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136 Cards in this Set
- Front
- Back
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ABCTs of emergency care
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airway, breathing, circulation, temperature
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naloxone
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administered if overdose from narcotics
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give comatose patient?
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iv naloxone, glucose, thiamine (none of these agents present a risk)
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what do blood gases tell you?
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patients condition, help identify toxicant
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give patient in shock?
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rapid iv crystalloid (ringer's lactate) or normal saline, also might have to give vasopressor (dopamine or norepinephrine)
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ringer's lactate
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rapid iv crystalloid given to a patient in shock, sometimes given with a vasopressor
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vasopressors (ex and use)
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dopamine, NE (sometimes given to a patient in shock in addition to a rapid iv crystalloid)
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control seizure
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give benzodiazepine (lorazepam, diazepam) or barbituate if first is not effective
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benzodiazepine (ex and use)
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lorazepam, diazepam given to control seizure and hyperthermia (brings down body temp)
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toxidromes
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symptoms resulting from a poisoning
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ideal time to prevent GI absorption
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within 60 min
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syrup of ipecac use
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for emesis, cause vomiting w/in 30min via direct stimulation of GI or later stimulation of CTZ
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syrup of ipecac disadvantages
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slow onset of action (20min or more), variable & incomplete emptying of stomach contents, own potential adverse effects, activated charcoal must be delayed until emesis stops
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syrup of ipecac contraindications
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coma (risk of aspiration), convulsions (risk of aspiration), age less than 9 mo (vomiting response not well dev), nontoxic ingestion (emesis has its own risks and discomfort), ingestion of caustic substances (don't expose esophagus a 2nd time), ingestion of petroleum distillate hydrocarbons (risk of aspiration)
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apomorphine use
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emesis w/in 1-3 min of sc injection
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apomorphine disadvantages
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respiratory depressant, so can be supplemented with naloxone to block the emetic and respiratory effects after emesis
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naloxone use
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given after emesis to block emetic and respiratory effects of apomorphine
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lavage def
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washing out stomach with water, saline, or other fluids.
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lavage disadvantages
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less effective than emesis (indicated if emesis too slow or contradindicated), discomfort of catheter, possible stomach perforation, some posions may be too large to enter small terminal pores of lavage tube
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activated charcoal use
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oral (usu 50-120g) to bind substances in stomach to prevent adsorption into circulation, w/in 30-60 min of poision ingestion, non-toxic (patient tolerance is limiting factor), may require multiple doses over several days (if drug is extended release of if known to undergo extensive enterohepatic circulation), given with sorbitol for constipation
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activated charcoal disadvantages
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not absorb acids and bases, alcohols, organic solvents, and metals, absorbs ipecac, constipating
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water
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dilute: topical toxicant, ocular exposure,orally ingested poison
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water
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dilute: topical toxicant, ocular exposure,orally ingested poison
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whole bowel irrigation definition
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large vol of physiologcial like solutions orally or through a nasogastric tube to quickly cause diarrhea
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whole bowel irrigation definition
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large vol of physiologcial like solutions orally or through a nasogastric tube to quickly cause diarrhea
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whole bowel irrigation use
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large quantity of toxic substance, late presentation, not absorbed by charcoal, oral overdose with delayed release medication bc of concretions, removal of drug packets (unless releasing drug-then surgery)
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whole bowel irrigation use
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large quantity of toxic substance, late presentation, not absorbed by charcoal, oral overdose with delayed release medication bc of concretions, removal of drug packets (unless releasing drug-then surgery)
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concretions
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intestinal masses of tablet aggregations from oral overdose with delayed release that become sticky when wet
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concretions
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intestinal masses of tablet aggregations from oral overdose with delayed release that become sticky when wet
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dialysis
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correct electrolyte imbalances through laws of osmosis
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peritoneal dialysis
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introduction of dialyzing soln into peritoneal cavity
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dialysis disadvantage
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does little to lower blood conentrations of substances that are highly bound to plasma prtns bc prtn prevent drug from passing through dialysis membrane, no sig dec of blood levels of toxicants that have a high Vd
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hemoperfusion def
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blood pumped through a cartridge that contains activated charcoal or ion-exchange resins
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hemoperfusion use
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for removal of chemical toxins esp if agent is lipid soluble or higly bound to plasma protein (more effective than hemodialysis)
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hemoperfusion disadvantages
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like dialysis, it can't significantly dec blood levels of toxicants that have high Vd, also has little effect on electrolyte imbalances
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Diuresis use
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rare, but use if toxin is excreted in urine, especially if it is not reabsorbed. more effective when coupled with acidification or alkalinization of urine
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diuretic agents
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mannitol, furosemide
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ion trapping
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acification or alkalinization of urine to ionize the chemical and dec reabsorption, but not routinely recommended bc of adverse effects
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acification
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clears basic chemicals (quinidine, amphetamine) faster with admin. of ascorbic acid or ammonium chloride
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alkalinization
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clears acids (salicylates, isoniazid) faster by admin. sodium bicarbonate
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freat acute ethanol intox
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supportive therapy: protect breathing and ventilation if necessary; correct hypothermia; adequate nutrition; glucose for hypoglycemia; thiamine as precaution for Wernicke's encephalopathy; seldom use lavage or dialysis, and activated charcoal not adsorb
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glucose use
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treat hypoglycemia (acute ethanol intox)
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thiamine
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precaution for Wernicke's encephalopathy
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gastric lavage use
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when emesis is too slow or contraindicated, after early isopropanol exposure
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isopropanol intoxication
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2nd most common alcohol exposure, even with bad taste!, more intoxicating than ethanol (worse respiratory depression), metabolizes to acetone (desired, so don't use ADH inhibitor) so can smell in breath in urine
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isopropanol treatment
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hemodialysis for very high conc, gastric lavage very early
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hemodialysis use
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very high conc of isopropanol
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acetone
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mild CNS depressant, odor o this in breath and urine strongly suggest intox with isopropanol
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methanol found in
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fouhd in windshield washing fluid, carburetor cleaners, camp stove fuels, and gas additives.
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methanol chemistry
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metabolizd through a formaldehyde intermediate to formic acid, which only slowly becomes CO2. so less intox than ethanol but intermediates are toxic
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formic acid effects
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severe metabolic acidosis and blindness
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ethylene glycol found in
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antifreeze, solvent for paints, lacquers
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ethylene glycol chemistry
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metabolized to glycolic acid`-> glyoxylic acid-> oxalic acid
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glycolic acid effects
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nephrotoxic, metabolic acidosis
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oxalic acid effects
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inc acidosis, binds ca so get urinary ca oxalate crystals (further inc renal toxicity) & dramatically lowers blood ca levels
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methanol treatment
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ADH inhibitor (ethanol, fomepizol) to prevent metabolism; sodium bicarbonate for acidosis, hemodialysis to remove high conc of the alcohol, the toxic aldehyde, and acid products; folic acid or folinic acid to convert formic acid to CO2
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ethylene glycol treatment
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thiamine and pyridoxine to divert metabolism from oxalic acid formation; soium bicarbonate to correct acidosis
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benzyl alcohol intox
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gasping syndrom in newborns, so should not use for injectable drug in neonates
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benzyl alcohol properties
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aromatic alcohol, preservative in parenteral solutions
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types of poisonous gases
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CO, cyanide, hydrogen sulfide
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CO properties
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binds to Hg much stronger than O2 (carboxyhemoglobin), interefere with normal association and dissociation of O2, normal half-life 4-5hrs
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CO intox
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O2 delivery severely diminished, reddish tint to skin (presence of carboxyHg)
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CO treatment
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remove victim from exposure, admin O2, no pharmacologic trtmnts
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O2 use
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100% O2- dec CO half-life from 4-5hrs to 80 min, hyperbaric to 23 min, puts more O2 in blood to compensate for O2 carrying capacity of Hg from CO poisoning
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cyanide treatment
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admin nitrites amyl nitrite first, then sodium nitite) and sodium thiosulfate (cyande antidote kit) or hyroxycobalamin (cyanokit)
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cyanide chemistry
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rapid acting ihibitor of cytochrome oxidase (terminal enzyme in ETC that transfers e- to oxygen), so O2 can't be used, ATP depleted.
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cyanide intox
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skin bright red (high O2 conc in blood)
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nitrite chemistry
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cyanide has high affinity for ferric iron, so use nitrite to convert iron in Hg to ferric state (methemoglobin), and any cyanide that has diffused away from cytochrome oxidase, can bind to a large pool of methemoglobin, so that ETC can occur
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nitrite administration
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first give amyl nitrite inhilation, until iv admin of sodium nitite can be started
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sodium thiosulfate
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speeds cyanide detox bc metabolism to thiocyanate requires thiosulfate. rxn is catalyzed by rhodanese enzyme
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hydroxocobalamin chemistry
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cyanide has a high affinity for cobalt, and binds to hydroxocobalamin, forming cyanobalamin (B12)
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Hydrogen Sulfide chemistry
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in sewer gas or refinery gases, inhibits cytochrome oxidase
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H2S treatment
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no specific antidotes, stop exposure, supportive therapy
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Hydrocarbon and Inhalant Ex.
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aliphatic, aromatic, halogenated
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aliphatic hydrocarbon ex., absorption, and effects
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gasoline, kerosine, lighter fluid; poor; GI
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aromatic hydrocarbon ex., absorption, and effects
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benzene, toluene, napthalene; well absorbed; liver, kidney, and other organs
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halogenated hydrocarbon ex., absorption,& effects
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chloroform, freon, trichloroethylene, many aerosol propellants; well absorbed from skin, GI, and lung; toxic to major organs, and risk of sensitizing heart to cathecholamines, so at risk of cardiac arrythmias and deah if frightened or stressed
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hydrocarbon treatment
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supportive care and management. emesis contradicted (risk of aspiration), activated charcoal ineffective (not significantly adsorbed), lavage considered if early and with protected airway
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pesticide ex
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insecticides, rodenticides, organophosphates, carbamate, organochloride
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organophosphate chem
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irreversible inhibitor of acetylcholinesterase bc acetylcholinesterase gets phosphorylated when it metabolizes the organophosphate ---> tightly bound
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organophosphate ex
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parathion, malathion
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organophosphate intox
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absorbed from all body surfaces, symptoms w/in 2-3hrs; constricted pupils, bradycardia, hypotension, excessive GI secretions, uncontrolled urination, headache, anxiety, convulsions (muscarinic receptors); muscle weakness and fasciculations (nicotinic receptors); death from respiratory failure (central depressant, weakness of respiratory m, pulmonary secretions)
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organophosphate treament
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maintain adequate respiration, dec absorption (emesis, activated charcoal), atropine, pralidoxime (2-PAM)
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atropine use and chem
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organophosphate intox; antagonized muscarinic receptors
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pralidoxime (2-PAM) use and chem
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organophosphate intox; regenerate acetylcholinesterase when used in first 2 days
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carbamate chem
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reversible inhibitor of acetylcholinesterase
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carbamate intox
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resemble organophosphate, but more transient, not as potent
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carbamate ex
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sevin
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carbamate treatment
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atropine but not pralidoxime (some carbamates inc by it)
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organochloride ex
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DDT, toxaphene, methoxyclor
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organochloride intox
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only toxic in intentional exposure, weak neurotoxins, excitation->convulsions
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organochloride treatment
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benzodiazepines (for convulsions in organochloride intox
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caustics and corrosive ex
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strong acids (auto battery, cleaner for auto battery, cleaning drains, toilet bowl, and metals); strong bases (cleaner for drains, dishwashing detergent, oven cleaner, bleaches, cement)
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acid tissue contact
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necrosis, but forms a protective coagulum (eschar)
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eschar
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protective coagulum that limits further penetration of acid burn
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base tissue contact
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saponify fats and cause liquefactive necrosis (deeper and more severe than acid burn)
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caustic/corrosive topical exposure treatment
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extensive flushing with water
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acid/base ingestion effects
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esophageal burns with high risk of stricture formation
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acid/base ingestion treatment
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emesis contraindicated (esophagus 2nd exposure); lavage may worsen gastric injury; activated charcoal ineffective; neutralization should never be done bc generates heat (add thermal burn to chemical injury); give small amount of water to dilute
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heavy metal treatment
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chelation therapy
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chelating agent ex
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dimercaprol, edetate, penicillamine, trientine, succimer, dereroxamine
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heavy metal states
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elemental (ground state), ionic, transition, alkyl
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elemental metal chem
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insolb, inert, rarely ingested (except mercury)
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ionic metal chem
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state most commonly associated with toxicity, react with electron-rich aa
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transition metals ex, chem
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iron, copper; participate in oxygen radical formation and oxidative stress
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alkyl metal chem
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lipid solb, readily abs from lungs/GI tractl. R-M complexes are directly toxic and can metabolize to realease ionic forms of the metal
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chelation therapy
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chelating agents have electron rich domains which tightly bind ionic metals. water solb chelates are excreted in urine. some chelates can be used for diff metals, but some are specific. they have little effect on uncharged alkylated metals
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dimercaprol (BAL) admin
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type of chelator that must be given i.m. injection, preffered chelator for mercury poison
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dimercaprol (BAL) side-effects
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nausea, headache, burning sensations from chelation of trace metals required in prosthetic groups of many enzymes
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edetate ex, admin
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calcium disodium edetate, EDTA; slow IV injection to prevent thromboplebitis
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edetate chem, disadvantage
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metals (lead) displace the ca in chelation site, and then the chelates are rapidly excreted in urine, but may cause mild, reversible kidney injury
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penicillamine
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from degradation of penicillin, oral admin
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penicillamine use
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wilson's disease, long-term chelation therapy (ex. mercury poisoning) to lower blood lead levels
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wilson's disease
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copper accumulates due to a ceruloplasmin deficiency, rheumatoid arthritis
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penicillamine disadvantage
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allergy (1/3 of ptnts)
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trientine use
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oral copper chelator for Wilson's disease who are intolerant of penicillamine, but less effective
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trientine disadvantages
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binds iron effectively, so dev iron deficiency anemia during long-term therapy
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succimer use
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oral, heavy metal chelator; lead poison in children, mercury, arsenic poison, little effect on urinary excretion of essential metals (iron, ca, Mg)
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succimer disadvantages
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GI symptoms (nausea, vomit, diarrhea) transient elevation of serum transaminases
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deferoxamine/desferrioxamine
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specific iron chelation agent. oral for iron in GI or injection fo systemic iron poisoning; aluminum overload
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heavy metal poison ex.
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iron, lead, mercury
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iron use
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prevention and treatment of anemia
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iron poison symptoms
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GI symptoms early followed by apparent recovery; shock, acidosis, cyanosis, liver injury following first few days after exposure
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iron poison treatment
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IV deferoxamine by continuous infusion preferred to IM injection. dose determined from serum iron levels
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lead treatment
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combo of edetate, dimercaprol, and penicillamine (succimer in children). cerebral edema treated with mannitol and dexamethasone. seizures controlled with diazepam; adequate dietary levels of iron circument roxic effect of lead
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lead symptoms
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acute lead poisoning is rare, usu from chronic exposure in lead-related industries; hypochromic micryocytic anemia, renal toxicity, lead palsy, Gi constipation, anorexia, and abdominal pain, lead encephalopathy in children
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hypochromic microcytic anemia
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in lead poisoining due to inhibition of two enzymes required for heme biosynthesis
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lead palsy
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neuromuscular condition due to demyelination of the nerve sheath
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lead absorption, excretion
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incompletely absorbed from GI tract, but alkyl forms readily absorned from lung in skin. lead then distributed to soft tissues and deposited to bone. blood levels often inc after chelation therapy, even if there is no additional exposure to the metal
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mercury chem
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metallic mercury is silver liquid with sig vapor pressure, oxidized after aborption to mercuric form (most toxic state). mercurous forms are insoluble and have little toxic potential. alkyl mercurials used as fungicides and readily absorbed from skin, lung, GI
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acute mercury poisoning
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direct toxic reactions along route of ingestion
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chronic mercury poisoning
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neurologic and psychiatric (mad hatter) symptoms, renal toxicity
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lead diagnosis
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50 micrograms per 100mL or more
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mercury diagnosis
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msr in blood or hair
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mercury treatment
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dimercaprol or penicillamine (or it's N-acetyl derivative). oral polythiol resins interfere with enterohepatic circulation of mercury
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polythiol resins use
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interfere with enterohepatic circulation in mercury poisoing
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