Block 1: Toxicology
Terms
undefined, object
copy deck
- incidence of toxicity (top 3)
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analgesics
cleaning substances
alcohols and hydrocarbons - 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 - tylenol and alcohol
- cyp2E1
- antidote for tylenol (acetaminophen)
- mucomyst = NAC
- 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 - 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 - tx aspirin toxicity
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alkalinize urine with bicarb
GI decontamination
activated charcoal - ethanol metabolism
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90% liver, 10% stomach
alcohol dehydrogenase
CYP450
catalase - ethanol toxicity treatment
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no antidote
supportive care - 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 - 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 - methanol toxicity mechanism
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methanol slowly met. to formaldehyde
formaldehyde quickly met. to formic acid
formic acid-> acidosis, ocular toxicity - methanol toxicity treatment
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high O2
lavage (<30 min)
alkalinize urine
folic acid
ETHANOL or FOMEPIZOLE - isopropanol toxicity mechanism
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CNS toxicity
high ketones (acetone)
abdominal pain, gastritis
no acidosis
hypotension and coma - isopropanol treatment
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removal and adsorption
supportive care
hemodialysis - CCl4 toxicity and treatment
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CNS depression
hepatic and renal toxicity
no treatment - gasoline toxicity and treatment
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WORST = ASPIRATION
CNS depression
lung inflammation
cardiac arrhythmias
DO NOT INDUCE VOMITING - 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 - 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) - lead treatment
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chelation:
CaNa2EDTA - MCC exposure to mecury
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inhalation
binds to and inhibits sulfhydryl containing enzymes - mercury treatment
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elemental- DMSA, D-penicillamine, dimpercaprol
organic- DMSA, D-penicillamine, NOT dimercaprol - 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 - cyanide treatment
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sodium nitrite
thiosulfate (speeds conversion)
methemoglobin (binds CN) - antidote competes with poison
- oxygen antidote for CO
- antidote accelerates excretion
- calcium salt antidote for radium
- antidote blocks metabolic formation of poison from less toxic precursor
- ethanol antidote for methanol and ethylene glycol
- antidote accelerates metabolic conversion or poison to nontoxic product
- thiosulfate antidote for cyanide
- 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