A 26-year-old man with no significant history presents to his primary care physician with complaints of episodic palpitations, morning headaches, and diaphoresis. He denies any illicit drug use. His physical examination is notable for a blood pressure of 230/120 mmHg. His ophthalmologic examination is significant for AV nicking.
What is the most appropriate next step?
Urine metanephrines. This patient’s medical history is consistent with a diagnosis of pheochromocytoma. Pheochromocytomas arise from chromaffin cells. These tumors are most commonly found in the adrenal glands, but may be present anywhere there are sympathetic nerves. Classic symptoms are episodic palpitations, headaches, and diaphoresis. Rarely, patients may present with orthostatic hypotension. Initial diagnostic testing would involve the evaluation of a urine specimen for urine metanephrines. A toxicology screen is not indicated given his clinical history. An MRI of the abdomen would be helpful to evaluate for intra-abdominal masses, but an MRI of the thorax would be of limited benefit. Starting a thiazide diuretic would be beneficial, but ultimately the patient requires surgical therapy for correction of his hypertension.
A 65-year-old man with a history of hypertension and dyslipidemia is admitted to the coronary care unit with a diagnosis of a myocardial infarction. He undergoes an emergent cardiac catheterization with insertion of a drug-eluting stent to his left circumflex coronary artery. His vital signs show a blood pressure of 170/90 mmHg with a heart rate of 85 bpm and no evidence of heart failure on examination.
Which of the following medications would be most appropriate to treat this patient’s hypertension?
Metoprolol. The initial choice of antihypertensive medication in this patient should be a β-blocker. Multiple studies have shown the benefit of βblockers in the post-myocardial infarction period. The morphine in acute myocardial infarction (MIAMI-1) and International Study of Infarct Survival (ISIS-1) trials in the fibrinolytic era both showed trends toward a decrease in mortality with the use of intravenous β-blockers. The clopidogrel and metoprolol in myocardial infarction (COMMIT) trial found decreases in the rate of reinfarction and ventricular fibrillation with intravenous metoprolol followed by oral metoprolol; however, there was a 30% increase in the risk of cardiogenic shock. A meta-analysis of the postmyocardial infarction use of β-blockers has shown up to a 40% decrease in cardiovascular mortality. The American Heart Association 2013 ST-segment elevation myocardial infarction (STEMI) guidelines recommend initiation of oral β-blockers in the first 24 hours, providing that heart failure signs, evidence of a low-output state, risk factors for cardiogenic shock, or other contraindications to β-blockers are absent. However, intravenous β-blockers carry a class IIa indication in STEMI, given the concern for possible complications.
Which of the following antihypertensive drug classes is most effective at reducing carotid intimal thickness?
Calcium channel blocker. Calcium channel blockers are the most effective of the antihypertensive regimens at reducing carotid atherosclerosis. Studies comparing various calcium channel blockers with thiazide diuretics, ACEIs, and β-blockers have shown that calcium channel blockers have greater ability to decrease carotid intimal thickness.
What is the long-term antihypertensive mechanism of action for thiazide diuretics?
Decreased peripheral resistance. The initial mechanism of action for lowering blood pressure is a decrease in plasma volume secondary to natriuresis. This triggers an increase in the activity of the rennin-angiotensin system, resulting in a return of plasma volume to normal. However, there is a long-term decrease in peripheral resistance that produces the chronic antihypertensive effects of thiazide diuretics.
A 46-year-old woman, status post orthotopic heart transplantation, is currently taking mycophenolate, prednisone, and tacrolimus as an immunosuppressive regimen. On routine laboratory evaluation, she is found to have leukopenia. Mycophenolate levels have not been elevated in the past few months.
Which of the following antihypertensive agents is the most likely culprit?
Captopril. Aside from mycophenolate, the ACEI captopril is the most likely cause of this patient’s leukopenia. When immunosuppressive therapy is combined with ACEIs, there are reports of the development of anemia, neutropenia, leukopenia, and agranulocytosis. The best treatment strategy in this patient would be to use an alternative antihypertensive agent and monitor blood counts closely.
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