This document provides an overview of benign prostatic hyperplasia (BPH), including relevant anatomy, etiology, pathophysiology, symptoms, complications, diagnosis, and treatment options. It discusses the prostate gland anatomy and development. Etiology sections cover the roles of androgens, estrogen, growth factors, and other signaling pathways. Pathophysiology involves increased urethral resistance and compensatory bladder changes. Symptoms include both voiding and storage issues. Complications include urinary retention, incontinence, and infection. Diagnosis involves history, exam, testing such as DRE, ultrasound and PSA. Treatment ranges from medications to minimally invasive procedures like TUNA and TUMT to surgeries

1. BENIGN PROSTATIC
HYPERPLASIA
PRESENTER
MODERATOR
DATE
DR SHAMPILE SYDNEY
DR NENAD
4TH FEBRUARY, 2014

2. Presentation layout
•
•
•
•
•
•
•
•
Relevant anatomy
Etiology
Pathophysiology
Symptoms
Complications of BPH
Diagnosis
Treatment
References

3. Prostate Gland Anatomy
•
•
•
•
•
•
Male sex gland
Pear-shape,wt7-16gm
Size of a walnut
Helps control urine flow
Produces fluid component of semen
Produces Prostate Specific Antigen (PSA

6. Development
• The prostatic part of the urethra develops from the
urogenital sinus (endodermal origin).
• It grows into the surrounding mesenchyme
• The glandular epithelium of the prostate differentiates
from these endodermal cells
• Mesenchyme differentiates into the dense stroma and
the smooth muscle of the prostate
• The prostate glands arises by the 9th week of
embryonic life
• Condensation of mesenchyme, urethra and Wolffian
ducts gives rise to the adult prostate gland, a
composite organ made up of several glandular and
non-glandular components tightly fused.

7. Arterial supply
• From the anterior division of the internal iliac
artery
Inferior vesical artery,
Middle rectal artery
Internal pudendal artery originates (hypogastric)
artery.
• The capsular artery is the second main branch of
the prostate. Supply the glandular tissue.

8. Venous drainage
• Prostatic plexus of veins
• Valveless communication exists between the
prostatic and vertebral plexus through which
prostatic carcinoma spread to vertebral
column and to skull

9. • Innervations
 from pelvic plexuses formed by the parasympathetic,
visceral, efferent, and preganglionic fibers that arise
from the sacral
• levels(S2-S4)
 sympathetic fibers from the thoracolumbar levels (L1L2).
 The pudendal nerve is the major nerve supply leading
to
• Somatic innervations of the striated sphincter and the
levator
• ani. The preprostatic sphincter and the vesicle neck or
internal sphincter is under alpha-adrenergic control.

10. Lymphatic drainage
• Obturator and the internal iliac lymphatic
channels.
• External iliac, presacral, and the para-aortic
lymph nodes.

11. ETIOLOGY
Role of Androgens
• Androgens do not cause BPH
• The development of BPH requires the
presence of testicular androgens
• Patients castrated before puberty or who are
affected by a variety of genetic diseases that
impair androgen action or production do not
develop BPH.

12. ETIOLOGY
Dihydrotestosterone and Steroid 5α-Reductase
• Intraprostatic DHT concentrations are
maintained but not elevated in BPH
• DHT is a more potent androgen than
testosterone because of its higher affinity for
the AR
• Moreover, the DHT-receptor complex may be
more stable than the testosterone receptor
complex.

13. • Two types of steroid 5α-reductase have been
discovered, each encoded by a separate
Type 1 5α-reductase, the predominant
enzyme in extraprostatic tissues, such as skin
and liver, is normally expressed in the 5αreductase deficiency syndrome
Type 2 5α-reductase is the predominant
prostatic 5α-reductase, although it is also
expressed in extraprostatic tissues

14. ETIOLOGY
Role of Estrogens
• There is animal model evidence to suggest that
estrogens play a role in the pathogenesis of BPH
• The role of estrogens in the development of
human BPH, however, is less clear
• There are at least two forms of ER
ER-α is expressed by prostate stromal cells
ER-β is expressed by prostate epithelial cells

15. ETIOLOGY
Regulation of Programmed Cell Death
• Programmed cell death (apoptosis) is a
physiologic mechanism crucial to the
maintenance of normal glandular homeostasis
• This is impaired in BPH

16. ETIOLOGY
Stromal-Epithelial Interaction
• Prostatic stromal and epithelial cells maintain
a sophisticated paracrine type of
communication
• Thus BPH may be due to a defect in a stromal
component that normally inhibits cell
proliferation, resulting in loss of a normal
“braking” mechanism for proliferation

17. ETIOLOGY
Growth Factors
• Interactions between growth factors and steroid
hormones may alter the balance of cell proliferation
versus cell death to produce BPH
• GF implicated in prostate growth.
bFGF (FGF-2)
acidic FGF (FGF-1)
Int-2 (FGF-3)
KGF, FGF-7)
β (TGF-β
EGF
• TGF-β (transforming ) is a potent inhibitor of
proliferation in normal epithelial cells in a variety of
tissues

18. ETIOLOGY
Other Signaling Pathways
• The early growth response gene-1 (EGR1)
• α2-macroglobulin
• IL-2, IL-4, IL-7, IL-17, interferon-γ (IFN-γ)
• Genetic and Familial Factors

19. PATHOPHYSIOLOGY
• The pathophysiology of BPH is complex
• BPH increases urethral resistance, resulting in
compensatory changes in bladder function
• Elevated detrusor pressure is required to
maintain urinary flow in the presence of
increased outflow resistance

20. LUTS
Voiding (obstructive)
symptoms
• Hesitancy
• Weak stream
• Straining to pass urine
• Prolonged micturition
• Feeling of incomplete
bladder emptying
• Urinary retention
Storage (irritative or
filling) symptoms
• Urgency
• Frequency
• Nocturia
• Urge incontinence
LUTS is not specific to BPH – not everyone with
LUTS has BPH and not everyone with BPH has LUTS

21. Common Symptoms
n
decrease in the urinary
stream
n Dribbling
or leaking
after urination
n Intermittency
n Hesitancy
n Pain
or burning
during urination
n Feeling
that the
bladder never
completely empties

22. Complications
Mortality
• 10 per 100,000
Bladder Stones
• bladder stone development is small
Urinary Tract Infections
• 0.1/100 patient-years
Bladder Decompensation
• progression from normal mucosa to advancing
trabeculation, diverticula and detrusor muscle
failure

23. Complications
Urinary Incontinence
• complications from surgical intervention for BPH
• secondary to overdistention of the bladder
(overflow incontinence)
• Due to detrusor instability (urge incontinence)
Acute Urinary Retention
• Long-term outcome resulting from BPH

24. Diagnosis of BPH
• History and Examination
• Digital rectal examination(DRE)
• inaccurate for size but can detect shape and consistency
• Ultrasonography
• Urodynamic analysis
• Measurement of prostate-specific antigen (PSA)
– high correlation between PSA and PV, specifically TZV
1
– men with larger prostates have higher PSA levels
– PSA is a predictor of disease progression and screening
tool for CaP
– as PSA values tend to increase with increasing PV and
increasing age, PSA may be used as a prognostic marker
for BPH

25. Other investigations
•
•
•
•
•
•
Serum Creatinine Measurement
Urinalysis
Postvoid Residual Urine Volume
Pressure-Flow Studies
Filling Cystometry (Cystometrography)
Urethrocystoscopy

26. TREATMENT
BPH needs to be treated ONLY IF:
n
The symptoms are severe enough to
bother patient and affect the quality
of life
n
Renal insufficiency
n
Frequent urinary tract infections

27. TREATMENT
• Medical
• Minimally Invasive and Endoscopic
• Surgical approaches

28. TREATMENT
•First line of defense against bothersome urinary
symptoms
–Manage the condition - don’t fix it
•Two major types:
•(Alpha-1-blocker) - relax the prostate and
provide a larger urethral opening
(prazosin,terazosin)
•Shrink the prostate gland (5-alpha reductase
inhibitor) (finasteride)

29. TREATMENT
• Combination therapy with both an αadrenergic receptor blocker and a 5αreductase inhibitor has been demonstrated to
be the most effective
• Antimuscarinic agents are useful adjuncts for
patients with “storage” symptoms or ED

30. Minimally Invasive and Endoscopic
Temporary Stents
• Temporary stents are tubular devices that are
made of either a nonabsorbable or a
biodegradable material
• designed for short-term use, to relieve
bladder outlet obstruction (BOO)

31. Temporary Stents
• Spiral Stents- e.g Urospiral,stent should
remain in the prostatic urethra for longer than
12 months
• Polyurethane Stents
• Biodegradable Stents

32. Permanent Stents
• were introduced as a definitive treatment for
prostatic obstruction, particularly for patients
unfit for prostatic surgery
• Patients were able to void satisfactorily in
most cases, but complications were relatively
high
• UroLume endourethral prosthesis

33. TRANSURETHRAL NEEDLE ABLATION
OF THE PROSTATE (TUNA)
• Heat treatment inducing necrosis of prostatic
tissue
• The aim is to increase prostatic temperature
to in excess of 60° C
• Uses low-level radiofrequency (RF) energy
that produces localized necrotic lesions in the
hyperplastic tissue.

34. Deployment of radiofrequency needles
in transurethral needle ablation

35. TRANSURETHRAL MICROWAVE
THERAPY
• These cover heat changes and differential
blood flow in the prostate
• Damages the sympathetic nerve endings
• Induction of apoptosis

36. The Prostatron antenna, treating the
prostatic transition zone.

37. LASERS
• “laser” stands for light amplification by the
stimulated emission of radiation
• There are four types of laser that can be used to
treat the prostate
1. Neodymium : Yttrium-Aluminum-Garnet Laser
2. Potassium-Titanyl-Phosphate Laser
3. Holmium : Yttrium-Aluminum-Garnet Laser
4. Diode Laser

38. LASERS
The energy from lasers can be delivered as follows:
• End firing
Bare tip
Sculptured tip
Sapphire tip
• Side firing
Metal or glass reflector
Prismatic internal reflector

39. TRANSURETHRAL RESECTION OF THE
PROSTATE (TURP)
• Gold Standard” of care for BPH
• Uses an electrical “knife” to surgically cut and
remove excess prostate tissue
• Effective in relieving symptoms and restoring
urine flow

40. TURP
Operation is performed through a modified
cystoscope
•
Prostatic tissue is resected using an electrically
energized wire loop
•
•
Prostatic capsule is usually preserved.
Continuous irrigation is necessary to distend
the bladder and to wash away blood and
dissected prostatic tissue.
•

41. SURGICAL PROCEDURE
•

42. IRRIGATION FLUID
Ideally the irrigation
solution should be:
• Isotonic
• electrically inert
• Nontoxic
• Transparent
• inexpensive
•
•
Nonhemolytic
Nonmetabolized

43. COMPLICATIONS
•TURP can be
associated with a number of
complications:
•TURP Syndrome (2%)
•Hemorrhage
•Bladder perforation (1%)
•Hypothermia
•Septicemia (6%)
•DIC
•The main challenges are blood loss and TURP
Syndrome due to excessive absorption of irrigant
fluid

44. TURP SYNDROME
•
•
TURP syndrome: constellation of signs and
symptoms caused by the absorption of large
volumes of isotonic irrigating fluids through
prostatic veins or breaches in the prostatic
capsule.
The syndrome is characterized by
• hypervolemia,
• hyponatremia
• hypo-osmolarity

45. TURP SYNDROME:
RISK FACTORS
TURP syndrome is more likely
to occur:
1. The hydrostatic pressure of the
irrigation solution is high.
2. An excessively distended
bladder
3. Prostatic gland is large.
4. The Prostatic Capsule is
violated during surgery.
5. Duration of surgery (>60mins)

46. Retropubic Prostatectomy
• Proper Positioning of the Patient
• Once anesthesia has been induced the patient
is positioned on the operating table in a
supine position
• Trendelenburg position without extension

47. Retropubic prostatectomy. The space of Retzius has
been opened and the periprostatic adipose tissue has
been dissected free from the superficial branch of the
dorsal vein complex. The endopelvic fascia is incised
bilaterally

48. A 2-0 chromic suture on a 58-inch circle-tapered needle is passed in the avascular plane between
the urethra and the dorsal vein complex at the apex of the prostate. A tie is grasped and tied
around the dorsal vein complex. B, With 2-0 chromic suture material on a CTX needle, a figure-ofeight suture is placed through the prostatovesicular junction just above the level of the seminal
vesicles to control the main arterial blood supply to the prostate gland. When placing this suture,
care must be taken to avoid entrapment of the neurovascular bundles located posteriorly and
slightly laterally

49. Retropubic prostatectomy. A, With the superficial branch of the
dorsal vein complex secured proximally and distally, a No. 15
blade on a long handle is used to make the transverse
capsulotomy. B, Metzenbaum scissors are used to develop the
plane anteriorly between the prostatic adenoma and the
prostatic capsule.

50. Retropubic prostatectomy. A, With blunt dissection with the index finger, the
prostatic adenoma is dissected free laterally and posteriorly. B, Metzenbaum
scissors are used to divide the anterior commissure to visualize the posterior
urethra and verumontanum. C, The index finger is then used to fracture the
urethral mucosa at the level of the verumontanum. With this last maneuver,
extreme care is taken not to injure the external sphincteric mechanism

51. Retropubic prostatectomy. A, After removal of the left lateral lobe of the
prostate, the right lateral lobe is excised with the aid of a tenaculum and
Metzenbaum scissors. B, Lastly, the median lobe is removed under direct
vision

52. Retropubic prostatectomy. A, View of the prostatic fossa and posterior urethra after enucleation
of all the prostatic adenoma. Note that the verumontanum and a strip of posterior urethra
remain intact. B, After placement of a urethral catheter and, if needed, a Malecot suprapubic
tube, the transverse capsulotomy is closed with two running 2-0 chromic sutures. The two
sutures are tied first to themselves and then to each other across the midline to create a
watertight closure of the prostatic capsule.

53. Suprapubic Prostatectomy
• Proper Positioning of the Patient
• After anesthesia has been induced, the patient is
positioned on the operating table in a supine
position.
• The table is placed in a mild Trendelenburg
position without extension
• 22-Fr catheter is inserted into the bladder. After
residual urine is drained, 250 mL of saline is
instilled into the bladder and the catheter is
clamped.

54. Suprapubic prostatectomy. A, A lower midline incision is made
from the umbilicus to the pubic symphysis. B, After developing
the prevesical space, a small, longitudinal cystotomy is made
with an electrocautery

55. With adequate exposure of the bladder neck, a circular incision
in the bladder mucosa is made distal to the trigone, using an
electrocautery

56. Starting at the bladder neck posteriorly, Metzenbaum scissors
are used to develop the plane between the prostatic adenoma
and the prostatic capsule (lateral view). B, Anterior view of the
same maneuver

57. Using the index finger, the prostatic adenoma is enucleated from
the prostatic fossa (lateral view). B, Anterior view of the same
maneuver. With extreme large prostate glands, the left, right,
and median lobes should be removed separately

58. After enucleation of the entire prostatic adenoma, a 0-chromic suture is used
to place two figure-of-eight sutures to advance bladder mucosa into the
prostatic fossa at the 5- and 7-o’clock positions at the prostatovesicular
junction to ensure control of the main arterial blood supply to the prostate.

59. suprapubic tube, the cystotomy is closed in two layers using a
running 2-0 Vicryl suture, enforced by tying of multiple
interrupted 3-0 Vicryl stay sutures. A closed Davol suction drain
is placed on one side of the bladder and exits via a separate stab
incision

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