MODULE: MALE ERECTILE DYSFUNCTION

Learning objective
After completing this module, the students are able to:

1. explain penile anatomy and physiology of erection

2. describe the classification of male erectile dysfunction (ED)
3. describe the etiology of ED
4. describe the pathophysiology of ED
5. take history patient with ED
6. communicate patient with ED

Overview:
Male erectile dysfunction (ED) has been defined as the persistent inability to attain and maintain an
erection sufficient to permit satisfactory sexual performance. Although ED is a benign disorder, it is
related to physical and psychosocial health, and has a significant impact on the quality of life of both
sufferers and their partners and families.

Simply stated, normal male sexual function can be divided into five phases, each of which is under
diverse regulation: libido, erection, ejaculation, orgasm, and detumescence. Male sexual dysfunction,
denoting the inability to achieve a satisfactory sexual relationship, may involve inadequacy of erection
or problem with emission, ejaculation, or orgasm. Erectile dysfunction is consistent inability to obtain or
maintain an erection for satisfactory sexual relationship. So, ED is part of sexual of sexual dysfunction.

Epidemiologi

The prevalence of erectile dysfunction increases dramatically with age. According to the Massachusetts
Male Aging Study the overall probability of complete impotence tripled from 5% in subjects 40 years
old to 15% in subjects 70 years old. These results are consistent with those from a number of other
epidemiological studies that have evaluated the relationship between erectile dysfunction and age. For
example Masumori et al compared the age related prevalence of erectile dysfunction among 289
Japanese and American men (the latter groups were from the Olmsted County study). Results from both
groups indicated an age related decrease in erectile function, sexual libido and sexual satisfaction.

In particular 71% of Japanese men 70 to 79 years old reported having erections only a little of the time
or less when sexually stimulated, and 80% perceived sexual drive once or less during the past month.
Marumo et al reported a similar increase in the prevalence of erectile dysfunction among 2,311
Japanese men between 23 and 79 years old.
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 Figure 1. Physiological Mechanism of Penile Smooth-
Muscle Relaxation.
The corpora cavernosa contain a network of smoothmuscle
cells and endothelial cells surrounded by an expansible tunica
albuginea. The sinusoid cavities are small in volume at rest as
the smooth-muscle cells are tonically contracted (Panel A).
With stimulation, smoothmuscle cells relax, which allows the
sinusoids to engorge with blood and causes the penis to
become tumescent.
As the sinusoids expand, they compress the subtunical
venous plexus, which causes an erection (Panel B). If
there is insufficient relaxation of smooth-muscle cells
(e.g., from a lack of endogenous nitric oxide associated
with endothelial disease) and decreased sinusoid compliance,
an inadequate number of smooth-muscle cells
(e.g., cell apoptosis from diabetes or neuropathy), or
tunical degeneration (e.g., Peyronie’s disease), then
insufficient compression of the subtunical veins results
in erectile dysfunction (Panel C).

The process of penile erection

While there have been substantial advances in our understanding of neural, hemodynamic and
molecular mechanisms involved in penile erection, this process is still incompletely understood. The
penis is innervated by autonomic and somatic nerves (fig. 1). Sympathetic and parasympathetic fibers in
the cavernous nerves regulate blood flow into the corpus cavernosum during erection and
detumescence. Erection begins with transmission of impulses from parasympathetic nerves and non-
adrenergic non-cholinergic nerves. This neural stimulus leads to release of nitric oxide from the non-
adrenergic non-cholinergic nerves and possibly the endothelial cells. Nitric oxide increases
intracellular levels of cyclic guanosine monophosphate (cGMP) in the cavernosal smooth muscle, which
acts to relax cavernosal tissue, perhaps by activating protein kinase G and stimulating phosphorylation
of proteins that regulate corporal smooth muscle tone. The actions of the parasympathetic nervous
system, nitric oxide and cGMP permit rapid blood flow into the penis and the development of an
erection. As pressure within the corporal body increases, small emissary veins transversing the tunica
albuginea are occluded, trapping blood in the corpus cavernosum. The erection is maintained until
ejaculation, which usually leads to detumescence. Phosphodiesterases, which hydrolyze cGMP and
cyclic adenosine monophosphate, have a key role in the physiology of erection.
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Table 1: Pathophysiology of erectile dysfunction

 Vasculogenic
 Neurogenic
- Central causes
- Peripheral causes
 Anatomical/structural
 Hormonal
 Drug-induced
 Psychogenic

Evaluation of male erectile dysfunction

Although the failure of erectile function is frequently the result of psychological disturbances, every
effort must be made to exclude a remedial, organic cause. Usually, the history is informative. Normally,
from early childhood through the eight decade, erection occurs during sleep.
Physical examination should include a thorough genital examination to rule out any abnormalities of
the penis itself. The testes should be palpated for size or abnormal masses; if the length is less than 4 cm,
hypoganadism should be considered. All pulses should be palpated, including the penile pulse, which
can be felt by pressing both corpora between the thumb and fore finger and palpating to either side of
the midline. If possible, penile blood pressure should be measured. If there is an indication from either
history or physical examination of a vascular etiology, an aortogram may be indicated.
A neurological examination to evaluate the erectile reflex is advisable including anal sphincter tone,
perineal sensation, and the bulbocavernosus reflex. An examination for peripheral neuropathy,
including distal muscle weakness, loss of tendon reflexes in the legs, and tests for impairment of
vibratory, position, tactile, and pain sensation, should also be performed.
Laboratory evaluation is probably of minimal value. Measurement of serum testosterone in the absence
of evidence of feminization or hypogonadism is seldom helpful.

Scenario:
A 65-year-old man presents to an outpatient clinic, reporting that he can no longer maintain an erection
sufficient for intercourse. His medical history includes wellcontrolled hypertension and stable coronary
artery disease. He smokes a pack of cigarettes daily. His medications include atenolol and low-dose aspirin
(81 mg daily). On physical examination, his body-mass index (the weight in kilograms divided by the square
of the height in meters) is 31; the examination is otherwise unremarkable, with normal external genitalia and
no loss of body hair.

Task:
1. Discuss a patient problem on the scenario
2. Explain the possibility mechanism. Why the patient suffered from those symptoms?
3. Describe the factors that make patient problem.
4. Do you need further examination to confirm your hypothesis about the patient problem? What for?
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5. What will the patient suffer from the next complication?

Suggested reading:
1. Purnomo BB. Disfungsi Ereksi. In: Dasar-dasar Urologi. Ed 2. Jakarta: CV Sagung Seto, 2007: p. 197 – 206.
2. Bella JA, Lue TF. Male Sexual Dysfunction. In: Smith’s General Urology. 17th ed. New York: Lange Medical
Book/McGraw-Hill, 2008: p. 589 – 610.
3. Lue TF, Broderick GA. Chapter 22 – Evaluation and Nonsurgical Management of Erectile Dysfunction and
Premature Ejaculation. In: Campbell’s–Walsh Urology. 9th ed. Philadelphia: WB Saunders – Elsevier, 2007.
4. McVary KT. Erectile Dysfunction. N Engl J Med 2007;357:2472-81. (Downloaded from www.nejm.org on
August 28, 2008)

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