Pentachlorophenol and Urea toxicosis

Question 1

What are pentachlorophenols used for?

Answer 1

Applicator as a wood preservative (protect from fungal rot and wood boring insects)

Question 2

How are animals usually exposed to pentachlorophenol?

Answer 2

Licking treated wood
Inhalation/skin contact of toxic amount from treated walls in sheds

Ingestion of contaminated feeds/water

Question 3

T/F: PCP salts are water soluble

Answer 3

True

Question 4

What factors increase toxicity of PCP?

Answer 4

High ambient temp 
Oily or organic solvents 
Previous exposure 
Poor condition 
Newborn 
Hyperthyroidism

Question 5

What factors decrease PCP toxicity?

Answer 5

Cold temp
Antithyroid drugs
Body fat

Question 6

What are the acute and chronic toxicities of PCP?

Answer 6

Acute 100-200mg/kg (moderate)

Chronic 40-70 mg/kg

Question 7

What is the distribution, metabolism, and excretion of PCP?

Answer 7

Distribution- throughout body with some accumulation in fat
Metabolized- conjugation to glucuronic acid
Excreted- urine

Question 8

What is the MOA of PCP ?

Answer 8

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

Question 9

What are signs of acute PCP toxicosis?

Answer 9

Fever, tachycardia, dyspnea, cyanosis, seizure, collapse,and death

Newborn pigs - hyperthermia, skin irritation, and rapid death

Question 10

What are signs of chronic toxicosis?

Answer 10

Weight loss, decreased milk production, anemia, fetal malformations/abortions

Question 11

What lesions can you see due to PCP toxicity?

Answer 11

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

Question 12

What samples can you take for chemical analysis of PCP?

Answer 12

Blood and urine -live animal

Kidney and skin- dead animal

Question 13

What is the DDX for toxicants causing respiratory insufficiency?

Answer 13

PCP (dark blood, fever) 
Nitrate (brown blood, no fever)
CO (bright red blood, no fever)
Pesticides (neuromuscular/autonomic signs)
Peracute infectious disease

Question 14

What is the treatment of PCP toxicity?

Answer 14

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

Question 15

What is the most commonly used non-protein nitrogen source?

Answer 15

Urea

-feed addivtive

Question 16

What are sources of non-protein nitrogen toxicosis?

Answer 16

Urea in feed as additive
Contamination of urea fertilizer
Ammonium salt and ammoniated feed products

Question 17

How does urea form protein ?

Answer 17

Urea changed to ammonia and CO2 (by urease)
Ammonia (NH3) aminates ketoacids to form amino acids
Amino acids —> bacterial protein —>animal protein

Question 18

An _________pH enhances hydrolysis of urea by urease

Answer 18

Alkaline (urea is basic)

Question 19

What speices are most susceptible to non-protein nitrogen toxicosis?

Answer 19

Ruminants

Horses are also susceptible

Question 20

What is the most toxic of all the NPN compounds

Answer 20

Urea

Question 21

What is the usual concentration of urea in the grain ration? Total ration?

Answer 21

Grain 3%

Total 1%

Question 22

T/F: cattle that are preconditioned have a higher lethal dose of NPN than non conditioned animals

Answer 22

True

Question 23

What animals are tolerant to NPN toxicosis

Answer 23

Very young

Question 24

Does fasting increase/deceased NPN toxicity

Answer 24

Increase

Question 25

How does dehydration/low water intake affect NPN toxicity?

Answer 25

Increases toxicity

Question 26

What feed is high in urease and will increase NPN toxicity?

Answer 26

Soybeans

Question 27

Is ammonia absorbed well in the rumen?

Answer 27

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

Question 28

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?

Answer 28

Hyperammonemia

Question 29

T/F: non-ionized ammonia cannot cross the BBB or the placenta

Answer 29

False | Can cross both

Question 30

What is the MOA of urea ?

Answer 30

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

Question 31

Restlessness, aggression, muscle tremors, salivation, teeth grinding, colic, sternal recumbency, bloat, and rumen stasis DDX?

Answer 31

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

Question 32

What lesions are seen in urea toxicity?

Answer 32

Main lesion due to vascular damage Congestion and degeneration in liver and kidney Ammonia odor

Question 33

What lab diagnostics do you do for urea toxicity?

Answer 33

Analysis of feed for urea content Analysis of ammonia in whole blood, rumen fluid, and vitreous fluid Elevated rumen pH

Question 34

What is the treatment for urea toxicity?

Answer 34

Relieve bloat ``` Acetic acid Treatment should be repeated every 4-5hrs Normal saline for dehydration Sodium bicarb for acidosis Rumenotomy ```