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Toxicology > Cardiovascular & Hematopoietic > Flashcards

Cardiovascular & Hematopoietic Flashcards

1
Q

First generation anticoagulant rodenticides

A

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

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2
Q

Second generation anticoagulant rodenticides

A

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

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3
Q

Mechanism of action of anticoagulant rodenticides

A

Inhibits Vitamin K epoxide reductase

Prevents formation of Vitamin K dependent clotting factors

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4
Q

Clinical signs of anticoagulant rodenticide toxicity

A

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

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5
Q

Diagnosis of anticoagulant rodenticide toxicity

A

Three methods:

  1. History of exposure
  2. Presence of coagulopathy
  3. Response to Vit K therapy
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6
Q

Treatment of anticoagulant rodenticide toxicity

A

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

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7
Q

Sources of nitrates in nitrate toxicosis

A

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

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8
Q

Mechanism of action of nitrate toxicosis

A

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

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9
Q

Species susceptibility nitrate toxicosis

A

Pigs>cattle>sheep>horses

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10
Q

Clinical signs of nitrate toxicosis

A 
Levels of MetHb
Brown blood!
Cyanosis
Ataxia
Seizures
Coma
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11
Q

Diagnosis of nitrate toxicosis

A

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

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12
Q

Treatment of nitrate toxicosis

A

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

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13
Q

Examples of cardiac glycosides

A

Foxglove
Oleander
Lilly of the valley

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14
Q

Mechanism of action of cardiac glycosides

A

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

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15
Q

Clinical signs of cardiac glycoside toxicity

A

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

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16
Q

Diagnosis of cardiac glycoside toxicity

A

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

17
Q

Treatment of cardiac glycoside toxicity

A

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

18
Q

Common sources of cyanide toxicity

A 
Plants (wild black cherry, white clover, Sorghum spp.)
Fertilizers
Pesticides/rodenticides
Fumigants
Combustion
19
Q

Cyanide is not toxic when

A

Dry

20
Q

Mechanism of cyanide toxicity

A

Inhibition of cytochrome oxidase and oxidative phosphorylation

21
Q

Clinical signs of cyanide toxicity

A

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

22
Q

Diagnosis of cyanide toxicity

A

History of ingestion
Unclotted red blood
Analysis of frozen stomach contents

23
Q

Treatment of cyanide toxicity

A

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

24
Q

Examples, sources of methylxanthines

A

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

25
Q

Mechanism of action of methylxanthine toxicity

A

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

26
Q

Clinical signs of methylxanthine toxicity

A 
Vomiting, diarrhea, diuresis
Hyperactivity, "bounce", panting
Tachycardia, hypertension
Ataxia
Tremors, seizures
Coma
Death
27
Q

Diagnosis of methylxanthine toxicity

A

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

28
Q

Treatment of methylxanthine toxicity

A 
GI decontamination
Monitor EKG
Treat seizures
Maintain respiration
Fluid diuresis may increase excretion
29
Q

What is gossypol?

A

Found in pigment glands of cottonseed

Provides insect resistance

30
Q

Mechanism of action of gossypol toxicity

A

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

31
Q

Clinical signs of gossypol toxicity

A

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

32
Q

Diagnosis of gossypol toxicity

A

Evidence of cottonseed ingestion

33
Q

Treatment of gossypol toxicity

A

High protein diet
Vit A
Iron
Lysine

Remove gossypol source

34
Q

What is cantharidin?

A

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

35
Q

Mechanism of action of cantharidin toxicity

A

Inhibits protein phosphatases

Mucosal irritant

36
Q

Clinical signs of cantharidin toxicity

A

Colic, frequent urination, diaphragm contraction with heart beat, shock, cardiac toxicity

Irritation, ulceration of oral, GI, and bladder

37
Q

Diagnosis of cantharidin toxicity

A 
Alfalfa hay consumption
Beetles in hay or stomach
Hypocalcemia
Increased BUN
Ulceration of mucous membranes
Cardiac necrosis
Sudden death
38
Q

Treatment of cardiac glycoside toxicity

A

GI decontamination
GI protectant (sucralfate)
Antibiotics

Toxicology (7 decks)

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