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
what is the order of sensitivity in species to anticoagulants
pigs, dogs, cats, ruminants, horses, chickens
26
moa of anticoagulants
inhibit vitamin K epoxide reductase which converts vitamin K epoxide to reduced form depleted reduced vitamin K -- cant make factors 2,7,9,10
27
which anticoagulant generation is more potent
second
28
how many days for the onset of clinical signs from anticoagulant tox
1-5 days | will see bleeding from anywhere because they cant clot
29
how long for anticoagulants to reach peak levels in blood
6-12 hours
30
T/F | anticoagulants are highly bound to plasma proteins
True
31
what factors can increase the toxicity of anticoagulants
vit k deficiency liver disease presence of drugs that cause hemorrhage/anemia corticosteroids
32
which test is the first noticed for anticoags
prolonged PT first
33
what three lab findings are common in bloodwork of animals poisoned by anticoags
thrombocytopenia anemia hypoproteinemia
34
differentials for anticoag tox
vitamin k deficiency | spoiled sweet clover ingestion
35
why is vitamin K1 not given IV for anticoag treatment
can cause anaphylaxis
36
treatment for anticoag toxicosis
vitamin K1 - po | whole blood transfusions when PCV <15
37
ingestion of this human medication will cause cholcalciferol toxicosis
psoriasis
38
dog ingesting large doses of vitamin D
cholcalciferol toxicosis
39
what species and what age are the most sensitive to cholcalciferol toxicosis
cats | young
40
T/F | cholcalciferol has a wide saftey margin and so it takes a large dose to be fatal
FALSE - very narrow
41
predisposing factors for cholcalciferol tox
renal disease hyperparatyroidism ingestion of a high Ca and Phos diet
42
cholcalciferol is metabolized in the liver by hydroxylation into
25-hydroxycholeclciferol
43
what is the main form of cholcalciferol in circulation
25-hydroxycholeclciferol
44
25-hydroxycholecalciferol is transported to the kidney and is metabolized into what
1,25-dihydroxycholcalciferol - calcitriol
45
what is the most potent form of cholcalciferol
calcitriol
46
T/F | vitamin D can be excreted in the milk in toxic levels
true
47
where is cholcalciferol mainly excreted
bile
48
this toxicant increases serum calcium due to increasing GI absorption and tubular reabsorption and calcium reabsoprtion
cholcalciferol
49
this toxicant causes hyperphosphatemia and soft tissue mineralization
cholcalciferol
50
how many hours for cholcalciferol tox clinical signs to appear
24-36 hours
51
in a dead patient what tissues can be tested for cholcalciferol tox
bile and kidney
52
T/F | cholcalciferol toxicosis will cause hemorrhagic enteritis and death due to heart and renal failure
TRUE
53
what can be done to lower serum calcium levels
calcitonin saline diuresis furosemide prednisone
54
who is most susceptible to bromethalin toxicosis
dogs | cats are more sensitive though
55
what species lacks an enzyme and therefore are resistant to bromethalin tox
guinea pigs
56
T/F | bromethalin is highly lipophilic
true
57
moa of bromethalin
uncoupling of oxidative phosphorylation leading to lack of ATP -- results in cerebral edema and increased csf pressure
58
bromethalin is metabolized by ____ in the liver to the metabolite desmethylbromathalin which is more toxic
N-desmethylation | this is lethal synthesis
59
where is bromethalin excreted
the bile
60
acute stage of bromethalin toxicosis signs
``` this is the convulsant stage hyperthermia running fits hyperexcitability ACUTE = in 24 hours ```
61
aubacute bromethalin toxicosis
paralytic stage -- in 2-3 days cats more hind limb ataxia, paresis, depression
62
T/F | to treat bromethalin give vitamin K1
no
63
drug for reducing cerebral edema
Mannitol
64
what treatment option is not recommended for bromethalin
mg sulfate
65
drug for seizures and muscle tremors
diazepam | phenobarb
66
most common source of lead toxicosis in animals
lead based paints
67
what conditions favor dissolution of lead
acidic
68
what species are more resistant to lead
goats pigs chickens
69
how is lead transported in the body
as lead proteinate on the erythrocyte membrane
70
T/F | lead can cross the BBB and the placenta
true
71
how many weeks does lead stay in soft tissues for
4-6
72
target tissues of lead
CNS GI hematopoietic system
73
this metal inhibits heme synthesis and causes anemia
lead
74
basophilic stippling caused from accumulation of ribosomal dna aggregates in this metal
lead
75
chronic lead tox
anemia
76
what do you test for lead in an alive patient
whole blood
77
what do you test in a dead patient for lead
kidneys,liver,gi
78
what might be seen on a radiograph in a young animal with chronic lead tox
metaphyseal sclerosis - lead lines
79
chelation agent to treat lead
calcium disodium EDTA
80
prognosis with lead tox
guarded especially when CNS signs are seen
81
ingestion of 5 pennies
subacute zinc toxicosis
82
acute LD50 of zinc
100mg/kg
83
chronic zinc toxicity is caused by ___ppm in diet
2000
84
what environment enhances zinc release and absorption
acid
85
metal that causes hemolytic anemia, icterus, and hemoglobinuria
zinc
86
how is zinc transported
plasma proteins - ALB/GLOB
87
white muscle disease
selenium deficiency in sheep
88
nutritional muscle dystrophy
selenium deficiency in lambs.calves.foals
89
hepatosis dietica
selenium deficiency in young pigs
90
exudative diathesis
selenium deficiency in young chicks
91
nutritional pancreatic atrophy
selenium deficiency in chickens
92
porcine stress syndrome
selenium deficiency in pigs
93
where can you find selenium deficient soil
north west, north east south east great lakes NOT florida
94
what is the daily requiirement of selenium
.1mg/kg
95
what does selenium smell like
rotten odors
96
list seleniferous plants
``` locoweed milkvetch princes plume golden wood woody aster ```
97
selenium contaminated water causes what in water fowl
teratogenic effects
98
this can be used to treat selenium toxicosis by increased elimination
organic arsenic
99
white muscle disease
selenium deficiency in sheep
100
nutritional muscle dystrophy
selenium deficiency in lambs.calves.foals
101
hepatosis dietica
selenium deficiency in young pigs
102
exudative diathesis
selenium deficiency in young chicks
103
nutritional pancreatic atrophy
selenium deficiency in chickens
104
porcine stress syndrome
selenium deficiency in pigs
105
where can you find selenium deficient soil
north west, north east south east great lakes NOT florida
106
what is the daily requiirement of selenium
.1mg/kg
107
what does selenium smell like
rotten odors
108
list seleniferous plants
``` locoweed milkvetch princes plume golden wood woody aster ```
109
selenium contaminated water causes what in water fowl
teratogenic effects
110
this can be used to treat selenium toxicosis by increased elimination
organic arsenic
111
T/F | selenium is an irritant to mucus membranes
true
112
selenium is readily absorbed here
small intestine
113
dramatically depletes tissue glutathione
selenium
114
acute oral selenium toxicosis signs
colic, bloat, and watery diarrhea | death in hours
115
blind staggers in cattle
subacute selenium toxicosus
116
causes a condition called porcine focal symmetrical poliomyelomalacia in pigs
subacute selenium toxicosis
117
chronic toxicosis of this metal results in loss of hair and hoof sloughing
selenium
118
what type of diet may help reduce selenium tox
high protein diet + copper
119
what glands do the bufo toad toxins come from
parotid
120
what makes bufotenine a schedule 1 substance
hallucinogenic effect
121
this is similar to the hallucinogen LSD
indole alkylamines
122
what dose can cause clinical signs from bufo toad toxins
1 mg/kg
123
where are bufogenins eliminated
the urine
124
bufogenins and bufotoxin have a digitalis like effect by what MOA
ihibiting Na/K ATPase
125
T/F | bufogenins cause direct irritation of the mucus membrane
true
126
clinical signs of bufotoxins
``` hypersalivation seizures circling vomiting red mucus membranes tachycardia collapse opisthotonos hyperthermia ```
127
rattlesnakes | copperheads, cottonmouths all belong to what familt
pit vipers -- crotalid
128
why are pit vipers named pit vipers
they have a temperature sensitive pit between nose and eyes - broad triangular head
129
nonenzymatic proteins and peptides in a snake are called
killing fractions
130
what states do not have venemous pit vipers
hawaii alaska maine
131
T/F | cats are more sensitive than dogs to pit viper vemon
false - dogs are more sensitive
132
what pit viper snake is the most toxic
rattlesnakes
133
this causes the snake venom to spread
hyaluronidase
134
this disrupts cell membranes, uncouples phosphorylation, and releases vasoactive amines during snake bites
phospholipase A2
135
primary effect of pit viper snake bite venom
hypocoagulation
136
what are some lab findings from a snake bite
echinocytosis hymolysis lowered coagulation times DIC
137
T/F | corticosteroids and NSAIDS help reduce the effects of venom in pit viper bites
false - they are contraindicated for use
138
snake found witha black head and alternating bands of black yellow and red
coral snake
139
what percent of coral snake bites are nonenvenomating
60%
140
primary effect of coral snake bites
neurotoxic -- nondepolarizing neuromuscular blockade, CNS depression, and muscle paralysis
141
what is an important complication of coral snake bites
aspiration pneumonia
142
what sign do dogs show that cats will not show in coral snake envonomation
intravascular hemolysis, anemia, and hemoglobinuria
143
what two factors will be elevated in lab diagnostics for coral snake bites
fibrinogen and creatine kinase
144
CNS stimulant that block the reuptake of norepinephrine and dopamine
amphetamines
145
this illicit drug is hydrolyzed by plasma and hepatic esterase and is methylated in the liver
cocaine
146
cns stimulant and sympathomimetic that blocks the reuptake of norepinephrine, epinephrine and serotonin and also increases catecholamine release
cocaine
147
T/F | cocaine has an indirect effect on the myocardium
false - direct
148
what lab diagnostics may be found in coke tox
high CK and systemic acidosis
149
T/F | cannabinoids have a narrow safety margin and are frequently fatal
FALSE - wide and rarely fatal
150
active constituent of marijuana
thc