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165 Cards in this Set
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What is the most common reason for a canine pet owner to call the poison control hotline |
Ingestion of human pharmaceuticals
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What is the most common reason for a feline pet owner to call the poison control hotline |
Exposure to insecticides (usually non feline topical application flea preventative)
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Majority of calls to the Pet Poison Helpline affect what species |
are canine related
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What are the most common recorded reasons for death in patients that had death as a recorded outcome |
Ingestion of human pharmaceuticals
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What were the most common foreign body calls in regards to |
Surprisingly, silica gel packets made up over 50% of the calls falling into the foreign body category. Affect labs most commonly
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What is the most common food related ingestion reported |
Chocolate
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What are the most common types of insecticides called about |
Pyrethrin-based insecticides accounted for over 80% of the insecticide calls, followed by avermectin or ivermectin, hydramethylnon, imidacloprid, and boric acid.
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Are silica dessicant packets harmful to dogs and cats |
Yes, Each of these ingredients may irritate the gastric mucosa; the iron-containing packets and color indicator–containing packets can be toxic to dogs and cats
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Are swifter pads hazardous to dogs |
No, the main ingredients are water and propylene glycol (not in a concentration to be hazardous)
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How toxic is bleach |
When used on surfaces, not overly hazardous, especially when diluted. Both ultra Clorox and regular Clorox bleach formulations contain 5.25% aqueous sodium hypochlorite but not sodium hydroxide (i.e., lye). However, sodium hypochlorite is still corrosive and may cause harm from eye or skin contact, ingestion, or inhalation. It is often used as a good premise disinfectant, but it is best to keep it away from pets.
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Are pot scrubbing brushes toxic |
No but can serve as a foreign body
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Is febreeze toxic to dogs |
NO, Zinc chloride, present in the pre-1998 formulation, was removed, and now the product is sold as a pump spray rather than as an aerosol that could have been an inhalation hazard to some birds in confined spaces. Febreze contains water, alcohol, a corn-derived odor eliminator, and fragrance. Toxicity is not expected with routine use, even with exaggerated exposure.
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Is resolve carpet cleaner toxic |
No, It is not a lethal formulation. It can cause temporary minor eye irritation and mild gastrointestinal upset if ingested. It is best to keep all household products out of a pet's reach.
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Are macadamia nuts toxic |
Yes, after ingestion can cause vomiting, weakness and depression in 6 hours. Toxic dose is 1 nut per kilogram of body weight, or more.
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Are grapes and raisins toxic |
Yes, Vomiting, polydipsia, and lethargy can occur 5 to 6 hours after ingestion, followed by anorexia, anuria, tremors, and diarrhea. One to two grapes per kilogram of body weight has been reported as sufficient to induce adverse clinical signs in some dogs.
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Are sugarless gums toxic |
Yes, Weakness, ataxia, and total collapse may occur 30 to 60 minutes following ingestion of significant amounts of sugarless candy, gum, or breath-mints. Xylitol promotes insulin release by the pancreas, which results in profound hypoglycemia. Absorption is rapid, and activated charcoal is not efficacious in most instances. Acute hypoglycemia is best treated with intravenous dextrose— an initial bolus followed by continuous intravenous drip, with blood glucose concentrations being monitored over the next 12 to 24 hours
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Is tea toxic to dogs and cats |
Yes, Tea contains 300 to 1200 mg/ oz of caffeine, whereas semisweet chocolate contains 22 to 138 mg/ oz, making tea on average 5 to 10 times more toxic than chocolate.
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How is chocolate toxic |
Chocolates contain the methylxanthines caffeine and theobromine, which can be toxic. Unsweetened baking chocolate contains the most methylxanthines (40 and 390 mg/ oz for caffeine and theobromine, respectively), and white chocolate has the least (0.8 and 0.2 mg/ oz, respectively). Hyperactivity, polydipsia, vomiting, diuresis, diarrhea, restlessness, tachycardia, cardiac arrhythmia, and seizures usually occur in a progressive fashion beginning shortly after significant ingestions. Treatment should be directed at decontamination , control of anxiety and seizures, and the support of renal elimination through fluid diuresis.
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Are onions and garlic toxic |
Yes, cause free radicals that cause Heinz bodies to form, damage to red blood cells, hemolysis , and methemoglobinemia. Effects persist for several days after exposure stops. Vitamin C and/ or administration of other antioxidants may have therapeutic benefits. Cooked onions and garlic are much less of a hazard than the raw food.
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Are herbal products safe |
No, The essential oils in such materials are irritants, which cause damage to sensitive respiratory cells, skin epithelium, and mucous membranes in general. Some herbal supplements may also contain steroids, benzodiazepines, heavy metals, analgesics, nonsteroidal antiinflammatory drugs, caffeine, atropine, and other constituents that are hazardous to pets that
Are easter lilies toxic |
Yes, Vomiting, hypersalivation, depression, and anorexia usually occur within 1 to 2 hours after ingestion, followed by anuria and severe renal failure 2 to 4 days later. All parts of the plant should be considered poisonous, and almost all species of Lilium should be considered toxic. Dogs only appear to be affected with gastrointestinal upset. Time is important part of prognosis
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Are poinsettas toxic |
Yes, This genus may contain a milk-like sap that contains diterpenoid esters. These compounds can act as irritants. On the other hand, cats or dogs chewing or ingesting the cultivated ornamental poinsettia flower or leaves rarely exhibit more than mild gastrointestinal upset or simply drool from the plant's taste. Serious consequences are rarely seen. Treatment usually consists of washing away the sap with a drink of water or milk.
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Are pennies toxic |
Yes, U.S. pennies minted since 1982 are copper coated, weigh 2.5 g, and contain 97.5% zinc. Although the adverse clinical signs of zinc poisoning, characterized by severe gastroenteritis and marked intravascular hemolysis, may be delayed following the ingestion of pennies, significant lodging of pennies in the acid media of the stomach increases the risk of zinc poisoning.
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Are centipedes toxic |
Yes, All species of the order Scolopendromorpha (i.e., centipedes having 21 or 23 pairs of legs) are venomous and can inflict harm by their bites or because they have been ingested. Venom contains: endopeptidase, cardiotoxin (toxin-S), serotonin, histamine, lipids, and various polysaccharides have been identified. Not fatal but ingestion can produce vomiting, anxiety, and an irregular heartbeat or may simply induce a mild digestive upset.
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Ingestion of catepillars, butterflies and moths toxic |
Yes, toxic. Several types of hair, setae, or bristles cover the bodies of butterflies, moths, and their caterpillars. These hairs are irritants and sometimes are associated with venomous glands. No less than 200 varieties of these insects are known to be poisonous. Harm may result as a dermatologic syndrome, an ophthalmic injury, or respiratory and digestive syndromes. Mild gastrointestinal upset appears to be the most common hazard.
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Is vitamin A toxic |
Excessive amounts of vitamin A promote bone lesions with potential development of exostoses, which in turn may cause pressure on spinal nerves, resulting in paresis or other nerve deficits.
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Is vitamin D toxic |
Excessive amounts of vitamin D lead to hypercalcemia and calcium deposition of soft tissues, resulting in gastrointestinal, cardiopulmonary, and renal pathophysiology
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Are mosquito repellants toxic to dogs and cats |
Yes, All DEET (N ,N-diethyl-meta-toluamide)– containing mosquito repellent products are potentially toxic to cats and dogs. Hypersalivation, vomiting, anxiety, tremors, ataxia, and seizures may occur within 6 hours following excessive exposure. Animals need to be decontaminated (dermal washing, oral-activated charcoal), their hydration monitored, and supportive therapy initiated as soon as possible following exposure. There is no antidote.
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Are other types of mosquito repellants (larvacides) toxic to dogs and cats like donuts, etc |
No, All mosquito prevention products containing BTI for use around the home (e.g., floating donuts, granules, liquids, briquettes ) are generally safe. They may potentially cause gastrointestinal upset 3 to 6 hours following ingestion, and on rare occasions ingestion of floating donuts could result in formation of a gastrointestinal obstruction.
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What are the two major types of antidotes |
Chemical, Pharmacological
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What are three emetics that can be used in veterinary medicine |
Xylazine, Apomorphine, Hydrogen peroxide
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Which ones can be reversed and with what |
Xylazine reversed with yohimbine, Apomorphine reversed with naloxone
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Name contraindications to inducing emesis |
Emesis should not be induced if the animal has been vomiting or if toxicant exposure has occurred over 3 hours before admission to the hospital. Moreover, it is not recommended to induce vomiting when a corrosive chemical has been ingested, if the animal cannot gag, or when there is evidence of preexistent or developing esophageal, cardiac, respiratory, or central nervous system disease. Marked sedation or loss of consciousness is a contraindication for emetics.
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When should activated charcoal not be used |
Caustic (alkaline) chemicals, petroleum distillates, or small molecules such as alcohols , some mineral acids, or ionized metals or minerals (e.g., sodium, lithium).
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What toxicities should receive multiple doses of activated charcoal |
Re-dosing at one half of the original dose can be considered at 4- to 8-hour intervals for toxicants that undergo enterohepatic recirculation including phenobarbital, methylxanthines (chocolate), theophylline, marijuana, ivermectin, and nonsteroidal antiinflammatory drugs
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What is a cathartic |
Reduces the amount of time a substance is in contact with the GI tract. Cathartics include sorbitol and magnesium or sodium sulfate salts. These may be incorporated into some commercial activated charcoal products or administered separately.
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When is intravenous lipid recommended |
ILE has been recommended as a potential antidote for lipophilic drug toxicosis.
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What drugs has ILE been demonstrated to help with |
bupivacaine , lidocaine, clomipramine, verapamil, bupropion , mepivacaine, ropivacaine , haloperidol, quetiapine, doxepin, carvedilol, carbamazepine, flecainide, hydroxychloroquine, amlodipine, propranolol, calcium channel blockers (e.g., diltiazem), and macrocyclic lactones (e.g., moxidectin, ivermectin).
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What are the proposed mechanisms of action for ILE |
Providing myocytes with energy substrates, thereby augmenting cardiac performance. Restoring myocardial function by increasing intracellular calcium concentration. Acting as a lipid sink by sequestration of lipophilic compounds into the newly created intravascular lipid compartment (a lipid or pharmacologic sink). With this lipid sink hypothesis, compartmentalization of the drug into the lipid phase results in a decreased free drug concentration available to tissues/ Increasing the overall fatty acid pool, which overcomes inhibition of mitochondrial fatty acid metabolism (e.g., bupivacaine toxicosis).Currently, the most supported hypotheses are that ILE improves cardiac performance and provides a lipid sink effect in the vascular compartment.
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What dangers are reported with ILE in human medicine |
Delayed or subacute reactions to ILE are commonly referred to as fat overload syndrome ( FOS). Reactions are often the result of accidental administration of excessive volumes or rates that overwhelms the endogenous lipid clearance mechanisms. FOS is characterized by hyperlipidemia, hepatomegaly, icterus, splenomegaly, thrombocytopenia, increased clotting times, hemolysis, and variable end-organ dysfunction.
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How does one treat Fat Overload Syndrome |
Management of FOS consists of both discontinuation of ILE administration and supportive care. Resolution of clinical signs is expected after the ILE is metabolized, but permanent organ damage has been reported. Plasma exchange has been recommended for cases of FOS that failed to respond to conservative therapy. Heparin, which elicits significant effects in lipid metabolism, has been clinically used to prevent adverse events from ILE administration. Although heparin can potentially minimize hyperlipidemia, its routine use with ILE therapy is not currently recommended.
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What are the names for human prescription amphetamines that an animal may be accidentally exposed to |
dextroamphetamine (Dexedrine), methylphenidate (Ritalin, Concerta), pemoline (Cylert), phentermine (Fastin), and the combination of dextroamphetamine and amphetamine (Adderall)
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What are some characteristics of amphetamines pharmacologically and their mechanism of action |
Amphetamines have a stimulant effect on the cerebral cortex through release of catecholamines, acting as a dopamine excitatory receptor agonist and enhancing release of serotonin. The are well absorbed and have peak effects within 1-3 hours.
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What are the clinical signs associated with ingestion of methamphetamines |
Restlessness , pacing, panting, and an inability to sit still. These signs can progress to pronounced hyperactivity, hypersalivation, vocalization, tachypnea, tachycardia , tremors , hyperthermia, seizures, and potentially death. In some cases animals may exhibit depression, weakness, and bradycardia.
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What is the recommended treatments for ingestion |
Ingestions of amphetamine products less than 30 minutes prior can undergo induction of emesis followed by activated charcoal and a cathartic. If already exhibiting signs of stimulation not be induced to vomit because of the risk of aspiration or if the product is rapidly absorbed with the possible rapid onset of signs, emesis is not recommended. For those cases gastric lavage followed by the instillation of activated charcoal and a cathartic is a safer approach. Stimulant signs associated with amphetamine intoxication can be treated with acepromazine or chlorpromazine. Phenothiazine tranquilizers have a protective effect. Phenobarbital, pentobarbital, and propofol also be used to treat CNS signs. Cyproheptadine, a serotonin antagonist, may help reduce the CNS signs. Tachyarrhythmias should be treated with a β-antagonist. Hyperthermia should be corrected using a water mist and fans. Animals should be monitored to prevent subsequent hypothermia and housed in a dark, quiet environment to avoid external stimulation. Fluid therapy is generally recommended
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What is not recommended as therapy for methamphetamine ingestion |
Diazepam is not recommended because it can exacerbate the stimulatory signs in some animals.
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What is the mechanism of action of cocaine |
CNS stimulant. It acts to block the reuptake of serotonin and norepinephrine and has the ability to block cardiac sodium channels
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What are the clinical signs of cocaine toxicoses |
Animals initially become restless and hyperactive. Signs can progress rapidly to tremors, tachycardia, hypotension, prolongation of QRS intervals, tachypnea, and seizures.
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How do you diagnose cocaine or methamphetamine toxicities |
Observational, history, or urine OTC kits available for humans
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What are the treatments for cocaine intoxication |
Gastric lavage with administration of activated charcoal and a cathartic. Tremors and seizures controlled with diazepam, chlorpromazine, or a barbiturate. Pretreatment with chlorpromazine effectively antagonized the effects of cocaine in experimentally dosed dogs. Sodium bicarbonate decreases the likelihood of development of ventricular arrhythmias, shortens the prolonged QRS complex duration, counteracts the reduction in mean arterial blood pressure, and reverses cocaine-induced sodium channel blockade, fluids, control body temperature
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What is THC |
Tetrahydrocannabinol (THC) marijuana
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What are the pharmacologic properties of THC |
Highly lipophilic, protein bound, has a large volume of distribution, and undergoes enterohepatic recirculation. Slow elimination from the body. Small amounts of metabolites are excreted in the urine, with the remainder through the feces via the bile. Marijuana has a wide margin of safety.
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What are the properties of THC intoxication |
Depression, disorientation, lethargy, ataxia, bradycardia, vomiting, tremor, mydriasis, hypothermia, and urine dribbling.
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What are the recommended treatments |
Repeated doses of activated charcoal, supportive, watch for hypothermia
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What is the mechanism of action and pharmacologic properties for most opioids |
Well absorbed from the gastrointestinal tract and rapidly metabolized in the liver. Morphine is glucuronidated, and the glucuronide is then excreted by the kidney. Most are agonist, antagonists, or partial agonists for mu receptors
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What are the clinical signs associated with opioid toxicity |
Vomiting, defecation, salivation, lethargy and depression, and ataxia. In severe cases respiratory depression, constipation, hypothermia, coma, seizures, and pulmonary edema
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What are the recommended treatments for opioid toxicity |
Emesis - Pylorospasm produced by the opioid may cause much of the drug to remain in the stomach; thus gastric lavage, activated charcoal, and a cathartic may be effective even several hours after ingestion.
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What are the severe concerning effects of opioid toxicity |
Respiratory depression is the most common cause of death with opioid overexposure and should be treated by establishment of a patent airway, assisted ventilation, and oxygen.
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What are the pharmacologic properties of Barbituates |
Lipid solubility of the drug determines the distribution of the barbiturate; The barbiturates are metabolized in the liver by hepatic microsomal enzymes and excreted in the urine
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What are the mechanisms of action for barbituates |
Barbiturates activate γ-aminobutyric acid A receptors and inhibit excitatory glutamate receptors.
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What are the clinical signs of barbiturate ingestion |
Clinical signs can include depression, ataxia, incoordination, weakness, disorientation, recumbency, coma, hypothermia, tachycardia or bradycardia, and death. Barbiturates can be detected in stomach contents, blood, urine, liver, and feces.
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What are the treatments recommended for barbiturate ingestion |
Activated charcoal acts as a sink, encouraging the barbiturate to diffuse back into the intestine from the circulation, even for compounds administered parenterally. Gastric lavage followed by activated charcoal and a cathartic is a safer alternative for animals exhibiting clinical signs
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What are contraindications for inducing emesis in a dog or cat that had ingested anti-depressants or anxiolytics |
Giving hydrogen peroxide or other home remedies to induce emesis in a cat, any patient demonstrating signs of toxicity especially CNS depression, magnesium based cathartics are not recommended because of the propensity of developing constipation, apomorphine is not recommended in cats
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Besides inducing emesis in patients that can safely undergo this, what else can be used to treat these drugs |
Activated charcoal with a cathartic such as sorbitol also may be administered in effort to adsorb the toxicants. In order to reduce the risk of aspiration, administration via an orogastric tube is advised in any symptomatic patient.
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What is the mechanism of action for SSRI’s |
SSRIs block the reuptake of serotonin in the presynaptic membrane, which results in an increased concentration of serotonin in the CNS.
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Which drugs are classified as SSRIs |
Fluoxetine (Prozac), citalopram (Celexa), escitalopram (Lexapro), paroxetine (Paxil), and sertraline (Zoloft), many of which are highly protein bound and all of which undergo hepatic metabolism.
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What clinical signs are seen in patients with SSRIs |
Tremors, seizures, nystagmus, dysphoria, vocalization, aggressive behavior, ataxia, and bradycardia. As the degree of overdose increases, so does the risk for serotonin syndrome: toxidrome characterized by central nervous, autonomic , and neurobehavioral signs such as muscle rigidity, increased reflexes, tremors, hyperthermia, hypertension, and transient blindness.
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What are other supportive therapies that can be utilized with SSRIs |
Cyproheptadine (a serotonin antagonist) is useful in reducing the severity of signs, especially vocalization and dysphoria. Agitation may be treated with acepromazine or chlorpromazine. Due to the risk for sedation and hypotension from phenothiazines, start at the low end of the dosage range For seizures in the absence of serotonin toxicity, benzodiazepines (e.g., diazepam) are effective. In cases of serotonin toxicity, benzodiazepines may exacerbate neurologic signs; therefore barbiturates (phenobarbital) are recommended. Additional treatments include methocarbamol for tremors and IV fluids for thermal cooling and to maintain hydration and adequate tissue perfusion. β-Blockers for tachycardia and hypertension.
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What is the mechanism of action of benzodiazepenes and non benzodiazepine hypnotics |
Effects through the inhibitory neurotransmitter γ-aminobutyric acid (GABA) and have similar clinical effects and treatment regimens. Common BZDs used off-label in veterinary medicine include alprazolam (Xanax), diazepam (Valium ), lorazepam (Ativan), midazolam (Versed), and zolazepam found in combination with tiletamine, a dissociative agent (Telazol). Other BZDs frequently used in human medicine include clonazepam (Klonopin), oxazepam (Serax), and temazepam (Restoril). Common non-BZD hyptnotics or sleep aids include zolpidem (Ambien), eszopiclone (Lunesta), and zaleplon (Sonata).
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What are the observed clinical signs with toxicity with BZD and non BZD hypnotics |
Chronic use of oral BZDs in cats, however, can result in fulminant hepatic failure and is not recommended. CNS depression, ataxia, and/ or aggression. Rare signs include hypotension , hypothermia , coma, or seizures. Paradoxically, approximately 50% of animals ingesting these agents display neurologic stimulation and excitement.
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What are the treatments for toxicities with these medications |
Appropriate decontamination, supportive care, and, if necessary, the reversal agent/ antidote flumazenil (Romazicon).
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How do tricyclic antidepressants worl |
TCAs are structurally similar to phenothiazines and act on numerous receptors by inhibiting the neuronal reuptake of norepinephrine, serotonin, and dopamine in the CNS. They also have an affinity for muscarinic and histamine (H 1)-receptors and can cause a sodium and potassium channel blockade to varying degrees. The most common TCAs used in veterinary medicine include amitriptyline and clomipramine (Clomicalm).
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What are the signs of toxicity with TCAs |
TCAs may lead to profound cardiac toxicosis in addition to neurologic signs. Clinical signs may develop within the first few hours: CNS depression, seizures, anticholinergic signs -mydriasis, tachycardia, urinary retention, and a slowed gastrointestinal (GI) transit time; bradycardia, hypotension, and arrhythmias secondary to inhibition of fast sodium channels in the cardiac ventricles. Cardiovascular collapse is often the cause of death in domestic animals following overdose.
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How are toxicities with TCAs treated |
Dextrose supplementation as needed, continuous electrocardiographic (ECG) monitoring, IV fluids, Cyproheptadine may be helpful. Diazepam or barbiturates for seizures. Phenothiazines should not be administered because these may exacerbate the clinical signs.
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Aside from appropriate decontamination of an OTC drug within 2 hours of its ingestion, what are the general recommendations for most of these toxicities |
Activated charcoal combined with an osmotic or saline cathartic
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What is the mechanism of action for NSAIDs |
Most NSAIDs act as nonselective inhibitors of the enzyme cyclooxygenase (COX), inhibiting both the cyclooxygenase -1 (COX-1) and cyclooxygenase-2 (COX-2) isoenzymes. COX catalyzes the formation of prostaglandins and thromboxane from arachidonic acid. Aspirin irreversibly inhibits COX, while the other commonly used NSAIDs (e.g., ibuprofen, naproxen) reversibly inhibit COX.
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Which species has a longer half life of aspirin |
Cats: the half-life of aspirin in cats approaches 40 hours, compared with 7.5 to 8 hours in dogs
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Which species has a longer half life of piroxicam |
Dogs: The plasma elimination half-life of piroxicam has been reported as 37 to 40 hours in dogs, 12 to 13 hours in cats
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What are the side effects or signs of toxicity with NSAIDS |
Vomiting, CNS depression, anorexia, diarrhea, and ataxia. Dogs are particularly sensitive to the ulcerogenic effects of NSAIDs. Renal disease can occur, onset of renal failure often occurs within the first 12 hours after NSAID exposure but may be delayed 3 to 5 days. Hepatopathies can occur but thought of as an idiosyncratic reaction. Additional effects: decreased platelet aggregation leading to increased bleeding time, bone marrow depression, allergic reactions, and seizures.
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What therapies are utilized with NSAID toxicity |
Fluid therapy, histamine (H 2)-receptor antagonists (ranitidine, famotidine, and cimetidine) and proton pump inhibitors (PPIs); Misoprostol.
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What is the mechanism of action for misoprostol |
Synthetic prostaglandin E 1 analog , prevents aspirin-induced gastric ulcers in dogs but is generally less effective after an ulcer forms
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What are the side effects for misoprostol |
Misoprostol also is associated with adverse side effects such as abdominal pain, vomiting, and diarrhea.
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What doses of ibuprofen have been shown to be well tolerated by dogs and cats |
100 mg/ kg for dogs and 50 mg/kg for cats. 250 to 300 mg/ kg in either dogs or cats have resulted in clinical signs of acute renal failure in addition to gastrointestinal lesions.
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What is the toxicity level for naproxen |
Naproxen is approximately 10 times more potent that aspirin as a COX inhibitor. In dogs-half-life of 35 to 74 hours and undergoes extensive enterohepatic recirculation. Toxicosis in a dog given 5.6 mg/ kg of naproxen for 7 days involved signs of anemia, melena, and renal and hepatic dysfunction.
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What was the toxicity level established for ketoprofen |
Ketoprofen at 2 mg/ kg PO for 4 days, followed by 1 mg/ kg daily PO for up to 90 days, was associated with prolonged bleeding time (by day 7 of dosing) and gastric lesions at the end of the study.
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In which ways is asprin different from other types of NSAIDS |
More extensive hepatic metabolism ( to salicylic acid), extensive phase II metabolic conjugation with glucuronic acid, and more widespread systemic delivery. Plasma half-life is 8 and 38 hours in dogs and cats, respectively.
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What is the toxic dose of aspirin |
Gastric ulcers developed in beagles within 2 hours after oral administration of aspirin at 100 mg/ kg. Adverse effects include (acidemia, severe CNS depression, cerebral edema, cardiac or renal failure)
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What is the mechanism of action for Tylenol |
Para-aminophenol derivative with antipyretic and analgesic activity, but minimal antiinflammatory effects.
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How is Tylenol different from other NSAIDS |
Does not inhibit neutrophil activation, has little ulcerogenic potential, and has no effect on platelets or bleeding time. May act by inhibiting COX or via interactions with the cannabinoid and serotonergic systems of the CNS.
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What makes acetaminophen toxic |
It’s metabolism involves cytochrome P-450 metabolism of the parent drug to a more toxic intermediate . Intermediate undergos conjugation (glucuronidation or sulfation), can be detoxified by conjugation with glutathione, or can react with tissue macromolecules, resulting in toxic effects. Toxicity develops when there are deficient glutathione stores or have inability to glucouronidate. Cats develop toxicity because they lack glucuronyl transferase and therefore cannot glucouronidate
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What are the toxic doses for dogs and cats |
Cats 10-40 mg/kg and dogs 100 mg/kg
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What are the clinical signs of acetaminophen toxicity |
CNS depression, vomiting, methemoglobinemia, tachycardia, hyperpnea, and weakness. Cats primarily develop methemoglobinemia within a few hours, followed by Heinz body formation. Clinical signs of methemoglobinemia have been reported dogs dosed at 200 mg/ kg. Icterus, vomiting, hypothermia, facial or paw edema (more common in cats), cyanosis, dyspnea, hepatic necrosis, and death.
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What type of liver damage is associated with Tylenol toxicity |
Liver damage (centrilobular necrosis) occurs most commonly in dogs and is often delayed, with signs and clinicopathologic changes appearing 24 or more hours after ingestion.
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How is acetaminophen toxicity treated |
Gastrointestinal decontamination (within 1 to 2 hours), Activated charcoal since acetaminophen undergoes enterohepatic recirculation. N-acetylcysteine. Ascorbic acid is used to decrease methemoglobin levels. Cimetidine, a cytochrome P-450 inhibitor, may help reduce formation of toxic metabolites and prevent liver damage
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How does N-acetylcysteine work |
This sulfhydryl-containing drug augments the animal's ability to use glutathione to detoxify reactive acetaminophen metabolites.
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What is the mechanism of action for proton pump inhibitors |
Inhibition of the H +/K + adenosine triphosphatase enzyme system at the surface of the gastric parietal cells involved in acid secretion.
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What side effects have been reported in people for PPIs |
Hypergastrinemia, headache, constipation, diarrhea, dizziness, and rash Anaphylactic and allergic reactions
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What are H1 antagonists used for |
Antihistamines include diphenhydramine, chlorpheniramine, dimenhydrinate, and cyclizine. Fexofenadine hydrochloride (Allegra).
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What are the side effects caused by antihistamines |
H1-antihistamines have antimuscarinic and α-adrenergic blockade activity and may cause dose-related prolongation of the QT interval, sedation, ataxia, vomiting, and diarrhea; however, CNS excitement or seizures also may be observed. Anticholinergic effects of H 1 antagonists may result in other clinical signs including dry mucous membranes, tachycardia, urinary retention, and hyperthermia.
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What are the side effects from cimetidine toxicity |
Inhibits cytochrome P-450 activity, slows the metabolism of drugs that are substrates for cytochrome P-450, and prolongs the half-life and thus increases the serum levels of phenytoin, theophylline, diazepam, lidocaine, procainamide, phenobarbital, propranolol, and warfarin. Can cause decreased heart rate, leukopenia and thrombocytopenia
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What are the side effects for famotidine |
Negative inotropic effect, rarely hyperthermia, CNS excitement
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What is the mechanism of action for nicotine |
Nicotine is a cholinergic (nicotinic) receptor agonist that exhibits both stimulant (low-dose) and depressant (high-dose) effects in the peripheral nervous system and CNS. Nicotine's cardiovascular effects are usually dose dependent. Nicotine may increase circulating levels of cortisol and catecholamines. May cause muscle tremors, hypertension, tachycardia , tachypnea, vomiting, hypersalivation, CNS depression or excitation, mydriasis, ataxia, weakness, seizures, and death from respiratory paralysis.
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Which common household plants can cause gastrointestinal irritation |
Araceae: elephant ear, Anthurium spp./ hyb. (e.g., flamingo flower), Caladium spp./ hyb., Dieffenbachia spp./ hyb. (e.g., dumb cane), Philodendron spp./ hyb., Zantedeschia spp./ hyb (e.g., calla lily)
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Which common household plants can cause cardiovascular effects |
Kalanchoe: Kalanchoe spp. Rhododendron: Azalea spp./ hyb, Rhododendron spp./ hyb. Oleander: Nerium oleander Yew: Taxus spp.
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Which common household plants cause renal effects |
Lilies: Lilium spp./ hyb., Hemerocallis spp./ hyb. Grapes/ raisins: Vitis spp./ hyb.
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Which common household plants cause hepatic or gastrointestinal effects |
Autumn crocus: Colchicum autumnale Castor beans: Ricinus communis Sago palms: Cycas spp./ hyb.
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How is blue green algae toxic |
Microcystis aeruginosa produces the hepatotoxic microcystins. Anabaena flos-aquae produce the neurotoxins anatoxin-a and anatoxin as. Aphanizomenon flos-aquae produce the neurotoxins saxitoxin and neosaxitoxin. Spirulina is not considered a toxigenic BG algae genus. However, some products have been found to be contaminated with mercury.
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How is ephedra toxic |
Contain stimulating and vasoactive effects. Biologic activity are the sympathomimetic alkaloids ephedrine and pseudoephedrine.
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What are the clinical signs associated with ephedra |
hyperactivity, tremors, seizures, behavioral changes, emesis, tachycardia, and hyperthermia.
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How is citrus aurantium similar to ephedra |
Is synephrine (structurally similar to epinephrine), octopamine (structurally similar to norepinephrine), and N-methyltyramine. The overall effect is that of stimulation. Causes tachycardia and increases in systolic and diastolic pressure. Similar toxicity to ephedra
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What is guarana |
Plant that contains caffeine. Toxic dose is as follow for dogs and cats:110 to 200 mg/ kg of body weight and 80 to 150 mg/ kg of body weight, respectively
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What is krypton |
Kratom, or Krypton, plant used for pain, depression, and anxiety. Potentially for opiate withdrawal. Active components including mitragynine and 7-hydroxymitragynine that are structurally similar to yohimbine, mitragynine acts as a mu opioid receptor partial agonist. The relatively minor component, indole alkaloid 7-hydroxymitragynine, is reported to be more potent than morphine.
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Noni juice causes what kind of adverse effects |
high potassium content that may predispose to interactions with potassium-sparing diuretics and certain antihypertensive medications. Has not been studied in animals.
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Aside from previous mentioned side effects from salicylates, what metabolic effects do they have |
Inhibit oxidative phosphorylation and Krebs cycle
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Goats rue (Galega officinalis) has been shown to cause what in sheep |
Pulmonary edema
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Lagerstroemia spesiosa has been shown to cause what in humans and animals |
There is evidence in both humans and animals to suggest a possible hypoglycemic effect
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What toxic effects does camphor oil cause |
Camphor is rapidly absorbed from the skin and gastrointestinal tract, and toxic effects can occur within minutes of exposure. Humans signs of intoxication include emesis, abdominal distress, excitement, tremors, and seizures followed by central nervous system (CNS) depression characterized by apnea and coma. Fatalities have occurred in humans and children
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What does citrus oil |
Fatal adverse reactions have been reported in cats following the use of an “organic” citrus oil. Clinical signs include hypersalivation, muscle tremors, ataxia, lateral recumbency, coma, and death were noted experimentally in three cats
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Adverse effects of pennyroyal oil includes what |
Used as a flea repellent. One case report of a dog dermally exposed to pennyroyal oil at approximately 2 g/ kg became listless and was vomiting. Later, developoed diarrhea, hemoptysis, and epistaxis, seizures and died. Histopathologic examination of liver tissue showed massive hepatocellular necrosis.
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Is it toxic for a dog to be exposed to lawns that have been treated with fertilizers |
Ingestion of grass or walking or laying on lawns treated with fertilizers, alone or in combination with herbicides or insecticides, by dogs should not result in toxicologic effects requiring treatment.
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Exposure to the herbicide glyphosate when directly ingested by dogs causes what |
Vomiting, hypersalivation, and diarrhea
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Exposure to the herbicide 2,4 D (2,4- dichlorophenoxyacetic acid) causes what clinical signs |
Gastrointestinal signs of vomiting, diarrhea, and abdominal pain, and possible electrolyte imbalances. Neurologic signs occur after high doses or chronic exposures and are characterized by myotonia (sustained muscle contractions)
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What kinds of cancers have been proposed to be associated with chronic exposure to 2,4 D |
Studies showed twofold increased risk of canine lymphoma in homes that used 2,4-D for 4 or more years and increased risk of development of TCC in Scottish Terriers
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Exposure to paraquat (bipyridyl herbicide) causes what kinds of clinical signs |
Gastrointestinal signs of vomiting and anorexia soon after exposure. Delayed signs: azotemia and progressive respiratory failure
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How does paraquat casue respiratory failure |
Causes oxidative injury to type I and type II alveolar cells. As degeneration and sloughing of pneumocytes occur, the animal develops respiratory difficulty with poor exchange of respiratory gases.
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What can be seen on thoracic radiographs in dogs that have been exposed to paraquat |
Often thoracic radiographs are normal in these cases, making ultimate diagnosis difficult unless the owner is aware of the paraquat exposure. In some patients, noncardiogenic pulmonary edema may be seen radiographically.
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What is the recommended treatment for paraquat poisoning |
Avoid oxygen supplementation as oxygen can accelerate further oxidative injury to pneumocytes. Keep in a quiet environment with minimal stimulation on room air. Most cases of paraquat poisoning are fatal, and treatment is supportive. Try gastric decontamination and activated charcoal.
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Are cocoa mulches toxic to dogs |
These mulches can contain the methylxanthines theobromine and caffeine Variability in the methylxanthine content in cocoa mulches, and not all ingestions result in significant toxicity. Treat as you would all chocolate toxicities
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What is the mechanism of action for anticoagulant rodenticides |
Inhibiting the recycling of vitamin K1 from vitamin K1 epoxide reductase. This inhibition leads to a reduction in the active forms of clotting factors II, VII, IX, and X in circulation, with factor VII and the extrinsic pathway affected initially
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What are the hallmark effects of a toxicity |
Development of a coagulopathy, however the coagulopathy is not always apparent on clinical presentation and typically is delayed for a number of days following ingestion.
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What type of bleeding occurs most commonly |
Intrapulmonary hemorrhage occurs commonly in anticoagulant rodenticide toxicosis
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What is the most definitive way to confirm toxicity from a rodenticide |
Detection of the specific anticoagulant rodenticide in serum; if postmortem, can test the liver
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How does one indirectly diagnose toxicity from rodenticide |
Demonstrating rapid response to vitamin K1 treatment. ACT, PT, and APTT are each dramatically shortened within 24 hours of initiating daily therapy
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What is a side effect of vitamin K-1 supplementation |
Can cause anaphylaxis regardless of route given (avoiding IV or IM is recommended to reduce chance of anaphylaxis)
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How long should vitamin K-1 therapy be continued in cases of toxicity |
3 to 5 days for warfarin. Treatment of brodifacoum, diphacenone, and chlorophacinone requires therapy for 2 to 4 weeks.
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Which type of vitamin K is contraindicated |
Vitamin K3 because it is not effective and may induce oxidative damage to red cells
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What does bromethalin toxicosis cause |
Uncoupling oxidative phosphorylation and leads acutely to hyperexcitability followed by depression in the chronic phase of toxicosis. tremors, seizures, hind limb hyperreflexia, and death may be observed within approximately 10 hours after exposure
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What is the therapy for bromethalin toxicosis |
No specific antidote exists. Aggressive charcoal therapy is aimed at reducing absorption and possible enterohepatic circulation of bromethalin. Mannitol and glucocorticoids have been used to reduce cerebral fluid pressure , but they may not reliably reverse clinical signs.
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What type of toxicity is caused by strychnine |
Strychnine inhibits the postsynaptic buffering effects of glycine on sensory stimulation of motor neurons and interneurons. Animals appear tense, and stiff within minutes to hours of exposure. Rectal temperature may be increased from muscular hyperactivity. Clinical signs progress to tonic extensor rigidity, especially after sensory stimulation by light, sound, or touch. Animals often die in opisthotonos because of paralysis of respiratory muscles.
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What is the treatment for patients poisoned with strychnine |
Sedating the patient to prevent seizures. This allows time for strychnine metabolism. Pentobarbital administered to effect, is the most often used sedative/ anticonvulsant. Methocarbamol may be administered for muscle relaxation. Other treatments may include intravenous fluids and urinary acidification (ammonium chloride) to assist with urinary excretion
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What are other differential diagnoses for strychnine poisoning |
Tetanus, hypocalcemia, mycotoxins, nicotine insecticides, and zinc phosphide
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What are the clinical signs of an animal poisoned with zinc phosphide |
Anorexia, lethargy , dyspnea, vomiting (occasionally with hematemesis), ataxia, agitation , muscle tremors, weakness, recumbency, and death. Signs develop within minutes to hours of ingestion of a toxic dose of zinc phosphide.
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What are the recommended treatments for zinc phosphide |
Increasing gastric pH may be helpful by reducing phosgene liberation. Milk of magnesia has been used as a home remedy; in the hospital gastric lavage with 5% sodium bicarbonate may be used. Diazepam or pentobarbital may be needed for excessive musculoskeletal activity or seizures. In addition to intravenous fluid therapy, liver-supportive agents may be considered.
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How are most dogs and cats exposed to organophosphate and carbamate compounds |
Dermal or oral exposures are commonly encountered by dogs or cats.
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What are the effects of organophosphates and carbamates on the body |
Inhibit acetylcholinesterase (AChE) and pseudocholinesterase. Animals poisoned with cholinesterase inhibitors often exhibit a mixture of clinical signs as a result of overstimulation of the nicotinic receptors of the somatic nervous system (skeletal muscle), sympathetic and parasympathetic preganglionic junctions, all parasympathetic postganglionic junctions (including a few sympathetic postganglionic junctions), and some neurons within the central nervous system.
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What do the clinical signs of organophosphate/carbamate poisonings look like |
Excessive salivation, anorexia, emesis, diarrhea, excessive lacrimation, miosis or mydriasis, dyspnea, excessive urination, and bradycardia or tachycardia. “SLUD”Diarrhea, urination, miosis, bronchospasm , bradycardia, emesis, lacrimation, salivation “DUMBBELS”
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What are the signs of nicotinic stimulation |
Ataxia, weakness, and muscle twitching. In acute high-dose oral exposures, seizures can occur within 10 to 20 minutes.
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How is death typically caused |
Respiratory failure and tissue hypoxia caused by excessive respiratory secretions, bronchoconstriction, paralysis of the respiratory muscles, and direct depression of the respiratory center in the medulla.
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How can one test for toxicity of organophosphates/carbamates |
Check PCV/TS as can alter accuracy of atropine test (cholinesterase testing). Administer atropine to see if symptoms resolve. Can have false negatives Postmortem-submit testing with body tissues including fat
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What systemic manifestation may result from organophosphate/carbamate toxicity |
Pancreatitis
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What medication can be given to help reduce muscle tremors from nicotinic stimulation |
Pralidoxime chloride ([ 2-PAM]
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What does Chlorpyrifos poisoning cause in cats |
Hyperesthesia, ataxia, anorexia , depression , and muscle tremors for several days or weeks after initial exposure.
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What is the difference between pyrethrin and pyrethroid compounds |
Pyrethrins are organic esters extracted with fat solvents from flower heads of the pyrethrum plant, Chrysanthemum cinerariifolium. Pyrethroids are their synthetic cohorts that vary in both structure and potency. Pyrethroids are more toxic and last longer.
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How are pyrethrins and pyrethroids toxic to mammals |
Reversibly prolonging sodium conductance, producing increased depolarizing afterpotentials that result in repetitive nerve firing.
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How do most toxicities occur in mammals |
Their toxicity to mammals is low and, when used according to label instructions, should not induce deleterious effects in mammals. Toxicoses observed when these products are ingested or when there is overzealous heavy topical application, particularly in cats and small dog- when “for use in dogs only” being used on cats.
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What are the clinical signs associated with pyrethrins and pyrethroids |
Excessive salivation, muscle tremors, depression, ataxia, anorexia, and vomiting. Less commonly reported adverse effects include weakness, dyspnea, diarrhea, hyperthermia or hypothermia, hyperesthesia (ear flicking, paw shaking; contractions of the superficial cutaneous muscles), and recumbency.
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How does one diagnose pyrethrin and pyrethroid toxicity |
Laboratory methods for analyzing pyrethrin /pyrethroid residues are not routinely available but can be done to confirm exposure if necessary. Since clinical signs often mimic organophosphate or carbamate poisonings, assessing blood or brain cholinesterase is recommended to rule out these differentials.
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What is the prognosis for pyrethrin and pyrethroid toxicity |
The prognosis for the majority of pyrethrin/ pyrethroid poisonings is excellent, with most animals recovering within 24 to 72 hours.
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What is amitraz and what is the mechanism of toxicity for this compound |
Formamidine pesticide that is present in some tick collars used on dogs. It is a monoamine oxidase inhibitor, an α2-adrenergic agonist, and an inhibitor of prostaglandin synthesis.
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What are the clinical signs of amitraz toxicity |
α2-adrenergic properties of amitraz and include depression, sedation, ataxia, bradycardia, mydriasis, hypothermia, vomiting, polyuria, and gastrointestinal stasis or diarrhea. Other signs that have been reported include hyperthermia, gastric dilation, hypersalivation, dyspnea, anorexia, shock, tachycardia, urinary incontinence, disorientation, tremors, and coma
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What additional diagnostics should be considered for amitraz toxicity |
Abdominal radiography is recommended to see if collar could be retrieved
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What medications are considered contraindicated with amitraz toxicity |
Xylazine, atropine and 2-PAM are contraindicated in the treatment of amitraz poisoning.
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What are the preferred treatments for amitraz |
Removal of collar if possible, gastric decontamination, alpha 2 antagonists yohimbine and atipamezole
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What is the mechanism of action of fipronil |
Fipronil acts on the γ-aminobutyric acid– mediated chloride channels of invertebrates, thereby interrupting nervous transmission and leading to rapid death of the fleas and ticks.
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What is the mechanism of action for Imidacloprid |
Adulticide that reportedly binds specifically to postsynaptic nicotinic acetylcholine receptors of insects and both kills adult fleas and exhibits some larvicidal action.
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What is the mechanism of action for nitenpyram |
Neonicotinoid derivative that binds and inhibits specific nicotinic acetylcholine receptors. It does not inhibit AChE activity. Pyriproxyfen is an insect growth regulator used topically to control insects. |
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