Inhalants, Gases, Weapons of Mass Destruction, Pesticides and Insecticides Flashcards
Which of the following is consistent with cyanide toxicity?
A) Lowered central venous oxygen saturation
B) Normal gap metabolic acidosis
C) Hypoglycemia
D) Hypophosphatemia
E) Elevated lactate level
Answer E. Cyanide results in anion gap metabolic acidosis and an increase in lactate concentrations. In fact, high lactate levels are suspicious of cyanide toxicity (>10 and refractory to resuscitation)
Cyanide Mechanism of action:
despite adequate oxygen, ATP cannot be formed which results in cellular hypoxia
Cyanide Sources
laetrile, cassava root, amygdalin, silver/gold extraction, products of combustion, acetonitrile (artificial nail remover)
Cyanide symptoms
headache, N/V, HTN hypotension, tachypnea bradypnea, altered LOC, collapse, seizures, cyanosis only occurs in late stages from shock – usually before death
Cyanide Treatment
nitrites/nitrates to purposely induce methemoglobinemia, hydroxocobalamin
Which statement about carbon monoxide (CO) toxicity is true?
A) Peak maternal COHgb (carboxyhemoglobin) exceeds peak fetal COHgb
B) Lower fetal PO2 diminishes adverse effects of fetal COHgb
C) Therapy with 100% oxygen may be discontinued when maternal COHgb returns to a normal level
D) Hyperbaric oxygen (HBO) should be administered for a period of time equal to twice the standard length of treatment
E) Fetal toxicity is generally greater than maternal toxicity
Answer E. CO toxicity may lead to adverse fetal effects even when maternal toxicity is inconsequential. Peak fetal COHgb generally exceeds maternal concentration and peaks at a later time. For this reason, it is recommended that oxygen be continued for a period of time 5 times as long as it takes to lower the maternal concentration to normal. Lower fetal PO2 and the greater affinity of fetal hemoglobin to CO exacerbates the effects of CO exposure. HBO should be considered in all cases of CO toxicity but is not necessarily for a longer time.
Carbon Monoxide Sources
products of combustion, propane powered vehicles (Zamboni, tractor exhaust, forklifts), gas stoves, kerosene heaters, indoor hibachi use (with poor ventilation), gas powered dryers and hot water heaters
Halogenated hydrocarbons metabolized into CO methylene chloride (varnish removers) and inhalational anesthetics (enflurane, desflurane, isoflurane)
Carbon Monoxide Mechanism of action:
CO binds with affinity to hgb of 250 times greater than oxygen; since CO cannot carry oxygen tissue hypoxia occurs. Also there is a shift to the left on the oxygen dissociation curve (shift to the Left means you hoLd onto your oxygen and don’t release it to the starved tissues).
CO also induces delayed lipid perioxidation in the CNS causing delayed neurological sequela (most commonly associated with loss of consciousness)
Cherry red color of the skin only occurs in 2-3% of patients
Carbon Monoxide Fetal Compromise
- Fetal Hgb has a higher affinity for CO than for maternal Hgb
- Maternal Hgb there fore does not reflect the degree of poisoning in the fetus
- Fetal demise and stillbirths may occur at low maternal COHgb levels
Carbon Monoxide CO half life
Room air ~ 4-6 hrs
on high flow oxygen ~ 40-90 mins
with HBO ~12-20 mins
Carbon Monoxide Indications for HBO
SMaLl Chest Pain:
Syncope Metabolic acidosis Level >25% Chest pain or EKG changes Pregnancy with > 15%
Which is the most significant difference between organophosphate (OP) and carbamate agents?
A) OP are more likely to lead to paralysis in acute toxicity
B) OP do not cross the blood-brain barrier
C) OP can undergo aging when bound to acetylcholinesterase
D) OP require metabolism by mixed function oxidases to become active
E) OP do no lead to dysrhythmias in acute toxicity
Answer C. OP agents have an OP-cholinesterase complex that “ages” over time. Once this has occurred that bond can not be broken and a new enzyme must be produced for the resolution of toxicity. With carbamates – the carbamate-acetylcholinesterase bond hydrolyzes spontaneously, reactivating the enzyme. So, the duration of cholinergic symptoms in carbamate toxicity is generally less than 24 hrs and they do not penetrate the blood-brain barrier well. But, seizures and CNS effects can occur with significant toxicity.
Which is true about irritant gases?
A) Mixing sodium hypochlorites and any acid may generate chloramine gas
B) Burning polyvinylchloride (PVC) plastic may liberate phosgene
C) Silo-fillers disease is relate to excess exposure to sulfur dioxide
D) Burning nitrocellulose (radiographic film) is expected to generate cyanide
E) Inhalation of hydrogen fluoride does not produce systemic findings typical of dermal hydrofluoric (HF) acid poisoning
Answer B. Combustion of PVC may liberate nitrogen dioxide, phosgene, and cyanide as well as other toxic gases. Chloramine is a toxic byproduct of bleach and AMMONIA. Mixing bleach with any other acid liberates chlorine gas. Burning x ray film liberates nitrogen from the nitrocellulose. Silo fillers disease is caused by oxides of nitrogen which are generated by decomposing fertilizer/dirt. HF acid can produce systemic reactions regardless of route.
The most important physical property of a XB within smoke that determines the location of lung injury is which factor? A) pH B) Molecular weight C) Particle size D) Water solubility E) Charge
Answer D. Water solubility is most important of an irritant XB in determining the level of respiratory tract injury.
Highly water soluble gases react with upper airway mucosal water to produce an intense inflammatory reaction. Unless the irritant gas concentrations are extremely high or prolonged exposure occurs, injury is limited to upper airways. Conversely, chemicals with low water solubility do not react with upper airway mucosa and are ABLE TO REACH LUNG PARENCHYMA
Barotrauma (pneumothorax, pneumopericardium, pneumomediastinum) is associated with which drug of abuse? A) Benzylpiperazine (BZP) B) Barbiturates C) Marijuana D) Methylenedioxy methamphetamine (MDMA) E) Gamma hydroxybutyrate (GHB)
Answer C. Barotrauma results from deep inhalation and Valsalva maneuver that follows abuse of inhaled XB like coke and marijuana and from direct pressure injury resulting from high-pressure nitrous oxide containers. It is not common with ingested drugs of abuse.
What mechanism best explains the reason for “sudden sniffing death”? A) Reperfusion injury B) Interference with K+ current C) Na channel blockade D) Simple asphyxiation E) Ca channel blockade
Answer B. It’s thought that inhalants “sensitize the myocardium” by blocking the potassium current (QT interval) and prolonging repolarization.
Sudden sniffing death can occur when a huffer/bagger/sniffer gets frightened by parents/police and a catecholamine surge (running) affects a sensitized myocardium causing a lethal dysrhythmia.
Which is a simple asphyxiant? A) Carbon monoxide B) Hydrogen sulfide C) Hydrogen chloride D) Nitrogen dioxide E) Nitrogen
Answer E. Simple asphyxiants have no direct pulmonary or systemic toxicity. Nitrogen is the only simple asphyxiant.
Which gas is a chemical asphyxiant? A) Propane B) Methane C) Hydrogen chloride D) Chloramine E) Cyanide
Answer E. Cyanide, hydrozoic acid ( liberator of azide) and hydrogen sulfide all poison the cytochrome oxidase chain leading to anaerobic respiration and metabolic organ failure by interfering with the oxygen loading and unloading.
Cyanosis, SOB, and tachypnea might be expected following which inhaled substance? A) Nitrous oxide B) Toluene C) Trichloroethane D) Isobutyl nitrite E) Methylene chloride
Answer D. Cyanosis suggests methemoglobinemia so look for the NITRITE answer. SOB and tachypnea are sxs of any inhalant.
Chronic toluene toxicity is clinically manifested by what symptom?
A) Methemoglobinemia
B) “sudden sniffer’s death”
C) Hepatocellular necrosis (similar to APAP toxicity)
D) Leukoencephalopathy
E) Sensorimotor peripheral neuropathy
Answer D. Patients with toluene leukoencephalopathy (dementia, ataxia, eye movement disorders, anosmia) display characteristic neurobehavioral deficits reflecting white matter involvement like inattention, apathy, impaired memory and visuospatial skills with preservation of language.
Which is true about carbon monoxide (CO)?
A) CO is denser than air
B) CO is irritating
C) CO is visible in high concentrations
D) CO is odorless
E) CO causes toxicity by binding to methemoglobin
Answer D. CO is colorless, odorless, and non irritating. It is lighter than air. It binds to hemoglobin and myoglobin.
A mass casualty event where victims collapse with respiratory failure is least consistent with exposure to what substance? A) Carfentanil B) Cyanogen chloride C) Lewisite D) Tabun E) Vx
Answer C. Carfentanil and cyanogen chloride cause sudden collapse. Mass casualty from lewisite should present with dermal, ocular, and respiratory tract sxs. The most severely poisoned lewisite victims can develop shock and respiratory failure in a delayed fashion.
Lewisite is a vesicant, used in chemical warfare, smells like geraniums, causes immediate intense eye, skin (vesicles form and rupture) and resp sxs, treated with BAL (British Anti Lewisite) and rapid decontamination. This can be differentiated from sulfur mustard since that has a delayed onset and frequently can be missed by HCP – increasing exposure.
Which is a potential source of cyanide poisoning? A) Automobile exhaust B) Ingestion of orange pits C) Burning of coal D) Burning of wood E) Nipride treatment
Answer E. Cyanide is a significant cause of death in fire victims, however, wood fires do not result in formation of cyanide. Cyanide can occur from Nipride administration when used for a prolonged period of time in the presence of renal failure. It is commonly administered in the same bag as sodium thiosulfate. The cyanide combines with the thiosulfate to form the less toxic sodium thiocyanate which is excreted.
Which is a source of hydrogen sulfide (HS)?
A) Decomposition of grain in silos
B) Incomplete combustion of silk
C) Combination of ammonia and hypochlorite
D) Sewers
E) Mercury refining
Answer D. HS is a byproduct of industrial processes such as paper and leather production, vulcanization of rubber and natural gas refining. HS is a natural product of bacterial decomposition of protein and sulfur-containing substances (SEWAGE) and of volcanoes, sulfur springs, and underground gas deposits.
