STUDY - Technical - New Dacian's Medicine
Impotence
Translation Draft
I've hardly managed to complete with a massive "chemistry" part of the human body, and I will now move on to a different kind of human chemistry.
Therefore, various endocrine, vascular, neurological and psychiatric disorders affect sexual and reproductive function in men. In addition, sexual dysfunction may be the symptom of a systemic disease.
But to see a sign of disease (a sign of abnormality) at this "level" is good to start with describing normal sexual function.
Penile erection is initiated by neuropsychological stimuli that ultimately produce vasodilation of the spaces and sinusoid arteries inside the two cavernous bodies (penians). The erection is normally preceded by sexual desire (or libido), which is partly regulated by androgen-dependent psychological factors. Although spontaneous nocturnal and diurnal erections are suppressed in men with androgenic deficiency, erections in response to erotic stimuli can continue for long periods.
Thus, the continuous action of testicular androgens seems to be necessary for normal libido, but not for the mechanism of erection itself. The penis is inervated by sympathetic, parasympathetic and somatic fibers. Somatic fibers in the dorsal nerve of the penis form the related pathway of the erectile reflex by transmitting the sensory impulses from the penile skin and gland to the ganglia of the posterior root S2-S4 through the shameful nerves.
Unlike corpuscular endings in the skin of the penis skin, most of the related endings in the gland are free nerve endings. The efferent pathway begins with the parasympathetic preganglionary fibers in S2-S4 that pass into the pelvic nerves towards the pelvic plexus. Sympathetic fibers that emerge from the intermediolateral grey areas T11-L2 pass through the sympathetic paravertebral ganglion chain, the upper hypogastric plexus and the hypogastric nerves to enter the pelvic plexus alongside the parasympathetic fibers.
Somatic efferent fibers from S3-S4 that pass through the shameful nerve to the hamstring and bulbocavernous muscles and postganglionary sympathetic fibers that irritate the smooth muscle of the epididymis, the deferential canals, the seminal vesicles and the internal bladder sphincter mediate the rhythmic contraction of these structures at the time of ejaculation. Autonomous nerve impulses, integrated into the pelvic plexus, are projected towards the penis through the cavernous nerves, which have the trajectory along the postero-lateral face of the prostate before penetrating the musculature of the pelvic floor immediately laterally after the urethra.
Distal to the membrane urethra some fibers enter the spongy body, while the others enter the cavernous bodies along with the terminal branches of the shameful artery and the efferent cavernous veins. If a disruption of cavernous nerves occurs as a result of pelvic trauma or surgery, erectile impotence may result.
The brain exerts an important modulating influence on the spinal reflex paths that control penile function. Variations visual, auditory, olfactory and imaginative stimuli causing erectile responses involving cortical, thalamic, rhinencephalic and limbic stimuli to the preoptic medial area of the anterior hypothalamus, which acts as an integration center. Other areas of the brain, such as the amygdala complex, can inhibit sexual function.
Although the parasympathetic nervous system is the main effector of erection, the transformation of the penis into an erect organ is a vascular phenomenon. In flaccid state, the arteries, arterioles and sinusoidal spaces of cavernous bodies are constricted due to the contraction of the smooth muscles in the walls of these structures, sympathetically mediated. The veins between the sinusoids and the dense albugine tunic that surround the cavernous bodies open freely into the emissary veins.
The erection begins when the relaxation of the smooth sinusoidal muscles causes the sinusoid to dilate and a decrease in peripheral resistance, causing a rapid increase in arterial blood flow through the shameful internal and cavernous arteries. The expansion of the sinusoidal system compresses the venulas on the internal face of the albugine tunic, leading to venous occlusion. Increased intracorporeal pressure leads to stiffness (incomplete expansion of sinusoidal spaces leads to incomplete stiffness).
Erection occurs when adrenergic-induced sinusoidal tone is antagonized by sacrate parasympathetic stimulation that produces sinusoidal relaxation primarily through the synthesis and release of nonadrenergic-noncolinergic neurotransmitter (NANC), nitric oxide (NO). The contribution of the acetylcholine-dependent release of NO from vascular endothelium is uncertain. In vitro, electrical stimulation of isolated bands in the cavernous body (with or without endothelium) causes sinusoidal relaxation by releasing neurotransmitters inside nerve endings, which is resistant to adrenergic and cholinergic blockers.
Inhibitors of nitric oxide or guanosine monophosphate (GMP) synthesis inhibitors, as well as nitric oxide purorators block sinusoidal relaxation. A variety of neuropeptides found in body tissues, including intestinal vasoactive peptide (VIP - vasoactive intestinal peptides) and genetically related peptide (CGRP - calcitonin gene-related peptides), produce turgidity when injected into the penis, but have uncertain physiological roles. Norepinephrine plays an important role in the adrenergic mechanism of detumescence.
Seminal emission and ejaculation are under the control of the sympathetic nervous system. The emission results from alpha-adrenergic-mediated contraction of the epidium, the deferent canal, seminal vesicles and the prostate, which causes the seminal fluid to enter the prostate urethra. Concomitant closure of the bladder neck prevents sperm reflux in the bladder and anterograde ejaculation results from contraction of the pelvic floor muscles, including the bullbocavernos and hamstring muscles.
Orgasm is a psychosensory phenomenon in which rhythmic contractions of the pelvic muscles are perceived as pleasant. Orgasm can also occur without erection or ejaculation or in the presence of retrograde ejaculation.
Detumescence after orgasm and ejaculation is incomplete understood. As it turns out, the active tone of the vessels in the sinusoidal spaces is restored by the contraction of the smooth muscles (probably mediated adrenergically), which decreases the flow of blood into the penis and supports the emptying of erectile tissue. After orgasm there is a refractory period that varies in duration with age, physical condition and psychological factors and during which erection and ejaculation are inhibited.
The time has come to address impotence. Simply defined, impotence is the impossibility of obtaining erection, ejaculation or both. Men with sexual dysfunction have a variety of symptoms, either separated or in combination: loss of desire (libidou), inability to initiate or maintain erection, impossibility of ejaculation, premature ejaculation or inability to achieve orgasm.
Sexual dysfunction may be secondary to systemic diseases or their treatment, specific disorders of the urogenital or endocrine system or psychological disorders. It was initially thought that the reason for dysfunction in most men with erectile impotence was psychological, but now it is believed that most impotent men have a component of an underlying organic condition. Since the selection and success of therapy depends on etiology, it is essential to evaluate all aspects of sexual function.
A decrease in sexual desire (or even loss of desire) may be due to androgenic deficiency (occurring in a condition either pituitary or testicular), psychological disorders or several types of drugs prescribed or usually abused. The possibility of androgenic deficiency can be tested by measuring testosterone and plasma gonadotropin levels. The minimum level of testosterone required for normal erectile function remains unknown. Hypogonadism may also result in the absence of emission, secondary to the decrease in ejaculation by seminal vesicles and prostate.
Organic causes of erectile impotence (even the impossibility of erection) can be grouped into endocrine, medicinal, local, neurological and vascular. The decrease in plasma testosterone secondary to testicular insufficiency is an unusual but easily recognizable and treatable disorder. A decrease in plasma testosterone to the lower limit of normal is not a cause of sexual dysfunction.
However, hyperprolactinemia may cause impotence in some men with pituitary tumors and may not be evidenced on physical examination, with hyperprolactinemia inhibiting the production of luteinizing hormone-releasing hormone and thus causing low or lower levels of normal testosterone and plasma gonadotropin. Bromocriptin, a dopaminergic agonist, can lower prolactin levels and recover potency in these men.
Although many drugs are associated with impotence, antihypertensive agents, cymetidine and monoaminoxidase inhibitors lead more frequently to erectile dysfunction. Peripheral and central sympatolytic antihypertensive drugs or beta-adrenergic receptor blockers are most commonly involved. Angiotensin conversion enzyme inhibitors, calcium channel blockers and peripheral vasodilators do not cause a significant incidence of sexual dysfunction.
Histamine receptor antagonists (H2) such as cimetidine have antiandrogenic properties, in addition to increased prolactin secretion. Finasteride, an inhibitor of 5 beta-reductase, usually used in the treatment of benign hypertrophy of the prostate, produces impotence, decreased libido or ejaculation disorders in 10-12% of men. Monoaminoxidase inhibitors, antipsychotic drugs and tricyclic antidepressants can affect sexual function through anticholinergic and sympatolytic action.
Penile disorders, including a history of priapism, penile trauma and Peyronie's disease, can cause impotence due to fibrosis of sinusoid spaces of cavernous bodies, occlusion of the body artery or neurogenic mechanisms. Peyroone's disease is not rare, with patients usually presenting with a painful closet on the dorsal face of the penis that can progress towards the development of a penis curvature and a decrease in the rigidity of erection.
Many types of neurological disorders cause impotence, including lesions of the anterior temporal lobe, spinal cord disorders, loss of sensory adhesion in the dorsal tabor or damage to parasympathetic nerves, for example following surgery such as prostatectomy or radical (total) cystectomy. In contrast, transurethral prostatectomy does not produce organic impotence.
In addition, the nerves that provide penis innervation (cavernous nerves) go to the posterolateral face of the prostate and if they are kept intact during radical surgery on the prostate or bladder, potency can be retained in most men. if the spinal cord injury is above the sacral region, the erection reflex may occur, while diffuse damage to the sacral marrow causes total impotence.
Up to half of men with diabetes develop impotence within 6 years of developing diabetes and impotence may be the first clinical manifestation of diabetic neuropathy. Vasculogenic dysfunction is a concomitant factor in most men with diabetic impotence. Several factors contribute to neuropathic impotence, including abnormalities of the sensory pathways, motor neuropathy of cavernous nerves (which bears the efferent pathway for vasodilation in the penis) and low levels of neurotransmitters in cavernous bodies.
In addition, the denervation of smooth sinusoidal muscles leads to the loss of contractile elements and fibrosis, which limits the dilation of spaces. Although the negative pathway in the penis can be tested by directly recording electrical activity in the smooth body muscle, the test may not be necessary because in most patients other manifestations of vegetative neuropathy are highlighted upon careful examination. Many other polyneuropathy associated with impotence have similar effects.
Men with vascurogen impotence may present with total erectile impotence, reduced penile stiffness or loss of erection during intercourse. Vascular insufficiency may be due to aortic occlusion (Leriche syndrome) or several distal atherosclerotic disorders in hypogastric, shameful or cavernous arteries. The function of the sinusoidal tissue itself can be negatively affected by atherosclerosis and the use of tobacco products containing a variety of vasoconstrictors.
A significant condition of the shameful and cavernous arteries may occur in the absence of other clinical manifestations of peripheral vascular disease. Impotence usually observed after irradiation of the pelvis is probably due to vasculogenous causes. Along with neuropathy, vascular insufficiency contributes to the impotence of many men with diabetes mellitus.
Early ejaculation rarely has an organic cause. It is usually related to anxiety in sexual situations, unreasonable expectations about performance or emotional disorders. Various successful therapeutic modalities have been described, but behavioral therapy is the most effective.
Absence of emission is a symptom that may be due to: 1. retrograde ejaculation, 2. sympathetic denervation, 3. androgenic deficiency and 4. Medicinal products. Retrograde ejaculation can occur after surgery on the bladder neck or develop spontaneously in a diabetic man. Highlighting sperm in a postcoital urine sample establishes the diagnosis.
After sympatectomy or sometimes after extensive retroperitoneal surgery, vegetative innervation of the prostate and seminal vesicles is lost, resulting in the absence of contraction of the smooth muscles during ejaculation. Androgenic deficiency causes a decrease in the secretion of the prostate and seminal vesicles and a decrease in the volume of ejaculate. Finally, drugs such as guanetidine, phenoxibenzamine, fentolamine and setraline affect ejaculation rather than erection or libido.
If libido and erectile function are normal, the absence of orgasm is almost always due to a psychiatric disorder.
Priapism (impossible to detumescent) is a persistent, painful erection, often unrelated to sexual activity. Priapism can be particularly normal erection by the absence of the turgidity of the penian gland. Priapism can be idiopathic, can be associated with siclemia, chronic granulocytic leukemia, spinal cord damage or the injection of vasodilatory agents (such as alprostadil) into the penis.
The disorder may be secondary to blood clotting in the sinusoidal spaces of the penis or abnormalities of the adrenergic mediated mechanism of detumescence. Failure in the prompt treatment of priapism usually causes fibrosis and subsequent loss of erectile function. In the early stages, detumescence can sometimes be achieved by suction, irrigation of cavernous bodies and injection of weak vasoconstrictors. If this fails, release surgery may be required through shunt procedures. In patients with secondary pyapism, conservative measures such as transfusion, oxygenation and irrigation are generally preferred to sanding procedures.
Let's move on to the impotence assessment. The relative frequency of organic causes, as opposed to psychogenic ones, of erectile impotence is still under debate. However, anxiety and depressive state are the common causes of impotence. Other psychological factors, such as disinterest in the sexual partner, fear of sexual incompetence, marital misunderstandings, guilt related to deviant sexual attitudes, concern, fatigue and poor health often act in various combinations to reduce sexual impulse.
The central problem in the assessment of impotence is to separate cases due to psychological factors from those due to organic causes. Often, separation can be done on the basis of anamnesis. With the exception of severe depression, men with psychogenic impotence usually have normal nocturnal and morning erections. From early childhood to the 8th decade, erections occur during normal sleep. This phenomenon called nocturnal penile tumescence (NPT) occurs during paradoxical sleep (REM) and the total duration of NPT is on average 100 minutes per night.
Therefore, if an impotent man recounts a history with rigid erections in any circumstances (often when he wakes up in the morning), the efferent and circulatory neurological systems that mediate the erection are intact and the dysfunction is likely due to a psychiatric disorder. In these patients, the investigation should be limited. Some patients with early sensory neuropathy may have nocturnal erections.
If the history of nocturnal erections is questionable, the measurement of NPTs can be made officially by using a voltage measuring device in a sleep laboratory or by attaching a recording device by instant shooting or home-monitor. Although false positive scans or false negatives are impossible, this procedure helps to differentiate psychogenic impotence from organic one. Patients with vasculogenic impotence may have a degree of penile tumescence without the development of adequate rigidity, which may cause a false positive NPT test.
An alternative to NPT testing is the visual sexual stimulation test, which uses recorded erotic video material in a laboratory where erection is monitored by a voltage measuring device. Other traits in support of organic impotence include a slow, insidious onset, not associated with any particular psychiatric symptomatology, an uninterrupted antecedent period of normal erectile functioning and persistent sexual desire. After deduction of an organic cause, the fundamental problem is the etiological differential diagnosis.
History should be tested for diabetes mellitus, manifestations of peripheral neuropathy or bladder dysfunction, symptoms related to the vascular system, such as intermittent claudication, and symptoms of penile disorders such as a history of priapism or penile curvature (Peyronie's disease). A thorough history of medication should be obtained and surgical history that could have caused neurological impairments should be investigated. Smoking is not only a risk factor for atherosclerotic disease, but can directly inhibit sinusoidal relaxation.
Physical examination should include a detailed genital examination to identify abnormalities of the penis, especially Peyroone's disease which usually feels like a fibrous plaque on the dorsal face of the penis. The testicles should be palpated for size, symmetry and abnormal formations (if the length is less than 3,5 cm, hypogonadism should be taken into account). Signs of feminization, such as gynecomastia and abnormal hair distribution on the body, should be sought. All pulses must be palpated and the presence of breaths must be searched.
Often you can feel the pulse in the dorsal artery of the penis. If anamnesis or physical examination indicates a vascular cause, direct measurement of penian blood flow may be recommended. With the exception of minimally invasive treatment options, laborious diagnostic procedures are rarely indicated. A prior presentation of therapeutic options should pre-order invasive diagnostic procedures. If the patient prefers nonsurgical therapy, further investigation, beyond anamnesis, physical examination and measurement of plasma testosterone, is unlikely to change the therapeutic behavior.
The arteriography of the shameful artery provides the most accurate assessment of penile arterial disease, but it is expensive and invasive. Furthermore, arterial distal lesions may remain unidentified, unless the procedure is performed under the conditions of a chemical erection (e.g. injection of alprostadil). The penile/brachial index can be used to estimate penile blood flow by dividing penile systolic blood pressure, determined by the Doppler technique, to the brachial systolic pressure determined simultaneously in clinostatism. An index of less than 0.6 is suggestive of vasculogenic impotence.
However, the test evaluates only the flow through the dorsal artery of the penis, which is not directly involved in the erection process. A significant condition may be present in the cavernous arteries despite normal flow through the dorsal artery. Pulsed Doppler investigation and high-resolution ultrasound can be used in combination with intracorporeal alprostadil injection to assess blood flow to cavernous arteries.
Alternatively, dynamic infusion cavernosonography that measures pressure directly inside cavernous bodies can be used to assess arterial influx. Anomalies of the venous occlusion mechanism in the penis may cause impotence due to venous leakage, but are usually the consequence of functional abnormalities of smooth sinusoidal muscles or damage to arterial influx rather than venous abnormalities. In addition, surgical attempts to eradicate venous leakage rarely restore long-term erectile function. However, investigations aimed at identifying venous leakage are rarely recommended.
Neurological examination should measure anal sphincter tone, perineal sensitivity and bulbocavernos reflex. This reflex is obtained by tightening the penis gland and observing the degree of constriction of the anal sphincter. An examination for peripheral neuropathy should include evaluation of distal muscle function, tendinous reflexes in the lower limbs and vibratory sensitivity of position, tactile and painful.
In the presence of peripheral neuropathy, tests to evaluate penile neuropathy are rarely necessary. In cases with an uncertain neurological component, the inclusion of the sacrat electromyographic signal of the bulbocavernos reflex or the direct electrical recording of cavernous bodies with point or surface electrodes may be helpful. A specific test to prove anomalies of the penile autonomous efferent pathway is not available.
In the absence of hypogonadism or feminization, serum testosterone levels are usually normal. Hyperprolactinemia, however, may not be suspected on the basis of anamnesis and physical examination. Although endocrine causes of erectile dysfunction are rare, measurement of serum prolactin, total serum testosterone and luteinizing hormone is indicated as abnormalities of these parameters are curable.
There's a little more to say about the treatment. Medical therapy with androgens offers slightly greater benefits than placebo, with the exception of hypogonadismal men, and empirical therapy may actually delay the identification of the organic cause. if a secreting pituitary tumour of prolactin is present, either surgical removal or bromocriptin treatment usually results in a return of potency. Yohimbina, an alpha2-adrenergic antagonist, is widely prescribed, but acts only in psychogenic impotence by placebo effect.
Surgical therapy may be useful in the treatment of low potency related to aortic obstruction (however, potency may be lost rather than improved after aortic surgery if the nervous eference to the penis is impaired). Penile revascularization is effective only in young men with traumatic arterial disorders. Very few men with impotence due to venous leakage had a benefit from venous ligatia. A variety of vasoactive substances can produce erection when injected into cavernous bodies.
Self-injection of prostaglandin E2 (alprostadil) produces erection in more than 90% of men with mild to moderate psychogenic, neurogenic and vasculogenic impotence. Adverse effects include occasional injection pain, priapism (1%) and penile fibrosis (2%). Commercially available mechanical devices that use a vacuum to produce erection and a rubber band at the base of the penis to limit venous return bring a successful non-surgical alternative to many patients, including those with diabetes and severe vascular disease.
Penile prostheses are a therapeutic alternative for impotent patients refractory to other forms of treatment. The malleable plastic rod inserted into the penis provides the simplest system and the lowest rate of complications (however, the functional and cosmetic performance of the device is not satisfactory in all cases). Hydraulic prostheses, multicomponents, offer the advantage of a more physiological erection and a larger increase in penis diameter, but these devices are prone to mechanical failure. Even in patients with organic impotence, psychotherapy is often beneficial in reducing concomitant psychogenic factors that limit the success of medical and surgical therapy.
Ready!!! I've done it...
I've hardly managed to complete with a massive "chemistry" part of the human body, and I will now move on to a different kind of human chemistry.
Therefore, various endocrine, vascular, neurological and psychiatric disorders affect sexual and reproductive function in men. In addition, sexual dysfunction may be the symptom of a systemic disease.
But to see a sign of disease (a sign of abnormality) at this "level" is good to start with describing normal sexual function.
Penile erection is initiated by neuropsychological stimuli that ultimately produce vasodilation of the spaces and sinusoid arteries inside the two cavernous bodies (penians). The erection is normally preceded by sexual desire (or libido), which is partly regulated by androgen-dependent psychological factors. Although spontaneous nocturnal and diurnal erections are suppressed in men with androgenic deficiency, erections in response to erotic stimuli can continue for long periods.
Thus, the continuous action of testicular androgens seems to be necessary for normal libido, but not for the mechanism of erection itself. The penis is inervated by sympathetic, parasympathetic and somatic fibers. Somatic fibers in the dorsal nerve of the penis form the related pathway of the erectile reflex by transmitting the sensory impulses from the penile skin and gland to the ganglia of the posterior root S2-S4 through the shameful nerves.
Unlike corpuscular endings in the skin of the penis skin, most of the related endings in the gland are free nerve endings. The efferent pathway begins with the parasympathetic preganglionary fibers in S2-S4 that pass into the pelvic nerves towards the pelvic plexus. Sympathetic fibers that emerge from the intermediolateral grey areas T11-L2 pass through the sympathetic paravertebral ganglion chain, the upper hypogastric plexus and the hypogastric nerves to enter the pelvic plexus alongside the parasympathetic fibers.
Somatic efferent fibers from S3-S4 that pass through the shameful nerve to the hamstring and bulbocavernous muscles and postganglionary sympathetic fibers that irritate the smooth muscle of the epididymis, the deferential canals, the seminal vesicles and the internal bladder sphincter mediate the rhythmic contraction of these structures at the time of ejaculation. Autonomous nerve impulses, integrated into the pelvic plexus, are projected towards the penis through the cavernous nerves, which have the trajectory along the postero-lateral face of the prostate before penetrating the musculature of the pelvic floor immediately laterally after the urethra.
Distal to the membrane urethra some fibers enter the spongy body, while the others enter the cavernous bodies along with the terminal branches of the shameful artery and the efferent cavernous veins. If a disruption of cavernous nerves occurs as a result of pelvic trauma or surgery, erectile impotence may result.
The brain exerts an important modulating influence on the spinal reflex paths that control penile function. Variations visual, auditory, olfactory and imaginative stimuli causing erectile responses involving cortical, thalamic, rhinencephalic and limbic stimuli to the preoptic medial area of the anterior hypothalamus, which acts as an integration center. Other areas of the brain, such as the amygdala complex, can inhibit sexual function.
Although the parasympathetic nervous system is the main effector of erection, the transformation of the penis into an erect organ is a vascular phenomenon. In flaccid state, the arteries, arterioles and sinusoidal spaces of cavernous bodies are constricted due to the contraction of the smooth muscles in the walls of these structures, sympathetically mediated. The veins between the sinusoids and the dense albugine tunic that surround the cavernous bodies open freely into the emissary veins.
The erection begins when the relaxation of the smooth sinusoidal muscles causes the sinusoid to dilate and a decrease in peripheral resistance, causing a rapid increase in arterial blood flow through the shameful internal and cavernous arteries. The expansion of the sinusoidal system compresses the venulas on the internal face of the albugine tunic, leading to venous occlusion. Increased intracorporeal pressure leads to stiffness (incomplete expansion of sinusoidal spaces leads to incomplete stiffness).
Erection occurs when adrenergic-induced sinusoidal tone is antagonized by sacrate parasympathetic stimulation that produces sinusoidal relaxation primarily through the synthesis and release of nonadrenergic-noncolinergic neurotransmitter (NANC), nitric oxide (NO). The contribution of the acetylcholine-dependent release of NO from vascular endothelium is uncertain. In vitro, electrical stimulation of isolated bands in the cavernous body (with or without endothelium) causes sinusoidal relaxation by releasing neurotransmitters inside nerve endings, which is resistant to adrenergic and cholinergic blockers.
Inhibitors of nitric oxide or guanosine monophosphate (GMP) synthesis inhibitors, as well as nitric oxide purorators block sinusoidal relaxation. A variety of neuropeptides found in body tissues, including intestinal vasoactive peptide (VIP - vasoactive intestinal peptides) and genetically related peptide (CGRP - calcitonin gene-related peptides), produce turgidity when injected into the penis, but have uncertain physiological roles. Norepinephrine plays an important role in the adrenergic mechanism of detumescence.
Seminal emission and ejaculation are under the control of the sympathetic nervous system. The emission results from alpha-adrenergic-mediated contraction of the epidium, the deferent canal, seminal vesicles and the prostate, which causes the seminal fluid to enter the prostate urethra. Concomitant closure of the bladder neck prevents sperm reflux in the bladder and anterograde ejaculation results from contraction of the pelvic floor muscles, including the bullbocavernos and hamstring muscles.
Orgasm is a psychosensory phenomenon in which rhythmic contractions of the pelvic muscles are perceived as pleasant. Orgasm can also occur without erection or ejaculation or in the presence of retrograde ejaculation.
Detumescence after orgasm and ejaculation is incomplete understood. As it turns out, the active tone of the vessels in the sinusoidal spaces is restored by the contraction of the smooth muscles (probably mediated adrenergically), which decreases the flow of blood into the penis and supports the emptying of erectile tissue. After orgasm there is a refractory period that varies in duration with age, physical condition and psychological factors and during which erection and ejaculation are inhibited.
The time has come to address impotence. Simply defined, impotence is the impossibility of obtaining erection, ejaculation or both. Men with sexual dysfunction have a variety of symptoms, either separated or in combination: loss of desire (libidou), inability to initiate or maintain erection, impossibility of ejaculation, premature ejaculation or inability to achieve orgasm.
Sexual dysfunction may be secondary to systemic diseases or their treatment, specific disorders of the urogenital or endocrine system or psychological disorders. It was initially thought that the reason for dysfunction in most men with erectile impotence was psychological, but now it is believed that most impotent men have a component of an underlying organic condition. Since the selection and success of therapy depends on etiology, it is essential to evaluate all aspects of sexual function.
A decrease in sexual desire (or even loss of desire) may be due to androgenic deficiency (occurring in a condition either pituitary or testicular), psychological disorders or several types of drugs prescribed or usually abused. The possibility of androgenic deficiency can be tested by measuring testosterone and plasma gonadotropin levels. The minimum level of testosterone required for normal erectile function remains unknown. Hypogonadism may also result in the absence of emission, secondary to the decrease in ejaculation by seminal vesicles and prostate.
Organic causes of erectile impotence (even the impossibility of erection) can be grouped into endocrine, medicinal, local, neurological and vascular. The decrease in plasma testosterone secondary to testicular insufficiency is an unusual but easily recognizable and treatable disorder. A decrease in plasma testosterone to the lower limit of normal is not a cause of sexual dysfunction.
However, hyperprolactinemia may cause impotence in some men with pituitary tumors and may not be evidenced on physical examination, with hyperprolactinemia inhibiting the production of luteinizing hormone-releasing hormone and thus causing low or lower levels of normal testosterone and plasma gonadotropin. Bromocriptin, a dopaminergic agonist, can lower prolactin levels and recover potency in these men.
Although many drugs are associated with impotence, antihypertensive agents, cymetidine and monoaminoxidase inhibitors lead more frequently to erectile dysfunction. Peripheral and central sympatolytic antihypertensive drugs or beta-adrenergic receptor blockers are most commonly involved. Angiotensin conversion enzyme inhibitors, calcium channel blockers and peripheral vasodilators do not cause a significant incidence of sexual dysfunction.
Histamine receptor antagonists (H2) such as cimetidine have antiandrogenic properties, in addition to increased prolactin secretion. Finasteride, an inhibitor of 5 beta-reductase, usually used in the treatment of benign hypertrophy of the prostate, produces impotence, decreased libido or ejaculation disorders in 10-12% of men. Monoaminoxidase inhibitors, antipsychotic drugs and tricyclic antidepressants can affect sexual function through anticholinergic and sympatolytic action.
Penile disorders, including a history of priapism, penile trauma and Peyronie's disease, can cause impotence due to fibrosis of sinusoid spaces of cavernous bodies, occlusion of the body artery or neurogenic mechanisms. Peyroone's disease is not rare, with patients usually presenting with a painful closet on the dorsal face of the penis that can progress towards the development of a penis curvature and a decrease in the rigidity of erection.
Many types of neurological disorders cause impotence, including lesions of the anterior temporal lobe, spinal cord disorders, loss of sensory adhesion in the dorsal tabor or damage to parasympathetic nerves, for example following surgery such as prostatectomy or radical (total) cystectomy. In contrast, transurethral prostatectomy does not produce organic impotence.
In addition, the nerves that provide penis innervation (cavernous nerves) go to the posterolateral face of the prostate and if they are kept intact during radical surgery on the prostate or bladder, potency can be retained in most men. if the spinal cord injury is above the sacral region, the erection reflex may occur, while diffuse damage to the sacral marrow causes total impotence.
Up to half of men with diabetes develop impotence within 6 years of developing diabetes and impotence may be the first clinical manifestation of diabetic neuropathy. Vasculogenic dysfunction is a concomitant factor in most men with diabetic impotence. Several factors contribute to neuropathic impotence, including abnormalities of the sensory pathways, motor neuropathy of cavernous nerves (which bears the efferent pathway for vasodilation in the penis) and low levels of neurotransmitters in cavernous bodies.
In addition, the denervation of smooth sinusoidal muscles leads to the loss of contractile elements and fibrosis, which limits the dilation of spaces. Although the negative pathway in the penis can be tested by directly recording electrical activity in the smooth body muscle, the test may not be necessary because in most patients other manifestations of vegetative neuropathy are highlighted upon careful examination. Many other polyneuropathy associated with impotence have similar effects.
Men with vascurogen impotence may present with total erectile impotence, reduced penile stiffness or loss of erection during intercourse. Vascular insufficiency may be due to aortic occlusion (Leriche syndrome) or several distal atherosclerotic disorders in hypogastric, shameful or cavernous arteries. The function of the sinusoidal tissue itself can be negatively affected by atherosclerosis and the use of tobacco products containing a variety of vasoconstrictors.
A significant condition of the shameful and cavernous arteries may occur in the absence of other clinical manifestations of peripheral vascular disease. Impotence usually observed after irradiation of the pelvis is probably due to vasculogenous causes. Along with neuropathy, vascular insufficiency contributes to the impotence of many men with diabetes mellitus.
Early ejaculation rarely has an organic cause. It is usually related to anxiety in sexual situations, unreasonable expectations about performance or emotional disorders. Various successful therapeutic modalities have been described, but behavioral therapy is the most effective.
Absence of emission is a symptom that may be due to: 1. retrograde ejaculation, 2. sympathetic denervation, 3. androgenic deficiency and 4. Medicinal products. Retrograde ejaculation can occur after surgery on the bladder neck or develop spontaneously in a diabetic man. Highlighting sperm in a postcoital urine sample establishes the diagnosis.
After sympatectomy or sometimes after extensive retroperitoneal surgery, vegetative innervation of the prostate and seminal vesicles is lost, resulting in the absence of contraction of the smooth muscles during ejaculation. Androgenic deficiency causes a decrease in the secretion of the prostate and seminal vesicles and a decrease in the volume of ejaculate. Finally, drugs such as guanetidine, phenoxibenzamine, fentolamine and setraline affect ejaculation rather than erection or libido.
If libido and erectile function are normal, the absence of orgasm is almost always due to a psychiatric disorder.
Priapism (impossible to detumescent) is a persistent, painful erection, often unrelated to sexual activity. Priapism can be particularly normal erection by the absence of the turgidity of the penian gland. Priapism can be idiopathic, can be associated with siclemia, chronic granulocytic leukemia, spinal cord damage or the injection of vasodilatory agents (such as alprostadil) into the penis.
The disorder may be secondary to blood clotting in the sinusoidal spaces of the penis or abnormalities of the adrenergic mediated mechanism of detumescence. Failure in the prompt treatment of priapism usually causes fibrosis and subsequent loss of erectile function. In the early stages, detumescence can sometimes be achieved by suction, irrigation of cavernous bodies and injection of weak vasoconstrictors. If this fails, release surgery may be required through shunt procedures. In patients with secondary pyapism, conservative measures such as transfusion, oxygenation and irrigation are generally preferred to sanding procedures.
Let's move on to the impotence assessment. The relative frequency of organic causes, as opposed to psychogenic ones, of erectile impotence is still under debate. However, anxiety and depressive state are the common causes of impotence. Other psychological factors, such as disinterest in the sexual partner, fear of sexual incompetence, marital misunderstandings, guilt related to deviant sexual attitudes, concern, fatigue and poor health often act in various combinations to reduce sexual impulse.
The central problem in the assessment of impotence is to separate cases due to psychological factors from those due to organic causes. Often, separation can be done on the basis of anamnesis. With the exception of severe depression, men with psychogenic impotence usually have normal nocturnal and morning erections. From early childhood to the 8th decade, erections occur during normal sleep. This phenomenon called nocturnal penile tumescence (NPT) occurs during paradoxical sleep (REM) and the total duration of NPT is on average 100 minutes per night.
Therefore, if an impotent man recounts a history with rigid erections in any circumstances (often when he wakes up in the morning), the efferent and circulatory neurological systems that mediate the erection are intact and the dysfunction is likely due to a psychiatric disorder. In these patients, the investigation should be limited. Some patients with early sensory neuropathy may have nocturnal erections.
If the history of nocturnal erections is questionable, the measurement of NPTs can be made officially by using a voltage measuring device in a sleep laboratory or by attaching a recording device by instant shooting or home-monitor. Although false positive scans or false negatives are impossible, this procedure helps to differentiate psychogenic impotence from organic one. Patients with vasculogenic impotence may have a degree of penile tumescence without the development of adequate rigidity, which may cause a false positive NPT test.
An alternative to NPT testing is the visual sexual stimulation test, which uses recorded erotic video material in a laboratory where erection is monitored by a voltage measuring device. Other traits in support of organic impotence include a slow, insidious onset, not associated with any particular psychiatric symptomatology, an uninterrupted antecedent period of normal erectile functioning and persistent sexual desire. After deduction of an organic cause, the fundamental problem is the etiological differential diagnosis.
History should be tested for diabetes mellitus, manifestations of peripheral neuropathy or bladder dysfunction, symptoms related to the vascular system, such as intermittent claudication, and symptoms of penile disorders such as a history of priapism or penile curvature (Peyronie's disease). A thorough history of medication should be obtained and surgical history that could have caused neurological impairments should be investigated. Smoking is not only a risk factor for atherosclerotic disease, but can directly inhibit sinusoidal relaxation.
Physical examination should include a detailed genital examination to identify abnormalities of the penis, especially Peyroone's disease which usually feels like a fibrous plaque on the dorsal face of the penis. The testicles should be palpated for size, symmetry and abnormal formations (if the length is less than 3,5 cm, hypogonadism should be taken into account). Signs of feminization, such as gynecomastia and abnormal hair distribution on the body, should be sought. All pulses must be palpated and the presence of breaths must be searched.
Often you can feel the pulse in the dorsal artery of the penis. If anamnesis or physical examination indicates a vascular cause, direct measurement of penian blood flow may be recommended. With the exception of minimally invasive treatment options, laborious diagnostic procedures are rarely indicated. A prior presentation of therapeutic options should pre-order invasive diagnostic procedures. If the patient prefers nonsurgical therapy, further investigation, beyond anamnesis, physical examination and measurement of plasma testosterone, is unlikely to change the therapeutic behavior.
The arteriography of the shameful artery provides the most accurate assessment of penile arterial disease, but it is expensive and invasive. Furthermore, arterial distal lesions may remain unidentified, unless the procedure is performed under the conditions of a chemical erection (e.g. injection of alprostadil). The penile/brachial index can be used to estimate penile blood flow by dividing penile systolic blood pressure, determined by the Doppler technique, to the brachial systolic pressure determined simultaneously in clinostatism. An index of less than 0.6 is suggestive of vasculogenic impotence.
However, the test evaluates only the flow through the dorsal artery of the penis, which is not directly involved in the erection process. A significant condition may be present in the cavernous arteries despite normal flow through the dorsal artery. Pulsed Doppler investigation and high-resolution ultrasound can be used in combination with intracorporeal alprostadil injection to assess blood flow to cavernous arteries.
Alternatively, dynamic infusion cavernosonography that measures pressure directly inside cavernous bodies can be used to assess arterial influx. Anomalies of the venous occlusion mechanism in the penis may cause impotence due to venous leakage, but are usually the consequence of functional abnormalities of smooth sinusoidal muscles or damage to arterial influx rather than venous abnormalities. In addition, surgical attempts to eradicate venous leakage rarely restore long-term erectile function. However, investigations aimed at identifying venous leakage are rarely recommended.
Neurological examination should measure anal sphincter tone, perineal sensitivity and bulbocavernos reflex. This reflex is obtained by tightening the penis gland and observing the degree of constriction of the anal sphincter. An examination for peripheral neuropathy should include evaluation of distal muscle function, tendinous reflexes in the lower limbs and vibratory sensitivity of position, tactile and painful.
In the presence of peripheral neuropathy, tests to evaluate penile neuropathy are rarely necessary. In cases with an uncertain neurological component, the inclusion of the sacrat electromyographic signal of the bulbocavernos reflex or the direct electrical recording of cavernous bodies with point or surface electrodes may be helpful. A specific test to prove anomalies of the penile autonomous efferent pathway is not available.
In the absence of hypogonadism or feminization, serum testosterone levels are usually normal. Hyperprolactinemia, however, may not be suspected on the basis of anamnesis and physical examination. Although endocrine causes of erectile dysfunction are rare, measurement of serum prolactin, total serum testosterone and luteinizing hormone is indicated as abnormalities of these parameters are curable.
There's a little more to say about the treatment. Medical therapy with androgens offers slightly greater benefits than placebo, with the exception of hypogonadismal men, and empirical therapy may actually delay the identification of the organic cause. if a secreting pituitary tumour of prolactin is present, either surgical removal or bromocriptin treatment usually results in a return of potency. Yohimbina, an alpha2-adrenergic antagonist, is widely prescribed, but acts only in psychogenic impotence by placebo effect.
Surgical therapy may be useful in the treatment of low potency related to aortic obstruction (however, potency may be lost rather than improved after aortic surgery if the nervous eference to the penis is impaired). Penile revascularization is effective only in young men with traumatic arterial disorders. Very few men with impotence due to venous leakage had a benefit from venous ligatia. A variety of vasoactive substances can produce erection when injected into cavernous bodies.
Self-injection of prostaglandin E2 (alprostadil) produces erection in more than 90% of men with mild to moderate psychogenic, neurogenic and vasculogenic impotence. Adverse effects include occasional injection pain, priapism (1%) and penile fibrosis (2%). Commercially available mechanical devices that use a vacuum to produce erection and a rubber band at the base of the penis to limit venous return bring a successful non-surgical alternative to many patients, including those with diabetes and severe vascular disease.
Penile prostheses are a therapeutic alternative for impotent patients refractory to other forms of treatment. The malleable plastic rod inserted into the penis provides the simplest system and the lowest rate of complications (however, the functional and cosmetic performance of the device is not satisfactory in all cases). Hydraulic prostheses, multicomponents, offer the advantage of a more physiological erection and a larger increase in penis diameter, but these devices are prone to mechanical failure. Even in patients with organic impotence, psychotherapy is often beneficial in reducing concomitant psychogenic factors that limit the success of medical and surgical therapy.
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