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30 Cards in this Set
- Front
- Back
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Toxidrome:
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A toxic syndrome; collectgion of vital signs and symptoms that is indicative of poisoning due to a specific class of poisons.
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Xenobiotic
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A chemical or substance that is foreign to a organism or biological system
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Dose-response relationship
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There is a dose below which no effect or respone is seen: threshold dose aka NOEL (no observed effect level)
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Phase 1 Rxn
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- microsomal monooxygenation, cytoslic and mitorchondrial oxidations, reductions and hydrolysis.
- Polar groups are introduced to be conjugated later |
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Phase 2 Rxn
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- takes products and other xenobiotics undergo conjugation with endogenous metabolites
- conjugation products are more polar, less toxic and more readily excreted |
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Metabolism of acetaminophen (weak acid)
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- 90% metabolized by phase 2 rxns: glucuronidation and sulfation
- 5% metabolized by CYP2E1 --> NAPQ1 (hepatotoxin): phase 1 rxn - 5% excreted in the urine unchanged |
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Enzyme necessary to metabolize NAPQ1
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CYP2E1
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Antidote for acetaminophen toxicity
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N-aceylcysteine (NAC) [mucomyst]
- prevents /treats acetaminophen induced hepatotoxicity |
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Metabolism of Methanol
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Methanol -(1)-> Formaldehyde -(2)-> Formic acid*
(1): Alcohol dehydrogenase (ADH), rate limiting step (2): Aldehyde dehydrogenase (ALDH) *Formic acid is toxic to the retina and optic nerves causing blindess due to formate formation |
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Antidote for methanol toxicity
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Fomepizole
- if given in time can prevent blindess - A competitive inhibitor of ADH, preventing the metabolism to its toxic metabolites |
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Oxalic acid
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A toxic metabolite as a result of ethylene glycol metabolism, damages kidneys
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Antidote for ethylene glcyol toxicity
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Fomepizole
- A competitive inhibitor of ADH, preventing the metabolism to its toxic metabolites |
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Teratogens: deleterious effects on the developmental process
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Thalidomide: cause phocomelia (abnormal limb formation)
- Tx: prevention Others: methyl mercury, alcohol, diethyl stilbestrol |
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Clinical manifestation of lead toxicity
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Weakness, seizures, peripheral neuropathy, headache, encephalopathy, abdominal pain, constipation, renal injury, anemia, fatigue, HTN
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Treatment for lead toxicity
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Remove from
Chelating agents Succimer (DMSA) |
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Clinical manifestations of mercury toxicity
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Renal toxin
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Clinical manifestations of arsenic toxicity
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GI, cardiac, hematologic, pheripheral neuropathy, dermal
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Treatment of arsenic toxicity
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Succimer
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Treatment of carbon monoxide toxicity
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- Remove from exposure
- Oxygen (hyperbaric if possible) |
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Clincal manifestations of cyanide toxicity
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Rapid syncope, hypotention, dysrhythmias, metabolic acidosis, and seizures
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Treatment of cyanide toxicity
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Hydroxycobalamin
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Other metals
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Copper: targets the kidney most
Iron: targets the liver the most - Tx: deferoxamine |
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Hepatotoxicity
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Liver is highly susceptible
- 1st organ to encounter xenobiotics when ingested |
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Nephrotoxicity
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Potent nephrotoxins:
- Heavy metals: Cadmium, mercury, and lead - Ethylene gycol: oxatic acid Effects: glosuria, proteinurea, renal necrosis and death |
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Hypersensitivity
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Types I-IV
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Treatment for hypersensitivity
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- Diphendydramine: H1 blocker
- Cimetidine: H2 blocker - EPI: ↓ of histamine release - Steroids: anti-inflammation |
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Type I hypersensitivity
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Mast cell mediated
Ex: Bees, penicillin |
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Type II hypersensitivity
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IgM/IgG mediated
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Type III hypersensitivity
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Immune system complex mediated
Serum sickness |
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Type IV hypersensitivity
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T-lymphocyte mediated
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