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toxicology lecture 2 Flashcards

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1
Q

what are the 4 rodenticide toxicities

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

what are anticoagulant rodenticides

A
  • 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
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3
Q

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

A

3-5 days between exposure and appearance of clinical signs

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4
Q

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

A

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

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5
Q

what is the 1st generation of anticoagulant rodenticide toxicity

A

warfarin base

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6
Q

what is warfarin base

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

what is the 2nd generation of anticoagulant rodenticide toxicity

A

coumarin base

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8
Q

what is a coumarin base

A

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

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9
Q

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

A

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

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10
Q

what are the LD50 values for warfarin

A

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

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11
Q

what are the clinic signs of anticoagulant rodenticide toxicity

A

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
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12
Q

what is the diagnosis of rodenticide toxicity

A

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

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13
Q

what is the treatment of rodenticide toxicity

A

antidote - vitamin K1

thoracocentesis

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14
Q

what is CNS rodenticide toxicity

A

bromethalin (fastra, tomcat)

decreases mitochronrial ATP production in brain and liver

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15
Q

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

A

1 -4 days

hind limb weakness, ataxia, tremors, loss of deep pain, decreased propriception

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16
Q

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

A

4 - 36 hrs

hyperthermia, seizures, hyperexcitability

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17
Q

what is calciferol rodenticide toxicity

A

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
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18
Q

what are the clinical signs of calciferol rodenticide toxicity

A

12 - 36 hrs post ingestion

anorexia, vomiting, muscle weakness, PU/PD, arrhythmia, seizures, hypercalcemia

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19
Q

what treatment can be used for calciferol rodenticide toxicity

A

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

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20
Q

what is zinc phosphide

A
  • sweeneys toxic peanuts, ACME gopher killer pellets, mold guard
  • forms phosphine gase -> interrupt mitochondria process -> cell death and cellular oxidative damage
21
Q

what are the clinical signs of zinc phosphide

A

appears rapidly after ingestion

  • vomiting, +/- hemorrhage, anorexia, deep/wheezy respirations, ataxia, and hypoxia
  • hard to detect because it degrades rapidly
22
Q

what are the treatment of zinc phosphide

A

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

23
Q

what is organophosphate and carbamate intoxication

A

-it inhibits acetylcholinesterase (AchE) and synatic cleft

AchE - is an enzyme that degrades the neurotrasmitter acetylcholine in the nervous system

24
Q

what does having excessive Ach do in the synapse

A

it accumulates with overstimulates muscarinic and nicotinic receptors

25
Q

what are the clinical signs of organophosphate and carbamate intoxication

A

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

26
Q

what are the nicotinic signs of organophosphate and carbamate intoxication

A

muscle tremors, twitiching, weakness and paralysis

27
Q

what the CNS signs of organophosphate and carbamate intoxication

A

seizures, and coma

28
Q

what is the treatment of organophosphate and carbamate intoxication

A
  • decomtamination
  • supportive care (fluid and oxygen)
  • atropine
  • pralidoxime
  • diazepram
29
Q

what is acetaminophen toxicity

A

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
Q

what should we know about cats and acetaminophen toxicity

A

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

31
Q

what are the toxic doses for dogs and cats for acetaminophen toxicity

A

dogs 75 to 100 mg/kg

cats 10 mg/kg

32
Q

what are the clinical signs of acetaminophen toxicity

A 
methemoglobinemia (cannot carry oxygen) 
-more than 200 mg/kg in dogs and 10 mg/kg in cats 
-brown/ muddy mm 
-resp signs - distress
hepatic dysfunction
renal failure
heinz body formation (cats)
33
Q

what is the treatment of acetaminophen toxicity

A

decontamination
transfusion
oxygen and fluid therapy

34
Q

what are the drugs used for acetaminophen toxicity

A

N-acetylcysteine
cimetidine
ascobric acid

35
Q

what does N-acetylcysteine do

A

it increases synthesis and replenishes cellular gluathione stores by providing a glutathione precursor

36
Q

what does cimetidine do

A

slowed metabolism of acetaminophen into toxic metabolites (not for cats)

37
Q

what does ascorbic acid do

A

it reduces the methemoglobin to hemoglobins

38
Q

what are permethrins and pyrethroids

A

insecticides frequently used in flea and tick meds
-extraction of chrysanthemom flowers
Pyrethroids are a deriative of pyrethrins - a more stable form which is more potent and toxic

39
Q

what is the mechanism of toxicity for permethrins and pyrethroids

A

dermal and GI absorption (ingestion and grooming)

-disruption of action potential -> repetitive firing of signals -> neurotoxicity -> affects CNS and PNS

40
Q

what is the clinical presentation of toxicity for permethrins and pyrethroids

A

within minutes/hours and up to 72 hours

  • no specific findings in usual bloodwork
  • few vet practices provide screening for presence of this toxicity
  • most pets have history of recent dermal application of an insecticide
41
Q

what are the clinical signs of toxicity for permethrins and pyrethroids

A

mild to moderately

hypersalivation, mild tremors, hypersensitivity/ depression, GI signs, V/D

42
Q

what are severe clinical signs of toxicity for permethrins and pyrethroids

A

disorientation, hyperthermia, muscle fasciculations, generalized tremors, seizures

43
Q

what is the treatment for pyrethrin toxicity

A

decontamination and supportive care (fluid/oxygen)
dermal exposure
oral exposure
medications - methocarbamol, diazepam/barbiturates

44
Q

what is the prognosis of permethrins and pyrethroids

A

excellent in general

  • fatal outcomes may occur (mostly in cats)
  • secondary brain injury may come from prolonged seizure activity/hyperthemia
  • severely overdosed (gave for dogs only to cats)
  • patient in which treatment and supportive care are withheld
45
Q

what is lily toxicitiy

A

can cause acute renal failure, we don’t know why but it has to deal with renal tubular necrosis

46
Q

what are the clinical signs of lily toxicity

A

lily induced gastritis within 2 hours can cause vomiting, anorexia, depression
uremia in approx 12 hours
acute renal faily in 24 to 72 hours
-polyuria,oliguria, anuria, depression, dehydration, enlarged/painful kidneys
-severe azotemia, elevated creatinine

47
Q

what is the treatment for lily toxicity

A 
no known antidote
fluid therapy, supportive care, intensive monitoring
GI Decontamination and fluid diuresis
peritoneal dialysis (only treatment in anuric cats)
48
Q

what is the prognosis of lily toxicity

A

ARF within 18 hours if treatment is delayed

death occurs approx 3 to 7 days without proper treatment

nursing vet tech (13 decks)

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