Tox 2 Flashcards
Gossypol- tox type
Cardiac/hematopoietic
Gossypol- source
Cotton seed
Gossypol- MOA
Binds and inhibits dehydrogenase in oxidative stress response and less energy and protein production; chelates iron causing anemia and reduces protein availability
Gossypol- species
Non-ruminants more sensitive, horses less effected
Gossypol- CS
Anemia, general weight loss, weakness; end result- myocardial necrosis and CHF
Gossypol- dx
History, chemical analysis
Gossypol- necropsy lesions
Cardiac necrosis, edematous, pale, mottled heart with vaculoization
Gossypol- tx
High protein diet with vitamin A, iron, lysine
Blister beetle- toxic agent
Cantharidin
Cantharidin- species effected
Horses
Cantharidin- lethal dose
6-250 beetles
Cantharidin- tox type
Heart and GI
Cantharidin- MOA
Inhibition of protein phosphatases leading to cardiac toxicity, mucosal irritant
Cantharidin- CS
Colic, PU, diaphragm contraction with heartbeat, severe iritation/ulceration of epithelia, cardiac toxicity
Cantharidin- dx
Presence of bugs; ulceration of MM; labs: hypocalcemia, increased BUN; cardiac necrosis
Cantharidin- tx
GI decontamination and protection (sucralfate), antibiotics
What is the most common toxicity site
Kidney- proximal convoluted tubule
Why is the proximal convoluted tubule most susceptible to toxicity
p450 and cysteine conjugation of B-lyase- leads to bioactivation of metabolites which cause damage; loose epithelium allows compounds to enter cells; increased anion, cation, metal transport can lead to accumulation and ischemic injury.
Describe acute kidney injury (AKI)
Decreased GFR, renal azotemia from damage to tubule/GFR/vasculature
AKI- CS
V, GI bleed, PUPD leading to olig/anuria
Chronic renal failure (CRF)- describe
Related to secondary compensatory changes in response to initial injury
CRF- CS
edema, hypocalcemia, PTH activity, reduced RBC count
Ethylene glycol- tox type
Renal, CNS
Ethylene glycol- MOA
Metabolites made by alcohol dehydrogenase: glycolic acid- acidosis; glyoxylic acid- CNS; oxalate- binds Ca to cause renal damage via calcium oxalate