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136 Cards in this Set

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ABCTs of emergency care
airway, breathing, circulation, temperature
naloxone
administered if overdose from narcotics
give comatose patient?
iv naloxone, glucose, thiamine (none of these agents present a risk)
what do blood gases tell you?
patients condition, help identify toxicant
give patient in shock?
rapid iv crystalloid (ringer's lactate) or normal saline, also might have to give vasopressor (dopamine or norepinephrine)
ringer's lactate
rapid iv crystalloid given to a patient in shock, sometimes given with a vasopressor
vasopressors (ex and use)
dopamine, NE (sometimes given to a patient in shock in addition to a rapid iv crystalloid)
control seizure
give benzodiazepine (lorazepam, diazepam) or barbituate if first is not effective
benzodiazepine (ex and use)
lorazepam, diazepam given to control seizure and hyperthermia (brings down body temp)
toxidromes
symptoms resulting from a poisoning
ideal time to prevent GI absorption
within 60 min
syrup of ipecac use
for emesis, cause vomiting w/in 30min via direct stimulation of GI or later stimulation of CTZ
syrup of ipecac disadvantages
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
syrup of ipecac contraindications
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)
apomorphine use
emesis w/in 1-3 min of sc injection
apomorphine disadvantages
respiratory depressant, so can be supplemented with naloxone to block the emetic and respiratory effects after emesis
naloxone use
given after emesis to block emetic and respiratory effects of apomorphine
lavage def
washing out stomach with water, saline, or other fluids.
lavage disadvantages
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
activated charcoal use
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
activated charcoal disadvantages
not absorb acids and bases, alcohols, organic solvents, and metals, absorbs ipecac, constipating
water
dilute: topical toxicant, ocular exposure,orally ingested poison
water
dilute: topical toxicant, ocular exposure,orally ingested poison
whole bowel irrigation definition
large vol of physiologcial like solutions orally or through a nasogastric tube to quickly cause diarrhea
whole bowel irrigation definition
large vol of physiologcial like solutions orally or through a nasogastric tube to quickly cause diarrhea
whole bowel irrigation use
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)
whole bowel irrigation use
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)
concretions
intestinal masses of tablet aggregations from oral overdose with delayed release that become sticky when wet
concretions
intestinal masses of tablet aggregations from oral overdose with delayed release that become sticky when wet
dialysis
correct electrolyte imbalances through laws of osmosis
peritoneal dialysis
introduction of dialyzing soln into peritoneal cavity
dialysis disadvantage
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
hemoperfusion def
blood pumped through a cartridge that contains activated charcoal or ion-exchange resins
hemoperfusion use
for removal of chemical toxins esp if agent is lipid soluble or higly bound to plasma protein (more effective than hemodialysis)
hemoperfusion disadvantages
like dialysis, it can't significantly dec blood levels of toxicants that have high Vd, also has little effect on electrolyte imbalances
Diuresis use
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
diuretic agents
mannitol, furosemide
ion trapping
acification or alkalinization of urine to ionize the chemical and dec reabsorption, but not routinely recommended bc of adverse effects
acification
clears basic chemicals (quinidine, amphetamine) faster with admin. of ascorbic acid or ammonium chloride
alkalinization
clears acids (salicylates, isoniazid) faster by admin. sodium bicarbonate
freat acute ethanol intox
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
glucose use
treat hypoglycemia (acute ethanol intox)
thiamine
precaution for Wernicke's encephalopathy
gastric lavage use
when emesis is too slow or contraindicated, after early isopropanol exposure
isopropanol intoxication
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
isopropanol treatment
hemodialysis for very high conc, gastric lavage very early
hemodialysis use
very high conc of isopropanol
acetone
mild CNS depressant, odor o this in breath and urine strongly suggest intox with isopropanol
methanol found in
fouhd in windshield washing fluid, carburetor cleaners, camp stove fuels, and gas additives.
methanol chemistry
metabolizd through a formaldehyde intermediate to formic acid, which only slowly becomes CO2. so less intox than ethanol but intermediates are toxic
formic acid effects
severe metabolic acidosis and blindness
ethylene glycol found in
antifreeze, solvent for paints, lacquers
ethylene glycol chemistry
metabolized to glycolic acid`-> glyoxylic acid-> oxalic acid
glycolic acid effects
nephrotoxic, metabolic acidosis
oxalic acid effects
inc acidosis, binds ca so get urinary ca oxalate crystals (further inc renal toxicity) & dramatically lowers blood ca levels
methanol treatment
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
ethylene glycol treatment
thiamine and pyridoxine to divert metabolism from oxalic acid formation; soium bicarbonate to correct acidosis
benzyl alcohol intox
gasping syndrom in newborns, so should not use for injectable drug in neonates
benzyl alcohol properties
aromatic alcohol, preservative in parenteral solutions
types of poisonous gases
CO, cyanide, hydrogen sulfide
CO properties
binds to Hg much stronger than O2 (carboxyhemoglobin), interefere with normal association and dissociation of O2, normal half-life 4-5hrs
CO intox
O2 delivery severely diminished, reddish tint to skin (presence of carboxyHg)
CO treatment
remove victim from exposure, admin O2, no pharmacologic trtmnts
O2 use
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
cyanide treatment
admin nitrites amyl nitrite first, then sodium nitite) and sodium thiosulfate (cyande antidote kit) or hyroxycobalamin (cyanokit)
cyanide chemistry
rapid acting ihibitor of cytochrome oxidase (terminal enzyme in ETC that transfers e- to oxygen), so O2 can't be used, ATP depleted.
cyanide intox
skin bright red (high O2 conc in blood)
nitrite chemistry
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
nitrite administration
first give amyl nitrite inhilation, until iv admin of sodium nitite can be started
sodium thiosulfate
speeds cyanide detox bc metabolism to thiocyanate requires thiosulfate. rxn is catalyzed by rhodanese enzyme
hydroxocobalamin chemistry
cyanide has a high affinity for cobalt, and binds to hydroxocobalamin, forming cyanobalamin (B12)
Hydrogen Sulfide chemistry
in sewer gas or refinery gases, inhibits cytochrome oxidase
H2S treatment
no specific antidotes, stop exposure, supportive therapy
Hydrocarbon and Inhalant Ex.
aliphatic, aromatic, halogenated
aliphatic hydrocarbon ex., absorption, and effects
gasoline, kerosine, lighter fluid; poor; GI
aromatic hydrocarbon ex., absorption, and effects
benzene, toluene, napthalene; well absorbed; liver, kidney, and other organs
halogenated hydrocarbon ex., absorption,& effects
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
hydrocarbon treatment
supportive care and management. emesis contradicted (risk of aspiration), activated charcoal ineffective (not significantly adsorbed), lavage considered if early and with protected airway
pesticide ex
insecticides, rodenticides, organophosphates, carbamate, organochloride
organophosphate chem
irreversible inhibitor of acetylcholinesterase bc acetylcholinesterase gets phosphorylated when it metabolizes the organophosphate ---> tightly bound
organophosphate ex
parathion, malathion
organophosphate intox
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)
organophosphate treament
maintain adequate respiration, dec absorption (emesis, activated charcoal), atropine, pralidoxime (2-PAM)
atropine use and chem
organophosphate intox; antagonized muscarinic receptors
pralidoxime (2-PAM) use and chem
organophosphate intox; regenerate acetylcholinesterase when used in first 2 days
carbamate chem
reversible inhibitor of acetylcholinesterase
carbamate intox
resemble organophosphate, but more transient, not as potent
carbamate ex
sevin
carbamate treatment
atropine but not pralidoxime (some carbamates inc by it)
organochloride ex
DDT, toxaphene, methoxyclor
organochloride intox
only toxic in intentional exposure, weak neurotoxins, excitation->convulsions
organochloride treatment
benzodiazepines (for convulsions in organochloride intox
caustics and corrosive ex
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)
acid tissue contact
necrosis, but forms a protective coagulum (eschar)
eschar
protective coagulum that limits further penetration of acid burn
base tissue contact
saponify fats and cause liquefactive necrosis (deeper and more severe than acid burn)
caustic/corrosive topical exposure treatment
extensive flushing with water
acid/base ingestion effects
esophageal burns with high risk of stricture formation
acid/base ingestion treatment
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
heavy metal treatment
chelation therapy
chelating agent ex
dimercaprol, edetate, penicillamine, trientine, succimer, dereroxamine
heavy metal states
elemental (ground state), ionic, transition, alkyl
elemental metal chem
insolb, inert, rarely ingested (except mercury)
ionic metal chem
state most commonly associated with toxicity, react with electron-rich aa
transition metals ex, chem
iron, copper; participate in oxygen radical formation and oxidative stress
alkyl metal chem
lipid solb, readily abs from lungs/GI tractl. R-M complexes are directly toxic and can metabolize to realease ionic forms of the metal
chelation therapy
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
dimercaprol (BAL) admin
type of chelator that must be given i.m. injection, preffered chelator for mercury poison
dimercaprol (BAL) side-effects
nausea, headache, burning sensations from chelation of trace metals required in prosthetic groups of many enzymes
edetate ex, admin
calcium disodium edetate, EDTA; slow IV injection to prevent thromboplebitis
edetate chem, disadvantage
metals (lead) displace the ca in chelation site, and then the chelates are rapidly excreted in urine, but may cause mild, reversible kidney injury
penicillamine
from degradation of penicillin, oral admin
penicillamine use
wilson's disease, long-term chelation therapy (ex. mercury poisoning) to lower blood lead levels
wilson's disease
copper accumulates due to a ceruloplasmin deficiency, rheumatoid arthritis
penicillamine disadvantage
allergy (1/3 of ptnts)
trientine use
oral copper chelator for Wilson's disease who are intolerant of penicillamine, but less effective
trientine disadvantages
binds iron effectively, so dev iron deficiency anemia during long-term therapy
succimer use
oral, heavy metal chelator; lead poison in children, mercury, arsenic poison, little effect on urinary excretion of essential metals (iron, ca, Mg)
succimer disadvantages
GI symptoms (nausea, vomit, diarrhea) transient elevation of serum transaminases
deferoxamine/desferrioxamine
specific iron chelation agent. oral for iron in GI or injection fo systemic iron poisoning; aluminum overload
heavy metal poison ex.
iron, lead, mercury
iron use
prevention and treatment of anemia
iron poison symptoms
GI symptoms early followed by apparent recovery; shock, acidosis, cyanosis, liver injury following first few days after exposure
iron poison treatment
IV deferoxamine by continuous infusion preferred to IM injection. dose determined from serum iron levels
lead treatment
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
lead symptoms
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
hypochromic microcytic anemia
in lead poisoining due to inhibition of two enzymes required for heme biosynthesis
lead palsy
neuromuscular condition due to demyelination of the nerve sheath
lead absorption, excretion
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
mercury chem
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
acute mercury poisoning
direct toxic reactions along route of ingestion
chronic mercury poisoning
neurologic and psychiatric (mad hatter) symptoms, renal toxicity
lead diagnosis
50 micrograms per 100mL or more
mercury diagnosis
msr in blood or hair
mercury treatment
dimercaprol or penicillamine (or it's N-acetyl derivative). oral polythiol resins interfere with enterohepatic circulation of mercury
polythiol resins use
interfere with enterohepatic circulation in mercury poisoing