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
Which drug may be helpful in treating serotonin syndrome and why?
Cyproheptadine; serotonin antagonist
Which pathway of metabolism of acetaminophen is assoc. with formation of toxic metabolite? What’s the name of the metabolite?
Metabolism by cytochrome P450 creates NAPQI
Normally, the toxic effect of NAPQI are mediated by?
Glutathione conjugation
Primary system affected by acetaminophen
1) dogs
2) cats
1) liver
2) hematologic (RBCs)
How does interpretation of an elevated ALT differ between dogs and cats
It’s more significant in cats bc it has a short half-life…so elevations typically mean ongoing damage
A specific antidote for acetaminophen toxicity and it’s MOA?
N-acetylcysteine (NAC)
replenishes glutathione & binds NAPQI
How can Glucagon and Insulin be used for treatment of Ca channel blocker intoxication
Both of these work to increases cAMP levels which stimulates release of intracellular Ca from the SR
What are the main cardio effects seen with Ca channel blockers? (2)
What do you expect to happen to serum Ca levels?
1) bradycardia
2) AV block (2nd & 3rd degree)
**Ca level remains normal
Baclofen is a ______ and is most life-threatening when it affects which body system?
Muscle relaxant
Respiratory (paralysis= death..need ventilator)
What two hematologic changes might you expect to see on a blood smear with lead toxicity
Basophilic stippling (disrupted heme synthesis)
Nucleated RBCs
Oral administration of what can help to decontaminate the GI tract of lead by inhibiting its absorption
Magnesium sulfate (MGSO4)
Concerning chelation therapy for lead toxicity
1) name the 3 chelation drug options
2) which drug is potentially nephrotoxic
3) which drugs would be good to give in combination…describe the MOA
1) Ca-EDTA, Succimer DMSA, Dimercaprol
2) Ca-EDTA
3) Ca-EDTA + Dimercaprol–> CaEDTA pulls it out of bone and dimercaprol enhances it’s excretion
The main disease seen with zinc toxicity is?
Hemolytic anemia
Which form of iron is assoc. with the greatest risk of toxicity
soluble salt forms
Free iron in systemic circulation is normally bound by _______ but this can become overwhlemed, leading to clinical signs
Transferrin
What chelation agent can be used for iron toxicity? What’s a unique side effect of this drug you should warn owners about?
Deferoxamine
Can turn urine bright red (normal)
Amanits phalloides mushrooms primarily impact which body system? What are the two principle toxins it produces?
Hepatic
1) amatoxins
2) Phallotoxins
The neuro signs caused by Hydrazine-containing mushrooms is primarily due to inhibition of?
GABA
With neuro toxic Amanita spp. why do clinical signs fluctuate between neuro depression and stimulation?
Because there a 2 principles toxins
1 toxin is glutamate agonist (excitation)–Ibotenic acid
the other toxin is GABA agonist (depression)–Muscimol
Muscarine containing mushrooms cause development of which type of clinical signs? A specific antidote for these?
muscarinic signs(SLUDDE)
**ATROPINE
Which spp. of mushroom is assoc. with the development of AKI (nephrotoxic)
Cortinaria spp.
Are grapes or raisins more likely to be assoc. with adverse effects?
Raisins (dried form)
Grapes/raisins primarily impact which body system?
Renal (nephrotoxic)
T/F: Dogs who ingest Macadamia nuts are unlikely to die and owners can probably offer supportive care at home
true!!
These dogs typically just get weak/depressed
What are the two methylxanthines we care about?
Caffeine
Theobromine (chocolate)
Treatment of _______ toxicity should include a urinary catheter. Why?
Thebromine (chocolate)
Metabolites can be reabsorbed from bladder
How does Xylitol causes most of it’s clinical signs
strong promoter of insulin release –> hypoglycemia
Spp. most susceptible to onions/garlic toxicity have low _____ ______ activity
erythrocyte catalase
What body system is primarily effected by onions/garlic?
Hematologic–oxidative injury (heinz bodies) and methemoglobinemia
Hemolysis later on
What are the two risks assoc. with ingestion of bread dough
1) ethanol toxicity
2) obstruction/GDV/rupture
Though sago palms initially cause GI upset, eventually clinical signs can progress and affect which two other systems?
neuro and hepatic
Cardiac glycosides primarily affect which system and by what mechanism?
Cardiovascular
disrupts function of Na/K ATPase pump
How do insoluble Ca oxalates cause clinical signs?
They are sharp and released during biting/chewing –> pain in mouth and edema of lips/tongue
The soluble Ca oxalata primarily affect which types of animals? Clinical signs are related to….
Large animals
hypocalcemia (oxalates bind systemic Ca)
*stones/renal failure less common
Two toxin types assoc. with Blue-green algae and the system they each affect. Which is more common?
1) Microcystins–liver (more common)
2) Anatoxin–neuro
