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912 Cards in this Set
- Front
- Back
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When are peak plasma concentrations reached with acetaminophen?
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1 hour
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When is complete absorption of acetaminophen achieved?
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4 hours
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What are the primary metabolic pathways for APAP?
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Conjugation with glucuronide (40-67%)
Sulfate (20-46%) |
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What is the cytotoxic metabolite of APAP?
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NAPQI
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How is NAPQI typically dealt with by the body?
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Combines with glutathione and other thiol containing compounds
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How does APAP cause liver damage?
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NAPQI covalently binds to critical cell proteins in the liver, it initially occurs in hepatic zone III - centrilobular region
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What are the clinical effects of severe APAP toxicity?
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Severe fulminant liver failure which causes multi organ failure, systemic inflammatory response syndrome, hypotension, cerebral edema, death
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How is NAC effective in APAP OD?
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-NAC enhances sulfation
-NAC serves as a glutathione precursor -NAC is a glutathione substitute -NAC may reduce systemic toxicity (scavenger or free radicles, decreasing edema) |
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What are the clinical stages of APAP toxicity?
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1 - pre-injury (0-12 hours) - nausea, vomiting, anorexia, may be completely asymptomatic (elevated APAP)
2- liver injury (8-36hours)- nausea, vomiting, RUQ tenderness (transaminitis) 3 - maximum liver injury (2-4 days)- liver failure (encephalopathy, coagulopathy, hemorrhage, acidosis) 4 - recovery (>4days) - none |
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Which liver enzyme rises and peaks first?
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AST (ALT, PT and bilirubin rise and peak shortly after AST)
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What are signs and symptoms consistent with fulminant liver failure?
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metabolic acidosis
coagulopathy hepatic encephalopathy |
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What is the definition of an acute ingestion of APAP?
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A single ingestion occurring within a 4-hour period (all other ingestions are considered chronic)
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What amount of APAP must be consumed before significant liver toxicity is evident?
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Significantly >150mg/kg
OR >7.5g |
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When does the risk of hepatoxicity after APAP ingestion increase?
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8 hours or longer after ingestion
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What should be done for patients at risk of toxicity whose serum APAP cannot be obtained prior to 6-8 hours after ingestion?
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Start NAC
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When can the APAP treatment nomogram not be used?
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-prior to 4 hours after ingestion
-chronic ingestion -APAP concentration cannot be obtained -Evaluation of patient >24h post ingestion -Time of ingestion is unknown |
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What increases the risk of hepatotoxicity from chronic ingestion?
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-increased total dose of APAP
-longer duration over which it has been ingested in supra therapeutic concentrations |
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What are possible higher risk factors for liver injury in patients taking therapeutic doses of APAP?
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chronic INH and chronic ETOH (increased CYP2E1 activity)
prolonged fasting (malnourished, AIDS, prolonged vomiting) -children with febrile illness |
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What is considered a significant elevation in AST in chronic APAP toxicity?
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AST >/= 50 IU
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What is the APAP serum concentration after a typical therapeutic dose?
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peaks below 30ug/L and less than 10ug/L at 4 hours
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Which patients is chronic APAP toxicity should be treated with NAC?
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AST >/= 50IU
[APAP] higher than expected |
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Does acetaminophen cross the placenta?
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Yes
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What is the approach to a pregnant female with APAP OD?
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-identical to that in any patient.
acute OD - plot on nomogram and treat as needed chronic - treat if AST >/= 50IU or serum APAP is above expected |
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Does activated charcoal bind APAP?
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YEs
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What is the risk of liver injury in patients with APAP OD treated within 6-8 hours? What is the risk of death?
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<4%
the risk of death approaches 0 |
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What is the rate of liver injury in patients treated within 8-24 hours post ingestion?
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~30%
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What route of NAC delivery should be used in patients with evidence of liver failure?
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IV (use of this route results in less hypotension, less cerebral edema, and death)
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What proportion of patients treated with IV NAC develop anaphylactoid reactions?
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2-6%
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What is the downside to PO NAC?
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50% of patients vomit (potentially delaying timely antidotal delivery)
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What should be done if a patient receiving PO NAC vomits?
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Any dose that is vomited within 1 hour of administration should be repeated
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What are the lengths of the various NAC protocols?
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IV NAC - 21 hours
PO NAC - 72 hours |
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What are the end points of the NAC protocol?
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-predetermined length of the protocol
AND AST concentration normal and serum APAP <10micrograms/mL |
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What are clinical predictors of severe hepatic failure?
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pH <7.3 or Cr >3.3 and INR >5 and grade III or IV encephalopathy
APACHE II >20 Lactate >3.5mmol/L prior to resuscitation |
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What clinical picture can salicylate toxicity cause?
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Metabolic acidosis
seizure hyperthermia pulmonary edema cerebral edema renal failure death |
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How long does it take for salicylic acid to be absorbed and for peak levels to occur?
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Absorbed - 30min
Peak levels - 2-4 hours |
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How do salicylates cause toxicity?
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By uncoupling mitochondrial oxidative phosphorylation
this results in increased pyruvate and lactic acid thereby increasing the metabolic rate, temperature and O2 consumption which results in hypoglycaemia inefficiency of anaerobic metabolism then results in hyperthermia |
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Is the majority of ASA in the blood ionized or nonionized?
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At physiological pH, ASA is primarily ionized but as pH decreases more particles become un-ionized markedly increasing the movement of salicylate into the tissues and CNS (only non-ionized particles can cross the cell membrane)
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What are reasons that patients with salicylate toxicity develop hypokalemia?
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-vomiting (stimulation of the CTX)
-increased renal excretion of Na+, HCO3-. and K+ in compensation of respiratory alkalosis -salicylate induced increased permeability of renal tubules -intracellular accumulation of Na+ and H20 -inhibition of active transport |
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What are RF for the development of pulmonary edema in salicylate toxicity?
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-age >30
-cigarette smoking -chronic salicylate ingestion -metabolic acidosis -neurologic symptoms -serum salicylate >40mg/dL |
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What is the most likely cause of an altered sensorium in salicylate toxicity?
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-cerebral edema
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How do salicylates cause toxicity?
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-they stimulate the respiratory centre, leading to hyperventilation and respiratory alkalosis
-they are weak acids and impair renal function which leads to the accumulation of inorganic acids -they interfere with Kreb's cycle and uncouple oxidative phosphorylation -> producing lactate and heat -they induce fatty acid metabolism and generate ketone bodies resulting in a wide anion gap metabolic acidosis |
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What do patients with salicylate ingestion that develop cerebral or pulmonary edema require?
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-immediate dialysis
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What happens in chronic salicylate ingestion?
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-decreased albumin binding which results in increased free salicylate
-this free salicylate enters the cell causing significant clinical illness with a relatively low serum salicylate |
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What is a toxic dose of ASA? What is a potentially lethal dose of ASA?
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toxic 200-300mg/kg
potentially lethal 500mg/kg |
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Is there a nomogram for ASA?
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Yes, it should not be used to determine prognosis or treatment
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What should be done if a patient with salicylate toxicity requires intubation?
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This patient requires dialysis
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What are 3 main objectives in the treatment of salicylate toxicity?
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-prevent further absorption
-correct fluid deficits/acid-base abnormalities -increase excretion |
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What is the target urine output in salicylate toxicity? What is the risk of too much fluid?
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2-3mL/kg/hr
excessive fluid can worsen cerebral and pulmonary edema |
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When is urine alkalization advisable in salicylate toxicity?
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salicylate level >35mg/dL
significant acid-base disturbance or increased salicylate levels |
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How does urine alkalization work?
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Alkaline urine traps the salicylate ion and increases excretion
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What is the dose of NaHCO3?
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1-2 mEq/kg over 1-2 hours
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What must be done prior to urine alkalization?
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correct K+ depletion
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When is HD advisable in Salicylate toxicity?
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Absolute serum level
-acute salicylate toxicity >7.2mmol/L -chronic salicylate toxicity >4.4mmol/L -rising ASA level -clinical deterioration despite adequate supportive care Manifestations of salicylism in vital end organs -AMS -ET intubation -coma -pulmonary edema -severe acid-base imbalance Unable to metabolize and eliminate drug -renal or hepatic failure |
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What is the order when you want to alkalinize the urine?
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bolus 1-2 mEq/kg of hypertonic sodium bicarb then IV infusion of 3 amps NaHCO3 (132mEq) in 1L of D5W at 1.5-2X maintenance
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When should alkalinization be considered
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tinnitus
CNS symptoms all patients with a salicylate concentration greater that 30-40mg/dL |
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What can be considered in small children with salicylate toxicity instead of HD?
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exchange transfusion
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What is ASA metabolized to?
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ASA-> salicylic acid-> glycine conjugation, glucuronyl transferase, hydrolysis (direct renal excretion)
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Which NSAIDs are available in OTC and prescription strength?
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ibuprofen
naproxen |
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How is the therapeutic anti-inflammatory effect of NSAIDs achieved?
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Inhibition of COX and blockade of prostaglandin production
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Where is COX-1 concentrated?
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-platelets
-vascular endothelial cells -gastric mucosal cells -renal collecting tubules |
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When is COX-2 expressed?
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-it is inducible, therefore it is only expressed in response to certain inflammatory stimuli
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Why do NSAIDs frequently cause GI symptoms?
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It becomes trapped in gastric mucosal cells
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What happens to the NSAIDs after they are absorbed?
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They become highly bound to albumin
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What are the main clinical findings of NSAID OD?
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Largely asymptomatic
+/- minor CNS or GI distrubance |
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At what dose of ibuprofen does symptomatic OD occur?
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100mg/kg
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When is renal dysfunction seen with ibuprofen OD?
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With massive acute OD associated with hypotension and hypovolemia. Typically this is reversible
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Which NSAID in OD is associated with a relatively high incidence of seizures?
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Mefanamic acid
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Should plasma NSAID concentrations be measured?
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No, they are not useful, but screening for APAP should be done
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At what level of ibuprofen ingestion, should children be evaluated?
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>300mg/kg
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Which NSAID OD should be managed more aggressively
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Pyrazolone
Fenamate |
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How long should you observe patient with non-trivial NSAID ODs
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4 hours post ingestion and until symptoms are noted to be mild or improving
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What are the 3 main groups of anticholinergics?
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-antimuscarinics
-neuromuscular blockers -ganglionic blockers |
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What plants have anticholinergic activity?
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Atropa belladonna -> atropine
Datura stramonium (jimson weed) -> scopolamine |
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What are current day uses for belladonna alkaloids?
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-mydriatics (pupillary dilators)
-anti-spasmodics -decreased gastric secretions -prevent motion sickness -treat asthma -treat bradycardia -dry airway secretions and block the vagal response to laryngoscopy |
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Which agents are central anti-muscarinics? what are they used for?
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Benztropine
Trihexylphenidyl -2nd line antiparkinsons agents and to counteract the effects of neuroleptics |
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What are other pharmacologic agents that possess anticholinergic activity
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TCA
phenothiazines anti-histamines carbamazepine cyclobenzaprine |
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Where are muscarinic receptors found?
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-smooth muscles in the eye, intestinal tract and urinary bladder
-they regulate sweat, salivary and mucosal gland activity |
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What does generalized inhibition of muscarinic receptors by atropine cause?
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Tachycardia
Pupillary dilatation loss of accommodation inability to sweat drying on mucosal surfaces GI paralysis urinary retention |
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What does muscarinic inhibition in the CNS cause?
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stimulation
seizures coma choreoathetosis memory impairment perceptual and cognitive dysfunction |
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What are the least sensitive organs to antimuscarinic drugs?
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the bladder
the GI tract |
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What CNS manifestations of anticholinergic poisoning do children typically exhibit?
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CNS stimulant effects
seizures preceded by CNS irritability or depression |
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What do patients with anticholinergic toxicity die of?
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-elevated temperature (due to increased motor activity and impaired heat exchange)
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What are manifestations of chronic anticholinergic poisoning?
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-organic mental symptoms with lack of significant peripheral anticholinergic signs
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What are 2 likely settings for chronic anticholinergic toxicity?
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1) elderly patients taking anticholinergic drugs for Parkinsonism or other chronic diseases
2)the psychiatric patient receiving neuroleptic therapy and started on another anticholinergic drug |
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How can you differentiate patients with sympathetic overload from those with anticholinergic effects?
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the presence or absence of diaphoresis
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What are findings suggestive of phencyclidine poisoning?
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-nystagmus
-diaphoresis -small pupils -extreme aggitation |
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What is often a distinguishing feature of serotonin syndrome?
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aggitation
tremor in the lower extremities |
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What can be a distinguishing feature of NMS?
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rigidity is a prominent physical exam feature
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What agents are suggested by antimuscarinic effects and ECG abnormalities?
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cardiotoxic agents with antimuscarinic side effects (TCA, carbamazepine, phenothiazines)
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How should agitation be controlled in the patient with anticholinergic poisoning?
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BZD
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How should hyperthermia be treated in patients with anticholinergic toxicity?
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Ice water or evaporative cooling (antipyretics, cooling blankets may be ineffective and there is no clear role for dantrolene)
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How should seizures be managed in a patient with anticholinergic toxicity?
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BZD (no role for phenytoin)
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What does physostigmine do?
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It is an acetylcholinersterase inhibitor that blocks the degradation of ACh which accumulates and overcomes the effect of ACh receptor blockade
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What are the risks of physostigmine?
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It can precipitate cholinergic excess causing seizures, muscle weakness, bradycardia, bronchoconstriction, lacrimation, salivation, bronchorrhea, vomiting and diarrhea
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What can occur if physostigmine is given to patients with TCA OD?
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asystole
(therefore TCA OD is a contraindication to physostigmine) |
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How is physostigmine given?
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1-2 mg over 5 min (0.02 mg/kg, max 0.5mg) for children
Can be repeated in 10-15 minutes |
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How long after ingestion should you monitor patients with anticholinergic ingestion?
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4 hours
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How long should you observe patients who have ingested datura stramonium?
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8 hours
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When do most serious complications from TCA occur?
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Within 30-60 minutes.
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Why is absorption prolonged in overdose with TCAs?
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The anticholinergic effect limits gastrointestinal motility and absorption.
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Which TCAs have active metabolites?
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All tertiary amines and amoxapine (a secondary amine_
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What are the major pharmacodynamic effects of TCAs?
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-sodium channel blockade
-alpha receptor antagonism -anticholinergic -antihistaminic -inhibit GABA receptors -impair serotonin and norepinephrine re-uptake -impair K+ efflux |
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What is the mechanism of cardiovascular collapse in TCA OD?
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-lactic acidosis which impairs myocardial sodium conduction
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What is the predictive value of altered LOC for TCA induced seizures?
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Mental status changes do not predict the occurrence of seizures and 23% of patients are awake and alert immediately before a seizure.
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Which TC have the highest incidence of seizures? Of cardiac toxicity?
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Amoxapine (seizures)
Maprotiline (cardiac and seizures) |
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What is the toxic dose of TCAs?
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10mg/kg or 1000mg
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What are ECG changes associated with TCA poisoning?
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Wide QRS
Prolonged QT Rightward deviation of the terminal 40msec QRS axis (R-wave in aVR >3mm) Brugada-like pattern |
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What is the value of quantitative TCA concentrations in the clinical setting?
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They have little value because they are not available in a timely manner and do not accurately predict the degree of toxicity
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Which patients with TCA intox should be intubated?
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Decreased LOC
Rapid Deterioration Any patient who will be receiving gastric lavage |
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By which mechanism does NAHCO3 help in TCA OD
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-provides an alkaline pH as well as a sodium load and hypertonicity that increases conductance through myocardial sodium channels.
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What is the usefulness of various vasopressors in TCA induced hypotension?
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Dopamin and NE should be used to treat refractory hypotension
Dobutamine can be used for inotropic support Vasopressin has also been used in refractory hypotension |
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Which antiarrythmic are contraindicated in TCA poisoning?
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Phenytoin (shown to prolong episodes of vtach)
Type Ia (quinidine, disopyramide, procainamide) Type Ic (flecanide, propafenone, moricizine) |
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How long does an asymptomatic patient need to be monitored after a TCA OD
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At least 6 hours
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What are signs that a TCA poisoned patient should be admitted to the ICU?
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-Ventilatory insufficiency
-Desaturation -QRS >100msec -sinus tachycardia >120bpm -dysrhythmias -hypotension -decreased LOC -seizures -abnormal or inactive bowel sounds |
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Define serotonin syndrome
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A constellation of signs and symptoms manifesting as autonomic, neuromuscular and mental status changes.
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List manifestations of SSRI poisoning?
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Gastrointestinal: emesis, abdo pain, nausea
Cardiovascular: sinus tach, hypertension, trigeminy and junctional rhythm CNS: drowsiness, tremor, euphoria, headache |
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What are factors that help distinguish serotonin syndrome from neuroleptic malignant syndrome?
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-history of precipitating medication (SSRI vs neuroleptic
-SS is more rapid in onset and more often exhibits clonus |
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How long after ingestion does it take to reach peak plasma concentrations of TCA?
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2-4hours (therapeutic dose)
longer with OD because of anticholinergic effects delay GI motility |
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Describe the pharmacokinetics of TCAs?
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highly lipophilic
extensively bound to plasm proteins large VD metabolized predominantly by the liver |
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What are the major pharmacodynamic effects of cyclic antidepressants?
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Sodium channel blockade
alpha blockade inhibition of biogenic amine re-uptake muscarinic receptor blockade histamine receptor blockade potassium efflux blockade indirect GABA antagonism |
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What phase of myocardial depolarization is prolonged in TCA OD?
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Phase 0 (sodium conductance is blocked through fast sodium channels)
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What is the result of the blocked fast sodium channels in TCA OD?
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-Decreased conduction with a prolonged QRS complex (>100msec)
--ve inotropic effects (secondary to impaired excitation-contraction coupling) |
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What is the result of alpha adrenoceptor blockade?
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decreased preload and afterload (decreased SVR, widened PP, decreased pupil size)
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What does 5-HT and NE reuptake inhibition in the CNS cause?
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Delirium
Seizures |
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What does K efflux blockade in TCA OD do?
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prolongs phase 3 of the myocardial action potential resulting in increased QT interval duration
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What does GABA inhibition cause?
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Increased CNS excitation and seizures
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Which patients should be considered to have cyclic antidepressant poisoning until proven otherwise?
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-QRS >100msec
-Rightward deviation of the terminal 40msec QRS axis (R-wave in aVR >3mm or R/S ratio in aVR >0.7) |
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What are the PNS effects of cyclic antidepressants?
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tachycardia, hyperthermia, mydriasis, anhydrosis, red skin, decreased BS, ileus, urinary retention, distended bladder (anticholinergic effects)
reflex tachycardia and miosis/mid-range pupils (alpha blockade) |
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Should tox screens for TCAs be done?
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Neither tox or lab tests are useful in clinical decision-making.
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Why may ventilatory support be required in TCA OD?
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To avoid respiratory acidosis, because acidosis inhibits conductance through fast sodium channels
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When should bicarb be administered in TCA OD?
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-QRS >100msec
-symptomatic patient with hypotension or dysrhythmia -acidemia -IV sodium bicarbonate |
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How is NaHCO3 administered?
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IV boluses of 1-2 mEq/kg until the QRS narrows or until serum pH increases to 7.50-7.53
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If symptoms of TCA OD are refractory to sodium bicarb what can be done?
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-hypertonic saline
-dopamine, NE |
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Which type of antidysrhythmic agents are contraindicated in wide complex tachycardia from TCA OD?
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Type Ia and Type Ic agents because they inhibit fast sodium channels)
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What else can be considered for polyventricular tachycardia?
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Transvenous pacemaker for overdrive pacing
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What should be used for agitation and seizures in TCA OD?
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BZD
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What else can be used for TCA associated seizures?
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phenobarbital
propofol |
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After how many hours of observation can patients be discharged after suspected TCA OD?
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6 hours if the following do not develop:
-ventilatory insufficiency -QRS >100msec -sinus tachycardia (>120bpm) -dysrhythmia -hypotension -decreased LOC -seizures -abnormal or inactive BS |
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How are SSRI's metabolized?
|
predominantly by the liver
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How long should you wait to start MAOI therapy after discontinuing SSRIs? why?
|
5 weeks
To avoid precipitating serotonin syndrome |
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What organ system are most affected by excessive serotonin?
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GI tract
CVS system CNS |
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What specific symptoms can SSRI OD cause?
|
sedation
-aggitation -tremor -hyper-reflexia -tachycardia -bradycardia -nausea and vomiting -abdo pain -facial flushing -dizziness |
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Which SSRI requires a prolonged observation period (beyond the routine 6 hours observation period) and why?
|
Citalopram
Seizures and QT prolongation followed by torsades with cardiac arrest have been observed as long as 8 hours after OD |
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WHat are Sternbach's suggested diagnostic criteria for serotonin syndrome?
|
-adding a serotonergic agent to patient's meds or increasing the dose of a patient's serotonergic agent
-at least 3 of the following symptoms agitation ataxia diaphoresis diarrhea hyperreflexia hyperthermia mental status changes myoclonus shivering tremor -a neuroleptic has not been started or increased -other aetiologies (infection, metabolic derangement and withdrawal) have been ruled out |
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What are helpful clues to differentiating serotonin syndrome from neuroleptic malignant syndrome?
|
-a history of precipitating medication use
-more rapid onset of symptoms -the presence of clonus |
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Is HD an option for SSRI ingestion?
|
no, SSRIs have large volumes of distribution and are highly bound to plasma proteins
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What medications have been proposed to treat the neurologic complications of SSRI OD and serotonin syndrome?
|
cyproheptadine
methysergide chlorpromazine propranolol (none are considered proven therapy) |
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How long should patients with SSRI OD be observed and how?
|
-6 hours (except citalopram and escitalopram which should be observed for up to 12 hours)
-with cardiac monitoring |
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What are the potential complications of serotonin syndrome?
|
-This entity can be fatal
-vtach -hypotension -coma -hyperthermia -rhabdomyolysis |
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What is the most significant toxic effect of bupropion?
|
seizure activity
(which may occur after OD or when the maximal daily dose is exceeded) |
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How should bupropion-induced seizures be treated?
|
BZD (+/- phenobarb load for recurrent seizures)
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WHat is the recommended observation period of immediate-release bupropion? extended-release bupropion?
|
8 hours
12 hours |
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What is the mechanism of action for bupropion?
|
-inhibits dopamine re-uptake
-enhances dopaminergic neurotransmission |
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What is the mechanism of action of Venlafaxine and its active metabolite O-desmethylvenlafaxine?
|
It inhibits the reuptake of serotonin to a greater extent than NE and dopamine
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What are clinical features of venlafaxine OD?
|
Common:
somnolence sinus tachycardia Rare: seizures hypotension prolonged QRS prolonged OTc rhabdomyolysis hepatic failure renal failure |
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What is the mechanism of action of mirtazipine?
|
-blocks pre-synaptic alpha 2 receptors and increases release of 5HT and NE
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What are the effects of monoamine oxidase inhibitors?
|
-inhibit MAO
-MAOI effect on indirect symptahomimetics such as amphetamine and methamphetamine and potential for enhanced CNS and PNS toxicity -depletion of NE stores -inhibitor of vit-B6 containing enzymes |
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What are the 3 presentations of MAOI toxicity?
|
MAOI OD
MAOI food or beverage interaction MAOI drug interaction |
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What are the 4 phases of MAOI OD?
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1) asymptomatic or latent
2) neuromuscular and cardiovascular excitation with sympathetic hyperactivity 3) CNS depression and CV collapse with hypotension + bradycardia 4) secondary complications |
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What is a lethal dose of MAOI OD?
|
2mg/kg
|
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What is the onset of sympathetic signs and symptoms with MAOI food or MAOI beverage interaction
|
minutes to hours
|
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What are signs and symptoms of MAOI drug interactions?
|
sympathetic storm or serotonin syndrome
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What are some typical drugs that are incompatible with MAOIs?
|
-Mixed-acting/indirect-acting sympathomimetics
-methylxanthines -antidepressants -opioids -other drugs that can cause serotonin syndrome |
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What is the management of hypertension in MAOI tox?
|
-mild hypertension does not require treatment
-HTN with signs of impending or ongoing target organ damage -> should be treated with sodium nitroprusside or phentolamine |
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What is the dosing of phentolamine?
|
5mg bolus or 0.02-0.1 mg/kg
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What is the management of bradycardia?
|
should not be treated unless associated with severe hypotension then IV atropine given until resolved then possibly pacemaker
|
|
|
What can be used to ttx life threatening hyperthermia in MAOI toxicity?
|
Dantrolene 2.5mg/kg IV
|
|
|
How long can it take to manifest the symptoms of MAOI OD?
|
up to 24 hours
|
|
|
What are the symptoms of SSRI discontinuation syndrome?
|
insomnia
nausea HA sensory disturbances hyperarousal anxiety agitation tachycardia tremor |
|
|
What is the definition of asphyxiation?
|
A condition of severely deficient supply of oxygen to the body
|
|
|
What happens when the Fi02 falls from 0.21 to 0.15
|
Autonomic stimulation
(tachycardia, tachypnea and dyspnea) cerebral hypoxia (ataxia, dizziness, incoordination, confusion) NB: dyspnea is not an early finding |
|
|
What is the management of exposure to asphyxiants?
|
-removal from exposure
-supportive care -administration of supplemental oxygen |
|
|
What is the definition of an asphyxiant?
|
Any gas that displaces sufficient oxygen from the breathable air
|
|
|
How do irritant gases result in disease?
|
-they dissolve in the respiratory tract mucus and alter the air-lung interface by invoking an irritant or inflammatory response
|
|
|
How are pulmonary irritants grouped?
|
highly water soluble - impact mucous membranes of the eyes and upper airways
Poorly water soluble - do not readily irritate the mucous membranes and may have pleasant odors, prolonged breathing allows the gas to reach the alveoli Intermediate water soluble - produce clinical syndromes that are composite of the other gases |
|
|
What is the management of exposure to pulmonary irritants?
|
-signs of upper airway dysfunction mandate direct visualization of the larynx
-bronchospasm may respond to inhaled beta agonists |
|
|
What additional therapy can be offered to patients exposed to chlorine or hydrogen chloride?
|
Inhaled 2% sodium bicarb
|
|
|
What is the disposition of patients exposed to pulmonary irritants?
|
-those exposed to water soluble agents can be discharged if asymptomatic or improve with symptomatic therapy
-those exposed to intermediate or poorly water soluble agents should be observed for increased dyspnea over several hours even if they are initially asymptomatic |
|
|
What is smoke inhalation?
|
It is a variant of irritant injury in which heated particulate and adsorbed toxins injure normal mucosa similar to other irritant gases
|
|
|
What do patients that are exposed to filtered or distant smoke inhale?
|
CO
cyanide and metabolic poisons (these patients do not inhale smoke) |
|
|
What laboratory findings suggest cyanide poisoning?
|
metaboic acidosis
serum lactate >10mmol/L |
|
|
Should corticosteroids be given to patients with smoke inhalation?
|
No, they are not indicated and amy be harmful in patients with cutaneous burns
|
|
|
What are worrisome clinical findings in smoke inhalation?
|
hoarseness
respiratory distress |
|
|
What are identifiers of substantial exposure to smoke?
|
closed-space exposure
carbonaceous sputum |
|
|
What industries is cyanide important in?
|
metallurgic
photographic |
|
|
In what occupations do most hydrogen sulfide poisonings occur?
|
petroleum refinery
sewage storage |
|
|
What is the odor of hydrogen sulphide?
|
rotten eggs
|
|
|
Why is the odor not a reliable predictor of hydrogen sulphide exposure?
|
Odor becomes unnoticeable with extremely high concentrations or prolonged exposures (olfactory fatigue)
|
|
|
How is cyanide toxic to tissues?
|
It inhibits oxidative metabolism by binding to complex IV of the electron transport chain within mitochondria
|
|
|
What are the toxic effects of hydrogen sulphide poisoning?
|
pulmonary irritant
cellular poison |
|
|
How is hydrogen sulphide different from cyanide?
|
hydrogen sulfide spontaneously dissociates from the mitochondria rapidly, allowing many patients to survive after brief exposure
|
|
|
Which organs manifest dysfunction in cyanide poisoning?
|
the heart and CNS (coma, seizures, dysrhythmia and CV collapse)
|
|
|
What happens to venous blood in cyanide/HS poisoning?
|
the oxygen content remains high (tissues cannot extract oxygen) "arterialization"
|
|
|
What symptoms in a fire victim suggest cyanide poisoning?
|
CV collapse, ventricular dysrhythmia and seizures
|
|
|
What is the goal of therapy in treatment of hydrogen cyanide exposure?
|
To reactivate the cytochrome oxidase system by providing an alternative binding site for cyanide ion
|
|
|
What does the cyanide antidote kit produce?
|
A high affinity source of ferric ions (Fe3+) for cyanide to bind to
|
|
|
What therapy should be administered by paramedics and during mass poisoning events for hydrogen cyanide poisoning?
|
sodium thiosulfate in combination with oxygen and sodium bicarbonate
|
|
|
What are the first 2 components of the HC kit and what is the goal of these therapies?
|
inhaled amyl nitrite and IV sodium nitrite
the goal is methemoglobin formation -> cyanomethemoglobin |
|
|
What is the purpose of sodium thiosulfate?
|
It increases the availability of sulfur donor to increase the rate of rhodonase function (cyanide + cyanomethnemoglobin are converted to thiocyanate by sulfur transferase/rhodonase
|
|
|
What is recommended in fire victims with possible simultaneous CO and CN poisoning?
|
The use of sodium thiosulfate alone (CO and MetHgb reduce O2 delivery to tissues)
|
|
|
What is the 2nd antidote for CN poisoning?
|
Hydroxycobalamin (vit B12)
it takes advantage of the high affinity of cobalt and CN |
|
|
What lab tests does hydroxycobalamin interfere with?
|
Carboxyhemoglobin and lactate
|
|
|
What is another therapy for CN tox (that is as of yet unproven)?
|
HBOT (superoxygenates plasma and tissues permitting higher levels of methemoglobinemia)
|
|
|
What is the treatment of HS toxicity?
|
removal from exposure
standard resuscitation techniques +/- nitrite portion of the cyanide antidote to form MetHgb |
|
|
How is CO generated?
|
Through incomplete combustion of virtually all carbon-containing products
|
|
|
What are the various mechanisms of CO poisoning?
|
decreased oxygen carrying capacity
CO binding to myoglobin -> rhabdomyolysis inhibits the final cytochrome complex involved in mitochondrial oxidative phosphorylation |
|
|
Should cherry red skin colour be used to aid in the diagnosis of CO or CN poisoning?
|
No, it is a post-mortem finding
|
|
|
What are the delayed neurologic sequelae of CO exposure?
|
Neurologic syndromes (focal deficits and seizures)
psychiatric and cognitive findings (apathy, memory deficits) |
|
|
What are RF that predict the development of delayed neurologic sequelae?
|
Age
Loss of consciousness |
|
|
Why is the calculated oxygen saturation on an ABG normal in the setting of CO poisoning?
|
Because the P02 is a measure of dissolved oxygen in the blood which remains normal even in the presence of substantial CO poisoning
|
|
|
What is the purpose of 02 therapy in CO exposure?
|
-It decreases the half life of COHb from 5 hours to 1 hour
-a sufficient P02 with HBOT can be achieved to sustain life in the absence of adequately functioning Hgb |
|
|
What is the benefit of HBOT?
|
HBOT is associated with a reduction in the rate of delayed neurologic sequelae from 12% to 1%
|
|
|
What are indications for HBOT in CO exposure?
|
1. Evidence of end-organ damage regardless of COHb level (neuro abnormality, cardiovascular instability)
2. Persistent symptoms after treatment with 100% O2 3. COHb >/=25% 4. COHb >/= 15% in pregnant women and children |
|
|
How long should you treat mildly CO poisoned patients?
|
~6hours
|
|
|
How does cocaine work?
|
It causes release of dopamine, epi, NE and serotonin
it inhibits the re-uptake of these stimulatory neurotransmitters from synaptic clefts It is a LA and results in Na+ channel blockade |
|
|
What happens when you mix EtOH and cocaine
|
May form cocaethylene which may potentiate the drug's stimulatory effects
|
|
|
What compound is identified by the urine cocaine tox screen?
|
benzoyl ecgonine
|
|
|
What can happen when yo give naloxone to someone who has been speed balling?
|
You may precipitate the underlying cocaine intoxication
|
|
|
What are the rapidly fatal complications of cocaine intoxication?
|
-hyperthermia
-hypertensive emergencies -cardiac dysrhythmias |
|
|
What are cardiovascular sequelae of cocaine intox?
|
Aortic dissection
pulmonary edema MI infarction intracranial hemorrhage strokes infarction of the anterior spinal artery |
|
|
How long after cocaine use can the urine tox remain positive?
|
3 days
|
|
|
When is a urine drug screen beneficial?
|
To document possible abuse or neglect in a child with suggested exposure
To confirm cocaine as an unknown substance in body packers To differentiate paranoia from drug-induced or psychiatric causes |
|
|
What are the large categories to consider in agitated delirium?
|
Metabolic
Structural lesions of the CNS Endocrine disease Infection Tox Heat stroke Post-ictal state |
|
|
What are the potential toxicologic causes of agitated delirium?
|
sympathomimetic/stimulant ( cocaine, amphetamine, caffeine, PCP/ketamine)
anticholinergic serotonin syndrome sedative hypnotic withdrawal |
|
|
What agents should be avoided in acutely intoxicated patients with sympathomimetic toxidrome?
|
Phenothiazines (droperidol and haloperidol)
|
|
|
What is the best way to cool a patient?
|
Ice water
Wet sheets with large fans packing the entire body in ice |
|
|
How is HTN managed in cocaine intox?
|
-BZD
-phentolamine IV 1-5 mg -avoidance of beta antagonists |
|
|
How should narrow complex dysrhythmias be treated in cocaine into?
|
BZD
|
|
|
How should wide complex dysrhythmias be treated in cocaine into?
|
-sodium bicarb 1-2 mEq/kg
-maybe lidocaine (if unresponsive to NaHCO3) |
|
|
What are possible causes of stimulant-iduced chest pain?
|
PTX
pneumomediastinum pneumopericardium AD pulmonary infarction infection FB aspiration endocarditis pericarditis ischemia/infarction coronary stent thrombosis |
|
|
What should be given to patients with ECG criterial for MI with persistent CP and HTN and a clear history of cocaine intox?
|
phentolamine 1mg IV (slowly)
|
|
|
Why are beta antagonists (including labetalol) contraindicated during acute cocaine intoxication?
|
because they may worsen coronary vasoconstriction
|
|
|
Can TPA be given in acute cocaine related MI?
|
Yes, the same contraindications apply though cardiac cath is preferable
|
|
|
What are "body packers"
|
Those who ingest cocaine (or other illicit substances) that have been wrapped tightly into condoms or other latex products and sometimes coated in wax
|
|
|
What is the single absolute criteria for surgical removal of body packs?
|
leaking or poorly secured packets - patient becomes symptomatic
|
|
|
How long should you monitor patients with cocaine-relatd CP?
|
12 hours
If everything is negative they can go home |
|
|
What criteria should body packers meet before they are discharged?
|
-3 packet free stools
-a reliable pack count consistent with ingestion -a negative contrast radiographic study |
|
|
What is the mechanism of action of amphetamines?
|
They enhance the release of catecholamines from pre-synaptic nerve terminals
|
|
|
WHat are patients with amphetamine intoxication at risk of?
|
hyperthermia
HTN emergency dysrhythmia myocardial ischemia increased potassium |
|
|
What is a "body stuffer"?
|
An individual who attempts to conceal evidence of cocaine possession by swallowing the drug while pursued by law enforcement officials
|
|
|
How long should you monitor patients with cocaine-relatd CP?
|
12 hours
If everything is negative they can go home |
|
|
What is the mechanism of action of amphetamines?
|
They enhance the release of catecholamines from pre-synaptic nerve terminals
|
|
|
WHat are patients with amphetamine intoxication at risk of?
|
hyperthermia
HTN emergency dysrhythmia myocardial ischemia increased potassium |
|
|
What is a "body stuffer"?
|
An individual who attempts to conceal evidence of cocaine possession by swallowing the drug while pursued by law enforcement officials
|
|
|
How long should you monitor patients with cocaine-relatd CP?
|
12 hours
If everything is negative they can go home |
|
|
What is the mechanism of action of amphetamines?
|
They enhance the release of catecholamines from pre-synaptic nerve terminals
|
|
|
WHat are patients with amphetamine intoxication at risk of?
|
hyperthermia
HTN emergency dysrhythmia myocardial ischemia increased potassium |
|
|
What is the main difference between amphetamine and cocaine?
|
the toxicity of amphetamines tends to be longer
|
|
|
What is the treatment for MDMA associated hyponatremia in the absence of seizures or other neurologic events?
|
Fluid restriction
|
|
|
What is different about methamphetamine ("crystal meth" "crank")?
|
The duration can be significantly longer
|
|
|
What do crystal meth labs contain?
|
anhydrous ammonia
HCl NaOH ether ephedrine |
|
|
What is the main difference between amphetamine and cocaine?
|
the toxicity of amphetamines tends to be longer
|
|
|
What specific life threatening emergency can MDMA precipitate
|
hyponatremia
|
|
|
What is the treatment for MDMA associated hyponatremia in the absence of seizures or other neurologic events?
|
Fluid restriction
|
|
|
What is different about methamphetamine ("crystal meth" "crank")?
|
The duration can be significantly longer
|
|
|
What do crystal meth labs contain?
|
anhydrous ammonia
HCl NaOH ether ephedrine |
|
|
What cardiovascular drugs account for the majority of fatalities?
|
digitalis
propranolol verapamil |
|
|
What are the effects of digitalis at therapeutic doses?
|
-Increasing the force of myocardial contraction to increase cardiac output
-decrease AV conduction to slow the ventricular rate in afib |
|
|
What is the biochemical basis for the effect of digitalis on conduction?
|
-inhibition of Na+ and K+ ATPase which increases intracellular Na+ and Ca++ and extracellular K+
|
|
|
Is digitalis toxicity characterized by brady and tachydysrhythmias?
|
Both, which can also alternate in the same patient
|
|
|
What are the effects of digitalis on Purkinje fibbers?
|
1) decreases resting potential slowed phase 0 depolarization and conduction velocity
2) decreased action potential duration 3) enhanced automaticity |
|
|
What is the most common ECG manifestation of digitalis toxicity?
|
PVCs
|
|
|
What happens to the ventricles at toxic extremes of dig toxicity?
|
Dangerous sensitivity to mechanical and electrical stimuli
|
|
|
How is digoxin eliminated? How is digitoxin eliminated?
|
Digoxin is primarily excreted in the urine.
Digitoxin is metabolized in the liver |
|
|
Describe the pharmacokinetics of digitalis and how that affects how we treat intoxication?
|
There is significant protein binding and a large volume of distribution which suggests that HD, hemoperfusion and exchange transfusion are ineffective
-the long half lives suggest that temporizing measures (pacemakers and atropine) might cost time, money and lives especially since Fab fragments are available |
|
|
What factors are associated with increased risk of digitalis toxicity?
|
Increased sensitivity to digoxin
underlying Heart disease Electrolyte imbalance hypoxia Increased digoxin levels renal failure drug interactions dehydration Cardiotoxic co-ingestants BB, CCB, TCA |
|
|
When should you consider chronic digitalis intoxication?
|
In any patient on maintenance therapy who develops consistent symptoms, especially with new conduction disturbances or dysrhythmias
|
|
|
What are the main differences of chronic vs acute digitalis intox?
|
Chronic intox has a higher mortality, normal to low K+, more commonly exhibit ventricular dysrhythmias, usually in elderly people, often need Fab, patients often have underlying heart disease
Acute into has K+ that's normal to high and more commonly exhibit bradycardia and AV block |
|
|
Which digoxin level correlates with tissue toxicity and when it it achieved?
|
Steady-state
6-8 hours after a dose or overdose |
|
|
What are typical K+ levels in digitalis toxicity?
|
Acute -> hyperkalemia
Chronic-> low serum and total body |
|
|
What organ systems are affected in digitalis toxicity?
|
Cardiac -> dysrhythmias
CNS visual distrubances gastrointestinal disturbances |
|
|
What is the antidote for digitalis toxicity?
|
digibind or digifab
|
|
|
How is hyperkalemia treatment in acute digitalis toxicity?
|
Serum K+ >5mEq/L warrants consideration of digitalis antibody if not immediately available.
IV glucose, insulin, NaHCO3 recent studies also suggest that Ca++ can be safely given |
|
|
What should be done about K+ in chronic dig toxicity?
|
-raising the serum K+ to 3.5-4mEq/L is an important early treatment - K+ can be administered orally or IV
-Mg++ should also be replaced (except in those with renal failure) |
|
|
What should be considered if you plan on cardioverting a patient with dig intoxication?
|
Cardioversion may cause asystole and lower energy settings may be less hazardous
|
|
|
Which drugs are believed to be the safest of antidysrhythmic drugs in the setting of digitalis intoxication?
|
phenytoin
lidocaine Though digoxin immune Fab are the preferred therapy for dysrhythmias |
|
|
What is the response rate to Dig Fab fragment?
|
90% in chronic or acute poisoning
|
|
|
What are expected reactions to Fab?
|
~1% hypersensitivity- erythema, urticaria, facial edema
-hypokalemia -exacerbation of CHF -increased ventricular rate with afib |
|
|
What is the primary indication for Fab fragment in acute dig toxicity?
|
hyperkalmia K+>5.5mEq/L or EKG changes
|
|
|
What is the empirical dosing of digibind or digifab and when should it be given?
|
10 vials over 30min - acute
4-6 vials - chronic life-threatening symptoms with appropriate history and no time to assess dig levels at 1 hour or steady-state |
|
|
What is the dose of digibind in cardiac arrest?
|
20 vials
|
|
|
What are 2 other approaches to determine the dosage of Digibind or DigiFab?
|
-Calculate based on ingested dose
-base the dosage on the steady-state dig or digitoxin level (after 6-8 hours) |
|
|
What happens to dig levels after Fab fragment administration?
|
It will remain elevated because both bound and unbound drug is measured.
|
|
|
Which children are at greatest risk of dig toxicity?
|
Those on chronic digitalis therapy for heart therapy
|
|
|
What accounts for the most paediatric digitalis intoxications and death?
|
Dosage calculation and administration errors
|
|
|
What are the signs and symptoms of digitalis intoxication in children?
|
-Obtundation and vomiting are more common than in adults
-Children may be asymptomatic at higher levels than adults -bradydysrhythmias and blocks are most common |
|
|
Who requires admission for dig toxicity?
|
-symptomatic patients
-all patients treated with Fab |
|
|
What beta blocking agent is most dangerous in OD?
|
Propranolol
|
|
|
What are beta 2 effects?
|
Vascular smooth muscle relaxation
Liver (glycogenolysis, gluconeogenesis) bronchodilation adipose tissue uterine smooth muscle relaxation |
|
|
When is the peak effect of normal-release beta blocker preparations observed?
|
1-4hours
|
|
|
Why is the bioavailability of PO vs IV beta blockers different?
|
First pass hepatic metabolism
|
|
|
What are the most common signs of Beta blocker OD?
|
-bradycardia
-hypotension -unconsciousness |
|
|
Why is propranolol much more toxic than other beta blockers?
|
Lipophilic nature and membrane stabilizing abilities allow it to penetrate the CNS
|
|
|
What is unique about labetalol?
|
It also blocks alpha adrenergic receptors
|
|
|
What is a main difference between dig and beta blocker OD?
|
Beta blocker has a more rapid onset
|
|
|
Why might multi dose activated charcoal be of use in Beta blocker OD?
|
Because these drugs undergo enterohepatic circulation
|
|
|
How is the order for whole bowel irrigation written?
|
Polyethylene glycol orally or via NG tube @ 1-2L/hour or 20cc/kg until clear effluent PR.
|
|
|
What is the first treatment of Beta blocker OD?
|
atropine, glucagon and crystalloid boluses
|
|
|
How is glucagon dosed?
|
5-10mg IV bolus followed by an infusion of 2-5mg/hour (diluted in D5W)
|
|
|
What are side effects of glucagon?
|
Nausea and vomiting
Hyperglycemia Hypokalemia Allergic reaction |
|
|
What drugs can be used in Beta blocker OD with persistent hypotension post fluid bolus?
|
Isoprenaline
dopamine epinephrine Importantly - do not timidly titrate catecholamine infusions, much higher doses may be required than we are clinically used to |
|
|
Should calcium be given in beta blocker OD?
|
Hyper/hypocalcemia can inhibit the action of glucagon therefore calcium should be given cautiously (infusion is safer than bolus)
|
|
|
What antidysrhythmic should be used in beta blocker toxicity with vtach and a pulse?
|
Lidocaine
(Class Ia and Ic agents should be avoided) |
|
|
Should HD or HP be considered for Beta blocker toxicity?
|
It can be considered for certain Beta Blocker OD but given that Be blockers do not destroy tissues, if circulation can be supported, complete recovery can be expected
|
|
|
What is much more common in paediatric beta blocker OD?
|
Symptomatic hypoglycemia
|
|
|
What are RF for hypoglycaemia in Beta blocker OD?
|
Young age
Fasting state Diabetes |
|
|
How long after an ingestion should patients become symptomatic?`
|
normal release -> 6 hours
|
|
|
What is the treatment of beta blocker poisoning?
|
1) glucagon, atropine, fluids
2) infusion of glucagon, insulin-glucose, catecholamines, phosphodiesterase inhibitors, pacing, arterial line, swan gantz, consider HD |
|
|
What are clinical applications of calcium channel blockers?
|
Angina pectoris
HTN SVT Hypertrophic Cardiomyopathy Migraine Prophylaxis |
|
|
How do calcium channel antagonists work?
|
They block slow calcium channels in the myocardium and vascular smooth muscle leading to coronary and peripheral vasodilation
|
|
|
Which CCA has the deadliest profile?
|
Verapamil (severe myocardial depression and peripheral vasodilation
|
|
|
What is the onset of action for CCA toxicity?
|
30-60min
|
|
|
What are the manifestations of Beta Blocker OD?
|
Bradycardia
Hypotension Unconsciousness Respiratory Arrest Hypoglycemia Seizures Bronchospasm VT or VF Hyperkalemia Hepatotoxicity |
|
|
Should atropine be used in CCA OD?
|
It can be tried but often the effect is short lived
|
|
|
What are second line agents for bradycardia and hypotension in CCA OD?
|
cardiac pacing
isoproterenol |
|
|
What is a reasonable dose of calcium in CCA OD?
|
6g
(10-20mL CaCl over 5-10 minutes then 5-10mL/hr) children: 10-30mg/kg |
|
|
What catecholamines have been reported to have success in CCA toxicity?
|
isoproterenol
dopamine |
|
|
What other therapy (other than atropine, calcium and catecholamines) can be done for CCA OD?
|
insulin euglycemia
|
|
|
How do you write the order for insulin-euglycemia?
|
-insulin bolus 1U/kg, then insulin infusion 0.5U/kg/hr
-glucose 10-30g/hr (using 5 or 10% dextrose solution) |
|
|
What is specific about nifedipine in children?
|
It is a medication that can kill a child with ingestion of a single tablet
|
|
|
What should be done in a patient who received nitrates after PDI type V ingestions (viagra/cialis etc)
|
IV fluids
If this is not enough then dopamine 5ug/kg/min |
|
|
What do nitrites cause?
|
vasodilatation
methemoglobin formation |
|
|
WHat are "poppers"
|
Inhaled alkyl nitrite in the hope of prolonging sexual pleasure
|
|
|
Who is particularly susceptible to the oxidative stress of nitrite exposure?
|
G6P-deficiency
|
|
|
At what levels of methemoglobin should you treat?
|
30%
|
|
|
How is methemoglobinemia treated?
|
methylene blue 1-2 mg IV over 5 minutes
|
|
|
What products are used in the clandestine production of methamphetamine?
|
Ammonium hydroxide
Anhydrous Lithium Metallic Lithium |
|
|
In what populations do we see caustic exposures?
|
intentional suicidal ingestions
Pediatric and elderly (accidental ingestion) |
|
|
What pills are most likely to stick and therefore cause pill esophagitis?
|
Doxycycline
Tetracyclines KCl ASA |
|
|
What factors influence the extent of injury from a caustic exposure?
|
Type of agent
Concentration Volume Viscosity Duration of Contact pH Presence or absence of food in the stomach |
|
|
What do acidic compounds cause?
|
coagulation necrosis
|
|
|
Why are acids less likely to cause esophageal or pharyngeal injury?
|
Squamous epithelial cells are somewhat resistant to coagulation necrosis
|
|
|
What does alkaline contact cause?
|
liquefaction necrosis
fat saponification protein disruption |
|
|
Why are alkali ingestions typically larger?
|
Alkalis are colourless, odorless and unlike acids, do to cause immediate pain on contact
|
|
|
What are the 4 steps of caustic ingestion?
|
1- necrosis
2- vascular thrombosis 3 - injured tissue begins to slough off 4 - granulation tissue forms |
|
|
How are caustic injuries categorized?
|
1st/2nd/3rd degree, similar to thermal burns
|
|
|
What characterizes 1st/2nd and 3rd degree caustic burns?
|
1- edema and hyperemia
2a - non-circumferential 2b - near circumferential (2nd degree is characterized by superficial ulvers, whitish membranes, exudate and friability) 3 - transmural involvement |
|
|
What are the emergent issues in caustic ingestions?
|
airway edema
esophageal/gastric perforation |
|
|
What clinical signs/symptoms are predictive of distal injury in caustic ingestions?
|
Prolonged drooling and dysphagia
|
|
|
What should be done immediately for hydrofluoric acid exposures?
|
Immediate cardiac monitoring (assess for prolonged QTc, torsades, ventricular dysrhythmia)
|
|
|
What is empirical intervention for life-threatening HF acid exposures with dysrhythmia?
|
High dose IV calcium
|
|
|
When is endoscopy contraindicated in caustic ingestions?
|
-possible or known perforation
->24 hours post ingestion (more hazardous because of wound softening) |
|
|
What are the 4 categories of caustic ingestion based on endoscopy?
|
1) no esophageal/gastric injury
2) gastric injury 3) linear burns of esophagus 4) circumferential burns |
|
|
When can water/mild dilution be considered?
|
Within the first few minutes after ingestion (in alert patients who are not vomiting and can tolerate liquids)
1-2 cups of milk or water can be given |
|
|
When is surgical intervention required in caustic ingestions?
|
Free air
Peritonitis Increasing chest or abdominal pain hypotension |
|
|
What should be done immediately for ocular alkali exposure?
|
Aggressive lavage with 2LNS per eye
|
|
|
What should be done in povidone-iondine ingestion?
|
Gastric irrigation with starch or milk (this converts the iodine to the much less toxic iodide)
|
|
|
What is the danger of phenol/formaldehyde ingestion?
|
They are protoplasmic poisons and cause protein denaturation and coagulation necrosis
|
|
|
What should be done in patients who ingest concentrated H2O2 and why?
|
Radiographic evaluation for the presence of gas in the chest/abdo/portal system because gas emboli can potentially be treated with HBOT
|
|
|
What is the treatment of ingested batteries?
|
Those lodged in the airway or esophagus require removal, while those that are gastric or intestinal are treated with watchful waiting.
|
|
|
What household products may contain methanol?
|
Antifreeze
Windshield washer fluid Carburator fluid Glass Cleaners Illicit Alcohol Production Formalin Embalming fluid |
|
|
How long does it take for Methanol to be absorbed?
|
30-60min
|
|
|
What is the smallest lethal dose of methanol in an adult?
|
15 mL of 40% methanol
|
|
|
What are the toxic metabolites of Methanol?
|
Methanol (alcohol dehydrogenase) -> formaldehyde (aldehyde dehydrogenase) formic acid
|
|
|
How is formic acid degraded?
|
Through a folate dependent pathway it is degraded to carbon dioxide and water
|
|
|
What are the main complications of methanol poisoning?
|
Optic neuropathy
Putaminal necrosis |
|
|
What is the latency period b/w methanol ingestion and onset of visual or metabolic disturbances?
|
12-24 hours
(though may even be longer if concomitant EtOH ingestion) |
|
|
What are early symptoms of methanol poisoning?
|
decreased MS, confusion, ataxia
|
|
|
What is the most common visual complaint in methanol poisoning?
|
central scotoma
|
|
|
What correlates with prognosis in methanol ingestion?
|
Degree of acidosis at the time of presentation and initiation of treatment within 8hours of exposure
|
|
|
Does the presence of a normal AG r/o methanol poisoning?
|
No
|
|
|
Apart from a wide AG what is another classic lab finding in Methanol toxicity?
|
Elevated osmolol gap
|
|
|
HOw do you calculate serum osmolality?
|
2Na+BUN+glucose+EtOH
|
|
|
What is the "normal" osmolal gap?
|
Often cited as <10mOsm/kg however there is considerable variability
|
|
|
Why should caution be used in ruling out a toxic alcohol ingestion with a normal osmolal gap?
|
-calculated osmalality may vary among laboratories
-in a later presentation there may be little or no osmolal gap because only the parent compound is osmotically active -toxic levels of methanol or ethylene glycol may be present with a gap of 10mOsm/kg |
|
|
What substances can cause elevated osmolal gaps?
|
Methanol
Ethylene glycol Isopropanol Ethanol Acetone Propylene glycol mannitol Glycerol Ethyl Ether |
|
|
What is a "double gap"?
|
Osmolal gap and anion gap
|
|
|
What substances may cause a "double gap"?
|
Ethanol
Methanol Ethylene Glycol Propylene Glycol DKA AKA multiorgan failure acetonitrile chronic renal failure |
|
|
What is an particular characteristic associated with methanol?
|
Ocular complaints
|
|
|
What is an particular characteristic of ethylene glycol?
|
Calcium oxalate crystaluria
|
|
|
What are sources of ethylene glycol?
|
Antifreeze
Airplane de-icing Hydraulic brake fluid Industrial solvents |
|
|
How long does it take to reach peak blood levels of ethylene glycol after ingestion?
|
1-4 hours
|
|
|
What are the reported toxic and lethal doses of ethylene glycol?
|
0.2 mL/kg and 1.4 mL/kg
|
|
|
What is the metabolic pathway of ethylene glycol?
|
ethylene glycol (alcohol dehydrogenase) ->glycoaldehyde ->(aldehyde dehydrogenase) -> glycolic acid -> glycoxylic acid -> oxalic acid
|
|
|
What are the four stages of ethylene glycol ingestion?
|
1) acute neurologic - similar to inebriation
2) cardiopulmonary - HTN, tachycardia, ARDS, hypocalcemia 3) Renal Stages - ATN 4) Delayed Neurologic Sequelae - cranial neuropathy |
|
|
Does ethylene glycol cause inebriation?
|
It causes the same degree of inebriation as EtOH
|
|
|
Does the absence of crystalluria r/o ethylene glycol ingestion?
|
No, it is a hallmark, less than 1/2 of patients have this finding
|
|
|
What shapes may the crystals in crystalluria take on?
|
Envelope-shaped
Needle - shaped Any shape |
|
|
Is urinary fluorescence useful in ethylene glycol toxicity?
|
No, a positive may be a false positive and a negative may be a false negative
|
|
|
What ECG changes can patients with ethylene glycol poisoning display?
|
QT prolongation secondary to hypocalcemia
|
|
|
Is Activated charcoal useful in toxic alcohol ingestion?
|
No
|
|
|
DO patients with inhalational exposure to Methanol need to go to the hospital?
|
Not necessarily
|
|
|
What are the treatment goals in patients with methanol or ethylene glycol toxicity?
|
-correction of metabolic acidosis with bicarbonate
-Alcohol dehydogenase blockade, inhibiting metabolism of methanol or ethylene glycol -removal of the parent alcohol and its metabolites by HD |
|
|
What should be considered when administering NaHCO3 to a patient with ethylene glycol ingestion?
|
The potential to worsen hypocalcemia
|
|
|
What are ways of blocking Alcoohol Dehydrogenase?
|
Antizol (fomepizole)
EtOH |
|
|
At what level of methanol or ethylene glycol should alcohol dehydrogenase be blocked?
|
20mg/dL
|
|
|
What is the target blood Ethanol level to block ADH?
|
100-150mg/dL
|
|
|
What is the dose of fomepizole?
|
15mg/kg followed by 10mg/kg q12 hours x 4 and then re-assess
|
|
|
What are general indications for HD in a patient with toxic alcohol ingestion?
|
-metabolic acidosis
-renal compromise -visual symptoms -deterioration despite intensive care -electrolyte imbalances unresponsive to conventional therapy -blood level >50mg/dL |
|
|
What else should be given to patients with methanol toxicity?
|
folinic acid
|
|
|
What else should be given to patients with ethylene glycol toxicity?
|
pyridoxine
thiamine |
|
|
Does isopropanol cause CNS depression?
|
It causes twice the CNS depression of EtOH
|
|
|
What is the metabolism of isopropanol?
|
isopropanol (alcohol dehydrogenase)-> acetone
|
|
|
What is a potentially lethal dose of isopropanol
|
2-4cc/kg
|
|
|
What symptoms predominate with isopropanol ingestion?
|
CNS and GI
|
|
|
What is a marker of severe poisoning in isopropanol ingestion?
|
hypotension
|
|
|
Do patients with isopropanol ingestion have a wide AG?
|
No, acetone is uncharged
|
|
|
What is "pseudo renal failure"?
|
Isolated false elevation of Cr with normal BUN because of interference of acetone and acetoacetone in the calorimetric determination of Cr
|
|
|
What is a distinguishing feature of isopropanol ingestion?
|
Ketosis without acidosis (from acetone)
|
|
|
What can be done for isopropanol ingestion?
|
Dialysis
|
|
|
What are indications for HD in isopropanol ingestion?
|
hypotension despite treatment and coma
|
|
|
What are the 4 types of hydrocarbon exposures that present to the ED?
|
1) accidental ingestion involving children
2) intentional inhalational abuse of volatile HCs 3) accidental inhalational and dermal exposure to HC 4) massive oral ingestion |
|
|
What do hydrocarbons contain?
|
Hydrogen and carbon
|
|
|
What are the 2 main categories of HC?
|
Aliphatic - straight chain
Aromatic - those containing a benzene ring |
|
|
What target organs are affected by HC toxicity?
|
The lungs
The CNS The heart |
|
|
What characteristics determine the potential for acute toxicity of HCs?
|
Viscosity - substances with low viscosity have higher toxicity
Volatility - high volatility allows a substance to displace O2 Surface Tension - low surface tension allows a substance to disperse easily Chemical side chains - increase the potential for toxicity |
|
|
What is the primary organ of HC toxicity?
|
the lung
|
|
|
How does pulmonary toxicity occur in HC poisoning?
|
By aspiration
|
|
|
How do HCs affect the lung?
|
-penetrate the lower airways and cause bronchospasm and inflammation
-displace O2 in the alveolar space -direct injury to alveoli and capillaries -inhibit surfactant function leading to alveolar instability and collapse |
|
|
What CNS symptoms do HCs cause?
|
Euphoria
Disinhibition Confusion Obtundation |
|
|
What CNS abnormalities does chronic HC exposure cause?
|
-peripheral neuropathy
-cerebellar degeneration -neuropsychiatric disorders -chronic encephalopathy -dementia |
|
|
What cardiac abnormalities are caused by HC?
|
They may cause sudden cardiac death secondary to sensitization to endogenous and exogenous catecholamines
|
|
|
What are signs of significant HC exposure?
|
tachypnea, tachycardia, wheezing, hypoxemia
|
|
|
What poisonings may mimic the symptoms of HC aspiration?
|
organophosphate
salicylate paraquat |
|
|
Should routine GI decontamination of HC be done?
|
routine gastric lavage or emesis should be avoided (HC is much more toxic to the lung) There are some exceptions to this
|
|
|
In what situations post HC exposure is full decon indicated?
|
C- Camphor (seizures)
H - halogenated HC (dysrhythmia or hepatotoxicity) A - aromatic HC (bone marrow suppression and CA) M - Metals (arsenic, mercury, lead) P - pesticides (cholinergic crisis, seizures, respiratory depression) |
|
|
What meds should be avoided in HC intoxication?
|
Epinephrine + isoproterenol
|
|
|
How long should you observe asymptomatic HC ingestion?
|
6 hours
|
|
|
How long should patients with aspiration be observed
|
Minimum 24 hours
|
|
|
How long should you observe recreational HC exposure?
|
4-6 hrs
-offer drug addiction counseling |
|
|
What are the most common iron exposures?
|
Ingestion of paediatric multivitamin formulations
|
|
|
What are normal serum iron levels?
|
50-150ug/dL
|
|
|
What is the total iron binding capacity (TIBC)?
|
A crude measure of the ability of serum proteins - including transferrin - to bind iron
|
|
|
What happens when iron levels rise following a significant iron OD?
|
Transferrin becomes saturated so that excess iron circulates as free iron - which is directly toxic to organs
|
|
|
What does the toxicity of an iron compound depend on?
|
The amount of elemental iron ingested
|
|
|
What is the risk stratification of iron ingestions?
|
<20mg/kg - no symptoms
20-60 - mild to moderate symptoms >60mg/kg moderate to severe morbidity |
|
|
What are the toxic effects of iron?
|
1-direct caustic injury to the gastrointestinal mucosa
2 - impairs cellular metabolism primarily of the heart, liver and CNS |
|
|
What are the five stages of acute iron poisoning?
|
I - corrosive effects of iron on the gut - vomiting and diarrhea
II - apparent recovery - asymptomatic period III - recurrence of GI symptoms, lethargy and coma, AG metabolic acidosis, leukocytosis, coagulopathy, renal failure, CV collapse IV - fulminant hepatic failure - 2-5d (rare) V - consequences of healing the injured gastric mucosa characterized by pyloric or proximal bowel scarring +/- obstruction |
|
|
When does the serum iron level peak?
|
3-5 hours after ingestion except for sustained-release or enteric coated preparations
|
|
|
Why may levels measured late be deceptive?
|
Iron is rapidly cleared from the serum and deposited in the liver therefore levels may be deceptively low
|
|
|
Should TIBC be used as an indicator of free iron?
|
No, TIBC is a crude test and cases of serious toxicity have been reported even when TIBC exceeds the serum iron level
|
|
|
Should gastric decontamination be used in iron OD?
|
No, AC does not bind iron and lavage/ipecac do not remove tablets
|
|
|
What method of decon is recommended for iron OD?
|
>20mg/kg -> WBI
Peg-lyte solution oral or NG 20-40cc/kg/hour or 1.5-2L/hr until rectal effluent is clear and no radiographic evidence of pill fragments |
|
|
When is WBI contraindicated?
|
Bowel obstruction, perforation or ileus
|
|
|
Can HD or HP be used for iron OD?
|
No, exchange transfusion has been recommended for severely symptomatic patients with iron >1000ug/dL
|
|
|
What does deferoxamine do?
|
It chelates iron to form the water soluble compound ferrioxamine which can be renal excreted or dialyzed
|
|
|
What does deferoxamine do to the urine?
|
turns it a "vin rose" color
|
|
|
Which patients should receive WBI?
|
-ingested >20mg/kg
-has pills visible on abdominal radiograph |
|
|
When should serum iron levels be checked?
|
3-5 hours after ingestion and 6-8 hours after ingestion to confirm the level is decreasing
|
|
|
What is the management of a patient with peak serum iron levels of </=300ug/dL?
|
If asymptomatic d/c home after 6 hours of observation
|
|
|
Which patients require chelation for Iron OD?
|
serum iron >500ug/dL
-systemic signs of toxicity (AMS, shock, AG metabolic acidosis) |
|
|
What tests are 100% specific for predicting serum iron >300ug/dL?
|
increased serum glucose and leukocyte count
|
|
|
What are potential sources of lead?
|
household paint
gasoline fushing weights pottery glaze bullets in bone bootleg whiskey ("moonshine") |
|
|
What is the mechanism by which lead is toxic?
|
Lead binds sulfhydryl groups and other ligands and interferes with critical enzymes
|
|
|
What systems are most affected by lead toxicity?
|
hematopoietic
neurologic renal GI |
|
|
What is the manifestation of hematopoietic toxicity in lead poisoning?
|
Anemia
|
|
|
What are neurologic signs of lead toxicity?
|
Wrist drop, foot drop
segmental demyelination and degeneration of motor axons acute toxicity may result in cerebral edema |
|
|
What are symptoms of acute lead exposure?
|
"lead colic" cramping abdominal pain, nausea, vomiting, constipation +/- diarrhea, fatigue, anemia, peripheral neuropathy, headache -> cerebral edema
|
|
|
What is the most important biomarker in lead toxicity?
|
Blood lead level (BLL)
|
|
|
What is a chronic toxic level of BLL in a child?
|
10ug/dL
|
|
|
What are the findings of lead toxicity on a peripheral smear?
|
basophilic stipling
|
|
|
What are "lead lines"?
|
Increased metaphyseal activity on wrist and knee radiographs that are characteristic of chronic lead exposure
|
|
|
What form of decontamination can be used for lead?
|
WBI
|
|
|
Which patients with lead expusure should be considered for chelation?
|
BLL>70ug/dL
signs suggestive of encephalopathy |
|
|
which initial chelator is used for lead exposure?
|
BAL (british antilewisite)/dimercaprol
|
|
|
Which chelator is used after dimercaprol?
|
CaNa2EDTA (NOT Na EDTA)
|
|
|
What is the key to managing chronic lead toxicity?
|
Identify and reduction of sources of primary exposure
|
|
|
Should ingested lead FB be removed?
|
THey can be allowed to pass but if still there in 2 weeks should be removed
|
|
|
Where is arsenic found?
|
Smelters, electric power plants than burn arsenic and rich coal, wood preservative, glass production
|
|
|
What are the inorganic forms of arsenic and their properties?
|
As3+ - highly lipid soluble, 5-10x more toxic
As5+ |
|
|
Where does arsenic concentrate?
|
in the liver, kidneys, spleen, lungs and GI tract
|
|
|
Why is arsenic toxic?
|
It bind sulfhydryl groups inhibiting critical enzymes (especially those involved in glycolysis)
-disrupts oxidative phosphorylation -arsine causes hemolysis |
|
|
What are the manifestations of exposure to arsine gas?
|
Severe hemolysis and renal tubular injury
|
|
|
What are the predominant effects of exposure to arsenic salts?
|
acute GI effects
metallic/garlicky taste in mouth later - encephalopathy, seizures, coma |
|
|
What are the chronic effects of arsenic poisoning?
|
Mees lines on the nails
sensorimotor neuropathy hyperkeratosis on the palms and soles |
|
|
What is the best way to diagnose arsenic poisoning?
|
24 hour urine collection (abnormal is >50ug/L)
|
|
|
Which substance can cause false positive urinary arsenic?
|
Arsenobetaine found in seafood
|
|
|
What decontamination should be considered in arsenic poisoning?
|
-orogastric lavage and WBI
(AC does not adsorb) -HD removes arsernic in ARF -exchange or plasma exchange should be considered very early after exposure |
|
|
What is the preferred chelator in arsenic poisoning?
|
IM dimercaprol
|
|
|
Is chelation useful for arsine?
|
No
|
|
|
What are the forms of mercury?
|
elemental, salts, organic
|
|
|
What industries use mercury in manufacturing?
|
-fluorescent lights
-batteries -polyvinyl choloride -latex paint |
|
|
What is a common root of elemental mercury exposure and what can it cause?
|
Inhalational - severe pneumonitis and ARDS
|
|
|
Is ingestion of elemental mercury dangerous?
|
No, it is not absorbed by the GI trace, unless it becomes trapped in a diverticulae
|
|
|
What happens with ingestion of inorganic mercury? (mercurous or mercuric)
|
Significant GI and renal toxicity
|
|
|
What are the manifestations of organic mercury compounds?
|
Primarily through ingestion
Neurotoxicity: ataxia, tremor, dysarthria, tunnel vision |
|
|
What is the timeline of symptoms of exposure to elemental, inorganic and organic mercury?
|
Elemental - inhalation - rapid
Inorganic salt ingestion - immediate Organic - symptoms over weeks to months |
|
|
What is the most helpful test for confirming exposure to mercury?
|
urine mercury
|
|
|
Is charcoal useful in mercury salt ingestion?
|
No, it adsorbs very little
|
|
|
When should BAL be used in mercury toxicity and when should it not be used?
|
It should be used in acute inorganic poisoning and it is contraindicated in patients poisoned with organic mercury
|
|
|
When do peak plasma concentrations occur in immediate release lithium ingestion? delayed-release?
|
immediate release 0.5-3 hours
delayed release - 6-12 hours |
|
|
What are the kinetics of lithium distribution?
|
Two - compartment -> initially extracellular then redistributes to various tissues
|
|
|
What medications may increase lithium levels?
|
NSAID
diuretics ACE Inhibitor |
|
|
What problems are associated with chronic lithium therapy? and what are their manifestations?
|
Nephrogenic diabetes which manifests as dehydration and hyponatremia
-inhibits the synthesis of thyroid hormone as hypothyroidism -leukocytosis (temporary) |
|
|
What are the classifications of lithium poisoning?
|
-acute toxicity
-chronic toxicity -acute on chronic |
|
|
What is the definition of acute lithium toxicity?
|
An OD of lithium in a patient without any lithium body stores
|
|
|
what are the manifestations of acute Li+ toxicity?
|
GI symptoms
ECG changes - bradycardia, T wave flattening and QT prolongation -delayed neurotoxicity |
|
|
How does chronic Li+ toxicity occur?
|
Increased absorption
decreased renal elimination |
|
|
What is the predominant presentation of chronic lithium toxicity?
|
tremor-> progressive drowsiness, hyper-reflexia, confusion, clonus, coma, seizures, EPS
|
|
|
What is SILENT syndrome?
|
Syndrome of irreversible lithium effectuated neurotoxicity
|
|
|
What is an acute on chronic lithium toxicity?
|
excess Li ingestion in a patient already taking Lithium
|
|
|
What are life-threatening syndromes that can be associated with Lithium
|
NMS
Serotonin syndrome |
|
|
What are the cornerstones in management of Li+ poisoning
|
Selective GI decontamination
Enhanced renal and extracoporeal elimination |
|
|
What form of GI decon is useful in Li and when?
|
WBI for sustained release Li
|
|
|
How do you maximize renal elimination of Li?
|
Fluid resuscitation with NaCl
IV NS at 2x maintenance - unless contraindicated |
|
|
What is the most effective technique for elimination of Li?
|
HD
|
|
|
When is HD used in Li tox?
|
Clinical deterioration
-inadequate endogenous Li clearance -inabiliyt to enhance renal elimination ->4.0mEq/L in acute ->2.5 mEq/L in chronic |
|
|
What are the elements of a toxicology risk assessment?
|
Obtain all prescription bottles and containers
Inquire about OD history Perform a pill count |
|
|
How reliable is the pupillary examination in a poisoned patient?
|
The pupillary exam in the poisoned patient may give misleading information, it is especially less reliable in multiple drug ingestions
|
|
|
Which opioids do not produce miosis?
|
Propoxyphene and pentazocin
|
|
|
Which toxins give a shoe polish door?
|
nitrobenzene
|
|
|
Which toxins give a garlic odor?
|
Arsenic
DMSO organophosphates yellow phosphorus selenium tellurium |
|
|
What toxins give rotten egg odor?
|
disulfiram
hydrogen sulfide NAC DMSA |
|
|
What toxins give off pear odor?
|
chloral hydrate
paraldehyde |
|
|
What toxins give off glue odor?
|
toluene
other solvents |
|
|
Give circumstances where physostigmine is indicated?
|
Physostigmine is a naturally occurring acetylcholinesterase inhibitor It is indicad in anticholinergic poisoning syndrome (in the absence of TCA OD)
Mild temperature elevation acute delirium with mumbling speech typical "picking" movements |
|
|
How do you give physostigmine?
|
It is given as 1-2 mg IV over 5 min (may be repeated in 10-15min)
|
|
|
What is Takutsubo cardiomyopathy? How does it present? How is it treated?
|
Takutsobo cardiomyopathy is a transient cardiac syndrome that results in left ventricular apical a kinesis and mimics ACS. It presents as chest pain, ST segment elevation and elevation of cardiac enzymes with no significant coronary stenosis on angiogram. Patients are treated as if they are having an ACS
|
|
|
What is the critical step in managing a patient with excited delirium?
|
Excited delerium is an extreme presentation of sympathomimetic excess. Patients are agitated hyperthermic, violent and possess "superhuman" strength.
It is critical to sedate and control hyperthermia aggressively. Also there is a need to treat the acidosis and hyperkalemia. |
|
|
What is the first hallmark of a severe sedative overdose?
|
Depressed sensorium. Then the patient becomes increasingly obtunded, the deep tendon reflexes diminish and vital signs deteriorate.
|
|
|
When is a CT head indicated in a poisoned patient?
|
In a comatose patient if there is suspicion for stroke, infection or head trauma
|
|
|
Which receptors are involved in producing serotonin toxicity?
|
5HT1A
5HT2A |
|
|
List 3 medications that can be used to alleviate serotonin toxicity? How are they given?
|
Cyproheptadine 4mg PO prn - liquid given through an NG tube
Methysergide Benzodiazepines - IV Activated charcoal may be considered PO IV NaHCO3 |
|
|
Which SSRI give ECG abnormalities? What is the abnormality?
|
Citalopram
QTc prolongation, QRS widening and ventricular fibrillation |
|
|
In which patients is it indicated to request a comprehensive drug screen?
|
Patients presenting with their first major psychotic episode
patients who are critically ill for unknown reasons when identification of an unsuspected toxin may change management |
|
|
What is the value of a urine tox screen?
|
The urine tox screen has little value because
1)the lab does not screen for many substances, even commonly ingested agents that are capable of causing critical illness 2) the urine screen is often performed soon after the ingestion when the drug concentration is too low for a positive result. Even the drug responsible for life-threatening symptoms may be negative on the urine screen soon after ingestion. 3) drugs found on screening may not be those responsible for the initial symptoms, especially if the drugs are not quantified. |
|
|
Which toxins are commonly associated with non cardiogenic pulmonary edema
|
Opioid
Salicylate |
|
|
Which classes of toxins are radio-opaque?
|
Heavy metals
Phenothiazines Potassium Calcium Chlorinated hydrocarbons (chloral hydrate) |
|
|
What are two formulations of activated charcoal? Which one is no longer recommended?
|
Oral slurry
AC with added sorbitol AC with added sorbitol is no longer recommended but cathartics have never been shown to be of benefit and repeated doses of sorbitol can cause dehydration |
|
|
What agents do not adsorb to charcoal?
|
Ions (acids, alkalies, lithium, borate, bromide)
hydrocarbons metals (iron) ethanol |
|
|
What is the proper decontamination for chemical gas exposure?
|
Exposure to a gas does not require decontamination because the patient and rescuers are not at risk once the patient is removed from the toxic environment. The exception is when the patient's skin or clothing is contaminated with a liquid that is evaporating.
If this is the case, remove all clothing as soon as possible. Skin should be irrigated with warm watery and with attention to skin folds and other areas that might be missed. |
|
|
List medications containing APAP that are available over the counter?
|
benadryl
dayquil dimetapp dristan excedrin midol nyquil robitussin sinutab sudafed vicks |
|
|
What is the toxic dose of APAP?
|
150mg/kg
|
|
|
Describe the metabolism of acetaminophen?
|
Conjugation with glucuronide or sulfate or oxidation by CYP4502E1 to NAPQI which rapidly combines with glutathione to form non-toxic metabolites excreted in the urine
|
|
|
In which organs is APAP metabolized?
|
Primarily the liver but may also be metabolized by the renal CYP enzymes
|
|
|
What are the characteristic histology findings with APAP hepatotoxicity? Why?
|
Centrilobular necrosis (hepatic zone III) because this is where oxidative metabolism is concentrated. In severe toxicity, the entire liver parenchyma may be affected.
|
|
|
List the mechanism of action of NAC?
|
It is:
glutathione precursor sulfur containing glutathione substitute enhances APAP conjugation with sulfate free- radical scavenger antioxidant |
|
|
Describe the clinical course of an APAP toxicity?
|
Stage 1 -preinjury - nausea, vomiting, anorexia (0-12)
Stage 2 - liver injury - nausea, vomining, RUQ pain (8-36 hours) Stage 3 - maximal liver injury - liver failure (2-4 days) Stage 4 - recovery (>4 days) |
|
|
List the different types of APAP exposure and their management?
|
Acute and chronic.
|
|
|
How is APAP overdose managed in the pregnant patient?
|
Same as other individuals
|
|
|
What is the risk of liver injury if NAC is given within 8 hours?
|
<4%, close to 0
|
|
|
When do NAC reaction occur? How are they treated? WHat is the pathophysiological mechanism?
|
IV NAC - anaphylactoid section within the first 15-60 min
PO NAC - anaphylactoid reaction (less frequent than IV) They are treated with antihistamines +/- slowing or stopping the infusion. You can also give glucocorticoids or epinephrine for more severe reactions |
|
|
When can NAC be stopped?
|
21hours after IV admin
72 hours after PO admin AND APAP <10ug/mL, AST normal |
|
|
When do patients with APAP induced hepatotoxicity need to be referred to a herpetology centre?
|
Established hepatotoxicity and at risk of fulminant hepatic failure.
|
|
|
Describe the mechanism of action of ASA?
|
ASA is converted to salizylate. Salicylate stimulates the respiratory center and increases the sensitivity of the respiratory centre to pH and carbon dioxide partial pressure.
Toxicity results primarily from interference with aerobic metabolism by uncoupling of mitochondrial oxidative phosphorylation. Salicyate is also a potent neurotoxin |
|
|
Contrast first-order vs zero-order kinetics
|
First order kinetics depend on the concentration of the drug, whereas zero order kinetics are independent of the drug concentration
|
|
|
At which serum concentration of ASA are zero order kinetics reached?
|
Serum concentrations grater than 30mg/dL
|
|
|
What is the mechanism of ASA induced hyperthermia?
|
Inefficiency of anaerobic metabolism results in less energy being used to create ATP and energy is released as heat causing hyperthermia
|
|
|
List 3 mechanisms contributing to the hypokalemia seen in ASA toxicity?
|
Vomiting secondary to stimulation of the CTZ
increased renal excretion of Na, HCO3 and K in response to respiratory alkalosis Salicylate induced increased permeability of renal tubules Intracellular accumulation of sodium and water Inhibition of the active transport system |
|
|
Which patients are more at risk of developing ASA induced NCPE?
|
Adults
->30year olds -cigarette smokers -chronic salicylate ingestions -metabolic acidosis -neurologic symptoms -serum salicylate >40mg/dL Children -high serum salicylate level -high anion gap -decreased serum potassium -low pco2 |
|
|
How many tablets of ASA are needed for a 70 kg patient to reach a toxic dose? A lethal dose?
|
Toxic - 175 80mg tabs
Lethal - 475 80mg tabs |
|
|
How are seizures treated?
|
HD
|
|
|
What are indications for HD in ASA toxicity?
|
-coma/seizures
-renal/hepatic/pulmonary failure -severe acid-base imbalance -deterioration of condition -serum salicylate level >100mg/dL in acute OD or >40 mg/dL in chronic OD |
|
|
What is the role of activated charcoal in ASA OD?
|
There is little role for AC in salicylate OD, it can limit the absorption of salicylates if given within 1 hour but has not been shown to alter the clinical outcome or morbidity
|
|
|
Why is dextrose given to these patients?
|
Tissue glycolysis (due to increased metabolic rate, temperature, tissue CO2 production and O2 consumption) results in hypoglycaemia. Rarely patient may display hyperglycemia
|
|
|
How is urinary alkalization performed?
|
Administer 1-2mEq/kg sodium bicarbonate over 1-2hours and then follow the urine pH which should ideally be maintained at a pH of 7.5-8. This should not come at the cost of alkalemia
|
|
|
What are the goals of alkalization?
|
increase the fraction of salicylate ion in the urine, thereby trapping it there and resulting in its excretion
|
|
|
How is ASA toxicity treated in the pregnant patient? In the postpartum period?
|
ASA toxicity should be treated the same way. If the fetus is viable, the fetus should be delivered since salicylate poisoning may result in fetal demise. In infants and congenital salicylism exchange transfusion may be considered
|
|
|
What is the definition of an illusion?
|
A misperception of a real object (as opposed to a hallucination)
|
|
|
What are serotonin-like agents?
|
lysergic acid
tryptamines |
|
|
What is the most common form of LSD?
|
A blotter which is placed sublingually or eaten whole
|
|
|
What is an example of a tryptamine?
|
Psilocybin and psilocin found in mushrooms
|
|
|
What receptors do serotonergic agents act on?
|
5-HT2A
|
|
|
What is the most common adverse reaction to psychedelics?
|
Acute panic reaction (paranoid delusions and fear of impending death)
|
|
|
What is the mainstay of treatment for serotonergic agents?
|
supportive
sedation |
|
|
What are enactogens?
|
Hallucinogenic stimulants that are analogues of amphetamines, mescaline, N-substituted piperazines
|
|
|
What are complications of MDMA?
|
Rhabdomyolysis
Hyperthermia Hyponatremia |
|
|
What is the mechanism of action of enactogens like MDMA?
|
Release serotonin, dopamine and NE from presynaptic terminal and inhibit catecholamine reuptake
|
|
|
What are the mechanisms responsible for hyponatremia in MDMA/
|
-excess intake of free water
-MDMA mediated release of antidiuretic hormone |
|
|
What are dissociative agents?
|
PCP
Ketamine Dextromethorphan |
|
|
What are the characteristics of dissociative agents?
|
Analgesic
Amnestic Lack of respiratory or cardiovascular depression |
|
|
What substances may cross react with the PCP urine assay?
|
Dextromethorphan
Chlorpromazine Methadone Ketamine Diphenhydramine |
|
|
What lab abnormality can be caused by chronic dextromethorphan use?
|
Hyperchloremia with negative anion gap (caused but bromide interference with the assay)
|
|
|
What is the main active ingredient in cannabinoids?
|
Delta-9-THC (tetrahydrocannabinol)
|
|
|
What are the most common effects from smoking marijuana?
|
Relaxation and euphoria
|
|
|
What is the difference between an opioid and opiate?
|
Opioid refers to all natural, synthetic and semi-synthetic agents with morphine-like actions.
Opiate refers only to natural agents |
|
|
What does the term endorphin refer to ?
|
enkephalin, beta endorphin and dynorphin (any of the 3 endogenous opioid families)
|
|
|
What are the opioid receptors
|
mu
kappa delta |
|
|
What opioids can cause seizures?
|
propoxyphene
meperidine (its metabolite) hypoxia (with OD of any opioid) |
|
|
What is the toxidrome of opioid toxicity?
|
hypoxia from CNS and respiratory depression
|
|
|
Which opioids have serotonergic properties?
|
meperidine
dextromethorphan |
|
|
Which opioids have may not produce miosis?
|
meperidine
propoxyphene lomotil pentazocin |
|
|
What cardiovascular problems can opioids cause?
|
hypotension (histamine release)
bradycardia propoxyphene may cause sodium channel blockade |
|
|
What opioids can cause seizures?
|
propoxyphene
meperidine (its metabolite) hypoxia (with OD of any opioid) |
|
|
What is the toxidrome of opioid toxicity?
|
hypoxia from CNS and respiratory depression
|
|
|
Which opioids have serotonergic properties?
|
meperidine
dextromethorphan |
|
|
Which opioids have may not produce miosis?
|
meperidine
propoxyphene lomotil pentazocin |
|
|
What cardiovascular problems can opioids cause?
|
hypotension (histamine release)
bradycardia propoxyphene may cause sodium channel blockade |
|
|
What is "cotton fever"?
|
A benign fever caused by cotton used to strain drug and remove particulates
|
|
|
What are signs of opioid withdrawal?
|
CNS excitation
tachypnea mydriasis |
|
|
Is opioid withdrawal life-threatening?
|
No
|
|
|
What commonly used opioid is missed on urine screens?
|
fentanyl
|
|
|
What can be done to hasten the passage of packets from body packers?
|
WBI
|
|
|
WHat route of administration cannot be used for naloxone?
|
PO
|
|
|
What is the duration of action of naloxone?
|
1-2 hours
|
|
|
What is the dose for a naloxone infusion?
|
2/3 the effective initial dose/hr
|
|
|
What agent is used for opioid withdrawal? How does it work?
|
Clonidine
(a central alpha agonist) It suppresses sympathetic hyperactivity |
|
|
How long should patients be observed if they receive naloxone?
|
2 hours
|
|
|
What is special about patients who have ingested and OD of lomotil?
|
They should be observed even if asymptomatic
|
|
|
What is the mechanism of action of barbiturates?
|
They enhance the activity of GABA and depress the activity of all excitable cells.
Barbituates have a separate binding site on GABA channels |
|
|
What are the effects of barbiturates?
|
Depressive effects
respiratory depression decreased pulse and BP |
|
|
How are barbiturates classified?
|
1) Ultra short acting (imm onset with IV)
2) Short acting (10-15 min onset) 3) intermediate acting (45-60 min onset 4) Long acting (onset 1hour) |
|
|
How can elimination of phenobarbital be enhanced? Can this be used with other barbiturates?
|
Alkalinization (this increases the amount of drug present in ionized form minimizing tubular absorption)
No, this cannot be used with other barbituates |
|
|
What are ultrashort acting barbiturates?
|
Methohexital
Thiopental |
|
|
What is the life threat in severe barbiturate toxicity?
|
respiratory depression
|
|
|
Is hypoventilation always apparent in barbiturate intoxication?
|
No, respirations can be shallow and rapid. Pulse oximetry or capnography will detect respiratory compromise
|
|
|
What are symptoms of barb withdrawal?
|
Tremors
Hallucination Seizures Delirium |
|
|
Do barb levels other than phenobarbital correlate with toxicity?
|
No, barbs have a high VD therefore serum levels do not accurately reflect CNS concentrations or correlate with clinical severity
|
|
|
What can occur to EEGs in the presence of barbs?
|
EEG may be silent as a result of barb OD therefore no patient should be declared brain dead if barbs are present in therapeutic levels
|
|
|
What GI decon can be considered in phenobarb OD?
|
MDAC 25g q 2hours
|
|
|
Why are BZD safer than other sedative hypnotics?
|
Cardiac effects and fatalities are rare
Respiratory depression is less pronounced than with barbs drug drug reactions are uncommon |
|
|
How do BZD work?
|
They enhance the inhibitory actions of GABA by binding to a BZD receptor. They decrease the ability of the nerve cell to initiate an action potential
|
|
|
Which BZDs have predictable IM absorption?
|
Lorazepam
Midazolam |
|
|
Which BZD have erratic IM absorption?
|
Diazepam
Chlordiazepoxide |
|
|
Where are BZD metabolized?
|
In the liver
|
|
|
Which BZDs have no active metabolites?
|
Oxazepam
Temazepam Lorazepam |
|
|
What are clinical features of BZD ingestion?
|
CNS depression
respiratory depression (large oral OD or IV admin) |
|
|
What is the most common sign of BZD toxicity?
|
ataxia
|
|
|
What is a contraindication to flumazenil
|
Any possibility of TCA OD
|
|
|
What complications can result from flumazenil?
|
Seizures
Cardiac Dysrhythmias |
|
|
When is flumazenil especially hazardous?
|
Pt habituated to BZD
When seizure-causing drugs (such as cocaine and TCA) have been ingested |
|
|
What are indications for flumazenil use?
|
Isolated BZD OD in non-habituated user (accidental paediatric exposure)
Reversal of conscious sedation |
|
|
Which patients are at risk of BZD withdrawal?
|
Continuous treatment for >4months
|
|
|
What is a potential date rape drug easily obtainable outside the US?
|
Flunitrazepam
|
|
|
What is buspirone?
|
A non-BZD agent used for generalized anxiety
|
|
|
Are zaleplon and zolpidem detected on urine drug screen?
|
no
|
|
|
Where do zolpidem and zaleplon act?
|
At a specific BZD receptor
|
|
|
What are the signs of chloral hydrate toxicity?
|
CNS and respiratory depression
Gastrointestinal irritation CV instability an dysrhythmia |
|
|
What is the treatment chloral hydrate induced ectopy?
|
propranolol
|
|
|
What are the only drugs found in non-prescription hypnotics?
|
Diphenhydramine
Doxylamine |
|
|
What is the most frequent finding with diphenhydramine OD?
|
Impaired consciousness
|
|
|
What may occur with severe diphenhydramine toxicity?
|
Seizures
Rhabdomyolysis |
|
|
What is a medical use for GHB
|
Narcolepsy
|
|
|
What is characteristic of GHB intox?
|
Periods of agitation alternating with periods of decreased LOC
|
|
|
In the absence of EtOH how long does it take for patients to awaken after GHB use? Otherwise, after what time interval should most patients with GHB ingestion awaken?
|
3-4 hours
8 hours |
|
|
Why should intubation be considered with GHB?
|
High incidence of emesis
|
|
|
Is there a withdrawal syndrome with GHB?
|
YEs
|
|
|
How is GHB withdrawal treated?
|
High dose BZD
Barbiturates (if severe) |
|
|
Is there delayed toxicity with GHB?
|
No
|
|
|
What are symptoms of GHB withdrawal?
|
Anxiety
Tremor Insomnia Delirium Autonomic instability |
|
|
What is the typical presentation of BZD OD?
|
Coma with normal vital signs
|
|
|
What is the starting dose of naloxone that should be given to a patient with opioid OD who is at risk of withdrawal?
|
0.04mg
|
|
|
In the context of caustic ingestion, which patients should not receive steroids?
|
Those at risk of mediastinitis
|
|
|
What are some of the subtle clinical signs that can help differentiate between beta blocker toxicity and CCB toxicity?
|
Beta Blockers are often associated with AMS, normal glucose (hypoglycaemia in children) and high degree AV blocks
CCB - normal mental status, hyperglycaemia (precent insulin release from the pancreas), complete AV block |
|
|
What is the clinical picture of clonidine OD?
|
Opioid toxidrome
|
|
|
Datura stramonium?
|
Jimson weed
anti-cholinergic |
|
|
What is an indication of severe snake envenomation?
|
metallic taste in the mouth
|
|
|
What are less commonly known sources of CO?
|
Banked blood
methylene chloride (converted to CO by CYP 2E1 in the liver) inhalational anesthetics |
|
|
Which metabolite of cocaine is atherogenic?
|
benzylechinine
|
|
|
Can you use a VBG for co-oximetry?
|
Yes
|
|
|
What are the lesions on CT scan most commonly found in CO poisoning?
|
bilateral lesions of the globus pallidus
|
|
|
What % of patients with ethylene glycol ingestion have calcium oxalate crystals in the urine?
|
50%
|
|
|
What is the classic shape of a calcium oxalate crystal?
|
Envelope but they can be any other shape i.e.. needles
|
|
|
What can result in a negative CO co-oximetry?
|
hydroxycobalamin
|
|
|
Which patients may have a negative reaction to methylene blue?
|
Those with G6PD deficiency
|
|
|
What is the treatment for sulfhemoglobin?
|
Remove the offending agent
x-change transfusion HBO? |
|
|
how do sulfonylureas work?
|
They close potassium channels on pancreatic cells and bring the cell to depolarization sooner
|
|
|
Which patients do not have large glycogen stores?
|
children
alcoholics cirrhotics |
|
|
Can you become hypoglycaemic while fasting on a sulfonylurea?
|
No, you should not become hypoglycaemic, if this happens you should check a creatinine because sulfonylureas are renal cleared.
|
|
|
What makes an animal poisonous?
|
If it has various toxins distributed in its tissues
|
|
|
What makes an animal venomous?
|
If it possess specific glands for producing venom connected to an apparatus for delivering that venom to another animal
|
|
|
What are life-threatening injuries related to venomous animals?
|
Venomous snake bites
Black widow spider bites Certain marine animal envenomations Anaphylactic reactions to insect stings |
|
|
What % of snakes species are venomous?
|
10-15%
|
|
|
Where do the majority of snake bites occur (anatomically)?
|
97% in the extremities
2/3 upper extremity 1/3 lower extremity |
|
|
What is the difference between a legitimate and an illegitimate snake bite?
|
legitimate - occurring accidentally
illegitimate - occurring when attempting to handle or disturb a snake |
|
|
What are the 5 venomous families of snakes?
|
colubriae
hydrophiidae elapidae viperidae crotalidae |
|
|
What snakes make up the crotalidae family?
|
pit vipers
|
|
|
What is the most prevalent snake in the US?
|
pit vipers (98% of all venomous snake bites)
|
|
|
What are the 3 main groups of pit vipers?
|
rattlesnakes
copperheads moccasins |
|
|
What snakes make up the elapidae family?
|
cobras
kraits mambas coral snakes |
|
|
What characterizes a coral snake?
|
The nose of the coral snake is black
The red and yellow bands are adjacent on the coral snake (they are separated by black on king snakes) |
|
|
What is a consistent way to identify pit vipers?
|
The presence of a heat sensitive pit midway between the eye and the nostril on both sides of the head
|
|
|
What are other characteristics used to identify venomous snakes?
|
-triangular shaped head
-the presence of an elliptic pupil -the arrangement of sub caudal plates -the tail structure -the presence of fangs |
|
|
What are the 2 venomous lizards?
|
the gila monster
the mexican beaded lizard |
|
|
What are the 2 predominant clinical responses to snake venom?
|
-neurotoxic
-hematotoxic |
|
|
in general which snake species venoms have predominantly systemic effects? local effects?
|
systemic - elapidae, hydrophiidae
local - colubridae, viperidae, crotalidae |
|
|
What is a dry bite?
|
A bite where no venom is injected
|
|
|
What systemic problems can be caused by envenomation?
|
DIC
pulmonary edema shock anaphylaxis |
|
|
How do pit viper envenomations cause death?
|
disruption of coagulation
increased capillary membrane permeability |
|
|
How do coral snakes cause death?
|
Compounds bock neuromuscular transmission at the ACh receptor causing direct inhibition on cardiac and skeletal muscle therefore death occurs by respiratory failure
|
|
|
What is the best first aid for a snakebite?
|
rapid transportation to a medical facility
|
|
|
What can be done to limit the spread of venom?
|
Calm the victim
immobilize the bitten area warp in an elastic bandage to collapse the lymphatics and superficial veins |
|
|
What is the only proven therapy for snake envenomation?
|
antivenin
|
|
|
What lab tests should be done in a snake bite?
|
cbc
coagulation profile fibrinogen fibrin split products SMA-7 type and crossmatch 4Units |
|
|
What is the grading of snake envenomation?
|
Grade O - IV
0 minimal no evidence of envenomation I - minimal envenomation II moderate envenomation III - severe envenomation IV - very severe envenomation |
|
|
Who is a candidate for antivenin?
|
Any victim of a venomous snake bite with moderate to severe envenomation
|
|
|
What precautions must be taken when administering antivenin?
|
prepare for possible anaphylaxis
|
|
|
What is fab AV
|
polyvalent antivenin less likely to produce allergic reactions
|
|
|
What is appropriate wound care for snake envenomations?
|
-cleansing
-immobilization -elevation at or above the heart -tetanus -constricting band |
|
|
How do arthropod fatalities mostly occur?
|
From an autopharmacologic response
|
|
|
What arthropods make up the hymenoptera family?
|
bees
wasps hornets yellow jackets ants |
|
|
In what time frame do most serious reactions to bee stings occur?
|
30 min
|
|
|
What are "killer bees"
|
More aggressive bees (they are not more)
|
|
|
What does a black widow spider look like?
|
Glossy black with bright red markings on the abdomen which may have an hourglass shape
|
|
|
How long should a patient receiving dpi be watched?
|
24hours
|
|
|
What ingredient of the black widow venom is most dangerous
|
neurotoxin
|
|
|
What are the clinical features of BW spider bite?
|
pinprick sensation with local swelling and redness
crampy pain especially in the chest or abdomen which may last several hours to days |
|
|
What is the management of BW spider bites?
|
Ice pack
transport to hospital cleanse wound tetanus symptomatic treatment with diazepam and analgesia consider antivenin especially in paediatric, pregnant and elderly The antivenin is derived from horse serum |
|
|
What is the most distinctive feature of the brown recluse spider?
|
Violin shaped area on the cephalothorax
|
|
|
What are the most concerning effects of brown recluse spider bites?
|
local tissue destruction
|
|
|
What is the most common mimic of loxosceles (brown recluse spider)?
|
MRSA skin infection
|
|
|
What species of scorpions is dangerous?
|
centuroides
|
|
|
What is the predominant characteristic of centuroides toxin?
|
neurotoxin
|
|
|
Is there scorpion antivenin?
|
yes
|
|
|
What should you think of in a patient presenting with ascending paralysis?
|
Tick paralysis
|
|
|
What is the most toxic (coelenterate) jelly fish?
|
box jelly fish
|
|
|
Which venomous snake bites should be treated empirically if there is a safe anti venom?
|
elapidae (because the venom is neurotoxic)
|
|
|
What type of decon should be done for theophylline
|
AC - it acts as gut dialysis by drawing drug out of the plasma
|
|
|
What is the treatment for a hypotensive patient with theophylline OD?
|
B blocker why?
|
|
|
What toxicity presents with "snowfield vision"?
|
Formic acid
|
|
|
What does 50% ethylene glycol mean
|
50g/100mL
|
|
|
What is the simplified mnemonic for AG metabolic acidosis
|
K - ketones
U - uremia L - lactate T - toxins S - salicylate |
|
|
How are organophosphates absorbed?
|
Derma, GI, Respiratory
|
|
|
How do organophosphates work?
|
They inhibit the enzyme acetylcholinesterase which results in accumulation and prolonged effect of acetylcholine
|
|
|
What is the classical syndrome of muscarinic acetylcholinesterase inhibition
|
Salivation
Lacrimation Urination Defectaion GI cramps Emesis |
|
|
What happens at the neuromuscular junction with excess acetylcholine?
|
Hyperstimulation of the muscles with secondary paralysis, the diaphragm becomes affected and respiratory arrest ensues
|
|
|
What is the timeline of organophosphate poisoning?
|
May be acute or chronic
|
|
|
What are mechanisms for early morbidity and mortality in acetylcholinesterase inhibitor poisoning?
|
Seizures
Pulmonary hypersecretion/bronchorrhea Bronchospasm |
|
|
What is the ultimate cause of morbidity and mortality in AChE Inhibition?
|
Skeletal muscle hyperactivation and subsequent paralysis from nicotinic hyperstimulation
|
|
|
What is "aging"?
|
The irreversible conformational change that occurs when an organophosphorus agent is bound to the cholinesterase enzyme for a prolonged time
|
|
|
On average, how long does aging take?
|
48 hours
|
|
|
How is exposure to cholinesterase inhibitors confirmed?
|
Plasma and erythrocyte cholinesterase levels.
|
|
|
What are the goals in management of AChI tox?
|
Decontamination
Supportive Care Reversal of ACh excess at muscarinic sites reversal of toxin binding on cholinesterase molecule |
|
|
What protective clothing should be used by HCP in organophosphorus poisoning?
|
Universal precautions
Nitrile or butyl rubber gloves eye shields protective clothing |
|
|
Which agent should be used for neuro muscarinic blockade in RSI?
|
Rocuronium (succinylcholine may have a prolonged duration)
|
|
|
Why do we treat with atropine?
|
It reverses the clinical effects of cholinergic excess at parasympathetic end organs and sweat glands
|
|
|
What is the endpoint for atropine administration?
|
Control of mucous membrane hyper secretion
Clear airways |
|
|
What do oximes do?
|
They restore cholinesterase activity
|
|
|
What are indications for oxime therapy?
|
Respiratory depression/apnea
Fasciculation Seizures Arrhythmias CV instability Large amounts of atropine (> 2-4mg atropine) |
|
|
What is the treatment for agitation, seizures, coma?
|
BZD after the airway has been secured
|
|
|
What are differences between nerve agents and organophosphates?
|
The nerve agents tend to age very quickly therefore reversal is very time sensitive. These agents do not require large doses of atropine but do require pralidoxime
|
|
|
What is IMS?
|
Intermediate syndrome that consists of proximal muscle and respiratory muscle weakness.
|
|
|
How are carbamates different from organophosphates?
|
-Much shorter duration
-carbamate-cholinesterase binding is reversible |
|
|
Should oximes be used in the management of carbamate toxicity?
|
If unsure, you should use it
|
|
|
What are chlorinated hydrocarbons used for?
|
DDT - insecticides
Lindane - scabies |
|
|
What are the predominant symptoms of chlorinated hydrocarbon pesticides?
|
Neurotoxicity - tremor, parethesia, seizure
Vent dysrhythmias (halogenated) |
|
|
How should seizures be controlled in chlorinated hydrocarbon exposure?
|
BZD or barbs
|
|
|
What are substituted phenols?
|
insecticides
termiticides wood preservative weight reduction agents |
|
|
How do substituted phenols work?
|
they uncouple oxidative phosphorylation
|
|
|
How do patients with phenol toxicity present?
|
Hypermetabolic
Hyperthermic hypovolemic renal and hepatic injury rhadomyolysis yellow staining of skin at the site of absorption |
|
|
What is agent orange?
|
chlorphenoxy pesticide used during the Vietnam war
|
|
|
What is the target organ of chlorphenoxy poisoning?
|
The skeletal muscle
|
|
|
What is specific about paraquat and diquat?
|
They are extremely corrosive and patients may die of esophageal perforation prior to developing the characteristic pulmonary injury
|
|
|
What is the classic finding in paraquat?
|
progressive pulmonary injury over 1-3 weeks
|
|
|
What is the key to successful treatment of acute paraquat exposure?
|
Early decontamination
Consider gastric lavage or AC Charcoal hemoperfusion vs HD and HP |
|
|
What are pyrethrins?
|
Naturally occurring insecticides of the yellow chrysanthemum
|
|
|
What is the most likely route of exposure with pyrethrins?
|
inhalation
|
|
|
What are clinical manifestations of pyrethrins?
|
Allergic manifestations
Local irritation Sodium channel and GABA mediated chloride channel effects -> neurologic signs and symptoms |
|
|
What are the clinical effects of DEET?
|
Contact dermatitis -> skin blisters (chronic LFT and neuro abnormalities)
|
|
|
How does capsaicin work?
|
Depletes nerve terminals of substance P causing a local inflammatory response, swelling, exudation and pain
|
|
|
Where do most capsaicin exposures occur?
|
pepper spray
causing chemical conjunctivitis +/- keratitis (rarely inhalation causes pulmonary edema and possibly ARDS) |
|
|
What is the treatment for pepper spray?
|
irrigation (eyes) and analgesics
|
|
|
What is one of the most commonly reported plant fatalities in the US?
|
water hemolck
|
|
|
What properties does datura stramonium have?
|
anticholinergic
jimson weed |
|
|
In what population do most plant exposures occur?
|
children<6years
|
|
|
What can occur if capsaicin is inhaled?
|
Severe pulmonary exudation and ARDS
|
|
|
What can occur if capsaicin is inhaled?
|
severe pulmonary exudation and ARDS
|
|
|
What is the most common manifestation of diffenbachia ingestion?
|
inability to talk because of severe pain and swelling and sensation of biting glass, this is due to calcium oxalate crystals found in idioblasts
|
|
|
Are poinsettias poisonous?
|
ingestions are benign/minimally toxic but contact dermatitis is very common
|
|
|
What toxins does oleander contain?
|
cardiac glycosides
|
|
|
Is the digoxin level reliable in oleander exposure?
|
Qualitatively it is valuable but there may be variable cross reactivity therefore you cannot use a level to rule it out
|
|
|
What is the treatment for oleander ingestion?
|
MDAC
digi FAB -> usually larger doses are needed than in digoxin poisoning |
|
|
What are 4 major types of problems associated with herbal product use?
|
-misidentification of an herbal plant and toxicity resulting from the substituted plant
-contamination with non-herbal toxic material -direct toxicity or OD of herbal products -drug-herbal interaction |
|
|
What are the most common undeclared pharmaceuticals in herbal products?
|
-ephedrine
-chlorpheniramine -methytestosterone -phenacetin |
|
|
Under what circumstances do mushroom exposures occur?
|
-Accidental ingestion by found children playing outdoors
-mistaken selection of poisonous mushroom while foraging for edible wild mushrooms -abuse of certain mushrooms for their mind altering potential |
|
|
which mushroom species is responsible for most deaths?
|
amanita
|
|
|
What is the onset of symptoms from mushrooms that have serious toxicity and potential for death?
|
>6hours post ingestion
|
|
|
Which mushroom groups are associated with CNS effects?
|
Ibotenic acid/muscimol (related to glutamic acid and GABA)
-psilocybin (related to LSD) |
|
|
What is the treatment for cholinergic syndrome from a mushroom?
|
atropine
no role for 2PAM |
|
|
What is the hallmark of coprine mushroom group ingestion?
|
disulfiram type reaction with EtOH
|
|
|
What groups of mushrooms cause late onset symptoms?
|
cyclopeptide
gyromitrin orelline |
|
|
What is the clinical presentation of cyclopeptide (amanita phylloides)
|
-6-24 GI symptoms
-hepatic toxicity followed by other end organ involvement over days-weeks |
|
|
What are useful treatment for amanita poisoning?
|
MDAC
|
|
|
What are the effects of ingestion of gyromitra mushrooms?
|
excitatory CNS effects - HA, agitation, seizures
|
|
|
What is a possible therapy for gyromitrin ingestion?
|
pyridoxine
|
|
|
What is the toxicity associated with orelline?
|
renal toxicity which can progress to CRF
|
|
|
What type of dcon should be done for theophylline?
|
AC - it acts as gut dialysis by drawing drug out of the plasma
|
|
|
What is the treatment for a hypotensive patient with theophylline OD?
|
Beta blocker
|
|
|
What toxicity presents with "snowfield vision"
|
Formic acid
|
|
|
What does 50% ethylene glycol mean?
|
50g/100mL
|
|
|
What is the simplified mnemonic for AG metabolic acidosis?
|
K - ketones
U - uremia L - lactate T - toxins S - salicylates |
|
|
Why may patients with a wide anion gap metabolic acidosis from toxic alcohols not have an osmolar gap?
|
Only parent compounds are osmotically active, toxic metabolites (which cause a wide AG) are charged so they are accounted for by the calculation. Therefore once the patient has a wide AG they are so far along in the poisoning that they don't have an osmotic gap anymore
|
|
|
What are features of valproid acid OD?
|
hypernatremia
hypocalcemia metabolic acidosis hypocarnitemia hyperammonemia |
|
|
What drugs may cause renal tubular acidosis?
(A hypercholoremic non-AG metabolic acidosis) |
topiramate
toluene |
|
|
What mechanisms result in seizures?
|
Na+ channels
Ca++ channels glutamate excess GABA depletion |
|
|
What is K2/spice?
|
a synthetic cannabinoid
|
|
|
What are bath salts? What are prominent features of bath salt ingestion?
|
synthetic amphetamines
psychotic halluciations |
|
|
What are the effects of synthetic cannabinoids?
|
sympathomimetic and THC
|
|
|
What is alcoholic hallucinosis?
|
Visual hallucinations with a clear sensorium not DTs (which have AMS as a prominent feature)
|
|
|
HOw can you determine if an alcohol withdrawal tremor is real?
|
Hand and tongue tremor simultaneously
|
|
|
WHy can symptoms of dissociated ingestion resemble other toxidromes?
|
At higher concentrations these agents bind other agents therefore they may have effects that are anticholinergic, sympathomimetic or opioid
|
|
|
Which patients are at risk of respiratory depression from BZD?
|
Elderly
very young those with OSA |
|
|
What is a reasonable initial dose of flumazenil?
|
0.05-0.1mg followed by titration (0.5mg/vial)
|
|
|
What is the preferred BZD for cocaine?
|
midazolam (quick on/quick off)
|
|
|
What is the preferred BZD for alcohol?
|
longer onset of action but longer CNS duration
|
|
|
How do you calculate the drip rate of naloxone?
|
2/3 the dose that arouses x 10 injected into a 1L bag of NS, run at 100cc/hr
|
|
|
When is flumazenil indicated?
|
Acute BZD OD in a patient known not to be a BZD user
|
|
|
in what patients does flumazenil carry a risk of seizures?
|
-chronic BZD user
-patient who ingests TCA |
|
|
Which opioid agonists may not produce characteristic miosis?
|
-propoxyphene
-pentazocine |
|
|
What should be done in critical patients suspected of body stuffing or packing?
|
rectal
vaginal abdo radiograph |
|
|
Under what circumstances are bowel sounds increased or decreased?
|
ingestion of agents affecting the cholinergic nervous system
|
|
|
What are the signs of anticholinergic CNS poisoning?
|
mild temperature elevation
acute delirium mumbling speech "picking movements" of the fingers |
|
|
What is a good way to distinguish between anticholinergic and sympathomimetic OD?
|
anticholinergic - dry, flushed skin
sympathomimetic - diaphoresis |
|
|
Which agent should be used for opioid OD of agent with long half life (methadone)?
|
nalmefene
|
|
|
Which drugs may cause serotonin syndrome in interactions with others?
|
SSRI
SRI MAOI tryptophans sympathomimetics dextromethorphan lithium |
|
|
What are the features of serotonin syndrome?
|
AMS
Temperature agitation tremor myoclonus increased reflexes ataxia diaphoresis shivering diarrhea |
|
|
Why is tox screen not useful?
|
-lab doesn't screen for many things
-if too soon, drug concentration may be too low in the urine -drugs found may not be responsible for the symptoms |
|
|
What toxins may cause non-cardiogenic pulmonary edema?
|
salicylates
opioids |
|
|
When should AC be considered?
|
-<1hr post ingestion
-type/amt of medication that are truly toxic beyond required for supportive care (BB, CCB, TCA) |
|
|
What agents do not adsorb to charcoal?
|
ions (acid, alkali, Li, borate, bromide)
hydrocarbon metals ETOH |
|
|
When may WBI be useful?
|
-recent ingestion of lithium, iron, lead
-sustained release formulation of highly toxic agents -body packers |
|
|
How is gastric lavage performed?
|
place 30F or greater OG
lavage with large bore tube |
|
|
What causes the majority of dermal injuries after chemical exposures?
|
Direct damage to the skin (as opposed to hyperthermic injury)
|
|
|
Describe the pathophysiology of acid injuries?
|
Acid injuries produce protein denaturation, coagulation necrosis and eschar formation which limits the extent of injury
|
|
|
By what mechanism does alkali produce injury?
|
Saponification and liquefactive necrosis
|
|
|
What is a hazardous material (HAZ-MAT)?
|
A substance that can cause physical injury or environmental damage if not handled properly
|
|
|
What are the two components of a contingency plan for HAZMAT situations?
|
Initiation of site plan
Evacuation |
|
|
How are individuals decontaminated in a HAZMAT incident?
|
Remove clothing
Brush off any powder Irrigate with copious amounts of H20 Collect H20 |
|
|
What are the minimum requirements for personal protective equipment in HAZMAT situations?
|
Chemical resistant clothing with hood
eye protection 2 pairs of gloves Boots Some form of respiratory protection |
|
|
What are priorities in decontamination?
|
Contaminated wounds, then eyes, then mucous membranes, then skin, then hair
|
|
|
How is hydrotherapy done?
|
Large amount
Low pressure Prolonged time |
|
|
Should high pressure irrigation be used?
|
No, it can drive chemicals into skin or splatter into the eyes
|
|
|
What are adjuncts for decontamination of elemental metals and phenols?
|
Elemental metals -> mineral oil
Phenols -> polyethylene glycol |
|
|
How long does hydrotherapy have to be continued to normalize pH in acid/alkali burns?
|
alkali - up to 12 hours
acid - up to 2 hours |
|
|
How are ocular burns classified?
|
Grade I-IV
|
|
|
How long should ocular irrigation continue?
|
Until ocular pH is 7.4, but for severe burns prolonged irrigation is needed regardless of a normal ocular pH
|
|
|
Where is hydrofluoric acid used?
|
Petroleum industry
Glass etching Removing rust Cleaning cement and bricks |
|
|
What part of HF results in the most damage?
|
The free fluoride ion which scavenges cations such as Ca++ and Mg++ resulting in hypocalcemia and hypomagnesemia, also inhibits Na+/K+/ATPase
|
|
|
What are the types of HF exposure?
|
-inhalation (often industrial)
-dermal -ocular |
|
|
What distinct characteristic does HF skin burn have?
|
The exposure causes progressive tissue destruction (over days)
|
|
|
What is the treatment for HF exposure?
|
-immediate irrigation
-if still severe pain then requires detox with Calcium salt formation -remove blisters -3.5g calcium gluconate in 150cc K-Y jelly -deep painful burns require infiltrative therapy 0.5cc/cm2 of 10% calcium gluconate -intraarterial catheter - 10xc of 10% calcium gluconate in 40-50cc of saline |
|
|
What are systemic manifestations of fluoride toxicity?
|
Similar to hypocalcemia
-abdo pain -muscle fasciculations -nausea -seizures -dysrhythmia |
|
|
How do you treat hypocalcemia secondary to HF toxicity?
|
IV 10% calcium gluconate
|
|
|
What are signs of systemic toxicity from formic acid?
|
Acidosis
Hemolysis Hemoglobinuria |
|
|
What has prompted an increase in anhydrous ammonia exposures?
|
Its use in methamphetamine production
|
|
|
What are the mechanisms of injury with anhydrous ammonia?
|
-freezes tissues
-chemical burns by liquefaction necrosis |
|
|
What happens with inhalational injury due to anhydrous ammonia?
|
Proximal airway injury
|
|
|
What is the pH of cement?
|
10-14
|
|
|
What is the treatment for cement burn?
|
Hydrotherapy
(excision and grafting are usually necessary) |
|
|
Where are phenols used?
|
agriculture
cosmetic medical fields |
|
|
What are signs of systemic phenol toxicity?
|
CNS - stimulation, lethargy, seizures
CVS - conduction disturbances |
|
|
What is the most effective treatment to reduce the severity of phenol burns?
|
Polyethylene glycol
|
|
|
How can white phosphorus be identified on the skin?
|
UV light or copper sulfate solution
|
|
|
What is methemoglobin?
|
When the ferrous ion (Fe2+) becomes oxidized to ferric (Fe3+)
|
|
|
How is methemoglobinemia treatment?
|
Asymptomatic -> remove offending agent
Symptomatic 2cc/kg 1% methylene blue over 3-5 minutes or exchange transfusion |
|
|
How long should you monitor a patient who has ingested hydrocarbons?
|
6 hours
if no symptoms and normal CXR may d/c home |
|
|
What should be done immediately with hot tar exposure?
|
cool with cold H20
|
|
|
Why does tar adhere to the skin?
|
because it is enmeshed in the hair
|
|
|
What happens when elemental metals (Li+, Na+, K+) come into contact with H20?
|
a violent exothermic reaction producing heat, H2 gas and OH
|
|
|
What should be done with known elemental exposure?
|
No H20 lavage
Cover metal with mineral oil |
|
|
Descrive the ED response to a chemical attack?
|
-triage outside the ED
-decon outside the ED -PPE: full face respirator mask, self-contained breathing apparatus, impermeable suits |
|
|
How are chemical attack agents classified?
|
-nerve agents
-vesicants -choking agents -cyanide |
|
|
What are vesicants?
|
A class of drug that produces blisters at the site of contact
|
|
|
What are examples of vesicants?
|
Mustard gas
Lewisite Phosgene |
|
|
What are choking agents?
|
Chemicals that induce the sensation of choking and can produce upper airway damage and pulmonary edema
|
|
|
What are examples of choking agents?
|
Phosgene
Chlorine Zinc containing smoke |
|
|
How do nerve agents work?
|
Prevent acetylcholinesterase from hydrolyzing ACh
|
|
|
What are symptoms of muscarinic excess?
|
Diarrhea
Urination Miosis Bronchorrhea Emesis Lacrimation Salivation |
|
|
What are manifestations of nicotinic excess?
|
Muscle fasciculations
Weakness |
|
|
WHy should succinylcholine be used with caution in nerve agent exposures?
|
Its duration of action will be significantly prolonged
|
|
|
What is the endpoint for atropine administration in nerve agent exposure?
|
Drying of bronchial secretions
|
|
|
What is given to treat seizures in nerve agent exposure?
|
BZD
|
|
|
What are the unique features of mustard gas?
|
Garlic or fishlike odor
does not cause pain immediately |
|
|
What is the management of vesicant injury?
|
Remove from environment
Decon with H2) or 0.5% hypochlorite solution |
|
|
How does cyanide work?
|
Binds and inactivates cytochrome oxidase part of cytochrome a3 on the electron transport chain
|
|
|
How does the Rumack-Matthew Nomogram work?
|
APAP concentrations must be measured between 4 and 24 hours after ingestion and plotted on the nomogram. Patients with APAP concentrations on or above the treatment line should be treated.
|
|
|
How do you evaluate ingestions of extended-release APAP preparations?
|
Peak plasma APAP occurs within 4 hours although some absorption can continue for up to 8 hours.
-use nomogram at 4 hours -then get a 2nd level 4 hours after the 1st one and treat if above the nomogram line |
|
|
What is the IV NAC protocol?
|
150mg/kg over 60min
50mg/kg over 4 hours 100mg/kg over 16hours One hour after the protocol is complete, recheck the LFTs and APAP. If APAP is >66umol/L or LFTs elevated restart the NAC at 100mg/kg |
|
|
What are side effects of PO and IV NAC?
|
PO - vomiting
IV - mild anaphylactoid reaction (rash, flushing, pruritus) (2-18%) Severe anaphylactoid reaction <1% |
|
|
What is the elimination of ASA?
|
Salicylate can be metabolized in the liver, however in overdose, hepatic metabolism becomes saturated and renal elimination of free salicylate becomes more important.
|
|
|
Describe the acid-base disturbance in ASA intox
|
-initial respiratory alkalosis (direct stimulation of the medulla)
-increased anion gap metabolic acidosis (interference with Krebs cycle, uncoupled oxidative phosphorylation, increased energy demand) -mixed respiratory alkalosis and metabolic acidosis -respiratory acidosis occurs when the patient becomes fatigued, suffers salicylate induced acute lung injury or blunted respiration due to co-ingestant) This is a poor prognostic marker and a preterminal event |
|
|
What electrolyte disturbances are seen in ASA intox?
|
Hypokalemia
Hyponatremia Low bicarb (increased renal excretion of Na and HCO3 to compensate for the respiratory alkalosis) |
|
|
What are the various degrees of salicylate toxicity?
|
Asymptomatic: occasional subjective but no objective manifestations
Mild: mild to moderate hyperpnea, tinnitus, sometimes lethargy Moderate: severe hyperpnea, prominent neuro disturbance Severe: severe hyperpnea, coma or semi coma, sometimes with convulsions |
|
|
What are sources of salicylate exposure other than ASA?
|
Methyl salicylate: oil of wintergreen, tiger balm
Acetyl salicylate: Percodan, fiorinal, peptobismol |
|
|
Describe chronic ASA intox
|
Primarily occurs in the elderly
insidious onset significant illness with low serum salicylate concentration Mortality = 25% |
|
|
What are the goals of urine alkalinization?
|
Serum pH 7.45-7.55
urine pH 7.5-9.0 |
|
|
Which drugs exhibit primarily anticholinergic toxicity
|
Belladonna alkaloids (atropine, scopolamine, cyclopentolate, topicamide)
Antiparkinsonians (benztropine, trihexylphenidyl, procyclidine) Prototypical H1 receptor blockers (diphenhydramine, chlorpheniramine, brompheniramine) Phenothiazines - promethazine |
|
|
What are the potential ECG findings in anticholinergic poisoning?
|
sinus tachycardia
|
|
|
What is the indication for physostigmine?
|
Severe, refractory pure anticholinergic intoxication
|
|
|
What is the toxic differential diagnosis of delirium?
|
Steroids
lithium Salicylates Anticholinergic Sympathomimetics PCP Mushrooms containing muscimol/ibotenic acid MOA solvents CO Sedative hypnotic withdrawal |
|
|
What specific presentation is associated with overdose of bupropion?
|
seizures
|
|
|
What specific presentation is associated with overdose of trazodone?
|
priapism
|
|
|
What medications are contraindicated in TCA overdose?
|
Physostigmine
Class Ia antidysrhythmics (quinidine, procainamide) Class Ic antidysrhythmics (flecanide, propafenone) Phenytoin |
|
|
what are the Hunter criteria for serotonin toxicity
|
1. Serotonin agent administered in the past 5 weeks
Any of the following -tremor and hyperreflexia -spontaneous clonus -muscle rigidity, temp >38, ocular or inducible clonus -ocular clonus and aggitation or diaphoresis -inducible clonus and aggitation or diaphoresis |
|
|
What are drugs associated with serotonin toxicity
|
Amphetamines
Cocaine Dextromethorphan Citalopram fluoxetine L-tryptophan sumatriptan |
|
|
What is the treatment for NMS?
|
Bromocriptine
|
|
|
List foods and beverages associated with MAOI toxicity
|
Aged meats
fava beans avocados ginseng chocolate figs ales beers wine sherry |
|
|
What is the digoxin effect?
|
Scooped ST segments
Prolonged PR |
|
|
What are specific dysrhythmias associated with digitalis toxicity
|
Atrial fibrillation with slow ventricular rate
nonparoxysmal junctional tachycardia atrial tachycardia with block bidirectional vtach |
|
|
What ar indications for administration of digiFab in adults?
|
Ventricular dysrhythmia
Symptomatic bradydysrhythmia unresponsive to atropine K+>5mEq/L Rapidly progressive rhythm disturbances or rising serum potassium co-ingestion of other cardiotoxic drugs ingestion of plant containing cardiac glycoside plus severe dysrhythmia acute ingestion >10mg plus any of above factors steady state >6ng/mL plus any of the above factors |
|
|
What are the indications for administration of digiFab in children?
|
-ingestion of 0.1-0.3mg/kg or steady state >5ng/mL plus rapidly progressive symptoms, potentially life-threatening dysrhythmias, conduction blocks or K+>6
-co-ingestion of cardiotoxic drugs -ingestion of plant containing cardiac glycosides plus severe dysrhythmia |
|
|
What is the distribution and function of different beta receptors?
|
B1
heart - increase HR, contractility and conduction velocity eye - stimulate aqueous humor production kidney - stimulate plasma renin secretion B2 smooth muscle - relaxation of bronchi, BV, intestine, uterus skeletal muscle - glycogenolysis liver - glycogenolysis heart B3 adipose tissue - lipolysis |
|
|
What is a caustic substance?
|
A substance that causes both clinical and histologic damage on contact with tissue surfaces.
|
|
|
What are indications for endoscopy in caustic ingestions?
|
Indicated in all patients with intentional ingestions
patients with unintentional ingestions with stridor, pain, vomiting and/or drooling |
|
|
What is crack dancing?
|
Transient choreoathetoid movement disorder after using cocaine
|
|
|
Why should haldol be avoided in a cocaine-intoxicated patient?
|
Haldol can limit cooling by impeding diaphoresis
Haldol may increase morbidity May have associated dysrhythmic effects that can be additive or even synergistic with cocaine |
|
|
What are admission criteria for cocaine related chest pain
|
persistent chest pain
ECG changes elevated enzymes dysrhythmias CHF/cardiogenic shock preexisting CAD multiple risk factors for CAD patient requires vasodilation |
|
|
What are indications for fomepizole (or EtOH)?
|
strong history or witnessed ingestion of ethylene glycol or methanol containing products
methanol concentration >/=6mmol/L or ethylene glycol >/=3mmol/L large osmol gap with suspicion of a toxic alcohol ingestion significant unexplained anion gap acidosis |
|
|
What are the benefits of fomepizole over ethanol?
|
No increased risk of CNS depression
No risk of respiratory depression from EtOH No absolute ICU admission Decreased risk of electrolyte imbalance Avoid EtOh induced hypoglycaemia No need for serial etOH measurements NO risk of subtherapeutic concentrations |
|
|
What are the different types of hallucinogens?
|
Serotonin like agents
LSD Tryptamines (psilocybin) Enactogens Designer amphetamines (MDMA, ecstasy) Mescaline Nutmeg Dissociative agents PCP Ketamine Dextromethorphan Plants Marijuana Salvia Absinthe Isoxazole mushrooms |
|
|
What is the mechanism of action of MDMA?
|
Release of 5-HT, DA, NE and inhibition of catecholamine reuptake
|
|
|
What are complications associated with MDMA?
|
Hypovolemia
Hyponatremia Rhabdomyolysis Renal Failure Hyperthermia Serotonin syndrome Dysrhythmias Seizures Hypertensive crisis in patients taking MAOI |
|
|
What is dextromethorphan?
|
-Similar in structure to PCP and opioids
-found in OTC antitussive preparations -clinical effects increased HR, increased BP, diaphoresis, euphoria, dysphoria, dissociative phenomenon, slurred speech, ataxia, rotary nystagmus |
|
|
What is the pathophysiology of iron toxicity?
|
GI toxicity
-direct irritant and corrosive effect on GI mucosa -N/V/diarrhea/GI bleeding Cardiovascular -potent vasodilator -negative inotrope -direct myocardial toxicity Metabolic acidosis -uncoupling of oxidative phosphorylation -disruption of the electron transport chain -free radical production |
|
|
How do you calculate the elemental iron load?
|
(#tabs) x (mg of iron salt/tab) x (%elemental iron)
|
|
|
What is the side effect of deferoxamine?
|
hypotension which is rate dependent
|
|
|
What are sources of mercury?
|
Elemental
Spill from mercury containing devices inhalational exposure deliberate injection or ingestions accidental ingestion Salts accidental disc battery ingestion deliberate ingestion laxative abuse Organic oral/dermal exposure to thimerosal occupational/agricultural accidents water/soil pollution contaminated seafood consumption paint |
|
|
What is the pathophysiology of mercury toxicity?
|
binds sulhydryl groups and inhibits multiple enzymes
|
|
|
Differentiate huffing and bagging?
|
Huffing: inhaling HCs through a saturated cloth
Bagging: pouring HCS in a bag and then inhaling them deeply |
|
|
What are the 4 mechanisms of inhaled toxins?
|
Pulmonary irritant - alter air lung interface by irritation or inflammation
simple asphyxiant - gas that displaces O2 and lowers FiO2 chemical asphyxiant - inhibits oxidative metabolism Poor Hb-O2 carrying capacity (CO) |
|
|
What are simple asphyxiant gases?
|
carbon dioxide
methane nitrogen nitrous oxide helium |
|
|
What are examples of highly water soluble gases
|
ammonia
chlorine hydrogen chloride hydrogen fluoride |
|
|
What are 6 sources of cyanide
|
-ingestion of cyanide salts as suicide or homicide
-smoke inhalation during fires -occupational exposure -medicinal sources (nitroprusside) -foot sources (plant pits) -cyanogenic chemicals (nitriles) |
|
|
Hoe does cyanide inhibit oxidative phosphorylation?
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It binds to complex IV of the electron transport chain within the mitochondria
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What is the dose of hydroxycobalamin?
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5g IV
70mg/kg in children |
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What are RF for cyanide toxicity in patients receiving nitroprusside?
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short term High dose therapy
long term therapy renal failure failure to protect the nitroprusside bottle from light (light increases the release of cyanide molecules) |
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What are potential sources of carbon monoxide?
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structure fires
clogged vents for home heating units gasoline powered generators indoors |
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What is the pathophysiology of CO intoxication?
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CO binds Hb ~250times greater affinity than oxygen
CO shifts the oxyhemoglobin dissociation curve to the left (decreased offloading of O2) CO binds to cytochrome oxidase in the mitochondria CO binds to myoglobin in muscles CO induces lipid peroxidation in the CNS |
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What are the fetal and neonatal concerns in CO intoxication?
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Fetal Hb has a greater affinity for CO than adult hemoglobin
Fetal COHb levels are 10-155 greater than the mother's |
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Why can patients be severely toxic with lithium levels in the therapeutic rance?
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because toxicity does not develop until lithium distributes into the cells
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How does acute on chronic lithium toxicity present?
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clinical presentation of both acute and chronic intoxication
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What are predisposing factors for chronic lithium toxicity?
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Dehydration
Hyponatremia thermal stress renal failure Drug interactions (NSAID, ACE, ARB, diuretics, metronidazole, carbemazepine, antipsychotics, SSRI) |
