Drug-food interactions US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Drug-food interactions. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Drug-food interactions US Medical PG Question 1: A 72-year-old man presents to the emergency department with a 1 hour history of bruising and bleeding. He says that he fell and scraped his knee on the ground. Since then, he has been unable to stop the bleeding and has developed extensive bruising around the area. He has a history of gastroesophageal reflux disease, hypertension, and atrial fibrillation for which he is taking an oral medication. He says that he recently started taking omeprazole for reflux. Which of the following processes is most likely inhibited in this patient?
- A. Sulfation
- B. Oxidation (Correct Answer)
- C. Filtration
- D. Acetylation
- E. Glucuronidation
Drug-food interactions Explanation: ***Oxidation***
- The patient is taking **omeprazole**, a proton pump inhibitor, which is a known **CYP450 inhibitor**.
- Since the patient is also on an **oral anticoagulant** for atrial fibrillation, inhibition of CYP450 enzymes can reduce the metabolism of the anticoagulant, leading to **increased anticoagulant effect** and subsequent bleeding and bruising.
*Sulfation*
- **Sulfation** is a phase II metabolic reaction that converts compounds into more polar and excretable forms, but omeprazole primarily affects phase I metabolism involving CYP450 enzymes.
- While sulfation can be important for the metabolism of some drugs, it is not the primary process inhibited by omeprazole to cause increased bleeding with oral anticoagulants.
*Filtration*
- **Filtration** is a renal process and not a metabolic enzyme pathway affected by omeprazole.
- Omeprazole's interaction with anticoagulants mainly occurs through hepatic metabolism, not renal filtration.
*Acetylation*
- **Acetylation** is a phase II metabolic reaction, primarily carried out by **N-acetyltransferases**.
- Omeprazole is primarily known to interact with **CYP450 enzymes** (phase I metabolism) rather than N-acetyltransferases.
*Glucuronidation*
- **Glucuronidation** is a phase II metabolic reaction involving **UGT enzymes** that typically inactivates and increases the excretion of drugs.
- While important for drug metabolism, omeprazole's primary drug interactions leading to increased anticoagulant effects are via **CYP450 inhibition** (phase I metabolism), not directly through glucuronidation.
Drug-food interactions US Medical PG Question 2: A 75-year-old female patient comes to the emergency department with altered mental status. She is brought in by her daughter with whom the patient lives. The patient’s daughter said they were watching TV when her mother became unresponsive. On exam the patient withdraws to pain but does not open her eyes or speak. An emergent head CT is done and shows an intracranial bleed. The patient is moved to the ICU and intubated. Further history is obtained from the daughter. The patient has a past medical history of diabetes and a previous stroke. Her medications are metformin and warfarin. The patient is compliant with all of her medications. The daughter says that the patient changed her diet about 1 month ago in response to a diet she saw on a talk show. Which of the following foods is most likely to cause the pathology seen in this patient?
- A. Grapefruit juice (Correct Answer)
- B. St. John’s wort
- C. Green tea
- D. Chili peppers
- E. Spinach
Drug-food interactions Explanation: ***Grapefruit juice***
- **Grapefruit juice** is a potent inhibitor of **cytochrome P450 3A4 (CYP3A4)**, which is involved in the metabolism of **warfarin**.
- Inhibition of warfarin metabolism leads to increased warfarin levels, subsequently potentiating its **anticoagulant effect** and significantly increasing the risk of **bleeding**, including dangerous **intracranial hemorrhage**.
*St. John’s wort*
- **St. John's wort** is a known **CYP3A4 inducer**, meaning it increases the metabolism of drugs like warfarin.
- This typically leads to **decreased warfarin efficacy** and thus an increased risk of **thrombosis**, not bleeding.
*Green tea*
- **Green tea** contains **vitamin K**, which can **antagonize the effects of warfarin**.
- Ingesting large amounts of green tea could potentially *reduce* warfarin's anticoagulant effect, increasing the risk of clotting, rather than bleeding.
*Chili peppers*
- **Chili peppers** do not have a well-documented significant interaction with **warfarin** that would lead to increased bleeding risk.
- Their primary effects relate to gastric irritation or altered sensation, not anticoagulant modulation.
*Spinach*
- **Spinach** is high in **vitamin K**, which is a crucial factor in blood clotting and is directly antagonized by **warfarin**.
- Increased intake of spinach would likely **decrease the efficacy of warfarin**, leading to a higher risk of **clotting**, not bleeding.
Drug-food interactions US Medical PG Question 3: A 58-year-old man comes to the physician because of severe muscle aches and fatigue for 3 days. Last week he was diagnosed with atypical pneumonia and treated with clarithromycin. He has hyperlipidemia for which he takes lovastatin. Physical examination shows generalized tenderness of the proximal muscles in the upper and lower extremities. Serum studies show an elevated creatine kinase concentration. This patient's current symptoms are most likely caused by inhibition of which of the following hepatic enzymes?
- A. CYP2E1
- B. CYP3A4 (Correct Answer)
- C. CYP2C9
- D. CYP1A2
- E. CYP2C19
Drug-food interactions Explanation: ***CYP3A4***
- The patient is taking **lovastatin**, which is metabolized by **CYP3A4**. **Clarithromycin** is a potent **CYP3A4 inhibitor**.
- Inhibition of **CYP3A4** by clarithromycin leads to increased lovastatin levels, causing statin-induced **myopathy** (muscle aches, fatigue, and elevated creatine kinase).
*CYP2E1*
- This enzyme is primarily involved in the metabolism of compounds like **ethanol** and **acetaminophen**, not lovastatin.
- Its inhibition would not explain the interaction between clarithromycin and lovastatin.
*CYP2C9*
- This enzyme metabolizes drugs such as **warfarin** and **NSAIDs**, but it is not the primary enzyme responsible for lovastatin metabolism or its interaction with clarithromycin.
- Inhibition of **CYP2C9** would not lead to the described myopathy in this context.
*CYP1A2*
- **CYP1A2** is involved in the metabolism of drugs like **caffeine** and **theophylline**.
- It does not play a significant role in the metabolism of lovastatin, and its inhibition would not cause the observed symptoms.
*CYP2C19*
- **CYP2C19** metabolizes drugs such as **clopidogrel** and **omeprazole**.
- It is not the target enzyme for the interaction between lovastatin and clarithromycin.
Drug-food interactions US Medical PG Question 4: A 25-year-old woman presents to her college campus clinic with the complaint of being unable to get up for her morning classes. She says that, because of this, her grades are being affected. For the past 6 weeks, she says she has been feeling depressed because her boyfriend dumped her. She finds herself very sleepy, sleeping in most mornings, eating more snacks and fast foods, and feeling drained of energy. She is comforted by her friend’s efforts to cheer her up but still feels guarded around any other boy that shows interest in her. The patient says she had similar symptoms 7 years ago for which she was prescribed several selective serotonin reuptake inhibitors (SSRIs) and a tricyclic antidepressant (TCA). However, none of the medications provided any long-term relief. She has prescribed a trial of Phenelzine to treat her symptoms. Past medical history is significant for a long-standing seizure disorder well managed with phenytoin. Which of the following statements would most likely be relevant to this patient’s new medication?
- A. “This medication is known to cause anorgasmia during treatment.”
- B. “You will have a risk for cardiotoxicity from this medication.”
- C. “A common side effect of this medication is sedation.”
- D. “While taking this medication, you should avoid drinking red wine.” (Correct Answer)
- E. “While on this medication, you may have a decreased seizure threshold.”
Drug-food interactions Explanation: ***"While taking this medication, you should avoid drinking red wine."***
- Phenelzine is a **monoamine oxidase inhibitor (MAOI)**. MAOIs inhibit the breakdown of **tyramine**, an amine found in fermented foods like red wine, aged cheeses, cured meats, and pickled foods.
- Consuming tyramine-rich foods with an MAOI can lead to a **hypertensive crisis**, characterized by a sudden, severe increase in blood pressure which can cause headaches, palpitations, and potentially stroke.
- This dietary counseling is **essential and immediately actionable** patient education when starting an MAOI.
*"This medication is known to cause anorgasmia during treatment."*
- While sexual dysfunction can occur with many antidepressants, **anorgasmia** is much more common and severe with **SSRIs (Selective Serotonin Reuptake Inhibitors)** than with MAOIs.
- MAOIs like phenelzine have a different mechanism of action and generally have a lower incidence of sexual side effects compared to SSRIs.
*"You will have a risk for cardiotoxicity from this medication."*
- **Cardiotoxicity** is a significant concern with **tricyclic antidepressants (TCAs)**, especially in overdose, due to their effects on cardiac sodium channels and potential for arrhythmias.
- While MAOIs can cause **orthostatic hypotension**, direct cardiotoxicity is not a primary concern with phenelzine.
*"A common side effect of this medication is sedation."*
- Phenelzine is generally considered **activating** rather than sedating, and can sometimes lead to insomnia or agitation.
- The patient's current hypersomnia is a symptom of her **atypical depression**, not a predicted side effect of phenelzine. In fact, phenelzine may help improve this symptom.
*"While on this medication, you may have a decreased seizure threshold."*
- This statement is actually **medically accurate** - MAOIs including phenelzine can lower (decrease) the seizure threshold, meaning they increase seizure risk.
- This is relevant given the patient's seizure disorder managed with phenytoin and warrants monitoring.
- However, the **dietary tyramine restriction** is the more critical and immediately actionable counseling point when initiating MAOI therapy, as hypertensive crisis can occur with the very first exposure to tyramine-rich foods.
Drug-food interactions US Medical PG Question 5: A 26-year-old man comes to the physician because of discoloration of the toenails. He has a history of peptic ulcer disease treated with pantoprazole. The physician prescribes oral itraconazole for a fungal infection and temporarily discontinues pantoprazole. Which of the following best describes the reason for discontinuing pantoprazole therapy?
- A. Decreased therapeutic effect of itraconazole due to cytochrome P450 induction
- B. Increased toxicity of itraconazole due to cytochrome P450 induction
- C. Decreased therapeutic effect of itraconazole due to decreased absorption (Correct Answer)
- D. Increased toxicity of itraconazole due to decreased protein binding
- E. Decreased therapeutic effect of itraconazole due to cytochrome P450 inhibition
Drug-food interactions Explanation: ***Decreased therapeutic effect of itraconazole due to decreased absorption***
- **Itraconazole** requires an **acidic gastric pH** for optimal absorption, as it is a weakly basic drug.
- **Pantoprazole**, a proton pump inhibitor, significantly raises gastric pH, thereby reducing itraconazole's absorption and its therapeutic effect.
*Decreased therapeutic effect of itraconazole due to cytochrome p450 induction*
- **Pantoprazole** does not primarily induce significant **cytochrome P450 enzymes** in a way that would lead to a clinically relevant decrease in itraconazole's therapeutic effect.
- While some PPIs can interact with CYP enzymes, this is not the main reason for discontinuing pantoprazole with itraconazole.
*Increased toxicity of itraconazole due to cytochrome p450 induction*
- **Cytochrome P450 induction** would generally lead to faster metabolism and **decreased levels of itraconazole**, thus reducing its efficacy rather than increasing its toxicity.
- This interaction mechanism is contrary to the clinical concern of increased toxicity.
*Decreased therapeutic effect of itraconazole due to cytochrome p450 inhibition*
- While both **pantoprazole** and **itraconazole** can interact with **cytochrome P450 enzymes** (itraconazole is a strong CYP3A4 inhibitor, and pantoprazole can be a weak CYP2C19 inhibitor), the primary concern when co-administering them is not a decrease in itraconazole's effect due to pantoprazole's P450 inhibition.
- If anything, inhibition of itraconazole's metabolism would theoretically increase its levels, which is not the reason for drug discontinuation.
*Increased toxicity of itraconazole due to decreased protein binding*
- There is no significant evidence that **pantoprazole** widely affects the **protein binding** of **itraconazole** to an extent that would lead to increased toxicity.
- Alterations in protein binding are not the primary mechanism behind this specific drug interaction.
Drug-food interactions US Medical PG Question 6: A 45-year-old female with a history of gastroesophageal reflux disease presents to her family physician with symptoms of epigastric pain right after a meal. The physician performs a urea breath test which is positive and the patient is started on appropriate medical therapy. Three days later at a restaurant, she experienced severe flushing, tachycardia, hypotension, and vomiting after her first glass of wine. Which of the following is the mechanism of action of the medication causing this side effect?
- A. Binds to the 30S ribosomal subunit preventing attachment of the aminoacyl-tRNA
- B. Blocks protein synthesis by binding to the 50S ribosomal subunit inhibiting protein translocation
- C. Blocks the synthesis of the peptidoglycan layer
- D. Inhibits the H+/K+ ATPase
- E. Forms toxic metabolites that damage bacterial DNA (Correct Answer)
Drug-food interactions Explanation: ***Forms toxic metabolites that damage bacterial DNA***
- The patient likely has a **_H. pylori_ infection** causing epigastric pain, diagnosed by a **positive urea breath test**.
- **Metronidazole**, a common treatment for _H. pylori_, causes a **disulfiram-like reaction** with alcohol, leading to flushing, tachycardia, hypotension, and vomiting. Metronidazole's mechanism involves forming **toxic free radicals** that damage bacterial DNA.
*Binds to the 30S ribosomal subunit preventing attachment of the aminoacyl-tRNA*
- This is the mechanism of action for **tetracyclines** (e.g., doxycycline) and **aminoglycosides** (e.g., gentamicin), which are sometimes used in _H. pylori_ regimens but do not typically cause this severe alcohol interaction.
- While tetracyclines are part of some _H. pylori_ treatment regimens, they are not primarily associated with a disulfiram-like reaction.
*Blocks protein synthesis by binding to the 50S ribosomal subunit inhibiting protein translocation*
- This describes the mechanism of action of **macrolide antibiotics** (e.g., clarithromycin), which are commonly used in _H. pylori_ treatment protocols.
- Although clarithromycin can cause gastrointestinal upset, it does not typically induce the severe disulfiram-like reaction described with alcohol.
*Blocks the synthesis of the peptidoglycan layer*
- This is the mechanism of action of **beta-lactam antibiotics** (e.g., amoxicillin), frequently included in _H. pylori_ eradication regimens.
- Amoxicillin does not cause a disulfiram-like reaction when combined with alcohol.
*Inhibits the H+/K+ ATPase*
- This describes **proton pump inhibitors (PPIs)** like omeprazole or pantoprazole, which are part of nearly all _H. pylori_ treatment regimens to reduce acid production.
- PPIs do not have a direct interaction with alcohol that causes this specific constellation of symptoms; their primary role is acid suppression, not antibacterial action leading to disulfiram effects.
Drug-food interactions US Medical PG Question 7: A 65-year-old male with diffuse large B cell lymphoma is treated with a chemotherapy regimen including 6-mercaptopurine. Administration of which of the following agents would increase this patient’s risk for mercaptopurine toxicity?
- A. Allopurinol (Correct Answer)
- B. Mesna
- C. Leucovorin
- D. Dexrazoxane
- E. Amifostine
Drug-food interactions Explanation: ***Allopurinol***
- **Allopurinol** inhibits **xanthine oxidase**, an enzyme responsible for metabolizing **6-mercaptopurine (6-MP)** into inactive metabolites.
- Concurrent administration significantly increases **6-MP levels**, leading to enhanced myelotoxicity and other severe adverse effects.
*Mesna*
- **Mesna** (2-mercaptoethane sulfonate) is a uroprotectant used to prevent **hemorrhagic cystitis** caused by oxazaphosphorine chemotherapy agents like **ifosfamide** and **cyclophosphamide**.
- It does not interact with the metabolism of **6-mercaptopurine**.
*Leucovorin*
- **Leucovorin** (folinic acid) is a rescue agent for **methotrexate toxicity** and enhances the efficacy of **5-fluorouracil**.
- It does not have a direct interaction with the metabolism or toxicity of **6-mercaptopurine**.
*Dexrazoxane*
- **Dexrazoxane** is a cardioprotective agent used to prevent **doxorubicin-induced cardiotoxicity**.
- It does not interact with the metabolic pathways of **6-mercaptopurine**.
*Amifostine*
- **Amifostine** is a cytoprotective agent that reduces the toxicity of **cisplatin** and **radiation therapy** to normal tissues, particularly the kidneys and salivary glands.
- It is not involved in the metabolism or potentiation of **6-mercaptopurine toxicity**.
Drug-food interactions US Medical PG Question 8: A 52-year-old man presents for a routine checkup. Past medical history is remarkable for stage 1 systemic hypertension and hepatitis A infection diagnosed 10 years ago. He takes aspirin, rosuvastatin, enalapril daily, and a magnesium supplement every once in a while. He is planning to visit Ecuador for a week-long vacation and is concerned about malaria prophylaxis before his travel. The physician advised taking 1 primaquine pill every day while he is there and for 7 consecutive days after leaving Ecuador. On the third day of his trip, the patient develops an acute onset headache, dizziness, shortness of breath, and fingertips and toes turning blue. His blood pressure is 135/80 mm Hg, heart rate is 94/min, respiratory rate is 22/min, temperature is 36.9℃ (98.4℉), and blood oxygen saturation is 97% in room air. While drawing blood for his laboratory workup, the nurse notes that his blood has a chocolate brown color. Which of the following statements best describes the etiology of this patient’s most likely condition?
- A. The patient’s condition is due to consumption of water polluted with nitrates.
- B. The patient had pre-existing liver damage caused by viral hepatitis.
- C. This condition resulted from primaquine overdose.
- D. It is a type B adverse drug reaction. (Correct Answer)
- E. The condition developed because of his concomitant use of primaquine and magnesium supplement.
Drug-food interactions Explanation: ***It is a type B adverse drug reaction.***
- The patient's symptoms (headache, dizziness, shortness of breath, cyanosis, chocolate brown blood) are consistent with **methemoglobinemia**, which is a known idiosyncratic reaction to **primaquine**. Type B adverse drug reactions are **unpredictable** and not dose-dependent, representing an individual's unique response to a drug.
- This reaction likely stems from an underlying **glucose-6-phosphate dehydrogenase (G6PD) deficiency**, making him susceptible to oxidative stress induced by primaquine, leading to methemoglobin formation. The occurrence of symptoms early in the course of medication (3rd day) also supports an idiosyncratic reaction rather than a typical dose-related effect.
*The patient’s condition is due to consumption of water polluted with nitrates.*
- While **nitrate poisoning** can cause methemoglobinemia, the patient’s symptoms appeared shortly after starting primaquine for malaria prophylaxis, making drug-induced methemoglobinemia a more direct and probable cause in this clinical context.
- Exposure to nitrate-polluted water is unlikely to cause a sudden onset of such severe symptoms within 3 days of arrival, especially considering he is taking a known oxidizing agent (primaquine).
*The patient had pre-existing liver damage caused by viral hepatitis.*
- Although **liver dysfunction** can alter drug metabolism, hepatitis A is an acute infection that does not typically cause chronic liver damage leading to altered drug metabolism for primaquine in the long term, especially 10 years after diagnosis.
- The primary risk factor for primaquine-induced methemoglobinemia is G6PD deficiency, not liver damage, which affects red blood cell susceptibility to oxidative stress.
*This condition resulted from primaquine overdose.*
- The prescribed dose of primaquine (one pill daily) is standard for malaria prophylaxis, and there is no indication the patient took more than prescribed. This reaction is likely due to an **idiosyncratic response** rather than an excessive dose.
- Methemoglobinemia from primaquine is often seen in individuals with **G6PD deficiency** even at therapeutic doses, making it an unpredictable Type B adverse reaction rather than a direct dose-dependent toxicity.
*The condition developed because of his concomitant use of primaquine and magnesium supplement.*
- There is no known direct significant **drug interaction** between primaquine and magnesium supplements that would lead to methemoglobinemia.
- The underlying cause of methemoglobinemia with primaquine is typically due to its **oxidative properties** in susceptible individuals (e.g., G6PD deficiency), not an interaction with magnesium.
Drug-food interactions US Medical PG Question 9: A 29-year-old woman presents with shortness of breath and chest pain for the past week. She says her chest pain is aggravated by deep breathing and she becomes short of breath while walking upstairs in her home. She also has been feeling feverish and fatigued for the past week, as well as pain in her wrists, hands, and left knee. Review of systems is significant for a 4.5 kg (10.0 lb) weight loss over the previous month. Past medical history consists of 2 spontaneous abortions, both of which occurred in the 1st trimester. On physical examination, there is a pink rash present over her face, which is aggravated by exposure to sunlight. There are decreased breath sounds on the right. A chest radiograph is performed which reveals evidence of a right pleural effusion. Serum ANA and anti-dsDNA autoantibodies are positive. Urinalysis is unremarkable. Errors with which of the following is most likely to lead to her disease?
- A. Intrinsic pathway
- B. Cytotoxic CD8+ T cells
- C. Bcl-2 overexpression
- D. Necrosis
- E. Fas-FasL interaction (Correct Answer)
Drug-food interactions Explanation: ***Fas-FasL interaction***
- This patient presents with multiple symptoms suggestive of **systemic lupus erythematosus (SLE)**, including photosensitive rash, arthritis, serositis (pleural effusion), weight loss, recurrent spontaneous abortions, and positive ANA/anti-dsDNA.
- Genetic defects in the **Fas** or **Fas ligand (FasL) apoptotic pathway** are strongly associated with increased risk of autoimmunity, particularly SLE, as they impair the deletion of autoreactive lymphocytes.
*Intrinsic pathway*
- The intrinsic apoptotic pathway is primarily activated by intracellular stress and mitochondria-dependent signals.
- While essential for cell death, defects in the intrinsic pathway are not as specifically implicated in the pathogenesis of SLE as the Fas-FasL (extrinsic) pathway.
*Cytotoxic CD8+ T cells*
- **CD8+ T cells** are primarily involved in killing virally infected or cancerous cells and are crucial for cellular immunity.
- While involved in some autoimmune processes, their dysfunction is not the primary or most common error leading to the development of SLE, which is largely mediated by autoantibodies.
*Bcl-2 overexpression*
- **Bcl-2** is an anti-apoptotic protein, and its overexpression inhibits apoptosis.
- While Bcl-2 overexpression could theoretically prevent the deletion of autoreactive cells, specific defects in the direct Fas-FasL signaling pathway are more directly and commonly linked to the immune dysregulation seen in SLE.
*Necrosis*
- **Necrosis** is an uncontrolled form of cell death often associated with inflammation and tissue damage.
- While certainly present in tissues affected by SLE due to inflammation, necrosis itself is a consequence of the disease process, not an upstream error in cell death regulation that leads to the autoimmunity of SLE.
Drug-food interactions US Medical PG Question 10: A 31-year-old woman is brought to the emergency department for a severe throbbing headache, nausea, and photophobia for 3 hours. She has severe occipital pain and chest tightness. Prior to onset of symptoms, she had attended a networking event where she had red wine and, shortly after, a snack consisting of salami and some dried fruits. The patient has recurrent migraine headaches and depression, for which she takes medication daily. She is mildly distressed, diaphoretic, and her face is flushed. Her temperature is 37.0°C (98.6 F), pulse is 90/min, respirations are 20/min, and blood pressure is 195/130 mmHg. She is alert and oriented. Deep-tendon reflexes are 2+ bilaterally. This patient's symptoms are most likely caused by a side effect of which of the following medications?
- A. Phenelzine (Correct Answer)
- B. Topiramate
- C. Ibuprofen
- D. Valproic acid
- E. Verapamil
Drug-food interactions Explanation: ***Phenelzine***
- This patient is experiencing a **hypertensive crisis**, characterized by a severe headache, nausea, chest tightness, diaphoresis, and significantly elevated blood pressure (195/130 mmHg). This is a classic presentation of a **tyramine-induced hypertensive crisis**, which can occur in patients taking **monoamine oxidase inhibitors (MAOIs)** like phenelzine.
- Phenelzine inhibits monoamine oxidase, which normally metabolizes **tyramine**. Ingestion of tyramine-rich foods (red wine, salami, dried fruits) leads to a buildup of tyramine, causing a massive release of **norepinephrine** and severe hypertension.
*Topiramate*
- Topiramate is an **anticonvulsant** commonly used for migraine prophylaxis.
- Its side effects typically include **paresthesias**, cognitive slowing, and weight loss, not acute hypertensive crisis from dietary interactions.
*Ibuprofen*
- Ibuprofen is a **non-steroidal anti-inflammatory drug (NSAID)** used for pain relief.
- While prolonged use can sometimes cause a mild increase in blood pressure or fluid retention, it does not typically lead to an acute, severe **hypertensive crisis** in response to specific food ingestion.
*Valproic acid*
- Valproic acid is an **anticonvulsant** and mood stabilizer, also used for migraine prophylaxis.
- Common side effects include **gastrointestinal upset**, tremor, and hepatotoxicity; it is not associated with dietary-induced hypertensive crises.
*Verapamil*
- Verapamil is a **calcium channel blocker** often used for hypertension, angina, and migraine prophylaxis.
- Its mechanism of action usually leads to a **decrease** in blood pressure, and it is not known to cause acute hypertensive reactions with specific food interactions.
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