Pentachlorophenol and Urea toxicosis Flashcards
What are pentachlorophenols used for?
Applicator as a wood preservative (protect from fungal rot and wood boring insects)
How are animals usually exposed to pentachlorophenol?
Licking treated wood
Inhalation/skin contact of toxic amount from treated walls in sheds
Ingestion of contaminated feeds/water
T/F: PCP salts are water soluble
True
What factors increase toxicity of PCP?
High ambient temp Oily or organic solvents Previous exposure Poor condition Newborn Hyperthyroidism
What factors decrease PCP toxicity?
Cold temp
Antithyroid drugs
Body fat
What are the acute and chronic toxicities of PCP?
Acute 100-200mg/kg (moderate)
Chronic 40-70 mg/kg
What is the distribution, metabolism, and excretion of PCP?
Distribution- throughout body with some accumulation in fat
Metabolized- conjugation to glucuronic acid
Excreted- urine
What is the MOA of PCP ?
Uncouples oxidative phosphorylation and blocks or decreases ATP
Increased O2 demand and effort to produce ATP (greater than O2supply)
—>overheating, metabolic acidosis, and dehydration
—>irritating to resp mucosa and intact skin
—>decreased cellular energy may cause neurotoxic and other effects
What are signs of acute PCP toxicosis?
Fever, tachycardia, dyspnea, cyanosis, seizure, collapse,and death
Newborn pigs - hyperthermia, skin irritation, and rapid death
What are signs of chronic toxicosis?
Weight loss, decreased milk production, anemia, fetal malformations/abortions
What lesions can you see due to PCP toxicity?
Rapid rigor mortis
Local skin and mm irritation
Pulmonary congestion and edema
Degenerative changes in liver and kidney
Dark blood (oxygen dep)
Hyperkeratosis of skin and villous like hyperplasia of urinary bladder mucosa in chronic cases
What samples can you take for chemical analysis of PCP?
Blood and urine -live animal
Kidney and skin- dead animal
What is the DDX for toxicants causing respiratory insufficiency?
PCP (dark blood, fever) Nitrate (brown blood, no fever) CO (bright red blood, no fever) Pesticides (neuromuscular/autonomic signs) Peracute infectious disease
What is the treatment of PCP toxicity?
Detox
- emetic and gastric lavage
- activated charcoal
- soap and water bath
Supportive
- oxygen therapy
- lower body temp
- IV fluids and electrolytes for dehydration and met acidosis
- prophylactic antibiotics and vitamins
What is the most commonly used non-protein nitrogen source?
Urea
-feed addivtive
What are sources of non-protein nitrogen toxicosis?
Urea in feed as additive
Contamination of urea fertilizer
Ammonium salt and ammoniated feed products
How does urea form protein ?
Urea changed to ammonia and CO2 (by urease)
Ammonia (NH3) aminates ketoacids to form amino acids
Amino acids —> bacterial protein —>animal protein
An _________pH enhances hydrolysis of urea by urease
Alkaline (urea is basic)
What speices are most susceptible to non-protein nitrogen toxicosis?
Ruminants
Horses are also susceptible
What is the most toxic of all the NPN compounds
Urea
What is the usual concentration of urea in the grain ration? Total ration?
Grain 3%
Total 1%
T/F: cattle that are preconditioned have a higher lethal dose of NPN than non conditioned animals
True
What animals are tolerant to NPN toxicosis
Very young
Does fasting increase/deceased NPN toxicity
Increase
How does dehydration/low water intake affect NPN toxicity?
Increases toxicity
What feed is high in urease and will increase NPN toxicity?
Soybeans
Is ammonia absorbed well in the rumen?
At normal rumenal pH (5 - 6.5) ammonia is ionized and not absorbed
At high levels of ammonia —> increase pH and non-ionized ammonia is absorbed
Normally ammonia is converted in the liver to urea, which is excreted. What happens if there is more ammonia than the capacity of the liver?
Hyperammonemia
T/F: non-ionized ammonia cannot cross the BBB or the placenta
False
Can cross both
What is the MOA of urea ?
Toxic due to ammonia
—> inhibit CAC —>lack of energy and decreased cellular resp—> tissue damage
—> increased blood ammonia, anaerobic glycolysis, blood lactate, and systemic acidosis, blood glucose, blood urea nitrogen, serum potassium, and phosphorus
—> death due to cardiac or respiratory failure
Restlessness, aggression, muscle tremors, salivation, teeth grinding, colic, sternal recumbency, bloat, and rumen stasis
DDX?
Urea toxicosis
Agents causing colic - inorganic arsenic
Lead, metaldehyde, and chlorinated hydrocarbon pesticides
-no abnormal posturing or maniacal behavior like seen in urea
Organophosphate
-PSNSmimetic
Grain engorgement, nitrate poisoning, enterotoxemia, and cyanide
What lesions are seen in urea toxicity?
Main lesion due to vascular damage
Congestion and degeneration in liver and kidney
Ammonia odor
What lab diagnostics do you do for urea toxicity?
Analysis of feed for urea content
Analysis of ammonia in whole blood, rumen fluid, and vitreous fluid
Elevated rumen pH
What is the treatment for urea toxicity?
Relieve bloat
Acetic acid Treatment should be repeated every 4-5hrs Normal saline for dehydration Sodium bicarb for acidosis Rumenotomy
