TOXICOLOGY 2 Flashcards
(23 cards)
on ethylene glycol toxicity: what is/are the toxic components?
-what type of crystals may form?
-not EG in itself: only its metabolites
-calcium oxalate crystals
on ethylene glycol toxicity: what are the 3 chronological phases of toxicity?
1 GI n neuro signs
2 apparent resolution
3renal failure
on ethylene glycol toxicity: describe challenges to testing for ethylene glycol levels/toxicity?
-patient can appear recovered between 12-24hrs
on ethylene glycol toxicity:
-blood changes in the early stage?
-blood changes in the late stage?
on ethylene glycol toxicity:
-what are these?
on ethylene glycol toxicity: what is a kidney sign that can be seen on ultrasound?
-medullary rim sign due to calcium oxalate crystal deposition
on ethylene glycol toxicity: -what is the antidote?
-how does it work?
-ethanol
-fomepizole
-ADH will instead break down the ethanol, and ethylene glycol is excreted unchanged
[therefore only effective in early changes]
on ethylene glycol toxicity: -what is the tx for late stages?
-prognosis?
-supportive for AKI
-horrible prognosis
on paracetamol toxicity: what are 3 reasons that cats are more susceptible?
-toxic dose is much lower in cats
-cats cannot do glucuronidation pathway, so more liekly to end up with NAPQI
-3: more prone to red cell oxidative damage
what is NAPQI?
the toxic component of paracetamol
[shows up when other forms of metabolism are overwhelmed due to toxicity, ends up using cytochrome pathway]
on paracetamol toxicity: what is the body’s normal defence mechanism against NAPQI
binds w glutathione
on paracetamol toxicity: some blood cell cahnges signs of NAPQI toxicity?
-oxidative injury
-necrosis n hepatotoxicity
-oxidative damage to haeme in RBCs
on paracetamol toxicity: -what are some (3) clinical signs?
-facial swelling-cats
-brown/muddy mucous membranes
-respiratory distress
on paracetamol toxicity: what is the antidote?
-how does it work?
N-acetylcysteine
-binds to NAPQI to form inactive metabolites
on anticoagulant rodenticide toxicity: this affects vitamin K dependant coagulation factor. which are those?
2,7,9,10
on anticoagulant rodenticide toxicity: MOA?
-depletion of vitamin K epoxide reductase
on anticoagulant rodenticide toxicity: bloodwork will show a greater increase in PT relative to the increase in aPTT. why?
because out of the vitamin K-dependant coag factors, factor VII has the shortest half life
on anticoagulant rodenticide toxicity: what are some common clinical signs?
-bleeding into body cavities::::
-hypovolaemic shock
[look for free fluid]
on NSAID toxicity: -two major susceptible organs to damage?
-how is this related to COX1 & COX2?
1-GI ulceration/perforation
2- kidney toxicity
-drug wants to be selective to only COX2 but often also has COX1 suppression. COX1 has protective gastric effects and afferent arteriolar vasodialation to maintain GFR
on NSAID toxicity:
-describe treatment(4 things)
-which patients should get GI decontamination: symptomatic or asymptomatic patients?
-fluids
-GI protectants
-monitor renal
-GI decontaminants in asymptomatic
on permethrin toxicity:
-what is permethrin?
-toxic to which animals?
-active ingredient in some ectoparasite drugs
-toxic to cats
on permethrin toxicity: what are some clinical signs of permethrin toxicity?
-muscle tremors
-seizures
-hypersalivation
on permethrin toxicity:
describe the treatment
-decontamination (clip fur around site, bathing)
-ILE
-diazepam for seizures, methocarbamol for muscle tremors
