Hepatobiliary Flashcards
(482 cards)
1
Q
What is the central role of hepatocytes in the liver?
A
Metabolism, detoxification, synthesis, and immune regulation
2
Q
Why do clinical signs of liver disease often appear late?
A
Due to the liver’s substantial reserve capacity and regenerative potential
3
Q
List common signs associated with hepatic dysfunction
A
- Hepatic encephalopathy (HE)
- Coagulopathies
- Portal hypertension
- Ascites
4
Q
What are the two main causes of hepatic encephalopathy?
A
- Severe hepatic insufficiency or failure
- Vascular anomalies such as portosystemic shunts (PSS)
5
Q
How is HE classified in veterinary medicine?
A
- Type A: Acute liver failure
- Type B: Portosystemic shunting
- Type C: Cirrhosis/portal hypertension
6
Q
What are the subcategories of Type C hepatic encephalopathy?
A
- Episodic
- Persistent
- Minimal (subclinical)
- Precipitated vs. spontaneous
- Mild vs. severe
7
Q
What is the grading scale for hepatic encephalopathy in veterinary medicine?
A
- Grade 0: Asymptomatic
- Grade 1: Mild decrease in mobility or apathy
- Grade 2: Severe apathy, mild ataxia
- Grade 3: Severe ataxia, hypersalivation, head pressing, blindness, circling
- Grade 4: Stupor, coma, or seizures
8
Q
What role does ammonia play in hepatic encephalopathy?
A
Ammonia is central to HE pathophysiology, with high CNS ammonia concentrations leading to neurologic deterioration
9
Q
What are the primary sources of ammonia in the body?
A
- Enterocyte metabolism
- Intestinal microbiota
10
Q
How does ammonia clearance occur in healthy animals?
A
- Periportal Hepatocytes convert ammonia to urea
- Perivenous Hepatocytes convert glutamate and ammonia into glutamine
11
Q
What is the impact of skeletal muscle on ammonia regulation?
A
Skeletal muscle buffers systemic ammonia by converting it to glutamine, which is then released into circulation
12
Q
What is the role of astrocytes in the CNS related to hepatic encephalopathy?
A
Astrocytes convert glutamate and ammonia into glutamine and are involved in neurotransmitter cycling
13
Q
How does inflammation contribute to advanced hepatic encephalopathy?
A
Systemic inflammation and infection can outweigh ammonia as primary contributors to clinical deterioration
14
Q
What trace element is associated with neurotoxicity in hepatic encephalopathy?
A
Manganese
15
Q
What are some common electrolyte and acid-base disturbances associated with HE?
A
- Alkalosis
- Hyponatremia
- Hypokalemia
16
Q
Fill in the blank: Non-absorbable disaccharides lower colonic pH, converting ammonia (NH₃) to non-absorbable _______.
A
ammonium (NH₄⁺)
17
Q
What is a clinical response to antibiotics in the context of HE?
A
Clinical response to antibiotics occurs without other identifiable improvement factors.
18
Q
What are the clinical caveats regarding antibiotic use in HE?
A
Avoid prolonged routine use unless clearly beneficial. Withdrawal should be considered once the HE trigger resolves.
19
Q
Why is protein restriction contraindicated in growing animals with congenital PSS?
A
It may impair growth, increase risk of metabolic bone disease, and promote sarcopenia.
20
Q
What does hypoalbuminemia contribute to in liver disease?
A
- Ascites
- Impaired drug and hormone transport
- Loss of antioxidant and immune-modulatory functions.
21
Q
What should be favored in protein management for liver disease?
A
High biological value proteins rich in essential amino acids.
22
Q
What are the mechanisms of hepatic sinusoidal PH?
A
- Structural resistance increases
- Dynamic resistance increases.
23
Q
What happens to the liver’s ability to accommodate fluctuations in portal blood flow due to portal hypertension?
A
It is impaired, leading to decreased production of vasodilators and increased production of vasoconstrictors.
24
Q
What is a common complication of ascites in liver disease?
A
It is generally a poor prognostic indicator in both acute and chronic liver disease.
25
What imaging indicators suggest portal hypertension?
* Increased portal vein to aorta ratio
* Reduced portal flow velocity on Doppler ultrasound.
26
What is the role of spironolactone in the medical management of ascites?
It is an aldosterone antagonist; onset may take 1–2 weeks.
27
What does the liver synthesize that is crucial for hemostasis?
* Pro-coagulants: Fibrinogen, Prothrombin, FV, FVIII, etc.
* Anticoagulants: Antithrombin, Protein C, etc.
28
What is a common coagulation abnormality in dogs with chronic liver disease?
Mild to moderate thrombocytopenia.
29
What coagulation profile changes are seen in congenital portosystemic shunts (CPSS)?
* Elevated vWF
* Mildly prolonged aPTT
* Reduced protein C.
30
What is the recommended pre-procedural coagulation testing for high-risk patients?
* Platelets < 50,000/µL
* PT or aPTT > 1.5× reference interval
* Fibrinogen < 100 mg/dL.
31
What is the initial management of active bleeding in liver disease?
Use fresh frozen plasma (FFP) for broad coagulation support.
32
What are the components of cryoprecipitate?
* Fibrinogen
* FVIII
* vWF
* FXIII.
33
What may exacerbate GI hemorrhage in portal hypertension?
Vitamin K1 administration
## Footnote
Preemptive vitamin K1 administration is advised before invasive procedures in cats, even if PT/aPTT are normal.
34
Therapy for hyperfibrinolysis is based on what findings?
TEG findings or rebleeding episodes.
35
Prophylactic anticoagulation is not routinely recommended in liver disease due to what risks?
* Risk of GI hemorrhage
* Unpredictable drug metabolism in hepatic insufficiency
36
Acute portal vein thrombosis (PVT) may present with what symptoms?
Abdominal pain, hypovolemic shock.
37
Chronic portal vein thrombosis (PVT) is often characterized by what?
Silence, especially with APSS; it contributes to worsening portal hypertension.
38
What is the recommended management for dogs with PVT?
* Heparin or Warfarin for 6-month course
* Survival benefit observed in studies
39
What is the detection threshold for bilirubin in plasma?
Bilirubin > 1 mg/dL
40
What are the four classifications of jaundice?
* Prehepatic Jaundice
* Hepatic Jaundice
* Sepsis-Associated (Intrahepatic) Jaundice
* Posthepatic (Extrahepatic) Jaundice
41
What causes prehepatic jaundice?
Excessive hemolysis that overwhelms hepatic clearance capacity.
42
Common causes of hepatic jaundice include what mechanisms?
* Hepatocellular dysfunction
* Intrahepatic cholestasis due to inflammation, hepatic lipidosis, or fibrosis
43
How is posthepatic jaundice caused?
Partial or complete bile duct obstruction, leading to conjugated bilirubin retention.
44
What is the formation process of bilirubin?
Derived from heme breakdown via macrophages converting heme to biliverdin and then to bilirubin.
45
How is unconjugated bilirubin transported to the liver?
Binds to albumin and is lipid-soluble.
46
What is delta bilirubin?
Formed when conjugated bilirubin binds covalently to albumin.
47
What does hyperbilirubinemia indicate in terms of prognosis?
Negative prognostic marker in gallbladder mucoceles, acute and chronic liver disease.
48
What are the neurologic consequences of severe unconjugated hyperbilirubinemia?
Kernicterus (bilirubin encephalopathy).
49
What is the significance of persistent jaundice post-resolution?
May reflect delta bilirubin.
50
What are the three major groups of congenital hepatic vascular anomalies?
* Congenital Portosystemic Shunts (PSS)
* Disorders of Abnormal Portal Perfusion or Portal Vein Hypoplasia (PVH)
* Disturbances in Hepatic Venous Outflow
51
What does Portal Vein Hypoplasia (PVH) refer to?
Diminutive or absent portal vein branches within the liver.
52
What are the two classifications of PVH based on portal hypertension?
* With portal hypertension
* Without portal hypertension
53
What are the hepatic consequences of decreased hepatic perfusion?
* Hepatic atrophy
* Reduced hepatotrophic stimulation
* Impaired protein synthesis
* Endothelial dysfunction
* Metabolic disruption
54
What are common clinical signs of hepatic vascular anomalies?
* Neurologic: Hepatic encephalopathy (HE)
* GI: Chronic vomiting, diarrhea
* Urinary: Cystolithiasis, pollakiuria
* Systemic: Poor growth, coagulopathies
55
What breeds are predisposed to Intrahepatic PSS (IHPSS)?
* Large-breed dogs (e.g., Irish Wolfhound, Labrador Retriever, Golden Retriever)
56
What breeds are predisposed to Extrahepatic PSS (EHPSS)?
* Small and toy breeds (e.g., Yorkshire Terrier, Maltese, Havanese)
57
What is the prevalence of congenital portosystemic shunts (CPSS) in dogs?
Reported in 0.18% of all dogs.
58
What characterizes PVH with portal hypertension?
Markedly underdeveloped intrahepatic portal veins, leading to high resistance and the development of multiple acquired shunts.
59
What are the clinical signs of Hepatic Encephalopathy (HE)?
* Dullness
* Ataxia
* Head pressing
* Seizures
* Ptyalism
60
What are common historical findings in dogs with congenital PSS?
* Failure to thrive
* Stunted growth
* Anesthetic intolerance
* Neurobehavioral abnormalities
61
What is the median age of diagnosis for Portal Vein Hypoplasia (PVH)?
3.25 years
62
What are the key laboratory findings in dogs with PSS?
* Microcytosis
* Low BUN and albumin
* Increased serum bile acids
* Low fasting cholesterol and glucose
* Increased blood ammonia
63
What is the prognosis for dogs with PVH without a macroscopic shunt?
Tend to present later in life, show milder signs, and have better prognosis with medical management.
64
What is a significant risk factor for developing hepatic arteriovenous malformations (HAVM)?
No breed predisposition has been identified.
65
What are the genetic associations found in Yorkshire Terriers regarding PSS?
Odds Ratio (OR) of 35.9, indicating a likely heritable condition.
66
What is the typical clinical manifestation of hepatic encephalopathy worsened by?
* GI bleeding
* High-protein meals
* Hypokalemia
* Infection or inflammation
67
What breeds are overrepresented for Extrahepatic Shunts in cats?
* Domestic Shorthair
* Persian
* Siamese
* Himalayan
* Burmese
68
What is the outcome of dogs with HAVM compared to CPSS or PVH?
Generally worse prognosis but favorable outcomes can still be achieved with management.
69
What is the prevalence of urinary tract signs in animals with IHPSS?
20–50%
## Footnote
Signs include hematuria, pollakiuria, stranguria, and urethral obstruction.
70
What are common urinary tract findings in animals with CPSS?
* Ammonium urate calculi or crystalluria (30–75.7%)
* Positive urine cultures (24% of dogs)
* Cystic calculi or debris (75.7%)
* Hematuria (39%)
* Bacteriuria (19.7%)
## Footnote
Urate uroliths in cats show a median age of 2 years compared to 7 years in cats without shunts.
71
What percentage of dogs with portocaval CPSS present preoperative signs?
88%
## Footnote
58% present with signs in portoazygous CPSS.
72
What is the most common clinical sign for splenocaval shunts?
CNS signs
73
In which type of shunt are urinary signs more frequent?
Right gastric vein origin shunt
74
What concurrent congenital defect is present in 30% of male cats with CPSS?
Cryptorchidism
75
What are common clinical signs in PVH without portal hypertension?
* Similar to mild congenital shunt
* Older age of onset
* Milder signs
* Better long-term prognosis with medical management
76
What are the typical clinical signs of PVH with portal hypertension?
* Purebred dogs, typically <4 years old
* >10 kg body weight
* Ascites (60%)
* PU/PD, GI upset, weight loss
77
What may cause anemia in CPSS?
* ↓ iron transport and serum iron
* ↓ total iron-binding capacity (TIBC)
* ↑ hepatic iron sequestration in Kupffer cells
78
What serum biochemistry abnormality is common in approximately 50% of dogs with CPSS?
Low Blood Urea Nitrogen (BUN)
79
What is the typical serum enzyme pattern seen in CPSS?
Mild to moderate increases (≤2–3×) in ALT and ALP
80
What is the significance of elevated hyaluronic acid in CPSS?
Indicates decreased hepatic clearance and may serve as a marker of liver function
81
What is the prevalence of ammonium biurate crystalluria in dogs with CPSS?
26–75%
82
What is the sensitivity of postprandial blood ammonia testing for detecting PSS?
91%
83
What does an elevated serum bile acid (SBA) indicate?
* Hepatic synthesis
* Secretion
* Enterohepatic recirculation
* Hepatocyte uptake and biliary excretion
84
What can cause false positives in serum bile acid testing?
* Non-shunt hepatobiliary disease
* Cholestasis
* Medications (glucocorticoids, anticonvulsants)
85
What is the typical fluid characteristic of abdominal effusion in CPSS?
Clear, acellular, pure transudate
86
What are common histopathological findings in dogs with CPSS?
* Hypoplasia or absence of intrahepatic portal tributaries
* Increased hepatic arterial profiles
* Kuppfer cell hypertrophy
* Bile duct proliferation
87
What is the histologic change prevalence in cats with CPSS?
* Portal vein hypoplasia (100%)
* Arterial hyperplasia (100%)
* Hepatocellular microvesicular change (50%)
* Fibrosis (42.5%)
88
What is the relationship between hepatic volume and lipid content in CPSS?
Larger liver volumes correlate with fewer lipid droplets per tissue field
89
What microRNA biomarkers are elevated in intrahepatic PSS?
* miR-34a
* miR-21
90
What are the CNS changes observed in Hepatic Encephalopathy (HE)?
CNS changes in HE include:
* Polymicrocavitation in brainstem
* Polymicrocavitation in cerebellar nuclei
* Polymicrocavitation in cerebral cortex
* Hypertrophy and hyperplasia of astrocytes in cerebellar cortex
## Footnote
These changes are indicative of brain response to metabolic disturbances.
91
Which microRNA biomarkers are elevated in intrahepatic portosystemic shunts (PSS)?
miR-34a and miR-21 are elevated in:
* Intrahepatic PSS
* Splenocaval and gastrocaval extrahepatic PSS
## Footnote
They are not overexpressed in splenophrenic or splenoazygous shunts.
92
What findings may indicate microhepatica in diagnostic imaging?
Microhepatica may be present in:
* 60–100% of dogs
* ~50% of cats
## Footnote
This condition is often visualized via radiography.
93
What is the sensitivity range for ultrasonography in diagnosing PSS?
Sensitivity: 74–95% overall
* 95–100% for intrahepatic PSS
## Footnote
Specificity ranges from 67–100%.
94
What does Doppler and flow assessment reveal about HAVMs?
HAVMs show hepatofugal flow on Doppler and flow assessment.
## Footnote
This indicates abnormal blood flow direction.
95
What is the significance of portal flow velocity alterations in EHPSS and IHPSS?
Portal flow velocity is altered in:
* 53% of EHPSS
* 92% of IHPSS
## Footnote
This is critical for diagnosing different types of shunts.
96
What are the general features of Computed Tomographic Angiography (CTA)?
General features of CTA include:
* Gold standard in humans and increasingly in veterinary patients
* Non-invasive and rapid
* Allows complete vascular assessment after a single peripheral contrast injection
## Footnote
It is ideal for intrahepatic PSS and HAVMs.
97
What does transcolonic scintigraphy with Technetium-99m Pertechnetate detect?
It is a non-invasive method for detecting portosystemic shunting.
## Footnote
The technique involves radioisotope infusion and imaging via gamma camera.
98
What indicates a shunt fraction of >60–80% in scintigraphy?
>60–80% is typical for congenital PSS.
## Footnote
Cats may have lower shunt fractions compared to dogs.
99
What is the sensitivity and specificity of Gadolinium-enhanced MRA?
Sensitivity: 63–79%
Specificity: up to 97%
## Footnote
Furumoxytol-enhanced MRA is experimental but shows improved image quality.
100
What is the role of Protein C Activity in distinguishing MVD from CPSS?
Protein C Activity >70% in 88% of MVD dogs, low in CPSS.
## Footnote
This helps differentiate between true shunting disorders and MVD.
101
What nutritional management should be followed for dogs with CPSS?
Nutritional management should include:
* 18–22% protein (dry matter basis)
* Low aromatic amino acids
* High branched-chain amino acids
## Footnote
This supports liver health and minimizes HE.
102
What is the uncommon occurrence in CPSS related to ascites?
Severe hypoalbuminemia or portal hypertension
## Footnote
Common in HAVM or NCPH.
103
What is the therapy for hypoalbuminemia?
Colloid support (e.g., plasma), assess and optimize dietary protein intake
104
What is the diuretic of choice for portal hypertension?
Spironolactone
## Footnote
Due to RAAS activation in portal hypertension.
105
What are the nutraceuticals that may benefit animals with MVD or NCPH?
* SAMe
* Vitamin E
* Ursodiol
* Silymarin (milk thistle)
* L-Carnitine (cats)
106
What is the prognosis for medical therapy in CPSS without surgical intervention?
Long-term outcomes are variable but generally inferior to surgical management
107
What was the euthanasia rate in a study of dogs with CPSS treated medically?
51.8% euthanized (median 9.9 months after diagnosis)
108
What is the mortality rate for medical management of CPSS?
88% mortality/euthanasia
109
What is the surgical goal for CPSS?
Complete attenuation of the shunt to redirect portal blood to the liver
110
What is the risk associated with small, debilitated patients during surgery?
Hypothermia, hypoglycemia, intraoperative hemorrhage
111
What type of anesthetics should be avoided in hepatic disease?
Anesthetics with high hepatic metabolism or protein binding
112
What are the outcomes for Ameroid Constrictors in shunt surgery?
* Complication rates: 7–20%
* Mortality rates: 0–17%
* Good to excellent outcomes: Up to 94%
113
What is the complication rate associated with Cellophane Band (CB) attenuation?
10–13%
114
What is a common postoperative complication after EHPSS surgery?
Hypoglycemia
## Footnote
Occurs in ~44% of dogs post-surgery.
115
What should be monitored postoperatively for portal hypertension?
Vomiting, abdominal distension, progressive ascites, abdominal pain, hypotension
116
What is the reported incidence of post-attenuation seizures?
Up to 12%
## Footnote
Not linked to HE or hypoglycemia.
117
What are the surgical techniques available for intrahepatic portosystemic shunt surgery?
* Suture ligation
* Ameroid constrictor (AC)
* Cellophane band (CB)
* Hydraulic occluder (HO)
* Percutaneous transvenous coil embolization (PTCE)
118
What are the potential contributors to severe GI ulceration in IHPSS dogs?
* Abnormal GI perfusion
* Hypoprostaglandinemia
* Abnormal mucus production
* Poor mucosal turnover or integrity
119
What is a key preoperative consideration in cats with PSS?
High rate of neurologic signs
## Footnote
Preoperative anticonvulsants like Keppra or Phenobarbital are recommended.
120
What are the outcomes of using a Hydraulic Occluder (HO) in surgery?
* 100% immediate survival
* 20% intraoperative complications
* 8/10 had long-term resolution of signs
121
What is the complication rate for suture ligation in intrahepatic shunt attenuation?
29–77%
122
What is the risk of persistent or recurrent clinical signs post-surgery?
Shunt remains patent, incorrect vessel attenuated, unrecognized second shunt, development of multiple acquired shunts
123
What is the treatment for post-attenuation seizures?
* Propofol
* Phenobarbital
* Keppra (levetiracetam)
* Midazolam / Diazepam
* Acepromazine
124
What should be avoided as a preoperative anticonvulsant in cats?
Potassium bromide
125
What are the surgical techniques used in cats for PSS?
* Suture ligation
* Ameroid constrictor (AC)
* Cellophane band (CB)
126
What complication rate is associated with suture ligation in cats?
24–62%
127
What is the good-to-excellent outcome percentage for suture ligation in cats?
75%
128
What percentage of cats survived to 6 months post-CB?
83%
129
What is a common neurologic sign reported in cats post-surgery?
Seizures
130
What is a noted risk factor NOT associated with postoperative neurologic signs in cats?
Pre-op Keppra use
131
What is the definition of Hepatic Arteriovenous Malformations (HAVMs)?
Rare congenital vascular malformations involving multiple high-pressure arterial communications with the portal vein.
132
What imaging techniques are essential for identifying HAVMs?
* CT angiography (CTA)
* Magnetic resonance angiography (MRA)
* Conventional angiography
133
What percentage of dogs with HAVMs develop multiple acquired portosystemic shunts?
Nearly all, except those with concurrent intrahepatic PSS
134
What is the best surgical treatment for focal lesions in HAVMs?
Liver lobectomy
135
What is the perioperative survival rate for surgery alone in HAVM treatment?
75–91%
136
What long-term medication is often used in IHPSS and HAVM patients?
Proton pump inhibitors (PPIs) such as Omeprazole
137
What is the median survival time for patients with Intrahepatic Portosystemic Shunts (IHPSS)?
1–3 years
138
What are positive prognostic factors for medical management of hepatic vascular anomalies?
* Older age at onset of clinical signs
* Minimal clinical signs
* Stable portal blood flow
139
What is a negative prognostic factor for medical management of hepatic vascular anomalies?
Occurrence of postoperative seizures
140
What is the mortality rate associated with the use of ameroid constrictors in EHPSS?
~7%
141
What long-term outcome percentage is associated with glue embolization in HAVM treatment?
10–70% good/fair outcomes
142
What percentage of cats with persistent CNS dysfunction may require euthanasia post-surgery?
33%
143
What is the complication rate associated with cellophane band treatment in cats?
66–100%
144
What is the primary source of blood supply in HAVMs?
Hepatic artery
145
What is the outcome for cats with microvascular dysplasia (MVD) when managed medically?
~92% long-term survival
146
What is the postoperative complication rate for cats undergoing PSS surgery?
Up to 75%
147
What is the risk of intraoperative hemorrhage noted in HAVM treatments?
High risk
148
What are ductal plate malformations (DPMs)?
A complex spectrum of developmental abnormalities arising from defective remodeling of the embryonic biliary ductal system
## Footnote
DPMs can manifest as discrete conditions or coexist as a continuum.
149
What does the ductal plate normally develop into?
Mature network of intrahepatic bile ducts and ductules
## Footnote
The ductal plate is a periportal sheet of biliary precursor cells.
150
What is the embryonic origin of the liver and biliary system?
Hepatic diverticulum (liver bud) from the endodermal epithelium of the ventral foregut
## Footnote
This process is broadly conserved across mammals.
151
What induces biliary differentiation in periportal hepatoblasts?
Activin/TGF-β gradients, Hepatocyte nuclear factor 6 (HNF6), NOTCH and WNT signaling pathways
## Footnote
These signals guide intrahepatic bile duct formation.
152
What are the histologic features of complete failure of ductal plate remodeling?
Dilated ring-like bile duct profiles encircling a central fibrovascular core
## Footnote
Partial remodeling may present as C-shaped ducts or curved luminal segments.
153
What abnormality is often associated with ductal plate malformations?
Abnormal portal vein development
## Footnote
Characterized by a dense plexiform network of hypoplastic, closely spaced portal vessels.
154
How can DPMs be clinically relevant in veterinary patients?
They may be mistaken for other hepatobiliary diseases
## Footnote
DPMs should be considered in young animals with progressive liver dysfunction.
155
What is the gold standard for diagnosing DPMs?
Histopathologic evaluation
## Footnote
Imaging and immunohistochemical markers can provide supportive evidence.
156
What are choledochal cysts?
Segmental dilatations of the extrahepatic and/or intrahepatic bile ducts
## Footnote
They communicate with the biliary system, hence not true cysts.
157
What are the two distinct phenotypes of Caroli disease?
* Caroli Disease: Isolated bile duct ectasia without hepatic fibrosis
* Caroli Syndrome: Bile duct ectasia with concurrent congenital hepatic fibrosis
## Footnote
Both are recognized as phenotypic variants of ductal plate malformation.
158
What are common clinical signs of Caroli disease and syndrome in dogs?
* Vomiting
* Polyuria/polydipsia
* Ascites
* Anorexia
* Weight loss
* Jaundice
* Neurologic signs
## Footnote
Clinical signs depend on the extent of bile duct dilatation and degree of hepatic fibrosis.
159
What laboratory findings may indicate Caroli disease or syndrome in dogs?
* Elevated ALT, AST, ALP, GGT, bilirubin, and bile acids
* Leukocytosis
* Non-regenerative anemia
* Azotemia and isosthenuria (if concurrent CKD is present)
## Footnote
These findings help in diagnosis.
160
What is the significance of portal mesenchyme in biliary tract development?
It induces hepatoblast differentiation and guides ductal remodeling
## Footnote
The ductal plate supports the development of intrahepatic arterial vessels.
161
What conditions may be associated with DPMs?
* Congenital hepatic fibrosis
* Caroli-like malformations
* Biliary cystic disease
## Footnote
These syndromes suggest a shared embryological basis.
162
What is an extrahepatic portosystemic shunt?
A vascular anomaly where blood bypasses the liver's normal filtration process.
163
What laboratory findings may indicate extrahepatic portosystemic shunt in dogs?
* Elevated ALT, AST, ALP, GGT, bilirubin, and bile acids
* Leukocytosis
* Non-regenerative anemia
* Azotemia and isosthenuria (if concurrent CKD is present)
164
What imaging findings are associated with extrahepatic portosystemic shunt?
* Multiple cystic intrahepatic biliary dilations that communicate with the biliary tree
* Calcification, renal cysts, portosystemic shunting, or cholelithiasis may also be present
* CT can reveal the 'central dot sign'
165
What is the gold standard for advanced diagnostics in humans for extrahepatic portosystemic shunt?
* Magnetic resonance cholangiopancreatography (MRCP)
* Endoscopic retrograde cholangiopancreatography (ERCP)
* Percutaneous transhepatic cholangiography
166
What is required for a definitive diagnosis of Caroli syndrome?
Liver biopsy showing cystic bile duct dilation and histologic evidence of congenital hepatic fibrosis.
167
What treatment options are available for extrahepatic portosystemic shunt?
* Supportive care: IV fluids, antibiotics for bacterial cholangitis, symptomatic management
* Medical therapy: Ursodiol, hepatic antioxidants
* Surgical options: Partial hepatectomy or liver lobectomy in localized disease
168
What is the prognosis for dogs and cats with extrahepatic portosystemic shunt?
Guarded due to risk of recurrent infection, portal hypertension, and liver failure.
169
What does polycystic liver disease (PLD) encompass?
A group of genetic disorders resulting in progressive expansion of fluid-filled hepatic cysts.
170
What is the hypothesized cause of polycystic liver disease (PLD)?
DPM of medium-sized intrahepatic bile ducts where cells proliferate abnormally.
171
What are common clinical signs of polycystic liver disease (PLD) in dogs?
* Organomegaly
* Hepatic failure
* Abdominal distension
172
What imaging findings are associated with polycystic liver disease (PLD)?
Ultrasound reveals thin-walled, fluid-filled, anechoic cysts within the hepatic parenchyma.
173
What is the recommended management for polycystic liver disease (PLD)?
* Supportive care (dietary management, hydration)
* CKD treatment (if present)
* Surgical options for localized cysts
174
What is congenital hepatic fibrosis (CHF)?
A condition resulting from defective remodeling of small intrahepatic bile ducts characterized by periportal or bridging fibrosis.
175
What laboratory findings may indicate congenital hepatic fibrosis (CHF)?
* Mild to moderate increases in ALT, AST, ALP, GGT
* Non-hyperbilirubinemia is common
* Elevated bile acids and ammonia may be noted
176
What are the clinical signs of congenital hepatic fibrosis (CHF)?
* Ascites
* Anorexia
* Vomiting
* Neurologic signs (hepatic encephalopathy)
177
What is the prognosis for congenital hepatic fibrosis (CHF)?
Varies based on severity of fibrosis and presence of portal hypertension; long-term survival is possible.
178
What are Von Meyenburg Complexes (VMCs)?
Rare, benign nodular malformations from abnormal remodeling of peripheral interlobular bile ducts.
179
What is the typical size of Von Meyenburg Complexes (VMCs) in humans?
Typically <1.5 cm in diameter.
180
What is the treatment and prognosis for Von Meyenburg Complexes (VMCs)?
No treatment is required; prognosis is excellent.
181
What is the definition of ALF in dogs and cats?
Acute onset of clinical signs of severe hepatocellular injury, hyperbilirubinemia, and coagulopathy with prolonged prothrombin time > 1.5× the upper reference interval
## Footnote
Encephalopathy is not required for diagnosis in veterinary patients.
182
What percentage of etiologies were identified in a study of dogs with ALF?
37%
183
What are the main triggers for systemic inflammatory responses in ALF?
* Kupffer cells
* Circulating monocytes
184
What cytokines are released during hepatocyte necrosis?
* Pro-inflammatory: TNF-α, IL-6, IL-1β
* Compensatory anti-inflammatory: IL-4, IL-10
185
What percentage of dogs with ALF showed signs of hepatic encephalopathy?
57%
186
What mediates cerebral edema in hepatic encephalopathy?
Cytokine-induced BBB permeability, astrocyte swelling, and cerebral hyperemia
187
What are the risk factors for developing intracranial hypertension in ALF?
* Severe HE
* High serum ammonia
188
What are some cardiovascular sequelae of liver failure?
* Mimics vasodilatory septic shock
* Relative adrenal insufficiency in 62% of humans with ALF
189
What is a particularly toxic drug for cats?
Acetaminophen
190
What are some neoplastic causes of liver disease?
* Lymphoma
* Histiocytic sarcoma
* Massive hepatocellular carcinoma
191
What are the signs of hepatic encephalopathy in dogs?
* Behavioral changes
* Neurologic signs: circling, head pressing, blindness
192
What are physical examination findings in acute liver disease?
* Icterus
* Oral ulceration
* Respiratory signs
* Abdominal pain
* Pyrexia
193
What percentage of dogs with ALF had thrombocytopenia according to one study?
92%
194
What urinary finding might indicate renal injury in acute liver disease?
Glucosuria
195
True or False: Hepatic encephalopathy is always present in cases of acute liver failure in veterinary patients.
False
196
What is the primary factor affecting thrombopoietin production?
Platelet clearance
## Footnote
Factors include SIRS, immune-mediated processes, splenic sequestration, and consumption due to hemorrhage, DIC, or thrombosis.
197
What urinalysis finding indicates possible renal injury?
Glucosuria, cylindruria, proteinuria, Fanconi-like syndrome
## Footnote
These findings may be seen with toxins such as leptospira, lomustine, carprofen, and others.
198
Which coagulation factors are synthesized in the liver?
All except factor VIII
## Footnote
This includes anticoagulants like antithrombin and protein C/S, as well as fibrinolytic proteins.
199
What may cause Vitamin K deficiency?
Cholestasis, malnutrition, antibiotics
## Footnote
These conditions affect the carboxylation of factors II, VII, IX, and X.
200
What imaging findings may thoracic radiographs reveal in acute liver disease?
Pleural effusion, metastasis, alveolar lung patterns
## Footnote
These patterns may be due to ARDS, aspiration pneumonia, atelectasis, hemorrhage, or pulmonary thromboembolism.
201
What are common ultrasound findings in acute liver disease?
Hepatomegaly, hyperechogenicity, hypoechogenicity, ascites
## Footnote
Renal changes may also include increased cortical echogenicity and pyelectasia.
202
What is the most common histologic diagnosis in acute liver disease?
Hepatic necrosis
## Footnote
This can be classified as centrolobular, periportal, or panlobular.
203
What is a significant cause of fatal acute liver disease in unvaccinated dogs?
Infectious Canine Hepatitis (CAV-1)
## Footnote
It is particularly common in young animals and is transmitted via oral-nasal exposure.
204
What factors may increase the risk of Drug-Induced Liver Injury (DILI)?
Genetic predisposition, pre-existing liver disease, co-administration of multiple drugs
## Footnote
Other factors include advanced age and immune-mediated responses.
205
What diagnostic techniques are used for confirming infectious causes of acute liver disease?
Histopathology, cytology, serology, immunohistochemistry, PCR
## Footnote
Bacterial hepatitis is diagnosed by bioculture and liver culture.
206
What are the clues suggesting DILI?
* Temporal association between drug initiation and onset of liver injury
* Known hepatotoxic potential of the drug
* Hypersensitivity signs: pyrexia, rash, arthralgia, eosinophilic leukocytosis
207
What does the R value classify in humans regarding liver injury?
* R > 5: hepatocellular (cytotoxic)
* R < 2: cholestatic
* R = 2–5: mixed pattern
208
What histopathological findings are associated with cytotoxic DILI?
Acute hepatic necrosis, minimal inflammation.
209
What histopathological findings are associated with cholestatic DILI?
Bile duct injury, cholestasis.
210
What is the role of corticosteroids in treating DILI?
May be useful in cases with hypersensitivity or immune-mediated acute liver failure.
211
What is the toxic metabolite associated with acetaminophen?
N-acetyl-p-benzoquinone imine (NAPQI).
212
What is the primary route of acetaminophen metabolism?
Glucuronidation/sulfation.
213
What is the hepatotoxic dose of acetaminophen in dogs?
>100 mg/kg.
214
What are common clinical signs of acetaminophen toxicity in dogs?
* Brown/cyanotic mucous membranes
* Facial and paw edema
* Depression, dyspnea
215
What treatment is recommended for acetaminophen toxicity?
N-acetylcysteine (NAC).
216
What are the histopathological findings associated with phenobarbital hepatotoxicity?
* Bridging portal fibrosis
* Nodular regeneration
* Biliary hyperplasia
217
What is a serious risk associated with zonisamide?
Idiosyncratic DILI reported within 3 weeks of treatment onset.
218
What is the mechanism of action for azathioprine?
Purine analog used in immune-mediated diseases.
219
What breed may be predisposed to azathioprine hepatotoxicity?
German Shepherds.
220
What should be monitored during the first 4 weeks of azathioprine treatment?
Liver enzymes.
221
What is the mechanism of action for azole antifungals?
Metabolized into oxidative intermediates that bind to hepatic proteins.
222
What is the most hepatotoxic aflatoxin?
Aflatoxin B1.
223
What is the mechanism of Sago Palm toxicosis?
Hepatotoxic, carcinogenic, neurotoxic, teratogenic.
224
What is the primary toxin in xylitol that causes hepatotoxicity?
Triggers acute insulin release, leading to hypoglycemia.
225
What is a key clinical sign of xylitol toxicity within 30 minutes?
Hypoglycemia.
226
What is the main mechanism of action for Amanita phalloides toxins?
Inhibit RNA polymerase II.
227
What treatment is effective against Amanita phalloides toxicosis?
Penicillin G and silymarin.
228
Fill in the blank: The primary clinical sign of methimazole-induced liver injury is _______.
cholestatic hepatopathy.
229
What is the mechanism of action for lomustine-induced hepatotoxicity?
Glutathione depletion and lipid peroxidation.
230
What is the typical timing for the onset of sulfonamide-induced hepatotoxicity?
5–36 days post-exposure.
231
What histopathological finding is associated with acute liver failure?
Panlobular hepatic necrosis
232
What is the mortality rate observed in one study of acute liver failure in dogs?
74% died or were euthanized; 26% survived
233
What indicators suggest autoimmune acute liver failure (ALF) in dogs?
Lymphoplasmacytic inflammation on biopsy, acute presentation
234
What is the initial treatment for autoimmune acute liver failure?
Steroids may be beneficial if initiated early
235
Which fluid is preferred over lactated Ringer's for rehydration in acute liver failure?
0.9% NaCl
236
What is a potential risk of fluid overload in patients with acute liver failure?
May exacerbate ARDS, portal hypertension, and cerebral edema
237
What is the mechanism of lactulose in managing hepatic encephalopathy?
Decreases colonic pH, converts ammonia to ammonium, increases fecal excretion
238
What type of antibiotics are used to target urease-producing gut flora?
* Rifaximin
* Neomycin
* Amoxicillin
* Metronidazole
239
What is one method to temporarily reduce intracranial pressure?
Hyperventilation
240
What are the benefits of using N-Acetylcysteine (NAC) in acute liver failure?
Replenishes intracellular glutathione, scavenges free radicals, improves microcirculatory function
241
What is the mechanism of Silymarin in treating acute hepatotoxicity?
Inhibits lipid peroxidation and cytochrome P450, acts as a free radical scavenger
242
What is the recommended approach for managing coagulopathy in acute liver failure in humans?
Focus on managing bleeding, not normalizing coagulation parameters
243
What is a negative prognostic indicator in dogs with acute liver failure?
* Hyperbilirubinemia
* Hypoalbuminemia
* Hypercholesterolemia
244
What does a >50% decline in ALT over several days indicate in dogs with acute liver failure?
May reflect viable hepatocytes with greater enzyme release
245
What is chronic hepatitis in dogs?
A histopathologic diagnosis characterized by hepatocellular apoptosis or necrosis, mononuclear or mixed inflammatory infiltrates, fibrosis, and regenerative changes.
## Footnote
It is an important cause of morbidity and mortality in dogs, identified in 12% of dogs examined in a necropsy-based study.
246
What are the liver enzyme changes in chronic hepatitis?
Variable to marked increase in liver enzymes.
## Footnote
In contrast, reactive hepatopathy shows mild elevation.
247
What is the significance of drug- and toxin-induced hepatitis in chronic hepatitis cases?
Certain agents can contribute to chronic hepatic inflammation despite most liver injuries being acute.
## Footnote
Important to obtain a thorough history of all medications, including herbal supplements.
248
Name some drugs implicated in chronic hepatitis.
* Phenobarbital
* Lomustine
* Primidone
* Phenytoin
* Carprofen
* Amiodarone
* Oxybendazole
249
What infectious agents may mimic chronic hepatitis in dogs?
* Leishmania
* Histoplasma
* Heterobilharzia americana
* Mycobacteria
* Leptospira
* Neospora
* Toxoplasma
* Sarcocystis
250
What is Copper-Associated Chronic Hepatitis (CACH)?
A condition where copper accumulates in hepatocytes due to impaired biliary excretion or excessive dietary intake.
## Footnote
It generates hydroxyl radicals that cause oxidative damage.
251
What breeds are predisposed to Copper-Associated Chronic Hepatitis?
* Bedlington Terrier
* Labrador Retriever
* Doberman Pinscher
* Dalmatian
* West Highland White Terrier
252
What are the clinical signs of chronic hepatitis in dogs?
* Decreased appetite (61%)
* Lethargy/depression (56%)
* Icterus (34%)
* Ascites (32%)
* PU/PD (30%)
* Vomiting (24%)
* Diarrhea (20%)
* Hepatic encephalopathy (7%)
* Melena (6%)
253
What is the median age at diagnosis for chronic hepatitis in dogs?
7.2 years
## Footnote
The range of ages can be wide.
254
What are the histopathologic features of immune-mediated chronic hepatitis?
* Lymphoplasmacytic infiltration
* Interface hepatitis
* Hepatocellular apoptosis and necrosis
* Progressive fibrosis
255
What is Lobular Dissecting Hepatitis (LDH)?
An aggressive variant of chronic hepatitis seen mostly in young dogs, characterized by bands of myofibroblasts and rapid progression to cirrhosis.
256
What are common laboratory findings in chronic hepatitis?
* Normocytic, normochromic, nonregenerative anemia
* Thrombocytopenia
* Increased ALT
* Increased ALP
* Prolonged PT, aPTT
257
What is the significance of copper quantification in chronic hepatitis?
It is vital in breeds at risk for copper-associated hepatitis, using methods such as atomic absorption spectroscopy.
258
What is the effect of chronic inflammation on the liver?
It initiates recruitment of immune cells and leads to oxidative stress, contributing to fibrosis and functional liver loss.
259
What are the potential complications of portal hypertension in chronic hepatitis?
* Ascites
* Acquired portosystemic shunts
* Ammonia dysmetabolism
* Hepatic encephalopathy
260
What must quantification consider regarding copper distribution?
Copper is unevenly distributed and regenerative nodules often have lower copper content
## Footnote
This is important for accurate assessment in cases of copper-associated chronic hepatitis.
261
Which additional stains should be used in histologic examination aside from H&E?
* Copper (rhodanine)
* Iron (Prussian blue)
* Connective tissue (Masson's trichrome)
* Lipofuscin
262
What additional testing should be performed if granulomatous or pyogranulomatous hepatitis is identified?
Testing for regional infectious agents (e.g., Leishmania, Heterobilharzia)
263
What role does fluorescence in situ hybridization (FISH) play in infectious disease testing?
May aid in detecting unculturable bacteria
264
What general supportive care should be provided while awaiting biopsy or in early management?
* High-quality, balanced diet
* Cytoprotective agents (e.g., SAMe, vitamin E)
* Treat complications (ascites, HE) as they arise
265
When is copper chelation recommended?
When hepatic copper concentration is:
* 1,000 µg/g dry weight
* Considered if 600–1,000 µg/g, depending on severity and histologic distribution
266
What rhodanine copper score supports chelation initiation?
A rhodanine copper score ≥3/5
267
What should be avoided when giving zinc and D-penicillamine?
They interfere with each other
268
What is the first-line treatment for ascites in dogs with chronic liver disease?
Avoid high-sodium diets
269
What medication is used to manage hepatic encephalopathy?
* Lactulose
* Metronidazole
* Ampicillin / Amoxicillin
270
What is the median survival time observed in a study of dogs with chronic hepatitis?
561 days
271
What negative prognostic indicators are associated with chronic hepatitis?
* Ascites
* Advanced hepatic fibrosis or cirrhosis
* Prolonged PT or aPTT
* Icterus (jaundice)
272
What are the three recognized forms of feline cholangitis according to WSAVA?
* Neutrophilic cholangitis
* Lymphocytic cholangitis
* Chronic cholangitis associated with liver flukes
## Footnote
WSAVA stands for World Small Animal Veterinary Association.
273
What is lymphocytic cholangitis?
A chronic, progressive inflammatory disease centered on the biliary tree, characterized by small lymphocyte infiltration of portal areas
## Footnote
It often includes portal fibrosis and biliary hyperplasia.
274
What percentage of feline liver biopsies in the UK show lymphocytic cholangitis?
6.8%
## Footnote
In New Zealand, the prevalence is 20%.
275
List common clinical signs of lymphocytic cholangitis in cats.
* Gradual weight loss
* Polyphagia or anorexia
* Vomiting
* Lethargy
* Polydipsia and polyuria
## Footnote
Clinical signs are often vague.
276
What are typical laboratory findings in lymphocytic cholangitis?
* Marked hyperglobulinemia
* Mild to moderate elevations in ALT and ALP
## Footnote
These findings may mimic feline infectious peritonitis (FIP).
277
What is the treatment of choice for lymphocytic cholangitis?
* Prednisolone: 1–2 mg/kg PO q24h
* Ursodiol: 10–15 mg/kg PO q24h
* Supportive care
## Footnote
Antibiotics are not recommended unless a bacterial infection is documented.
278
What is the prognosis for cats treated for lymphocytic cholangitis?
Generally good with treatment, median survival times range from 26 to 36 months
## Footnote
Some cats achieve complete resolution of ascites.
279
What are the two trematode families that infect the feline biliary system?
* Platynosomidae
* Opisthorchiidae
## Footnote
Platanosomum spp. is common in tropical/subtropical regions.
280
What is the primary clinical sign associated with liver fluke infestation?
Jaundice
## Footnote
Other signs include dehydration, hepatomegaly, abdominal pain, and ascites.
281
What is the treatment of choice for liver fluke infestation?
Praziquantel
## Footnote
Dosage is typically 20–40 mg/kg SQ, IM, or PO.
282
What is the histopathological hallmark of hepatic amyloidosis?
Congo red staining viewed under polarized light shows apple-green birefringence
## Footnote
This is pathognomonic for amyloid.
283
What are the two types of copper-associated hepatopathies in cats?
* Primary (inborn error of metabolism)
* Secondary to chronic biliary disease
## Footnote
Secondary copper hepatopathy is often associated with conditions like lymphocytic cholangitis.
284
What are common clinical signs of vitamin A toxicosis in cats?
* New bone formation of cervical and thoracic vertebrae
* Soft tissue mineralization due to hypercalcemia
* Hepatic changes
## Footnote
Chronic ingestion of excessive vitamin A is the cause.
285
What is the newly discovered virus related to hepatitis in cats?
Domestic Cat Hepadnavirus (DCH)
## Footnote
This virus was discovered in 2018.
286
What is stellate cell lipidosis?
A condition involving lipid accumulation in hepatic stellate cells
287
What can happen to cats consuming vitamin A doses near the upper safe limit?
They can develop milder but similar hepatic lesions
288
Is the clinical significance of vitamin A-induced hepatic fibrosis in cats established?
No, it is not yet established
289
What conditions is DCH being investigated as a possible cause of?
* Chronic hepatitis
* Hepatocellular carcinoma (HCC)
290
What are the DCH DNA detection rates in feline populations?
<1% to >18%
291
What are the risk factors for DCH viremia?
* Concurrent retrovirus infection
* Elevated ALT
292
What percentage of hepatic biopsies in cats report chronic hepatitis?
2.4%
293
What percentage of feline liver neoplasms does hepatocellular carcinoma account for?
27%
294
What is the potential impact of DCH if confirmed as a pathogenic agent?
Strategies from HBV research, including vaccination, may be applicable
295
What is the histopathologic finding in primary copper-associated hepatitis in cats?
* Inflammation and fibrosis
* Multifocal, mixed, centrilobular hepatitis
* Eosinophilic cytoplasmic granules
* Hepatocyte vacuolation
* Severe diffuse hepatic necrosis
296
What staining methods are used for diagnosing copper-associated hepatitis?
* Rhodanine
* Rubeanic acid
297
Where does copper accumulate in primary copper hepatopathy?
Centrilobular (zone 3) hepatocytes
298
What is the prognosis for cats with primary copper-associated hepatitis?
Variable; may survive several years with treatment
299
What are some clinical manifestations of hypervitaminosis A?
* New bone formation
* Pain and restricted mobility
* Hepatic effects like severe hepatic fibrosis
300
What are the key characteristics of chronic hepatitis in cats?
Relatively uncommon, representing 2.4% of hepatic biopsies
301
What is the percentage of primary hepatic tumors among all feline cancers?
1–2.9%
302
What is a potential diagnostic method for measuring hepatic copper?
Flame atomic absorption spectroscopy
303
What are the adverse effects associated with penicillamine treatment?
Reversible hemolytic anemia
304
What are the main biliary tract diseases of dogs and cats with potential infectious etiologies?
Neutrophilic cholangitis and cholecystitis
## Footnote
Bacterial infection is the most common cause in both species.
305
Which species is more frequently affected by neutrophilic cholangitis?
Cats
## Footnote
This is likely due to anatomical differences in their biliary systems.
306
What is the most common cause of neutrophilic cholangitis in dogs and cats?
Bacterial infection
307
What is the role of microbiota in the gallbladder and bile of healthy individuals?
They host a complex microbiota with homeostatic mechanisms that help defend against pathogen invasion and immune dysregulation.
308
What are the key protective mechanisms of biliary microbiota?
* Secretory IgA and mucus to prevent bacterial adhesion
* Bile flow (bacteriostatic)
* Sphincter of Oddi to prevent reflux
309
What organisms are most commonly associated with biliary disease in dogs and cats?
* Escherichia coli
* Enterococcus spp.
* Bacteroides spp.
* Clostridium spp.
310
What histopathologic feature characterizes acute neutrophilic cholangitis?
Neutrophilic infiltration of periportal and intrahepatic bile ducts.
311
What are the common clinical signs of neutrophilic cholangitis in cats?
* Anorexia/inappetence
* Vomiting
* Lethargy
* Fever (30–40%)
* Icterus (63%)
* Abdominal discomfort (24%)
* Weight loss (50%)
312
What laboratory findings may indicate neutrophilic cholangitis or cholecystitis?
* Inflammatory leukogram
* Hyperbilirubinemia
* Increased liver enzyme activity
313
True or False: Absence of laboratory findings rules out cholangitis or cholecystitis.
False
314
What imaging technique can identify biliary obstruction?
Ultrasound
315
What is the gold standard for definitive diagnosis of neutrophilic cholangitis and cholecystitis?
Histopathology from multiple liver and biliary sites.
316
What is the first-line antimicrobial therapy for biliary infections?
Amoxicillin-clavulanate, with or without metronidazole.
317
What duration is typically recommended for antimicrobial therapy in biliary infections?
6–8 weeks
318
What adjunctive therapy is proposed for its choleretic and cytoprotective effects?
Ursodeoxycholic acid (ursodiol)
319
What are the poor outcomes associated with neutrophilic cholangitis?
* Gallbladder rupture
* Bile peritonitis
* Severe cholecystitis
* Complications from mucoceles or choleliths
320
What is the median age of cats diagnosed with neutrophilic cholangitis?
10 years
321
What is the normal gallbladder wall thickness in cats?
≤ 1.0 mm
322
What is the normal gallbladder wall thickness in dogs according to new studies?
≤ 1.3 mm
323
What is the common bile duct diameter considered normal in cats?
Up to 4 mm
324
What percentage of cats with neutrophilic cholangitis have concurrent pancreatitis?
50–90%
325
What is the significance of culture-negative cases in cholangitis?
They may reflect prior antimicrobial use or a dysregulated immune response.
326
What is a common complication rate associated with cholecystocentesis?
2–7% overall
327
What is the proposed treatment strategy when bacteria are not confirmed?
Empirical antimicrobial therapy initially.
328
What concurrent diseases must be managed for long-term resolution of biliary disease in cats?
* Pancreatitis
* Inflammatory bowel disease (IBD)
329
What is the prognosis for neutrophilic cholangitis and uncomplicated cholecystitis?
Typically favorable, with reported survival of several years.
330
What uncommon infectious organism can be identified in rare cases of cholecystitis in immunosuppressed cats?
Toxoplasma gondii
331
What is the upper limit of common bile duct diameter in dogs?
1.3 mm
## Footnote
This measurement is particularly relevant in fasted or unsedated patients, reflecting improved ultrasonographic resolution and measurement accuracy.
332
What is considered a normal common bile duct diameter in cats?
Up to 4 mm
## Footnote
A diameter larger than this may indicate potential health issues.
333
What conditions may cause dilation of the common bile duct?
* Biliary obstruction
* Cholangitis
* Cholelithiasis
## Footnote
These conditions can lead to significant health complications in affected animals.
334
What are the clinical signs that may indicate neutrophilic cholangitis and/or cholecystitis?
* Anorexia
* Vomiting
* Fever
* Icterus
## Footnote
These signs are frequently observed in affected patients.
335
Which laboratory findings support a presumptive diagnosis of neutrophilic cholangitis and/or cholecystitis?
* Elevated liver enzyme activities (ALT, AST, ALP)
* Hyperbilirubinemia
* Inflammatory leukogram
## Footnote
These findings are critical for diagnosing liver-related issues.
336
What ultrasound findings are indicative of neutrophilic cholangitis and/or cholecystitis?
* Gallbladder wall thickening
* Common bile duct dilation
* Gallbladder sediment
* Hepatomegaly or echogenicity changes
## Footnote
These findings help in visualizing the condition of the biliary system.
337
What microbiological evidence can support the diagnosis of neutrophilic cholangitis?
Presence of bacteria in bile via culture or cytology
## Footnote
This evidence is crucial for confirming the bacterial involvement in the condition.
338
What is the significance of a patient's response to antimicrobials in the context of neutrophilic cholangitis?
Response to antimicrobials suggests a bacterial etiology in the absence of other causes
## Footnote
This response can help guide treatment decisions.
339
What is considered the gold standard for definitive diagnosis of neutrophilic cholangitis?
Histopathology
## Footnote
This method is particularly important when treatment response is poor or surgery is required.
340
What is the hepatobiliary system responsible for?
Bile formation and transport, facilitating fat digestion and absorption, as well as excretion of metabolic waste
341
What are gallbladder mucoceles (GBMs) characterized by?
Accumulation of inspissated, immobile mucus and bile within the gallbladder
342
What is the median age of dogs diagnosed with gallbladder mucoceles?
10 years (range: 1.5–17 years)
343
Which breeds are predisposed to gallbladder mucoceles?
* Shetland Sheepdogs
* Cocker Spaniels
* Miniature Schnauzers
* Border Terriers
* Pomeranians
* Beagles
344
What environmental factor is suspected to be associated with gallbladder mucoceles in Shetland Sheepdogs?
Imidacloprid
345
What are common clinical signs of gallbladder mucoceles in dogs?
* Vomiting
* Lethargy
* Diarrhea
* Anorexia
* Abdominal pain
* Jaundice
346
What is the diagnostic modality of choice for gallbladder mucoceles?
Ultrasonography
347
What is the classic appearance of gallbladder mucoceles on ultrasound?
Kiwi fruit appearance with gravity-independent hyperechoic material and a peripheral hypoechoic rim
348
What is the recommended treatment for symptomatic dogs with gallbladder mucoceles?
Cholecystectomy
349
What factors increase the risk of complications in dogs with gallbladder mucoceles?
* Gallbladder rupture
* Bile peritonitis
* Sepsis
* Multi-organ dysfunction syndrome (MODS)
* Death
350
What medical management is recommended for mild or subclinical gallbladder mucoceles?
* Low-fat diet
* Ursodeoxycholic acid (10–15 mg/kg PO q24h)
* S-adenosylmethionine (SAMe)
351
What is the prognosis for dogs undergoing cholecystectomy for gallbladder mucoceles?
Generally good long-term prognosis if they survive the immediate postoperative period
352
What is the prevalence of cholelithiasis in dogs?
0.97% to 13%
353
What type of stones are predominantly found in dogs with cholelithiasis?
Pigment stones composed of calcium bilirubinate, carbonate, calcium phosphate, and free fatty acids
354
What are common clinical signs of cholelithiasis when they occur?
* Vomiting
* Anorexia
* Lethargy
* Abdominal pain
* Diarrhea
* Jaundice
355
What is the preferred diagnostic modality for cholelithiasis?
Abdominal ultrasound
356
What surgical intervention is preferred for cholecystolithiasis?
Cholecystectomy
357
What is the prognosis for animals that survive the first 7 postoperative days after surgery for cholelithiasis?
Good long-term prognosis
358
What is the most common type of biliary neoplasia in dogs?
Intrahepatic cholangiocarcinoma
359
What are common clinical signs of biliary neoplasia?
* Vomiting
* Anorexia
* Lethargy
* Weight loss
* Diarrhea
* Jaundice
360
What imaging techniques are used for the diagnosis of biliary neoplasia?
* Radiographs
* Ultrasound
* CT
361
What is the gold standard for diagnosing biliary neoplasia?
Histopathology
362
What is the primary curative option for biliary neoplasia?
Surgical intervention
363
What percentage of cholangiocarcinoma cases are solitary lesions?
37–46%
364
What percentage of cholangiocarcinoma cases are multifocal?
Up to 54%
365
What is the range of diffuse involvement in cholangiocarcinoma cases?
17–54%, with or without metastasis
366
In cats with bile duct adenomas, what is the distribution of single vs. multifocal lesions?
Roughly equal distribution
367
What percentage of cats with bile duct carcinomas experience carcinomatosis and intraperitoneal metastasis?
~70%
368
What is the primary curative option for focal biliary tract neoplasia in dogs and cats?
Surgical intervention
369
What factors determine the appropriate surgical procedure for biliary neoplasia?
Tumor type and anatomical location
370
What is the prognosis for liver lobectomy for bile duct adenomas?
Generally carries a good prognosis
371
What are the regional or distant metastasis rates for cholangiocarcinomas in dogs and cats?
Dogs: 88%, Cats: 80%
372
What is associated with a poor prognosis in cholangiocarcinomas?
High rates of metastasis
373
What is a significant risk associated with surgical resection of common bile duct tumors?
High perioperative mortality
374
What is the median survival time reported for dogs after cholecystectomy for gallbladder neuroendocrine tumors?
1,358 days (range: 432–1,834 days)
375
What is gallbladder agenesis?
A rare congenital malformation in dogs
376
What causes gallbladder agenesis?
Aberrant embryologic development of the pars cystica
377
What other hepatobiliary malformations frequently co-occur with gallbladder agenesis?
* Ductal plate malformation
* Lobe hypoplasia
378
Which breed is overrepresented in cases of gallbladder agenesis?
Small breed dogs, particularly Chihuahuas
379
What is the median age of dogs affected by gallbladder agenesis?
~2 years
380
What percentage of dogs are subclinical at the diagnosis of gallbladder agenesis?
Approximately 50%
381
What clinical signs may occur in dogs with gallbladder agenesis?
* Vomiting
* Anorexia
* Diarrhea
* Ascites
* Lethargy
* Seizures
382
What imaging technique is used to suspect gallbladder agenesis?
Ultrasound
383
What is the typical management for asymptomatic individuals with gallbladder agenesis?
Dietary fat restriction
384
What is a potential treatment for symptomatic humans with gallbladder agenesis?
* Antibiotics
* NSAIDs
* Smooth muscle relaxants
385
What is the prognosis for dogs with isolated gallbladder agenesis?
Typically have a normal lifespan
386
What is destructive cholangitis?
Defined by progressive loss and destruction of bile ducts in the portal triads
387
How many canine cases of destructive cholangitis have been reported in the last 20 years?
Six
388
What are potential triggers for destructive cholangitis in dogs?
* Idiosyncratic drug reactions
* Immune-mediated mechanisms
* Viral infections (theoretical)
389
What are the clinical signs associated with destructive cholangitis?
* Vomiting
* Anorexia
* Diarrhea
* Lethargy
* Weight loss
* Jaundice
390
What is required for the diagnosis of destructive cholangitis?
Histopathologic analysis from multiple liver lobes
391
What treatment may be included in the management of destructive cholangitis in humans?
* Withdrawal of suspected offending drugs
* High-dose ursodiol
* Immunosuppressive therapy (e.g., corticosteroids)
392
What is the prognosis for humans with destructive cholangitis?
Variable outcomes from irreversible bile duct loss to epithelial regeneration
393
What is the prognosis for dogs with destructive cholangitis?
Remains uncertain, but recovery is possible based on limited reports
394
What can vacuoles in hepatocytes contain?
* Fat
* Glycogen
* Water
395
What systemic diseases can lead to vacuolar hepatopathy?
* Diabetes mellitus
* Hyperadrenocorticism
* Toxicoses
* Congenital cobalamin deficiency
* Hepatic congestion
* Inflammatory hepatobiliary diseases
* Portosystemic shunting
* Dyslipidemias
396
What is steroid hepatopathy?
The most common form of vacuolar hepatopathy in dogs, resulting from glucocorticoid overproduction or therapy.
397
What are the pathologic features of steroid hepatopathy?
* Vacuolation in zone 3
* Cytoplasmic glycogen accumulation
* Dramatic increases in ALP
* Mildly elevated ALT
* Clear cell change without significant inflammation
398
What breed is predisposed to glycogen-associated hepatopathy?
Scottish Terriers
399
What are common clinical features in Scottish Terriers with glycogen hepatopathy?
* Moderate to marked increase in serum ALP
* Mild increase in ALT
* Median age for carcinoma: ≥8 years
* 50% show signs of hyperadrenocorticism
400
What is hepatic steatosis also known as?
Lipidosis
401
What are some causes of hepatic steatosis?
* Diabetes mellitus
* Hypothyroidism
* Hyperthyroidism
* Toxins
* Congenital portosystemic shunts
* Disorders of fat metabolism
* Obesity-related insulin resistance
402
What is the primary inciting event for feline hepatic lipidosis?
Anorexia lasting more than 2–14 days
403
What are some common clinical signs of feline hepatic lipidosis?
* Anorexia
* Weight loss
* Vomiting
* Lethargy
404
How is feline hepatic lipidosis diagnosed?
Through clinical findings, laboratory abnormalities, and imaging.
405
What is a common laboratory finding in feline hepatic lipidosis?
Increased ALP activity (100% of cases)
406
What is the role of ultrasound in diagnosing vacuolar hepatopathies?
To identify hypoechoic liver or hepatic nodules, though findings are non-specific.
407
What complications can arise from severe vacuolar hepatopathy?
* Cirrhosis
* Portal hypertension
* Hepatic insufficiency
* Hepatocellular carcinoma
408
What is the prognosis for cholesterol ester storage disease in dogs?
Unclear; considered benign in humans.
409
True or False: Vascular hepatopathies are always benign.
False
410
What is the significance of monitoring liver enzyme levels in dogs with vascular hepatopathy?
They are not predictive of progression or phenotype.
411
What medical therapy may be beneficial for glycogen-associated hepatopathy?
S-adenosylmethionine (SAMe)
412
What is the median age for cats affected by feline hepatic lipidosis?
7 years
413
What are the hematology findings in cats with feline hepatic lipidosis?
* Mild to moderate anemia
* Poikilocytosis
* Heinz bodies
414
What electrolyte disturbances are common in feline hepatic lipidosis?
* Hypokalemia
* Hypochloremia
* Hypophosphatemia
* Hypomagnesemia
415
What is the correlation between obesity and feline hepatic lipidosis?
Obese cats are at higher risk due to increased adipose reserves and pro-inflammatory adipokines.
416
What is the recommended dosage of Vitamin K before biopsy in cats?
1 mg/kg SQ Q24h x 3–5 days
417
What platelet count increases the risk of severe bleeding during invasive procedures?
<80,000/µL
418
What PTT value is associated with increased risk of severe bleeding?
>1.5× upper reference interval
419
What are the typical ultrasound findings in cases of feline hepatic lipidosis?
* Enlarged, diffusely hyperechoic liver
* Liver echogenicity often exceeds that of surrounding falciform fat
420
What are the differential diagnoses for hyperechoic liver?
* Obesity
* Cholangiohepatitis
* Fibrosis
* Lymphoma
421
What is required for a definitive diagnosis of feline hepatic lipidosis?
Demonstration of lipid vacuoles in ≥50–80% of hepatocytes
422
What are the histologic findings consistent with feline hepatic lipidosis?
* Diffuse vacuolar change consistent with lipid accumulation
* Secondary cholestasis
* Potential underlying structural liver disease
423
What are the limitations of cytology (FNA) in diagnosing feline hepatic lipidosis?
* False positives: May misdiagnose lymphoma or cholangitis as FHL
* False negatives: In cases of focal disease
424
When should a liver biopsy be reserved for feline hepatic lipidosis?
* Non-responders to therapy
* Strong suspicion of underlying hepatopathy
425
What is the mainstay of therapy for feline hepatic lipidosis?
Nutritional Support
426
What is the impact of early enteral feeding on mortality in feline hepatic lipidosis?
Reduces mortality from 90% to ≤40%
427
What feeding strategy should be followed during treatment?
Begin with 25–33% of Resting Energy Requirement (RER), increase over 3–4 days
428
What should be avoided to prevent complications during feeding?
* Forced oral feeding
* Appetite stimulants
429
What are the dietary recommendations for feline hepatic lipidosis?
* High-protein, high-calorie recovery diets
* Supplement L-carnitine, Vitamin B12, Thiamine, Vitamin K, SAMe, Vitamin E
430
What is the role of SAMe in the treatment of feline hepatic lipidosis?
20 mg/kg PO Q24h (on empty stomach)
431
What supportive medical management should be provided?
* Antiemetics: Maropitant, ondansetron
* Fluid therapy
* Monitor and correct electrolyte abnormalities
432
True or False: Protein restriction is recommended in managing hepatic encephalopathy.
False (feed smaller meals more frequently)
433
What factors influence the prognosis of feline hepatic lipidosis?
* Timeliness of intervention
* Nutritional support
* Presence and treatment of underlying disease
* Prevention of complications
434
What is the reported range of mortality rates for feline hepatic lipidosis?
12% to 70%
435
What are negative prognostic indicators at presentation for feline hepatic lipidosis?
* Older age
* Hypoproteinemia
* Hypocholesterolemia
* Increased creatine kinase (CK) activity
436
What are positive prognostic indicators during hospitalization?
Decreases in serum beta-hydroxybutyrate (BHBA) and bilirubin concentrations
437
What is another name for Superficial Necrolytic Dermatitis (SND)?
Hepatocutaneous Syndrome
438
What are common associated conditions with Superficial Necrolytic Dermatitis?
* Glucagon-secreting tumors
* Diabetes mellitus
* Phenobarbital therapy
439
What is the median age for dogs affected by Superficial Necrolytic Dermatitis?
8–10 years
440
What are common locations for skin lesions in Superficial Necrolytic Dermatitis?
* Paw pads
* Nose
* Periorbital area
* Perianal/genital regions
* Pressure points
441
What diagnostic findings are common in Superficial Necrolytic Dermatitis?
* Elevated ALP and ALT
* Hypoaminoacidemia
* Aminoaciduria
442
What is the typical ultrasound appearance of the liver in Superficial Necrolytic Dermatitis?
"Honeycomb" or "Swiss cheese" appearance
443
What is the prognosis for dogs with Superficial Necrolytic Dermatitis?
Poor, with most dogs dying or euthanized within 6 months of diagnosis
444
What nutritional support is recommended for Superficial Necrolytic Dermatitis?
High-quality, digestible, high-protein diet
445
What should be avoided in the treatment of Superficial Necrolytic Dermatitis?
Corticosteroids (may make things worse)
446
What percentage of all tumors do primary tumors of the liver and biliary tree represent in dogs?
0.6–1.5%
447
What percentage of all tumors do primary tumors of the liver and biliary tree represent in cats?
1–3%
448
Metastatic tumors occur how many times more frequently than primary hepatic tumors in dogs?
Approximately 3 times
449
In cats, which type of tumors are more common, primary or metastatic?
Primary tumors
450
In cats, at what age do malignant hepatic tumors typically occur compared to benign tumors?
Younger age
451
What is the most common primary hepatic tumor in dogs?
Hepatocellular adenomas and carcinomas
452
What percentage of tumors were hepatocellular in a histologic classification study of canine liver tumors?
77%
453
In cats, what type of tumors were reported to be most common in a UK study of feline liver biopsies?
Hematopoietic tumors
454
What percentage of older dogs may have nodular hyperplasia?
15–60%
455
What breed was noted to have a 16% occurrence of hepatocellular carcinoma?
Miniature Schnauzers
456
What is the metastatic potential of massive HCC?
0–37% of cases
457
What common metastatic sites are associated with nodular/diffuse HCC?
* Regional lymph nodes
* Peritoneum
* Lungs
458
What is the prevalence of neuroendocrine tumors in dogs as primary hepatic tumors?
~3%
459
What is the typical biological behavior of neuroendocrine tumors?
Aggressive
460
What is the percentage of metastatic rate for bile duct tumors in dogs?
~90%
461
What is the most frequently reported mesenchymal tumor in dogs?
Hemangiosarcoma
462
What is the morphology of mesenchymal tumors in terms of distribution?
* Massive: 33%
* Nodular: 67%
463
What is the risk of disseminated intravascular coagulation (DIC) in animals with hepatic hemangiosarcoma?
Present in ~20% of dogs with advanced hepatocellular carcinoma
464
In cats, how often do hepatobiliary tumors show no clinical signs?
~50%
465
What is the clinical finding noted in ~75% of cases during physical examination of hepatic tumors?
Abdominal mass or hepatomegaly
466
What is the risk associated with hepatic hemangiosarcoma in animals?
DIC (Disseminated Intravascular Coagulation) is a risk.
467
What are the differences in biochemical abnormalities between primary and metastatic tumors?
* Primary tumors are more likely to cause hypoproteinemia and hypoglycemia
* Higher ALT/ALP in primary tumors
* Less likely to cause hyperbilirubinemia
468
What does an AST:ALT ratio of <1 suggest?
Suggestive of HCC (Hepatocellular Carcinoma) or bile duct carcinoma.
469
What does an AST:ALT ratio of >1 indicate?
More likely in neuroendocrine or mesenchymal tumors.
470
What percentage of dogs show elevated serum bile acids with hepatobilliary neoplasia?
Elevated in 50-75% of dogs.
471
What is alpha-fetoprotein (AFP) and its significance?
Glycoprotein produced by fetal, regenerative, or neoplastic hepatocytes; elevated in ~75% of dogs with hepatocellular carcinoma.
472
What are the advantages of abdominal ultrasound over radiography?
* Identifies mass type
* Localizes lesions
* Evaluates relationship to surrounding structures
473
What are some ultrasound features seen in hepatic tumors?
* Hypoechoic, heterogeneous, or multifocal nodules/masses
* Hyperechoic or normal appearance in some cases
* Cystic components in specific tumors
474
What is the diagnostic accuracy of FNA cytology in dogs?
Low diagnostic agreement: ~30%.
475
What are common complications following liver biopsy?
* Mild-to-moderate hemorrhage
* Vascular compromise
* Hypoglycemia
* Liver dysfunction
476
What is the median survival time for dogs with massive hepatocellular carcinoma after surgical lobectomy?
Not reached (>1,460 days).
477
What is the prognosis for nodular or diffuse HCC?
Poor prognosis.
478
What is the median survival time for dogs with nodular HCC treated with gemcitabine?
983 days.
479
What type of tumors are bile duct carcinomas and their prognosis?
Prognosis is very poor; no effective treatment.
480
What is the prognosis for myelolipoma in cats?
Excellent prognosis with liver lobectomy.
481
What is the treatment for systemic hepatic neoplasia?
Systemic chemotherapy.
482
What percentage of dogs with massive HCC showed a partial response to 3D conformal radiation therapy?
5/6 dogs (approximately 83%).
