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64 Cards in this Set
- Front
- Back
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what are the 5 major steps in the management of acute poisoning?
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supportive care: airway, breathing, circulation, disability, exposure
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dextrose
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hypoglycemia can present as any alteration in mental status (confusion, seizures, coma)
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thiamine
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to treat/prevent precipitating acute Wernicke's encephalopathy, deficiency (due to chronic disease, malnutrition, eating disorders or alcoholism)
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naloxone
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to reverse respiratory depression with known or suspected opiate toxicity
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preferred method for gastrointestinal decontamination
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activated charcoal
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what does activated charcoal not work on?
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caustics
corrosives heavy metals alcohols cyanide aliphatic hydrocarbons laxatives |
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when is gastric lavage indicated in general?
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not recommended fro routine use- used when AC won't work and only removes dissolved drugs
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when (in general) do you induce emesis?
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immediately following witnessed poisoning in prehospital setting
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complications of gastric lavage
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force of procedure may force gastric contents into small bowel
esophageal perforation (acid alkali) aspiration risk (petroleum) |
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complications of emesis
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aspiration
protracted vomiting vagal induced bradycardia esophageal tearing |
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contraindications to gastric lavage
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corrosive agents
strong acid or alkali petroleum uconscious patients with no ET tube |
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emesis contraindications
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depressed mental status
<6 months old inability to protect airway ingestion of agents causing a rapid mental status change ingestion of acids, alkali, petroleum, or sharp objects |
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description of and indications for whole bowel irrigation
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enteral administration of PEG that cleans the GI tract of contents to stop absorption
drug packets sustained release formulations enteric-coated preps substances not absorbed by AC |
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cathartics: description and indications
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limit absorption by increased rectal evacuation and decreased passage time; prevent constipation and enhance elimination of the charcal-poison complex
never used as a single agent therapy |
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urinary alkalinization
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hastens elimination
1st treatment for moderate salicylate poisoning along with AC |
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osmotic diuresis
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decreased reabsorption and increased flow through renal tubule; may cause volume overload
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hemodialysis
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for severe poisoning, it has limited use; not good for drugs with large VD
readily corrects electrolyte disturbances and metabolic acidosis caused by some drugs used for: alcohols, salicylates, ethyline glycol, litihm |
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symptoms of acute CO poisoning
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psychomotor impairment
headache confusion loss of visual acuity coma convulsions |
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symptoms of prolonged exposure to CO
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coma
convulsions damage to brain and heart shock respiratory failure |
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moa of CO poisoning- heme
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CO reversibly binds to Fe of heme and has a 200x greater affinity for Fe than O2- displaces O2 from Hb
O2 can't bind heme O2 that is bound to heme can't be released-> O2 can't be transferred to tissues-> tissues deprived of O2 |
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moa of CO poisoning: direct cellular toxicity
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myoglobin binding: direct skeletal and cardiac muscle tox
cytochrome binding: impaired oxidative metabolism, free radical formation, metabolic acidosis CO stimulates guanylate cyclase: cerbral vasodilation leading to syncope |
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treatment of CO poisoning
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decrease exposure and maintain vital functions
keep patient at rest to decrease O2 demand give 100% O2- specific antidote |
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MOA of cyanide poisoning
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affects virtually all body tissues by inactivating ubiquitous metalloenzymes
primary: binds to Fe3+ to prevent it from being reduced to Fe2+ (involved in cytochrome oxidase ETC) the body is unable to generate ATP even though plenty of O2 is available in the blood and tissues (can't use it!) cells switch to anaerobic metabolism for energy and there is an accumulation of pyruvate and lactate metabolic acidosis |
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histotoxic hypoxia
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apparently good oxygenation (no cyanosis) but intense respiratory distress
due to cyanide |
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symptoms of cyanide poisoning
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hyperpnea
gasping collapse d/t CNS and cardiac effects convulsions cardiac arrhythmias |
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treatment and MOA of tx for cyanide poisoning
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sodium nitrite (IV)promotes the formation of methemoglobin to detoxify cyanide to cyanmethemoglobin-> metHb competes with cytochrome oxidase for CN- and up to 25% methemoglobinemia is formed
thiosulfate given second- facilitates enzyme-catalyzed conversion of cyanide to less-toxic thiocyanate; as free CN- in the blood decreases, more dissociates from CNmetHb and is eliminated |
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alternative tx for CN poisoning
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inhaled amyl nitrite is sometimes used while prepping the 1st line treatments, but it has questionable efficacy- only 5% methemoglobinemia
hydroxycobalamin- IV dosing- forms a harmless vitamin B12a cyanocobalamin which can be eliminated in the urine; works within the intravascular and cellular spacing |
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is there hyperpnea in in CO poisoning?
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no. CO is potent enough to have its toxic fx at a concentration too low to trigger the chemoreceptors
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is there hyperpnea in CN poisoning?
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yes, as a direct result of chemoreceptor stimulation (aortic and carotid receptors)
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organophosphates-human toxicity
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common poisoning, but rarely death
well-absorbed through skin, GI and respiratory tract cholinesterase inhibitor |
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carbamate human toxicity
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poisoning is common but death is rare; less toxic than organophosphates and readily reversible
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chlorinated hydrocarbons human toxicity
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not used as often
less poisonous, but worse for environment and stayed around longer |
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organophosphates vs. carbamate: which is more toxic?
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organophosphates
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pralidoxime (2-PAM) is the treatment for
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organophosphates
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primary delayed toxicity of paraquat ingestion
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respiratory distress due to progressive fibrosis of lungs
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prompt removal because you need to prevent systemic absorption
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once paraquat absorption has occurred, treatment is less than 50% successful
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warfarin MOA and sx of tox?
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antagonizes action of vitamin K in activation of clotting
induces bleeding |
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treatment of warfarin tox
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vitamin K
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methyl bromide moa and sx
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highly reactive and cytotoxic
headaches visual disturbances seizures CNS depression coma pulmonary edema |
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treatment of methyl bromide poisoning
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symptomatic
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strychnine MOA and sx
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competitive agonist of glycine that acts at the postsynaptic receptor in motor neurons of the spinal cord's neural horn
antagonizes inhibitory tone powerful and uncontrollable muscle contractions also CNS excitation leading to severe seizures and death also respiratory paralysis |
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treatment for strychnine poisoning
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minimize external stimulation
support respiration with diazepam |
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risks of petroleum hydrocarbons
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low concentration:
dizziness high concentration: CNS depression convulsions death coma oral: most of the symptomatic causes are due to aspiration |
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tox of aromatic hydrocarbons
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readily absorbed via GI and respiratory route with systemic toxicity
cardiac arrhythmia occurs due to myocardial sensitization with CNS depression |
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primary symptoms of lead poisoning
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constipation is early
hematologic symptoms neuromuscular nephropathy hyperuricemia with gout most severe: CNS fx |
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symptoms of lead poisoning in adults vs. children
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children are more sensitive to encephalopathy
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diagnosis of lead poisoning
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blood lead level
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treatment for lead poisoning
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chelation
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how does lead produce anemia?
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binds to Hb in erythrocytes and inhibits heme formation
inhibits ALA dehydratase and ferrochatase RBC's more fragile and have a decreased lifespan anemia |
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basophilic stippling
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seen in anemia due to lead poisoning
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acute arsenic poisoning
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GI- nausea, projectile vomiting, excruciating abdominal pain
diarrhea= rice-water stools cardiopulmonary fx BM depression convulsions death |
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chronic arsenic poisoning
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weight loss
hair loss muscle weakness aching garlic odor sensorimotor peripheral neuropathy BM depression skin problems liver damage |
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tx of arsenic poisoning
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limit exposure
empty stomach activated charcoal supportive tx chelation therapy |
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mercury acute poisoning
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(kidneys, CNS)
pulmonary fx- dyspnea, cough, NVD, gingivostomatitis neuro fx corrosive presentation ashen- grey mucous membranes due to preciptation |
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mercury chronic poisoning
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neuropsychiatric disorders (depression, irritability, confusion, shyness, withdrawal, explosive anger)
tremors gingivostomatitis weakness, goiter, tachycardia |
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mercury poisoning tx
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remove from exposure
monitor pulmonary function chelation supportive care |
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iron acute poisoning
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GI damage
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iron chronic poisoning
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hepatic damage
gi obstruction/damage |
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iron poisoning treatment
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empty stomach
lavage or emesis x-ray to count pills deferoxamine |
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EDTA used for
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lead
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dimercaprol
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arsenic, lead, mercury
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succimer
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lead, arsenic, mercury
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penicillamine
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copper, mercury
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deferoxamine
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iron
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