Qaseem, A., Snow, V., Denberg, T. D., Casey, D. E., Forciea, M. A., Owens, D. K., & Shekelle, P. (2009). Hormonal testing and pharmacologic treatment of erectile dysfunction: A clinical practice guideline from the American College of Physicians. Annals of internal medicine, 151(9), 639-649. Retrieved from http://annals.org/aim/article/745155/hormonal-testing-pharmacologic-treatment-erectile-dysfunction-clinical-practice-guideline-from
Dr. Liou says that some men come to him after getting a prescription from their primary care doctors, claiming that the drug doesn't work. Sometimes it's because they used it incorrectly. "The biggest misconception is that these drugs are an on/off switch for erections," Dr. Liou says. But the drugs don't work well without sexual stimulation. "During that time, you need to be with your partner and have foreplay," Dr. Liou says. "Don't take it, do the taxes or the dishes, and then meet at the bedroom thinking you'll be ready to go. It's not like that."
Other medical therapies under evaluation include ROCK inhibitors and soluble guanyl cyclase activators. Melanocortin receptor agonists are a new set of medications being developed in the field of erectile dysfunction. Their action is on the nervous system rather than the vascular system. PT-141 is a nasal preparation that appears to be effective alone or in combination with PDE5 inhibitors. The main side effects include flushing and nausea. These drugs are currently not approved for commercial use.
The drugs are worth trying, but don’t expect miracles. Everyone has heard of Viagra, but Cialis is actually more popular because it’s effective longer—24 to 36 hours instead of three to five. Erection drugs improve erections in around two-thirds of men. They don’t work for about one-third. When they work, they do not produce porn-star erections. Over time, many men need larger doses. But as dosage increases, side effects become more likely, notably, headache and nasal congestion. Finally, the drugs have no effect on arousal, so men may raise erections but don't feel particularly interested in sex. Many men feel disappointed with the drugs. Fewer than half refill their prescriptions.
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Injection therapy involves injecting a substance into the penis to enhance blood flow and cause an erection. The Food and Drug Administration (FDA) approved a drug called alprostadil (Caverject) for this purpose in July of 1995. Alprostadil relaxes smooth muscle tissue to enhance blood flow into the penis. It must be injected shortly before intercourse. Another, similar drug that is sometimes used is papaverine—not yet been approved by the FDA for this use. Either drug may sometimes cause painful erections or priapism (uncomfortable, prolonged erections) that must be treated with a shot of epinephrine.
Sildenafil (Viagra) was the first oral phosphodiesterase type 5 (PDE5) inhibitor approved by the FDA in the United States for the treatment of erectile dysfunction (it is not approved for women). Sildenafil inhibits PDE5, which is an enzyme that destroys cGMP. By inhibiting the destruction of cGMP by PDE5, sildenafil allows cGMP to accumulate. The cGMP in turn prolongs relaxation of the smooth muscle of the corpora cavernosa. Relaxation of the corpora cavernosa smooth muscle allows blood to flow into the penis resulting in increased engorgement of the penis. In short, sildenafil increases blood flow into the penis and decreases blood flow out of the penis.
ED means no erections from masturbation. According to the American Urological Association, ED is “the inability to achieve or maintain an erection sufficient for satisfactory sexual performance.” Huh? That’s absurdly vague. If you define “an erection” as what you see in porn, and “satisfactory sexual performance” as porn sex—instant, hard-as-rock erections that last forever with climaxes always on cue—then just about every guy has ED. What is ED, really? For practical purposes, it means that a man who’s sober (no alcohol or other erection-impairing drugs) cannot raise even a semi-firm erection after extended masturbation.
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Damage to the autonomic pathways innervating the penis may eliminate "psychogenic" erection initiated by the central nervous system. Lesions of the somatic nervous pathways may impair reflexogenic erections and may interrupt tactile sensation needed to maintain psychogenic erections. Spinal cord lesions may produce varying degrees of erectile failure depending on the location and completeness of the lesions. Not only do traumatic lesions affect erectile ability, but disorders leading to peripheral neuropathy may impair neuronal innervation of the penis or of the sensory afferents. The endocrine system itself, particularly the production of androgens, appears to play a role in regulating sexual interest, and may also play a role in erectile function.
Depression and anxiety: Psychological factors may be responsible for erectile dysfunction. These factors include stress, anxiety, guilt, depression, widower syndrome, low self-esteem, posttraumatic stress disorder, and fear of sexual failure (performance anxiety). It is also worth noting that many medications used for treatment of depression and other psychiatric disorders may cause erectile dysfunction or ejaculatory problems.
Erectile dysfunction (ED) affects 50% of men older than 40 years,  exerting substantial effects on quality of life.  This common problem is complex and involves multiple pathways. Penile erections are produced by an integration of physiologic processes involving the central nervous, peripheral nervous, hormonal, and vascular systems. Any abnormality in these systems, whether from medication or disease, has a significant impact on the ability to develop and sustain an erection, ejaculate, and experience orgasm.
While studies are limited, it has been shown that male sexual dysfunction can also negatively impact the sexual function of female partners. A study comparing the sexual function of women with partners with erectile dysfunction to those without showed that sexual arousal, lubrication, orgasm, satisfaction, pain and total score were significantly lower in those who had partners with erectile dysfunction. Later in that study, a large proportion of the men with erectile dysfunction underwent treatment. Following treatment, sexual arousal, lubrication, orgasm, satisfaction and pain were all significantly increased. It was concluded that female sexual function is impacted by male erection status, which may improve following treatment of male sexual dysfunction.
In addition to Viagra, other ED drugs available in the United States include avanafil (Stendra), tadalafil (Cialis) and vardenafil (Levitra). These all improve blood supply to the penis. In combination with sexual stimulation, the drugs can produce an erection sufficient to initiate and complete intercourse. There is also a fast-dissolving form of Levitra, called Staxyn, that you put under your tongue.
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
This is similar to magnetic resonance imaging. Magnetic resonance angiography uses magnetic fields and radio waves to provide detailed images of the blood vessels. Doctors may inject a "contrast agent" into the patient's bloodstream that causes vascular tissues to stand out against other tissues. The contrast agent provides for enhanced information regarding blood supply and vascular anomalies.
Vacuum constriction devices may be effective at generating and maintaining erections in many patients with erectile dysfunction and these appear to have a low incidence of side effects. As with intracavernosal injection therapy, there is a significant rate of patient dropout with these devices, and the reasons for this phenomenon are unclear. The devices are difficult for some patients to use, and this is especially so in those with impaired manual dexterity. Also, these devices may impair ejaculation, which can then cause some discomfort. Patients and their partners sometimes are bothered by the lack of spontaneity in sexual relations that may occur with this procedure. The patient is sometimes also bothered by the general discomfort that can occur while using these devices. Partner involvement in training with these devices may be important for successful outcome, especially in regard to establishing a mutually satisfying level of sexual activity.
While impotence may be the presenting symptom of vascular disease, in neurologic disease impotence generally occurs in the setting of an obvious nervous system disorder, typically in patients known to have spinal cord pathology or neuropathy. Impotent patients should be questioned about decreased genital sensation, which would suggest diabetic, alcoholic, or other forms of neuropathy; weakness, which may accompany multiple sclerosis or spinal cord tumors; and back pain, bowel, and bladder symptoms, which raise concern for cauda equina syndrome. A careful drug history is important in the evaluation of impotence. Drugs that cause impotence (Table 187.3) generally do so by interfering with neurotransmission.
The 1985 National Ambulatory Medical Care Survey indicated that there were about 525,000 visits for erectile dysfunction, accounting for 0.2 percent of all male ambulatory care visits. Estimates of visits per 1,000 population increased from about 1.5 for the age group 25-34 to 15.0 for those age 65 and above. The 1985 National Hospital Discharge Survey estimated that more than 30,000 hospital admissions were for erectile dysfunction.
To examine what is known about the demographics, etiology, risk factors, pathophysiology, diagnostic assessment, treatments (both generic and cause-specific), and the understanding of their consequences by the public and the medical community, the National Institute of Diabetes and Digestive and Kidney Diseases and the Office of Medical Applications of Research of the National Institutes of Health, in conjunction with the National Institute of Neurological Disorders and Stroke and the National Institute on Aging, convened a consensus development conference on male impotence on December 7-9, 1992. After 1 1/2 days of presentations by experts in the relevant fields involved with male sexual dysfunction and erectile impotence or dysfunction, a consensus panel comprised of representatives from urology, geriatrics, medicine, endocrinology, psychiatry, psychology, nursing, epidemiology, biostatistics, basic sciences, and the public considered the evidence and developed answers to the questions that follow.
The lab testing obtained for the evaluation of erectile dysfunction may vary with the information obtained on the health history, physical examination, and recent lab testing. A testosterone level is not necessary in all men; however, a physician will order labs to determine a patient's testosterone level if other signs and symptoms of hypogonadism (low testosterone) such as decreased libido, loss of body hair, muscle loss, breast enlargement, osteoporosis, infertility, and decreased penile/testicular size are present.
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