FMGE 2023 — Pharmacology

Q: A 50-year-old woman was prescribed a diuretic by a doctor to manage hypertension. Which of the following diuretics acts on site 'A' as marked in the given image?

Hydrochlorothiazide. ***Hydrochlorothiazide*** - Hydrochlorothiazide is a **thiazide diuretic** that acts on the **Distal Convoluted Tubule (DCT)**, which is indicated by the letter 'A' in the provided diagram. - It works by inhibiting the **Na+/Cl- cotransporter** in the early DCT, leading to increased excretion of sodium and water, which helps lower blood pressure. *Furosemide* - Furosemide is a potent **loop diuretic** that acts on the **thick ascending limb of the loop of Henle** (labeled as 'G'). - It inhibits the **Na+/K+/2Cl- cotransporter**, causing a significant increase in sodium and water excretion, making it more powerful than thiazides. *Acetazolamide* - Acetazolamide is a **carbonic anhydrase inhibitor**, and its primary site of action is the **Proximal Convoluted Tubule (PCT)** (labeled as 'D'). - It is a weak diuretic and is more commonly used for glaucoma, metabolic alkalosis, or altitude sickness rather than as a primary agent for hypertension. *Mannitol* - Mannitol is an **osmotic diuretic** that exerts its effect primarily in the **Proximal Convoluted Tubule (PCT)** and the **descending limb of the loop of Henle**. - It is administered intravenously and is used to reduce intracranial or intraocular pressure, not for the chronic management of hypertension. [Practice more Pharmacology PYQs on OnCourse]

Q: Which of the following diuretics primarily acts on the part labeled 'D' in the given diagram of a nephron?

Hydrochlorothiazide. ***Hydrochlorothiazide*** - The part labeled 'D' in the diagram is the **Distal Convoluted Tubule (DCT)**. **Thiazide diuretics**, such as hydrochlorothiazide, primarily act on this segment of the nephron. - They work by inhibiting the **Na+/Cl- cotransporter** in the DCT, which reduces the reabsorption of sodium and chloride from the tubular fluid, leading to increased water excretion. *Furosemide* - Furosemide is a **loop diuretic** that acts on the **thick ascending limb of the Loop of Henle** (part of B), not the DCT. - It is a more potent diuretic than thiazides because it inhibits the **Na+-K+-2Cl- cotransporter**, which is responsible for reabsorbing a significant portion of filtered sodium. *Acetazolamide* - Acetazolamide is a **carbonic anhydrase inhibitor** that primarily acts on the **Proximal Convoluted Tubule (PCT)** (labeled 'A'). - Its mechanism involves reducing the reabsorption of **bicarbonate (HCO3-)**, which leads to a mild diuretic effect and can cause metabolic acidosis. *Mannitol* - Mannitol is an **osmotic diuretic** that acts mainly in the **Proximal Convoluted Tubule (PCT)** and the **descending limb of the Loop of Henle**. - It is a pharmacologically inert substance that increases the **osmolarity** of the tubular fluid, thereby preventing water reabsorption. [Practice more Pharmacology PYQs on OnCourse]

Q: Which of the following statement is correct regarding the mechanism of action of labetalol?

Blocks both alpha and beta-adrenergic receptors.. ***Blocks both alpha and beta-adrenergic receptors*** - Labetalol is a unique **non-selective beta-blocker** (blocking $\beta_1$ and $\beta_2$) that also possesses **selective $\alpha_1$-adrenergic blocking activity**. - This combined mechanism makes it effective for conditions like **hypertensive emergencies**, providing both reduced heart rate (via beta block) and peripheral vasodilation (via alpha block). *Directly acts as arterial vasodilator resulting in indirect effect tachycardia* - While labetalol causes **vasodilation** (due to $\alpha_1$ blockade), it also **blocks $\beta$-receptors**, preventing the typical **reflex tachycardia** that occurs with direct vasodilators like hydralazine. - Its primary mechanism is receptor blockade, not direct smooth muscle relaxation. *Primarily acts as a vasodilator with little effect on arterioles* - Labetalol acts as a potent **arteriolar vasodilator** (via $\alpha_1$ blockade), which is crucial for lowering systemic vascular resistance and blood pressure. - Its vasodilatory effect is significant and targeted at arterioles. *Decreases peripheral vascular resistance by directly acting as a relaxant for vascular smooth muscles* - Labetalol decreases **peripheral vascular resistance (PVR)** through **antagonism of $\alpha_1$ receptors** in vascular smooth muscles, preventing vasoconstriction. - It does not act as a direct smooth muscle relaxant like nitroprusside or hydralazine. [Practice more Pharmacology PYQs on OnCourse]

Q: A psychiatrist prescribes lithium for a patient who is diagnosed with bipolar disorder. Which of the following statements is incorrect regarding lithium?

Hemodialysis is not useful in lithium overdose. ***Correct Answer: Hemodialysis is not useful in lithium overdose*** - This statement is **INCORRECT** (making it the right answer to this negation question) - **Hemodialysis IS actually very useful** in severe lithium toxicity - Lithium has low molecular weight (~7 Da), minimal protein binding, and small volume of distribution, making it effectively removed by hemodialysis - **Indications for hemodialysis in lithium toxicity:** Lithium levels >4 mEq/L, severe clinical toxicity (seizures, altered consciousness), or renal failure *Incorrect Option: Lithium is teratogenic if given to pregnant females* - This statement is TRUE, so it's not the answer - Lithium causes **Ebstein's anomaly** (downward displacement of tricuspid valve) when given in first trimester - Risk is 1-2% (20x higher than general population) - FDA pregnancy category D *Incorrect Option: Lithium toxicity is exacerbated with thiazide* - This statement is TRUE, so it's not the answer - Thiazide diuretics decrease renal lithium clearance by promoting sodium depletion - This leads to **compensatory increase in proximal tubular reabsorption** of both sodium and lithium - NSAIDs and ACE inhibitors also increase lithium levels similarly *Incorrect Option: Lithium can decrease thyroid hormone levels* - This statement is TRUE, so it's not the answer - Lithium inhibits thyroid hormone synthesis and release, causing **hypothyroidism in 5-35%** of patients - Mechanism: Inhibits iodine uptake and blocks thyroid hormone release - Requires regular thyroid function monitoring (TSH, T3, T4) during lithium therapy [Practice more Pharmacology PYQs on OnCourse]

Q: Which of these drugs stimulates PPAR-alpha (Peroxisome proliferator-activated receptor alpha)?

Gemfibrozil. ***Gemfibrozil***- It belongs to the **fibrate class** of lipid-lowering drugs, and its primary mechanism is activating the **Peroxisome Proliferator-Activated Receptor alpha (PPAR-alpha)**.- PPAR-alpha activation leads to increased synthesis of **lipoprotein lipase (LPL)**, enhancing the catabolism of **VLDL** and chylomicrons, which effectively lowers **triglyceride** levels.*Ezetimibe*- This drug selectively inhibits the absorption of dietary and biliary cholesterol by blocking the **NPC1L1 (Niemann-Pick C1-Like 1)** transporter protein located on the brush border of the small intestine enterocytes.- It does not interact with PPAR-alpha but is typically used to reduce **LDL cholesterol**, often in combination with statins.*Colestipol*- It is a **bile acid sequestrant** (resin) that binds negatively charged bile acids in the intestinal lumen, forming a non-absorbable complex that is excreted in stool.- The loss of bile acids forces the liver to increase the synthesis of new bile acids from cholesterol, thereby upregulating hepatic **LDL receptors** and reducing plasma LDL levels.*Simvastatin*- This drug is an HMG-CoA reductase inhibitor (**statin**), which is the rate-limiting enzyme in hepatic cholesterol synthesis.- By reducing intracellular cholesterol synthesis, it causes upregulation of surface **LDL receptors** on hepatocytes, increasing LDL clearance from the blood. [Practice more Pharmacology PYQs on OnCourse]

20 Previous Year Questions with Answers & Explanations

Questions

A 50-year-old woman was prescribed a diuretic by a doctor to manage hypertension. Which of the following diuretics acts on site 'A' as marked in the given image?

Which of the following diuretics primarily acts on the part labeled 'D' in the given diagram of a nephron?

Which of the following statement is correct regarding the mechanism of action of labetalol?

A psychiatrist prescribes lithium for a patient who is diagnosed with bipolar disorder. Which of the following statements is incorrect regarding lithium?

Which of these drugs stimulates PPAR-alpha (Peroxisome proliferator-activated receptor alpha)?

Which drug is most appropriate for treating diarrhea in a patient treated for colorectal carcinoma with 5-fluorouracil?

Which of the following drugs are used to treat chemotherapy-induced nausea and vomiting?

A patient on anti-cancer therapy developed an infection. Blood analysis revealed neutropenia. Which of the following drugs is likely to be effective in this patient?

A 38-year-old professor with depression requests you to prescribe an antidepressant that would be least likely to cause sexual dysfunction. Which of the following drugs would you prescribe?

Q10

A 50-year-old factory worker was brought to the emergency room with complaints of headache, vomiting, and blurring of vision after he consumed local spirit. Which of the following is used for the treatment of his condition?

FMGE 2023 - Pharmacology FMGE Practice Questions and MCQs

Question 1: A 50-year-old woman was prescribed a diuretic by a doctor to manage hypertension. Which of the following diuretics acts on site 'A' as marked in the given image?

A. Acetazolamide
B. Mannitol
C. Hydrochlorothiazide (Correct Answer)
D. Furosemide

Explanation: ***Hydrochlorothiazide*** - Hydrochlorothiazide is a **thiazide diuretic** that acts on the **Distal Convoluted Tubule (DCT)**, which is indicated by the letter 'A' in the provided diagram. - It works by inhibiting the **Na+/Cl- cotransporter** in the early DCT, leading to increased excretion of sodium and water, which helps lower blood pressure. *Furosemide* - Furosemide is a potent **loop diuretic** that acts on the **thick ascending limb of the loop of Henle** (labeled as 'G'). - It inhibits the **Na+/K+/2Cl- cotransporter**, causing a significant increase in sodium and water excretion, making it more powerful than thiazides. *Acetazolamide* - Acetazolamide is a **carbonic anhydrase inhibitor**, and its primary site of action is the **Proximal Convoluted Tubule (PCT)** (labeled as 'D'). - It is a weak diuretic and is more commonly used for glaucoma, metabolic alkalosis, or altitude sickness rather than as a primary agent for hypertension. *Mannitol* - Mannitol is an **osmotic diuretic** that exerts its effect primarily in the **Proximal Convoluted Tubule (PCT)** and the **descending limb of the loop of Henle**. - It is administered intravenously and is used to reduce intracranial or intraocular pressure, not for the chronic management of hypertension.

Question 2: Which of the following diuretics primarily acts on the part labeled 'D' in the given diagram of a nephron?

A. Acetazolamide
B. Mannitol
C. Hydrochlorothiazide (Correct Answer)
D. Furosemide

Explanation: ***Hydrochlorothiazide*** - The part labeled 'D' in the diagram is the **Distal Convoluted Tubule (DCT)**. **Thiazide diuretics**, such as hydrochlorothiazide, primarily act on this segment of the nephron. - They work by inhibiting the **Na+/Cl- cotransporter** in the DCT, which reduces the reabsorption of sodium and chloride from the tubular fluid, leading to increased water excretion. *Furosemide* - Furosemide is a **loop diuretic** that acts on the **thick ascending limb of the Loop of Henle** (part of B), not the DCT. - It is a more potent diuretic than thiazides because it inhibits the **Na+-K+-2Cl- cotransporter**, which is responsible for reabsorbing a significant portion of filtered sodium. *Acetazolamide* - Acetazolamide is a **carbonic anhydrase inhibitor** that primarily acts on the **Proximal Convoluted Tubule (PCT)** (labeled 'A'). - Its mechanism involves reducing the reabsorption of **bicarbonate (HCO3-)**, which leads to a mild diuretic effect and can cause metabolic acidosis. *Mannitol* - Mannitol is an **osmotic diuretic** that acts mainly in the **Proximal Convoluted Tubule (PCT)** and the **descending limb of the Loop of Henle**. - It is a pharmacologically inert substance that increases the **osmolarity** of the tubular fluid, thereby preventing water reabsorption.

Question 3: Which of the following statement is correct regarding the mechanism of action of labetalol?

A. Blocks both alpha and beta-adrenergic receptors. (Correct Answer)
B. Primarily acts as a vasodilator with little effect on arterioles
C. Decreases peripheral vascular resistance by directly acting as a relaxant for vascular smooth muscles.
D. Directly acts as arterial vasodilator resulting in indirect effect tachycardia.

Explanation: ***Blocks both alpha and beta-adrenergic receptors*** - Labetalol is a unique **non-selective beta-blocker** (blocking $\beta_1$ and $\beta_2$) that also possesses **selective $\alpha_1$-adrenergic blocking activity**. - This combined mechanism makes it effective for conditions like **hypertensive emergencies**, providing both reduced heart rate (via beta block) and peripheral vasodilation (via alpha block). *Directly acts as arterial vasodilator resulting in indirect effect tachycardia* - While labetalol causes **vasodilation** (due to $\alpha_1$ blockade), it also **blocks $\beta$-receptors**, preventing the typical **reflex tachycardia** that occurs with direct vasodilators like hydralazine. - Its primary mechanism is receptor blockade, not direct smooth muscle relaxation. *Primarily acts as a vasodilator with little effect on arterioles* - Labetalol acts as a potent **arteriolar vasodilator** (via $\alpha_1$ blockade), which is crucial for lowering systemic vascular resistance and blood pressure. - Its vasodilatory effect is significant and targeted at arterioles. *Decreases peripheral vascular resistance by directly acting as a relaxant for vascular smooth muscles* - Labetalol decreases **peripheral vascular resistance (PVR)** through **antagonism of $\alpha_1$ receptors** in vascular smooth muscles, preventing vasoconstriction. - It does not act as a direct smooth muscle relaxant like nitroprusside or hydralazine.

Question 4: A psychiatrist prescribes lithium for a patient who is diagnosed with bipolar disorder. Which of the following statements is incorrect regarding lithium?

A. Lithium is teratogenic if given to pregnant females
B. Lithium toxicity is exacerbated with thiazide
C. Hemodialysis is not useful in lithium overdose (Correct Answer)
D. Lithium can decrease thyroid hormone levels

Explanation: ***Correct Answer: Hemodialysis is not useful in lithium overdose*** - This statement is **INCORRECT** (making it the right answer to this negation question) - **Hemodialysis IS actually very useful** in severe lithium toxicity - Lithium has low molecular weight (~7 Da), minimal protein binding, and small volume of distribution, making it effectively removed by hemodialysis - **Indications for hemodialysis in lithium toxicity:** Lithium levels >4 mEq/L, severe clinical toxicity (seizures, altered consciousness), or renal failure *Incorrect Option: Lithium is teratogenic if given to pregnant females* - This statement is TRUE, so it's not the answer - Lithium causes **Ebstein's anomaly** (downward displacement of tricuspid valve) when given in first trimester - Risk is 1-2% (20x higher than general population) - FDA pregnancy category D *Incorrect Option: Lithium toxicity is exacerbated with thiazide* - This statement is TRUE, so it's not the answer - Thiazide diuretics decrease renal lithium clearance by promoting sodium depletion - This leads to **compensatory increase in proximal tubular reabsorption** of both sodium and lithium - NSAIDs and ACE inhibitors also increase lithium levels similarly *Incorrect Option: Lithium can decrease thyroid hormone levels* - This statement is TRUE, so it's not the answer - Lithium inhibits thyroid hormone synthesis and release, causing **hypothyroidism in 5-35%** of patients - Mechanism: Inhibits iodine uptake and blocks thyroid hormone release - Requires regular thyroid function monitoring (TSH, T3, T4) during lithium therapy

Question 5: Which of these drugs stimulates PPAR-alpha (Peroxisome proliferator-activated receptor alpha)?

A. Ezetimibe
B. Colestipol
C. Simvastatin
D. Gemfibrozil (Correct Answer)

Explanation: ***Gemfibrozil***- It belongs to the **fibrate class** of lipid-lowering drugs, and its primary mechanism is activating the **Peroxisome Proliferator-Activated Receptor alpha (PPAR-alpha)**.- PPAR-alpha activation leads to increased synthesis of **lipoprotein lipase (LPL)**, enhancing the catabolism of **VLDL** and chylomicrons, which effectively lowers **triglyceride** levels.*Ezetimibe*- This drug selectively inhibits the absorption of dietary and biliary cholesterol by blocking the **NPC1L1 (Niemann-Pick C1-Like 1)** transporter protein located on the brush border of the small intestine enterocytes.- It does not interact with PPAR-alpha but is typically used to reduce **LDL cholesterol**, often in combination with statins.*Colestipol*- It is a **bile acid sequestrant** (resin) that binds negatively charged bile acids in the intestinal lumen, forming a non-absorbable complex that is excreted in stool.- The loss of bile acids forces the liver to increase the synthesis of new bile acids from cholesterol, thereby upregulating hepatic **LDL receptors** and reducing plasma LDL levels.*Simvastatin*- This drug is an HMG-CoA reductase inhibitor (**statin**), which is the rate-limiting enzyme in hepatic cholesterol synthesis.- By reducing intracellular cholesterol synthesis, it causes upregulation of surface **LDL receptors** on hepatocytes, increasing LDL clearance from the blood.

Question 6: Which drug is most appropriate for treating diarrhea in a patient treated for colorectal carcinoma with 5-fluorouracil?

A. Ciprofloxacin
B. Atropine
C. Ornidazole
D. Loperamide (Correct Answer)

Explanation: ***Loperamide*** - **Loperamide** is the standard, first-line agent used for controlling **chemotherapy-induced diarrhea (CID)**, especially that caused by 5-fluorouracil (5-FU). - High doses of loperamide are often required in a fixed, scheduled regimen (e.g., 2 mg every 2 hours) until diarrhea resolves, to decrease gut motility and intestinal fluid secretion. *Ciprofloxacin* - **Ciprofloxacin** is an antibiotic used when diarrhea is suspected to be infectious or for prophylaxis against **neutropenic fever**, but it is not the symptomatic treatment for 5-FU toxicity. - It does not address the underlying pathology of 5-FU induced enteritis, which involves mucosal damage and malabsorption. *Atropine* - **Atropine** is primarily used to treat acute **cholinergic syndrome** (early diarrhea, sweating, lacrimation) which is a major toxicity associated with the chemotherapy drug **Irinotecan**, not 5-FU. - As an anticholinergic, it is not the preferred or protocol-driven agent for managing severe, non-infectious 5-FU-induced diarrhea. *Ornidazole* - This is an **antibiotic/antiprotozoal** medication, mainly effective against organisms like *Giardia* or *Amoeba*. - It is not indicated for symptomatic management of non-infectious **chemotherapy-induced toxicity** resulting from the direct mucosal damage inflicted by 5-FU.

Question 7: Which of the following drugs are used to treat chemotherapy-induced nausea and vomiting?

A. Doxylamine + domperidone + aprepitant
B. Prochlorperazine + metoclopramide + domperidone
C. Dexamethasone + metoclopramide + domperidone
D. Granisetron + dexamethasone + aprepitant (Correct Answer)

Explanation: ***Granisetron + dexamethasone + aprepitant***- This triple-therapy combination represents the gold standard for preventing and treating highly emetogenic chemotherapy (HEC)-induced nausea and vomiting (CINV).- **Granisetron** (a **5-HT3 receptor antagonist**) blocks acute CINV, **dexamethasone** (a corticosteroid) enhances the antiemetic effect, and **aprepitant** (an **NK-1 receptor antagonist**) covers the delayed phase of CINV.*Doxylamine + domperidone + aprepitant*- **Doxylamine** is primarily used for nausea in pregnancy (mixed with pyridoxine) and is not a standard first-line agent for CINV prophylaxis.- **Domperidone** (a D2 antagonist) is infrequently used for CINV due to concerns over QT prolongation and is significantly less effective than 5-HT3 antagonists.*Prochlorperazine + metoclopramide + domperidone*- This combination consists primarily of **dopamine D2 receptor antagonists** and is insufficient for prophylaxis against moderately or highly emetogenic chemotherapy.- It lacks both a **5-HT3 inhibitor** (crucial for acute CINV) and an **NK-1 inhibitor** (crucial for delayed CINV and highly emetogenic regimens).*Dexamethasone + metoclopramide + domperidone*- This regimen is missing the key highly potent antiemetics: the **5-HT3 receptor antagonist** (like granisetron or ondansetron) and the **NK-1 receptor antagonist** (like aprepitant), which are indispensable for highly emetogenic chemotherapy.- While **dexamethasone** is standard, relying solely on **metoclopramide** and **domperidone** (D2 antagonists) is an inadequate primary strategy against severe CINV.

Question 8: A patient on anti-cancer therapy developed an infection. Blood analysis revealed neutropenia. Which of the following drugs is likely to be effective in this patient?

A. Filgrastim (Correct Answer)
B. Epoetin alfa
C. Oprelvekin
D. Romiplostim

Explanation: ***Filgrastim***- It is a recombinant form of **granulocyte colony-stimulating factor (G-CSF)**, which stimulates the proliferation and differentiation of neutrophil precursors in the bone marrow.- It is the standard treatment for **chemotherapy-induced neutropenia** (as seen in patients on anti-cancer therapy) to raise neutrophil counts and reduce infection risk.*Romiplostim*- This drug is a **thrombopoietin (TPO) receptor agonist** used to stimulate platelet production.- It is indicated for conditions like **immune thrombocytopenia** and would not be effective in stimulating neutrophil recovery in neutropenia.*Oprelvekin*- It is a recombinant form of **interleukin-11 (IL-11)**, indicated specifically for the prevention of severe **thrombocytopenia** following myelosuppressive chemotherapy.- While it has some broad hematopoietic effects, its primary clinical use is platelet restoration, making it ineffective for acute **neutropenia** in this context.*Epoetin alfa*- This drug is a recombinant form of **erythropoietin (EPO)**, primarily used to stimulate red blood cell production to treat **anemia**.- It specifically targets the erythroid lineage and has no clinical utility in increasing **neutrophil** counts.

Question 9: A 38-year-old professor with depression requests you to prescribe an antidepressant that would be least likely to cause sexual dysfunction. Which of the following drugs would you prescribe?

A. Bupropion (Correct Answer)
B. Venlafaxine
C. Fluoxetine
D. Escitalopram

Explanation: ***Bupropion***- Bupropion is a **norepinephrine-dopamine reuptake inhibitor (NDRI)** that differs structurally and mechanically from SSRIs and SNRIs. - It is known for its relatively neutral effect on sexual function, often having the **lowest incidence** of sexual side effects among commonly prescribed antidepressants, and is sometimes used to treat SSRI-induced sexual dysfunction.*Escitalopram*- As a **selective serotonin reuptake inhibitor (SSRI)**, escitalopram frequently causes sexual side effects such as decreased libido, delayed orgasm, and anorgasmia.- This class of drugs elevates **serotonin levels**, which is strongly implicated in causing sexual dysfunction.*Venlafaxine*- Venlafaxine is a **serotonin-norepinephrine reuptake inhibitor (SNRI)**, and its serotonergic component carries a medium-to-high risk of causing sexual dysfunction.- The common sexual side effects include **erectile dysfunction** in men and reduced arousal in women.*Fluoxetine*- Fluoxetine is a commonly prescribed **SSRI** with a significant association with sexual side effects, including inhibited orgasm and reduced libido.- Its long half-life means that these adverse effects, if they occur, can persist following **discontinuation**.

Question 10: A 50-year-old factory worker was brought to the emergency room with complaints of headache, vomiting, and blurring of vision after he consumed local spirit. Which of the following is used for the treatment of his condition?

A. Fomepizole (Correct Answer)
B. Flumazenil
C. N-acetyl cysteine
D. Naloxone

Explanation: ***Fomepizole***- Fomepizole is the preferred antidote for **methanol** and **ethylene glycol** poisoning because it competitively inhibits the enzyme **alcohol dehydrogenase** (ADH).- By inhibiting ADH, it prevents the metabolism of methanol into its toxic metabolite, **formic acid**, which is responsible for the characteristic **ocular toxicity** (blurring of vision) and **metabolic acidosis** seen in this patient.*Flumazenil*- Flumazenil is a competitive antagonist used to reverse the effects of **benzodiazepines**, primarily in cases of overdose or to reverse procedural sedation.- It has no role in the treatment of **methanol poisoning**, which causes toxicity via the accumulation of **formic acid**.*N-acetyl cysteine*- **N-acetyl cysteine (NAC)** is the specific antidote for **acetaminophen** (paracetamol) overdose, as it replenishes **glutathione** stores in the liver.- It is ineffective in the treatment of **methanol poisoning**, which requires ADH inhibition or **hemodialysis** to remove the toxins.*Naloxone*- **Naloxone** is an opioid antagonist used specifically to rapidly reverse the effects of **opioid overdose** by competing for the opioid receptors.- The patient's symptoms (headache, vomiting, blurring of vision) are classic for **methanol toxicity** and are not indicative of opioid overdose.