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admin | Category: Male Dysfunction Treatment 2016 | 15.07.2014
The goals of patient evaluation, are to assess the likely cause of the erectile dysfunction and identify medical or psychologic conditions that may be contributing to the dysfunction or that may influence treatment options.
Often one can get an excellent clue to the etiology by the history and physical examination which can then be tested by precise laboratory tests. History and Clinical ExaminationAnatomic, psychogenic, endocrinologic, neurologic, and vascular abnormalities may all contribute to impotence. A thorough history is the most important factor in the evaluation of the patient with erectile dysfunction. Psychogenic disorders may occasionally be primary factors contributing to erectile dysfunction. Once a concern with the patient's sexual function is identified, the next step is to differentiate erectile dysfunction from other sexual problems, such as loss of libido or ejaculatory problems.
The full 15 question IIEF which helps in distinguishing what type of sexual dysfunction is present can be accessed here.
The shortened 5 question IIEF which helps in judging the severity of true erectile dysfunction can be accessed here. Early recognition of psychogenic disturbances allows the physician to avoid costly and confusing evaluation for other etiologies of impotence.
Because impotence is known to be associated with many common medical conditions and medications, a careful medical history may yield insights into the etiology of impotence.
Careful physical examination with particular attention to sexual and genital development may occasionally reveal an obvious cause of impotence. The cardiovascular examination should include assessment of vital signs (especially blood pressure and pulse) and signs of hypertensive or ischemic heart disease.
In many cases, a careful history and physical exam will direct the physician to the most expedient cost-effective evaluation and eliminate the need for unnecessary diagnostic tests.
Sildenafil was originally developed for heart disease, but was found to have a unique mechanism of action that targeted only factors in the penis, even though it is taken orally. The rationale for the use of sildenafil is based upon the role of nitric oxide-induced vasodilation (which is mediated by cyclic GMP) in initiating and maintaining an erection. In order to understand the action of sildenafil as well as some of its side effects, it would be worthwhile to briefly recall the physiology of penile erection. With sexual arousal through imaginative, visual, auditory, tactile, olfactory, and other erotic stimuli, nitric oxide (NO) is released by nonadrenergic, noncholinergic (NANC) neurons. Dilation of the helicine arterioles and relaxation of the sinusoids lead to engorgement of sinusoidal spaces with blood. The intracellular decline in Ca++ ions suppresses the activity of myosin light chain (MLC) kinase and thus increases the intracellular content of dephosphorylated MLC, which enables the smooth muscle cell to relax. The PDEs are responsible for enzymatic degradation of the biologically active cGMP and cAMP to the biological inactive molecules GMP and AMP. The prototype of this new class of selective PDE5 inhibitors for the treatment of ED was sildenafil. Penile erection is a complex physiologic process that occurs through a coordinated interaction between the nerves, the blood vessels and the hormones. In the flaccid penis, a balance exists between blood flow in and out of the erectile bodies. ErectionWhen a man gets sexually aroused, the nerves trigger a series of events which leads to the release of a substance of called nitric oxide (NO).
Nerves and vascular endothelium release nitric oxide in response to sexual arousal, which activates cytoplasmic guanylate cyclase, converting GTP into cGMP. Cyclic AMP (cAMP) and cyclic GMP (cGMP), the intracellular second messengers mediating smooth-muscle relaxation, activate their specific protein kinases, which phosphorylate certain proteins to cause opening of potassium channels, closing of calcium channels, and sequestration of intracellular calcium by the endoplasmic reticulum. During the return to the flaccid state, cyclic GMP is hydrolyzed to GMP by phosphodiesterase type 5. Although I have tried to keep the discussion to the basics, the mechansms leading to flaccidity or detumescence are fairly complicated as seen below. Molecular Mechanism of Penile Smooth-Muscle Contraction.Norepinephrine from sympathetic nerve endings, and endothelins and prostaglandin F2 from the endothelium, activate receptors on smooth-muscle cells to initiate the cascade of reactions that results in elevation of intracellular calcium concentrations and smooth-muscle contraction.

As we saw above, the central role in the penis becoming flaccid again is the decrease in the levels of cGMP which is hydrolyzed to GMP by phosphodiesterase type 5.
In the flaccid state, the smooth muscle cells of the penile arteries and the corpora cavernosa are in a state of tone (contraction). At the same time, some have multiple causes, such as a person with diabetes who is also on certain antihypertensive medications. Therefore, the evaluation of impotence begins with a comprehensive history and physical examination. Recognition of these patient characteristics should lead the clinician to entertain the possibility of a primary psychogenic etiology of impotence.
The physician should use appropriate vocabulary, avoiding slang or excessively technical terminology.
Moreover, many patients complain of erectile dysfunction when they mean something lese such as premature ejaculation etc., and again this needs to be recognized before embarking on the detailed evaluation. Particular attention should be given to the cardiovascular, neurologic and genitourinary systems, as these systems are directly involved with erectile function. Careful examination of the penis may reveal an anatomic abnormality such as a micropenis, the presence of chordee, or a Peyronie's plaque. Abdominal or femoral artery bruits and asymmetric or absent lower extremity pulses are indicative of vascular disease. Patients with diabetes or neurodegenerative disorders may show evidence of peripheral neuropathy.
Sildenafil is the first orally administered treatment of proven efficacy for erectile dysfunction. Detumescence is associated with catabolism of cyclic GMP by type 5 cyclic GMP phosphodiesterase.
Originally termed endothelial-derived relaxing factor, NO is known to be the most important physiologically occurring vasoactive molecule in the entire cardiovascular system. Expansion against the tunica albuginea compresses blood-draining subtunical venules, resulting in blockade of cavernous venous outflow. It is well established that NO and cGMP are the most important transmitters for onset and maintenance of erection. Although some events in the cascade resulting in penile erection await clarification, NO, a gas with intrinsic vasodilator properties, activates guanylate cyclase and in turn stimulates the formation of cGMP This substance then acts as a second messenger, playing a pivotal role in vasodilatation and relaxation of corporal smooth muscle, the structural changes responsible for penile erection. PDE5 and, to a much lesser extent, PDE2 and PDE3, are localized to the corpus cavernosum of the penis, where they catalyze the transformation of cGMP to its inactive form 5_-GMP. 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. This leads to a series of biochemical reactions ending in the increased formation of a substance called cyclic guanosine monophosphate or cGMP for short.
The increased levels of cGMP, result in cavernosal smooth muscle relaxation, dilatation of cavernosal and helicine arteries and engorgement of lacunar spaces. After ejaculation or cessation of erotic stimuli, sympathetic tonic discharge resumes, resulting in contraction of the smooth muscles around sinusoids and arterioles. This leads to a decrease in the cGMP levels and consequently, the smooth muscles of the erectile tissues contract. Protein kinase C is a regulatory component of the calcium-independent, sustained phase of agonist-induced contractile responses.
It is important to remember this as this where the oral drug sildenalfil citrate (the famous "Viagra") works, as we shall see later. Relaxation of the smooth muscle (arterial and cavernosal) causes increased inflow of blood into the lacunar spaces of the corpora cavernosa. A careful sexual history and knowledge of concurrent illnesses and medications are essential. Having the patient define the terms in his own words will help the physician and patient communicate more effectively. Many common medications such as psychotropic drugs and antihypertensives have been associated with impotence.

Taken for one hour before planned sexual intercourse, it is effective for a wide range of disorders causing erectile dysfunction.
Sildenafil acts by blocking the latter enzyme and as a result increases both the number and duration of erections in men with erectile dysfunction.
This also applies to corpus cavernosum function, where local smooth muscle relaxation, and in turn erection, is mediated predominantly by NO release. This leads to complete filling of the cavernous sinusoids and subsequently to a considerable increase of the intracavernous pressure. The expanding lacunar spaces compress the subtunical venous plexus against the tunica albuginea, decreasing cavernosal venous outflow, increasing intracavernosal pressure, with resulting penile rigidity. Sildenafil inhibits the action of phosphodiesterase (PDE) type 5, thus increasing the intracellular concentration of cGMP.
Arterial flow is diminished to flaccid levels, much of the blood from the sinusoidal spaces is expelled, and the venous channels reopen. Vasoconstriction of the penile arteries and contraction of the trabecular muscle, result in reduction of arterial inflow and collapse of lacunar spaces, respectively. The arterial pressure expands the relaxed trabecular walls, thus expanding the tunica albuginea with subsequent elongation and compression of the draining venules. The sexual history should include the duration of impotence, level of libido, and a complete inventory of sexual partners. The International Index of Erectile Function (IIEF) is a valuable tool for defining the area of sexual dysfunction.
Similarly, a patient's surgical history may also provide clues to the possible causes of impotence. Certain genetic syndromes such as Kallmann's or Klinefelter's syndrome may present with obvious physical signs of hypogonadism or distinctive body habitus. The superficial anal reflex, indicative of normal somatic function of sacral cord levels S24, is assessed by touching the perianal skin and noting contraction of the external anal sphincter muscles.
In the phase of full rigidity, intracavernous pressure reaches values considerably higher than systemic (systolic) blood pressure.During male sexual arousal, NO is released either at parasympathetic NANC nerve terminals on the cavernous smooth muscle cell or at parasympathetic cholinergic nerve terminals on the endothelial cell lining of the sinusoids. Venous outflow drops as the expanding cavernosal spaces compress the venous plexus and the larger veins passing through the tunica albuginea. Contraction of the trabecular muscle causes decompression of the drainage venules from the cavernous bodies, thus allowing the blood to drain out of the lacunar spaces and reulting in the penis becoming flaccid. The IIEF is designed to be a self-administered measure of erectile dysfunction, but it also assesses a patient's function in other phases of sexual function. Prior radical pelvic surgery (eg, prostatectomy, abdominoperineal resection), radiation, and pelvic trauma are known to be associated with impotence.
Through membrane-bound G proteins, NO activates guanylate cyclase, which induces cleavage of guanosine triphosphate to 3',5'-cyclic guanosine monophosphate (3',5'-cGMP).The smooth muscle-relaxing effects of NO are mediated by this second messenger (cGMP). After ejaculation or cessation of the erotic stimuli, the smooth muscle surrounding the arteries and the lacunar spaces contracts.
The IIEF also establishes a reliable baseline that can be used to monitor changes related to treatment.
It is performed by placing a finger in the rectum and noting contraction of the anal sphincter and bulbocavernosus muscle when the glans penis is squeezed.
Cyclic GMP activates protein kinase G (PKG), which phosphorylates proteins at the so-called maxi-potassium channels. The inflow of blood is reduced and the venous drainage of the corporeal spaces is opened, returning the penis to the flaccid state. This results in an outflow of potassium (K+) ions into the extracellular space with subsequent hyperpolarization, with inhibition or blockade of voltage-dependent calcium (Ca++) channels and therefore a decrease in intracellular Ca++ ion concentrations. Erection of the penis is thus a haemodynamic event under the control of the autonomic nervous system.

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