4 - Specific Poisons

• Malathion

• Parathion

[Pesticides]

Examples of Organophosphate pesticides

a. Red phosphorus and white phosphorus
b. Malathion, parathion
c. Violet and black phosphorus
d. Match and fireworks chemicals

c. Inhibits Acetylcholinesterase leading to increased Ach (irreversible after "bond aging" 24-48 hours)

[Pesticides]

Mechanism of toxicity of Organophosphates

a. Inhibits heme synthesis leading to anemia
b. Competes with divalent ions (Ca, Mg)
c. Inhibits Acetylcholinesterase leading to increased Acetylcholine
d. Inhibits SOD and catalase leading to increased free radicals

d. 24-48 hours

[Pesticides]

Organophosphate inhibition of Acetylcholinesterase becomes irreversible after bond aging occurs within this time frame

a. 12-24 hours
b. 48-72 hours
c. 6-12 hours
d. 24-48 hours

• Diarrhea

• Urination

• Miosis (pupillary constriction)

• Bradycardia

• Bronchospasm

• Emesis (vomiting)

• Lacrimation (tearing)

• Salivation

• Sweating

📌Mnemonic: “DUMBBELSS”

[Pesticides]

Clinical presentation of Organophosphate include:

• Atropine (preferred; given anytime)

• Pralidoxime (enzyme regenerator; given before aging has set in)

[Pesticides]

Treatment for Organophosphate poisoning [2]

d. Atropine

[Pesticides]

Preferred treatment for Organophosphate poisoning that can be given anytime

a. Pralidoxime
b. EDTA
c. BAL
d. Atropine

c. Pralidoxime

[Pesticides]

Treatment for Organophosphate poisoning that acts as an enzyme regenerator but must be given before aging has set in

a. Atropine
b. BAL
c. Pralidoxime
d. EDTA

d. Red phosphorus

[Pesticides]

Phosphorus form used in matches and fireworks

a. White phosphorus
b. Violet phosphorus
c. Black phosphorus
d. Red phosphorus

• Violet phosphorus

• Black phosphorus

[Pesticides]

Phosphorus forms used in electronics

a. Red and white phosphorus
b. White and black phosphorus
c. Violet and black phosphorus
d. Red and violet phosphorus

d. White phosphorus

[Pesticides]

Most toxic form of Phosphorus that is banned as pesticide but currently used in warfare, grenades, explosives, and fire starters

a. Red phosphorus
b. Black phosphorus
c. Violet phosphorus
d. White phosphorus

d. White phosphorus

This phosphorus is currently used in warfare, grenades, explosives, and fire starters

a. Red phosphorus
b. Black phosphorus
c. Violet phosphorus
d. White phosphorus

• Luminous stool/vomitus

• Garlic odor breath

• Phossy jaw (necrosis of jaw)

[Pesticides]

Clinical presentation of White Phosphorus poisoning

a. Ataxia, weakness of muscle, loss of vision and hearing
b. Anemia, decreased IQ, burton's line
c. Luminous stool/vomitus, garlic odor breath, phossy jaw (necrosis of jaw)
d. Severe joint pain, bone softening

• Ergonovine

• Methylsergide

[Medications]

Examples of Ergot alkaloids used for migraine

a. Nitroglycerin and ISDN
b. Ergonovine and methylsergide
c. Ergotamine and methysergide
d. ISMN and ergotamine

d. Ergonovine

[Medications]

Ergot alkaloid used for:

• Uterine contraction

• Post-partum bleeding

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

c. Abortifacient

[Medications]

Off-label use of Ergot alkaloids

a. Vasodilator
b. Antihypertensive
c. Abortifacient
d. Anticoagulant

d. Vasoconstriction

[Medications]

Mechanism of toxicity of Ergot alkaloids

a. Vasodilation
b. Inhibits Acetylcholinesterase
c. Increased free radicals
d. Vasoconstriction

c. Gangrenous ergotism ("walang dadaloy na dugo at oxygen")

[Medications]

Clinical presentation of Ergot alkaloid toxicity

a. Minamata disease
b. Itai-Itai disease
c. Gangrenous ergotism
d. Mad hatter's disease

• Amputation

• Vasodilator (nitrates)

[Medications]

Treatment for Ergot alkaloid toxicity (gangrenous ergotism)

a. Atropine and Pralidoxime
b. BAL and EDTA
c. Deferoxamine IV and Deferasirox PO
d. Amputation; vasodilator (nitrates)

• Nitroglycerin (sublingual)

• ISDN (sublingual)

• ISMN (PO)

[Medications]

Examples of Nitrates used as medications

a. Ergotamine, methysergide, ergonovine
b. Malathion, parathion
c. Nitroglycerin (sublingual), ISDN (sublingual), ISMN (PO)
d. Atropine and Pralidoxime

c. Vasodilation

[Medications]

Mechanism of action of Nitrates

a. Vasoconstriction
b. Inhibits Acetylcholinesterase
c. Vasodilation
d. Increased free radicals

• Headache (most common)

• Tolerance (Increased dose needed to achieve same effect)

[Medications]

Clinical Presentation for Nitrates [2]

c. Headache

[Medications]

Most common clinical presentation of Nitrate toxicity

a. Tolerance requiring increased dose to achieve same effect
b. Gangrenous ergotism
c. Headache
d. Vasoconstriction leading to gangrene

b. Increased dose needed to achieve same effect

[Medications]

Nitrate toxicity presenting as tolerance is defined as

a. Decreased dose needed to achieve same effect
b. Increased dose needed to achieve same effect
c. No change in dose needed
d. Drug becomes ineffective completely

a. Tolerance

[Medications]

Increased dose needed to achieve same effect
a. Tolerance
b. Dependence
c. Withdrawal
d. Sensitization

c. Factory workers exposed to nitroglycerin or organic nitrates

[Medications]

Monday sickness syndrome" caused by Nitrates occurs in this population

a. Elderly patients taking nitroglycerin
b. Pregnant women taking ISMN
c. Factory workers exposed to nitroglycerin or organic nitrates
d. Immunocompromised patients taking ISDN

a. Nitrates

[Medications]

Monday sickness syndrome is caused by ______
a. Nitrates
b. Organophosphates
c. Phosphorus
d. Carbamates

a. Monday sickness syndrome

[Medications]

An occupational phenomenon where industrial workers exposed to nitroglycerin or organic nitrates develop drug tolerance over the workweek due to loss of tolerance (resensitization)
a. Monday sickness syndrome
b. Friday sickness syndrome
c. Weekend sickness syndrome
d. Holiday sickness syndrome

c. Loss of tolerance (resensitization) over the weekend

[Medications]

"Monday sickness syndrome" occurs due to _____

a. Increased tolerance over the weekend
b. Drug accumulation over the workweek
c. Loss of tolerance (resensitization) over the weekend
d. Increased dose taken over the workweek

c. Increases NAPQI (N-acetyl-p-benzoquinone imine) via CYP2E1 leading to hepatotoxicity

[Medications]

Mechanism of toxicity of Paracetamol

a. Inhibits Na/K ATPase leading to arrhythmias
b. Inhibits SOD and catalase leading to increased free radicals
c. Increases NAPQI (N-acetyl-p-benzoquinone imine) via CYP2E1 leading to hepatotoxicity
d. Vasoconstriction leading to gangrenous ergotism

a. CYP2E1

[Medications]

BEQ: Paracetamol increases NAPQI (N-acetyl-p-benzoquinone imine) via______ leading to hepatotoxicity
a. CYP2E1
b. CYP1A2
c. CYP2D6
d. CYP3A4

d. 4 g/day

[Medications]

Maximum dose of Paracetamol per day

a. 2 g/day
b. 6 g/day
c. 8 g/day
d. 4 g/day

c. 15-20 g/day

[Medications]

Fatal dose of Paracetamol

a. 4-8 g/day
b. 8-12 g/day
c. 15-20 g/day
d. 10-15 g/day

• Anorexia

• Abdominal pain

• Jaundice

[Medications]

Clinical presentation of Paracetamol toxicity

a. Arrhythmias, hallucination, xanthopsias
b. Headache, tolerance, Monday sickness syndrome
c. Luminous stool, garlic odor breath, phossy jaw
d. Anorexia, abdominal pain, jaundice

c. N-acetylcysteine (NAC)

[Medications]

Antidote for Paracetamol toxicity

a. Atropine
b. Pralidoxime
c. N-acetylcysteine (NAC)
d. Penicillamine

c. Inhibits Na/K ATPase resulting in (+) inotropy and (-) dromotropy

[Medications]

Mechanism of toxicity of Digoxin

a. Increases NAPQI leading to hepatotoxicity
b. Inhibits SOD and catalase leading to increased free radicals
c. Inhibits Na/K ATPase resulting in (+) inotropy and (-) dromotropy
d. Vasoconstriction leading to gangrenous ergotism

c. Positive inotropy (increased contractility)

[Medications]

Effect of Digoxin toxicity on inotropy

a. Negative inotropy (decreased contractility)
b. No change in inotropy
c. Positive inotropy (increased contractility)
d. Alternating inotropy

d. Negative dromotropy (decreased conduction)

[Medications]

Effect of Digoxin toxicity on dromotropy

a. Positive dromotropy (increased conduction)
b. No change in dromotropy
c. Alternating dromotropy
d. Negative dromotropy (decreased conduction)

• Arrhythmias

• Hallucination

• Xanthopsias (yellow-green color blindness)

[Medications]

Clinical presentation of Digoxin toxicity

a. Anorexia, abdominal pain, jaundice
b. Headache, tolerance, Monday sickness syndrome
c. Arrhythmias, hallucination, xanthopsias (yellow-green color blindness)
d. Luminous stool, garlic odor breath, phossy jaw

a. Xanthopsia

[Medications]

Yellow-green color blindness seen in Digoxin toxicity is called ______
a. Xanthopsia
b. Erythropsia
c. Chloropsia
d. Cyanopsia

c. Dinoflagellates

[Toxins]

Source of Saxitoxins

a. Amanita phalloides mushroom
b. Aspergillus flavus mold
c. Dinoflagellates
d. Contaminated fish and seafood

a. Dinoflagellates

[Toxins]

The organism that causes red tide

a. Dinoflagellates

b. Diatoms

c. Cyanobacteria

d. Euglenoids

a. Inhibits Na channels leading to hyperpolarization

[Toxins]

The mechanism of toxicity of saxitoxins
a. Inhibits Na channels leading to hyperpolarization
b. Hepatotoxicity leading to liver cancer
c. Inhibits RNA Pol II (transcription)
d. Inhibits acetylcholinesterase leading to increased Ach

a. Paralytic shellfish poisoning

[Toxins]

Clinical presentation of Saxitoxin poisoning

a. Paralytic shellfish poisoning
b. Neurotoxic shellfish poisoning
c. Liver cancer
d. Jaundice and hepatomegaly

a. True

[Toxins]

Brevetoxin have same SOURCE and MOT as saxitoxin

a. True

b. False

b. Brevetoxin

[Toxins]

The toxin that is associated with the brain and causes neurotoxic shellfish poisoning

a. Saxitoxin

b. Brevetoxin

c. Aflatoxin

d. Mycotoxin

a. Dinoflagellates (red tide)

[Toxins]

The source of brevetoxin
a. Dinoflagellates (red tide)
b. Aspergillus flavus
c. Improper dried legumes
d. Peanuts and grains

a. Inhibits Na channels leading to hyperpolarization

[Toxins]

The mechanism of toxicity of brevetoxin
a. Inhibits Na channels leading to hyperpolarization
b. Hepatotoxicity leading to liver cancer
c. Inhibits RNA Pol II (transcription)
d. Inhibits acetylcholinesterase leading to increased Ach

b. Neurotoxic shellfish poisoning

[Toxins]

The presentation of brevetoxin poisoning
a. Paralysis (paralytic shellfish poisoning)
b. Neurotoxic shellfish poisoning
c. Liver cancer
d. Jaundice and hepatomegaly

b. Neurotoxic shellfish poisoning

[Toxins]

Clinical presentation of brevetoxin poisoning
a. Paralytic shellfish poisoning
b. Neurotoxic shellfish poisoning
c. Liver cancer
d. Jaundice and hepatomegaly

b. Aspergillus flavus (mold that grows on improper dried legumes (peanuts) and grains)

[Toxins]

The source of aflatoxin
a. Dinoflagellates (red tide)
b. Aspergillus flavus
c. Improper dried legumes
d. Peanuts and grains

b. Aspergillus flavus

[Toxins]

Mold that grows on improper dried legumes (peanuts) and grains
a. Aspergillus niger
b. Aspergillus flavus
c. Aspergillus fumigatus
d. Penicillium chrysogenum

b. Hepatotoxicity leading to liver cancer

[Toxins]

Mechanism of toxicity of aflatoxin
a. Inhibits Na channels leading to hyperpolarization
b. Hepatotoxicity leading to liver cancer
c. Inhibits RNA Pol II (transcription)
d. Inhibits acetylcholinesterase leading to increased Ach

c. Liver cancer

[Toxins]

Clinical presentation of aflatoxin poisoning
a. Paralytic shellfish poisoning
b. Neurotoxic shellfish poisoning
c. Liver cancer
d. Jaundice and hepatomegaly

• Amanita phalloides mushrooms (death cap)

• Amanita virosa (destroying angel)

[Toxins]

Sources of Amatoxin

a. Dinoflagellates and Aspergillus flavus
b. Amanita phalloides (death cap) and Amanita virosa (destroying angel) mushrooms
c. Red tide and contaminated grains
d. Aspergillus flavus and Amanita phalloides

a. Amanita phalloides

[Toxins]

The mushroom known as "death cap"
a. Amanita phalloides
b. Amanita virosa
c. Amanita muscaria
d. Amanita pantherina

b. Amanita virosa

[Toxins]

The mushroom known as "destroying angel"
a. Amanita phalloides
b. Amanita virosa
c. Amanita muscaria
d. Amanita pantherina

b. Fatal toxin

[Toxins]

Amatoxin is classified as

a. Non-fatal toxin
b. Fatal toxin
c. Mildly toxic
d. Moderately toxic

a. Amatoxin

[Toxins]

The fatal mushroom toxin
a. Amatoxin
b. Saxitoxin
c. Brevetoxin
d. Aflatoxin

a. Inhibits RNA Pol II (transcription)

[Toxins]

Mechanism of toxicity of Amatoxin

a. Inhibits RNA Pol II (transcription)
b. Inhibits Na channels leading to hyperpolarization
c. Hepatotoxicity leading to liver cancer
d. Inhibits acetylcholinesterase leading to increased Ach

a. RNA Pol II (transcription)

[Toxins]

The enzyme inhibited by amatoxin
a. RNA Pol II (transcription)
b. RNA Pol I (transcription)
c. RNA Pol III (transcription)
d. DNA polymerase

a. Acute liver failure → death

[Toxins]

Clinical presentation of amatoxin poisoning:

a. Acute liver failure → death

b. Paralytic shellfish poisoning

c. Neurotoxic shellfish poisoning

d. Liver cancer

a. Death

[Toxins]

The outcome of acute liver failure caused by amatoxin
a. Death
b. Paralysis
c. Neurotoxicity
d. Liver cancer

a. rRNA

📌Mnemonic: “RMT”

• I - rRNA

• II - mRNA

• III - tRNA

[Toxins]

RNA Polymerase I transcribes
a. rRNA
b. mRNA
c. tRNA
d. DNA

b. mRNA

📌Mnemonic: “RMT”

• I - rRNA

• II - mRNA

• III - tRNA

[Toxins]

RNA Polymerase II transcribes
a. rRNA
b. mRNA
c. tRNA
d. DNA

c. tRNA

📌Mnemonic: “RMT”

• I - rRNA

• II - mRNA

• III - tRNA

[Toxins]

RNA Polymerase III transcribes
a. rRNA
b. mRNA
c. tRNA
d. DNA

c. Latrodectus mactans (black widow spider)

[Toxins]

Source of Latrotoxin

a. Amanita phalloides (death cap) mushroom
b. Dinoflagellates = red tide
c. Latrodectus mactans (black widow spider)
d. Pufferfish (fugu)

a. Black widow spider

[Toxins]

Latrodectus mactans
a. Black widow spider
b. Brown recluse spider
c. Funnel-web spider
d. Tarantula

d. Increases Acetylcholine release

[Toxins]

Mechanism of toxicity of Latrotoxin

a. Blocks Na channel
b. Inhibits RNA Pol II (transcription)
c. Inhibits Na channels = hyperpolarization
d. Increases Acetylcholine release

• Diarrhea

• Urination

• Miosis (pupillary constriction)

• Bradycardia

• Bronchospasm

• Emesis (vomiting)

• Lacrimation (tearing)

• Salivation

• Sweating

📌Mnemonic: “DUMBBELSS”

[Toxins]

Clinical presentation of Latrotoxin poisoning from black widow spider bite

a. Flaccid paralysis
b. Paralytic shellfish poisoning
c. DUMBBELSS
d. Acute liver failure = death

d. Pufferfish (fugu)

[Toxins]

Source of Tetrodotoxin

a. Latrodectus mactans (black widow spider)
b. Dinoflagellates = red tide
c. Aspergillus flavus mold
d. Pufferfish (fugu)

c. Blocks Na channel

[Toxins]

Mechanism of toxicity of Tetrodotoxin

a. Increases Ach release
b. Inhibits Na channels , leading to hyperpolarization
c. Blocks Na channel
d. Inhibits RNA Pol II (transcription)

d. Flaccid paralysis

[Toxins]

Clinical presentation of Tetrodotoxin poisoning from pufferfish

a. DUMBBELSS
b. Neurotoxic shellfish poisoning
c. Acute liver failure = death
d. Flaccid paralysis

• Saxitoxin inhibits Na channels → hyperpolarization

• Tetrodotoxin blocks Na channel

[Toxins]

Difference between Saxitoxin and Tetrodotoxin in terms of mechanism of action

a. Saxitoxin blocks Na channel; Tetrodotoxin inhibits Na channels = hyperpolarization
b. Saxitoxin increases Ach release; Tetrodotoxin blocks Na channel
c. Both have the same mechanism of action
d. Saxitoxin inhibits Na channels → hyperpolarization; Tetrodotoxin blocks Na channel

• Latrotoxin → DUMBBELSS

• Tetrodotoxin = flaccid paralysis

[Toxins]

Difference between Latrotoxin and Tetrodotoxin in terms of clinical presentation

a. Latrotoxin = flaccid paralysis; Tetrodotoxin = DUMBBELSS
b. Latrotoxin = neurotoxic shellfish poisoning; Tetrodotoxin = flaccid paralysis
c. Latrotoxin = DUMBBELSS; Tetrodotoxin = flaccid paralysis
d. Both present with flaccid paralysis

• Coma

• Pinpoint pupil

• Respiratory depression

[Drug of Abuse]

Opioid overdose triad
a. Comma, pinpoint pupil, respiratory depression
b. Comma, mydriasis, respiratory depression
c. Coma, pinpoint pupil, respiratory depression
d. Coma, mydriasis, respiratory depression

a. Naloxone (full opioid antagonist)

[Drug of Abuse]

Treatment for opioid overdose
a. Naloxone
b. Naltrexone
c. Methadone
d. Buprenorphine

a. Lysergic acid diethylamine

[Drug of Abuse]

LSD means ______
a. Lysergic acid diethylamine
b. Lysergic acid dimethylamine
c. Lysergic acid diethylamide
d. Lysergic acid dimethylamide

a. Acid

[Drug of Abuse]

Lysergic acid diethylamine (LSD) is also known as
a. Acid
b. Angel dust
c. Ecstasy
d. Shabu

• Increased BP

• Hallucination

• Profound mydriasis

[Drug of Abuse]

Clinical presentation of LSD
a. Increased BP, hallucination, profound mydriasis
b. Decreased BP, hallucination, profound miosis
c. Increased BP, hallucination, profound miosis
d. Decreased BP, hallucination, profound mydriasis

a. Angel dust

[Drug of Abuse]

Phencyclidine (PCP) is also known as
a. Angel dust
b. Acid
c. Ecstasy
d. Shabu

b. Phencyclidine (PCP)

[Drug of Abuse]

The most dangerous hallucinogen resulting in death
a. LSD
b. Phencyclidine (PCP)
c. Mescaline
d. Psilocybin

• Dissociative anesthesia

• Reckless behavior

• Paranoia

• Fatal seizures

[Drug of Abuse]

Presentation of Phencyclidine (PCP)
a. Dissociative anesthesia, reckless behavior, paranoia, fatal seizures
b. Increased BP, hallucination, profound mydriasis
c. Coma, pinpoint pupil, respiratory depression
d. Dissociative anesthesia, reckless behavior, euphoria, fatal seizures

a. Cocaine

[Drug of Abuse]

The stimulant also known as coke, crack, snow, nose, and candy
a. Cocaine
b. Methamphetamine
c. MDMA
d. Marijuana

b. Methamphetamine

[Drug of Abuse]

The stimulant also known as shabu, bato, and poor man's cocaine
a. Cocaine
b. Methamphetamine
c. MDMA
d. Marijuana

c. MDMA (Methyleneoxymethamphetamine)

[Drug of Abuse]

The stimulant also known as ecstasy, molly, and party drug
a. Cocaine
b. Methamphetamine
c. MDMA (Methyleneoxymethamphetamine)
d. Marijuana

a. Methyleneoxymethamphetamine

[Drug of Abuse]

MDMA stands for
a. Methyleneoxymethamphetamine
b. Methylenedioxymethamphetamine
c. Methyleneoxymethylamphetamine
d. Methylenedioxymethylamphetamine

• Sympathomimetic effects

• Delusional parasitosis

• Bruxism

[Drug of Abuse]

Clinical presentation of stimulants
a. Sympathomimetic effects, delusional parasitosis, bruxism
b. Sympatholytic effects, delusional parasitosis, bruxism
c. Sympathomimetic effects, delusional parasitosis, miosis
d. Sympatholytic effects, delusional parasitosis, miosis

a. Bruxism

[Drug of Abuse]

The grinding of teeth caused by stimulants
a. Bruxism
b. Trismus
c. Lockjaw
d. Tardive dyskinesia

• Weed

• Pot

• MJ

• Chongke

• Kush

• Hashish

• Damo

• Gulay

• Salad

• Bhang

• Tiririt

[Drug of Abuse]

Marijuana (Cannabis Sativa) is also known as
a. Weed, pot, MJ, chongke, kush, hashish, damo, gulay, salad, bhang, tiririt
b. Weed, pot, MJ, coke, crack, snow
c. Weed, pot, MJ, ecstasy, molly
d. Weed, pot, MJ, shabu, bato

a. Tetrahydrocannabinol (THC) and Cannabidiol (CBD)

[Drug of Abuse]

The active components of Marijuana (Cannabis Sativa)
a. Tetrahydrocannabinol (THC) and Cannabidiol (CBD)
b. Tetrahydrocannabinol (THC) and Cannabinol (CBN)
c. Cannabidiol (CBD) and Cannabinol (CBN)
d. Tetrahydrocannabinol (THC) only

a. Tetrahydrocannabinol (THC)

[Drug of Abuse]

The addictive component of marijuana
a. Tetrahydrocannabinol (THC)
b. Cannabidiol (CBD)
c. Cannabinol (CBN)
d. Cannabigerol (CBG)

b. Cannabidiol (CBD)

[Drug of Abuse]

The medically active component of marijuana
a. Tetrahydrocannabinol (THC)
b. Cannabidiol (CBD)
c. Cannabinol (CBN)
d. Cannabigerol (CBG)

• Runny nose

• Hunger

• Uncontrollable hunger

• Alters depth and time perception

• Increases attention span

• Increases memory

[Drug of Abuse]

Clinical presentation of marijuana
a. Runny nose, hunger, uncontrollable hunger, alters depth and time perception, increases attention span, increases memory
b. Runny nose, hunger, uncontrollable hunger, alters depth and time perception, decreases attention span, decreases memory
c. Runny nose, hunger, uncontrollable hunger, alters depth and time perception, increases attention span, decreases memory
d. Runny nose, hunger, uncontrollable hunger, alters depth and time perception, decreases attention span, increases memory