Toxicology Flashcards
What is the antidote to ropinirole?
(Metoclopramide)
What are the emetic options for cats?
(Hydromorphone (SQ), xylazine (SQ or IM), and dexmedetomidine (IM); dex is the superior choice)
What are the emetic options for dogs?
(Apomorphine and ropinirole/Clevor)
Should you stabilize a patient first or make them vomit first?
(Stabilize)
When should you not induce emesis?
(If the agent is caustic/corrosive, if it has been greater than 6 hours since ingestion, if the animal is predisposed to aspiration, and if the animal is neurologic with an inability to swallow well or unconsciousness)
When is gastric lavage necessary?
(Comatose patients or large ingestions cases where emesis was unsuccessful)
What is the point of giving activated charcoal?
(Binds toxins to prevent hepatic recirculation)
What gastrointestinal sign is most common after ingestion of methylxanthines (caffeine, theobromine, theophylline)?
(Vomiting)
Methylxanthines will cause tachycardia/bradycardia (choose) and arrhythmias.
(Tachycardia and tachyarrhythmias)
Are methylxanthines uppers or downers in animals?
(Uppers → hyperactivity, restlessness, agitation, trembling, seizures)
When do signs typically occur post methylxanthine ingestion?
(1-4 hours post ingestion)
For a case of severe methylxanthine toxicity, what drugs would you use for management of the following possible signs?
- Tachyarrhythmias and hypertension
- Hyperactivity
- Seizures
- Tachyarrhythmias and hypertension (Propranolol and lidocaine)
- Hyperactivity (Acepromazine, hefty doses)
- Seizures (Diazepam/midazolam)
For the following organ systems, give the clinical signs that NSAID toxicity can cause associated with them:
- GI
- Renal
- Neurologic
- Cardiovascular
- GI (Hematemesis, abdominal pain, melena)
- Renal (PU/PD early, decreased to absent urine output later, halitosis)
- Neurologic (Seizures, obtundation; associated with carprofen and ibuprofen specifically)
- Cardiovascular (Hypovolemic shock)
What are some drugs that can be used for ulcer prevention and support (i.e. there is already an ulcer and you want to keep it happy) associated with NSAID toxicity?
(Omeprazole (ulcer prevention), sucralfate (keeps current ulcers happy), and misoprostol (provides prostaglandins for GI healing but has ADEs of GI cramping/diarrhea so can make tx confusing))
In addition to hepatic/hematologic related clinical signs (pale gums, icterus, melena, petechiae, ecchymosis), xylitol toxicity causes neurologic signs (weakness, depression, tremors, ataxia, collapse, seizures); how does xylitol toxicity cause neurologic signs?
(It can be related to the severe hypoglycemia xylitol induces or from hepatic encephalopathy once the liver is toast)
What does treatment for a patient in the hypoglycemic xylitol dose range entail?
(Dextrose CRI or boluses and monitoring BG)
What does treatment for a patient in the hepatic necrosis xylitol dose range entail?
(Monitor/treat coagulopathy, support hepatic function with supplements (N-acetylcysteine in hospital, denamarin, SAM-e, milk thistle, vitamin E for at home), and will still be hypoglycemic so dextrose CRI/boluses and BG monitoring)
Which of the following organ systems and clinical signs pair appropriately with wild mushroom toxicity?
- GI (Hypersalivation, vomiting, diarrhea)
- Neurologic (Dull to comatose, ataxia, tremors, agitation, vocalization)
- Hepatic (Jaundice, signs of hepatic encephalopathy)
- Renal (Urinary incontinence, PU/PD)
(All of them, renal signs more consistent with more dangerous mushrooms not available in the US but you never know)
What is the primary treatment for mushroom toxicity?
(Decontamination when possible and supportive care depending on the organ system affected)
What organ systems are targeted by Sago/Cycad Palms?
(GI (melena, hypersalivation, V/D), hepatic (jaundice, PU/PD, hepatic encephalopathy), and CNS (seizures, dull to obtunded mentation, ataxia, CP deficits)
What is the primary target organ of marijuana/THC/CBD and what signs will be shown?
(CNS → lethargy, somnolence to hyperesthetic, ataxia, agitation, seizures, comatose)
How quickly can marijuana signs crop up after exposure and how long can they last?
(C/S can begin as soon as 20-30 minutes post exposure and last 2-3 days)
When is emesis and activated charcoal indicated with marijuana toxicity?
(When a moderate to large amount has been ingested and the patient is minimally affected (don’t want to make a comatose patient try to vomit))
What treatment can improve a marijuana toxicity patient in 30 mins to an hour if rapidly administered?
(Intralipids)
What is the primary target organ of SSRIs/MAOIs and what signs will be shown in toxicity cases?
(CNS → agitation, vocalization, disorientation, mydriasis, tremors, seizures, absent menace; also can cause cardiovascular signs (usually tachy but sometimes brady) and hyperthermia)
In cases of SSRI/MAOI toxicity, signs typically occur 1-2 hours after ingestion but what should you keep in mind if an owner comes to you with a torn up bottle of SSRIs and a dog that is totally fine?
(Ask if they are extended release, signs may not develop for 12 hours post ingestion)
What is the purpose of giving an SSRI/MAOI toxicity case cyproheptadine?
(It is a serotonin antagonist → prevents serotonin syndrome; also give ace for sedation and methocarbamol for tremors)
Which type of rodenticide is neurotoxic?
(Bromethalin, will cause weakness, ataxia, tremors, dull mentation, hyperexcitability, circling, hyperesthesia, seizures, head-pressing, and paralysis)
There is no antidote for neurotoxic rodenticides like there are for anticoagulant rodenticides so what does treatment for neurotoxic rodenticides entail?
(Activated charcoal (q8h for up to 2 days for larger ingestions), intralipid therapy, seizure control, and mannitol or hypertonic saline for cerebral edema)
Pyrethroid toxicity causes hyperexcitability, tremors, and seizures in cats within 1-2 hours of exposure and routine labs will be consistent with muscle trauma, what does that mean?
(Will see increased CK, signs of kidney injury subsequent to excess CK, and dehydration)
The treatment plan for pyrethroids include tremor and seizure management (methocarbamol, midazolam/diazepam, propofol, phenobarbital) and intralipid therapy works well, what is something you should suggest to the owner before they even leave the house when appropriate?
(A bath)
What is the primary target organ that is damaged in cases of vitamin D toxicosis and what signs might you see?
(Kidney → PU/PD early, oliguric/anuric later, halitosis, uremic ulcers, and secondary cardiac effects d/t electrolyte changes; may also see GI (V/D, melena, hematemesis, and abdominal pain) and neurologic (seizures, paresis) signs)
Cholecalciferol is converted into calcitriol in the kidneys which increases/decreases (choose) the excretion and increases/decreases (choose) the gut absorption of what two electrolytes?
(Decreases excretion and increases gut absorption of calcium and phosphorus)
What are the treatments for vitamin D toxicosis?
(Normal saline (decreases calcium absorption in renal tubules), furosemide (increases calcium excretion at the loop of henle), prednisone (promotes renal excretion); also intralipid therapy is useful early on and cholestyramine can be used at home)
What is considered the most likely toxic principle associated with grapes/raisins?
(Tartaric acid)
What is the primary target organ that is damaged in cases of grape/raisin toxicity?
(Kidney → PU/PD; can see some secondary GI effects)
Ethylene glycol toxicosis often presents with an acute neurologic phase with signs such as ataxia, blindness, disorientation, weakness, dull to comatose, and seizures, lots of people describe it as inebriation/drunk; this may be confused with what other toxicity?
(That good ol’ devils lettuce (I say having never smoked pot before 😂), want to differentiate because if you don’t tx ethylene glycol within 6 hours of ingestion, the prognosis is grave; may also have GI and renal signs)
What are the treatment options for ethylene glycol toxicity?
(4MP and ethanol; also can include supportive therapies, urinary output, weight monitoring, hemodialysis, and peritoneal dialysis)
How does lily toxicosis lead to kidney tubule obstruction?
(Lilies cause proximal tubule damage and necrosis of the epithelial cells leads to sloughing into the lumen and obstruction)
How long can it take for signs of bleeding (hematuria, dyspnea, lameness, lethargy, bruising, epistaxis, melena/hematochezia, distended abdomen, shock, muffled heart sounds) to be apparent in cases of anticoagulant rodenticide toxicity?
(Signs of bleeding may not be seen for up to a week after exposure)
How does the treatment for the following anticoagulant rodenticide patients differ → patient 1 is stable with signs of hemorrhage and prolonged PT/PTT times; patient 2 is in hypovolemic shock.
(Patient 1 → fresh frozen plasma, adm vitamin K PO or SQ, monitor for worsening of bleeding; patient 2 → whole blood transfusion, adm vitamin K SQ, monitor)
What is the primary sign that indicates acetaminophen toxicity?
(Cyanosis d/t methemoglobinemia, usually occurs within 4 hours of exposure, can also see dyspnea, dark/brown gums, weakness, facial and paw swelling, dull to obtunded mentation, seizures due to hypoglycemia, jaundice, and signs of hepatic encephalopathy)
What might you see on CBC in a case of acetaminophen toxicity?
(Regenerative anemia, Heinz bodies, anisocytosis, polychromasia, and spherocytes)
