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74 Cards in this Set
- Front
- Back
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cathartic to use with activated charcoal
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corbitol
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narcan gtt
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hourly rate=initial dose needed to produce arousal
**may need repeat bolus of 50% initial dose about 30 minutes into infusion |
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Substances not adsorbed by activated charcoal
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small ions (Fe, Li)
Alcohols Acids/alkali |
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narcan t 1/2
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20-30 minutes
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button battery removal ?
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ear or esophagus- need immediate removal
stomach-depends on size of battery relative to patient |
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stratagy for narcan use in a opiate dependent patient
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first 0.1-0.2 mg
repeat q 2-5 minutes, doublng each dose until respiratory effort/mental status improves up to 10 mg total |
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button batteries- pathology
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damage by-
alkali leakage electric current pressure necrosis can lead to esophageal perforation in 4-6 hours |
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necrosis caused by alkali exposure
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liquefaction
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tx of corrosive ingestions
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lavage and charcoal contraindicated (unless co-ingestant)
NPO irrigation (skin/eyes) antiemetic H2 blocker steroids/abx (controversial) |
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endoscopy in corrosive ingestions
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ideally at 6-24 hours post-exposure in all symptomatic patients
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necrosis caused by acid exposure
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coagulation
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components of King's college criteria for APAP toxicity needing transplant evaluation
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pH
lactate coags phosphorus creatinine encephalopathy |
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tx for APAP ingestion
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confirmed 1 time ingestion, within 24 hours
-check level at 4 hours (or later) -tx with IV NAC if level over line everyone else -no treatment if APAP=0 and LFTs are normal, otherwise treat with NAC |
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toxic dose of APAP
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7.5 g in 24 hours (adult)
150 mg/kg (pediatrics) |
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tx for sympathomimetic toxicity
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benzos
bicarbonate no haldol (seizure) no beta blockers (unopposed alpha agonism) |
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tx of anticholinergic toxicity
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benzos
consider physostigmine (only if NO TCA--> may cause asystole in TCA OD) |
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general approach to the poisoned patient
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toxidrome?
antidote? Decontamination? supportive care? |
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tx of cholinergic toxicity
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atropine
2-PAM (must be given early) |
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pressor of choice for poisoned patient
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norepinephrine (levophed)
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syrup of Ipecac
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activates 5HT3 receptors on vomiting center and GI tract
consider in large toxic ingestion with no expected change in mental status that is not ammendable to charcoal |
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activated charcoal
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adsorbtion of drug
begins at 1 minute, equilibrium at 10-25 mintues desorbtion may occur if in GI tract too long (consider cathartic/WBI) may also work on already absorbed drug via "GI dialysis" |
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flumazenil- adverse effects
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can precipitae withdrawal and seizure in bzd dependant patient
can induce seizure/arrythmia in patients taking TCAs, carbeazepine and others |
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flumazenil
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competetive bzd antagonist
dose 0.2 mg then 0.3mg if no response in 30 seconds t 1/2 -1 hour best used to reverse sedation in benzo naive patients |
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glucagon as an antidote
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beta bolcker OD (works!)
CCB (may be beneficial) hypoglycemia (takes time to work, relies on stores; D50 is much faster) relies on normal calcium to have cardiovascular effect hyper or hypo Ca will blunt response |
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adverse efffects of narcan
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acute opiate withdrawal in dependant patient
unmasking of dangerous coingestant |
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glucagon adverse effects
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vomiting
hyper/hypoglycemia hypokalemia (due to insulin surge) prolonged use-dilated cardiomyopathy in pheochromocytoma patients- hypertensive crisis |
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digoxin and calcium
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dig increases cardiac myocyte intracellular calcium
giving calcium to a dig OD patient can exacerbate dysrhythmia and/or lead to hypercontractility/arrest (stone heart) |
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dig level after giving Dig Fab
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total Dig level not useful; check free dig level if avilable
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osmolal gap
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measured serum osm-calculated serum Osm
[2 x NA] + [glucose/18] + [BUN/2.8] + [serum EtOH /4.6} |
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normal range serum osm and osm gap
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serum osm-280-300
osm gap- 2-6 |
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lab features of ethelyene glycol ingestion
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AG metabolic acidosis
Low Biacarb Osm Gap hypocalcemia proteinuria/hematuria/ Ca Oxalate crystals evidence of AKI |
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clinical manifestations of ethylene glycolol poisoning
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CNS-lethargy --> stupor/coma, meningoencephalitis and/or cerebral edema, with generalized or focal signs (hyperreflexia, nystagmus, axtazia, crania neuropathies, seizure)
Renal-flank pain, ATN Cardiopulmonary-hypertension, tachycardia, dysrhythmias, and pulmonary edema |
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estimate of serum ethylene glycol level
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=osm gap x 6.2note;
**must sbtract EtOH contribution to gap 1st |
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Management of ethylene glycolol poisoning
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ABCs
IVF to maitain UOP- speeds excretion NG aspiration if very recent ingestion NaHCo3- to correct acidosis Ca- to correct symptomatic hypocalcemia Fomepizole or EtOH- to inhibit production of toxic metabolites CoFactors- (Mg, thiamine, B6) to shunt metabolites to less toxic pathways hemodialysisdispo- typically ICU |
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Fomepizole (pharmacology, use)
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Alcohol dehydrogenase inhibitor
Used in ethylene glycol and methanol poisonining |
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Toxic Vital Signs
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Reg (HR, BP, Tem, RR, O2)+Finger stick
EKG BHCG Tylenol/ASA level |
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PE findings for Toxic patients
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Mental Status (hyper- or hypo-)
Pulpil size GI (bowel sounds) Skin (Dry/diaphoretic/flushed)Mucous membranes (dry/wet)GU (?full bladder) |
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anticholinergic vs sympathomimetic toxicity
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anticholinergic sympathomimetic
bowel sound hypoactive hyperactive skin dry diaphoretic bladder urinary retention normal |
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types of Hgb measured by co oximietry
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oxyhemoglobin
deoxyhemiglobin carboxyhemoglobin methemoglobin (***may be mistaken for sulfhemiglibin***) |
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treatment for sympathomimetic toxicity
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benzos
sodium bicarb (for QRS widenieng) Avoid Haldol or Beta Blockers |
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Treatment for cholinergic toxicity
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Atropine +/- 2-PAM (pralidoxime)
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time to peak ASA concentration
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theraputic dose- 30-60 mintoxic dose- 4-6 hours, maybe longer if enteric coated, bezoar, etc
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Clinical Manifestations of Acute salicylate toxicity
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Respiratory- hyperventilation, respiratory alkalosis, acute lung injury
AG Metabolic acidosis--due to salicylates + lactate + ketones(typically seen after resp alk) CNS- tinnitus, agitation/delerium--->coma Muscular ridgidity GI- n/v, gastritis Acute renal failure |
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Chronic salicylate toxicity
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most often seen in elderly
frequently misdiagnosed due to insidious onset of sx same sx as acute toxicity |
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Importance of pH in salicylate poisoning
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Acidemia increases passage of salicylate into CNS---> dramatically increases toxicity and mortality-pH shoudl be followed along with serum concentration
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Management of Salicylate toxicity
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consider GI decontamination- charcoal/lavage/WBI
correct volume status/electorolyes Alkalinize blood/urine with NaHCO3 to goal urine pH 7.5-8 (consider for anyone with tinnitus/CNS sx and or serum lever >30) Avoid intubation!!! Consider hemodialysis(sick pts, severe electrolyte disturbances, serum level >100, pt inability to clear drug) |
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calcium channel blocker ingestion presentation
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hypotension, decreased contractility, bradycrdia,AV block
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Ca therapy in CCB exposure
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may be helpful, but not adequate in the sickest Pts
improves ionotropy but not HR or conduction may require high/ multiple doses |
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Ca in digoxin toxicity
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may exacerbate hemodynamic instability
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hydrofluoric Acid exposure
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severe burns and systemic hypocalcemia
tx-topical/subQ Ca Gluconate for burns: consider IA Ca as wellIV/nebulized Ca gluconate for hypocalcemia monitor Ca and mag |
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black widow spider bites
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sever abdominal and back pain, muscle spasm
tx c IV calcium and analgesia |
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dose of dig FAB
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can use quantity ingested or serum concentration to estimate total body dig load
then give1 vial per 0.5 mg. or adult emperic dosing -acute -10-20 vials -chronic- 3-6 vials required dose may be high several hours after acute ingestion, once drug distributes to tissue |
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examples of cardioactive steroids
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digoxin
digitoxin oleanders quilltoad venom |
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digoxin FAB
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commercially available as Digibind or DigiFab
bind to intravascular and interstitial dig, cause efflux then binding of intracellular dig onset- (mean) 19 minutes |
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Dig FAB in renal patients
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T 1/2 is substantially increased
may see rebound bump in free dig level several days later |
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sodium bicarb in TCA overdose
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NaHCo3 increase # of Na channels open and decreases drug binding effect likely due to pH and Na effects
result decrease QRS duration Indications-QRS >100, terminal R in aVR > 3mm, hypotension increase risk of seizure at QRS>;100, dysrhythmias at QRS>160 |
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Sodium Bicarb dosing
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TCA OD- 1-2 mEq/kg Bolus, then gtt (3 amps in 1L D5W @ 2xMIVF)
Goal- narrow QRS and pH 7.50-7.55 Salicylates- 1-2 mEq/kg (IF acedemic) then gtt as above Goal- UOP-3-5 cc/kg/hr, pH Contrast Nephropathy PPX154 mEq/L, run at 3 cc/kg over 1 hr, then 1 cc/kg/hr x 6 hours |
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Drugs that may have enhanced elimination or decreased toxicity from NaCO3
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***Generally weak aacids, and things that act on Na Channels
Tyle IA and IC antiarrhythmics Verapamil Cocaine Phenibarbial Chlorpropamide (NOT other sulfonylureas) Phenobarbital (NOT other Barbs) Chlorphenoxy Herbacides Ethylene Glycol Methanol Methotrexate Clorine Gas (nebulized NaHCO3 can neutralize HCl formed in lungs after inhalation) |
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Ca in digoxin toxicity
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may exacerbate hemodynamic instability
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hydrofluoric Acid exposure
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severe burns and systemic hypocalcemia
tx-topical/subQ Ca Gluconate for burns: consider IA Ca as wellIV/nebulized Ca gluconate for hypocalcemia monitor Ca and mag |
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black widow spider bites
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sever abdominal and back pain, muscle spasm
tx c IV calcium and analgesia |
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dose of dig FAB
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can use quantity ingested or serum concentration to estimate total body dig load
then give1 vial per 0.5 mg. or adult emperic dosing -acute -10-20 vials -chronic- 3-6 vials required dose may be high several hours after acute ingestion, once drug distributes to tissue |
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examples of cardioactive steroids
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digoxin
digitoxin oleanders quilltoad venom |
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digoxin FAB
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commercially available as Digibind or DigiFab
bind to intravascular and interstitial dig, cause efflux then binding of intracellular dig onset- (mean) 19 minutes |
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Dig FAB in renal patients
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T 1/2 is substantially increased
may see rebound bump in free dig level several days later |
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sodium bicarb in TCA overdose
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NaHCo3 increase # of Na channels open and decreases drug binding effect likely due to pH and Na effects
result decrease QRS duration Indications-QRS >100, terminal R in aVR > 3mm, hypotension increase risk of seizure at QRS>;100, dysrhythmias at QRS>160 |
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Sodium Bicarb dosing
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TCA OD- 1-2 mEq/kg Bolus, then gtt (3 amps in 1L D5W @ 2xMIVF)
Goal- narrow QRS and pH 7.50-7.55 Salicylates- 1-2 mEq/kg (IF acedemic) then gtt as above Goal- UOP-3-5 cc/kg/hr, pH Contrast Nephropathy PPX154 mEq/L, run at 3 cc/kg over 1 hr, then 1 cc/kg/hr x 6 hours |
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Drugs that may have enhanced elimination or decreased toxicity from NaCO3
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***Generally weak aacids, and things that act on Na Channels
Tyle IA and IC antiarrhythmics Verapamil Cocaine Phenibarbial Chlorpropamide (NOT other sulfonylureas) Phenobarbital (NOT other Barbs) Chlorphenoxy Herbacides Ethylene Glycol Methanol Methotrexate Clorine Gas (nebulized NaHCO3 can neutralize HCl formed in lungs after inhalation) |
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NaHCO3 in salicylate toxicity
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-increase pH increase ionizd for of salicylate
-alkaliniation traps NaHCO3 in blood (OUT of CNS) and in urine (OUT of body completely |
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indications for physostigmine
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anti-muscarinic toxicity without QRS or QTc prolongation
*****risk outweighs benefits in tx of anticholinergic effects of TCAs, GHB and antipsychotics |
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adverse effects of physostigmine
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excessive use can cause cholinergic toxicity muscarinic-bronchorrhea, bradycardia, nicotinic-fasciculation-->weakness
Tremor->seizure may require atropine +/- pralidoxime |
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digoxin toxicity
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Cardiac effects-conduction delay increased automaticity, dysthythmias,
electorolytes-hyperkalemia, hypomagnesemia GI-nausea/vomiting/ abd pain |
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drug interactions with physostigmine
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drugs that rely on plasma cholinesterase will have prolonged effect (i.e. cocaine, succinylcholine)
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indications for Dig Fab
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know/suspected dig toxicity with-symptomatic Bradycardia.
-2nd/3rd AV block unresponsive to atropine -ventricular dysrhythmia -K >5 -serum dig >10 -ingestion of >10 mg in healthy adult or > 0.1 mg/kg in healthy child -suspected CCB or B blocker + dig ingestion (give prior to Ca !!!) |
