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toxicology lecture 2 Flashcards

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
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
31
what are the toxic doses for dogs and cats for acetaminophen toxicity
dogs 75 to 100 mg/kg | cats 10 mg/kg
32
what are the clinical signs of acetaminophen toxicity
``` 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
what is the treatment of acetaminophen toxicity
decontamination transfusion oxygen and fluid therapy
34
what are the drugs used for acetaminophen toxicity
N-acetylcysteine cimetidine ascobric acid
35
what does N-acetylcysteine do
it increases synthesis and replenishes cellular gluathione stores by providing a glutathione precursor
36
what does cimetidine do
slowed metabolism of acetaminophen into toxic metabolites (not for cats)
37
what does ascorbic acid do
it reduces the methemoglobin to hemoglobins
38
what are permethrins and pyrethroids
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
what is the mechanism of toxicity for permethrins and pyrethroids
dermal and GI absorption (ingestion and grooming) | -disruption of action potential -> repetitive firing of signals -> neurotoxicity -> affects CNS and PNS
40
what is the clinical presentation of toxicity for permethrins and pyrethroids
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
what are the clinical signs of toxicity for permethrins and pyrethroids
mild to moderately | hypersalivation, mild tremors, hypersensitivity/ depression, GI signs, V/D
42
what are severe clinical signs of toxicity for permethrins and pyrethroids
disorientation, hyperthermia, muscle fasciculations, generalized tremors, seizures
43
what is the treatment for pyrethrin toxicity
decontamination and supportive care (fluid/oxygen) dermal exposure oral exposure medications - methocarbamol, diazepam/barbiturates
44
what is the prognosis of permethrins and pyrethroids
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
what is lily toxicitiy
can cause acute renal failure, we don't know why but it has to deal with renal tubular necrosis
46
what are the clinical signs of lily toxicity
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
what is the treatment for lily toxicity
``` no known antidote fluid therapy, supportive care, intensive monitoring GI Decontamination and fluid diuresis peritoneal dialysis (only treatment in anuric cats) ```
48
what is the prognosis of lily toxicity
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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