drug toxicology
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- Acetaminophen toxicity
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increased drug > lots through p450> increase NAPQI > liver toxicity
NAPQI usually can be broken down by GSH but that is overwhelmed at excess NAPQI - Acetaminophen Tox Management
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use NAC (N-aceytlcystein): substitutes for GSH, replenish GSH levels, act directly as antioxident
Kids: more resistant due to higher turnover of GSH - Acetaminophnen and alcohol
- Eth induces CYP2E1, more Rx shifted to P450 route, and more NAPQI produced
- Salicylates (aspirin) toxicity
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metabolized normally through conjugation::: toxicity by: uncouple oxid phosph. leading to low ATP and metabolic acidosis, direct stimulation of resp. center >> resp alkalosis, GI irritation, decreased PT, platelet dysfunction
In chronic tox, will see cerebral edema - Salicylate (aspirin) tox management
- alkalynize urine, GI decon, activated charcoal
- Alcohol toxicity
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mainly metabolized by ADH, some by 2E1... excessive acetic acid production, acidosis
supportive treatment - Methanol toxicity
- Methanol via ADH to formaldehyde then via Ald Dehydrog. to formic acid (a much stronger acid)
- Methanol tox mgmt
- oxygen, lavage, induce emesis, sodium bicarb, folic acid to convert formic acid to CO2 and H20) ethanol or fomepizole)
- Ethylene Glycol Tox
- acid lead to anion gap and acidosis, calcium oxalate crystals formed >> tubular necrosis
- Ethylene Glycol Tox Mgmt
- lavage, charcoal, alkalinize urine, block ADH with fomeprizole or Eth, folic acid, hemodialysis
- Isopropanol tox (rubbing alcohol)
- removal and adsorption, supp care, hemodialysis
- Carbon tetracholoride tox
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CNS depression, hepatic, renal tox
No spec. treatment - Gasoline
- worst tox by aspiration, do NOT induce vomiting>>> lung inflammation, arrhthmias, CNS depression
- CO tox
- formation of COHb, Dx: cherry red cyanosis seen only post-mortem, living pts usually cyanotic and pale
- CO treatment
- 100% O2, hyperbaric chamber
- Lead tox
- 8% GI absorption in adult, 50% in children, resp tract absorption quick, most moves to bones and teeth, slow turnover:::/// Path: constip, metallic taste, delayed devp, encephalopathy, anemia... by inhibiting enzymes by binding sulfhydryl groups (heme biosynthesis)
- Lead tox treatment
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Chelation.
CaNa2EDTA: for lead
Dimercaprol (BAL): arsenic and mercury.
DMSA: lead, arsenic, mercury.
Penicillamine: copper
Dferoxamine: iron - Mercury tox
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peripheral peeling rash, CNS tremor, personality change (erethism: shyness, depression with explosive anger or blushing)
Mech: inhibits sulfhydryl enzyems, inhibits ChAT >> motor dysfunction - Mercury tox mgmt
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Elemental: DMSA, penicillamine, dimercaprol.//
Organic Hg: above but not dimercaprol which causes redistribution of chemical to brain!!! *** - Arsenic Tox
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binds SH groups, substitues phosphate groups: Sx: acute: GI, hypotension, metab. acidos./// chronic: neuropathy, skin changes
Trt: dimercaprol - Cadmium Tox
- tissue irritation , GE, pulmonary edema, liver and kidney damage w/ GSH depletion. Trt w/ CaNa2EDTA
- Thalium tox
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colorless, odorless, tasteless: acts as K+, impairs cation-activated enzyems: ATPases, ADH..>> Mitchondrial swelling, cell death
TRT: purssian blue radiogardase - Radioactive metals(Cs, U, Po)
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Cs: substitue K+ or Na+
Po: alpha particles damage DNA
U; dirty bombs
TRT: prussian blue radiogardase - Cyanide Tox
- binds ferric iron (cyt oxid in mitochondria), inhibits oxid. phosph. >> lactice acidosis and hypoxia.// sx: venous blood red, almond breath, elev respiration, agitation, coma, death
- Cyanide Tox Mgmt
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Amyl nitrite (inhaled) then sodium nitrite (IV): oxidizes iron to Fe3+ >>> less inhibition of oxid. phosph.//
sodium thiosulfite(IV)convert cyanide to thiocyante