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Small A. Emergency > Toxicology > Flashcards

Toxicology Flashcards

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1
Q

What is the antidote to ropinirole?

A

(Metoclopramide)

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2
Q

What are the emetic options for cats?

A

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

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3
Q

What are the emetic options for dogs?

A

(Apomorphine and ropinirole/Clevor)

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4
Q

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

A

(Stabilize)

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5
Q

When should you not induce emesis?

A

(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)

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6
Q

When is gastric lavage necessary?

A

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

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7
Q

What is the point of giving activated charcoal?

A

(Binds toxins to prevent hepatic recirculation)

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8
Q

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

A

(Vomiting)

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9
Q

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

A

(Tachycardia and tachyarrhythmias)

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10
Q

Are methylxanthines uppers or downers in animals?

A

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

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11
Q

When do signs typically occur post methylxanthine ingestion?

A

(1-4 hours post ingestion)

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12
Q

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

  • Tachyarrhythmias and hypertension
  • Hyperactivity
  • Seizures
A
  • Tachyarrhythmias and hypertension (Propranolol and lidocaine)
  • Hyperactivity (Acepromazine, hefty doses)
  • Seizures (Diazepam/midazolam)
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13
Q

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

  • GI
  • Renal
  • Neurologic
  • Cardiovascular
A
  • 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)
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14
Q

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?

A

(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))

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15
Q

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?

A

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

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16
Q

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

A

(Dextrose CRI or boluses and monitoring BG)

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17
Q

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

A

(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)

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18
Q

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)
A

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

19
Q

What is the primary treatment for mushroom toxicity?

A

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

20
Q

What organ systems are targeted by Sago/Cycad Palms?

A

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

21
Q

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

A

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

22
Q

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

A

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

23
Q

When is emesis and activated charcoal indicated with marijuana toxicity?

A

(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))

24
Q

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

A

(Intralipids)

25
Q

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

A

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

26
Q

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?

A

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

27
Q

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

A

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

28
Q

Which type of rodenticide is neurotoxic?

A

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

29
Q

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

A

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

30
Q

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?

A

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

31
Q

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

(A bath)

32
Q

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

A

(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)

33
Q

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?

A

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

34
Q

What are the treatments for vitamin D toxicosis?

A

(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)

35
Q

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

A

(Tartaric acid)

36
Q

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

A

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

37
Q

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?

A

(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)

38
Q

What are the treatment options for ethylene glycol toxicity?

A

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

39
Q

How does lily toxicosis lead to kidney tubule obstruction?

A

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

40
Q

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?

A

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

41
Q

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.

A

(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)

42
Q

What is the primary sign that indicates acetaminophen toxicity?

A

(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)

43
Q

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

A

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

Small A. Emergency (16 decks)

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