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Transcript
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