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125 Cards in this Set
- Front
- Back
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What is one of the most important recommendations you can make to your client when they're concerned about the type of household chemical their pet may have consumed?
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BRING THE LABEL TO THE CLINIC!
Household chemicals have a wide range of toxicities, so it is important to know EXACTLY what the animal was exposed to. |
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For household chemicals that are mostly GI irritants, though may be caustic & corrisive, what is the general treatment regime for them?
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Dilution is the Solution!
No need for activated charcoal |
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Activated charcoal may be necessary in the treatment of toxicity from what classes of household chemicals?
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Anionic surfactants
Cationic surfactants Disinfectants |
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Match the Label/Signal word the the Oral LD50:
No label 50 - 500mg/kg Caution <5 - 50mg/kg Warning 5-15+ g/kg Danger: Poison 0.5 - 5 g/kg |
No label = 5-15+ g/kg
Caution = 0.5 - 5 g/kg Warning = 50 - 500 mg/kg Danger: Poison = <5 - 50 mg/kg |
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Soaps and Shampoos are usually a combination of what 2 household toxicants?
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Anionic & nonionic solutions/surfactants
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What do "dandruff" shampoos pose a potentially greater risk of toxicity than "normal" shampoo?
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Many dandruff shampoos have added zinc & selenium compounds, adding an additional metal toxicity to the detergent/surfactant toxicity
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When ranking household chemicals as toxicants, where do soaps fall in the range of fatal?
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Rarely if ever fatal
Sometimes added essential oils can contribute to their toxicity |
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What is the LD50 of Soap?
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7 - 20 g/kg
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Rank the following shampoos from most toxic to least toxic:
Rug, Hair, Dandruff What are their LD50's? |
Hair < Rug < Dandruff
Hair Shampoo >10 g/kg Rug Shampoo = 7-9g/kg Dandruff Shampoo = 3-10 g/kg |
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What system(s) is/are primarily affected by Soaps & Shampoos?
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GI
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What is the typical onset time for clinical signs associated with Soap & Shampoo toxicity?
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<2hrs.
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What are the treatment goals for a Soap/Shampoo toxicity case?
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Treat the symptoms (vomitting, diarrhea)
DILUTE!!! with milk or water. Since this is NOT a systemic problem (i.e. the toxicant is NOT being absorbed), there is NO NEED to include activated charcoal |
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What is the difference between a soap and a detergent?
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Soaps are salts of fatty acids obtained from animal or vegetable sources and are typically LESS TOXIC than detergents
Detergents are cleaning products based on non-soap surfactants. |
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How do surfactants work?
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Surfactants have both a hydrophobic & a hydrophilic end to them that lowers the surface tension of water to allow it to wet surfaces more easily.
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What are the different types of detergent surfactants? Give examples/compounds of each
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Anionic = alkyl sodium sulfate/sodium laurel sulfate
Nonionic = alyl-aryl polyehter sulfates/alkyl thoxylate (low-sudsing products). Cationic = Quaternary ammonIUM derivates such as benzalkonium chloride, benzethonium chloride. Amphoteric = combo of cationic & anionic. |
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What type of surfactant are most granular detergents? How toxic are they?
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Mostly anionic & nonionic surfactants.
Not very toxic |
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List the types of detergent surfactants from least toxic to most toxic:
Cationic, Non-ionic, Amphoteric, Anionic |
Nonionic < Anionic < Amphoteric < Cationic
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What physiologic effect will anionic surfactants have in the body?
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Change surface tension associated with RBCs, leading to HEMOLYSIS
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What body system(s) do cationic surfactants affect?
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CNS = major effects
Dermal = may also cause ulceration GI, as always |
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What is the typical onset period of a granular soap or detergent?
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< 2 hours
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What types of clinical signs can you expect to see in a cationic surfactant toxicosis?
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Muscle tremors, seizures
Bladder atony Oral/esophageal ulcers Stomach ulcers Salivation Dermal/corneal ulcers Acidosis & shock PARESIS & PARALYSIS |
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What are the primary treatment goals for a case of granular detergent toxicosis?
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Treat the symptoms!
Anionic --> MAY require activated charcoal IF HUGE amounts were ingested. Cationic -> Dependent on Dose, Concentration, Time since exposure. You may add activated charcoal if a concentrated amount was ingested. There's not much we can do for the ganglionic blockade... |
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Exposure to a substance above what pH is expected to cause ulcers & dermal erosions?
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pH 12+
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What system(s) is/are affected by exposure to automatic dishwasher detergent?
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GI
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What clinical signs are associated with exposure to automatic dishwasher detergent?
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Vomiting
Diarrhea Salivation GI pain Oral/esophageal/gastric erosion (possible) Hypocalcemia with muscle tremors (RARE) |
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What methods of treatment can you give to a patient with an automatic dishwasher detergent toxicosis?
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Dilution with milk or water --> Milk is better, since it contains some calcium
Take radiographs to look for GI lesions. Esophagoscopy & possible steroids for circumferential ulcers. Analgesics |
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Of all the liquid dishwashing detergents. which is the least toxic?
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DAWN! Typically used to clean animals caught in oil spills, etc.
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What are the 3 main types of Disinfectant cleaners?
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Phenolic compounds with soap or detergent
Pine-oil based compounds with soap or detergent Cationic surfactants straight or mxed with nonionic detergents |
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How do "builders" cause toxicity in animals?
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Builders are concentrated salts that bind up Calcium and make water softer.
Often include silicates, carbonates, phosphates, all with a high alkalinity. |
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TRUE/FALSE: All disinfectants are more toxic than soaps & plan detergents.
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TRUE!
Think about it...they are specifically made to kill things... |
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What are the LD50's for the 3 different disinfectants commonly found in households?
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Phenols = <0.5 g/kg
Pine oils = 1-2.5 mL/kg Cationic surfactants = ... not in the notes ... >0.1% to 5% cause damage |
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What system(s) is/are affected by Household Disinfectants?
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GI
CNS |
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What are the clinical signs associated with Household Disinfectant toxicosis?
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Vomiting, diarrhea
GI PAIN & EROSIONS Dermatitis, corneal ulcers DEPRESSION, LETHARGY CONVULSIONS (Cationic) ICTERUS & RENAL DAMAGE (PINE OIL, phenols) MET-HB (Phenol) |
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What lesions are typically seen with a Household Disinfectant toxicosis?
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Ulcers of skin, cornea, GI
Hepatic & renal necrosis |
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What are the recommended treatments for a Household Disinfectant toxicosis?
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DILUTION with milk/egg whites (or water) --> toxicants will preferrentially denature proteins in milk & eggs
Activated charcoal +/- saline cathartic Sucralfate for ulcers Acetylcysteine for GSH conjugation (pine oils & phenols) SAM for liver sparing action. +/- Emesis |
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Under what circumstances would emesis NOT be recommended in a Household Disinfectant toxicosis treatment?
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If the toxicant was >5% concentrated.
At this concentration, the toxicant is likely to cause ulcers, so emesis would not be a good thing... |
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What are some common "Alkaline" Household toxicants?
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Household Ammonia
Oven Cleaners Drain Cleaners |
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Which of the household chemicals has the worst prognosis for its toxicosis?
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Drain cleaners!
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At what precentages are the common Alkaline Household toxicants corrosive/toxic/etc.
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Household ammonia = >8.8% are corrosive
Oven cleaners = 4% (sodium hydroxide) All are corrosive Drain cleaners = Range from 2% to 50-100% sodium/potassium hydroxide. All are corrosive. |
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What are some of the primary differences between alkaline solution-derived necrosis & acidic solution-derived necrosis?
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Alkaline solutions with pH >12 cause LIQUEFACTIVE necrosis. The solutions continue to penetrate the mucosa until they reach body fluids that can neutralize them. Lesions are usually more serious & deeper than acid solution lesions.
Acid solutions with pH <2 cause COAGULATIVE necrosis. Usually show less penetration than alkaline solutions with a characteristics gray-black discoloration. |
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What system(s) is/are affected by Alkaline Household cleaners?
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GI
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What clinical signs are associated with an Alkaline cleaner toxicosis?
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Vomiting, Salivation
dysphagia, stridor Abdominal pain Hematemesis GI Ulceration, especially around pylorus Dyspnea with esophageal perforations |
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Is it recommended to administer a neutralizing acid to a patient that has consumed an Alkaline household cleaner? Why/why not?
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NO!!!
Giving a weak acid to neutralize the alkaline cleaner will cause an exothermic reaction that has adverse effects of its own. |
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What are the recommended treatments for Alkaline cleaner toxicosis?
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Dilution with milk/water (slowly neutralize pH)
Esophagoscopy Steroids (if circumferential ulcers WITHOUT perforation are present) Sucralfate for non-perforating ulcers Analgesics |
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TRUE/FALE: Emesis, Lavage and administration of activated charcoal are immediately recommended for toxicosis from Alkaline cleaners.
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FALSE!!! Emesis, lavage & activated charcoal/cathartics are absolutely CONTRAINDICATED
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What are some common household sources of Acid cleaners?
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Toilet bowl cleaners
Phosphoric acid (Lime-a-way) Antirust compounds Swimming pool cleaners |
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What are the 2 main acids that cause the damage from TB Cleaner & Acid toxicosis?
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Hydrochloric acid
Sulfuric Acid |
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The clinical signs and treatment of acid cleaner toxicosis is the same as for what other household toxicant?
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Alkaline cleaners
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What are some common sources of bleach?
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Liquid bleach (Chlorox)
Tile mildew removers Scouring powders |
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Why are scouring powders considered more toxic than household, liquid bleach?
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Prolonged contact with granular powders
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Of the types of bleach products commonly found in a home, which is the most toxic & which is the least?
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Most = Mildew removers (usually have Warning label)
Least = Liquid bleach (usually just below pH needed for ulcer formation. No label) |
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What system(s) is/are affected by bleach products? What are the clinical signs?
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GI
Vomiting Abdominal pain |
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How do you treat a bleach toxicosis?
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DILUTION with milk or water
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List the following Household Hydrocarbons from MOST volatile to LEAST volatile:
Rubbing alcohol, Gasoline/Kerosene, Motor Oil, Furniture polish |
Furniture polish > Gasoline/Kerosene > Rubbing alcohol > Motor Oil
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What routes of absorption do household hydrocarbons typically go through?
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Most are absorbed well Orally, Dermally or via Inhalation
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What is the LD 50 for most Hydrocarbons?
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0.5 - 5 g/kg
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Why are cats more sensitive than dogs to hydrocarbon toxicosis?
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Because they often have the added ingestion factor from grooming themselves.
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Are hydrocarbons more likely to induce CNS depression or seizures?
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CNS depression!
Hydrocarbons almost NEVER induce seizures. |
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How can heart failure & death result from hydrocarbon toxicosis?
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Volatile fumes may sensitive the heart to endogenous catecholamines & lead to sudden death +/- pulmonary edema
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What system(s) is/are affected by hydrocarbon toxicosis?
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CNS
Respiratory |
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What is the typical onset time for a hydrocarbon toxicosis?
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TRICK QUESTION!
It depends on the dose AND the route |
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What are the clinical signs associated with a hydrocarbon toxicosis?
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Depression/lethargy
Ataxia COMA VOMITING DIARRHEA Dyspnea, tachypnea, coughing Tachycardia SKIN IRRITATION |
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What is a major complication that can result from emesis of a volatile hydrocarbon?
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ASPIRATION pneumonia is "very" common with volatile hydrocarbon toxicosis
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How can you diagnose a hydrocarbon toxicosis?
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History of exposure with clinical signs
Chest radiographs showing aspiration pneumonia, leukocytosis, fever |
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After how long post exposure to a hydrocarbon is an animal likely to NOT develop aspiration pneumonia? Nor a clinical toxicosis?
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Over 1 hour post exposure = no aspiration pneumonia
Over 6-12 hours post exposure = No toxicosis |
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Treatment of hydrocarbon toxicoses is dependent on what factors?
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Volatility of hydrocarbon
Amount ingested (Time since ingestion) |
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Oxygen and/or detergents/hand degreasers are included in hydrocarbon toxicosis treatment when?
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Oxygen - for aspiration pneumonia
Detergents/degreasers - dermal exposures (aka, wash the animals) |
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TRUE/FALSE: Most toxicoses associated with household fertilizers are non-lethal and involve dogs more than cats.
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TRUE!
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What system(s) is/are affected by household fertilizers? What are the clinical signs associated with them?
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GI - vomiting, diarrhea, anorexia
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What is the treatment recommended for household fertilizer toxicosis?
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Symptomatic treatment
Dilution rather than activated charcoal Demulcents may be required |
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What general chemical property do the Neonicotinoids have?
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Agonistic then antagonistic actions at nicotinic sites.
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What is the most likely source for Nicotine in an animal?
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Smoking/antismoking product
No longer widely used as insecticide |
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What toxicokinetic properties make Nicotine toxic?
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Easily absorbed orally AND dermally
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TRUE/FALSE: Nicotine has a general toxicity that is not specific to insects.
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TRUE!
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What are the sites of action for Nicotine?
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Nicotinic receptor sites in ganglia of Autonomic Nervous System
NM junction |
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What is the prognosis for a Nicotine toxicosis?
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Poor
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If Nicotine is a CNS stimulant acting at nicotinic sites in autonomic ganglia & NMJ, what kind of clinical signs might you expect?
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Activation/Stimulation = Muscular signs, including muscle tremors, seizures, hyperesthesia, etc.
Block of receptors = ataxia, paralysis/paresis, muscle weakness, etc. |
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What are the sources/uses of Imidacloprid?
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Used as a crop protectant from sucking (but NOT chewing) insect.
Used as a topic flea adulticide for cats & dogs. |
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How does the chemistry of Imidacloprid & Nicotine differ?
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Imidacloprid is a chlorinated derivative of Nicotine that has been MODIFIED sufficiently to be much more selective for INSECTS rather than mammals.
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What properties of Imidacloprid make it MORE safe than Nicotine?
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Long enough to control insects, BUT not stable enough to accumulate in environment/patient
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What toxicokinetic properties make Imidacloprid a potential toxin for animals?
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Widely distributes on skin to kill fleas
Can be orally absorbed. |
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At what times the concentration of the labeled dose is Imidacloprid still safe, as per an FDA requirement?
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5 times the labeled dose!
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How does an overdose of imidacloprid manifest?
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Stimulates then blocks nicotinic receptors
Appears as muscle tremors/rigidity followed by muscle weakness & laxity. |
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What antidote used to treat Imidacloprid toxicoses?
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NONE! There is no antidote!
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Insecticides that act on Ion channels typically affect what channels?
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Na and Cl channels
Cl channels affected are usually GABA channels Na channels associated with neurons most notably affected by Ion Channel Insecticides. |
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Why do convulsions typically result from a toxicosis of Ion Channel Insecticides?
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Acute toxicity of Ion Channel Insecticides BLOCKS Cl channels (like GABA), preventing inhibition of ganglia while ENHANCING Na channels, resulting in repetitive firing & depolarization. All of this stimulates the nervous system.
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What is the general mode of treatment for Ion Channel Insecticide toxicoses?
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REMOVAL of insecticide, TIME and SUPPORT are the major players in the treatment of these insecticides.
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What are the toxicokinetics of Fipronil?
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DOESN'T readily penetrate skin
IF it enters the body, undergoes enterohepatic circulation. |
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How does the toxicity of a Fipronil toxicosis manifest?
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GABA receptor blocker mostly affects invertebrates, BUT...
Expected signs in mammalians include muscle fasciculations, temors, convulsion, lethargy, ataxia. |
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What is the time course of a Fipronil toxicosis?
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Onset in <7 hours.
Recovery within 12-24 hours. |
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What is the main treatment plan for a Fipronil toxicosis?
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TIME
Possible administration of GABA agonists (barbiturates, benzodiazepines) |
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What is the MOST common insecticide used?
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Pyrethrins/Pyrethroids
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What are the benefits of using a Pyrethrin/Pyrethroid?
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Narrow spectrum
Biodegradable Non-volatile Contact insecticide |
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What chemical structure do ALL Pyrethroids/Pyrethrins have in common?
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Esters!
All have sites for mixed function oxidase & esterase actions |
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What is the difference in the chemical structure between type I and II Pyrethroids?
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Type II have a -CN attached by Type I do not.
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What kinetic factors affect the absorption of Pyrethroids?
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Pyrethroids are polar molecules, therefore their absorption is influenced by their polarity and the solvent their mixed with.
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By what mechanisms are Pyrethroids metabolized?
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Esterases
Mixed function oxidases Glucoronidation |
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What is the difference in the toxicities of Type I and II Pyrethroids?
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"T" syndrome from Type I = tremors and hyperexcitability
"CS" syndrome from Type II = Tonic clonic seizures |
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Which of our domestic species are most susceptible to Pyrethroid toxicoses?
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CATS!
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What treatments are recommended for Pyrethroid toxicoses?
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No specific antidotes
WASH THE ANIMALS!!! Remove them from exposure Include anticonvulsants as needed |
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What is the prognosis of Pyrethroid toxicoses?
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Good, usually
Recovery typically occurs within <24 hours. |
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What are the 2 main chemical structures found in Organochlorine insecticides? How do their structures affect their actions?
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(1) Aliphatic structure = more likely top prevent closing of Na channel
(2) Multicyclic/Cyclodiene = more likely to be GABA receptor agonists |
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What properties do the aliphatic and multicyclic Organochlorines have in common?
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Lipophilic
Very stable Able to biomagnify |
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Why are Organochlorine toxicoses less likely to occur than with other insecticides?
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Most of them have been banned or are subjected to restricted use (require licensure to use!)
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What are some important facts about DDT?
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Organochlorine
Banned for general use in USA in 1970's May have contaminated other insecticides Acts on Na channel May still be used outside of USA |
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How does the lipophilic nature of Organochlorines affect their toxicokinetcs?
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Absorbed by ALL routes
Distributes into ALL tissues Stores in fat Gets into milk |
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Metabolism of Organochlorines is affects what factors?
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Metabolisms increases Organochlorine polarity and water solubility.
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What implications does a two-stage excretion have on the clearance of Organochlorines?
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Two stage clearance means rapid initial stage followed by SLOWER, long-term excretion
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How long is the t1/2 of Organochlorines?
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Terminal half life can range from 1 week to 2 months depending on the compound.
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BY what routes are Organochlorines excreted?
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Milk
Kidney Feces |
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Even though Organochlorines are not used much in the united states anymore, how might they still be a source of toxicosis?
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Many OC's remain in the environment & can be a source of secondary exposures & toxicities.
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Which would be more likely to have a higher concentration of OC's: a fish-eating bird of prey living in an OC contaminated habitat or a bloom of algae in an OC contaminated environment?
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Bird of prey --> due to OC's bioaccumulation properties, concentration of OC's in animals' bodies as they climb higher on the food chain.
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What is the mechanism of action for a chronic OC toxicosis?
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Increased induction of microsomal enzymes that leads to reduction of steroid hormones.
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What clinical signs are apparent from a chronic OC exposure?
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Endocrine disruption
Reproductive/dermal effects Anorexia Adrenal involution Hepatomegaly OC's in blood and fat |
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What treatment(s) is/are recommended for OC toxicoses?
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Limit exposure = TIME
Enhance metabolism (for OC's with Short T1/2) Enhance excretion |
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What is the mechanism of action of Amitraz?
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Alpha 2-agonist (like Xylazine!)
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What clinical signs may be apparent from an Amitraz toxicosis?
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Depression
Bradycardia Hypotension Vomiting Convulsions Elevated glucose (Humans) |
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What treatment(s) is/are recommended for an Amitraz toxicosis?
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Alpha 2 antagonist = Yohimbine, Tolazoline
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What is Hydramethylnon used for? How can you treat its toxic effects?
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Stomach poison for fire ants and roaches.
SYMPTOMATIC |
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What insecticide is very similar to Hydramethylnon in its use and treatment?
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Boric acid!
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What is one of the most common insect repellants used today? How does it work?
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DEET!
Decreases ability of insect to detect warmth and moisture |
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How do DEET toxicities manifest?
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Well, DEET is not really absorbed very well, so toxicosis is rare.
May cause dermatitis or ocular effects If it is absorbed systemically, it can cause encephalopathy with ataxia, confusion and temors being seen. |
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What are 2 common Insect Growth Regulators? What is their mechanism of action?
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Lufenuron - Interferes with chitin synthesis
Methoprene - Decreases maturation |
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What adverse effects are observed with Insect Growth Regulator toxicoses?
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GI upset mostly
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What is/are the primary use(s) of Rotenone?
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Topical insecticide for lice and mites
Fish anesthetic |
