Environmental Toxicology

Question 1

Carbon monoxide mechanism

Answer 1

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

Question 2

Carbon monoxide symptoms

Answer 2

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)

Question 3

Carbon monoxide treatment

Answer 3

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

Question 4

Cyanide- sources

Answer 4

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

Question 5

Cyanide posioning

Answer 5

Results from prolonged use of nitroprusside, smoke inhalation in enclosed space, ingestion of cyanide, or terrorism with hydrogen cyanide

Question 6

Cyanide poisoning- mechanism

Answer 6

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

Question 7

Cyanide poisoning sx

Answer 7

Initial- flushing, tachycardia, tachypnea, HA, dizziness, N/V with ingestion
Worsening- LOC, coma, hemodynamic compromise, arrhythmia’s, seizures, apnea, cardiac arrest, and death.

Question 8

Cyanide poisoning diagnosis

Answer 8

labs- ABG, serum electrolytes, and carboxyhemoglobin (in smoke ventilation)
Elevated Oxygen in venous blood is often present
Serum lactate of > or = 10mmol/L

Question 9

Cyanide poisoning treatment

Answer 9

Decontamination
Stabilization
Antidote- hydroxocobalamin, each molecule binds one cyanide ion forming (not allowing it to bind the mitochondrial oxidase_ cyanocobalamin which is eliminated through the urine.

Question 10

Lead Poisoning

Answer 10

Toxic to central nervous system

Causes a disruption of the BBB allowing lead and other potential neurotoxins in.

Question 11

Lead encephalopathy

Answer 11

Lethargy, vomiting, irritability, and dizziness that can progress to altered mental status, coma, and death.

Question 12

Lead poisoning mechanism

Answer 12

Interferes with the synthesis of hemoglobin

Causes both reversible and irreversible kidney damage

Question 13

Chelators

Answer 13

EDTA- used to bind lead
Dimercaprol (BAL)- binds lead, arsenic, and mercury
Succimer- binds lead, arsenic, and mercury

Question 14

Metal Antidotes

Answer 14

Iron- defuroxamine, deferasirox (oral option)

Copper (wilsons disease)- penicillamine or trientine

Question 15

Pesticides

Answer 15

Parathion, malathion, diazinon
Organophosphates
Acetylcholinesterase inhibitors- producing acute muscarinic and nicotinic toxicity

Question 16

Pesticide treatment

Answer 16

Atropine- muscarinic antagonist

Pralidoxime- regenerated ACHE