A 59-year-old man with a history of major depressive disorder, asthma, and erectile dysfunction presents to his family physician complaining of depressed mood, amotivation, overeating, and anhedonia. He currently takes no medications. The patient has a 3 pack-year smoking history and would like to quit but has been unsuccessful in the past. His BMI is 29 kg/m^2. The physician suggests starting an antidepressant for the patient's mood symptoms. The patient is reluctant, as he used to take sertraline, but stopped it after his erectile dysfunction worsened. Which of the following antidepressants would be most appropriate for this patient?
Q862
A 32-year-old woman presents for a follow-up visit. She was diagnosed with type 2 diabetes mellitus a month ago but refused to start medications despite counseling due to her fear of gaining weight. She tried exercising and eating healthy in an attempt to ''cure'' her diabetes. She managed to lose 1.8 kg (4 lb) in a month. Today she still complains of increased urinary frequency, the same symptom that leads to her initial suspicion of diabetes. No other significant past medical history. She is happily married and plans on having kids in the next few years. The patient is a non-smoker, denies illicit drug use, and drinks socially. Her vital signs show a pulse of 80/min, a respiratory rate of 16/min, a blood pressure of 120/80 mm Hg, and a temperature of 36.9°C (98.4°F). Her BMI is 33.0 kg/m2. Physical exam findings are unremarkable. Her fingerstick glucose today is 214 mg/dL. Laboratory findings reveal the following:
Glycated Hemoglobin (HbA1c) 7.1%
Blood glucose (fasting) 130 mg/dL
Serum:
Sodium 142 mEq/L
Potassium 3.9 mEq/L
Chloride 101 mEq/L
Serum creatinine 0.8 mg/dL
Blood urea nitrogen 9 mg/dL
Urinalysis shows:
Glucose Positive
Ketones Negative
Leukocytes Negative
Nitrites Negative
RBCs Negative
Casts Negative
Which of the following is the best treatment option for this patient?
Q863
A 48-year-old woman presents to the emergency room because of severe back pain after a fall. She says that she was walking home from work when she slipped on a patch of ice on the sidewalk. Since she did not have anything to hold onto, she fell backwards and landed on her posterior iliac crests bilaterally. Immediately after the fall, she started experiencing back pain and tenderness that concerned her enough to call for an ambulance. Her past medical history is significant for arthritis, diabetes, and hypertension. On arrival, her temperature is 99°F (37.2°C), blood pressure is 129/86 mmHg, pulse is 112/min, respirations are 19/min. Physical exam reveals tenderness to palpation over the middle of her lower back. A drug that may have predisposed this patient to this outcome most likely has which of the following mechanisms?
Q864
A 71-year-old woman presents to the clinic after an X-ray that revealed compression fractures of her L1 and L2 vertebral bodies due to osteoporotic changes. The patient has a history of hypertension for which she takes hydrochlorothiazide, and rheumatoid arthritis, for which she has been taking prednisone for the last 2 years. The patient states that she had a dual-energy X-ray absorptiometry (DEXA) scan 3 years ago that was normal and attributes that finding to regularly taking calcium and vitamin D supplements since then. The patient states that her pain from the fractures is stopping her from participating in her regular activities, such as exercising and gardening. Which of the following is the main cause of her osteoporosis?
Q865
You are working in the emergency room of a children's hospital when a 4-year-old girl is brought in by ambulance due to "difficulty breathing." The patient had been eating lunch on a school field trip when she suddenly complained of abdominal pain. Shortly thereafter, she was noted to have swelling of the lips, a rapidly developing red rash and difficulty breathing. In the ambulance her blood pressure was persistently 80/50 mmHg despite intramuscular epinephrine. In the course of stabilization and work up of the patient, you note an elevated tryptase level. What is the mechanism behind this elevated tryptase level?
Q866
A research team is studying the effects of a novel drug that was discovered to treat type 2 diabetes. In order to learn more about its effects, they follow patients who are currently taking the drug and determine whether there are adverse effects that exceed anticipated levels and may therefore be drug-related. They discover that the drug causes an excess of sudden cardiac death in 19 patients with renal failure out of 2 million total patients that are followed. Based on these results, an additional warning about this serious adverse effect is added to the investigator brochure for the drug. Which of the following clinical phase studies does this study most likely describe?
Q867
A 55-year-old woman comes to the physician because of involuntary hand movements that improve with alcohol consumption. Physical examination shows bilateral hand tremors that worsen when the patient is asked to extend her arms out in front of her. The physician prescribes a medication that is associated with an increased risk of bronchospasms. This drug has which of the following immediate effects on the cardiovascular system?
Stroke volume | Heart rate | Peripheral vascular resistance
Q868
A 30-year-old obese female presents with new-onset headaches, ringing in her ears, and blurry vision. Ibuprofen and avoidance of light has not relieved her symptoms. She denies a history of recent trauma, fever, chills, and fatigue. Past medical history is significant for type 2 diabetes mellitus managed with metformin. She has had 20/20 vision her whole life and wonders if she might need to get eyeglasses. She has 2 healthy school-age children. Her temperature is 36.8°C (98.2°F), heart rate is 90/min, respiratory rate is 15/min, and blood pressure is 135/80 mm Hg. Physical exam is notable for decreased lateral eye movement, and the funduscopic findings are shown in the picture. Laboratory findings are within normal limits and brain imaging is normal. Lumbar puncture demonstrates an elevated opening pressure and normal CSF composition. Which of the following is a side effect of the medication used to treat this condition?
Q869
A 66-year-old man with congestive heart failure presents to the emergency department complaining of worsening shortness of breath. These symptoms have worsened over the last 3 days. He has a blood pressure of 126/85 mm Hg and heart rate of 82/min. Physical examination is notable for bibasilar crackles. A chest X-ray reveals bilateral pulmonary edema. His current medications include metoprolol succinate and captopril. You wish to add an additional medication targeted towards his symptoms. Of the following, which statement is correct regarding loop diuretics?
Q870
A 26-year-old woman (gravida 3 para 1) with no prenatal care delivers a boy at 37 weeks gestation. His Apgar score is 5 at 1 minute and 8 at 5 minutes. His weight is 2.1 kg (4.2 lb) and length is 47 cm (1 ft 7 in). The mother’s history is significant for chronic pyelonephritis, atrial fibrillation, and gastroesophageal reflux disease. She has a 5-pack-year smoking history and also reports alcohol consumption during pregnancy. Examination of the infant shows a short depressed nasal bridge, wide nose, brachydactyly, and a short neck. Ophthalmoscopy reveals bilateral cataracts. What is the most likely cause of the newborn’s symptoms?
Autonomic/CV Drugs US Medical PG Practice Questions and MCQs
Question 861: A 59-year-old man with a history of major depressive disorder, asthma, and erectile dysfunction presents to his family physician complaining of depressed mood, amotivation, overeating, and anhedonia. He currently takes no medications. The patient has a 3 pack-year smoking history and would like to quit but has been unsuccessful in the past. His BMI is 29 kg/m^2. The physician suggests starting an antidepressant for the patient's mood symptoms. The patient is reluctant, as he used to take sertraline, but stopped it after his erectile dysfunction worsened. Which of the following antidepressants would be most appropriate for this patient?
A. Citalopram
B. Bupropion (Correct Answer)
C. Sertraline
D. Mirtazapine
E. Amitriptyline
Explanation: **Bupropion**
- **Bupropion** is an antidepressant that does not typically cause **sexual dysfunction** and can aid in **smoking cessation**, addressing two key concerns for this patient.
- It acts by inhibiting the reuptake of **norepinephrine** and **dopamine**, which can also help with **amotivation** and **anhedonia**.
*Citalopram*
- **Citalopram** is an **SSRI** (selective serotonin reuptake inhibitor), a class of drugs commonly associated with causing or worsening **sexual dysfunction**, which is a significant concern for this patient.
- While effective for depression, it does not offer the additional benefit of aiding in **smoking cessation**.
*Sertraline*
- The patient previously stopped **sertraline** due to worsening **erectile dysfunction**, indicating that this **SSRI** is not a suitable option for him.
- Reintroducing **sertraline** would likely lead to similar adverse effects and patient non-adherence.
*Mirtazapine*
- **Mirtazapine** is an antidepressant that can cause **weight gain** and **sedation**, which would be undesirable for a patient with a BMI of 29 kg/m^2 who also needs to quit smoking.
- Although it has a lower incidence of sexual dysfunction compared to SSRIs, it does not offer benefits for **smoking cessation**.
*Amitriptyline*
- **Amitriptyline** is a **tricyclic antidepressant (TCA)** known for significant side effects such as **anticholinergic effects** (e.g., dry mouth, constipation, urinary retention), **sedation**, and **cardiac toxicity** in overdose.
- Given the patient's age and history, a TCA would likely be poorly tolerated and poses higher risks compared to other options.
Question 862: A 32-year-old woman presents for a follow-up visit. She was diagnosed with type 2 diabetes mellitus a month ago but refused to start medications despite counseling due to her fear of gaining weight. She tried exercising and eating healthy in an attempt to ''cure'' her diabetes. She managed to lose 1.8 kg (4 lb) in a month. Today she still complains of increased urinary frequency, the same symptom that leads to her initial suspicion of diabetes. No other significant past medical history. She is happily married and plans on having kids in the next few years. The patient is a non-smoker, denies illicit drug use, and drinks socially. Her vital signs show a pulse of 80/min, a respiratory rate of 16/min, a blood pressure of 120/80 mm Hg, and a temperature of 36.9°C (98.4°F). Her BMI is 33.0 kg/m2. Physical exam findings are unremarkable. Her fingerstick glucose today is 214 mg/dL. Laboratory findings reveal the following:
Glycated Hemoglobin (HbA1c) 7.1%
Blood glucose (fasting) 130 mg/dL
Serum:
Sodium 142 mEq/L
Potassium 3.9 mEq/L
Chloride 101 mEq/L
Serum creatinine 0.8 mg/dL
Blood urea nitrogen 9 mg/dL
Urinalysis shows:
Glucose Positive
Ketones Negative
Leukocytes Negative
Nitrites Negative
RBCs Negative
Casts Negative
Which of the following is the best treatment option for this patient?
A. Start empagliflozin.
B. Start glipizide.
C. Start metformin. (Correct Answer)
D. Start exenatide.
E. Start insulin.
Explanation: ***Start metformin*** is the correct answer.
- **Metformin is the first-line pharmacological treatment** for type 2 diabetes mellitus according to ADA and AACE guidelines due to its proven efficacy, safety profile, and multiple benefits.
- It has a **weight-neutral to modest weight loss effect** (~2-3 kg), directly addressing this patient's primary concern about weight gain from medications.
- **Low risk of hypoglycemia** when used as monotherapy, making it safe for this active patient.
- **Cardiovascular benefits** and potential reduction in microvascular complications with long-term use.
- **Cost-effective** and well-tolerated, with GI side effects that typically diminish over time.
- The patient has **normal renal function** (Cr 0.8 mg/dL), so metformin is safe to use (contraindicated only when eGFR <30 mL/min/1.73m²).
*Start empagliflozin* is incorrect.
- Empagliflozin is an **SGLT2 inhibitor** that promotes glycosuria, leading to weight loss (~2-4 kg) and provides cardiovascular and renal protective benefits.
- While increasingly popular and beneficial for weight management, it is typically used as **second-line therapy** or added to metformin, or used first-line specifically in patients with established atherosclerotic cardiovascular disease, heart failure, or chronic kidney disease.
- Not the standard initial monotherapy choice in this uncomplicated T2DM patient.
*Start glipizide* is incorrect.
- Glipizide is a **sulfonylurea** that stimulates pancreatic beta cells to release insulin, effectively lowering blood glucose.
- However, it is **strongly associated with weight gain** (2-5 kg), which directly contradicts the patient's primary concern and motivation.
- **Significant risk of hypoglycemia**, particularly with missed meals or increased activity.
- Now considered a later-line option due to these adverse effects.
*Start exenatide* is incorrect.
- Exenatide is a **GLP-1 receptor agonist** that enhances glucose-dependent insulin secretion, suppresses glucagon, and delays gastric emptying.
- **Promotes significant weight loss** (3-5 kg) and has cardiovascular benefits, making it attractive for this patient's profile.
- However, it is **injectable** (requires patient training), more expensive than metformin, and commonly causes GI side effects (nausea, vomiting).
- Typically used as **second-line therapy** after metformin or as first-line in specific cases with compelling cardiovascular indications.
- Not the standard initial choice for uncomplicated T2DM.
*Start insulin* is incorrect.
- Insulin therapy is the most potent glucose-lowering agent and is essential for type 1 diabetes and advanced type 2 diabetes with beta-cell failure.
- However, it is **strongly associated with weight gain** (2-4 kg) and carries a **high risk of hypoglycemia**, both of which are undesirable for this patient.
- Reserved for patients who have failed multiple oral agents or have severe hyperglycemia (e.g., HbA1c >10%, symptomatic hyperglycemia).
- This patient's HbA1c of 7.1% does not warrant insulin as initial therapy.
Question 863: A 48-year-old woman presents to the emergency room because of severe back pain after a fall. She says that she was walking home from work when she slipped on a patch of ice on the sidewalk. Since she did not have anything to hold onto, she fell backwards and landed on her posterior iliac crests bilaterally. Immediately after the fall, she started experiencing back pain and tenderness that concerned her enough to call for an ambulance. Her past medical history is significant for arthritis, diabetes, and hypertension. On arrival, her temperature is 99°F (37.2°C), blood pressure is 129/86 mmHg, pulse is 112/min, respirations are 19/min. Physical exam reveals tenderness to palpation over the middle of her lower back. A drug that may have predisposed this patient to this outcome most likely has which of the following mechanisms?
A. Inhibition of leukotriene and prostaglandin production
B. Inhibition of circulating cytokine
C. Inhibition of folate processing
D. Stimulation of adipocyte transcription factor (Correct Answer)
E. Inhibition of prostaglandin production alone
Explanation: ***Stimulation of adipocyte transcription factor***
- The patient's presentation with a **vertebral fracture** after a minor fall, combined with a history of **arthritis**, strongly suggests **osteoporosis** as a predisposing factor.
- **Glucocorticoids** are commonly used to treat arthritis and stimulate **adipocyte transcription factors** (like PPAR-γ), leading to **reduced bone formation** and increased bone resorption, causing osteoporosis.
*Inhibition of leukotriene and prostaglandin production*
- This mechanism describes **NSAIDs**, which are used for pain and inflammation but do not typically cause osteoporosis or increase fracture risk through this specific mechanism.
- While NSAIDs can have gastrointestinal side effects, they are not directly linked to the bone fragility seen in this case.
*Inhibition of circulating cytokine*
- This mechanism is characteristic of **biologic agents** used in immunosuppression, such as TNF-α inhibitors.
- These drugs are not typically associated with increased fracture risk or osteoporosis in the same way glucocorticoids are.
*Inhibition of folate processing*
- This mechanism is characteristic of **methotrexate**, a disease-modifying antirheumatic drug (DMARD) used in arthritis.
- While methotrexate has side effects, it is not primarily known to induce osteoporosis or increase fracture risk as seen with glucocorticoids.
*Inhibition of prostaglandin production alone*
- This mechanism broadly refers to drugs like **NSAIDs** (non-selective COX inhibitors) or selective COX-2 inhibitors.
- As mentioned, these drugs do not typically cause the bone fragility leading to spontaneous fractures seen with long-term glucocorticoid use.
Question 864: A 71-year-old woman presents to the clinic after an X-ray that revealed compression fractures of her L1 and L2 vertebral bodies due to osteoporotic changes. The patient has a history of hypertension for which she takes hydrochlorothiazide, and rheumatoid arthritis, for which she has been taking prednisone for the last 2 years. The patient states that she had a dual-energy X-ray absorptiometry (DEXA) scan 3 years ago that was normal and attributes that finding to regularly taking calcium and vitamin D supplements since then. The patient states that her pain from the fractures is stopping her from participating in her regular activities, such as exercising and gardening. Which of the following is the main cause of her osteoporosis?
A. Hydrochlorothiazide (HCTZ) therapy
B. Calcium malabsorption
C. Decreased estrogen levels
D. Undiagnosed hyperparathyroidism
E. Bone depletion due to chronic corticosteroid use (Correct Answer)
Explanation: ***Bone depletion due to chronic corticosteroid use***
- The patient's long-term **prednisone** use for rheumatoid arthritis for **2 years** is a significant risk factor for **secondary osteoporosis**.
- **Glucocorticoids** directly inhibit osteoblast activity, increase osteoclast activity, and impair calcium absorption, leading to accelerated bone loss.
*Hydrochlorothiazide (HCTZ) therapy*
- **Thiazide diuretics** like HCTZ are often associated with a **reduced risk of osteoporosis** because they decrease urinary calcium excretion, potentially leading to increased bone mineral density.
- Therefore, HCTZ is unlikely to be the cause of her current osteoporosis.
*Calcium malabsorption*
- While **calcium malabsorption** can contribute to osteoporosis, the patient's history of taking **calcium and vitamin D supplements** suggests she is actively trying to mitigate this risk.
- Furthermore, chronic **corticosteroid use** is a more direct and potent cause of bone loss than general calcium malabsorption in this clinical context.
*Decreased estrogen levels*
- Decreased estrogen levels are a primary cause of **postmenopausal osteoporosis** in women. While this patient is 71 and postmenopausal, her **corticosteroid use** is a more dominant and specific cause of bone loss in this case.
- Her normal DEXA 3 years ago implies that postmenopausal bone loss alone might not fully explain the rapid development of severe osteoporosis leading to vertebral fractures.
*Undiagnosed hyperparathyroidism*
- **Hyperparathyroidism** causes increased bone resorption due to elevated **parathyroid hormone (PTH)**, leading to osteoporosis.
- However, there is no information in the vignette to suggest hyperparathyroidism, such as elevated calcium levels or specific symptoms like kidney stones. **Chronic corticosteroid use** is a much more direct and established cause in this patient's history.
Question 865: You are working in the emergency room of a children's hospital when a 4-year-old girl is brought in by ambulance due to "difficulty breathing." The patient had been eating lunch on a school field trip when she suddenly complained of abdominal pain. Shortly thereafter, she was noted to have swelling of the lips, a rapidly developing red rash and difficulty breathing. In the ambulance her blood pressure was persistently 80/50 mmHg despite intramuscular epinephrine. In the course of stabilization and work up of the patient, you note an elevated tryptase level. What is the mechanism behind this elevated tryptase level?
A. IgM mediated complement activation
B. Cross-linking of IgE on mast cells (Correct Answer)
C. IgG production by plasma cells
D. Antibody-antigen immune complexes
E. Cross-linking of IgG on mast cells
Explanation: **Cross-linking of IgE on mast cells**
- The rapid onset of symptoms like **lip swelling**, **rash**, and **difficulty breathing** after eating, along with **hypotension** despite epinephrine, points to **anaphylaxis**, which is primarily mediated by **IgE**.
- **Tryptase** is a serine protease selectively stored in the secretory granules of **mast cells** and is released upon mast cell activation, making it a reliable marker for **anaphylaxis**.
*IgM mediated complement activation*
- **IgM-mediated complement activation** is primarily involved in host defense against infections and in autoimmune conditions, but not typically in acute allergic reactions like anaphylaxis.
- While complement activation can occur in severe allergic reactions, the direct trigger and primary mechanism for tryptase release in anaphylaxis is **IgE cross-linking**.
*IgG production by plasma cells*
- **IgG production by plasma cells** is part of the adaptive immune response, responsible for long-term immunity and neutralizing toxins and pathogens.
- It is not the immediate mechanism for **mast cell degranulation** and **tryptase release** in an acute allergic reaction such as anaphylaxis.
*Antibody-antigen immune complexes*
- **Antibody-antigen immune complexes** are typically associated with Type III hypersensitivity reactions, which involve deposition of complexes in tissues, leading to inflammation (e.g., lupus, serum sickness).
- These reactions generally have a delayed onset and a different clinical presentation, not the acute, systemic symptoms of **anaphylaxis** seen here.
*Cross-linking of IgG on mast cells*
- While **IgG** can play a role in some immune responses, the primary immunoglobulin involved in immediate hypersensitivity reactions like anaphylaxis, leading to mast cell degranulation, is **IgE**, not IgG.
- Mast cells have **Fc receptors** for IgE, not IgG, that, when cross-linked by allergen, trigger the release of mediators including **tryptase**.
Question 866: A research team is studying the effects of a novel drug that was discovered to treat type 2 diabetes. In order to learn more about its effects, they follow patients who are currently taking the drug and determine whether there are adverse effects that exceed anticipated levels and may therefore be drug-related. They discover that the drug causes an excess of sudden cardiac death in 19 patients with renal failure out of 2 million total patients that are followed. Based on these results, an additional warning about this serious adverse effect is added to the investigator brochure for the drug. Which of the following clinical phase studies does this study most likely describe?
A. Phase IV (Correct Answer)
B. Phase II
C. Phase V
D. Phase III
E. Phase I
Explanation: ***Phase IV***
- This study occurs **after a drug has been approved and marketed**, focusing on post-marketing surveillance for long-term safety, effectiveness, and real-world side effects in a large and diverse patient population.
- The discovery of a rare but serious adverse effect (sudden cardiac death) in a large patient population (2 million) after the drug is already in use is characteristic of a **Phase IV clinical trial**.
*Phase II*
- Phase II trials involve a **larger group of patients (hundreds)** and focus on evaluating the drug's effectiveness and further assessing safety in patients with the target condition.
- This phase is typically conducted **before widespread marketing** and would not involve 2 million patients.
*Phase V*
- There is **no widely recognized "Phase V"** in standard clinical trial terminology (Phases I-IV focus on drug development and post-marketing surveillance).
- This term is sometimes used informally to refer to **health economics and outcomes research** or implementation studies, which are not described in the scenario.
*Phase III*
- Phase III trials are large-scale studies involving **thousands of patients** to confirm effectiveness, monitor side effects, compare the drug to standard treatments, and collect information for safe use.
- While large, these trials are conducted **before regulatory approval** and marketing, and would not typically follow 2 million patients already taking the drug in the real world.
*Phase I*
- Phase I trials are the **first stage of human testing**, involving a small group of healthy volunteers (20-100) to assess safety, dosage, and pharmacokinetics.
- The primary goal is to determine if the drug is safe enough for further testing, not to identify rare adverse events in a large patient population.
Question 867: A 55-year-old woman comes to the physician because of involuntary hand movements that improve with alcohol consumption. Physical examination shows bilateral hand tremors that worsen when the patient is asked to extend her arms out in front of her. The physician prescribes a medication that is associated with an increased risk of bronchospasms. This drug has which of the following immediate effects on the cardiovascular system?
Stroke volume | Heart rate | Peripheral vascular resistance
A. ↓ ↓ ↓
B. ↓ ↓ ↑ (Correct Answer)
C. ↓ ↑ ↑
D. ↑ ↑ ↑
E. ↑ ↑ ↓
Explanation: ***↓ ↓ ↑***
- This patient likely has **essential tremor**, which is characterized by **bilateral hand tremors** that improve with alcohol and worsen with intention (postural tremor). The prescribed medication is a **beta-blocker** (e.g., propranolol), which is associated with an increased risk of bronchospasms due to blocking **beta-2 receptors** in the airways.
- Beta-blockers **decrease heart rate** (negative chronotropic effect) and **stroke volume** (negative inotropic effect) by blocking beta-1 receptors in the heart, reducing cardiac output.
- **Peripheral vascular resistance increases** acutely due to: (1) **unopposed alpha-1 adrenergic tone** in blood vessels (loss of beta-2 mediated vasodilation), and (2) baroreceptor-mediated reflex vasoconstriction in response to decreased cardiac output. This helps maintain blood pressure despite reduced cardiac output.
*↓ ↓ ↓*
- While beta-blockers decrease **heart rate** and **stroke volume**, peripheral vascular resistance does not decrease acutely. A decrease in all three parameters would cause severe hypotension.
- The loss of beta-2 receptor-mediated vasodilation and baroreceptor reflexes lead to increased, not decreased, peripheral vascular resistance.
*↓ ↑ ↑*
- Beta-blockers **decrease heart rate** through beta-1 blockade, not increase it. This is their primary cardiac mechanism of action.
- An increase in heart rate would be expected with sympathomimetic drugs or anticholinergics, not beta-blockers.
*↑ ↑ ↑*
- This combination indicates increased cardiovascular activity, which is the opposite effect of **beta-blockers**.
- Beta-blockers reduce heart rate and stroke volume by blocking beta-1 receptors; they do not increase these parameters.
- This pattern would suggest sympathetic activation or administration of an adrenergic agonist.
*↑ ↑ ↓*
- Beta-blockers **decrease** (not increase) both heart rate and stroke volume through beta-1 receptor blockade.
- While decreased peripheral vascular resistance occurs with vasodilators, beta-blockers acutely **increase** PVR due to unopposed alpha-adrenergic tone.
Question 868: A 30-year-old obese female presents with new-onset headaches, ringing in her ears, and blurry vision. Ibuprofen and avoidance of light has not relieved her symptoms. She denies a history of recent trauma, fever, chills, and fatigue. Past medical history is significant for type 2 diabetes mellitus managed with metformin. She has had 20/20 vision her whole life and wonders if she might need to get eyeglasses. She has 2 healthy school-age children. Her temperature is 36.8°C (98.2°F), heart rate is 90/min, respiratory rate is 15/min, and blood pressure is 135/80 mm Hg. Physical exam is notable for decreased lateral eye movement, and the funduscopic findings are shown in the picture. Laboratory findings are within normal limits and brain imaging is normal. Lumbar puncture demonstrates an elevated opening pressure and normal CSF composition. Which of the following is a side effect of the medication used to treat this condition?
A. Elevated liver function tests
B. Rhabdomyolysis
C. Kidney stones (Correct Answer)
D. Pancreatitis
E. Decreased white blood cell count
Explanation: ***Kidney stones***
- The patient's symptoms (headaches, tinnitus, blurry vision), **obesity**, normal brain imaging, and **elevated CSF opening pressure with normal CSF composition** are classic for **idiopathic intracranial hypertension (IIH)**, also known as pseudotumor cerebri.
- The first-line medical treatment for IIH is **acetazolamide**, a carbonic anhydrase inhibitor, which commonly causes **kidney stones** due to altered urine pH and reduced citrate excretion.
*Elevated liver function tests*
- While some medications can cause elevated liver function tests, this is not a typical or common side effect of **acetazolamide**.
- **Acetaminophen** overdose or certain antibiotics are more frequently associated with this side effect.
*Rhabdomyolysis*
- **Rhabdomyolysis** is characterized by muscle breakdown and is often associated with statin use, significant trauma, or certain illicit drugs.
- It is not a known side effect of **acetazolamide**.
*Pancreatitis*
- **Pancreatitis** can be a side effect of various medications (e.g., thiopurines, certain diuretics), but it is not commonly associated with **acetazolamide**.
- The patient's history of Type 2 Diabetes is a risk factor for pancreatitis, but not directly linked to the treatment of IIH.
*Decreased white blood cell count*
- A decrease in white blood cell count (leukopenia or agranulocytosis) is a serious but rare side effect of certain medications, such as **clozapine** or **methimazole**.
- It is not a typical side effect of **acetazolamide**.
Question 869: A 66-year-old man with congestive heart failure presents to the emergency department complaining of worsening shortness of breath. These symptoms have worsened over the last 3 days. He has a blood pressure of 126/85 mm Hg and heart rate of 82/min. Physical examination is notable for bibasilar crackles. A chest X-ray reveals bilateral pulmonary edema. His current medications include metoprolol succinate and captopril. You wish to add an additional medication targeted towards his symptoms. Of the following, which statement is correct regarding loop diuretics?
A. Loop diuretics can cause metabolic acidosis
B. Loop diuretics can cause ammonia toxicity
C. Loop diuretics can cause hyperlipidemia
D. Loop diuretics decrease sodium, magnesium, and chloride but increase calcium
E. Loop diuretics inhibit the action of the Na+/K+/Cl- cotransporter (Correct Answer)
Explanation: ***Loop diuretics inhibit the action of the Na+/K+/Cl- cotransporter***
- Loop diuretics, like furosemide, directly block the **Na+/K+/2Cl- cotransporter** in the **thick ascending limb of the loop of Henle**, preventing the reabsorption of these ions.
- This inhibition leads to increased excretion of water, sodium, potassium, and chloride, which is beneficial in conditions like **pulmonary edema** due to **congestive heart failure**.
*Loop diuretics can cause metabolic acidosis*
- Loop diuretics typically cause **metabolic alkalosis**, not acidosis, because they increase the excretion of hydrogen ions and potassium, leading to a compensatory increase in bicarbonate.
- The increased delivery of sodium to the collecting duct can also stimulate potassium and hydrogen secretion, contributing to alkalosis.
*Loop diuretics can cause ammonia toxicity*
- Loop diuretics do not directly cause **ammonia toxicity**; this is more commonly associated with conditions like **hepatic encephalopathy** or certain other medications.
- Their primary mechanism of action is on renal ion transport, not ammonia metabolism.
*Loop diuretics can cause hyperlipidemia*
- While some diuretics like **thiazide diuretics** can cause mild increases in **lipid levels**, loop diuretics are not typically associated with significant **hyperlipidemia**.
- The most common metabolic side effects of loop diuretics include electrolyte imbalances.
*Loop diuretics decrease sodium, magnesium, and chloride but increase calcium*
- Loop diuretics decrease the reabsorption of **sodium**, **magnesium**, and **chloride**, leading to their increased excretion.
- They also increase **calcium excretion** (cause hypocalcemia), rather than increasing serum calcium levels, by inhibiting its reabsorption in the thick ascending limb of the loop of Henle.
Question 870: A 26-year-old woman (gravida 3 para 1) with no prenatal care delivers a boy at 37 weeks gestation. His Apgar score is 5 at 1 minute and 8 at 5 minutes. His weight is 2.1 kg (4.2 lb) and length is 47 cm (1 ft 7 in). The mother’s history is significant for chronic pyelonephritis, atrial fibrillation, and gastroesophageal reflux disease. She has a 5-pack-year smoking history and also reports alcohol consumption during pregnancy. Examination of the infant shows a short depressed nasal bridge, wide nose, brachydactyly, and a short neck. Ophthalmoscopy reveals bilateral cataracts. What is the most likely cause of the newborn’s symptoms?
A. Omeprazole
B. Warfarin (Correct Answer)
C. Atenolol
D. Alcohol
E. Gentamicin
Explanation: **Warfarin**
- The constellation of **nasal hypoplasia (short depressed nasal bridge, wide nose)**, **stippled epiphyses (brachydactyly)**, and **ophthalmologic abnormalities (bilateral cataracts)** are classic features of **warfarin embryopathy (fetal warfarin syndrome)**.
- Warfarin crosses the placenta and inhibits **vitamin K-dependent carboxylation**, affecting bone and cartilage development and leading to these characteristic fetal anomalies.
*Omeprazole*
- **Omeprazole** is a proton pump inhibitor generally considered **safe in pregnancy** and is not associated with teratogenic effects like those described.
- It is commonly used to treat **gastroesophageal reflux disease** during pregnancy.
*Atenolol*
- **Atenolol** is a beta-blocker that can cause **fetal growth restriction** and **neonatal bradycardia** or **hypoglycemia** if used in late pregnancy.
- However, it does not typically cause the specific craniofacial or skeletal malformations seen in this infant.
*Alcohol*
- **Fetal alcohol syndrome** is characterized by **growth restriction**, **facial dysmorphology (e.g., short palpebral fissures, smooth philtrum, thin upper lip)**, and **CNS abnormalities**.
- While the infant has growth restriction, the specific facial and skeletal features do not align with fetal alcohol syndrome.
*Gentamicin*
- **Gentamicin** is an aminoglycoside antibiotic that can cause **ototoxicity** (hearing loss) and **nephrotoxicity** in both the mother and fetus.
- It is not associated with the **craniofacial, skeletal, or ocular anomalies** described in this case.
