Tuesday, May 30, 2023
This activity is intended for urologists, primary-care physicians, and internists.
The central goals of this educational activity are to enhance recognition of, and care for, erectile dysfunction (ED) by exploring the epidemiology of this underrecognized condition, discussing interview and other diagnostic techniques, and considering the evidence supporting distinct treatment approaches.
Upon completion of this self-study activity, participants will be able
to:
Medical Education Collaborative, a nonprofit education organization, is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.
Medical Education Collaborative designates this educational activity for a maximum of 1.5 hours in Category 1 credit towards the AMA Physician's Recognition Award. Each physician should claim only those hours of credit that he/she actually spent in the educational activity.
For questions regarding the content of this activity, contact the accredited provider for this CME/CE activity noted above. For technical assistance, contact [email protected]
There are no fees for participating in or receiving credit for this
online educational activity. For information on applicability and
acceptance of continuing education credit for this activity, please
consult your professional licensing board.
This activity is designed to be completed within the time
designated on the title page; physicians should claim only those
credits that reflect the time actually spent in the activity. To
successfully earn credit, participants must complete the activity
online during the valid credit period that is noted on the title page.
Follow these steps to earn CME/CE credit:
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The 3',5'-cyclic nucleotide PDEs are key regulators of intracellular cGMP and cAMP activity and, hence, relaxation of corporal smooth muscle.[13,14] Known to occur in at least 11 isoforms and isoenzymes, these enzymes are distributed in nearly all body tissues, with clearly distinct concentrations, depending on the respective functions of the tissues. The PDEs are responsible for enzymatic degradation of the biologically active cGMP and cAMP to the biological inactive molecules GMP and AMP.
Within the corpus cavernosum and other tissues, multiple PDE isoforms are expressed as products of either different genes or the same gene produced by alternative splicing. Messenger RNA for at least 13 PDE5 isoforms and isoenzymes were identified within the human corpus cavernosum,[15] a finding that was indicative of the complexity of penile erection physiology.
By inhibiting the degradation of cGMP, PDE5 inhibitors prolong the activity of this cyclic nucleotide second messenger within the cavernous vasculature and smooth musculature, thus potentiating the erectile response. The prototype of this new class of selective PDE5 inhibitors for the treatment of ED was sildenafil. The new selective PDE5 inhibitor tadalafil, which is now under review with the Food and Drug Administration (FDA) and the European Agency for the Evaluation of Medicinal Products, significantly potentiated relaxant responses of human corporal smooth muscle tissues to sodium nitroprusside (Figure 5), acetylcholine, and electrical stimulation. Similar potentiating effects were observed when human penile resistance arteries were exposed to sodium nitroprusside or acetylcholine (Figure 6) in the presence of tadalafil. Consistent with the mechanism of action for PDE5 inhibitors, tadalafil induces no physiologic erection in the absence of sexual stimulation.
