4.2 Household Toxicants Flashcards
acid vs alkali burns
-acids cause coagulation necrosis > a barrier to further penetration
-alkalis cause liquefaction necrosis > facilitates rapid, deep dissolution of tissue (much more severe)
how are soaps made? what toxic signs do they cause?
- Made by reacting alkali with fat
- Primarily GI signs
- Alkali may cause caustic burns
- Homemade soaps, dishwasher detergents often contain free alkali (lye = NaOH/KOH)
Toxicity generally low, ingestion uncommon
treatment options for ingestion of soap
- Emesis (only if non-alkali)
- Dilution (oral milk or water)
- Fluids/electrolytes if vomiting/diarrhea severe (or if cardiac signs)
what are non-ionic detergents? how toxic are they? what signs do they cause when ingested?
e.g. many hand dishwashing detergents, shampoos, some laundry detergents
* Generally low toxicity
* Usually GI signs, mild corneal damage
* Ingestion is uncommon
what is a treatment for ingestion of non-ionic detergents?
- Decontamination (flush skin/eyes)
- Dilution (oral milk or water)
- Fluids if vomiting/diarrhea severe
what are anionic detergents? how toxic are they? what issues do they cause when ingested?
e.g. sulfates, sulfonates in laundry detergent automatic dishwasher detergents, some shampoos
* Toxicity mild to moderate (usually not fatal)
* Esophageal damage a major concern
* Ocular lesions more severe
* Ingestion uncommon but very harmful, intravascular hemolysis possible
how do we treat ingestion of anionic detergents?
- Decontamination (flush skin/eyes)
- Dilution (oral milk/water)
- Activated charcoal
- Fluids if vomiting/diarrhea severe
what are cationic detergents? how toxic are they? what problems do they cause when ingested?
- Quaternary ammonium compounds
- e.g. some detergents, fabric softeners, sanitizers
- Toxicity high to extreme
- Severe oral & esophageal caustic burns, severe ocular damage
- Profuse salivation, hematemesis, weakness, seizures, coma, death
how do we treat ingestion of cationic detergents? What should we be careful of, in particular?
- Decontamination (flush skin/eyes)
- Dilution/deactivation (milk, egg whites)
- Activated charcoal?
- Fluids to correct electrolyte imbalances
- DO NOT INDUCE VOMITING
- DO NOT NEUTRALIZE ALKALI WITH ACID > heat > burns
how toxic are other alkali products such as toilet bowl and drain cleaners, or bleach? what sort of effects do they cause? how can they be treated and what is the prognosis?
- Ingestions of these products are rare but contact can occur with spills
- Toxicity HIGH to EXTREME
- Effects similar to cationic detergents or
worse - May obliterate esophagus; gastric perforation
- Dilution & supportive care
- AC will not bind**
- Analgesics to control severe pain
- Prognosis grave
what is the timeframe and mechanism of ibuprofen toxicosis? what signs do we see?
Ibuprofen toxicosis: 30 minutes to 3 hours after ingestion
GI adverse effects are seen at lower doses, e.g. gastric ulcers (higher doses > multiple organ toxicity)
> Inhibits gastric mucus secretion, increases gastric acid production > ulceration & hemorrhage
Higher doses cause renal vasoconstriction, kidney damage, bleeding may be seen due to inhibition of platelet function
Corticosteroids exacerbate NSAID toxicity; do not use concurrently!!!
**why do corticosteroids exacerbate NSAID toxicity? what are the mechanisms of these two drugs?
Mechanism:
Phospholipids > arachadonic acid
=>leukotrines > inflammation
OR
=>prostaglandins > inflammation
-Steroids block the synthesis of arachadonic acid from phospholipids
-NSAIDS (eg. ibuprofen) block the synthesis of prostaglandins from arachadonic acid
>compounding effect?
most common signs of ibuprofen toxicosis
Most common signs: (worse if pre-existent dz present)
GI (vomiting, anorexia, diarrhea, melena)
Depression, ataxia
Renal
> Gastric hemorrhage less common in cats, primary signs usually renal
ibuprofen toxicosis treatment
If detected early, treatment aimed at reducing absorption (emesis, activated charcoal, cathartics)
IV fluids may be required to ensure adequate renal perfusion
GI perforations require surgery
Severe blood loss may necessitate transfusion
Omeprazole: proton pump inhibitor - inhibits gastric acid secretion > shortens recovery time
Misoprostol: PGE1 analogue that protects GI mucosae, decreases gastric acid secretion, increases bicarbonate secretion (more of a preventative)
what doses of acetaminophen (tylenol) cause toxicity?
Dogs: therapeutic dosage is 15 mg/kg TID
Toxicity seen with acute dosages of ~600 mg/kg, and occasionally with chronic therapy
Cats: far more sensitive, drug is not used therapeutically
Toxicity seen at dosages as low as 10 mg/kg
**what is the mechanism of acetaminophen toxicosis?
Metabolism in dogs:
Most of the drug is conjugated via hepatic glucuronidation & sulfation pathways to yield non- toxic metabolites > excreted in urine & bile > also some enterohepatic recycling
Ordinarily only a small minority of molecules undergo P450 metabolism > toxic intermediate metabolite NAPQI (N-acetyl benzoquinoneimine) that is then conjugated with glutathione
Glucuronidation & sulfation pathways are finite, so high doses result in increasing P450 metabolism
Acetaminophen also inhibits glutathione synthesis
> even more unconjugated toxic metabolite accumulates
Cats are deficient in enzymes required for hepatic glucuronidation, so even higher amounts of NAPQI toxic metabolite accumulate > essentially no safe dose
how can we treat an acetaminophen overdose?
Within limits, glutathione conjugation can inactivate this reactive intermediate > administer source of glutathione (n-acetylcysteine) > minimizes hepatic damage
what specifically does acetaminophen toxicosis damage? what clinical signs will we see in dogs and cats?
Metabolite directly damages plasma membranes
> damage most severe in liver, blood
Dogs: clinical signs are those of hepatic injury (vomiting, anorexia, tachycardia, tachypnea)
Cats: feline RBCs far more prone to oxidative injury (different hemoglobin structure)
> methemoglobinemia is the most prominent feature of feline acetaminophen toxicity
treatment steps for acetamiphen toxicosis and prognosis?
Treatment
1. minimize absorption (emesis or gastric lavage, followed by activated charcoal)
2. supportive therapy (for electrolyte disturbances, etc.)
3. source of glutathione (N-acetyl-cysteine) to speed conjugation of toxic metabolites > administer immediately to affected cat; repeat every 4 hours for 5 treatments
Prognosis depends on dose and delay before treatment
most common illicit drug conumed by animals, and most important thing to do with client in cases of illicit drug consumption
- Most common is dog eating marijuana (particularly edibles)
- Whatever the source, important to gain trust of client in order to help animal
effects of marijuana consumption on pets? signs? recovery time?
- Rarely fatal
- Stimulates cannabinoid receptor 1 in brain
- CNS signs: bradycardia, depression, ataxia, mydriasis; also urinary incontinence, vomiting, hypothermia, other
- Supportive care – control temperature; recovery may take up to 5 days
what are the effects of amphetamine consumptions? how do we treat?
Amphetamines: treat narcolepsy, ADD
* CNS stimulation: seizures
* Arrhythmias
* Supportive treatment and AC (inhibit enterohepatic recycling)
what can result in a false positive for amphetamines in a urine drug test?
- Decongestants containing pseudoephedrine can result in false positives on urine drug tests
what do barbituates do? what are the signs of overdose and how do we treat?
Barbiturates: sedatives, anticonvulsants
* CNS depression, extreme hypotension
* Supportive treatment, emesis (not if unconscious)/gastric lavage + AC
