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Vocabulary-style flashcards covering the clinical progression, diagnosis, treatment components, and prognosis of Sago palm toxicity based on the lecture notes.
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Sago palm (Cycad family)
A plant toxic to all species (especially dogs) that targets the gastrointestinal system, the central nervous system (CNS), and the liver.
Early clinical signs of Sago palm toxicity (1−4h)
Severe gastrointestinal (GI) upset and lethargy, which can sometimes resolve completely before further symptoms develop.
Delayed clinical signs of Sago palm toxicity (2−3d)
Neurological signs (weakness, ataxia, tremors, seizures) and liver failure (icterus, abdominal pain, hemorrhage).
Labwork markers of Sago palm-induced liver failure
Hyperbilirubinemia, hypoalbuminemia, hypoglycemia, and prolonged clotting times (PT, PTT).
Treatment: Decontamination
Induction of emesis and administration of activated charcoal (AC) for 2−3 doses.
Hepatoprotectants for Sago palm toxicity
Medications including N-acetylcysteine and S-adenosylmethionine.
Methocarbamol
A treatment used to manage tremors associated with Sago palm poisoning.
Sago palm monitoring protocol
Monitoring liver enzymes q24h×3d, and addressing glucose and clotting times if hepatic necrosis occurs.
Sago palm seeds
The most poisonous part of the plant; just 1−2 seeds can kill a medium-size dog.
Prognosis for Sago palm liver failure
Poor to grave, with a mortality rate of 67% in dogs and possible long-term liver dysfunction.
Common source of Sago palm exposure
Though native to tropical areas, most exposure occurs from indoor ornamentals.