PROSTATE GLAND

By

DR. NGWOGU K. O.
 INTRODUCTION
 The prostate is a retroperitoneal organ encircling the
bladder neck and urethra.
 In the adult, the prostate weighs approximately 20g.
 It has 4 anatomically distinct zones viz peripheral,
central, transitional and the region of the anterior
fibromuscular stroma (peri-urethral zone).
 The types of proliferative lesion are different in each
region e.g. most hyperplasia arise in the transitional zone
while most carcinomas originate in the peripheral zone.
 Three pathologic processes affect the prostate gland viz
inflammation, benign nodular enlargement, and tumours.
BPH is the commonest.
 PROSTATITIS
 It can be divided into acute and chronic bacterial
prostatitis.
 They result from bacteria that cause UTI viz strains
of E. coli, other gram -ve rods, staphylococci, etc.
 Occasionally, prostatitis is 2o to surgical
manipulations on the urethra or prostate gland itself
such as catheterization, cystoscopy, urethral dilation
or resection procedures on the prostate.
 Clinically, prostatitis is associated with fever, chills
and dysuria.
 On DRE, the gland is quite tender and boggy. Urine
 BENIGN ENLARGEMENT OF THE PROSTATE
 It is also called benign prostatic hyperplasia (nodular hyperplasia).
 This is a common disorder in men > 50years.
 It is characterized by hyperplasia of the prostatic stromal and epithelial cells,
resulting in the formation of large, discrete nodules in the periurethral zone of
the prostate.
 When it is sufficiently large, the nodules compress and narrow the urethral
canal to cause partial or complete obstruction of the urethra.
 The enlarged prostate weighs between 60-100g and the hyperplasia originates
almost exclusively in the inner aspect of the prostate gland in the transition
zone.
 Histologically, the hallmark of BPH is nodularity due to glandular proliferation
or dilatation and fibrous or muscular proliferation of the stroma.
 Diagnosis of BPH cannot be made on needle biopsy because of the limited
sampling.
 Also, needle biopsies do not typically sample the transition zone where BPH
occurs.
 CLINICAL COURSE
 Symptoms of nodular hyperplasia, when present, relate to 2 secondary
effects:
 Compression of the urethra with difficulty in urination
 Retention of urine in the bladder with subsequent distention and
hypertrophy of the bladder, infection of the urine, and development of
cystitis and renal infections.
 Patient experiences frequency of urination, nocturia, hesitancy of urine,
overflow dribbling and dysuria.
 Sudden acute urinary retention may appear for unknown reason, requiring
emergency catheterization.
 Also, there is incomplete bladder emptying during micturition due to raised
level of urethral floor. This generates residual urine that is prone to infection
after catheterization.
 Nodular hyperplasia is not considered to be a premalignant lesion.
 Transurethral resection of the prostate (TURP) is effective in reducing
symptoms, improving flow rates and decreasing post-void residual urine
 PROSTATE CANCER (ADENOCARCINOMA)

 CAP is the commonest cancer in males and the

second leading cause of cancer death.
 It is typically a disease of men > 50years, hence
screening is started at age 40.
 ETIOLOGY
 Exact cause remains unknown but risk factors include: age, race,
+ve family history, hormone levels, environmental influences and
increased fat consumption.
 However, other dietary products which are said to prevent, inhibit
or delay progression of CAP include: lycopenes (found in
tomatoes), vitamin A, E, selenium and soya bean products.
 As with BPH, androgens are believed to play a role in the
pathogenesis of CAP.
 Support for this observation lies in the inhibition of these tumours
when orchiectomy is carried out.
 The role of hormones in this malignancy also stems from the fact
that androgens are required for the maintenance of prostatic
epithelium.
 African – Americans have the highest incidence and mortality of
 MORPHOLOGY

 About 70% of CAP arise in the peripheral zone of the gland,

classically in a posterior location, making it palpable on DRE.
 Characteristically, on cross-section, the neoplastic tissue is
gritty and firm.
 Histologically, most lesions are adenocarcinomas that produce
well-defined gland patterns.
 The neoplastic glands are typically smaller than benign glands
and are lined by a single uniform layer of cuboidal or low
columnar epithelium.
 In contrast to benign glands, CAP glands are more crowded,
characteristically lacking branching and papillary unfolding.
 SPREAD

 Spread of CAP occurs by direct local invasion and

through the blood stream and lymph.
 Hematogenous spread is mainly to the bones and
viscera.
 SYMPTOMS
 Because of peripheral location of CAP, away from
the urethra, urinary symptoms occur late.
 Patients with clinically advanced prostate cancer
may present with urinary symptoms like dysuria,
frequency, difficulty in starting or stopping the
stream or hematuria; back pain caused by vertebral
metastases.
 INVESTIGATIONS
 Biopsy, DRE
 Ultrasound guided biopsy more accurate than random
 CT scanning (for assessing extent of spread and staging)
 PSA (for screening men at risk > 40years)
 PSA is useful in the diagnosis and management of CAP.
 Prostate Specific Antigen (PSA) is a product of prostatic epithelium
and is secreted in the serum.
 Elevated levels (> 0-4ng/ml) occur in association with CAP and to a
lesser extent BPH with overlap.
 Other causes of increased PSA include: prostatitis, infarct,
instrumentation of the prostate, ejaculation.
 Therefore PSA is organ specific but not cancer specific.
 Few patients of CAP may have normal PSA values.
 Serial measurements of PSA are of great value in assessing the
 CAP is treated by surgery, radiotherapy, and
hormonal manipulation.
 Most common treatment for clinically localized
CAP is radical prostatectomy.
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