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.
How is toxic hepatopathy diagnosed?
Based on compatible history and clinical signs. liver enzyme elevation is moderate to severe and primarily hepatocellular or mixed. Bile acids and bilirubin may be normal or elevated. Hypoglycaemia and hypokalaemia may be present. Azotaemia either prerenal or concurrent acute kidney injury may be present.
What is the treatment for toxic hepatopathy?
Some toxicities have specific treeatments. Try to reduce/withdraw offending toxins. Primarily treatment consists of supportive care including IVFT, gastroprotectants, anti oxidants (more specifically indicated for hepatotoxicosis than with other causes of liver disease) and vitamin K if coagulopathy is present.
What is vacuolar Hepatopathy?
Glycogen accumulates in hepatocytes which leads to cell swelling and cholestasis. It is often secondary to corticosteroid or other drug therapy but is recognised as a primary disorder in some breeds such as Scottish terriers. Any breed may develop secondary disorder.
How is vacuolar hepatopathy diagnosed?
Diagnosis: elevation in ALt, GGT and bile acids may be seen. Abdominal ultrasound usually shows hepatomegaly and a diffusely hyperechoic liver. Cytology will show vacuolar change though biopsy needed for definitive diagnosis.
What is the treatment for vacuolar hepatopathy?
No definitive treatment is indicated. Secondary VH is usually reversible with withdrawal of offending agent. No treatment for scottish terrier VH. May be a link between VH and hepatocellular carcinoma in scottish terriers.
What is infectious hepatitis?
Infectious causes of hepatitis. Leptospirosis can cause hepatitis, L grippotyphosa is recognised to cause hepatitis. May be acute or chronic, compatible with efefct on liver function and presence of systemic infection. Characteristic changes of acute hepatitis. Leptospirosis PCR or serology should be performed on suspect cases.
What is cholecystitis/cholangitis?
Bacterial or unidentified pathogen causes biliary tract inflammation/infection which is usually neutrophilic. There may be recent history of enteritis or pancreatitis. Any age or breed may be affected. May include anorexia, jaundice, vomiting and pyrexia.
How is diagnosis of cholecystitis made?
Minimum database can show anaemia of chronic inflammation, neutrophilic leukocytosis and cholestatic liver enzyme elevation, including potentially elevated bilirubin and bile acids. Abdominal ultrasound is indicated to rule out presence of a mucocele and extrahepatic bile duct obstruction. Bile cytology and culture can comfirm presence of neutrophilic inflammation and presence of bacterial infection.
What is a gallbladder mucocele?
Mucoid concretions within the gallbladder can result in biliary obstruction. Numerous endocrinopathies, including diabetes mellitus, hyperadreenocorticism, hypothyroidism and pancreatitis can result in changes to biliary secretions, increasing risk of mucocele. It is recognised as a primary disorder in some breeds.Usually occurs in middle aged to older dogs. Shetland sheepdogs, cocker spaniel and miniature schnauzers seem predisposed. May be incidental.
How is diagnosis made of a gallbladder mucocele and what is the treatment?
minimum databse often shows cholestatic enzyme elevation and elevated bil acid.s abdominal ultrasound shows a classic kiwi gall bladder. Deefinitive treatment is cholecystectomy. Medical therapy includes ursodeoxycholic acid and low fat diet as well as management of any concurrent underlying endocrinopathies.
What is hepatic lipidosis in cats?
A period of anorexia induces a negative energy balance and mobilises fat stores from peripheral fat to the liver. Concurrently, dietary deficiencies of methionine, carnitine and taurine result in inability to process fats for energy metabolism. Hepatocyte swelling leads to cholestasis.
What are the clinical signs of hepatic lipidosis in the cat?
Signs can include jaundic, vomiting, diarrhoea, hepatomegaly as well as signs of hepatic encephalopathy. HE in cats is usually milder and commonly includes Ptyalism and depression. There may be signs of underlying disease which leads to anorexia.
How is hepatic lipidosis diagnosed?
Minimum database can show anaemia of chronic inflammation. Alkaline phosphatase is clasically elevated, moreso than GGT. Alanine transferase is also usually abnormal. Bilirubin may be increased and urea may be decreased with hepatic dysfunction. Hypokalaemia, hypophosphataemia and hypomagnesemia may be present secondary to anorexia and hypokalaemia is associated with a poorer prognosis.
What is the treatment for hepatic lipidosis?
Th most important aspect of treatment is restoration of a positive energy balance which typically requires placement of a feeding tube. Oesophageal feeding tube/nasoesophageal feeding tube placed. Small frequent meals are typically better tolerated. IV fluids and electrolyte supplementation. Vitamin K should be administered for coagulopathy. Anti oxidants are used to replace deficits in glutathionee. Prognosis is good with adequate treatment and management of underlying disease.
What is a neutrophilic cholangitis?
An ascending bacterial infection of the biliary tract which leads to neutrophilic inflammation of the bile ducts and portal tracts, similar to cholangitis in dogs. Most frequently isolated bacteria include E. coli, streptococcus, clostridium and other enteric bacteria. The gallbladder may also be affected. All aged cats may be affected but younger to middle aged cats are more frequently diagnosed.
How is neutrophilic cholangitis diagnosed?
Minimum database typically shows a neutrophilic leukoocytosis with possible left shift. Alanine transferase and bilirubin are most commonly elevated. Abdominal radiographs are usually normal and ultarsound may show biliary tract dilation. Biliary cytology and culture can isolate infective organism and give sensitivity.
What is the treatment for neutrophilic cholangitis?
Cats should be treated with an extended period with appropriate antibiotics (usually 4-6 weeks) until there is resolution of clinical signs and bloodwork changes. Potentiatied amoxicillin can be used pending culture results. Ursodeoxycholic acid would be appropriate to increase choleresis and reduce cell membrane damage.
What is lymphocytic cholangitis?
Lymphocytes infiltrate portal tracts, leading to proliferation of the bile ducts and portal fibrosis. It is likely immune mediated and may present similarly in some respects to FIP. Affects mostly young to middle aged cats. Persians overrepresented. Clinical signs: often present as a chronic waxing and waning illlness. Signs include jaundice, weight loss, anorexia and lethargy. Cats may have high protein ascites.
How is lymphocytic cholangitis diagnosed?
Neutrophilic leukocytosis, liver enzymes may be mild to moderately elevated, hyperglobulinaemia may be present, coagulation times may be prolonged, ultrasound could show biliary tract dilation that can appear like EHBO and ascites may be present.
What is Extrahepatic bile duct obstruction?
Compression of bile duct can occur secondary to intraluminal or extraluminal causes which can include cholangitis, duodenitis, pancreatitis or some bcombination. Biliary neoplasia can also cause EHBO. Choleliths are a rare cause.
What is the treatment for EHBO?
depends on underlying cause. Cats require vitamin K supplementation along with UDCA and anti oxidants. Biliary tract surgery should be avoided if possible because of high perioperative morbidity.
describe Congenital portosystemic shunts in Cats?
Pure bred cats overrepresented. Hepatic encephalopathy signs are more consistent in cats than dogs and may be waxing and waning. Minimum database include decreased urea and microcytosis, remaining changes on bloodwork are less common in cats than dogs. Bile acids tolerance test will be elevated. Abdominal ultrasound may show microhepatica and shunt vessel may be visualised.
What are the clinical signs of liver disease?
Gastrointestinal signs including anoreia vomiting diarrhoea weight loss. Weight loss may occur due to decreased absorption. Jaundice - due to hyperbilirubinaemia (prehepatic from haemolysis, hepatic from decreased liver processing, post hepatic from decreased excreetion). Bleeding - prolonged clotting times can occur, decreased production of clotting facotrs, PU/PD - decreased urea production with liver dysfunction leads to renal medullary washout, altered steroid metabolism, hepatic encephaopathy. Ascites - via decreased oncotic pressure, increased hydrostatic pressure (portal hypertension) or bile peritonitis. Hepatic encephalopathy - ammonia and other bacterial metabolites > brain. increased drug sensitivity - hepatic metabolized drugs have increased plasma levels with hepatic dysfunction.
Describe haematology tests with liver disease?
RBC - iincreased with dehydration, decreased with anaemia of chronic inflammatory disease or chronic GI blood loss or PSS. PSS might have microcytosis without anaemia. Schistocytes, acanthocytes can be seen with liver disease. WBC - sterss or inflammatory leukocgram, platelets- mild to moderately decreased with chronic GI blood loss/ DIC.
Describe the typical biochemistry panel with liver disease?
Elevated ALT: in hepatocyte cytoplasm > indicates hepatocellular damage. Elevated ALP > synthesised by bile caniliculi > indicates biliary stasis. Also produced by bone. 1. Elevated ALP is always significant in cats! Elevated GGT - associated with biliary epithelial cells - indiates biliary hyperplasia/stasis. Usually normal in causes of cholestsis that are outside of biliary treee. More consistently elevated with primary biliary disease. Glucose - decreased with imapired glucoeogenesis or glycogenolysiis by liver 1 - usually lost late in disease process. e. cholesterol - decreased with impaired hepatic production. Urea - decreased with impaired protein metabolism by liver. Albumin - decreased with impaired hepatic production. Bilirubin - increased with prehepatic: hemolysis, hepatic: decreased conjugation and excretion, 3. post hepatic: decreased excretion. Bile acids: bile acids secreted with bile into duoodenum > resorbed in ileum and recycled via portal circulation to liver > absorbed from portal circulation within liver. With PSS there is decreased recycling of bile acids > increased serum bile acids.
What would show in urinalysis with liver disease?
Urine specific gravity - increased with dehydration, decreased with polyuria/polydipsia. Bilirubinuria - dogs normally conjugate some bilirubin in kidneys that reacts with urine test so small amounts can be normal. Always abnormal in cats. Urate/bilirubin crystals or stones may be present in bladder and can be supportive of liver disease.
What would A coagulation panel show in Liver disease?
PT/PTT would be increased due to decreased production of clotting factors and decreased recycling of vitamin K. Fibrinogen - decreased due to impaired hepatic production or increased consumption. Or may be increased in some chronic inflammatory diseases. D-dimers - increased with liver disease or DIC.
What would happen to ammonia in liver disease?
Normally produced by gut bacteria and absorbed in portal circulation > removed by first pass metabolism and converted to urea by liver > excreted via kidneys. Increased with PSS or svere liver dysfunction. Often causes HE - can occur without hyperammonemia. Lactulose used to treat elevated ammonia orally or rectally - traps ammonia in gut as ammonium to reduce absorptiion. Given a enema will work fairly quickly usually 10-15 minutes.
What will happen to protein C with liver disease?
Protein C is an anticoagulant protein produced by the liver. It is decreased with liver dysfunction. A degree of derangement may help differentiate between PSS and non PSS liver disease dogs. May also differentiate between congenital PSS and portal vein hypoplasia. Improves with correction of congenital PS.
What will appear on abdominal radiographs when liver disease is present?
Liver size is approximated by looking at gastric axis. Normal > approximately parallel to last ribs. Hepatomegaly > higher angle of gastric axis. Microhepatica > decreased angle of axis. May see hepatic masses or choleliths. Decreased abdominal detail may indicate ascites. Overall relatively insensitive for liver disease.
Describe what will be seen on abdominal ultrasound with liver disease?
Allow for assessment of hepatic and biliary tract size, architecture and presence of masses/tumours. Variable sensitivity to detect portosystemic shunts. Allows fr FNA of liver cytology.
What will hepatic cytology show in liver disease?
May b e diagnostic for infiltrative neoplastic diseases. May be suggestive of infiltrative non neoplastic diseases but does not rule out concurrent separate liver disease. Quite poor for cirrhosis, some liver tumours, copper storage disease, many forms of hepatitis/cholangitis.
What is nuclear scintigraphy and how is it used in liver disease?
A radioisotope is injected into colonic lumen via catheter or splenic parenchyma > absorption of isotope tracked > degree of shunting of isotope bypassing liver directly to hear it is quantified. Shunt fraction can be diagnostic for PSS. Does not differentiate acquired from congenital. May be normal with smaller degree of shunting. Largely replaced by CT angiography but may be done with sedation.
What is CT angiography?
CT scan of abdomen with injection of contrast to delineate portal vasculature. Usually confirms the presence or absence of PSS. Allows for assessment of hepatic biliary size/architecture.
