Toxicology

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Do not induce emesis w poisoning caused by:

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petroleum distillates, alkali/acids, convulsants

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SO2 and lung damage

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forms sulfurous acid - causes reflex bronchoconstriction

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NO2 and lung damage

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lung damage via direct irritation - causes pulmonary edema - “silo-fillers lung”

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paraquat and lung damage

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herbicide - pulmonary fibrosis

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asbestos and lung damage

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mesothelioma and pulmonary fibrosis

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cotton and lung damage

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byssinosis

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bleomycin and lung damage

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oxygen free radicals damage tissue

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High O2 concentration damages retina and CNS via

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formation of superoxide ion

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Carbon monoxide (CO) pharm effects

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a. forms carboxyHb which cannot carry oxygen and interferes w the release of oxygen from oxyHb = arterial O2 content is 50% of normal
b. reduces oxygen carrying capacity (content) of blood but not the PaO2
c. CO also directly toxic to cellular cytochromes

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Carbon monoxide (CO) S/S

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headache w tightness in temporal region; confusion & loss of visual acuity, psychomotor impairment; syncope, tachycardia, tachypnea

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Carbon monoxide (CO) poisoning tx

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oxygen

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Phenytoin tx of pregnant female results in:

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baby born w cleft lip & palate and seizures

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Benzene toxicity

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bone marrow depression = aplastic anemia or leukemia

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toxicity of phosgene (COCl2)

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a highly toxic suffocating gas

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MOA of strychnine -

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blocks postsynaptic inhibition caused by glycine released from Renshaw cells; no inhibition of muscle activity; tonic extension os muscles causes stiffness; excitability of muscle increased

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Tx organophosphate poisoning w

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atropine (first drug given) + pralidoxime (2-PAM)

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Tx Carbamate insecticide poisoning. e.g., aldicarb

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tx w atropine alone

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mercury (Hg) toxicity, tx w

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dimercaprol (BAL) or penicillamine (chelating agents)

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mercury (Hg) toxicity S/S

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gingivitis. loose teeth, neuropathy (tremor in fingers, arms & legs),
Hg deposits in lens, personality changes, fearful, irritable, can’t concentrate

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lead (Pb) toxicity tx

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EDTA (a chelating agent)

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lead (Pb) toxicity S/S

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lead interfers with heme synthesis, so precursors of heme accumulate

peripheral neuropathy consisting of wristdrop (painless weakness of extensor muscles), gastric colic, lead encephalopathy c severe toxicity, renal damage after
years of exposure

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lead (Pb) toxicity labs

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hypochromic microcyctic anemia with increased urinary excretion of delta-aminolevulinic acid (DAA)

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dioxin causes

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dermatitis amd chloracne

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arsenic (Ar) toxicity tx w

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dimercaprol (BAL)

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arsenic (Ar) toxicity S/S

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garlic odor or sweet breath; anemia; cutaneous dilation (“milk and roses” complexion), hyperkeratosis of palms and soles, transverse white lines in fingernails (Mee’s lines)

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Fe overdose S/S

(seen in children whose mother has been taking Fe for pregnancy)

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severe gastric distress w bleeding, including bloody diarrhea

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Fe overdose, tx w

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gastric lavage, deferoxamine into stomach, deferoxamine i.v.

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Antidotes to Fe

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deferoxamine

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Antidotes to Pb

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EDTA

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Antidotes to Hg and Ar

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dimercaprol (BAL)

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Antidotes to Hg and Cu

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penicillamine

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cyanide toxicity S/S

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lactic acidosis, increased respiratory rate/depth, venous blood bright red, cytotoxic hypoxia, convulsions, respiratory arrest

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cyanide toxicity MOA

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reacts w ferric iron of cytochrome oxidase in mitochondria to inhibit cellular respiration, prevents reuction of ferric iron to ferrous iron in cytochrome a3, so no electron transport - same effect as no oxygen

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cyanide toxicity, tx w

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d. tx ( must be rapid) = nitrite + thiosulfate
e. tx w nitrite to convert Hb (Fe++) to MetHb (Fe+++) because CN likes Fe+++, MetHb competes w cytochrome oxidase for CN, MetHb converted to cyanometHb with restoration of cytochrome oxidase, cyanometHb acted on by rhodanese in presence of thiosulfate to form thiocyanate which is eliminated by renal excretion can treat w hydroxycobalamin which reacts w CN to form cyanocobalamin, hydroxycobalamin used to treat CN poisoning from sodium nitroprusside

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aspirin OD S/S

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tinnitus!
respiratory alkalosis at first
inc CO2 production, hyperpyrexia, sweating
increased rate/depth of respiration

metabolic acidosis with large doses

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aspirin OD MOAs

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uncouples oxidative phosphorylation,
c. increased rate/depth of respiration via increased CO2 and direct effect on medulla
d. respiratory alkalosis - followed by increased renal excretion of HCO3- in an attempt to compensate for increased production of CO2

f. large increase in CO2 inhibits medullary respiration center in the presence of continued production of CO2 and low plasma HCO3- = acidosis
g. salicylate also interferes w citric acid cycle - inc [lactate/pyruvate] = acidosis

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acetaminophen OD S/S

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inc AST/ALT, liver damage by radicals

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acetaminophen OD tx

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Tx with N-acetylcysteine
(acetylcysteine is a precursor of glutathione), replinishes glutathione stores to combine with toxic metabolite of acetaminophen

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S/S excessive ACh stimulation, tx w

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atropine

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S/S atropine poisoning

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hot, red, dry skin, fever, dry - tx w physostigmine