Cardiovascular & Hematopoietic

Question 1

First generation anticoagulant rodenticides

Answer 1

Short half-life (15 hours)
Low potency, requires multiple ingestions for toxicity
Example: warfarin

Question 2

Second generation anticoagulant rodenticides

Answer 2

Long half-life (20 days)
High potency, kills with single ingestion
Example: brodifacoum

Question 3

Mechanism of action of anticoagulant rodenticides

Answer 3

Inhibits Vitamin K epoxide reductase

Prevents formation of Vitamin K dependent clotting factors

Question 4

Clinical signs of anticoagulant rodenticide toxicity

Answer 4

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

Question 5

Diagnosis of anticoagulant rodenticide toxicity

Answer 5

Three methods:

1. History of exposure
2. Presence of coagulopathy
3. Response to Vit K therapy

Question 6

Treatment of anticoagulant rodenticide toxicity

Answer 6

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

Question 7

Sources of nitrates in nitrate toxicosis

Answer 7

Fertilizers
Plants (lambsquarter, black nightshade, pigweed)
Contamination of water

Question 8

Mechanism of action of nitrate toxicosis

Answer 8

Nitrate anion causes vasodilation and oxidizes ferrous iron in hemoglobin to ferric state forming methemoglobin
Results in oxygen starvation of tissue

Question 9

Species susceptibility nitrate toxicosis

Answer 9

Pigs>cattle>sheep>horses

Question 10

Clinical signs of nitrate toxicosis

Answer 10

Levels of MetHb
Brown blood!
Cyanosis
Ataxia
Seizures
Coma

Question 11

Diagnosis of nitrate toxicosis

Answer 11

Test nitrate levels in feed or water (not blood!)

Question 12

Treatment of nitrate toxicosis

Answer 12

Ruminants: IV new methylene blue (will turn urine green), feed corn to cattle
Cats, Horses: ascorbic acid
Educate owners

Question 13

Examples of cardiac glycosides

Answer 13

Foxglove
Oleander
Lilly of the valley

Question 14

Mechanism of action of cardiac glycosides

Answer 14

Inhibits Na/K ATPase pump through competition with K binding sites

Question 15

Clinical signs of cardiac glycoside toxicity

Answer 15

Can occur 1hr to weeks after ingestion
Trembling, staggering, dyspnea
Increase Ca++, Na+, and K+
Tachycardia, arrhythmia, weak pulse

Question 16

Diagnosis of cardiac glycoside toxicity

Answer 16

Based on history, access to plants, clinical signs, analysis of vomit

Question 17

Treatment of cardiac glycoside toxicity

Answer 17

GI decontamination
Propanolol for arrhythmias
Treat hyperK
Use digoxin immune Fab fragments if propanolol ineffective

Question 18

Common sources of cyanide toxicity

Answer 18

Plants (wild black cherry, white clover, Sorghum spp.)
Fertilizers
Pesticides/rodenticides
Fumigants
Combustion

Question 19

Cyanide is not toxic when

Answer 19

Dry

Question 20

Mechanism of cyanide toxicity

Answer 20

Inhibition of cytochrome oxidase and oxidative phosphorylation

Question 21

Clinical signs of cyanide toxicity

Answer 21

15min-few hours after consumption
Cherry red blood that is slow to clot*
Sudden death, dyspnea, weakness, tremors

Question 22

Diagnosis of cyanide toxicity

Answer 22

History of ingestion
Unclotted red blood
Analysis of frozen stomach contents

Question 23

Treatment of cyanide toxicity

Answer 23

Two steps:

1. Induce methemoglobin formation with sodium nitrite to bind cyanide
2. Give sodium thiosulfate to increase formation of thiocyanate by rhodanese

If necessary, treat MetHb with methylene blue

Question 24

Examples, sources of methylxanthines

Answer 24

Examples: caffeine theobromine, theophylline
Sources: coffee, chocolate (esp. unsweetened baking chocolate, cocoa been mulch), medications

Question 25

Mechanism of action of methylxanthine toxicity

Answer 25

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

Question 26

Clinical signs of methylxanthine toxicity

Answer 26

``` Vomiting, diarrhea, diuresis Hyperactivity, "bounce", panting Tachycardia, hypertension Ataxia Tremors, seizures Coma Death ```

Question 27

Diagnosis of methylxanthine toxicity

Answer 27

Chemical analysis of stomach contents, plasma, serum, urine or liver Theobromine can be detected in serum for 3-4 days after ingestion

Question 28

Treatment of methylxanthine toxicity

Answer 28

``` GI decontamination Monitor EKG Treat seizures Maintain respiration Fluid diuresis may increase excretion ```

Question 29

What is gossypol?

Answer 29

Found in pigment glands of cottonseed | Provides insect resistance

Question 30

Mechanism of action of gossypol toxicity

Answer 30

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

Question 31

Clinical signs of gossypol toxicity

Answer 31

Weight loss, weakness, dyspnea Anemia, edema, congestive heart failure Myocardial necrosis Sudden death

Question 32

Diagnosis of gossypol toxicity

Answer 32

Evidence of cottonseed ingestion

Question 33

Treatment of gossypol toxicity

Answer 33

High protein diet Vit A Iron Lysine Remove gossypol source

Question 34

What is cantharidin?

Answer 34

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

Question 35

Mechanism of action of cantharidin toxicity

Answer 35

Inhibits protein phosphatases | Mucosal irritant

Question 36

Clinical signs of cantharidin toxicity

Answer 36

Colic, frequent urination, diaphragm contraction with heart beat, shock, cardiac toxicity Irritation, ulceration of oral, GI, and bladder

Question 37

Diagnosis of cantharidin toxicity

Answer 37

``` Alfalfa hay consumption Beetles in hay or stomach Hypocalcemia Increased BUN Ulceration of mucous membranes Cardiac necrosis Sudden death ```

Question 38

Treatment of cardiac glycoside toxicity

Answer 38

GI decontamination GI protectant (sucralfate) Antibiotics