Tox Flashcards
common clinical signs with houseplant ingestion
ptyalism, vomiting, diarrhea
Which houseplants can cause renal failure
ones containing oxalate - lilies, coffee bean, grapes, begonias, philodenderons
Which plants can cause hemolysis, methemoglobinemia, and/or anemia, hemoglobinuria
oxidants or cytotoxins causing RBC damage red maple (for EQ), onions (allium family), periwinkle
If an animal ingests foxglove or deadly nightshade, what effects do you expect?
Cardiac problems b/c cardiac glycoside
Which houseplants can cause neuro signs or hallucinations?
Allspice, macadamia nut - dogs, catnip, poppy
Which houseplants can cause liver disease?
jasmine, tea tree, some palms
Which houseplants can cause sudden death
glory lily, heavenly bamboo, chokecherry, yew
What’s with lily and cats?
all spp if lilium are toxic –> renal failure –> death
esp. flowers, but also consumption of leaves
toxin not ID’d
most common plants assoc’d w/ nitrate poisoning in rum
red rooted pig weed kochia weed sunflower lambs quarter sudan grass russian thistle
MOA of nitrate poisoning
nitrate –> nitrite in rumen –> binds to hgb –> methemoglobinemia –> hypoxia, abortion, death
what is brown mucosa a key sign of
methemoglobinemia –> nitrate poisoning
How do you treat for nitrate poisoning
methylene blue reduces methemoglobin
most common plants assoc’d w/ cyanide poisoning in rum (8)
Sorghums: Johnson grass, sudan grass or hybrids (choke cherry)
Service berry, Elderberry, Mountain mahogony, Arrow grass, Poison Suckle
Key parts about cyanide poisoning
- reduced better in highly acidic stomach
- block cytochrom oxidase activity –> no oxygen use in cells –> cell anoxia
- ataxia, tremors,, mydriatic, resp signs, sudden death
what is cherry red venous blood a key sign of
HCN (cyanide) poisoning
MOA and clin signs for larkspur poisoning in cattle
Bloch ACh at NMJ –> paralysis, bloat, sudden death
would treat with AChesterase inhibitors
MOA and clin signs for water hemlock (cicutoxin) poisoning in cattle
toxin Accums in roots –> inhibits GABA –> convulsions, seizure –> resp failure, sudden death
MOA and clin signs for yew poisoning in horses (most sensitive)
Taxine A,B inhibits cardiac Ca/Na channels
Taxane damages microtubules –> bradyarrythmias, vomiting/diarrhea, death
MOA and clin signs for milkweed or foxglove poisoning in cattle
cardiac glycosides (digoxin in foxglove) alter heart rate and rhythm –> cardia arrhythmia, 2nd degree heart block, GI issues, sudden death
MOA of oxalates, clin signs, treatment
- nephrotoxic - oxalates precipitate calcium –> oxalate crystals deposit in kidney, muscle
- Get muscle issues, hemorrhage, kidney failure, coma, death
- Ca borogluconate, hydration
5 major plants seen with oxalate poisoning
usually plants with red stem
greasewood, halogeton, shamrock, red-rooted pigweed, kochia weed
What is the concern with oak
gallotannins in new leaves, acorns –> denatures proteins –> hemorrhagic enteritis, icterus, bloody urine/diarrhea –> death
2 plants assoc’d w/ tremetol-induced myopathy/neurotoxicity & clin signs
white snake root & rayless golden rod milk sicknees (passed in milk), muscle tremors, choke --> heart block, death
Black walnut shavings are associated with what clin signs?
laminitis, tachypnea, colic
MOA and clin signs for Selenium toxicity in EQ
Se alters protein function –>oxidative damage –> wt/ loss, hair/skin changes, liver/kidney/muscle degen, diarrhea, death
Se accumulating plants (6)
Prince’s plume, milk vetch, woody aster, pain brush, gum weed, 4 wing saltbrush
Plants that cause primary photosensitization
carrot/celery family
St. Johns wort, bishop’s weed
buckwheats
What is secondary photosensitization
pyrrolizidine alkaloids metablized into bad pyrroles –> liver damage
Liver can’t metabolize phylloerythrin from chlorophyll –> accum –> photosensitization
Plants that cause secondary photosensitization
Groundsel/tansy ragwort (green picket fence), hounds tongue, heliotrope, fiddle neck, crotolaria (rattlepod)
How do steroidal sapogenins (agave family) contribue to secondary photosensitization?
form crystalloid material –> blocks biliary system
4 plants that produce steroidal sapogenins
Agave, bear grass, lantana, puncture vine/goats head
why are cats more susceptible to heniz body anemia
glucuronidation
How does the brassica family (kale, mustard, cabbage, etc) cause toxicity
disulfide toxin causes heinz body anemia –> hemoglobinuria, hepatotoxicity
How does moldy sweet clover cause toxicity? (Mycotoxic leukoencephalomalacia)
- Penicillium/Aspergillus spp ingested –> Coumarin converted to dicoumarol –> Vit k depletion –> hematomas, hematuria, decreased clotting
- Treat with whole blood, vit K
Also get hemorrhage of subcortical white matter
Bracken fern - primary toxin and dz seen
Thiaminase, Ptaquiloside
Causes thiamine deficiency (–>PEM), acute hemorrhage, retinal degen in sheep, bladder/UGI cancer
Toxins in locoweed (3)
Swainsonine from endophytes - lysosomal storage dz
Miserotoxins - cracker heels
Se accumulators - lameness, hair loss
Clin signs of locoweed/milk vetch poisoning
CNS signs - esp. unpredictable behav, repro probs, teratogenic effects, poor growth, CHF
- no treatment
Chewing disease in EQ is from what plants (2)? causes what clin signs? (Aka negropallidal encephalomalacia)
Prolong ingestion of Russian knapweed, yellow star thistle
Hypertonic facial/tongue muscles –> difficulty eating, inhalation pneumonia –> dehydrate/starve to death
brain damage irreversible
Classic brain lesion of chewing disease
nigropallidalencephalomalacia
bilateral liquefactive necrosis/ cavitation of globus pallidus/substantia nigra
Plants containing nicotine & nicotine-like alkaloids (e.g. hemlock) have what MOA
nicotinic ACH receptor agonists –> CNS, CV –> resp failure & death
How socrates died
4 teratogenic plants causing crooked calf dz & their MOA
Tobacco, poison hemlock, lupine, locoweed
neuromuscular blockade –> decreased fetal movement –> congenital contracture +/- cleft palate
What causes cyclopia in cattle
Mom ingesting verratum spp (e.g. western false helbore) on days 13-14 of gestation
pine needle abortion is most common in who? d/t what MOA?
cattle, bison
isocupressic acid inhibits uterine blood flow –> fetal stress
Gossypol toxicity
from cottonseed
binds protein & iron –> causes ROS, damage –> organ failure, pulmonary edema, decreased sperm counts (MALE fertility issue)
affects monogastrics (pigs, calves) - limit amt in diet
MOA of organophosphates/carbamates causing acute pesticide toxicity & clin signs
inhibit AChE –> excess ACh signaling
see SLUDGE clin signs, muscle effects up to paralysis
Die by resp or CV arrest
Which toxicity is more reversible: carbamate vs. organophosphate
- carbamate induced-AChE inhibition is reversible b/c short enz half life (mins vs. days for OP)
- But 2-PAM only helps treat OP toxicity
Pyrethrin/Pyrethroid insecticide tox: MOA, animal most affected, clin signs
- binds lipid membranes –> slows Na channel activation
- CATS have strong adverse reactions d/t given product dosed/labeled for dogs or licking off dog
- salivation, twitching, seizures, trying to rub back
- supportive care only but can resolve it
Ivermectin/Selamectin toxicity and herding breeds
herding breeds have ABCB1 mutation –> decreased transporter activity –> failure to remove drugs from BBB, sensitive to doses that wouldn’t affect normal dogs (CNS signs)
Most common route of exposure for Amitraz toxicity & clin signs
treatment?
- eating tick collar –> alpha 2 agonist –> decreased adrenergic signaling –> CNS/resp depression, profound bradycardia
- yohimbine/atipamezole can reverse (alpha 2 adrenergic antagonists)
Most effective way to avoid DEET (diethyltoluamide) toxicity?
use products w/ less than 50% DEET
anticoagulant rodenticide toxicity - MOA and clin signs
- blocks metabolism of vitamin K –> active clotting factors not formed
- delayed effect: 3-7 days between ingestion and tox
- see coag probs & vague signs + dyspnea if chest bleed, lameness if joint bleed, neuro if brain bleed etc.
- PT and aPTT increased,
- decontam, give vit K & supportive care
Bromethalin toxicity - MOA and clin signs (used for warfarin-resistant rodents)
- highly lipiphilic - goes to brain & fat –> uncouples ox phos –> depletes ATP
- Neuro signs - paresis/ataxia, tremors –> paralysis, seizures, death
- long half life (relay tox), 2-7 days between ingestion and signs
Cholecalciferol (Vit D3) toxicity - MOA, clin signs
- metabolized in liver, kidneys
- high dose = buildup while metabolizing –> increased Ca, P in serum altering cell activity, soft tissue mineralization
- acute tox: vomiting, diarrhea, PU/PD, kidney probs, msk & cardiac fx changes
NSAIDs (Ibuprofen) and dogs
- can use in dogs (at much lower dose than for humans0, but other dog-specific nsaids (carprofen) work better (more specific to cox-2)
- tox = GI probs, ulcers –> renal damage/failure
NSAIDs (Ibuprofen or aspirin) and cats
NOPE
super sensitive d/t glucuronidation
What big clin sign does acetominophen tox cause in cats
metabolite build up –> liver injury –> methemoglobinemia (muddy mucous mem, hematuria etc)
Cats don’t have enz to process acetaminophen
Venlafaxine (anti-depressant)
cats wierdly attracted to
serotonin/NE reuptake inhibitor = super sympathetic drive (mydriatic, vomiting, tachypnea/cardia, etc)
Xylitol intoxiation
GI, liver signs, seizures
insulin released in response to xylitol –> hypoglycemia –> liver damage
Theobromine/caffine/theophylline aka methylxanthines aka whats in chocolate
increases intracellular Ca –> increase CV (tachycardiarrhtyhmias), CNs issues (hyperexcite, seizure) –> tachypnea/resp failure
ethylene glycol tox (antifreeze) MOA & clin signs
metabilized into oxalic acid which binds Ca –> calcium oxalate deposits in kidney
- GI, CNS signs, metbolic acidosis, renal dz –> failure
Treat ethylene glycol tox
- fomepizol or ethanol to outcompete binding & inhibit metab
- Ca gluconate for hypocalcemia, bicarb if acidodic, supportive care
What agent is used to induce emesis in dogs
Apomorphine - acts directly on chemoreceptor trigger zone, emesis in 4-6 min
What agent is used to induce emesis in cats
Xylazine - centrally acting alpha 2 agonist, emesis in 10-20 min
Delivery of venom for Elapidae vs. crotalidae
Elapidae (e.g. coral snake) - venom drips onto fangs with bite so evenomation depends on bite time
Crotalidae (e.g. rattlesnakes, cottonmouth, copperheads) - retractible fangs w/ forced expulsion of venom - often whole venom load delivered
Elapidae vs. crotalidae venom MOA/clin signs & treatment
E - neurotoxic, little reaction at site, delayed uptake = signs ~12 hrs later, antivenin discontinued
C - toxin pre-digests tissue - tissue damage, swelling at bite site, petichiation, coag issues, hematuria. show up hours later, can continue to show up to 36 hrs. Crofab antivenin only treats length of recovery
What spider bite are cats super sensitive to?
Black widows - latrotoxin causes lactrodecticm - paralysis, vocalizing, sludge
Antivenin available
Which two spider bites both cause a bullseye lesion? and why does that lesion form
Brown recluse, Hobo spiders (pacific NW)
Venom is necrotizing, long time to heal
When are hymenoptera (wasps etc) stings concerning
dogs can go into anaphylactic shock and get secondary IMHA
MOA of botulism (Clostridium botulinum) and clin signs
Toxin blocks ACH release presynaptically –> flaccid paralysis, shaker foal synd
Vaccinate w/ toxoid vacc to avoid
MOA of tetanus (Clostridium tetani) and clin signs
Blocks glycine relase and other inhibitory NT’s —> uncontrolled muscle contractions, grin, lockjaw, sensitivity to sound/light
Tetanus vacc important preventative
MOA of cyanobacterial tox
ACH agonist –> resp paralysis, sludge
PREVENT, can give atropine (inhibits ACH)
MOA of cantharidin exposure in EQ
crushed blister beetles in alfalfa–> cantharidin is vesicant –> erodes/ulcerates GI and bladder –> colic, hematuria, etc
Dogs licking toads (bufodienolide tox) MOA
cardiac glycoside –> inhibits Na/K/ATPase pumps –> decreased AP’s –> salivation, vomiting –> convulsions, coma, death
Aflatoxin causes hepatoxicosis vs. ochratoxins cause renal tox, why?
A - metabolized in liver into a reactive metabolite
O - enterohepatic recycling = long half life, accums in kidneys
What mycotoxin causes hyperestrogenism & swelling/hyperemia of female parts? In who?
Zearalenone from Fusarium fungi
Pigs most sensitive, sometimes ewes
What two disease states does fumonisin tox cause
ELEM - EQ leukoencephalomalacia
PPE - porcine pulmonary edema (d/t toxin causing left sided HF)
(keep levels low in feed - no tx)
MOA for slaframine causing slobber syndrome
metabolized in liver to active form –> accum in GI –> parasympathomimetic –> sludge
(atropine can stop but not reverse activity)
Why are pigs super susceptible to Trichothecene tox from contaminated feed?
can’t metabolize vomitoxin –> see vomiting
Types of acute radiation syndromes
- cerebrovascular - die in 3 days
- hematopoietic/pancytopenia - die in 3-8 days (can can progress to pulmonary synd - die at 30 days)
- GI - die in 3-10
- cutaneous
medical vs. work exposure to radiation
medical - radiation risk is high, but benefits outweigh
work - how much will repeat low dose exposure increase chance of cancer? take precautions
ALARA
as low as reasonably achievable
- provide training, follow the rules
- protect self via time, distance, shielding
Molybdenum tox & copper deficiency
- d/t low Cu or high Mo in diet (or high sulfer intake which facilitates effect of Mo
- Mo binds Cu in rumen –> Cu deficit = chronic diarrhea, bleached dull hair, random fx
- Treat by supp Cu - but careful in sheep, can cause Cu tox
Why does Molybdenum tox & copper deficiency cause swayback in lambs but not cattle?
sheep fetus doesn’t accumulate copper in liver during gestation, but cattle fetus does
Main cause for copper tox in sheep and goats
getting fed EQ/pig/poultry mineral feeds to sheep
or grazing w/ pig/poultry manure, or oversupp in own feed
MOA/diagnose copper tox
- Accums in liver way before increase in serum Cu
- causes liver damage, hemolysis, kidney damage
- Diagnose - test liver and kidney Cu levels, gunmetal kidney, friable liver
Major source of zinc tox in dogs, MOA/clin signs, treat
ingesting pennies –> ox damage to RBC’s –> GI probs, Hgbemia/uria, anemia w/ basophilic stippling, heinz bodies –> take rads, or test for serum Zn
Sources for sulfur tox (4)
High sulfur in water
high S soil = plant accum
molasses based diet or corn gluten
Sulfur tox MOA/clin signs
Sulfur reduced in rumen into H2S –> absorbed into blood/lungs –> inhibits cytochrome –> decreased E, CNS signs (blindness, head pressing, recumbent)
- test water, diet for S levels
- give Thiamine if suspect PEM
What disease can sulfer tox cause
PEM
If you have a neuro cow (blindness, head pressing), top ddx’s (4)
Lead tox
Sulfer tox/PEM
water dep/salt tox
Thiamine deficiency
how does salt tox/water dep occur?
restricted water –> excess serum Na in body pulls fluid from brain –> decreased glycolysis/E use in brain traps Na there –> CNS signs
Why do you not rehydrate a salt tox case rapidly
don’t want to drop serum Na lower than brain Na - mo problems
hypertonic saline to reduce cerebral edema
What’s the main issue with non-prot nitrogen (urea) tox (feed additive)
converted into ammonia –> ammonia build-up increases lactate –> rumen pH >8
treat - put acetic acid (vinegar) in rumen, feed diet w/ low NPN
Why ionophores added to feeds
promote growth in cattle by increasing the amount of propionate fermented from rumen
tox occurs w/ feeding mix error, poor prognosis
