household hazards Flashcards
ethylene glycol (antifreeze) species, exposure scenarios and lethal dose
- All species are susceptible
- Most poisonings in dogs and cats
- Exposure scenario in animals
- Sweet taste previously
- Seasonal?
- Leakage from machinery
- Left in garage with access
ethylene glycol mechanism of toxicity and target organ
- Target organ: kidneys
- Secondary: CNS, cardiovascular system
-first phase acts like alcohol reaction but undergoes Bioactivation reaction in the liver.
2 rate limiting steps so rxn only goes so fast so you get a build up, can only metabolize at a set rate.
* Oxalic acid sequesters/binds calcium
* Urinary filtrate: precipitation of calcium oxalate crystals →
obstructive nephropathy
EG clinical phase 1
- Phase 1: due to unmetabolized EG which is an alcohol metabolite
- 30 minutes to 12 hours post-exposure
- CNS depression: resembles ethanol intoxication, appear drunk
- Nausea, vomiting, depression, ataxia, hypothermia, polyuria (dogs only) and polydipsia
- With worsening CNS depression, animals drink less= dehydration
EG clinical phase 2
- Phase 2: due to EG metabolites, glycolic acid, oxalic acid
- Species differences: 12-24 hrs in cats, 36-72 hours in dogs
- Severe metabolic acidosis → myocardial depression, tachypnea, tachycardia
- Severe lethargy progressing to coma
- Oliguria progressing to anuria
EG clin path features
- Hypocalcemia**, hyperphosphatemia
-High anion gap, titration type metabolic acidosis (↓ HCO3-)**
* Why? Accumulation of glyoxylic acid, decreased GFR
urinalysis: Hallmark: calcium oxalate crystals**
-azotemia
-aciduria
EG histology features
- Histologic pathology: acute tubular necrosis with calcium oxalate crystals**
- Kidney, other locations (gastrointestinal tract, heart, brain)
- Birefringent crystals under polarized light
EG management
decontaminate: no AC or emesis due to alcohol base and cns signs
Antidotes:
* Ethanol (alcohol) IV: competition for alcohol dehydrogenase
- 4-methylpyrazole (fomepizole): inhibition of alcohol dehydrogenase
- Timing is key – give antidote prior to complete bioactivation of EG**
- Disadvantages to using ethanol: CNS depression, metabolic acidosis
- Symptomatic and supportive care for the kidneys, dialysis
- Good prognosis if treated by 5 hours post-ingestion (dogs), 3 hours (cats)
EG diagnosis
- Examine muzzle, paws, vomitus, urine with a Woods Lamp
-send out tests - Supportive findings on clinical pathology: blood gas, chemistry,
-Histologic findings – CaOx crystals are basically pathognomonic
Nicotine poisoning , exposure, target, toxicity
- Ingestion of cigarette butts, e-cigarette cartridges,
nicotine gum and patches, chewing tobacco - Toxicity: clinical signs at >1 mg/kg BW
- One cigarette can cause symptoms in a small dog
-target: CNS
- Mechanism: activation of nicotinic acetylcholine receptors in autonomic ganglia, CNS stimulant
nicotine clinical features
- Onset: within an hour of exposure
- Lower doses: CNS/neuromuscular excitation
- Higher doses: CNS excitation followed by CNS depression
- GI: vomiting, defecation, salivation
- CV: bradycardia or tachycardia,
- CNS: agitation, hyperexcitability, tremors, convulsions
high doses: * Progressive descending paralysis and neuromuscular
blockade → respiratory failure
bleach target
Mucosal irritation**
* Ingestion: corrosive injury to GIT
* Inhalation: irritation and respiratory symptoms
* Ocular: corneal irritation, damage
bleach clinical features
- Dilute products: hypersalivation, mild vomiting, anorexia, diarrhea, depression
- Concentrated products:
- Corrosive injury to the gastrointestinal tract
- Pain, anorexia, hypersalivation, vomiting ± blood, diarrhea
- Can lead to serious secondary problems
- Perforation, septic peritonitis
- Stricture formation
-corneal ulcers,
-resp damage, pulmonary edema
bleach management and diagnosis
- Decontamination:
- Oral: do not induce vomiting
- Dermal: gentle washing + E-collar
- Respiratory: fresh air
- Ocular: rinse with physiologic saline
- Oral administration of milk or water
- Anti-emetic, gastroprotectants
- Diagnosis: history of possible exposure; smell of bleach on the patient or see bleached hair
smoke inhalation different types of asphyxiants
Categories of toxic combustion products:
* Irritants: produce local effects on the respiratory tract
* Hydrophilic vs. lipophilic
* Ammonia, acrolein, PVC, sulfur dioxide, chlorine, phosgene,
isocyanates
- Simple asphyxiants: displace oxygen (Carbon dioxide, methane, oxygen-deprived environments)
- Chemical asphyxiants: prevent oxygen utilization
- CO, HCN, H2S, nitrogen oxide
smoke inhalation clinical
- Severe respiratory problems
- Cough, stridor
Injury of face, lips, eyes, nasopharynx - Dyspnea, tachypnea,
-cyanotic or cherry red MM
Cause of death: asphyxiation
* CNS depression due to asphyxiation
