[TOXICOLOGY] Medical Toxicology

Proverbs 16:3

c. 200 mg/kg

Aspirin poisoning becomes potentially lethal at doses greater than:

a. 50 mg/kg
b. 100 mg/kg
c. 200 mg/kg
d. 500 mg/kg

d. Aspirin

Reye’s Syndrome is caused by

a. Acetaminophen
b. Isoniazid
c. Digoxin
d. Aspirin

b. Children after a viral infection

Reye's syndrome is associated with aspirin use in:

a. Elderly patients with hypertension
b. Children after a viral infection
c. Pregnant women
d. Patients with diabetes

b. Fatty liver and hepatic encephalopathy

Reye's syndrome is characterized by:

a. Pulmonary fibrosis and renal failure
b. Fatty liver and hepatic encephalopathy
c. Nephrotic syndrome and edema
d. Myocarditis and arrhythmias

b. Respiratory alkalosis + bicarbonaturia

The initial acid-base disturbance in aspirin poisoning is:

a. Metabolic acidosis
b. Respiratory alkalosis
c. Respiratory acidosis
d. Metabolic alkalosis

d. Stimulates the CNS respiratory center causing hyperventilation

Respiratory alkalosis in salicylate poisoning occurs because aspirin:

a. Depresses the respiratory center immediately
b. Causes bronchoconstriction
c. Inhibits bicarbonate excretion
d. Stimulates the CNS respiratory center causing hyperventilation

a. Respiratory acidosis

A severe aspirin overdose may eventually cause:

a. Respiratory acidosis
b. Metabolic alkalosis
c. Hypernatremia
d. Polycythemia

d. Uncoupling of oxidative phosphorylation

Hyperthermia in salicylate poisoning results from:

a. Increased thyroid hormone production
b. Acetylcholinesterase inhibition
c. Excess insulin release
d. Uncoupling of oxidative phosphorylation

a. Inhibition of aminotransferase in the Krebs cycle

Aspirin causes metabolic acidosis partly by:

a. Inhibition of aminotransferase
b. Increased bicarbonate synthesis
c. Increased insulin secretion
d. Enhanced gluconeogenesis

a. Metabolic acidosis

Salicylic acids → _____

a. Metabolic acidosis
b. Respiratory alkalosis
c. Respiratory acidosis
d. Metabolic alkalosis

a. Tinnitus

Which symptom is characteristic of mild salicylate poisoning (salicylism)?

a. Tinnitus
b. Bradycardia
c. Jaundice
d. Hematuria

a. Hyperventilation

Which finding is commonly seen in mild salicylate poisoning?

a. Hyperventilation
b. Constipation
c. Miosis
d. Edema

a. Hallucinations
b. Fever
c. Acid-base disturbances

• Headache is seen in mild salicylism

• Mild (Salicylism) = Tinnitus, Hyperventilation, Headache

• Fatal = respiratory depression

Severe salicylate poisoning may present with:

a. Hallucinations
b. Fever
c. Acid-base disturbances
d. Headache

b. Respiratory depression

The most common cause of death (fatal) in severe aspirin poisoning is:

a. Renal failure
b. Respiratory depression
c. GI hemorrhage
d. Cardiac arrest

a. Activated charcoal

Treatment for aspirin toxicity

a. Activated charcoal
b. Atropine
c. Penicillamine
d. Vitamin K

b. Forced alkaline diuresis

Treatment for aspirin toxicity

a. Acidification of urine
b. Forced alkaline diuresis
c. Vitamin K administration
d. Chelation therapy

b. Sodium bicarbonate (NaHCO₃)

Agent is used to correct acidosis in aspirin poisoning

a. Calcium gluconate
b. NaHCO₃
c. Protamine sulfate
d. Naloxone

a. Ice blanket

A patient with aspirin poisoning and hyperthermia may benefit from:

a. Ice blanket
b. Heating pad
c. Copper sulfate
d. Vitamin C

a. Gastric lavage &
c. Emesis

Which GI decontamination method may be used in aspirin poisoning?

a. Gastric lavage
b. Whole Bowel Irrigation (WBI)
c. Emesis
d. Cathartics

Answer Key

• 110 – 160 mg/kg → B (Vascular collapse), E (Hypoprothrombinemia)

• 50 – 80 mg/kg → D (Salicylism), A (Hyperventilation)

• > 160 mg/kg → G (Renal failure), C (Respiratory failure → may lead to death)

• 80 – 110 mg/kg → F (Metabolic acidosis), H (Hyperthermia)

  

Matching Type Quiz: Salicylate Toxicity

Column A – Toxic Dose (mg/kg)

1. 110 – 160

2. 50 – 80

3. >160

4. 80 – 110

Column B – Effects

A. Hyperventilation

B. Vascular collapse

C. Respiratory failure → may lead to death

D. Salicylism

E. Hypoprothrombinemia

F. Metabolic acidosis

G. Renal failure

H. Hyperthermia

b. Hepatic injury

Acetaminophen poisoning primarily causes:

a. Renal stones
b. Hepatic injury
c. Pulmonary fibrosis
d. Bone marrow suppression

b. Nausea and vomiting

Which symptom is commonly seen early in acetaminophen poisoning?

a. Tinnitus
b. Nausea and vomiting
c. Wrist drop
d. Tremor

a. Acetaminophen poisoning

A patient presents with nausea, vomiting, and abdominal pain after a drug overdose. Which poisoning should be suspected?

a. Acetaminophen poisoning
b. Copper poisoning
c. Mercury poisoning
d. Lead poisoning

a. Jaundice

Which of the following is a later manifestation of acetaminophen toxicity?

a. Jaundice
b. Burton's line
c. Kaiser-Fleischer rings
d. Acrodynia

b. N-acetylcysteine (Fluimucil®)

The antidote for acetaminophen poisoning is:

a. Deferoxamine
b. N-acetylcysteine
c. Penicillamine
d. Atropine

d. Replenish glutathione (GSH) stores

The primary action of N-acetylcysteine is to:

a. Chelate iron
b. Increase vitamin K synthesis
c. Inhibit acetylcholine receptors
d. Replenish glutathione (GSH) stores

d. Isonicotinylhydrazide

Isoniazid is also known as:

a. Acetylsalicylic acid
b. Ethambutol
c. Para-aminosalicylic acid
d. Isonicotinylhydrazide

c. Inhibition of pyridoxal phosphokinase

The mechanism of toxicity of isoniazid is:

a. Inhibition of acetylcholinesterase
b. Inhibition of MAO
c. Inhibition of pyridoxal phosphokinase
d. Inhibition of ferrochelatase

b. Vitamin B6 (Pyridoxine)

INH toxicity primarily causes deficiency of:

a. Vitamin B1 (Thiamine)
b. Vitamin B6 (Pyridoxine)
c. Vitamin B12 (Cobalamin)
d. Vitamin C (Ascorbic acid)

a. Irritability and seizures

A patient with INH overdose is most likely to present with:

a. Irritability and seizures
b. Burton's line
c. Pulmonary fibrosis
d. Acrodynia

c. Liver

The toxic metabolites of isoniazid primarily affect the:

a. Heart
b. Lungs
c. Liver
d. Bone marrow

a. Signs of liver failure

Which finding suggests hepatotoxicity from INH overdose?

a. Signs of liver failure
b. Hyperreflexia
c. Mydriasis
d. Proteinuria

c. 1:1

Pyridoxine is administered in INH poisoning at what ratio?

a. 1:10
b. 1:5
c. 1:1
d. 10:1

b. Digitalis lanata and Digitalis purpurea

Digoxin is derived from:

a. Atropa belladonna
b. Digitalis lanata and Digitalis purpurea
c. Papaver somniferum
d. Cinchona officinalis

d. Inhibition of Na⁺-K⁺ ATPase

The mechanism of action of digoxin is:

a. Inhibition of acetylcholinesterase
b. Calcium channel blockade
c. Blockade of β₁ receptors
d. Inhibition of Na⁺-K⁺ ATPase

c. Hypokalemia

Which electrolyte abnormality increases the risk of digoxin toxicity?

a. Hyperkalemia
b. Hypernatremia
c. Hypokalemia
d. Hypermagnesemia

b. Hypercalcemia

Which electrolyte disturbance potentiates digoxin toxicity?

a. Hypocalcemia
b. Hypercalcemia
c. Hyponatremia
d. Hypophosphatemia

a. Hypercalcemia + Hypokalemia

Which combination increases the likelihood of digoxin toxicity?

a. Hypercalcemia + Hypokalemia
b. Hypocalcemia + Hyperkalemia
c. Hypernatremia + Hypermagnesemia
d. Hyponatremia + Hypophosphatemia

c. Increases digoxin absorption

Chronic antibiotic use may increase digoxin toxicity because it:

a. Enhances renal excretion
b. Blocks digoxin receptors
c. Increases digoxin absorption
d. Inactivates digoxin

c. Quinidine

Which antiarrhythmic drug increases the risk of digoxin toxicity?

a. Lidocaine
b. Procainamide
c. Quinidine
d. Esmolol

a. Confusion &
c. Hallucinations

Which neuropsychiatric manifestation may occur in digoxin toxicity?

a. Confusion
b. Coma
c. Hallucinations
d. Aphasia

b. Xanthopsia

The classic visual disturbance associated with digoxin toxicity is:

a. Diplopia
b. Xanthopsia
c. Hemianopsia
d. Nyctalopia

c. Yellow-green visual discoloration

Xanthopsia refers to:

a. Red color blindness
b. Blue-green visual discoloration
c. Yellow-green visual discoloration
d. Complete blindness

c. Fatal arrhythmia

The most feared complication of digoxin toxicity is:

a. Hepatic failure
b. Renal failure
c. Fatal arrhythmia
d. Pulmonary fibrosis

b. Ventricular tachycardia

Which life-threatening arrhythmia may occur in severe digoxin toxicity?

a. Atrial flutter
b. Ventricular tachycardia
c. Sinus bradycardia
d. First-degree AV block

a. Cardiac automaticity

Digoxin-induced ventricular tachycardia results from stimulation of:

a. Cardiac automaticity
b. Hepatic metabolism
c. Renal secretion
d. Skeletal muscle contraction

d. All of the above

Which cardiac structures are stimulated in digoxin toxicity?

a. SA node
b. AV node
c. Bundle of His and ventricular muscle
d. All of the above

sedation = μ (Mu)

modulation of hormone and neurotransmitter release = μ (Mu) and δ (Delta)

psychotomimetic effects = κ (Kappa)

slowed gastrointestinal transit = μ (Mu)

inhibition of respiration = μ (Mu)

supraspinal and spinal analgesia = All

slowed gastrointestinal transit = κ (Kappa)

OPIOIDS AND OPIATES: μ (Mu) or δ (Delta) or κ (Kappa)?

sedation = ____

modulation of hormone and neurotransmitter release = ____

psychotomimetic effects = ____

slowed gastrointestinal transit = ____

inhibition of respiration = ____

supraspinal and spinal analgesia = ____

slowed gastrointestinal transit = ____

modulation of hormone and neurotransmitter release = ____

1. κ

2. δ

3. μ

OPIOIDS AND OPIATES: μ (Mu) or δ (Delta) or κ (Kappa)?

1. Dynorphins >> endorphins and enkephalins

2. Enkephalins > endorphins and dynorphins

3. Endorphins > enkephalins > dynorphins

b. Stimulation of opioid receptors

The mechanism of toxicity of opioids and opiates is:

a. Inhibition of acetylcholinesterase
b. Stimulation of opioid receptors
c. Blockade of dopamine receptors
d. Inhibition of Na⁺-K⁺ ATPase

✅Pinpoint pupils (Miosis)

Mydriasis

Agitation

✅Coma

✅Respiratory depression

Seizures

Triad is most characteristic of opioid poisoning

(Put check)

Pinpoint pupils (Miosis)

Mydriasis

Agitation

Coma

Respiratory depression

Seizures

c. Naloxone

The antidote for opioid overdose is:

a. Atropine
b. Flumazenil
c. Naloxone
d. Pralidoxime

b. Competitive opioid antagonist

Naloxone acts as a:

a. Opioid agonist
b. Competitive opioid antagonist
c. Benzodiazepine antagonist
d. Cholinergic agonist

b. Benzodiazepines and Barbiturates

Sedative-hypnotics commonly include:

a. Opioids and NSAIDs
b. Benzodiazepines and Barbiturates
c. Organophosphates and Carbamates
d. Digoxin and Quinidine

d. Drowsiness and ataxia

A patient who overdosed on benzodiazepines is most likely to present with:

a. Agitation and seizures
b. Miosis and diarrhea
c. Hyperthermia and tremors
d. Drowsiness and ataxia

a. Somnolence

An overdose of benzodiazepines commonly produces:

a. Somnolence
b. Hallucinations
c. Hypertension
d. Hyperglycemia

a. Confusion

Which mental status change may occur in sedative-hypnotic poisoning?

a. Confusion
b. Euphoria
c. Mania
d. Psychosis

c. Flumazenil

Which antidote is used for benzodiazepine overdose?

a. Naloxone
b. Pyridoxine
c. Flumazenil
d. Atropine

c. Hallucinogen

Lysergic Acid Diethylamide (LSD) is classified as a:

a. Opioid
b. Sedative-hypnotic
c. Hallucinogen
d. Stimulant

b. Ergot

LSD is derived from:

a. Belladonna
b. Ergot
c. Digitalis
d. Cinchona

c. Activation of 5-HT₂A receptors

The primary mechanism of LSD is:

a. Stimulation of μ-opioid receptors
b. Blockade of dopamine receptors
c. Activation of 5-HT₂A receptors
d. Inhibition of acetylcholinesterase

HTN

Tremors

Vomiting

Profound mydriasis

LSD Clinical Presentation:

HTN or hypotension?

Stiffness or Tremors?

Nausea or Vomiting?

Profound miosis or mydriasis?

c. MDMA (Ecstasy)

Which of the following is considered an amphetamine-related drug?

a. Morphine
b. Digoxin
c. MDMA (Ecstasy)
d. Diazepam

a. Cocaine

Which illicit drug is classified as an amphetamine-related compound?

a. Cocaine
b. Warfarin
c. Aspirin
d. Acetaminophen

b. Stimulation of adrenergic receptors with release of norepinephrine

The mechanism of toxicity of amphetamines primarily involves:

a. Inhibition of acetylcholinesterase
b. Stimulation of adrenergic receptors
c. Blockade of opioid receptors
d. Inhibition of Na⁺-K⁺ ATPase

c. Norepinephrine (NE)

Amphetamines produce their effects mainly by increasing:

a. Acetylcholine
b. GABA
c. Norepinephrine (NE)
d. Histamine

b. Teeth grinding

Bruxism, due to Amphetamine, refers to:

a. Tooth discoloration
b. Teeth grinding
c. Jaw fracture
d. Difficulty swallowing

b. Hyperthermia

The most dangerous manifestation of amphetamine toxicity is:

a. Mydriasis
b. Hyperthermia
c. Bruxism
d. Insomnia

c. Hypertension

Which cardiovascular effect is commonly seen in amphetamine poisoning?

a. Bradycardia
b. Hypotension
c. Hypertension
d. HF

d. Pinpoint pupils

Which finding is LEAST consistent with amphetamine toxicity?

a. Bruxism
b. Hyperthermia
c. Hypertension
d. Pinpoint pupils

b. Labetalol

Which drug may be used to manage hypertension associated with amphetamine toxicity?

a. Naloxone
b. Labetalol
c. Pyridoxine
d. Flumazenil

a. Sodium nitroprusside

Which vasodilator may be used in severe amphetamine-induced hypertension?

a. Sodium nitroprusside
b. Vitamin K
c. Deferoxamine
d. Atropine

b. Angel Dust

Phencyclidine (PCP) is commonly known as:

a. Ecstasy
b. Angel Dust
c. Speed
d. Crack

c. Dissociative anesthesia

Phencyclidine produces a state similar to:

a. Opioid analgesia
b. General anesthesia
c. Dissociative anesthesia
d. Local anesthesia

b. Ketamine

PCP is most closely related pharmacologically to:

a. Morphine
b. Ketamine
c. Aspirin
d. Digoxin

Aphasia

General anesthesia

✅Disorganized thought process

Sedation

✅Nystagmus

✅HTN

Miosis

Xanthopsia

Phencyclidine Clinical Presentation:

(Put check)

Aphasia

General anesthesia

Disorganized thought process

Sedation

Nystagmus

HTN

Miosis

Xanthopsia

b. Hashish &

d. Hashoids

Marijuana is also known as:

a. Angel Dust
b. Hashish
c. Ecstasy
d. Hashoids

b. Δ⁹-Tetrahydrocannabinol (THC)

The principal psychoactive component of marijuana is:

a. Cannabidiol (CBD)
b. Δ⁹-Tetrahydrocannabinol (THC)
c. Morphine
d. Mescaline

a. The most commonly used illegal drug

Marijuana is considered:

a. The most commonly used illegal drug
b. The most common prescription opioid
c. A synthetic stimulant
d. A hallucinogenic mushroom

a. Stimulation of cannabinoid receptors

The mechanism of action of marijuana is:

a. Stimulation of cannabinoid receptors
b. Inhibition of acetylcholinesterase
c. Blockade of opioid receptors
d. Activation of α₁ receptors

Tachycardia

Rhinitis

Increase appetite

Impaired short-term memory

Impaired rxn time

Acute psychosis

Bizarre behavior

Motor disturbances

Marijuana Clinical Presentation:

Bradycardia or Tachycardia

Rhinitis or Sinusitis

Increase or Decrease appetite

Impaired short-term memory or Amnesia

Bradykinesia or Impaired rxn time

Acute psychosis or Mania

Bizarre behavior or Paranoia

Motor disturbances or GI disturbances

b. CNS depression

The primary mechanism of alcohol toxicity is:

a. CNS stimulation
b. CNS depression

c. Rostral to caudal progression

Alcohol produces CNS depression in a:

a. Caudal to rostral progression
b. Peripheral to central progression
c. Rostral to caudal progression
d. Random pattern

a. GABA-ergic activity

The CNS effects of alcohol are primarily due to its:

a. GABA-ergic activity
b. Cholinergic activity
c. Adrenergic activity
d. Histaminergic activity

c. Depression of the CNS respiratory center

Respiratory acidosis in alcohol intoxication results from:

a. Hyperventilation
b. Increased bicarbonate loss
c. Depression of the CNS respiratory center
d. Excessive sweating

b. Metabolic alkalosis

Repeated vomiting in alcohol intoxication may lead to:

a. Respiratory acidosis
b. Metabolic alkalosis
c. Respiratory alkalosis
d. Metabolic acidosis

c. Lactic acid

Alcohol intoxication may cause metabolic lactic acidosis due to accumulation of:

a. Ketoacids
b. Sulfuric acid
c. Lactic acid
d. Uric acid

CORI Cycle

Metabolic acidosis

Coma

Hyperthermia

Hypoglycemia

ALCOHOL Clinical Presentation:

Metabolic acidosis or Metabolic alkalosis

Coma or Seizure

Hyperthermia or Hypothermia

Hypoglycemia or Hyperglycemia

c. Vitamin B1 (Thiamine)

Which vitamin should be administered before glucose in chronic alcohol intoxication?

a. Vitamin B6 (Pyridoxine)
b. Vitamin B12 (Cobalamin)
c. Vitamin B1 (Thiamine)
d. Vitamin K

b. Wernicke-Korsakoff syndrome

Administration of thiamine before glucose helps prevent:

a. Reye's syndrome
b. Wernicke-Korsakoff syndrome
c. Fetal alcohol syndrome
d. Hepatic encephalopathy

b. Vitamin B1 then glucose

A chronic alcoholic presenting with confusion and malnutrition should receive:

a. Glucose alone
b. Vitamin B1 then glucose
c. Naloxone then glucose
d. Vitamin K then glucose

c. Hemodialysis

In severe alcohol poisoning, which extracorporeal method may be utilized?

a. Hemoperfusion
b. Plasmapheresis
c. Hemodialysis
d. Exchange transfusion

a. IV fluids and supportive care

A dehydrated patient with acute alcohol intoxication should receive:

a. IV fluids and supportive care
b. Vitamin K
c. Activated charcoal
d. EDTA

a. Claviceps purpurea

Ergot alkaloids are derived from:

a. Claviceps purpurea
b. Digitalis purpurea
c. Papaver somniferum
d. Atropa belladonna

c. Ergotamine

Which drug is an ergot alkaloid used for acute migraine treatment?

a. Methysergide
b. Ergonovine
c. Ergotamine
d. Sumatriptan

b. Ergonovine

Which ergot alkaloid is commonly used for postpartum bleeding?

a. Ergotamine
b. Ergonovine
c. Digoxin
d. Morphine

b. Postpartum bleeding

Methysergide and ergonovine uses

a. Acute migraine treatment
b. Postpartum bleeding
c. Anticoagulation therapy
d. Treatment of seizures

d. Both B and C

Which of the following is an abortifacient ergot derivative?

a. Ergotamine
b. Ergonovine
c. Methysergide
d. Both B and C
e. Both A and B

b. Convulsive and gangrenous

Ergot toxicity may present in which two major forms?

a. Respiratory and cardiac
b. Convulsive and gangrenous
c. Acute and chronic
d. Hepatic and renal