Toxicology Flashcards
Antiemetic dose of 3% hydrogen peroxide
1-2mL/kg with max dose of 45mL/dog; If unsuccesful you can repeat x1
What are the adverse effects/mechanisms of hydrogen peroxide administration?
- 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
What is the MOA of intravenous lipids?
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
What are some toxins ILEs may be used for?
Loperamide, Vit D, Bromethalin, Naproxen, ivermectin, synthetic cannabinoids, THC, permethrin, macrocyclic lactose’s, diltiazem, lidocaine, ibuprofen, beta-blockers
What compound is responsible for CNS signs with eythylene glycol in cats?
Glycoaldehyde
What body system is most affected with castor bean toxicity?
GI
What is the toxic dose of ethylene glycol in dogs and cats?
Dog: 4.2-6.6mL/kg; Cat: 1.5mL/kg
What is the rate limiting step of ethylene glycol toxicity?
Oxidation in the liver via alcohol dehydrogenase
What is the major metabolite of ethylene glycol?
Glycoaldehyde
What metabolite of ethylene glycol causes metabolic acidosis?
Glycolate/glycolic acid
What clinical signs are associated with each stage of ethylene glycol toxicosis?
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
What type of crystals can be found on UA if a patient ingested ethylene glycol?
Calcium oxalate - monohydrate (picket fences)»_space;» diphydrate (envelope-shaped)
What clin path findings might you see with ethylene glycol toxicosis?
Hyperosmolality, high anion gap metabolic acidosis, hypocalcemia, hyperphosphatemia, hyperkalemia, hyperglycemia, isosthenuria, azotemia
What are the two substances that can be used to treat dogs that ingest ethylene glycol?
Ethanol - competitive inhibitor of ADH; 4-methylpyrazole (Antizol) - DOGS ONLY similar MOA to ethanol
Through what mechanism does strychnine cause clinical signs?
Inhibition of glycine, which is normally an inhibitory neurotransmitter. By inhibiting glycine you increase excitability of neurons
What are the clinical signs of strychnine toxicosis?
Apprehension, tension, stiff muscles +/- hyperthermia hours after exposure
How is strychnine toxicosis treated?
Sedate to prevent seizures, Methocarbamol for muscle tremors, Avoid stimulation, Acidify urine with ammonium chloride –> promotes urinary excretion
Why do patients with strychnine typically die?
Paralysis of respiratory muscles - will be in opisthotonus
What species of Lillies are toxic to cats?
Lilian and Memerocallis
Lilly ingestion causes what in cats?
Acute renal failure - all parts of the plant are toxic
Why is aspirin more toxic to cats than dogs?
They have reduced glucuronyl-conjugating capacity
How is aspirin metabolized?
Glucuronidation in the liver
What are clinical signs of aspirin toxicosis?
GI signs, renal, bleeding/methemoglobinemia
What is the mechanism through which cardiac glycoside plants cause toxicity?
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
What plants are considered cardiac glycosides?
Common oleander, yellow oleander, foxglove, lily of the valley, kalanchoe
What are clinical signs of cardiac glycoside toxicosis?
GI signs, cardiovascular changes (bradycardia, 1-3rd degree AV block, ventricular arrhythmias, asystole), sudden death
What is the mechanism of toxicity of yew plants?
Contain taxine which is a cardio toxic alkaloid
What are clinical signs of lead toxicity in dogs?
GI signs (with chronic low level exposure); Anemia; CNS signs (with acute, high level exposure –> causes ataxia, tremors, seizures, coma
What CBC changes might you see with lead toxicity in a dog?
Nucleated RBCs, basophilic stippling of RBCs, anemia
What is the half life of lead in dogs?
Triphasic - 12d, 184d, 4591d
What form of lead is most readily absorbed in the GIT?
Organolead (then lead salts, then metallic lead)
What happens in the GIT when lead is ingested?
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
Once absorbed, how much of the lead is bound to RBCS?
> 90%
What are the effects of lead toxicity?
- 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
How is lead toxicity treated?
Decontamination, chelation, supportive care
T/F: Chelation can be nephrotoxic so you should check the patient’s renal status before starting
TRUE
How does chelation work?
Binds lead into a soluble complex to be excreted in urine
What are some chelators that can be used to treat lead toxicosis?
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
What is the prognosis for dogs with CNS signs from lead toxicosis?
Guarded to severe; Prognosis is favorable with mild-moderate clinical signs
What is the mechanism for acteaminophen toxicity in cats?
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
