Antiepileptic drug interactions US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Antiepileptic drug interactions. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Antiepileptic drug interactions US Medical PG Question 1: A 57-year-old man calls his primary care physician to discuss the results of his annual laboratory exams. The results show that he has dramatically decreased levels of high-density lipoprotein (HDL) and mildly increased levels of low-density lipoprotein (LDL). The physician says that the HDL levels are of primary concern so he is started on the lipid level modifying drug that most effectively increases serum HDL levels. Which of the following is the most likely a side effect of this medication that the patient should be informed about?
- A. Hepatotoxicity
- B. Gallstones
- C. Flushing (Correct Answer)
- D. Malabsorption
- E. Myalgia
Antiepileptic drug interactions Explanation: ***Flushing***
- The medication that most effectively increases HDL levels is **niacin (vitamin B3)**.
- A common and well-known side effect of niacin, especially at therapeutic doses, is **cutaneous flushing**, often accompanied by itching and warmth, due to prostaglandin release.
*Hepatotoxicity*
- While some lipid-modifying drugs, particularly statins, can cause hepatotoxicity, it is less characteristic of niacin directly affecting the liver.
- **Niacin** can cause mild liver enzyme elevations but severe hepatotoxicity is rare with standard doses and monitoring.
*Gallstones*
- **Fibrates** (e.g., gemfibrozil, fenofibrate) are known to increase the risk of gallstone formation by increasing cholesterol excretion into bile.
- Fibrates primarily lower triglycerides and can moderately increase HDL, but are not the *most effective* for significantly raising HDL.
*Malabsorption*
- **Bile acid sequestrants** (e.g., cholestyramine, colestipol) can cause malabsorption of fat-soluble vitamins and other drugs.
- These drugs primarily lower LDL and have minimal effects on HDL levels.
*Myalgia*
- **Statins** (HMG-CoA reductase inhibitors) are well-known to cause muscle-related side effects, including myalgia, myopathy, and in severe cases, rhabdomyolysis.
- Statins primarily lower LDL, and their effect on HDL is generally modest.
Antiepileptic drug interactions US Medical PG Question 2: 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
Antiepileptic drug 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.
Antiepileptic drug interactions US Medical PG Question 3: 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.”
Antiepileptic drug 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.
Antiepileptic drug interactions US Medical PG Question 4: A case-control study is conducted to investigate the association between the use of phenytoin during pregnancy in women with epilepsy and the risk for congenital malformations. The odds ratio of congenital malformations in newborns born to women who were undergoing treatment with phenytoin is 1.74 (P = 0.02) compared to newborns of women who were not treated with phenytoin. Which of the following 95% confidence intervals is most likely reported for this association?
- A. 0.36 to 0.94
- B. 1.75 to 2.48
- C. 0.56 to 1.88
- D. 0.83 to 2.19
- E. 1.34 to 2.36 (Correct Answer)
Antiepileptic drug interactions Explanation: ***1.34 to 2.36***
- A **95% confidence interval** that does not include **1.0** indicates a statistically significant association, consistent with the given **p-value of 0.02** (which is less than 0.05).
- This interval contains the **point estimate (odds ratio of 1.74)**, making it the most plausible range for the true effect.
- The confidence interval must always encompass the point estimate from which it is derived.
*0.36 to 0.94*
- This confidence interval is **entirely below 1.0**, suggesting a protective effect, which contradicts the given odds ratio of **1.74** indicating an increased risk.
- This interval does not contain the point estimate of **1.74**.
*1.75 to 2.48*
- While this interval indicates an increased risk and does not include 1.0, it **does not contain the stated odds ratio of 1.74**, as its lower bound is 1.75.
- A confidence interval must always encompass the point estimate from which it is derived.
*0.56 to 1.88*
- This confidence interval **includes 1.0**, which would imply no statistically significant association between phenytoin use and congenital malformations.
- This contradicts the given **p-value of 0.02**, which indicates statistical significance.
*0.83 to 2.19*
- This confidence interval **includes 1.0**, suggesting **no statistically significant association**.
- This contradicts the given **p-value of 0.02**, which demonstrates statistical significance.
Antiepileptic drug interactions US Medical PG Question 5: A 19-year-old man with a history of generalized tonic-clonic seizures comes to the physician for a routine health maintenance examination. He is a known user of intravenous cocaine. His vital signs are within normal limits. Physical examination shows multiple hyperpigmented lines along the forearms. Oral examination shows marked overgrowth of friable, ulcerated gingival mucosa. Which of the following is the most likely cause of this patient's oral examination findings?
- A. Cyclosporine
- B. Lacosamide
- C. Carbamazepine
- D. Phenytoin (Correct Answer)
- E. Lamotrigine
Antiepileptic drug interactions Explanation: ***Phenytoin***
- **Phenytoin** is a common cause of **gingival hyperplasia**, presenting with marked overgrowth of friable, ulcerated gingival mucosa due to its effect on fibroblast proliferation and collagen production.
- This medication is frequently used to manage **tonic-clonic seizures**, consistent with the patient's history.
*Cyclosporine*
- While **cyclosporine** can cause **gingival hyperplasia**, it is an **immunosuppressant** primarily used in organ transplantation or autoimmune conditions, which is not indicated in the patient's seizure history.
- The patient's presentation does not suggest any condition for which cyclosporine would be prescribed.
*Lacosamide*
- **Lacosamide** is an anticonvulsant that stabilizes hyperexcitable neuronal membranes, but it is **not typically associated with gingival hyperplasia**.
- Its known side effects are primarily neurological, such as dizziness, headache, and nausea.
*Carbamazepine*
- **Carbamazepine** is an anticonvulsant effective for focal and tonic-clonic seizures, but **gingival hyperplasia is a rare side effect** with this medication.
- More common side effects include dizziness, drowsiness, and bone marrow suppression.
*Lamotrigine*
- **Lamotrigine** is an anticonvulsant used for various seizure types, but **gingival hyperplasia is not a recognized side effect**.
- It is more commonly associated with skin rashes, including severe reactions like **Stevens-Johnson syndrome**.
Antiepileptic drug interactions US Medical PG Question 6: A 20-year-old woman presents to the emergency department with painful abdominal cramping. She states she has missed her menstrual period for 5 months, which her primary care physician attributes to her obesity. She has a history of a seizure disorder treated with valproic acid; however, she has not had a seizure in over 10 years and is no longer taking medications for her condition. She has also been diagnosed with pseudoseizures for which she takes fluoxetine and clonazepam. Her temperature is 98.0°F (36.7°C), blood pressure is 174/104 mmHg, pulse is 88/min, respirations are 19/min, and oxygen saturation is 98% on room air. Neurologic exam is unremarkable. Abdominal exam is notable for a morbidly obese and distended abdomen that is nontender. Laboratory studies are ordered as seen below.
Serum:
hCG: 100,000 mIU/mL
Urine:
Color: Amber
hCG: Positive
Protein: Positive
During the patient's evaluation, she experiences 1 episode of tonic-clonic motions which persist for 5 minutes. Which of the following treatments is most appropriate for this patient?
- A. Phenobarbital
- B. Magnesium (Correct Answer)
- C. Phenytoin
- D. Propofol
- E. Lorazepam
Antiepileptic drug interactions Explanation: ***Magnesium***
- The patient's presentation with **painful abdominal cramping**, **elevated blood pressure (174/104 mmHg)**, **proteinuria**, a **positive hCG** (100,000 mIU/mL), and a **new-onset tonic-clonic seizure** strongly indicates **eclampsia**.
- **Magnesium sulfate** is the first-line treatment for seizure prophylaxis and management in patients with preeclampsia and eclampsia.
*Phenobarbital*
- While effective for seizure control, **phenobarbital** is a less preferred agent for eclampsia compared to magnesium sulfate.
- Its use in eclampsia is typically reserved for cases refractory to magnesium sulfate.
*Phenytoin*
- **Phenytoin** is not recommended as a first-line agent for eclamptic seizures, as magnesium sulfate has demonstrated superior efficacy.
- It carries a risk of adverse effects such as **cardiac arrhythmias** and **hypotension**, especially with rapid administration.
*Propofol*
- **Propofol** is an anesthetic and sedative used for continuous seizure control, often in status epilepticus, but is not the primary treatment for eclampsia.
- Its use can lead to significant **respiratory depression** and **hypotension**, requiring close monitoring and intubation.
*Lorazepam*
- Although **lorazepam** is a benzodiazepine used to acutely stop seizures, it is not the preferred agent for eclampsia.
- Benzodiazepines may cause **sedation** and **respiratory depression**, and their efficacy in eclampsia is inferior to magnesium sulfate.
Antiepileptic drug interactions US Medical PG Question 7: A 28-year-old woman comes to the emergency department because of a 2-day history of dark urine, increasing abdominal pain, and a tingling sensation in her arms and legs. She has a history of epilepsy. Her current medication is phenytoin. She is nauseated and confused. Following the administration of hemin and glucose, her symptoms improve. The beneficial effect of this treatment is most likely due to inhibition of which of the following enzymes?
- A. Uroporphyrinogen decarboxylase
- B. Porphobilinogen deaminase
- C. Aminolevulinic acid synthase (Correct Answer)
- D. Ferrochelatase
- E. Aminolevulinate dehydratase
Antiepileptic drug interactions Explanation: ***Aminolevulinic acid synthase***
- The patient's symptoms (dark urine, abdominal pain, neurological symptoms like tingling and confusion) and improvement with **hemin** and **glucose** strongly suggest an acute porphyria, most likely **acute intermittent porphyria (AIP)**.
- **Hemin** and **glucose** work by downregulating **aminolevulinic acid synthase (ALAS)**, the rate-limiting enzyme in heme synthesis, thereby reducing the production of neurotoxic porphyrin precursors (ALA and PBG).
*Uroporphyrinogen decarboxylase*
- Deficiency in **uroporphyrinogen decarboxylase** is associated with **porphyria cutanea tarda (PCT)**, which primarily causes cutaneous photosensitivity, not acute neurovisceral symptoms.
- PCT does not typically present with acute life-threatening attacks or respond acutely to hemin and glucose.
*Porphobilinogen deaminase*
- Deficiency of **porphobilinogen deaminase (PBG deaminase)** is the underlying genetic defect in **acute intermittent porphyria (AIP)**.
- While this is the enzyme deficient in AIP, hemin and glucose don't directly inhibit this enzyme; their action is upstream on ALAS to prevent the accumulation of toxic precursors.
*Ferrochelatase*
- Deficiency of **ferrochelatase** causes **erythropoietic protoporphyria (EPP)**, leading to painful photosensitivity and sometimes liver disease, but generally not acute neurovisceral attacks.
- The symptoms presented and the treatment response are not consistent with EPP.
*Aminolevulinic acid dehydratase*
- Deficiency in **aminolevulinic acid dehydratase** causes **ALA dehydratase deficiency porphyria**, a very rare form of porphyria with symptoms similar to lead poisoning.
- While it involves elevated ALA, it's less common than AIP, and the broad clinical picture with the dramatic response to hemin points more directly to the regulation of ALAS.
Antiepileptic drug interactions US Medical PG Question 8: A 55-year-old male presents to his primary care physician for a normal check-up. He has a history of atrial fibrillation for which he takes metoprolol and warfarin. During his last check-up, his international normalized ratio (INR) was 2.5. He reports that he recently traveled to Mexico for a business trip where he developed a painful red rash on his leg. He was subsequently prescribed an unknown medication by a local physician. The rash resolved after a few days and he currently feels well. His temperature is 98.6°F (37°C), blood pressure is 130/80 mmHg, pulse is 95/min, and respirations are 18/min. Laboratory analysis reveals that his current INR is 4.5. Which of the following is the most likely medication this patient took while in Mexico?
- A. Griseofulvin
- B. Rifampin
- C. St. John’s wort
- D. Trimethoprim-sulfamethoxazole (Correct Answer)
- E. Phenobarbital
Antiepileptic drug interactions Explanation: ***Trimethoprim-sulfamethoxazole***
- **Trimethoprim-sulfamethoxazole** is a potent inhibitor of **CYP2C9**, the primary enzyme responsible for metabolizing **warfarin**, leading to significantly increased INR and bleeding risk.
- The patient's **elevated INR (4.5)** from a previous stable level of 2.5 strongly suggests an interaction with a medication that inhibits warfarin metabolism, and trimethoprim-sulfamethoxazole is a common culprit.
- TMP-SMX is commonly used to treat **cellulitis** and other skin infections, which aligns with the clinical presentation of a painful red rash.
*Griseofulvin*
- **Griseofulvin** is an antifungal agent that acts as a **CYP inducer**, which would *increase* warfarin metabolism and lead to a *decreased* INR, not the elevated INR seen in this patient.
- While it could treat fungal skin infections (e.g., tinea), it would cause the opposite effect on warfarin levels.
*Rifampin*
- **Rifampin** is a strong **CYP inducer**, meaning it would *increase* warfarin metabolism and thus *decrease* INR, leading to a higher risk of clotting, which is the opposite of what is seen in this patient.
- It is often used for tuberculosis or serious bacterial infections, not typically for a simple skin rash.
*St. John's wort*
- **St. John's wort** is a known **CYP inducer**, similar to rifampin, and would lead to a *decrease* in warfarin levels and INR.
- It is an herbal supplement primarily used for depression and would not typically be prescribed by a physician for a rash.
*Phenobarbital*
- **Phenobarbital** is a potent **CYP inducer**, which would *accelerate* warfarin metabolism and result in a *decreased* INR, increasing the risk of thrombosis.
- It is an anticonvulsant and sedative, not a medication typically prescribed for a rash.
Antiepileptic drug interactions US Medical PG Question 9: A 50-year-old woman presents with acute onset fever and chills for the past hour. She mentions earlier in the day she felt blue, so she took some St. John’s wort because she was told by a friend that it helps with depression. Past medical history is significant for hypertension, diabetes mellitus, and depression managed medically with captopril, metformin, and fluoxetine. She has no history of allergies. Her pulse is 130/min, the respiratory rate is 18/min, the blood pressure is 176/92 mm Hg, and the temperature is 38.5°C (101.3°F). On physical examination, the patient is profusely diaphoretic and extremely irritable when asked questions. Oriented x 3. The abdomen is soft and nontender with no hepatosplenomegaly. Increased bowel sounds are heard in the abdomen. Deep tendon reflexes are 3+ bilaterally and clonus is elicited. The sensation is decreased in the feet bilaterally. Mydriasis is present. Fingerstick glucose is 140 mg/dL. An ECG shows sinus tachycardia but is otherwise normal. Which of the following is the most likely cause of this patient’s condition?
- A. Sepsis
- B. Anaphylactic reaction
- C. Diabetic ketoacidosis
- D. Neuroleptic malignant syndrome
- E. Serotonin syndrome (Correct Answer)
Antiepileptic drug interactions Explanation: ***Serotonin syndrome***
- The patient's presentation with **fever, diaphoresis, hypertension, tachycardia, hyperreflexia, clonus, mydriasis**, and **agitation** after combining an **SSRI (fluoxetine)** with **St. John's wort** (a serotonin-enhancing herbal supplement) is highly characteristic of serotonin syndrome.
- This condition results from excessive serotonergic activity in the central and peripheral nervous system.
*Sepsis*
- While **fever, chills, and tachycardia** can be indicators of sepsis, the presence of specific neurological and neuromuscular signs like **hyperreflexia, clonus, and mydriasis** points away from it.
- The patient's **irritable state and normal mental orientation** is less typical for severe sepsis, which often involves altered mental status.
*Anaphylactic reaction*
- **Anaphylaxis** presents with rapid onset of symptoms such as **urticaria, angioedema, bronchospasm, and hypotension**, which are not observed in this patient.
- There is no history of allergen exposure, and the prominent neurological symptoms are not typical of anaphylaxis.
*Diabetic ketoacidosis*
- **DKA** is characterized by **hyperglycemia, metabolic acidosis, and ketonemia**, often presenting with Kussmaul respirations and fruity breath odor.
- The patient's **fingerstick glucose (140 mg/dL)** is not significantly elevated, and there is no mention of deep, rapid breathing or other DKA-specific symptoms.
*Neuroleptic malignant syndrome*
- **NMS** is typically associated with exposure to **dopamine antagonists (antipsychotics)** and is characterized by **severe muscle rigidity, hyperthermia, altered mental status, and autonomic instability.**
- While some symptoms overlap, this patient's history of St. John's wort and fluoxetine points to increased serotonin, and the specific neuromuscular findings like clonus are more indicative of serotonin syndrome.
Antiepileptic drug interactions US Medical PG Question 10: A 63-year-old man with high blood pressure, dyslipidemia, and diabetes presents to the clinic for routine follow-up. He has no current complaints and has been compliant with his chronic medications. His blood pressure is 132/87 mm Hg and his pulse is 75/min and regular. On physical examination, you notice that he has xanthelasmas on both of his eyelids. He currently uses a statin to lower his LDL but has not reached the LDL goal you have set for him. You would like to add an additional medication for LDL control. Of the following, which statement regarding fibrates is true?
- A. Fibrates inhibit the rate-limiting step in cholesterol synthesis
- B. Fibrates can potentiate the risk of myositis when given with statins (Correct Answer)
- C. Fibrates can cause significant skin flushing and pruritus
- D. Fibrates can increase the risk of cataracts
- E. The primary effect of fibrates is to lower LDL
Antiepileptic drug interactions Explanation: ***Fibrates can potentiate the risk of myositis when given with statins***
- **Fibrates** and **statins** can both independently cause muscle toxicity (myopathy, rhabdomyolysis).
- When used concomitantly, especially **gemfibrozil** with statins, there is an **increased risk of muscle adverse events** due to pharmacokinetic interactions that raise statin levels.
- This combination requires careful monitoring and is often avoided; **fenofibrate** is preferred over gemfibrozil when combination therapy is needed.
*Fibrates inhibit the rate-limiting step in cholesterol synthesis*
- This statement describes the mechanism of action of **statins**, which inhibit **HMG-CoA reductase**, the rate-limiting enzyme in cholesterol synthesis.
- Fibrates, on the other hand, act primarily by activating **PPAR-alpha receptors**, leading to altered lipid metabolism (increased lipoprotein lipase activity, decreased VLDL synthesis).
*Fibrates can cause significant skin flushing and pruritus*
- **Niacin (nicotinic acid)** is the lipid-modifying agent most commonly associated with significant **skin flushing and pruritus**, mediated by prostaglandin release.
- Fibrates do not cause significant flushing; their side effects include GI disturbances, gallstones, and potential muscle toxicity.
*Fibrates can increase the risk of cataracts*
- This is **not an established adverse effect** of the fibrate class.
- While **clofibrate** (an older, largely discontinued fibrate) showed some association with cataracts in older studies, this is not a recognized risk with modern fibrates like **fenofibrate** and **gemfibrozil**.
- Current fibrate therapy does not require routine ophthalmologic monitoring for cataracts.
*The primary effect of fibrates is to lower LDL*
- The primary effect of **fibrates** is to significantly **lower triglycerides** (by 30-50%) and **increase HDL cholesterol** levels (by 10-20%).
- While they can cause a modest decrease in LDL cholesterol (10-15%), this is not their primary or most pronounced lipid-modifying effect.
- Fibrates are primarily indicated for **hypertriglyceridemia** and mixed dyslipidemia.
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