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25 Cards in this Set

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Review Set 7
keeton is a bastard
when not to induce emesis?
-do not induce emesis w/poisoning caused by...
-petroleum distillates
stuff that causes lung damage?
- SO2 - forms sulfurous acid - causes reflex bronchoconstriction

- NO2 - lung damage via direct irritation - causes pulmonary edema - “silo-fillers lung”

- paraquat - herbicide - pulmonary fibrosis

- asbestos - mesothelioma and pulmonary fibrosis

- cotton - byssinosis

- bleomycin - oxygen free radicals damage tissue
High O2 conc damages retina and CNS via formation of superoxide ion
-does that make me crazy?
Carbon Monoxide
-forms carboxyHb which cannot carry oxygen and interferes w/ the release of
oxygen from oxyHb = arterial O2 content is 50% of normal

-reduces oxygen carrying capacity (content) of blood but not the PaO2

-CO also directly toxic to cellular cytochromes

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

-tx w/ oxygen
pregnant female given phenytoin...whats gonna happen?
-baby has cleft lip/palate and seizures
-Halogenated HC’s are directly mutagenic

-Polycyclic aromatic HC’s mutagenic aftermetabolized by CYP450
-Benzene - bone marrow depression = aplastic anemia or leukemia
-MOA of strychnine-blocks postsynaptic inhibition caused by glycine released from Renshaw cells
-no inhibition of muscle activity;tonic extension os muscles causes stifness; excitability of muscle increased
Toxicity of PHOSGENE (COCl2)
-toxicity of phosgene (COCl2) - a highly toxic suffocating gas
tx of organophosphate poisoning?
-atropine (first drug given) + pralidoxime (2-PAM)
tx of carbamate insecticide poisoning?
-Carbamate insecticides. e.g., aldicarb - tx w/ atropine alone
Mercury toxicity
-TX:dimercaprol (BAL) or penicillamine

-S/S:chelating agents gingivitis. loose teeth, neuropathy (tremor in fingers, arms & legs),Hg deposits in lens, personality changes, fearful, irritable, can’t concentrate
Lead toxicity
-lead interfers with heme synthesis, so precursors of heme accumulate
-Tx: EDTA(a chelating agent)
-S/S:peripheral neuropathy consisting of wristdrop (painless weakness of extensor muscles), gastric colic, lead encephalopathy c severe toxicity, renal damage after years of exposure

-Labs:hypochromic microcyctic anemia with increased urinary excretion of delta-aminolevulinic acid (DAA)
Arsenic Toxicity
-TX: dimercaprol (BAL)
-S/S: garlic odor or sweet breath, anemia, cutaneous dilation ("milk and rose" complexion), hyperkeratosis of palms and soles, transverse white lines in fingernails (Mee's lines)
Iron overdose
-seen in children whose mother is takin iron during pregnancy

-TX: gastric lavage, deferoxamine into stomach, deferoxamine iv

-S/S: severe gastric distress w/bleeding->bloody diarrhea
Antidotes for heavy metal poisoning
(a great band name would be anecdotes on heavy metal poisoning!!!)
-Hg and Arsenic=dimercaprol(BAL)
-Hg and Cu=penicillamine
cyanide toxicity
-smoke from burning plastic, fumigants, metal polishes, electroplating solutions
-cyanide has a "bitter almond" smell
cyanide toxicity
-MOA - 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
cyanide toxicity
-S/S = lactic acidosis, increased respiratory rate/depth, venous blood bright red, cytotoxic hypoxia, convulsions, respiratory arrest
cyanide toxicity
-tx (must be rapid)
-tx: nitrite + thiosulfate

-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
Aspiring OD (TINNITUS)
1.acute phase of mild poison-resp alkalosis
2.uncouples oxidative phosph-incCO2production,hyperpyrexia,sweating
3.increased rate/depth of respiration via incCO2 and direct effect on medulla
4.resp alkalosis-followed by inc renal excretion of HCO3- in attempt to compensate for inc prod of CO2
5.severe poisoning-combination of resp and met acidosis
6.large inc in CO2 inhibits medullary resp center in the presence of continued prod of CO2 and low plasma HCO3- =acidosis
7.salicylate interferes w/ citric acid cycle -inc lactate/pyruvate
Acetaminophen OD
-acetaminophen OD - ass. with inc AST/ALT

-Tx with N-acetylcysteine
(acetylcysteine is a precursor of glutathione)
-replinishes glutathione stores to combine with toxic metabolite of acetaminophen
Toxicity of plant materials
-S/S excessive ACh stimulation -> tx w/ atropine

-S/S atropine poisoning - hot, red, dry skin, fever, dry -> tx w/ physostigmine
-Dioxin causes dermatitis and chloracne