The laboratory results should be discussed with the patient and, if possible, with his sexual partner. This educational process allows a review of the basic aspects of the anatomy and physiology of the sexual response and an explanation of the possible etiology and associated risk factors (eg, smoking and the use of various medications). Treatment options and their benefits and risks should be discussed. This type of dialogue allows the patient and physician to cooperate in developing an optimal management strategy.

Then you have to be able to make the right diagnosis. What is the basis for their erectile dysfunction? Is it psychogenic? Is it some sort of neurological or blood vessel or hormonal issue? So you have to make a diagnosis. You have to be able to make an assessment. And then only after those things are done, then you start to think about medications.
The laboratory results should be discussed with the patient and, if possible, with his sexual partner. This educational process allows a review of the basic aspects of the anatomy and physiology of the sexual response and an explanation of the possible etiology and associated risk factors (eg, smoking and the use of various medications). Treatment options and their benefits and risks should be discussed. This type of dialogue allows the patient and physician to cooperate in developing an optimal management strategy.

The most common treatment for erectile dysfunction is drugs known as phosphodiesterase-5 (PDE-5) inhibitors. These include tadalafil (Cialis), vardenafil (Levitra), and sildenafil citrate (Viagra). These are effective for about 75% of men with erectile dysfunction. They are tablets that are taken around an hour before sex, and last between 4 and 36 hours. Sexual stimulation is required before an erection will occur. The PDE-5 inhibitors cause dilation of blood vessels in the penis to allow erection to occur, and help it to stay rigid. Men using nitrate medication (e.g. GTN spray or sublingual tablets for angina) should not use PDE-5 inhibitors.


Intraurethral alprostadil is contraindicated in individuals who have abnormal penile anatomy (for example, urethral stricture, severe hypospadias with penile curvature), patients with acute or chronic irritation/infection of the urethra, individuals prone to priapism such as those with sickle cell anemia, thrombocytopenia, polycythemia, multiple myeloma, or are prone to blood clots. Intraurethral alprostadil should not be used for sexual intercourse with a pregnant woman.
Diabetes is an example of an endocrine disease that can cause a person to experience impotence. Diabetes affects the body’s ability to utilize the hormone insulin. One of the side effects associated with chronic diabetes is nerve damage. This affects penis sensations. Other complications associated with diabetes are impaired blood flow and hormone levels. Both of these factors can contribute to impotence.

Patients with both ED and cardiovascular disease who receive treatment with an oral PDE5 inhibitor require education regarding what to do if anginal episodes develop while the drug is in their system. Such education includes stressing the importance of alerting emergency care providers to the presence of the drug so that nitrate treatment is avoided.
Inside the cell, NOS catalyzes the oxidation of L-arginine to NO and L-citrulline. Endogenous blockers of this pathway have been identified. The gaseous NO that is produced acts as a neurotransmitter or paracrine messenger. Its biologic half-life is only 5 seconds. NO may act within the cell or diffuse and interact with nearby target cells. In the corpora cavernosa, NO activates guanylate cyclase, which in turn increases cyclic guanosine monophosphate (cGMP). Relaxation of vascular smooth muscles by cGMP leads to vasodilation and increased blood flow.
Look, ED can have many causes. Most of the time, it’s physiological. But there are also lots of psychological reasons why someone may experience ED. Treating ED isn’t all about medication. Dealing with some of these psychological issues can help you battle ED, too. I’m talking about depression, anxiety, loss of desire, sense of inadequacy, guilt, fatigue, anger, relationship dysfunction. Working through these types of psychological challenges can help you achieve the happy, healthy manhood you deserve.

Exercise regularly. Make it a priority to get outside or go to the gym to walk, run, swim, bike, or do strength training at least 4 times a week. According to a study conducted by Harvard, walking 30 minutes a day caused a 41% drop in risk for ED.[3] Getting regular exercise aids circulation, getting your blood pumping through your entire body. When it's time to sustain an erection, better circulation is key.[4]
Recognized risk factors for ED include cardiovascular disease (CVD) (hypertension, atherosclerosis, and hyperlipidemia), diabetes, depression, alcohol use, smoking, pelvic/perineal surgery or trauma, neurologic disease, obesity, pelvic radiation, and Peyronie’s disease. One study suggested that the relationship between arterial disease and ED is very strong, with 49% (147 of 300) of patients with coronary artery disease noted on cardiac catheterization reporting significant erectile dysfunction.6 Endothelial dysfunction has been indicated as the pathophysiologic mechanism responsible for both CVD and ED.7 The Boston Area Community Health survey demonstrated a dose-response between smoking and incidence of erectile dysfunction.8 Animal studies have demonstrated both smooth-muscle disruption and decreased production of neural nitric oxide synthase in cigarette-exposed animals.9

The device consists of an acrylic cylinder placed over the penis that uses a lubricant to achieve a good seal between the penile body and cylinder. An erection is then achieved by creating a vacuum inside the cylinder with a pump connected to the cylinder. Once an erection is achieved, a constriction band is applied to the base of the penis to maintain the erection. The cylinder can then be removed and the patient can engage in intercourse with the constriction band at the base of the penis maintaining the erection. The band can remain on for approximately 30 minutes and then must be removed. The erection produced by the device differs from a normal erection likely because of venous occlusion from the constriction band resulting in generalized swelling of the entire penis, with probable preservation of arterial inflow.
Due to the risk of hypotension, caution should be used in patients using alpha blockers for prostate hyperplasia and patients using other antihypertensive medications and alpha blockers, which should not be co-administered with PDE5 inhibitors. In patients who take 50 mg of sildenafil or more and use alpha blockers, sildenafil dosing should be avoided for at least 4 hours after the dose of the alpha blocker. In patients who take 25 mg of sildenafil, use of any alpha blockers is considered safe.
In a 2005 study, three months of twice-daily sets of kegel exercises combined with biofeedback and advice on lifestyle changes, such as quitting smoking, losing weight, and limiting alcohol, worked far better than just giving the participants advice. “Wearing tight pants will affect impotence along with some other medical conditions like diabetes and heart disease,” which can also affect a man’s degree of impotence, Dr. Jennifer Burns, specializing in family practice with an emphasis on gastrointestinal health at the BienEtre Center, told Medical Daily.
The sympathetic pathway originates from the 11th thoracic to the 2nd lumbar spinal segments and goes via the white rami to enter the sympathetic chain ganglia. Subsequently nerves travel through the lumbar splanchnic to inferior mesenteric and superior hypogastric nerves to the pelvic plexus. The T10 through T12 segments are most often the origin of sympathetic fibers, and the sympathetic chain ganglia that innervate the penis are located in the sacral and caudal ganglia (3).
The somatosensory pathways for erections originate in the penile skin, glans and urethra. Glans afferent sensory free nerve endings are 10-fold more than their corpuscular receptors, and are derived from Aδ and unmyelinated C fibers. The nerve endings coalesce to form the dorsal penile nerve along with other sensory nerve fibers. Through the pudendal nerve they enter the S2-4 nerve roots to terminate on spinal neurons and interneurons. The dorsal nerve is not purely somatic, however. Nerve bundles within the dorsal nerve contain nitric oxide (NO) synthase, found typically in autonomic nerves, and stimulation of the sympathetic chain can leak to evoked potentials from the dorsal nerve and vice versa (10-12).

You have to desensitize yourself to stimulation. One way to do this is to masturbate about an hour beforehand, achieving another orgasm shortly after that will be more difficult. If you continue to have trouble, talk to your partner about changes to the timing of your sexual routine, you may need to give them oral or manual stimulation first or after you ejaculate, etc.
Obesity and metabolic syndrome can cause changes in blood pressure, body composition, and cholesterol which may lead to ED. Other conditions that may contribute to erectile dysfunction include Parkinson’s, multiple sclerosis, Peyronie’s disease, sleep disorders, alcoholism, and drug abuse. Taking certain medications can also increase your risk for ED.
The Food and Drug Administration (FDA) does not recommend alternative therapies to treat sexual dysfunction.[27] Many products are advertised as "herbal viagra" or "natural" sexual enhancement products, but no clinical trials or scientific studies support the effectiveness of these products for the treatment of ED, and synthetic chemical compounds similar to sildenafil have been found as adulterants in many of these products.[28][29][30][31][32] The FDA has warned consumers that any sexual enhancement product that claims to work as well as prescription products is likely to contain such a contaminant.[33]
The American Urological Association Guideline on the Management of ED states oral PDE5i are considered first line therapy for the treatment of ED, unless contraindicated (57). Sildenafil, the first oral PDE5i, was introduced in 1998 and has revolutionized ED therapy due to its broad applicability, effectiveness and safety profile. PDE5i work by preventing hydrolysis of cGMP by the PDE5 enzyme in the smooth muscle of the corpora cavernosa. cGMP degradation typically leads to smooth muscle contraction and detumescence prevented by PDE5i administration. Two other PDE5i, vardenafil and tadalafil are other PDE5i with different pharmacokinetics, PDE receptor selectivity and side effect profiles.
You’ve probably heard of Viagra, but it’s not the only pill for ED. This class of drugs also includes Cialis, Levitra,  Staxyn, and Stendra. All work by improving blood flow to the penis during arousal. They're generally taken 30-60 minutes before sexual activity and should not be used more than once a day. Cialis can be taken up to 36 hours before sexual activity and also comes in a lower, daily dose. Staxyn dissolves in the mouth. All require an OK from your doctor first for safety.
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