Liver & Pancreatic Diseases In Animals

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. 07/25/09

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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. 07/25/09

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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 07/25/09

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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. 07/25/09

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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. 07/25/09

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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 solution should Dr.be substituted. 07/25/09 8 Ghalib's Lectures

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). 07/25/09

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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. 07/25/09

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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. 07/25/09

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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. 07/25/09

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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. 07/25/09

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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. 07/25/09

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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. 07/25/09

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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. 07/25/09

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