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35 Cards in this Set

  • Front
  • Back
Mech of CO Poisoning
Forms CarboxyHb that can't carry O2
Reduces ability of OxyHb to dissociate O2
Threshold for CO fatality
>0.1% in air
CO Poisoning Treatment
100% O2 or Hyperbaric O2
Sulfur Oxides
Air pollutants that form sulfurous acid on contact with moist membranes
Ozone/Hydrocarbons
Air pollutant found in polluted urban air and upper atmosphere
Particulate Matter
Pneumoconiosis and Asbestosis from dust inhalation
Bronchial cancer associated with Asbestosis
Nitrogen Oxides
Air pollutants that are deep lung irritants capable of producing pulmonary edema
Carbon Tetrachloride, Chloroform, Trichloroethylene
Halogenated Aliphatic Hydrocarbons
Industrial solvents that cause CNS depression
No treatment
Benzene
Aromatic Hydrocarbon
Industrial solvent that causes CNS depression
Acute effects seen in CNS
Chronic effects on bone marrow
Parathion, Malathion, TEPP, Dichlorvos
Organophosphate Insecticide
Irreversible AChE inhibitors
Phosphorylate enzyme "ages" by losing alkyl group
Delayed Toxicity of Organophosphates
Axonal degeneration and demyelination unrelated to AChE inhibition
Treatment for organophosphate poisoning
Atropine and AChE reactivator Pralidoxime within 24 hours
Carbaryl, Baygon
Carbamates- garden insecticide
Reversible AChE inhibitors
Treatment of Carbamate Poisoning
Administer Atropine but Pralidoxime is contraindicated because enzyme not phosphorylated
(Additive affect of carbamate in inhibiting AChE)
Chlordane, DDT, Lindane
Chlorinated Hydrocarbons- insecticide
Acute CNS stimulation by targeting Na and Ca
Chronically stored in body fat
Pyrethrins
Botanical Insecticides
Contact dermatitis or asthmatic rxn is common as lethal dose is large
CNS excitation/convulsion by inhibition of ion channels
Paraquat
Herbicide that produces superoxide anions
causes respiratory distress due to fibroblast proliferation
Treatment of Paraquat Poisoning
Gastric lavage, hemodialysis or cyclophosphamide (to inhibit fibroblasts)
Chlorophenoxy Compounds
AKA Agent Orange
Herbicide that causes excessive GH action
Chronic toxicity due to dioxin (teratogen and carcinogen)
Ethanol
Distributes to total body water
Zero Order Kinetics
CNS Depressant
Prevention of Ethanol Toxicity
Disulfiram (Antabuse) blocks ALDH
Methanol
Distributes to total body water
Metabolized at one fifth the rate of ethanol
Toxicity related to amount of Formic Acid produced
Treatment of Methanol Toxicity
Lavage with Bicarb
Ethanol to delay breakdown time
Hemodialysis
Fomepizole- inhibits ADH so no formic acid
Ethylene Glycol
Metabolized by ADH and ALDH into glycolic acid then to oxalate, a calcium chelator
Treatment of Ethylene Glycol Toxicity
Ethanol to compete for enzymes and Fomeprizone
Cyanide
Present in fruit seeds and burning plastic
CN combines with FE3+ of cytochrome oxidase
Venous blood is bright red
Cyanide Poisoning Treatment
Step 1: Use Amyl or Sodium Nitrite to oxidixe Hb Fe2+ to Fe3+
Step 2: Supply thiosulfate to remove CN from Hb
Lead
Binds rbcs and widely distributed to soft tissue and bone
Binds sulfhydryl groups of proteins
Interferes with divalent cations
Lead Poisoning Treatment
EDTA (Versene) IV or IM
Succimer orally
Mercury
Forms covalent bonds with sulfhydryl groups
CNS and GI Tract involved
Treatment for Mercury Poisoning
Dimercaprol IM
Crosses BBB
Also Penicillamine or Succimer orally
Arsenic
Binds SH groups to disrupt cellular metabolism
Treat with Dimercaprol followed by penicillamine or succimer
3 Phases of Acute Iron Poisoning
1. Corrosive effect on GI Tract
2. Quiescent Period (6-24hrs)
3. Edema, Acidosis, Convulsions, Coma
Treatment of Iron Toxicity
Milk to induce emesis
Gastric lavage
Deferoxamine orally or IV
Activated Charcoal effectively binds
Acetominophen, Salicylates, Ipecac, Arsenic, and Organophosphates