Cardiac and hemostatic toxins, heavy metals Flashcards

1
Q

Toxicants that cause Cardiotoxicity

A

Beta-Blockers
Calcium Channel Blockers
Zinc/Aluminum Phosphide
Sodium Monofluoroacetate (1080)
Yew Plants

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2
Q

toxicants that cause RBC hemolysis

A

Onions/Garlic (Dogs)
Red Maple (Horses)
Chlorates
Copper
Zinc
Snake Envenomation

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3
Q

toxins that cause Methemoglobinemia

A

Acetaminophen
Onions/Garlic (Dogs)
Phenol Disinfectants
Chlorates
Zinc/Aluminum Phosphide
Nitrates (Ruminants)

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4
Q

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

A

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

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5
Q

Explain how red maple leaves cause hemolysis in horses

A

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

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6
Q

Know the mechanism of toxicity of anticoagulant rodenticides and antidote

A

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

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7
Q

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

A

PT: early detection (factor 7-extrinsic depletes fastest)
PTT
ACT

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8
Q

Explain why ruminants are susceptible to nitrate toxicity
and recommended treatments

A

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

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9
Q

Know what distinguishes a venom from poison

A

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

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10
Q

Know the 4 types of enzymatic proteins in pit viper venom

A

Coagulants: use up clotting factors
hemorrhagins/hemolytics: damage blood vessels
mycotoxins: destruction of muscle
cytotoxins: necrosis and breakdown of proteins

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11
Q

Know the 2 types of pit vipers most commonly found in Virginia

A

Copperheads
Timber rattlesnakes

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12
Q

Know what part of the body that animals, particularly dogs and horses, are most commonly bitten by pit vipers

A

face, extremities

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13
Q

Describe the clinical presentation of diarrhea associated with some arsenic cases

A

Movement of fluids in to GI mucosa causes swelling
Loss of GI mucosa = “bloody rice water” diarrhea: huge loss of fluids, hypovolemia & shock

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14
Q

Know the most common source of arsenic poisoning in animals

A

water/soil, commercial products, pesticides
cattle: Ashes from burned, treated wood

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15
Q

arsenic mechanism

A

Inhibits ATP synthesis
makes reactive oxygen species= damage to DNA, RNA, proteins

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16
Q

Know the preferred chelator used to treat arsenic toxicity in large animals

A

Sodium Thiosulfate
Binds free arsenic

17
Q

Explain what copper storage disease is in dogs and how it occurs

A

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

18
Q

Describe the 2 phases of chronic toxicity that occur with copper toxicosis

A
  1. Accumulation or pre-hemolytic phase
    Accumulates in liver if inadequate biliary excretion
  2. Hemolytic phase > hepatic necrosis, nephrotoxicity
19
Q

Explain why sheep are more susceptible to copper toxicity when compared to other animals

A

sheep cannot excrete copper into bile efficiently in response to dietary increase
accumulates in liver > copper dumps into blood
* hemolysis

20
Q

Explain how molybdenum can affect copper absorption and utilization in animals

A

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

21
Q

Know the preferred chelators used to treat copper toxicity

A

D-penicillamine or Trientine

22
Q

Know the preferred chelator used to treat iron toxicity

A

Deferoxamine mesylate (Desferal®)
Siderophore – specifically binds iron

23
Q

Iron mechanism of toxicity

A

Direct corrosive action on the gastrointestinal tract due to lipid peroxidation
metabolic acidosis

24
Q

Know the most common source of lead poisoning in large animals (cattle)

A

Lead containing batteries, Lead shot

25
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
26
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
27
Explain how calcium disodium EDTA treats lead toxicosis
removes lead from bones/tissues
28
Know the most common source of zinc poisoning in animals
U.S. **Pennies** minted after 1982
29
Which heavy metal causes Nephrotoxicity
arsenic copper lead mercury zinc
30
which heavy metals cause Hepatotoxicity
arsenic copper iron lead zinc
31
which heavy metals cause Gastrointestinal toxicity
arsenic copper iron lead mercury NaCl
32
which heavy metals cause Red blood cell hemolysis
zinc copper
33
which heavy metal causes Metabolic acidosis
iron