Toxicology Mechanism of Actions Flashcards
ionophore MOA
bind and transport cations down concentration gradients -> uncontrolled ion transport leading to electrolyte imbalances -> loss of ATP in mitochondria -> cell death -> necrosis
nitrate MOA
rumen microbes convert nitrate -> nitrite -> ammonia
nitrite oxidizes Fe2+ -> Fe3+ -> methemoglobin -> hypoxia
NPN MOA
urea -> ammonia -> neuro signs
ATP depletion?
Na ion intoxiation/water deprivation MOA
rapid rehydration -> edema -> increased intracranial pressure -> decreased perfusion -> ischemia/necrosis/PEM
sulfur MOA
converted to hydrogen sulfite by ruminal microbes -> inhibit cytochrome C oxidase -> decreased ATP -> PEM
mycotoxins MOA
protein synthesis inhibitors
tremorgenic mycotoxins cross BBB -> block glycine and cause presynaptic Ach release
methylxanthines (theobromine, caffeine) MOA
-increased intracellular Ca
-release of catecholamines
allium spp MOA
oxidative damage; disulfides, thiosulfate
Hb oxidation; heinz bodies, eccentrocytes
RBC + Na/K pump damage; hemolysis
methemoglobin; hypoxia
grape/raisin MOA
unknown. tartaric acid suspected
macadamia nut MOA
unknown
xylitol MOA
depletion of ATP -> oxidation damage from ROS
hypoglycemia -> liver necrosis
NSAID MOA
inhibition of COX enzymes -> decreased PG synthesis
marijuana MOA
CB1 and CB2 agonist
meth MOA
release catecholamines
inhibit monoamine esterase
lead MOA
gamma-aminolevulinic acid -> protoporphyrin
binds to RBCs and inhibits maturation = rubricytosis, basophilic stippling
copper MOA
hepatic injury / inflammation / fibrosis; RBC oxidation and hemolysis, hyperbilirubinemia, hyperbilirubinuria, nephrosis
iron MOA
oxidative stress (fenton reaction) -> lesions in GI and liver
mercury MOA
reduced protein synthesis, lipid peroxidation (ROS), crosses BBB causing neuronal degeneration