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Capstone 2 > Tox > Flashcards

Tox Flashcards

1
Q

common clinical signs with houseplant ingestion

A

ptyalism, vomiting, diarrhea

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2
Q

Which houseplants can cause renal failure

A

ones containing oxalate - lilies, coffee bean, grapes, begonias, philodenderons

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3
Q

Which plants can cause hemolysis, methemoglobinemia, and/or anemia, hemoglobinuria

A 
oxidants or cytotoxins  causing RBC damage
red maple (for EQ), onions (allium family), periwinkle
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4
Q

If an animal ingests foxglove or deadly nightshade, what effects do you expect?

A

Cardiac problems b/c cardiac glycoside

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5
Q

Which houseplants can cause neuro signs or hallucinations?

A

Allspice, macadamia nut - dogs, catnip, poppy

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6
Q

Which houseplants can cause liver disease?

A

jasmine, tea tree, some palms

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7
Q

Which houseplants can cause sudden death

A

glory lily, heavenly bamboo, chokecherry, yew

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8
Q

What’s with lily and cats?

A

all spp if lilium are toxic –> renal failure –> death
esp. flowers, but also consumption of leaves
toxin not ID’d

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9
Q

most common plants assoc’d w/ nitrate poisoning in rum

A 
red rooted pig weed
kochia weed
sunflower
lambs quarter 
sudan grass 
russian thistle
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10
Q

MOA of nitrate poisoning

A

nitrate –> nitrite in rumen –> binds to hgb –> methemoglobinemia –> hypoxia, abortion, death

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11
Q

what is brown mucosa a key sign of

A

methemoglobinemia –> nitrate poisoning

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12
Q

How do you treat for nitrate poisoning

A

methylene blue reduces methemoglobin

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13
Q

most common plants assoc’d w/ cyanide poisoning in rum (8)

A

Sorghums: Johnson grass, sudan grass or hybrids (choke cherry)
Service berry, Elderberry, Mountain mahogony, Arrow grass, Poison Suckle

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14
Q

Key parts about cyanide poisoning

A
  • reduced better in highly acidic stomach
  • block cytochrom oxidase activity –> no oxygen use in cells –> cell anoxia
  • ataxia, tremors,, mydriatic, resp signs, sudden death
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15
Q

what is cherry red venous blood a key sign of

A

HCN (cyanide) poisoning

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16
Q

MOA and clin signs for larkspur poisoning in cattle

A

Bloch ACh at NMJ –> paralysis, bloat, sudden death

would treat with AChesterase inhibitors

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17
Q

MOA and clin signs for water hemlock (cicutoxin) poisoning in cattle

A

toxin Accums in roots –> inhibits GABA –> convulsions, seizure –> resp failure, sudden death

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18
Q

MOA and clin signs for yew poisoning in horses (most sensitive)

A

Taxine A,B inhibits cardiac Ca/Na channels

Taxane damages microtubules –> bradyarrythmias, vomiting/diarrhea, death

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19
Q

MOA and clin signs for milkweed or foxglove poisoning in cattle

A

cardiac glycosides (digoxin in foxglove) alter heart rate and rhythm –> cardia arrhythmia, 2nd degree heart block, GI issues, sudden death

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20
Q

MOA of oxalates, clin signs, treatment

A
  • nephrotoxic - oxalates precipitate calcium –> oxalate crystals deposit in kidney, muscle
  • Get muscle issues, hemorrhage, kidney failure, coma, death
  • Ca borogluconate, hydration
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21
Q

5 major plants seen with oxalate poisoning

A

usually plants with red stem

greasewood, halogeton, shamrock, red-rooted pigweed, kochia weed

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22
Q

What is the concern with oak

A

gallotannins in new leaves, acorns –> denatures proteins –> hemorrhagic enteritis, icterus, bloody urine/diarrhea –> death

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23
Q

2 plants assoc’d w/ tremetol-induced myopathy/neurotoxicity & clin signs

A 
white snake root & rayless golden rod
milk sicknees (passed in milk), muscle tremors, choke --> heart block, death
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24
Q

Black walnut shavings are associated with what clin signs?

A

laminitis, tachypnea, colic

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25
Q

MOA and clin signs for Selenium toxicity in EQ

A

Se alters protein function –>oxidative damage –> wt/ loss, hair/skin changes, liver/kidney/muscle degen, diarrhea, death

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26
Q

Se accumulating plants (6)

A

Prince’s plume, milk vetch, woody aster, pain brush, gum weed, 4 wing saltbrush

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27
Q

Plants that cause primary photosensitization

A

carrot/celery family
St. Johns wort, bishop’s weed
buckwheats

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28
Q

What is secondary photosensitization

A

pyrrolizidine alkaloids metablized into bad pyrroles –> liver damage
Liver can’t metabolize phylloerythrin from chlorophyll –> accum –> photosensitization

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29
Q

Plants that cause secondary photosensitization

A

Groundsel/tansy ragwort (green picket fence), hounds tongue, heliotrope, fiddle neck, crotolaria (rattlepod)

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30
Q

How do steroidal sapogenins (agave family) contribue to secondary photosensitization?

A

form crystalloid material –> blocks biliary system

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31
Q

4 plants that produce steroidal sapogenins

A

Agave, bear grass, lantana, puncture vine/goats head

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32
Q

why are cats more susceptible to heniz body anemia

A

glucuronidation

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33
Q

How does the brassica family (kale, mustard, cabbage, etc) cause toxicity

A

disulfide toxin causes heinz body anemia –> hemoglobinuria, hepatotoxicity

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34
Q

How does moldy sweet clover cause toxicity? (Mycotoxic leukoencephalomalacia)

A
  • 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
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35
Q

Bracken fern - primary toxin and dz seen

A

Thiaminase, Ptaquiloside

Causes thiamine deficiency (–>PEM), acute hemorrhage, retinal degen in sheep, bladder/UGI cancer

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36
Q

Toxins in locoweed (3)

A

Swainsonine from endophytes - lysosomal storage dz
Miserotoxins - cracker heels
Se accumulators - lameness, hair loss

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37
Q

Clin signs of locoweed/milk vetch poisoning

A

CNS signs - esp. unpredictable behav, repro probs, teratogenic effects, poor growth, CHF
- no treatment

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38
Q

Chewing disease in EQ is from what plants (2)? causes what clin signs? (Aka negropallidal encephalomalacia)

A

Prolong ingestion of Russian knapweed, yellow star thistle
Hypertonic facial/tongue muscles –> difficulty eating, inhalation pneumonia –> dehydrate/starve to death
brain damage irreversible

39
Q

Classic brain lesion of chewing disease

A

nigropallidalencephalomalacia

bilateral liquefactive necrosis/ cavitation of globus pallidus/substantia nigra

40
Q

Plants containing nicotine & nicotine-like alkaloids (e.g. hemlock) have what MOA

A

nicotinic ACH receptor agonists –> CNS, CV –> resp failure & death
How socrates died

41
Q

4 teratogenic plants causing crooked calf dz & their MOA

A

Tobacco, poison hemlock, lupine, locoweed

neuromuscular blockade –> decreased fetal movement –> congenital contracture +/- cleft palate

42
Q

What causes cyclopia in cattle

A

Mom ingesting verratum spp (e.g. western false helbore) on days 13-14 of gestation

43
Q

pine needle abortion is most common in who? d/t what MOA?

A

cattle, bison

isocupressic acid inhibits uterine blood flow –> fetal stress

44
Q

Gossypol toxicity

A

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

45
Q

MOA of organophosphates/carbamates causing acute pesticide toxicity & clin signs

A

inhibit AChE –> excess ACh signaling
see SLUDGE clin signs, muscle effects up to paralysis
Die by resp or CV arrest

46
Q

Which toxicity is more reversible: carbamate vs. organophosphate

A
  • 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
47
Q

Pyrethrin/Pyrethroid insecticide tox: MOA, animal most affected, clin signs

A
  • 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
48
Q

Ivermectin/Selamectin toxicity and herding breeds

A

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)

49
Q

Most common route of exposure for Amitraz toxicity & clin signs
treatment?

A
  • eating tick collar –> alpha 2 agonist –> decreased adrenergic signaling –> CNS/resp depression, profound bradycardia
  • yohimbine/atipamezole can reverse (alpha 2 adrenergic antagonists)
50
Q

Most effective way to avoid DEET (diethyltoluamide) toxicity?

A

use products w/ less than 50% DEET

51
Q

anticoagulant rodenticide toxicity - MOA and clin signs

A
  • 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
52
Q

Bromethalin toxicity - MOA and clin signs (used for warfarin-resistant rodents)

A
  • 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
53
Q

Cholecalciferol (Vit D3) toxicity - MOA, clin signs

A
  • 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
54
Q

NSAIDs (Ibuprofen) and dogs

A
  • 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
55
Q

NSAIDs (Ibuprofen or aspirin) and cats

A

NOPE

super sensitive d/t glucuronidation

56
Q

What big clin sign does acetominophen tox cause in cats

A

metabolite build up –> liver injury –> methemoglobinemia (muddy mucous mem, hematuria etc)
Cats don’t have enz to process acetaminophen

57
Q

Venlafaxine (anti-depressant)

A

cats wierdly attracted to

serotonin/NE reuptake inhibitor = super sympathetic drive (mydriatic, vomiting, tachypnea/cardia, etc)

58
Q

Xylitol intoxiation

A

GI, liver signs, seizures

insulin released in response to xylitol –> hypoglycemia –> liver damage

59
Q

Theobromine/caffine/theophylline aka methylxanthines aka whats in chocolate

A

increases intracellular Ca –> increase CV (tachycardiarrhtyhmias), CNs issues (hyperexcite, seizure) –> tachypnea/resp failure

60
Q

ethylene glycol tox (antifreeze) MOA & clin signs

A

metabilized into oxalic acid which binds Ca –> calcium oxalate deposits in kidney
- GI, CNS signs, metbolic acidosis, renal dz –> failure

61
Q

Treat ethylene glycol tox

A
  • fomepizol or ethanol to outcompete binding & inhibit metab
  • Ca gluconate for hypocalcemia, bicarb if acidodic, supportive care
62
Q

What agent is used to induce emesis in dogs

A

Apomorphine - acts directly on chemoreceptor trigger zone, emesis in 4-6 min

63
Q

What agent is used to induce emesis in cats

A

Xylazine - centrally acting alpha 2 agonist, emesis in 10-20 min

64
Q

Delivery of venom for Elapidae vs. crotalidae

A

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

65
Q

Elapidae vs. crotalidae venom MOA/clin signs & treatment

A

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

66
Q

What spider bite are cats super sensitive to?

A

Black widows - latrotoxin causes lactrodecticm - paralysis, vocalizing, sludge
Antivenin available

67
Q

Which two spider bites both cause a bullseye lesion? and why does that lesion form

A

Brown recluse, Hobo spiders (pacific NW)

Venom is necrotizing, long time to heal

68
Q

When are hymenoptera (wasps etc) stings concerning

A

dogs can go into anaphylactic shock and get secondary IMHA

69
Q

MOA of botulism (Clostridium botulinum) and clin signs

A

Toxin blocks ACH release presynaptically –> flaccid paralysis, shaker foal synd
Vaccinate w/ toxoid vacc to avoid

70
Q

MOA of tetanus (Clostridium tetani) and clin signs

A

Blocks glycine relase and other inhibitory NT’s —> uncontrolled muscle contractions, grin, lockjaw, sensitivity to sound/light
Tetanus vacc important preventative

71
Q

MOA of cyanobacterial tox

A

ACH agonist –> resp paralysis, sludge

PREVENT, can give atropine (inhibits ACH)

72
Q

MOA of cantharidin exposure in EQ

A

crushed blister beetles in alfalfa–> cantharidin is vesicant –> erodes/ulcerates GI and bladder –> colic, hematuria, etc

73
Q

Dogs licking toads (bufodienolide tox) MOA

A

cardiac glycoside –> inhibits Na/K/ATPase pumps –> decreased AP’s –> salivation, vomiting –> convulsions, coma, death

74
Q

Aflatoxin causes hepatoxicosis vs. ochratoxins cause renal tox, why?

A

A - metabolized in liver into a reactive metabolite

O - enterohepatic recycling = long half life, accums in kidneys

75
Q

What mycotoxin causes hyperestrogenism & swelling/hyperemia of female parts? In who?

A

Zearalenone from Fusarium fungi

Pigs most sensitive, sometimes ewes

76
Q

What two disease states does fumonisin tox cause

A

ELEM - EQ leukoencephalomalacia
PPE - porcine pulmonary edema (d/t toxin causing left sided HF)
(keep levels low in feed - no tx)

77
Q

MOA for slaframine causing slobber syndrome

A

metabolized in liver to active form –> accum in GI –> parasympathomimetic –> sludge
(atropine can stop but not reverse activity)

78
Q

Why are pigs super susceptible to Trichothecene tox from contaminated feed?

A

can’t metabolize vomitoxin –> see vomiting

79
Q

Types of acute radiation syndromes

A
  • 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
80
Q

medical vs. work exposure to radiation

A

medical - radiation risk is high, but benefits outweigh

work - how much will repeat low dose exposure increase chance of cancer? take precautions

81
Q

ALARA

A

as low as reasonably achievable

  • provide training, follow the rules
  • protect self via time, distance, shielding
82
Q

Molybdenum tox & copper deficiency

A
  • 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
83
Q

Why does Molybdenum tox & copper deficiency cause swayback in lambs but not cattle?

A

sheep fetus doesn’t accumulate copper in liver during gestation, but cattle fetus does

84
Q

Main cause for copper tox in sheep and goats

A

getting fed EQ/pig/poultry mineral feeds to sheep

or grazing w/ pig/poultry manure, or oversupp in own feed

85
Q

MOA/diagnose copper tox

A
  • 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
86
Q

Major source of zinc tox in dogs, MOA/clin signs, treat

A

ingesting pennies –> ox damage to RBC’s –> GI probs, Hgbemia/uria, anemia w/ basophilic stippling, heinz bodies –> take rads, or test for serum Zn

87
Q

Sources for sulfur tox (4)

A

High sulfur in water
high S soil = plant accum
molasses based diet or corn gluten

88
Q

Sulfur tox MOA/clin signs

A

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
89
Q

What disease can sulfer tox cause

A

PEM

90
Q

If you have a neuro cow (blindness, head pressing), top ddx’s (4)

A

Lead tox
Sulfer tox/PEM
water dep/salt tox
Thiamine deficiency

91
Q

how does salt tox/water dep occur?

A

restricted water –> excess serum Na in body pulls fluid from brain –> decreased glycolysis/E use in brain traps Na there –> CNS signs

92
Q

Why do you not rehydrate a salt tox case rapidly

A

don’t want to drop serum Na lower than brain Na - mo problems

hypertonic saline to reduce cerebral edema

93
Q

What’s the main issue with non-prot nitrogen (urea) tox (feed additive)

A

converted into ammonia –> ammonia build-up increases lactate –> rumen pH >8
treat - put acetic acid (vinegar) in rumen, feed diet w/ low NPN

94
Q

Why ionophores added to feeds

A

promote growth in cattle by increasing the amount of propionate fermented from rumen
tox occurs w/ feeding mix error, poor prognosis

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