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PCTExam1
| Question | Answer |
|---|---|
| what age group does poisonings occur most often? | <6 years old |
| what time of day are poisonings most prevalent? | early evening-late morning |
| what percentage of poisonings are unintentional? intentional? | 81.4%; 14.7% |
| how many poison control centers are there in the US? | 57 |
| data collections thru AAPCC includes what? | substance/amount, symptoms, treatment, outcome, location, age, reason for exposure, and name |
| how many deaths occurred of the 33,000 calls the palmetto poison center got in 2010? | 6 |
| why should neutralization not be performed? | exothermic rxn |
| what are the 3 drugs that might be started in the ED if a poisoned patient is in a coma or has AMS? | Dextrose, Thiamine, Naloxone |
| milk should only be used if what is ingested? why? | toothpaste; binds fluoride |
| how long does it take for Ipecac to work? how much stomach contents is emptied? | 20 minutes; 30-40% |
| how can chronic use of Ipecac cause cardiotoxicity and myopathy? | Emetine is an alkaloid that causes inhibition of protein synthesis and a blockade of sodium and calcium channels |
| what is the mechanism of gastric lavage? | push fluid in with syringe, drawn out with a syringe (Water or Saline) |
| highly adsorbent powder made from distillation of wood pulp | activated charcoal |
| what is activated charcoal mixed with to form an aqueous slurry? | water |
| what can be added to activated charcoal to decrease the risk of constipation? | sorbitol (cathartic use) |
| how long after ingestion should activated charcoal be given? | within one hour |
| what is the mechanism of WBI? | wash out intestines |
| how long should you administer WBI? | until rectal effluents are clear |
| what ingredient is in WBI? | PEG |
| when do we see increased LFTs in APAP ingestion? | phase 3 - 72-96 hours |
| how can you predict toxicity of APAP if not a single ingestion? | amount - 7.5grams/24 hours |
| what are treatment strategies for APAP overdose? | GI decontamination (Activated Charcoal), NAC, and Supportive Care |
| LD of NAC? maintenance? | 140mg/kg; 70mg/kg x 17 doses q |
| when do you order APAP levels? | 4 hours post ingestion |
| what strength is NAC given? how does it come? | 5%; 10 & 20% |
| ER APAP have been shown to have toxic levels how long after ingestion? | 11-14 hours |
| toxic doses of what can cause bezoar? | salicylates |
| 1 concentrated tsp of oil of wintergreen equals what? | 7.5g of ASA |
| difference in acute and chronic toxicity with salicylates | chronic - no significant gastroenteritis, acidotic, usually mental deterioration, severe dehydration Acute - N/V, stomach pain, hyperventilation, respiratory alkalosis, dehydration |
| why is it important to continue drawing levels of salicylates q 4 hours? | bezoar and EC/SR tablets |
| what is thought to be the causes of most of the effects seen with NSAID toxicity? | decreased prostaglandin synthesis (COX inhibition) |
| toxic amounts of NSAIDs in pediatrics? | >250mg/kg |
| why can't enhanced elimination be preformed with NSAIDs? | highly protein bound |
| what are the most common salt forms of iron that are seen in toxicity | sulfate, gluconate, or fumarate |
| what is the calculation for elemental iron? | FSG=359 |
| what is the mechanism of toxicity with iron? | direct corrosive effect on mucosal tissue and may cause hemorrhagic necrosis and perforation (Fluid Loss); absorbed iron causes cellular dysfunction and death, resulting in lactic acidosis and organ failure |
| what is deferoxamine? when is it used? | Iron Chelator; Fe>500 or >350 + Serious Sx |
| why is lead toxicity more serious and common in children? | 40-50% absorption in children and only 10-15% in adults |
| what is the cornerstone of treatment for all heavy metal toxicities? | chelation |
| what is BAL used for? | High Lead Levels with Symptoms of Toxicity/Encephalopathy |
| what is CaNa2EDTA used for? | Lead Toxicity |
| what is Succimer used for? | Asymptomatic Lead Toxicity with Levels 45-69%, Lead Levels of 35-44% in <2y/o, elevated erythrocyte protoporphyrin, or hint of mild sx |
| key in lead toxicity treatment | prevent re-exposure |
| drugs with narrow therapeutic indexes, <10x daily dose can cause severe intoxication | cyclic antidepressants |
| what is the primary cause of death in cyclic antidepressant overdose | CV (QRS Widening) |
| what is the order of CV events in cyclic antidepressant toxicity? | sinus tachy, conduction defects, ventricular tachy, ventricular fibrillation |
| why are blood levels generally not drawn for cyclic antidepressants? | they are qualitative not quantitative (not a good measure of severity) |
| why are children at an increased risk of toxicity with cyclic antidepressant toxicity? | smaller lipid compartment, low capacity for binding to albumin, and more free drug |
| what should you do upon discovery of cyclic antidepressant overdose? | call 911 |
| what should you treat rhythm disturbances due to cyclic antidepressant toxicity with? | lidocaine |
| why should physostigmine not be used in refractory dysrhythmias due to cyclic antidepressant toxicity? | can cause seizure and CV effects |
| how long should you monitor an asymptomatic cyclic antidepressant overdose patient? | at least 6 hours |
| why is hemodialysis not recommended in cyclic antidepressant toxicity? | highly lipophillic, high protein binding, and lg VoD |
| cyclic antidepressant that has less cardiac SE and more prominent CNS effects and can have excessive muscular hyperactivity | amoxapine |
| cyclic antidepressant that has a higher incidence of seizures, cardiac dysthythmias and duration of coma than TCAs | maprotiline |
| cyclic antidepressant that interferes with SE reuptake with little effect on adrenergic system, little to no effect on heart, toxicity is mostly CNS depression and some hypotension | trazodone |
| which 2 SSRIs can cause QTc widening? | citalopram and escitalopram |
| what can be seen in SSRI overdose? | SE Syndrome |
| most bites occur during what month range? | may-october |
| 7 Poisonous Snakes in SC | Eastern Diamondback Rattlesnake, Timber Rattlesnake, Canebrake Rattlesnake, Pigmy Rattlesnake, Cottonmouth Moccasin, Copperhead Moccasin, Eastern Coral |
| pit vipers are all members of what genus? | crotalidae |
| eastern coral snake is member of what family? | elapidae |
| what type of toxin is associated with eastern coral snake? | neuro toxin |
| reaction to foreign antigens | serum sickness |
| how long does it take for serum sickness to present following tx with antivenom? | 7-14 days |
| what is the antivenom for coral snakes and black widows derived from? | horses |
| what tx is available for poisonous snake bites? coral snake bites? | crofab; antivenin derived from horses |
| what tx is available for brown recluse bites? | supportive care |
| what is a unique diagnostic feature of a black widow bite? | diaphoresis around bite site |
| how long must you monitor a patient with a black widow bite? | minimum of 6-8 hrs |
| act primarily by phosphorylation of acetylcholinesterase at nerve endings which blocks AChE lead to accumulation of Acetylcholine at muscarinic and nicotinic receptors and the CNS | Organophosphates |
| aging (permanent inhibition of AChE Thru Covalent Binding) can occur following 24-48 exposure to what? | Organophosphates |
| what is seen following massive exposures of organophosphates? | SLUD Symptoms |
| what do organophosphates smell like? | garlicky or solvent odor |
| how long must you monitor a patient with organophosphate toxicity? | at least 72 hours |
| therapeutic endpoints desired with atropine given to patient with organophosphate toxicity | drying of bronchial secretions, reversal of wheezing and bradycardia |
| what is the goal in giving pralidoxime to a patient with organophosphate toxicity? | reactivate the phosphorylated cholinesterase enzyme which treats the nicotinic effects |
| what organochorine insecticide is still used? | lindane |
| where are pyrethrins derived from? | chrysanthemum plant |
| natural insecticide | pyrethrins |
| why is there low toxicity associated with pyrethrins and pyrethroids? | limited absorption and rapid degradation |
| what is the treatment for skin contact with pyrethrins or pyrethroids? | vitamin E |
| paraquat is used on what type of plants? diquat? | land plants; aquatic plants |
| formed during production of some organochlorines | dioxins |
| L-type channels are located where? | in the plasma membrane of all types of muscle cells |
| allows for normal propagation of electrical impulses via the specialized myocardial conduction tissues, particularly the AV node | calcium |
| what does skeletal muscle depend on for excitation contraction coupling? | intracellular calcium stores |
| what type of tissue is calcium influx critical? | cardiac and smooth muscle |
| what class of CCB is diltiazem in? | benzothiazepine |
| what class of CCB is verapamil in? | phenylalkylamine |
| what class of CCB are nifedipine, amlodipine, and felodipine in? | dihydropyridines |
| which CCB is the most potent inhibitor of cardiac conductions and has the mot prominent effects electrophysiologically | verapamil |
| CCB that has essentially no effect on SA/AV conduction but is a potent peripheral vasodilator | nifedipine |
| CCB that displays the effects of verapamil and nifedipine but less prominently | diltiazem |
| what is the doc in BB toxicity? | glucagon |
| how long should a patient be monitored following CCB toxicity? | minimum of 24 hours even if asymptomatic if SR & 8 hrs if IR |
| what causes the positive ionotropic effects of digoxin? | inhibition of Na-K ATPase Pump & Increased intracellular Ca++ |
| why in chronic digoxin overdose is there only normal-mild digoxin levels? | tissues and receptors are saturated |
| why are chronic digoxin overdose patients usually seen with hypokalemia? | usually also on diuretic |
| when should a digoxin level be drawn? | 6 hours after acute ingestion |
| antidote for digoxin | digoxin-specific antibody fragments |
| each vial of digoxin-specific antibody fragments will bind how much digoxin? | 0.5mg |
| schedule I drugs | LSD, marijuana, heroin, cocaine |
| schedule II drugs | morphine, methadone, topical cocaine, PCP |
| schedule III drugs | anabolic steroids, codeine, hydrocodone, some barbituates |
| schedule IV drugs | benzos, talwin |
| georgia home boy, vita g, liquid ecstasy are all slang terms for what? | gamma hydroxybutyric acid |
| what is converted by alcohol dehydrogenase and aldehyde dehydrogenase to GHB? | 1, 4 butanediol (Found on Aquadots) |
| semisynthetic opioids | heroin, oxycodone |
| synthetic opioids | methadone, meperidine |
| opiates | morphine, codeine |
| opiate receptor responsible for spinal and supraspinal analgesia, & cough suppression | delta |
| opiate receptor responsible for spinal analgesia, miosis, and diuresis | kappa |
| opiate receptor responsible for supraspinal analgesia, peripheral analgesia, sedation, euphoria, respiratory depression, GI dysmotility, pruritus, and bradycardia | mu |
| what receptor is naloxone most potent at? | mu |
| what is naloxone's onset? duration? | 1-2 min; 20-90 min |
| inhalation of volatile substance directly from container (i.e. airplane glue, rubber cement) | sniffing |
| pouring a volatile liquid onto fabric and placing over nose/mouth | huffing |
| spraying a solvent into a plastic/paper bag and rebreathing from the bag several times | bagging |
| sodium and potassium account for what percentage of extracellular cations? | 95% |
| chloride and bicarb account for what percentage of extracellular anions? | 85% |
| what causes blindness with methanol toxicity? | formic acid |
| is osmolality usually measured or calculated? osmolarity? | measured; calculated |
| what are the toxins associated with ethylene glycol? | glycoaldehyde & oxalic acid |
| what happens to oxalic acid in the body? | precipitates with calcium in the kidneys (envelope-like crystals) |
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