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29 Cards in this Set
- Front
- Back
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incidence of toxicity (top 3)
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analgesics
cleaning substances alcohols and hydrocarbons |
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phases of acetaminophen toxicity
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I- (30 in-4 hrs)- anorexia, nausea, vomitting, diaphoresis
II (24-48 hrs)- decreased sx but begin liver problems III (3-5 days)- hepatic damage,necrosis of zone 3 hepatocytes jaundice, coagulopathy, renal failure, encephalopathy, cardiomyopathy, death IV (4-days- 2 wks)- hepatic failure and death OR complete resolution and recovry |
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tylenol and alcohol
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cyp2E1
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antidote for tylenol (acetaminophen)
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mucomyst = NAC
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aspirin metabolism
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90% bound to protein
conjugated in liver by 5 pathways conjugates excreted in urine peak levels in 30 min, t1/2 = 2-4 hrs |
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aspirin toxicity mechanisms (4)
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uncoupling ox-phos -> inc anion gap
stim resp center -> resp alkylosis irritate GI tract dec prothrombin and platelet dysfunction |
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tx aspirin toxicity
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alkalinize urine with bicarb
GI decontamination activated charcoal |
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ethanol metabolism
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90% liver, 10% stomach
alcohol dehydrogenase CYP450 catalase |
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ethanol toxicity treatment
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no antidote
supportive care |
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ethylene glycol toxicity mechanism (5)
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acid -> anion gap acidosis
calcium oxylate crystals -> tissue inj. calcium oxylate crystals-> renal tubules acute tubular necrosis and renal failure cardiac failure and pulmonary edema |
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ethylene glycol toxicity treatment
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lavage (<2hrs)
activated charcoal alkalinize urine ETHANOL (block alcohol dehyrogenase)or FOMEPIZOLE (block ADH) folic acid, pyridoxine, thiamine |
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methanol toxicity mechanism
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methanol slowly met. to formaldehyde
formaldehyde quickly met. to formic acid formic acid-> acidosis, ocular toxicity |
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methanol toxicity treatment
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high O2
lavage (<30 min) alkalinize urine folic acid ETHANOL or FOMEPIZOLE |
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isopropanol toxicity mechanism
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CNS toxicity
high ketones (acetone) abdominal pain, gastritis no acidosis hypotension and coma |
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isopropanol treatment
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removal and adsorption
supportive care hemodialysis |
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CCl4 toxicity and treatment
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CNS depression
hepatic and renal toxicity no treatment |
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gasoline toxicity and treatment
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WORST = ASPIRATION
CNS depression lung inflammation cardiac arrhythmias DO NOT INDUCE VOMITING |
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Lead absorption in kids and adults
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GI- kids = 50%
adults = 8% Resp- into blood rapidly most moves to bones and teeth >10 years to turn over 1/2 of stored lead |
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lead pathology
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gi- constipation, metallic taste, lead colic
CNS- delayed development, encephalopathy blood- hypochromic, microcytic anemia, basophilic stippling mechanism- inhibits enzymes by binding to sulfhydryl groups (heme biosynthesis) |
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lead treatment
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chelation:
CaNa2EDTA |
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MCC exposure to mecury
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inhalation
binds to and inhibits sulfhydryl containing enzymes |
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mercury treatment
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elemental- DMSA, D-penicillamine, dimpercaprol
organic- DMSA, D-penicillamine, NOT dimercaprol |
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cyanide poisoning
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chemical asphyxia
binds ferric iron inhibits cellular resp, inhibits ox-phos venous blood is RED bitter almond breath inc. respiration agitation, coma, death |
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cyanide treatment
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sodium nitrite
thiosulfate (speeds conversion) methemoglobin (binds CN) |
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antidote competes with poison
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oxygen antidote for CO
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antidote accelerates excretion
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calcium salt antidote for radium
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antidote blocks metabolic formation of poison from less toxic precursor
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ethanol antidote for methanol and ethylene glycol
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antidote accelerates metabolic conversion or poison to nontoxic product
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thiosulfate antidote for cyanide
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antidote complexes with poison making in inert
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dimercaprol and DMSA- arsenic and mercury
EDTA- lead penicillamine and EDTA- copper methemoglobin- cyanide |
