How to Treatment of male sexual dysfunction. Causes of ERECTILE DYSFUNCTION.

male sexual dysfunction and erectile dysfunction this post are very important for male sexual Disease.and how to Treatment of erectile dysfunction.

Normal male sexual function requires (1) an intact libido, (2) the
ability to achieve and maintain penile erection, (3) ejaculation, and
(4) detumescence.

Libido refers to sexual desire and is influenced by a
variety of visual, olfactory, tactile, auditory, imaginative, and hormonal
Sex steroids, particularly testosterone, act to increase libido.
Libido can be diminished by hormonal or psychiatric disorders and
by medications.


Epidemiology Erectile dysfunction (ED) is not considered a nor-
mal part of the aging process. Nonetheless, it is associated with certain
physiologic and psychological changes related to age.

In the Massachu-
setts Male Aging Study (MMAS), a community-based survey of men
aged 40–70, 52% of responders reported some degree of ED. Complete
ED occurred in 10% of respondents, moderate ED in 25%, and minimal
ED in 17%. The incidence of moderate or severe ED more than doubled
between the ages of 40 and 70..

2)Pathophysiology ED may result from three basic mechanisms:
(1) failure to initiate (psychogenic, endocrinologic, or neurogenic),
(2) failure to fill (arteriogenic), and (3) failure to store adequate blood
volume within the lacunar network (venoocclusive
dysfunction). These
categories are not mutually exclusive, and multiple factors contribute
to ED in many patients.

3)Vasculogenic The most common organic cause of ED is a distur-
bance of blood flow to and from the penis.
Atherosclerotic or traumatic
arterial disease can decrease flow to the lacunar spaces, resulting in

decreased rigidity and an increased time to full erection. Excessive
outflow through the veins despite adequate inflow also may contrib-
ute to ED.

4)Neurogenic Disorders that affect the sacral spinal cord or the
autonomic fibers to the penis
preclude nervous system relaxation of
penile smooth muscle, thus leading to ED. In patients with spinal cord
injury, the degree of ED depends on the completeness and level of the
lesion. Patients with incomplete lesions or injuries to the upper part
of the spinal cord are more likely to retain erectile capabilities than
are those with complete lesions or injuries to the
lower part.

5)Endocrinologic Androgens increase libido, but their exact role
in erectile function is unclear.
Individuals with castrate levels of
testosterone can achieve erections from visual or sexual stimuli.
Nonetheless, normal levels of testosterone appear to be important for
erectile function, particularly in older males…

6)Diabetic ED occurs in 35–75% of men with diabetes mellitus.
Pathologic mechanisms are related primarily to diabetes-associated
vascular and neurologic complications. Diabetic macrovascular com-
plications are related mainly to age, whereas microvascular complica-
tions correlate with the duration of diabetes and the degree of glycemic

7)Psychogenic Two mechanisms contribute to the inhibition of
erections in psychogenic ED
. First, psychogenic stimuli to the sacral
cord may inhibit reflexogenic responses, thereby blocking activation
of vasodilator outflow to the penis. Second, excess sympathetic stim-
ulation in an anxious man may increase penile smooth-muscle tone.
The most common causes of psychogenic ED are performance anxiety,
depression, relationship conflict, loss of attraction, sexual inhibition,
conflicts over sexual preference, sexual abuse..

8)Medication-Related Medication-induced ED is esti-
mated to occur in 25% of men seen in general medical outpatient clin-
ics. The adverse effects related to drug therapy are additive, especially
in older men. In addition to the drug itself, the underlying disease
being treated is likely to contribute to sexual dysfunction. Among
the antihypertensive agents, the thiazide diuretics and beta blockers
have been implicated most frequently. Calcium channel blockers and
angiotensin converting-enzyme inhibitors are cited less frequently.


Male Sexual Dysfunction

Patient and partner education is essential in the treatment of ED.
In goal-directed therapy, education facilitates understanding of.

the disease, the results of the tests, and the selection of treatment.
Discussion of treatment options helps clarify how treatment is best
offered and stratify first- and second-line therapies.

Patients with
high-risk lifestyle issues such as obesity, smoking, alcohol abuse,
and recreational drug use should be counseled on the role those
factors play in the development of ED.

Therapies currently employed for the treatment of ED include
oral phosphodiesterase type 5 inhibitor therapy (most commonly
used), injection therapies, testosterone therapy, penile devices, and
psychological therapy.

In addition, limited data suggest that treat-
ments for underlying risk factors and comorbidities—for example,
weight loss, exercise, stress reduction, and smoking cessation—may
improve erectile function. Decisions regarding therapy should take
into account the preferences and expectations of patients and their

Sildenafil, tadalafil, vardenafil, and avanafil are the only approved
and effective oral agents for the treatment of ED.

These four med-
ications have markedly improved the management of ED because
they are effective for the treatment of a broad range of causes, includ-
ing psychogenic, diabetic, vasculogenic, post-radical prostatectomy
(nerve-sparing procedures), and spinal cord injury

They belong to a
class of medications that are selective and potent inhibitors of PDE-5,
the predominant phosphodiesterase isoform found in the penis. They
are administered in graduated doses and enhance erections after
sexual stimulation The onset of action is ~30–120 min,

depending on the medication used and other factors, such as recent
food intake. Reduced initial doses should be considered for patients
who are elderly, are taking concomitant alpha blockers, have renal
insufficiency, or are taking medications that inhibit the CYP3A4
metabolic pathway in the liver (e.g., erythromycin, cimetidine, keto-
conazole, and possibly itraconazole and mibefradil), as they may
increase the serum concentration of the PDE-5 inhibitors (PDE-5i) or
promote hypotension.

Initially there were concerns about the cardiovascular safety of
these drugs. It is known that these agents can act as mild vasodila-
tors and warnings exist about orthostatic hypotension with concom-
itant use of alpha blockers.

The use of PDE5i is not contraindicated
in men who are also receiving alpha blockers, but they must be sta-
bilized on this blood pressure medication prior to initiating therapy.
Earlier concerns that the use of PDE5i would increase cardiovascular
events have been mitigated by the results of several controlled trials
showing no increase in myocardial ischemic events or overall mor-
tality compared to the general population.

Several randomized trials have demonstrated the efficacy of this
class of medications. There are no compelling data to support the
superiority of one PDE-5i over another. Subtle differences between
agents have variable clinical relevance ..
Patients may fail to respond to a PDE-5i for several reasons
Some patients may not tolerate PDE-5i secondary to
adverse events from vasodilation in nonpenile tissues expressing
PDE-5 or from the inhibition of homologous nonpenile isozymes
(i.e., PDE-6 found in the retina).

Abnormal vision attributed to the
effects of PDE-5i on retinal PDE-6 is of short duration, reported only
with sildenafil and not thought to be clinically significant. A more
serious concern is the possibility that PDE-5i may cause nonarteritic
anterior ischemic optic neuropathy (NAION); although data to
support that association are limited, it is prudent to avoid
the use
of these agents in men with a prior history of nonarteritic anterior
ischemic optic neuropathy.

Testosterone supplementation combined with a PDE-5i may be
beneficial in improving erectile function in hypogonadal men with
ED who are unresponsive to PDE-5i alone. These drugs do not affect
ejaculation, orgasm, or sexual drive. Side effects associated with
PDE-5i include headaches (19%), facial flushing (9%), dyspepsia
(6%), and nasal congestion (4%).

Approximately 7% of men using
sildenafil may experience transient altered color vision (blue halo
effect), and 6% of men taking tadalafil may experience loin pain.
PDE-5i is contraindicated in men receiving nitrate therapy for
cardiovascular disease, including agents delivered by the oral, sub-
lingual, transnasal, and topical routes.

These agents can potentiate
its hypotensive effect and may result in profound shock. Likewise,
amyl/butyl nitrate “poppers” may have a fatal synergistic effect
on blood pressure. PDE-5i also should be avoided in patients with
congestive heart failure and cardiomyopathy because of the risk
of vascular collapse. Because sexual activity leads to an increase in

Sildenafil Tmax 30–120 min
Duration 4 h
High-fat meal decreases absorption.
Alcohol use may affect efficacy.
2–5 h 25–100 mg
Starting dose 50 mg
Headache, flushing,
dyspepsia, nasal
congestion, altered vision
Cardiovascular risk factors
Retinitis pigmentosa
Change dose with some antiretrovirals
Should be on stable dose of alpha
Vardenafil Tmax 30–120 min
Duration 4–5 h
High-fat meal decreases absorption.
ETOH may affect efficacy.
4.5 h 5–10 mg Headache, flushing,
rhinitis, dyspepsia
Same as sildenafil
May have minor prolongation of QT
Concomitant use of Class I
Tadalafil Tmax 30–60 min
Duration 12–36 h
Plasma concentration not affected by food
10 mg, 20 mg;
2.5 or 5 mg for daily
Headache, dyspepsia,
backpain, nasal
congestion, myalgia
Same as sildenafil
Avanafil Tmax 30 min
Duration 2 h
Plasma concentration not affected by food
50 mg 100 mg and
200 mg dose
Headache, flushing,
nasal congestion
nasopharyngitis back
Same as sildenafil

physiologic expenditure [5–6 metabolic equivalent tasks (METs)], 2821
physicians have been advised to exercise caution in prescribing any
drug for sexual activity to those with active coronary disease, heart
failure, borderline hypotension, or hypovolemia and to those on
complex antihypertensive regimens.

Although the various forms of PDE-5i have a common mecha-
nism of action, there are a few differences among the four agents
(Table 390-2). Tadalafil is unique in its longer half-life and avanafil
appears to have the fastest onset of action. All four drugs are effective
for patients with ED of all ages, severities, and etiologies. Although
there are pharmacokinetic and pharmacodynamic differences among
these agents, clinically relevant differences are not clear.

Testosterone replacement is used to treat both primary and second-
ary causes of hypogonadism Androgen supplementa-
tion in the setting of normal testosterone is rarely efficacious in the
treatment of ED and is discouraged. Methods of androgen replace-
ment include transdermal patches and gels, including cutaneous
nasal and axillary gels. Parenteral administration of long-acting
testosterone esters (enanthate and cypionate), long-acting subcu-
taneous pellets, and oral preparations (17 α-alkylated derivatives)
are also available Oral androgen preparations have the
potential for hepatotoxicity and should be avoided.

The increased scrutiny of testosterone caused the U.S. Food
and Drug Administration (FDA) to issue a warning that there is a
“weak signal” that testosterone replacement therapy increases the
risk of thromboembolic events and may have addictive properties.

Though testosterone therapy has known risks, such as water reten-
tion in heart failure patients, and worsening sleep apnea, increas-
ing evidence suggests that, when monitored appropriately, this
therapy decreases the risk for metabolic syndrome, changes body
composition by increasing lean muscle mass, and improves insulin
sensitivity and average hemoglobin A1c.

This evidence, combined
with the fact that hypogonadism is a known risk factor for metabolic
syndrome and cardiovascular disease, has led to the conclusion that
testosterone therapy for age-related hypogonadism in fact improves
overall health and decreases risk of cardiovascular events. It is
important to note that men with secondary hypogonadism who
desire fertility should not be treated directly with testosterone, but
with an alternative such as the selective estrogen-receptor modula-
tor (SERM) clomiphene citrate, which increases gonadotropin levels,
stimulating testicular T production.

Testosterone circulates in the body in two forms: free and unbound
or bound to proteins such as albumin or sex hormone-binding glob-
ulin (SHBG). SHBG has a very high affinity for testosterone and,
thus testosterone bound to SHBG does not bind to the androgen
receptor and is not bioavailable. Bioavailable testosterone is any tes-
tosterone that is not bound to SHBG.

Unfortunately, reliable assays
to directly measure bioavailable testosterone or free testosterone
are expensive and difficult to perform, and are thus not offered by
most laboratories. However, direct measurement of SHBG is inex-
pensive and reliable, allowing free and bioavailable testosterone to
be calculated.

Men who receive testosterone should be reevaluated after
3–6 months and at least annually thereafter for testosterone levels,
erectile function, and adverse effects, which may include gyne-
comastia, sleep apnea, development or exacerbation of LUTS or
BPH, prostate cancer, lowering of HDL, erythrocytosis, elevations
of liver function tests, and reduced fertility. Periodic reevaluation
should include measurement of CBC and PSA and digital rectal
examination. Therapy should be discontinued in patients who do
not respond within 3–6 months without an alternate explanation
(e.g., elevated estradiol).


Vacuum constriction devices (VCDs) are a well-established non-
invasive therapy. They are a reasonable treatment alternative for
select patients who cannot take sildenafil or do not desire other

VCDs draw venous blood into the penis and use a
constriction ring to restrict venous return and maintain tumescence.
Adverse events with VCD include pain, numbness, bruising, and
altered ejaculation. Additionally, many patients complain that the
devices are cumbersome and that the induced erections have a non-
physiologic appearance and feel.

If a patient fails to respond to oral agents, a reasonable next choice is
intraurethral or self-injection of vasoactive substances. Intraurethral
prostaglandin E1
(alprostadil), in the form of a semisolid pellet (doses
of 125–1000 μg), is delivered with an applicator. Approximately 65%
of men receiving intraurethral alprostadil respond with an erection
when tested in the office, but only 50% achieve successful coitus at
home. Intraurethral insertion is associated with a markedly reduced
incidence of priapism in comparison to intracavernosal injection.

Injection of synthetic formulations of alprostadil is effective in
70–80% of patients with ED, but discontinuation rates are high
because of the invasive nature of administration.

Doses range
between 1 and 40 μg. Injection therapy is contraindicated in men
with a history of hypersensitivity to the drug and men at risk for
priapism (hypercoagulable states, sickle cell disease). Side effects
include local adverse events, prolonged erections, pain, and fibrosis
with chronic use. Various combinations of alprostadil, phentola-
mine, and/or papaverine sometimes are used.

A less frequently used form of therapy for ED involves the surgi-
cal implantation of a semirigid or inflatable penile prosthesis. The
choice of prosthesis is dependent on patient preference and should
take into account body habitus and manual dexterity, which may
affect the ability of the patient to manipulate the device.

Because of
the permanence of prosthetic devices, patients should be advised
to first consider less invasive options for treatment. These surgical
treatments are associated with a low rate of potential complications
but generally are reserved for treatment
of refractory ED or in men
who cannot tolerate less invasive treatments. Despite their cost and
the requirement for surgery, penile prostheses are associated with
very high rates of patient and partner satisfaction.
A course of sex therapy may be useful for addressing specific inter-
personal factors that may affect sexual functioning. Sex therapy
generally consists of in-session discussion and at-home exercises
specific to the person and the relationship.

Psychosexual therapy
involves techniques such as sensate focus (nongenital massage), sen-
sory awareness exercises, correction of misconceptions about sexual-
ity, and interpersonal difficulties therapy (e.g., open communication
about sexual issues, physical intimacy scheduling, and behavioral
interventions). These approaches may be useful in patients who
have psychogenic or social components to their ED, although data
from randomized trials are scanty and inconsistent. It is preferable
to include both partners in therapy if the patient

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