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A 65-year-old man comes to your office to ask about "ED" after seeing a television advertisement about potential treatments. For 3 years, he has noted progressive difficulty attaining erections adequate for sexual intercourse. He sheepishly tells his story and wonders if the medicines advertised on television would be right for him. He also asks about whether his blood pressure medication could be causing his symptoms and whether hormone treatments might help.

  • How do you make him feel more comfortable discussing his concerns?
  • What organic disorders could be causing—or be associated with—his erectile dysfunction (ED)? How might those factors affect his treatment options?
  • What effects do medications have on sexual function?
  • How often are treatable hormone deficiencies responsible for ED?

Erectile dysfunction (ED) is the inability to attain and sustain an erection of sufficient rigidity for sexual activity. It affects nearly 1 in 5 men over 20 years of age, and the prevalence increases dramatically with advancing age. Seventy-eight percent of men over 75 years are affected and Hispanic men are more likely to report it.1

Although patients may be reluctant to discuss this problem it is important for physicians to inquire about it. Effective treatments based on improved understanding of the mechanisms of ED are now available. ED may be a sign of important comorbid cardiovascular disease. ED is a strong predictor of both coronary artery disease and peripheral artery disease as endothelial dysfunction contributes to all 3 conditions.

There are many associated or contributing conditions that should be explored, including urologic problems, diabetes, hormonal disturbances, depression, obstructive sleep apnea, neurologic disorders, and the use of medications.

α-Adrenergic sympathetic tone limits blood flow to the penis and maintains the flaccid state. Erection occurs when erotic stimuli inhibit sympathetic tone and release nitric oxide and other vasoactive substances from nerve endings and endothelial cells in the penile arterioles. The cavernosal sinusoids become engorged with blood, and erection ensues. This is aided by a passive inhibition of venous outflow as the subtunical venous plexus is compressed between the expanding sinusoids and unyielding tunica albuginea. Forcible compression of the base of the penis by the ischiocavernous muscles then further increases the intracavernous pressure.

Any derangement in these events can cause ED, commonly the failure of nitric oxide release due to endothelial dysfunction. Improved understanding of these mechanisms has led to ...

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