Exam 2 Flashcards
Give 2 examples of 2nd generation anti-coagulants
Brodifacoum
Bromadiolone
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
factor 7
prothrombin time (PT) prolongs first
At what time frame after ingestion do we check PT? If it’s prolonged, what therapy do we provide?
after 48hr
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:
1) dogs
2) cats
1) 90ml/kg
2) 40-50ml/kg
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 _______
neurotoxic;
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 widows
Black widow venom is primarily a ______ and causes release of?
Neurotoxin;
release of Norepi & ACh
Name 2 types of rodenticides that are not anti-coagulant
Cholecalciferol
Bromethalin
Net result of cholecalciferol toxicity?
Hypercalcemia
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
50,000ppm
*300ppm is normal ambient level
