SOLVENTS

Question 1

Produces FORMIC ACID

Answer 1

Methanol

Question 2

Produces GLYCOLIC ACID & OXALIC ACID

Answer 2

Ethylene Glycol

Question 3

Methanol and Ethylene Glycol Antidote

Answer 3

FOMEPIZOLE (or ETHANOL)

Yes. Both fomepizole and ethanol are antidotes for both methanol and ethylene glycol.

Why they work for both:
• Methanol and ethylene glycol are not very toxic by themselves.
• Their danger comes from being metabolized by alcohol dehydrogenase (ADH) into toxic acids:
• Methanol → formaldehyde → formic acid (blindness, acidosis)
• Ethylene glycol → glycolaldehyde → glycolic & oxalic acids (acidosis, renal failure)

Role of the antidotes:
• Fomepizole = direct inhibitor of alcohol dehydrogenase
• Ethanol = competitive substrate with higher affinity for ADH

Both:
→ Block ADH
→ Prevent formation of toxic metabolites
→ Allow methanol or ethylene glycol to be excreted unchanged

Question 4

formic acid → metabolic acidosis, optic nerve damage

Answer 4

Methanol

MRationale (step-by-step):
1. Methanol itself is not very toxic.
The danger comes from how the body metabolizes it.
2. Liver metabolism:
• Methanol → (alcohol dehydrogenase) → Formaldehyde
• Formaldehyde → (aldehyde dehydrogenase) → Formic acid
3. Formic acid causes metabolic acidosis:
• Formic acid is a strong organic acid.
• It accumulates in blood → lowers pH → high anion gap metabolic acidosis.
4. Formic acid damages the optic nerve:
• Formic acid inhibits mitochondrial cytochrome oxidase.
• This blocks cellular respiration, especially in tissues with high energy demand like the optic nerve and retina.
• Result: optic neuritis → blurred vision → “snowfield” vision → possible blindness.

Summary:

Methanol poisoning is dangerous because it is converted into formic acid, which:
• Acidifies the blood → metabolic acidosis
• Blocks cellular respiration in optic nerve → visual toxicity and blindness

Question 4

are dangerous because their toxic metabolites (acids) cause organ damage, and fomepizole or ethanol block their metabolism.

Answer 4

methanol and ethylene glycol

Question 5

glycolic acid + oxalic acid → metabolic acidosis, renal failure (oxalate crystals)

Answer 5

Ethylene glycol

Rationale (step-by-step):
1. Ethylene glycol itself is not very toxic.
Its toxicity comes from metabolism in the liver.
2. Liver metabolism of ethylene glycol:
• Ethylene glycol → (alcohol dehydrogenase) → Glycoaldehyde
• Glycoaldehyde → → Glycolic acid
• Glycolic acid → → Glyoxylic acid → Oxalic acid
3. Glycolic acid causes metabolic acidosis:
• Accumulates in blood → lowers pH → high anion gap metabolic acidosis.
4. Oxalic acid causes renal toxicity:
• Oxalic acid binds calcium → calcium oxalate crystals
• Crystals deposit in renal tubules → tubular obstruction and acute renal failure.
5. Key features of ethylene glycol poisoning:
• Early: CNS depression (like alcohol)
• Later: metabolic acidosis (glycolic acid)
• Renal failure (oxalate crystals in urine)

Summary:
Ethylene glycol is metabolized to glycolic acid (causing acidosis) and oxalic acid (forming calcium oxalate crystals → renal failure).

Question 6

What is another name for Methanol?

Answer 6

Wood Alcohol

Question 7

Visual disturbances
Metabolic acidosis

Answer 7

Methanol poisoning

Question 8

What are the sources of ethylene glycol?

Answer 8

Antifreeze, Paints, Lacquers

Question 9

What is the treatment (TX) for Methanol poisoning?

Answer 9

Sodium Bicarbonate (NaHCO₃)

Question 10

Renal Failure
Metabolic Acidosis

Answer 10

Ethylene Glycol Poisoning

Question 11

What are the main antidotes of ethylene glycol?

Answer 11

Pyridoxine (VB6)
Thiamine (VB1)

Question 12

How does Pyridoxine help in ethylene glycol poisoning?

Answer 12

Glyoxylic Acid → (+ Pyridoxine) → Glycine → Hippuric Acid (Detoxification)

Rationale (step-by-step):
1. Context:
• Glyoxylic acid is a toxic metabolite of ethylene glycol.
• Without detoxification, glyoxylic acid can be further metabolized to oxalic acid, which causes renal toxicity.
2. Role of Pyridoxine (Vitamin B6):
• Pyridoxine acts as a cofactor for transamination reactions.
• It facilitates the conversion of glyoxylic acid → glycine, a harmless amino acid.
3. Formation of Hippuric Acid:
• Glycine conjugates with benzoic acid (or related intermediates) → forms hippuric acid, which is water-soluble and easily excreted in urine.
4. Therapeutic significance:
• Administration of pyridoxine in ethylene glycol poisoning shifts metabolism away from oxalate formation.
• This reduces renal toxicity and prevents calcium oxalate crystal deposition.

Summary:
Pyridoxine enables glyoxylic acid detoxification → glycine → hippuric acid → safe excretion, preventing oxalate-related renal damage in ethylene glycol poisoning.

Question 13

How does Thiamine help in ethylene glycol poisoning?

Answer 13

A: Glyoxylic Acid → (+ Thiamine) → α-hydroxy-β-ketoadipic Acid → Non-toxic

Rationale (step-by-step):
1. Context:
• Glyoxylic acid is a toxic intermediate of ethylene glycol metabolism.
• If left unchecked, it can be converted into oxalic acid, leading to renal failure.
2. Role of Thiamine (Vitamin B1):
• Thiamine acts as a cofactor for transketolase and related enzymes in amino acid metabolism.
• In this pathway, thiamine helps convert glyoxylic acid → α-hydroxy-β-ketoadipic acid, which is a non-toxic metabolite.
3. Therapeutic significance:
• Administration of thiamine in ethylene glycol poisoning helps shunt glyoxylic acid away from oxalate formation.
• This prevents calcium oxalate crystal deposition in kidneys and reduces renal toxicity.
4. Outcome:
• Instead of forming harmful oxalic acid, glyoxylic acid is converted to a harmless metabolite that can be safely excreted.

Summary:
Thiamine detoxifies glyoxylic acid by forming α-hydroxy-β-ketoadipic acid, a non-toxic product → reduces renal damage in ethylene glycol poisoning.

Question 14

Why are Pyridoxine and Thiamine given together in ethylene glycol poisoning?

Answer 14

Both antidotes redirect Glyoxylic Acid into non-toxic pathways, decreasing the formation of Oxalic Acid.

Rationale: By enhancing these alternative metabolic routes, they reduce renal toxicity and support safe excretion of metabolites.

Question 15

What is the first step in ethylene glycol metabolism?

Answer 15

Ethylene Glycol → (Alcohol Dehydrogenase) → Glycolaldehyde

Rationale & Concept: Alcohol dehydrogenase converts ethylene glycol into its first toxic intermediate. This step is crucial because inhibiting this enzyme (with ethanol or fomepizole) prevents formation of downstream toxic metabolites.

Question 16

What happens to glycolaldehyde in ethylene glycol metabolism?

Answer 16

Glycolaldehyde → (Aldehyde Dehydrogenase) → Glycolic Acid

Rationale & Concept: Aldehyde dehydrogenase oxidizes glycolaldehyde to glycolic acid, which is highly acidic and causes metabolic acidosis. Controlling this step is key to preventing systemic acid-base disturbances.

Question 17

correct sequence in ethylene glycol metabolism is

Answer 17

Ethylene Glycol Metabolism and Detoxification
1. Stepwise metabolism:
• Ethylene glycol → (Alcohol dehydrogenase) → Glycolaldehyde
• Glycolaldehyde → (Aldehyde dehydrogenase) → Glycolic acid
• Glycolic acid is partly toxic → causes metabolic acidosis
• Glycolic acid → Glyoxylic acid
2. Glyoxylic acid – the key branching point:
• From here, metabolism can go in toxic or non-toxic directions:
Non-toxic pathways (enhanced by vitamins):
• Glyoxylic acid + Pyridoxine (Vitamin B6) → Glycine → Hippuric acid → safely excreted
• Glyoxylic acid + Thiamine (Vitamin B1) → α-Hydroxy-β-ketoadipic acid → non-toxic
Toxic pathway (to avoid):
• Glyoxylic acid → Oxalic acid (+ Formic acid in methanol poisoning) → binds calcium → Calcium oxalate crystals → renal toxicity
3. Concept / Rationale:
• Glycolic acid is partly toxic (causes metabolic acidosis), but Glyoxylic acid is the critical branching metabolite.
• Antidotes (Pyridoxine and Thiamine) work at the Glyoxylic acid step, redirecting it into non-toxic pathways and preventing oxalate formation, which protects the kidneys.

Question 18

Which metabolite mainly causes metabolic acidosis?

Answer 18

Glycolic Acid

Rationale & Concept: Glycolic acid accumulates in the blood, increasing hydrogen ion concentration. Understanding this explains why patients develop high-anion-gap metabolic acidosis.

Question 19

What happens to the remaining toxic metabolites if antidotes are not given?

Answer 19

Glyoxylic Acid → Oxalic Acid & Formic Acid → Toxicity (Renal Failure + Metabolic Acidosis)

Rationale & Concept: Without cofactors, more Glyoxylic Acid is converted to Oxalic Acid and Formic Acid, which explains why untreated poisoning leads to kidney injury and severe acidosis.

Question 20

How can the formation of toxic metabolites be prevented in methanol and ethylene glycol

Answer 20

Ethanol / Fomepizole in Ethylene Glycol Poisoning
1. Mechanism of action:
• Ethanol and Fomepizole competitively inhibit alcohol dehydrogenase (ADH).
• ADH is the enzyme that converts ethylene glycol → glycolaldehyde (the first toxic metabolite).
2. Effect of inhibition:
• By blocking ADH, ethylene glycol is not metabolized into:
• Glycolaldehyde
• Glycolic acid (causes metabolic acidosis)
• Glyoxylic acid → Oxalic acid (causes renal toxicity)
• Essentially, toxicity is prevented or greatly reduced.
3. Concept / Rationale:
• The toxicity of ethylene glycol is due to its metabolites, not ethylene glycol itself.
• Competitive inhibition at ADH keeps ethylene glycol in its relatively non-toxic form, allowing renal excretion without causing acidosis or kidney damage.

Question 21

Colorless, pungent odor

Answer 21

formaldehyde

Question 22

formaldehyde commonly used?

Answer 22

used as EMBALMING fluid and preservative in VACCINES

Question 23

Local: Mucosal irritation
Systemic: CNS depression, coma, metabolic acidosis

Answer 23

Formaldehyde Poisoining

Formaldehyde Toxicity
1. Local effect – Mucosal irritation:
• Formaldehyde is highly reactive and a strong electrophile.
• It denatures proteins on contact with mucous membranes.
• Result: burning sensation, irritation of eyes, nose, throat, and respiratory tract.
2. Systemic effect:
• If absorbed (inhalation, ingestion, or skin):
• CNS depression – formaldehyde interferes with normal neuronal function.
• Coma – high doses can severely depress the central nervous system.
• Metabolic acidosis – formaldehyde is rapidly metabolized in the liver:
• Formaldehyde → Formic acid
• Accumulation of formic acid → high anion gap metabolic acidosis
3. Concept / Rationale:
• Local toxicity: direct protein denaturation → irritation.
• Systemic toxicity: liver metabolism produces formic acid, which is responsible for CNS depression, acidosis, and potential organ damage.

Question 24

What is the antidote for formaldehyde poisoning?

Answer 24

NaHCO₃ (Sodium Bicarbonate)

Question 25

Primary ingredient in fingernail polish remover, airplane glues, varnish, and rubber cement

Answer 25

Acetone

Question 26

What are the clinical presentations of acetone exposure?

Answer 26

Acetone → CNS Depression, Coma, Respiratory Depression Rationale: 1. High lipid solubility: • Acetone is highly lipid‑soluble, so it easily crosses the blood–brain barrier. 2. Depresses neuronal activity: • In the brain, acetone acts like other organic solvents and alcohols: • It enhances inhibitory neurotransmission (GABA‑like effect). • It suppresses excitatory neuronal firing. • Result: general CNS depression. 3. Dose‑dependent effect: • Low levels → dizziness, euphoria, drowsiness • Higher levels → confusion, stupor • Very high levels → coma 4. Effect on respiratory center: • The medullary respiratory center is sensitive to CNS depressants. • Acetone suppresses this center → slowed and shallow breathing. • Severe suppression → respiratory depression and possible arrest. 5. Concept summary: • Acetone’s lipid solubility lets it rapidly enter the brain. • It depresses neuronal signaling in a dose‑dependent manner. • At high concentrations, this leads to coma and respiratory failure.

Question 27

What is the antidote/treatment for acetone toxicity?

Answer 27

Neutralization with milk or H₂O RATIONALE • Milk or water acts as a diluent: • Dilutes acetone in the GI tract → lowers local concentration. • Reduces mucosal irritation → prevents nausea, vomiting, and burning sensation. Systemic effects (CNS depression, respiratory depression) require supportive care, not dilution.

Question 28

What are hydrocarbons derived from?

Answer 28

Petroleum Distillation

Question 29

How are hydrocarbons classified?

Answer 29

By Volatility and Viscosity Volatility: • The tendency of a substance to evaporate or vaporize at a given temperature. • High volatility → evaporates easily (e.g., gasoline). Viscosity: • The resistance of a fluid to flow. • High viscosity → flows slowly (e.g., motor oil). Inverse relationship: • High viscosity → low volatility • Low viscosity → high volatility • Reason: • Viscosity reflects intermolecular attractions that also control ease of vaporization. • Strong intermolecular forces → molecules stick together → harder to flow and harder to evaporate.

Question 30

Give examples of hydrocarbons with high volatility and very low viscosity.

Answer 30

Methane, Butane

Question 31

Give examples of hydrocarbons with intermediate volatility and low viscosity.

Answer 31

Turpentine, Gasoline

Question 32

Give examples of hydrocarbons with low volatility and intermediate viscosity.

Answer 32

Kerosene

Question 33

Give examples of hydrocarbons with very low volatility and high viscosity.

Answer 33

Mineral Oil

Question 34

What are the routes of administration (ROA) for hydrocarbons?

Answer 34

Ingestion (PO) — accidental Dermal, Inhalational — intentional

Question 35

What is the mechanism of toxicity (MOT) of hydrocarbons?

Answer 35

Cannot be metabolized → CNS depression, pneumonitis, cytotoxicity, mutagenicity Rationale / MOT: 1. Not metabolized effectively: • Many simple hydrocarbons (e.g., gasoline, kerosene, benzene derivatives) are poorly metabolized or metabolized very slowly. • They persist in tissues, especially fat and brain because they are lipid-soluble. 2. CNS depression: • Being highly lipid-soluble, hydrocarbons cross the blood–brain barrier easily. • They dissolve in neuronal membranes and disrupt ion channels and neurotransmission. • Result: dizziness → drowsiness → CNS depression → coma. 3. Pneumonitis (especially by aspiration): • Low viscosity and high volatility allow hydrocarbons to be easily aspirated into lungs. • They dissolve pulmonary surfactant and damage alveolar cells. • Leads to chemical pneumonitis. 4. Cytotoxicity: • Hydrocarbons dissolve lipid membranes of cells. • This causes membrane disruption, enzyme dysfunction, and cell death. 5. Mutagenicity (some hydrocarbons): • Aromatic hydrocarbons (e.g., benzene, PAHs) can form reactive metabolites or directly interact with DNA. • This leads to DNA damage, mutations, and cancer risk. Concept Summary: Because many hydrocarbons are not easily metabolized and are lipid-soluble, they accumulate in tissues, depress the CNS, damage lungs when aspirated, disrupt cell membranes (cytotoxicity), and some can damage DNA (mutagenicity).

Question 36

Q: What are the general clinical presentations of hydrocarbon exposure?

Answer 36

Cough, Atelectasis (lung collapse)

Question 37

Blood cancers

Answer 37

Benzene

Question 37

Euphoria, satiety (bisyo), rhabdomyolysis (severe muscle wasting) (RUGBY)

Answer 37

Toluene Rationale: 1. Euphoria: • Toluene is highly lipid-soluble, so it rapidly enters the brain. • It enhances inhibitory neurotransmission (GABA-like effect) and suppresses excitatory pathways. • Result: euphoria, intoxication, “high” feeling. 2. Satiety / addiction (“bisyo”): • Repeated exposure stimulates the dopamine reward pathway. • This causes craving and habitual use (sniffing, glue-sniffing). • Users feel a false sense of satisfaction or “busog sa high,” leading to addiction behavior. 3. Rhabdomyolysis (RUGBY): • Toluene causes: • CNS depression → prolonged immobility • Direct muscle toxicity • Hypoxia and metabolic disturbances • These lead to muscle cell breakdown → release of myoglobin → rhabdomyolysis. • Myoglobin can damage kidneys → acute renal failure.

Question 38

Arrhythmia

Answer 38

CFCs or Butane

Question 39

General presentations of hydrocarbon exposure:

Answer 39

Cough Atelectasis (lung collapse) Specific compound-related presentations: Toluene: 3. Euphoria 4. Satiety (bisyo) 5. Rhabdomyolysis (severe muscle wasting) (RUGBY) Benzene: 6. Blood cancers CFCs / Butane: 7. Arrhythmia

Question 40

What are the general treatments/antidotes for hydrocarbon toxicity?

Answer 40

Aspiration (for volatile substances in lungs), O₂ support, β₂-agonists 1. Short-acting β₂-agonists (SABAs) – rapid relief • Salbutamol / Albuterol (most common) • Terbutaline • Fenoterol 2. Long-acting β₂-agonists (LABAs) – maintenance therapy • Salmeterol • Formoterol

Question 41

Treatment/Antidote for Hydrocarbon Exposure: If lungs are affected (volatile substances already in the lungs):

Answer 41

Aspiration

Question 42

Treatment/Antidote for Hydrocarbon Exposure: Trap volatile oil that might be inhaled

Answer 42

Mineral Oil

Question 43

What is the odor of carbon tetrachloride?

Answer 43

Freshly mowed hay

Question 45

use in Non-flammable cleaning fluids and fire extinguishers

Answer 45

Carbon Tetrachloride

Question 46

What is the mechanism of toxicity (MOT) of carbon tetrachloride?

Answer 46

Displaces O₂ → Tissue hypoxia → Cell death Rationale/Concept: Carbon tetrachloride is a volatile solvent that reduces oxygen availability in tissues, leading to cellular hypoxia and necrosis.

Question 47

What are the toxic metabolites of carbon tetrachloride?

Answer 47

Epoxide, Phosgene Rationale/Concept: These metabolites are highly reactive and cause oxidative damage to cells, especially in the liver and kidneys.

Question 48

What are the clinical presentations of carbon tetrachloride toxicity?

Answer 48

Tissue hypoxia, Cell death

Question 49

What is the antidote/treatment for carbon tetrachloride poisoning?

Answer 49

O₂ supplementation