Diseases of the liver

Introduction
 Examination of the liver is greatly concerned with an
investigation of the symptoms and signs of disturbance of liver
functions.

 It is a large organ in the body and probably possesses the

greatest number and variety of functions. e.g. secretion of bile,
protein metabolism, deamination of amino acids, formation of
urea, conversion of glucose, ketone bodies and other materials
used in metabolism.

 The liver uses the amino acids to form plasma protein (albumin,
globulin and fibrinogen), prothrombin, choline estrase, tissue
protein and also it stores proteins.

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The liver also play an important role in
– CHO metabolism,
– formation of lipids,
– vitamins metabolism & storage (vitamins A, D, E, K,
thiamine, riboflavin),
– detoxicative metabolism,
– erythropoesis,
– fat metabolism and s
– torage of blood with the spleen.

Primary diseases of the liver occur in farm animals as a result

of poisoning.
Secondary diseases occur as a part of generalized diseases
process or spread from another organ, are more common. In
primary diseases the clinical manifestations are caused only by
the liver lesions while in secondary involvement the syndrome
may include clinical signs unrelated to the hepatic lesions.
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 Manifestations of liver and biliary diseases
A) Dermatological signs:
a- Icterus (jaundice): It is common in horses with acute
liver diseases while in ruminants biliary obstruction is
the most likely cause of icterus.

b- Photodermatitis: Phylloerythrin which acts as a

photodynamic agent accumulates in the circulation
and binds to the skin in patient with cholestasis.

C- Pruritus: It is attributed to accumulation of bile salts

in the skin has been reported in horses with liver
failure.

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B) Neurological signs:
Signs of hepatoencephalopathy may occur and it may be
attributed to
– Hypoglycemia,
– Hyperammonemia
– Increased concentration of mercaptan, sulfur-containing
amino acids and short chain fatty acids in the plasma.

C) Gastrointestinal signs:
Weight loss is attributed to anorexia and failure of hepatic
metabolic function.
Diarrhea is common in cattle with chronic liver diseases
attributed to increase hydrostatic pressure associated with
portal hypertension.
Tenesmus followed by rectal prolapses is observed in some
cattle with liver diseases

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 Ascites is common findings in cattle with liver
cirrhosis. Hyperalbuminemia may be possible cause.
Recurrent subacute abdominal pain has been reported
in horses with liver failure.

D) Hematological signs:
a- Bleeding diathesis, coagulopathy leading to
hemorrhage as in epistaxis, bleeding from
venipuncture sites may accompany severe terminal
liver failure and is caused by inadequate hepatic
synthesis of clotting factors. Beside decreased
absorption of fat soluble vitamin K which is required by
the liver for production of certain factors.
b- Hemolytic crisis: which may be attributed to increased
RBCs fragility has been reported in horses with liver
failure.
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Diagnosis
1- Clinical signs as mentioned above.

2- Laboratory tests
A) Liver enzymes such as
– Gamma-glutamyl transferase (GGT)
– Alkaline phosphatase (AP)
– Dehydrogenases
- Sorbitol dehydrogenases (SDH)
- Lactate dehydrogenases (LDH)
- Glutamate dehydrogenase (GDH)
B) Serum bilirubin assessment.
C) Bile acid concentration.
D) Dye excretion tests.
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3- Other diagnostic modalities
A) Hepatic ultrasound to diagnose hepatomegaly
and space-occupying lesions in the liver.

B) Percutaneous liver biopsy to determine the

presence and causes of liver diseases.

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Treatment
1- For management of hepatic encephalopathy.
Sedation: for convulsing animal and restless, xylazine
(0.5-1 mg/kg) and diazepam 0.4 mg/kg are effective
sedatives.
Minimize production and absorption of toxic
metabolites using minerals and lactulose (0.3 ml/kg) to
decrease ammonia absorption from the gut and
neomycin (10-100 mg/kg) orally to decrease
production of ammonia by gut microflora.
Diet: in form of low protein with high energy feeds rich
in amino acids.

2- IV fluid therapy: 5% dextrose (2 ml/ kg hour) should

be used for first 24 hours in animals with
hypoglycemia, after 24 hours, 2.5 dextrose in lactated
ringer
07/25/09 solution should Dr.be substituted.
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3- Vitamins supplementations
Vitamin K1 (40 mg/ 450 kg. once weekly) is indicated
to prevent coagulopathies.
Vitamin B1 and folic acid, once weekly.

4- Antimicrobial therapy based on culture and sensitivity

including administration of B-lactam and an
aminoglycosides or trimethoprim-sulfanamides.
Metronidazole should be added if anaerobic infection
suspected.

5- Corticosteroids may benefit animals with chronic

active hepatitis (0.5-1.5 mg / Kg twice daily).
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 Diffuse diseases of the liver
Hepatitis
It is include all diffuse degenerative and inflammatory
diseases which affect the liver.
Etiology:
1) Toxic hepatitis: The lesion may be mild manifested
by cloudy swelling or severe accompanied by
extensive necrosis leading to fibrosis. The common
causes are:
– Inorganic poison such as copper, phosphorus, arsenic &
selenium, or
– Organic poison such as carbon tetrachloride,
hexachloroethan & chloroform.
– Poisonous plants, fungi (such as aspergillus, penicillium &
fusarium) and algae.

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 2) Infectious hepatitis: It may occur in cases
of:
– Salmonellosis
– Leptospirosis
– Systemic mycoses (histoplasmosis) and
– Infectious necrotic hepatitis due to infection with
clostridium novyi.
3) Parasitic hepatitis: It occur in cases of:
– Massive liver fluke infestation
– Migration of ascaris larvae.

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 4) Nutritional hepatitis: liver cirrhosis caused by
methionine deficiency and acute hepatic necrosis
caused by cystine deficiency in diets of rats are not
known to have an importance in farm animals.

5) Congestive hepatopathy: Congestive heart

failure cause increase pressure in sinusoids of the
liver causing anoxia and compression resulting in
degeneration

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Pathogenesis:
The usual lesion in toxic hepatitis varies from
cloudy swelling to acute necrosis with terminal
veno-occlusive lesion in some plant poisoning.

In infectious hepatitis the lesion vary from necrosis

of local isolated cells to diffuse necrosis.

In parasitic hepatitis, the changes depend upon the

number and type of migrating larvae. Massive fluke
infestation may cause acute hepatic insufficiency.
In liver fibrosis, the signs develop more slowly.

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Clinical findings:
1- Anorexia accompanied by constipation punctuated
by attack of diarrhea. The feces is lighter in color
than normal.

2- Nervous signs such as yawing or coma to

hyperexcitability with muscle tremors and
convulsions may occur due to hypoglycemia and
failure of detoxification mechanism of the liver.

3- Dummy syndrome with signs of animal push with

head, not responding to stimuli and may be blind.

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 4- Subacute abdominal pain may be present
manifested by arching of the back and pain on
palpation of the liver due to distension with increase
tension of liver capsule.

5- Jaundice and edema particularly in horses may or

may not be present.

6- Photosensitization may occur in animal fed green

food and exposed to sunlight.

7- In chronic hepatic fibrosis, the signs are similar to

those of hepatitis but developed more slowly and
persist for months. Ascitis and the dummy syndrome
are more common than in hepatitis.
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 Focal diseases of the liver
Hepatic abscess
It does not cause clinical signs unless they are massive and
metastatic.
Liver abscess cause significant loss in feedlot and grain-fed
cattle because chemical ruminitis leading to hepatic abscess.
Omphalophelebitis, ruminal parakeratosis or ruminitis may
also lead to hepatic invasions by fusobacterium necrophorum
or other organisms including actionmyces, streptococcus &
staphylococcus spp.

Tumors of the liver

The commonest neoplasm in calves is lymphmatosis.
Adenoma, adenocarcinoma and metastasis through portal
veins are not uncommon in ruminants.

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 Diseases of the pancrease
Diabetes mellitus:
Lesions of the pancrease causing diabetes mellitus
are recorded in cows, horses and monkies.

Clinical signs in horses include weight loss, polydipsia,

polyuria and high blood glucose and cholesterol. It
occurs in old horses due to pancreatic injury related to
migration of strongyl larvae.

In cow, there is emaciation, polydipsia, ketonuria,

glucosuria and hyperglycemia.
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