Lecture 12 2/10/25 Flashcards by Danika Boltz

What are the different classifications for hepatobiliary dz?

-inflammatory vs. non-inflammatory
-hepatocellular vs vascular vs biliary
-primary vs secondary

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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

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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

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What are the congenital hepatic vascular diseases?

-macroscopic congenital portosystemic shunts; extrahepatic and intrahepatic
-primary portal vein hypoplasia; with or without portal hypertension

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What is the acquired hepatic vascular disease?

multiple extrahepatic shunts, secondary to hepatic fibrosis or hepatic arteriovenous malformations

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What are the characteristics of CPSS etiology?

-heritable disease
-single genetic causal mutation NOT identified
-likely has a complex polygenic etiology

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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

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What is the pathophysiology of microvascular dysplasia?

-abnormal blood flow through the hepatic sinusoids
-minimal systemic consequences

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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

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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

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What is the clinical presentation of microvascular dysplasia?

-same signalment as small breed dogs with extrahepatic CPSS
-can occur simultaneously with extrahepatic CPSS

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What are the neurologic signs seen in patients with hepatic vascular dz?

-reduced mentation
-altered behavior
-ataxia
-head pressing
-circling
-tremors
-blindness
-seizures
-coma

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What are the GI signs seen in patients with hepatic vascular dz?

-vomiting
-diarrhea
-pica
-GI bleeding/melena

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What are the urinary tract signs seen in patients with hepatic vascular dz?

-hematuria
-dysuria
-stranguria

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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

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What are the differential diagnoses for hepatic vascular dz based on clinical signs?

-reactive hepatopathy
-portal hypertension with multiple acquired PSS

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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

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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

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What are the characteristics of CT angiography for patients with vascular dz/PSS?

-gold standard imaging modality
-used for surgical planning of shunt attenuation

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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