Cardiovascular & Hematopoietic Flashcards
First generation anticoagulant rodenticides
Short half-life (15 hours)
Low potency, requires multiple ingestions for toxicity
Example: warfarin
Second generation anticoagulant rodenticides
Long half-life (20 days)
High potency, kills with single ingestion
Example: brodifacoum
Mechanism of action of anticoagulant rodenticides
Inhibits Vitamin K epoxide reductase
Prevents formation of Vitamin K dependent clotting factors
Clinical signs of anticoagulant rodenticide toxicity
Delayed onset of clinical signs (3-5 days) as clotting factors in plasma are consumed
Depression, anorexia, anemia, dyspnea, nosebleeds, bleeding gums, bloody feces
Hemorrhage (abdominal cavity)
Prolonged bleeding from injection sites
Diagnosis of anticoagulant rodenticide toxicity
Three methods:
- History of exposure
- Presence of coagulopathy
- Response to Vit K therapy
Treatment of anticoagulant rodenticide toxicity
Emesis, absorbent, cathartics
Vitamin K administration
May need transfusion
May need to treat for 10-14 days for 1st gen or 30 days for 2nd gen
Sources of nitrates in nitrate toxicosis
Fertilizers
Plants (lambsquarter, black nightshade, pigweed)
Contamination of water
Mechanism of action of nitrate toxicosis
Nitrate anion causes vasodilation and oxidizes ferrous iron in hemoglobin to ferric state forming methemoglobin
Results in oxygen starvation of tissue
Species susceptibility nitrate toxicosis
Pigs>cattle>sheep>horses
Clinical signs of nitrate toxicosis
Levels of MetHb Brown blood! Cyanosis Ataxia Seizures Coma
Diagnosis of nitrate toxicosis
Test nitrate levels in feed or water (not blood!)
Treatment of nitrate toxicosis
Ruminants: IV new methylene blue (will turn urine green), feed corn to cattle
Cats, Horses: ascorbic acid
Educate owners
Examples of cardiac glycosides
Foxglove
Oleander
Lilly of the valley
Mechanism of action of cardiac glycosides
Inhibits Na/K ATPase pump through competition with K binding sites
Clinical signs of cardiac glycoside toxicity
Can occur 1hr to weeks after ingestion
Trembling, staggering, dyspnea
Increase Ca++, Na+, and K+
Tachycardia, arrhythmia, weak pulse
Diagnosis of cardiac glycoside toxicity
Based on history, access to plants, clinical signs, analysis of vomit
Treatment of cardiac glycoside toxicity
GI decontamination
Propanolol for arrhythmias
Treat hyperK
Use digoxin immune Fab fragments if propanolol ineffective
Common sources of cyanide toxicity
Plants (wild black cherry, white clover, Sorghum spp.) Fertilizers Pesticides/rodenticides Fumigants Combustion
Cyanide is not toxic when
Dry
Mechanism of cyanide toxicity
Inhibition of cytochrome oxidase and oxidative phosphorylation
Clinical signs of cyanide toxicity
15min-few hours after consumption
Cherry red blood that is slow to clot*
Sudden death, dyspnea, weakness, tremors
Diagnosis of cyanide toxicity
History of ingestion
Unclotted red blood
Analysis of frozen stomach contents
Treatment of cyanide toxicity
Two steps:
- Induce methemoglobin formation with sodium nitrite to bind cyanide
- Give sodium thiosulfate to increase formation of thiocyanate by rhodanese
If necessary, treat MetHb with methylene blue
Examples, sources of methylxanthines
Examples: caffeine theobromine, theophylline
Sources: coffee, chocolate (esp. unsweetened baking chocolate, cocoa been mulch), medications
Mechanism of action of methylxanthine toxicity
Competitive antagonist of adenosine receptors
Causes CNS stimulation, vasoconstriction, tachycardia
Prevents Ca++ reuptake leading to increased skeletal and cardiac muscle contractility
Inhibits phosphodiesterase -> increased cAMP and GMP concentrations
Clinical signs of methylxanthine toxicity
Vomiting, diarrhea, diuresis Hyperactivity, "bounce", panting Tachycardia, hypertension Ataxia Tremors, seizures Coma Death
Diagnosis of methylxanthine toxicity
Chemical analysis of stomach contents, plasma, serum, urine or liver
Theobromine can be detected in serum for 3-4 days after ingestion
Treatment of methylxanthine toxicity
GI decontamination Monitor EKG Treat seizures Maintain respiration Fluid diuresis may increase excretion
What is gossypol?
Found in pigment glands of cottonseed
Provides insect resistance
Mechanism of action of gossypol toxicity
Chelates iron and causes anemia, reduces protein availability
Inhibition of dehydrogenase leading to decreased energy and stress
Ruminants tolerate higher levels then monogastrics
Horses are resistant
Clinical signs of gossypol toxicity
Weight loss, weakness, dyspnea
Anemia, edema, congestive heart failure
Myocardial necrosis
Sudden death
Diagnosis of gossypol toxicity
Evidence of cottonseed ingestion
Treatment of gossypol toxicity
High protein diet
Vit A
Iron
Lysine
Remove gossypol source
What is cantharidin?
Toxin produced by blister beetle or spanish fly
Eggs develop on grasshopper larvae, so beetle numbers are tied to grasshopper numbers
Beetles found in alfalfa, usually in large groups
Usually effects horses
Mechanism of action of cantharidin toxicity
Inhibits protein phosphatases
Mucosal irritant
Clinical signs of cantharidin toxicity
Colic, frequent urination, diaphragm contraction with heart beat, shock, cardiac toxicity
Irritation, ulceration of oral, GI, and bladder
Diagnosis of cantharidin toxicity
Alfalfa hay consumption Beetles in hay or stomach Hypocalcemia Increased BUN Ulceration of mucous membranes Cardiac necrosis Sudden death
Treatment of cardiac glycoside toxicity
GI decontamination
GI protectant (sucralfate)
Antibiotics
