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exam 2 Flashcards

1
Q

what two species are most susceptible to phenoxy derivatives of fatty acids (2,4-D)

A

cattle and dogs

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2
Q

what species are most sensitive to phenoxy derivatives of fatty acids (2,4-D)

A

dogs

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3
Q

T/F
pastures sprayed with phenoxy derivatives of fatty acids (2,4-D) in the recommended concentrations do not cause poisoning unless young or weak animal

A

true

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4
Q

What is the LD50 in dogs of phenoxy derivatives of fatty acids (2,4-D)

A

100mg/kg – this is moderately toxic

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5
Q

what is the MOA for phenoxy derivatives of fatty acids (2,4-D)

A

it alters the metabolism of plants which increases their toxicity by increasing accumulation of nitrate or cyanide

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6
Q

T/F

phenoxy derivatives of fatty acids (2,4-D) alters rumen microflora

A

FALSE – it is not degraded by microflora in the rumen

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7
Q

T/F

meat residues of phenoxy derivatives of fatty acids (2,4-D) are very common in sheep and cattle

A

FALSE

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8
Q

phenoxy derivatives of fatty acids (2,4-D) is metabolized mainly by _____

A

hydrolysis

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9
Q

what would enhance renal excretion of phenoxy derivatives of fatty acids (2,4-D)

A

alkanization

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10
Q

T/F

phenoxy derivatives of fatty acids (2,4-D) is a chronic toxicity and accumulates in the body

A

FALSE – acute and no accumultion

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11
Q

within an hour of a dog ingesting phenoxy derivatives of fatty acids (2,4-D) what would you seee

A

anorexia
weakness of muscles and ataxia with rigidity of skeletal muscles
opisthotonos and posterior paralysis

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12
Q

T/F

CPK levels will decrease with phenoxy derivatives of fatty acids (2,4-D) toxicity

A

FALSE - will increase

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13
Q

restricted use dipyridyl herbicide

A

paraquat

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14
Q

general use dipyridyl herbicide

A

diquat

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15
Q

T/F

dipyridyl herbicides are stable in the environment

A

false – rapidly inactivated by light and soil

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16
Q

what does paraquat do with oxygen

A

reaction causing tissue damage

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17
Q

toxicity of paraquat is enhanced by these 3 things

A

selenium vitamin E deficiency
depletion of tissue glutathione
oxygen therapy

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18
Q

T/F

paraquat binds strongly to soil

A

TRUE

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19
Q

dipyridyl herbicide are caustic to ______

A

mucus membranes

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20
Q

which is more absorbed by the GIT

paraquat or diquat

A

paraquat

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21
Q

paraquat is distributed all over the body and achieves 10X the concentrations in this body part

A

lungs

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22
Q

how long does paraquat take to be excreted in the urine

A

24 hours – but the lung clinical signs are delated up to 48 hours up to 7 days !!

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23
Q

where are the main lesions caused by paraquat

A

the lungs – respiratory pulmonary fibrosis, congestion, edema, collapsed lungs

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24
Q

T/F

give oxygen as part of the supportive therapy treating paraquat toxicosis

A

FALSE – it is contraindicated as it may increase lung damage

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25
Q

what is the prognosis of paraquat

A

guarded or grave

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26
Q

what are sources of pentachlorophenol (PCP)

A

licking wood
inhalation
vapors penetrating skin

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27
Q

what factors increase PCP toxicity

A 
high ambient temperature 
oily or organice solvent vehicles 
previous exposure 
poor condition
newborn 
hyperthyroid
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28
Q

MOA of PCP

A

blocks ATP and there is an increased oxygen demand
overheating acidosis and dehydration occur
decreased cellular energy

“animal gets roasted”

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29
Q

newborn piglet shows hyperthermia, skin irritation and rapid death

A

PCP toxicosis

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30
Q

T/F

PCP may cause abortions or fetal malformations

A

TRUE

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31
Q

what does the blood look like in PCP tox

A

it is dark colored because it has been deprived of oxygen

also will see rapid rigor mortis – does not help you save the animal though because they are dead

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32
Q

1 part NPN is how many parts protein

A

3 – used as a cheap way to give protein additives to cattle

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33
Q

Important in growth, cell proliferation, Skeletal development, collagen formation, skin, feathering, wound healing

A

zinc

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34
Q

what is the most common source of zinc toxicity

A

ingestion -

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35
Q

how many pennies will a dog eat for subacute toxicity of zinc

A

5

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36
Q

T/F

zinc in a dog diet typically ranges from 80 to 120 ppm

A

TRUE

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37
Q

chronic zinc toxicity is a low dose >____ ppm in diet over time

A

2000

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38
Q

for acute zinc toxicity: LD50 is about ___ mg/kg zinc salts

A

100

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39
Q

T/F

A basic environment increases zinc release

A

FALSE – acidic

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40
Q

T/F

zinc is rapidly excreted from the body through the urine and liver metabolism

A

FALSE – it is HIGHLY conserved

30 to 40% extracted from the liver and returns back to circulation via bile, small intestine, and absorption – enterohepatic circulation

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41
Q

how is zinc transported to the liver

A

largely bound to plasma proteins (albumins, globulins)

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42
Q

what is the most consistent form of zinc toxicity

A

intravascular hemolysis - hemolytic anemia

secondary is renal failure

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43
Q

major organ of zinc metabolism

A

liver –

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44
Q

sequesters metal ions for excretion

A

metallothionein

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45
Q

sequester free radicals associated with Zn toxicity

A

glutathione

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46
Q

Use these test tubes for chemical dx of zinc tox

A

Use trace element tubes for analysis

= Royal/Dark blue tube top

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47
Q

why could a radiograph help in dx of zinc

A

foreign body ingestion - pennies?!?!

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48
Q

________ may increase zinc redistribution and absorption from the intestines and cause further damage to pancreas, kidneys, liver

A

chelation therapy

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49
Q

what is the prognosis for zinc

A

bad once they have severe hemolytic anemia – otherwise can be good

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50
Q

which is more of an irritant

organic or inorganic iron

A

inorganic

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51
Q

what state is iron absorbed as

A

ferrous state – in the Small intestine

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52
Q

greater than what ppm of iron fed to piglets can cause rickets

A

5000ppm – interferes with phosphate absorption

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53
Q

absorbed ferrous iron is oxidized to ___

A

ferric iron

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54
Q

ferric iron binds to ____ in the plasma and is distributed throughout the body

A

transferrin

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55
Q

3 iron binding proteins for stability, transport, and storage

A

Hemosiderin, ferritin, and transferrin

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56
Q

most common source of iron

A

oral supplements

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57
Q

which form of exposure of iron is the most toxic and which is the least

A

IV is most

oral is least

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58
Q

what is iron dextran

A

injected in newborn pigs, 150 to 200 mg

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59
Q

What condition can make risk of iron toxicity increased in sows and piglets

A

selenium and vitamin E deficiency

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60
Q

T/F

iron is highly conserved and there is not a good excretion method in animals

A

true

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61
Q

T/F

chelation with sodium EDTA can result in hypercalcemia

A

FALSE – hypocalcemia

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62
Q

what is the primary effect of iron toxicosis

A

effect is on the GIT, cardiovascular system, and liver – leading to shock and death

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63
Q

T/F

bound iron is highly reactive and can lead to free radical lipid peroxidation and direct damage to cell membranes

A

FALSE – free iron does this

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64
Q

what serum levels of iron show toxicosis

A

> 300 mcg/dL

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65
Q

T/F

Acid conditions favor dissolution of metal ions (Pb+2) and absorption

A

TRUE

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66
Q

T/F

metallic lead is more readily absorbed than organic lead

A

False

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67
Q

A thumbnail sized chip of lead-based paint may contain ____ mg of lead

A

50- 200 mg of lead

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68
Q

what is the loswest lethal dose of lead in dogs

A

191 mg/kg

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69
Q

most common source of lead toxicosis in animals is what

A

lead based paints

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70
Q

what 3 species are most resistant to lead

A

chickens
goats
swine

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71
Q

T/F

adult animals are more susceptible than puppies to lead

A

FALSE - puppies eat whatever they wanna

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72
Q

what does lead bind to for transportation

A

erythrocyte membrane for transport and then 60-90% is taken up by bone

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73
Q

T/f

lead crosses the BBB and placenta

A

true

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74
Q

what do you test for antemortem cases of lead

A

whole blood

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75
Q

what do you test for postmortem cases of lead

A

kidneys and liver

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76
Q

liver chelating protein involved in cellular detoxification of inorganics - sequesters metal ions present in elevated concentrations

A

Metallothionein

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77
Q

3 main systems affected by lead

A

GIT
Blood - anemia
CNS – edema in brain, hyperexcitability, seizures

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78
Q

what would you see on radiographs of a young animal with lead toxicosis

A

metaphyseal sclerosis - lead line

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79
Q

T/F

lead tox causes regenerative anemia

A

false – non regenerative

bone marrow responds inadequately

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80
Q

T/F

to treat lead poisoning give activated charcoal

A

false – charcoal does not bind metals!!! give cathartics

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81
Q

what is the most commonly used chelating agent

A

Calcium disodium EDTA

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82
Q

the lethal dose of inorganic arsenic

A

1-25 mg/kg

this is very potent and highly toxic~~~

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83
Q

most susceptible to inorganic arsenic

A

herbivores

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84
Q

3 oxidative states of inorganic arsenic

A

elemental
pentavelant
trivalent

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85
Q

how is inorganic arsenic excreted

A

rapidly in the urine - 48 hours

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86
Q

most sensitive cells to inorganic arsenic

A

capillary endothelial – causes edema, hemorrhage, bloat

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87
Q

what is the cause of sudden death in peracute inorganic arsenic poisoining

A

hypovolemic shock

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88
Q

what tissues are most sensitive to inorganic arsenic

A

ones that are rich in oxidative enzymes such as intestines, liver and kidnet

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89
Q

arsanillic acid is mainly used in ___

A

swine

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90
Q

roxarsone is mainly used in ___

A

poultry

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91
Q

feed additive to improve weight gain and feed efficiency in swine and poultry

A

organic arsenicals

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92
Q

what conditions enhance the toxicity of organic arsenicals

A

dehydration, water deprivation, and renal insufficeny

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93
Q

what signs does arsenillic acid cause in pigs

A

acute tox is 3-5 days

ataxia and partial paralysis but normal appetite

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94
Q

MOA of organic arsenic is perihperal nerve demyelination and axonal damage which is very similar to what deficiency

A

Vitamin B

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95
Q

T/F

inorganic arsenic causes erythema in pigs

A

FALSE – organic arsenic

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96
Q

what causes death in acute copper toxicosis

A

hypovolemic shock

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97
Q

what is the normal copper:molybedenum ratio

A

6:1

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98
Q

what species are resistant to copper

A

swine and poutry

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99
Q

T/F

excess molybdenum can cause copper toxicosis

A

false – deficiency of Mb can

can tx copper tox by giving molyb

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100
Q

copper accumulation in sheep takes how long

A

2-10 weeks

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101
Q

what is the significance of having liver damage with copper toxicosis

A

damaged hepatocytes will result in more accumulation – secondary copper toxicosis

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102
Q

what lesions are see in copper toxicosis

A

icterus
hemolysis
methemoglobin
enlarged yellow friable liver

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103
Q

most common species to get copper tox

A

sheep

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104
Q

most common species to get molybdenum tox

A

cattle

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105
Q

this is a component of xanthine oxidase which converts the purine xanthine into uric acid

A

molybdenum

106
Q

elevated molybdenum intereferes with ___ absorption

A

Copper

107
Q

causes hepatosis dietetica in young pigs

A

selenium deficiency

108
Q

causes exudative daithesis in chicks

A

selenium deficiency

109
Q

causes nutritional pancreatic atrophy in chickens

A

selenium deficiency

110
Q

causes white muscle disease

A

selenium deficiency

111
Q

causes nutritional muscle dystrophy in calves and foals

A

selenium deficiency

112
Q

daily rewuiremnet of selenium

A

0.1 ppm – aka .1 mg/kg

113
Q

T/F

selenium is highly palatable

A

false and smells rotton

114
Q

what plants have selenium

A 
locoweed 
milk vetch 
princes plume
golden wood 
woody aster
115
Q

selenium contaminated water will cause teratogenic effects in ____

A

water fowl

116
Q

what oxidative state of selenium is not very toxic and is poorly absorbd

A

selenite

117
Q

organic arsenic can be used to treat ____ toxicosis by increasing elimination

A

selenium

118
Q

what type of diet reduces toxicity of selenium

A

high protein

119
Q

why is elemental Se not absorbed

A

it is insoluble in water

120
Q

chronic Se exposure accumulates where

A

hair and hoof

121
Q

T/f

in acute tox of selenium (probably oral) they die in hours

A

ya true

122
Q

urea is normally what percent of the grain ration

A

3% – and 1% of the total ration

123
Q

what are good sources for testing for ammonium

A

vitreous/ocular fluid
whole blood
rumen content

124
Q

what should be relieved first during Tx of NPN toxicosis

A

bloat

125
Q

most toxic of all NPN compounds

A

urea

126
Q

who is most susceptible to NPN

A

ruminants

127
Q

what pH enhances hydrolysis of urea by urease

A

alkaline

128
Q

most common ionophore

A

monensin

129
Q

what species is most sensitive to monensin

A

horses and adult turkeys

130
Q

who is least sensitive to ionophores

A

poultry

131
Q

anticoccidial in cattle, poultry, and goats

A

ionophores

132
Q

T/F

monensin is approved to improve milk efficiency in dairy cattle

A

true

133
Q

how much of ionophores do horses absorb

A

100%

134
Q

T/F

monensin accumulates in tissues when fed in high doses

A

false - does not accumulate

135
Q

how much do ruminants absorb of ionophores

A

about 50%

136
Q

what is the drug of choice to treat micoplasma or erhlicia

A

tetracycline/oxycycline – intracellular antibiotics

137
Q

main target in the body of ionophores

A

mitochondria of highly energetic tissues – then causes cell death due to disrupting homeostatic mechanisms

138
Q

what is the best sample to test for ionophores

A

the feed

139
Q

what enzymes will be elevated by ionphore tox

A

CPK

AST

140
Q

main lesions in horses from monensin

A

cardiac muscle lesions - pale/necrosis streaks

141
Q

this plant causes myoglobinuria and skeletal / cardiac muscle damage similar to ionophores do

A

coffee senna - cassia occidentalis

142
Q

if horses survive monensin toxicity what is their life like

A

they can die at any moment if too stressed - pasture pony

143
Q

what is sodium chloride normalyl present in feed at

A

0.5-1%

144
Q

if animals have free access to water, they can tolerate more than ___% of salt in feed

A

10%

145
Q

sodium enters the brain by ___ diffusion and is removed by _____ transport

A

passive diffusion

active transport

146
Q

most susceptible species to water deprivation-sodium ion toxicosis

A

pigs
cattle
poutly

147
Q

normal sodium level in plasma

A

135-145 meq/ml

148
Q

normal sodium level in CSF

A

130-140

149
Q

what is an issue of sodium trapped in the brain

A

water is attracted and cerebral edema occurs

150
Q

fluid to test for sodium ion tox

A

serum
csf
ocular fluid

sodium will be 160 or more meq/ml

151
Q

brain sodium concentration over ____ support soium ion tox diagnosis

A

2000ppm

152
Q

T/F

water deprivation can cause intermittent seizures

A

TRUE

153
Q

T/F

treat water deprivation by giving animal water asap

A

FALSE – give small amounts of water over 2-3 days graduallt

154
Q

what is a concern if large amount of water is given at one time to treat water deprevation

A

death by aggrevating cerebral edema

155
Q

how many spelling errors are in this brainscapre

A

limit does not exist

156
Q

also called Compound 1080

A

Sodium fluoroacetate

157
Q

T/F

Fluoroacetate is an irritant with a strong odor

A

False - no odor

158
Q

T/F

birds are the most sensitive to Fluoroacetate

A

FALSE - birds most resistant followed by rodents

carnivores are the most sensitive

159
Q

how much Fluoroacetate does it take a rodent to be poisoned

A

Rodents 5-8 mg/kg

compared to Dogs 0.06-0.2 mg/kg

160
Q

T/F

Fluoroacetate undergoes lethal sysnthesis

A

true –Metabolized to fluorocitrate “lethal synthesis” in mitochondria

161
Q

how long does Fluoroacetate take to be excreted by the urine

A

24 hours

162
Q

Fluoroacetate MOA

A

Blocks the TCA cycle - energy depletion
Inhibition of aconitase interferes with cellular respiration
Accumulation of citrate binds with serum calcium – hypocalcemia and heart failure

163
Q

Fluoroacetate target organs

A

brain, CNS, cardiopulmonary

164
Q

T/F

Fluoroacetate clinical signs will take 12 or more hours to develop

A

FALSE - very fast onset – 30 min up to 4 hours

death in 2-12 hours

165
Q

Fluoroacetate cardiac signs predominate in this animal

A

horses – Death may be due to arrhythmias or resp failure/anoxia

166
Q

what is a consistent feature in cats poisoned by Fluoroacetate

A

vocalization

167
Q

what will be elevated on lab analysis from Fluoroacetate poisoning

A

citrate levels !

168
Q

what specimen is chem analysis run on for Fluoroacetate toxicosis

A

GIT contents

169
Q

TX for Fluoroacetate

A

since onset and death happens so fast, may not have time

emetics and lavage tho

170
Q

Registered with EPA as restricted use pesticide (RUP) – highly toxic

A

Strychnine

171
Q

Strychnine persists in the environment for how long

A

40 days

172
Q

What species is most frequently poisoned by Strychnine

A

dogs - maliciously :(

dogs are also more sensitive than cats

173
Q

Strychnine toxic dose in dogs

A

Dogs: 0.5-1.2 mg/kg

174
Q

Strychnine toxic dose in cats

A

2mg/kg

175
Q

T/F

vomiting decreases toxicity of Strychnine

A

TRUE

176
Q

where is Strychnine absorbed

A

mucosa of the GIT

177
Q

this toxin antagonizes glycine, binds to the chlorine ion channel, and results in increased neuronal excitability and an exaggerated reflex arc

A

Strychnine

178
Q

how can you differentiate between Strychnine and compound 1080 poisoning

A

with Strychnine Intermittent muscle contractions are triggered by emotional, auditory or minimal physical stimuli

179
Q

Strychnine onset of signs? and death is caused by?

A

10 min - 2 hours … rapid death from resp failure

180
Q

a form of vitamin D needed to maintain calcium balance by enhancing absorption of
calcium from the GIT and kidneys

A

Cholecalciferol

181
Q

Toxic doses of this lead to high calcium and phosphorus level in the body, resulting in acute or chronic kidney failure

A

Cholecalciferol

182
Q

T/F

young animals can be exposed to Cholecalciferol through milk

A

TRUE

183
Q

T/F

Cholecalciferol has a wide safety margin

A

FALSE - very narrow small amounts can lead to severe signs and death

184
Q

what does Cholecalciferol do to calcium and phosphorus levels

A

increases them both
PTH will be decreased
mineralization onto soft tissue organs

185
Q

T/F

Bromethalin is an anticoagulant

A

FALSE - non-coagulant

186
Q

T/F

Bromethalin and its main metabolite desmobromethalin are strong couplers of oxidative phosphorylation

A

FALSE - strong uncouplers

187
Q

T/F

treat Bromethalin with Vitamin K1 as an antidote

A

false

188
Q

Single-dose, non-anticoagulant rodenticide

A

Bromethalin

189
Q

T/F

cats are more sensitive than dogs and dogs are more susceptible than cats to Bromethalin

A

TRUE

190
Q

T/F

Bromethalin is highly lipophobic

A

false - highly lipophilic

191
Q

T/F Bromethalin is mainly excreted by urine

A

FALSE

it is bile – undergoes hepatic recirculation!!!

192
Q

surfactant or a mixture of surfactants derived from petrochemicals (hydrocarbons) with cleaning properties

A

detergent

193
Q

which are the highest toxicity detergents:
nonionic
anionic
cationic

A

cationic are highest toxicity - positively charged

Fabric softeners, germicides

194
Q

T/F

phenolic compounds have low toxicity

A

false - high

195
Q

Derived from coal tar - a type of alcohol that denatures

proteins and dissolves lipids

A

phenolic compounds

196
Q

how are phenolics metabolized

A

metabolized by glucuronidation

197
Q

detergent or phenol moa:

direct denature and precipitation of proteins leading to coagulative necrosis

A

phenols

198
Q

detergents or phenols MOA :

direct irritation of skin and mucous membranes, degree of caustic damage is relative to the agent

A

detergents

199
Q

T/F

Calcium hypochlorite is a bleaching liquid

A

false – bleaching powder

Sodium hypochlorite is a bleaching liquid

200
Q

Toxicity primarily due to absorption of phosphine gas

A

Zinc Phosphide

201
Q

Zinc Phosphide death …

A

occurs in 3-48 hours due to tissue anoxia

202
Q

how do antacids help with Zinc Phosphide decontamination

A

they raise the gastic ph above 4

203
Q

Acetylene, garlic or fishy odor to vomitus/GI contents is from???

A

zinc phosphide tox

204
Q

what is the lethal dose for most animals with zinc phosphide

A

Lethal dose for most animals ~20-40mg/kg

205
Q

Which of the following are the ‘vitamin K dependent’ coagulation factors?

A

9, 10, 7, 2

206
Q

odor and taste of rodenticides

A

none

207
Q

T/F

the action of anticoaguant rodenticides is fast and quicker than 24 hours

A

FALSe - Action is slow
Generally not less than 24-36 hours for any product

for 1st generation ones it could take a week

208
Q

how do first generation anticoagulant rodenticides work

A

take about a week –Single dose toxicity may be 50-100x multiple dose toxicity
meant to kill rats and mice by them eating a bit over 6 days

209
Q

how do second generation anticoagulant rodenticides work

A

effective after one dose.

Acute oral LD50 for a dog: Warfarin 20-50mg/kg Brodifacoum 0.2-4mg/kg

210
Q

who is the most sensitive to anticoagulant rodenticides

A

dogs

211
Q 
put animals in the correct order of sensitivity to anticoagulant rodenticides 
dogs
cats
ruminants 
chickens 
pigs
horses
A

Pigs, dogs and cats, ruminants, horses and chickens

212
Q

what factors will enhance Anticoagulant Rodenticides toxicity

A 
vitamin k deficiency 
preexisting liver disease
enzyme inhibitors 
conditions like hemorrhage, surgery 
steroid admin
213
Q

Anticoagulant Rodenticides reach peak level in the blood after how many hours

A

6-12

214
Q

T/F

Anticoagulant Rodenticides do not bind to plasma proteins which is why they cause such an issue

A

false - highly bound

215
Q

T/F warfarin is a second generation Anticoagulant Rodenticide

A

FALSE - first

216
Q

what is warfarin half life

A

19 hours

217
Q

Brodifacoum half life

A

6 days !! – second generation

218
Q

Anticoagulant Rodenticides MOA

A

Inhibit vitamin K epoxide reductase – leads to vitamin K depletion

219
Q

T/F

first generation anticoagulant rodenticides are more potent than second generation

A

FALSE - reverse

220
Q

how do anticoagulant rodenticides cause abortion in cattle

A

placental hemorrhage

221
Q

T/F

there is always evidence of external bleeding with anticoagulant rodenticides

A

false - animals may even die without

222
Q

what is a secondary lesion of anticoagulant rodenticides

A

bacterial pneumonia

223
Q

what is the treatment for anticoag rodenticide tox

A

Vitamin K1 – vitamin K3 is NOT effective
given orally
will improve in 24 hours

224
Q

T/F

to tx anticoagulant rodenticide tox give vitamin K1 IV to act fast

A

FALSE -risk of anaphylaxis

oral or parenteral – have same absorption

225
Q

how to treat a dog that got warfarin and has Clinical – bleeding, PCV < 15%, unstable

A

Give clotting factors and RBCs (fresh whole blood or FFP with packed RBCs)
Start vitamin K, monitor closely, supportive care

226
Q

Rich in low-temperature distillates such as

gasoline, kerosene and naphtha

A

sweet crude oil

227
Q

Contains high sulfur high-temp distillates, such as lubricating oil and gas oil

A

sour crude oil,

228
Q

which is more lethal: sweet crude oil or sour crude oil

A

sweet crude oil - gasoline

229
Q

The minimal lethal dose based on death caused by aspiration pneumonia over a week for sweet crude oil

A

Sweet crude oil, 48 mL/kg

230
Q

The minimal lethal dose based on death caused by aspiration pneumonia over a week for sour crude oil

A

Sour crude oil, 74 mL/kg

231
Q

T/F

petroleum is an irritant and is oily in nature

A

true – caustic and dissolve cell membranes

232
Q

what can chronic exposure to petroleum on the skin cause

A

hyperkeratosis

233
Q

T/F

Short-chain aliphatics cause aspiration pneumonia

A

FALSE - long chain do

234
Q

Chlorinated aliphatic hydrocarbon toxicity effects what system

A

CNS

235
Q

Aromatic hydrocarbons at 60 ppm in air following chronic exposure can cause____________

A

bone marrow suppression

236
Q

______ are the most susceptible to crude petroleum substances

A

cattle

237
Q

T/F
low boiling point petroleums are generally less toxic than high boiling point ones because of more absorption via inhalation

A

FALSE – low bp are more toxic

Low boiling points = low viscosity = low surface tension generally have more pneumotoxic (lung) effects through inhalation, thus impairing respiration

238
Q

Highly volatile aliphatics (short-chain) are partly metabolized and excreted through the _____

A

lungs

239
Q

how does petroleum cause aspiration pneumonia

A

ingestion leads to vomiting
direct contact can rapidly dissolve the cell - cause edema and bronchoconstriction
oily in the lungs cannot be coughed up

240
Q

T/F

activated charcoal and emetics tx petroleum

A

true

241
Q

fluoride has a high affinity to this mineral

A

calcium

242
Q

acute fluoride toxicosis (fluorosis) is the most

common

A

FALSE - chronic is

243
Q

T/F
Soluble sodium fluoride (NaF) is more toxic than
calcium fluoride (CaF2)

A

TRUE

244
Q

what age animals are most susceptible to fluoride tox

A

young bc bones and teeth developing

245
Q

best specimen to test for fluoride

A

bone – Levels >1500 ppm are significant

246
Q

how to treat fluoride

A

once it is in the bone and teeth it can not be mobilized – need to prevent by keeping out of food or levels low

247
Q

antifreeze ingestion

A

ethylene glycol

248
Q

Some commercial antifreeze products have ____ rust inhibitor

A

phosphate

249
Q

taste of antifreeze

A

sweet – but is colorless and odorless

250
Q

ethylene glycol half life in dogs

A

3-4 hours

251
Q

how is ethylene glycol metabolized

A

in the liver INTO toxic metabolites – lethal synthesis

252
Q

Ethylene Glycol is oxidized by alcohol dehydrogenase to

A

glycoaldehyde

253
Q

Glycoaldehyde is oxidized by aldehyde dehydrogenase to

A

glycolic acid

254
Q

what do the toxic metabolites of ethylene glycol cause

A

metabolic acidosis and acute renal failure

255
Q

what crystals form that are diagnostic of EG

A

Calcium oxalate monohydrate

256
Q

signs of ethylene glycol appear within 30 min - 12 hours

A

Signs include nausea/vomiting, anorexia, CNS depression, ataxia, incoordination, hypothermia, muscle fasciculations, tachycardia, tachypnea, polyuria, polydipsia, dehydration, coma, and death

257
Q

T/F

ethylene glycol toxicosis lowers the anion gap

A

FALSE - increases it

258
Q

T/F

ethylene glycol causes hyophosphatemia

A

false - hyperphosphatemia

also hyperkalemia , hypocalcemia, hyperglycemia

259
Q

Catachem Ethylene Glycol test

A

no false positive with ethanol

260
Q

ethylene glycol antidote

A

Inhibitors of alcohol dehydrogenase Inhibit formation of toxic metabolites
Most effective if started within 3hr of EG ingestion

261
Q

best treatment for EG given IV to dogs and cats

A

Fomepizole (4-methylpyrazole, 4-MP) Antizol-Vet®

20% ethanol is slower recovery but can also be used

TOX (5 decks)

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