Cardiac and hemostatic toxins, heavy metals Flashcards
Toxicants that cause Cardiotoxicity
Beta-Blockers
Calcium Channel Blockers
Zinc/Aluminum Phosphide
Sodium Monofluoroacetate (1080)
Yew Plants
toxicants that cause RBC hemolysis
Onions/Garlic (Dogs)
Red Maple (Horses)
Chlorates
Copper
Zinc
Snake Envenomation
toxins that cause Methemoglobinemia
Acetaminophen
Onions/Garlic (Dogs)
Phenol Disinfectants
Chlorates
Zinc/Aluminum Phosphide
Nitrates (Ruminants)
Know what toxin is present in yew plants that is responsible for their cardiotoxicity and Explain how the toxins in yew plants affects the heart rate in poisoned animals
Taxines
Ca+2 and Na+ channel antagonists/blockers
* Increases cytoplasmic calcium > decreased calcium in cardiomyocytes and in arteries
* Decreased smooth muscle contraction decreased heart contractility, increased vasodilation & hypotension
* Bradycardia, vasodilation
Explain how red maple leaves cause hemolysis in horses
Bacteria in ileum convert gallic acids/tannins to pyrogallol > oxidizing agent
RBC membrane damage = hemolysis (acute hemolytic anemia)
Oxidation of hemoglobin = Heinz body anemia (denatured hemoglobin) with or without methemoglobinemia
Know the mechanism of toxicity of anticoagulant rodenticides and antidote
vitamin K antagonists
* Inhibit vitamin K-epoxide reductase (VKOR) in the liver
* Depletion of active vitamin K-dependent clotting factors: Factors II, VII, IX, X, Protein C, Protein S
antidote= vitamin K
Know what clinical laboratory tests that should be performed to assess exposure to and recovery from anticoagulant rodenticide toxicity and which is best for early detection
PT: early detection (factor 7-extrinsic depletes fastest)
PTT
ACT
Explain why ruminants are susceptible to nitrate toxicity
and recommended treatments
Rumen microflora converts: Nitrate > Nitrite > Ammonia > Protein
Intake of nitrate and conversion to nitrite exceed microflora capacity to reduce nitrite
* Nitrites absorbed into blood and oxidize hemoglobin (Fe+2 > Fe+3)
* Methemoglobin and RBCs cannot release oxygen to tissues
* Vasodilation, methemoglobinemia, hypoxia
Treatment: IV 1 % - 2 % Methylene blue, Vitamin C
Know what distinguishes a venom from poison
Poison: A toxin/toxicant that enters the body through being ingested, absorbed through the skin, inhaled
Venom: A toxin that enters the body through injection
Know the 4 types of enzymatic proteins in pit viper venom
Coagulants: use up clotting factors
hemorrhagins/hemolytics: damage blood vessels
mycotoxins: destruction of muscle
cytotoxins: necrosis and breakdown of proteins
Know the 2 types of pit vipers most commonly found in Virginia
Copperheads
Timber rattlesnakes
Know what part of the body that animals, particularly dogs and horses, are most commonly bitten by pit vipers
face, extremities
Describe the clinical presentation of diarrhea associated with some arsenic cases
Movement of fluids in to GI mucosa causes swelling
Loss of GI mucosa = “bloody rice water” diarrhea: huge loss of fluids, hypovolemia & shock
Know the most common source of arsenic poisoning in animals
water/soil, commercial products, pesticides
cattle: Ashes from burned, treated wood
arsenic mechanism
Inhibits ATP synthesis
makes reactive oxygen species= damage to DNA, RNA, proteins
Know the preferred chelator used to treat arsenic toxicity in large animals
Sodium Thiosulfate
Binds free arsenic
Explain what copper storage disease is in dogs and how it occurs
Autosomal recessive trait due to lack of a gene (COMMD1) coding for a liver protein involved in excretion of copper in bile
Livers abnormally accumulate copper
Hepatitis and progressive scarring and cirrhosis
Describe the 2 phases of chronic toxicity that occur with copper toxicosis
- Accumulation or pre-hemolytic phase
Accumulates in liver if inadequate biliary excretion - Hemolytic phase > hepatic necrosis, nephrotoxicity
Explain why sheep are more susceptible to copper toxicity when compared to other animals
sheep cannot excrete copper into bile efficiently in response to dietary increase
accumulates in liver > copper dumps into blood
* hemolysis
Explain how molybdenum can affect copper absorption and utilization in animals
Molybdenum is a copper antagonist
* When present in high concentrations, copper utilization and absorption is decreased
* When present at low concentrations, copper accumulation increases
* Occurs when copper to molybdenum ratio is > 10:1 in the feed
Know the preferred chelators used to treat copper toxicity
D-penicillamine or Trientine
Know the preferred chelator used to treat iron toxicity
Deferoxamine mesylate (Desferal®)
Siderophore – specifically binds iron
Iron mechanism of toxicity
Direct corrosive action on the gastrointestinal tract due to lipid peroxidation
metabolic acidosis
Know the most common source of lead poisoning in large animals (cattle)
Lead containing batteries, Lead shot
Explain why young animals exposed to lead will primarily exhibit neurological clinical signs
Younger animals more readily absorb lead in GI tract
Blood brain barrier immature > lead crosses over into CNS
Know the distribution of lead in an animal’s body after it is absorbed into the blood stream
Bound to hemoglobin
distributes to:
* liver
* brain
* kidney
* bone
Explain how calcium disodium EDTA treats lead toxicosis
removes lead from bones/tissues
Know the most common source of zinc poisoning in animals
U.S. Pennies minted after 1982
Which heavy metal causes Nephrotoxicity
arsenic
copper
lead
mercury
zinc
which heavy metals cause Hepatotoxicity
arsenic
copper
iron
lead
zinc
which heavy metals cause Gastrointestinal toxicity
arsenic
copper
iron
lead
mercury
NaCl
which heavy metals cause Red blood cell hemolysis
zinc
copper
which heavy metal causes Metabolic acidosis
iron
