C12 pt 2 Flashcards
liver fibrosis involves activation of what cells?
- when reversible? permanent?
o Potentially reversible in acute, self-limiting injury
o In severe injury, cross-links and becomes resistant to degradation, leading to
permanent scarring
o In persistent injury, becomes progressive and can lead to cirrhosis
o Variety of possible patterns…
Fibrosis along the Space of Disse leads to
o Fibrosis along the Space of Disse leads to loss of endothelial fenestration
(capillarization) and impairs exchange between hepatocytes and blood
o Hypoxia leads to accompanying hepatocellular atrophy
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Dissecting fibrosis – worst prognosis
liver cirrhosis: when do we see it?
Cirrhosis: nodular regeneration, bridging fibrosis, vascular disruption, biliary hyperplasia
o Associated with hepatic insufficiency
o End result of multiple pathological processes
o Nodules have increased cellular mass but
less sinusoidal space
o Fibrosis contributes to portal hypertension
(ascites)
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* Nodules do not always mean cirrhosis!
o Dogs are the only species that tend to form
regenerative nodules
signs of liver dysfunction often manifest where?
- Signs of dysfunction often manifest in other organs (brain, skin, gut)
acute liver failure
- is it common? causes?
Acute liver failure is uncommon and due to severe and rapid injury
o Usually toxins, sometimes hyperthermia or acute ischemia
Chronic liver failure subdivisions and what they are
Chronic liver failure is subdivided into end stage liver (failure due to progressive fibrosis and loss of functional mass) and acute-on-chronic (a compensated failing liver suddenly flips into acute failure)
Hepatic encephalopathy cause, signs, prognosis
o Ammonia toxicity is important (mostly derived from dietary protein, detoxified and removed by the liver)
o Ammonia crosses the blood-brain barrier, damages astrocytes and reduces brain metabolism
o Variable neurologic signs
§ Ruminants: blindness, dullness
§ Horses: mania
§ Dogs and cats: subtle (inappetence, vomiting)
o Can cause death due to cerebral edema
o Poor prognosis in acute disease, less negative indicator in chronic disease
Cholestasis - whats this? leads to? types?
Cholestasis: impaired bile secretion and/or flow
o Leads to increased bilirubin in the blood
o Can be hepatocellular (altered function) or obstructive
Jaundice
- what is it? where to look?
Jaundice: yellow pigmentation of tissues due to excess plasma bile pigments
o Most prominent in the sclerae
o Do not mistake carotenoids in fat for jaundice! (horses, channel island cows: look
for pigment in connective tissue of dermis and periosteum to confirm jaundice)
Cholestasis and jaundice
- cateogires of jaundice?
- cholestasis always associated with what?
- NO JAUNDICE in what type of cholestasis?
o Jaundice can be prehepatic (ex. hemolysis), hepatic (altered function), or posthepatic (ex. obstruction) in cause
o Cholestasis is always associated with ductular reaction; in later stages may develop concentric fibrosis around bile ducts
o NO JAUNDICE in focal cholestasis – unaffected regions are still working
Photosensitization - what is it
- primary?
- hepatogenous?
o Inflammation of skin (usually unpigmented) due to action of UV light on photodynamic compounds bound to dermal cells
o Primary: the liver excretes unchanged native compounds that the animal ingested (ex. St. John’s wort)
o Hepatogenous: caused by cholestasis in herbivores eating green forages
> Plant porphyrins are catabolized to phytoporphyrins and normally excreted in
bile, but if retained they can cause photosensitization
Coagulopathy/hemorrhage
- more likely in what liver pahtology?
- will we see hemorrhage in chronic disease?
o Uncommon in acute liver failure, but more likely in acute liver necrosis
o Necrosis causes consumption of clotting factors in the necrotic areas
o In chronic disease, there is usually no hemorrhage due to reduced clotting
factor production unless there is increased pressure on the clotting cascade
o Ex. surgical procedures
Edema/ascites
- what is it, when do we see?
o Ascites is low protein fluid, can form in chronic liver failure but more commonly seen with venous congestion
o Reduced protein production by the liver can contribute but ascites mainly forms due to increased sinusoidal pressure
Hepatocutaneous syndrome
- what species? signs?
o Also called superficial necrolytic dermatitis (SND), mostly seen in dogs
o Erythema, crusting, exudate, ulceration and alopecia of the footpads, periocular/perioral region, anogenital region, pressure points
Congenital portosystemic shunt (PSS) - what is not connected properly?
- types?
- compare with acquired PSS?
- signs
- Tx
o Aberrant connection between the portal vein and vena cava (portocaval) or azygous vein (portoazygous)
o Can be extrahepatic or intrahepatic, most common in dogs and cats o Regardless of location, always a single vessel (compare with
acquired PSS later…)
o Clinical signs: failure to thrive, +/- hepatic encephalopathy
o Hypoplastic liver (not getting growth factors from the gut)
o No portal hypertension = no ascites
o Typically respond well to shunt ligation but not always
