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Diagnosis of Liver Disease in Dogs & Cats

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Diagnosis of Liver Disease in Dogs & Cats by Dr. Kanwarpal Singh Dhillon

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Diagnosis of Liver Disease in Dogs & Cats

  1. 1. DIAGNOSISOF LIVERDISEASES & HEPATIC ENCEPHALOPATHY Submitted by: Kanwarpal Singh Dhillon M.V.Sc (Medicine)
  2. 2. Location of liver in dog  It located cranial part of stomach & intestine , caudal to diaphram.  Bulk of liver located on the right side.
  3. 3. Location of liver of cat
  4. 4. Function of liver Liver plays a central role in a many of processes Including :-  Carbohydrate, lipid,& protein metabolism ,  Detoxification of metabolites and xenobiotics,  Storage of vit, trace minerals, fat, glycogen.  Production of bile, release into GIT to help breakdown of fats.  Production of several clotting factors, & protein mainly albumin.
  5. 5. General Considerations Clinical & laboratory abnormalities associated with liver failure are diverse. The diagnostic strategy include:  Clinical, laboratory & radiographic studies to identify the liver disease  Characterization of the functional aspects of the hepatic disease  Determination of an etiologic or histologic diagnosis – req. a liver biopsy  In acute hepatic failure – toxic or infectious causes are common, & intensive supportive care is req. for hepatic regeneration  In chronic disorders – irreversible changes (cirrhosis); long term prognosis may be favorable
  6. 6. Clinical Signs  Vomiting – common sign of liver disease. Hematemesis suggests gastroduodenal ulceration  Diarrhea – occurs less frequently than vomiting  Polyuria & polydipsia (PU/PD)  Pigmented urine (bilirubinuria) & jaundice (icterus) of the sclera, oral mm.,& skin  Alcholic (gray-colored) feces occur secondary to severe cholestasis  Excessive bleeding (hemorrhages of the skin, melena, hematuria) due to clotting abnormalities, vit. K malabsorption.  Ascites – in severe chronic liv.disease. - ascites & edema formation in liv.disease includes: - hypoalbuminemia - portal hypotension - renal retention of Na+ & H2O
  7. 7. Ascites Alcholic
  8. 8.  Hepatic Encephalopathy : - metabolic encephalopathy - occurs secondary to severe liv. disease & portosystemic shunting of blood - Ammonia, Mercaptans, short-chain fatty acids & gamma-aminobutyric acid (GABA) are potential encephalopathic toxins - produced in the colon by bacterial action on various subtrates - normally, liver detoxifies these subtances, systemic conc. are low - With severe liv. disease or portosystemic shunting, these potential toxins reach high conc. in syst.circulation & CNS - High protein diet causes exacerbation of encephalopathy, bcz protein is subtrate for toxins (ammonia & mercapans)
  9. 9.  Clinical signs : - Behaviour changes - Altered consciousness -Motor disturbances -Seizures - Coma
  10. 10. History & Signalment  Breed predilections for specific liv.diseases.  Congenital hepatic disorders (portosystemic shunt) are common in Young animals.  To characterize the clinical course of liv.disease as Acute or Chronic.  History of drugs intolerance, which normally metabolized by liver (sedatives, transquilizers, anticonvulsants, anesthetics)  Determine current vaccination status – exposure for infectious agents which affect the liver (Lepto. ICH, FIP).
  11. 11. Physical examination  Evaluate the sclera, oral m.m, skin for Jaundice (detected when serum bilirubin conc. are >2.5-3.0 gm/dl)  Abd. palapation for liver - edges are normally sharp, not rounded –  Hepatomegaly – caused by passive venous congestion, diffuse inflammation, nodular hyperplasia, bile engorgement, & infiltration by fat, glycogen, & neoplastic cells.  Hepatodynia (pain on palpation of the liver)  Morderate to severe abd. effusion may be detected  Neurologic examination  Rectal examination – evaluate for melena & acholic feces.  Evaluate skin & m.m for evidence of bleeding – ‘Pallor’ in blood loss anemia
  12. 12. Pallor mm.
  13. 13. Laboratory Evaluation Hepatic disease may not be suspected until biochemical tests identify elevated liver enzyme activity or other evidence of hepatic dysfunction. 1. Complete Blood Count (CBC)  Mild to moderate anemia-  blood loss (gastroduodenal ulceration, cougulopathy)  Chronic disease (normocytic-normochromic anemia)  Erythocytic microcytosis without hypochromic or anemia common in dogs & cats with portosystemic shunts  Targets cells & acathocytes occur in dogs & cats in hepatic disease, due to altered RBC membranes.
  14. 14. Erythocytic microcytosis
  15. 15. 2. Urinalysis  The specific gravity may be isothenuric or hypothenuric, if liv.disease is associated with PU/PD.  Bilirubinuria is sensitive indicator of abnormal metabolism (hyperbilirubinuria & jaundice).  Bilirubinuria imparts a yellow-orange color to the urine
  16. 16. 3. Liver enzymes  Alanine Aminotransferase (ALT)/ SGPT :  Hepatocyte injury with leakage of enzymes from the cytoplasm of the hepatocyte – ALT activity  Hepatocellular necrosis & inflammation – largest ALT activity  Corticosteriod therapy or hyperadrenocorticism & Anticonvulsant drug therapy in dogs – ALT activity.  Small amt. of ALT are present in canine skeletal muscle, in severe muscle injury - ALT activity  ALT is considered liver-specific in Dog & Cat
  17. 17.  Aspartate Aminotransferase (AST)/SGOT:  Hepatocyte injury with leakage of enzymes from the cytoplasm of the hepatocyte - AST  AST is not liver-specfic in Dogs & Cats – present in hepatocytes & skeletal muscle tissue.  Comparison of activities of ALT, AST & Creatine kinase (CK), a muscle enzymes, can indicate whether AST activity is increased due to hepatic or muscle injury.  In Cats with liver disease, AST may more sensitive than ALT in detecting hepatic disease.
  18. 18.  Alkaline Phosphatase (ALP) :  Young growing animals or animals with severe bone disease – ALP activity due to bone isoenyme.  Cats generally have smaller inc.in serum ALP activity than Dogs do.  Corticosteriod-induced ALP, in Dogs, but not in Cats.  Anticonvulsant drug therapy – ALP in Dogs, but not in Cats.  Inc.of ALP indicates intra-hepatic & extra hepatic cholestasis
  19. 19. Gamma Glutamyltransferase (GGT) :  Increased serum GGT activity usually reflects intra-hepatic & extra-hepatic cholestasis & pancretitis.  Corticosteriod-induced GGT, in Dogs.  Anticonvulsant drug therapy – GGT activity in Dogs.  In hepatobiliary diseases – GGT activity exceeds ALP activity, in Cats
  20. 20. Other Biochemical Tests BILIRUBIN: - serum bilirubin level >2.5-3.0 mg/dl result in clinical icterus. - Bilirubin level inc.due to prehepatic causes (hemolysis) or extrahepatic cholestasis. ALBUMIN: - during hepatic disease it can be dec. due to dec.synthesis or inc.vol.of distribution (ascites). - dec. albumin lev.indicate severe or chronic disease. - if serum alumin is <1.5 gm/dl, hypoalbuminemia contributes – dev. of Ascites & Edema GLOBULIN: - serum globulin that are synthesis in the liver (alpha & beta-globulin) – dec. in chronic liv.disease, but immunoglobulin (gamma-globulin) level are in liv.dsease due to inflammatory or immune stimulation
  21. 21.  Blood Urea Nitrogen (BUN) :  BUN can be dec.in animal with liv.disease bcz of dec. conversion of Ammonia to Urea.  Anorexia & low protein diet – dec. BUN values.  If the animal is dehyrated , inc. BUN may be seen in hepatic disease.  GLUCOSE :  Hypogycemia can be seen with liv.disease bcz liver is essential for glucose metabolism.  CHOLESTEROL :  Cholesterol values may be normal  Inc. due to dec. excreation & Inc. production with cholestasis  Dec. due to dec. synthesis, malabsorption, or inc. bile acid synthesis.
  22. 22. Liver function test  BILE ACID :  Measurement of serum bile acids after Fasting & Postprandially reflect the 3 component fo Enterohepatic pathway –  Hepatocyte uptake  Biliary secretion  Portal circulation  In liver dysfunction-  Fasting level in Dogs >20umol/L & In Cats > 15umol/L.  Postprandially level in Dogs >25umol/L & In Cats >20umol/L  Postprandially bile acids – more sensitive than fasting sample in determing liver dysfunction.
  23. 23.  Other methods of evaluating liver function- Blood Ammonia (BA) Conc. & Ammonia Tolerance Test (ATT) If fasting blood ammonia levels are within normal limits, but liv.disease is suspected, then an ammonia tolerance test can be conducted. ATT should be done with caution when Hepatic encephalopathy is suspected ( it exacrebate clinical signs in these animals).
  24. 24. Parameters of hemostasis  Liver is responsible for synthesis of all coagulation factors (expect factor VIII), plasminogen, antithrombin III & alpha2 antiplasmin.  Mech.of excessive bleeding associated with liver failure include failure of hepatocytes to synthesize clotting factors, & malabsorption of vit. K .  Prothrombin Time (PT) & Activated Partial Coagulation system – abnormal results in liv.disease.
  25. 25.  Blood Gas Analysis ◦ Various acid-base imbalances may occur secondary to liver disease (resp. alkalosis, metabolic alkalosis, & metabolic acidosis.  Abdominal Fluid Analysis ◦ Ascitic fluid that accumulate secondary to liver disease. ◦ With hepatic venous congestion, protein conc. of fluid is >2.5gm/dl
  26. 26. Radiographic Evalution  Survey Radiography :  Abdominal radiographs are useful to evaluate for:  Changes in liver size (hepatomegaly, microhepatica)  Altered tissue characteristics such as mineralized hepatic densities (choleliths) & radiolucencies (abscesses)  Presence of abdominal effusion.  Hepatic neoplasia.
  27. 27.  Ultrasonography :  Detect focal parenchymal abnormalities –  Masses, abscesses, cysts & regenerative nodules.  The USG appreance of these focal lesions often similar, & biopsy is req. for differentation.  Detect vascular lesions – portosystemic shunts, hepatic arteriovenous congestion.  Angiography :  Useful to diagnosis vascular disorders involving the liver
  28. 28. Liver Biopsy  Often req.to - ◦ Definitively characterize the nature & severity of hepatic disease ◦ Differentiate acute from chronic disorders ◦ Assess response to therapy  Biopsy Methods ◦ Fine-Needle Aspiration  For cytologic evaluation of the liver  For e.g : Feline hepatic lipidosis, & hepatic neoplasia ◦ Blind Percutaneous Needle Biopsy  Advantage – req. minimal sedation & take little time  Disadvantage – excessive bleeding & trauma to adjacent organs may occur  Contraindicated – in hepatic abscess or cyst, vascular tumours, bile duct obstuction, peritonitis, abdominal adhesions & extreme obesity.  Keyhole Needle Biopsy  Similar to percutaneous tech.  Performed under general anaesthesia
  29. 29. Fine-Needle Aspiration
  30. 30.  Ultrasound-Guided Needle Biopsy ◦ Difficult if the liver is small  Laproscopy ◦ Provide direct visualization of the liver & adjacent structures. ◦ When liver is small, laproscopy is useful alternative method to UGNB. ◦ Req. heavy sedatives or anesthesia & clinical expertise.  Laprotomy ◦ Advantages – obtain large sample of liver tissue ◦ Disadvantage –  req. general anesthesia  High risk of complication  Delay wound healing in hypoalbuminemic patients
  31. 31. Ultrasound-Guided Needle Biopsy
  32. 32. Laprotomy Laproscopy
  33. 33. References  Merck manual  Saunders manual of small animals practice
  34. 34. THANK YOU

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