Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
146 Cards in this Set
- Front
- Back
Other DD's for OP toxicity signs?
|
Carbamates, nicotine
|
|
Is nicotine an acid or a base?
|
It is a base
|
|
how to we trap nicotine in the urine to excrete it more quickly
|
We acidify the urine with ammonium chloride
|
|
why do we see muscarinic signs with nicotine toxicity?
|
The nicotinic receptors are stimulated, and then in turn, stimulate the muscarinic receptors
|
|
What is the difference between a low dose and a high dose of nicotine?
|
At a low dose you will see NM excitement. A a high dose, you will see NM blockade
|
|
What are the clinical signs you would see with nicotine toxicity?
|
Tremors, parasympathetic signs. NM stimulation is transient, as we will see a secondary depression
|
|
What do carbamates, op's, and nicotine all have in common?
|
They are all CNS stimulants, but ALSO have parasympathetic effects. Other CNS stimulants do not have that
|
|
What 3 toxic agents cause CNS stimulation and parasympathetic effects?
|
CON! (as in they are trying to con you into thinking they are only stimulants) Carbamate, OP's, Nicotine
|
|
What insecticide is the most likely cause of tremors?
|
Pyrethrins and pyrethroids
|
|
With pyrethroid toxicity, are there parasympathetic signs?
|
No
|
|
What drug is found to be best when treating tremors?
|
Methocarbymol
|
|
what do we find pyrethrin in?
|
Topical flea/tick treatments and chrysanthemum
|
|
Of the two types of pyrethroids, which one is more toxic and why?
|
Type 2 is more toxic because it contains alpha cyanomoiety
|
|
Advantage is a flea product. What is added to it to make it 'advantix'
|
pyrethrin
|
|
What specie is most sensitive to pyrethrins?
|
Fish and some birds
|
|
What do we add to pyrethrins to slow down its metabolism (and therefore making it more toxic)
|
Piperonyl butoxide
|
|
What it piperonyl butoxide added to?
|
Pyrethrins
|
|
What is the MOA of pyrethrins?
|
It opens Na channels, so you get a repeated firing of the neurons in the CNS. This causes tremors. After time, it becomes desensitized and you get a CNS depression
|
|
What toxins act on sodium channels and keep them open?
|
Pyrethrins and chlorinated hydrocarbons that are DDT (Diphenyl aliphatics)
|
|
What is the MOA of Diphenyl aliphatics
|
These are organic chlorines, and act by keeping the sodium channels open. You gget repeated firing of neurons in the CNS, then subsequent CNS depression
|
|
what is a type one allergic reaction?
|
It is associated with histamine release and is mediated by IgE
|
|
What are other DD's for tremors in dogs?
|
Tremorgenic mycotoxins such as moldy compost
|
|
What was rotenone originally used for?
|
To be put on arrowheads to kill fish, and as a pesticide in water to kill fish
|
|
What animal is resistant to rotenone?
|
Chickens
|
|
What animal is most sensitive to rotenone?
|
Fish
|
|
What form of rotenone has the highest toxicity?
|
The emulsified form
|
|
MOA of rotenone
|
It inhibits NADH from becoming NAD. We need NAD for the electron transport chain. Without NAD, we are inhibiting this chain, therefore decreaing energy production.
|
|
Does rotenone respond well to enzyme inhibitors?
|
Yes, it does. Rotenone undergoes lethal synthesis, so we want to slow down metabolism
|
|
What are the clinical signs associated with rotenone toxicity?
|
GIT (vomiting) and neurologic (ataxia, CNS depression, tremors and possible seizures and Hypoglycemia!
|
|
If you see hypoglycemia and CNS depression, what toxic agent can you assume is the culprit?
|
Rotenone
|
|
how is the prognosis with rotenone
|
Excellent
|
|
In what species is amitraz used?
|
Swine and cattle and dogs
tick collars |
|
In what species is amitraz never used?
|
Horses, as it causes GI stasis
|
|
What is the MOa of amitraz?
|
it is an alpha 2 agonist - so it works similar to xylazine and domitor
|
|
Where is amitraz metabolized?
|
Liver
|
|
what are the clinical signs of amitraz?
|
CNS depression due to alpha 2 stimulation, and potentially seizures due to alpha 1 stimulation. Bradycardia, vasodilation
|
|
Antidote to amitraz?
|
Alpha 2 antagonists such as yohimbine or antisedan
|
|
What toxin is in the preventick collars?
|
Amitraz
|
|
With DEET, what are the neurological signs?
|
Tremors, excitement, ataxia and seizures. It causes CNS excitement
|
|
What is the specimen of choice with DEET?
|
Stomach contents
|
|
what animals should not be treated with Selemectin?
|
Collies and dogs with white feet
|
|
MOA of macrocyclic lactones
|
Ivermectin is a macocyclic lactone --> it is a GABA agonist. therefore you get CNS depression
|
|
Antidote for ivermectin?
|
Picrotoxin
|
|
What is the "sink" organ of chorinated hydrocarbons
|
fat
|
|
What is the specimen of choice with organochlorine toxicosis?
|
Brain
|
|
How does DDT work?
|
It keeps the Na channels open, causing a rapid continuous firing of the nuerons in the CNS
|
|
what is the major issue with organochlorines?
|
They persist in the environment for a very long time and can bio accumulate in food chains
|
|
If something has a high risk factor does it have a lot of risk associated with it?
|
No, there isnt a lot of risk associated with it
|
|
How does lindane work?
|
GABA inhibitor
|
|
How do cyclodienes work?
|
Don't know
|
|
Do we see stimulation or depression of the cns with organochlorines?
|
stimulation
|
|
"cattle walking backwards" think...
|
organochlorines
|
|
Antidote for organochlorines?
|
Nope
|
|
What are 2 causes of bounding pulses?
|
Anemia and shock
|
|
what are 3 causes of anemia
|
Destruction of RBS's, decreased production of RBC's, blood loss
|
|
What causes heinz bodies?
|
Oxidation of RBC's
|
|
What does oxidation of iron in RBC's cause?
|
Methemoglobinemia
|
|
What does napthelene smell like?
|
Moth balls
|
|
What rbc changes will be seen with nathalene toxicity?
|
methemoglobinemia and heinz body formation
|
|
What are the clinical signs of napthelene toxicity?
|
GI (salivation, vomiting, diarrhea, etc) RBC destruction, and secondary renal/liver injury
|
|
What inseticide is known for skin lesions?
|
D-Limonene
|
|
What is a good first line antibiotic to treat skin lesions associated with D limonene?
|
Ampicillin
|
|
What causes the sepsis related to d-limonene toxicity
|
The skin lesions
|
|
D Dimer vs FDP
|
D dimer shows breakdown product that has already formed a thrombus. FDP can be breakdown product before a thrombus forms. D Dimer is a more reliable test for DIC
|
|
When do we usually see D-limonene toxicity
|
When dog products are used on cats.
|
|
With which toxin can we see reactions that resemble erythema multiforme? (necrosis with inflammation) or toxic epidermal necrosis (necrosis with minimal inflammation)
|
D-Limonene
|
|
SIRS
|
Systemic inflammatory response syndrome
|
|
What are the sings of SIRS?
|
Increase or decrease in heart rate, dec in resps, dec in wbc's, toxic changes, left shift, severe inflammation. If you have 2 of these things, its considered SIRS
|
|
How is the progosis in animals with D-Limonene toxicity?
|
It is good in most cases unless they have skin lesions. The worse the lesion, the worse the prognosis
|
|
How does warfarin work?
|
it inhibits epoxide reductase, and therefore doesnt allow K dependant clotting factors to activate
|
|
Clotting factors that are K dependant
|
2, 7, 9, 10
|
|
With Warfarin toxicity, which clotting text would you want to run first?
|
PT as it tests factor 7, and 7 has the shortest half life, so if there is a decrease in it, you will notice a prolonged time with this factor most quickly
|
|
Is warfarin a first or second generation anticoagulant?
|
First
|
|
Pindone and chlorophacinone are what generation?
|
First generation anticoagulant
|
|
Anticoagulants aer derivitives of either -
|
hydroxycoumarin or indandione
|
|
What is the the toxic difference between first and second generation anticoagulants?
|
First genreation need multiple doses to see clinical signs, where second generation need just one dose
|
|
what animal is most sensitive to anticoagulants?
|
Pigs, then dogs
|
|
What factors will decrease toxicity of anticoagulants?
|
Pregnancy and enzyme inducers
|
|
in the second phase of blood loss in a dog, what is the PVC and TS?
|
The TS drops, but the PCV will remain
|
|
What kind of vitamin K doe we use in anticoagulant toxicosis
|
K1 only!!
|
|
what factors does frozen plasma lack?
|
Factors 5 and 8
|
|
Bromethalin is not effective in what species?
|
Guinea pigs
|
|
Is there bait shyness with bromethalin
|
nope. It is green and tasty
|
|
Where are the highest distributions of bromethalin?
|
Brain and fat
|
|
How is bromethalin affected by enzyme inducers?
|
It is metabolized and becomes more toxic. Lethal sythnesis
|
|
MOA of bromethalin
|
Uncoupling of oxidative phosphorylation, resulting in loss of ATP
|
|
How does bromethalin cause cerebral damage?
|
Via lipid peroxidation
|
|
What are the clinical signs of bromethalin stoxiciy?
|
Acute CNS signs. Tremors, hyper excitability, running fits
|
|
What 2 toxins cause running fits?
|
Fluoroacetate and bromethalin
|
|
What 2 toxins cause tremors and seizures that are precipitated by light or noise?
|
Bromethalin and strychnine
|
|
Do you see depression or exicitability in Bromethalin toxicity?
|
Excitability
|
|
Bromethalin toxicity causes signs that are typical of lesions in which section of the spine?
|
T3 - L3
|
|
Antidote for bromethalin?
|
Nope
|
|
What is compound 1080?
|
Fluroacetate
|
|
What is fluroacetate used for?
|
To deter wolves from eating sheep
|
|
What animal is most sensitive to fluroacetate?
|
Dogs
|
|
What animal is most resistant to furoacetate?
|
Birds
|
|
What animals are very sesitive to strychnine?
|
Farm animals
|
|
MOA of fluroacetate
|
Tightly binds to aconitase inhibiting the TCA cycle. This inhibits energy production
|
|
What could you look for in bloodwork if you suspect fluroacetate?
|
Increase in citrate (as it cant be used in tca cycle while aconitase is bound) and hypocalcemia (due to citrate binding calcium)
|
|
What are the clinical signs of fluroacetate?
|
CNS stimulation, running in circles, seizures, then coma
|
|
concerning fluroacetate, what is the general cause of death?
|
cardiac or from convulsions/resp failure
|
|
In addition to activated charcoal and emetics, what is something else we can give for decontamination with fluroacetate?
|
Limewater. It will precipitate out the fluroacetate, thereby preventing absorption
|
|
Antidote for fluroacetate
|
ethanol 50% and acetic acid 5%.
|
|
What is the prognosis of fluroacetate toxicosis
|
grave
|
|
Is strychnine an acid or a base?
|
Base
|
|
What would we use to change the pH of urine to trap strychnine and excrete it faster?
|
Ammonuim chloride
|
|
Who is resistant to strychnine?
|
Poultry
|
|
how long does it take for the body to excrete the lethal dose of strychnine?
|
24 hours
|
|
MOA of strychnine
|
Glycine inhibitor. Glycine is an inhibitor that works at the level of the spine. This is why we see the spine "stretching" so much
|
|
what specimens do we sample from animals with strychnine toxicity?
|
urine in live animals, stomach contents in dead animals
|
|
what drug is best for seizures concerning strychnine toxicity?
|
Methocarbomol
|
|
What are the clinical signs of strychnine toxicosis?
|
ellicitable seizures, opisthotonos
|
|
What can a dog get into to cause vitamin D toxicosis?
|
Psoriasis creams, certain plants, cholecalceferol
|
|
what are the top rule outs for hypercalcemia?
|
Renal failure, hyperparathyroidism, Vit D toxicity, neoplasia
|
|
Which animals are most sensitive to Vit D toxicity?
|
Young animals, and cats
|
|
Can vitamine D be excreted in milk?
|
Yes
|
|
What will you see with a vit d toxicity on blood work?
|
Hypercalcemia, and hyperphosphotemia
|
|
At what point do we see mineralization of tissues??
|
When calcium x phosphorus >70
|
|
Clinical signs of Vit D toxicty
|
effects aer due to hypercalcemia on cellular membranes and soft tissue mineralization. - GIT, anorexia, **bloody diarrhea** , hyper acidity and ulceration, renal failure, PU/PD, arrythmias, coma and death
|
|
Why do we see a hyper gastric acidity and ulceration in cases of vit d toxicity?
|
Hyper calcemia directly stimulates gastrin secretion (gastric acid)
|
|
Why with Vit D toxicty do we see hyponatremia and hypokalemia?
|
It competes for reabsorption in tubules with calcium. The body would try to reabsorb as much calcium as possible and would pee out the na and k
|
|
Treatment of Vit D toxicosis
|
Pamidronate, saline, low calcium diet
|
|
what toxin smells like rotten fish
|
Zinc phosphide
|
|
What animal is most senstive to zinc phosphide?
|
Birds
|
|
What system in the body, enhances toxicity of zinc phosphide?
|
Gastric Secretion in the GIT
|
|
Do we cause emesis in animals with zinc phosphide toxicity?
|
Yes, it reduces absorption even though zinc phosphide can be corrosive
|
|
how is zinc phosphide eliminated from the body
|
Most of it is eliminated in gaseous form from the lungs.
|
|
Are people effected by animals that have zinc phosphide toxicity?
|
yes. As the toxin is breathed out, people can breathe it in if the are handling the pet
|
|
MOA of zinc phosphide
|
interupts oxidative phosphorylation. Inhibits energy production. Ellicitable seizures. Also, corrosive nature of zinc phosphide results in vomiting blood. Barin, heart, lungs, liver, blood vessels all are effected.
|
|
Running in circles
|
Fluracetate, zinc phosphide
|
|
Specimen used in zinc phosphide?
|
stomach contents, vomitus. maybe see methemoglobinemia in blood
|
|
Acetylene odor?
|
Dead fish smell
|
|
CS of zinc phosphide toxicity
|
Nonspecific - GI, pulmonary, excitement of the cns and rapid death
|
|
Antidote for zinc phosphide
|
Nope
|
|
What are metaldehydes mixed with to create a snail killer?
|
Carbamates
|
|
how do metaldehydes react to enzyme inducers?
|
Quite well. Decreases toxicity
|
|
MOA of metaldehyde toxicosis
|
Causes direct GI irritation and CNS excitement by decreasing GABA, norepi, and serotonin which will lead to seizures
|
|
Clinical signs of metaldehyde
|
Convulsive seizures, ataxia, hyperthermia, etc "Shake and bake"
|
|
Why do we give b12 in cns animals?
|
It is thought to be neuroprotective
|
|
With which 4 toxins, do we see entero hepatic circulation?
|
Chlorinated hydrocarbon, D-Limonene, Bromethalin, Vit D
|
|
What the MOA of Rotenone?
|
Stops NAD from changing into NADH --> loss of ATP
|
|
Which 2 toxins have a MOA of uncoupling phosphorylation?
|
Zinc Phosphate and Bromethalin (also PCP but we didnt go over it yet)
|
|
What 2 toxins undergo lethal synthesis
|
Bromethaline and rotenone (not including OP's bc not all of them do)
|
|
To which 3 toxins are chicken resistant?
|
Strychnine, rotenone, and fluroacetate
|
|
Which 4 toxins have ellicitable seizures?
|
Strychnine, Zinco Phosphide, bromethalin, metaldehyde
|