Urea And ammonia toxicity.pptx

Ammonia Colorless gas with a pungent ammoniacal smell
Extremely soluble in water forming a caustic alkaline solution of ammonium hydroxide (NH4OH)
Used as a refrigerant, fertilizer
Gas leak.
Fertilizers.
The spillage of Household and industrial cleaners
Ammonia is produced by decaying manure.
Increased ammonia levels of 25–30 ppm can damage the mucociliary apparatus of the upper respiratory tract, and higher levels (50–75 ppm) can cause decreased feed intake as well as caustic burns to the cornea, which can result in blindness.
Urea, also called carbamide, is an organic compound with the chemical formula CO(NH2)2.
Diamide of carbonic acid
Easily soluble in water
White crystalline powder and odourless
Liberates ammonia smell
MECHANISM OF ACTION
Toxicity of urea and non-protein nitrogen is due to ammonia absorbed from the stomach.
When the level of ammonia is high, the animal cannot detoxify ammonia fast because the urea and glutamine synthesizing mechanisms are saturated.
Increased ammonia leads to inhibition of citric acid cycle.
There is an increase in anaerobic glycolysis, blood glucose and blood lactate.
A decreased energy production and cellular respiration leads to convulsions.
In animals that are not too ill, cold water-acetic acid treatment can be given. 19-38 litres of water and 3.8litres of 5% acetic acid can be administered to an adult cow
Intravenous fluids should be administered.

1. Ammonia and urea Toxicity Urusha Ghimire Roll nO 37​

2. Ammonia Colorless gas with a pungent ammoniacal smell Extremely soluble in water forming a caustic alkaline solution of ammonium hydroxide (NH4OH) Used as a refrigerant, fertilizer 2

3. 3 Source of ammonia poisoning Gas leak. Fertilizers. The spillage of Household and industrial cleaners Ammonia is produced by decaying manure. Increased ammonia levels of 25–30 ppm can damage the mucociliary apparatus of the upper respiratory tract, and higher levels (50–75 ppm) can cause decreased feed intake as well as caustic burns to the cornea, which can result in blindness. Pullets exposed to high levels of ammonia in wet litter developed blindness as a result of corneal ulcers.

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5. 5 Both  ammonia and urea are nitrogen-containing compounds.  Ammonia is the simplest nitrogen containing compound where as urea is a derivative of ammonia. Because ammonia is toxic, it is excreted immediately by fish, converted into uric acid by birds, and converted into urea by mammals.  Ammonia is smaller, more volatile and more mobile than urea. If allowed to accumulate, ammonia would raise the pH in cells to toxic levels. Why does the body convert ammonia into urea? Ammonia  is produced from leftover amino acids, and it must be removed from the  body . The liver produces several chemicals (enzymes) that change  ammonia into  a form called  urea , which the  body  can remove  in the  urine. If this process is disturbed,  ammonia  levels begin to rise.

6. Urea urea 6 Urea, also called carbamide, is an organic compound with the chemical formula CO(NH2)2. Diamide of carbonic acid Easily soluble in water White crystalline powder and odourless Liberates ammonia smell Urea and other commonly used non-protein nitrogen have the ability to liberate ammonia. Hydrolysis of urea is speeded up by urease and an alkaline pH.

7. 7 urea Source of Urea poisoning Fertilizers Urea and other organic and inorganic sources of nitrogen are added to ruminant rations as a source of non-protein nitrogen Ammonium salts Poachers use urea to kill wild animals Toxic dose 100gms in cattle and 10-25 gms in goat/sheep Blood ammonia nitrogen reaches 0.84mg to 1.3mg%

8. Toxicosis results from the accumulation of ammonia in the animal factors, which enhance urea toxicosis, are Rapid ingestion A diet low in energy and protein and high in fiber Ingestion of palatable urea concentrate such as urea molasses mixtures High pH in the rumen High body temperature Water deficiency and Feeds rich in urease like soyabeans Stress Hepatic insufficiency 8

9. ABSORPTION AND FATE In the rumen, ammonia liberated is in the form of ammonium ion and hence it cannot be absorbed. At rumen pH 6.2 charged ion is highly water soluble and poorly absorbed. If rumen pH is elevated to 10 or above, then ammonia will be in soluble form and lacks charge and can be absorbed. In the blood at a pH of 7.4, almost all the ammonia is in the form of ions and cannot cross the cell membrane. In the normal course, liver ammonia is converted into urea by the urea cycle or incorporated into glutamic acid in the synthesis of glutamine. 9

10. MECHANISM OF ACTION Toxicity  of urea and non-protein nitrogen is due to ammonia absorbed from the stomach. When the level of ammonia is high, the animal cannot detoxify ammonia fast because the urea and glutamine synthesizing mechanisms are saturated. Increased ammonia leads to inhibition of citric acid cycle. There is an increase in anaerobic glycolysis, blood glucose and blood lactate. A decreased energy production and cellular respiration leads to convulsions. 10

11. CLINICAL SYMPTOMS AND PM LESIONS Sometimes affected animal is found dead Behavioural abnormalities like restlessness and dullness initially, later signs of excitation, head pressing, abnormal posturing, jumping over unseen objects Nervous phenomena like tremors, twitching, and spasm of muscles beginning from the eyelids and proceeding towards the tail are noticed. Autonomic manifestations include salivation, bradycardia, hypertension and severe colic. Gastrointestinal signs include rumen atony, bloat, teeth grinding, groaning, kicking at the abdomen and other evidence of colic. Locomotor disturbances like initial in-coordination and later staggering and stumbling prior to collapse. 11

12. Post mortem lesions No characteristic lesions are noticed in urea poisoning. Mild pulmonary edema with lung congestion and petichiae are also noticed. Animals bloat rapidly and the carcasses decompose more rapidly. Liver is enlarged and pale Kidney cloudy and necrotic foci present Stomach- Hemorrhagic patches, ulceration and odema 12

13. DIAGNOSIS AND TREATMENT 13 Diagnosis  is based on history,  clinical symptoms , post mortem lesions, laboratory investigations like BUN, blood ammonia concentration, ruminal pH, and analysis of feed, stomach, and ruminal contents for urea or ammonia. Treatment In animals that are not too ill, cold water-acetic acid  treatment  can be given. 19-38 litres of water and 3.8litres of 5% acetic acid can be administered to an adult cow Intravenous fluids should be administered. Emptying the rumen provides prompt relief from urea toxicosis. Convulsions can be controlled by pentobarbital sodium administration.