Blakley Flashcards
How are organochlorines absorbed
Well absorbed through skin and MM
Poorly absorbed through lungs and GIT
Distribution of organochlorines
Accumulate in lipid tissues; Readily detectable in liver, kidney brain and fetus
metabolism of organochlorines
dechlorinated slowly in the liver; many metabolites are highly toxic
how are organochlorines excreted
through the bile; enterohepatic recycling occurs
what is organochlorines mechanism of action
K efflux is hindered and Na depolarization is prolonged –> decreasing transmembrane resting potential (decreased firing threshold)
other mechanisms of action for organochlorines
increased synaptic activity, increased neurotransmitter release from presynaptic terminals and inhibition of GABA
what is the susceptibility of cats to organochlorines
5 times more susceptible than most species
what are the clinical manifestations of organchlorines
behavioral abberations (anciety, apprehension, head between legs, licking excessively), nervous phenomena (hypersensitivity, muscle twitching, jaw clamping, clonic tonic convulsions, opisthotonus), autonomic manifestations (minimal but do occur – salivation, diarrhea, dyspnea), locomotor disturbance (stiff gait, ataxia, incoordination)
PM findings with organochlorines
non-specific; GIT (hemorrhage and congestion), mild fatty degeneration of liver and kidney, degenerative changes in thyroid, pancreas, testis and adrenal glands
Treatment of organochlorines
Wash off skin, gastric lavage, activated charcoal, mineral oil (to force through and bind), sedation, IV lipid emulsion
residue concerns of organochlorines
milk and meat residues are a major concern due to reproductive, carcinogenic and immunosuppresive effects
diagnosis of organochlorines
analyze fat, milk, liver, kidney and GI contents
3 major groups of anticholinesterase compounds
organophosphates insecticides, carbamate insecticides and nicotinoid insecticides
residue concerns with anticholinesterase compounds
not a concern because rapidly degraded with short half life
absorption of anticholinesterase compounds
well absorbed by all routes including dermal and respiratory
distribution of anticholinesterase compounds
rapidly to all tissues; no accumulation in fat
excretion of anticholinesterase compounds
excreted rapidly in a few days
mechanism of action of anticholinesterase compounds
inhibition of acetylcholinesterase prevents break down of acetylcholine
enzymes affected by anticholinesterase compounds
pseudo(plasma) cholinesterase (non-specific) and true (RBC) cholinesterase (80%)
specific mechanism of action of organophosphate
forms a stable enzyme-organophosphate complex that is practically irreversible
specific mechanism of action of carbamates
carbamate enzyme complex is not as stable so enzyme inhibition is reversible
nicitinoid compound mechanism of action
binds to nicotinic receptors therefore no inhibition of acetylcholinesterase BUT need extreme high doses to bind a sufficient number of receptors to cause signs
clinical manifestations of anticholinesterase compounds
excessive muscarinic and nicotinic stimulation starting 5 minutes to 1-2 hours after exposure; diarrhea, vomiting, salivation, dyspnea due to bronchoconstriction, decreased HR, pupil constriction
with what anticholinesterase compound does delayed neurotoxicity occur with
organophosphates
clinical signs of delayed neurotoxicity (organophosphates)
develops 10D to 3M after exposure; irreversible effects of muscle weakness especially in hind limbs, knuckling, ataxia (flaccid paralysis), cats unable to retract claws, normal acetylcholinesterase
PM findings of delayed neurotoxicity (organophosphates)
axonal degeneration, peripheral neuropathy, degeneration of myelin sheath
diagnosis of delayed neurotoxicity (organophosphates)
histo exam of spinal cord, chemical analysis of tissues and history of previous exposure
PM findings for anticholinesterase compounds
few lesions, petechial hemorrhage and congestion on viscera, slight pulmonary edema
Diagnosis of anticholinesterase compounds
history, cholinesterase activity in heparinized blood (measured by Michel’s change in pH for organophosphates only or titrimetric pH stat for carbamates/organophosphates
factors that influence the measurement of cholinesterase activity
aging, enzyme denaturation, spontaneous reaction (carbamate)
treatment of anticholinesterase toxicity
atropine (non-competitive antagonist that blocks muscarinic receptors), 2-PAM (for organophosphates only, contraindicated in carbamates), wash, activated charcoal, bicarb and fluids
mechanisms of action of lead
based on the affinity of lead for SH or imidazole groups; binds to various macromolecules to impair their function
(enzymes, decreases cellular respiration and ATP production due to effect on mitochondria, embryotoxic, teratogenic, immunosuppression)
absorption of lead
1-2% in adults, 30-40% in young
distribution of lead
cumulative toxin; distributes to liver and kidney within the day, chronic exposure displaces Ca in bone (does NOT go to brain)
excretion of lead
kidney and minor excretion in milk
effect of lead on the GIT
irritation and gastroenteritis
effect of lead on nervous system
encephalopathy – capillary damage causes hemorrhage and congestion in the brain followed by edema and malacia +/- blindness and peripheral nerve damage
effect of lead on hemopoetic system
anemia associated with decreased iron uptake, increased RBC fragility, and impaired heme synthesis; can see basophilic stippling
effect of lead on kidney
degenerative changes – tubular necrosis, nephritis, fibrosis and hyaline degeneration (acid fast inclusion bodies)
effect of lead on respiratory system
swallowing mechanisms can be impaired by neuro dysfunction leading to aspiration pneumonia
duration of acute lead poisoning
short; typically less than 24 hours
clinical manifestations of acute lead poisoning (cattle)
behavioral changes (mania, bellowing, head pressing), locomotor disturbances (staggering and muscle tremors), nervous phenomena (clamping jaws, blindness, hyperaesthesia, intermittent tonic-clonic convulsions, opisthotonus), GIT (rumen stasis, salivation, abdominal pain)
clinical manifestation of subacute lead poisoning (cattle)
dullness and head pressing, variable locomotor disturbances, blindness, depression, hyperaesthesia, NO CONVULSIONS, grinding teeth, anorexia
lead poisoning in sheep
usually subacute and may have osteoporosis
lead poisoning in horses
usually chronic – colic, diarrhea, pharyngeal paralysis, aspiration pneumonia, inspiratory dyspnea, roaring
lead poisoning in swine
primarily GI signs, vomiting, few CNS signs
lead poisoning in dogs
anorexia, vomiting, colic, hyperexcitability, convulsions, hysterical bark
diagnosis of lead poisoning
lead analysis of liver and kidney
antemortem diagnosis of lead poisoning
heparinized blood, rumen contents, fecal contents
clinical pathology of lead poisoning
anemia, basophilic stipling, increased ESR, hypochromia, leptocytes, proteinuria, glucosuria
treatment of lead poisoning
chelation therapy (penicillamine, BAL, Ca EDTA)
supportive care of lead poisoned animals
force feeding, oral fluids, mannitol
residue concerns of lead poisoning
treatment of food animals is not recommended due to meat and milk residues
lead half life
many months
3 forms of mercury
elemental metal mercury, inorganic mercury, organic mercury
absorption of metal mercury
well absorbed by inhalation
inorganic mercury absorption
poor; burns skin
absorption of inorganic mercury
well absorbed by skin and GIT (lipophilic)
metabolism of mercury
converted to inorganic forms but in environment be converted to organic mercury (methyl mercury)
distribution of mercury
liver and kidney accumulate high quantities; fetus acts as a sink and protects mother)
excretion of inorganic mercury
urinary
excretion of organic mercury
bile and feces; 70D half life
mechanism of action of inorganic mercury
causes corrosive damage and tissue necrosis (irritation); binds with sulfhydryl groups causing reduced metabolic activity and degenerative change)
mechanism of action of organic mercury
interferes with metabolic activity causing degenerative changes
clinical manifestation of inorganic mercury
GIT and neurological syndrome; anorexia, vomiting, salivation, diarrhea, stomatitis, ulcers, ataxia, tremors, terminal convulsions, depression, paresis, hematuria, proteinuria, uremia, epistaxis, dyspnea, (alopecia and keratinization occur with chronic)
clinical manifestations of organic mercury
ataxia, tremors, terminal convulsions, depression, paresis, hematuria, proteinuria, uremia, epistaxis, dyspnea, (alopecia and keratinization occur with chronic)
PM of inorganic mercury
gastroenteritis, stomatitis, mucosal hemorrhage and edema, ulcers, interstitial nephritis, tubular necrosis, edema, bronchitis, hydrothorax, mild liver necrosis, encephalomalacia, cerebellar atrophy of offspring
PM of organic mercury
interstitial nephritis, tubular necrosis, edema, bronchitis, hydrothorax, mild liver necrosis, encephalomalacia, cerebellar atrophy of offspring
diagnosis of mercury
clinical manifestations and pathology of CNS and GIT; analysis of blood, liver or kidney for mercury
treatment of mercury
success is limited by long half life and degenerative organ change; sodium thiosulfate, egg whites, milk, astringents; chelators such as BAL are used to treat pets
residue concerns of mercury
major concerns due to milk and meat residues being lengthy and highly teratogenic nature
forms of arsenic
organic (less toxic, CNS) and inorganic (severe GI signs and CNS)
arsenic absorption
readily absorbed through skin or GIT
arsenic distribution
accumulates in energy rich tissues (liver, kidney, GI epithelium); with chronic exposure will be in hair and hoof as well
excretion of arsenic
bile or urine
arsenic mechanism of action
metabolic poison that impairs cellular respiration and uncouples oxidative phosphorylation (degenerative changes)
mechanism of action of inorganic arsenic
chemical irritation, tissue degeneration and metabolic poison
clinical manifestation of acute inorganic arsenic
high mortality, sudden onset, vomiting, abdominal pain, weakness, ataxia, recumbency, shock, diarrhea and death within 3-4 hours
clinical manifestations of subacute inorganic arsenic
duration of 2-7 days with more neuro signs; colic, vomiting, diarrhea, salivation, grinding teeth, dehydration and shock, muscle tremors, incoordination, clonic convulsions, hind end paralysis
clinical manifestations of chronic inorganic arsenic
vague, unthrifty animals with poor growth, indigestion, reduced milk production, abortion and buccal cavity ulceration
diagnosis of inorganic arsenic
clinical signs, analysis of liver, kidney, hair, or food
arsenic half life
only a few days
treatment of inorganic arsenic poisoning
BAL is first choice because will pull out of brain; sodium thiosulfate (sulfur binds arsenic), fluid therapy is essential for shock
types of organic arsenic used as feed additives
arsanilic acid (least toxic), roxarsone, nitrophenylarsonic acid (5x more toxic than arsanilic)
elimination rate of organic arsenic
rapidly eliminated – short withdrawal times
clinical manifestation of acute organic arsenic
symptoms in about 1 week, incoordination, ataxia, paralysis, blindness, not anorexia and no GI signs (CONSUME FOOD UNTIL LATE STAGES)
clinical manifestations of chronic organic arsenic
similar signs to acute but to a lesser extent
diagnosis of acute arsenic poisoning
history, neuro signs, feed analysis is best
what does glutathione peroxidase assess
selenium deficiency
normal function of selenium
stabilize cell membrane
plant sources of selenium
astragalus (locoweed)
absorption of selenium
well absorbed
distribution of selenium
found in all tissues; will be at highest levels in oxidative and energy rich tissues (liver and kidney), can displace sulfur in hair and hoof, accumulates in fetus
excretion of selenium
urine mostly; bile, sweat, lungs, hair and hooves
selenium toxicity mechanism of action
causes lipid peroxidation and membrane damage; high levels reduces ATP formation; irritating orally
clinical manifestations of acute selenium poisoning
sudden onset in 1-2 days with quick death; anorexia, depression, dyspnea, cyanosis, colic and shock
PM of acute selenium toxicity
congestion, hemorrhage, enteritis with oral exposure, degenerative changes to liver and kidney
manifestation of subacute selenium toxicity (blind staggers)
often a plant source, onset is days to weeks; wander aimlessly, anorexia, blind, impaired swallowing, head pressing, emaciation, dyspnea, death
PM of subacute selenium toxicity
pulmonary edema, hydrothorax, gastroenteritis, ulcers, rumen necrosis and hyperemia
chronic selenium poisoning manifestations (alkali disease)
onset is months, dullness, rumen stasis, impaction, hoof deformities, hair loss
PM of chronic selenium poisoning
mild gastroenteritis, atrophy and dilation of heart, other organs show degeneration
PM of selenium poisoning in swine
symmetrical spinal poliomalacia, necrosis of grey horns of L6-L9 leading to paralysis, continue to eat and drink
diagnosis of selenium toxicity
tissue and feed analysis
treatment and prevention of selenium toxicity
fluids for shock therapy, acetylcysteine, dietary supplementation with copper, arsenic or sulfur containing AA may bind Se
factors influencing iron toxicity
young animals, especially pigs, have no mechanism to excrete excess iron until 8D of age; animals born with high iron stores are more susceptible; animals born with low Vit E/Se status are more susceptible.
mechanism of action of iron toxicity
not fully understood! CV collapse and death from shock; observe increased permeability leading to fluid loss and hepatic necrosis (leading to hemorrhage)
clinical manifestations of peracute iron toxicosis
anaphylactoid like reaction then death from shock within minutes to 1-2 hours; (injectables)
clinical manifestations of subacute/classical iron poisoning
drowsiness, depression, coma and death in 4-5 hours, vomiting, diarrhea, melena, necrosis, icterus, hemoglobinuria, pale skin, dyspnea, acidosis, hemorrhage
presenting complaint for subacute/classical iron poisoning
liver damage
clinical manifestations of chronic iron poisoning
rickets and poor growth due to iron binding P and altering bone growth
PM of iron toxicity
subacute will show periportal necrosis and iron deposits in kupffer cells; icterus
treatment of iron toxicity prior to GI signs
milk of magnesia can be used to form insoluble iron hydroxide salts
treatment of iron toxicity after GI signs
fluids for shock and acidosis, chelators such as deferoxamine (Ca EDTA has low affinity), vitamin E
most effective treatment of iron toxicity
vitamin E because antioxidant activity prevents further liver damage
differences in species susceptibility regarding copper
ruminants more susceptible monogastrics; sheep more susceptible than catte; llamas comparable to sheep but without the hemolytic crisis; bedlington terriers are predisposed; pigs/horses metabolize copper differently so not affected
absorption of copper
well absorbed
distribution of copper
found extensively in plasma bound to albumin, ceruloplasmin, oxidase enzyme or metallothionein; liver is primary storage organ
can blood be used to diagnose copper toxicity
No; ceruloplasmin will be low with copper deficiency but remains within normal reference in copper toxicity
excretion of copper
primarily in the feces; biliary excretion, though limited, is critical for homeostasis (bedlington terriers don’t have this –> chronic copper poisoning)
acute copper toxicity mechanism of action
protein coagulant at high levels leading to severe gastroenteritis
chronic copper toxicity mechanism of action (primary)
Cu has oxidative properties that occur when liver exceeds storage – lipid peroxidation begins (glutathione is depleted causing Hg in RBC to be oxidized to methemoglobin, damaged erythrocytes undergo hemolysis)
what color is the blood with copper poisoning
chocolate brown
phytogenous chronic copper poisoning (secondary)
copper is normal but low molybdenum – increased Cu absorption and decreased excretion, no liver damage present
hepatogenous chronic copper poisoning
related to ingestion of plants that cause liver damage (pyrrolizidine alkaloids impair bile excretion leading to chronic Cu poisoning) or chronic active hepatitis
factors preceding Cu exceeding liver storage capacity
declining plane of nutrition, shipping, lactation, exercise, stress
manifestations of acute copper poisoning
death within 24 hours; abdominal pain, nausea, vomiting, salivation, shock, feces (green color), mild jaundice, gastroenteritis primarily (erosion and ulceration), congestion of other organs, no methemoglobin
manifestations of chronic copper poisoning
hemoglobinuria, hemoglobinemia, methemoglobinemia (portwine urine, red plasma, chocolate brown blood), jaundice and increased liver enzymes, trembling and weakness
PM changes with chronic copper poisoning
liver will have generalized icterus, enlargement and friable; kidney – hemorrhage, friable, degeneration, tubular necrosis, gun metal color; spleen – enlarged, black currant jam appearance; methemoglobin causes brown discoloration of tissues
diagnosis of acute copper poisoning
signs of sudden death and gastroenteritis, GI contents may be blue green color, normal tissue levels
diagnosis of chronic copper poisoning
analysis of feed for copper molybdenum levels (normal is 6-10:1); elevated liver enzymes, methemoglobin and hemoglobinuria; 1 or 2 sick and the rest on the brink of disaster
treatment of copper poisoning
unsuccessful once hemolytic crisis occurs; ammonium molybdate orally, sodium thiosulfate, thiomolybdate (ideal but not available commercially)m chelators, add Mo/Zn to diet
what mineral does molybdenum toxicity manifest as a deficiency of
copper
differences of susceptibility of molybdenum toxicity
cattle/ruminants are more susceptible; young are more susceptible; pigs can tolerate high levels
mechanism of action of molybdenum toxicity
interferes with copper storage by reducing absorption and enhancing secretion (also competes with Cu for Cu dependent enzymes); interferes with P absorption and mineral metabolism in bones (faulty bone development); interferes with phospholipid synthesis causing reduced growth and maintenance of myeline
clinical manifestations of molybdenum toxicity in sheep
swayback, incoordination, ataxia, occasionally blind, depigmented stringy wool, usually young, rapidly growing animals
clinical manifestations of molybdenum toxicity in cattle
emaciation, diarrhea, anemia, achromotrichia, enlarged joints, osteoporosis, reduced fertility and reduced milk production
diagnosis of molybdenum toxicity
forage levels of Cu/Mo (2/1), tissue levels of Cu and Mo, response to Cu therapy
treatment of molybdenum toxicity
copper sulfate as a mineral mix; injectable copper; copper oxide needles; chelated mineral mix
absorption of zinc
well absorbed
distribution of zinc
found in most tissues
excretion of zinc
excreted in urine and bile
zinc half life
2-3 days; may be longer if there is kidney damage associated with Zn exposure
mechanism of action of zinc toxicity
oxidative damage; hapten induced immune dysfunction and DIC can also occur
clinical manifestations of Zn (dogs)
anorexia, salivation, vomiting, diarrhea, bleeding, jaundice, intravascular hemolysis, heinz bodies, leukocytosis with left shift, regenerative anemia, bilirubinemia, hemoglobinuria, tubular nephrosis
diagnosis of zinc toxicity
elevated blood zinc levels (must use proper tube for diagnosis to be accurate), radiographs, clin path
treatment of zinc toxicity
surgery, blood, transfusions, heparin or dicoumarol, cimetidine to reduce acid secretion and decrease dissolving Zn
what is the most necessary treatment for zinc toxicity
heparin or dicoumarol to prevent DIC
complication of zinc toxicity
pancreatitis and DIC
what time of year is blue-green algae toxicity seen
hot summer months
why do you need to collect a water sample ASAP with blue-green algae
toxin can disappear from water within 24 hours
factors affecting blue-green algae toxicity
species of algae, bacterial presence in bloom (cl. botulinum), growth conditions, sunlight/temperature, acummulation, decompisition, LPS endotoxins, after rapid growth there may be rapid lysis with release of endotoxins
what N/P ratio favors green algae
high N/P ratio
what N/P ratio favors blue-green algae growth
low N/P ratio (high P favors)
what are the 3 species of blue-green algae
microcystis, anabena, aphanizomenon (mike, annie and fannie)
what toxin is present in anabena (blue-green)
anatoxin-a; alkaloid, very fast death factor, not stable
what is the mechanism of action of anatoxin-a (anabena)
postsynaptic depolarizing neuromuscular block, nicotinic agonist, anticholinesterase activity
clinical manifestations of anabena (blue-green)
paralysis, tremors, convulsions (3-5 minutes after drinking), salivation, vomiting, diarrhea, dyspnea, death within 4 minutes
PM of anabena toxicity (blue-green)
few distinct changes; agonal hemorrhage and congestion
diagnosis of anabena toxicity (blue-green)
mouse bioassay
treatment of anabena toxicity (blue-green)
artificial respiration for at least 30 hours; (anatoxin irreversibly binds cholinesterase enzymes – animals usually found dead); atropine may offer relief
components of microcystis toxin (blue-green)
hepatotoxic and post-synaptic neuromuscular block (two peptides) – fast death factor
mechanism of action of microcystis (blue-green)
hyperphosphorylation of proteins and keratin, tumor promotor, hepatotoxin induces necrosis and apoptosis
clinical manifestation of microcystis (blue-green)
death within one hour, vomiting, hemorrhagic diarrhea, icterus, photosensitzation in survivors, convulsions
PM of microcystis (blue-green)
liver will be swollen, mottled, congested, hemorrhage, necrosis and apoptosis; tubular nephritis; pulmonary hemorrhage; cardiac degeneration
diagnosis of microcystis
mouse bioassay with water sample; liver pathology; hepatic enzymes elevated within 45 minutes
aphanizomenon toxins
saxitoxin (paralytic shell fish poison, Na channel blocker, inhibits axonal transmission of nerve impulses); neurotoxins (neuromuscular action and inhibition of nerve conduction)
clinical manifestations of aphanizomenon toxicity (blue-green)
paralysis, death associated with respiratory depression/depression of respiratory center
PM of aphanizomenon toxicity (blue-green)
no specific lesions
treatment of aphanizomenon toxicity (blue-green)
symptomatic; activated charcoal
prevention of blue-green algae toxicity
copper sulfate in water, diquat, shade, lime (standard treatment), duckweed, chlorine, increase N/P ratio
what is the standard prevention of blue-green algae toxicity
lime: removes P and increase N/P ratio to favor green algae growth; changes pH and may make cattle not want to drink it
thiram (fungicide)
relatively non-toxic; hepatotoxic and skin irritant; rotten egg smell from cows; zero residues
chorophenols (fungicide) – trichlorophenol and pentachlorophenol
uncouples oxidative phosphorylation; temperature of animal sky rockets (need to cool down); irritant;
pentachlorophenol mechanism of action (fungicide)
powerful uncoupler of oxidative phosphorylation, inactivates respiratory enzymes, direct irritant
clinical manifestations of pentachlorophenol (fungicides)
muscle weakness, incoordination, anorexia, immense increase in BT, dyspnea, sweating, dehydration, irritation to skin/resp tract, cardiac malfunction, terminal convulsions
absorption and excretion of pentachlorophenols (fungicides)
rapid absorption and excretion (glucoronidation) – cats can’t metabolize
treatment of pentachlorophenols (fungicide)
cold water bath, wash, lavage
pentachlorophenols are present in (fungicide)
wood preservative, molluscacide and rug shampoo
Maneb (carbamate fungicide)
contains Mg; causes depressio, anorexia and diarrhea; PM shows liver and kidney degeneration, congestion of lungs, thyroid hyperplasia
Captan (fungicide)
low toxicity; clinical signs are dyspnea, anorexia, depression; PM shows hydrothorax, ascites and gastroenteritis
what is dinitroorthocresol
an insecticide, herbicide and wood preservative
absorption of dinitroorthocresol
fat soluble; absorbed by vapors, oral or cutaneous exposure
mechanism of action of dinitroorthocresol
uncouples oxidative phosphorylation so increases body temperature
symptoms of dinitroorthocresol
fever, weakness, dyspnea, anorexia, acidosis, liver/kidney damage, possible abortion, stains organs yellow
treatment of dinitroorthocresol
lavage, bicarb, activated charcoal, cathartic and ice pacls
effect of sulfur toxicity (fungicide)
irritation causing superpurgation and diarrhea; erythema, colic, dullness, ataxia, gastroenteritis, ulcers, erosions, liver and kidney congestion
thiabendazole (fungicide and anthelmintic)
depression, anorexia and GIT disturbance
mechanism of action of chlorates (herbicides)
strong oxidizing agent; methemoglobin formation, RBC damage, irritation (rumen stasis)
symptoms of chlorate toxicity
diarrhea, vomiting, colic, hematuria, dyspnea, cyanosis, tissues are chocolate brown (looks like chronic Cu but no liver damage)
treatments of chlorate toxicity
lavage, demulcent, methylene blue (none very effective)
what rule is paraquat (herbicide) considered the exception to
the rule that herbicides are not very toxic; paraquat is quite toxic but there are species differences
manifestation of acute paraquat toxicity
excitation, incoordination, ataxia, diarrhea, dyspnea, death within 10 days
manifestation of chronic paraquat toxicity (herbicide)
progressive fibrosing pneumonitis
mechanism of action paraquat (herbicide)
reduction of oxygen to superoxide anion – free radical damage in lung, lipid peroxidation, cell damage and impaired cell function
other organ affects of paraquat (herbicide)
edema and hyaline membrane formation in lung, GIT irritation and ulcer, kidney and liver degeneration, eye and skin irritant
treatment of paraquat toxicity (herbicide)
soap wash, lavage, adsorbents
what is TCDD
a phenoxyderivative herbicide
TCDD skin lesions (highest toxicity of phenoxyderivative herbicides)
hepatotoxic, carcinogenic, teratogenic, immunosuppresion, chloroacne (skin), fat accumulation
what are 2,4 D derivative
phenoxyderivative herbicides
2,4 D absorption and half life
oral and dermal absorption; excreted unchanged in urine with 18 hour half life
mechanism of action of 2,4 D (herbicide)
uncouples oxidative phosphorylation so increases BT, decreased ribonuclease synthesis and damages muscle membranes
clinical signs of 2,4 D (herbicide)
anorexia, rumen stasis, hind limb paralysis
PM of 2,4 D (herbicide)
congestion and degeneration of organs, some hemorrhage
what species is most sensitive to 2,4 D toxicity (herbicide)
dogs – myotonia, vomiting, bloody diarrhea, posterior weakness
treatment of 2,4 D (herbicide)
wash, activated charcoal and fluids
food residue concern with 2,4 D (herbicide)
low
rotenone absorption and metabolism (acaricide)
poor absorption and rapid metabolism
rotenone symptoms (acaricide)
nausea, vomiting, salivation, dyspnea, tremors, incoordination, paralysis
treatment of rotenone (acaricide)
sedation (atropine is ineffective), good prognosis, residues are not a concern
pyrethrins/pyrethroids (acaricide) absorption
well absorbed by lungs, orally or dermally
mechanism of action of pyrethrins (acaricide)
alters Na channels to decrease ion fluxes; binds GABA
clinical signs of pyrethrin toxicity (acaricide)
muscle tremors, excitation, paralysis, salivation, vomiting, dyspnea
treatment of pyrethrin toxicity (acaricide)
rapid recovery usually; wash, emetics, activated charcoal, sedation
amitraz absorption, metabolism and excretion (acaricide)
well absorbed, metabolized by oxidation and excreted in urine (limited residue concern because rapid)
mechanism of action of amitraz toxicity (acaricide)
alpha adrenergic agonist, monoamine oxidase inhibitor, CV collapse and respiratory depression
clinical manifestations of amitraz toxicity (acaricide)
decreased HR, ataxia, depression, vomiting, diarrhea, seizures
PM of amitraz (acaricide)
non-specific with enlarged liver
treatment of amitraz
wash, emetic, activated charcoal
