Flashcards in Exam 2 Deck (50)
Give 2 examples of 2nd generation anti-coagulants
Describe how 2nd generation anti-coag rodenticides work (MOA)
antagonize the action of vitamin K1 epoxide reductase --> can't make active vitamin K --> depletion of vitamin K1 dependent factors (2,7,9,10)
Which coag factor has the shortest half-life? Bc of this, which coag panel test becomes prolonged first
prothrombin time (PT) prolongs first
At what time frame after ingestion do we check PT? If it's prolonged, what therapy do we provide?
oral vitamin K1 for 4 weeks
Two important products of COX pathway that can be inhibited by NSAIDs & their general effect on platelets
Thromboxane A2-- increases platelet aggregation
Prostacyclin (PGI2)-- inhibits platelet aggregation
What is the shock fluid dose for:
Which type of fluids (generally) should be avoided with pit viper envenomation
Colloids (may interfere with coagulation)
When choosing an analgesic for a patient follow pit viper bite, which category of drug should be avoided and why?
NSAIDs--inhibitory effects on platelet aggregation
Coral snake venom is primarily _____ and therefore causes minimal _______
minimal tissue reaction & pain
Describe how coral snake venom works
it's a post-synaptic alpha-neurotoxin--> blocks nicotinic ACh receptors of NMJs
Cats are extremely sensitive to the venom of ____ and it is often fatal
Black widow venom is primarily a ______ and causes release of?
release of Norepi & ACh
Name 2 types of rodenticides that are not anti-coagulant
Net result of cholecalciferol toxicity?
Describe the MOA of bromethalin toxicity
uncouples oxidative phosphorylation (decreased ATP--> messed up Na/K ATPase--> Na builds in cells)
Why would multiple doses of activated charcoal be indicated for cholecalciferol or bromethalin toxicity?
Due to enterohepatic circulation
*esp. bromethalin which is excreted in bile*
What is the risk assoc. with inducing emesis in a dog that's ingested zinc phosphide?
the gas that comes up (phosphine gas) can be toxic to staff!
Which route of exposure to zinc phosphide is worse and why?
Inhalation--readily absorbed into systemic circulation
*with ingestion, it's corrosive to the mucosa and induces vomiting*
How does strychnine cause clinical signs (MOA)?
blocks the inhibitory actions of glycine (CNS upregulated)
Which toxic gases are
1) heavier than air
2) lighter than air
1) CO2, H2S
2) NH3, CO
Acute levels of ____ppm of which gas can lead to olfactory paralysis
>100ppm of H2S
Primary source of H2S as it relates to animal exposure?
decomposition of fecal material
(gets mixed or stirred, releasing the gas)
Why are pulse oximeters not helpful in diagnosis of CO toxicity?
They only measure dissolved gas in the blood--cannot tell if it's Hgb bound to O2 or CO
Levels of CO2 must reach _____ppm for clinical signs to appear
*300ppm is normal ambient level
How do amyl nitrite and sodium nitrite treat HCN toxicity
they induce the formation of methemoglobin which has a higher affinity for HCN
GOAL= 25% MetHgb
Which spp. is highly susceptible to heated teflon (PTFE)
Lethal dose of ethylene glycol in
1) 4 ml/kg
2) 1.5 ml/kg
EG toxicity requires early diagnosis and treatment. What is the treatment window (time frame) in dogs? Cats?
Dogs: < 8-12hr
Cats: < 3 hr
Two treatment options for EG toxicity? Their MOAs?
4-MP--> inhibits alcohol dehydrogenase
Ethanol--> shifts alcohol dehydrogenase to itself for metabolism so EG doesn't get broken down
Why is methanol associated with formation of blindness in humans and primates?
inability to breakdown formic acid (metabolite)
Ethanol and 4-MP are not indicated in the tx of?
Which toxic substance is assoc. with heinz body anemia in cats
Why might we see a strong metabolic acidosis with proplyene glycol ingestion?
one of it's breakdown products is lactic acid (high lactate= metabolic acidosis)
Would 4-MP be indicated for tx of propylene glycol?
Pyrethrin & pyrethroid MOA?
Name a few clinical signs you might see
Prolonged Na channel conduction
hyperesthesia (tx somewhere quiet), muscle tremors, ear twitching
Lipid therapy would be effective for any drug with a Log P _____
*higher number= more it mixes with fat
How do Organophosphates and Carbamates differ? (2)
OPs--> irreversible inhibition of AChE
Carbamates--> REVERSIBLE inhibition of AChE
OPs undergo "aging" which strengthens their bond to the enzyme & carbamates do not
OPs and carbamates primarily cause ______ signs. Name 4
SLUD (salivation, lacrimation, urination, defecation)
Tx of choice for OPs and carbamate toxicity? What is our main goal?
Goal= treat bradycardia & bronchial secretions
**Atropine doesn't help nicotinic signs!!**
Which drug is considered an antidote for OP/Carbamate toxicity
*helps nicotinic signs
The presence of muscle tremors combined with HYPOthermia might be indicative of which toxicity?
Toxin assoc. with snail/slug bait? Assoc. clinical signs?
"Shake and bake"--> muscle tremors + secondary hyperthermia
On which channels does Ivermectin exert its effects?
activates glutamate-gated chloride channels
Dogs with the ____ mutation can only handle ____ mg/kg of ivermectin.
Is HW prevention safe for these affected dogs?
MDR1 mutation can only get 0.15mg/kg
HW prevention is safe (0.006mg/kg)
How does Amitraz cause clinical signs?
increases alpha-2 adrenergic activity (sedation, ataxia, bradycardia)
Concerning Amitraz toxicity:
1) why might we see hyperglycemia
2) what drug can be used for tx
1) alpha-2 agonists inhibit insulin release
2) Atipamezole (alpha-2 antagonist)
If you're not sure which type of moth ball a dog or cat ate, which test can you use?
Mix salt with water
Bad type will float, other will sink
2 reasons corrosive alkalies are worse than corrosive acids
corrosive acids are painful upon ingestion which limits the amount ingested (unlike alkalines...large amounts can be ingested)
Alkalines cause more severe necrosis (liquefactive compared to coagulative)
Treatment for corrosives includes decontamination? (T/F)
FALSE--no emesis or activated charcoal
DILUTE with water or milk instead