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Flashcards in toxicology lecture 2 Deck (48)
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1

what are the 4 rodenticide toxicities

1. warfarin
2. bromethalin
3.cholecalciferol (vitamine D3)
4. zinc phosphide

2

what are anticoagulant rodenticides

- they are Vit K antagonists (our body can recycle and reuse Vitamin K)
-interferes with the production of vitamin K dependent clotting factors in the liver

3

what is the lag period of the coagulation system when vitamin K is depleted

3-5 days between exposure and appearance of clinical signs

4

how long does is take to see clinical signs if vitamin K is depleted

about 3 days, because then all the stored of vitamin K will have been consumed

5

what is the 1st generation of anticoagulant rodenticide toxicity

warfarin base

6

what is warfarin base

-warfarin, diphacinone, pidone
-short acting anticoagulant
- depress clotting factors for about 7 to 10 days

7

what is the 2nd generation of anticoagulant rodenticide toxicity

coumarin base

8

what is a coumarin base

bromadiolone, brodifacoum, super-warfarin - greater potency and accumulation effects in the liver
-depressed clotting factos for approx a month

9

what are the LD50 values for bromadiolone (super-warfarin)

rats 1.125 mg/kg b.w.
mice 1.75 mg/kg b.w.
rabbits 1 mg/kg/ b.w.

10

what are the LD50 values for warfarin

rats 3mg/kg
mice 437 mg/kg
rabbits 800 mg/kg

11

what are the clinic signs of anticoagulant rodenticide toxicity

3- 5 days post ingestion =
1. intracavital bleeding (lungs and abd), melena, epistaxis etc.
2. lethargy, excercise tolerance, inappetence, pallor, dyspnea
3. sudden death - paricardium, cranium, thorax etc
4.mild thrombocytopenia (secondary to blood loss, do not interfere with platelet production or function
**check poo

12

what is the diagnosis of rodenticide toxicity

-prolongation of PT (prothrombin time) and greater than PTT (thromboplastin time) and development of CS

13

what is the treatment of rodenticide toxicity

antidote - vitamin K1
thoracocentesis

14

what is CNS rodenticide toxicity

bromethalin (fastra, tomcat)
decreases mitochronrial ATP production in brain and liver

15

in CNS rodenticide toxicity less than LD50 what are the paralytic signs and when do they start

1 -4 days
hind limb weakness, ataxia, tremors, loss of deep pain, decreased propriception

16

in CNS rodenticide toxicity more than LD50 what are the convulsant signs and when do they start

4 - 36 hrs
hyperthermia, seizures, hyperexcitability

17

what is calciferol rodenticide toxicity

cholecalciferol (vitamin D#)
-orhto-mouse-B-gone, quintox, rampage
-increase calcium absorption from food and bones -> soft tissues calcification, nephrosis, cardiac arrhythmia
-free calcium levels are high and lead to mieralization of blood vessels and tissues (organs) = system calcification

18

what are the clinical signs of calciferol rodenticide toxicity

12 - 36 hrs post ingestion
anorexia, vomiting, muscle weakness, PU/PD, arrhythmia, seizures, hypercalcemia

19

what treatment can be used for calciferol rodenticide toxicity

furosamide, prednisone, calcitonin (lowers the calcium level by excreting or slowing down)

20

what is zinc phosphide

- sweeneys toxic peanuts, ACME gopher killer pellets, mold guard
-forms phosphine gase -> interrupt mitochondria process -> cell death and cellular oxidative damage

21

what are the clinical signs of zinc phosphide

appears rapidly after ingestion
-vomiting, +/- hemorrhage, anorexia, deep/wheezy respirations, ataxia, and hypoxia
-hard to detect because it degrades rapidly

22

what are the treatment of zinc phosphide

sodium bicarbonate slows the hydrolysis into gas, induce vomit in a well ventilated area to prevent exposure

23

what is organophosphate and carbamate intoxication

-it inhibits acetylcholinesterase (AchE) and synatic cleft
AchE - is an enzyme that degrades the neurotrasmitter acetylcholine in the nervous system

24

what does having excessive Ach do in the synapse

it accumulates with overstimulates muscarinic and nicotinic receptors

25

what are the clinical signs of organophosphate and carbamate intoxication

V/D, urination, miosis, bronchospasm, bronchorrhea, lacrimation, salivation, bradycardia

26

what are the nicotinic signs of organophosphate and carbamate intoxication

muscle tremors, twitiching, weakness and paralysis

27

what the CNS signs of organophosphate and carbamate intoxication

seizures, and coma

28

what is the treatment of organophosphate and carbamate intoxication

-decomtamination
-supportive care (fluid and oxygen)
-atropine
-pralidoxime
-diazepram

29

what is acetaminophen toxicity

NSAID - 90% is metabolized by the sulfate and glucuronide pathways (liver and kidneys) -> nontoxic metabolites
5% is metabolized by NAPQI
-can be neutralized by bind with endogenous glutathione and then excretes it out

30

what should we know about cats and acetaminophen toxicity

they have reduced glucuronide metabolism and they are deficient in glutathione and less than 3% of acetaminophen in excreted