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29 Cards in this Set

  • Front
  • Back
incidence of toxicity (top 3)
cleaning substances
alcohols and hydrocarbons
phases of acetaminophen toxicity
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
antidote for tylenol (acetaminophen)
mucomyst = NAC
aspirin metabolism
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)
uncoupling ox-phos -> inc anion gap
stim resp center -> resp alkylosis
irritate GI tract
dec prothrombin and platelet dysfunction
tx aspirin toxicity
alkalinize urine with bicarb
GI decontamination
activated charcoal
ethanol metabolism
90% liver, 10% stomach
alcohol dehydrogenase
ethanol toxicity treatment
no antidote
supportive care
ethylene glycol toxicity mechanism (5)
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
lavage (<2hrs)
activated charcoal
alkalinize urine
ETHANOL (block alcohol dehyrogenase)or FOMEPIZOLE (block ADH)
folic acid, pyridoxine, thiamine
methanol toxicity mechanism
methanol slowly met. to formaldehyde
formaldehyde quickly met. to formic acid
formic acid-> acidosis, ocular toxicity
methanol toxicity treatment
high O2
lavage (<30 min)
alkalinize urine
folic acid
isopropanol toxicity mechanism
CNS toxicity
high ketones (acetone)
abdominal pain, gastritis
no acidosis
hypotension and coma
isopropanol treatment
removal and adsorption
supportive care
CCl4 toxicity and treatment
CNS depression
hepatic and renal toxicity

no treatment
gasoline toxicity and treatment
CNS depression
lung inflammation
cardiac arrhythmias

Lead absorption in kids and adults
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
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
MCC exposure to mecury
binds to and inhibits sulfhydryl containing enzymes
mercury treatment
elemental- DMSA, D-penicillamine, dimpercaprol
organic- DMSA, D-penicillamine, NOT dimercaprol
cyanide poisoning
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
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
dimercaprol and DMSA- arsenic and mercury
EDTA- lead
penicillamine and EDTA- copper
methemoglobin- cyanide