Lindsay Mitchell, ARNP is a Board Certified Family Nurse Practitioner and graduated with high honors from South University in Savannah, GA. She has a background in primary care, women’s health and focusing on evidence based practices. She has a strong passion for providing efficient and accessible patient care, along with caring for underserved patient populations. Prior to becoming an ARNP, she worked as a registered nurse in the emergency department in Jacksonville, Fl.
The availability of phosphodiesterase-5 (PDE5) inhibitors—sildenafil, vardenafil, tadalafil, and avanafil—has fundamentally altered the medical management of ED. In addition, direct-to-consumer marketing of these agents over the last 15 years has increased the general public’s awareness of ED as a medical condition with underlying causes and effective treatments.
As blood flows into the penis, the corpora cavernosa swell, and this swelling compresses the veins (blood vessels that drain the blood out of the penis) against the tunica albuginea. Compression of the veins prevents blood from leaving the penis. This creates a hard erection. When the amount of cGMP decreases by the action of a chemical called phosphodiesterase type 5 (PDE5), the muscles in the penis tighten, and the blood flow into the penis decreases. With less blood coming into the penis, the veins are not compressed, allowing blood to drain out of the penis, and the erection goes down.
Alprostadil may also be administered into the urethral opening of the penis. In MUSE (medical urethral system for erection), the man inserts a thin tube the width of a vermicelli noodle into his urethral opening and presses down on a plunger to deliver a tiny pellet containing alprostadil into his penis. The drug takes about 10 minutes to work and the erection lasts about an hour. The main side effect is a sensation of pain and burning in the urethra, which can last about five to 15 minutes.
Conditions associated with reduced nerve and endothelium function (eg, aging, hypertension, smoking, hypercholesterolemia, and diabetes) alter the balance between contraction and relaxation factors (see Pathophysiology). These conditions cause circulatory and structural changes in penile tissues, resulting in arterial insufficiency and defective smooth muscle relaxation. In some patients, sexual dysfunction may be the presenting symptom of these disorders.
Impotence, also called erectile dysfunction, in general, the inability of a man to achieve or maintain penile erection and hence the inability to participate fully in sexual intercourse. In its broadest sense the term impotence refers to the inability to become sexually aroused; in this sense it can apply to women as well as to men. In common practice, however, the term has traditionally been used to describe only male sexual dysfunctions. Professional sex therapists, while they identify two distinct dysfunctions as forms of impotence, prefer not to use the term impotence per se. Thus, because of its pejorative connotation in lay usage and because of confusion about its definition, the word impotence has been eliminated from the technical vocabulary in favour of the term “erectile dysfunction.”
For the past few months I’ve been dating a lovely man but our relationship is at risk because he can’t get it up. He says he fancies me and always seems turned on. Sometimes he gets hard - but when we try for sex he loses his erection. On the few occasions he has got hard, he doesn’t orgasm. I’ve always been a very sexual person and would like a lot of sex. We’re hardly having any. I find it difficult to orgasm even if he tries other things because I keep thinking. Why can’t he have proper sex with me?
Frankly, I sympathize with you: He’s got a bad credit history (and likely a history of making similarly poor financial decisions) and you are anxious to pay this debt back before anything else, to the extent that you’re “basically” spending your whole paycheck on debt. Should he be paying more right now? Maybe he should pay more — but, then again, maybe it’s not all or nothing: Maybe you could compromise.
Normal erectile function depends on the release of NO and endothelial-dependent vasodilation of the penile arteries. The ‘artery size’ hypothesis, first described by Dr Montorsi, offers an explanation why men are more likely to develop ED before a myocardial infacrtion. It is believed that atherosclerosis affects all vascular beds equally but smaller arteries are more likely to become occluded than larger arteries.31 32 The penile arteries are 1–2 mm while the coronary arteries are 3–4 mm. Thus, the same degree of endothelial dysfunction and atherosclerosis is more likely to occlude blood flow in the penile arteries compared with the coronary arteries. The penile arteries therefore serve as a sensitive indicator for subsequent CVD. This theory is supported by the fact that ED occurs approximately 3 years prior to cardiac symptoms in virtually all patients with chronic coronary syndrome whereas patients with acute coronary syndrome have a much lower prevalence of sexual dysfunction.32
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The link between chronic disease and ED is most striking for diabetes. Men who have diabetes are two to three times more likely to have erectile dysfunction than men who do not have diabetes. Among men with erectile dysfunction, those with diabetes may experience the problem as much as 10 to 15 years earlier than men without diabetes. Yet evidence shows that good blood sugar control can minimize this risk. Other conditions that may cause ED include cardiovascular disease, atherosclerosis (hardening of the arteries), kidney disease, and multiple sclerosis. These illnesses can impair blood flow or nerve impulses throughout the body.