The document discusses hepatic (liver) functions and manifestations of liver disease. It covers topics such as jaundice, hepatic encephalopathy, and different types of jaundice (prehepatic, hepatic, post-hepatic). Liver diseases discussed include toxic hepatitis, infectious hepatitis, parasitic hepatitis, and nutritional hepatitis. Clinical signs, nervous system signs, and laboratory tests for assessing liver function and disease are also summarized.

2. Hepatic functions
The maintenance of normal blood glucose levels by
providing the source as glycogen
The formation of some of the plasma proteins
The formation and excretion of bile salts and the
excretion of bile pigments
The formation of prothrombin
The detoxification and excretion of many toxic
substances, including photodynamic agents

3. Manifestations of liver and biliary disease
 Jaundice
 Hepatic encephalopathy: hypoglycemia and failure of normal hepatic
detoxification mechanisms, leading to the accumulation of excess amino acids and
ammonia, or of acetylcholine, and the liberation of toxic breakdown products of
liver parenchyma, causes Hepatic encephalopathy
Nervous signs include:
 Hyperexcitability
 Convulsions
 Muscle tremor and weakness
 Dullness
 " Yawning
 Compulsive walking
 Head-pressing
 Failure to respond to signals
 Mania
 Edema and emaciation: fall in plasma protein. This may be sufficiently
severe to cause edema because of the lowered osmotic pressure of the plasma.
 Diarrhea and constipation: partial or complete absence of bile salts from
the alimentary tract deprives it of the laxative

4.  Abdominal pain: distension of the organ with increased
tension of the capsule, and lesions of the capsule
 Alteration in size of the liver
 Photosensitization: In hepatic or biliary insufficiency
excretion Most photosensitizing substances, including
Phylloerythrin is retarded and photosensitization
occurs
 Haemorrhagic diathesis: deficiency in prothrombin
formation and a consequent prolongation of the
clotting time of the blood
 Displacement of the liver: displaced from its normal
position and protrude into the thoracic cavity through
a diaphragmatic hernia, causing respiratory distress
 Rupture of the liver

5. Jaundice
Jaundice is the yellowish staining of the
skin and sclerae (the whites of the eyes)
that is caused by high levels in blood of
the chemical bilirubin. The color of the
skin and sclerae vary depending on the
level of bilirubin. When the bilirubin
level is mildly elevated, they are
yellowish. When the bilirubin level is
high, they tend to be brown.

6. Physiology of jaundice
Obstructive Jaundice

7. Prehepatic (Hemolytic) jaundice
Occurs in case of hemolytic anemia.
Total bilirubin level is increased due to increased blood indirect
bilirubin level.
The color of urine remains normal, because indirect bilirubin is
bind to albumin, and subsequently unable to pass the glomerular
filter.
Higher level of blood indirect bilirubin, results in higher bilirubin
uptake by the liver and increased the rate of formation of direct
bilirubin, and increased the direct bilirubin that pass to the small
intestine. This results in dark brown color of the feces.
The increased stercobilinogen level in the small intestine results
in increase the formation of urobilinogen, which is excreted in
urine.
The most important changes in pre-hepatic jaundice are
increased total and indirect bilirubin in blood, normal urine color,
dark brown feces and increased urobilinogen in urine.

8. Hepatic jaundice
Occurs in case of hepatitis.
Serum levels of total bilirubin are increased
because ofretention of direct bilirubin,
passes out in the urine, causing an
elevation of urine levels.
The urobilinogen levels in the urine also
rise.
Dark brown color of urine, as a result of
excretion of direct bilirubin in urine.
Normal color of feces

9. Post-hepatic (Obstructive) Jaundice
Occurs in case of obstruction of main bile duct.
Total bilirubin increased due to increase blood direct
bilirubin level.
Dark brown color of urine.
Clay color of feces
Absence of urobilinogn from urine
Obstructive jaundice = failure of bilirubin to reach
the gut > light colored stool, dark urine

10. Principles of treatment
 Oral or intravenous injections of glucose , eg. Dextrose 5%
 Amino acid mixtures, especially those ontaining
methionine, are used with apparently good results.eg.
Hermin
 Diets high in carbohydrate, calcium and protein of high
biological value and a number of specific substances are
known to have a protective effect against hepatotoxic
agents.
 Administration of lipotrophic factors including choline
and maintenance on a diet low in fat and protein may
reduce the compressive effects of fibrous tissue
contraction.

11. Hepatitis
Diffuse, degenerative and inflammatory diseases that
affect the liver
Only difference between hepatitis and hepatosis
being that the onset of the disease is slower and less
acute than in hepatitis.

12. Toxic hepatitis
 The common causes of toxic hepatitis in farm animals
are:
 Inorganic poisons – copper, phosphorus, arsenic,
selenium
 Organic poisons – carbon tetrachloride,
hexachloroethane, Gossypol, creosols and coal tar pitch,
chloroform and copper diethylamine quinoline sulfonate

13. Infectious hepatitis
 Rift Valley fever
 Bacillus pilijormis, associated with Tyzzer's disease in
foals
Equid herpesvirus 1
Dcltaproteobacterium "
Postvaccinal hepatitis of horses, also known as serum
hepatitis,
Idiopathic acute hepatic disease,
Theiler's disease
Systemic mycoses, e.g. histoplasmosis,
Infectious equine anemia,
Salmonellosis, septicemic listeriosis, leptospirosis
Clostridium novyi

14. Parasitic hepatitis
Acute and chronic liver fluke infestation
Migrating larvae of Ascaris sp.
chronic shistosomiasis1
Hepatic sarcocystosis in a horse
Nutritional hepatitis (Trophopathic hepatitis)
Selenium and vitamin E deficiency

15. Pathogenesis
Toxic agent Swelling
causes form
lesion
Characterized by
cloudy swelling to
acute necrosis
fibrosis
develop
Infectious agent Endotoxin
1. Multifocal hepatocellular necrosis,
2. Decreasedhepatic gluconeogenesis
3. Decreased hepatic blood flow
causes
a. lysosomal damage, release lysosomal
enzymes, prostaglandins, collagenase,
Hepatocytes
damage
Decreased mitochondrial function
Reduce liver function

16. Clinical findings
Anorexia
 Mental depression- with excitement
 Muscular weakness
Jaundice
Recumbency
coma
intermittent convulsion.
Photosensitization may also occur
but only when the animals are on a
diet containing green feed and are
exposed to sunlight.
Weight loss,
Tachycardia,
Intennittent fever
 Abdominal pain,
 Ventral body wall edema
Clotting deficiency.
Diarrhea or constipation

17. Nervous signs
Ataxia and lethargy
Yawning
Coma
Hyperexcitability
Muscle tremor
Mania, including aggressive behavior, and convulsions.
A characteristic syndrome is the dummy syndrome, in which
affected animals push with the head, do not respond to normal
stimuli and may be blind.
There may be subacute abdominal pain
pain on palpation of the liver.

18. Most common cause of acute hepatic failure in the horse.
administration of tetanus antitoxin.
 Lactating mares appear to be at a higher risk than other horses.
Clinical findings include
Serum Hepatitis (TheHer's disease
Sudden anorexia,
Marked lethargy,
Stiff gait,
 Subcutaneous edema of the distal
aspects of all four limbs and body
wall,
Blindness,
Head pressing
Circling
 Abdominal pain,
Tachycardia,
Icterus
a marked reduction in gastrointestinal
sounds.
Death in a few days

19. Examination of the liver
 Palpation and percussion
 Biopsy
 Ultrasonography
 Radiography
 ,

20. Laboratory tests for hepatic disease
and function
 Serum bile acids, arginase and gamma-glutamyl transferase
(GGT) –sensitive indicator of cholestasis and/or hepatocellular
necrosis
 serum activities of sorbitol dehydrogenase (SDH),GGT and
aspartate aminotransferase (AST, formerly known as SGOT),
and the BSP clearance' test – sensitive indicators of
hepatocellular injury in cattle
 Chronic hepatic
 leukocytosis
 neutrophilia,
 hypoalbuminemia,
 hyperbetaglobulinemia,
 increased ALP and GGT
 increases in AST, SDH, total lactate dehydrogenase

21. Hepatic function
 The sulfobromophthalein sodium clearance- - test has been
used in cattle, sheep and horses.
 The time required by the normal liver to reduce the plasma
concentration of BSP to half the initial concentration is
taken as the standard BSP half-life
 Cattle is 2.5-5.5 minutes,
 Sheep 2.0 minutes
 Normal horses about 2.0 minutes

22. Icteric index
 Measurement of the icteric index of plasma, by comparing
its color with a standard solution of potassium dichromate
Serum hepatic enzymes
Sorbitol dehydrogenase (also called L-iditol dehydrogenase
(ID) - sheep and cattle Lactate dehydrogenase (LDH)- abundant in
liver, kidney, muscle and myocardium Aspartate aminotransferase
or L-alanine aminotransferase (ALT, previously known as
SGPT)- Dog
Arginase
Gamma-glutamyl transferase- cattle, sheep and horses. GGT is
a sensitive indicator of liver damage in horses
Glutamate dehydrogenase (GD)- ruminants and horses
Ornithine carbamoyl-transferase (OCT)