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primary hepatic tumors, metastatic disease, nodular hyperplasia, vascular anomalies (congenital, acquired portosystemic shunts, portal vein hypoplasia, arteriovenous malformations)
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What percentage of hepatic masses in dogs are primary tumors versus metastatic?
~50% are metastatic, ~50% are primary.
What is the most common primary hepatic neoplasm in dogs?
Hepatocellular carcinoma (HCC).
What is the most common primary hepatic neoplasm in cats?
Biliary (cholangiocellular) carcinoma.
What are the three morphologic forms of hepatic neoplasia?
Massive, nodular, and diffuse.
Which form of hepatic neoplasia is most amenable to surgical resection?
Massive (solitary large mass in one lobe).
Which form of hepatic neoplasia is usually metastatic or infiltrative?
Diffuse (multilobar or infiltrative lesions).
What are common clinical signs of hepatic neoplasia?
Lethargy, anorexia, weight loss, vomiting, hepatomegaly, icterus, sometimes ascites or hypoglycemia.
What laboratory abnormalities are typical in hepatic neoplasias?
Mild to marked ALT/ALP increases, hyperbilirubinemia, sometimes hypoglycemia (from paraneoplastic insulin-like growth factor).
What imaging features suggest neoplasia over inflammation?
Focal mass effect, distortion of hepatic margins, variable echogenicity, or vascular invasion.
What are the three forms of hepatocellular carcinoma (HCC) in dogs?
Massive, nodular, and diffuse.
Which is most common and most surgically resectable form of HCC in dogs?
Massive HCC — typically a single mass in the left lateral lobe.
What is the behavior of the massive form of HCC?
Usually non-metastatic and slow-growing.
What is the behavior of the nodular and diffuse forms of HCC?
Often multicentric and may metastasize to lungs or lymph nodes.
What are the imaging features of HCC?
Large, heterogeneous, hyperechoic or mixed echogenicity mass with vascular invasion possible.
What diagnostic methods confirm HCC?
Cytology (suggestive), histopathology (definitive), and contrast-enhanced CT (vascular mapping).
What is the treatment of choice for resectable HCC?
Surgical lobectomy.
What is the prognosis for resectable massive HCC?
Excellent — median survival > 3–4 years.
What is the prognosis for diffuse HCC?
Poor to grave; rarely resectable.
What paraneoplastic syndromes can occur?
Hypoglycemia, hypercholesterolemia, erythrocytosis.
What is the most common hepatic tumor in cats?
Biliary carcinoma (cholangiocellular carcinoma).
What cells does biliary carcinoma (cholangiocellular carcinoma) originate from?
Bile duct epithelium.
What is the biological behavior of biliary carcinoma?
Highly malignant, infiltrative, and often metastatic to lungs and lymph nodes.
What are common clinical signs of biliary carcinoma?
Icterus, vomiting, weight loss, and palpable hepatomegaly.
What does ultrasound typically show with biliary carcinoma?
Irregular, hypoechoic or mixed echogenicity nodules, possibly with biliary dilation.
How is diagnosis of biliary carcinoma confirmed?
Biopsy and histopathology showing glandular or ductular epithelial proliferation.
What is the treatment of choice for biliary carcinoma?
Surgical resection if localized; palliative care for diffuse disease.
What is the prognosis of biliary carcinoma?
Guarded to poor — median survival ~6 months for cats, 1 year for dogs.
What is hepatic nodular hyperplasia?
A benign, age-related proliferation of hepatocytes.
Which species is most commonly affected by hepatic nodular hyperplasia?
Older dogs (>10 years).
What is the clinical significance of hepatic nodular hyperplasia?
Usually incidental, but may elevate ALT/ALP mildly.
How can hepatic nodular hyperplasia be differentiated from neoplasia?
Regular margins, homogeneous appearance, and no invasion on imaging; confirmed by biopsy.
Is treatment needed for hepatic nodular hyperplasia?
No; monitor with periodic imaging and liver enzymes.
What are other less common primary hepatic tumors?
Hepatoblastoma, hemangiosarcoma, leiomyosarcoma, neuroendocrine carcinoma.
What is the most common malignant vascular tumor?
Hepatic hemangiosarcoma.
What are typical signs of hemangiosarcoma?
Sudden collapse, hemoabdomen, anemia, and hypovolemic shock.
How is hepatic hemangiosarcoma diagnosed?
Imaging (cavitated mass, free fluid), cytology (bloody aspirate), biopsy.
What is the treatment for hemangiosarcoma?
Surgery ± chemotherapy (doxorubicin-based).
What is the prognosis for hepatic hemangiosarcoma?
Poor — median survival <6 months.
What is the most common cause of multiple hepatic nodules in older animals?
Metastatic neoplasia (from spleen, pancreas, GI tract, mammary, adrenal).
How are metastatic lesions distinguished from primary tumors in the liver?
Multiple lesions in multiple lobes, irregular margins, often with known primary elsewhere.
Define portosystemic shunt (PSS).
An abnormal vascular connection allowing portal blood to bypass the liver and enter systemic circulation.
What are the two main categories of PSS?
Congenital and acquired.
What is the key difference between congenital and acquired PSS?
Congenital: single large vessel, no portal hypertension.
Acquired: multiple small vessels secondary to portal hypertension.
What breeds are predisposed to congenital extrahepatic PSS?
small breeds (Yorkshire Terrier, Maltese, Mini Schnauzer).
What breeds are predisposed to intrahepatic PSS?
Large breeds (Irish Wolfhound, Labrador Retriever).
What are the clinical signs of PSS?
Stunted growth, neurologic signs (HE), PU/PD, vomiting, ammonium biurate crystalluria.
What are key lab findings of PSS?
Low BUN, low albumin, hypocholesterolemia, elevated bile acids, high ammonia.
What imaging findings are characteristic for PSS?
Small liver, large kidneys, abnormal shunt vessel seen on CT angiography or ultrasound.
What is the gold-standard diagnostic tool for PSS?
CT angiography or nuclear scintigraphy.
What is the treatment of choice for congenital PSS?
Gradual surgical attenuation using ameroid constrictor or cellophane banding.
What preoperative management is necessary prior to PSS sx?
Control HE (lactulose, diet), correct electrolytes, give antibiotics.
What are potential postoperative complications for PSS?
Seizures, portal hypertension, ascites.
What is the prognosis for congenital PSS with surgery?
Good to excellent — ~80–90% clinical improvement.
What is the management for acquired PSS?
Medical only — treat underlying portal hypertension and HE; surgery contraindicated.
What is portal vein hypoplasia (PVH)?
A congenital reduction in the size or number of intrahepatic portal veins.
What breeds are predisposed to portal vein hypoplasia (PVH)?
Yorkshire Terrier, Maltese, Cairn Terrier, Dachshund.
How does PVH differ from congenital PSS?
No macroscopic shunt vessel; microscopic portal underperfusion.
What are clinical signs of PVH?
Often asymptomatic or mild hepatic encephalopathy.
What are typical lab findings of PVH?
Mild increases in bile acids, mild ALT elevation.
How is PVH diagnosed?
Biopsy (decreased or absent portal veins, arteriolar proliferation)
What is the treatment for PVH?
Medical management for HE if symptomatic (diet, lactulose, antibiotics).
What is the prognosis for PVH?
Excellent — most dogs live normal lives.
What is a hepatic arteriovenous malformation (AVM)?
Abnormal communication between hepatic artery and portal vein.
What are the effects of AVM?
Increases portal pressure → portal hypertension and ascites.
How is AVM diagnosed?
Doppler ultrasound or CT angiography showing turbulent, mixed arterial/venous flow.
What is the treatment of AVM?
Surgical ligation or coil embolization if localized.
What causes portal vein thrombosis?
Inflammation, neoplasia, hypercoagulability, pancreatitis, or sepsis.
What are clinical signs of portal vein thrombosis?
Acute abdominal pain, ascites, vomiting, or GI bleeding.
How is portal vein thrombosis diagnosed?
Ultrasound showing echogenic thrombus with absent or reversed flow.
How is portal vein thrombosis treated?
Anticoagulants (heparin, clopidogrel), supportive therapy, and treating the underlying cause.