Inhalants, Gases, Weapons of Mass Destruction, Pesticides and Insecticides

Question 1

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 1

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)

Question 2

Cyanide Mechanism of action:

Answer 2

despite adequate oxygen, ATP cannot be formed which results in cellular hypoxia

Question 3

Cyanide Sources

Answer 3

laetrile, cassava root, amygdalin, silver/gold extraction, products of combustion, acetonitrile (artificial nail remover)

Question 4

Cyanide symptoms

Answer 4

headache, N/V, HTN  hypotension, tachypnea  bradypnea, altered LOC, collapse, seizures, cyanosis only occurs in late stages from shock – usually before death

Question 5

Cyanide Treatment

Answer 5

nitrites/nitrates to purposely induce methemoglobinemia, hydroxocobalamin

Question 6

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 6

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.

Question 7

Carbon Monoxide Sources

Answer 7

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)

Question 8

Carbon Monoxide Mechanism of action:

Answer 8

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

Question 9

Carbon Monoxide Fetal Compromise

Answer 9

1. Fetal Hgb has a higher affinity for CO than for maternal Hgb
2. Maternal Hgb there fore does not reflect the degree of poisoning in the fetus
3. Fetal demise and stillbirths may occur at low maternal COHgb levels

Question 10

Carbon Monoxide CO half life

Answer 10

Room air ~ 4-6 hrs
on high flow oxygen ~ 40-90 mins
with HBO ~12-20 mins

Question 11

Carbon Monoxide Indications for HBO

Answer 11

SMaLl Chest Pain:

        Syncope
	Metabolic acidosis
	Level >25% 
	Chest pain or EKG changes
	Pregnancy with > 15%

Question 12

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 12

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.

Question 13

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 13

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.

Question 14

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 14

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

Question 15

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 15

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.

Question 16

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 16

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.

Question 17

Which is a simple asphyxiant?
A) Carbon monoxide
B) Hydrogen sulfide
C) Hydrogen chloride
D) Nitrogen dioxide
E) Nitrogen

Answer 17

Answer E. Simple asphyxiants have no direct pulmonary or systemic toxicity. Nitrogen is the only simple asphyxiant.

Question 18

Which gas is a chemical asphyxiant?
A) Propane
B) Methane
C) Hydrogen chloride
D) Chloramine
E) Cyanide

Answer 18

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.

Question 19

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 19

Answer D. Cyanosis suggests methemoglobinemia so look for the NITRITE answer. SOB and tachypnea are sxs of any inhalant.

Question 20

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 20

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.

Question 21

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 21

Answer D. CO is colorless, odorless, and non irritating. It is lighter than air. It binds to hemoglobin and myoglobin.

Question 22

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 22

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.

Question 23

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 23

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.

Question 24

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 24

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.

Question 25

As nicotine toxicity progresses from early phase to the late phase, which change is likely to occur?
A) Muscle fasciculation  muscle paralysis
B) CNS stimulation  CNS depression
C) Tachycardia  bradycardia
D) Hypertension  hypotension
E) All of the above

Answer 25

Answer E. All of the above

Question 26

Which statement about DEET (diethyl-meta-toluamide) is correct?
A) It is available to the consumer in concentration 5-10%
B) It is often combined with pyrethrins
C) DEET is poorly absorbed through the skin
D) DEET and several active metabolites can be found in fat for up to 2 months after dermal application
E) Lower concentrated products are not as effective as the higher concentrated products

Answer 26

Answer D. DEET and several active metabolites can be found in fat for up to 2 months after dermal exposure. Currently the lower concentrated products are of comparable efficacy to the higher concentrated products.

Question 27

Fun Facts about Organochlorines

Answer 27

Insecticides that have slow metabolism, lipid soluble, chemically stable, and persist in the environment. Commonly used for lice applications (Lindane).

Well absorbed orally and by inhalation; not well absorbed dermally unless it is dissolved in a hydrocarbon solvent.

They are lipophilic and significant fat storage increases the body burden in chronically exposed people.

Majority of their toxicity is in the CNS by causing hyperexcitability and seizures from keeping the sodium channel open

Lindane frequently has the presenting symptom being a grand mal seizure

Aging: OP become permanently bound to the cholinesterase enzyme by a process known as aging. When this occurs, cholinesterase function only returns to normal with synthesis of new cholinesterase.

Speed of aging varies between Ops

Discard both clothing and leather as 90% of the toxin can be removed with the clothes alone.

Emesis is also potentially toxic to HCP

Question 28

Fun Facts about Weapons of Mass Destruction

Answer 28

Nerve Agents – organaophosphates
G series (German origin) – GA (Tabun), GB (sarin), GD (soman)
V series (British origin) – Vx

Vesicants – blistering agents
Sulfur mustard
Phosgene
Lewisite

Vx – the most toxic OP
rapid onset – sxs within a few seconds
longest aging half time 48 hours
very low volatility – slowest to evaporate from liquid to a vapor
longest persistence in soil - 2-6 days
Tends to linger on clothes and surfaces
lowest amount of lethal dose 50 for skin - 10mg

Question 29

Which is true regarding inorganic and organic rodenticides?
A) All organic rodenticides are considered highly toxic
B) All organic rodenticides are considered moderately toxic
C) All inorganic rodenticides are considered highly toxic
D) All inorganic rodenticides are either highly or moderately toxic
E) Low toxicity rodenticides may be found in both organic and inorganic groups

Answer 29

Answer C. According to the Federal Insecticide, Fungicide, and Rodenticide Act – those rodenticides with a single dose of LD 50 (median lethal dose for 50% of test subjects) of less than 50mg/kg are considered highly toxic. All the inorganic rodenticides fall into this category.

Question 30

What is the most common symptom of intermediate syndrome with respect to organophosphate (OP) toxicity?
A) Proximal limb and cranial nerve palsies
B) Mydriasis
C) Bronchorrhea
D) Ventricular dysrhythmias
E) Vomiting and diarrhea

Answer 30

Answer A. Cranial nerve palsies and motor weakness (usually arms) are often the first sxs of intermediate syndrome.

The following OPs can cause intermediate syndrome:
metholate, malathion, diazinon, fenthion, parathion and methylparathion

Question 31

Which respiratory irritant has the greatest solubility?
A) Ammonia
B) CO2
C) Hydrogen sulfide
D) Methyl bromide
E) Ozone

Answer 31

Answer A. Ammonia is a highly water soluble irritant gas approximately 90 grams per 100 ml of water (90 gm%)

CO2 0.2 gm%
Hydrogen sulfide 0.4 gm%
Methyl bromide 2 gm%
Ozone 0.001 gm%

Question 32

Which is true regarding occupational (occ) asthma?
A) Occ asthma occurs when preexisting asthma is exacerbated by an exposure in the workplace
B) Occ exposure accounts for nearly all adult-onset asthma
C) There may be a long latency period between first exposure and onset of sxs
D) Cleaning materials (such as ammonia) are typically indicated
E) Sxs may improve with nebulized Na HCO3

Answer 32

Answer C. Occ asthma is caused by workplace factors only and accounts for 10-15% of adult-onset asthma. There may be a period of yrs between the first exposure and onset of sxs. Ammonia and hypochlorites more commonly are associated with reactive airway dysfunction syndrome, which is more acute in nature. Occ asthma is thought to be triggered by large organic molecules.

Question 33

Which is true about carbon monoxide?
A) Affinity 100x > oxygen for hemoglobin
B) Affinity 100x > oxygen for myoglobin
C) A product of hemoglobin formation
D) Binds to cytochrome oxidase
E) Causes shift to the right on the oxygen-dissociation curve

Answer 33

Answer D. Affinity for hemoglobin is 200-250x greater than oxygen and 40x greater than oxygen for myoglobin. CO is a byproduct of hemoglobin degradation and binds to cytochrome oxidase. In the presence of CO and formation of carboxyhemoglobin – the remaining oxyhemoglobin offloads oxygen less readily. There is a shift to the left on the oxyhemoglobin dissociation curve.

Question 34

Mass casualty with the following sxs: c/o eye pain, lacrimation, rhinorrhea, cough, N/V are least likely to occur to exposure to which biological warfare agent?
A) Adamsite
B) Chloracetophenone
C) Hydrogen cyanide
D) Sarin
E) Sulfur mustard

Answer 34

Answer C. The described toxidrome is typical for riot control agents. Hydrogen cyanide is a weak acid and produces rapid loss of consciousness but no mucous membrane irritation.

Question 35

What best characterizes the primary effect of excessive ingestion to Chlorphenoxy herbicides?
A) Acute tubular necrosis and peripheral neuropathy
B) GI upset and CNS depression
C) Muscle pain and hypothermia
D) Urticaria and wheezing
E) Bradycardia and excess secretions

Answer 35

Answer B. When ingested in large amounts, Chlorphenoxy herbicides can cause oral/GI damage, CNS depression (paralysis and coma), inhibition of oxidative phosphorylation (causing fever), widespread muscle damage and rhabdomyolysis.

After substantial dermal exposure, a mixed sensory-peripheral neuropathy has occurred after a latent period of time.

Agent orange had chlorphenoxy included in its ingredients.

Question 36

What is the most likely clinical symptom following exposure to cyanide gas?
A) V tach
B) Bloody emesis
C) Seizures
D) Abdominal pain
E) Cyanosis

Answer 36

Answer C. The CNS is the system most sensitive to cyanide. Sxs include headache agitation, confusion, and seizures/coma/death. Progressive cardiac failure and bradycardia (not ventricular dysrhythmias) occur. GI sxs are not common. Cyanide may occur late in profound shock but is not common.

Question 37

What symptom of OP toxicity is of the greatest life-threatening concern after acute exposure?
A) Bronchorrhea
B) Bradydysrhythmias
C) Respiratory insufficiency
D) Prolonged QTc 
E) Increased GI motility

Answer 37

Answer C. Excessive cholinergic stimulation resulting in depolarization of the neuromuscular junction can lead to effects to those of succinylcholine: paralysis and respiratory arrest.

Question 38

Nicotine is least well absorbed from which site?
A) Oral mucosa
B) Lung
C) Small intestine
D) Skin
E) Stomach

Answer 38

Answer E. Nicotine is poorly absorbed in the stomach in acidic environments. Alkaline environs (oral, skin, lungs and small intestine) have better absorption. Recall that green-leaf tobacco sickness occurs with workers harvesting tobacco leaves without skin protection.