Plant-Related Toxicants Flashcards
Describe the accumulation of nitrate by plants
- nitrate is absorbed from the soil by the plant and converted to nitrite by nitrate reductase
- nitrite is converted to ammonia
- ammonia is converted to amino acids, then to vegetable protein
- accumulation occurs with the conversion of nitrate to nitrite is reduced, but nitrate is still being taken up
Which part of the plants/what age have the highest concentrations of nitrate?
- stalks contain the highest
- young plants have higher concentrations
What are the properties of nitrate?
solubility, palatability
- soluble in water
- salty and palatable
Which species are the most susceptible to nitrate poisoning?
Which are the least?
- ruminants are most susceptible
- pigs are resistant
Describe the toxicokinetics of nitrate poisoining
- rumen microflora convert nitrate to nitrite faster than nitrite is converted to ammonia
- excess nitrite is absorbed and enters erythrocytes in exchange for Cl ions
- crosses placenta
Describe the mechanism of action of nitrate poisoning
- nitrite interacts with hemoglobin: ferrous oxidized to ferric and hemoglobin converts to methemoglobin
- high mHb causes death from anoxemia
- abortions occur
What are the clinical signs of nitrate poisoning?
- sudden death without signs
- rapid breathing, restlessness, weakness, ataxia, cyaosis, convulsions and death
- abortion
What are the observed lesions in nitrate poisoning?
- congestion of organs
- brown colored blood
How is nitrate poisoning treated?
- methylene blue 1% IV
- activated charcoal, rumen lavage, or oral antibiotics
How are large animals usually poisoned with cyandide?
Small animals?
LA: ingestion of cyanogenic plants (wild cherry, sudan grass, johnson grass, and sorghums)
SA: ingestion of hydrogen cyanide and cyanide salts in many materials
Which animals are more susceptible to cyanide poisoning?
- ruminants are most susceptible
- sheep less than cattle
Describe the toxicokinetics of cyanide poisoning
- HCN absorbed through GI tract, inhalation, and intact skin
- distributed throughout body
- CN with thiosulfate is metabolized to thiocyanate which is less toxic and excreted in urine
Describe the mechanism of action of acute cyanide toxicity
- excess cyanide in blood and tissue binds with ferric iron and copper
- blocks electron transport and inhibit cells from using oxygen
- metabolic acidosis
- decreases cellular energy
- vasoconstriction
- neuronal damage from anoxia
- irritation of mucus membranes
Describe the mechanism of action of chronic cyanide toxicity
- neuronal degeneration and demyelination of spinal cord and brain
- low levels of cyanide are goitrogenic
What are the clinical signs of acute cyanide toxicosis?
- rapid onset
- tachypnea, anxiety, severe panting, gasping, and behavioral alarm
- death in 4-5 minutes
What are the clinical signs of chronic cyanide toxicosis?
- posterior paralysis, urinary incontinence, and cystitis
- constipation due to lower spinal cord degeneration
- possible goitrogenic effect
What lesions are found in cyanide toxicosis?
- mucus membranes bright red
- blood is cherry red and may not clot
- congestion and petechiae in GI and lungs
- cyanide smell
How is cyanide toxicosis diagnosed?
- elevated thiocyanate levels in urine
- lactic acidosis and increased anion gap
- sodium picrate paper test
How is cyanide toxicosis treated?
- sodium nitrate 20% IV (vasodilation and methemoglobin)
- sodium thiosulfate 20% IV (converts cyanide to thiocyanate)
- sodium thiosulfate orally
- oxygen
- mineral oil, vinegar
Which species are the most susceptible to soluble oxalate poisoning?
sheep and cattle
What will reduce the toxicity of soluble oxalate?
- ruminants allowed to graze small quantities of oxalate containing plants
- presence of food in rumen
- calcium or calcium rich diets
Describe the mechanism of action of soluble oxalate poisoning
- after absorption, oxalates combine with calcium ion to form insoluble ca oxalate
- leads to hypocalcemia and tetany, or affects bone and milk production
- precipitation of ca oxalate crystals in kidney tubules
What are the clinical signs of soluble oxalate poisoning?
- colic, dullness, depression, muscle weakness and twitching, head and neck pulled to one side, prostration, coma, and death
- rapid breathing and blood-tinged froth around mouth
- fatal renal tubular toxicosis, oliguria, hyperkalemia, and cardiac failure
What lesions are seen in soluble oxalate toxicosis?
- excess fluid in abdomen and thoracic cavities
- petechial hemorrhage in GI mucosa
- emphysema of lungs
- blood tinged froth in mouth and esophagus
- kidneys have dark red cortex and medullar separated by a gray line
How is soluble oxalate toxicosis diagnosed?
- presence of Ca oxalate crystals in kidney tubules
- hypocalcemia
- high BUN
