Diseases of the Liver Flashcards

1
Q

What are the 2 intracellular markers?

A

ALT

AST

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2
Q

Of ALT and AST, and increase in which is more indicative of severe hepatocellular damage?

A

AST

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3
Q

Where is ALT stored?

A

In the cytosol of liver cells

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4
Q

Where is AST stored?

A

In the mitochondria and cytosol of cells

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5
Q

Which is more liver specific, AST or ALT?

A

ALT

AST is also in skeletal and cardiac muscle

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6
Q

T/F: Severity of elevation of AST correlates to degree of liver damage, and is an indicator of prognosis.

A

False.

Severity of elevation of AST correlates to degree of liver damage, but is NOT always an indicator of prognosis.

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7
Q

What is important to remember with regards to the half-lives of AST and ALT?

A

They’re short, so if concentration has dropped 50% in 2.5 days, inciting cause is gone

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8
Q

If AST>ALT, what else should you check and why?

A

Check CK because AST is also in skeletal muscle, will help you figure out what’s going on.

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9
Q

What are the 2 membrane-bound markers?

A

ALKP

GGT

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10
Q

Where are ALKP and GGT bound?

A

canicular membrane of gall bladder

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11
Q

What is the other difference between ALT&AST and ALKP&GGT?

A

Half-lives

ALKP and GGT have longer half-lives

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12
Q

What will induce an increase in ALKP and GGT?

A

Choleostasis

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13
Q

In the dog, which is less specific, ALKP or GGT?

A

ALKP is less specific in the dog

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14
Q

Where do we see ALKP isoenzymes (5 places)

A
Intesines
Kidneys
Placenta
Bones (yonung, old and neoplasia)
Drugs (corticosteroids and phenobarbitone)
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15
Q

What 2 drugs act as ALKP isoenzymes?

A

Corticosteroids

Phenobarbitone

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16
Q

Why is increased ALKP in a cat so significant?

A

Because they don’t have corticosteroid-associated ALKP so ALKP is VERY liver specific

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17
Q

Where does bilirubin come from?

A

RBCs

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18
Q

Where is bilirubin stored?

A

Gall bladder

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19
Q

How is bilirubin normally eliminated?

A

Conjugated and excreted via bile ducts to get broken down in GI to urobilinogen.

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20
Q

What are the 3 general disorders of bilirubin?

A

Pre-hepatic jaundice
Hepatic jaundice
Post-hepatic jaundice

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21
Q

What is an example of pre-hepatic jaundice?

A

Hemolysis (IMHA)

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22
Q

What is an example of post-hepatic jaundice?

A

Bile duct obstruction

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23
Q

What can tell you if you have pre-hepatic jaundice?

A

PCV

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24
Q

What is a good way to tell if post-hepatic jaundice?

A

US

If you don’t have signs associated with EHBA, can conclude liver dysfxn.

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25
Q

How can you tell if you have hepatic jaundice?

A

Rule out Pre- and Post-hepatic, consider a biopsy

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26
Q

When do you start seeing signs of compromised liver function?

A

70% destruction

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27
Q

What is the best test for liver function?

A

Ammonia Tolerance Testing

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28
Q

What is the second best test for liver function?

A

Serum Bile Acids

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29
Q

How do you perform a serum bile acid test?

A

12hr fast, take blood sample, challenge with protein (usually tbsp of A/D is good enough), second blood sample take n2hrs post-prandially.

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30
Q

In the serum bile acids test, which sample is the most sensitive and specific test?

A

Post-prandial sample

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31
Q

T/F: Post-prandial bile acids is equivalent in sensitivity and specificity to ammonia tolerance test in detecting PSS.

A

True

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32
Q

T/F: Post-prandial bile acids is equivalent in sensitivity and specificity to ammonia tolerance test in detecting parenchymal liver dz.

A

False

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33
Q

When do you start to see hypoalbuminemia?

A

With less than 33% liver fxn

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34
Q

If albumin is significantly low, what will that lead to?

A

Development of ascites

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35
Q

What 2 things does ascites do to us?

A

Makes biopsy more tricky

Is a negative prognostic indicator

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36
Q

What should we remember about dogs with hypoglycemia?

A

It’s uncommon

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37
Q

If we have a dog with hypoglycemia, what should be on our ddx?

A

Hepatic encephalopathy

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38
Q

If we have a dog with hypoglycemia, what 2 tests should be on our list to perform?

A

BG

Basal ammonia

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39
Q

T/F: Hyperglycemia is more common in cats with liver dz.

A

True

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40
Q

If you have a hyperglycemic cat, what do you want to try to do right away and why?

A

Regulate glucose

Impact on outcome
Effect on brain fxn and myocardial health

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41
Q

What 3 additional tests would you run if you suspect liver dz?

A

Hematology
Urinalysis
Coagulation panel

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42
Q

What would you expect to find on hematology in a liver dz patient?

A

Non-specific changes

Mild non-regenerative anemia and thrombocytopenia

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43
Q

What is microcytic, hypochromic anemia indicative of (especially in yorkies and danes)?

A

Abnormal iron metabolism secondary to PSS

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44
Q

What would be important to note on a UA of a cat with suspected liver dz?

A

Increased bilirubin

NOTE: Cats normally have a high threshold for bilirubin so if you’re seeing it in the urine, is significant.
NOTE: Small amount in dogs can be normal

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45
Q

What are urate crystals on UA of a yorkie pretty diagnostic for?

A

PSS

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46
Q

How much coagulation factor depletion do you need to see prolonged clotting times?

A

70%

Note very sensitive

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47
Q

Which coagulation factor does the liver NOT produce?

A

Factor VIII

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48
Q

What is abdominal radiology good for with liver dz?

A

Assessing liver size

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49
Q

What is abdominal US good for investigating?

A

Hepatobiliary dz

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50
Q

Can a normal US scan exclude hepatic disease?

A

No, poor correlation between US and surgical/histo findings

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51
Q

When would you consider a liver biopsy?

A

Primary dz of unknown origin in a STABLE animal

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52
Q

According to WSAVA, you should not treat with steroids until..?

A

We have biopsy proven signs of chronicity (fibrosus and mononuclear infiltrate)

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53
Q

When is a liver biopsy contraindicated?

A

If coagulopathy is present

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54
Q

If clotting times are prolonged, what should you consider before doing a liver biopsy?

A

Treat with plasma or Vit K

NOTE: Some people will still give Vit K even if clotting times are normal

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55
Q

What parameter should you check before performing a FNA on the liver?

A

Platelet numbers

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56
Q

How is a liver FNA performed?

A

23G needle with US guidance

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57
Q

What should you do while obtaining a liver FNA?

A

Aspirate multiple areas

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58
Q

What is the most sensitive sample for diagnosing cholangeohepatitis?

A

Bile

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59
Q

What parameter should you consider before performing a liver biopsy?

A

Coagulation factors

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60
Q

What is the name of the trigger biopsy needle?

A

Tru-cut

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61
Q

T/F: Tru-cut is the gold standard.

A

False

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62
Q

What is a step you should do before you send your tru-cut biopsy away for histo?

A

Do an impression for cytology

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63
Q

What liver biopsy needle is used for the largest amount of tissue?

A

Menghini

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64
Q

What is the Menghini typically used for?

A

Investigating copper associated liver dz

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65
Q

What is a MAJOR thing to remember with regards to trigger biopsy needles in cats?

A

Associated with vagal shock and sudden death

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66
Q

What is the gold standard for liver histopathology?

A

Wedge sample via laparoscopy or celiotomy

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67
Q

Why is it so good to gain a liver sample via laparoscopy or celiotomy (2 reasons)?

A

Can visualize and control bleeding

Can get larger sample

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68
Q

What is another thing you can gain from a larger liver sample?

A

Quantitative copper concentrations

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69
Q

What is H&E stain for?

A

Routine histology

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70
Q

What is Masson’s trichome stain for?

A

Cirrhosis and fibrosis (chronic liver pathology)

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71
Q

What is PAS stain for?

A

Vacuolar hepatopathy

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72
Q

What is Rubeanic acid/Rhodanine stain for?

A

Copper

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73
Q

What is Congo Red stain for?

A

Amyloid

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74
Q

What is Perl’s stain for?

A

Iron

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75
Q

What is a trasnudate?

A

Low protein (

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76
Q

What is a modified transudate?

A
Low protein (2.5-7.5 g/dL)
Low cellularity (1000-1500 cells/mL)
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77
Q

What is a non-septic exudate?

A
High protein (>3 g/dL)
High cellularity (>5000 cells/mL, neuts with NO bacteria)
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78
Q

What is a septic exudate?

A
High protein (>3 g/dL)
High cellularity (>5000 cells/mL, neuts with intracellular bacteria)
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79
Q

What are 2 causes of a transudate?

A

Hypoalbuminemia (PLE, PLN, Liver failure)

Portal hypertension

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80
Q

What are 3 causes of a modified transudate?

A

R-sided CHF
Neoplasia
Liver dz

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81
Q

What is a cause of an exudate?

A

FIP

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82
Q

What is a cause of a septic exudate?

A

GI perforation

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83
Q

How do you define acute liver disease?

A

Less than 2 weeks duration

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84
Q

What are 5 different causes of acute liver dz?

A
Toxic
Hypoxic
Traumatic
Metabolic
Infectious
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85
Q

What are the 3 subdivisions of acute liver dz?

A

Single cell necrosis
Acute hepatic failure
Fulminant hepatic failure

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86
Q

What is single cell necrosis?

A

Isolated cells damaged

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87
Q

What might we detect with single cell necrosis?

A

Usually subclinical/clinically silent.

Enzyme increases present on routine analysis

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88
Q

What is acute hepatic failure?

A

Widespread necrosis

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89
Q

What might we see with acute hepatic failure?

A

Mental dullness, vomition, PU/PD, icterus
ALT up, ALKP possibly up
Fxn may be maintained

NOTE: Could also be subclinical

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90
Q

What is fulminant hepatic failure?

A

Massive necrosis resulting in coagulopathies and hepatic encephalopathies

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91
Q

What do we see in fulminant hepatic failure?

A

Anorexia, V&D

ALT markedly increased, ALKP increase follows

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92
Q

What is there an increased risk of with fulminant hepatic failure?

A

Increased risk of the dog dying before discharge

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93
Q

What must you address in fulminant helpatic failure?

A

Colloid and oncotic pressure because these dogs become hypoalbuminemic and suffer from hypoglycemia.

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94
Q

How do we diagnose acute liver dz?

A

Need history to see what/if dog was exposed to
Biochem (looking for elevated enzymes)
Coagulopathies?
US -> diffuse hypoechogenicity? hepatomegaly?

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95
Q

What is the standard treatment for acute liver disease?

A
Decontamination
Fluids
Antiemetics (REALLY nauseous, want centrally acting)
PPIs
N-acetyl cysteine or SAMe
Silymarin
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96
Q

What doe N-acetyl cystein and SAMe do to help the liver?

A

Both are glutathione donors, so they protect the liver from oxidative damage

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97
Q

Why is LRS not good to use in liver failure patients?

A

Converted in the liver so it can manifest a hyperlactatemia

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98
Q

What fluids should you use instead of LRS in a liver failure patient?

A

Saline solution

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99
Q

Although saline would be better than LRS in liver failure dogs, why would you choose LRS instead in a dog with hepatic encephalopathy?

A

Because saline will acidify the patient, with allows ammonium to pass the BBB more easily which is what we do NOT want

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100
Q

Nutritionally, how do we treat acute liver dz?

A

Provide a good quality, normal protein content

NOTE: Be aware of aromatic amino acids which come from animal proteins. Plant proteins are better

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101
Q

What happens if we protein restrict a patient with acute liver dz?

A

Their BMR will be increased, so if they don’t get enough protein in their diet, they will breakdown muscle which also exacerbates hepatic encephalopathy

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102
Q

What is the only time you should restrict protein?

A

If visible clinical hepatic encephalopathy is present

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103
Q

What are 4 etiologies for acute liver dz?

A

Toxins
Metabolic
Infectious
Hypoxia

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104
Q

What are 4 toxins that can cause acute liver dz?

A

Acetaminophen
Carprofen
Diazepam
Aflatoxin

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105
Q

What do we see in cats with acetaminophen toxicosis?

A

Heinz bodies
Hemolytic anemia
Methemoglobinemia

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106
Q

What is important to remember about cats with acetaminophen toxicosis?

A

Cats will die before they develop acute hepatic necrosis

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107
Q

What do we see in dogs with acetaminophen toxicosis?

A

Acute hepatic failure

NOTE: Dogs have a higher tolerance, takes 150-200mg to get to toxic levels

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108
Q

Why is a side effect of the “-conazoles” liver failure?

A

Because it is a P450 enzyme inhibitor

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109
Q

What do you do to treat acetaminophen toxicosis?

A
N-acetylcystein
SAMe
Ascorbic acid (Vit. C)
Cimetidine
Support (O2, gastric lavage, emetics, charcoal)
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110
Q

What 2 things does carprofen cause in labradors?

A

Idiosyncratic fulminant hepatic injury

Acute renal injury

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111
Q

What should you do if you deicde to put a lab on carprofen?

A

Warn the owner of the risks and monitor liver enzymes

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112
Q

What formulation of diazepam do cats have trouble with?

A

Oral diazepam

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113
Q

What do we see in cats who have been given oral diazepam?

A

Centrilobular necrosis, myocyte and muscle necrosis

Hypoglycemia, coagulopathies, icterus and ARF

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114
Q

How do you treat a cat who has ingested diazepam?

A

Support
Vit. K
Blood
N-acetyl cystine

115
Q

What is the most common cause of aflatoxicosis?

A

Spoiled and contaminated food, usually pre-procesing, the corn is spoiled.

116
Q

What signs do we see of aflatoxicosis?

A

Groups of dogs affected, high mortality rate

Bleeding and hypoalbuminemia

117
Q

How do we treat dogs with aflatoxicosis?

A

Need blood transfusions, FFP and support

118
Q

What is the prognosis for dogs with aflatoxicosis?

A

Poor

119
Q

What does xylitol do?

A

Stimulates insulin release and hypoglycemia -> marekdly elevates liver enxymes -> necrosis

120
Q

What do we see with xylitol toxicosis?

A

Icterus

Bleeding

121
Q

How do we treat dogs with xylitol toxicosis?

A

Admit them and start SAMe

122
Q

What are 3 plants that cause acute liver dz?

A

Cycads
Mushrooms
Chinberry

NOTE: Most of the time, cause will not be apparent

123
Q

How do we treat dogs that have a plant toxicosis causing acute liver dz?

A

Emesis
Charcoal
Proactively prevent further liver damage

124
Q

How long do we expect to keep a dog with plant toxicosis in the ICU?

A

About 3 days

125
Q

After discharge, how often do we want to see plant toxicosis dog in again and what are we monitoring?

A

Want to see them every ~2.5 days to monitor liver enzymes and make sure they’ve dropped by at least 50% if they haven’t returned to normal already.

126
Q

What is the most important liver dz in cats?

A

Hepatic lipidosis

127
Q

How does hepatic lipidosis occur?

A

Imbalance in lipid metabolism causes lipid accumulation in the hepatocytes and subsequent loss of fxn

Usually associated with starvation

128
Q

Why do we see hepatic lipidosis so often in cats who are being fed kibble?

A

Because kibble has a lot of CHO which cats can’t metabolize.

129
Q

How can we decrease risk or prevent hepatic lipidosis?

A

Increase protein content in the diet

130
Q

What cats are most at risk of developing hepatic lipidosis?

A

Obese cats

131
Q

What signs do we see in hepatic lipidosis?

A

Vomiting, diarrhea, bleeding, icterus, ALKP increased

132
Q

How do we treat hepatic lipidosis?

A

As soon as can, place a feeding tube to get nutrition into the cat
Supplement with L-carnitine, Taurine and Arginine

NOTE: L-carnitine assists mitochondrial fatty acid oxidation; Taurine important to conjugate bile acids; Arginine is part of the urea cycle

133
Q

Why should you not force feed a cat with hepatic lipidosis?

A

Cat will develop a very strong food aversion

134
Q

In dogs, drooling is often a sign of nausea. In cats, it means something else, what does it mean?

A

Sign of hepatic encephalopathy

135
Q

What are 2 infectious causes of acute liver dz?

A

Infection canine hepatitis

Lepto

136
Q

Who do you see most commonly with ICH?

A

Young, unvaccinated dogs

137
Q

What are the signs of ICH?

A

V&D, GI bleeding, glomeulonephritis

NOTE: ICH can be mistaken for Parvo

138
Q

What is the hallmark feature of ICH?

A

Corneal edema

139
Q

How do you dz lepto?

A

Serum titers

140
Q

How do you treat lepto?

A

Abx

141
Q

What do you need to remember about dogs with suspected lepto?

A

EVERYONE should be wearing PPE, highly zoonotic

142
Q

How can you prevent shedding of lepto in urine?

A

Treat with a combo of penecillin and tetracycline

143
Q

When might you see hepatic encephalopathy?

A

Acute or chronic liver dz

PSS

144
Q

How does an animal with hepatic encephalopathy present?

A

Mental dullness, stupor/coma
Disoriented, blindness
Head pressing, circling, ataxia
Sometimes seizures

NOTE: Cats will salivate, DO NOT assume this is nausea

145
Q

What is hepatic encephalopathy?

A

A neurologic syndrome that is potentiall reversible

146
Q

What 4 things are on your Ddx if you have hepatic encephalopathy?

A

Acute liver injury
PSS
Cirrhosis
Urea enzyme cycle deficiency

147
Q

How does hepatic encephalopathy occur?

A

Circulating toxins cross the BBB

148
Q

What 3 toxins may cause hepatic encephalopathy?

A

Aromatic amino acids
Ammonia
Benzodiazapine-like substances

149
Q

Which toxin in hepatic encephalopathy is measurable?

A

Ammonia

150
Q

What can hepatic encephalopathy progress to?

A

Cerebral edema and death

151
Q

How can you prevent hepatic encephalopathy from progressing to cerebral edema and death?

A

Mannitol or hypertonic saline

152
Q

What are 7 things that can aggravate hepatic encephalopathy?

A

High protein diet
GIT bleeding (most dangerous trigger, ulcers)
Constipation (prolonged GI transit)
Metabolic alkalosis or Hypokalemia (if no H+ available, no excretion of ammonia at the kidney)
Excess benzodiazepines (dog is sedate MUCH MUCH longer than anticipated)
Stored blood trasnfusion (RBCs produce ammonia)

153
Q

How do you treat hepatic encephalopathy?

A

Prevent formation and absorption of toxic substances from GIT
Correct fluids, pH and electrolytes
Treat primary cause if possible
Supportive care

154
Q

What general therapies would you use in acute cases of hepatic encephalopathy?

A

Retention enema with lactulose, Povidone iodine or Neomycin sulfate) **First thing you will do if emergency
Fluids & glucose & potassium CRI
Cleansing enema (every 6hrs)
Use ion-trapping effect of lactulose
Half-dose of metronidazole to kill bacteria responsible for producing ammonia

155
Q

What is the “ion-trapping effect” of lactulose?

A

Keeps ammonia in ammonium form which is not absorbed.

156
Q

What is the prognosis of acute hepatic dz?

A

Generally good if event was overcome, cause was removed, damage did not exceed 50% and damage didn’t prevent regeneration

157
Q

What is chronic liver dz?

A

No improvement for 6+ months, inflammation that progresses to fibrosis and cirrhosis

158
Q

Do we often find the cause of chronic liver dz?

A

No

159
Q

What 2 dog breeds commonly have copper associated chronic liver dz?

A

Bedlington terriers

Westies

160
Q

What breed commonly has idiopathic hepatic fibrosis?

A

Young GSD

NOTE: Fibrosis in these dogs extends across the entire lobule

161
Q

What are 6 main categories for causes of chronic hepatic dz?

A
Copper associated
Idiopathic
Chronic cholangiohepatitis
Drug induced
Infectious
Vacuolar hepatopathies
162
Q

What is chronic cholangiohepatitis?

A

Inflammation around the biliary tract

163
Q

What are 3 drugs that cause chronic liver dz?

A

Anticonvulsants
Carprofen (labs)
Steroids

NOTE: Steroid hepatopathy is transient

164
Q

When we say a steroid hepatopathy is transient, what does that mean?

A

When we stop the steroids, the liver is allowed to heal

165
Q

What are some major infectious causes of chronic liver dz?

A

Infectious canine hepatitis
Lepto
Acidophil cell hepatitis

166
Q

What are vacuolar hepatopathies usually?

A

Reactive hepatopathies

167
Q

What are 3 causes for vacuolar hepatopathy?

A

DM
Hyperadrenocorticism
Storage dz

168
Q

What 2 things are often in the vacuoles of vacuolar hepatopathy?

A

Fat

Glycogen

169
Q

T/F: Increased ALKP in a dog is an indication that we should investigate the liver.

A

False. Increased ALKP in a dog is NOT an indication to investigate the liver

170
Q

If you have increase ALKP in a dog, what 2 systems should you focus on before the liver?

A

Endocrine system
GI

NOTE: ALKP is usually an innocent bystander in the dog

171
Q

What are the first 2 cells to respond to injury around the portal triads?

A

Lymphocytes

Plasma cells

172
Q

Where does liver dz in the dog usually start?

A

Periportal rather than centrilobular

173
Q

As liver dz progresses, what is the pathogenesis?

A

Damage progresses from periportal towards the central vein, results in distorted architechture

174
Q

What causes hepatic fibrosis and cirrhosis?

A

It’s secondary to inflammation

175
Q

Who is responsible for hepatic fibrosis and cirrhosis?

A

Ito cells

176
Q

How is hepatic fibrosis and cirrhosis formed?

A

Ito cells produce collagen -> excessive extracellular matrix is produced and that ECM affects hepatocyte function and sinusoidal blood flow

177
Q

What effect does fibrosis and cirrhosis have on blood flow?

A

Less elasticity causes increased pressure, portal hypertension and we see acquired PSS

178
Q

Where can fibrosis occur?

A

Any of the 3 acinar zones

179
Q

What zone has the best prognosis if it develops fibrosis?

A

Zone 1

180
Q

What does the liver look like grossly if it’s got fibrosis and cirrhosis?

A

Nodular

181
Q

T/F: Chronic hepatitis is a diagnosis.

A

True

182
Q

What enzyme should you not ignore in predisposed dog breeds

A

ALT

183
Q

What cells are involved with chronic hepatitis?

A

CD3+ lymphocytes

184
Q

What age group is typically affected by chronic hepatitis?

A

4-7years

185
Q

Is there a sex predisposition with chronic hepatitis?

A

Females more likely than males

186
Q

What is the clue or chronic hepatitis?

A

Increased ALT

187
Q

What can you do to try to diagnose chronic hepatitis early?

A

Screen all at risk dogs

188
Q

What is the most common and sometimes only sign you would see with chronic hepatitis?

A

PU/PD

NOTE: Rest of signs are very general

189
Q

If you suspect chronic hepatitis, why would you do a liver function test?

A

Because the clinical signs are so vague

190
Q

If you have vague clinical signs, PU/PD and suspect chronic hepatitis, what 2 tests should you do?

A

US (Can often find microhepatica)

Biopsy!!

191
Q

What 6 general steps do you take to treat a chronic liver?

A
Treat underlying cause
Diet (only protein restrict in HE)
Treat inflammation
Prevent fibrosis
Supplement vitamins and micronutrients
Give antioxidants
192
Q

How long would you give abx for in chronic liver dz?

A

2-3 months

NOTE: can use fluoroquinolones, clavamox or 1/2 dose metronidazole

193
Q

If you have a copper storage issue, what 2 things can you use to treat?

A

Penicillamine
Zinc-gluconate (binds Cu in the diet nd excretes in intestines)

Both are chelators

NOTE: DO NOT use chelators unless confirmed storage dz or else you will deplete copper available to animal

194
Q

When should you also be supplementing vitamins and micronutrients?

A

If the patient is clinically ill in hospital

195
Q

What is the best antioxidant to use for the chronic liver?

A

SAMe (S-adenosil-L-methionine)

196
Q

How does Ursadiol help chronic liver?

A

Promotes bile flow and targets T lymphoctes to prevent fibrosis

197
Q

If you are treating with metronidazole, why do you only give half the dose in a liver patient?

A

Because they have altered drug metabolism (metronidazole is metabolized in the liver)

198
Q

What are 3 other thins you might consider when treating chronic liver?

A

Coagulopaties (give vit. K, FFP)
GIT complication (ulcers)
Secondary infections

199
Q

How does ascites form with chronic hepatitis?

A

Portal hypertension in the absence of severe hypoalbuminemia

200
Q

What should you NOT do to a chronic hepatitis case with ascites?

A

Don’t drain the fluid via abdominocentesis! Could be fatal. Can do for diagnostics, but bandage well!!!

Only exception is if animal is dyspneic, and even then only drain a little bit.

201
Q

How do you manage ascites in a chronic hepatitis patient?

A

Spironolactone, then add furosemide

NOTE: Not furosemide right away because shifts fluids too fast and also causes K loss which will exacerbate HE!

202
Q

How can you monitor the ascites?

A

Measure girth at L2

203
Q

Once you stabilize your ascites patient, how can you help manage them?

A

Low sodium diet

204
Q

What are 3 causes of feline inflammatory liver dz?

A

Suppurative cholangitis
Lymphocytic cholangitis
Lymphocytic portal hepatitis (flukes)

205
Q

What is triaditis?

A

Hepatitis
Pancreatitis
Inflammatory bowel dz

206
Q

Because cats get triaditis, what should you do?

A

Biopsy the triad!!! (US guided)

207
Q

What US changes do you see with cholangitis?

A

Enlarged liver with mixed echogenicity (fibrosis)
Biliary tracts thickened (esp. common bile duct)
Common bile duct becomes tortuous

NOTE: These are hallmark for cholangitis, just can’t tell which one yet.

208
Q

When you find cholangitis on US, what would your next step(s) be?

A

Biopsy for dx

Cholecystocentesis to completely empty gall bladder (reduce chance of leakage) and send bile for culture and cytology

209
Q

What age do we typically see suppurative cholangitis and cholangiohepatitis?

A

Middle-age to older cats

210
Q

What causes the hepatocyte necrosis in suppurative cholangitis and cholangiohepatitis?

A

Neutrophilic infiltrate into periportal space

211
Q

What enzyme changes will you see with suppurative cholangitis and cholangiohepatitis?

A

Increased bilirubin, ALT, ALKP and GGT

212
Q

What do you see on the hemogram with suppurative cholangitis and cholangiohepatitis?

A

Neutrophilic left shift

213
Q

How do you treat suppurative cholangitis and cholangiohepatitis?

A

Broad spectrum abx

  • Clavamox
  • Cephalosporins
  • Fluoroquinolones

NOTE: NO enrofloxacin in cats!

214
Q

How long would you expect to have a cat in hospital with suppurative cholangitis and cholangiohepatitis?

A

7-14 days ICU

NOTE: Place a feeding tube

215
Q

What are 3 other things (besides abx) that you would use with a cat who had suppurative cholangitis and cholangiohepatitis?

A

Vit. K
SAMe
UDCA (Ursadiol etc.)

216
Q

What is the prognosis in suppurative cholangitis and cholangiohepatitis?

A

Fair, but difficult if triaditis

217
Q

What is lymphocytic cholangitis?

A

Lymphocytic infiltrates

218
Q

What cats would you expect to find lymphocytic cholangitis in?

A

Young cats
Persians

NOTE: US mean age is older than Japan’s which is about 4yrs

219
Q

What are the clinical signs of lymphocytic cholangitis?

A

Jaundice and ascites
Might still be eating
Hepatomegaly
Lymphadenopathy

220
Q

What does lymphocytic cholangitis closely resemble?

A

FIP

221
Q

How do you diagnose lymphocytic cholangitis?

A

Histopath!!

See increase ALT, ALKP, GGT
Hyperglobulinemia
Ascitic fluid is thick with high globulins

HISTOPATH IS THE ONLY WAY TO DX!!!

222
Q

Besides FIP, what else would be on your Ddx for lymphocytic cholangitis?

A

Lymphoma

223
Q

How do you treat lymphocytic cholangitis?

A

Methotrexate is DoC
Prednisolone
Chlorambucil (instead of azothiaprine - for dogs)

Immunosuppressives

224
Q

What are the 2 functions of bile?

A

Digestion and absorption of fat

Excretion of cholesterol and bilirubin

225
Q

Describe drainage of the liver.

A

Canaliculi merge to form terminal bile ducts and progressively larger bile ducts -> hepatic duct -> cystic ducts -> common bile duct -> duodenum

226
Q

How is bile released?

A

Protein and fat stimulate contraction of the gall bladder via cholecystikinin (CCK)

227
Q

What can happen if bile isn’t released?

A

Cholecystitis

Biliary mucoceal

228
Q

What is an important cause of bile dysmotility?

A

Hypothyroid

229
Q

What is extrahepatic biliary obstruction (EHBO)?

A

Obstruction of flow of bile from the gall bladder into the duodenum.

230
Q

What are 4 causes of EHBO?

A

Stricture
Intraluminal obstruction
Extrinsic compression
Various diseases

231
Q

What is the most common cause o EHBO in dogs?

A

Pancreatitis

232
Q

What are the 2 most common causes of EHBO in cats?

A
Tumors
Inflammatory dz (FIP)
233
Q

What is a good differential for EHBO?

A

Choledocholithiasis (primary or secondary)

234
Q

What are 3 less likely causes of EHBO?

A

Neoplasia
Chronic duodenitis
Rupture of gall bladder or ducts

235
Q

What is the cardinal clinical sign of EHBO?

A

Icterus

236
Q

What are the other 5 main signs of EHBO?

A
Abdominal pain
Mental dullness
Vomition
Dehydration
Anorexia
237
Q

What blood chem results would help you diagnose EHBO?

A

Slight increase in total bilirubin
Increase in ALKP/GGT
Increase in cholesterol

238
Q

Are RADs helpful in diagnosing EHBO?

A

Only if mineralized choeleliths present

239
Q

What type of imaging is best for diagnosing EHBO?

A

US

240
Q

What 3 things might you see on abdominal US of the gall bladder when EHBO is present?

A

Distended gall bladder
Dilated tortuous bile duct
Thickened gall bladder wall

241
Q

What sort of hemogram would you expect with EHBO?

A

Inflammatory leukogram with left-shift

242
Q

What might you also notice increased in the blood work of an EHBO patient?

A

Increased cholesterol

NOTE: Because of the obstruction, don’t ignore possibility of this as well.

243
Q

What sort of ultrasonographic changes do you see with EHBO?

A

Retrograde dilation of CBD and GB and tortuous CBD

NOTE: looks like “too many tube”, if remains for 5-7 days you can see intrahepatic dilation.

244
Q

What is the average diameter of the common bile duct in a cat?

A

2mm

245
Q

What is the average diameter of the common bile duct in a dog?

A

3mm

246
Q

How do you treat EHBO?

A

General supportive treatment
Surgery if obstruction or rupture
May require Abx on culture of bile

247
Q

What is cholecystitis?

A

A non-obstructive inflammation of the gall bladder which could become necrotic.

248
Q

There are 3 classes of cholecystitis, what are they?

A

Class I: No rupture
Class II: Bile peritonitis
Class III: Omental adhesion

249
Q

How is each class of cholecystitis managed?

A

Class I: Medically (chronic management though, surgical will remove the issue)
Class II: Surgical
Class III: Surgical

250
Q

What bacterial infection can progress to a necrotizing cholecystitis?

A

E. coli

251
Q

What 2 bacteria can cause emphysematous cholecystitis?

A

E. coli and Clostridum

252
Q

How do you diagnose cholecystits?

A

RADs or US (better)

253
Q

What can you do with a case of cholecystitis to figure out the cause?

A

Percutaneous US guided cholecystocentesis for C&S

254
Q

What can you do for a case of cholecystitis to minimize risk?

A

Drain completely

255
Q

What 3 things should you check before you perform a cholecystectomy?

A

Is there an inflammatory leukogram? (Give broad spectrum Abx)
Is patient hypotensive? (if yes, stabilize)
Is patient hypokalemic? (if yes, associated with worse outcome)

256
Q

What is the progression of a biliary mucocele?

A

Too much fat + not enough fiber = cholesterol accumulates
Inflammation + abnormal absorption = Cholesterol precipitates

NOTE: Often, owners think this is a cholelith, but these are rare in dogs

257
Q

What is a biliary mucocele?

A

Abnormally distended gall bladder with mucous and congealed bile salts

258
Q

How is a biliary mucocele confirmed?

A

Non-dependent sludge on US

259
Q

What breed is at risk of developing a biliary mucocele?

A

Shetland sheepdogs

260
Q

What endocrinopathy is a risk factor to developing a biliary mucocele?

A

Hyperadrenocorticism

261
Q

What is a major risk factor to developing a biliary mucocele?

A

Hyperlipidemia

262
Q

What sort of clinical signs will you see with a biliary mucocele?

A

Non-specific signs
Concurrent pancreatitits (miniature schnauzer)
Icterus if sludge is obstructing CBD
Often an incidental finding (Shetlands/HAC)

263
Q

What 4 things would you expect to see on your lab results with a biliary mucocele?

A

Severely elevated liver enzymes***
Hypercholesterolemia
Hypertriglyceridemia
Hyperbilirubinemia

264
Q

How can you obtain a definitive diagnosis of a biliary mucocele?

A

Abdominal US

NOTE: can also exclude other etiologies of acute vomiting and can evaluate the CBD

265
Q

What is a hallmark sign of necrosis in the gallbladder on US?

A

Edema

266
Q

What are 2 things that signify edema in the gall bladder on US?

A

Lamellation (strips)

Wall is thickened

267
Q

What 3 things might you see on US that signify a gall bladder rupture?

A

Discontinuity of the wall
Free fluid
Surrounding fat is hyperechoic

268
Q

What is the definitive treatment for a biliary mucocele?

A

Surgery

269
Q

What should you be sure to take with you when you surgically remove the gall bladder?

A

Two pieces of the liver from the left and right side along with a biopsy of the gall bladder.

This is because if the patient has a chronic cholangiohepatitis, you’re going to want to know about it.

270
Q

When you remove a gall bladder, what should you do with the bile?

A

Send for aerobic and anaerobic culture

271
Q

What is a very important surgical rule of thumb when removing a gall bladder?

A

Ensure the CBD is still patent or else you won’t have any way to allow drainage of the liver.

272
Q

Why is medical management of a biliary mucocele not very effective?

A

Because we are unable to convert the semi-solid mucocele into liquid bile

273
Q

Why should you also treat biliary mucocele patients with Ursodiaol?

A

It promotes choleresis by cholehepatic shunting

NOTE: Choleresis = The secretion of bile by the liver into the gallbladder.

274
Q

Why would you treat a biliary mucocele patient with SAMe?

A

Need to protect the liver as well, so good to give antioxidant

275
Q

What comordib dzs do biliary mucocele patients sometimes have?

A

Bile peritonitis and pancreatitis

276
Q

What 2 things do you do in cases of biliary mucocele which also have bile peritonitits and pancreatitis?

A

Address hypotensive shock

Supportive care for the peritonitis and pancreatitis

277
Q

How does a gall bladder rupture affect the outcome of the patient?

A

It doesn’t, hypotensive shock is what you need to be worried about

278
Q

How common are primary hepatobiliary neoplasias?

A

Uncommon

279
Q

What 4 tumors can send mets to the hepatobiliary system?

A

Lymphoma
Pancreatic adenocarcinoma
Hemangiosarcoma
Intestinal sarcoma

280
Q

What type of hepatobiliary neoplasia is benign in old cats?

A

Biliary cystadenoma

281
Q

54% of all primary tumors in the dog are hepatocellular carcinomas, where do these almost always start in the liver?

A

Left lateral lobe

282
Q

Hepatobiliary neoplasias can be clinically silent, how do you often pick them up in geriatric dogs?

A

Increased ALKP

Don’t ignore ALKP in a geriatric dog

283
Q

What are 3 ways you can diagnose hepatobiliary neoplasias?

A

US
FNA
Biopsy**

284
Q

What is the prognosis usually in hepatobiliary neoplasias?

A

Poor