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Fundamentals of Diagnostics Exam 2 > Toxicology > Flashcards

Toxicology Flashcards

1
Q

what does % equal

A

grams/100g or mL/100mL

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2
Q

how many mL per oz

A

30

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3
Q

what is 1 ppm

A

1:1,000,000 = 1 mg/kg = 0.0001%

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4
Q

how do you calculate a mg/kg dose of drug in feed

A

ppm in feed x % body weight eaten per day as a decimal

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5
Q

how many pounds in a ton

A

2000

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6
Q

what is 1 g/ton equal to

A

1.1 ppm

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7
Q

what general organ system do insecticides target

A

CNS

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8
Q

where do organophosphates, carbamates, and neonicotinoid insecticides work

A

acetylcholine receptors

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9
Q

what do pyrethroids, avermectins, and fipronil target

A

sodium or chloride chanels

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10
Q

what signs do cholinesterase inhibiting OPs and carbamates cause

A

parasympathetic, neuromuscular, and CNS

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11
Q

what should you do if signs and history are SUGGESTIVE of OP/carbamate toxicity

A

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

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12
Q

how do you confirm diagnosis of organophosphate or carbamate toxicity

A

measure acetylcholinesterase activity of heparinized whole blood and/or brain tissue
(>70% reduction in activity is diagnostic)
analyze bait residues, stomach contents, and urine

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13
Q

what action do organophosphates and carbamates have

A

inhibit acetylcholinesterase

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14
Q

what is the treatment for known cholinesterase inhibitor toxicity

A

immediate atropine (0.1-0.5mg/kg 1/4 IV, the rest IM or SQ)
then 2-PAM
decontamination when stable

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15
Q

what is the MOA of atropine

A

muscarinic receptor antagonist (parasympatholytic)

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16
Q

what is the MOA of 2-PAM

A

regeneration of AChE, especially useful for nicotinic signs

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17
Q

what are signs of OP toxicosis

A

trembling, salivating, bradycardia, seizure, death

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18
Q

what animal is especially sensitive to pyrethrins

A

cats

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19
Q

what is the target of pyrethrins

A

sodium channels

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20
Q

what is the treatment for pyrethrin toxicosis

A

decontaminate

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21
Q

what is the target of bromethalin

A

nervous system

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22
Q

what is the treatment for bromethalin toxicosis

A

no antidote. induce emesis
toxic at 0.25-1.5 mg/kg

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23
Q

what is the target of vitamin K antagonists

A

hematopoietic system

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24
Q

what is the action of warfarin

A

vitamin K antagonist

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25
Q

what is the treatment for warfarin

A

vitamin K

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26
Q

what is cholecalciferol

A

vitamin D

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27
Q

what is the effect of cholecalciferol

A

increases calcium absorption

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28
Q

what is the target of cholecalciferol

A

kidney

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29
Q

what is the target of strychnine

A

nervous system, causes tetanic seizures

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30
Q

what is the action of zinc phosphide

A

changes to volatile phosphine gas

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31
Q

what is the target of lead

A

multi-systemic (CNS, GI, kidney)

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32
Q

what is the effect of sodium

A

CNS toxicity from water deficiency

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33
Q

what is the mechanism of copper toxicity

A

chronic exposure via feed additive with acute release from liver in stressed sheep; also in copper wire
targets kidney

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34
Q

what is the effect of zinc

A

hematopoietic

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35
Q

what is the target of arsenic

A

GI

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36
Q

what is the target of iron

A

GI and liver

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37
Q

what is the target of selenium deficiency

A

muscle

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38
Q

what is the treatment for lead toxicosis

A

calcium EDTA 75mg/kg
very long withdrawal period in food animals

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39
Q

where is aflatoxin found and what is its target

A

hot, dry season mainly in corn
GI (liver)

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40
Q

where is vomitotoxin found and what is its target

A

cool, wet season mainly in small grains
GI

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41
Q

where is zealenone found and what is its target

A

cool, wet season mostly in small grains
reproductive system

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42
Q

where is slaframine found and what is its target

A

in clover
limited cholinergic effect

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43
Q

where is penitrem A found and what is its target

A

in rotting dairy products and garbage
neurotoxic

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44
Q

where is roquefortine found and what is its target

A

in rotting compost and garbage
neurotoxic

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45
Q

where is fumonisin found and what is its target

A

moldy corn
neurotoxic

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46
Q

how do you test for mycotoxins

A

no diagnostic test in biological samples
must test the food

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47
Q

what are some toxic bulbs

A

daffodils/jonquils, tulips, iris, hyacinths, crocus, amaryllis, gladiolas

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48
Q

what is the effect of toxic bulbs

A

usually not lethal, irritant resins, alkaloids and/or insoluble calcium oxalate
GI signs (salivation, diarrhea, vomiting)
mostly affects dogs, onset <1 hour

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49
Q

what is the treatment for toxic bulbs

A

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

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50
Q

what is the toxin in daffodils, narcissus, jonquil, paper-whites, and lent lilies

A

all parts of plant toxic
phenanthridine alkaloids (lycorine), insoluble calcium oxalate crystals

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51
Q

what is the effect of daffodils, narcissus, jonquil, paper-whites, and lent lilies

A

contact irritant, allergen, centrally acting emetic, decreased protein synthesis
GI and skin signs (salivation, vomiting, diarrhea, pain, dermatitis)
typically transient, rarely fatal

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52
Q

what animals are most susceptible to onion/garlic tox

A

cattle and cats>dogs
(toxic dose 0.5% of BW)

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53
Q

what is the MOA of onion/garlic tox

A

metabolized to disulfides, which cause oxidative damage to RBCs. hemoglobin denaturation means reduced oxygen delivery and RBC lysis

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54
Q

treatment for onion/garlic tox

A

decontamination and symptomatic treatment
prognosis is dose-dependant

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54
Q

clinical signs of onion/garlic tox

A

odor on breath, vomiting, anemia, hemoglobinuria

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55
Q

what is the MOA of mistletoe

A

phoratoxin is a weak toxalbumin that binds to ribosomal cell receptors primarily in the GI epithelium

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56
Q

what is the MOA of holly and poinsettias

A

saponins in holly berries and euphorbol esters in poinsettias are general irritants of the GIT

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57
Q

what is the MOA of christmas trees

A

phenols and pine-oils are general protoplasmic poisons that denature and precipitate proteins
possible liver, kidney and CNS involvement

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58
Q

what species is especially sensitive to christmas trees

A

cats are sensitive to the phenols b/c they are deficient in glucuronidation

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59
Q

what clinical signs are seen with the christmas plants

A

salivation, anorexia, depression, lethargy, vomiting, diarrhea, colic, gastroenteritis

only with christmas trees: icterus, hepatic necrosis, nephrosis

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60
Q

what is the treatment for christmas plant tox

A

symptomatic tx; fluids, antiemetics, demulcents

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61
Q

which are specifically more toxic to cats?
a. tulip bulbs
b. onions
c. mistletoe
d. pine

A

b and d

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62
Q

which plants have cardioactive steroids

A

christmas kalanchoe, oleander (oleandrin), foxglove (digitoxin and digoxin), lily of the valley

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63
Q

what is the MOA of cardiotoxic plants

A

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

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64
Q

clinical signs of cardiotoxic plants

A

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

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65
Q

how can you diagnose cardiotoxic plant tox

A

the usual (history, signs, plant in GIT), hyperkalemia!, ECG abnormalities!!, serum/urine analysis for toxin

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65
Q

treatment for cardiotoxic plants

A

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

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65
Q

what is the target of tobacco

A

nervous system, GIT and can cause indirect cardiotoxicity

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65
Q

what is the toxin in dogbane and milkweed? onset/duration? species susceptible?

A

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

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65
Q

how do you diagnose dogbane/milkweed tox

A

usual (hx, clinical signs, plant in GIT)
hyperkalemia!, ECG abnormalities!, serum/urine analysis for cardenolide

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65
Q

what is the toxin in tobacco and the toxic dose

A

nicotine 1 mg/kg

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66
Q

clinical signs of tobacco tox? who is usually affected?

A

shaking, trembling, twitching, nausea, salivation, mouth and stomach irritation, weak, staggering, resp problems, erratic HR and BP
puppies usually affected

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67
Q

treatment for tobacco tox

A

remove residual, assist resp as needed, stabilize heart and BP

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68
Q

T/F: cardiotoxic plants can be found in home gardens and in fields

A

true

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69
Q

T/F: many cardiotoxic plants are toxic in a manner similar to the cardiac drug digoxin

A

true

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70
Q

T/F: HR increases when animals ingest typical cardiotoxic plants

A

false - they cause bradycardia, but end stage can cause arrhythmias and tachycardia

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71
Q

what is the toxin in yew? who is susceptible?

A

taxine alkaloids
all parts toxic except the berry things
all animals susceptible

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72
Q

what is the effect of yew

A

direct effect on the myocardium with depression of AV conduction, bradycardia, hypotension, and diastolic cardiac arrest

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73
Q

clinical signs and onset/duration of yew tox

A

onset 15 min to 24 hours, course <12 hours
dyspnea, bradycardia, convulsion (dogs), trembling, diarrhea, incoordination, depression, lethargy, diarrhea, SUDDEN DEATH

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74
Q

what lesions are found on necropsy with yew tox

A

plant in stomach or mouth, enlarged globular heart, increased pericardial fluid, lung edema and congestion

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75
Q

how do you diagnose yew tox

A

hx of access, taxine analysis of stomach contents, pile of dead animals, widened QRS

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76
Q

treatment of yew tox

A

if you’re lucky enough to find them alive; avoid excitation, IM atropine, activated charcoal and saline cathartic once HR normalizes
prognosis is guarded

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77
Q

what is the toxin in rhododendron, azalea, and mt laurel? who is affected?

A

grayanotoxins
all parts of plant toxic
sheep and goats most likely affected, but can also affect cattle, dogs, horses, and you

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78
Q

MOA of rhododendron, azalea, and mt laurel

A

stimulates the vagal nerve and vomiting center in the brain, causing decreased HR, arrhythmias and persistent vomiting. can get sudden death

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79
Q

if you have a vomiting ruminant, what is the toxin

A

rhododendron, azalea, or mt laurel

80
Q

clinical signs, onset/duration of rhododendron, azalea, and mt laurel

A

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

81
Q

treatment for rhododendron, azalea, and mt laurel

A

stop vomiting with 1/10 tranq dose of acepromazine
once vomit stops, activated charcoal and saline cathartic
cardiac drugs for arrhythmias

82
Q

T/F: poisonous shrubs can be in home gardens and fields

A

true

83
Q

T/F: ingestion of some shrubs can cause cardiac arrest

A

true - yew for sure
rhododendron, azalea, and mt laurel can cause death from arrhythmias

84
Q

T/F: vomiting is more likely to occur with yew than rhododendron poisoning

A

false

85
Q

what is the toxin in buckeye? who is affected?

A

aesculin in all parts, but especially the seed
cattle most susceptible
possible in sheep, pigs, chickens, horses, dogs

86
Q

clinical signs of buckeye tox

A

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

87
Q

treatment for buckeye tox

A

sedatives until symptoms resolve so they don’t hurt themselves

88
Q

how do animals get exposed to black walnut

A

shavings from the dark heartwood

89
Q

what is the effect of black walnut and who does it affect

A

enhances constriction of blood vessels in hoof wall thought to be the mechanism of laminitis in horses

90
Q

clinical signs of black walnut

A

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

91
Q

how do you diagnose black walnut tox

A

analysis of wood shavings from bedding. chocolate brown color

92
Q

treatment of black walnut tox

A

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

93
Q

what part of the oak tree is toxic and who is susceptible

A

acorns, cattle

94
Q

MOA of oak tox

A

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

95
Q

clinical signs of oak tox

A

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

96
Q

diagnosis of oak tox

A

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

97
Q

treatment/prevention of oak tox

A

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!

98
Q

what is the major differential for oak tox

A

redroot pigweed - causes perirenal edema and myocardial degeneration in pigs>cattle>sheep

99
Q

which maple tree is the most toxic

A

red maple

100
Q

who is affected by maple tox and in what time of year

A

horses, zebras, alpacas most. can affect cattle, sheep, goats
in the fall

101
Q

what is the toxin and MOA of maple tox

A

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

102
Q

clinical signs of maple tox

A

weak, tachypnea, pyrexia (fever) from hemolysis, methemoglobinemia, heinz body anemia, cyanosis, tachycardia, hemogloninuria, icterus, colic

103
Q

necropsy findings with maple tox

A

icterus with centrilobular hepatic necrosis, splenomegaly, reddish-black kidneys with tubular nephrosis and hemoglobin casts, very dark blood

104
Q

diagnosis of maple tox

A

history, decreased PCV, heinz bodies, eccentrocytes, metHb (>20%), incerased bilirubin, increased AST/SDH, azotemia, isosthenuria

105
Q

treatment for maple tox

A

activated charcoal and saline cathartics, blood transfusion if severely hypoxic, asorbic acid (antioxident) to reduce metHb, fluids, pain control, NO STEROIDS (increases mortality)

106
Q

what are some cyanogenic plants

A

black cherry, chokecherry, sudan grass, sorghum, sudex, milo, millet, Johnson grass, apricots, flax, sugar beets, arrow grass, crabapple trees

107
Q

when are cyanogenic plants toxic and who is susceptible

A

during wilting stage when they have volatile cyanide
ruminants, esp goats susceptible. also possible in horses and dogs

108
Q

MOA of cyanide tox

A

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!

109
Q

ddx for cyanide tox

A

nitrate poisoning has the same signs, but see brown blood

110
Q

why is it important to differentiate nitrate from cyanide poisoning prior to treatment

A

cyanide poisoning is treated by making methemoglobin. if already methemoglobinemic from nitrate, will make it worse

111
Q

clinical signs and onset/duration of cyanide tox

A

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

112
Q

cyanide tox treatment

A

thiosulfate, nitrate, hydroxocobalamine (vit B12a)

113
Q

which is the most likely to cause sudden death?
a. buckeye
b. oak
c. maple
d. black walnut
e. wild cherry

A

e

114
Q

which is a special concern for horses?
a. buckeye
b. oak
c. maple
d. black walnut
e. wild cherry

A

c and d

115
Q

which causes a non-lethal neurotoxicity?
a. buckeye
b. oak
c. maple
d. black walnut
e. wild cherry

A

a

116
Q

which cause lesions in the same organ?
a. buckeye
b. oak
c. maple
d. black walnut
e. wild cherry

A

b and c - renal
c and e - RBCs

117
Q

what is the most important factor in your toxin differential list

A

body systems involved

118
Q

what body systems are usually involved with onset <24 hours

A

nervous system and heart

119
Q

what body systems are usually involved with onset 1-5 days

A

kidney and liver

120
Q

what are the 4 major points for a toxin differential list?
what other factors are considered?

A

top 4: systems involved, onset time, morbidity, mortality
others: species susceptibility, seasonality, age susceptibility, progression of signs

121
Q

what should your initial exam of a tox case focus on

A

“bleeding, beating, breathing”
respiratory, cardiovascular, shock, electrolytes, coagulation status

122
Q

what should your first treatment be with any toxin

A

treat the patient, not the poison
assess and stabilize animal

123
Q

what is a concern with using royal blue blood tubes

A

false elevation of Zn with exposure to rubber

124
Q

what basic tissues should be saved for tox analysis

A

brain, liver, kidney, urine, GI contents

125
Q

what factors go into risk for toxicity

A

hazard and exposure

126
Q

how many ounces in a pint

A

8

127
Q

what are the initial actions taken in a tox case

A

first priority is to stabilize, then prevent further absorption, protect personnel, calculate exposure and treat for suspected toxicant

128
Q

what are the types of decontamination

A

remove, dilute, eliminate
it’s all about preventing further absorption

129
Q

what cases require decontamination

A

all tox cases. asymptomatic patients may not require treatment, but decontamination is still important

130
Q

what are contraindications for emetics/gastric lavage

A

volatile compounds, solvents, caustics, corrosives, convulsing patients
the stomach wall is weakened and may burst, plus potential for aspiration
(take home message)

131
Q

when is activated charcoal not useful

A

metals and alcohols

132
Q

T/F: three important items on a differential list are systems involved, onset time, and morbidity/mortality

A

true

133
Q

T/F: tox sampling and analysis is necessary for diagnosis of all cases of poisoning

A

false

134
Q

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

A

b

135
Q

which household cleaning products are the most toxic

A

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)

136
Q

household products come with warning labels in categories 1-6. what does each category mean

A

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

137
Q

rank the following signal words in order of most to least concerning: danger, caution, warning

A

most concerning: danger
next: warning
least: caution

138
Q

describe the toxicity and give examples of non-ionic detergents

A

lowest toxicity. non-phosphate or low suds laundry products, shampoos, dishwashing detergents (alkyl-aryl polyether sulfate, alkyl ethoxylate)

139
Q

describe the toxicity and give examples of anionic detergents

A

can be irritating. dishwashing soap, laundry detergent, shampoo (alkyl sodium sulfate, sodium lauryl sulfate)

140
Q

describe the toxicity and give examples of cationic detergents

A

most toxic type, dose important! disinfectants, algicides, applicator tank mixes, fabric softeners
quaternary ammonium derivatives!!, (benzalkonium chloride, benzethonium chloride)

141
Q

describe amphoteric detergents

A

combo of anionic and cationic, more in industrial cleaning products, not common in the house

142
Q

list the following in order from most to least toxic:
anionic, cationic, nonionic, amphoteric

A

cationic, amphoteric, anionic, nonionic
(cationic is worst! take home message)

143
Q

what is the effect of cationic surfactant tox

A

irritation, possible neuromuscular or ganglionic blockade
(take home message)

144
Q

describe the MOA of quaternary ammonium (“quat”)

A

acts where ACh does and causes neuro signs

145
Q

what are the clinical signs and onset/course for granular soap and detergents

A

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

146
Q

name some alkali cleaning products

A

ammonia, oven cleaner, drain cleaner

147
Q

what effect does ammonium hydroxide have

A

3% - mild irritation, warning label
10% - corrosive

148
Q

what kind of label do oven cleaners (4% NaOH) have

A

danger

149
Q

what is the MOA of alkali cleaners

A

more lipophilic than acids and penetrate deeper into tissues, causing liquefactive necrosis!
(take home message)

150
Q

what is the treatment for alkali substances

A

dilute and protect
(emesis, activated charcoal, lavage and cathartics are CONTRAINDICATED b/c the substance is irritating)

151
Q

what type of label do acids like toilet bowl cleaners have

A

danger

152
Q

what type of label do oxidizers like bleach have

A

warning

153
Q

what type of label do hydrocarbon solvents have, where are they found, and how are they absorbed

A

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)

154
Q

what are the types of disinfectant cleaners

A

cationic surfactants, phenolic compounds, pine-oil based (terpenes/phenolics)

155
Q

what are the clinical signs of disinfectant cleaner tox and how does their toxicity compare to detergents

A

GI irritation, pain
all more toxic than soaps and plain detergents

156
Q

what animals are most sensititve to disinfectant cleaners

A

cats - don’t handle pine oil and phenols well
(take home message)

157
Q

what is the treatment for disinfectant cleaner tox

A

dilution with milk or water, irrigate exposed surfaces, symptomatic treatment

158
Q

what is the unique effect of anionic surfactants

A

hemolysis
(take home message)

159
Q

what effect do acid cleaners have

A

coagulative surface necrosis
(take home message)

160
Q

what alcohol should not be used for antiseptic use and what is the risk

A

methanol
absorbed thru skin, causes vomiting, CNS depression, hypothermia, acidosis

161
Q

what is the effect of fertilizer toxicity and who is usually affected

A

fertilizers with certain percentages of N-P-K are irritating. target GI system - vomiting, diarrhea, anorexia
most cases in small animals, mostly nonlethal

162
Q

what is unique about rose fertilizers

A

may have 5% iron, which can cause iron tox and hepatic damage

163
Q

what is the treatment for fertilizer tox

A

symptomatic, dilution rather than activated charcoal, demulcent may be needed

164
Q

what is the treatment for corrosives

A

irrigation with water or milk
corticosteroids may be used with airway edema, but do not help with preventing strictures

165
Q

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

A

b and c

166
Q

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

A

b
a,c,d,e are true of all animals

167
Q

how many ounces per gallon

A

128

168
Q

in general are herbicides very toxic? why? what is the exception?

A

most are not very toxic because they target plant specific stuff
paraquat is very toxic!

169
Q

how toxic is glyphosphate? clinical signs?

A

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)

170
Q

what is the treatment for glyphosphate tox

A

most cases mild and self limiting. with high dose/concentration, treat as a caustic agent
symptomatic tx, dilution with milk or water

171
Q

what is the MOA of glufosinate

A

irreversibly inhibits glutamine synthetase, causing hyperammonemia.
if it penetrates the CNS, neurotoxic. similar structure to glutamate

172
Q

what are the clinical signs and onset/duration of glufosinate tox

A

nausea and vomiting early, then seizures and resp depression
onset 4-50 hrs, lasts days

173
Q

what is the treatment for glufosinate tox

A

monitor for 48 hours due to delayed onset. diazepam for seizures, IV fluids to increase excretion, resp support as needed

174
Q

what is the MOA on plants of 2,4-D? what are they used for?

A

analogues of auxin, disrupt hormone balance and protein synthesis causing abnormal plant growth
used on broadleaf weeds

175
Q

what is the toxic potential for 2,4-D

A

for clinical signs, would need direct exposure to concentrated formula or animal susceptible due to poor health

176
Q

who is more sensitive to 2,4-D and why?

A

dogs b/c decreased ability to excrete organic acids in urine

177
Q

what are the clinical signs of 2,4-D herbicides?

A

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

178
Q

what is the toxic potential and onset of 2,4-D herbicides?

A

only toxic if exposed to concentrate
onset <12 hours with small doses, <2 hours at high dose

179
Q

how do 2,4-D herbicides cause myotonia? in what animals?

A

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)

180
Q

what is the treatment for 2,4-D herbicide tox? prognosis?

A

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

181
Q

what is another name for 2,4-D

A

phenoxy/chloroacetic acid herbicides

182
Q

what is unique about paraquat

A

need a license to use it. very toxic. nonselective and fast acting

183
Q

describe the movement of paraquat through the body

A

poorly absorbed from GIT or skin, rapid distribution to tissues. accumulates in lungs and kidney, excreted unchanged in urine

184
Q

what is the MOA of paraquat

A

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

185
Q

what is the effect of paraquat

A

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

186
Q

what are the clinical signs of acute, high dose paraquat tox? onset?

A

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)

187
Q

what are the clinical signs of chronic or acute sublethal dose paraquat tox? onset?

A

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

188
Q

how is diquat different from paraquat

A

use is not restricted. it does not concentrate in the lungs

189
Q

what is the MOA of diquat

A

distribution to GIT, kidney, eye, and liver
like paraquat, superoxide anion is formed

190
Q

what are the clinical signs of diquat tox

A

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)

191
Q

what chronic lesions are seen on necropsy with paraquat tox

A

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

192
Q

what necropsy lesions are seen with diquat tox

A

GI ulceration/necrosis, cerebral hemorrhage, renal tubular necrosis, cataracts in dogs

193
Q

what lab tests can be done to detect paraquat/diquat tox

A

sodium dithionite test on plasma and urine
also analysis of stomach contents, plasma, urine, lung, kidney

194
Q

what is the treatment and prognosis for paraquat/diquat tox

A

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

195
Q

what is the most common triazine herbicide and where does it persist?

A

atrazine persists in aquatic environments
EPA tolerance ≤ 3ppb in drinking water
(key point: potential association with frog defects, repro)

196
Q

what is the toxic potential for triazine herbicides? MOA?

A

low acute toxicity via oral and dermal routes
MOA unknown, but can cause direct articular vasodilation

197
Q

what are the clinical signs of triazine herbicide tox? onset?

A

anorexia, salivation
CNS in cattle - ataxia, prostration, hyperesthesia!, muscle tremors
onset <24 hours
(key point: hyperesthesia in cattle)

198
Q

how do you diagnose triazine herbicide tox? treat?

A

test stomach contents or liver
symptomatic tx

199
Q

what toxin can be used as a “hit and run”/malicious use

A

paraquat
(key point: moderate dose used as a lung toxicant)

200
Q

are fungicides more or less toxic than herbicides?

A

less

201
Q

what effects are possible with fungicides? name some examples of products

A

mutagenic and carcinogenic potential
ex: captan, folpet, thiram

202
Q

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

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

203
Q

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

a. atrazine
b. paraquat
c. paraquat
d. paraquat

204
Q

T/F: diquat has a unique toxicity

A

true - the eye in dogs

205
Q

What is the classic clin path presentation of ethylene glycol toxicity

A

Azotemia, acidosis, markedly increased anion gap, marked hypocalcemia

Fundamentals of Diagnostics Exam 2 (5 decks)

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