A 27-year-old woman presents for a checkup. She is 20 weeks pregnant and has been admitted to the hospital multiple times during her pregnancy for seizures. She has a known seizure disorder but discontinued her valproic acid when she became pregnant. The patient's past medical history is otherwise unremarkable. She does not smoke, drink alcohol, or use any drugs. She generally prefers not to take medications and sees a shaman for her care typically. Given her recent hospitalization, the patient agrees to start carbamazepine. Which of the following is the most appropriate treatment for this patient at this time?
Q782
A 34-year-old woman comes to the emergency department complaining of severe headache and anxiety, diaphoresis, and palpitations for the last 30 minutes. She has had several similar episodes over the past few weeks. She has no significant past medical history and has a 10 pack-year smoking history. She takes no illicit drugs. Her blood pressure on arrival is 181/80 mmHg and her pulse is 134/min. If this patient was given metoprolol, how would her blood pressure respond?
Q783
A 43-year-old woman comes to the physician with a 2-week history of new pruritic plaques on the scalp and extensor surfaces of the elbows and knees. Ten years ago, she was diagnosed with psoriasis. Her only medication is topical calcipotriene. Physical examination shows well-demarcated, symmetrical, erythematous plaques with silvery scale. There is pitting of the nails on all fingers. Therapy with a high-potency topical medication that inhibits NF-κB and phospholipase A2 is begun. Long-term use of this agent is most likely to result in which of the following?
Q784
A 52-year-old woman status-post liver transplant presents to her transplant surgeon because she has noticed increased urination over the last 3 weeks. Six months ago she received a liver transplant because of fulminant liver failure after viral hepatitis. Since then, she has noticed that she has been drinking more water and urinating more. Her husband has also noticed that she has been eating a lot more. She says that she never had these symptoms prior to her transplant and has been taking her medications on time. After confirmatory tests, she is started on a medication that binds to an ATP-gated potassium channel. The drug that increases the risk of the complication experienced by this patient most likely has which of the following mechanisms of action?
Q785
A 33-year-old woman presents with weight gain and marks on her abdomen (as seen in the image below). She does not have any significant past medical history. She is a nonsmoker and denies any alcohol use. Her blood pressure is 160/110 mm Hg and pulse is 77/min. A T1/T2 MRI of the head shows evidence of a pituitary adenoma, and she undergoes surgical resection of the tumor. Which of the following therapies is indicated in this patient to ensure normal functioning of her hypothalamic-pituitary-adrenal (HPA) axis?
Q786
A 4-year-old boy presents to the Emergency Department with wheezing and shortness of breath after playing with the new family pet. Which of the following immunological factors is most involved in generating the antibodies necessary for mast cell Fc-receptor cross-linking and degranulation?
Q787
A 62-year-old woman is brought to the emergency room at a nearby hospital after being involved in a roadside accident in which she sustained severe chest trauma. Enroute to the hospital, morphine is administered for pain control. Upon arrival, the patient rapidly develops respiratory failure and requires intubation and mechanical ventilation. She is administered pancuronium in preparation for intubation but suddenly develops severe bronchospasm and wheezing. Her blood pressure also quickly falls from 120/80 mm Hg to 100/60 mm Hg. Which of the following best explains the most likely etiology of this complication?
Q788
A 45-year-old man is brought into the emergency department after he was hit by a car. The patient was intoxicated and walked into oncoming traffic. He is currently unconscious and has a Glasgow coma scale score of 3. The patient has been admitted multiple times for alcohol intoxication and pancreatitis. The patient is resuscitated with fluid and blood products. An initial trauma survey reveals minor scrapes and abrasions and pelvic instability. The patient’s pelvis is placed in a binder. After further resuscitation the patient becomes responsive and states he is in pain. He is given medications and further resuscitation ensues. One hour later, the patient complains of numbness surrounding his mouth and in his extremities. Which of the following is the most likely explanation of this patient’s current symptoms?
Q789
A 37-year-old woman is brought to the emergency department by police after being found naked outside a government building. She is accompanied by her husband who reports that she has been having "crazy" ideas. The patient's speech is pressured and she switches topics quickly from how she is going to be president one day to how she is going to learn 20 languages fluently by the end of the year. Upon further questioning, it is revealed that she has struggled with at least 2 depressive episodes in the past year. Her medical history is significant for hypertension, hyperlipidemia, gout, and chronic migraines. She was recently diagnosed with a urinary tract infection and given nitrofurantoin. She has also been taking indomethacin for an acute gout flare. Her other medications include atorvastatin, allopurinol, metoprolol, and acetazolamide. She is prescribed lithium and instructed to follow-up with a primary care physician. At a follow-up appointment, she complains of nausea, vomiting, and increased urinary frequency. On examination, she has a coarse tremor and diffuse hyperreflexia. Which of the following medications is most likely responsible for the patient's current presentation?
Q790
A 9-year-old boy is brought to the emergency department by his mother because of painful swelling in his right knee that started after he collided with another player during a soccer game. He has no history of serious illness except for an episode of prolonged bleeding following a tooth extraction a few months ago. Physical examination shows marked tenderness and swelling of the right knee joint. There are multiple bruises on the lower extremities in various stages of healing. Laboratory studies show a platelet count of 235,000/mm3, partial thromboplastin time of 78 seconds, prothrombin time of 14 seconds, and bleeding time of 4 minutes. The plasma concentration of which of the following is most likely to be decreased in this patient?
Autonomic/CV Drugs US Medical PG Practice Questions and MCQs
Question 781: A 27-year-old woman presents for a checkup. She is 20 weeks pregnant and has been admitted to the hospital multiple times during her pregnancy for seizures. She has a known seizure disorder but discontinued her valproic acid when she became pregnant. The patient's past medical history is otherwise unremarkable. She does not smoke, drink alcohol, or use any drugs. She generally prefers not to take medications and sees a shaman for her care typically. Given her recent hospitalization, the patient agrees to start carbamazepine. Which of the following is the most appropriate treatment for this patient at this time?
A. Vitamin B12
B. Folate (Correct Answer)
C. Iron
D. Magnesium
E. Vitamin D
Explanation: ***Folate***
- **Carbamazepine**, a common anti-epileptic drug (AED), is known to interfere with **folate metabolism**, making supplementation crucial during pregnancy.
- Adequate **folate** intake is vital to prevent **neural tube defects** (NTDs) in the developing fetus, a risk exacerbated by AEDs like carbamazepine.
*Vitamin B12*
- While important for neurological health and red blood cell formation, **vitamin B12** deficiency is not directly caused or worsened by carbamazepine in a way that necessitates immediate supplementation more than folate in this context.
- Routine B12 supplementation is not a primary recommendation for pregnant women on carbamazepine when compared to folate.
*Iron*
- **Iron** supplementation is commonly recommended during pregnancy to prevent **anemia**, but it is not specifically indicated for women on carbamazepine, nor does carbamazepine interfere with iron absorption significantly.
- Although important, iron deficiency is a general obstetric concern rather than a specific interaction with carbamazepine.
*Magnesium*
- **Magnesium** is important for various bodily functions, including muscle and nerve function, but there is no direct interaction with **carbamazepine** that would necessitate its supplementation over other nutrients.
- Magnesium is not primarily used to mitigate the adverse effects of carbamazepine or prevent congenital malformations.
*Vitamin D*
- There is some evidence that certain AEDs can affect **vitamin D metabolism** and bone health, but this is less critical than folate in preventing immediate, severe birth defects like NTDs.
- While vitamin D supplementation may be beneficial in pregnancy, it does not address the most urgent risk associated with carbamazepine exposure during fetal development.
Question 782: A 34-year-old woman comes to the emergency department complaining of severe headache and anxiety, diaphoresis, and palpitations for the last 30 minutes. She has had several similar episodes over the past few weeks. She has no significant past medical history and has a 10 pack-year smoking history. She takes no illicit drugs. Her blood pressure on arrival is 181/80 mmHg and her pulse is 134/min. If this patient was given metoprolol, how would her blood pressure respond?
A. Hypotension due to alpha-1-adrenergic receptor blockade
B. Hypertension due to alpha-1-adrenergic receptor blockade
C. Hypertension due to alpha- and beta-adrenergic receptor blockade
D. Hypotension due to beta-adrenergic receptor blockade (Correct Answer)
E. Hypertension due to alpha-1-adrenergic receptor stimulation
Explanation: ***Hypotension due to beta-adrenergic receptor blockade***
- The patient's symptoms (severe headache, anxiety, diaphoresis, palpitations, hypertension, and tachycardia) are highly suggestive of a **pheochromocytoma**, which releases excessive amounts of **norepinephrine** and **epinephrine**.
- Metoprolol is a **selective beta-1 adrenergic receptor antagonist**. Blocking beta-1 receptors would counteract the effects of excess catecholamines on the heart (e.g., reducing heart rate and contractility), leading to a decrease in **cardiac output** and subsequently **blood pressure** (hypotension).
*Hypotension due to alpha-1-adrenergic receptor blockade*
- While alpha-1 antagonists can cause hypotension, metoprolol primarily blocks **beta-1 receptors**, not alpha-1 receptors.
- Using an alpha-1 blocker alone in a pheochromocytoma crisis can lead to a reflex **tachycardia** due to unopposed beta stimulation, but the primary mechanism of hypotension from metoprolol is beta-blockade.
*Hypertension due to alpha-1-adrenergic receptor blockade*
- **Alpha-1 blockade** typically leads to **vasodilation** and **hypotension**, not hypertension. This option misaligns the effect of alpha-1 blockade with the outcome.
- Metoprolol does not block alpha-1 receptors, so this mechanism is not relevant to metoprolol's action.
*Hypertension due to alpha- and beta-adrenergic receptor blockade*
- This statement is incorrect because simultaneous blockade of both alpha and beta receptors (e.g., with labetalol) would primarily lead to a **reduction in blood pressure**, although the immediate effect of *unselective* beta blockade in a pheochromocytoma (due to unopposed alpha-1 vasoconstriction) can initially worsen hypertension if not preceded by alpha blockade.
- Metoprolol does not block alpha receptors, making this explanation inaccurate for the drug in question.
*Hypertension due to alpha-1-adrenergic receptor stimulation*
- Metoprolol is a **beta-adrenergic receptor blocker**, not an alpha-1 adrenergic receptor stimulator. Stimulation of alpha-1 receptors would indeed cause **vasoconstriction** and hypertension, but this is the opposite of metoprolol's action.
- In an unblocked pheochromocytoma crisis, there is already significant alpha-1 stimulation from excess catecholamines. Metoprolol's action would be to block beta-receptors, which could indirectly lead to *unopposed alpha-1 stimulation* if used alone without alpha blockade, but the drug itself does not stimulate alpha-1 receptors.
Question 783: A 43-year-old woman comes to the physician with a 2-week history of new pruritic plaques on the scalp and extensor surfaces of the elbows and knees. Ten years ago, she was diagnosed with psoriasis. Her only medication is topical calcipotriene. Physical examination shows well-demarcated, symmetrical, erythematous plaques with silvery scale. There is pitting of the nails on all fingers. Therapy with a high-potency topical medication that inhibits NF-κB and phospholipase A2 is begun. Long-term use of this agent is most likely to result in which of the following?
A. Hair growth on upper lip
B. Dermal collagen loss (Correct Answer)
C. Nonblanchable pinpoint macules
D. Dysplastic nevi
E. Decreased sebum production
Explanation: ***Dermal collagen loss***
- This patient is being treated with a **high-potency topical corticosteroid**. Long-term use of such medications can lead to **atrophy of the skin**, characterized by thinning due to loss of collagen and elastic fibers.
- Clinical manifestations of dermal collagen loss include **skin thinning, striae, telangiectasias, and easy bruising**.
*Hair growth on upper lip*
- **Hirsutism**, or excessive hair growth, is typically associated with systemic corticosteroid use or conditions causing androgen excess, not commonly with topical corticosteroids applied to the scalp and extensor surfaces.
- While systemic absorption can occur, it's less likely to cause localized hirsutism on the upper lip compared to other systemic side effects.
*Nonblanchable pinpoint macules*
- **Petechiae**, which are nonblanchable pinpoint macules, are usually indicative of capillary bleeding and can be a side effect of prolonged corticosteroid use due to skin thinning and fragility.
- However, **dermal collagen loss** is a more direct and fundamental structural change leading to the overall skin atrophy and fragility seen with long-term topical steroid use.
*Dysplastic nevi*
- **Dysplastic nevi** are atypical moles that can be precursors to melanoma and are primarily linked to genetic factors and sun exposure, not a direct side effect of topical corticosteroid use.
- Topical corticosteroids do not have a known association with the development of dysplastic nevi or increased risk of melanoma.
*Decreased sebum production*
- Topical corticosteroids do not significantly alter **sebum production**. In fact, they can sometimes promote **steroid acne**, which involves follicular changes rather than a decrease in sebum.
- **Sebum production** is primarily regulated by hormonal factors, particularly androgens.
Question 784: A 52-year-old woman status-post liver transplant presents to her transplant surgeon because she has noticed increased urination over the last 3 weeks. Six months ago she received a liver transplant because of fulminant liver failure after viral hepatitis. Since then, she has noticed that she has been drinking more water and urinating more. Her husband has also noticed that she has been eating a lot more. She says that she never had these symptoms prior to her transplant and has been taking her medications on time. After confirmatory tests, she is started on a medication that binds to an ATP-gated potassium channel. The drug that increases the risk of the complication experienced by this patient most likely has which of the following mechanisms of action?
A. Targeting the a-chain of the IL-2 receptor
B. Conversion into 6-mercaptopurine
C. Inosine monophosphate dehydrogenase inhibitor
D. Binding to FKBP-12 to inhibit calcineurin (Correct Answer)
E. Binding to cyclophilin A to inhibit calcineurin
Explanation: ***Binding to FKBP-12 to inhibit calcineurin***
- The patient's symptoms of **increased urination, thirst (polydipsia), and appetite (polyphagia)**, especially after an organ transplant, are highly suggestive of **new-onset diabetes mellitus (NODM)**, a known complication of immunosuppressive therapy.
- **Tacrolimus**, a calcineurin inhibitor given post-transplant, binds to **FKBP-12** and is known to cause **NODM** by impairing insulin secretion and increasing insulin resistance.
*Binding to cyclophilin A to inhibit calcineurin*
- This describes the mechanism of **cyclosporine**, another calcineurin inhibitor, which also causes NODM. However, given the context of a drug binding to an **ATP-gated potassium channel** to treat the complication, the question is asking about the mechanism of the *original* drug that caused the diabetes, not the treatment.
- While cyclosporine does inhibit calcineurin, the specific binding protein mentioned (FKBP-12) points more directly to tacrolimus, which is a stronger contributor to NODM.
*Targeting the a-chain of the IL-2 receptor*
- This mechanism describes **basiliximab** and **daclizumab**, which are anti-CD25 antibodies used for **induction therapy** in transplant patients.
- These drugs are generally associated with a lower risk of diabetes compared to calcineurin inhibitors and are not typically the sole maintenance immunosuppressants causing such a prominent side effect.
*Inosine monophosphate dehydrogenase inhibitor*
- This mechanism belongs to **mycophenolate mofetil (MMF)**, an immunosuppressant commonly used in transplant patients.
- While MMF has various side effects, **new-onset diabetes** is less commonly associated with it compared to calcineurin inhibitors.
*Conversion into 6-mercaptopurine*
- This describes the mechanism of **azathioprine**, another immunosuppressant widely used in transplantation.
- Azathioprine is primarily associated with **bone marrow suppression** and **gastrointestinal side effects**, with **new-onset diabetes** being a rare complication compared to calcineurin inhibitors.
Question 785: A 33-year-old woman presents with weight gain and marks on her abdomen (as seen in the image below). She does not have any significant past medical history. She is a nonsmoker and denies any alcohol use. Her blood pressure is 160/110 mm Hg and pulse is 77/min. A T1/T2 MRI of the head shows evidence of a pituitary adenoma, and she undergoes surgical resection of the tumor. Which of the following therapies is indicated in this patient to ensure normal functioning of her hypothalamic-pituitary-adrenal (HPA) axis?
A. Hydrocortisone (Correct Answer)
B. Fludrocortisone
C. Methotrexate
D. Bilateral adrenalectomy
E. Mometasone
Explanation: ***Hydrocortisone***
- This patient presents with signs and symptoms consistent with **Cushing's syndrome** (weight gain, hypertension, striae), likely caused by a **pituitary adenoma** (Cushing's disease).
- Following surgical resection of a pituitary adenoma causing Cushing's disease, the chronically suppressed adrenal glands may not immediately resume normal **cortisol production**. Therefore, **glucocorticoid replacement therapy** (e.g., hydrocortisone) is crucial to prevent acute adrenal insufficiency, gradually tapered as the HPA axis recovers.
*Fludrocortisone*
- **Fludrocortisone** is a potent synthetic **mineralocorticoid** primarily used to treat conditions associated with mineralocorticoid deficiency, such as Addison's disease or congenital adrenal hyperplasia.
- While it can be used for adrenal insufficiency, this patient's primary need after pituitary surgery for Cushing's disease is **glucocorticoid replacement** for suppressed cortisol production, not mineralocorticoid effects unless specifically determined to be deficient.
*Methotrexate*
- **Methotrexate** is an **immunosuppressant** and **chemotherapeutic agent** used in conditions like cancer, rheumatoid arthritis, and psoriasis.
- It has no role in the management of pituitary adenomas or the restoration of HPA axis function post-surgical resection.
*Bilateral adrenalectomy*
- **Bilateral adrenalectomy** is a surgical procedure to remove both adrenal glands, used in cases of intractable Cushing's syndrome where other treatments have failed.
- While it effectively reduces cortisol, it induces permanent **adrenal insufficiency**, requiring lifelong glucocorticoid and mineralocorticoid replacement, and is typically a last resort, not the initial post-surgical therapy for a resected pituitary adenoma.
*Mometasone*
- **Mometasone** is a **synthetic corticosteroid** primarily used topically (e.g., for skin conditions or asthma) for its anti-inflammatory effects.
- It is not an appropriate systemic therapy for replacing cortisol and supporting HPA axis recovery after pituitary surgery due to its different potency and formulation.
Question 786: A 4-year-old boy presents to the Emergency Department with wheezing and shortness of breath after playing with the new family pet. Which of the following immunological factors is most involved in generating the antibodies necessary for mast cell Fc-receptor cross-linking and degranulation?
A. IL-5
B. IL-13
C. IL-2
D. IL-4 (Correct Answer)
E. IL-10
Explanation: **IL-4**
- **IL-4** is a primary cytokine responsible for promoting **Th2 differentiation** and inducing **B cell class switching to IgE**, which is critical for allergic reactions.
- The IgE antibodies then bind to **Fc receptors on mast cells**, leading to cross-linking and degranulation upon re-exposure to the allergen.
*IL-5*
- **IL-5** is primarily involved in the growth, differentiation, and activation of **eosinophils**, which are important in late-phase allergic reactions and parasitic infections.
- While it plays a role in allergic inflammation, it does not directly drive the production of IgE antibodies crucial for initial mast cell sensitization.
*IL-13*
- **IL-13** shares many functions with IL-4, including promoting **IgE production** and contributing to airway hyperresponsiveness and mucus secretion in asthma.
- However, **IL-4** is considered the foundational cytokine for initial IgE class switching, even though IL-13 can synergize or contribute later.
*IL-2*
- **IL-2** is primarily known for its role in the **proliferation and differentiation of T cells**, including regulatory T cells, and general immune activation.
- It does not directly promote B cell class switching to IgE or directly induce allergic antibody production.
*IL-10*
- **IL-10** is an **immunosuppressive cytokine** that *inhibits* the production of pro-inflammatory cytokines and can downregulate immune responses.
- Its role is generally to *suppress* allergic responses rather than generate the antibodies (IgE) necessary for mast cell degranulation.
Question 787: A 62-year-old woman is brought to the emergency room at a nearby hospital after being involved in a roadside accident in which she sustained severe chest trauma. Enroute to the hospital, morphine is administered for pain control. Upon arrival, the patient rapidly develops respiratory failure and requires intubation and mechanical ventilation. She is administered pancuronium in preparation for intubation but suddenly develops severe bronchospasm and wheezing. Her blood pressure also quickly falls from 120/80 mm Hg to 100/60 mm Hg. Which of the following best explains the most likely etiology of this complication?
A. Autonomic stimulation
B. Histamine release (Correct Answer)
C. Underlying neuromuscular disease
D. Drug interaction
E. Skeletal muscle paralysis
Explanation: ***Histamine release***
- In this clinical scenario, the **bronchospasm, wheezing, and hypotension** occurring after drug administration suggest **histamine release**.
- **Morphine** (administered enroute) is well-known to cause **direct histamine release** from mast cells, which can lead to bronchospasm, hypotension, and urticaria.
- While **pancuronium** itself has **minimal histamine-releasing properties** (unlike atracurium, mivacurium, or tubocurarine), the combination of morphine-induced histamine release followed by the stress of intubation preparation may have precipitated this **anaphylactoid reaction**.
- The temporal relationship and clinical presentation are most consistent with a **histamine-mediated adverse effect**.
*Autonomic stimulation*
- Pancuronium has **vagolytic (antimuscarinic) effects** that typically cause **tachycardia and increased blood pressure**, not hypotension and bronchospasm.
- While autonomic responses can influence respiratory and cardiovascular function, they do not explain the acute bronchospasm and hypotension seen here.
*Underlying neuromuscular disease*
- Neuromuscular diseases affect the response to neuromuscular blockers by altering receptor numbers or function (e.g., prolonged paralysis in myasthenia gravis, resistance in denervation injuries).
- They do not cause acute bronchospasm and hypotension with drug administration.
*Drug interaction*
- While morphine and pancuronium can both be used together safely in anesthesia, there is no specific pharmacokinetic or pharmacodynamic interaction between them that would precipitate this severe reaction.
- The clinical presentation is more consistent with a direct pharmacological effect (histamine release) rather than a drug interaction.
*Skeletal muscle paralysis*
- Pancuronium's primary effect is **skeletal muscle paralysis** by blocking nicotinic acetylcholine receptors at the neuromuscular junction.
- Muscle paralysis itself does not cause bronchospasm, wheezing, or hypotension; these are adverse effects related to histamine release or other pharmacological mechanisms.
Question 788: A 45-year-old man is brought into the emergency department after he was hit by a car. The patient was intoxicated and walked into oncoming traffic. He is currently unconscious and has a Glasgow coma scale score of 3. The patient has been admitted multiple times for alcohol intoxication and pancreatitis. The patient is resuscitated with fluid and blood products. An initial trauma survey reveals minor scrapes and abrasions and pelvic instability. The patient’s pelvis is placed in a binder. After further resuscitation the patient becomes responsive and states he is in pain. He is given medications and further resuscitation ensues. One hour later, the patient complains of numbness surrounding his mouth and in his extremities. Which of the following is the most likely explanation of this patient’s current symptoms?
A. Transfusion complication (Correct Answer)
B. Trauma to the spinal cord
C. Hypokalemia
D. Medication complication
E. Late-onset edema surrounding the spinal cord
Explanation: ***Transfusion complication***
- The patient's symptoms of **perioral numbness** and **extremity paresthesias** after massive transfusion are highly suggestive of **citrate toxicity**. Citrate, used as an anticoagulant in blood products, can chelate calcium and magnesium, leading to **hypocalcemia** and **hypomagnesemia**.
- This is exacerbated by **hypothermia**, **liver dysfunction** (common in chronic alcoholics), and **rapid transfusion rates**, all of which can impair citrate metabolism.
*Trauma to the spinal cord*
- While spinal cord injury can cause numbness and paresthesias, it typically presents with a **dermatomal distribution** or clear sensory level, and often motor deficits.
- The described numbness around the mouth and general extremity involvement is less typical for a focal spinal cord injury.
*Hypokalemia*
- **Hypokalemia** can cause muscle weakness, cramps, and cardiac arrhythmias, but **paresthesias** and **perioral numbness** are not classic symptoms.
- The presenting symptoms are more consistent with electrolyte disturbances involving calcium or magnesium.
*Medication complication*
- While medications can cause side effects, the specific constellation of **perioral paresthesia** and **extremity numbness** following massive transfusion points strongly to **citrate toxicity** rather than a generic medication reaction.
- The context of **massive transfusion** makes a direct link to transfusion-related electrolyte shifts far more probable.
*Late-onset edema surrounding the spinal cord*
- Acute spinal cord edema causing neurological symptoms would typically manifest with more localized, dermatomal deficits and potentially motor weakness.
- The rapid onset of widespread paresthesias and perioral numbness is not a typical presentation of delayed spinal cord edema.
Question 789: A 37-year-old woman is brought to the emergency department by police after being found naked outside a government building. She is accompanied by her husband who reports that she has been having "crazy" ideas. The patient's speech is pressured and she switches topics quickly from how she is going to be president one day to how she is going to learn 20 languages fluently by the end of the year. Upon further questioning, it is revealed that she has struggled with at least 2 depressive episodes in the past year. Her medical history is significant for hypertension, hyperlipidemia, gout, and chronic migraines. She was recently diagnosed with a urinary tract infection and given nitrofurantoin. She has also been taking indomethacin for an acute gout flare. Her other medications include atorvastatin, allopurinol, metoprolol, and acetazolamide. She is prescribed lithium and instructed to follow-up with a primary care physician. At a follow-up appointment, she complains of nausea, vomiting, and increased urinary frequency. On examination, she has a coarse tremor and diffuse hyperreflexia. Which of the following medications is most likely responsible for the patient's current presentation?
A. Nitrofurantoin
B. Indomethacin (Correct Answer)
C. Acetazolamide
D. Metoprolol
E. Atorvastatin
Explanation: ***Indomethacin***
- This patient is likely experiencing **lithium toxicity**, characterized by nausea, vomiting, increased urinary frequency, coarse tremor, and hyperreflexia. **NSAIDs** like indomethacin can decrease renal lithium clearance, leading to elevated lithium levels and toxicity.
- **Lithium** is primarily cleared by the kidneys, and NSAIDs inhibit prostaglandin-mediated renal vasodilation, thus reducing **glomerular filtration rate** and increasing lithium reabsorption in the renal tubules.
*Nitrofurantoin*
- This antibiotic is used for **urinary tract infections** and is generally well-tolerated.
- It is not known to significantly interact with lithium to cause toxicity or the presented symptoms.
*Acetazolamide*
- This **carbonic anhydrase inhibitor** actually increases lithium excretion.
- It would typically cause a *decrease* in lithium levels, making lithium toxicity less likely.
*Metoprolol*
- This **beta-blocker** primarily affects the cardiovascular system.
- It does not have a significant interaction with lithium that would lead to increased lithium levels or toxicity.
*Atorvastatin*
- This **statin** is used to lower cholesterol.
- It is not known to interact with lithium or cause the symptoms of lithium toxicity described.
Question 790: A 9-year-old boy is brought to the emergency department by his mother because of painful swelling in his right knee that started after he collided with another player during a soccer game. He has no history of serious illness except for an episode of prolonged bleeding following a tooth extraction a few months ago. Physical examination shows marked tenderness and swelling of the right knee joint. There are multiple bruises on the lower extremities in various stages of healing. Laboratory studies show a platelet count of 235,000/mm3, partial thromboplastin time of 78 seconds, prothrombin time of 14 seconds, and bleeding time of 4 minutes. The plasma concentration of which of the following is most likely to be decreased in this patient?
A. Plasmin
B. Factor VII
C. Protein C
D. Thrombin
E. Von Willebrand factor (Correct Answer)
Explanation: ***Von Willebrand factor***
- The patient's history of **prolonged bleeding** after a tooth extraction, **joint hemorrhage** (hemarthrosis) after minor trauma, and **multiple bruises** are classic signs of a **coagulation disorder**.
- The laboratory results showing a **normal platelet count**, **normal prothrombin time (PT)**, **normal bleeding time**, and **prolonged partial thromboplastin time (PTT)** are highly suggestive of **hemophilia A or B**, or **severe von Willebrand disease (VWD)**. However, considering the typical presentation (hemarthrosis) of hemophilia and knowing that vWF is a carrier of factor VIII, severe vWD is the most common hereditary bleeding disorder.
- Severe VWD can cause sufficiently low Factor VIII levels to result in a prolonged PTT.
*Plasmin*
- **Plasmin** is involved in fibrinolysis (breaking down clots) and is not directly related to the **prolonged PTT** seen in this patient.
- A decrease in plasmin would typically lead to a **pro-thrombotic state**, not a bleeding disorder.
*Factor VII*
- **Factor VII** is part of the **extrinsic coagulation pathway**. A deficiency in Factor VII would primarily prolong the **prothrombin time (PT)**, not the PTT.
- This patient has a normal PT, making Factor VII deficiency unlikely.
*Protein C*
- **Protein C** is a natural anticoagulant that inactivates coagulation factors Va and VIIIa.
- A deficiency in Protein C would lead to a **hypercoagulable state** (increased risk of clotting), which contradicts the patient's bleeding symptoms.
*Thrombin*
- **Thrombin** is a key enzyme in the coagulation cascade that converts fibrinogen to fibrin.
- While overall coagulation is impaired in this patient, the individual measurement of thrombin concentration is not directly indicated by the prolonged PTT. A low factor VIII (which can be caused by low vWF) is primarily responsible for the prolonged PTT.