Exam I - Rodenticides and Molluscicides Flashcards
1
Q
What type of rodenticides are there?
A
Anticoagulant rodenticides Cholecalciferol Bromethalin Strychnine Zinc phosphide Fluoroacetate (compound 1080)
2
Q
What type of molluscicides are there?
A
Methaldehyde
3
Q
What are the first generation anticoagulant rodenticides?
A
Warfarin
Pindone
Chlorphacinone
4
Q
What are the second generation anticoagulant rodenticides?
A
Brodifacoum
Diphacinone
Bromadialone
5
Q
What is relay toxicosis?
A
Secondary toxicosis - animal being poisoned by eating an animal that ate the poison.
6
Q
What animals can be poisoned by relay toxicosis?
A
Pigs, cats and dogs
7
Q
T/F Anticoagulant rodenticides are odorless and tasteless, they are resistant in the environment for weeks to months and action is fast
A
False - action is slow - generally not less than 24-36 hrs
Over 1 week for first generation
8
Q
When are first generation anticoagulant rodenticides most toxic?
A
When ingested daily for about a week
9
Q
When are second generation anticoagulant rodenticides most toxic?
A
effective after one dose
10
Q
What is the order of sensitivity to anticoagulant rodenticides in other species?
A
Pigs Dogs/Cats Ruminants horses chickens
11
Q
What enhances the anticoagulant rodenticide effects?
A
Vitamin K deficiency (oral sulfonamide therapy)
Liver disease
Enzyme inhibitors (cimetidine)
Anything that causes hemorrhage, anemia, hemolysis
Drugs that displace the anticoagulant from protein binding sites - (Phenylbutazone, salicylates, sulfonamides, corticosteroids)
12
Q
What would the administration of steroids or thyroxine in an animal with anticoagulant rodenticide poisoning cause?
A
Increase receptor site affinity
13
Q
What factors decrease anticoagulant rodenticide toxicity?
A
Pregnancy Enzyme inducers (phenytoin)
14
Q
T/F Anticoagulant rodenticide absorption is complete, largely bound to plasma protein, achieve higher concentrations in the liver, cross the placenta, and reach peak blood level in 6-12 hrs
A
True
15
Q
T/F first generation anticoagulant rodenticides have longer plasma half lives than second generation
A
False - second generation have long half lives
Diphenadione - 4.5 days
Brodifocoum - 6 days
Warfarin - 19 hrs (1st generation)
16
Q
What is the MOA of anticoagulant rodenticides?
A
Inhibit vitamin K epoxide reductase
17
Q
What does the vitamin K epoxide reductase do? and what does the inhibition of this enzyme lead to?
A
Converts vitamin K epoxide to reduced form
Leads to depletion of reduced vitamin K, which leads to reduced carboxylation and activation of precursors of clotting factors II, VII, IX, X
18
Q
How long does it take to see onset of clinical signs with anticoagulant rodenticides?
A
1-5 days
19
Q
What clinical signs will you see on an animal with anticoagulant rodenticide?
A
Epistaxis, bloody discharge from orifices, hematuria, bleeding from venipuncture site, hematoma, weakness, shock, tachypnea/dyspnea, anorexia, lethargy
20
Q
What coagulation parameters are prolonged when anticoagulant rodenticide toxicity occurs?
A
Activated clotting time (ACT)
One stage prothrombin time (OSPT, PT)
Activated partial thromboplastin time (APTT)
Proteins induced by vitamin K antagonist (PIVKA)
21
Q
What laboratory findings will you see in an animal with anticoagulant rodenticide toxicity?
A
Anemia
thrombocytopenia
Hypoproteinemia
Radiographic changes (hemorrhage)
22
Q
What are your ddx for anticoagulation rodenticide toxicity?
A
Spoiled sweet clover (cattle, horses) Vitamin K deficiency (swine, poultry) Other toxins that cause hemorrhage - Ricin (caster beans) Saponis (coffee weeds) Monocrotaline (crotalaria) Gossypol (cotton seed) Aflatoxins
23
Q
What vitamin K should be used to give in an animal with anticoagulant rodenticide toxicity?
A
Vitamin K1 (phytonadione) orally Vit. K3 not effective
24
Q
Why don’t you want to give vitamin K IV?
A
risk of anaphylaxis
25
How would you treat an animal with anticoagulant rodenticide toxicity?
```
Emesis/activated charcoal
Vitamin K
Clotting factors (FFP, cryoprecipitate)
```
26
What is cholecalciferol?
Early form of vitamin D3
27
Is cholecalciferol soluble in water or oil?
Insoluble in water, soluble in most organic solvents/oil
28
T/F More bioavailable forms of cholecalciferol are toxic at higher doses
False - more bioavailable forms are toxic at far lower doses
29
Cholecalciferol is absorbed from the GI tract, binds to vitamin D binding protein in plasma for transportation to the liver, its metabolized and turned into
Calcidiol - main form in circulation
30
Calcidiol is transported to the kidney and metabolized to
Calcitriol - very potent!
31
Where are highest concentrations of cholecalciferol found?
Plasma, liver, kidneys, fat (very fat soluble)
32
Could cholecalciferol under enterohepatic recirculation?
yes
33
What may predispose an animal to cholecalciferol toxicity?
Renal disease
Hyperparathyroidism
High calcium/phos in the diet
34
What is the MOA of cholecalciferol rodentocides?
Causes hypercalcemia and hyperphosphatemia
35
What does the increase in calcium cause?
deposition of calcium in soft tissues (mineralization), tissue damage, increased capillary permeability, renal ischemia, renal loss of Na and K
36
What does calcitriol do?
Causes increase absorption of Ca from the GI tract,
decreases Ca storage in bone,
decreased of Ca excretion from the kidneys
37
T/F When there is a cholecalciferol rodenticide overdose, calcidiol itself, instead of calcitriol, has effects on the GI, bone and kidneys, which continues to increase Ca levels
True
38
When will you start to see clinical signs of cholecalciferol rodenticide toxicity?
within 24-36 hrs
39
What GI clinical signs will you see with cholecalciferol rodenticide toxicity?
GI - anorexia, vomiting, +/- HEMATEMESIS (vomiting blood), abdominal pain, constipation (+/- MELENA - dark stool - blood in stool)
40
What renal, CV, neurologic clinical signs will you see with cholecalciferol rodenticide toxicity?
PU/PD (hyposthenuria)
Arrhythmias, hypertension
Depression, weakness, muscle twitching, seizures, coma/death
41
What lesions might you see on an animal with cholecalciferol rodenticide toxicity?
Hemorrhagic gastroenteritis
| Mineralization of kidneys, myocardium, lungs stomach, major vessels
42
what lab findings will you see on animal with cholecalciferol rodenticide toxicity?
```
Hypercalcemia
Hyperphosphatemia
Increased Calcidiol and Calcitriol
Decreased PTH
Azotemia
proteinuria
Glucosuria
```
43
What are your ddx for cholecalciferol rodenticide toxicity?
```
HARD IONS
Hyperparathyroidism
Addison disease, aluminum, Vitamin A toxicity,
Renal disease, Raisins
D - Vit. D toxicosis
Idiopathic
Osteolytic
Neoplasia
Spurious
```
44
How would you treat cholecalciferol rodenticide?
Treat hypercalcemia -
In hospital -saline diuresis, furosemide, sodium bicarb
At home - Glucocorticoids, salmon calcitonin, bisphosphonates
45
Bromethalin is a GUP, what does that mean?
General use pesticide
46
T/F Bromethalin is effective agains warfarin resistant rodents, has no bait shyness, and has possible secondary (relay) toxicosis of non target animals (even though its not been reported)
True
47
What animal is resistant to bromethalin?
Guinea pigs - lack correct metabolic enzymes
48
What animal is most sensitive to bromethalin and what animal is more susceptible?
Cats are more sensitive
| Dogs are more susceptible
49
What are the toxicokenetics of bromethalin?
Highly lipophilic
Rapidly absorbed orally
Highly distributed
50
What tissue would have the highest concentration of bromethalin?
fat and brain
51
Bromethalin is metabolized in the liver by N-demethylation to a metabolite _____
desmethylbromethalin - which is more toxic
52
What is the half life of bromethalin in the rat?
5-6 days
53
What is the MOA for bromethalin?
Uncoupling of oxidative phosphorylation
Lack of adequate ATP
Insufficiency energy for Na+/K+ ion pumps
54
What are primary organ targets for bromethalin?
Brain and spinal cord
55
What does ion pump dysfunction with bromethalin toxicity lead to?
fluid imbalance, edema and increased pressure
56
Bromethalin may have acute or delayed (subacute) signs, which one is more common?
Delayed - subacute signs (2-3 days to onset)
57
What signs might you see on a subacute bromethalin toxicity case?
Hind limb ataxia, proprioceptive deficits and paresis, paralysis, loss of deep pain response, patellar hyperreflexia, UMN bladder
58
What lesions will you see on an animal with bromethalin toxicity?
Cerebral edema
| Diffuse white matter vacuolization through CNS
59
What should you avoid giving an animal with bromethalin toxicity?
Magnesium containing cathartics - CNS depressive
60
How could you treat bromethalin toxicity?
```
No specific antidote
Decontamination - emesis/activated charcoal with sorbitol
Supportive care -
Cerebral edema - mannitol, furosemide
Seizures - diazepam, phenobarbitol
```
61
Strychnine is a RUP, what does that stand for?
Restricted use pesticide
62
Strychnine is used to control what animals?
```
Gophers
Squirrels
Deer mice
Moles
Prairie dogs
Rats
Porcupines
Chipmunks
Rabbits
Pigeons
```
63
T/F Strychnine is a weak base, has a bitter taste, moderately water soluble, and persist in the environment up to ~40 days
True
64
What animals are susceptible and what animus are more sensitive to strychnine?
All animals are susceptible
| Dogs are most sensitive and most frequently poisoned than cats
65
T/F Strychnine is rapidly absorbed from the GI tract, dose not accumulate in tissue, its highly protein bound, does cross the BBB, and undergoes enterohepatic recirculation
False- its not highly protein bound, all else is true
66
What is the MOA for Strychnine?
Block post synaptic effect of glycine in the spinal cord
Glycine is an important inhibitory neurotransmitter to motor neurons and interneurons in the spinal cord/brainstem/thalamus
67
What does strychnine lead too?
Highly exaggerated reflex arcs
Muscle spasms
Severe extensor rigidity
Tonic seizures
68
How long does it take to see clinical signs with strychnine toxicity?
Rapid onset - 10mins - 2hrs and rapid death
69
What clinical signs will you see with strychnine poisoning?
Mydriasis, stiffness, muscle twitching, hyperthermia, tonic seizures and opisthotonos,
70
How do animals die from strychnine poisoning?
Respiratory failure
71
How would you treat strychnine poisoning?
Decontaminate - emesis if not contraindicated, activated charcoal
Enhance renal excretion with ammonium chloride or methionine (if patient is not acidotic)
72
What do you want to avoid in strychnine toxic patients?
Bicarbonate or antacids in the lavage fluid - will cause them to absorb it faster
Opioids, phenothiazines, neuromuscular blockers and dissociative anesthetics
73
What is the most important thing to do with a strychnine patient?
KEEP IN A QUIET PLACE, avoid stimulation
74
What is the prognosis for strychnine toxic animals?
Reasonably good if alive, early and aggressive therapy for 24-72 hrs
75
Is Zinc phosphide a GUP or RUP?
RUP - restricted use pesticide
76
What is a grey/black powder, has a acetylene, garlic or dead fish odor and its stable when dry and decomposes in environment within 2 weeks
Zinc phosphide
77
What does zinc phosphide do when exposed to acid?
liberates phosphine gas
78
T/F zinc phosphide is relatively insoluble in water, phosphine liberation is slower in water, and the gas is toxic, flammable and a irritant
True
79
What is the acute toxicity of zinc phosphine due to?
the phosphine gas
80
What is the chronic toxicity of zinc phosphine due to?
Both zinc phosphine and phosphine gas
81
What enhances zinc phosphide toxicity?
Acid (gastric)
| Dogs have been reported to eat large amounts of it on an empty stomach (more alkaline) and survive
82
Hydrolysis and liberation of phosphine gas occurs at a pH of ___
4 or lower
83
Why would you not want to induce emesis on an animal that consumed zinc phosphide?
Its corrosive (GI irritant)
84
What is the MOA for zinc phosphide?
Exact mechanism unknown
Direct irritation of GI mucosa
Toxicity primarily due to phosphine
85
What effects does phosphine have?
May inhibit oxidative phosphorylation and cellular energy production, leading to cell death
increases oxygen radicals resulting in peroxidation and cell damage
86
How fast is the onset of clinical signs with zinc phosphide toxicity?
rapid (mins to hrs)
87
What clinical signs will you see with zinc phosphide?
anorexia, vomiting (hematemesis), abdominal pain and bloat in cattle, increase resp. CNS excitation, compulsive hyper motility (mad dog running), yelping, convulsions,
88
How will an animal die from zinc phosphide and how fast?
Death within 3-48 hrs due to tissue anoxia
89
How would you be able to tell an animal has zinc phosphide toxicity?
Acetylene, garlic or fishy odor to vomitus/GI content
Gastroenteritis (hemorrhagic)
Congestion of liver/kidneys/lungs
90
If you want to test for zinc phosphide and send samples to a lab, what should you do?
Send specimens in an airtight container and frozen ASAP. they could release gas!
91
You should be cautious when dealing with zinc phosphide toxicities because phosphine gas is easily liberated, what is the EPA safe limit exposure for 15 min?
1 ppm
| 8 hrs = 0.3ppm
92
What should you tell an owner that calls with a concern of pet ingesting zinc phosphide?
DO NOT MAKE THEM VOMIT. gas could escape and affect them.
| If pet vomits in the car, make sure to open the windows and dispose of the vomit properly
93
How could you treat zinc phosphide toxicity?
No specific antidote
Decontaminate - Emesis (No H2O2)
Antacids - raise gastric pH above 4 with combination Mg.
Supportive care - IV fluids, trat seizures, hypomagnesemia, hypocalcemia,
94
What should you not use to make an animal vomit with zinc phosphide toxicity?
Hydrogen peroxide
95
What yellow toxin is used in livestock protection collar (LPC) for controlling coyotes preying on sheep and goats?
Fluoroacetate (compound 1080)
96
T/F Fluoroacetate is odorless, water soluble, relatively insoluble in organic solvents, its an irritant, and degraded by soil microorganisms and plant enzymes
True
97
How are fluoroacetate compounds absorbed?
GI tract, lung or open wound
98
Will you see fluoroacetate relay (secondary) toxicosis?
Yes, because doses to kill rodents are soo high and doses for dogs are so low
99
Fluoroacetate is metabolized to monofluoroacetic acid by hydrolysis, is this toxic?
Yes, its also toxic
100
What is the mechanics of action for Fluoroacetate?
condenses with oxaloacetate to fluorocitrate and competes with regular citrate as a substrate for aconite in the TCA cycle
101
What does fluoroacetate cause?
- Slowing of the TCA cycle and decreasing cellular respiratory and energy
- Build up of citrate - citrate toxicity binds Ca_
- inhibits enzymes (glutamate, PFK)
102
How long before you start seeing clinic signs when an animal has fluoroacetate toxicity?
Clinical signs are rapid in onset - 30 mins- 2-4 hrs
103
What signs will you see on a dog?
CNS stimulation and GI signs
GI - V/D, Urination, hyperirritability, tenesmus
CNS - running in a straight line, barking, helping, opisthotonos
Hyperthermia, mydriasis, coma
Death within 2-12 hrs
104
What signs will you see on horses, cattle, sheep and goats with fluoroacetate toxicity?
Cardiac signs predominate in horses!
heart failure, staggering, arrhythmias
Colic, terminal convulsions, death
105
What signs will you see on cats and pigs with fluoroacetate toxicity?
BOTH CNS sings and cardiac sings in cats
Bradycardia/arrhythmias
vocalization, hyperesthesia, hypothermia
106
What lab findings will you see on an animal with fluoroacetate?
Elevated citrate levels
Hyperglycemia
Metabolic acidosis
Low ionized Ca+
107
How would you treat an animal with fluoroacetate toxicity?
```
Onset rapid, may not get to treat
Emesis?
Activated charcoal
Glyceryl monoacetate (IV/IM)
Acetic acid/ethanol (PO)
Acetamide/dextrose
```
108
T/F Metaldehyde is a restricted use pesticide, used as fuel camp stoves outside of NA, Soluble in water, and products can release Metaldehyde for 10-14 days under moderately moist conditions
False - its poorly soluble in water
109
What animals are susceptible to metaldehyde poising? which ones are most sensitive? which are more likely to ingest?
Dogs, cats, livestock and horses are susceptible
Cats are more sensitive
Dogs more likely to ingest
110
Hedgehogs are considered an endangered species in the UK why?
because they feed on slugs/snails and they are being killed with metaldehyde
111
What routes could metaldehyde be absorbed? which one is more toxic?
Inhalation is more toxic
| Ingestion is more common
112
What occurs to metaldehyde in the gastric environment?
Undergoes acid hydrolysis to acetaldehyde
113
T/F metaldehyde is readily absorbed from the GI tract, both metaldehyde and acetaldehyde cross the BBB, and may undergo enterohepatic recirculation
True
114
Metaldehyde is metabolized in the liver by a microsomal enzyme (P450 enzymes), what could decrease the toxicity of metaldehyde?
Phenobarbital - enzyme inducer
115
Acetaldehyde is also metabolized by hepatic aldehyde dehydrogenase, what is it converted into?
CO2 and exhaled
116
What is the MOA of metaldehyde?
In mice, metaldehyde decreases brain GABA, norepinephrine and serotonin (5-HT) - may lead to seizures/CNS excitation,
117
What does metaldehyde cause?
GI irritation
Metabolic acidosis
CNS excitation lead to HYPERTHERMIA
118
What is the cause of death in animals with metaldehyde toxicity?
Respiratory failure
119
What may occur to dogs that survive the acute disease of metaldehyde?
Liver failure may develop (not reported in cats)
120
What clinical signs will you see on an animal with metaldehyde toxicity?
Acute neurotoxicosis/hyperthermia
"shake and bake"
Salivation, V/D.
Incordination, muscle tremors, hyperesthesia, convulsions, opisthotonos
121
What signs might you see in cats with metaldehyde toxicity?
Nystagmus, mydriasis
122
How would you treat an animal with metaldehyde toxicity?
```
Decontaminate - emesis (1-2 hrs)
Activated charcoal
Enemas
Fluid therapy
Mange hyperthermia
Phenobarbital - enzyme inducer
Methocarbamol (muscle relaxant)
```
123
How could you treat horses with metaldehyde toxicity?
Xylazine and acepromazine
