Toxicology Flashcards
(98 cards)
1
Q
Why is hydrogen peroxide not recommended for decontamination in dogs & cats?
A
Cats - you will kill them
Dogs - causes significant erosion of esophagus & stomach
2
Q
What is the route of administration for apomorphine?
A
IV injection (often compounded)
3
Q
What is the route of administration of Clevor?
A
Eye drops
4
Q
An aggressive dog presents to your clinic for a known toxin ingestion and you want to induce emesis. Are you going to use Apomorphine or Clevor? (Assuming you have both options)
A
Apomorphine because w/ Clevor you have to get close to the animal’s face to administer the eye drops & often have to re-dose
5
Q
Does Apomorphine have an antidote? If so, what is it?
A
No, but Cerenia usually works well
6
Q
Does Clevor have an antidote? If so, what is it?
A
Yes, antidote is metoclopramide (dopamine antagonist)
7
Q
In what species would you use Hydromorphone, Xylazine, or Dexmedetomidine to induce emesis?
A
Cats
8
Q
What is the reversal agent for Dexmedetomidine?
A
Antisedan
9
Q
What is the reversal agent for Xylazine?
A
Yohimbine
10
Q
What is the reversal agent for Hydromorphone (or Apomorphine)?
A
Naloxone
11
Q
When is inducing emesis indicated?
A
- If ingestion has occurred within the last 2-3 hours
- If there is a risk for foreign body obstruction
- Ingestion of substances with delayed release
Most toxins warrant emesis unless otherwise noted
12
Q
When is inducing emesis contraindicated?
A
- Caustic/corrosive agents (cleaners/chemicals)
- > 6hr post-ingestion
- Predisposed to aspiration
- Neurologic & cannot swallow well/unconscious
13
Q
What other products (besides those for inducing emesis) can be used to aid in decontamination?
A
- Adsorbents (activated charcoal +/- Sorbitol or Cholestyramine
- Gastric lavage
- Enemas
14
Q
Which adsorbent can be administered as a single dose for most intoxicants?
A
Activated charcoal
15
Q
What can be added to activated charcoal to promote rapid transit of the toxin through the gut?
A
Sorbitol
16
Q
Describe how Cholestyramine works
A
- Used for specific intoxicants
- Binds bile acids in intestine thereby preventing re-absorption of intoxicants from the gut
17
Q
When is gastric lavage recommended for decontamination?
A
For comatose patients or large ingestions of toxins where emesis was attempted but unsuccessful
18
Q
T/F: In most cases of toxicant ingestions, fluids are utilized to create diuresis thereby getting it out of the body faster.
A
F, there are some specific indications for fluid therapy, but mostly it is used to take care of subclinical dehydration
19
Q
What is/are the main target organs of methylxanthines (caffeine, theobromine (chocolate), theophylline)?
A
Mutli-organ targets (specifically GI, cardiovascular, & neurologic)
20
Q
How long after ingestion of methylxanthines are clinical signs typically present?
A
1-4 hours post-ingestion
21
Q
What is the treatment plan for methylxanthine ingestion?
A
- AC w/ sorbitol + EKG + fluids if hospo indicated for 6-12h (if severe, repeat doses of AC & still give fluids + EKG for 24-48h)
- Tachyarrhythmia & hypertension control w/ propranolol, lidocaine
- Hyperactivity controlled with Ace
- Seizure control w/ diazepam & midazolam
22
Q
What is the prognosis for methylxanthine ingestion?
A
Excellent for most patients, esp. if appropriate decontamination
23
Q
What target organs are affected by NSAID toxicosis?
A
Multi-organ targets (specifically GI, renal, neuro, & cardiovascular if severe enough; can see hepatic damage/failure too)
24
Q
T/F: Hepatic damage/failure from NSAID toxicosis is idiosyncratic and not dose dependent.
A
T
25
T/F: Development of gastric ulcers are more common w/ NSAID toxicosis, and not as common with chronic administration
F, gastric ulceration more common with chronic, appropriate use of NSAIDs
26
You have a patient who ingested a toxic dose of Carprofen and you want to give them something for ulcer prevention and support just to be safe. They are doing okay clinically after general treatment. Are you going to prescribe Omeprazole or Sucralfate?
Omeprazole; Sucralfate only effective if you KNOW there is ulceration present.
27
Describe a general treatment plan for NSAID toxicity
- Ulcer prevention & support
- Renal support (weight & urinary output monitoring, fluid support)
- Tx hypovolemic shock if present
- Intravenous lipids
- Can do blood purification techniques but $$$
28
What target organs are affected with xylitol toxicity?
Multi-organ targets, specifically neurologic (weakness, depression, tremors, ataxia) & hepatic/hematological
29
How long after ingestion of xylitol would you expect to see neurologic signs? What about hepatic/hematologic signs?
Neurologic - within 1 hour of ingestion
Hepatic/hematologic - can take up to 3 days post-ingestion
30
What is the emergency treatment (i.e. P is having seizures) for xylitol toxicity?
Dextrose 50% 0.25-0.5ml/kg IV (diluted 1:1 with saline)
31
What is the treatment plan for a patient with xylitol toxicity when hypoglycemia is present? What about if they ingested enough to be in the hepatic necrosis range (500mg/kg)?
Hypoglycemia range - Dextrose CRI (boluses as indicated), Central line or freestyle libre to monitor BG
Hepatic necrosis range - monitor & tx coagulopathy, supplements to support hepatic function, N-acetylcysteine
32
T/F: Mushroom toxicity can cause a variety of unexplainable acute clinical signs, but hepatotoxic mushrooms can have a worse prognosis as compared to other mushrooms.
T
33
For Sago/Cycad palm toxicity, which part of the plant is toxic & what organs are targeted?
1. All parts of plant are toxic
2. Targets the GIT, liver, & CNS
34
Sago/cycad palm ingestion can present diagnostic findings similar to what other toxic substance?
Xylitol (tx will be the same too - dextrose CRI w/ boluses as needed, hepatic support +/- monitoring for coagulopathy)
35
The prognosis for sago/cycad palm toxicity is highly variable, and is based on what 3 factors?
1. Amount of plant ingested
2. Time to presentation
3. Severity of clinical signs
36
Hops is becoming a more common intoxicant due to in-home brewing hobbies. What effect does this have on the body?
Causes malignant hyperthermia resulting in multi-organ failure
37
What is the primary target organ associated with marijuana/THC/CBD ingestion?
Neurologic - will appear jumpy/startle easily (hyperesthesia), ataxic, cats may pace/wander, stare into space, etc.
38
With marijuana/THC/CBD ingestion, is the patient more likely to be bradycardic or tachycardic? Are they more likely to be hypothermic or hyperthermic?
1. Bradycardic
2. Hypothermic
39
How soon will you see clinical signs of marijuana/THC/CBD ingestion & how long can they last?
Can begin as little as 20-30 minutes after ingestion & may last appx. 2-3 days
40
What is the treatment plan for MOST patients that have ingested small amounts of marijuana/THC/CBD?
Benign neglect (unless they are very clinical)
41
What is the treatment plan for patients who have ingested moderate to large amounts of marijuana/THC/CBD (even if they are minimally affected/asymptomatic)?
Emesis + activated charcoal w/ sorbitol & rapid utilization of intralipids
42
What is the primary target organ for SSRIs/MAO inhibitor toxicity?
Primarily neurologic (agitation, vocalization, disorientation, absent menace, etc.) but may also be tachycardic & hyperthermic
43
How long after ingestion would you see clinical signs of SSRI/MAO inhibitor toxicity?
1-2 hours after ingestion; ER/CR formulations may not develop signs until 12 hours after ingestion
44
What is the treatment plan for patients who have accidentally ingested SSRIs/MAO inhibitors?
- Sedate with acepromazine
- Methocarbamol for tremors
- Cyproheptadine (serotonin antagonist) or Chlorpromazine
45
What is the prognosis for toxicity associated with SSRI/MAO inhibitor ingestion?
Very good with supportive therapies
Clinical signs may take up to 2 days to resolve
46
Does the presence of green colored feces tell you if the rodenticide ingested was neurotoxic or anticoagulant?
No, both can present with green feces
47
Why is it important to identify the specific rodenticide that was ingested?
Because it will affect your treatment plan and the prognosis
48
What is the most common neurotoxic rodenticide?
Bromethalin
49
How early will you see clinical signs of neurotoxic rodenticide toxicity & how long has progression of clinical signs been reported?
Signs as early as 24 hours post-ingestion with progression of signs reported up to 2 weeks after
50
T/F: Neurotoxic rodenticides have an antidote available, but anticoagulant rodenticides do not.
F - other way around
51
Why might you give a dog with a known neurotoxic rodenticide ingestion Mannitol or hypertonic saline?
To control cerebral edema
52
What is the primary target organ of pyrethroids (permethrin)?
Neurologic (hyperexcitable, tremors, seizures)
53
Are dogs or cats more sensitive to pyrethroids?
Cats
54
How long after exposure to pyrethroids will you see clinical signs?
1-2 hours
55
An owner calls you because they have accidentally put K9 advantix on their cat. What do you recommend they do before coming to the hospital?
Bathe the cat quickly! Then bring to the hospital for treatment
56
In addition to getting the pyrethroid product off of the cat, what else is part of your treatment plan?
Tremor & seizure management (methocarbamol, anti-epileptics, +/- propofol), intralipid therapy, & supportive fluids as indicated
57
T/F: You do not have to be azotemic to have an AKI.
T
58
What is the mechanism of action of vitamin d toxicosis?
Cholecalciferol is converted to calcitriol in the kidneys which decreases Ca & P excretion while increasing gut absorption
59
Why might a patient with vitamin D toxicosis have an irregular EKG?
They are likely hyperkalemic from the kidney failure
60
What is the target organ for vitamin D toxicosis?
Kidneys
61
What treatments are indicated for vitamin D toxicosis?
- 0.9% saline to decrease Ca absorption in renal tubules
- Furosemide to increase Ca excretion at Loop of Henle
- Prednisone to promote renal excretion
- Phosphate binders to decrease GIT absorption
Will give you credit if you also said cholestyramine & even intralipid therapy if used early in course of disease
62
What does monitoring look like for patients with vitamin D toxicosis?
Monitor chemistry + lytes in asymptomatic patients q24h for 3-5 days. If hypercalcemia normalizes, then can taper off to a weekly then biweekly schedule for monitoring
63
What are possible sequelae of vitamin D toxicosis?
1. Metastatic calcification of tissues
2. Permanent renal injury
64
A patient ingested a low dose of vitamin D and presented with mild hypercalcemia. Like the good Dr. that you are, you performed prompt decontamination. What is this patient's prognosis?
Good
- Prognosis will be guarded at higher dosages & those patients with clinical signs
65
What is the mechanism of action of grapes/raisin toxicity?
Idiosyncratic toxicity
66
What is the most likely toxic principle associated with grape/raisin toxicity?
Tartaric acid
67
What is the target organ associated with grape/raisin toxicity?
Kidneys
68
Grapes/raisin ingestion produce similar findings to what other toxic substance?
Vitamin D
69
Grapes/raisin ingestion produces similar findings to vitamin D toxicosis EXCEPT for what?
Hypercalcemia less likely
70
What is the treatment plan for a clinical patient with grapes/raisin toxicosis?
- Fluid support
- Nausea control
- Urinary output monitoring
- Nutritional support
- Hemodialysis if oliguric or anuric
71
A patient presents to you for dribbling urine. What toxicoses are on your differential list?
1. Marijuana/THC/CBD
2. Ethylene glycol
72
In the first few hours of toxication, ethylene glycol toxicity can look like what other toxicity?
Marijuana/THC/CBD
Later, it presents very similar to grape/raisin & vitamin D toxicosis
73
Patients that have ingested ethylene glycol MUST receive the antidote within what time period or else their prognosis decreases signifcantly?
Need it within 6 hours of ingestion
74
What is the prognosis of ethylene glycol toxicosis?
- Guarded to good when interventions sought within 6 hours
- Grave if ingestion is 8-12 hours prior to presentation, clinical signs present, or larger ingestions
75
What is the treatment plan for ethylene glycol toxicosis?
- 4MP ($$$) or ethanol ($)
- Supportive therapies
- Urinary output & weight monitoring
- Hemodialysis & peritoneal dialysis
76
What is the primary target organ associated with lily toxicosis?
Renal
May also present with seizures
77
What parts of lilies are toxic?
All
78
What is the toxic principle of lilies?
Unknown
79
Lily toxicosis causes similar clinical findings as what other toxicoses?
Vitamin D toxicity (except hypercalcemia) & grapes/raisins
80
Why are Mannitol & Furosemide ineffective for treating lily toxicosis?
Lilies cause tubule obstruction from necrotic epithelial cells
81
What is the treatment plan for lily toxicosis?
- Bath (pollen exposure)
- Seizure management
- Fluids
- Peritoneal dialysis & hemodialysis
- Urinary output & weight monitoring
82
How long after anticoagulant rodenticide exposure can you see signs of bleeding?
Can take up to a week after exposure
83
With anticoagulant rodenticide toxicity, which factor is affected first?
Factor 7
84
List 5 common anticoagulants
1. Bromadiolone
2. Chlorophacinone
3. Difethialone
4. Brodifacoum
5. Warfarin
85
Prolonged PT/PTT that is greater than 2x the reference interval is most likely indicative of what?
Anticoagulant rodenticide toxicity
86
If there was a known recent ingestion of anticoagulant rodenticide, what is your treatment plan?
- Decontamination
- Oral Vitamin K for 14-30d.
87
You have a patient that got into anticoagulant rodenticide. Hemorrhage is present, but the patient is stable. Both PT & PTT are still prolonged. What is your treatment plan?
Plasma transfusion, vitamin K orally or SQ if P not eating, monitor for worsening bleeding
88
You have a patient with suspected anticoagulant rodenticide toxicity that is in hypovolemic shock. What do you do?
- Whole blood transfusion
- Vitamin K SQ until P able to eat
89
How long after discontinuation of Vitamin K should you recheck PT/PTT?
48-72 hours after discontinuation
90
Why is it important to check the ingredients when a patient is known to have ingested acetaminophen?
Some formulations contain codeine too, which would require treatment for 2 potential toxicities
91
Why does toxicity occur with acetaminophen ingestion (particularly in cats)?
Utilization of minor pathways creating toxic metabolites (limited glucuronidation pathways)
92
Why are patients with acetaminophen ingestion cyanotic?
Due to methemoglobinemia (patients present as dyspneic, dark/brown gums, weakness, facial & paw swelling w/in 4 hours)
93
What are 2 poor prognostic indicators associated with acetaminophen toxicosis?
1. Presence of methemoglobinemia
2. Presence of liver injury
94
What species of plants create oxalate crystals that are irritating to the GIT when ingested?
Dieffenbachia & Philodendron spp. (calla lily, peace lily, dumbcane, philodendrons)
95
T/F: Cats reportedly ingest amphetamine/ADHD medications more frequently than other medications.
T
96
What toxins are on your differential list when a patient has increased liver enzymes?
Sago palm, blue-green algae, xylitol, acetaminophen, aflatoxins, anti-fungals, amatoxic mushrooms, iron, & NSAIDs
97
What toxins are on your differential list for coagulopathies?
Vitamin K rodenticide, hepatotoxic substances, NSAIDs
98
What toxins are on your differential list for azotemia?
Lilies in cats, ethylene glycol, raisins/grapes, veterinary or human NSAIDs, aminoglycosides, cholecalciferol
