Toxicology Flashcards
Basic tenet of toxicology
The dose makes the poison
What is the difference between a toxin, toxicant, and hazard
Toxin = naturally derived Toxicant = man-made substance Hazard = anything that CAN cause adverse effect, but must be applied in a deleterious manner
How is dosing defined in toxicology?
Defined by the time frame of exposure:
Acute 3mo repeated exposure
How is the dose-response curve different in toxicology?
Bucket shaped curve. Most important parts are the thresholds (point on curve that demonstrates significant change in response) and slope (describes severity/toxicity of change)
What are the general differences between reducing and oxidizing pollutants?
Reducing - mainly SO2 and smoke from incomplete combustion of coal
Oxidizing - characterized by hydrocarbons, oxides of nitrogetn, secondary photochemical oxidants. result of auto exhaust
What are major sources of indoor pollution?
Infiltration of outdoor pollution, building material exposure, radon, CO, particulate matter, nitrogen oxides. Sick-Building Syndrome
What is selective toxicity and why is it important?
Pest-specific toxicants, only affects a targeted population. Allows use in pesticides to be “safe” for humans
Inhalant abuse
To get “high”. all solvents can be abused as inhalants.
Endocrine disruptors
Interfere with the production, release, transport, metabolism, and/or action of natural hormones. Eg: Diethylstilbestrol (DES), PCBs, bis-phenol A, PFOA
Paraquat
Bipyridyl derivative, herbicide. High mortality rate, 3-4 wk due to pulmonary toxicity.
Tx: gastric lavage, give Fuller’s earth (kaolin)
Anticoagulants
May cause hemorrhage by antagonizing actions of Vit K in synthesis of clotting factors. Delay between ingestion and toxicity. Used as rodenticide
Toxicogenomics
The “fingerprint” of individual response? eg: CYP polymorphisms
How do pesticides work?
Carbamate pesticides and organophosphates inhibit acetylcholinesterase (AChE) resulting in increase of ACh. Differences between are rate of dephosphorylation or decarbamylation.
DUMBELS
What is Arsenic’s mechanism of action?
inorganic arsenicalss cycle, glycolysis) Arsine gas - binds Hb cause hemolysis
What are the effects of acute and chronic Arsenic poisoning?
Acute: GI disturbances, vomiting, diarrhea. Rice water stools, muscle cramps, thirst.
Chronic: muscle weakness, edema, hyperkeratosis, alopecia, hepatic/renal dysfunction, Mee’s lines
Essential trace elements
Metals that are essential for normal physiological and biochemical functions eg: Cu, Fe, Mg…
What are effects of Arsine gas?
GI disturbances, shortness of breath, dark/bloody urine, jaundice. Blockage of renal tubules by Hb-> renal failure, fatal hemolysis.
What is treatment for Arsenic poisoning?
Supportive care, chelation with BAL (dimercaprol), succimer.
What do you use to biologically monitor arsenic?
blood and urine concentrations.
Cadmium’s mechanism of action?
Interaction with functional macromolecules (proteins). Half life of 10-30 years. Carried in blood by metallothionein.
Effects of Cadmium?
Acute: local irritation, GI irritation, diarrhea, cramping, vomiting. Inhaled -> pneumonitis progressing to pulmonary edema
Chronic: renal problems, osteopenia-osteomalacia (MSK pain = itai-itai), yellow teeth lines
Treatment for Cadmium?
supportive/symptomatic treatment. vitamin D may be effective for osteomalacia. EDTA salts may reduce body burden
Biological monitoring of Cd?
Blood, urine subject to change, should be creatinine-corrected.
Lead
Both inorganic and organic harmful. Children absorb more (40%) than adults (5-15%). Affects soft tissues (kidney, liver, brain). Half life 20 yrs.
