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TOX > final exam - cumulative things (not plant things) > Flashcards

final exam - cumulative things (not plant things) Flashcards

1
Q

how long can organophosphates persist in the environment

A

2-4 weeks

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2
Q

this pesticide can penetrate the skin and waxy coating of plants and fruits

A

organophosphates

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3
Q

T/F

muscle relaxants and neuromuscular blockers decrease toxicity of organophosphates

A

FALSE - increases

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4
Q

MOA of organophosphates

A

irreversible inhibition of choliesterases – increases ACH at all cholinergic sites

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5
Q

what receptors are most sensitive to OP toxicosis

A

muscarinic

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6
Q

what is the cause of death in high exposure of organophosphate toxicosis

A

respiratory failure

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7
Q

what samples can be tested for OP

A

stomach/rumen contents

hair and skin for dermal exposure

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8
Q

A patient is suspected of OP poisoning so you give it atropine. It displays dry mucous membranes, tachycardia, and dilated pupils … was it poisoned with OP

A

no

if none of these signs were seen with atropine then it would have been yes

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9
Q

treatment of dyspnea and cyanosis

A

oxygen therapy

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10
Q

treament for organophosphate poisoning

A

atropine sulfate

2PAM cholide

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11
Q

which age animals are most sensitive to carbamates

A

young

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12
Q

causes reversible inhibition of acetylcholinesterases

A

carbamate

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13
Q

T/F

2PAM is the treatment of choice for organophosphate and carbamate

A

FALSE – it is not effective with carbamate

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14
Q

which has a longer duration and more severe clinical signs carbamate or OP

A

OP

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15
Q

commonly used as flea and tick control in dogs and cats

A

pyrethrins/pyrethroids

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16
Q

T/F

pyrethrins are esters and are water soluble

A

false - they are esters, but they are LIPID soluble

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17
Q

pyrethrin conjugated metabolites are excreted where

A

in the urine

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18
Q

who is the most sensitive to pyrethrins

A

birds and fish

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19
Q

MOA is to delay the closure of the sodium ion channels in the axonal membrane of the insect – “knockdown effect:

A

pyrethrins

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20
Q

what are the clinical signs in pyrethrin tox

A 
salivation
vomiting 
diarrhea 
 hyperexcitability 
tremors 
seizures 
death
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21
Q

smell and taste of warfarin

A

odorless

tasteless

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22
Q

which generation of anticoagulant is most toxic after 1 dose

A

second generation

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23
Q

which generation of anticoagulant is most effective when ingested over a week

A

first generation - warfarin is a first gen

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24
Q

which species is most susceptible to anticoag toxicosis

A

dogs

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25
Q

what is the order of sensitivity in species to anticoagulants

A

pigs, dogs, cats, ruminants, horses, chickens

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26
Q

moa of anticoagulants

A

inhibit vitamin K epoxide reductase which converts vitamin K epoxide to reduced form
depleted reduced vitamin K – cant make factors 2,7,9,10

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27
Q

which anticoagulant generation is more potent

A

second

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28
Q

how many days for the onset of clinical signs from anticoagulant tox

A

1-5 days

will see bleeding from anywhere because they cant clot

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29
Q

how long for anticoagulants to reach peak levels in blood

A

6-12 hours

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30
Q

T/F

anticoagulants are highly bound to plasma proteins

A

True

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31
Q

what factors can increase the toxicity of anticoagulants

A

vit k deficiency
liver disease
presence of drugs that cause hemorrhage/anemia
corticosteroids

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32
Q

which test is the first noticed for anticoags

A

prolonged PT first

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33
Q

what three lab findings are common in bloodwork of animals poisoned by anticoags

A

thrombocytopenia
anemia
hypoproteinemia

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34
Q

differentials for anticoag tox

A

vitamin k deficiency

spoiled sweet clover ingestion

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35
Q

why is vitamin K1 not given IV for anticoag treatment

A

can cause anaphylaxis

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36
Q

treatment for anticoag toxicosis

A

vitamin K1 - po

whole blood transfusions when PCV <15

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37
Q

ingestion of this human medication will cause cholcalciferol toxicosis

A

psoriasis

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38
Q

dog ingesting large doses of vitamin D

A

cholcalciferol toxicosis

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39
Q

what species and what age are the most sensitive to cholcalciferol toxicosis

A

cats

young

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40
Q

T/F

cholcalciferol has a wide saftey margin and so it takes a large dose to be fatal

A

FALSE - very narrow

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41
Q

predisposing factors for cholcalciferol tox

A

renal disease
hyperparatyroidism
ingestion of a high Ca and Phos diet

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42
Q

cholcalciferol is metabolized in the liver by hydroxylation into

A

25-hydroxycholeclciferol

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43
Q

what is the main form of cholcalciferol in circulation

A

25-hydroxycholeclciferol

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44
Q

25-hydroxycholecalciferol is transported to the kidney and is metabolized into what

A

1,25-dihydroxycholcalciferol - calcitriol

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45
Q

what is the most potent form of cholcalciferol

A

calcitriol

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46
Q

T/F

vitamin D can be excreted in the milk in toxic levels

A

true

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47
Q

where is cholcalciferol mainly excreted

A

bile

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48
Q

this toxicant increases serum calcium due to increasing GI absorption and tubular reabsorption and calcium reabsoprtion

A

cholcalciferol

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49
Q

this toxicant causes hyperphosphatemia and soft tissue mineralization

A

cholcalciferol

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50
Q

how many hours for cholcalciferol tox clinical signs to appear

A

24-36 hours

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51
Q

in a dead patient what tissues can be tested for cholcalciferol tox

A

bile and kidney

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52
Q

T/F

cholcalciferol toxicosis will cause hemorrhagic enteritis and death due to heart and renal failure

A

TRUE

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53
Q

what can be done to lower serum calcium levels

A

calcitonin
saline diuresis
furosemide
prednisone

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54
Q

who is most susceptible to bromethalin toxicosis

A

dogs

cats are more sensitive though

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55
Q

what species lacks an enzyme and therefore are resistant to bromethalin tox

A

guinea pigs

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56
Q

T/F

bromethalin is highly lipophilic

A

true

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57
Q

moa of bromethalin

A

uncoupling of oxidative phosphorylation leading to lack of ATP – results in cerebral edema and increased csf pressure

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58
Q

bromethalin is metabolized by ____ in the liver to the metabolite desmethylbromathalin which is more toxic

A

N-desmethylation

this is lethal synthesis

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59
Q

where is bromethalin excreted

A

the bile

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60
Q

acute stage of bromethalin toxicosis signs

A 
this is the convulsant stage 
hyperthermia 
running fits 
hyperexcitability 
ACUTE = in 24 hours
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61
Q

aubacute bromethalin toxicosis

A

paralytic stage – in 2-3 days
cats more
hind limb ataxia, paresis, depression

62
Q

T/F

to treat bromethalin give vitamin K1

A

no

63
Q

drug for reducing cerebral edema

A

Mannitol

64
Q

what treatment option is not recommended for bromethalin

A

mg sulfate

65
Q

drug for seizures and muscle tremors

A

diazepam

phenobarb

66
Q

most common source of lead toxicosis in animals

A

lead based paints

67
Q

what conditions favor dissolution of lead

A

acidic

68
Q

what species are more resistant to lead

A

goats
pigs
chickens

69
Q

how is lead transported in the body

A

as lead proteinate on the erythrocyte membrane

70
Q

T/F

lead can cross the BBB and the placenta

A

true

71
Q

how many weeks does lead stay in soft tissues for

A

4-6

72
Q

target tissues of lead

A

CNS
GI
hematopoietic system

73
Q

this metal inhibits heme synthesis and causes anemia

A

lead

74
Q

basophilic stippling caused from accumulation of ribosomal dna aggregates in this metal

A

lead

75
Q

chronic lead tox

A

anemia

76
Q

what do you test for lead in an alive patient

A

whole blood

77
Q

what do you test in a dead patient for lead

A

kidneys,liver,gi

78
Q

what might be seen on a radiograph in a young animal with chronic lead tox

A

metaphyseal sclerosis - lead lines

79
Q

chelation agent to treat lead

A

calcium disodium EDTA

80
Q

prognosis with lead tox

A

guarded especially when CNS signs are seen

81
Q

ingestion of 5 pennies

A

subacute zinc toxicosis

82
Q

acute LD50 of zinc

A

100mg/kg

83
Q

chronic zinc toxicity is caused by ___ppm in diet

A

2000

84
Q

what environment enhances zinc release and absorption

A

acid

85
Q

metal that causes hemolytic anemia, icterus, and hemoglobinuria

A

zinc

86
Q

how is zinc transported

A

plasma proteins - ALB/GLOB

87
Q

white muscle disease

A

selenium deficiency in sheep

88
Q

nutritional muscle dystrophy

A

selenium deficiency in lambs.calves.foals

89
Q

hepatosis dietica

A

selenium deficiency in young pigs

90
Q

exudative diathesis

A

selenium deficiency in young chicks

91
Q

nutritional pancreatic atrophy

A

selenium deficiency in chickens

92
Q

porcine stress syndrome

A

selenium deficiency in pigs

93
Q

where can you find selenium deficient soil

A

north west, north east
south east
great lakes

NOT florida

94
Q

what is the daily requiirement of selenium

A

.1mg/kg

95
Q

what does selenium smell like

A

rotten odors

96
Q

list seleniferous plants

A 
locoweed 
milkvetch
princes plume
golden wood
woody aster
97
Q

selenium contaminated water causes what in water fowl

A

teratogenic effects

98
Q

this can be used to treat selenium toxicosis by increased elimination

A

organic arsenic

99
Q

white muscle disease

A

selenium deficiency in sheep

100
Q

nutritional muscle dystrophy

A

selenium deficiency in lambs.calves.foals

101
Q

hepatosis dietica

A

selenium deficiency in young pigs

102
Q

exudative diathesis

A

selenium deficiency in young chicks

103
Q

nutritional pancreatic atrophy

A

selenium deficiency in chickens

104
Q

porcine stress syndrome

A

selenium deficiency in pigs

105
Q

where can you find selenium deficient soil

A

north west, north east
south east
great lakes

NOT florida

106
Q

what is the daily requiirement of selenium

A

.1mg/kg

107
Q

what does selenium smell like

A

rotten odors

108
Q

list seleniferous plants

A 
locoweed 
milkvetch
princes plume
golden wood
woody aster
109
Q

selenium contaminated water causes what in water fowl

A

teratogenic effects

110
Q

this can be used to treat selenium toxicosis by increased elimination

A

organic arsenic

111
Q

T/F

selenium is an irritant to mucus membranes

A

true

112
Q

selenium is readily absorbed here

A

small intestine

113
Q

dramatically depletes tissue glutathione

A

selenium

114
Q

acute oral selenium toxicosis signs

A

colic, bloat, and watery diarrhea

death in hours

115
Q

blind staggers in cattle

A

subacute selenium toxicosus

116
Q

causes a condition called porcine focal symmetrical poliomyelomalacia in pigs

A

subacute selenium toxicosis

117
Q

chronic toxicosis of this metal results in loss of hair and hoof sloughing

A

selenium

118
Q

what type of diet may help reduce selenium tox

A

high protein diet + copper

119
Q

what glands do the bufo toad toxins come from

A

parotid

120
Q

what makes bufotenine a schedule 1 substance

A

hallucinogenic effect

121
Q

this is similar to the hallucinogen LSD

A

indole alkylamines

122
Q

what dose can cause clinical signs from bufo toad toxins

A

1 mg/kg

123
Q

where are bufogenins eliminated

A

the urine

124
Q

bufogenins and bufotoxin have a digitalis like effect by what MOA

A

ihibiting Na/K ATPase

125
Q

T/F

bufogenins cause direct irritation of the mucus membrane

A

true

126
Q

clinical signs of bufotoxins

A 
hypersalivation
seizures 
circling
vomiting
red mucus membranes
tachycardia 
collapse 
opisthotonos 
hyperthermia
127
Q

rattlesnakes

copperheads, cottonmouths all belong to what familt

A

pit vipers – crotalid

128
Q

why are pit vipers named pit vipers

A

they have a temperature sensitive pit between nose and eyes - broad triangular head

129
Q

nonenzymatic proteins and peptides in a snake are called

A

killing fractions

130
Q

what states do not have venemous pit vipers

A

hawaii
alaska
maine

131
Q

T/F

cats are more sensitive than dogs to pit viper vemon

A

false - dogs are more sensitive

132
Q

what pit viper snake is the most toxic

A

rattlesnakes

133
Q

this causes the snake venom to spread

A

hyaluronidase

134
Q

this disrupts cell membranes, uncouples phosphorylation, and releases vasoactive amines during snake bites

A

phospholipase A2

135
Q

primary effect of pit viper snake bite venom

A

hypocoagulation

136
Q

what are some lab findings from a snake bite

A

echinocytosis
hymolysis
lowered coagulation times
DIC

137
Q

T/F

corticosteroids and NSAIDS help reduce the effects of venom in pit viper bites

A

false - they are contraindicated for use

138
Q

snake found witha black head and alternating bands of black yellow and red

A

coral snake

139
Q

what percent of coral snake bites are nonenvenomating

A

60%

140
Q

primary effect of coral snake bites

A

neurotoxic – nondepolarizing neuromuscular blockade, CNS depression, and muscle paralysis

141
Q

what is an important complication of coral snake bites

A

aspiration pneumonia

142
Q

what sign do dogs show that cats will not show in coral snake envonomation

A

intravascular hemolysis, anemia, and hemoglobinuria

143
Q

what two factors will be elevated in lab diagnostics for coral snake bites

A

fibrinogen and creatine kinase

144
Q

CNS stimulant that block the reuptake of norepinephrine and dopamine

A

amphetamines

145
Q

this illicit drug is hydrolyzed by plasma and hepatic esterase and is methylated in the liver

A

cocaine

146
Q

cns stimulant and sympathomimetic that blocks the reuptake of norepinephrine, epinephrine and serotonin and also increases catecholamine release

A

cocaine

147
Q

T/F

cocaine has an indirect effect on the myocardium

A

false - direct

148
Q

what lab diagnostics may be found in coke tox

A

high CK and systemic acidosis

149
Q

T/F

cannabinoids have a narrow safety margin and are frequently fatal

A

FALSE - wide and rarely fatal

150
Q

active constituent of marijuana

A

thc

TOX (5 decks)

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