4.3 Household Toxicants Flashcards

1
Q

what are common food toxicants

A

chocolate/caffine, ethanol, grapes, hopps, macadamia nuts, onions, play dough, bread dough, xylitol

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2
Q

list some common examples of toxicants in the following classes:
1) OTC drugs
2) prescription drugs
3) recreational drugs
4) miscellaneous

A

1) OTC drugs: acetaminophen, NSAIDs (ibuprofen)
2) prescription drugs: apomorphine, baytril, ivermectin, metronidazole, opioids
3) recreational drugs: marijuana, cocaine, methamphetamine
4) miscellaneous: ethylene glycol (antifreeze)

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3
Q

what is the name for the toxins produced by coffee and chocolate

A

methylxanthines

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4
Q

what is the MOA of methylxanthines (chocolate and caffeine)

Note, there is 2

A

increased intracellular calcium
- phosphorylates proteins in Ca transport

release of catecholamines

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5
Q

peak caffeine absorption occurs in ____ and peak chocolate absorption occurs in ____

A

< 1h; 10h

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6
Q

how is chocolate and caffeine metabolized and excreted

A

metabolized in liver; excreted in enterohepatic circulation; minor reabsorption in kidney

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7
Q

what are some clinical signs of chocolate and caffeine toxicity (methylxanthines)

A

vomiting, diarrhea, tachycardia, arrhythmia, heart failure, excitability, tremors, ataxia, seizures, rep. failure

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8
Q

what is the name of the toxicant produced by chocolate

A

theobromine

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9
Q

methylxanthines can be divided into (2)

A

chocolate (theobromine) and caffine

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10
Q

how do we treat methylxanthine (theobromine, caffeine) toxiciy

A
  • supportive care (treat seizures and arrhythmias)
  • decontamination (emesis, lavage)
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11
Q

onions, leeks, garlic and chives belong to what species

A

allium spp.

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12
Q

what is the MOA of allium spp. toxicity (6)

A

oxidative damage:
- Hb oxidation
- Heinz bodies
- eccentrocytes
- RBC fragility causing hemolysis
- Na/K pump damage causing hemolysis
- methemoglobinemia causing hypoxia

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13
Q

is garlic or onion more toxic

A

garlic

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14
Q

would you expect to see a regenerative or non-regenerative anemia in a patient with onion/garlic toxicosis

A

regenerative, due to hemolysis

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15
Q

what are the clinical signs of allium spp. toxicosis

A
  • anemia
  • depression
  • pale mm
  • tachypnea
  • tachycardia
  • pigmenturia (due to hemolysis)
  • vomiting
  • diarrhea
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16
Q

what can onion be used to treat in cats

A

primary erythrocytosis (a myeloproliferative neoplasm)

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17
Q

T/F grape and raisin toxicity is not always dose-dependent

A

T

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18
Q

what is the MOA of grape and raisin toxicity

A

exact MOA unknown but tartaric acid suspected

causes ARF: acute tubular necrosis, renal failure, death

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19
Q

what are the clinical signs of grape/raisin toxicity and what is consistent

A

vomiting (consistent), diarrhea, anorexia, lethargy

20
Q

how is grape/raisin toxicity diagnosed

A

chemistry: azotemia, elevated K/P/Ca

urinalysis: casts/sediments, isothenuria, proteinuria, glycosuria

21
Q

how do we treat grape/raisin toxicity

A
  • perfuse kidneys (IV fluids and diuretic)
  • minimize absorption (emesis, charcoal)
22
Q

what is the MOA of macadamia nut toxicity

A

unknown

23
Q

what are the clinical signs of macadamia nut toxicity (5)

A

vomiting, depression, ataxia, hyperthermia, tremors

24
Q

dogs typically recover from macadamia nut toxicity after how long

A

1-2 days

25
Q

what are some potential sources of xylitol

A

low levels in fruits and veggies; gum, candy, toothpaste, nutritional supplements

26
Q

what is the MOA of xylitol

A

hypoglycemia and liver necrosis

ATP depletion and oxidative damage from ROS

27
Q

what are some signs of xylitol toxicity

A

vomiting, weakness, collapse, ataxia, tremors, seizures, elevated liver parameters, prolonged coagulation

28
Q

what is one of the top calls to pet poison control centres

A

ibuprofen (NSAID) overdose

29
Q

what are some clinical signs of NSAID toxicity

A

vomiting, diarrhea, inappetence, hematemesis, hematochezia, GI ulceration, perforation, peritonitis, anorexia, oliguria/anuria, uremic breath, decreased mentation, seizures, respiratory depression

30
Q

how do we treat NSAID toxicity

A

fluids, reduce absorption, surgery for GI perforations, transfusion for blood loss, omeprazole/misoprostol

31
Q

what is the MOA of marijuana toxicity

A

THC is a CB1 and CB2 receptor agonist:

CB1: psychoactive
CB2: immune system -> anti-inflammatory

32
Q

where does THC go once it is absorbed

A

distributed to fat, brain and liver, before being eliminated in the bile (90%) and urine (10%) as well as undergoing enterohepatic circulation

33
Q

what are some signs of THC toxicity

A

mydriasis, vomiting, weakness, ataxia, depression, coma, urinary incontinence

34
Q

T/F a human on-site test is effective for diagnosing marijuana toxicity in pets

A

F; unreliable in animals

35
Q

how do we diagnose marijuana toxicity

A

GC-MS

36
Q

what is the MOA of methamphetamine toxicity

A

release catecholamines; inhibit monoamine oxidase; may impact dopamine and serotonin receptors

37
Q

how is methamphetamine metabolized and excreted

A

metabolized in liver, excreted in urine

38
Q

T/F methamphetamine is commonly combined with other substances, such as caffeine and phenylpropanolamine

A

T

39
Q

what are the clinical signs of methamphetamine toxicosis

A

tachycardia, hyperactivity, tremors, seizures, myoglobinuric nephrosis, hyperthermia

40
Q

how do we diagnose methamphetamine toxicosis

A

chromatography, history, clinical signs

41
Q

how do we treat methamphetamine toxicosis

A

supportive care, manage neurologic signs, prevent further absorption, cool body temperature

42
Q

how is cocaine metabolized and excreted

A

metabolized in liver, excreted in urine

43
Q

T/F cocaine can cross the BBB

A

T

44
Q

T/F cocaine is commonly contaminated with caffeine, lidocaine and amphetamines

A

T

45
Q

what are the clinical signs of cocaine toxicity

A

hyperactivity, seizures, hyperthermia, tremors, mydriasis, vomiting, tachycardia

46
Q

_______________ is a test we can use to evaluate toxicity of what 4 recreational drugs

A

QuickScreen; phencyclidine, AMP, THCA, cocaine metabolite