QUESTIONS

1. How does vitamin D act to elevate serum calcium? (Hint: 3 tissues are involved.)
    
2. What is the difference between metastatic mineralization & dystrophic mineralization?
    
3. What are the 3 main brands of vitamin D based rodenticides in the U.S.?
    
4. With anti-coagulant rodenticides it is a problem if a pet eats a rodent that has been poisoned. Is this a problem w/the vitamin D based rodenticides.
    
5. The toxic dose of cholecalciferol reported on the package is 88 mg/kg.  Experimentally, what has been found to be the true toxic dose?
    
6. What is the half life of vitamin D3?
    
7. Can this toxicosis be diagnosed by measuring calcitriol levels?
    
8. The antidote in the literature is _________________ but this drug is very short-lived.  It can also cause vomiting & anorexia.
   
   
   
   
    

ANSWERS

1. In the intestine, vitamin D leads to increased absorption of calcium.  In bone, calcium is mobilized.  In the kidney, vitamin D leads to increased calcium resorption.
   
   
   
   
    
2. Metastatic mineralization occurs when the product of calcium & Phosphorus is elevated & mineralization of soft tissues is occuring spontaneously.  In dystrophic calcification, calcium is deposited secondary to necrosis.  In vitamin D toxicosis, we think dystrophic calcification occurs first. If the Ca x P product is not fixed, you will get metastatic calcification next.
   
   
   
   
    
3. The 3 main vitamin D rodenticides of the U.S. are:  Rampage, Quintox, & Rat-B-Gone.
   
   
   
   
    
4. Secondary poisoning does not seem to be a problem with the vitaimin D based rodenticides.
   
   
   
   
    
5. Experimental toxicity starts at 12-20 mg/kg.
   
   
   
   
    
6. In one study the half life was 10.7 days  (pretty long).
   
   
   
   
    
7. Calcitriol levels have been either normal or increased. This parameter is not so reliable.  All intoxicated dogs had elevated calciums, normal PTHs, most had elevated Phosphorus.  Calcium elevation plus knowing that exposure occurs seems to be a reliable method of diagnosis. MI state runs 25 (OH) cholecalciferol  levels weekly & the diagnosis can also be made this way.
   
   Remember:  cholecalciferol is the toxin. 25 (OH) cholecalciferol (calcidiol) is the what you get when the liver hydroxylates cholecalciferol at the 25th Carbon & is what MI State will measure for you. 1,25 (OH) cholecalciferol (calcitriol) is the stuff after another hydroxyl is added in the kidney.
   
   **However, these pellets are BLUE so blue vomit or diarrhea is a big hint!
   
   
   
   
    
8. The literature antidote is salmon calcitonin.  You may do as well with steroids (to reduce Gi calcium absorption), Lasix (to reduce renal resorption - be sure the patient is hydrated first), Saline IV (to help w/renal excretion) & low calcium diet.  There is also a new product called "calcibind" which will bind intestinal calcium.
   
   Median time to normocalcemia is 13.5 days.
   
   Survivors may well go into CRF.