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ACVIM SAIM (2023) > Toxicology > Flashcards

Toxicology Flashcards

1
Q

Antiemetic dose of 3% hydrogen peroxide

A

1-2mL/kg with max dose of 45mL/dog; If unsuccesful you can repeat x1

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2
Q

What are the adverse effects/mechanisms of hydrogen peroxide administration?

A
  1. Corrosive damage: peroxidation of membrane lipids resulting in gastric ulceration. 2. Gas production: gastric dilation or gas emboli (portal vein, gastric wall, brain) —> 1mL of 3% H2O2 = 10mL O2. 3. Oxidative damage: to lipid membranes —> RBC hemolysis has been reported in a dog treated with 5x the max dose of H2O2
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3
Q

What is the MOA of intravenous lipids?

A

Lipid sink theory: ILE creates lipophilic circulating blood volume to which the lipid soluble toxins can translocate from tissue to plasma, enabling more rapid toxin elimination

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4
Q

What are some toxins ILEs may be used for?

A

Loperamide, Vit D, Bromethalin, Naproxen, ivermectin, synthetic cannabinoids, THC, permethrin, macrocyclic lactose’s, diltiazem, lidocaine, ibuprofen, beta-blockers

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5
Q

What compound is responsible for CNS signs with eythylene glycol in cats?

A

Glycoaldehyde

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6
Q

What body system is most affected with castor bean toxicity?

A

GI

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7
Q

What is the toxic dose of ethylene glycol in dogs and cats?

A

Dog: 4.2-6.6mL/kg; Cat: 1.5mL/kg

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8
Q

What is the rate limiting step of ethylene glycol toxicity?

A

Oxidation in the liver via alcohol dehydrogenase

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9
Q

What is the major metabolite of ethylene glycol?

A

Glycoaldehyde

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10
Q

What metabolite of ethylene glycol causes metabolic acidosis?

A

Glycolate/glycolic acid

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11
Q

What clinical signs are associated with each stage of ethylene glycol toxicosis?

A

Stage 1 (30m-12h): CNS depression, ataxia, vomiting, PU/PD; Stage 2 (12-24h): Pulmonary changes (NCPE), tachycardia, anorexia; Stage 3 (24-72h): Oliguric/anuric renal failure, vomiting, uremia, +/- seizures

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12
Q

What type of crystals can be found on UA if a patient ingested ethylene glycol?

A

Calcium oxalate - monohydrate (picket fences)&raquo_space;» diphydrate (envelope-shaped)

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13
Q

What clin path findings might you see with ethylene glycol toxicosis?

A

Hyperosmolality, high anion gap metabolic acidosis, hypocalcemia, hyperphosphatemia, hyperkalemia, hyperglycemia, isosthenuria, azotemia

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14
Q

What are the two substances that can be used to treat dogs that ingest ethylene glycol?

A

Ethanol - competitive inhibitor of ADH; 4-methylpyrazole (Antizol) - DOGS ONLY similar MOA to ethanol

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15
Q

Through what mechanism does strychnine cause clinical signs?

A

Inhibition of glycine, which is normally an inhibitory neurotransmitter. By inhibiting glycine you increase excitability of neurons

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16
Q

What are the clinical signs of strychnine toxicosis?

A

Apprehension, tension, stiff muscles +/- hyperthermia hours after exposure

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17
Q

How is strychnine toxicosis treated?

A

Sedate to prevent seizures, Methocarbamol for muscle tremors, Avoid stimulation, Acidify urine with ammonium chloride –> promotes urinary excretion

18
Q

Why do patients with strychnine typically die?

A

Paralysis of respiratory muscles - will be in opisthotonus

19
Q

What species of Lillies are toxic to cats?

A

Lilian and Memerocallis

20
Q

Lilly ingestion causes what in cats?

A

Acute renal failure - all parts of the plant are toxic

21
Q

Why is aspirin more toxic to cats than dogs?

A

They have reduced glucuronyl-conjugating capacity

22
Q

How is aspirin metabolized?

A

Glucuronidation in the liver

23
Q

What are clinical signs of aspirin toxicosis?

A

GI signs, renal, bleeding/methemoglobinemia

24
Q

What is the mechanism through which cardiac glycoside plants cause toxicity?

A

Inhibits Na/K ATPase pump —> slowed electrical conductivity w/decreased active transport of Na and and efflux of K —> RBC fragility and shortened life span

25
Q

What plants are considered cardiac glycosides?

A

Common oleander, yellow oleander, foxglove, lily of the valley, kalanchoe

26
Q

What are clinical signs of cardiac glycoside toxicosis?

A

GI signs, cardiovascular changes (bradycardia, 1-3rd degree AV block, ventricular arrhythmias, asystole), sudden death

27
Q

What is the mechanism of toxicity of yew plants?

A

Contain taxine which is a cardio toxic alkaloid

28
Q

What are clinical signs of lead toxicity in dogs?

A

GI signs (with chronic low level exposure); Anemia; CNS signs (with acute, high level exposure –> causes ataxia, tremors, seizures, coma

29
Q

What CBC changes might you see with lead toxicity in a dog?

A

Nucleated RBCs, basophilic stippling of RBCs, anemia

30
Q

What is the half life of lead in dogs?

A

Triphasic - 12d, 184d, 4591d

31
Q

What form of lead is most readily absorbed in the GIT?

A

Organolead (then lead salts, then metallic lead)

32
Q

What happens in the GIT when lead is ingested?

A

It is ionized in the acidic environment of the GIT. Ionization increases absorption. Absorption is also increased in animals deficient in Fe, Zn, Ca, or VIt D

33
Q

Once absorbed, how much of the lead is bound to RBCS?

A

> 90%

34
Q

What are the effects of lead toxicity?

A
  1. Competes with Ca and alters flux across membranes (lead can substitute for Ca in activation of protein kinase C) 2. Inhibition of cytochrome P-450 leading to aberrant neurotransmission of serotonergic levels. 3. Impaired growth hormone secretion . 4. Increased catecholamine levels. 5. Compete with other cations (ferrous iron, zinc) to alter enzyme function . 6. Interferes with cellular energy and metabolism in mitochondria. 7. Toxic to fetus/young animals - inhibits dendritic arborization in the brain. 8. Binds with sulfhydryl groups of enzymes –> interferes with enzymes involved in heme synthesis which results in RBC abnormalities and anemia. 9. Basophilic stippling of RBCs is due to accumulated ribosomal RNA aggregates
35
Q

How is lead toxicity treated?

A

Decontamination, chelation, supportive care

36
Q

T/F: Chelation can be nephrotoxic so you should check the patient’s renal status before starting

A

TRUE

37
Q

How does chelation work?

A

Binds lead into a soluble complex to be excreted in urine

38
Q

What are some chelators that can be used to treat lead toxicosis?

A

Calcium disodium EDTA (clinical improvement in 24-48h); British anti-lewisite (contraindicated in hepatic dysfunction); Succimer (PO admin; less nephrotoxic, doesn’t bind essential minerals); D-penicillamine (binds essential nutrients like Cu, Zn, Fe), chelates may be nephrotoxic

39
Q

What is the prognosis for dogs with CNS signs from lead toxicosis?

A

Guarded to severe; Prognosis is favorable with mild-moderate clinical signs

40
Q

What is the mechanism for acteaminophen toxicity in cats?

A

Acetaminophen is converted to NAPQI (more toxic metabolite) by cytochrome p450. NAPQI can then be detoxified by glutathione, but cats have a relative deficiency in this enzyme system

ACVIM SAIM (2023) (19 decks)

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