HEPATOBILIARY SYSTEM

Berhanu M., SVM, HawU

2013
 Liver performs many vital functions, some of these
functions are
 synthesis of cholesterol and bile acids, degradation of
glycogen, metabolism and conjugation of bile pigments and

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xenobiotics

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 production of plasma proteins and clotting factors

 production of bile

 provides a vast filter for blood entering the liver through

the portal vein (Kupffer cells)

 production of energy by oxidative phosphorylation and

oxidation of fatty acids
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Hepatic dysfunction and failure
 In healthy animals more than two third of the hepatic
parenchyma can be removed without impairment of

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hepatic function
 Signs of liver damage are observed when a

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considerable reserve and regenerative capacity is lost
and biliary outflow is obstructed.
 Hepatic failure is the loss of normal hepatic function
as a result of either acute or chronic liver damage
 Cholestasis, jaundice, hepatic encephalopathy, a
variety of metabolic disturbances, vascular and
hemodynamic changes and photosensitization are the
common sequel
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1. Cholestasis and jaundice

I. Cholestasis is a reduced canalicular flow of bile.

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a. Extrahepatic cholestasis
 Choleliths, parasites, neoplasms, inflammation

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 If chronic, hepatocellular necrosis and biliary fibrosis(
throughout the portal tract).

b. Intrahepatic cholestasis
 Swelling on hepatocytes  narrow canaliculi. When?

II. Jaundice (ictrus) is a yellowish discoloration of

tissue
 resulted from hyperbilirubinaemia, when? 4
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Cholengitis: chronic, fibrosis, liver fluke

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2. Portosystemic encephalopathy (Hepatic
encephalopathy)
 amines absorbed from GIT and hepatic dysfunction
 If not detoxified, amines can exert toxic effect on the

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brain
 common in ruminants and horses with hepatic failure.

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 Neurological signs range from depression and other
behavioral change to mania and convulsion.

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3. Metabolic disturbances
Bleeding disorder (haemorrhagic diathesis), why?
 usually occurs following acute hepatic failure

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Hypoalbuminaemia
 occur in severe, diffuse hepatic disease (chronic)

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 Edema!!!

 Glycogen metabolism

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4. Vascular and haemodynamic alterations
 extensive and diffuse fibrosis  ↑ resistance to blood
flow through the liver.
 ↑ pressure within the portal vein (portal hypertension)

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and other hepatic vasculature  transudation of fluid
in to the peritoneal cavity (ascitis).

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 Ascitis is further increased due to  colloidial osmotic
pressure (hypoalbuminaemia).

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BOTTLE JAW

Berhanu M.
HawU
ACA research
2002EC
Dog: Ascites. Note the prominent superficial blood vessels
but the absence of a caput medusa

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5. Photosensitization
 Reaction on lightly or non-pigmented areas of the skin

photodynamic pigments + ultraviolet light  free

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
radicals!

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 It can be classified as 10 and 20 (hepatogenous)

 Hepatocellular dysfunction or biliary obstruction

prevents normal excretion and allows high
concentrations of phylloerythrin to accumulate in blood
and cutaneous tissues.


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Chronic passive congestion
 CPC  persistent hypoxia in centrilobular areas.

 Because of oxygen and nutrient deprivation

 centrilobular hepatocytes atrophy and necrotized 

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sinosoides in these areas dilated and congested
 periportal hepatocytes usually undergo fatty change and

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appear yellowish.
 Such lung is called Nutmeg liver

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Cholelithiasis
 they are formed secondary to chronic mild cholecystitis
and disturbance of resorptive activity of the gall
bladder

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 are composed of a mixture of cholesterols, bile
pigments, salts of bile acids, calcium salts and a

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protenaceous matrix
 obstruct bile ducts to cause jaundice and vitamin K
deficiency (how?)
 pressure necrosis on the wall of bile duct and gall
bladder and hence diverticula

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Biliary obstruction
 could be by

 choleliths,

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 adult Ascaris (mechanical obstruction),
 tumors of pancrease and duodenum,

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 tumors and abscesses of the hilus of the liver and
portal nodes
 the consequence of biliary obstruction depends on the
site and duration of the obstruction
 rupture followed by an acute chemical peritonitis, can
be rapidly fatal, particularly if Clostridia are
involved

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Biliary calculus and chronic biliary fibrosis of the liver:
diffusely firm and slightly tan liver. Hard, oval, 5 cm stone in
duct.

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 VIRAL DISEASES OF THE LIVER
1. Infectious Canine Hepatitis (ICH)
 It is caused by canine adenovirus 1 (CAV-1)

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 excreted in the urine for long periods by infected
animals

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 edematous gallbladder, linear hemorrhage on the serosa
of the anterior surface of the stomach and intestine are
the common postmortem findings
 slightly enlarged liver with sharp edges and friable
consistency
 large intranuclear inclusion bodies in endothelium and
hepatic parenchyma (believed to be diagnostic)
 corneal edema

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2. Rift valley fever
 it is chiefly a disease of the young, causing heavy
mortality among lambs and calves and abortion in ewes
and cows

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 widespread hemorrhage, ranging from serosal
petechiae to severe GIT bleeding

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 the liver tend to be darker and show scattered pale foci
of necrosis 1-2 mm in diameter
 eosinophilic intranuclear inclusion bodies, often
elongated, are sometimes seen in degenerate
hepatocytes

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Mottled, pale and red, soft and friable

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Multiple hemorrhages and congestion: RVF; lamb

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BACTERIAL DISEASES OF THE LIVER
 bacteria enter the liver by
 direct implantation (e.g. TRP)

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 invasion of the capsule from an adjacent focus of
suppurative peritonitis,

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 hematogenously via the hepatic artery, portal
veins and umbilical vein, or via the bile duct
 L. monocytogenous- in fetal and neonatal lambs,

calves and piglets

 Campylobacter fetus- in fetal and neonatal lambs

 Actinobacillus equuli - in foals

 Mycobacterium sp.- miliary tuberculosis

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Hepatic abscesses: C.pyogenes, look the color!

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Liver(neonate): necrobacillosis

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Necrotic hepatitis Fusobacterium necrophorum

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Liver granulomatous hepatitis: tuberculosis

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1. Black disease (infectious necrotic hepatitis)
 Caused by exotoxin (,  and zeta) of Clostridium
novyi

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 Damage induced by Fasciola hepatica create suitable
environment for germination of C.novyi

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 Principally a disease of sheep but it occurs in cattle
too. It is seen occasionally in horses.
 Affected animals are usually in good condition and
postmortem decomposition occurs rapidly.

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 Unusual degree of subcutaneous venous congestion and
edema of the Sternal subcutis
 Serous cavities contain an abundant fluid that clots on

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exposure to air
 Subendocardial hemorrhages in the left ventricle are

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almost constant
 Several yellowish white areas (2 to 3 cm in diameter) of
necrosis surrounded by inflammatory zone on the liver

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Large irregular dark and pale areas scattered, adult
sheep.

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3. Hepatic abscess
 hematogenous or extension of omphalophlebitis or
direct implantation
 omphalogenic abscesses are more common in calves

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 mixed bacteria, but C.pyogenes, Streptococci and
Staphylococci are predominat

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 hepatic abscesses in feedlot is much important
economically
 hepatic abscesses of biliary origin

 F. necrophorum as a complication of ruminitis in adult

cattle
 Multiple, elevated, rounded, dry areas of coagulative
necrosis, with inflammatory zone/capsule

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 fates

 sterilization of the focus with calcification,

resorption or encapsulation

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 generalized abscessation (if the hepatic vein

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is involved)
 death, when the abscesses are multiple and
fresh and are necrobacillary in origin (death
is due to toxemia)

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 PARASITIC (HELMINTHIC) INFLAMMATION OF
THE LIVER AND BILE DUCTS
 Parasites +zone of coagulative necrosis and eosinophils
(other WBC too)

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 commonly seen parasites/their immature stages

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 Cysticercus tenuicollis in wandering phase (sheep)
 larvae of Ascaris suum and Stephanurus dentatus in pigs
 migrating larvae of strongyles in horse
 adults of Ascaris, esp. in pigs, may migrate to the bile duct
 metacestodes of Echinococcus granulosus
 Stilesia hepatica in the bile ducts of ruminants
 Fasciola
 Dicrocoelium dendraticum in ruminants, horses, pigs, dogs
and cats
 Opistorchis tenuicollis and O.sinensis in bile ducts of39
carnivores
Cysticercus tenuicollis (close up)

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Hydatidosis: cross sec of vesicles

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TOXIC LIVER DISEASES
 liver is the most common site of toxic injury for two
reasons

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 It receives about 80% of its blood supply from the portal
vein, so what?
 Production of potent toxic metabolites in the attempt

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detoxification
 The balance between MFO / cytochrome P-450 system
and antioxidants will determine the extent of damage.
 Major causes are
 Plant toxins (pyrrolizidine alkaloids),
 mycotoxins (aflatoxins and sporidesmin),
 chemotherapeutics (e.g. phenobarbiturate),
 metals (e.g. Cu, Fe etc.)
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
Copper poisoning (copper toxicosis)
 mainly seen in sheep, because Cu storage is poorly
managed/ regulated
 Cu is toxic if the amount is slightly increased and not

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properly sequestrated
 In domestic animals, causes of Cu toxicosis are

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1. Dietary excess in ruminants
2. Pasture which is normal in [Cu] but low [Mo]
3. Plants rich in hepatotoxic phytotoxins
 intravascular hemolysis and hepatocellular necrosis

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 Any cause of cholestasis can aggravate copper toxicity
 Carcass become jaundiced

 deep reddish brown kidney, hemoglobinuria

 liver slightly soft and swollen and deep orange in color

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 bile is dark and granular

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Copper poisoning: dark urine and yellow tissues. The liver is slightly
fatty and slightly enlarged. The kidneys are dark (gun metal kidneys). The
urine is very dark; and the fat is decidedly icteric, or yellow and the spleen
is slightly enlarged.

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Fatty liver (fatty degeneration)
 Lipids arrive in the liver via the plasma from two
sources;
 as triglycerides from fat depots and

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 as chylomicrons from the intestine (diet)

 Mechanisms for fatty degeneration of the liver;

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 interference with protein production
 interference with the release of lipoproteins
 impaired combination of lipid with protein
 blockage of oxidation of fatty acid;
 Excess fatty acid presented to the liver
 enhanced fatty acid synthesis
 In Diabetes (dogs) and in ketosis, why?
 Gross and Microscopically appearance

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Fatty liver/fatty change: pregnancy toxemia

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LIVER KETOSIS
End stage liver (disease) or cirrhosis
 it is characterized by
1.Nodular regeneration of parenchyma (regeneration nodules)
2. Fibrosis

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3. Bile duct hyperplasia
 The hallmark of such liver is the total absence of any

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normal lobular architecture
 Chronic toxic insults are the major causes
 Plants containing pyrrolizidine alkaloids
 Chronic extrahepatic biliary obstruction and cholestasis
 Chronic hepatitis of any cause, alcohol abuse and iron
overload
 Signs are similar with hepatic failure (but it can be
clinically silent too)
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LIVER CIRRHOSIS
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Biliary cirrhosis: Fibrosis about each and every periportal area

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CHOLANGIOADENOCARCINOMA WITH RUPTURE

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