Tox Exam 2 Herbicides and Fungicides Flashcards
Source of phenoxy derivatives of fatty acids (2, 4-D) poisoning in cattle?
accidental ingestion of concentrates or sprays, grazing freshly sprayed pastures
Source of 2,4-D poisoning in pets?
freshly sprayed lawns
T/F 2,4-D sprayed forages at recommended concentrations can cause poisoning.
FALSE. do NOT cause poisoning
Which species are most susceptible to 2,4-D poisoning?
cattle & dogs
Which species are most sensitive to 2,4-D poisoning?
dogs
ADME of 2,4-D?
A=readily from GIT, poorly from skin
D=all over, liver, kidney, brain
M=1/2 life short (few hrs) but longer in dogs (up to 3-4 days)–mainly metabolized by hydrolysis
E=mainly unchanged in urine–tubular secretion
Is 2,4-D an acidic or basic toxin?
acidic
T/F Acidifying the urine will increase 2,4-D toxin excretion?
FALSE–alkalinization
T/F Meat residues in cattle/sheep are unlikely unless exposed to high concentrations of 2,4-D.
TRUE
Chemical properties of 2,4-D?
Alters metabolism of plants which increases toxicity by increasing accumulation of nitrate or cyanide. May increase palatability of plant.
Not stable in environment, not degraded by rumen microflora, do NOT alter rumen microflora.
MOA of 2,4-D?
irritation of GI mucosa, affects skeletal muscle in dogs, degeneration of liver/kidneys
Clinical signs of 2,4-D?
mainly GI & neuromuscular signs
Clinical signs of 2,4-D in ruminants?
anorexia, rumen atony, bloat, D+, ulcers in gastric mucosa
Clinical signs of 2,4-D in dogs?
anorexia, V+, bloody D+, muscle weakness (esp posterior muscles), ataxia, rigidity of skeletal muscles
Clinical signs of 2,4-D in swine?
V+, D+, muscle weakness, depression
T/F Rumen stasis with ingested food is a characteristic finding of 2,4-D poisoning.
TRUE
Specimens used in the diagnosis of 2,4-D poisoning?
forage, water, kidney, urine, liver, stomach contents, poo
Lab diagnosis of 2,4-D poisoning?
elevated ALP (alkaline phosphatase), LDH (lactate dehydrogenase), CPK (creatine phosphokinase)
Treatment of 2,4-D poisoning?
no specific antidote, detox by washing skin or activated charcoal, supportive/symptomatic–IV fluids, antidiarrheals, rumenatorics
Name the 2 dipyridyl herbicides that we discussed in lecture.
paraquat & diquat
Is paraquat (PQ) a RUP or a GUP?
RUP
Is diquat (DQ) a RUP or a GUP?
GUP
Are PQ & DQ stable in the environment?
NO! rapidly degraded by light and soil
PQ binds strongly to soil
Are PQ & DQ stable in neutral, acidic & alkali conditions?
stable in neutral and acidic–but destroyed in alkali
T/F PQ/DQ are caustic to membranes & cause characteristic ulcers.
TRUE
What species are susceptible to dipyridyl herbicidal toxicity?
ALL, esp dogs
What factors increase PQ toxicity?
selenium-vit E deficiency, depletion of tisssue glutathione & oxygen therapy
ADME of dipyridil herbicides?
A= (DQ)--poorly absorbed from GIT, (PQ)--absorbed from GIT & skin D= (PQ) all over body--high concentration in lung (10x other tissues) M= (PQ) minimal metabolism E= (PQ) w/in 24 hrs unchanged in urine
MOA of dipyridil herbicide toxicity?
Reduced by NADPH to produce singlet oxygen which reacts with lipids in cell membranes to form hydroperoxidases. Production of free radicals, membrane damage, cellular degeneration & necrosis–esp lungs.
Clinical signs of acute dipyridyl herbicide toxicity?
early–> V+, anorexia, depression, high doses may cause ataxia, dyspnea, seizures
delayed–> 2-7 days, resp signs–tachypnea, dyspnea, harsh sounds, cyanosis, decreased pulmonary compliance
Clinical signs of subacute or chronic dipyridyl herbicide toxicity?
after 7 days up to 3 wks, resp signs d/t pulmonary fibrosis
Pathology of dipyridyl herbicide toxicity?
pulmonary edema, congestion & enlargement of liver, kidneys and spleen, hemorrhage, fibrosis, failure of lung to collapse, lingual ulcers
Specimens that are used to diagnose dipyridyl herbicide toxicity?
suspected plant, stomach contents, urine in acute cases, lung in chronic cases
T/F Radiology can be used to detect mild changes in the lungs due to PQ/DQ toxicity.
TRUE
Differential diagnosis for dipyridyl herbicide toxicity?
pneumonias, inhalant toxicants such as toxic gases/vapors/dusts, zinc phosphide also stimulates CNS/convulsions + resp signs
Treatment for dipyridyl herbicide toxicity?
no specific antidote detox-->emetics, charcoal, bentonite/fuller's earth choice, saline cathartics after adsorbent supportive-->fluids, hemo/peritoneal dialysis biochemical antags (antioxidants)-->orgotein (superoxide dismutase), acetylcysteine, ascorbic acid, niacin, riboflavin
T/F Giving O2 early in dipyridyl herbicide toxicity is crucial in preventing further lung damage.
FALSE–O2 contraindicated early bc may increase lung damage
T/F Treatment for dipyridul herbicide toxicity must be started before 24 hrs post exposure for it to be helpful.
TRUE
Prognosis for dipyridul herbicaide toxicity?
guarded or grave
Is pentachlorophenol (PCP) a herbicide or a fungicide?
fungicide–prevents fungal infections in plants
PCP is used as a _____ preservative.
wood–protects limber from fungal rot & wood boring insects
Causes of pentachlorophenol toxicosis in livestock & pets?
licking wood treated w/ PCP, ingesting contaminated water or feeds, vapors can penetrate skin, inhalation of toxic amounts from treated walls in sheds & barns
T/F An animal can still get pentachlorophenol toxicosis by inhaling treated walls in sheds and barns even months/years post application.
TRUE
T/F PCP is still used in wood preserving solutions, insecticides & herbicides for home & garden use.
FALSE–no longer used for these purposes
Factors increasing PCP toxicity?
high temp–can give off toxic vapors, oily/organic solvent vehicle, previous exposure, poor condition, newborn, hyperT
Factors decreasing PCP toxicity?
cold temp, antithyroid drugs, presence of body fat
ADME of PCP?
A=readily through GIT, inhalation, intact skin
D=throughout body–accumulation in fat
M=1/2 life 1.5-2 days
E=glucuronides excreted in urine; residue in tissues/fats depleted from body w/in 1 wk of exposure
Chemical properties of PCP?
irritant to mucous membranes, resp tract, skin–older preparation contained dioxins which are carcinogenic/teratogenic
T/F PCP persists in water, sewage & soil.
FALSE–bacterial decomposition prevents their persistence in the environment
T/F There are 3 different types of PCP toxicosis–subacute, acute & chronic.
FALSE–just 2 types–acute & chronic
Describe the clinical signs of acute PCP toxicity.
very fast onset–fever, tachycardia, dyspnea, cyanosis, seizure, collapse, death
newborn pigs–hyperthermia, skin irritation, rapid death
Describe the clinical signs of chronic PCP toxicity.
anorexia, decreased milk production, anemia, fetal malformations, abortions–fever & resp distress may be absent
MOA of PCP toxicity?
uncouples oxidative phosphorylation & blocks/decreases ATP–increased O2 demand to produce ATP–O2 demand > O2 supply
Pathology of PCP toxicity?
rapid rigor mortis, local irritation of skin & MM, pulmonary congestion & edema, degenerative changes in liver/kidneys, dark blood due to hypoxia
chronic cases–hyperkeratosis of skin & villous like hyperplasia of urinary bladder mucosa
Lab diagnosis of PCP toxicity?
antemortem–>chem analysis of blood/urine
postmortem–>skin & kidney
Differential diagnosis of PCP toxicity?
heat stoke, toxicants causing resp insufficiency–nitrate (brown blood, no fever), CO (bright red blood, no fever), pesticides (marked neuromuscular signs, autonomic signs), parachute infectious dz
Treatment of PCP toxicity?
no specific antidote
detox–>emetics, gastric lavage w/ 5% Na bicarb, activated charcoal or mineral oil, soap/water on skin
symptomatic–>O2 therapy, lower body temp (cold water/ethanol), IV fluids (NO glucose), electrolytes, prophylatic use of ABs & vitamins to prevent secondary bacT infections d/t liver/kidney/GI damage
Prognosis of PCP toxicity?
survives past 24 hrs–chances of complete recovery are far
