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DACVIM Literature 2018-2023 > Liver > Flashcards

Liver Flashcards

1
Q

A defect in what basic cellular component results in ductal plate malformation?

A

Primary cilia

JVIM 2021, Siebert

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2
Q

Which ductal plate malformation results in abundant malformed bile ducts in fibrosis expanding the portal tracts?

A

Proliferative-like DPM

JVIM 2021, Siebert

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3
Q

Name two histopath findings that differentiate proliferative-like ductal plate malformation from other hepatopathies that result in scarring.

A

1) Minimal inflammation
2) Normal orientation of hepatic chords

JVIM 2021, Siebert

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4
Q

Which ductal plate malformation causes malformed medium to large bile ducts, diverticula, etc?

A

Caroli DPM

JVIM 2021, Siebert

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5
Q

What chronic condition does Caroli DPM mimic histologically? What differentiates it from this condition?

A

Can look like chronic EHBDO histologically but usually doesn’t clinically present that way.

JVIM 2021, Siebert

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6
Q

Which ductal plate malformation incurs increased risk for choleliths?

A

Caroli DPM

JVIM 2021, Siebert

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7
Q

Which ductal plate malformation results in cysts-like offshoots along the CBD or cystic duct? Where do these most frequently occur in the biliary tract?

A

Choledochal cyst DPM; usually at the duodenal papilla

JVIM 2021, Siebert

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8
Q

Which ductal plate malformation causes lots of teeny cystic malformations in fibrosis, which effaces the normal liver parenchyma? Which side of the liver is usually affected?

A

Expansive cystadenoma DPM

JVIM 2021, Siebert

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9
Q

Name at least two additional congenital malformations that may accompany expansive cystadenoma ductal plate malformation.

A

1) GB agenesis or hypoplasia
2) liver lobe agenesis or hypoplasia
3) Congenital PSS (rare)

JVIM 2021, Siebert

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10
Q

Which ductal plate malformations are more common in cats > dogs?

A

Choledochal cyst DPM, expansive cystadenoma DPM

JVIM 2021, Siebert

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11
Q

Which ductal plate malformations can progress to congenital hepatic fibrosis?

A

Proliferative-like DMP, Caroli DPM

JVIM 2021, Siebert

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12
Q

In people, what is the only effective treatment for congenital hepatic fibrosis? Why do immunomodulatory medications not work?

A

1) Liver transplant
2) The fibrosis is not caused by inflammation

JVIM 2021, Siebert

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13
Q

What proportion of animals with peritoneopericardial diaphragmatic hernia (PPDH)/congenital central diaphragmatic hernia (CCDH) also have liver and/or renal DPM? What does this imply as a possible mechanism for the development of PPDH/CCDH?

A

> 70%. Means primary cilia may be involved.

JVIM 2021, Siebert

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14
Q

Should you biopsy herniated or nonherniated liver lobes in cases of peritoneopericardial diaphragmatic hernia (PPDH)/congenital central diaphragmatic hernia (CCDH)? How many lobes should you bx for most accurate diagnosis?

A

> 2 nonherniated lobes

JVIM 2021, Siebert

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15
Q

Does bloodwork differentiate animals with peritoneopericardial diaphragmatic hernia (PPDH)/congenital central diaphragmatic hernia (CCDH) that DO vs DO NOT also have ductal plate malformation?

A

Only if liver fibrosis (presumably dysfunction?) and/or shunt present

JVIM 2021, Siebert

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16
Q

What is the typical signalment for hepatocutaneous syndrome (including a few predisposed breeds)?

A

–Older, small breed, male
–Cockers, shelties, shih tzu, westies

JVIM 2021, Loftus

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17
Q

Which endocrinopathy frequently accompanies hepatocutaneous syndrome?

A

Diabetes mellitus

JVIM 2021, Loftus

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18
Q

Which two amino acids are frequently found in the urine of dogs with hepatocutaneous syndrome?

A

Lysine, methionine

JVIM 2021, Loftus

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19
Q

Does the amino acid profile predict which ACHES dogs do or do not have concurrent SND?

A

No – lots of overlap

JVIM 2021, Loftus

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20
Q

What is presumed to cause hepatocutaneous syndrome in people?

A

Glucagonoma

JVIM 2021, Loftus

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21
Q

What two CBC abnormalities are associated with ACHES-SND vs ACHES without SND?

A

SND –> anemia, microcytosis

JVIM 2021, Loftus

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22
Q

What proportion of ACHES dogs do not have SND at the time of diagnosis? What proportion of these will develop it later on?

A

50%, 20%

JVIM 2021, Loftus

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23
Q

What liver histopath finding is pathognemonic for ACHES?

A

Proliferative hepatocellular foci (different from regenerative nodules)

JVIM 2021, Loftus

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24
Q

What liver condition can ACHES potentially progress to? What type of monitoring is indicated?

A

Dysplastic foci or hepatocellular carcinoma; monitor with serial AUS

JVIM 2021, Loftus

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25
Q

Which medication is associated with developing ACHES? How does discontinuing it affect survival?

A

Phenobarbital; d/c’ing does not seem to affect survival

JVIM 2021, Loftus

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26
Q

What are the three basic pillars of ACHES treatment? List them in order of anticipated relative benefit.

A

Home-cooked diet, AA +/- lipid infusions, enteral supplements

JVIM 2021, Loftus

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27
Q

What is the dosing frequency of AA +/- lipid infusions in dogs with SND?

A

q7-10d until skin lesions resolve, then q3-6 weeks

JVIM 2021, Loftus

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28
Q

How quickly do SND lesions respond to AA +/- lipid infusions?

A

Highly variable – after 1-13 transfusions, so even if does not respond for a while, doesn’t mean they WON’T respond

JVIM 2021, Loftus

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29
Q

Name at least three enteral supplements to consider for ACHES.

A

Proline, lysine, arginine/ornithine, glutathione, SAMe (not proven to be low in ACHES dogs but easy to supplement)

JVIM 2021, Loftus

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30
Q

What is the downstream product of SAMe?

A

Glutathione

JVIM 2021, Loftus

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31
Q

What is the target protein % for diet in treatment of ACHES? Is a balanced commercial diet or home cooked preferred?

A

50% of metabolizable energy (ME) from protein. Home cooked (developed by nutritionist) > commercial diet.

JVIM 2021, Loftus

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32
Q

How does diabetes mellitus affect prognosis of ACHES?

A

ACHES dogs with DM did better but may have been type II error; at the very least, can infer ACHES dogs with DM can still do well

JVIM 2021, Loftus

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33
Q

What is the MST for ACHES dogs with optimal treatment (>2 AA +/- lipid transfusions, >3 prioritized enteral supplements, home cooked diet)? How does this compare with all other tx combinations?

A

Optimal tx MST >4.8 years, other tx combos 7mo

JVIM 2021, Loftus

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34
Q

Does hepatic lead correlate positively or negatively with hepatic copper? This is especially true at what copper threshold?

A

Positive, esp at Cu >400

JVIM 2021, Gori

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35
Q

What peripheral and bone marrow effects are seen with acute lead poisoning? What are the two basic mechanisms?

A

–Anemia (most common), basophilic stippling, decr M:E, ineffective erythropoiesis
–Interferes with heme synth, causes RBC oxidative stress

JVIM 2021, Gori

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36
Q

What are the three possible etiologies of hepatic copper accumulation? Which of these may play a role in lead accumulation?

A

1) genetic defect in hepatic Cu metabolism
2) cholestasis –> impaired biliary excretion of Cu
3) excessive dietary Cu

1 and 2 may play a role in lead accumulation, but previous studies have ruled out 3 (no significant lead in dog food)

JVIM 2021, Gori

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37
Q

What are three underlying mechanisms that can cause incr bile acids?

A

1) liver dysfunction –> decr portal BA clearance
2) PSS
3) bile stasis

JVIM 2021, Pena-Ramos

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38
Q

Can pre/post BA differentiate between different types of hepatopathies?

A

No – lots of overlap between diseases

JVIM 2021, Pena-Ramos

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39
Q

Can normal dogs have high bile acids, and vice versa?

A

Yes. Even dogs with liver vascular anamolies can have normal BA.

JVIM 2021, Pena-Ramos

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40
Q

Can normal dogs have high bile acids, and vice versa?

A

Yes. Even dogs with liver vascular anomalies can have normal BA.

JVIM 2021, Pena-Ramos

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41
Q

Are pre or post BA more sensitive for liver disease? Which is more specific?

A

Pre BA are more specific, post BA are more sensitive

JVIM 2021, Pena-Ramos

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42
Q

What is the typical BCAA:AAA in healthy dogs vs APSS dogs?

A

Healthy 3-4
APSS <1.5

JVIM 2021, Devriendt

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43
Q

BCAA vs AAA
Which are typically metabolized by the liver vs muscle?

A

BCAA - muscle
AAA - liver

JVIM 2021, Devriendt

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44
Q

Other than high ammonia and low BCAA:AAA, name at least two other causes for hepatic encephalopathy.

A

High glutamine, glutamate, Mn, systemic inflamm

JVIM 2021, Devriendt

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45
Q

How does medical management (diet, medications) affect the amino acid profile of PSS dogs?

A

Incr methionine and serine (lots of these in the diet and probably not being metabolized by the liver appropriately) but does not improve the AA profile overall.

JVIM 2021, Devriendt

46
Q

In a small study of cPSS treated with surgical attenuation, what was their BCAA:AAA at 3 months?

A

1.5 – significantly better than at dx (0.6) but not as good as it should be (normal = 3-4)

JVIM 2021, Devriendt

47
Q

Which seems more important in PSS/HE dogs, BCAA or AAA? Why?

A

AAA because typically out of ref range. BCAA were low end preop and high end postop, but still WNL.

JVIM 2021, Devriendt

48
Q

What is this test trying to assess? How does it work? What is the sens/spec? How does this compare with other tests?
Test: Low dose lidocaine IV –> measure monoethylglycylxylidide (MEGX) 15 min later

A

1) Looking for successful APSS attenuation.
2) Lidocaine is mostly metabolized by the liver (CYP450) and it mainly depends on its blood flow. MEGX is a metabolite. If normal liver blood flow (ie, attenuated APSS), expect high MEGX at 15min.
3) Sens 96, Spec 83
4) Better performance than other tests (pre/post BA, fasting ammonia, ammonia tolerance test)

JVIM 2021, Devriendt

49
Q

At what time interval post op can the lidocaine/MEGX test detect complete APSS closure?

A

3mo (not at 1mo) – probably b/c it takes time for ameroid to completely constrict AND liver/CYP450 to recover function.

JVIM 2021, Devriendt

50
Q

Are GB mucoceles associated with a primarily HYPER or HYPOcoagulable state?

A

HYPERcoagulable

JVIM 2021, Pavlick

51
Q

Is proteinuria positively, negatively, or not associated with GB mucocele? Does illness severity and/or cholesterol affect this?

A

Proteinuria is positively associated with GB mucocele and correlates with illness severity; does not correlate with cholesterol

JVIM 2021, Lindaberry

52
Q

A dog presents with acute collapse and he has GB wall edema on A-FAST. What are your top two differentials? What quick test should you do next, and what might you find?

A

DDX anaphylaxis vs R CHF. Check T-FAST. Most R CHF dogs with GB wall edema also have pericardial and peritoneal effusion. If distended CVC+hepatic veins and lack of change during cardiac/resp cycles, R CHF is more likely than anaphylaxis.

JVIM 2021, Lisciandro

53
Q

What is the typical presentation (CS, PE) of cats with EHBO?

A

CS nonspecific (v+, hyporexia, lethargy, weight loss, icterus)
PE usually pretty stable, variable BCS but mean 4/9, 74% icteric

JVIM 2021 Griffin

54
Q

True or False:
A lack of clinical icterus rules out severe hyperbilirubinemia.

A

False

JVIM 2021 Griffin

55
Q

What are at least 3 common AUS findings in cats with EHBO?

A

–Distended biliary elements (CBD most common > cystic duct, intrahepatic biliary ducts, GB)
–Biliary wall thickening
–Abnormal pancreas, pancreatitis
–60% choleliths, sludge

JVIM 2021 Griffin

56
Q

How does tbili prior to discharge affect prognosis in cats with EHBO treated with biliary stenting?

A

It doesn’t affect prognosis. Only 68% of cats had improvement prior to discharge and most had not normalized by that time point.

JVIM 2021 Griffin

57
Q

What proportion of EHBO cats treated with surgical biliary stenting survive to discharge? How quickly did nonsurvivors typically die post op, and what was usually the cause? What pre-op factor was significantly associated with increased risk of death?

A

–78% survived to discharge
–Half of nonsurvivors died within 24hrs post op, usually due to systemic illness (none due to recurrent obstruction)
–Peritoneal effusion pre-op –> incr risk of death post op (but several effusion cats also did fine)

JVIM 2021 Griffin

58
Q

Regarding biliary stenting:
–How can you tell a temporary stent has passed? How quickly does it pass post op?
–How can you make the stent permanent?

A

–Usually AUS (pretty much never observed passing in feces); may pass as early as 1 week post op (though no sutures used in this cat), mean 6 weeks
–Can’t really make it permanent – even if you use nonabsorbable suture, will still pass

JVIM 2021 Griffin

59
Q

What proportion of cats that survive biliary stent placement will develop recurrent EHBO, and which disease was overrepresented for this? How quickly does it happen post op?

A

–39% EHBO recurrence, most commonly with stones (stricture vs new stones)
–1/3 within a week, the rest months to years later

JVIM 2021 Griffin

60
Q

True or False:
Dogs with cholelithiasis are usually sick but signs are typically vague.

A

False; most are asymptomatic (but when present, CS are vague)

JVIM 2021, Allan

61
Q

What is the difference between typical cholelith composition in people vs dogs?

A

Humans: cholesterol based
Dogs: Calcium carbonate + chol + bili

JVIM 2021, Allan

62
Q

What are the three MoA’s of ursodiol?

A

Displaces hydrophobic BA, choleretic, anti-inflammatory

JVIM 2021, Allan

63
Q

Choleliths were discovered on AUS during a workup for unrelated concerns. Liver enzymes are normal and the dog is clinically well. What should you do?

A

Monitor only. Most dogs with incidental choleliths will not go on to develop issues from these. Treatment is not necessarily indicated.

JVIM 2021, Allan

64
Q

A dog presents with vague signs of vomiting and hyporexia. Choleliths are found on AUS and liver enzymes are marginally elevated. How likely is it that the choleliths explain his clinical signs?

A

Unlikely. Most symptomatic dogs have choledocoliths and more significantly elevated LEs.

JVIM 2021, Allan

65
Q

A small study found that what proportion of medically managed (ie, ursodiol +/- abx) cholelith dogs had improvement (dissolution vs passage) of stones?

A

38%; most of these had complete resolution

JVIM 2021, Allan

66
Q

Dogs with symptomatic cholelithiasis tend to be younger or older?

A

Younger – also seen in people

JVIM 2021, Allan

67
Q

What is the frequency of any hemorrhage (PCV drop >6%) and major hemorrhage associated with percutaneous liver bx? What is one risk factor for each?

A

–Hemorrhage 42%, associated with higher pre-bx PCV (contradicts other studies), most asymptomatic
–Major hemorrhage 2%, associated with neoplasia

JVIM 2020, Reece

68
Q

What dog breed with GB mucocele can have decr CCK and incr transglutaminase-2-IgA? What condition is this similar to in people?

A

Border terriers
Celiac

JSAP 2020 Barker

69
Q

True or False: Cats with intrahepatic PSS can be successfully treated with coil embolization.

A

True. Teeny study N=4 cats. 3/4 did well, those who initially had neuro signs resolved, 1 cat developed acquired shunts.

JAVMA 2020 Culp

70
Q

True or False: De novo lipogenesis is a significant driver of hepatic lipidosis.

A

False. HL vs normal cats did not have different levels of peroxisome receptors and FA synthase. Sterol regulatory element-binding factor was downregulated.

JFMS 2020 Vatolina

71
Q

True or False: Cholestatic liver disease in cats is not associated with low vit D.

A

False. 33% have low vit D compared with 17% of extrahepatic illness cats.

JVIM 2020 Kibler

72
Q

True or False: microRNA-122 can differentiate healthy vs hepatopathy dogs.

A

True. Sens 77, spec 97 at cutoff >3K.

JVIM 2018 Oosthuyzen

73
Q

How does body condition affect portal blood flow in dogs?

A

Overweight –> lower portal velocity and lower flow volume

JVIM 2018 Belotta

74
Q

Can RBC and/or plasma glutathione be used to estimate liver glutathione?

A

No - no correlation

JVIM 2018 Barry

75
Q

What is the clinical significance of branching mineralization of the biliary tree? What breed is overrepresented?

A

Means nothing
CKCS

JSAP 2018 Genain

76
Q

Shear wave elastography is a type of imaging. Can it differentiate the following groups of dogs?

Clinically relevant liver fibrosis
Mild hepatitis +/- fibrosis
Healthy

A

Higher velocity in dogs with clinically relevant fibrosis (no overlap with other groups) BUT could not diff mild liver disease vs healthy

JVIM 2019 Tamura

77
Q

Can plasma free amino acid profiles differentiate the following groups?

HCC
Benign hepatopathy
Healthy

A

No

JVIM 2019 Leela-arporn

78
Q

Are the following higher, lower, or similar liver bx of HCC dogs vs healthy?

Cu
Zn

A

Higher Cu, lower Zn

JVIM 2019 Harro

79
Q

Which correlates best with copper quantification:
Digital image analysis
Spectroscopy

Which groups of dogs have higher Cu?
Younger vs older
Small vs large breed

A

Digital image analysis

Older, large breed
Also high Cu in necroinflamm disease

JAVMA 2021 Miller

80
Q

True or false: Copper staining in feline liver biopsies correlates well to copper quantification.

A

False. Study found that 31% were above RI, but only 11% stained positive and 2.5% score >3

JFMS 2021 Yamkate

81
Q

In cats with cholestatic liver disease assessed via TEG:
% hypercoag?
% hypocoag? Significance?

A

50% hypercoag
22% hypocoag – prolonged PT/PTT agreed with TEG. Synthetic liver failure.

JFMS 2021 Kakar

82
Q

Answer the following regarding canine cholangitis/cholangiohepatitis.

–Proportion that have fever, leukocytosis?
–Proportion that have a GB obst?
–Most common type of inflamm on liver bx?

A

–30% each
–About half
–Almost all are chronic neutrophilic inflamm

JVIM 2018 Harrison

83
Q

Answer the following regarding canine vs feline cholangitis/cholangiohepatitis.

–Proportion with positive liver and/or bile culture? Two most common pathogens?
–MST post op in dogs?
–Incr risk of death? (Dogs - 2; Cats - 4)

A

Dogs (liver and/or bile): about half – E. coli, Enterococcus

Cats (liver, bile, crushed cholelith): >90% – E. coli, Enterococcus

Dog MST 1.8yrs

Incr risk of death:
–Dogs: no cholecystectomy or age >13yrs
–Cats: no sx, leukocytosis, ALP >2x RI, hyperbilirubinemia

JVIM 2018 Harrison

84
Q

Which are helpful in a diagnosis of chronic hepatitis?

Which correlate with severity of inflamm and fibrosis?

Which correlates with survival?

microRNA-122
microRNA-29
IL-6
CCL2 (stimulates cytokine production)
p21 (IHC marker of cell senescence - liver bx)

A

High miRNA-122 and -29 correlate with severity of hepatitis and fibrosis in labs with CH

High p21 (90% immunopositivity in CH dogs vs <15% healthy controls). >92% –> shorter survival.

IL-6 and CCL2 are too variable to be helpful

JVIM 2018 Sakai
JVIM 2018 Raghu
JVIM 2018 Kortum

85
Q

What proportion of chronic hepatitis dogs will go into remission with cyclosporine?
How long does it take on average?
How does evidence of liver dysfunction affect likelihood and/or time to respond?

A

80%
2.5mo
No effect

JVIM 2019 Ullal

86
Q

What is tetrathiomolybdate (TTM)? What is it used to treat in people and experimentally in dogs? How does it work?

A

Copper chelator. Binds Cu+alb –> bile excretion. Tx Wilson’s disease in people, experimentally Cu hepatopathy in dogs.

JVIM 2019 Langlois

87
Q

In a small study (N=10) of Cu hepatopathy dogs treated with ammonium tetrathiomolybdate (TTM):
–What proportion had decr Cu (by median >650mcg/g) at 6wks?
–Effect on liver enzymes and histologic score?
–What element accumulated in the liver (and probably other tissues)? Potential concerns with this?
–Other adverse effects?

A

80%

No effect – no better but no worse

Molybdenum. Good b/c Mo+Cu in liver –> nontoxic. Potentially bad in other tissues (sheep –> endocrinopathy, ill thrift). In people, AEs incl anemia/leukopenia (d/t Cu deficiency) and uncommonly direct hepatotox.

Sporadic GI effects but didn’t preclude tx. Evan’s in one dog – unclear if secondary to TTM or not (doesn’t happen in people).

JVIM 2019 Langlois

88
Q

What is ATP7B? Mutations in this are associated with what disease?

A

Gene that makes liver intracellular Cu transport protein needed to make ceruloplasmin and excrete Cu into bile

Defective ATP7B –> primary Cu hepatopathy. Association found in dobies and in cats (75% of affected cats).

JSAP 2021 Vincent
JFMS 2020 Asada

89
Q

Are renin and aldosterone higher, lower, or no difference in acquired PSS vs congenital extrahepatic PSS vs healthy dogs?

For aPSS, how does underlying etiology affect it?

How does presence of ascites affect this?

A

Higher in aPSS. No difference EH CPSS vs healthy.

Higher in CH (prob b/c worse portal hypertension) > portal hypoplasia

No effect

JVIM 2019 Sakamoto

90
Q

How do the following affect likelihood of recovery from PSS surgery?

Albumin
DHD
ERLEC1
LRSMD2

A

Higher alb –> more likely to recover

Others had no effect

JVIM 2019 Van den Bossche

91
Q

Dogs with congenital PSS completely attenuated via sx generally have an excellent outcome. Based on one study, what proportion of dogs with only partial attenuation have a similar outcome?

A

20%

JSAP 2018 Tivers

92
Q

How long on average does it take for thin film to cause complete PSS occlusion?

A

8 weeks

JVIM 2019 Serrano

93
Q

How can an Ameroid accidentally cause an acute occlusion of PSS?

A

If it causes a kink

JVIM 2019 Serrano

94
Q

Based on a 2019 meta-analysis, what PSS closure achieves the best occlusion and QoL outcome?

Suture ligation
Thin film
Ameroid
Coil

A

Ameroid

JVIM 2019 Serrano

95
Q

Sodium benzoate and sodium phenylacetate bind glycine (which contains nitrogen) –> urinary excretion. It can effectively lower ammonia in people. What is its effect in congenital PSS dogs?

A

Small study (N=10) – no effect on ammonia or CS

JVIM 2019 Straten

96
Q

What is the most common presentation in cats with congenital PSS?
–Signalment
–CS (name three)
–Extra vs intrahepatic

A

–Young male DSH
–Neuro/abnormal behavior 82%, ptyalism 73% (rare in PSS dogs), copper iris inappropriate for breed 38%
–Extrahepatic

JVIM 2019 Valiente

97
Q

Regarding a study of CPSS cats treated with thin film attenuation:
–Most common complication? Can you do anything pre-op to prevent?
–One uncommon but weird complication? Does this tend to be permanent or transient?
–Two other uncommon but significant potential complications?

A

Seizures 23%. Pre-op keppra didn’t make a difference.

Reduced vision/blindness 5% (more common in other studies), usually resolves within 2mo

Coma, acquired PSS

JVIM 2019 Valilente

98
Q

Regarding a study of CPSS cats treated with thin film attenuation:
–Post op mortality rate?
–Proportion that do well if they survive the immediate post op period?
–Median time to normalized BA?

A

12%

90%

3mo

JVIM 2019 Valiente

99
Q

If cPSS dogs treated with surgical attenuation develop post op neuro signs:

Proportion that had sz? Proportion of recurrent sz?

Proportion that hand non-sz neuro signs? Proportion that eventually resolved?

A

Sz: 60% post op, 50% recurrent

Non-sz neuro: 40% post op, resolved in 70%

JAVMA 2020 Carrera

100
Q

Regarding cats with hepatopathy given mirtazapine:

Is time to max concentration shorter or longer than healthy cats?

T1/2 shorter or longer? Does it correlate with ALT and/or Tbili?

How should you change dosing recommendations?

A

Longer (4hrs vs 1hr)

Longer (14hr vs 7hr) – correlated with ALT and Tbili.

Increase the dose interval

JVIM 2018 Fitzpatrick

101
Q

Are the following higher, lower, or no difference in cats with hepatic lipidosis vs healthy:

LDL
HDL
Chol
TG

A

Higher LDL
Lower HDL
No difference Chol, TG

JFMS 2019 Minamoto

102
Q

Regarding death due to multiple acquired PSS (MAPSS):
–MST?
–Three factors that incr risk of dying from MAPSS related cause vs non-MAPSS related cause?
–No effect on risk (two factors)?

A

MST 1.5yrs

Higher body weight, biochem evidence of progressive liver dysfunction, mentation changes at diagnosis

Prior PSS attenuation, ascites

JAVMA 2021 Anglin

103
Q

Name six breeds with incr risk of GB mucocele (hint – all are small or medium sized).

A

Sheltie
American cocker
Chi
Pom
Mini schnauzer
Border terrier (85x risk in the UK)

JVIM 2019 Allerton

104
Q

What proportion of dogs with GB mucocele and cholecystectomy have cholecystitis? Was this associated with mortality?
How many were culture positive (note – most had pre-op abx)?

A

30%, no association with mortality
14%

JVECC 2019 Rogers

105
Q

True or False: CT cholangiography can somewhat estimate patency in dogs with GB mucocele.

A

True

JSAP 2019 Hayakawa

106
Q

Are GB wall thickness and albumin correlated?

A

No

JSAP 2021 Sparago

107
Q

In dogs with GB mucocele:
–Mortality for elective vs sick/nonelective cholecystectomy?
]–Factors that increased risk of mortality? (CS, biochem, sx findings)

A

20-23% sick/nonelective, 2-6% elective

Incr mortality:
–Sick
–GB rupture – OR 2.7
–Higher ALT, Tbil, azotemia
–Lower Alb

JAVMA 2018 Youn
JVIM 2019 Parkanzky
JVIM 2019 Jaffey
JSAP 2021 Friesen

108
Q

How do the following affect mortality in dogs with GB mucocele treated surgically?

Bacterial cholangitis
Abx
Time from AUS identification of mucocele to time of sx

A

No effect

JVIM 2018 Jaffey

109
Q

In general, how does AUS perform in identifying GB rupture?

A

Overall seems like sensitivity is poor and specificity is variable depending on the study. Probably operator dependent.

JVIM 2019 Jaffey
JVIM 2019 Parkanzky

110
Q

Compare MST for medically vs surgically managed GB mucocele.

A

Med - MST 3.7yrs
Sx (if survives post op period): MST 5yrs

JVIM 2019 Parkanzky

111
Q

In dogs who underwent cholecystectomy for non-gravity dependent biliary sludge:
–Most common histopath findings (name 3)?
–Was there clinical benefit?

A

Cholecystitis (usually lymphoplasmacytic) 75%
Reactive hepatitis 56%
Enteritis 75%

Most had improvement or resolution of CS

JSAP 2021 Vijoen

112
Q

Most common findings in dogs with GB agenesis:
–Signalment
–CS
–Labwork abnormality
–Concurrent structural changes
–Liver histopath diagnosis

What two big tests offer the best diagnostic approach?

A

–Young, chihuahua, boxer
–Nonspecific GI, ascites
–Incr ALT
–CBD dilation, malformed liver lobes, acquired PSS (30%)
–DPM 94%

CT cholangiography + lap liver bx

JVIM 2019 Sato

DACVIM Literature 2018-2023 (13 decks)

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