Pharmacology Quiz: Mood Stabilizers
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Mood StabilizersQuestion 1 of 20

A patient calls their psychiatrist four weeks after starting lamotrigine, which has been slowly titrated to 50 mg daily. The patient reports developing a new rash.

Which of the following descriptions of the rash would be most concerning for Stevens-Johnson syndrome and warrant immediate discontinuation of the drug?

A tender, purpuric rash on the face and trunk accompanied by fever and painful oral erosions.
A faint, non-pruritic macular rash on the trunk that is not spreading.
An itchy, red rash localized to areas of sun exposure.
A well-demarcated, scaly plaque on the elbow that has been present for several months.
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Pharmacology Quiz

Pharmacology Quiz: Mood Stabilizers

Practice Mood Stabilizers in Pharmacology with focused quiz questions that help you check what you know, review explanations, and build confidence with test-style prompts.

What this quiz covers

This quiz focuses on Mood Stabilizers, giving you a quick way to practice the rules, question types, and explanations that matter most for Pharmacology.

How to use this quiz

Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

All questions

Question 1

A patient calls their psychiatrist four weeks after starting lamotrigine, which has been slowly titrated to 50 mg daily. The patient reports developing a new rash.

Which of the following descriptions of the rash would be most concerning for Stevens-Johnson syndrome and warrant immediate discontinuation of the drug?

  1. A tender, purpuric rash on the face and trunk accompanied by fever and painful oral erosions. (correct answer)
  2. A faint, non-pruritic macular rash on the trunk that is not spreading.
  3. An itchy, red rash localized to areas of sun exposure.
  4. A well-demarcated, scaly plaque on the elbow that has been present for several months.
Explanation: When you encounter questions about drug-induced rashes, especially with lamotrigine, you need to immediately assess for life-threatening conditions like Stevens-Johnson syndrome (SJS). SJS is a severe cutaneous adverse reaction that can progress to toxic epidermal necrolysis and carries significant mortality risk. Answer A correctly describes the classic presentation of SJS: tender, purpuric lesions (indicating vascular involvement and tissue damage) on the face and trunk, accompanied by systemic symptoms like fever and mucosal involvement (painful oral erosions). The combination of purpura, mucosal involvement, and systemic symptoms creates the "triad of terror" that demands immediate drug discontinuation and emergency care. Answer B describes a benign-appearing rash that's faint, non-itchy, and not spreading—characteristics that suggest a mild cutaneous reaction rather than SJS. Answer C presents a photosensitivity reaction localized to sun-exposed areas, which is unrelated to SJS and doesn't involve mucous membranes or systemic symptoms. Answer D describes a chronic, localized lesion that predates lamotrigine initiation, making it irrelevant to drug-induced pathology. The key distinguishing features of SJS are mucosal involvement (oral, ocular, or genital erosions), systemic symptoms (fever, malaise), and the morphology of skin lesions (purpuric, tender, often with epidermal detachment). Remember that lamotrigine carries a black box warning for serious rashes, particularly when titrated too rapidly or combined with valproate. Any mucosal involvement with lamotrigine-associated rash should trigger immediate discontinuation—don't wait to see if it worsens.

Question 2

A patient with bipolar disorder has been well-managed on lithium. The patient is prescribed hydrochlorothiazide for newly diagnosed hypertension.

What is the most likely effect of initiating hydrochlorothiazide on the patient's lithium therapy?

  1. A decrease in lithium levels due to increased renal excretion.
  2. An increase in lithium levels due to increased proximal tubular reabsorption. (correct answer)
  3. No significant change in lithium levels, as the drugs act on different parts of the nephron.
  4. An increase in hand tremor due to a pharmacodynamic interaction, with no change in lithium level.
Explanation: Thiazide diuretics, such as hydrochlorothiazide, block sodium reabsorption in the distal convoluted tubule. This leads to a compensatory increase in sodium (and lithium, which is handled similarly to sodium) reabsorption in the proximal convoluted tubule. The net effect is a reduction in lithium clearance by up to 25-50%, which can cause lithium levels to rise into the toxic range. Therefore, initiating a thiazide diuretic in a patient on lithium requires close monitoring and often a pre-emptive reduction in the lithium dose.

Question 3

An elderly patient with bipolar disorder and dementia, maintained on divalproex, is brought in for evaluation of waxing and waning confusion, lethargy, and asterixis. Liver function tests are normal.

Which laboratory test should be prioritized to investigate a likely metabolic cause of the patient's encephalopathy related to their mood stabilizer?

  1. Serum divalproex level.
  2. Serum ammonia level. (correct answer)
  3. Serum calcium level.
  4. Thyroid stimulating hormone (TSH) level.
Explanation: Divalproex can cause hyperammonemic encephalopathy even in the absence of significant liver dysfunction. This is particularly true in elderly patients or those with underlying urea cycle defects. The symptoms of confusion, lethargy, and asterixis are classic for this condition. While checking a drug level is reasonable, the encephalopathy can occur even with therapeutic divalproex levels. Therefore, checking a serum ammonia level is the key diagnostic step. Calcium and thyroid abnormalities are not characteristic adverse effects of divalproex.

Question 4

A 45-year-old patient with bipolar I disorder has a history of Stage 3 Chronic Kidney Disease (CKD). Their mood has not been adequately controlled with an atypical antipsychotic alone, and the addition of a mood stabilizer is being considered.

Given the patient's significant renal impairment, which of the following mood stabilizers should be avoided?

  1. Lithium. (correct answer)
  2. Divalproex.
  3. Lamotrigine.
  4. Carbamazepine.
Explanation: Lithium is almost exclusively eliminated by the kidneys, with its clearance being directly proportional to the glomerular filtration rate (GFR). In a patient with pre-existing CKD, lithium clearance is significantly impaired, leading to a very high risk of accumulation and toxicity, even at standard doses. Divalproex, lamotrigine, and carbamazepine are primarily metabolized by the liver and are therefore much safer options in patients with renal disease.

Question 5

A 50-year-old on chronic divalproex therapy for mood stabilization is scheduled for an elective hernia repair. Pre-operative laboratory work is performed.

Which finding, directly attributable to the medication, would be most likely to increase the patient's risk of surgical bleeding and potentially delay the procedure?

  1. Elevated serum ammonia.
  2. Mildly elevated transaminases.
  3. Decreased serum carnitine.
  4. Dose-dependent thrombocytopenia. (correct answer)
Explanation: Divalproex can cause a dose-dependent thrombocytopenia (low platelet count). Platelets are essential for primary hemostasis and clotting. A significantly low platelet count would increase the risk of perioperative bleeding and would be a major concern for the surgical and anesthesia teams, potentially leading to postponement of the surgery until the count recovers after dose reduction or discontinuation. While the other options are known effects of divalproex, they do not directly impact the risk of surgical bleeding to the same degree as thrombocytopenia.

Question 6

A 48-year-old woman has been maintained on lithium for bipolar disorder for 10 years. She reports several months of progressive fatigue, constipation, and a 15-pound weight gain despite no changes in diet or exercise. Her mood has been stable.

Which of the following is the most appropriate initial management step?

  1. Discontinue lithium and switch to lamotrigine due to intolerable side effects.
  2. Check a TSH and free T4 level to assess for lithium-induced hypothyroidism. (correct answer)
  3. Reassure the patient that these are common, benign side effects of long-term lithium use.
  4. Decrease the lithium dose by half and re-evaluate in one month.
Explanation: The patient's symptoms are classic for hypothyroidism, a common long-term adverse effect of lithium therapy. Lithium interferes with thyroid hormone synthesis and release. The first step in management is to confirm the diagnosis by checking thyroid function tests (TSH and free T4). If hypothyroidism is confirmed, the standard of care is to initiate levothyroxine supplementation while continuing the lithium, especially since it is effective for her mood. Discontinuing an effective mood stabilizer is a last resort.

Question 7

A patient on a stable dose of lamotrigine 200 mg daily for bipolar depression has carbamazepine added to their regimen for mood stabilization.

What is the expected impact of adding carbamazepine on the patient's lamotrigine therapy, and what adjustment is likely needed?

  1. Carbamazepine will inhibit lamotrigine metabolism, requiring a decrease in the lamotrigine dose.
  2. Carbamazepine will induce lamotrigine metabolism, requiring an increase in the lamotrigine dose. (correct answer)
  3. There is no significant interaction, so no dose adjustment is needed for lamotrigine.
  4. Carbamazepine will displace lamotrigine from plasma proteins, requiring a decrease in the lamotrigine dose.
Explanation: Carbamazepine is a potent inducer of UGT enzymes, which are responsible for glucuronidating and eliminating lamotrigine. The addition of carbamazepine can decrease lamotrigine concentrations by approximately 40-50%. To maintain therapeutic efficacy, the dose of lamotrigine often needs to be increased, sometimes doubled, when co-administered with an enzyme inducer like carbamazepine. This is the opposite of the interaction with valproate, an enzyme inhibitor.

Question 8

A 34-year-old patient taking divalproex sodium for bipolar II disorder presents with several days of severe epigastric pain radiating to the back, accompanied by nausea and vomiting. The patient has no history of alcohol use.

Which laboratory finding would be most specific for confirming a serious, known adverse effect of divalproex sodium in this patient?

  1. Serum aspartate aminotransferase (AST) of 250 U/L.
  2. Serum ammonia of 95 µmol/L.
  3. White blood cell count of 15,000/mm³.
  4. Serum lipase of 980 U/L. (correct answer)
Explanation: The patient's presentation is classic for acute pancreatitis, a known and serious adverse effect of divalproex sodium. A significantly elevated serum lipase level (typically >3 times the upper limit of normal) is the most specific laboratory marker for acute pancreatitis. While elevated liver enzymes (AST) and hyperammonemia are also associated with valproate, they do not align with the specific clinical picture of epigastric pain radiating to the back. Leukocytosis is a non-specific inflammatory marker.

Question 9

A physician is considering prescribing carbamazepine for a 31-year-old patient of Southeast Asian ancestry with a new diagnosis of bipolar I disorder.

Which of the following is the most critical screening to perform before initiating therapy to mitigate the risk of a potentially fatal cutaneous reaction?

  1. Complete blood count with differential to establish a baseline for monitoring aplastic anemia.
  2. HLA-B*1502 allele testing to screen for genetic risk of Stevens-Johnson syndrome. (correct answer)
  3. CYP2C9 genotype testing to determine the patient's metabolic capacity for carbamazepine.
  4. Serum sodium level to establish a baseline for monitoring syndrome of inappropriate antidiuretic hormone (SIADH).
Explanation: The presence of the HLA-B*1502 allele, which is more common in people of Asian descent, is strongly associated with an increased risk of developing carbamazepine-induced Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). The FDA recommends screening for this allele in this patient population before initiating carbamazepine. While monitoring CBC and sodium are important during therapy, the genetic screening is the most critical step before initiation to prevent this specific life-threatening reaction.

Question 10

A 48-year-old woman has been maintained on lithium for bipolar disorder for 10 years. She reports several months of progressive fatigue, constipation, and a 15-pound weight gain despite no changes in diet or exercise. Her mood has been stable.

Which of the following is the most appropriate initial management step?

  1. Discontinue lithium and switch to lamotrigine due to intolerable side effects.
  2. Check a TSH and free T4 level to assess for lithium-induced hypothyroidism. (correct answer)
  3. Reassure the patient that these are common, benign side effects of long-term lithium use.
  4. Decrease the lithium dose by half and re-evaluate in one month.
Explanation: The patient's symptoms are classic for hypothyroidism, a common long-term adverse effect of lithium therapy. Lithium interferes with thyroid hormone synthesis and release. The first step in management is to confirm the diagnosis by checking thyroid function tests (TSH and free T4). If hypothyroidism is confirmed, the standard of care is to initiate levothyroxine supplementation while continuing the lithium, especially since it is effective for her mood. Discontinuing an effective mood stabilizer is a last resort.

Question 11

A 24-year-old woman of childbearing potential is being treated with valproic acid for bipolar disorder. During a medication review, she states she is considering becoming pregnant.

When counseling the patient on the teratogenic risks of her current medication, it is most important to emphasize the significantly increased risk for which of the following fetal abnormalities?

  1. Ebstein's anomaly of the tricuspid valve.
  2. Congenital hypothyroidism.
  3. Neural tube defects such as spina bifida. (correct answer)
  4. Limb and digit malformations.
Explanation: Valproic acid is a potent teratogen with a well-established, dose-dependent risk of causing major congenital malformations. The most significant and characteristic risk is for neural tube defects (e.g., spina bifida, anencephaly), with an incidence many times higher than in the general population. Ebstein's anomaly is classically associated with first-trimester lithium exposure. Congenital hypothyroidism is a risk with maternal hypothyroidism, which can be caused by lithium. Limb malformations are less specific to valproate.

Question 12

A 34-year-old patient taking divalproex sodium for bipolar II disorder presents with several days of severe epigastric pain radiating to the back, accompanied by nausea and vomiting. The patient has no history of alcohol use.

Which laboratory finding would be most specific for confirming a serious, known adverse effect of divalproex sodium in this patient?

  1. Serum aspartate aminotransferase (AST) of 250 U/L.
  2. Serum ammonia of 95 µmol/L.
  3. White blood cell count of 15,000/mm³.
  4. Serum lipase of 980 U/L. (correct answer)
Explanation: The patient's presentation is classic for acute pancreatitis, a known and serious adverse effect of divalproex sodium. A significantly elevated serum lipase level (typically >3 times the upper limit of normal) is the most specific laboratory marker for acute pancreatitis. While elevated liver enzymes (AST) and hyperammonemia are also associated with valproate, they do not align with the specific clinical picture of epigastric pain radiating to the back. Leukocytosis is a non-specific inflammatory marker.

Question 13

A 45-year-old patient with bipolar I disorder has a history of Stage 3 Chronic Kidney Disease (CKD). Their mood has not been adequately controlled with an atypical antipsychotic alone, and the addition of a mood stabilizer is being considered.

Given the patient's significant renal impairment, which of the following mood stabilizers should be avoided?

  1. Lithium. (correct answer)
  2. Divalproex.
  3. Lamotrigine.
  4. Carbamazepine.
Explanation: Lithium is almost exclusively eliminated by the kidneys, with its clearance being directly proportional to the glomerular filtration rate (GFR). In a patient with pre-existing CKD, lithium clearance is significantly impaired, leading to a very high risk of accumulation and toxicity, even at standard doses. Divalproex, lamotrigine, and carbamazepine are primarily metabolized by the liver and are therefore much safer options in patients with renal disease.

Question 14

A 62-year-old man on lithium therapy for over a decade presents with polyuria and nocturia. A 24-hour urine collection shows a volume of 5 liters. A water deprivation test demonstrates a failure to concentrate urine, with minimal response to desmopressin administration.

These findings are most consistent with lithium-induced damage to which part of the nephron, leading to the patient's condition?

  1. The proximal convoluted tubule, impairing sodium reabsorption.
  2. The glomerulus, causing a protein-losing nephropathy.
  3. The collecting ducts, causing resistance to antidiuretic hormone (ADH). (correct answer)
  4. The loop of Henle, disrupting the countercurrent multiplier.
Explanation: The clinical picture is classic for nephrogenic diabetes insipidus (NDI), a well-known long-term complication of lithium therapy. Lithium enters the principal cells of the collecting ducts and interferes with the ADH signaling cascade, primarily by downregulating aquaporin-2 water channels. This makes the collecting ducts resistant to the effects of ADH, impairing water reabsorption and leading to the excretion of large volumes of dilute urine. The lack of response to desmopressin (an ADH analog) confirms the nephrogenic (renal) origin rather than a central (pituitary) cause.

Question 15

A 50-year-old on chronic divalproex therapy for mood stabilization is scheduled for an elective hernia repair. Pre-operative laboratory work is performed.

Which finding, directly attributable to the medication, would be most likely to increase the patient's risk of surgical bleeding and potentially delay the procedure?

  1. Elevated serum ammonia.
  2. Mildly elevated transaminases.
  3. Decreased serum carnitine.
  4. Dose-dependent thrombocytopenia. (correct answer)
Explanation: Divalproex can cause a dose-dependent thrombocytopenia (low platelet count). Platelets are essential for primary hemostasis and clotting. A significantly low platelet count would increase the risk of perioperative bleeding and would be a major concern for the surgical and anesthesia teams, potentially leading to postponement of the surgery until the count recovers after dose reduction or discontinuation. While the other options are known effects of divalproex, they do not directly impact the risk of surgical bleeding to the same degree as thrombocytopenia.

Question 16

An elderly patient with bipolar disorder and dementia, maintained on divalproex, is brought in for evaluation of waxing and waning confusion, lethargy, and asterixis. Liver function tests are normal.

Which laboratory test should be prioritized to investigate a likely metabolic cause of the patient's encephalopathy related to their mood stabilizer?

  1. Serum divalproex level.
  2. Serum ammonia level. (correct answer)
  3. Serum calcium level.
  4. Thyroid stimulating hormone (TSH) level.
Explanation: Divalproex can cause hyperammonemic encephalopathy even in the absence of significant liver dysfunction. This is particularly true in elderly patients or those with underlying urea cycle defects. The symptoms of confusion, lethargy, and asterixis are classic for this condition. While checking a drug level is reasonable, the encephalopathy can occur even with therapeutic divalproex levels. Therefore, checking a serum ammonia level is the key diagnostic step. Calcium and thyroid abnormalities are not characteristic adverse effects of divalproex.

Question 17

A 45-year-old patient has been stable on lithium carbonate for bipolar I disorder for three years. His last set of monitoring labs, performed six months ago, showed a lithium level of 0.7 mEq/L, a serum creatinine of 1.0 mg/dL, and a TSH of 2.5 mIU/L.

According to standard clinical practice guidelines for a stable patient on long-term lithium, what is the most appropriate frequency for monitoring serum creatinine and TSH?

  1. Every 6 to 12 months. (correct answer)
  2. Every 3 months.
  3. Every month.
  4. Only if symptoms of toxicity or thyroid dysfunction develop.
Explanation: When you encounter questions about lithium monitoring, think about balancing patient safety with practical clinical care. Lithium has a narrow therapeutic window and can cause serious long-term effects, particularly on kidney and thyroid function, which requires systematic monitoring even in stable patients. For stable patients on long-term lithium therapy, clinical guidelines recommend monitoring serum creatinine and TSH every 6 to 12 months. This frequency reflects the chronic, gradual nature of lithium's potential adverse effects on renal and thyroid function. Since this patient has been stable for three years with normal lab values six months ago, continuing this established monitoring interval is appropriate and follows evidence-based practice standards. Let's examine why the other options miss the mark. Option B (every 3 months) represents monitoring frequency typically reserved for patients who are newly initiated on lithium, have unstable levels, or show signs of organ dysfunction. Option C (monthly monitoring) is excessive for stable patients and typically used only during initial dose titration or when managing toxicity concerns. Option D (monitoring only with symptoms) is dangerous because both nephrotoxicity and thyroid dysfunction can develop insidiously without obvious clinical symptoms until significant damage has occurred. Remember that lithium monitoring follows a risk-stratified approach: more frequent monitoring during initiation and dose changes, then standard intervals (6-12 months) for stable patients. The key is understanding that "stable" doesn't mean "no monitoring needed" – it means you can follow routine surveillance rather than intensive monitoring protocols.

Question 18

A patient on a stable dose of lamotrigine 200 mg daily for bipolar depression has carbamazepine added to their regimen for mood stabilization.

What is the expected impact of adding carbamazepine on the patient's lamotrigine therapy, and what adjustment is likely needed?

  1. Carbamazepine will inhibit lamotrigine metabolism, requiring a decrease in the lamotrigine dose.
  2. Carbamazepine will induce lamotrigine metabolism, requiring an increase in the lamotrigine dose. (correct answer)
  3. There is no significant interaction, so no dose adjustment is needed for lamotrigine.
  4. Carbamazepine will displace lamotrigine from plasma proteins, requiring a decrease in the lamotrigine dose.
Explanation: Carbamazepine is a potent inducer of UGT enzymes, which are responsible for glucuronidating and eliminating lamotrigine. The addition of carbamazepine can decrease lamotrigine concentrations by approximately 40-50%. To maintain therapeutic efficacy, the dose of lamotrigine often needs to be increased, sometimes doubled, when co-administered with an enzyme inducer like carbamazepine. This is the opposite of the interaction with valproate, an enzyme inhibitor.

Question 19

A patient with bipolar I disorder has been stable on lithium 900 mg daily. Their most recent 12-hour trough level was 1.4 mEq/L (therapeutic range 0.6-1.2 mEq/L). The patient reports a persistent fine hand tremor and mild nausea but is otherwise euthymic and without overt signs of severe toxicity.

What is the most appropriate next step in management?

  1. Continue the current dose and add propranolol to manage the tremor.
  2. Discontinue lithium immediately and admit the patient for observation.
  3. Hold the next dose, decrease the total daily dose, and recheck the level in one week. (correct answer)
  4. Obtain an EKG and a basic metabolic panel immediately.
Explanation: A lithium level of 1.4 mEq/L is in the mild toxicity range. While the patient's symptoms are not severe, the elevated level is the root cause and must be addressed. The most appropriate management is to hold a dose or two and then restart at a lower total daily dose to bring the level back into the therapeutic range. Adding a beta-blocker treats the symptomatic tremor but ignores the underlying supratherapeutic level. Immediate discontinuation and admission are not necessary for mild, asymptomatic toxicity. While an EKG and BMP are not unreasonable, the primary action is dose adjustment.

Question 20

A patient begins carbamazepine for mood stabilization. A trough level drawn 1 week after reaching a dose of 400 mg twice daily is 8.0 mg/L (therapeutic range 4-12 mg/L). The patient remains on this dose and reports excellent adherence. A repeat level 4 weeks later is 4.5 mg/L, and the patient notes a mild return of symptoms.

What is the most likely pharmacological principle responsible for the decrease in the carbamazepine level?

  1. Auto-induction of hepatic CYP3A4 enzymes. (correct answer)
  2. Development of receptor-site tolerance.
  3. Saturation of plasma protein binding.
  4. Decreased gastrointestinal absorption over time.
Explanation: Carbamazepine is a potent inducer of hepatic enzymes, including CYP3A4, which is the primary enzyme responsible for its own metabolism. This process, known as auto-induction, begins after a few days of therapy and is typically complete within 3-5 weeks. The induction leads to an accelerated rate of carbamazepine clearance, resulting in a lower serum concentration despite a constant dose and good adherence. This often necessitates a dose increase after the first few weeks of therapy.