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10 Cards in this Set

  • Front
  • Back
carbon monoxide
chemical asphyxiant, binds irreversibly to hemoglobin-200x's> than O2. resultant carboxyhb can't transport O2.
Tx: Hyperbaric O2
Binds Fe3+ , cyt A3, halts ETC-preventing O2 consumption.
~nitrite makes MetHb, soaking up CN.
~thiosulfate: makes SCN, which is non-toxic
sulfur dioxide
Upper respiratory tract irritant-atmospheric pollutant that gets dissolved in water-->acid formed, tissue damage.
NO2 (nitrogen dioxide),
O3 (ozone)
Deep lung irritant, oxidizing agent.
breaks down membrane-->lipid peroxidation, delayed reaction. Toxic to macrophages, high risk of infection
Particulate toxins: inhaled non-gases: silica-lung necrosis, fibrotic lesions. presence-->increased macrophages, lymphocytes
asbestos: fibrotic lesions, sits, absorbs other carcinogens
aromatic hydrocarbon
Solvent toxicity:dizzy, headache, decrease CNS arrhythmia.
Systemic toxicity: P450 metabolizes benzene to epoxide-->mutagenesis, myelosuppression> AML
metabolized by ADH-->formaldehyde-->formic acid. Accumulation of formic acid is toxic. it blocks mit cyt oxidase-->superimposed lactic acidosis. retina and optic nerve damage-->blindness
Clinical: visual impairment
Metabolic acidosis-->increase anion gap, increase plasma osmolality gap.
Symptoms delayed for 12=36 hrs
ETOH, competitive substrate for ADH
~Fomepizole: inhibitor of ADH that can be used instead of ETOH
~Folate administration: formic acid slowly metabolized to CO2 in a folate dependent manner.
~oral charcoal: decrease absorption of methanol; NaHCO3; hemodialysis
aromatic hydrocarbon; less systematically toxic than benzene b/c it's less readily metabolized and less epoxides generated.
aromatic hydrocarbon; less systematically toxic than benzene b/c it's less readily metabolized and less epoxides generated
aliphatic hydrocarbons
petroleum distallates: methane, octane, kerosene.
Toxicity via ingestion/inhalation-solvent properties, depress CNS and destroy lung tissue-disrupt/disorganize neuronal membranes
Depress gag reflex