Final--New Material Flashcards
Name 4 conditions that are required in order for a mold to grow
1) aerobic conditions
2) feed moisture >14%
3) relative humidity >70%
4) temperature–warm
+/- plant damage
Definitive diagnosis of mycotoxicosis comes from identification of ______
the toxin
NOT the mold
Of the many toxin types, ___ is the most toxic and oncogenic of the aflatoxins
B1
What are the 3 outcomes of aflatoxin binding to cellular components?
1) oncogenesis (most potent natural hepatocarcinogen)
2) altered anabolic/catabolic processes (i.e. protein synthesis, inhibited lipid transport, and decreased glycogen)
3) immunosuppression
What are the two toxin types assoc. with Tricothecens? Which is more toxic?
1) DON (vomitoxin)
2) DAS (T-2) **more toxic
Which body system(s) are primarily impacted by Fumonisin and in which spp.?
Hepatic and neuro
Horses
**Equine leukoencephalomalacia (Moldy corn dz)
Fumonisin is assoc. with which type of food/feedstuffs?
corn, corn-based feeds
Citrinin & Ochratoxins primarily affect which body system? How? In which TYPES of animals does this most commonly occur?
Citrinin & Ochratoxins= KIDNEYS
Degeneration of proximal tubules–alters reabsorption
**MONOGASTRICS
Which toxin can cause early development of mammary tissue and red, swollen vulvas in Gilts? Also describe it’s MOA
Zearalenone–binds to estradiol 17-beta receptor and causes hyperestrogenism
Describe Fescue’s interactions at the following receptors and the response/outcome
1) D1 dopaminergic receptor
2) D2 dopaminergic recepot
1) Inhibition–> vasoconstriction
2) stimulation –> decreases prolactin secretion
4 clinical syndromes assoc. with fescue ingestion?
Summer slump
Fescue foot
Fat necrosis
Repro Disorders
Though they cause many of the same types of syndromes, what’s the primary difference between Ergotism and fescue?
Ergotism does NOT cause fat necrosis like fescue
Ergot= Claviceps spp.
A horse showing excessive salivation may have ingested which mycotoxin?
Slaframine
Describe the mechanism whereby NSAIDs can cause renal disease?
NSAIDs inhibit prostaglandins that are important for vasodilation–> decreased perfusion pressure to kidney –> ischemia
**NOT directly nephrotoxic
NSAIDs primarily cause coagulopathy via inhibition of?
Thromboxane A2 (TXA2) which comes from platelets and normally causes vasoconstriction and platelet aggregation
**remember the function of PGI2
For how long must you treat NSAID toxicity? Which NSAID has the longest tx time?
At least THREE HALF-LIVES
Naproxen (Aleve)–> 72hr half-life
Salicylates (Aspirin) primarily cause their clinical effect through which mechanism?
Uncoupling of oxidative phosphorylation
Most the clinical effects of Amphetamines are due to?
Stimulation of CNS and Sympathetic nervous system
Cocaine causes its clinical signs via which TWO mechanisms?
1) reuptake inhibitor (serotonin, dopamine, NE)
2) Blockage of voltage-gated Na channels
What is the main MOA of Tricyclic antidepressants (TCAs) and how do the CV signs differ from cociane or amphetamines
reuptake inhibitor (5-HT & NE) *also blocks alpha-1 and muscarinic*
causes tachycardia with HYPOTENSION due to alpha-blockade
The primary clinical sign assoc. with serotonin elevations in dogs? (Serotonin syndrome)
Tremors
Death from TCAs primarily occurs due to?
Cardiac failure