1
Q
What is the “Pringle maneuver”
A
It is the simultaneous manual occlusion of the hepatic artery and portal vein at the level of the epiploic foramen during a laparotomy (to control hemorrhage)
2
Q
In case of bile peritonitis secondary to blunt trauma, where does the leakage most commonly come from
A
Common bile duct > hepatic ducts
3
Q
Once in surgery, what is a contra-indication for cholecystectomy
A
Obstruction of the common bile duct that cannot be flushed
4
Q
What are surgical options for extra-hepatic biliary obstruction
A
- If the common bile duct is not patent even with catheterization, cholecystoduodenostomy (preferably) or cholecystoenterostomy is required
- If the common bile duct can be patent when passing a catheter, biliary stenting is possible (mostly for reversible causes: pancreatitis, cholangiohepatitis, trauma or palliative with neoplasia)
- For very temporary obstructions (pancreatitis), a cholecystostomy tube can be placed
- If the common bile duct is patent but the gallbladder is damaged, cholecystectomy
5
Q
What bile duct needs to be ligated for a cholecystectomy
A
Cystic duct
6
Q
What bacteria are most common in liver abscesses
A
E Coli, Staphylococcus, Enterococcus, Klebsiella, Clostridium
7
Q
What lobe is most commonly affected by liver lobe torsion
A
Left lateral lobe (very large)
8
Q
What is the most common composition of choleliths in dogs and cats? Where do they typically form?
A
Dogs: calcium bilirubinate > calcium carbonate
Cats: calcium carbonate > calcium bilirubinate / cholesterol
(Mostly cholesterol in humans)
Form mostly in the gallbladder
9
Q
What is the treatment of choice for choleliths? When is treatment indicated?
A
Flushing any choleliths present in the bile duct back in the gallbladder, then cholecystectomy
Indicated if there are associated signs of gallbladder disease (cholecystitis) or bile duct distension
10
Q
What are the 3 classes of congenital liver vascular diseases
A
- Macrovascular porto-systemic shunts
- Primary hypoplasia of the portal vein (PVH) with portal hypertension (“non-cirrhotic portal hypertension”) or without portal hypertension (“microvascular dysplasia)
- Disturbances in portal outflow
11
Q
What are the different types of porto-systemic shunts
A
- Intra-hepatic porto-systemic shunts
- Left divisional (most frequent)
- Right divisional
- Central divisional - Extra-hepatic porto-systemic shunts (most frequent)
- Porto-caval
- Porto-azygous
12
Q
What is the most common extra-hepatic porto-systemic shunt
A
Solitary porto-caval shunt
13
Q
Where does shunting of blood happen in portal vein hypoplasia (PVH) with portal hypertension / without portal hypertension
A
- PVH with portal hypertension = idiopathic portal hypertension with secondary acquired extra-hepatic porto-systemic shunts
- PVH without portal hypertension = microvascular dysplasia = intra-hepatic microvascular communication between portal and systemic circulations
14
Q
What is a consequence of hepatic arteriovenous malformation
A
Arterial blood flow communicating directly with portal circulation -> severe portal hypertension -> acquired porto-systemic shunts
15
Q
What factors can lead to exacerbation of hepatic encephalopathy
A
- GI bleed
- Stored blood transfusions
- Drugs (benzodiazepines, opioids, etc)
- NSAIDs
- High-protein meals
- Hypokalemia
16
Q
What dog breed can have an elevated ammonia despite being healthy
A
Irish Wolfhound puppies (should resolve after a few months)
17
Q
What is the long term survival rate for dogs with porto-systemic shunts treated medically vs surgically
A
- Medically: 50%
- Surgically: 88%
18
Q
What are 3 options to occlude an extra-hepatic PSS
A
- Ameroid constrictor (casein surrounded by stainless steel)
- Cellophane band
- Hydraulic occluder
19
Q
What is the maximum change in portal pressure that should be tolerated after PSS occlusion
A
9-10 cmH2O (absolute max pressure of 17-24 cmH2O)
20
Q
What is the normal range for pre-prandial and post-prandial bile acids
A
- Pre-prandial: <10 umol/L
- Post-prandial: <15 umol/L
Suggestive of disease when > 25-30 umol/L in dogs, > 25 umol/L in cats
(cannot be interpreted in patients with cholestasis)
21
Q
Name 4 post-operative complications PSS attenuation and their prevalence
A
- Hypoglycemia (~40%), sometimes refractory to dextrose supplementation
- Portal hypertension (2-14%)
- Seizures / encephalopathy (neuro signs 3-27% dogs, 8-37% cats but up to 60% ; seizures ~3-10% in dogs and 0-32% in cats)
- (Can also have coagulopathy pre-op that is exacerbated with surgery)
22
Q
True or false: ligature removal is recommended with patients exhibiting signs of portal hypertension following PSS attenuation
A
False in most cases, they can be supported medically (GI protectants) and ascites will resolve with time
Ligature removal is recommended in patients with refractory hypotension and DIC
23
Q
What are predisposing factors for gallbladder mucocele
A
- Breed: Shetland Sheepdog, Miniature Schnauzer, Cocker Spaniel
- Hyperlipidemia
- Hypothyroidism
- Hyperadrenocorticism
24
Q
What are the most common causes of acquired porto-systemic shunts
A
Portal hypertension –> PVH with portal hypertension (congenital) / hepatic fibrosis, cirrhosis / hepatic arterio-venous malformation
25
What are risk factors for post-attenuation neurological signs in dogs with PSS
- Older dogs
- Porto-azygous shunt
- Neurological signs just before surgery
- EHPSS vs IHPSS
26
What are the most sensitive lab test and imaging modalities to diagnose a PSS? (Both are very rarely performed)
- Lab test = ammonia tolerance test
- Imaging = nuclear scintigraphy
27
Name at least 7 substances involved in hepatic encephalopathy
- Ammonia
- Glutamate / glutamine
- Tryptophan
- Gamma-aminobutyric acid (GABA)
- Manganese
- Bile acids
- Endogenous benzodiazepines
- Endogenous opioids
- Aromatic amino-acids
- False neurotransmitters (octopamine, phenylethanolamine, mercaptan)
- Short chain fatty acids
28
What are the 3 categories of hepatic encephalopathy
- Type A = acute fulminant liver dysfunction
- Type B = abnormal liver perfusion / bypass (porto-systemic shunt)
- Type C = chronic / cirrhotic (end stage)
29
What is the most important feature of acute hepatic encephalopathy
Cytotoxic brain edema
30
Name confounding factors implicated in worsening signs of hepatic encephalopathy
- Hypoglycemia
- Metabolic alkalosis (increases NH3:NH4+ ratio)
- Hypokalemia (worsens metabolic alkalosis + increases renal ammonia production)
- Hyponatremia
- GI bleeding
- Protein ingestion
- Constipation
- Sepsis
- Drugs (benzodiazepines, opioids)
- Renal insufficiency
- Diuretic administration, dehydration
31
What bacteria are involved in emphysematous cholecystitis
- E Coli
- Clostridium spp
32
What is the mortality rate for elective cholecystectomy vs non-elective cholecystectomy
2% when elective, 20% when not elective
33
What is the prognosis for gallbladder mucocele
Peri-operative mortality up to 20-40% but good long term survival for those surviving the post-op period
34
Name causes of cholecystitis in dogs and cats
- Infectious (mostly bacterial, can be parasitic)
- Extra-hepatic biliary obstruction (pancreatitis, cholangitis, neoplasia, choleliths, duodenal FB)
- Gallbladder mucocele
- Gallbladder infarction
35
What are the 2 types of cholangitis? Which type is more frequent
- Neutrophilic (more commonly associated with infection, more acute)
- Lymphocytic (more chronic and suspected to have an immune-mediated component)
Same frequency in cats, neutrophilic more frequent in dogs
36
What chelator can be used for copper-associated hepatopathy? What breeds are predisposed?
D-penicillamine
Bedlington Terrier, Dalmatian, Labrador Retriever, Doberman Pinscher
37
What Lepto serovars are more likely to cause hepatic involvement
- L. icterohaemorrhagiae
- L. pomona
38
What are differentials for hepatitis / cholangiohepatitis in dogs and cats
1. Idiopathic (canine chronic hepatitis, feline cholangitis complex)
2. Viral:
- Infectious canine hepatitis (adenovirus type I)
- FIP
3. Bacterial:
- Canine / feline cholangitis
- Leptospirosis
- Salmonellosis
- Brucellosis
4. Protozoal
- Toxoplasmosis
- Neosporosis
- Leishmaniasis
- Hepatozoonosis
5. Parasitic
- Visceral larval migrans
- Dirofilariasis (in caudal vena cava)
- Echinococcus
6. Fungal
- Histoplasmosis
- Blastomycosis
- Aspergillosis
7. Rickettsial
- Ehrlichiosis
- Rocky Mountain Spotted Fever (Rickettsia rickettsii)
7. Toxins
- Acetaminophen
- Aflatoxin
- Amiodarone
- Azathioprine
- Azole antifungals
- Oral diazepam
- Methimazole
- Phenobarbital
- Trimethoprim - sulfadiazine
- Xylitol
- Zonisamide
39
What are causes of hepatic failure in cats and dogs
1. Infectious:
- CAV-1
- Canine Herpes virus
- Leptospirosis
- Toxoplasmosis
- Liver abscess
- Blastomycosis
- Histoplasmosis
- Rickettsia rickettsii
- Ehrlichia canis
2. Drugs:
- Acetaminophen
- Aspirin
- Phenobarbital
- Trimethoprim-sulfa
- Ketoconazole / itraconazole
- Griseofulvin
- Zonisamide
- Lomustine
- Phenytoin
- Methimazole in cats
- Oral diazepam in cats
3. Toxins:
- Sago palm
- Envenomation
- Heavy metals (Cu, Fe, Pd)
- Mushrooms (Amanita phalloides)
- Aflatoxins
- Blue-green algae
- Xylitol (dogs)
4. Miscellaneous
- Chronic hepatitis / cirrhosis
- Hepatic amyloidosis
- Hepatic neoplasia
- Porto-systemic shunting
- Feline hepatic lipidosis
- Cholangitis / cholangiohepatitis
- Septicemia / endotoxemia
5. Traumatic / hypoxic:
- Diaphragmatic hernia
- Heat stroke
- Liver torsion
- Massive ischemia
40
How much liver parenchyma loss is required to start having liver failure
70-75%
41
Why is liver failure often associated with sepsis
- Liver cannot efficiently remove pathogens from portal circulation before they reach systemic circulation (mostly GI pathogens)
- Decreased hepatic synthesis of complement
- Decreased activity of granulocytic cells, cell adhesion, chemotaxis
42
What morphological changes of RBC can be seen with hepatic failure
- Target cells
- Acanthocytes
- Anisocytosis
43
Where is ALT found in the liver? What is its half-life in circulation?
In the cytosol of hepatocytes
Half-life 24-60h
44
Where is ALP found in the liver?
Membranes of hepatocyte canalicular cells and biliary epithelial cells
45
How high does serum bilirubin need to be to cause icterus
40-60 umol/L
46
What is the recommended dose for a lactulose retention enema
0.1-1 mL/kg lactulose diluted 1:3 in warm water
47
What is the recommended protein content recommended in diets fed to patients with hepatic encephalopathy
- Dog: 18-22%
- Cat: 30-35%
Prefer diary or vegetable proteins (higher branched:aromatic amino-acid ratio)
48
Name hepatoprotective medications and their beneficial properties
- S-adenosylmethionine (SAMe) = glutathione precursor + anti-inflammatory
- Vitamin E = anti-oxidant
- Silymarin = anti-oxidant (inhibits lipid peroxidation and increases hepatic glutathione)
- N-acetylcysteine = glutathione precursor
- Ursodeoxycholic acid = anti-inflammatory, immunomodulatory, antifibrotic + promotes choleresis by increasing gallbladder contractility and liquifying bile (which prevents hepatocyte injury by hydrophobic bile acids)
- Zinc = enhances ureagenesis, copper chelation, immune function, glutathione metabolism + anti-fibrotic
- D-penicillamine, colchicine, prednisone = anti-fibrotic
49
What causes increased intrahepatic venous resistance in liver injury
- Changes in hepatic architecture caused by fibrosis and regenerative nodules
- Microthrombi
- Increased vasomotor tone from sinusoidal endothelial cells and hepatic stellate cells
50
How is the splanchnic arterial resistance in portal hypertension
Decreased due to shear stress (vasodilation)
51
What maladaptive response contributes to worsening portal hypertension in patients with chronic portal hypertension
Activation of RAAS system and ADH secretion due to decreased effective circulating volume (from splanchnic vasodilatation) -> water and Na retention -> worsening portal hypertension, ascites
52
What is the classification of portal hypertension? Name examples of causes for each class
1. Pre-hepatic portal hypertension:
- Secondary to PSS attenuation
- Portal vein thrombus
- Extraluminal compression of portal vein
- Congenital portal vein atresia
2. Intra-hepatic portal hypertension:
a. Pre-sinusoidal:
- Hepatic arterio-venous fistulas
- Chronic cholangitis
- Nodular hyperplasia
b. Sinusoidal:
- Chronic hepatitis / cirrhosis
- Primary hypoplasia of the portal vein
c. Post-sinusoidal:
- Veno-occlusive disease
3. Post-hepatic portal hypertension:
- Right heart failure
- Pericardial disease
- Pulmonary hypertension
- Budd-Chiari syndrome (= obstruction of flow in caudal vena cava due to thrombus, neoplasia, extrluminal compression, stenosis)
53
What is a normal portal pressure
~8-9 mmHg (10-12 cmH2O)
54
How is the protein content of ascites correlated with class of portal hypertension
- Pre-hepatic and pre-sinusoidal portal hypertension -> TP < 2.5 g/dL in ascites
- Sinusoidal, post-sinusoidal, post-hepatic portal hypertension -> TP > 2.5 g/dL (leak from lymphatic vessels with more proteins)
55
What are ultrasonographic signs of portal hypertension
- Decreased portal vein blood flow velocity (< 10 cm/s)
- Increase portal vein / aorta ratio
- Hepatofugal flow
- Dilated left gonadal vein
56
What is the management of ascites due to portal hypertension
- Treat underlying cause of portal hypertension if possible
- Sodium restriction
- Spironolactone (+/- furosemide but ideally not)
- Abdominocentesis as needed - recommend emptying 20-50% of volume
57
What is the delay for occurrence of seizures after PSS attenuation
Can take up to 72h in dogs and up to 5 days in cats
58
What is the peri-operative mortality with EHPSS / IHPSS attenuation
- 2.6-7.1% for EHPSS
- 12.% for IHPSS (but might be better with minimally-invasive)
59
What is a proposed mechanism for the development of post-attenuation neurological signs in PSS
Possible abrupt decrease in inhibitory mediators that were elevated due to the PSS (GABA, endogenous benzodiazepines, etc.)
60
What is the incidence of post-attenuation neurological signs in dogs with PSS
~ 3-27%
61
What is the mortality rate for post-attenuation neurologic signs with seizures
~ 70%
62
What is the long-term outcome of dogs that developed neurologic signs after surgical treatment of a congenital portosystemic shunt and survived > 30 days
Overall good outcome (76% survival at 1300 days) but frequent persistent / recurrent neuro signs or seizures
63
How can you differentiate hemolytic icterus from obstructive icterus?
- Hemolytic: unconjugated bilirubin
- Obstructive: conjugated bilirubin
- Total obstruction: no urobilinogen, clay coloured stool
64
Up to what % of liver volume removal is tolerated in dogs?
65-70%
65
How does liver regeneration occur?
- Hepatic arterial buffer response: intrinsic regulatory mechanisms leading to increased arterial perfusion secondary to a lack of washout of adenosine via portal circulation
- Increases in cytokines (IL-6, TNF-alpha), growth factors (hepatocyte growth factor, epidermal growth factor, transforming growth factor-β); vasoregulators (NO, PGE2); and hormones (insulin, estrogen)
66
Name 2 endocrinopathies that have been associated with gallbladder mucocele
- Hypothyroidism
- Hyperadrenocorticism
67
True or false: metastatic tumors of the liver are more common than primary ones
True
68
What are the 4 general types of hepatobiliary tumours? Give examples.
What is the most common primary hepatic tumor in the dog and in the cat?
- Hepatocellular (benign adenomas, hepatocellular carcinoma)
- Cholangiocellular (hepatocellular carcinoma, biliary cystandenoma)
- Neuroendocrine (carcinoma)
- Mesenchymal (hemangiosarcoma - usually metastatic, leiomyosarcoma, osteosarcoma, fibrosarcoma, mesenchymoma, chondrosarcoma)
Most common in dogs: hepatocellular carcinoma
Most common in cats: biliary cystadenomas
69
What is a symptom of hepatic encephalopathy specific to cats?
Ptyalism
70
Biochemical signs of synthetic liver dysfunction
- Hypoglycemia
- Hypoalbuminemia
- Hypocholesterolemia
- Low BUN
- Abnormal bile acids (elevated)
71
What is the role of lactulose in HE?
The role of metronidazole?
Lactulose:
- Allows conversion of NH3 to NH4+ in the gut, preventing absorption of ammonia
- Osmotic cathartic --> decreases GI transmit time
Metronidazole:
- Reduces number of urease producing bacteria in the gut
72
What are the 3 types of necrotizing cholecystitis?
- Type I: Areas of necrosis without GB rupture
- Type II: acute inflammation with rupture
- Type III: Chronic inflammation with adhesions/fistulae to adjacent organs
73
What is the timeline for dilation of the gallbladder, cystic duct and intrahepatic bile ducts in EHBO?
GB and cystic duct ligation within 24h
Intrahepatic bile ducts within 5-7 days
74
What are coleliths most commonly composed of?
Calcium carbonate & bilirubin pigments
75
Describe the hallmark ultrasonographic appearance of GB mucocele.
Echogenic, non mobile material fills the distended gallbladder in either a stellate or finely striated pattern, often with a hypo echoic rim along the wall.
76
True or false: Bacterial infections of the GB are uncommon in dogs with GB mucoceles.
True
77
What has been associated with a poor prognosis in the post-op period of GB mucocele?
Hyperlactatemia and hypotension
78
Why is excessive copper bad?
Damaging to the hepatocytes - oxidative stress, cellular degeneration, death with associated inflammation
79
What are the most common lesions seen in acute vs chronic liver disease?
Acute: hepatocellular necrosis
Chronic: hepatocellular necrosis, fibrosis, inflammation, hyperplasia
80
Explain how ammonia is associated to HE-induced seizures
Ammonia is associated with an increased release of glutamate (major excitatory neurotransmitter in the brain)
--> Overactivation of glutamate receptors (N-methyl-D-aspartate) --> seizures
81
Name causes of coagulopathy in liver failure
- Decreased factor synthesis
- Increased factor utilization
- Decreased factor turnover
- Increased fibrinolysis and tissue thromboplastin release
- Synthesis of abnormal coagulants
- Decreased PLT function and numbers
- Vitamine K deficiency
- Increased production of anticoagulants
82
Explain why PU/PD are commonly seen with liver failure
- Failure of liver to produce urea --> defective renal medullary concentrating ability
- Decreased release and/or responsiveness of collecting ducts to ADH
83
Conversion of bilirubin from umol/L to mg/dL
umol/L x 0.058
84
Biochemical parameter that is a hallmark of chronic liver dysfunction
Hypoalbuminemia - long half life (8 days)
85
When does liver failure have a very good prognosis?
When it is associated with PSS
86
87
Name 4 poor prognostic indicators of hepatic failure
- PT > 100 sec
- Very young or very old animals
- Viral or idiosyncratic drug reaction
- Marked hyperbilirubinemia
Hepato-biliary
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