Urinary Obstruction &
Benign Prostatic Hyperplasia
(BPH)
Xiao Huang, MD; PhD
Department of Urology,1st Affiliated Hospital of
Zhejiang University, School of Medicine
Urinary Obstruction
 Urinary Tract Anatomy
 Urinary Obstruction
 Reason of Urinary Obstruction
 Hydronephrosis
Urinary Tract Anatomy
Urinary Obstruction
Reason of Urinary Obstruction
Obstruction Reason Classification
 Dynamic and structural
 Congenital and aquired
 Populations




Child: congenital
Adults: stone, injury, tumor ,TB
Women: pelvic disease
Old men: BPH
 Locations




Kidney: calculus, tumor, infection, TB, UPJ stricture, congenital
deformity
Ureter: stone, tumor, iatrogenic injury, ureteritis,TB , Metastatic
carcinoma
Bladder: BPH, bladder neck contracture, tumor, calculus, Neurogenic
bladder
Urethral: urethral stricture, Phimosis ,Congenital Posterior urethral
valve ,stone.
Hydronephrosis
 What is hydronephrosis?
 Hydronephrosis is a "stretching" or dilation
of the inside, or collecting part, of the
kidney.
 It often results from a blockage in the
ureter where it joins the kidney that
prevents urine from draining into the
bladder.
 Urine is trapped in the kidney and causes
it to stretch.
 Hydronephrosis may also be due to
abnormal backwash or "reflux" of urine
into the bladder.
Degrees of Hydronephrosis
Kidney function:
Minimally affected
compensation
damage
Benign Prostatic Hyperplasia (BPH)
Objectives
 What is a BPH
 How to approach a patient with LUTS (lower
urinary tract symptoms)
 Treatment of BPH
Outline
1. Definition of BPH
2. Anatomy and Physiology
3. Microscopic Appearance
4. Prevalence of BPH
5. Etiology
6. Natural History of BPH
7. LUTS
8. Approach to a patient with BPH
9. IPSS
10. Differential Diagnosis
11. Management of BPH
12. Treatment of BPH
1.Definition
 BPH is a nonmalignant enlargement of the prostate gland caused by
cellular hyperplasia of both glandular and stromal elements that leads
to troublesome lower urinary tract symptoms (LUTS) in some men
 It is the most common benign tumor in men and is not a precancerous
condition
2.Anatomy and physiology

The prostate is a compound
tubuloalveolar exocrine gland of the male
mammalian reproductive system

Function is to store and secrete a clear,
slightly alkaline fluid that constitutes 1030% of the volume of the seminal fluid
that along with the spermatozoa,
constitutes semen

Secret is composed of simple sugars and
proteins (proteolytic enzymes, acid
phosphatase, prostate-specific
antigen);zinc and citric acid
Lower urinary tract
2. Anatomy and physiology

A healthy human prostate is slightly larger
than a walnut (4cm by 3cm). It surrounds
the urethra just below the urinary bladder
and can be felt during a rectal exam. It
has anterior, median, posterior and two
lateral lobes

Relations: Posterior: rectal ampulla
(Denonvilliers’ fascia);Superior: bladder
neck ; Anterior:pubic symphysis
(retropubic space of Retzius); Inferior:
urogenital diaphragm

It’s work is regulated by androgens which
are responsible for male sex
characteristics
2.Anatomy and physiology




Glandular cells produce milky fluid that
liquefies semen
Smooth muscle cells, which contract
during sex and squeeze the fluid from the
glandular cells into the urethra, where it
mixes with sperm and other fluids to
make semen. The muscle cells are
stimulated by alpha adrenergic receptors
Stromal cells (which form the structure of
the prostate)
The prostate gland also contains an
enzyme - 5 alpha-reductase that converts
testosterone to dihydrotestosterone
2.1. Zonal Anatomy(McNeal-1972)

Peripheral Zone 70% of the young
adult (60-70% of CaP)

Central Zone 25% (5-10% CaP)

Transition Zone 5% ( 10-20% CaP)
BPH
Zonal Anatomy
3.Microscopic Appearance

Prostate consists of a thin fibrous capsule under
which are circulary oriented smooth muscle
fibres and collagenous tissue. Prostatic stroma
lies deep to this layer and is composed of
connective and ellastic tissue and smooth
muscle where epithelial cells are embeded

As a male ages, there are more likely to be
small concretions within the glandular lumina,
called corpora amylacea, that represent
laminated concretions of prostatic secretions.
The glands are normally separated by stroma

The thin layer of connective tissue that
surrounds the prostate merges with surrounding
soft tissues, including nerves
4.Prevalence of BPH
 In men 20 to 30 years of age, the prostate
weighs about 20 g;
 however, the mean prostatic weight increases
after the age of 50.
4.Prevalence of BPH
 20% of men age 41-50
 50% of men age 51-60
 65% of men age 61-70
 80% of men age 71-80
 90% of men age 81-90
lower urinary tract symptoms associated with BPH
increase with age.
Pathophysiology of Clinical BPH: Predictive
Risk Factors
 Increasing age
 Prostatic enlargement
 Lower-urinary-tract symptoms (LUTS)
 Decreased urinary flow rate
 Elevated prostate-specific antigen (PSA)
Slide I.4
5.Etiology of BPH
 Androgens
 Estrogens
 Lifestyle
 Hereditary(genetic)/Race
5.1 Androgens

Testosterone and related hormones play a permissive role in BPH

Androgens have to be present for BPH to occur

Administering exogenous testosterone is not associated with a significant
increase in the risk of BPH symptoms

Didhydrotestosterone (DHT), a metabolite of testosterone is a critical mediator of
prostatic growth. DHT is synthesized in the prostate from circulating
testosterone by the action of the enzyme 5α-reductase, type 2. This enzyme is
localized principally in the stromal cells; hence, these cells are the main site for
the synthesis of DHT

DHT can act in an autocrine fashion on the stromal cells or in paracrine fashion
by diffusing into nearby epithelial cells. In both of these cell types, DHT binds to
nuclear androgen receptors and signals the transcription of growth factors that
are mitogenic to the epithelial and stromal cells. DHT is 10 times more potent
than testosterone because it dissociates from the androgen receptor more
slowly

the active androgen, DHT, is important in promoting growth of prostate that
would eventually lead to symptomatic BPH.
Regulation of Prostate Growth: Intrinsic and
Extrinsic Factors
Extrinsic factors
Testicular
• Androgens
• Estrogens
• Nonandrogenic
Intrinsic factors
(prostate)
Nontesticular
• Endocrine organs
• Neurotransmitters
• Immunologic
Epithelium
• Luminal
• Basal
• Neuroendocrine
Stroma
• Fibroblast
Genetic
• Smooth muscle
•
Homeobox
genes
• Extracellular matrix
• Hereditary
diseases
Urethra
• Urine
• Testis-epididymal
fluid
Environmental
• Dietary
• Micro-organisms
(immune response)
Extrinsic factors
Adapted from Lee C et al. In Benign Prostatic Hyperplasia. Plymouth, United Kingdom: Health Publication, 2001:79-106.
Slide III.1
Regulation of Prostate Growth:Role of
Androgens
 DHT is the principal androgen responsible for
prostatic growth
and BPH
 5-reductase mediates
the conversion OH
of
OH
testosterone to DHT
5-reductase
O
O
H
Testosterone
Dihydrotestosterone
Adapted from Bartsch G et al Eur Urol 2000;37(4):367-380.
Slide III.2
5.2 Estrogen





BPH occurs when men generally have elevated estrogen levels and relatively
reduced free testosterone levels
Prostate tissue becomes more sensitive to estrogens and less responsive to
DHT
Cells taken from the prostates of men who have BPH have been shown to grow
in response to high estradiol levels with low androgens present
Estrogens may render cells more susceptible to the action of DHT
Androgen/estrogen ratio change
5.3 Lifestyle

On a microscopic level, BPH can be seen in the vast majority of men over the
age of 70 years, around the world

Men who lead a western lifestyle have a much higher incidence of symptomatic
BPH than men who lead a traditional or rural lifestyle
6.Natural History of BPH

Pathological or first phase of BPH asymptomatic and involves a progression from
microscopic to macroscopic BPH

Clinical or second phase of BPH - progression
from pathological to ‘clinical BPH’ =development
of LUTS

Mechanical and dynamic components are
responsible for the progression from pathological
to clinical BPH

In clinical BPH, the ratio of stroma to epithelium
is 5: 1

Asymptomatic hyperplasia the ratio is 2.7:1
Pathophysiology of Clinical BPH: Overlapping but
Independent Features
Enlarged
prostate
LUTS
BOO
Adapted from Nordling J et al. In Benign Prostatic Hyperplasia. Plymouth, United Kingdom: Health Publication, 2001:107-166.
Slide I.2
7. Lower Urinary Tract Symtoms-LUTS
7.1.Voiding/Obstructive symptoms:
7.2.Storage/Irritative symptoms:

Hesitancy

Frequency of urination

Intermittency

Nocturia

Incomplete voiding


Weak urinary stream
Urgency (compelling need to void
that can not be deferred)

Straining to pass urine

Urge incontinence

Prolonged micturition

Terminal dribbling
7. Obstructive and irritative symptoms origin

Obstructive symptoms-mechanical obstruction due to glandular enlargement as well as
dynamic obstruction secondary to contraction of the smooth muscle of the prostate, urethra
and bladder neck. This dynamic obstruction is a result of sympathetic nervous system
mediated stimulation of alpha-1adrenoceptors

Irritative symptoms - detrusor instability related to detrusor muscle changes in response to
obstruction, such as bladder wall hypertrophy and collagen deposition in the bladder

Adrenoceptors may be further sub-divided into alpha1A and alpha1D subtypes, with alpha1A
predominant in the prostate and alpha 1D in the bladder. Thus blockade of alpha1A may be
necessary for reduction of obstruction whereas the blockade of alpha1D may be required to
relieve storage symptoms
8. Differential Diagnosis
10.2. Prostatic
10.1. Pre-prostatic
 Prostatitis
 Urethral stricture
 Bladder neck contracture
 Bladder tumors
 Neurogenic bladder
 Bladder calculi
 Urinary tract infections
 Prostate Cancer
9. Approach to a patient with BPH

History: (LUTS, previous surgery in the GU tract, STD and Hx of urethral
stricture, prescription meds and over the counter meds). Use IPSS

Physical Examination :digital rectal exam ( R/O Ca:nodules, asymmetry,
hardened ridges, induration; R/O prostatitis: tenderness, bogginess; R/O anal
malignancy and detect undiagnosed neurologic conditions by evaluating the
sphincter tone and perianal sensation;Abdomianl exam-distended bladder)

Urinalysis- by dipstick and routine microscopy, urine culture and sensitivity to
R/O infections and hematuria

Serum PSA-optional to R/O Prostate Cancer
9. Approach to a patient with BPH
(cont’d)

Upper tract imaging (IVP,CT, U/S) only in presence of concomitant urinary tract
disease or complications-hematuria, UTI, renal insufficiency, Hx of stone disease

Cystoscopy- only for patients who don’t respond to medical Trx to determine the
need for surgical approach

Cystometrograms and urodynamic profile -for patients with suspected neurologic
disease or those who failed prostate surgery

Flow rate, post-void residual urine determination and pressure flow- optional
10. IPSS
 Mild (score 0-7)
 Moderate (score 8-19)
 Severe (score 20-35)
11. Management of BPH
 Goal- rapid and sustained relief of symptoms:
 Decrease bladder outlet obstruction
 Improve bladder emptying
 Lower detrusor instability
 Reverse renal insufficiency
 Prevent future episodes of gross hematuria, UTI and urinary retention
 Quality of life and sexuality
 Management depends on severity
12. Treatment of BPH

Lifestyle modification

Watchful Waiting

Medical Therapy

Phytotherapy (alternative)

Surgical Treatment : Conventional Surgical or Minimally Invasive Treatment
12. Treatment Algorithm
Initial Presentation:
Typical Man with LUTS secondary to BPH
No surgical Indications
Mild Symptoms
Small or Large Prostate
Moderate-Severe Symptoms
No Significant Bother
Moderate-Severe Bother
Small Prostate
Large Prostate
Small Prostate
Large Prostate
Watchful waiting
Watchful waiting or
consider 5-alphareductase therapy
Alpha blocker therapy
or surgical option
Alpha blocker or
5 alpha reductase Trx
or combination
or surgical option
Watchful waiting
12.1. Lifestyle Changes

Enriched diet with ample amounts of fresh fish, fruits and vegetables

Reduce stress

Exercise on a regular basis

Weight within normal limits

Limit fluid intake, decrease bladder irritants-caffeine, alcohol; avoid
anticholinergic drugs, narcotics and skeletal muscle relaxants

See your doctor if you develop nocturia

Be aware of interaction of botanical and medical treatment
12.2. Watchful Waiting

The risk of progression or complications is uncertain

In men with symptomatic BPH, progression is not inevitable and some men undergo
spontaneous improvement or resolution of their symptoms

Retrospective studies on the natural history of BPH are inherently subject to bias, related to
patient selection and the type and extent of follow-up. Very few prospective studies
addressing the natural history of BPH have been reported. A large randomized study
compared finasteride with placebo in men with moderately to severely symptomatic BPH
and enlarged prostates on DRE (McConnell et al, 1998). Patients in the placebo arm of the
study had a 7% risk of developing urinary retention over 4 years

Appropriate management of men with mild symptom scores (0-7)

Men with moderate or severe symptoms can also be managed in this fashion if they so
choose

Neither the optimal interval for follow-up nor specific endpoints for intervention have been
defined
12.3. Medical Treatment
 Alpha blockers
 5α-Reductase inhibitors
 Combination Therapy
12.3. Medical Treatment
Alpha blockers

Initially used for treatment of high blood
pressure
Alpha Blockers

The human prostate and bladder base contain
alpha-1-adrenoreceptors and the prostate
contracts to corresponding agonists. The
contractile properties of the prostate and bladder
neck are mediated primarily by the subtype α1a
receptors
Alpha-1 short-acting:
Prazosin
2mg BID
Alpha-1, long-acting:
Terazosin
Doxazosin
5 or 10 OD
4 or 8 OD

Alpha blockade improves both objective and
subjective symptoms and signs of BPH in some
patients

Alpha blockers can be classified according to
their receptor selectivity as well as their half-life
Oral Dosage
Alpha-1a selective:
Tamsulosin
0.4 or 0.8 OD
12.3. Medical Treatment,
Alpha blockers
(cont’d)

Short Acting: Prazosin

Long-acting: Alfuzosin, Doxazosin mesylate, Tamsulosin, Terazosin

Side Effects: dizziness, postural hypotension, fatigue, retrograde ejaculation, rhinitis, and
headaches. May potentiate other antihypertensive medications

Studies have shown that all of them have comparable effectiveness and the future research
is focussed on improving convenience and tolerability

Terazosin and doxazosin may decrease the total cholesterol as well as LDL fraction. Both
may cause first-dose syncope so titration is required

Alfuzosin and tamsulosin -have alpha 1A selectivity and dose titration is not required
12.3. Medical Treatment,
Alpha blockers
(cont’d)

A study performed at the University of Maryland, Baltimore, USA, published in Jan. 2007,
Title:”A review of the clinical efficacy and safety of 5alpha-reductase inhibitors for the
enlarged prostate”

Conclusion: alpha-blockers in men with enlarged prostate have reported improvements in
total symptom scores of 10% to 20% compared with placebo

Do not reduce the risk of long-term complications nor disease progression
12.3. Medical Treatment
5α-Reductase inhibitors

Finasteride is a 5α-reductase inhibitor that blocks the conversion of testosterone to
dihydrotestosterone. It affects the epithelial component of the prostate, resulting in a
reduction in the size of the gland and improvement in symptoms

Six months of therapy are required to see the maximum effects on prostate size (20%
reduction) and symptomatic improvement

Several randomized, double-blind, placebo-controlled trials have compared finasteride with
placebo. Efficacy, safety, and durability are well established

Symptomatic improvement is seen only in men with enlarged prostates (> 40 mL)

Side effects include decreased libido, decreased ejaculate volume, and impotence. Serum
PSA is reduced by approximately 50% in patients being treated with finasteride, but
individual values may vary, thus complicating cancer detection

Cost: $ 73 for 30 day supp.
12.3. Medical Treatment
5α-Reductase inhibitors (cont’d)


Dutasteride: not enough data! In 3 double-blind trials it reduced acute urinary retention
(1.8% versus 4.2%- placebo) and need for surgery (2.2% vs 4.1%) but increased impotence
( 7.3% vs 4.0%), ejaculation disorder, and gynecomastia and lowered libido
Cost: $84 for 30 day supp.
12.3. Medical Treatment
5α-Reductase inhibitors (cont’d)

Summary:

Significantly reduced the relative risk for acute urinary retention(AUR) and enlarged
prostate-related surgery, slowed the disease progression, and showed greater relief of
symptoms compared to placebo
Dutasteride, improved symptom scores greater after 4 years of therapy compared with 2
years (-6.4 vs -4.3 points, respectively) and flow rates were better (2.6 vs 2.3 mL/sec).
Finasteride showed maintenance of the decreased risk for AUR and enlarged prostaterelated surgery over 4 year period
Generally well tolerated, with sexual dysfunction the most frequently reported adverse effect
(1%-8%)



12.3. Medical Treatment
Combination therapy

Short term

Veterans Affairs Cooperative Study, 1229 men with BPH randomly assigned to placebo,
finasteride, terazosin or both for one year. Results as follow:

Terazosin lowered the symptom score and increased the peak urinary flow rate when
compared with placebo

Finasteride alone was no better than placebo

The combination of finasteride and terazosin was no better than terazosin alone
12.3. Medical Treatment
Combination therapy (cont’d)

Short term

PREDICT trial in which 1095 men were randomly assigned to doxazosin, finasterid or both
for one year. Resluts as follow:

Doxazosin more effective than finasteride or placebo for urinary symptoms and flow rate

Combination no more effective than doxazosine alone

Conclusion: Combination treatment with an alpha-blocker and a 5ARI is beneficial for
immediate relief of symptoms ( with discontinuation of the alpha-blocker after several
months of therapy)
12.3. Medical Treatment
Combination therapy (cont’d)

Long term

Medical Therapy of Prostatic Symptoms (MTOPS) trial-3047 men with BPH randomly assign.
to doxazosin, finasteride, combination therapy or placebo were evaluated for symptomatic
improvement and overall clinical progression of the BPH. Follow up 4.5 years. Results as
follow:

Risk of overall progression- reduced to a similar degree by doxazosin and finasteride (39
and 34% when compared to placebo)

Combination therapy reduced the risk of clinical progression by 66 %

Symptom scores improved with all therapies, but to a greater degree with combined therapy
Combination Therapy for BPH ( MTOPS Study )
12.3. Medical Treatment
Combination therapy(cont’d)

Combination therapy or finasteride alone (but not doxazosin alone), reduced the risk of
acute urinary retention and the need for invasive therapy

NNT(# needed to treat) to prevent one instance of overall clinical progression was 8.4 for
combination therapy, 13.7 for doxazosin, and 15.0 for finasteride

AE -similar with combination therapy and monotherapy, with the exception of abnormal
ejaculation, peripheral edema, and dyspnea, which were more common with combination
therapy

Conclusion: long-term combination therapy lowered the risk of overall clinical progression of
BPH significantly more than treatment with either drug alone. In addition, combination
therapy or finasteride alone (but not doxazosin alone), reduced the risk of acute urinary
retention and the need for invasive therapy
12.4. Phytotherapy

Saw Palmetto Extracts

Beta-sitosterol plant extract

Rye Grass Pollen Extract

Pygeum Africanum
12.5. Surgical Treatment
Conventional Surgical Treatment
 For patient who do not experience response to medical treatment in 12-
24 months; for those whose symptoms progress
 TURP (transurethral resection of the prostate)- Gold standard
 A resectoscope loaded with diathermy loop is introduced to the bladder
and strips of prostatic adenoma are resected and dropped into the
bladder. The prostate chips are extracted from the bladder and
hemostasis is achieved with electrocautery
 Under general anesthesia or with a regional block; 60-90 min.
Procedure.Requires 24-48 hours observation in hospital
12.5. Surgical Treatment
Conventional Surgical Treatment
12.5. Surgical Treatment
Conventional Surgical Treatment
 Efficacy- decrease in symptom scores and increase in maximal urinary
flow rates
 Complications: bleeding, urethral stricture/bladder neck contracture,
hyper/hypovolemia, retrograde ejaculation (75%), nausea, vomiting,
confusion, hypertension, bradycardia, and visual disturbances
 Treatment of complications : diuresis and hypertonic saline
administration for severe cases
12.5. Surgical Treatment
Conventional Surgical Treatment
 TUIP
(Transurethral incision of the prostate)

For moderate to severe symptoms and small prostate

Patients had posterior commisure hyperplasia or an “elevated bladder neck”; a
muscle resection is performed

Short-term improvement in BPH symptoms is about the same for TUIP as for
TURP

Lower rate of retrograde ejaculation (25%)
12.5. Surgical Treatment
Conventional Surgical Treatment
 Open Prostatectomy

Not done routinely

When prostate too large for TURP
(>100mL)

Concomitant conditions - bladder
diverticulum or bladder stone
present,recurrent or persistent urinary
tract infections,acute urinary
distention,bladder outlet
obstructions,recurrent gross hematuria of
prostate origin,pathological changes in
the bladder, ureters, or kidneys due to
prostate obstruction
12.5. Minimally Invasive
Surgical treatment
 TUMT-transurethral microwave therapy
 TUNA- transurethral needle ablation
 Urinary Stents
 Laser Prostatectomy
12.5. Minimally Invasive
Surgical treatment

TUMT(transurethral microwave therapy)

Performed as a single outpatient visit under local
anesthesia and an oral analgesic. Improves symptom
scores and urinary flow rates

(TUMT) uses a special catheter with a tip containing an
antenna to deliver microwave energy to the prostate, thus
causing high temperatures within the prostate without
affecting adjacent structures. The heat will kill prostate
cells, so the prostate will effectively become smaller and
less obstructing to urine flow. Sensors on the catheter and
on a tube in the rectum enable monitoring of the
temperatures throughout the procedure, and a cooling
system circulates water within the catheter to protect the
urethra

Disadvantages: the prostate may swell up right after
therapy due to the heat and a catheter is placed for a
week. The damaged prostate cells will be broken by the
body and its molecules re-used for several months

Symptoms may start decreasing after 3 weeks
12.5. Minimally Invasive
Surgical treatment

TUNA

An office procedure performed under local anesthesiaimproves symptom scores and urinary flow rates

It uses specially designed catheter through which
interstitial radio-frequency needles are deployed from the
tip of it. They will heat the tissue resulting in coagulative
necrosis

The entire procedure lasts 30-60 minutes

A catheter is left for 1-4 days after the procedure
(transurethral needle ablation)
12.5. Minimally Invasive
Surgical treatment
 Intraurethral Stent

Limited long term experience

Increases urine flow rates but causes secondary
obstruction by exuberant granulation tissue
growth through and around the stent

Difficult to remove it; formation of bladder calculi
in 50% of patients

Usually for patients with limited life expectancy
that are not good surgical or anesthetic
candidates

Abandoned by most urologists
12.5. Minimally Invasive
Surgical treatment

Laser Therapy- “The wave of the future”

Neodymium: yttrium-aluminium-garnet (Nd:YAG) -Visual
Laser ablation of the Prostate
The final result is coagulative necrosis of the prostatic
urethra and adjacent inner prostatic tissue. The obstructive
tissue starts to slough 4-8 weeks post-op leading to an
open prostatic urethra






Green light laser -Laser Vaporization of Prostate- causes
rapid vaporization of the superficial tissue, with a minimal
rim (2 mm) of coagulation
Advantage: immediate TUR-like efect of the prostatic
urethra, resulting in shorter duration of Foley
catheterization in the initial post-op period

Holmium-YAG- Laser resection- prostatic lobes are
resected into multiple small prostate chips that fall into the
bladder, similar to standard electrocautery TURP
Advantage:immediate anatomical patency of the prostatic
urethra, resulting in shorter duration of Foley
catheterization and higher peak flow rates in the initial
post-op period

12.5. Minimally Invasive
Surgical treatment
 Transurethral balloon dilation of the prostate

Performed with specially designed catheters

Most effective in small prostate (<40mL)

Does not produce retrograde ejaculation

May be of value in younger patients wishing to avoid or delay TURP, but is
unlikely to achieve wider application because of the transient effects

Very rarely used today
In Summary
 BPH (Benign prostatic hyperplasia) becomes increasingly common as
men age
 Many men with BPH are asymptomatic or have only mild symptoms,
and may not require therapy
 Men who develop upper or lower tract injury will require surgery
 Alpha-adrenergic antagonists provide immediate therapeutic benefits
and are first line treatment for smaller prostates <40mL and mild
symptoms
 5-alpha-reductase inhibitors require long-term treatment for efficacy
and are beneficial for larger prostates >40 mL mild to moderate
symptoms
In Summary
 Combined alpha adrenergic antagonist and 5-alpha-reductase inhibitor
therapy appears to be superior to either agent alone for long-term Trx
 The choice of medical treatment may be made on the basis of cost and
side-effect profile of the drug
 TURP is the GOLD STANDARD for men who require an invasive
procedure and are in good health
 Men that are poor candidates for surgery and require an invasive
surgical procedure should be advised on TUNA
 Other surgical therapies (TUMT, Laser) may be reasonable options
based on local expertise
Thank you
Questions???