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Function of liver
Liver plays a central role in a many of
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.
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
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
In chronic disorders – irreversible changes (cirrhosis);
long term prognosis may be favorable
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
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
- portal hypotension
- renal retention of Na+ & H2O
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
- 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)
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).
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
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
Rectal examination – evaluate for melena & acholic feces.
Evaluate skin & m.m for evidence of bleeding – ‘Pallor’ in
blood loss anemia
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.
The specific gravity may be isothenuric or
hypothenuric, if liv.disease is associated with
Bilirubinuria is sensitive indicator of abnormal
metabolism (hyperbilirubinuria & jaundice).
Bilirubinuria imparts a yellow-orange color to the
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
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
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
In Cats with liver disease, AST may more sensitive
than ALT in detecting hepatic disease.
Alkaline Phosphatase (ALP) :
Young growing animals or animals with
severe bone disease – ALP activity due to
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
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
- serum bilirubin level >2.5-3.0 mg/dl result
in clinical icterus.
- Bilirubin level inc.due to prehepatic causes
(hemolysis) or extrahepatic cholestasis.
- during hepatic disease it can be dec. due to
dec.synthesis or inc.vol.of distribution
- dec. albumin lev.indicate severe or chronic
- if serum alumin is <1.5 gm/dl, hypoalbuminemia
contributes – dev. of Ascites & Edema
- 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
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.
Hypogycemia can be seen with liv.disease bcz
liver is essential for glucose metabolism.
Cholesterol values may be normal
Inc. due to dec. excreation & Inc. production with
Dec. due to dec. synthesis, malabsorption, or inc.
bile acid synthesis.
Liver function test
BILE ACID :
Measurement of serum bile acids after Fasting &
Postprandially reflect the 3 component fo
Enterohepatic pathway –
In liver dysfunction-
Fasting level in Dogs >20umol/L & In Cats >
Postprandially level in Dogs >25umol/L & In Cats
Postprandially bile acids – more sensitive than
fasting sample in determing liver dysfunction.
Other methods of evaluating liver
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).
Parameters of hemostasis
Liver is responsible for synthesis of all
coagulation factors (expect factor VIII),
plasminogen, antithrombin III & alpha2
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
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
◦ With hepatic venous congestion, protein conc.
of fluid is >2.5gm/dl
Survey Radiography :
Abdominal radiographs are useful to
Changes in liver size (hepatomegaly,
Altered tissue characteristics such as
mineralized hepatic densities (choleliths) &
Presence of abdominal effusion.
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.
Useful to diagnosis vascular disorders involving
Often req.to -
◦ Definitively characterize the nature & severity of hepatic disease
◦ Differentiate acute from chronic disorders
◦ Assess response to therapy
◦ 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
Contraindicated – in hepatic abscess or cyst, vascular tumours,
bile duct obstuction, peritonitis, abdominal adhesions & extreme
Keyhole Needle Biopsy
Similar to percutaneous tech.
Performed under general anaesthesia
Ultrasound-Guided Needle Biopsy
◦ Difficult if the liver is small
◦ Provide direct visualization of the liver & adjacent
◦ When liver is small, laproscopy is useful
alternative method to UGNB.
◦ Req. heavy sedatives or anesthesia & clinical
◦ Advantages – obtain large sample of liver tissue
◦ Disadvantage –
req. general anesthesia
High risk of complication
Delay wound healing in hypoalbuminemic patients