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drug toxicology


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Acetaminophen toxicity
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
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
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
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
CNS depression, hepatic, renal tox

No spec. treatment
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
CaNa2EDTA: for lead
Dimercaprol (BAL): arsenic and mercury.
DMSA: lead, arsenic, mercury.
Penicillamine: copper
Dferoxamine: iron
Mercury tox
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
Elemental: DMSA, penicillamine, dimercaprol.//
Organic Hg: above but not dimercaprol which causes redistribution of chemical to brain!!! ***
Arsenic Tox
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
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)
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
Amyl nitrite (inhaled) then sodium nitrite (IV): oxidizes iron to Fe3+ >>> less inhibition of oxid. phosph.//

sodium thiosulfite(IV)convert cyanide to thiocyante

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