-adenosylmethionine (SAMe)
Silymarin

187
Q

What is S-adenosylmethionine (SAMe)?

A

S-adenosylmethionine (SAMe) is a precursor of glutathione and thus has antioxidant effects

188
Q

What is silymarin?

A

Silymarin is derived from the milk thistle plant and has antioxidant effects

189
Q

What is N-acetylcysteine?

A

N-acetylcysteine is a pro drug of cysteine which helps to replenish hepatocellular cysteine and consequently glutathione concentrations

190
Q

What is the clinical use of N-acetylcysteine?

A

N-acetylcysteine is used in cases of acute hepatopathies due to hepatotoxic drugs and toxins

191
Q

(T/F) Bile acids can be hepatotoxic

A

TRUE. Hydrophobic bile acids can be hepatotoxic, however the reason for this is unknown

192
Q

What is ursodeoxycholic acid (UDA)?

A

Ursodeoxycholic acid (UDA) is a synthetic hydrophillic bile acid which can displace hydrophobic toxic bile acid and promote bile flow

193
Q

What are the clinical uses of ursodeoxycholic acid (UDA)?

A

Management of gallbladder mucocoeles
Management of acute hepatopathies with cholestasis
Management of chronic hepatopathies with cholestasis

194
Q

When is ursodeoxycholic acid (UDA) contraindicated?

A

Ursodeoxycholic acid (UDA) is contraindicated in patients with biliary obstruction

195
Q

When is vitamin K indicated in the management of hepatic disease?

A

Vitamin K is indicated when a patient has evidence of a coagulopathy secondary to hepatic disease

196
Q

When would you have to administer vitamin K subcutaneously?

A

Vitamin K should be administered subcutaneously when a patient is anorexic or a biliary disease as fat is required to absorb vitamin K from the gastrointestinal tract

197
Q

Why should you avoid giving vitamin K intravenously?

A

Intravenous administration of vitamin K can cause anaphylaxis

198
Q

When are antibiotics indicated in the management of hepatic disease?

A

Primary bacterial infection
Secondary bacterial infection
Hepatic encephalopathy

199
Q

Which antibiotics should be used in the management of hepatic disease?

A

Ideally, choose antibiotics based on culture and sensitivity. However, if this is not possible choose antibiotics based on the most likely bacteria to be involved which is enteric bacteria. Also be mindful of antibiotics which are metabolised by the liver and can be hepatotoxic

200
Q

What are the features of hepatic prescription diets?

A

Low protein
Low copper
High in zinc
Vitamins B and E (antioxidants)

201
Q

What are the indicators for prescribing hepatic diets?

A

Hepatic encephalopathy
Copper-associated liver disease

Liver diets are low in proteins and thus are contraindicated in some diseases and should not be given if you don’t know the cause of liver disease

202
Q

What is hepatic fibrosis?

A

Hepatic fibrosis is the excessive deposition of collagen within the liver

203
Q

Describe the progression of hepatic fibrosis

A

Myofibroblasts are triggered in response to chronic inflammation resulting in excessive collagen deposition and hepatic fibrosis. As the fibrosis advances, fibrotic tracts will extend across the hepatic lobules. Eventually, the liver will become cirrhotic

204
Q

How can hepatic fibrosis cause portal hypertension?

A

Hepatic fibrosis of the sinusoids will increase the resistance of portal blood flow into the liver resulting in portal hypertension due to increased hepatic resistance

205
Q

How do you diagnose hepatic fibrosis?

A

Liver biopsy and histological evaluation

206
Q

How do you stop progression of hepatic fibrosis?

A

Treat the underlying cause
Anti-fibrotic drugs (however no clinical evidence that these work)

207
Q

Which drugs potentially have anti-fibrotic effects?

A

Prednisolone
Penicillamine
S-adenosylmethionine (SAMe)
Silymarin

208
Q

What is hepatic cirrhosis?

A

Hepatic cirrhosis is a chronic, irreversible state where the normal hepatic tissue has been replaced by fibrotic tissue, resulting in end-stage liver failure

209
Q

How does hepatic fibrosis appear on histology?

A

Inflammation
Progressive, bridging fibrosis
Nodular regeneration

210
Q

What is portal hypertension?

A

Portal hypertension is increased blood pressure in the hepatic portal system

211
Q

What are the potential causes of portal hypertension?

A

Cirrhosis
Vascular obstruction

212
Q

What are some of the potential complications of portal hypertension?

A

Ascites
Acquired portosystemic shunts
Gastrointestinal ulceration
Hepatic encephalopathy

213
Q

How do you manage ascites?

A

Diuretics
Abdominocentesis

214
Q

Which diuretics can be used to manage ascites?

A

Spironolactone
Furosemide

215
Q

How do you treat gastrointestinal ulceration?

A

Antiemetics
Gastroprotectants
Small frequent meals
Treat the underlying cause

216
Q

Which gastroprotectants are typically used in combination for the treatment of gastrointestinal ulcers?

A

Omeprazole
Histamine (H2) blockers
Sucralfate

217
Q

Which histamine (H2) blocker is contraindicated for the treatment of gastrointestinal ulcers secondary to hepatic disease?

A

Cimetidine

218
Q

Why is cimetidine contraindicated in the treatment of gastrointestinal ulcers secondary to hepatic disease?

A

Cimetidine is contraindicated for the treatment of gastrointestinal ulcers secondary to hepatic disease a cimetidine can decrease hepatic blood flow and delay hepatic drug metabolism

219
Q

How can gastrointestinal ulceration cause hepatic encephalopathy?

A

Gastrointestinal bleeding causes loss of proteins into the gastrointestinal tract. These proteins will br broken down into ammonia by intestinal bacteria. This increased protein breakdown into ammonia can overwhelm the liver’s ability to detoxify ammonia, especially in patients with pre-existing liver dysfunction, with the elevated ammonia levels in the bloodstream a key factor in the development of hepatic encephalopathy

220
Q

What is hepatic encephalopathy?

A

Hepatic encephalopathy is a neurological condition resulting from liver dysfunction

221
Q

What is one of the most common causes of hepatic encephalopathy?

A

Portosystemic shunts

222
Q

Which toxin is the main cause of hepatic encephalopathy?

A

Ammonia

223
Q

What are the potential clinical signs of hepatic encephalopathy?

A

Altered mentation
Ataxia
Head pressing
Ptyalism (cats)
Seizures
Blindness

All of which will worsen after eating

224
Q

Why do the clinical signs of hepatic encephalopathy worsen following a meal?

A

Eating a meal exacerbates the clinical signs of hepatic encephalopathy by providing more dietary proteins which are broken down into ammonia which builds up in the bloodstream, exacerbating hepatic encephalopathy

225
Q

How do you manage hepatic encephalopathy?

A

Small, frequent, low protein meals
Antibiotics
Lactulose
Treat factors that can worsen the hepatic encephalopathy
Treat seizures

226
Q

Which diets can be used in the management of hepatic encephalopathy?

A

Hepatic prescription diets
Purina hypoallergenic food

227
Q

What is the main risk of hepatic prescription diets in young growing animals?

A

Hepatic prescription diets are very low in protein which in young growing animals can cause break down endogenous proteins in order to maintain adequate growth and development

228
Q

What can be added to hepatic prescription diets for young growing animals to slightly increase to protein content?

A

Cottage cheese
Tofu

229
Q

What should never be fed to patients with hepatic encephalopathy?

A

Red meat as it is very high in protein

230
Q

Why are antibiotics used in the management of hepatic encephalopathy?

A

Antibiotics are used to reduce the enteric bacteria which break down dietary proteins into ammonia

231
Q

Which antibiotics can be used in the management of hepatic encephalopathy?

A

Ampicillin
Neomycin
Metronidazole
Amoxicillan and Clavulanic acid

232
Q

What should you be aware of if using metronidazole to manage hepatic encephalopathy?

A

Metronidazole can be hepatotoxic so you should use a lower than normal dose

233
Q

Why is lactulose used in the management of hepatic encephalopathy?

A

The breakdown of lactulose to lactate in the colon leads to acidification of the colon contents, which will favour the conversion of ammonia (NH3) to ammonium (NH4) which cannot be absorbed across the cell membranes into the bloodstream. Furthermore, lactulose is a laxative which will increase the rate of excretion of ammonium (NH4) in the faeces

234
Q

What are the routes of administration for lactulose when managing hepatic encephalopathy?

A

Oral
Rectal enema (if the patient is unstable)

235
Q

Which factors can exacerbate the clinical signs of hepatic encephalopathy?

A

Dehydration
Hypokalaemia
Alkalaemia
Gastrointestinal haemorrhage

236
Q

How should you manage seizures secondary to hepatic encephalopathy?

A

Initially you may not know what is causing the seizures so use diazepam or midazolam for emergency treatment. Be aware that diazepam and midazolam are metabolised by the liver so if the seizures are secondary to hepatic encephalopathy this can cause the patients to becaome quite sedated. If you determine that hepatic encephalopathy is the cause of the seizures, use levetiracetam. Be aware patients may require propofil continuous rate infusions (CRIs)

237
Q

What is another cause of seizures secondary hepatopathies other than hepatic encephalopathy?

A

Hepatopathies can cause decreased glucose production which can result in seizures so it is important to measure glucose levels on a glucometer when a patient starts to seize as they may require dextrose infused IV fluids

238
Q

What are the indicators for the use of steroids (immunosuppressive therapy) for managing hepatic disease?

A

Biopsy evidence of chronic inflammation *(i.e. chronic hepatitis and lymphocytic cholangitis) with no evidence of infection, and no to mild fibrosis

239
Q

What are the contraindications for the use of steroids (immunosuppressive therapy) for managing hepatic disease?

A

Signs of portal hypertension
Signs of gastrointestinal ulceration
Hepatic encephalopathy
Evidence of infection
Evidence of bridging fibrosis
Acute hepatopathies

240
Q

Why are steroids contraindicated for managing hepatic disease in patients with hepatic encephalopathy?

A

Steroids can induce protein breakdown, increasing ammonia production which will worsen hepatic encephalopathy

241
Q

Why are steroids contraindicated for managing hepatic disease in patients with hepatic infections?

A

Steroids cause immunosuppression which will worsen infections

242
Q

Why are steroids contraindicated for managing hepatic disease in patients with bridging fibrosis?

A

Bridging fibrosis is a key indicator there may also be portal hypertension so it is contraindicated as portal hypertension can cause both hepatic encephlopathy and gastrointestinal ulceration

243
Q

Why are steroids contraindicated for managing acute hepatopathies?

A

Steroids are contraindicated as acute hepatopathies tend to have infectious or toxic aetiologies

MODULE 16 - Alimentary Tract Disease (19 decks)

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