Toxicology Flashcards
what does % equal
grams/100g or mL/100mL
how many mL per oz
30
what is 1 ppm
1:1,000,000 = 1 mg/kg = 0.0001%
how do you calculate a mg/kg dose of drug in feed
ppm in feed x % body weight eaten per day as a decimal
how many pounds in a ton
2000
what is 1 g/ton equal to
1.1 ppm
what general organ system do insecticides target
CNS
where do organophosphates, carbamates, and neonicotinoid insecticides work
acetylcholine receptors
what do pyrethroids, avermectins, and fipronil target
sodium or chloride chanels
what signs do cholinesterase inhibiting OPs and carbamates cause
parasympathetic, neuromuscular, and CNS
what should you do if signs and history are SUGGESTIVE of OP/carbamate toxicity
start with preanesthetic dose of atropine (0.01-0.04mg/kg) IV
if eyes dilate, HR increases, and/or salivation stops in 5-10 min, stop there. if no change, give antidotal dose (0.2 mg/kg)
in small animals also give 2-PAM
how do you confirm diagnosis of organophosphate or carbamate toxicity
measure acetylcholinesterase activity of heparinized whole blood and/or brain tissue
(>70% reduction in activity is diagnostic)
analyze bait residues, stomach contents, and urine
what action do organophosphates and carbamates have
inhibit acetylcholinesterase
what is the treatment for known cholinesterase inhibitor toxicity
immediate atropine (0.1-0.5mg/kg 1/4 IV, the rest IM or SQ)
then 2-PAM
decontamination when stable
what is the MOA of atropine
muscarinic receptor antagonist (parasympatholytic)
what is the MOA of 2-PAM
regeneration of AChE, especially useful for nicotinic signs
what are signs of OP toxicosis
trembling, salivating, bradycardia, seizure, death
what animal is especially sensitive to pyrethrins
cats
what is the target of pyrethrins
sodium channels
what is the treatment for pyrethrin toxicosis
decontaminate
what is the target of bromethalin
nervous system
what is the treatment for bromethalin toxicosis
no antidote. induce emesis
toxic at 0.25-1.5 mg/kg
what is the target of vitamin K antagonists
hematopoietic system
what is the action of warfarin
vitamin K antagonist
what is the treatment for warfarin
vitamin K
what is cholecalciferol
vitamin D
what is the effect of cholecalciferol
increases calcium absorption
what is the target of cholecalciferol
kidney
what is the target of strychnine
nervous system, causes tetanic seizures
what is the action of zinc phosphide
changes to volatile phosphine gas
what is the target of lead
multi-systemic (CNS, GI, kidney)
what is the effect of sodium
CNS toxicity from water deficiency
what is the mechanism of copper toxicity
chronic exposure via feed additive with acute release from liver in stressed sheep; also in copper wire
targets kidney
what is the effect of zinc
hematopoietic
what is the target of arsenic
GI
what is the target of iron
GI and liver
what is the target of selenium deficiency
muscle
what is the treatment for lead toxicosis
calcium EDTA 75mg/kg
very long withdrawal period in food animals
where is aflatoxin found and what is its target
hot, dry season mainly in corn
GI (liver)
where is vomitotoxin found and what is its target
cool, wet season mainly in small grains
GI
where is zealenone found and what is its target
cool, wet season mostly in small grains
reproductive system
where is slaframine found and what is its target
in clover
limited cholinergic effect
where is penitrem A found and what is its target
in rotting dairy products and garbage
neurotoxic
where is roquefortine found and what is its target
in rotting compost and garbage
neurotoxic
where is fumonisin found and what is its target
moldy corn
neurotoxic
how do you test for mycotoxins
no diagnostic test in biological samples
must test the food
what are some toxic bulbs
daffodils/jonquils, tulips, iris, hyacinths, crocus, amaryllis, gladiolas
what is the effect of toxic bulbs
usually not lethal, irritant resins, alkaloids and/or insoluble calcium oxalate
GI signs (salivation, diarrhea, vomiting)
mostly affects dogs, onset <1 hour
what is the treatment for toxic bulbs
decontamination (multiple doses activated charcoal), antiemetics
symptomatic tx for GI upset, metabolic acidosis, pain
gastric lavage is not recommended as calcium oxalate is an irritant
what is the toxin in daffodils, narcissus, jonquil, paper-whites, and lent lilies
all parts of plant toxic
phenanthridine alkaloids (lycorine), insoluble calcium oxalate crystals
what is the effect of daffodils, narcissus, jonquil, paper-whites, and lent lilies
contact irritant, allergen, centrally acting emetic, decreased protein synthesis
GI and skin signs (salivation, vomiting, diarrhea, pain, dermatitis)
typically transient, rarely fatal
what animals are most susceptible to onion/garlic tox
cattle and cats>dogs
(toxic dose 0.5% of BW)
what is the MOA of onion/garlic tox
metabolized to disulfides, which cause oxidative damage to RBCs. hemoglobin denaturation means reduced oxygen delivery and RBC lysis
treatment for onion/garlic tox
decontamination and symptomatic treatment
prognosis is dose-dependant
clinical signs of onion/garlic tox
odor on breath, vomiting, anemia, hemoglobinuria
what is the MOA of mistletoe
phoratoxin is a weak toxalbumin that binds to ribosomal cell receptors primarily in the GI epithelium
what is the MOA of holly and poinsettias
saponins in holly berries and euphorbol esters in poinsettias are general irritants of the GIT
what is the MOA of christmas trees
phenols and pine-oils are general protoplasmic poisons that denature and precipitate proteins
possible liver, kidney and CNS involvement
what species is especially sensitive to christmas trees
cats are sensitive to the phenols b/c they are deficient in glucuronidation
what clinical signs are seen with the christmas plants
salivation, anorexia, depression, lethargy, vomiting, diarrhea, colic, gastroenteritis
only with christmas trees: icterus, hepatic necrosis, nephrosis
what is the treatment for christmas plant tox
symptomatic tx; fluids, antiemetics, demulcents
which are specifically more toxic to cats?
a. tulip bulbs
b. onions
c. mistletoe
d. pine
b and d
which plants have cardioactive steroids
christmas kalanchoe, oleander (oleandrin), foxglove (digitoxin and digoxin), lily of the valley
what is the MOA of cardiotoxic plants
GI irritants (saponin glycosides)
cardiotoxicity - inhibition of Na/K-ATPase pump causes increased intracellular Na and Ca and increased extracellular K
increased K reduces resting membrane potential, causing impaired conduction, bradycardia and dysrhythmias
clinical signs of cardiotoxic plants
GI and cardiac signs: anorexia, hypersalivation, vomiting/diarrhea +/- blood, colic, depression/lethargy, marked weakness and stupor, arrhythmias (bradycardia, AV block, tachycardia, weak, irregular pulses)
death usually from asystole and vfib
onset 1-8 hr, course of 1-2 days
how can you diagnose cardiotoxic plant tox
the usual (history, signs, plant in GIT), hyperkalemia!, ECG abnormalities!!, serum/urine analysis for toxin
treatment for cardiotoxic plants
aggressive decontamination if caught early (multiple doses activated charcoal)
bradycardia: atropine! or glycopyrrolate
arrhythmia: lidocaine!, procainamide, or phenytoin +/- beta blocker
digibind - antibodies to bind digitalis and similar glycosides in small animals
what is the target of tobacco
nervous system, GIT and can cause indirect cardiotoxicity
what is the toxin in dogbane and milkweed? onset/duration? species susceptible?
all parts of plant toxic, usually in contaminated hay
cardenolide based cardioglycosides
all animals susceptible, most likely to affect horses and cattle
onset <24 hours. lasts 2-5 days
how do you diagnose dogbane/milkweed tox
usual (hx, clinical signs, plant in GIT)
hyperkalemia!, ECG abnormalities!, serum/urine analysis for cardenolide
what is the toxin in tobacco and the toxic dose
nicotine 1 mg/kg
clinical signs of tobacco tox? who is usually affected?
shaking, trembling, twitching, nausea, salivation, mouth and stomach irritation, weak, staggering, resp problems, erratic HR and BP
puppies usually affected
treatment for tobacco tox
remove residual, assist resp as needed, stabilize heart and BP
T/F: cardiotoxic plants can be found in home gardens and in fields
true
T/F: many cardiotoxic plants are toxic in a manner similar to the cardiac drug digoxin
true
T/F: HR increases when animals ingest typical cardiotoxic plants
false - they cause bradycardia, but end stage can cause arrhythmias and tachycardia
what is the toxin in yew? who is susceptible?
taxine alkaloids
all parts toxic except the berry things
all animals susceptible
what is the effect of yew
direct effect on the myocardium with depression of AV conduction, bradycardia, hypotension, and diastolic cardiac arrest
clinical signs and onset/duration of yew tox
onset 15 min to 24 hours, course <12 hours
dyspnea, bradycardia, convulsion (dogs), trembling, diarrhea, incoordination, depression, lethargy, diarrhea, SUDDEN DEATH
what lesions are found on necropsy with yew tox
plant in stomach or mouth, enlarged globular heart, increased pericardial fluid, lung edema and congestion
how do you diagnose yew tox
hx of access, taxine analysis of stomach contents, pile of dead animals, widened QRS
treatment of yew tox
if you’re lucky enough to find them alive; avoid excitation, IM atropine, activated charcoal and saline cathartic once HR normalizes
prognosis is guarded
what is the toxin in rhododendron, azalea, and mt laurel? who is affected?
grayanotoxins
all parts of plant toxic
sheep and goats most likely affected, but can also affect cattle, dogs, horses, and you
MOA of rhododendron, azalea, and mt laurel
stimulates the vagal nerve and vomiting center in the brain, causing decreased HR, arrhythmias and persistent vomiting. can get sudden death
if you have a vomiting ruminant, what is the toxin
rhododendron, azalea, or mt laurel
clinical signs, onset/duration of rhododendron, azalea, and mt laurel
persistent, projectile vomiting/regurg, retching in horses, anorexia, hypersalivation, ruminal atony, bloat, diarrhea, colic, bradycardia, hypotension, arrhythmias, seizure, death from arrythmias
onset 6 hrs, course 1-2 days
treatment for rhododendron, azalea, and mt laurel
stop vomiting with 1/10 tranq dose of acepromazine
once vomit stops, activated charcoal and saline cathartic
cardiac drugs for arrhythmias
T/F: poisonous shrubs can be in home gardens and fields
true
T/F: ingestion of some shrubs can cause cardiac arrest
true - yew for sure
rhododendron, azalea, and mt laurel can cause death from arrhythmias
T/F: vomiting is more likely to occur with yew than rhododendron poisoning
false
what is the toxin in buckeye? who is affected?
aesculin in all parts, but especially the seed
cattle most susceptible
possible in sheep, pigs, chickens, horses, dogs
clinical signs of buckeye tox
CNS signs onset 16 hours, course 1-3 days
- ataxia, muscle tremors, lateral recumbency, paralysis, incoordination with hypermetria (goose-stepping), hyperesthesia, nystagmus/strabismus, prostration, clonic-tonic seizures, coma
not usually fatal
treatment for buckeye tox
sedatives until symptoms resolve so they don’t hurt themselves
how do animals get exposed to black walnut
shavings from the dark heartwood
what is the effect of black walnut and who does it affect
enhances constriction of blood vessels in hoof wall thought to be the mechanism of laminitis in horses
clinical signs of black walnut
acute laminitis! more in front legs onset less than a few hours, course 2 days to several weeks
also depression, lethargy, anorexia, stiff gait, reluctant to move, shifting weight, edema below the carpus/tarsus, increased body and hoof temp, increased gut sounds, colic
how do you diagnose black walnut tox
analysis of wood shavings from bedding. chocolate brown color
treatment of black walnut tox
signs subside with removal of shavings and washing down the legs
activated charcoal, cathartic, mineral oil, acepromazine, DMSO, prazosin (vasodilator), pain control, soft supportive bedding/ mechanical support
what part of the oak tree is toxic and who is susceptible
acorns, cattle
MOA of oak tox
gallotannin in acorns contains gallic acid. gallic acid and its metabolite, pyrogallol, are astringents. phenols inactivate and denature proteins, causing gastroenteritis and GI ulcers. enter vasculature and cause destruction of endothelial cells and proteins. damage to proximal renal tubular cells
clinical signs of oak tox
GI, cardiovascular, renal
onset 3-14 days, course 7-10 days
depression, lethargy, anorexia, gaunt, ventral edema!, epistaxis, dyspnea!, pu/pd, severe dehydration!, rumen atony/constipation, black tarry fetid diarrhea!, colic!
can die from renal failure, but this takes a long time
diagnosis of oak tox
evidence of consumption and renal failure
azotemia, low Na, Cl, Ca, +/- K, high Mg
necropsy - melena, perirenal edema!, acorns in GIT, myocardial degeneration, ascites, hydrothorax
treatment/prevention of oak tox
prevention is key. hard to treat
fluid therapy, electrolytes, rumenatorics (restore rumen motility with vit B, transfaunation, propylene glycol), pelleted concentrate with 10% CaOH! to precipitate tannins, high proline feeds may bind tannins, pasture management!
what is the major differential for oak tox
redroot pigweed - causes perirenal edema and myocardial degeneration in pigs>cattle>sheep
which maple tree is the most toxic
red maple
who is affected by maple tox and in what time of year
horses, zebras, alpacas most. can affect cattle, sheep, goats
in the fall
what is the toxin and MOA of maple tox
aceritannin breaks down into gallic acid and pyrogallol (same 2 as with oak), which cause oxidative damage and heinz body formation (denatured hemoglobin), hemolysis, and methemoglobin formation
clinical signs of maple tox
weak, tachypnea, pyrexia (fever) from hemolysis, methemoglobinemia, heinz body anemia, cyanosis, tachycardia, hemogloninuria, icterus, colic
necropsy findings with maple tox
icterus with centrilobular hepatic necrosis, splenomegaly, reddish-black kidneys with tubular nephrosis and hemoglobin casts, very dark blood
diagnosis of maple tox
history, decreased PCV, heinz bodies, eccentrocytes, metHb (>20%), incerased bilirubin, increased AST/SDH, azotemia, isosthenuria
treatment for maple tox
activated charcoal and saline cathartics, blood transfusion if severely hypoxic, asorbic acid (antioxident) to reduce metHb, fluids, pain control, NO STEROIDS (increases mortality)
what are some cyanogenic plants
black cherry, chokecherry, sudan grass, sorghum, sudex, milo, millet, Johnson grass, apricots, flax, sugar beets, arrow grass, crabapple trees
when are cyanogenic plants toxic and who is susceptible
during wilting stage when they have volatile cyanide
ruminants, esp goats susceptible. also possible in horses and dogs
MOA of cyanide tox
inhibits cytochrome oxidase in the oxidative phosphorylation chain in mitochondria, so cells are unable to use their oxygen to make ATP. cells suffer toxic anoxia. blood is unable to give up its oxygen to cells, becoming superoxygenated and cherry red!
ddx for cyanide tox
nitrate poisoning has the same signs, but see brown blood
why is it important to differentiate nitrate from cyanide poisoning prior to treatment
cyanide poisoning is treated by making methemoglobin. if already methemoglobinemic from nitrate, will make it worse
clinical signs and onset/duration of cyanide tox
onset <1 hour, course of <2 hours
excitement/apprehension, muscle tremors, tonic-clonic convulsions, bright red mucous membranes!, staggering, polypnea, severe dyspnea, jerky eyes, recumbency, prostration, coma, sudden death!
necropsy - bitter almond or bleach smell to rumen!, bright red lungs, epicardial hemorrhage
cyanide tox treatment
thiosulfate, nitrate, hydroxocobalamine (vit B12a)
which is the most likely to cause sudden death?
a. buckeye
b. oak
c. maple
d. black walnut
e. wild cherry
e
which is a special concern for horses?
a. buckeye
b. oak
c. maple
d. black walnut
e. wild cherry
c and d
which causes a non-lethal neurotoxicity?
a. buckeye
b. oak
c. maple
d. black walnut
e. wild cherry
a
which cause lesions in the same organ?
a. buckeye
b. oak
c. maple
d. black walnut
e. wild cherry
b and c - renal
c and e - RBCs
what is the most important factor in your toxin differential list
body systems involved
what body systems are usually involved with onset <24 hours
nervous system and heart
what body systems are usually involved with onset 1-5 days
kidney and liver
what are the 4 major points for a toxin differential list?
what other factors are considered?
top 4: systems involved, onset time, morbidity, mortality
others: species susceptibility, seasonality, age susceptibility, progression of signs
what should your initial exam of a tox case focus on
“bleeding, beating, breathing”
respiratory, cardiovascular, shock, electrolytes, coagulation status
what should your first treatment be with any toxin
treat the patient, not the poison
assess and stabilize animal
what is a concern with using royal blue blood tubes
false elevation of Zn with exposure to rubber
what basic tissues should be saved for tox analysis
brain, liver, kidney, urine, GI contents
what factors go into risk for toxicity
hazard and exposure
how many ounces in a pint
8
what are the initial actions taken in a tox case
first priority is to stabilize, then prevent further absorption, protect personnel, calculate exposure and treat for suspected toxicant
what are the types of decontamination
remove, dilute, eliminate
it’s all about preventing further absorption
what cases require decontamination
all tox cases. asymptomatic patients may not require treatment, but decontamination is still important
what are contraindications for emetics/gastric lavage
volatile compounds, solvents, caustics, corrosives, convulsing patients
the stomach wall is weakened and may burst, plus potential for aspiration
(take home message)
when is activated charcoal not useful
metals and alcohols
T/F: three important items on a differential list are systems involved, onset time, and morbidity/mortality
true
T/F: tox sampling and analysis is necessary for diagnosis of all cases of poisoning
false
in most cases, which is the DVM’s most reasonable approach to a tox patient
a. administration of an antidote
b. decontamination
c. enhancement of elimination
d. redistribution
b
which household cleaning products are the most toxic
automatic dishwasher detergent, commercial bleach, ammonia, toilet bowl cleaner, oven cleaner, drain cleaner
(take home message: drain cleaner is alkali and has the worst prognosis)
household products come with warning labels in categories 1-6. what does each category mean
1 - no label, LD50 >15g/kg
2 - no label, LD50 5-15 g/kg
3 - caution, LD50 0.5-5 g/kg
4 - warning, LD50 50-500 mg/kg
5 - danger: poison, LD50 5-50 mg/kg
6 - danger:poison, LD50 <5 mg/kg
rank the following signal words in order of most to least concerning: danger, caution, warning
most concerning: danger
next: warning
least: caution
describe the toxicity and give examples of non-ionic detergents
lowest toxicity. non-phosphate or low suds laundry products, shampoos, dishwashing detergents (alkyl-aryl polyether sulfate, alkyl ethoxylate)
describe the toxicity and give examples of anionic detergents
can be irritating. dishwashing soap, laundry detergent, shampoo (alkyl sodium sulfate, sodium lauryl sulfate)
describe the toxicity and give examples of cationic detergents
most toxic type, dose important! disinfectants, algicides, applicator tank mixes, fabric softeners
quaternary ammonium derivatives!!, (benzalkonium chloride, benzethonium chloride)
describe amphoteric detergents
combo of anionic and cationic, more in industrial cleaning products, not common in the house
list the following in order from most to least toxic:
anionic, cationic, nonionic, amphoteric
cationic, amphoteric, anionic, nonionic
(cationic is worst! take home message)
what is the effect of cationic surfactant tox
irritation, possible neuromuscular or ganglionic blockade
(take home message)
describe the MOA of quaternary ammonium (“quat”)
acts where ACh does and causes neuro signs
what are the clinical signs and onset/course for granular soap and detergents
irritation depends on concentration, vomiting, diarrhea, hemolysis (anionic), neurologic (cationic), acidosis (cationic), shock (cationic), ulcers of GI, dermis, and cornea possible (cationic)
onset <2 hours, duration depends on surfactant
name some alkali cleaning products
ammonia, oven cleaner, drain cleaner
what effect does ammonium hydroxide have
3% - mild irritation, warning label
10% - corrosive
what kind of label do oven cleaners (4% NaOH) have
danger
what is the MOA of alkali cleaners
more lipophilic than acids and penetrate deeper into tissues, causing liquefactive necrosis!
(take home message)
what is the treatment for alkali substances
dilute and protect
(emesis, activated charcoal, lavage and cathartics are CONTRAINDICATED b/c the substance is irritating)
what type of label do acids like toilet bowl cleaners have
danger
what type of label do oxidizers like bleach have
warning
what type of label do hydrocarbon solvents have, where are they found, and how are they absorbed
caution
glues, furniture polishes, non-water cleaners, paint removers and thinners, spot removers
absorbed orally, dermally, or by inhalation
(take home message: solvents and bleach can be inhaled)
what are the types of disinfectant cleaners
cationic surfactants, phenolic compounds, pine-oil based (terpenes/phenolics)
what are the clinical signs of disinfectant cleaner tox and how does their toxicity compare to detergents
GI irritation, pain
all more toxic than soaps and plain detergents
what animals are most sensititve to disinfectant cleaners
cats - don’t handle pine oil and phenols well
(take home message)
what is the treatment for disinfectant cleaner tox
dilution with milk or water, irrigate exposed surfaces, symptomatic treatment
what is the unique effect of anionic surfactants
hemolysis
(take home message)
what effect do acid cleaners have
coagulative surface necrosis
(take home message)
what alcohol should not be used for antiseptic use and what is the risk
methanol
absorbed thru skin, causes vomiting, CNS depression, hypothermia, acidosis
what is the effect of fertilizer toxicity and who is usually affected
fertilizers with certain percentages of N-P-K are irritating. target GI system - vomiting, diarrhea, anorexia
most cases in small animals, mostly nonlethal
what is unique about rose fertilizers
may have 5% iron, which can cause iron tox and hepatic damage
what is the treatment for fertilizer tox
symptomatic, dilution rather than activated charcoal, demulcent may be needed
what is the treatment for corrosives
irrigation with water or milk
corticosteroids may be used with airway edema, but do not help with preventing strictures
soaps, detergents, surfactants for household use: why are they usually not considered particularly dangerous?
a. intrinsic hazard low
b. active ingredient in low concentration
c. labeling and/or packaging
b and c
cats are more sensitive than dogs to some disinfectants. which type and why?
a. cationic surfactants b/c they cause neuromuscular blockade
b. phenolic disinfectants b/c cats lack mechanism for elimination
c. ammonia-containing products b/c they can be inhaled
d. acids and alkali products b/c they’re corrosive
e. bleach b/c it can produce chloramine gas
b
a,c,d,e are true of all animals
how many ounces per gallon
128
in general are herbicides very toxic? why? what is the exception?
most are not very toxic because they target plant specific stuff
paraquat is very toxic!
how toxic is glyphosphate? clinical signs?
low mammalian toxicity. adverse effects are likely due to surfactant irritation of GIT and resolve within 24 hours
salivation, abdominal pain, anorexia, vomiting, depression, lethargy
(key point: GI problems with surfactant)
what is the treatment for glyphosphate tox
most cases mild and self limiting. with high dose/concentration, treat as a caustic agent
symptomatic tx, dilution with milk or water
what is the MOA of glufosinate
irreversibly inhibits glutamine synthetase, causing hyperammonemia.
if it penetrates the CNS, neurotoxic. similar structure to glutamate
what are the clinical signs and onset/duration of glufosinate tox
nausea and vomiting early, then seizures and resp depression
onset 4-50 hrs, lasts days
what is the treatment for glufosinate tox
monitor for 48 hours due to delayed onset. diazepam for seizures, IV fluids to increase excretion, resp support as needed
what is the MOA on plants of 2,4-D? what are they used for?
analogues of auxin, disrupt hormone balance and protein synthesis causing abnormal plant growth
used on broadleaf weeds
what is the toxic potential for 2,4-D
for clinical signs, would need direct exposure to concentrated formula or animal susceptible due to poor health
who is more sensitive to 2,4-D and why?
dogs b/c decreased ability to excrete organic acids in urine
what are the clinical signs of 2,4-D herbicides?
ocular, dermal or mucosal irritation
dogs - anorexia, vomiting, diarrhea +/- blood, myotonia(muscle weakness with rigidity)!, hyperthermia, tachypnea, ataxia, depression, myalgia, rhabdomyolysis, paresis (esp hind legs)
ruminants - anorexia, depression, salivation, prostration, bloat/rumen atony, muscle weakness, diarrhea
swine - vomiting, diarrhea, ataxia, depression, weakness
what is the toxic potential and onset of 2,4-D herbicides?
only toxic if exposed to concentrate
onset <12 hours with small doses, <2 hours at high dose
how do 2,4-D herbicides cause myotonia? in what animals?
dogs
alters muscle membrane, inhibiting voltage gated Cl channels in muscle, causing hyperpolarization of cell membrane and thus myotonia
(key point: acute exposure causes myotonia in dogs)
what is the treatment for 2,4-D herbicide tox? prognosis?
treatment=prevention
symptomatic and decontamination, provide fluids with NaHCO3- for ion trapping in urine, activated charcoal, restrict grazing area for cattle
prognosis is good for rapid recovery
what is another name for 2,4-D
phenoxy/chloroacetic acid herbicides
what is unique about paraquat
need a license to use it. very toxic. nonselective and fast acting
describe the movement of paraquat through the body
poorly absorbed from GIT or skin, rapid distribution to tissues. accumulates in lungs and kidney, excreted unchanged in urine
what is the MOA of paraquat
caustic on contact
induces oxidative stress (reduces to a free radical that reoxidizes to superoxide anion). oxygen free radicals in the body cause cellular, lipid, membrane, and protein damage
what is the effect of paraquat
concentrated in the lung and causes severe fibrosis!!!
also concentrates in kidney, causing direct damage to glomerulus and tubules. the necrosis in turn reduces elimination of the drug
what are the clinical signs of acute, high dose paraquat tox? onset?
GI, pulmonary!, renal, hepatic, and CNS effects
fulminating pulm edema, hemorrhage, interstitial pneumonia, acute renal tubular necrosis, hepatic necrosis, and death. multi-organ failure!!, convulsions
onset <2 hours, death within a few days
(key point: convulsive syndromes with hight doses of paraquat and diquat)
what are the clinical signs of chronic or acute sublethal dose paraquat tox? onset?
GI, resp!, renal, hepatic effects
anorexia, depression, lethargy, ulceration of GIT, vomiting, diarrhea, colic - onset 1-3 days
fatal, progressive pulmonary fibrosis! causing dyspnea 2-7 days after initial exposure
how is diquat different from paraquat
use is not restricted. it does not concentrate in the lungs
what is the MOA of diquat
distribution to GIT, kidney, eye, and liver
like paraquat, superoxide anion is formed
what are the clinical signs of diquat tox
cataracts in dogs
anorexia, depression, mouth and esophagus ulcers, vomiting, diarrhea, colic, renal impairment, seizure
(key point: convulsive syndromes with hight doses of paraquat and diquat)
what chronic lesions are seen on necropsy with paraquat tox
lung - hyaline membrane formation within alveoli, type 2 pneumocyte proliferation, alveolar septal fibrosis
also with acute and chronic see GI ulceration/necrosis, proximal renal tubule necrosis, hepatic necrosis
what necropsy lesions are seen with diquat tox
GI ulceration/necrosis, cerebral hemorrhage, renal tubular necrosis, cataracts in dogs
what lab tests can be done to detect paraquat/diquat tox
sodium dithionite test on plasma and urine
also analysis of stomach contents, plasma, urine, lung, kidney
what is the treatment and prognosis for paraquat/diquat tox
can only treat animals presenting in <6 hours of exposure
GI decontamination (emesis, activated charcoal, etc), forced diuresis, scavengers to reduce reactive oxygen species (N-acetylcysteine, vit E, vit C), anti-inflammatories, salicylates (reduce reactive oxygen)
prognosis extremely guarded for paraquat
what is the most common triazine herbicide and where does it persist?
atrazine persists in aquatic environments
EPA tolerance ≤ 3ppb in drinking water
(key point: potential association with frog defects, repro)
what is the toxic potential for triazine herbicides? MOA?
low acute toxicity via oral and dermal routes
MOA unknown, but can cause direct articular vasodilation
what are the clinical signs of triazine herbicide tox? onset?
anorexia, salivation
CNS in cattle - ataxia, prostration, hyperesthesia!, muscle tremors
onset <24 hours
(key point: hyperesthesia in cattle)
how do you diagnose triazine herbicide tox? treat?
test stomach contents or liver
symptomatic tx
what toxin can be used as a “hit and run”/malicious use
paraquat
(key point: moderate dose used as a lung toxicant)
are fungicides more or less toxic than herbicides?
less
what effects are possible with fungicides? name some examples of products
mutagenic and carcinogenic potential
ex: captan, folpet, thiram
Glyphosphate and 2,4-D are popular herbicides with low toxicities. When tox occurs, could any of these factors contribute to toxicity? (yes or no)
a. inappropriate dilution of concentrates
b. species
c. additives/contaminants
d. use of structural relatives rather than the drugs themselves
a. yes
b. yes, dogs more sensitive to 2,4-D
c. yes
d. yes, i think she is talking about glufosinate, a relative to glyphosphate. it is more toxic and not commonly used. CNS and resp signs
chose either paraquat or atrazine for the following:
a. more available for use
b. lower acute LD50
c. target organ is the lung
d. causes free radical damage to tissues
a. atrazine
b. paraquat
c. paraquat
d. paraquat
T/F: diquat has a unique toxicity
true - the eye in dogs
What is the classic clin path presentation of ethylene glycol toxicity
Azotemia, acidosis, markedly increased anion gap, marked hypocalcemia
