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Ettinger Old > Hepatobiliary disease > Flashcards

Hepatobiliary disease Flashcards

1
Q

What gene is associated with copper storage disease and in which breed?

A

COMMD1
Bedlington Terrier

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2
Q

Which breeds are predisposed to hepatic amyloidosis?

A

Abyssinian, Oriental, Siamese, Chinese Shar-Pei

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3
Q

What is the median age of presentation of animals with multiple acquired PSS?

A

3y

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4
Q

What breed is predisposed to progressive vacuolar hepatopathy? What other condition is it associated with?

A

Scottish Terriers
Hepatocellular carcinoma

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5
Q

What are the presenting signs of hepatocutaneous syndrome in dogs and cats?

A

Dogs - hyperkeratosis footpads, erythema/ulcerations of perioral, perianal, perivulval, preputial skin
Cats - ulceration/crusting of mucocutaneous junction, pinnae, periocular, interdigital areas, central abdomen (NOT FOOTPADS)

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6
Q

How is portal hypertension classified - give examples

A

Pre-hepatic - extra hepatic portal vein (atresia, fibrosis, thrombosis, neoplasia), arteriovenous fistulas
Intra-hepatic - pre sinusoidal, sinusoidal, post sinusoidal (chronic hepatitis with fibrosis)
Post-hepatic - post hepatic CVC/RA - R-CHF, pulmonary hypertension, Budd Chiari

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7
Q

How does peritoneal fluid differ between conditions causing ascites through PH?

A

Pre-hepatic/pre sinusoidal/sinusoidal - low protein content (<2.5g/dL)
Post hepatic, post sinusoidal, sinusoidal - high protein content (>2.5g/dL)

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8
Q

What is the mechanism of HE in cats with hepatic lipidosis?

A

Cat’s can’t synthesis arginine - depleted with fasting
Arginine necessary for completion of urea cycle

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9
Q

Which liver enzymes are leakage or inducible?

A

Leakage - ALT/AST
Inducible - ALP/GGT

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10
Q

What % of hepatic neoplasia have normal liver enzymes?

A

50%

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11
Q

What is the T1/2 of ALT in dogs/cats?

A

D - 48-60h
C - 6h

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12
Q

What is the T1/2 of AST in dogs/cats?

A

D - 22h
C - 77mins

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13
Q

Where is AST found?

A

Liver, muscle, RBCs

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14
Q

Where is ALT found?

A

Liver&raquo_space;> muscle

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15
Q

What can cause AST > ALT

A

Muscle/RBC origin

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16
Q

Where in the cell are ALT/AST found?

A

ALT - cytosol
AST - 80% cytosol, 20% mitochondria

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17
Q

Where is ALP found (list in descending order)

A

Intestinal mucosa, renal cortex, placenta, liver, bone

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18
Q

What is the T1/2 of ALP in dogs and cats?

A

D - 70h
C - 6h

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19
Q

What is the sensitivity/specificity for of ALKP for liver disease in dogs/cats

A

D - 81/50%
C - 50/93%

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20
Q

What is the mechanism of ALKP elevation in hyperthyroid cats?

A

Bone isoenzyme

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21
Q

Where is GGT found (list in descending order)

A

Kidney, pancreas, liver, gallbladder, intestine, spleen, lungs, erythrocytes

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22
Q

In cats how to ALKP and GGT compare with a) hepatic lipidosis, b) necroinflammatory liver disease?

A

a) ALP > GGT
b) GGT > ALP

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23
Q

How much hepatic function must be lost for hypoglycaemia to occur?

A

75%

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24
Q

How much hepatic function must be lost for hypoalbuminaemia to occur?

A

70%

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25
Q

What liver condition has been associated with hyperalbuminaemia?

A

Hepatocellular carcinoma

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26
Q

What condition other than about it disease or anaemia is associated with jaundice?

A

Sepsis
Cytokines inhibit the expression of hepatocyte transporters necessary for bilirubin transport

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27
Q

What is the mechanism for a patient remaining jaundiced after the resolution of bile duct obstruction?

A

Conjugated bilirubin binds irreversibly with albumin forming delta-bilirubin. T1/2 2 weeks

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28
Q

Which hormone stimulates gallbladder contraction?

A

Cholecystokinin, secreted from the duodenal mucosa in response to fat or protein

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29
Q

Where are bile acids absorbed?

A

Ileum

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30
Q

What is the reported sensitivity and specificity of bile acid stimulation for diagnosis of a PSS?

A

99%/95-100%

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31
Q

What is the reported sensitivity and specificity of fasted ammonia for diagnosis of a PSS?

A

98/89%

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32
Q

How does the liver affect haemostasis?

A

1 - produces all clotting factors except VW-subtype of FVIII
2 - cholestasis causes malabsorption of vit K
3 - AT III, protein C and S synthesised in liver
4 - PH => splanchnic pooling and increased capturing of platelets
5 - fibrinogen - acute phase proteins produced in excess = increased fibrinogen consumption

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33
Q

How can PSS and PVH be differentiated?

A

Reduced protein C activity in PSS but not PVH

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34
Q

Which breeds are predisposed to the formation of ammonium urate crystals without hepatic insufficiently?

A

Dalmatian, English bulldog, Siamese cats

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35
Q

What are the mechanisms for polyuria in patients with hepatic disease?

A

Loss of renal medullary hypertonicity, impaired hormone metabolism and psychogenic polydipsia

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36
Q

Which radiographic view has the best correlation with liver weight in dogs?

A

Right lateral

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37
Q

What is the reported agreement of cytologic and histologic diagnosis in the liver sampling?

A

30-60%

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38
Q

What percentage of patients with a histopathological diagnosis of hepatic neoplasia had neoplastic cells detected on cytology?

A

50%

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39
Q

What is the reporter discordance between tru-cut and wedge liver biopsy?

A

50%

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40
Q

What is the mechanism of SAMe?

A

Central role in synthesis of glutathione - essential antioxidant
May have anti-inflammatory, anti-carcinogenic and apoptosis modulating effects

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41
Q

What is the mechanism of N acetylcysteine?

A

Replenishes intracellular cysteine and glutathione concentrations

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42
Q

What is a concern about the long-term use of N acetylcysteine?

A

May lead to impairment of ammonia metabolism by the urea cycle

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43
Q

What is the mechanism of sillymarin?

A

Free radical effects, anti-inflammatory effects, may inhibit hepatic fibrosis, may act as choleretic

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44
Q

What medication has proven effective for Amanita mushroom toxicity?

A

Silymarin (IV)

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45
Q

What is the mechanism of UDCA?

A

Hydrophilic bile acid, displaces harmful hydrophobic bile acids, choleretic, cytoprotective, immunomodulatory.

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46
Q

What is the mechanism of D-penicillamine?

A

Chelaitng agent, combines with copper allowing mobilisation from the liver and excretion in the urine. May have antifibrotic effect.

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47
Q

What are the short and long term side effects of D-penicillamine.

A

GI
Copper deficiency - microcytic hypo chromic anaemia, anorexia. vomiting, weight loss

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48
Q

What is an alternative medication that can be used in dogs who do not tolerate D-penicillamine?

A

Trientine

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49
Q

How does trientine differ from penicillamine. When might it be a good first option?

A

Removes more copper from circulating pool and less from tissue pool
Cu-related haemolysis

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50
Q

How does zinc reduce copper?

A

Induces metallothionein by enterocytes - bind Cu, prevents absorption

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51
Q

What non-hepatic clinical signs are associated with CAV-1 infection?

A

Bronchopneumonia, conjunctivitis, anterior uveitis and corneal oedema

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52
Q

What infectious agents have been associated with acute hepatitis in dogs?

A

CAV-1, lepto, clostridium, E. canis

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53
Q

In which zones of the liver does copper accumulate in a) copper storage disease and b) secondary copper accumulation?

A

a) Zone 3 (centrilobular)
b) Zone 1 (periportal)

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54
Q

According to WSAVA classification, what are the 4 types of cholangitis?

A

Neutrophilic, lymphocytic, destructive, chronic associated with liver fluke

55
Q

Which liver enzyme is most consistently elevated in feline cholangitis?

A

AST

56
Q

How often is bile culture in cats positive? What are the common isolates?

A

36%
E.Coli + anaerobes

57
Q

What is the most common biochemical abnormality in cats with lymphocytic cholangitis?

A

Hypergammaglobulinaemia

58
Q

Which parasite is associated with infectious chronic cholangitis in cats?
Where is it seen geographically?
What are its hosts?
How is it treated?

A

Platynosomum
North, South, Central America, Caribbean, parts of Africa and Asia
Lizards, snails, isopods
Praziquantel

59
Q

What viral diseases are associated with liver disease in cats?

A

FeLV, FCV, FIP, FIV

60
Q

Which fungal diseases are associated with liver disease in cats?

A

Histoplasma, Coccidioidomycosis, Blastomyces, Aspergillosis, Cryptococcus, Sprothrix

61
Q

How much blood is supplied to the liver by the portal vein and hepatic artery respectively?

A

80/20%

62
Q

Are IH or EH PSS associated with more severe clinical signs?

A

IH

63
Q

Which breeds are predisposed to EHPSS?

A

D - YT, Havanese, Maltese, Dandie Diamont, Pug, Miniature Schnauzer
C - DSH, Persian, Siamese, Himalayan, Burmese

64
Q

What type of PSS is most commonly seen in cats?

A

EHPSS

65
Q

Which breeds are predisposed to IHPSS and what type do they get?

A

Left divisional - Irish Wolfhound
Right divisional - Australian Cattle Dog
Retrievers and Australian Shepherds - either

66
Q

What aspects of shunt morphology are associated with the degree of clinical signs observed?

A

High
Portocaval, insertion caudal to liver, splenocaval (CNS), right gastric (urinary)

67
Q

What haematological changes are reported in dogs/cats with PSS?

A

Microcytic normochromic anaemia
D - Target cells
C - Poikilocytes

68
Q

How to coagulation abnormalities differ in dogs with acute and chronic liver failure?

A

Chronic - PT elevation only
Acute - PT/aPTT

69
Q

What testing should be done in an animal with HE and hyperammonemia without evidence of a PSS?

A

Urine metabolic screen
For urea cycle abnormalities (ornithine carbamylase deficiency, methymalanic acidemia)

70
Q

What are positive prognostic indicators for dogs with PSS managed medically?

A

Older age and higher urea level

71
Q

What is the prognosis for medical management of PSS?

A

> 50% PTS within 10 months
~33% can survive long term

72
Q

What proportion of dogs with EH / IH PSS tolerate complete occlusion?

A

EH - 32-52%
IH - <15%

73
Q

What are the potential manifestations of acute/chronic portal hypertension following PSS ligation?

A

Acute - ascites, intestinal congestion, diarrhoea, hypoxaemia, bowel death
Chronic - MAPSS

74
Q

What proportion of dogs are reported to redevelop clinical signs following shunt attenuation?

A

40-50%

75
Q

Following temporary shunt occlusion what portal pressures are associated with increased postoperative complications?

A

> 9-10cm water above resting
17-24cm water absolute

76
Q

What gradual occlusion devices for PSS are available?

A

Ameroid constrictors
Cellophane bands

77
Q

With ameroid constrictor placement what is the;
a - complication rate
b - mortality rate
c - rate of good to excellent outcomes

A

a - 7-20%
b - 0-17%
c - 94%

78
Q

With cellophane band placement what is the;
a - complication rate
b - mortality rate
c - rate of good to excellent outcomes

A

a - 10-13%
b - 3-9%
c - 84%

79
Q

What is the reported surgical complication rate with IHPSS?

A

29-77%

80
Q

What is the reported incidence of post ligation seizures unrelated to HE following PSS attenuation?

A

12%

81
Q

What clinical signs post PSS attenuation indicate worrisome portal hypertension?

A

Vomiting, ascites, abdominal pain, hypotension

82
Q

What is a specific complication seen following attenuation of IHPSS? How can the risk be reduced?

A

GI bleeding
Lifelong gastric acid suppression

83
Q

How does the prognosis of PSS in cats and dogs differ?

A

Cats have higher post operative complication rates and worse long term outcomes (particularly due to neurological sequelae)

84
Q

What is the pathophysiology of HAVM?

A

Increased portal pressure due to high pressure arterial blood shunting into PV => multiple acquired shunts

85
Q

What factors are associated with poor long term outcome in dogs with EHPSS?

A

Hypoalbuminaemia, leukocytosis, post-op seizures, persistent shunting at 6-10 weeks

86
Q

What factors are associated with good short term outcome in dogs with IHPSS?

A

Higher bodyweight, TP, albumin, BUN

87
Q

What are the treatment options for HAVM and the prognosis?

A

Surgery along - 75-91% survival
Glue embolisation - 100%

88
Q

What is the complication rate in PSS attenuation in cats?

A

Complications in 75%
0-23% mortality rate

89
Q

On histopathology how can hepatic glycogen and fat accumulation be differentiated?

A

PAS - glycogen
Oil red O - fat

90
Q

What are the possible causes of vacuolar hepatopathy in dogs and cats?

A

Steroid (endogenous/exogenous)
Vacuolar hepatopathy of Scottish Terriers
Cobalamin deficiency (dogs)
Secondary (CHF, neoplasia, hepatobilliary disease, GI, renal, infectious)

91
Q

Where are changes seen in different stages of steroid hepatopathy?

A

Starts in centrilobular region (one 3)
Becomes generalised when chronic

92
Q

What biochemical changes are seen with steroid hepatopathy in dogs?

A

ALKP elevation - poss due to reduced clearance of intestinal isoenzyme

93
Q

Which breed is associated with glycogen-like vacuolar hepatopathy? What other disease is associated with it?

A

Scottish Terriers
HCC
50% have clinical signs of HAC - poss related to precursor form

94
Q

What conditions are associated with hepatic steatosis?

A

Hepatic lipidosis (C)
Vit A toxicosis (C)
Aflatoxicosis (D)
Secondary to hyperlipidaemia
Endocrine disease (hypothyroidism, DM, hyperthyroidism)
PSS

95
Q

What types of steatosis are described histopathologically? Which types are typically seen with DM and HL?

A

Microvesicular - vacuoles smaller than cell nucleus
Macrovesicular - larger vacuoles, often displacing nucleus
DM - micro
HL - micro + macro

96
Q

What types of FHL are recognised?

A

Primary - overweight cats after prolonged fasting
Secondary - associated with other disease

97
Q

What are the common clinical examination findings in FHL?

A

Hepatomegaly and jaundice

98
Q

What are the typical biochemical findings in FHL?

A

Elevated ALT, ALKP, bilirubin
GGT often normal if primary

99
Q

What is the diagnostic test of choice for FHL? What is the limitation of other options

A

Histopath
Cytology can give false +ve

100
Q

What are the mortality rates of FHL with and without assisted feeding?

A

Without - 90%
With - 40%

101
Q

What food is most appropriate to feed cats with HL?

A

High protein - shown to reduce hepatic lipid effectively in experimentally induced FHL

102
Q

What is the pathogenesis of the skin lesions in SND?

A

Amino acid deficiency

103
Q

What % of cases of SND have signs of DM?

A

25-40%

104
Q

What is the classical histological findings of SND?

A

Parakeratotic hyperkeratosis with inter and intracellular oedemas
Red, white and blue on H + E

105
Q

What is the cause of hemochromatosis?

A

Iron overload of the liver
Only secondary reported in dogs - normally associated with Cu

106
Q

What are the 2 forms of amyloid?

A

Normal - soluble
Abnormal - auto-aggregating fibrillar form of beta-pleated sheets

107
Q

Which breeds of cats are associated with amyloidosis and how do they present?

A

Abyssinian - renal (+/- hepatic involvement)
Siamese - often hepatic

108
Q

How do cats with hepatic amyloidosis present?

A

Acute abdominal bleed secondary to liver fracture
Jaundice, hepatomegaly

109
Q

Which lysosomal storage disease with predominantly hepatic signs is reported? Which breed is affected?

A

Lipid storage disorder, Fox Terriers

110
Q

What are the two mechanisms of drug induced hepatotoxicosis?

A

Cytotoxic
Cholestasis

111
Q

What are R values? How are they calculated and used?

A

Used in people to differentiate cytotoxic and cholestatic liver injury
R = (ALT/upper limit normal)/(ALKP/upper limit normal)
<2 cholestatic, 2-5 mixed, >5 hepatocellular

112
Q

What is the rationale of treating paracetamol toxicity with NAC?

A

Reactive metabolite; NAPQI detoxified by conjugation with glutathione. NAC = glutathione precursor

113
Q

What has been suggested as a treatment for methaemoglobinaemia secondary to paracetamol toxicity?

A

Ascorbate

114
Q

What has been reported as an effective treatment for blue-green algae toxicosis?

A

Cholestyramine

115
Q

What has been reported as an effective treatment for Amanita toxicosis?

A

Silybin

116
Q

Are primary or metastatic liver tumours more common in cats/dogs?

A

D - metastatic
C - primary

117
Q

What are the 4 tissue types of liver tumours?

A

Hepatocellular, bile duct, neuroendocrine, mesenchymal

118
Q

What is the most common liver tumour in dogs?

A

Hepatocellular adenoma/carcinoma

119
Q

What is the most common liver tumour in cats?

A

Bile duct adenoma

120
Q

What predilections are reported for canine bile duct tumours?

A

Breed - Labradors
Sex - Female

121
Q

What neuroendocrine tumours are reported in dogs and cats, how do they typically behave?

A

Carcinoids
Biologically aggressive and diffuse

122
Q

What are the most common primary mesenchymal hepatic tumours in dogs/cats?

A

D - leiomyosarcoma
C - Haemangiosarcoma

123
Q

How to biochemical abnormalities differ between primary and metastatic liver tumours?

A

Primary - more likely to have low protein, low glucose, increased ALKP, less likely to have elevated TBil

124
Q

What biomarker has been reported to be elevated in HCC and bile duct carcinoma?

A

Alpha-fetoprotein

125
Q

What chemotherapy has been described for treatment of nodular/diffuse HCC?

A

Gemcitabine, mitoxantrone

126
Q

What are the treatment options for nodular/diffuse bile duct carcinomas?

A

No effective treatment described

127
Q

Which breeds are predisposed to cholelithiasis?

A

Mini Schnauzers and Mini Poodles

128
Q

What types of choleliths are reported in dogs?

A

Cholesterol, bilirubin and mixed

129
Q

What is the significance of biliary sludge in dogs/cats?

A

Dogs - common incidental finding
Cats - often indicative of cholecystitis

130
Q

What gallbladder wall thickness accurately predicts gallbladder disease in cats?

A

> 1.0mm

131
Q

What rare manifestation of cholecystitis is described? What is it’s aetiology and what treatment should be recommended?

A

Empysematous cholecystitis
Usually associated with E Coli and Clostridium
Surgery

132
Q

What risk factors have been associated with GBM?

A

Dyslipidaemia, gallbladder dysmotility, endocrine disease (HAC), exogenous steroids

133
Q

What is the link between steroids and GBM formation?

A

Steroids increase levels of unconjugated bile acids - more hydrophobic => biliary injury => mucin secretion increases

Ettinger Old (13 decks)

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