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40 Cards in this Set
- Front
- Back
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In acetaminophen poisoning, why should blood levels not be drawn before 4 hours after the exposure?
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In overdose, the absorption is delayed
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How is acetaminophen metabolized?
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It is metabolized in the liver by glucuronidation or sulfation to non-toxic metabolites and by CYP450s to an active intermediate which is toxic
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What is the toxic intermediate of acetaminophen and why does toxicity not occur with every dose?
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N-acteyl-p-benzoquinone-imine (NAPQI); under normal circumstances it is detoxified by glutathione, but in overdose the glutathione is depleted
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What is generally seen in the first phase (0-24 hours) of acetaminophen overdoes?
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Mostly asymptomatic, may show nausea, anorexia, vomiting
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What is seen in the second phase of acetaminophen toxicity (24-72 hours)?
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Initial symptoms (if present), become less pronounced
chemical evidence of hepatic dysfunction and RUQ pain |
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What happens 72-96 hours after a toxic acetaminophen dose?
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Frank hepatic necrosis with symptoms of encephalopathy and coagulopathy
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How often should acetaminophen levels be drawn in toxicity?
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They shouldn't. It is generally unnecessary unless the initial draw was before 4 hours
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When is the nomogram used in acetaminophen toxicity?
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Only in acute cases
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What is used to treat acetaminophen toxicity?
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N-acetylcysteine given within 8 hours of ingestion
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What are simple asphyxiants?
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Gases that displace oxygen and have no toxicity of themselves
Examples include helium, methane, and ethane |
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What are chemical asphyxiants and what are some examples?
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This is asphyxiation by mechanisms such as toxins binding to Hg and cytochrome oxidase
Examples include CO, cyanide, and HS |
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What is the treatment for chemical asphyxiation with CO? CN?
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High flow oxygen and possibly hyperbaric oxygen for CO poisoning
Hydroxycobalamin for CN poisoning |
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What are irritant gases?
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Compounds that produce injury to the mucosal lining of the respiratory tract
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What are some examples of high water solubility gases and what sort of injury do they cause?
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Ammonia, chloramine, HCl
They cause rapid onset of oral, nasal, and throat pain, cough and stridor |
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What is an intermediate water soluble irritant gas and what sort of injury do they cause?
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Chlorine gas
It results in both lower and upper respiratory effects It causes less irritation and delays the onset of symptoms |
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What is a low water soluble irritant gas and what are it's symptoms of toxicity?
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Phosgene
It lacks irritant properties, resulting in delayed onset of effects and lower respiratory tract effects |
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The toxicity of hydrocarbons is related to what factors?
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It is related to the volatility and the viscosity of the hydrocarbons
If a hydrocarbon has a low viscosity and high volatility, it can spread over a larger area and cause significant lung injury |
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What hydrocarbons have a high volatility and low viscosity?
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kerosene and gasoline
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What are the major symptomatic components of toxicity related to aromatic and halogenated hydrocarbons?
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CNS depression- sedation, coma, ect.
Cardiac dysrhythmias |
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What kind of agents produce the most lung injury?
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Low viscosity hydrocarbons
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What are some systemic manifestations of hydrocarbon toxicity?
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1) CNS depression - sedation, lethargy, coma, ect.
2) cardiac dsyarhthymias 3) GI - N and V |
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Describe the pulmonary injury in hydrocarbon toxicity
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Chemical pneumonitis leading to ARDS with alteration or destruction of surfactant and inflammatory reactions
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What are the three factors of hydrocarbons that determine their potential toxicity?
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viscosity
volatility agent |
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When do you remove hydrocarbons from the stomach?
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If it is a mixed ingestion or a very large dose of an aliphatic hydrocarbon or if they are aromatic or complex hydrocarbons (they are more toxic)
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Should emesis be induced when hydrocarbons are ingested?
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Most of the time, NO
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What are the three patterns of inhalation abuse?
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experimenters
intermittent chronic inhalant abusers |
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What is the most frequent cause of death from volatile substance abuse and how does it occur?
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Sudden sniffing death syndrome - hydrocarbon induced myocardial sensitivity to epinephrine and a sudden surge of epi secondary to startle reflex with a resultant fatal cardiac dysarhthmyia
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What are the psychosocial findings associated with potential VSA?
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deliquency
school failure socail maladjustment unusual location of products of abuse |
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What are clinical findings with VSA?
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Vivid hallucinations
appearance of intoxication perioral pyoderma chest pain feeling of omnipotenece |
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On what is the relative toxicity of iron preparations based?
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The amount of elemental iron in the preparation
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What happens to the GI tract when a large amount of iron is ingested?
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Corrosive mucosal damage initially with hydrogen ion production as well as histamine (vasdilation leading to shock)
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What causes the toxicity in patients who overdose on large amounts of iron containing drugs?
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The circulating free iron in the serum
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What is the effect of iron on the CNS?
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It is a CNS depressant
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Describe the symptoms seen in the first phase of iron toxicity (0-6 hours)
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GI - N and V, hematemesis,
tacycardia, hypotension potentially shock if vasodilation and fluid loss is great enough |
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What is seen 6-24 hours after toxic iron ingestion?
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temporary recovery
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What is seen in the third phase of iron toxicity (8-24 hours)?
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Abrupt return of symptoms - GI, cardiovascular, shock and seizures
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What happens 2 days to 3 weeks after toxic iron ingestion?
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ARDS
Cirrhosis Sepsis with Yersina gastric scaring with pyloric stenosis |
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What is the diagnostic test to get in iron toxicity?
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Serum iron
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What is used to decontaminate iron toxicity patients?
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Cathartic or GI lavage and deferoxamine
Emesis is not induced! Charcoal is not used |
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What is the mechanism of action of deferoxamine? Who should receive it?
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It pulls iron out of the mitochondria and forms water-soluble ferrioxamine; Indications for use are serum iron over 500 mcg/dL or significant signs and symptoms regardless of level
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