Lecture 12 2/10/25 Flashcards
What are the different classifications for hepatobiliary dz?
-inflammatory vs. non-inflammatory
-hepatocellular vs vascular vs biliary
-primary vs secondary
How does the occurrence of primary vs secondary hepatobiliary dz differ between dogs and cats?
-dogs are more likely to have inc. liver enzymes due to secondary dz
-cats are more likely to have inc. liver enzymes due to primary dz
What are hepatic vascular diseases?
-conditions causing abnormal blood flow within or around the liver
-lead to liver atrophy and buildup of toxins within the system
What are the congenital hepatic vascular diseases?
-macroscopic congenital portosystemic shunts; extrahepatic and intrahepatic
-primary portal vein hypoplasia; with or without portal hypertension
What is the acquired hepatic vascular disease?
multiple extrahepatic shunts, secondary to hepatic fibrosis or hepatic arteriovenous malformations
What are the characteristics of CPSS etiology?
-heritable disease
-single genetic causal mutation NOT identified
-likely has a complex polygenic etiology
What is the pathophysiology of hepatic venous hypoperfusion?
-leads to decreased hepatic clearance of nutrients and waste products from GI portal drainage
-leads to reduced hepatic size, histologic changes in the liver, and alteration of normal metabolic function
-can cause hepatic encephalopathy due to decreased metabolism of ammonia and other substances from portal circulation
What is the pathophysiology of microvascular dysplasia?
-abnormal blood flow through the hepatic sinusoids
-minimal systemic consequences
What is the clinical presentation of extrahepatic CPSS?
-usually identified within first 2 years of life
-can be detected at any age
-more common in small breeds
-no gender predisposition
What is the clinical presentation of intrahepatic CPSS?
-usually more severe signs
-detected before 1 year of age
-more common in large breeds
-no gender predisposition
What is the clinical presentation of microvascular dysplasia?
-same signalment as small breed dogs with extrahepatic CPSS
-can occur simultaneously with extrahepatic CPSS
What are the neurologic signs seen in patients with hepatic vascular dz?
-reduced mentation
-altered behavior
-ataxia
-head pressing
-circling
-tremors
-blindness
-seizures
-coma
What are the GI signs seen in patients with hepatic vascular dz?
-vomiting
-diarrhea
-pica
-GI bleeding/melena
What are the urinary tract signs seen in patients with hepatic vascular dz?
-hematuria
-dysuria
-stranguria
What are the miscellaneous clinical signs seen with hepatic vascular dz?
-PU/PD
-small stature
-poor BCS
-intolerance to sedatives/anesthetics
-hypersalivation
-copper-colored irises
-intermittent pyrexia
What are the differential diagnoses for hepatic vascular dz based on clinical signs?
-reactive hepatopathy
-portal hypertension with multiple acquired PSS
What are the common abnormalities found on CBC/chem/UA in animals with CPSS?
-microcytosis +/- anemia
-hypoalbuminemia
-decreased BUN
-hypocholesterolemia
-hypoglycemia
-increased liver enzyme activities
-low USG
-ammonium biurate crystals
What are more specific tests that can be run in patients with suspected hepatic vascular dz/CPSS?
-paired total serum bile acids (rule out parenchymal hepatic dz and cholestasis)
-plasma NH3
-protein C
What are the characteristics of CT angiography for patients with vascular dz/PSS?
-gold standard imaging modality
-used for surgical planning of shunt attenuation
What are the characteristics of abdominal ultrasound for patients with vascular dz/PSS?
-operator dependent
-can identify microhepatica, renomegaly, nephrolithiasis, urolithiasis, and decreased portal vein to aorta ratio
What are the limitations of trans-splenic scintigraphy?
-use of radionuclide
-suboptimal shunt localization
What are the characteristics of microvascular dysplasia?
-malformed intrahepatic portal microvasculature
-usually no signs of illness
-possible to see mild increase of hepatic transaminases
-no other clin path abnormalities
-serum bile acids elevated
How is microvascular dysplasia diagnosed/managed?
-protein C to distinguish from macroscopic PSS
-CT angiography/scintigraphy to confirm
-no specific therapy indicated; be careful with use of drugs metabolized via liver
What are the characteristics of PSS medical management?
-should be done in all dogs with PSS regardless of whether attenuation sx is planned
-lifelong if attenuation is not an option
-goal is to reduce elevated systemic NH3
-involves dietary modification, acceleration of GI transit, and modulation of gut microbiota
What are the three goals when managing hepatic encephalopathy?
-reduce incidence of predisposing factors
-alleviate neurologic signs
-identify underlying hepatic condition for more specific management
What are the characteristics of appropriate nutrition for patients with PSS?
-commercially available liver diets are a good starting point
-start low with protein and gradually increase to levels that can be tolerated without causing hepatic encephalopathy signs
-soy and dairy proteins are best
-avoid red meat, fish, and organ meat
Which products can be used for gut microbiota modulation?
-antibiotics
-probiotics
What are the characteristics of nonabsorbable disaccharides?
-laxative effects decrease gut transit time
-decrease activity of bacterial ureases and enteric peptidases to increase bacterial nitrogen fixation
-acidify enteric pH to trap ammonia in the gut as ammonium ions and prevent absorption
What are the treatment steps for patients with severe overt encephalopathy?
-fluids
-elevate head to reduce aspiration risk
-IV antibiotics to modify gut flora
-cleansing enema
-lactulose retention enemas to reduce NH3 resorption
What are the treatment options for pets experiencing seizures due to hepatic encephalopathy?
-IV levetiracetam
-propofol CRI
-mannitol to induce osmotic diuresis
Why should benzos be avoided in seizuring patients?
they can worsen the encephalopathy signs
What are the surgical options for extrahepatic congenital PSS attenuation?
-silk suture ligation
-ameroid constrictor application
-cellophane banding
What are the surgical options for intrahepatic congenital PSS attenuation?
-suture ligation
-endovascular coil embolization
What are the perioperative management steps for patients undergoing shunt attenuation?
-levetiracetam for at least 1 day prior to surgery to reduce post-op seizure risk
-proton pump inhibitors pre- and post-op to decrease incidence of GI ulcers
-post-op rechecks at 2 weeks, 1 month, 3 months, and 6 months
-tapering of medical therapy as signs improve
-protein C evaluation at re-checks
-additional surgery or medical management in animals not improving
What is the prognosis of hepatic vascular dz?
-depends on severity of signs and management strategy
-PSS attenuation provides longer survival than medical management
-microvascular dysplasia has good prognosis
What is acute liver injury?
severe hepatocellular damage in a patient without previous hx of liver dz
What does acute liver failure manifest with?
-hyperbilirubinemia
-impaired coagulation
-overt hepatic encephalopathy
What are the most common causes of ALI/ALF?
-toxic
-infectious
-neoplastic
-idiopathic
What is the pathophysiology of ALI/ALF?
-severe acute hepatocellular injury results in cell death and organ dysfunction
-death and dysfunction leads to synthetic failure
-mechanism of action varies with etiology
What are the clinical signs of ALI/ALF?
-acute hepatic encephalopathy
-acute GI signs
-icterus
-ascites
-hypotension
-circulatory/hemorrhagic shock
What is the clin path seen in ALI/ALF patients?
-increased leakage enzymes; ALT, AST
-abnormal liver function parameters; decreased GUAC, increased bilirubin
-abnormal coagulation; prolonged PT/PTT, decreased fibrinogen
What is seen on diagnostic imaging in patients with ALI/ALF?
-often non-specific
-normal or enlarged liver size
-rounded edges
-diffusely hypo- or hyperechoic
How is ALI/ALF diagnosed?
Presumptive:
-history
-clinical signs
-clin path +/- cytology
-diagnostic imaging
Definitive:
-liver biopsy
What are the treatment steps for ALI/ALF patients?
-fluid therapy
-vasopressors for hypotension not responding to fluids
-decontamination in toxin ingestion cases
-antidotes for intoxication/ingestion where indicated
-hepatoprotectants
-vitamin K if coagulation is abnormal
What is the treatment for hepatic encephalopathy?
mild, overt: oral lactulose and GI flora modulation
severe, overt: intensive supportive care
What are the treatment options available for patients with secondary conditions such as GI ulcers and ascites?
GI ulceration: omeprazole and antiemetics
ascites: spironolactone +/- furosemide
Why is it questionable to use antibiotics in ALI/ALF patients?
-reason for wanting to use antibiotics is to protect against infectious complications
-cannot use agents metabolized by liver or that are hepatotoxic; limits drug choices
What should be monitored in ALI/ALF patients?
-CBC
-chem
-UA
-coag. panel
-hepatic transaminase reduction
-bilirubin and hepatic synthetic factors
What is the prognosis for ALI/ALF?
-variable
-severely elevated transaminases are NOT poor prognostic indicators
-normal albumin in ALF is a good survival indicator
