Toxicology and misc. pharmacology

Question 1

What is the antidote for amitraz toxicity?

Answer 1

Atipamezole or yohimbine

Question 2

What are the antidotes for organophosphate toxicity?

Answer 2

Atropine or pralidoxime

Extra note: Pralidoxime reactivated cholinesterase which has become inactivated by organophosphates.

Question 3

What drug can be used in the management of SSRI and Baclofen toxicity?

Answer 3

Cyproheptadine

Question 4

What is the antidote for digoxin toxicity, what other toxicity could this be used for?

Answer 4

Digoxin immune FAB which can also be usef in Bufo toad toxicity

Question 5

What drug is used in the management of permethrin, metaldehyde and styricine toxicity?

Answer 5

Methocarbamol

Question 6

What non anti-coagulant rodenticides are there to be aware of

Answer 6

Bromethalin
Phosphides
Cholecalciferol

Question 7

What is the MoA of bromethalin toxicity?

Answer 7

Uncoupling of oxidative phosphorylation in the liver and brain. The Na/KATPase pump fails leading to intracellular odema.

Question 8

How is bromethalin toxicity treated

Answer 8

Emesis and administration of AC
Otherwise supportive aimed at controlloing ICP

Question 9

What is the MoA of phosphide rodenticides?

Answer 9

Phosphine gas is liberated from the solid form in the presence of moisture (e.g. GI tract) it is then corrosive

Question 10

How is phosphide rodenticide toxicity treated?

Answer 10

Emesis and AC are the main things to do but the gas is a risk to human health so this needs to be performed in a well ventillated area with appropriate precautions taken. Otherwise it is supportive care.

Question 11

How should you approach the management of a suspected rodenticide toxicity?

Answer 11

Emesis and AC can still be used.
PT can be taken at 36 - 48 hours post-ingestion (this is the T 1/2 of VII)
Treat with vitamin K if this is prolonged for a time dependent on the generation of anti-coagulant (7d for first gen, 30 days for second gen).

Question 12

What is the MoA of pyrethroid toxicity? Why does this affect cats more commonly than dogs?

Answer 12

Pyrethroids cause prolonged sodium conduction in the CNS which has the result of increaseing AcH release. This therefore can cause GI signs and CNS (tremoring).

Question 13

What is the treatment of pyrethroid toxicity?

Answer 13

Topical decontamination
Methocarbamol +/- benzodiazapines
Supportive care.

Question 14

What is the MoA of organophosphate toxicity? What are the clinical signs?

Answer 14

Competetive inhibition of acetylxholine esterase results in Ach activation of neurons.

Clinical signs can be remembered with ‘SLUDGE-M’
Salivation, lacrimation, urination, defecation, gastroenteritis, emesis, miosis

Question 15

What is the MoA of metaldehyde toxicity?

Answer 15

Reduced CNS GABA

Question 16

What are the major consequences of CCB overdose?

Answer 16

Vasodilation (may result in reflex tachycardia) and bradycardia which results from effects on L-type calcium channels on the AVN.

Question 17

What are the treatment options for CCB overdose?

Answer 17

Need to consider electrolyte monitoring, IV calcium can be given if significant cardiac effects are seen. Intralipid and high dose insulin therapy have also been described.

Question 18

What is the MoA of cyprohepatdine?

Answer 18

It is a H1 antagonist but also has serotonin antagonistic properties.

Question 19

What drug may be contraindicated in the management of serotonin syndrome?

Answer 19

Benzodiazapines

Question 20

What are the clinical effects of TCAs?

Answer 20

These inhibit the re-uptake of nEP, serotonin and dopamine. It can also activate muscariniic and H1 receptors and block sodium and potassium channels so effects can include cardiac toxicosis through inhibition of Na channels, neurologic signs, anticholinergic signs and hypoglycaemia.

Question 21

How long after NSAID toxicity might AKI occur?

Answer 21

Full clinical effects can take 48 - 72 hours to occur but if nephrotoxicity does not occur within 3 - 5 days then AKI is not likely to occur.

Question 22

What are the main effects of amphetamine toxicity and its management? N.B that cocaine is similar.

Answer 22

amphetamines stimulate nEP, dopamine and serotoning.
Cardiovascular effects are therefore possible along with CNS stimulatory effects.

Specific treatments include ACP, chlorpromazine and cyproheptadine (if serotonin syndrome occurs)

Question 23

What are the main clinical signs of mnarijuhana intoxication? How is this treated.

Answer 23

Hypothermia, anlgesia, cataplexy and locomotor suppression. Urine drippling and incontinance can also occur. Mostly supporitve therapy but intralipids can also be given.

Question 24

How does lilly toxicity progress

Answer 24

It has a biphasic toxicity so in the first 6 - 12 hours salivation and vomiting are the clincial signs. After 12 hours renal failure will ensue and may be accompanied by CNS signs.

Question 25

What is the mechanism of cycad palm toxicity?

Answer 25

Azoxyglycosides within the plant are hydrolysed by intestinal flora to aglycone which will result in fulminant hepatic failure.

Question 26

What is the mechanism of toxicity of rhododendrons?

Answer 26

Grayanotoxin binds to sodium channels thus prolonging depolarisation of the CNS. This can result in CNS signs (seizures), positive inotropy and cardiac arrest as well as arrythmias.

Question 27

What is the mechanism of toxicity of castor beans?

Answer 27

Castor beans contain ricin which inactivated ribosomal RNA.

Question 28

What is the clinical presentation of castor been toicity?

Answer 28

Initially can pesent with severe HGE followed by leukop[enia, haemolysis, renal failure and CNS signs.

Question 29

What is the mechanism of toxicity of allium species?

Answer 29

They contain sulfoxides which are broken down into N-porpyl disulfide which results in oxidative RBC damage.