Liver Flashcards
(112 cards)
1
Q
A defect in what basic cellular component results in ductal plate malformation?
A
Primary cilia
JVIM 2021, Siebert
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
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
4
Q
Which ductal plate malformation causes malformed medium to large bile ducts, diverticula, etc?
A
Caroli DPM
JVIM 2021, Siebert
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
6
Q
Which ductal plate malformation incurs increased risk for choleliths?
A
Caroli DPM
JVIM 2021, Siebert
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
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
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
10
Q
Which ductal plate malformations are more common in cats > dogs?
A
Choledochal cyst DPM, expansive cystadenoma DPM
JVIM 2021, Siebert
11
Q
Which ductal plate malformations can progress to congenital hepatic fibrosis?
A
Proliferative-like DMP, Caroli DPM
JVIM 2021, Siebert
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
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
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
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
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
17
Q
Which endocrinopathy frequently accompanies hepatocutaneous syndrome?
A
Diabetes mellitus
JVIM 2021, Loftus
18
Q
Which two amino acids are frequently found in the urine of dogs with hepatocutaneous syndrome?
A
Lysine, methionine
JVIM 2021, Loftus
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
20
Q
What is presumed to cause hepatocutaneous syndrome in people?
A
Glucagonoma
JVIM 2021, Loftus
21
Q
What two CBC abnormalities are associated with ACHES-SND vs ACHES without SND?
A
SND –> anemia, microcytosis
JVIM 2021, Loftus
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
23
Q
What liver histopath finding is pathognemonic for ACHES?
A
Proliferative hepatocellular foci (different from regenerative nodules)
JVIM 2021, Loftus
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
25
Which medication is associated with developing ACHES? How does discontinuing it affect survival?
Phenobarbital; d/c'ing does not seem to affect survival
JVIM 2021, Loftus
26
What are the three basic pillars of ACHES treatment? List them in order of anticipated relative benefit.
Home-cooked diet, AA +/- lipid infusions, enteral supplements
JVIM 2021, Loftus
27
What is the dosing frequency of AA +/- lipid infusions in dogs with SND?
q7-10d until skin lesions resolve, then q3-6 weeks
JVIM 2021, Loftus
28
How quickly do SND lesions respond to AA +/- lipid infusions?
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
29
Name at least three enteral supplements to consider for ACHES.
Proline, lysine, arginine/ornithine, glutathione, SAMe (not proven to be low in ACHES dogs but easy to supplement)
JVIM 2021, Loftus
30
What is the downstream product of SAMe?
Glutathione
JVIM 2021, Loftus
31
What is the target protein % for diet in treatment of ACHES? Is a balanced commercial diet or home cooked preferred?
50% of metabolizable energy (ME) from protein. Home cooked (developed by nutritionist) > commercial diet.
JVIM 2021, Loftus
32
How does diabetes mellitus affect prognosis of ACHES?
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
33
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?
Optimal tx MST >4.8 years, other tx combos 7mo
JVIM 2021, Loftus
34
Does hepatic lead correlate positively or negatively with hepatic copper? This is especially true at what copper threshold?
Positive, esp at Cu >400
JVIM 2021, Gori
35
What peripheral and bone marrow effects are seen with acute lead poisoning? What are the two basic mechanisms?
--Anemia (most common), basophilic stippling, decr M:E, ineffective erythropoiesis
--Interferes with heme synth, causes RBC oxidative stress
JVIM 2021, Gori
36
What are the three possible etiologies of hepatic copper accumulation? Which of these may play a role in lead accumulation?
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
37
What are three underlying mechanisms that can cause incr bile acids?
1) liver dysfunction --> decr portal BA clearance
2) PSS
3) bile stasis
JVIM 2021, Pena-Ramos
38
Can pre/post BA differentiate between different types of hepatopathies?
No -- lots of overlap between diseases
JVIM 2021, Pena-Ramos
39
Can normal dogs have high bile acids, and vice versa?
Yes. Even dogs with liver vascular anamolies can have normal BA.
JVIM 2021, Pena-Ramos
40
Can normal dogs have high bile acids, and vice versa?
Yes. Even dogs with liver vascular anomalies can have normal BA.
JVIM 2021, Pena-Ramos
41
Are pre or post BA more sensitive for liver disease? Which is more specific?
Pre BA are more specific, post BA are more sensitive
JVIM 2021, Pena-Ramos
42
What is the typical BCAA:AAA in healthy dogs vs APSS dogs?
Healthy 3-4
APSS <1.5
JVIM 2021, Devriendt
43
BCAA vs AAA
Which are typically metabolized by the liver vs muscle?
BCAA - muscle
AAA - liver
JVIM 2021, Devriendt
44
Other than high ammonia and low BCAA:AAA, name at least two other causes for hepatic encephalopathy.
High glutamine, glutamate, Mn, systemic inflamm
JVIM 2021, Devriendt
45
How does medical management (diet, medications) affect the amino acid profile of PSS dogs?
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
In a small study of cPSS treated with surgical attenuation, what was their BCAA:AAA at 3 months?
1.5 -- significantly better than at dx (0.6) but not as good as it should be (normal = 3-4)
JVIM 2021, Devriendt
47
Which seems more important in PSS/HE dogs, BCAA or AAA? Why?
AAA because typically out of ref range. BCAA were low end preop and high end postop, but still WNL.
JVIM 2021, Devriendt
48
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
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
At what time interval post op can the lidocaine/MEGX test detect complete APSS closure?
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
Are GB mucoceles associated with a primarily HYPER or HYPOcoagulable state?
HYPERcoagulable
JVIM 2021, Pavlick
51
Is proteinuria positively, negatively, or not associated with GB mucocele? Does illness severity and/or cholesterol affect this?
Proteinuria is positively associated with GB mucocele and correlates with illness severity; does not correlate with cholesterol
JVIM 2021, Lindaberry
52
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?
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
What is the typical presentation (CS, PE) of cats with EHBO?
CS nonspecific (v+, hyporexia, lethargy, weight loss, icterus)
PE usually pretty stable, variable BCS but mean 4/9, 74% icteric
JVIM 2021 Griffin
54
True or False:
A lack of clinical icterus rules out severe hyperbilirubinemia.
False
JVIM 2021 Griffin
55
What are at least 3 common AUS findings in cats with EHBO?
--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
How does tbili prior to discharge affect prognosis in cats with EHBO treated with biliary stenting?
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
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?
--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
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?
--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
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?
--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
True or False:
Dogs with cholelithiasis are usually sick but signs are typically vague.
False; most are asymptomatic (but when present, CS are vague)
JVIM 2021, Allan
61
What is the difference between typical cholelith composition in people vs dogs?
Humans: cholesterol based
Dogs: Calcium carbonate + chol + bili
JVIM 2021, Allan
62
What are the three MoA's of ursodiol?
Displaces hydrophobic BA, choleretic, anti-inflammatory
JVIM 2021, Allan
63
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?
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
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?
Unlikely. Most symptomatic dogs have choledocoliths and more significantly elevated LEs.
JVIM 2021, Allan
65
A small study found that what proportion of medically managed (ie, ursodiol +/- abx) cholelith dogs had improvement (dissolution vs passage) of stones?
38%; most of these had complete resolution
JVIM 2021, Allan
66
Dogs with symptomatic cholelithiasis tend to be younger or older?
Younger -- also seen in people
JVIM 2021, Allan
67
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?
--Hemorrhage 42%, associated with higher pre-bx PCV (contradicts other studies), most asymptomatic
--Major hemorrhage 2%, associated with neoplasia
JVIM 2020, Reece
68
What dog breed with GB mucocele can have decr CCK and incr transglutaminase-2-IgA? What condition is this similar to in people?
Border terriers
Celiac
JSAP 2020 Barker
69
True or False: Cats with intrahepatic PSS can be successfully treated with coil embolization.
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
True or False: De novo lipogenesis is a significant driver of hepatic lipidosis.
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
True or False: Cholestatic liver disease in cats is not associated with low vit D.
False. 33% have low vit D compared with 17% of extrahepatic illness cats.
JVIM 2020 Kibler
72
True or False: microRNA-122 can differentiate healthy vs hepatopathy dogs.
True. Sens 77, spec 97 at cutoff >3K.
JVIM 2018 Oosthuyzen
73
How does body condition affect portal blood flow in dogs?
Overweight --> lower portal velocity and lower flow volume
JVIM 2018 Belotta
74
Can RBC and/or plasma glutathione be used to estimate liver glutathione?
No - no correlation
JVIM 2018 Barry
75
What is the clinical significance of branching mineralization of the biliary tree? What breed is overrepresented?
Means nothing
CKCS
JSAP 2018 Genain
76
Shear wave elastography is a type of imaging. Can it differentiate the following groups of dogs?
Clinically relevant liver fibrosis
Mild hepatitis +/- fibrosis
Healthy
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
Can plasma free amino acid profiles differentiate the following groups?
HCC
Benign hepatopathy
Healthy
No
JVIM 2019 Leela-arporn
78
Are the following higher, lower, or similar liver bx of HCC dogs vs healthy?
Cu
Zn
Higher Cu, lower Zn
JVIM 2019 Harro
79
Which correlates best with copper quantification:
Digital image analysis
Spectroscopy
Which groups of dogs have higher Cu?
Younger vs older
Small vs large breed
Digital image analysis
Older, large breed
Also high Cu in necroinflamm disease
JAVMA 2021 Miller
80
True or false: Copper staining in feline liver biopsies correlates well to copper quantification.
False. Study found that 31% were above RI, but only 11% stained positive and 2.5% score >3
JFMS 2021 Yamkate
81
In cats with cholestatic liver disease assessed via TEG:
% hypercoag?
% hypocoag? Significance?
50% hypercoag
22% hypocoag -- prolonged PT/PTT agreed with TEG. Synthetic liver failure.
JFMS 2021 Kakar
82
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?
--30% each
--About half
--Almost all are chronic neutrophilic inflamm
JVIM 2018 Harrison
83
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)
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
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)
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
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?
80%
2.5mo
No effect
JVIM 2019 Ullal
86
What is tetrathiomolybdate (TTM)? What is it used to treat in people and experimentally in dogs? How does it work?
Copper chelator. Binds Cu+alb --> bile excretion. Tx Wilson's disease in people, experimentally Cu hepatopathy in dogs.
JVIM 2019 Langlois
87
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?
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
What is ATP7B? Mutations in this are associated with what disease?
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
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?
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
How do the following affect likelihood of recovery from PSS surgery?
Albumin
DHD
ERLEC1
LRSMD2
Higher alb --> more likely to recover
Others had no effect
JVIM 2019 Van den Bossche
91
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?
20%
JSAP 2018 Tivers
92
How long on average does it take for thin film to cause complete PSS occlusion?
8 weeks
JVIM 2019 Serrano
93
How can an Ameroid accidentally cause an acute occlusion of PSS?
If it causes a kink
JVIM 2019 Serrano
94
Based on a 2019 meta-analysis, what PSS closure achieves the best occlusion and QoL outcome?
Suture ligation
Thin film
Ameroid
Coil
Ameroid
JVIM 2019 Serrano
95
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?
Small study (N=10) -- no effect on ammonia or CS
JVIM 2019 Straten
96
What is the most common presentation in cats with congenital PSS?
--Signalment
--CS (name three)
--Extra vs intrahepatic
--Young male DSH
--Neuro/abnormal behavior 82%, ptyalism 73% (rare in PSS dogs), copper iris inappropriate for breed 38%
--Extrahepatic
JVIM 2019 Valiente
97
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?
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
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?
12%
90%
3mo
JVIM 2019 Valiente
99
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?
Sz: 60% post op, 50% recurrent
Non-sz neuro: 40% post op, resolved in 70%
JAVMA 2020 Carrera
100
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?
Longer (4hrs vs 1hr)
Longer (14hr vs 7hr) -- correlated with ALT and Tbili.
Increase the dose interval
JVIM 2018 Fitzpatrick
101
Are the following higher, lower, or no difference in cats with hepatic lipidosis vs healthy:
LDL
HDL
Chol
TG
Higher LDL
Lower HDL
No difference Chol, TG
JFMS 2019 Minamoto
102
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)?
MST 1.5yrs
Higher body weight, biochem evidence of progressive liver dysfunction, mentation changes at diagnosis
Prior PSS attenuation, ascites
JAVMA 2021 Anglin
103
Name six breeds with incr risk of GB mucocele (hint -- all are small or medium sized).
Sheltie
American cocker
Chi
Pom
Mini schnauzer
Border terrier (85x risk in the UK)
JVIM 2019 Allerton
104
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)?
30%, no association with mortality
14%
JVECC 2019 Rogers
105
True or False: CT cholangiography can somewhat estimate patency in dogs with GB mucocele.
True
JSAP 2019 Hayakawa
106
Are GB wall thickness and albumin correlated?
No
JSAP 2021 Sparago
107
In dogs with GB mucocele:
--Mortality for elective vs sick/nonelective cholecystectomy?
]--Factors that increased risk of mortality? (CS, biochem, sx findings)
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
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
No effect
JVIM 2018 Jaffey
109
In general, how does AUS perform in identifying GB rupture?
Overall seems like sensitivity is poor and specificity is variable depending on the study. Probably operator dependent.
JVIM 2019 Jaffey
JVIM 2019 Parkanzky
110
Compare MST for medically vs surgically managed GB mucocele.
Med - MST 3.7yrs
Sx (if survives post op period): MST 5yrs
JVIM 2019 Parkanzky
111
In dogs who underwent cholecystectomy for non-gravity dependent biliary sludge:
--Most common histopath findings (name 3)?
--Was there clinical benefit?
Cholecystitis (usually lymphoplasmacytic) 75%
Reactive hepatitis 56%
Enteritis 75%
Most had improvement or resolution of CS
JSAP 2021 Vijoen
112
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?
--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
