•
From the primitive urethra as a series of solid epithelial buds which in
a matter of weeks become canalised
•
Surrounding mesenchyme forms the muscular and connective tissue of the
gland and has a major role in differentiation (stromal epithelium interactions)
•
Skene’s tubules opening on either side of the female urethra are the
homologue of the prostate
Surgical
anatomy
The
contemporary classification of the prostate into different zones was based on
the work of McNeal (Fig. 66.1). He showed that it is divided into: the
peripheral zone (PZ) which lies mainly posteriorly and from which most
carcinomas arise, and a central zone (CZ) which lies posterior to the urethral
lumen and above the ejaculatory ducts as they pass through the prostate; the two
zones are rather like an egg in its egg-cup. There is a also periurethral
transitional zone (TZ) from which most benign prostatic hyperplasia (BPH)
arises. Smooth muscle cells are found throughout the prostate, but in the upper
part of the prostate and bladder neck, there is a separate sphincter muscle that
sub serves a sexual function, closing during ejaculation. Resection of this
tissue during prostatectomy is responsible for retrograde ejaculation. The
distal striated urethral sphincter muscle is found at the junction of the
prostate and the membranous urethra, it is horse-shoe shaped with the bulk lying
anteriorly; it is quite distinct from the muscle of the pelvic floor (Fig. 65.1).
The
glands of the peripheral zone (Fig. 66.2), lined by columnar epithelium, lie in
the fibromuscular stroma and their ducts which are long and branched open into
posterolateral grooves on either side of the verumontanum. The glands of the CZ
and TZ are shorter and un
Benign
prostatic hyperplasia (BPH) starts in the periurethral transitional zone and
as it increases in size it compresses the outer PZ of the prostate which becomes
the false capsule. There is also the
outer true fibrous anatomical capsule; and
external to this lie condensations of endopelvic fascia known as the periprostatic
sheath of endo pelvic fascia. Between the anatomical capsule and the
prostatic sheath lies the abundant prostatic venous plexus. The prostatic sheath
is contiguous with the strong fascia of Denonvillier that separate the prostate
and its coverings from the rectum. The neurovascular bundles supplying autonomic
innervation to the corpora of the penis are in very close relationship to the
posterolateral aspect of the prostatic capsule and are at risk of damage during
radical cystoprostatectomy or radical prostatectomy; inadvertent diathermy in
the region of these nerves may be the cause of erectile impotence after
transurethral prostatectomy.
Physiology
The prostate has a sexual function, but it is
a little unclear how important its secretions are to human fertility. That the
normal adult prostate undergoes atrophy after castration was known to John
Hunter.
Systemic
hormonal influences (endocrine) and local growth factors (paracrine and
autocrine)
The growth of the prostate is governed by many
local and systemic hormones whose exact functions are not yet known. The main
hormone acting on the prostate is testosterone which is secreted by the Leydig
cells of the testes under the control of luteinizing hormone (LH), which is
secreted from the anterior pituitary under the control of hypothalamic
luteinizing hormone-releasing hormone (LHRH). Testosterone is converted to
5-di-hydrotestosterone (DHT) by the enzyme 5a-reductase, which is found in high
concentration in the prostate and the perigenital skin. Other androgens are
secreted by the adrenal cortex, but their effects are minimal. Oestrogenic
steroids are also secreted by the adrenal cortex and in the ageing male may play
a part in disrupting the delicate balance
between DHT and local peptide growth factors, and hence increase the risk of BPH.
Increased levels of serum oestrogens, by acting on the hypothalamus, decrease
the secretion of LHRH (and hence LH) and thereby decrease serum testosterone
levels. Therefore, pharmacological levels of oestrogens cause atrophy of the
testes and prostate by means of reductions in testosterone.
Other
locally acting peptides are secreted by the prostatic epithelium and mesenchymal
stromal cells in response to steroid hormones. These include epidermal growth
factor, insulin-like growth factors, basic fibroblast growth factor and
transforming growth factors a and 3. These undoubtedly play a part in normal and
abnormal prostatic growth, but as yet their functions are unclear.
Elaboration and
secretion of prostate-specific antigen (PSA) and acid phosphatase
PSA is a glycoprotein which is a serine
protease. Its function may be to facilitate liquefaction of semen, but it is a
marker for prostatic disease. It is measured by an immunoassay and the normal
range can differ a little from laboratory to laboratory. The normal upper limit
is about 4 nmollml. Its level in men with metastatic prostate cancer is usually
increased to >30 nmol/ml and falls to low levels after successful androgen
ablation. Men with locally confined prostate cancer usually have serum PSA
levels <—15 nmol/ml. Although PSA
is a reliable marker for the progress of advanced disease it is neither specific
nor sensitive in the differential diagnosis of early prostate cancer and BPH, as
both diseases are compatible with PSA in the range of 4—12 nmol/ml. PSA
measurement has superseded measurement of serum acid phosphatase.
Benign prostatic hyperplasia
BPH
occurs in men over 50 years of age; by the age of 60 years 50 per cent of men
have histological evidence of BPH and 15 per cent have significant lower urinary
tract symptoms
Aetiology of
benign prostatic hyperplasia
Hormones
Serum testosterone levels slowly but
significantly decrease with advancing age; however, levels of oestrogenic
steroids are not decreased equally. According to this theory the prostate
enlarges because of increased oestrogenic effects. It is likely that the
secretion of intermediate peptide growth factors plays a part in the development
of BPH.
Pathology
BPH affects both glandular epithelium and
connective tissue stromal to variable degrees. These changes are similar to
those occurring in breast dysplasia (see Chapter 45), where adenosis, epitheliosis and stromal proliferation are seen
in differing proportions. BPH typically affects the submucous group of glands in
the transitional zone, forming a nodular enlargement. Eventually, this
overgrowth compresses the PZ glands into a false capsule and causes the
appearance of the typical ‘lateral’ lobes.
When
BPH affects the sub cervical central zone glands, a‘middle’ lobe develops which projects up
into the bladder within the internal sphincter (Fig.
66.3). Sometimes both
lateral lobes also project into the bladder, so that when viewed from within,
the sides and back of the internal urinary meatus are surrounded by an
intravesical prostatic collar.
Effects of
benign prostatic hyperplasia
It is important to realise that the
relationship between anatomical prostatic enlargement (BPH), symptoms of
prostatism
and urodynamic evidence of bladder outflow obstruction (BOO) is complex (Fig.
66.4). Pathophysiologically, bladder outflow obstruction may be caused in part
by increased smooth muscle tone which is under the control of alpha-adrenergic
agonists. Consequences of BPH
• No symptoms, but urodynamic
evidence of BOO
• Symptoms of prostatism, no
evidence of BOO
• Symptoms of prostatism and BO
• Others (acute/chronic
retention, haematuria, urinary infection and stone formation)
Anatomically,
the effects are as follows.
Urethra
The
prostatic urethra is lengthened, sometimes to twice its normal length, but it is
not narrowed anatomically. The normal posterior curve may be so exaggerated that
it requires a curved catheter to negotiate it. When only one lateral lobe is
enlarged, distortion of the prostatic urethra occurs.