Rodenticides

Question 1

strychnine kinetics

Answer 1

rapid absorptions– Ka = 15 mins; metabolize via N-oxidation; excretion via the urine

Question 2

strynchnine mech of ac?

Answer 2

competitive antagonism; imitates glycine and acts as an inhibitory neurotransmitter; intermittent convulsions; extensor rigidity;

Question 3

treatment for strychnine?

Answer 3

sedation; activated charcoal; acidify the urine; KMNO4 (oxidizes strychnine in the gut)

Question 4

anticoagulant rodenticide examples?

Answer 4

warfarin, 2nd gen–diphacinone, brodifacoum; coumadin, dicouporal, heparin

Question 5

anticoag mech of ac?

Answer 5

inhibition of vit k epoxide reductase; decreases synthesis of clotting factors II, VII, IX, X

Question 6

clinical manifestations of anticoag rodenticides?

Answer 6

massive bleeding

Question 7

treatment of anticoag rodent?

Answer 7

vit K1, and blood transfusion

Question 8

drug interactions of anticoags?

Answer 8

anticoags decrease vit K synthesis–> cannot take with sulfonamides, which kill the bacteria in your gut which makes vit K to begin with;
anticoags decrease protein binding–> cannot take with sulfonamides also, which displaces warfarin–>more warfarin available to cause harm
increases fat in diet

Question 9

kinetics of anticoags?

Answer 9

2nd gen more strongly bound to proteins; 2nd gen has a much longer half life; all are well-absorbed, metabolized by hydroxylation

Question 10

fluoroacetate mech of action?

Answer 10

replaces A-CoA in the Krebs cycle; inhibits aconitase; this blocks cell resp and subsequently E production

Question 11

clinical manifestations of fluoroacetate?

Answer 11

convulsions; running fits; cardiac arrhythmia; also terminal anoxic convulsions

Question 12

treatment of fluoroacetate?

Answer 12

sedation for convulsions; 2C fragment–>jumpstarts the krebs cycle; CaCl2–>required by heart to beat (prevents cardiac arrhythmia); Ca Ketoglutarate–> @C fragment

Question 13

Postmortem clinical manifestations of fluoroacetate?

Answer 13

no liver damage; rigor mortis sets in quickly because energy is messed up

Question 14

zinc phosphide subcellular target (mech of ac), and consequential target organs?

Answer 14

targets mitochondria–>liver and kidney contain lots of mito, so they are target organs;

Question 15

zinc phosphide kinetics

Answer 15

rapidly absorbed

Question 16

ZP treatment?

Answer 16

treat shock with fluids, and seizures–sedate

Question 17

clinical manifestations of ZP poisoning?

Answer 17

vomiting, seizures (tonic clonic–>stiffening and paddling), shock

Question 18

What is ANTU, it’s kinetics, and mech of action?

Answer 18

Alpha-naphthyl thiourea; rapidly metabolized, must perform autopsy ASAP; not an enviro issue
Increases permeability in palm capillaries–>massive pulmonary edema

Question 19

Cholecalciferol mech of AC and kinetics?

Answer 19

Rapid absorption, reabsortio , increased mobilization of bone–> increased blood Ca

Well absorbed and metabolized, not an enviro issue

Question 20

Cholecalciferol clinical manifestations?

Answer 20

Cardiac dysfunction

Calcification of the heart, kidney, etc

Question 21

Cholecalciferol treatment?

Answer 21

Activated charcoal
Steroids–shifts calcification
Calcitonin–hormone–drops blood Ca
Give lipid emulsions