Liver Flashcards
What is the signalment for chronic hepatitis?
Any age or b reed, though Labrador retrievers, west highland white terriers, skye terriers, doberman pinschers, cocker spaniels and english springer spaniels have been described as more frequently affected.
What is chronic hepatitis?
The underlying cause is usually unidentified but may be infectious or toxic insult that sets up chronic inflammation or may in some cases be primarily autoimmune. Inflammation is mixed, most often lymphocytic-plasmacytic. Chronic inflammation leads to fibrosis, which can cause portal hypertension and lead to the development of acquired portosystemic shunts.
What are the clinical signs of chronic hepatitis?
Typically occur late in the disease process when there had been over 75% functional liver capacity lost. May include vomiting, diarrhoea, anorexia, weight loss, pu/Pd, jaundice ascites, and Hepatic encephalopathy.
How is chronic hepatitis diagnosed?
Haematology is often normal but may include anaemia of chronic inflammatory disease and or neutrophilic leukocytosis. early on in the disease process, liver enzymes may be mild to moderately elevated. Later on with more fibrosis, liver enzymes may be normal but indicators of liver function (urea, bbile acids, bilirubin, albumin, cholesterol, glucose) may be abnormal. Coagulation times may be prolonged. Liver size may be decreased on abdominal radiographs and abdominal utlrasound. Bile acids tolerance test is abnormal once dysfunction has occurs or acquired portosystemic shunts are present. Hepatic biopsy needed to confirm diagnosis and provide prognostic information.
How is chronic hepatitis treated?
Manage as with hepatic dysfunction. Diet should be moderately restricted, high quality protein that is easily diigestible. Cottage cheese may be added to increase palatability and provide a good protein source. antioxidant therapy including s-adenosylmethionine, vitamin E and milk thistle may be of benefit, though there is no medical evidence to support its use. Ursodeoxycholic acid promotes choleresis and decreases toxic bile salts. Also little evidence to support use but may be of benefit, also little evidence to support use but may be of benefit. Antibiotics may be indicated: metronidazole or amoxicillin for hepatic encephalopathy. Amoxicillin if leptospirosis is considered possible. Anti inflammatory doses of glucocorticoids may be helpful to reduce inflammation.
What is the prognosis for chronic hepatitis?
Varied, depending on severity of the disease. Best outcomes if treated early but if significant cirrhosis is present, especially with concurrent severe liver dysfunction or portal hypertension, prognosis is guarded (weeks to a month or two with supportive care)
What is copper storage hepatitis?
Copper is normally excreted in bile. With defects in copper excretion (perhaps via an identified mutation), copper accumulates leading to secondary inflammation and eventual fibrosis. Copper may accumulate also as a secondary process to primary inflammatory hepatitis but the distribution of copper within the portal triad is typically different.
What is the signalment for copper storage hepatitis?
Multiple breeds have been identified to have suspected primary copper accumulation causing hepatitis: Bedlington terrier, Labrador retriever dalmation, doberman, WHWT, skye terrier. A mutation in copper excretion has only been identified in bedlingtons. Dogs can present at any age.
What are the clinical signs of copper storage hepatitis?
Typically occur late in the disease process and may be waxing/waning or more acute on chronic (vague signs of illness chronically with sudden deterioration). Clinical signs will be as for chronic hepatitis. Susceptible breeds with elevated liver enzymes should be investigated with biopsy.
How is copper storage hepatitis diagnosed?
Bloockwork/liver function changes will be identical to chronic hepatitis. Biopsy with copper quantification is needed to differentiate. Distribution of copper in this disease is usually centrilobular (around central vein); if copper accumulates secondary to chronic hepatitis it is typically milder and periportal.
What is the treatment for copper storage hepatitis?
General medical management as with chronic hepatitis. Specific treatment for opper storage disease includes addition of zinc acetate or zinc gluconate to diet to bind dietary copper. Patients that are systemically ill or have very high hepatic copper levels may need copper chelation therapy with D -penicillamine for several months but then dogs can typicaly be maintained on hepatic diet and zinc supplementation.
What is a congenital portosystemic shunt?
A congenital vascular anomaly remains persistently patent after birth, connecting portal circulation directly to systemic circulation bypassing the hepatic parenchyma. Because the anomalous vessel is a lower pressure system the hepatic parenchyma, blood preferentially shunts past the liver. May be extrahepatic or intrahepatic.
What is the signalment for PSS?
Small breed dogs more frequently, Yorkshire terrier, WHWT, Maltese terrier, miniature schauzer, other small breed. Larger breed dogs more frequently have intrahepatic shunts, Labrador retriever, irish wolfhound etc. Dogs typically present under 1 year, t hough dogs with some normal portal circulation may have milder signs and present as adults.
What are the clinical signs of a PSS?
Presenting signs can be neurologic,GI, urinary or general body condition. Hepatic encephalopathy: depression, lethargy, circling, blindness, seizures. GI: vomiting, diarrhoa, anorexia. Urinary: PU PD, cystolith, urate crystals.
How is PSS diagnosed?
Minimum database most often shows a microcytic hypocrhomic anaemia, normal to mildly elevated liver enzymes, and low urea though may be unremarkable. Bile acid tolerance test is extremely sensitive for PSS but not specific - many other liver and non liver diseases may give abnormal bile acids without PSS. Abdominal ultrasound is essentially the opposite - it is specific but not sensitive.
What is treatment for PSS?
Attenuation of the shunt vessel via surgery (extrahepatic) or transjugular coil embolixation (intrahepatic). Cases are usually medically managed before definitive treamtne to make them more stable. Medical management may adequately control signs of patients for whom definitive treatment is not an option due to cost. Medical management consists of hepatic diet, oral lactulose and metronidazole or amoxicillin for HE signs and anti epileptics.
What is portal vein hypoplasia?
The portal vasculature within the liver is under developed.
What is the signalment for Portal vein hypoplasia?
As with extrahepatic PSS, though typically patients are slightly older at time of presentation.
How is Portal vein hypoplasia diagnosed?
As with PSS, though bile acids tolerance test is usually less elevated than with congenital PSS. Diagnostic imaging is used to rule out PSS. Hepatic biopsy is used to confirm diagnosis though often medical management is instituted in suspected patients based on breed, clinical signs and lack of pss.
What is non cirrhotic portal hyeprtension?
Similar to portal vein hypoplasia but with Secondary portal hypertension, may develop multiple acquired PSS but do not have cirrhosis. Occurs in any breed, usually presents as young adult, more often large than small breed.
How is non cirrhotic portal hypertension diagnosed?
As with PSS, though on ultrasound and CT the liver is typically small. There is usually ascites, portal hypertension and may be multiple acquired extrahepatic shunts visualised. Liver biopsy needed for definitive diagnosis.
What is the treatment for non cirrhotic portal hypertension
Medical management as with PSS. Gastroportectants may be indicated. Drainage of ascitic fluid should be avoided whenever possible because it will exacerbate concurrent hypoalbuminaemia.
What is drug/toxic hepatopathy?
Ingestion of hepatotoxin treatment with hepatotoxic drug may lead to oxidant injury and subsequent inflammation eventually leading to fibrosis. Common offenders include paracetamol, phenobarbital , xylitol, aflatoxin, lomustine. May affect any age or breed of dog.
What are the clinical signs of drug/toxic heptopathy?
Usually acute and may include vomiting, diarrhoea, anorexia, weight loss, PU/PD HE, jaundice, bleeding from acquired coagulopathy.
