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toxins Flashcards

1
Q

what are our go to decontamination methods with cats

A

hydromorphone SQ
xylazine
dexdomitor IM

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2
Q

decontamination methods in dogs

A

apomorphine
clevor eye drops
hydrogen peroxide

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3
Q

you have a patient come in with toxin ingestion. what do you do

A

stabilize first. make sure they have good enough mentation to vomit. decontaminate in almost all cases

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4
Q

when do we not want to induce emesis

A

corrosive agents, neurologic patients that cant swallow
aspiration risk patients (ME)
>6hr post ingestion

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5
Q

after inducing emesis what next?

A

decontaminate with charcoal, gastric lavage, or enemas

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6
Q

when do we want to give fluids

A

only if they are hypovolemic. shocky. we do not “dilute” the toxins

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7
Q

what are multi organ target toxins

A

caffeine, chocolate= methylxanthines
NSAIDS
sago palms
wild mushrooms
xylitol

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8
Q

vomiting, tachycardic, agitation, trembling, seizures

A

methylxanthines

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9
Q

treatment for chocolate or caffeine

A

activated charcoal, EKG, +- lidocaine for tachys, +- ace for hyperactivity

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10
Q

MOA of NSAID toxicity

A

blocks COX1&2 in the GI mucosa and kidneys.

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11
Q

hematemesis, melena, PU/PD, decreased urine output, seizures

A

NSAID toxicity

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12
Q

treatment for NSAID tox

A

ulcer prevention
hypovolemic shock treatment
IV lipids

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13
Q

which toxins can carry a poor prognosis

A

NSAID if anuric renal failure
xylitol if hepatic failure

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14
Q

Petechiae, hypovolemic shock, icterus CS of what

A

hepatic injury

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15
Q

xylitol MOA

A

stimulates insulin secretion

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16
Q

what doses of xylitol causes hypoglycemia vs hepatic necrosis

A

hypoglycemia- 100 mg/kg
hepatic necrosis - 500 mg/kg

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17
Q

weakness, depression, seizures, +- hetechiae, hypovolemia, icterus

A

xylitol

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18
Q

treatment for xylitol

A

emergency seizure treatment with dextrose, +- liver support for hepatic injury

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19
Q

treatment for wild mushroom toxicity

A

liver support, decontaminate if possible, supportive care

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20
Q

what CS can we see from mushroom toxicity

A

GI, SLUDDE signs, Neuro, hepatic

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21
Q

when do you see cliical signs from sago palms

A

2-3 days after exposure

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22
Q

GI- melena, hypersalivation, injury and dysfunction to liver

A

sago palm

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23
Q

what are the target organs from sago palm

A

GIT, liver, CNS

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24
Q

primary neurotoxic substances

A

marijuana, SSRIs, rodenticides, pyrethroids

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25
when do you see clinical signs from marijuana
20-30 minutes and can last for days
26
what does a cat look like after weed ingestion
pace and wander around, disoriented, staring into space, aggression + other normal signs vomiting, urinary incontinence, jumpy
27
what are general CS from weed
vomiting, easily agitated, urinary incontinence, brady and hypothermic
28
treatment for weed
denign neglect +- emesis and intralipids if ate an insane amount
29
tachycardia, hyperthermia, mydriasis, absent menace, agitation, vocalization
SSRIs
30
MAO of SSRIs
extreme serotonin dump because serotonin reuptake is inhibited
31
treatment for SSRI toxicity
acepromazine sedation methocarbamol for tremors serotonin antagonist cyproheptadine PO or enema
32
when do you see CS post SSRI ingestion
1-12 hours post ingestion
33
clinical signs from rodenticides
green feces and vomitus, neurologic, anisocoria, nystagmus
34
when do CS signs start in rodenticides
24 hours post ingestion
35
MOA of rodenticides
couples the oxidative phosphoroylation pathway. No ATP to the brain
36
treatment for neurogenic rodenticides
supportive care, seizure control, intralipids, charcoal e8hr
37
what is a pyrethroid
insecticide/flea and tick control
38
who is most sensitive to pyrethroids
cats
39
MOA of pyrethroids
persistent cellular excitation
40
treatment for pyrethroids
bath, tremor and seizure management, intralipid therapy
41
treatment for tremors
methocarbamol
42
clinical signs of pyrethroids
hyperexcitability, tremors, seizures
43
signs of nephrotoxicity
Pu/PD, azotemia, acidemia, hyperkalemia, irregular EKG, hypertension
44
clinical signs of vitamin D tox
GI, renal, neuro
45
how to ddx vitamin D tox from other nephrotoxins
hypercalcemia seen with vit D from
46
what are our nephrotoxic ddx
vitamin D, grapes, ethylene glycol, lilies
47
treatment for vitamin D tox
cholestyramine. phosphate binders
48
MOA of grape tox
tartaric acid
49
grape treatment
supportive care, insulin, dextrose
50
what moves potassium into the cells and out of the blood
insulin
51
what to remember about ethylene glycol
there are two phases drunken phase and the renal injury phase
52
timing of clinical signs of ethylene glycol
1-6hrs neurotoxic 12-24hrs renal
53
lily clinical signs
renal, seizures
54
MOA of lily toxicity
proximal tubule damage and necrosis of the tubules
55
treatment for lily ingestion
bath, seizure management, monitor renal function
56
what to ddx lily tox from
vitamin D, rasins, ethylene glycol
57
clinical signs of anticoagulent rodenticides
multicompartment hemorrhage. green feces,
58
treatment for recent ingestion of anticoag rodenticides
decontamination and vitamin K
59
general treatment for anticoag rodenticides
plasma, vitamin K, blood if hypovolemic, activity restriction
60
what to remember about tylenol toxicosis
could also have codeine in the formulation
61
CS of tylenol toxicosis
dyspnea, cyanosis, muddy mm, edema, dull mentation, jaundice
62
muddy mm, weakness, ADR, paw swelling
ddx acetaminophen
63
MOA of acetaminophen
toxic metabolites created in the minor pathways
64
treatment for acetaminophen
supportive care, liver supplements

ER (3 decks)

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