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POD from G > 4.3 Household Toxicants > Flashcards

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

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

25
what are some potential sources of xylitol
low levels in fruits and veggies; gum, candy, toothpaste, nutritional supplements
26
what is the MOA of xylitol
hypoglycemia and liver necrosis ATP depletion and oxidative damage from ROS
27
what are some signs of xylitol toxicity
vomiting, weakness, collapse, ataxia, tremors, seizures, elevated liver parameters, prolonged coagulation
28
what is one of the top calls to pet poison control centres
ibuprofen (NSAID) overdose
29
what are some clinical signs of NSAID toxicity
vomiting, diarrhea, inappetence, hematemesis, hematochezia, GI ulceration, perforation, peritonitis, anorexia, oliguria/anuria, uremic breath, decreased mentation, seizures, respiratory depression
30
how do we treat NSAID toxicity
fluids, reduce absorption, surgery for GI perforations, transfusion for blood loss, omeprazole/misoprostol
31
what is the MOA of marijuana toxicity
THC is a CB1 and CB2 receptor agonist: CB1: psychoactive CB2: immune system -> anti-inflammatory
32
where does THC go once it is absorbed
distributed to fat, brain and liver, before being eliminated in the bile (90%) and urine (10%) as well as undergoing enterohepatic circulation
33
what are some signs of THC toxicity
mydriasis, vomiting, weakness, ataxia, depression, coma, urinary incontinence
34
T/F a human on-site test is effective for diagnosing marijuana toxicity in pets
F; unreliable in animals
35
how do we diagnose marijuana toxicity
GC-MS
36
what is the MOA of methamphetamine toxicity
release catecholamines; inhibit monoamine oxidase; may impact dopamine and serotonin receptors
37
how is methamphetamine metabolized and excreted
metabolized in liver, excreted in urine
38
T/F methamphetamine is commonly combined with other substances, such as caffeine and phenylpropanolamine
T
39
what are the clinical signs of methamphetamine toxicosis
tachycardia, hyperactivity, tremors, seizures, myoglobinuric nephrosis, hyperthermia
40
how do we diagnose methamphetamine toxicosis
chromatography, history, clinical signs
41
how do we treat methamphetamine toxicosis
supportive care, manage neurologic signs, prevent further absorption, cool body temperature
42
how is cocaine metabolized and excreted
metabolized in liver, excreted in urine
43
T/F cocaine can cross the BBB
T
44
T/F cocaine is commonly contaminated with caffeine, lidocaine and amphetamines
T
45
what are the clinical signs of cocaine toxicity
hyperactivity, seizures, hyperthermia, tremors, mydriasis, vomiting, tachycardia
46
_______________ is a test we can use to evaluate toxicity of what 4 recreational drugs
QuickScreen; phencyclidine, AMP, THCA, cocaine metabolite

POD from G (46 decks)

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