Flashcards in Environmental Toxicology Deck (16):
Carbon monoxide mechanism
Binds heme iron in hemoglobin 200 fold more strongly than O2 resulting in hypoxia. Carboxymetheglobin shifts dissociation curve for oxyhemoglobin left, impeding disociation of O2
Carbon monoxide symptoms
Initial sx are non-specific
HA, dizziness, and irritability
Levels (COHb concentration) correspond to sx
30-40%- sever HA, vominting, visual disturbance
50-60% collapse and convulsions
70%- death (and perhaps at lower concentrations)
Carbon monoxide treatment
Hyperabaric oxygen therapy reduces 1/2 life of COhb from 5 hrs at room air to 20 minutes.
Appears to protect against long term brain injury and is indicated for most exposures
Plants- fruits and leaves of prunus species (almonds, apricots, cherries, peaches, and plums) and some other plants such as apples, cassava, elderberry, hydrangea. (Such a small amount alot must be consumed.
Industrial uses- gold/silver extraction, stainless steel manufacturing, and petroleum refining
Results from prolonged use of nitroprusside, smoke inhalation in enclosed space, ingestion of cyanide, or terrorism with hydrogen cyanide
Cyanide poisoning- mechanism
Cyanide forms complexes with cation-containing enzymes. Most significant rapid and irreversible binding to gerric ion (Fe3+) contained in mitochondrial cytochrome oxidase.
By inhibiting cytochrome oxidase cyanide inhibits aerobic metabolism, stops generation of ATP and arrests cellular respiration resulting in tissue hypoxia.
Cessation of aerobic metabolism leads to accumulation of lactic acid
Cyanide poisoning sx
Initial- flushing, tachycardia, tachypnea, HA, dizziness, N/V with ingestion
Worsening- LOC, coma, hemodynamic compromise, arrhythmia's, seizures, apnea, cardiac arrest, and death.
Cyanide poisoning diagnosis
labs- ABG, serum electrolytes, and carboxyhemoglobin (in smoke ventilation)
Elevated Oxygen in venous blood is often present
Serum lactate of > or = 10mmol/L
Cyanide poisoning treatment
Antidote- hydroxocobalamin, each molecule binds one cyanide ion forming (not allowing it to bind the mitochondrial oxidase_ cyanocobalamin which is eliminated through the urine.
Toxic to central nervous system
Causes a disruption of the BBB allowing lead and other potential neurotoxins in.
Lethargy, vomiting, irritability, and dizziness that can progress to altered mental status, coma, and death.
Lead poisoning mechanism
Interferes with the synthesis of hemoglobin
Causes both reversible and irreversible kidney damage
EDTA- used to bind lead
Dimercaprol (BAL)- binds lead, arsenic, and mercury
Succimer- binds lead, arsenic, and mercury
Iron- defuroxamine, deferasirox (oral option)
Copper (wilsons disease)- penicillamine or trientine
Parathion, malathion, diazinon
Acetylcholinesterase inhibitors- producing acute muscarinic and nicotinic toxicity