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OBJECTIVES: The knowledge of penile anatomy is basic to perform a proper diagnosis and direct the most adequate treatment of the various diseases that may appear: urethral stenosis, erectile dysfunction, congenital or acquired penile curvature, etc.; being its anatomical knowledge essential for a proper surgical management.The penis is the male organ involved in both voiding and sexual functions: the body of the penis is composed by three erectile bodies, (i.e the deep structures): the corpora cavernosa and the corpus spongiosum, this last surrounding and covering the urethra. Buck’s fascia is in relation to the deep structures of the penis. The superfi-cial fascia, dartos, is made up from a more areolar tissue and is in relation to skin and vessels. The vascularization of the deep structures comes from the common penile artery, a branch of the internal pudendal artery. Penile blood drains through three venous systems: superficial, intermediate and deep systems. Pudendal nerves are in charge of the sensitive and motor somatic innervations. Cavernosal nerves are a combination of parasympathetic and sympathetic afferent fibers, corresponding to the nerves of the autonomic system of the penis.
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In these article we review the main mechanisms involved in human erection. We review and update in detail the biochemical (nitric oxide and Rhokinase pathways), cellular (smooth muscle relaxation mechanisms), neural (autonomic and somatic pathways) and microscopic penile principles.
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The penis physiological states of flaccidity or erection, result from the contraction or relaxation, respec-tively, of smooth muscle cells in the corpora cavernosa (CSMCs). They result from the interaction of various inter- and intracellular molecular signaling pathways. During the more usual state of flaccidity seems to pre-dominate a tonic sympathetic activity, releasing nora-drenaline (NA) and other agonists that generate con-tractile signals in the CSMCs, with the likely cooperation of endothelium-derived messengers. Through activation of membrane receptors in the CSMCs they raise the intracellular messengers inositol triphosphate (IP3) and diacylglycerol (DAG). This results in a transient increase in cytosolic calcium concentration [Ca2+]i that starts the contractile response which is further sustained by the parallel agonist-induced activation of a “calcium sensitizing” mechanism involving the RhoA/Rho-kinase pathway. Overexpression of the latter might contribute to several vascular disorders as hypertension, vasospasm or erectile dysfunction.On sexual stimulation the cavernous nerves release nitric oxide (NO) that starts the erectile response. They also release acetylcholine that stimulates the endothelium to generate a more sustained release of NO. NO diffuses into CSMCs and increases their intracellular levels of cyclic guanosin monophosphate (cGMP) which decrea-ses [Ca2+]i and deactivates the calcium sensitizing mechanism, thus relaxing CSMCs. This main physiological pathway for CSMCs relaxation is helped by the cyclic adenosin monophosphate (cAMP) pathway activated by various intercellular messengers from neural or paracrine sources, including prostaglandins E (PGE). Different phosphodiesterase enzymes (PDEs) inactivate the cyclic nucleotides thereby limiting their erectogenic action. Indeed the pharmacological inhibition of PDEs, especially the cGMP- specific PDE5, greatly enhances the erectile responses. There are cross-talk mechanisms between the cGMP and cAMP signaling pathways that offer additional possibilities for the pharmacotherapy of erectile dysfunction.
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OBJECTIVES: To review the different as-pects of psychogenic erectile dysfunction (PED).METHODS: To review the bibliography and our personal experience.CONCLUSION: PED is more frequent than curren-tly thought and may grow in the future, especially in young men, linked to the present style of life. Performan-ce anxiety related to different circumstances is the most common cause of PED. Other causes are given by an inadequate sexual education, traumatic sexual experien-ces during childhood, a conflictive couple relationship, stressful situations of any nature or psychiatric disorders, like depression, among others.PED may be associated with other sexual disorders. Usually occurs abruptly and it is easy to diagnose when there are normal erections in any circumstances.
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Neurogenic erectile dysfunction is a consequence of alterations in neural pathways, autonomic, somatic, the combination of both or brain components that induce erection. This review aims to explain the physiopathological mechanisms of the most frequent neurological alterations causing erectile dysfunction and sexual disorders.
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Vascular etiology is present in up to 60% of the patients with erectile dysfunction (ED). Both small vessel disease, such as that in diabetes mellitus, and arteriosclerosis of bigger size arteries, as in hypertension, cause arterial insufficiency and erectile dysfunction.Tobacco smoking alters the arterial hemodynamics in the penis, causing erectile dysfunction in a high percentage of advanced age smokers: pelvic arteries fibrosis and stenosis accelerates the existing arteriosclerosis. Venous occlusive dysfunction may be due to the decrease of corpora cavernosa compliance or tunica albuginea inherent anomalies.Vascular endothelial growth factor may play a role in the modulation of vascularization of the normal penile architecture.Various events, all of them important, may cause erectile dysfunction. Moreover, no cause can participate independently. A cascade of situations (including psychological factors as well as organic) may lead to erectile dysfunction. A continuous understanding of organic causes of erectile dysfunction will allow physicians to discover treatments for their correction, as well as to give confidence to the patient.
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The proper function of erection mecha-nisms depend on correct interrelationship between psy-chological, vascular, neurological and hormonal factors.Endocrine diseases affect sexual function, and sexualdysfunction may be one of the symptoms of some hor-monal anomalies.Diabetes mellitus is the endocrine disease most frequen-tly causing erectile dysfunction due to the frequent vas-cular and neurological complications associated. It isimportant to determine blood glucose in the initial eva-luation of a male with erectile dysfunction, as well asto try an adequate control of blood glucose levels toavoid worsening. Diabetic male erectile dysfunction ismultifactorial, more severe and has worse response tooral treatment.Hyperprolactinemia causes disorders of the sexual sphe-re because it produces a descent of testosterone. In the-se cases, sexual symptoms are treated by correcting thelevels of prolactin. Routine determination of prolactin isnot clear and it seems it should be determined whentestosterone levels are diminished.Thyroid hormone disorders (both hyper and hypotyroi-dism) are associated with erectile dysfunction, whichwill subside in half the patients with thyroid hormonenormalization. The role of adrenal hormones in erectilefunction is not clear and their routine determination isnot considered in the diagnostic evaluation of erectiledysfunction. The role of estradiol in the regulation of theerection mechanism is not well known either, although itis known that high levels may cause erectile dysfunction.Among endocrine-metabolic disorders we point out dys-lipemias, with hypercholesterolemia as an important riskfactor for erectile dysfunction and, though its correctionmay prevent vascular system deterioration, the role ofstatins in erectile dysfunction is not clear
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The delicate harmony by which the various elements in the penis work may be altered by different pathologies that damage its structure. Structural anomalies in the penis cause a failure of the hemodynamic event and erectile dysfunction, which is usually severe, resistant to medical treatment and generally non reversible. The most frequent physiopathologic mechanisms of these dysfunctions are loss of compliance in the erectile tissue, abnormal drainage, or severe alterations of penile geometry. Among possible etiologies are La Peyronie disease, priapism, diabetes, penile trauma, infiltration of corpora cavernosa by an inflammatory or neoplasic processes, and others.
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In 1993 the NIH (National Institute of Health) Consensus Conference on Impotence defined erectile dysfunction as the permanent incompetence to start or maintain an erection enough to enable satisfactory sexual intercourse.Erectile dysfunction (ED) is a frequent disorder that affects negatively quality of life of males suffering it. Its prevalence varies between different countries, cultures and races. The first population studies published date from early 90`s and still keep their validity. All of them show the influence of age on prevalence of ED, as well as its close relationship with cardiovascular diseases. Depending on the definition used and study design prevalence varies from 10 to 52%, mainly in men between 40-70 years, with an incidence in western countries between 25-30 new cases per 1000 inhabitants year.
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OBJECTIVES: Erectile Dysfunction (ED) is one of the most negatively impacting complications associated with pelvic surgery. To date, several technical approaches and therapeutics options are available to limit the impact of pelvic surgical treatment on sexual health. The present article focuses on the short- and long term outcomes of pelvic surgery in terms of erectile dysfunction.METHODS: A Medline search was conducted to identify original and review articles as well as editorials addressing the functional outcome after surgery. Keywords included radical prostatectomy, radical cystectomy, rectal cancer and erectile dysfunction.RESULTS: Erectile function impairment represents the most significant complication of pelvic surgery, negatively impacting the overall sexual health. The rates of ED range from 25-100% of patients, according to the extension of the pelvic dissection, the conservation of the neurovascular structures, as well as in consideration of the pre-operative erectile function of the patients. Recent advances in the knowledge of pelvic anatomy resulted in an increase in the rates of erectile function recovery, especially in patients subjected to radical prostatectomy. The use of pro-erectile drugs significantly improves the outcomes of patients treated with nerve-sparing approach. Radical cystectomy for muscle-invasive bladder cancer is still associated with a high rate of erectile dysfunction. Similarly, pelvic surgery for rectal cancer is often a cause of ED in patients surviving to cancer treatment. Presence of urinary or faecal diversions surely represent a limitation to sexual activity in men.CONCLUSION: Recent advances in surgical technique and in the awareness of pelvic anatomy led to a better comprehension of the structures responsible for erectile function in pelvic surgery. New strategies are necessary in order to further reduce the rates of ED after this frequent surgical approach.
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Erection is a vascular phenomenon under a psychologic control in a hormonal environment. Erectile dysfunction is defined as the inability to obtain and to maintain sufficient erection for satisfactory intercourse.Organic erectile dysfunction results mainly from vascular problems due to atherosclerosis, a process that begins during childhood, and becomes clinically evident from middle age.Endothelial dysfunction is the first step of atherosclerosis. As the endothelial cells recover the sinusoid spaces in the cavernous tissue and because common risk factors for atherosclerosis have been frequently found in patients with erectile dysfunction, it is logical that vascular impotence presents the same pathophysiology of the other vascular diseases. They share a similar pathogenic involvement of nitric oxide pathway leading to impairment of endothelium dependent vasodilatation and structural vascular abnormalities. Circulating markers of endothelial cell damage have been reported in patients with erectile dysfunction while they have not yet presented any other vascular pathology.Endothelial progenitor cells of bone marrow origin that play a role in promoting endothelial repair are also reduced in vascular abnormalities.As penile arteries have the smallest diameter in the vascular network and because atherosclerosis is a systemic disease, erectile dysfunction could be a sentinel symptom of a more generalized vascular pathology.Modifications of reversible causes or risk factors at the base of the pathogenesis of atherosclerosis remain the first approach toward improving endothelial function and associated with chronic exposure to PDE5-I, they could improve or even cure ED and could avoid fatal cardiovascular attacks in the future.
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OBJECTIVES: The relationship between lower urinary tract symptoms (LUTS) and erectile dysfunction (ED) is the result of their greater association in advanced age. Nevertheless, several investigations show that urinary tract symptoms have an independent relationship with sexual dysfunction and lower satisfaction. Likewise, the severity of LUTS correlates with the magnitude of sexual dysfunction in all age groups, which suggests a possible causal relationship.A series of hypothesis have been posed to explain the existence of a common physiopathology for LUTS and ED. Currently, this relationship between LUTS and ED issupported on four theories, which are not mutually excluding, (a) autonomic hyperactivity and metabolic syndrome hypothesis, (b) changes in nitric oxide/nitric oxide (NOS/NO) synthetase in the guanine monophosphatase pathway in penis and prostate, (c) the activation of Rho kinase and the endothelin pathway, and (d) the physiopathological consequences of pelvic arteriosclerosis.Given the contribution of sexual function to keep the quality of life, possible negative effects on sexual function should be taken into consideration when choosing treatment for benign prostatic hyperplasia.The combined therapeutic approach of these two entities (ED and LUTS) brings a benefit to the patient both in urinary symptoms and sexual sphere, although placebo controlled studies are required to confirm these data and to ascertain the role of combination therapy in the treatment of both conditions.
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OBJECTIVES: To analyze the relationship between testosterone deficit syndrome (TDS) and erectile dysfunction and its diagnostic and therapeutic implications.METHODS: Bibliographic review in the Pub Med database of the US National Library of Medicine.RESULTS: The real TDS is unknown, due to the lack of uniform diagnostic criteria on what fraction should be measured (total, free or bioavailable) and what the diagnostic values are. Despite this fact, it is estimated that between 5-15% of males with erectile dysfunction show diminished testosterone levels. There is a solid research base demonstrating that testosterone plays an essential role in the physiology of erection, both at central and peripheral levels. Nevertheless, evidence obtained in human studies is not that strong, mainly in old patients with TDS. The results of some metaanalysis show that substitutive treatment with testosterone improves erections and sexual desire. However, not every patient with TDS will benefit from testosterone substitution therapy, probably because in some cases the origin of erectile dysfunction is multifactorial. Combined treatment with testosterone plus phosphodiesterase 5 (PDE 5) seems to be an adequate alternative to rescue patients with erectile dysfunction and hypogonadism not responding to monotherapy, be it with testosterone alone or PDE 5 inhibitors alone.CONCLUSIONS: Systematic determination of serum testosterone in patients consulting for erectile dysfunction is highly recommendable, because testosterone substitution therapy enables, in a number of patients, improvement of erections and sexual desire. Moreover, testosterone substitution therapy may improve the other symptoms of TDS and increase the efficacy of PDE5 inhibitors when they are not effective in monotherapy.
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OBJECTIVES: To update a syndrome that has increased the number of pathologies included such as obesity, hypertension, hypercholesterolemia, type II diabetes mellitus, and the recent addition of erectile dysfunction and androgen deficiencyMETHODS: Global review of bibliography taking the last articles as a reference and mainly those from Prof. M. Serrano Rios and his group in Madrid.RESULTS: Metabolic syndrome seems to be consolidated as a universally accepted term, despite its complex semantic and gnoseologic itinerary. The inclusion of erectile dysfunction and androgen deficiency gives more pathogenic solidity and makes the professional field of endocrinology closer to two mainly urological processes.The urologist has a new perspective of processes that are of his own, that he has to take care of in a comprehensive manner, with physical examination, blood tests and therapy.CONCLUSIONS: Metabolic syndrome may be more frequently than suspected recognized in the urologist office. Urologists are compelled, in this typically medical process, to exercise with more dedication and fullness the medical compromise of our medical-surgical specialty
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OBJECTIVES: We aim in this work to es-tablish directions for data collection in the chart of the patient with erectile dysfunction (ED), to characterize the presenting problem, reveal possible associated risk factors, evaluate the need of additional complementary tests, and decide if a multidisciplinary approach is ne-cessary.METHODS: Bibliographic review about directions and recommendations on initial and clinical management of ED.CONCLUSIONS: Sexual history is the most important part of the basic routine with a patient with ED, and the purpose of the andrologist is to identify the type of sexual dysfunction, time of start, severity, duration, and treatment expectations.
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The introduction of PDE 5 inhibitors has widen the ambit of health care in erectile dysfunction (ED), which now includes family doctors, urologists, endocrinologists, neurologists, angio-cardiologists, psychiatrists, psychologists and other specialists. To make a proper diagnosis, it is convenient to know there are many diseases associated with ED. To evaluate ED we have to identify sexual problems and to use certain means, such as adequate questionnaires and symptom scores, a detailed sexual and clinical history, physical exam and elementary lab tests. In most cases of ED it is not necessary to perform invasive tests or refer the patient to a specialist, but the doctor needs to know there are cases that require such reference, and sometimes more studies and tests are required.
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OBJECTIVES: Sexuality on the whole and erectile response particularly are not alien to psychoso-cial and couple features. We review al psychological and couple features that interfere on erection and also point out the interventional directions of couple therapy that give the best results in the treatment of erectile dys-function.METHODS: We performed a bibliographic review about the psychological and social features under the current way of life in relation to erectile response phy-siology, in addition to review different models of couple therapy.RESULTS/CONCLUSIONS: The separation of the couple reproduction-pleasure achieved in the 50`s ena-bled a progressive claim from women of their need to be satisfied, representing one of the reasons that led to the phenomenon of “performance anxiety” that, al-together with some toxic habits (Tobacco consumption, alcohol, drugs, sedentary life, etc) help the appearance of erectile dysfunction. When psychological factors are an important part of the problem, couple sexual therapy in combination with phosphodiesterase 5 inhibitors is the therapy of choice.
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OBJECTIVE: To review the available published literature relating to the use of oral therapy in the treatment of erectile dysfunction.METHODS: A literature review was undertaken using techniques of systematic review via Medline and other comparable databases. Only data relating to peer-reviewed published articles was considered. Data available in abstract form was not considered.RESULTS: Currently there are 4 orally active drugs which are licensed, orally active and widely available. Three of these drugs (namely sildenafil, tadalafil and vardena-fil) are inhibitors of the enzyme phosphodiesterase type 5 (PDE5) and work peripherally within the penis to potentiate the smooth muscle relaxation that is needed for a penile erection. The fourth drug (namely apomorphine) works centrally on dopaminergic receptors, probably within the paraventricular nucleus. There is considerable evidence to support the efficacy, tolerability and safety of these agents. Comparator trials have failed to show significant differences in efficacy between the PDE5 inhibitors, but have demonstrated superiority for sildenafil over apomorphine in terms of efficacy. There are currently a number of new PDE5 inhibitors under development.CONCLUSION: Oral therapy is the first line therapy for most men with erectile dysfunction. There are a number of commercially available drugs that demonstrate good efficacy, tolerability and safety.
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OBJECTIVE: To explore the mechanism of action, as well as the risks and benefits of two popular and effective treatment modalities for erectile dysfunction (ED). Intracavernosal injection (ICI) therapy involves direct injection of vasoactive agents into cavernosal tissue to facilitate erection. Commonly perscribed agents include PGE1 (alprostadil), papaverine, and phentolamine. Though there are some risks associated with improper injection technique, these agents have a low side effect profile and have proven to be very effective, especially in combination. Patients may also chose the less invasive option of a vacuum erection device (VED), which are often successful in ED of any etiology.
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The introduction of penile prosthesis in the early 1970s has been the first breakthrough in the treatment of erectile dysfunction. Since then a variety of treatment options for erectile dysfunction have been de-veloped, including penile vascular surgery, injection the-rapy, vacuum erection device therapy, intraurethral and oral pharmacotherapy. Although the percentage of men newly diagnosed with erectile dysfunction who undergo surgical treatment has declined, the number of men presenting with erectile dysfunction continues to increase out of proportion to this decline. Moreover, many men that are now effectively managed with medical treatment are likely to require penile prosthesis implantation as their erectile dysfunction progresses. This chapter will focus on the surgical management of erectile dysfunction and in particular on penile prosthesis implantation.
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About 30-40 % of ED patients are nonresponders to PDE 5 inhibitor monotherapy. Lifestyle modifications and physical activity with weight loss enhance PDE 5 inhibitor responsiveness. The same applies for combination therapies such PDE 5 inhibitors + L-Arginine 3.000mg, PDE 5 inhibitors + statins and PDE 5 inhibitors + Yohimbine. Combination of daily dosing with Tadalafil 5 mg and on demand application of sildenafil or vardenafil can improve responsiveness and erection hardness (personal experiences).Guanylate cyclase activators or RhoA-kinase inhibitors, either as monotherapy or in combination with PDE 5 inhibitors have shown in preclinical settings the potential to improve erectile function and represent targets for new ED drugs in the future. Immunophilin ligands were able to ameliorate erectile function after cavernous nerve injury due to pelvic surgery.Although having shown convincing efficacy both in animals and humans the centrally acting Melanocortin Receptor (MCR) Agonists were given up for ED treatment because of unfavorable side-effects.Promising targets for ED therapy in the future is gene therapy with several targets as well as stem cell therapy with adipose-derived or muscle-derived stem cells.
