Rodenticides Flashcards
strychnine kinetics
rapid absorptions– Ka = 15 mins; metabolize via N-oxidation; excretion via the urine
strynchnine mech of ac?
competitive antagonism; imitates glycine and acts as an inhibitory neurotransmitter; intermittent convulsions; extensor rigidity;
treatment for strychnine?
sedation; activated charcoal; acidify the urine; KMNO4 (oxidizes strychnine in the gut)
anticoagulant rodenticide examples?
warfarin, 2nd gen–diphacinone, brodifacoum; coumadin, dicouporal, heparin
anticoag mech of ac?
inhibition of vit k epoxide reductase; decreases synthesis of clotting factors II, VII, IX, X
clinical manifestations of anticoag rodenticides?
massive bleeding
treatment of anticoag rodent?
vit K1, and blood transfusion
drug interactions of anticoags?
anticoags decrease vit K synthesis–> cannot take with sulfonamides, which kill the bacteria in your gut which makes vit K to begin with;
anticoags decrease protein binding–> cannot take with sulfonamides also, which displaces warfarin–>more warfarin available to cause harm
increases fat in diet
kinetics of anticoags?
2nd gen more strongly bound to proteins; 2nd gen has a much longer half life; all are well-absorbed, metabolized by hydroxylation
fluoroacetate mech of action?
replaces A-CoA in the Krebs cycle; inhibits aconitase; this blocks cell resp and subsequently E production
clinical manifestations of fluoroacetate?
convulsions; running fits; cardiac arrhythmia; also terminal anoxic convulsions
treatment of fluoroacetate?
sedation for convulsions; 2C fragment–>jumpstarts the krebs cycle; CaCl2–>required by heart to beat (prevents cardiac arrhythmia); Ca Ketoglutarate–> @C fragment
Postmortem clinical manifestations of fluoroacetate?
no liver damage; rigor mortis sets in quickly because energy is messed up
zinc phosphide subcellular target (mech of ac), and consequential target organs?
targets mitochondria–>liver and kidney contain lots of mito, so they are target organs;
zinc phosphide kinetics
rapidly absorbed
