Pentachlorophenol (PCP) Flashcards
What are PCPs used for?
wood preservatives - protection from fungal rot and insects
How are animals exposed to PCPs?
licking treated wood, inhalation of toxic amounts from treated walls in sheds or barns
Vapors can also penetrate the skin
Ingestion of contaminated feeds or water
Are PCPs water soluble?
not very much - but they are soluble in oils and organic solvents
**the SALT forms are soluble in water
What temperatures promote increased vapors from PCPs?
high ambient temp - can increase the concentration of toxic vapors
What do older PCP preparations include that is a carcinogenic and teratogenic?
Dioxins
What is the acute oral or dermal LD50 of PCPs for domestic animals? What category of toxicity do they belong to?
ranges from 100 - 200mg/kg
Moderately toxic
**Chronic toxicity ranges from 40-70 mg/kg
What factors will increase the toxicity of PCPs?
High ambient temperature, oily or organic solvent vehicles, previous exposure, poor condition of animal, newborn, hyperthyroidsim (increased metabolism =increased body temp)
Where can/do PCPs get stored in the body?
Adipose tissue
***lipophilic
What factors will decrease the toxicity of PCPs?
Cold temp, antithyroid drugs, and the presence of body fat (since it will go to the fat for storage - where it is inactive)
How are PCPs absorbed?
Lipophilic = readily absorbed from the GIT, inhalation, thru intact skin
Where are PCPs distributed throughout the body
All over - with some accumulation in fat
What is the average half life of PCPs in the body?
a day and a half to two days
How are PCPs metabolized and excreted?
Conjucation to glucuronic acid –> Glucuronides are excreted in the urine
Cats are deficient
Residues of PCPs in tissues and fat are depleted from the body within ____ days of exposure
7 days / 1 week
What is the MOA of PCPs?
irritant to resp. tract, mm, and skin
uncouples oxidated phosphorylation and blocks or decreased ATP –> lack of energy = increased oxygen demand in efforts to produce ATP –>
- overheating
- metabolic acidosis
- dehydration
decreased cellular energy = neuro toxic, wt loss, decreased milk production, repro problems
What clinical signs are associated with acute PCP toxicosis?
“animal cooks in it’s own heat”
fever, tachycardia, dyspnea, cyanosis, sz, collapse, death
***newborn pigs = hyperthermia, skin irritation, rapid death
What clinical signs are associated with chronic PCP toxicosis?
Wt. loss, decreased milk production, anemia, fetal malformations/abortions
Fever and resp. distress may be ABSENT
T/F: PCP toxicosis will increase the onset of rigor mortis
TRUE
hyperthermia will increase the onset of rigormortis and that is one of the main clinical signs
What lesions will be noted with PCP toxicosis?
Fast onset of rigor mortis
local irritation to MM and skin
degenerative lesions in the liver and kidney
Dark blood = oxygen deprived
Hyperkeratosis of the skin and villous like hyperplasia of urinary bladder in chronic cases (this is pathopneumonic but RARELY seen)
What samples can be used for PCP chemical analysis?
blood and urine from a live animal
kidney and skin of a dead animal
How is a PCP toxicosis diagnosis made?
History of exposure + signs of rapid overheating and respiratory distress, rapid rigor mortis, dark blood, and chemical analysis
What are ddx for PCP poisoning?
Heat stroke (differentiated via hx)
Toxicants causing resp distress:
Nitrate (should have brown blood + no fever)
CO (bright red blood + no fever)
Pesticides (Neuromuscular signs/autonomic signs)
Peracute infections
What is the course of tx for PCP poisoning?
General and symptomatic
emetics or G.L. with sodium bicarb
ACTIVATED CHARCOAL or mineral oil
Soap/water detox bath
O2 therapy, IVF, decrease body temp, prophylactic ABs
What is the prognosis for animals with PCP toxicosis?
If the animal survives the first 24 hours - chances for a complete recovery are fair
