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NAME : TOBECHUKWU O. OGBONNA
MATRIC NUMBER :
13/MHS01/080
DEPARTMENT: MEDICINE AND
SURGERY
COLLEGE: MEDICINE AND HEALTH
SCIENCES
COURSE: REPRODUCTIVE
PHYSIOLOGY
COURSE CODE : PHS 204
TITLE: PHSIOLOGY OF COITUS AND
MALE ERECTION
A DETAILED STUDY OF COITAL PHYSIOLOGY,
WITH SPECIAL REFERENCE TO THE PHYSIOLOGY OF MALE ERECTION
TOBECHUKWU O. OGBONNA
DEPARTMENT OF MEDICINE AND SURGERY, AFE BABALOLA UNIVERSITY, ADO
EKITI .NIGERIA.
Physiology of Normal Erection and Coitus
Structure and Function of the Male Reproductive System.
COMPONENTS OF THE MALE REPRODUCTIVE SYSTEM
 Bladder Ureter
 Urethra
 Penis
 Vas deferens
 Testis
 Scrotum
 Epididymis Cowper's (bulbourethral) gland
 Prostate gland
 Ejaculatory duct
 Seminal vesicle
Testes form in the human embryo, they develop seminiferous tubules beginning at around 43
to 50 days after conception. The seminiferous tubules are the sites of sperm production. At
about 9 to 10 weeks the Leydig cells, located in the interstitial tissue between the
seminiferous tubules begin to secrete testosterone (the major male sex hormone, or androgen)
Testosterone secretion during embryonic development converts indifferent structures into the
male external genitalia, the penis and the scrotum, a sac that contains the testes. In the
absence of testosterone, these structures develop into the female external genitalia.
In an adult, each testis is composed primarily of the highly convoluted seminiferous tubules .
Although the testes are actually formed within the abdominal cavity, shortly before birth they
descend through an opening called the inguinal canal into the scrotum, which suspends them
outside the abdominal cavity. The scrotum maintains the testes at around 34°C, slightly lower
than the core body temperature (37°C). This lower temperature is required for normal sperm
development in humans.
Production of Sperm
The wall of the seminiferous tubule consists of germinal cells, which become sperm by
meiosis, and supporting Sertoli cells. The germinal cells near the outer surface of the
seminiferous tubule are diploid (with 46 chromosomes in humans), while those located closer
to the lumen of the tubule are haploid (with 23 chromosome each). Each parent cell
duplicates by mitosis, and one of the two daughter cells then undergoes meiosis to form
sperm; the other remains as a parent cell. In that way, the male never runs out of parent cells
to produce sperm. Adult males produce an average of 100 to 200 million sperm each day and
can continue to do so throughout most of the rest of their lives.
The diploid daughter cell that begins meiosis is called a primary spermatocyte. It has 23 pairs
of homologous chromosomes (in humans) and each chromosome is duplicated, with two
chromatids. The first meiotic division separates the homologous chromosomes, producing
two haploid secondary spermatocytes. However, each chromosome still consists of two
duplicate chromatids. Each of these cells then undergoes the second meiotic division to
separate the chromatids and produce two haploid cells, the spermatids. Therefore, a total of
four haploid spermatids are produced by each primary spermatocyte. All of these cells
constitute the germinal epithelium of the seminiferous tubules because they “germinate” the
gametes.
In addition to the germinal epithelium, the walls of the seminiferous tubules contain
nongerminal cells known as Sertoli cells. The Sertoli cells nurse the developing sperm and
secrete products required for spermatogenesis (sperm production). They also help convert the
spermatids into spermatozoa by engulfing their extra cytoplasm.
Spermatozoa, or sperm, are relatively simple cells, consisting of a head, body, and tail . The
head encloses a compact nucleus and is capped by a vesicle called an acrosome, which is
derived from the Golgi complex. The acrosome contains enzymes that aid in the penetration
of the protective layers surrounding the egg. The body and tail provide a propulsive
mechanism: within the tail is a flagellum, while inside the body are a centriole, which acts as
a basal body for the flagellum, and mitochondria, which generate the energy needed for
flagella movement.
The testis and spermatogenesis. Inside the testis, the seminiferous tubules are the sites of
spermatogenesis. Germinal cells in the seminiferous tubules give rise to spermatozoa by
meiosis. Sertoli cells are nongerminal cells within the walls of the seminiferous tubules. They
assist spermatogenesis in several ways, such as helping to convert spermatids into
spermatozoa. A primary spermatocyte is diploid. At the end of the first meiotic division,
homologous chromosomes have separated, and two haploid secondary spermatocytes form.
The second meiotic division separates the sister chromatids and results in the formation of
four haploid spermatids.
Acrosome
Head
Body
Tail
Nucleus
Centriole
Mitochondrion
Flagellum
Male Accessory Sex Organs
After the sperm are produced within the seminiferous tubules, they are delivered into a long,
coiled tube called the epididymis. The sperm are not motile when they arrive in the
epididymis, and they must remain there for at least 18 hours before their motility develops.
From the epididymis, the sperm enter another long tube, the vas deferens, which passes into
the abdominal cavity via the inguinal canal.
The vas deferens from each testis joins with one of the ducts from a pair of glands called the
seminal vesicles, which produce a fructose-rich fluid. From this point, the vas deferens
continues as the ejaculatory duct and enters the prostate gland at the base of the urinary
bladder. In humans, the prostate gland is about the size of a golf ball and is spongy in texture.
It contributes about 60% of the bulk of the semen, the fluid that contains the products of the
testes, fluid from the seminal vesicles, and the products of the prostate gland. Within the
prostate gland, the ejaculatory duct merges with the urethra from the urinary bladder. The
urethra carries the semen out of the body through the tip of the penis. A pair of pea-sized
bulbourethral glands secrete a fluid that lines the urethra and / lubricates the tip of the penis
prior to coitus (sexual intercourse).
In addition to the urethra, there are two columns of erectile tissue, the corpora cavernosa,
along the dorsal side of the penis and one column, the corpus spongiosum, along the ventral
side . Penile erection is produced by neurons in the parasympathetic division of the
autonomic nervous system. As a result of the release of nitric oxide by these neurons,
arterioles in the penis dilate, causing the erectile tissue to become engorged with blood and
turgid. This increased pressure in the erectile tissue compresses the veins, so blood flows into
the penis but cannot flow out. The drug sildenafil (Viagra) prolongs erection by stimulating
release of nitric oxide in the penis. Some mammals, such as the walrus, have a bone in the
penis that contributes to its stiffness during erection, but humans do not.
The result of erection and continued sexual stimulation is ejaculation, the ejection from the
penis of about 5 milliliters of semen containing an average of 300 million sperm.
Successful fertilization requires such a high sperm count because the odds against any one
sperm cell successfully completing the journey to the egg and fertilizing it are extraordinarily
high, and the acrosomes of several sperm need to interact with the egg before a single sperm
can penetrate the egg. Males with fewer than 20 million sperm per millilitre are generally
considered sterile. Despite their large numbers, sperm constitute only about 1% of the volume
of the semen ejaculated.
Hormonal Control of Male Reproduction
The anterior pituitary gland secretes two gonadotropic hormones: FSH and LH. Although
these hormones are named for their actions in the female, they are also involved in regulating
male reproductive function. In males, FSH stimulates the Sertoli cells to facilitate sperm
development, and LH stimulates the Leydig cells to secrete testosterone. The principle of
negative feedback inhibition discussed in chapter 56 applies to the control of FSH and LH
secretion. The hypothalamic hormone, gonadotropinreleasing hormone (GnRH), stimulates
the anterior pituitary gland to secrete both FSH and LH. FSH causes the Sertoli cells to
release a peptide hormone called inhibin that specifically inhibits FSH secretion. Similarly,
LH stimulates testosterone secretion, and testosterone feeds back to inhibit the release of LH,
both directly at the anterior pituitary gland and indirectly by reducing GnRH release. The
importance of negative feedback inhibition can be demonstrated by removing the testes; in
the absence of testosterone and inhibin, the secretion of FSH and LH from the anterior
pituitary is greatly increased.
An adult male produces sperm continuously by meiotic division of the germinal cells
lining the seminiferous tubules. Semen consists of sperm from the testes and fluid
contributed by the seminal vesicles and prostate
gland. Production of sperm and secretion of testosterone from the testes are controlled
by FSH and LH from the anterior pituitary.
Male Reproductive Hormones
Follicle-stimulating hormone (FSH) Stimulates spermatogenesis,
Luteinizing hormone (LH) Stimulates secretion of testosterone by Leydig cells,
Testosterone Stimulates development and maintenance of male secondary sexual
characteristics and accessory sex organs.
Hormonal interactions between the testes and anterior pituitary. LH stimulates the Leydig
cells to secrete testosterone, and FSH stimulates the Sertoli cells of the seminiferous tubules to
secrete inhibin.
SEXUAL AROUSAL IN MALES
Sexual arousal (also sexual excitement) is the arousal of sexual desire, during or in anticipation
of sexual activity. A number of physiological responses occur in the body and mind as preparation
for sex and continue during it. Genital responses are not the only changes, but noting Mental
stimuli such as touch, and the internal fluctuation of hormones, can influence sexual arousal.
Sexual arousal has several stages and may not lead to any actual sexual activity, beyond a
mental arousal and the physiological changes that accompany it. Given sufficient sexual
stimulation, sexual arousal in humans reaches its climax during an orgasm. It may also be
pursued for its own sake, even in the absence of an orgasm.
Erotic stimuli
Depending on the situation, a person can be sexually aroused by a variety of factors, both
physical and mental. A person may be sexually aroused by another person or by particular
aspects of that person, or by a non-human object. The welcome physical stimulation of an
erogenous zone or acts of foreplay can result in arousal, especially if it is accompanied with
the anticipation of imminent sexual activity. Sexual arousal may be assisted by a romantic
setting, music or other soothing situation. The potential stimuli for sexual arousal vary from
person to person, and from one time to another, as does the level of arousal.
Stimuli can be classified according to the sense involved: somatosensory (touch), visual, and
olfactory (scent). Auditory stimuli are also possible, though they are generally considered
secondary in role to the other three.] Erotic stimuli which can result in sexual arousal can
include conversation, reading, films or images or a smell or setting, any of which can
generate erotic thoughts and memories in a person. Given the right context, these may lead to
the person desiring physical contact, including kissing, cuddling, and petting of an erogenous
zone. This may in turn make the person desire direct sexual stimulation of the breasts,
nipples, buttocks and/or genitals, and further sexual activity.
Erotic stimuli may originate from a source unrelated to the object of subsequent sexual
interest. For example, many people may find nudity, erotica or pornography sexually
arousing, which may generate a general sexual interest which is satisfied with sexual activity.
When sexual arousal is achieved by or dependent on the use of objects, it is referred to as
sexual fetishism, or in some instances a paraphilia.
Physiological response in males
Male sexual arousal. On the left of the image the male genitalia are in
regular, flaccid state; on the right the male is sexually aroused and his
penis has become erect.
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Penile tumescence and erection
The veins in the penis may become more prominent
Tightening and/or retraction of the foreskin often exposing the glans
penis
Emission of pre-ejaculatory fluid
Swelling of the testes
Ascension of the testes
Tensing and thickening of the scrotum
Pupil dilation
It is normal to correlate the erection of the penis with male sexual arousal. Physical or
psychological stimulation, or both, leads to vasodilation and the increased blood flow
engorges the three spongy areas that run along the length of the penis (the two corpora
cavernosa and the corpus spongiosum). The penis grows enlarged and firm, the skin of the
scrotum is pulled tighter, and the testes are pulled up against the body. However the
relationship between erection and arousal is not one-to-one. After their mid-forties, some men
report that they do not always have an erection when they are sexually aroused. Equally, a
male erection can occur during sleep (nocturnal penile tumescence) without conscious sexual
arousal or due to mechanical stimulation (e.g. rubbing against the bed sheet) alone. A young
man — or one with a strong sexual drive — may experience enough sexual arousal for an
erection to result from a passing thought, or just the sight of a passerby. Once erect, his penis
may gain enough stimulation from contact with the inside of his clothing to maintain and
encourage it for some time.
As sexual arousal and stimulation continues, it is likely that the glans or head of the erect
penis will swell wider and, as the genitals become further engorged with blood, their color
deepens and the testicles can grow up to 50% larger. As the testicles continue to rise, a
feeling of warmth may develop around them and the perineum. With further sexual
stimulation, the heart rate increases, blood pressure rises and breathing becomes quicker. The
increase in blood flow in the genital and other regions may lead to a sex flush sometimes, in
some men.
As sexual stimulation continues, the muscles of the pelvic floor, the vas deferens (between
the testicles and the prostate), the seminal vesicles and the prostate gland itself may begin to
contract in a way that forces sperm and semen into the urethra inside the penis. This is the
onset of orgasm and it is likely, once this has started, that the man will continue to ejaculate
and orgasm fully, with or without further stimulation.
Equally, if sexual stimulation stops before orgasm, the physical effects of the stimulation,
including the vasocongestion, will subside in a short time. Repeated or prolonged stimulation
without orgasm and ejaculation can lead to discomfort in the testes.
After orgasm and ejaculation, men usually experience a refractory period characterised by
loss of erection, a subsidence in any sex flush, less interest in sex, and a feeling of relaxation
that can be attributed to the neurohormones oxytocin and prolactin. The intensity and
duration of the refractory period can be very short in a highly aroused young man in what he
sees as a highly arousing situation, perhaps without even a noticeable loss of erection. It can
be as long as a few hours or days in mid-life and older men.
Psychological response
Psychological sexual arousal involves appraisal and evaluation of a stimulus, categorization
of a stimulus as sexual, and an effective response. The combination of cognitive and
physiological states elicits psychological sexual arousal. Some suggest that psychological
sexual arousal results from an interaction of cognitive and experiential factors, such as
affective state, previous experience, and current social context.
Male
The relationship between sexual desire and arousal in men is complex, with a wide range of
factors increasing or decreasing sexual arousal. Physiological responses, such as heart rate,
blood pressure, and erection, are often discordant with self-reported subjective perceptions of
arousal. This inconsistency suggests that psychological, or cognitive aspects, also have a
strong effect on sexual arousal. The cognitive aspects of sexual arousal in men are not
completely known, but it does involve the appraisal and evaluation of the stimulus,
categorization of the stimulus as sexual, and an effective response .Research suggests that
cognitive factors, such as sexual motivation, perceived gender role expectations, and sexual
attitudes, contribute to sex differences observed in subjective sexual arousal. Specifically,
while watching visual stimuli, men are more influenced by the sex of an actor portrayed in
the stimulus, and men typically prefer a stimulus that allows objectification of the actor and
projection of themselves into the scenario. There are reported differences in brain activation
to sexual stimuli, with men showing higher levels of amygdala and hypothalamic responses
than women. This suggests the amygdala plays a critical role in the processing of sexually
arousing visual stimuli in men].This whole process leads to PENILE ERECTION
PENILE ERECTION
Penile erection is a complex physiologic process that occurs through a coordinated cascade of
neurologic, vascular, and humoral events.
Erection, also called Penile Erection, enlargement, hardening, and elevation of the male
reproductive organ, the penis. From an anatomic standpoint, the penis is highly vascular, invested
with a rich supply of smooth muscle erectile tissue, and harbors numerous sinusoids, all of which
rende
r it well suited to accommodate the enhanced perfusion of the penis
underlying physiologic erection.
Internally, the penis has three long masses of cylindrical tissue, known as erectile tissue, that are
bound together by fibrous tissue. The two identical areas running along the sides of the penis are
termed corpora cavernosa; the third mass, known as the corpus spongiosum, lies below the
corpora cavernosa, surrounds the urethra—(a tube that transports either urine or semen),—and
extends forward to form the tip (or glans) of the penis. All three masses are spongelike; they
contain large spaces between loose networks of tissue. When the penis is in a flaccid, or resting,
state, the spaces are collapsed and the tissue is condensed. During erection, blood flows into the
spaces, causing distention and elevation of the penis. The amount of blood entering the penis can
be increased by physical or psychological stimulation. As blood enters, there is a temporary
reduction in the rate and volume of blood leaving the penis. The arteries carrying blood to the
penis dilate; this, in turn, causes tissue expansion. The veins leading from the penis have funnelshaped valves that reduce the outflow of blood. As the erectile tissue begins to enlarge, the
additional pressure causes the veins to be squeezed against the surrounding fibrous tissue, and this
further diminishes the outflow of blood. Essentially, blood becomes temporarily trapped in the
organ.
The corpus spongiosum does not become as erect as the corpora cavernosa. The veins are more
peripherally located, so that there is a continual outflow of blood in this region. This constant
circulation prevents the urethra from being collapsed by the adjacent tissue, which would prevent
release of the semen.
The penis returns to its flaccid state when the arteries relax and begin to contract. Blood flow is
once again reduced to its usual rate and volume. As blood drains from the erectile tissue spaces,
pressure is reduced on the veins, and flow continues at its normal pace.
Within the penis, erection begins with vasodilatation of the cavernous artery and helicine
arterioles in association with relaxation of the trabecular erectile tissue. These actions cause
engorgement of blood in the sinusoidal spaces of the corpora cavernosa and spongiosum, and
penile erection results. The expansion of penile blood volume leads to compression of subtunical
venules by the resistant fibrous outer covering, the tunica albuginea, with occlusion of venous
outflow and physiologic erection.
Voluntary or reflexogenic contraction of the ischiocavernous and bulbocavernous musculature
contributes to the increase in intracavernosal pressure, which may reach or exceed mean arterial
pressure.
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 NOdependent 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. 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.
Physiology of Sexual Response And Coitus
The physiology of arousal in the male is elicited in numerous ways. The neurological
mechanisms are what we have an interest in for this course. Sensory organs detect anal
stimulation, skin stimulation, perineal stimulation as well as friction on the glans penis. All of
these sensations are transmitted via the pudendal nerve to the sacral plexus. In addition, an
inflamed/irritated urethra, bladder, prostate, seminal vesicles, testes and/or vas deferens
drives transmissions to the sacral plexus. Likewise, the male's sexual drive causes sexual
organs to overfill causing increased secretions and vasocongestion. These signals are also
transmitted to the sacral plexus. Signals from the sacral plexus travel two directions: 1) back
to the penis, causing the penile arterial pressure to increase and blocking venous sinusoidal
drainage and 2) to an "uncharted" region of the cerebrum. The bottom line is that these
signals all "cause" sexual sensation.
The physiology of arousal in the female is elicited in numerous ways. The neurological
mechanisms are what we have an interest in for this course. Sensory organs detect anal
stimulation, groin stimulation, perineal stimulation as well as friction on the glans clitoris and
labia or in the labial groove. All of these sensations are transmitted via the pudendal nerve to
the sacral plexus. In addition, an inflamed/irritated urethra or bladder drives transmissions to
the sacral plexus. Likewise, the female's sexual drive causes sexual organs to overfill causing
increased secretions and vasocongestion. Furthermore, emotional states, learned behaviors
and blood levels of estrogens, progesterone and corticoids govern the female's sexual drive.
These signals are also transmitted to the sacral plexus. Signals from the sacral plexus travel
two directions: 1) back to the clitoris, causing the clitoral arterial pressure to increase and
blocking venous sinusoidal drainage and 2) to an "uncharted" region of the cerebrum. The
bottom line is that these signals all "cause" sexual sensation. Nipple erection during this stage
is due to small muscle fiber contraction during sexual excitement.
In both sexes, the psyche is important, i.e., thinking, dreaming, fantasizing about things of a
sexual nature enhances the stage of arousal. Ultimately, this all leads to orgasm in the female
and ejaculation in the male (particularly nocturnal emission in the pubescent male).
The physiology of male erection depends upon the degree of sexual stimulation he is
receiving. Erection is caused by parasympathetic impulses from the sacral cord (S2, S3, S4)
to the penis. These same motor nerves innervate the ischiocavernosus and bulbospongiosus
muscles. The result is that penile arterioles dilate and the penile venules constrict. This puts
high-pressure blood flow into the corpus spongiosum and the corpora cavernosa. The penis
becomes erect it is said to be in a state of TUMESCENCE, i.e., a condition of being swollen,
or a swelling. The scrotum also begins to elevate as the penis becomes erect.
The physiology of female erection depends upon the degree of sexual stimulation he is
receiving. Erection is caused by parasympathetic impulses from the sacral cord (S2, S3, S4)
to the clitoris. These same motor nerves innervate the ischiocavernosus muscle. These same
nerves cause the clitoris to retract under the clitoral hood, later. The result is that clitoral
arterioles dilate and the clitoral venules constrict. This puts high-pressure blood flow into the
corpora cavernosa. The clitoris becomes erect it is said to be in a state of TUMESCENCE,
i.e., a condition of being swollen, or a swelling. During tumescence in the female, the
introitus tightens by at least one-third due to venous congestion at the outer third of the
vaginal barrel (location of the corpus spongiosum in the female). The vaginal barrel and labia
minora thicken (called the orgasmic platform) due to VASOCONGESTION. The orgasmic
platform "grips" the penis during intercourse, hence, penile size is only important
psychologically, NOT physiologically. Vasocongestion is one of TWO primary physiological
responses to sexual intercourse in both the male and female. NOTE: vaginal secretions
increase and the uterus "swings" more to a posteroflexed position.
Lubrication in the male is a parasympathetic response. Cowper's glands secrete mucous
through the urethra. This mucous washes out residual urine in the urethra and increases the
pH for the sperm (sperm require an alkaline pH for survival). Cowper's glands are a SMALL
aid to lubrication for coitus as they only secrete 2-3 drops of lubricant. MOST of the
lubrication for coitus is from the female. Without lubrication, the sexual sensations are
decreased and pain is sensed, instead. The scrotum (dartos, cremaster) contracts. The testes
increase about 50% in size (vasocongestion) and elevate more. The penis changes colors due
to vasocongestion from "skin color" to pink to bright/deep red.
Lubrication in the female is a parasympathetic response. Bartholin's glands secrete a slight
amount of mucous. This mucous is NOT the primary mucous for coitus. MOST of the
lubrication for coitus is due to the female's vaginal wall vasocongestion. Lubrication
"squeezes" through the congested wall as a transudate. It provides for lubrication and it
buffers the acidity (with semen) of the vagina for an appropriate sperm environment. It may
be in levels so as to flow from the vagina and introitus moistening all tissues in its path,
including the labia. Without lubrication, sexual sensations are decreased and pain is sensed,
instead. The vagina changes colors due to vasocongestion from "skin color" to pink to
bright/deep red..
Orgasm is the sudden discharge of accumulated sexual tension in a peak of sexual arousal.
Male orgasm, as mentioned, earlier, is a two-staged process. Emission is due to sympathetic
impulses from L1 and L2. They innervate the urethral crest and muscles of the epididymis,
vas deferens, seminal vesicles, prostate and penile shaft (the genital organs). Emission is the
"forerunner" to ejaculation. Epididymal, vas deferens and ampullary contractions expel sperm
to the internal urethra. Contractions of the seminal vesicles and prostate expel fluids and ALL
fluids mix to make semen.
Ejaculation occurs when the internal urethra fills with semen. Signals are sent to the pudendal
nerve via the sacral plexus/cord. Rhythmic nerve impulses are transmitted from L1 and L2.
Once the prostate contracts, ejaculation is inevitable, i.e., nothing will stop ejaculation at this
point, a point of no return. Skeletal perineal muscles at the base of the erectile tissues contract
with wave-like increases in pressure ("squirts"). These spasms number about 4 to 5 in the
prostate, seminal vesicles, vas deferens and urethra at 0.8-second intervals. Accompanying
this are involuntary contractions of the internal and external sphincters. This last 3-15
seconds and is associated with a slight clouding of consciousness. Semen is ejaculated from
the urethra to the exterior. The ejaculatory spurt is about 30-50 cm at 18 YOA and decreases
from there to seepage by about 70 YOA. Muscles relax decreasing vasocongestion. The penis
undergoes detumescence (unswelling) and the genitals disengorge. A sense of relaxation is
felt.
In some instances (multiple sclerosis, diabetes, after some prostate surgeries), a male may
experience retrograde ejaculations, i.e., he may ejaculate into his bladder -- this is due to
destruction of his sphincter vesiculi.
Sympathetic nerves drive the female orgasm, as well. OT is secreted during orgasm in both
sexes (causes uterus to contract in female and prostate in male). Perineal muscles contract
giving 3-15 rhythmic spasms of the lower third of the vagina and uterus (from the fundus to
the cervix). It is also known that the cervix "dips" down towards the vagina during orgasm
associated with a decrease in pressure in the vagina. It is thought that this facilitates sperm
movement into the uterus (if semen is present, of course). Involuntary spasms of both anal
sphincters occur as well. Contractions/spasms occur at 0.8-second intervals for 3-15 seconds.
Orgasm in females is also accompanied by a slight clouding of consciousness, a sense of
satisfaction, peace and relaxation. Orgasm increases uterine and fallopian tube motility to
increase chances of fertilization -- may be due to an increased rate of sperm transport.
Orgasm is analogous to ejaculation in the male. The clitoris and vaginal barrel undergo
detumescence just as the penis and testes. Ejaculatory inevitability does NOT happen in
women, i.e., a female's orgasm can be stopped at any time.
MYOTONIA is the second of the two primary physiological responses to sexual intercourse.
It is a temporary rigidity after muscular contraction just before and peri-orgasm. BP also
rises, as does the respiratory rate.
In both sexes, detumescence is rapid. It is described as a "sense of well being" for both sexes.
In males, there is a refractory period that may run from minutes to hours with no further
erection/orgasm. This increases as the male ages. In females, a refractory period does NOT
exist. A female is capable of having multiple and successive orgasms with appropriate
stimulation.
In the male, detumescence occurs in two phases: 1) partial disengorgement occurs due to
contractions of orgasm (pumps blood out of erectile/genital tissues) and 2) a slower phase
where genital blood flow returns to levels at the pre-arousal state.
In the female, the orgasmic platform disappears with orgasm (contractions "pump" blood
away from the genitals). The uterus "re-depresses" and "drops" the cervix into seminal pool -see above graphic. The labia change colors back to normal and the vaginal length and width
decreases. The clitoris disengorges and emerges from the hood. Stimulation of the genitals
and breasts MAY be unpleasant post-orgasm.
If vasocongestion is not relieved in the male, PARTICULARLY if very high levels of
arousal were reached, he may experience testicular aching and swelling of the vas deferens
("blue balls"). If vasocongestion does not occur in women, this leads to pelvic congestion and
breast congestion with a secondary increase in size.
Patterns of Sexual Response
In adults, sexual response follows generally predictable patterns that have been documented
by a number of researchers. However, there is some variation in the ways in which these
patterns have been formalized. In this module, we will describe the sexual response cycle in
five key stages, on the basis of a combination of models.
Although both men and women experience the same general stages of response, the amount
of time needed to achieve each stage and the progression between stages may vary. In
addition, psychological and emotional responses may vary greatly from person to person.
Progression from one stage to the next is not inevitable: several of the stages can be achieved,
lost, and regained many times without progression. The next page describes the five-stage
sexual response cycle and examines each stage in more detail.
The Sexual Response Cycle
There are five main stages to the sexual response cycle:
1. Desire (also called libido). This stage, in which a man or woman begins to want or
"desire" sexual intimacy or gratification, may last anywhere from a moment to many
years.
2. Excitement (also called arousal). This stage, which is characterized by the body’s
initial response to feelings of sexual desire, may last from minutes to several hours.
3. Plateau. This stage, the highest point of sexual excitement, generally lasts between 30
seconds and three minutes.
4. Orgasm. This stage, the peak of the plateau stage and the point at which sexual
tension is released, generally lasts for less than a minute.
5. Resolution. The duration of this stage—the period during which the body returns to
its preexcitement state—varies greatly and generally increases with age.
Comparison of Sexual Response in Women and Men
Body changes
Phase
Both Sexes
Women
Men
Desire
(Duration:
anywhere
from a
moment to
many
years)
Not applicable
Not applicable
Not applicable
Excitement
(Duration:
anywhere
from a few
minutes to
several
hours)
Heart rate and
blood pressure
increase, body
muscles tense,
sexual flush
occurs,
nipples
become erect,
genital and
pelvic blood
vessels
become
engorged, and
involuntary
and voluntary
muscles
contract.
The vagina
lengthens and
widens, the clitoris
swells and enlarges,
breasts increase in
size, the labia swell
and separate, the
vagina becomes
lubricated, and the
uterus rises slightly.
Vaginal lubrication
is the key indicator
of sexual
excitement.
The penis becomes erect,
the scrotum thickens,
and the testes rise closer
to the body. Erection of
the penis is the key
indicator of sexual
excitement.
Breathing
rate, heart
rate, and
blood pressure
further
increase,
sexual flush
deepens, and
muscle
tension
increases.
There is a
sense of
impending
orgasm.
The clitoris
withdraws, the
Bartholin’s glands
lubricate, the
areolae around
nipples become
larger, the labia
continue to swell,
the uterus tips to
stand high in the
abdomen, and the
“orgasmic platform”
develops (the lower
vagina swells,
narrows, and
Plateau
(Duration:
between 30
seconds
and 3
minutes)
Note: Men generally
reach this stage faster
stage than women do.
Note: Women
generally reach this
stage more slowly
than men do.
The ridge of the glans
penis becomes more
prominent, the Cowper’s
glands secrete
preejaculatory fluid, and
the testes rise closer to
the body.
tightens).
Orgasm
(Duration:
less than 1
minute)
Resolution
(Duration:
varies
greatly)
Heart rate,
breathing, and
blood pressure
reach their
peak, sexual
flush spreads
over the body,
and there is a
loss of muscle
control
(spasms).
The uterus, vagina,
anus, and muscles
of the pelvic floor
contract 5 to 12
times at 0.8-second
intervals.
Heart rate and
blood pressure
dip below
normal,
returning to
normal soon
afterward; the
whole body,
including the
palms of
hands and
soles of feet,
sweats; there
is a loss of
muscle
tension,
increased
relaxation,
and
drowsiness.
Blood vessels dilate
to drain the pelvic
tissues and decrease
engorgement; the
breasts and areolae
decrease in size;
nipples lose their
erection; the clitoris
resumes its
prearousal position
and shrinks slightly;
the labia return to
normal size and
position; the vagina
relaxes; the cervix
opens to help semen
travel up into the
uterus—closing 20–
30 minutes after
orgasm; and the
uterus lowers into
the upper vagina
(location of semen
after male orgasm
during penile–
vaginal intercourse).
Note: Women can
have orgasm, move
back into plateau
stage, and achieve
another orgasm
(called “multiple
orgasms”).
Ejaculation occurs
(contractions of the
ejaculatory duct in the
prostate gland cause
semen to be ejected
through the urethra and
penis), and the urethra,
anus, and muscles of
pelvic floor contract 3 to
6 times at 0.8-second
intervals.
Nipples lose their
erection; the penis
becomes softer and
smaller; the scrotum
relaxes, and the testes
drop farther away from
the body. Depending on
a number of factors
(including age), the
refractory period in men,
during which erection
cannot be achieved, may
last anywhere from 5
minutes to 24 hours or
more.
Special Notes:

Penetration is not necessary for sexual gratification to occur. Sexual
stimulation and orgasm can take place for both sexual partners without
penetration.


Completing the five phases of the sexual response cycle is not necessary
for sexual fulfillment.
Orgasm may vary in intensity from one person to another. For some, it
may involve intense spasm and loss of awareness; for others, it may be
signaled by as little as a sigh or subtle relaxation.
The Stages of Sexual Response
STAGE 1: Desire
Our minds and bodies can respond sexually to a variety of stimuli—including sight, sound,
smell, touch, taste, movement, fantasy, and memory. These stimuli can create sexual
desire—a strong wanting for sexual stimulation (either by oneself or with another person) or
sexual intimacy that may cause one to seek sexual satisfaction. Societal and cultural values
influence the range of stimuli that provoke sexual desire, and ideals about the stimuli
considered “sexual” or “attractive” can vary greatly between cultures and among subsets of a
single culture. In addition, each individual reacts to sets of stimuli that are idiosyncratic—
based on his or her own thoughts, feelings, and experiences.
Indications of Desire. Desire is a prelude to sexual excitement and sexual activity—it occurs
in the mind rather than the body and may not progress to sexual excitement without further
physical or mental stimulation. Desire may be communicated between potential sexual
partners either verbally or through body language and behavior (for example, through
“flirting”). This communication, which is shaped by sociocultural factors, may be subtle and
easily misread. In different cultures, behaviors meant to communicate desire may vary greatly
along gender lines; for example, in some cultures, women are expected not to express overt,
verbal communication of their sexual desire, whereas such communication from men is
expected.
STAGE 2: Excitement (arousal)
Excitement is the body’s physical response to desire. (A person who manifests the physical
indications of excitement is termed to be “aroused” or “excited.”) The progression from
desire to excitement depends on a wide variety of factors—it may be brought on by sensory
stimulation, thoughts, fantasy, or even the suggestion that desire may be reciprocated. For
some persons (particularly for some adolescents), the excitement stage may be achieved with
very little physical or mental stimulation, whereas for others, significant intimacy, physical
stimulation, or fantasy may be required. It generally takes longer for women to achieve full
arousal than for men to do so. Excitement may lead to intimacy and sexual activity, but this is
not inevitable: for both sexes, initial physical excitement may be lost and regained many
times without progression to the next stage.
Indications of Excitement. Excitement can be communicated between partners verbally,
through body language, through behavior, or through any of the following body changes:


For both sexes: Heart rate and blood pressure increase, body muscles tense, sexual
flush occurs, nipples become erect, genital and pelvic blood vessels become engorged,
and involuntary and voluntary muscles contract.
For women: The vagina lengthens and widens, the clitoris swells and enlarges,
breasts increase in size, the labia swell and separate, the vagina becomes lubricated,

and the uterus rises slightly. Vaginal lubrication is the key indicator of sexual
excitement.
For men: The penis becomes erect, the scrotum thickens, and the testes rise closer to
the body. Erection of the penis is the key indicator of sexual excitement.
STAGE 3: Plateau
If physical or mental stimulation (especially stroking and rubbing of erogenous zones or
sexual intercourse) continues during full arousal, the plateau stage may be achieved. This
stage, the highest moment of sexual excitement before orgasm, may be achieved, lost, and
regained several times without the occurrence of orgasm.
Indications of the Plateau Stage. The plateau stage can be communicated between partners
verbally, through body language, through behavior, or through any of the following
physiological changes:



For both sexes: Breathing rate, heart rate, and blood pressure further increase, sexual
flush deepens, and muscle tension increases. There is a sense of impending orgasm.
For women: The clitoris withdraws, the Bartholin’s glands lubricate, the areolae
around the nipples become larger, the labia continue to swell, the uterus tips to stand
high in the abdomen, and the “orgasmic platform” develops (that is, the lower vagina
swells, narrows, and tightens).
For men: The ridge of the glans penis becomes more prominent, the Cowper’s glands
secrete preejaculatory fluid, and the testes rise closer to the body.
STAGE 4: Orgasm
Orgasm occurs at the peak of the plateau phase. At the moment of orgasm, the sexual tension
that has been building throughout the body is released, and the body releases chemicals called
endorphins, which cause a sense of well-being. Orgasm can be achieved through mental
stimulation and fantasy alone, but more commonly is a result of direct physical stimulation or
sexual intercourse (although many women report difficulty in achieving orgasm through
vaginal intercourse alone). Women are capable of multiple orgasms (moving immediately
from orgasm back into the plateau stage and to orgasm again), whereas men must pass
through the resolution stage before another orgasm can be achieved.
Indications of Orgasm. The intensity of orgasm can vary among individuals and can vary
for an individual from one sexual experience to another. Orgasm may involve intense spasm
and loss of awareness, or it may be signaled by as little as a sigh or subtle relaxation. Orgasm
can be communicated between partners verbally, through body language, through behavior,
or through any of the following physiological changes:



For both sexes: Heart rate, breathing, and blood pressure reach their highest peak,
sexual flush spreads over the body, and there is a loss of muscle control (spasms).
For women: The uterus, vagina, anus, and muscles of the pelvic floor contract five to
12 times at 0.8-second intervals.
For men: Ejaculation (contractions of the ejaculatory duct in the prostate gland cause
semen to be ejected through the urethra and penis) occurs, and the urethra, anus, and
muscles of the pelvic floor contract three to six times at 0.8-second intervals.
STAGE 5: Resolution
Resolution is the period following orgasm, during which muscles relax and the body begins
to return to its preexcitement state. Immediately following orgasm, men experience a
refractory period, during which erection cannot be achieved (the duration of this period varies
among individuals and increases with age). Women experience no refractory period—they
can either enter the resolution stage or return to the excitement or plateau stage immediately
following orgasm.
Indications of Resolution. Resolution can be communicated between partners verbally,
through body language, through behavior, or through any of the following body changes:



For both sexes: Heart rate and blood pressure dip below normal, returning to normal
soon afterward; the whole body (including the palms of hands and soles of feet)
sweats; there is a loss of muscle tension, increased relaxation, and drowsiness.
For women: Blood vessels dilate to drain the pelvic tissues and decrease
engorgement; the breasts and areolae decrease in size; nipples lose their erection; the
clitoris resumes its prearousal position and shrinks slightly; the labia return to normal
size and position; the vagina relaxes; the cervix opens to help semen travel up into the
uterus (closing 20–30 minutes after orgasm); and the uterus lowers into the upper
vagina (location of semen after male orgasm during penile-vaginal intercourse).
For men: Nipples lose their erection; the penis lightens in color and becomes softer
and smaller; the scrotum relaxes, and the testes drop farther away from the body.
Depending on a number of factors (including age), the refractory period in men may
last anywhere from five minutes to 24 hours or more.
The Effect of Diseases and Drugs on Sexual Response
Short- and long-term use of recreational drugs (such as alcohol, marijuana, cocaine,
amphetamines, and psychotropic drugs) can affect sexual function. For example, alcohol use
can inhibit sexual function in both the short and the long run. Amphetamines can enhance
sexual desire initially, but long-term use can lead to sexual dysfunction.
Chronic and debilitating diseases can also affect sexual desire and function. The medications
used to manage many chronic conditions can also affect sexual response and performance;
however, it is not always possible to predict which clients will experience these effects before
the medication is prescribed.
The effect of drugs on sexual function is often underemphasized by health care providers and
medical researchers, and there has been significantly more research into the effects of drugs
on sexual function in men than in women. Providers rarely mention the sexual side effects of
the drugs that they prescribe, sometimes out of the fear that clients will be reluctant to take
the medications if they know about the sexual side effects in advance. There are a number of
ways that medicines can interfere with sexual function or satisfaction. Some drugs cause
drowsiness, lethargy, or depression; others interfere with the chemical messengers of the
brain that are critical for sexual interest and function. Some drugs interfere with the ability to
achieve orgasm, while others delay or prevent ejaculation.
APPLIED PHYSIOLOGY
Drugs That Affect Sexual Function
There are number of ways that medications can interfere with sexual function and
satisfaction. The following list, while not exhaustive, includes commonly prescribed drugs
that have been implicated as affecting sexual functioning:
Note: Tranquilizers (such as Valium and Librium) and alcohol may increase sexual desire
among inhibited individuals, but diminish both arousal and orgasm.
Antihypertensive drugs (drugs used to treat high blood pressure)








Thiazide diuretics-blockers (Propranol, Atenolol, Pindolol)
Clonidine
Guanethidine
Alpha methyldopa
Prozasin
Hydralazine
Reserpine
Spironolactone
Psychoactive agents (drugs used to treat depression, anxiety, insomnia, and other
psychological conditions)






Tricyclic antidepressants
Imipramine
Doxepin
Amitryptyline
Major tranquilizers (Chlorpromazine, Butyrophenone, Prochlorperazine, Perpheasine,
Trifluoperazine, Thioridazine)
Monoamine oxidase inhibitors (Pargyline, Phenelzine)
Other drugs









Digoxin
Cimetidine
Clofibrate
Blofibrate
Drugs used in cancer chemotherapy
Acetazolamide
Heparin
Estrogen
Anorectic agents
The following list, while not comprehensive, describes common conditions that affect sexual
function. Other conditions that affect sexual function include cancer, thyroid disorder,
Parkinson’s disease, chronic obstructive pulmonary disease, malnutrition, and alcoholism.
What Is “Sexual Dysfunction”?
Sexual dysfunction is the persistent or recurrent inability to react emotionally or physically
to sexual stimulation in a way expected of the average healthy person or according to one’s
own standards of acceptable sexual response. Sexual dysfunction can occur during the desire,
excitement, plateau, or orgasm stage of the sexual response cycle.
For example, one of the most common dysfunctions is inhibited arousal during the
excitement stage. This presents as erectile dysfunction (impotence) in men or lack of
lubrication in women. Occasional inhibited arousal is common and not dysfunctional;
however, chronic inhibited arousal is a sexual dysfunction that can be caused by recreational
drug use, certain medications, certain diseases, physical damage, or psychological factors.
Any of the following factors can contribute to sexual dysfunction:




Psychological/emotional factors, including stress, negative body image, performance
anxiety, expectation of failure, fear of pregnancy, memory of negative sexual
experiences, and fear of acquiring or transmitting a sexually transmitted disease
Biological/physiological factors, including changes related to aging, certain medical
conditions (arthritis, reproductive cancers, diabetes, cardiac disease, hypertension),
physical injury (such as spinal cord injuries), the effects of hormonal contraceptive
methods, pregnancy, and substance abuse
Interpersonal/social factors, including peer pressure, poor communication with a
partner, sexual abuse, attitudes toward sexual orientation, uncertainty of how to
behave, and conflicts with one’s partner
Environmental factors, including cultural influences, gender dynamics, availability
of partners (partner ratio), and physical setting (lack of privacy)
Common Sexual Dysfunctions
In diagnosis and history taking, it is important to remember that each dysfunction covered in
this lecture can be lifelong (has always been present), acquired (has not always been
present), situational (occurs in some situations and not others), or generalized (occurs
regardless of the situation). The following list, while far from exhaustive, describes common
sexual dysfunctions, their possible causes, and treatments.
Note: Sexual dysfunctions should be assessed objectively and managed according to the
cause—not according to the status, orientation, or age of the affected client. The range of
dysfunction encountered among adolescents, older clients, unmarried adults, homosexuals,
and bisexuals is the same as that found among married heterosexual adults of reproductive
age. If you feel unable to provide professional, impartial services to particular clients, refer
the clients to another provider, if possible.
Inhibited sexual desire (ISD) (frigidity)
Sexual desire changes over the course of our lives, and occasional loss of desire in either sex
is not uncommon. In ISD, however, there is persistent loss of desire that disrupts sexual
relationships. It is characterized by diminished sexual attraction, decreased sexual activity,
few or no sexual dreams or fantasies, and diminished attention to erotic material by one or
both partners. ISD is the most common presenting sexual dysfunction in women and is less
commonly reported in men. Female sexual arousal disorder (FSAD) is the name for
persistent or recurrent inability to achieve or maintain an adequate lubrication-swelling
response. (A woman with FSAD may or may not find enjoyment in physical contact.)
Causes of ISD:



Contributing factors to ISD include hormone deficiencies, depression, alcoholism,
liver or kidney disease, and chronic illness, as well as the side effects of drugs (e.g.,
antihypertensives and antidepressants). Psychological contributing factors include
stress, relationship problems, sexual trauma, major life changes, and the pairing of
negative memories with sexual interactions.
In women. Testosterone plays a vital role in women’s sexual desire. Reduction in
testosterone (e.g., due to removal of ovaries, chemotherapy, menopause) can be
treated through supplementation of the hormone. Life events affecting hormonal
patterns (though not fully understood) include premenstrual tension, childbirth,
pregnancy, and menopause.
In men. Sexual desire in men can be inhibited by many physical and psychological
factors. In the presence of testosterone deficiency, signs and symptoms include loss of
facial and body hair, decrease in lean muscle mass, fatigue, loss of energy or lethargy,
and erectile dysfunction (ED).
Treatment of ISD:


ISD can be difficult to treat. Replacement therapy is indicated if testosterone
deficiency is the cause of ISD. Determine if there are any relationship, situational, or
physical or psychological issues that may be contributing to the loss of desire. (If the
cause is psychological, most studies of outcome indicate that response to
psychological interventions for ISD is very poor.)
Treat or refer the client to a sex therapist, urologist, or other appropriate specialist on
the basis of the underlying cause, if possible.


Premature ejaculation (PE)
Premature ejaculation is a condition in men characterized by persistent or recurrent
ejaculation with minimal sexual stimulation before, on, or shortly after penetration and before
the person wishes it. PE occurs when a man is unable to exert reasonable voluntary control of
his ejaculatory response and is unaware of erotic sensations leading to the “point of
inevitability” and ejaculation. PE is most common among younger men and men with limited
sexual experience. The condition is often associated with performance anxiety.
Causes of PE:


Causes are rarely physical. Some infections of the urethra and prostate, neglected
gonorrhea, and overly tight foreskin have been considered as possible physical causes.
More commonly, the affected man has not learned to recognize the sensory feedback
that indicates ejaculation is imminent. This is common among men who have taught
themselves to ignore this sensory feedback and “think of other things” as a means of
avoiding ejaculation before they are satisfied or before their partner is satisfied.
Treatment of PE:



Interventions may include psychological approaches aimed at reducing anxiety,
special techniques to improve ejaculatory control (such as the “pause and squeeze”
technique), and drug therapy with the use of formulations that delay ejaculation,
thereby improving sexual satisfaction in the client and his partner.
Refer the client to a sex therapist, psychologist, or urologist, if possible.
Male orgasmic disorder
Male orgasmic disorder is persistent or recurrent involuntary delay in orgasm and ejaculation
or the inability of the man to have orgasm. (Note: This is sometimes confused with retrograde
ejaculation—a condition in which the man ejaculates into his bladder instead of out through
the urethra. Retrograde ejaculation is common in gay men and may be related to fears of
infection believed to be brought on by “safer sex” campaigns.)
Causes and treatment of male orgasmic disorder:



The cause is rarely physical and rather is associated with a traumatic sexual
experience, strict religious upbringing, hostility, overcontrol, or lack of trust.
Psychological exploration and counseling is the indicated treatment.
Erectile dysfunction (ED)
ED (also known as impotence) is the persistent or recurrent inability in men to attain an
erection or to maintain an erection until completion of sexual activity. (Note: Occasional
inability to achieve erection may cause undue stress and result in performance anxiety, which
affects future functioning and creates a cycle of impotence. Occasional impotence is
common; this is usually situational and is not considered dysfunctional.) Erectile dysfunction,
usually of an organic type, is being seen increasingly in those with late stage HIV. It is not
yet clear whether ED is an effect of the virus or of the antiviral drugs used to treat infection.
Causes of ED:



Drugs, alcohol, diabetes, Parkinson’s disease, multiple sclerosis, HIV, other diseases,
and spinal cord lesions can cause ED.
Approximately one-third of cases are psychological, one-third physical, and the
remaining third have a mix of both causes.
Performance anxiety is often associated with ED.
Treatment of ED:


Where possible, refer the client to a sex therapist, psychologist, or urologist. As part
of treatment, both partners should be counseled about the risks involved in some
treatment approaches.
Approaches to treatment depend on the cause of the dysfunction and commonly
include intracavernosal injection (with Papaverine, Alprostadil, Vasoactive intestinal
polypeptide, or combinations of these); intraurethral pellets (prostaglandin); oral
medications (Yohimbine, Sildenafil [Viagra]); hormonal treatment (testosterone, in
the presence of low levels); surgical interventions; and psychological therapy.


One approach to ED includes the use of vacuum devices (manual or battery operated)
that involve placing the penis is a plastic tube with suction, thus drawing venous
blood into the penis to create an erection. Once the penis is erect, a rubber constriction
ring is placed at the base of the penis to prevent the erection from being lost, thus
allowing sexual intercourse. However, tissue damage may result using this method if
the erection is maintained for more than 30 minutes.
Surgical interventions for the insertion of an inflatable penile prosthetic can allow
erection sufficient for sexual intercourse. These prostheses are used with men who
have had pelvic surgery, diabetes, or atherosclerosis; they can also be used for
conditions such as Peyronie’s disease (which is characterized by a hard fibrous
formation in the penile tissue layer causing curvature of the penis on erection and
sometimes pain, making sexual intercourse difficult or impossible). Risks associated
with the surgical procedure include infection, trauma to the urethra, compression or
damage to the blood vessels in the penis, and drooping of the glans.
Contributing Factors
Infertility
Infertility may be a contributing cause of sexual dysfunction. For example, sexual function
may be affected by infertility when investigations and treatments alter a couple’s mode of
sexual relations. Alternatively, a man may feel excessive pressure to perform, which
negatively affects his erectile or ejaculatory ability when the couple tries to conceive.
Both men and women can develop arousal difficulties because of the associated anxiety and
stress of performing. In addition, some partners may feel their self-worth compromised by
being sought only when conception is more likely. These stresses usually diminish the
pleasurable aspect of sexual expression and focus sex solely on reproduction. Erectile failure
during sexual intercourse due to pressure to perform may begin a vicious cycle of fear of
failure, with anxiety leading to further failures. Consequently, men may experience loss of
desire and decreased sexual activity, erectile problems, premature ejaculation, or delayed
ejaculation. Women may experience loss of desire, vaginismus, dyspareunia, or anorgasmia.
When clients first present with infertility, providers should investigate the possibility of
retrograde ejaculation (ejaculation into the male urinary bladder), as well as the possibility
that the client does not fully understand reproductive functioning and is engaging in sexual
activities that are not associated with pregnancy—for example, deposit of sperm into
locations other than the vagina (e.g., rectum).