Toxicology Lecture – Cyanide, Nitrate/Nitrite & Corrosives

These flashcards cover major points from the lecture on cyanide toxicity, nitrate/nitrite poisoning, and corrosive agents—including sources, mechanisms, clinical features, treatment, complications, and forensic aspects such as acid attacks.

What characteristic odor is often associated with cyanide poisoning?

A smell of bitter almonds on the breath or at the scene.

Which enzyme is inhibited by cyanide, resulting in cellular hypoxia?

Cytochrome oxidase (binds to ferric ion in the enzyme).

Why can cyanide salts ingested by mouth have a delayed onset of symptoms (15–30 min)?

In gastric juice they liberate hydrogen cyanide gas, which is absorbed more slowly than inhaled gas.

What are the primary target organs for cyanide toxicity?

Central nervous system and cardiac tissue.

Death may occur within how many minutes after inhaling a high dose of cyanide gas?

6–8 minutes.

Which two-part antidote regimen is used for cyanide poisoning?

Sodium nitrite followed by sodium thiosulfate.

Describe the chemical reaction underlying the nitrite component of the cyanide antidote.

Sodium nitrite converts hemoglobin (Hb) to methemoglobin (MetHb) which then binds cyanide to form cyanomethemoglobin.

What metabolic disturbance is characteristic of cyanide poisoning?

Severe metabolic acidosis due to shift to anaerobic metabolism.

List three common industrial or environmental sources of cyanide.

Combustion of plastics/synthetic rubber, vehicle exhaust, laboratories using cyanide salts.

Small-dose cyanide exposure causes which early neurological sign?

Dizziness or drowsiness followed by restlessness.

What is the taste sensation sometimes reported by victims of cyanide poisoning?

A salty or saltish taste in the mouth.

Which form of nitrates is 4–5 times more toxic: nitrate (NO₃⁻) or nitrite (NO₂⁻)?

Nitrite (NO₂⁻).

Explain how nitrate ingestion leads to methemoglobinemia.

Nitrate (NO₃⁻) is converted in the body to nitrite (NO₂⁻), which oxidizes hemoglobin to methemoglobin, impairing oxygen transport.

What pediatric condition is classically associated with acute nitrate/nitrite poisoning?

Blue baby syndrome (infant methemoglobinemia).

At what percentage of methemoglobin conversion can anoxia and death occur?

When 70–80 % of hemoglobin is converted to methemoglobin.

Chronic nitrate exposure may produce which class of carcinogenic compounds?

Nitrosamines (nitrite combines with amines).

Define a ‘corrosive’ in toxicology.

A highly reactive substance that causes rapid, destructive damage to living tissue upon contact.

Give two examples of common inorganic corrosive acids.

Hydrochloric acid (HCl) and sulfuric acid (H₂SO₄).

What type of necrosis do strong acids typically cause?

Coagulative necrosis.

Which part of the gastrointestinal tract is mainly affected after ingestion of strong acids?

The stomach.

Strong alkalis such as caustic soda cause what type of necrosis?

Liquefactive necrosis with saponification of fats.

Following alkali ingestion, which GI segment is most severely damaged?

The esophagus.

List four factors that determine the severity of corrosive injury.

Physical form, concentration, amount of agent, duration of contact (also pH and stomach contents for ingestions).

State two immediate clinical signs after corrosive ingestion.

Severe oral pain/burns and vomiting (often hematemesis).

Name three serious complications of corrosive poisoning.

Airway obstruction, perforation of the GI tract, circulatory shock.

In autopsy of acid ingestion, what external sign is often present on clothing and skin?

Brownish-black stains and corroded areas from trickling acid on chin, neck, and chest.

What simple bedside test helps distinguish acid from alkali exposure?

Litmus paper test of saliva (red for acid, blue for alkali).

Define ‘vitriolage’.

Criminal assault involving throwing corrosive acid, usually sulfuric acid, to disfigure or kill.

What is the primary aim in most acid attacks?

Disfigurement of the victim’s face leading to permanent scarring and possible blindness.

Why are concentrated alkalis often more dangerous than concentrated acids?

They penetrate deeper, producing liquefactive necrosis and extensive tissue destruction with less immediate pain to warn the victim.

How does oxalic acid differ from many inorganic acids in its toxic profile?

It is an organic acid that can be absorbed systemically, causing remote (systemic) effects in addition to local damage.

Explain the mechanism by which corrosives ‘burn’ tissue.

They extract water, liberate heat, coagulate/precipitate cellular proteins, and in acids convert hemoglobin to hematin, leading to tissue destruction.

What occupational setting might expose individuals to cyanide gas aside from fire smoke?

Industries manufacturing cyanide or laboratories handling cyanide solutions.

Which bodily fluid is used for excretion of the detoxified cyanide metabolite thiocyanate?

Urine.

What immediate supportive care is given to a cyanide-exposed patient before antidotes?

Administration of 100 % oxygen via mask or endotracheal tube.

List two hallmarks of severe cyanide poisoning on physical exam.

Dilated non-reactive pupils and rapid progression to convulsions, coma, and cardiac arrest.