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NAME: ONOTU ROSELINE OHUNENE MATRIC NUMBER: 13/MHS01/099 COLLEGE: MEDICINE AND HEALTH SCIENCES DEPARTMENT: MEDICINE AND SURGERY COURSE: ENDOCRINOLOGY PHYSIOLOGY AND REPRODUCTIVE COURSE CODE: PHS204 DATE: 6/06/2015 LECTURER IN CHARGE: CHRISTOPHER AKINTAYO ASSIGNMENT 1) Write on the physiology of erection 2) Write on the physiology of coitus THE PHYSIOLOGY OF ERECTION INTRODUCTION An erection is the hardening of the penis that occurs when sponge-like tissue inside the penis fills up with blood. Usually, an erection causes the penis to enlarge and stand away from the body. There are three types of erection 1) Psychogenic erection -this occur as a result of visual or auditory stimuli, or as a result of fantasy 2) Reflexogenic erection -this occurs as a result of tactile stimulation of the penis, and are important in maintaining the erection during sexual activity 3) Nocturnal erection-this occurs during REM sleep The physiological mechanism by which an erection occurs begins with an increase in blood flow to the penis, filling the sinusoids of the corpora cavernosum. The cavernosal smooth muscle relaxes to allow the expansion to facilitate the extra volume of blood. This expansion presses on the venous plexus, which creates an outflow obstruction, thereby increasing the pressure within the penis and aiding rigidity. The relaxation of the smooth muscle of the penis relies on the parasympathetic nervous system. The sympathetic nervous system controls ejaculation, and also causes constriction of smooth muscle. This constricts the blood containing lacunar spaces of the penis and empties them of blood, therefore aiding detumescence. Penile erection is initiated by sexual stimuli, including auditory, visual, and olfactory stimuli, and erotic cognitions. Spinal cord sexual arousal occurs as a result of tactile stimulation of the penis. The neurotransmitter mediating these sexual signals is nitric oxide (NO), initially termed endothelium-derived relaxing factor. NO is produced by the endothelium in the absence of cholinergic or adrenergic influences. NO stimulates smooth muscle guanylate cyclase, upregulating synthesis of cyclic guanine monophosphate (cGMP), which plays a pivotal role in penile arteriolar vasodilatation and relaxation of penile corporeal smooth muscle. Oxygen levels are important in NO-mediated responses, which vary widely from penile flaccidity to erection. Decreasing oxygen tension levels progressively inhibit NO responses, and elevation of oxygen to normal levels restores NO-dependent activities. Both cholinergic and adrenergic influences are significant in penile erection and detumescence. Parasympathetic fibers and acetylcholine, the release of which may be stimulated by tactile sensory stimuli to the penis, enhance penile blood flow and smooth muscle relaxation. Sympathetic (adrenergic) fibers and norepinephrine neurotransmission help to maintain the penis in its flaccid state. Detumescence is mediated by adrenergic nerve terminals whose neurotransmitter, norepinephrine, activates alpha-adrenergic receptors (found chiefly in the thoracolumbar region of the spinal cord). Activation of these receptors produces vasoconstriction of the penile vasculature and decompression of penile venules, which result in detumescence. Incomplete corporeal smooth muscle relaxation resulting from impairment of the NO-induced relaxing mechanism or from augmented alpha-adrenergic activity has been proposed as a mechanism of ED. Prostaglandin E1 (PGE1) is produced during erection by the penile musculature and activates adenylate cyclase, which alters ion-channel permeability and results in calcium release by the smooth muscle cells. (Although the PGE1 pathway is not thought to play a major intrinsic proerectile role, it is considered to be important as a therapeutic approach.) These smooth muscle cells then relax, allowing increased blood flow. Dynamic vascular studies have demonstrated that venous outflow obstruction and the resultant entrapment of arterial blood in the penis are essential in the initiation and maintenance of a rigid erection. Failure of these vascular phenomena, as seen with venous leakage, can result in ED. Venous leakage may be of traumatic origin, resulting in abnormal venous communication between the corpora cavernosa and the glans penis. Leakage may also result from the failure of emissary veins to close, as in Peyronie's disease. [59] An unusual cause of ED is a traumatic or congenital arteriovenous fistula between the pudendal artery and a pelvic vein. An elevated penile content of corporeal connective tissue, possibly related to a decrease in oxygen, has been proposed as a mechanism for defective veno-occlusion. Phosphodiesterases are essential in regulating intracellular cGMP activity through enzymatic hydrolysis (to 5'-GMP), thus terminating its second-messenger function.. Multiple PDEs exist throughout the body; their isoforms vary depending on the specific function that they perform. In cGMP penile activity, the PDE5 isoform terminates the vasodilator and smooth muscle-relaxing effects of cGMP. Inhibition of this process by PDE5 inhibitors forms the basis for recent developments in the oral therapy of ED. The maintenance of an erection and the tone of the cavernosal smooth muscle are determined by an integrated response to neural stimulation and paracrine or autocrine systems. THE PHYSIOLOGY OF COITUS IN MALE INTRODUCTION Coitus means sexual intercourse or copulation. It is principally the insertion and thrusting of a male’s penis, usually when erect, into a female’s vagina for the purposes of sexual pleasure or reproduction, or both. The male sexual response cycle consists of excitement, plateau, orgasm, and resolution. The initial event, penile erection, is produced by arteriolar dilatation and increased blood flow to the erectile tissue of the penis. Erection is a reflex response initiated by visual, olfactory, or imaginative stimuli impinging upon supraspinal centers or by genital stimulation that in turn activates spinal reflex mechanisms. Sacral parasympathetic and thoracolumbar sympathetic nerves provide the efferent vasodilator input to the penis. Parasympathetic nerves also stimulate secretion from the seminal vesicles and prostate and Cowper's glands during the plateau phase. The orgasmic phase is characterized by seminal emission and ejaculation and the accompanying sensations. Emission of semen into the urethra depends on sympathetic nerves that elicit contractions of smooth muscles in the vas deferens, seminal vesicles, and prostate. Rhythmic contractions of striated muscle (bulbocavernosus and ischiocavernosus) generated by efferent pathways in the pudendal nerve eject semen from the urethra. APPLIED PHYSIOLOGY Erectile dysfunction (ED) or impotence is sexual dysfunction characterized by the inability to develop or maintain an erection of the penis during sexual activity. Psychological impotence is where erection or penetration fails due to thoughts or feelings (psychological reasons) rather than physical impossibility; this is somewhat less frequent but can often be helped. Notably in psychological impotence, there is a strong response to placebo treatment SIGNS AND SYMPTOMS Erectile dysfunction is characterized by the regular or repeated inability to obtain or maintain an erection. It is analyzed in several ways: Obtaining full erections at some times, such as nocturnal penile tumescence when asleep (when the mind and psychological issues, if any, are less present), tends to suggest that the physical structures are functionally working. Other factors leading to erectile dysfunction are diabetes mellitus (causing neuropathy). CAUSES Drugs (anti-depressants (SSRIs) and nicotine are most common) Neurogenic disorders Cavernosal disorders (Peyronie's disease) Psychological causes: performance anxiety, stress, and mental disorders Surgery Aging. It is four times more common in men aged in their 60s than those in their 40s. Kidney failure Diseases such as diabetes mellitus and multiple sclerosis (MS). While these two causes have not been proven they are likely suspects as they cause issues with both the blood flow and nervous systems. Lifestyle: smoking is a key cause of erectile dysfunction. Smoking causes impotence because it promotes arterial narrowing. TREATMENTS Treatment depends on the cause. Exercise, particularly aerobic exercise during midlife is effective for preventing ED; exercise as a treatment is under investigation. For tobacco smokers, cessation results in a significant improvement. Oral pharmacotherapy and vacuum erection devices are first-line treatments followed by injections of drugs into the penis, and penile implants. REFERENCES 1) 2) 3) 4) www.ncbi.nlm.nih.gov/pubmed/7356224 Coitus/wikepedia.com www.endocrinesurgeon.co.uk/index.php/the-physiology-of-an-erection http://en.wikipedia.org/wiki/Erectile_dysfunction