Toxicology

Question 1

What is the antidote to ropinirole?

Answer 1

(Metoclopramide)

Question 2

What are the emetic options for cats?

Answer 2

(Hydromorphone (SQ), xylazine (SQ or IM), and dexmedetomidine (IM); dex is the superior choice)

Question 3

What are the emetic options for dogs?

Answer 3

(Apomorphine and ropinirole/Clevor)

Question 4

Should you stabilize a patient first or make them vomit first?

Answer 4

(Stabilize)

Question 5

When should you not induce emesis?

Answer 5

(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)

Question 6

When is gastric lavage necessary?

Answer 6

(Comatose patients or large ingestions cases where emesis was unsuccessful)

Question 7

What is the point of giving activated charcoal?

Answer 7

(Binds toxins to prevent hepatic recirculation)

Question 8

What gastrointestinal sign is most common after ingestion of methylxanthines (caffeine, theobromine, theophylline)?

Answer 8

(Vomiting)

Question 9

Methylxanthines will cause tachycardia/bradycardia (choose) and arrhythmias.

Answer 9

(Tachycardia and tachyarrhythmias)

Question 10

Are methylxanthines uppers or downers in animals?

Answer 10

(Uppers → hyperactivity, restlessness, agitation, trembling, seizures)

Question 11

When do signs typically occur post methylxanthine ingestion?

Answer 11

(1-4 hours post ingestion)

Question 12

For a case of severe methylxanthine toxicity, what drugs would you use for management of the following possible signs?

• Tachyarrhythmias and hypertension
• Hyperactivity
• Seizures

Answer 12

• Tachyarrhythmias and hypertension (Propranolol and lidocaine)
• Hyperactivity (Acepromazine, hefty doses)
• Seizures (Diazepam/midazolam)

Question 13

For the following organ systems, give the clinical signs that NSAID toxicity can cause associated with them:

• GI
• Renal
• Neurologic
• Cardiovascular

Answer 13

• 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)

Question 14

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?

Answer 14

(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))

Question 15

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?

Answer 15

(It can be related to the severe hypoglycemia xylitol induces or from hepatic encephalopathy once the liver is toast)

Question 16

What does treatment for a patient in the hypoglycemic xylitol dose range entail?

Answer 16

(Dextrose CRI or boluses and monitoring BG)

Question 17

What does treatment for a patient in the hepatic necrosis xylitol dose range entail?

Answer 17

(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)

Question 18

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)

Answer 18

(All of them, renal signs more consistent with more dangerous mushrooms not available in the US but you never know)

Question 19

What is the primary treatment for mushroom toxicity?

Answer 19

(Decontamination when possible and supportive care depending on the organ system affected)

Question 20

What organ systems are targeted by Sago/Cycad Palms?

Answer 20

(GI (melena, hypersalivation, V/D), hepatic (jaundice, PU/PD, hepatic encephalopathy), and CNS (seizures, dull to obtunded mentation, ataxia, CP deficits)

Question 21

What is the primary target organ of marijuana/THC/CBD and what signs will be shown?

Answer 21

(CNS → lethargy, somnolence to hyperesthetic, ataxia, agitation, seizures, comatose)

Question 22

How quickly can marijuana signs crop up after exposure and how long can they last?

Answer 22

(C/S can begin as soon as 20-30 minutes post exposure and last 2-3 days)

Question 23

When is emesis and activated charcoal indicated with marijuana toxicity?

Answer 23

(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))

Question 24

What treatment can improve a marijuana toxicity patient in 30 mins to an hour if rapidly administered?

Answer 24

(Intralipids)

Question 25

What is the primary target organ of SSRIs/MAOIs and what signs will be shown in toxicity cases?

Answer 25

(CNS → agitation, vocalization, disorientation, mydriasis, tremors, seizures, absent menace; also can cause cardiovascular signs (usually tachy but sometimes brady) and hyperthermia)

Question 26

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?

Answer 26

(Ask if they are extended release, signs may not develop for 12 hours post ingestion)

Question 27

What is the purpose of giving an SSRI/MAOI toxicity case cyproheptadine?

Answer 27

(It is a serotonin antagonist → prevents serotonin syndrome; also give ace for sedation and methocarbamol for tremors)

Question 28

Which type of rodenticide is neurotoxic?

Answer 28

(Bromethalin, will cause weakness, ataxia, tremors, dull mentation, hyperexcitability, circling, hyperesthesia, seizures, head-pressing, and paralysis)

Question 29

There is no antidote for neurotoxic rodenticides like there are for anticoagulant rodenticides so what does treatment for neurotoxic rodenticides entail?

Answer 29

(Activated charcoal (q8h for up to 2 days for larger ingestions), intralipid therapy, seizure control, and mannitol or hypertonic saline for cerebral edema)

Question 30

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?

Answer 30

(Will see increased CK, signs of kidney injury subsequent to excess CK, and dehydration)

Question 31

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?

Answer 31

(A bath)

Question 32

What is the primary target organ that is damaged in cases of vitamin D toxicosis and what signs might you see?

Answer 32

(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)

Question 33

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?

Answer 33

(Decreases excretion and increases gut absorption of calcium and phosphorus)

Question 34

What are the treatments for vitamin D toxicosis?

Answer 34

(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)

Question 35

What is considered the most likely toxic principle associated with grapes/raisins?

Answer 35

(Tartaric acid)

Question 36

What is the primary target organ that is damaged in cases of grape/raisin toxicity?

Answer 36

(Kidney → PU/PD; can see some secondary GI effects)

Question 37

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?

Answer 37

(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)

Question 38

What are the treatment options for ethylene glycol toxicity?

Answer 38

(4MP and ethanol; also can include supportive therapies, urinary output, weight monitoring, hemodialysis, and peritoneal dialysis)

Question 39

How does lily toxicosis lead to kidney tubule obstruction?

Answer 39

(Lilies cause proximal tubule damage and necrosis of the epithelial cells leads to sloughing into the lumen and obstruction)

Question 40

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?

Answer 40

(Signs of bleeding may not be seen for up to a week after exposure)

Question 41

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.

Answer 41

(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)

Question 42

What is the primary sign that indicates acetaminophen toxicity?

Answer 42

(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)

Question 43

What might you see on CBC in a case of acetaminophen toxicity?

Answer 43

(Regenerative anemia, Heinz bodies, anisocytosis, polychromasia, and spherocytes)