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31 Cards in this Set
- Front
- Back
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How does acetominophen excess cause liver centrilobular necrosis?
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Acetominophen ---> N-benzoquinoneimine (NAPQI)
2) NAPQI interacts with glutathione to form nontoxic metabolite. If excess NAPQI, glutathione used up, and NAPQI reacts with hepatic proteins and lipids --> centrilobular necrosis. |
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How do you treat acetominophen toxicity?
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N-acetylcysteine.
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What is mechanism of N-acetylcysteine?
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1) Can reduce oxidized glutathione
2) Directly bind toxic free radicals. |
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What is mechanism of toxicity of methanol?
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Metabolized by alcohol dehydrogenase to formaldehyde and then again into formic acid.
Formic acid --> directly toxic |
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What are the toxic effects of methanol poisoning?
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Formic acid causes retinal damage and metabolic acidosis.
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How do you treat methanol poisoning?
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Administration of ethanol, because alcohol dehydrogenase has 10 fold greater affinity for ethanol than other alcohols.
2) 4-methylpyrazole (alcohol dehydrogenase inhibitor)? |
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What is an alcohol dehydrogenase inhibitor than can be used to treat methanol poisnoning?
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4-methylpyrazole.
Also give sodium bicarbonate to correct the metabolic acidosis. |
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What is the toxicity of aspiring?
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Mechanism: uncouples oxidative phosphorylation and can result in respiratory stimulation.
1) Respiratory alkalosis followed by metabolic acidosis. |
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What are other side effects of aspirin toxicity?
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1) Tinnitus, Peptic ulcer disease, hemorrhage, GI bleeding.
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How do you treat aspirin toxicity?
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Alkalinize the urine since salicylates are organic acids.
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What is mechanism of ethylene glycol poisoning?
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Converted to oxalic acid or formic acid, by alcohol dehydrogenase.
Nephrotoxicity due to formation of calcium oxalate stones. |
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how do you treat etyhlene glycol poisoning?
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Ethanol of 4-methylpyrazole
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How do you treat opiate overdose?
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Opiate anatagonist naloxone or naltrexone. They can displace opiates at opioid receptor sites.
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What is mechanism of toxicity in arsenic poisoning?
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Binds sulfhydrl groups on proteins interfering with enzyme systems.
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What are toxic effects of arsenic poisoning?
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Nausea
Pulmonary Edema! Peripheral neuropathy! Hemolysis! Mees lines: horizontal white bands on finger nails!! |
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How do you treat arsenic toxicity?
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Dimercaprol or succimer.
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What is mechanism of toxicity of iron overdose?
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Iron accumulation in hepatic, and tissues leading to cell dysfunction.
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How do you treat iron overdose?
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Deferoxamine!! You get hematemasis and bloody diarrhea and hypotension; extremely toxic to GI tract. Metabolic acidosis!
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What are the toxic effects of lead poisoning?
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Thirst and metallic taste in mouth
2) Abdominal pain and milky vomit 3) Shock |
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what are the chronic toxic effects of lead poisoning?
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Neurologic: sleep disturbance, slowed reaction time
Peripheral neuropathy and memory loss Anemia Nephrosclerosis/HTN **Lead lines in gingivae Lead lines in epiphyses of long bones. |
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How do you treat lead toxicity?
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Dimercaprol (EDTA).
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What is toxic effects of inhaled mercury?
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Gingivostomatitis
Pulmonary edema Tx: chelation therapy using dimercaprol. |
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What is mechanism of Diisopropylfluorophosphate, nerve gas, and malathion?
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Covalent inhibition of acetylchollinesterase: make too much acetylcholine.
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What are toxic effects of nerv gas, malation, DFP?
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S alivation
L acrimation U rination D defecation Emesis |
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How do you treat organic phosphate poisoning?
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Atropine or pralidoxime (2-PAM).
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What is meant by the term aging in organophosphate poisoning?
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These organophosphate compounds phosphorylate the active site of acetylcholinesterase. This bond is very stable and not easily reversible. The stability of the bond is further increased by loss of alkyl group --> this is aging.
Pralidoxime can be given to increase rate of regeneration of acetylcholinesterase following exposure to organophosphorous compound, but it wont work if enzyme-inhibitor complex has aged!! |
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What is toxicity of DDT: Dichlorodiphenyltrichloroethane?
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Interferes with na+ channels in excitable membranes, causing repetitive neuronal firing and excessive stimulation.
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What is toxicity of paraquat (herbicide)?
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Acccumulation in lung with pulmonary edema and fibrosis.
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What is toxic mechanism of strychinine?
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competitive antagonist at glycine receptor, blocking inhibitory effects of glycine within spinal cord.
Causes muscle contraction, tetanus, and cessation of respiration due to diaphragmatic contraction. |
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What is sulfur dioxide toxicity?
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Irritation of eyes, mucous membranes, and skin, and pulmonary edema. Follows burning of fossil fuels.
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What are nitrogen oxide toxicity?
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Fibrotic destruction of terminal bronchioles.
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