Benign Prostate Hyperplasia: Aetiology, Pathology , Diagnosis and Medical therapy is a document that discusses benign prostate hyperplasia (BPH). It covers the etiology, pathology, diagnosis, and medical therapy of BPH. The document discusses risk factors for BPH like age, genetics, and hormones. It describes the pathological features of BPH including epithelial and stromal cell hyperplasia. Diagnosis involves history, exam, lab tests like PSA and ultrasound. Medical therapy options presented are watchful waiting, alpha blockers, 5-alpha-reductase inhibitors, and anticholinergics.

1. Benign Prostate Hyperplasia:
Aetiology, Pathology , Diagnosis and Medical therapy
Dr Mohamed Elsawy
Tutor: Dr Mostafa El-Missiry
5th Jan 2021

2. Agenda
• Introduction including modern terminology.
• Etiology
• Pathology
• Diagnosis
• Medical Therapy
• F/U

3. Terminology
BPH
Histologic
diagnosis
BPE
Enlargement due
to benign growth
(can be without
obstruction)
BPO
Urodynamically
proven BOO
BPH = benign prostatic hyperplasia; BPE = benign prostatic enlargement; BPO =
benign prostatic obstruction; BOO = bladder outlet obstruction
1.2

4. LUTS
• Symptoms attributable to lower urinary tract dysfunction
– storage (irritative) symptoms
– emptying (obstructive) symptoms
– may be associated with BPH, BPE, and BPO, but not exclusive to these
Nordling J et al. Benign Prostatic Hyperplasia. 5th International Consultation
on Benign Prostatic Hyperplasia. Paris, France. June 25-28, 2000:107-166.
1.4

5. Differential Diagnosis
• Urethral stricture
• Bladder neck
contracture
• Bladder stones
• Urinary tract infection
• Interstitial cystitis
• Neurogenic bladder
• Inflammatory prostatitis
• Medications
• Carcinoma of the prostate
• Carcinoma in situ of the
bladder
1.8

6. Berry SJ, et al. J Urol. 1984;132:474-479.
CDC. 2020 National Diabetes Fact Sheet.
Available at http://www.cdc.gov/diabetes/pubs/estimates.htm.
CDC. 2020 Forecasted State-Specific Estimates of Self-Reported Asthma Prevalence.
Available at http://www.cdc.gov/mmwr/preview/mmwrhtml/00055803.htm.
BPH
(Men Ages 61 to 72)
Diabetes
(Adults Over 65)
Asthma
(Entire Population)
0 25 50 75
Prevalence of BPH Versus
Other Common Conditions

7. Prevalence of Histologic BPH
Incidence is age dependent with BPH being
present in approximately 70% and 90% of
males in their seventh and ninth decades of
life, respectively.

8. Risk Factors
• Religion: Jewish associated with a high prostatectomy rate.
• Socioeconomic factors:
-Higher rate of BPH in higher income groups.
-Higher rate of surgery in lower income groups.
• Sexual activity: decreased SA and ED associated with BPH( could be
cofounding effect of age)
• Alcohol &cirrhosis: have been associated with lower rates of BPH as Alcohol
decrease testosterone level.

9. Risk Factors
• Hypertension: alpha adrenergic sympathetic fibers may play an imp. Role in
both BPH and HTN
• Obesity: Large adenoma are present in obese and may be due to increase
estrogen levels due to aromatization of testosterone to estrogen in adipose
tissues.
• Diet: Beef intake and lower consumption of vegetables associated with
development of BPH.

10. Risk Factors
• Smoking: associated with BPH as it increases testosterone.
• Medications exacerbate BPH:
- Cold meds containing alpha sympathomimetics
-Antihistamines
-Antidepressants.
-Bronchodilators.
• Vasectomy: no effect

11. Etiology
-BPH (hyperplasia) is characterized by an increased number of
epithelial and stromal cells in the peri-urethral area of the
prostate, through (proliferation or impaired programmed
cell death)
-Androgens, estrogens, stromal-epithelial interactions, growth
factors, and neurotransmitters may play a role

12. Role of Androgen
• It maintains ability to respond to androgens throughout life.
• AR levels remains high throughout life.
• Although androgens do not cause BPH, the development of BPH requires the
presence of testicular androgens during prostate development, puberty, and aging.
• Androgen suppress programed cell death in the gland leading to its growth.
• Patients castrated prior to puberty or who are affected by a variety of genetic
disease that impair androgen action do not develop BPH.
• Androgen withdrawal leads to partial involution of established BPH and drastic
vasoconstriction of blood vessels

13. Role of Androgen
• 90% of total prostatic androgen is in the form of DHT, principally derived from testicular
androgens.
• DHT is a more potent androgen in the prostate because of its higher affinity for the AR.
• Types of 5 α reductase enzyme
Type1 Type2
• (skin, liver, prostatic epithelium)
• Still made in 5 α reductase deficiency syndrome.
• Inhibited by Dutasteride.
• Prostatic stroma
• Involved in 5 α reductase deficiency syndrome.
• Inhibited by Dutasteride and Finasteride.

14. Role of Estrogens
• It is less clear.
– Serum estrogen levels increase in men with age.
– estrogen appears to be involved in induction of the AR

15. Stromal-Epithelial Interaction
• one class of stromal cell excretory protein (i.e., extracellular
matrix) partially regulates epithelial cell differentiation. 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.

16. Growth factors
• Growth stimulatory factors (eg FGF-
1, FGF-2, FGF-7, and FGF-17
families, vascular endothelial growth
factor (VEGF), and insulin-like
growth factor (IGF) ) may play a
role, with DHT augmenting or
modulating the growth factor effects.
• In contrast, TGF-β, which is known
to inhibit epithelial cell proliferation,
may normally exert a restraining
influence over epithelial proliferation
that is lost or downregulated in BPH

17. Potential Role of Inflammatory Pathways and Cytokines in BPH

18. Adrenergic Nervous System & BPH
– It may promote hyperplastic growth

19. Genetic & Familial Factors
– Autosomal dominant inheritance pattern
– Familial BPH was characterized by large prostate
• Mean PV 82.7ml in familial BPH compared to mean PV 55.5ml in
sporadic BPH
– 50% of men undergoing prostatectomy when younger than 60
years of age could be attributable to an inheritance form of
disease
– 9% of men undergoing prostatectomy when older than 60 would
have familial risk (Sanda et al 1994)

20. Pathophysiology

21. Pathology – Anatomic features

22. Pathology
• BPH first develops in the periurethral & transition zone of the
prostate as increased no. of epithelial and stromal cells.
• Epithelial budding occurs from the ducts with appearance of
mesenchymal nodules.
• Early in disease development there is an increased number of
nodules, then later there is a significant increase in large nodules.
• Predominant growth at the periurethral region near BN  middle
lobe
• Predominant growth at transitional zone lateral lobe

23. Pathophysiology
• Prostatic capsule plays an important role in the development
of LUTS.
– The capsule transmits the “pressure” of tissue expansion to the
urethra and leads to an increase in urethral resistance.
– Incision of the prostatic capsule (transurethral incision of the
prostate) results in a significant improvement in outflow
obstruction, despite the fact that the volume of the prostate remains
the same.
• The size of the prostate does not correlate with the degree of
obstruction.

24. Importance of Prostatic Smooth Muscle
• Prostatic smooth muscle represents a significant volume of
the gland
• Smooth muscle cells in the prostate/prostatic urethra are
under adrenergic nervous control.
• Thus, stimulation of this system will result in increase in
prostatic urethral resistance & blockage of this stimulation
will diminish that response (α1-receptor blockers)

25. Importance of Prostatic Smooth Muscle
• Other factors that may influence smooth muscle contraction
– Endothelin and endothelin receptors
– Kallikrein-kinin system
– Type 4 and type 5 phosphodiesterase isoenzymes in the prostate
and the detrusor muscle
– adrenergic neurotransmitters may play a role in prostatic smooth
muscle cell regulation.

26. The Bladder’s Response to Obstruction
• Increased IVP 
• Smooth muscle hypertrophy.
• Trabeculation.
• Development of cellules, saccules and diverticula.
• Sever trabeculation is associated with significant residual urine.
• Reduced bladder contractility or detrusor failure.
• Aging produces some of the same changes in bladder function, histology, and
cellular function.
• Atherosclerosis and chronic bladder ischemia or hypoxia induced by other
mechanisms (e.g., increased bladder wall tension) may contribute to bladder
pathology
• These changes leads to:
– Detrusor instability /decreased compliance: Storage symptoms
– Decreased detrusor contractility : Voiding symptoms

27. Presentation
• LUTS
• - storage symptoms: (frequency, nocturia, urgency)
• - voiding symptoms: (hesitancy, straining, weak stream,
intermittency, sense of incomplete emptying)
• AUR
• UTI
• Bladder stone
• Renal impairment.

28. Diagnosis
1. Detailed History.
2. Examination.
3. Micturition Diary.
4. Investigations.
5. Uroflowmetry.
6. Urodynamics.
7. Cystoscopy.

29. Detailed History
• IPSS

30. Detailed History
• Medical history: Hematuria, UTI, AUR, DM, Neurogenic
disease like parkinsonism, co-morbidities.
• Surgical history: prior LUT surgery raise the possibility of
urethral stricture or BN contracture.
• Drug History: identify drugs that impair bladder
contractility.
• Sexual function

32. Examination:
• Abdominal Ex.:
- Check for overdistended palpable bladder.
- Any hernia or masses.
• Penile Ex:
- Urethral discharge.
- Meatal stenosis.
- Phimosis
- Palpable urethral mass.

33. Examination
• DRE:
-Prostate is smooth , symmetrical, firm with exaggerated median
and 2 lateral sulci.
-Estimate size by evaluating degree of rectal bulging
1-2 finger mild
2-3 fingers moderate
>3 fingers huge
however it is poor estimation and TRUS is more accurate
-Check for changing consistency ( hard) or presence of nodularity

35. • Frequency volume charts and bladder diaries:
• Day-time and night-time voiding frequency,
• Total voided volume,
• The fraction of urine production during the night (nocturnal polyuria index),
• Volume of individual voids.

37. Laboratory Investigation
• Urine Analysis (dipstick or sediment)
-must be included to identify (UTI), microhaematuria and
diabetes mellitus.

38. Laboratory Investigation
• PSA:
• The potential benefits and harms of using serum PSA testing to diagnose PCa in
men with LUTS should be discussed with the patient.
• A strong association between PSA and prostate volume was found in a large
community-based study in the Netherlands . A PSA threshold value of 1.5
ng/mL could best predict a prostate volume of > 30 mL, with a positive
predictive value (PPV) of 78%.

39. Laboratory Investigation
• Patients with BPO seem to have a higher PSA level and larger prostate volumes
• The risk for treatment was higher in men with a baseline PSA of > 1.4 ng/mL.
• Serum PSA is a stronger predictor of
-prostate growth than prostate volume.
-changes in symptoms, QoL/bother, and maximum flow-rate (Qmax).
-clinical progression.
-baseline serum PSA predicted the risk of acute urinary retention (AUR) and BPE-
related surgery.
-elevated free PSA levels could predict clinical BPH, independent of total PSA levels.

40. Laboratory Investigation

41. Laboratory Investigation
• Urine Cytology:
Considered in men with sever irritative symptoms and
dysuria especially if they have a smoking history

42. • Serum Createnine measurement:
-To exclude renal insufficiency caused by obstructive BPO ( about 11% of men with LUTS had
renal insufficiency)
-Hydronephrosis, renal insufficiency or urinary retention are more prevalent in patients with
signs or symptoms of BPO.
-patients who presented with LUTS, decreased Q-max, a history of hypertension and/or
diabetes were associated with CKD
-Patients with renal insufficiency are at an increased risk of developing post-operative
complications
- Those with an elevated creatinine level require investigational ultrasound (US) of the kidney.

44. • Ultrasound KUB with Full UB & PVR:
( Cheap and provide imp. Data about)
It allows for characterization of renal hydroureteronephrosis, masses, evaluation of bladder,
prostate, and PVR
• Prostate size and shape
• Assessment of prostate size is important for the selection of interventional treatment.
• Prostate volume predicts symptom progression and the risk of complications .
• Transrectal US is superior to transabdominal volume measurement.
• The presence of a median lobe may guide treatment choice in patients scheduled for a minimally
invasive approach since medial lobe presence can be a contraindication for some minimally
invasive treatments .

45. • Post-void residual (PVR)
• High PVR volumes can be a consequence of obstruction and/or detrusor underactivity
• A large PVR is not a contraindication to watchful waiting (WW) or medical therapy, although it may
indicate a poor response to treatment and especially to WW.
• In MTOPS study, a high baseline PVR was associated with an increased risk of symptom progression.
• Monitoring of changes in PVR over time may allow for identification of patients at risk of AUR.
• It is of particular importance for the treatment of patients using antimuscarinic medication.
• No PVR threshold for treatment decision has yet been established; this is a research priority.

46. • Bladder Shape:
• Max volume.
• Wall thickness.
• Diverticula.
• Bladder stones.

48. • VCUG and ascending urethrography:
• Not routinely used unless VUR and urethral stricture are
suspected

49. • Uroflowmetry:
• Key parameters are Q-max & flow pattern
• An abnormal flow rate is below 15 ml/sec which may
indicate infra-vesical obstruction or detrusor underactivity.
• Preferable evaluated with voided volume of about 125ml.
• Used for monitoring treatment outcome.

51. • Pressure Flow Study:

52. Interpretation of P/Q stud
 P det.
& Normal
flow
Unobstructed
 Pdet.
 flow
 Pdet.
+ Normal
flow
 Pdet
 flow
Det under
activity Obst. +
 det.
activity
Obst.
Grey zones

53. • Videourodynamics
• It provides additional anatomical and functional information
and may be recommended if the clinician considers this is
needed to understand the pathophysiological mechanism of
an individual patient’s
• LUTS.

54. • Non invasive pressure flow testing:
• The penile cuff method in which the flow is interrupted to
estimate isovolumetric bladder pressure, shows promising
data.

55. • Cystourethroscopy:

56. Complication of BPH
AUR 5%
• The risk of AUR increase with increasing prostate size,
increase PSA
• Types: precipitated(26%underwent surgery)or
spontaneous(75%underwent surgery)
• Risk factors: medications, prostatic infection, constipation,
sexual activity, excessive fluid intake, bladder
overdistension, bed rest.

57. Hematuria 2.5%
• Ep compress prostatic venous plexus leads to venous
congestion and venous rupture.
• Other pathology as Ca bladder must be excluded.
• Finasteride is the first line therapy as it influencing the
expression of VEGF.

58. UTI:
• High PVR may predispose to UTI.
Bladder stones(0.7%):
• 8 times higher in men with BPH than the control group.
Upper tract deterioration and Azotemia 13%
• Renal failure increase the risk for operative complication and
mortality rate after TURP.

59. Bladder decompensation
• Due to bladder changes (wall thickening, diverticula) which
end with DUA
Urinary incontinence
• Overflow or UI

60. SEVERITY INDEX

61. CURRENT TREATMENT OPTIONS
• Non-surgical management:
– Conservative treatment (Watchful Waiting)
– Medical management:
• Alpha blockers
• 5-alpha-reductase inhibitors (5ARIs)
• Anticholenergics
• PDE5I
• Combination therapy
• Phytotherapy
• Surgical management:
– Minimally invasive techniques
– Surgery

62. GOAL OF TREATMENT
• ↓ symptoms (IPSS/AUA)
• ↓ bother (bother score) and ↑ QOL
• ↓ prostate size or arrest further growth
• ↑Increase in peak flow rate / Relieve obstruction
• Prevention of long-term outcomes/complications
• Acceptable adverse events profile

63. WW

64. WHICH PATIENT ??
Watchful waiting is suitable for mild-to-moderate
uncomplicated
LUTS minimally bothered by their symptoms

65. EDUCATION AND REASSURANCE
• Discuss the causes of LUTS, including normal prostate and bladder function.
• Discuss the natural history of BPH and LUTS, including the expected future symptoms.
• Reassure that symptoms not caused by cancer .
• FLUID MANAGEMENT
• Advise a daily fluid intake of 1500 to 2000 mL
(minor adjustments made for climate and activity).
• Avoid inadequate or excessive intake
on the basis of a frequency-volume chart.
• Advise fluid restriction when symptoms are most inconvenient (e.g., during long journeys or when out in
public).
• Advise evening fluid restriction for nocturia
(no fluid for 2 hours before retiring).
• Avoid caffeine and carbonated drinks.
•Avoid alcohol in the evening if nocturia is bothersome.

66. • TYPES OF TOILETING AND BLADDER RETRAINING
• Advise men to double-void.
• Advise urethral milking for men with postmicturition dribble.
• Advise bladder retraining.(distraction techniques, increase the minimum time between voids, urge to
void should be suppressed
•Avoid constipation
•CONCURRENT MEDICATION
• Adjust the time when medication with an effect on the urinary system is taken, to improve LUTS at times
of greatest inconvenience (e.g., during long journeys and when out in public).
• Replace antihypertensive diuretics with suitable alternatives with fewer urinary effects (via the patient’s
general practitioner).
•F/U:
• Periodic monitoring is advised .
• Failure rate over period of 5 years was 20% .
• Increasing IPPS score and PVR are strong predictors of failure.

67. Medical Treatments for
BPH, LUTS, BOO
– 1-adrenergic blockers
– Dynamic component
– 5 -reductase inhibitors
– Anatomic component
– Anticholinergic Therapy
– Storage Sx’s
– Phosphodiesterase 5 inhibitors
– Dynamic component
– Beta 3 agonist
– Storage Sx’s
– Phytotherapy

68. Alpha Blockers
1-ARs and Human LUTS
Smooth muscle
contraction
1A
Lumbosacral
1D
Instability
Irritative
symptoms
1D>1A
Resistance
vessels
1A
Aging effects
1B>1A
Spinal cord
Prostate Detrusor Vessels
Schwinn DA. BJU Int. 2000;86:11-22.
Jardin A et al. Benign Prostatic Hyperplasia. 5th International Consultation on Benign
Prostatic Hyperplasia. Paris, France. June 25-28, 2000:459-477.
Rudner XL et al. Circ. 1999;100:2336-2343.
2.8

69. Comparison of -Adrenergic Blockers
Agent Dosing Titration Uroselective
Terazosin
(Hytrin®)
1 mg, 2 mg,
5 mg, 10
mg, 20 mg
+ NO
Doxazosin
(Cardura®)
1 mg, 2 mg,
4 mg, 8 mg,
16 mg
+ NO
Alfuzosin 10 mg - YES
(Highly diffused in prostatic
tissue vs serum)
Tamsulosin
(Flomax®)
0.4 mg,
0.8 mg
+/-
(for improved
efficacy)
YES
(Relative affinity for 1A
receptors over 1B )
Silodosin 8 mg - Yes
Relative affinity for 1A

70. • Mechanism of action:
• Inhibit the effect of noradrenaline on smooth ms cells of
prostate reducing prostate tone and BOO.
• Alpha 1 receptors located outside the prostate(UB & spinal
cord) and alpha 1 adrenoreceptors subtypes (Alpha 1 B or
alpha 1D) may play a role as mediators.

71. • Efficacy:
• α1-blockes have a similar efficacy in appropriate dose.
• Effect over placebo takes few hours and takes a few weeks
to be fully develop .
• Reduce IPPS by 40%, and increase q-max by 25%.
• It is neither reduce prostate size nor prevent AUR.
• It is more efficacious on small prostate <40 ml in long term
studies.

72. • Tolerability and Safety:
• Dizziness
• Postural hypotension.
• VD ( more for doxazocin, Terazosin & alfuzosin, less for Tamsulosin and silodosin) caution
should be taken with other CVS medications causing VD to avoid (induced VD that leads to
hypotension).
• Silodosin has no VD effect.
• IFIS affecting cataract Surgery ( Not to be given before cataract surgery and ophthalmologist
should be aware about its use).
• Abnormal ejaculation with young age being an apparent risk factor. (more with Silodosin and
Tamsulosin), not present in doxazocin and alfuzosin. Silodosin higher than Tamsulosin
(P<0.00001).
• Meta analysis showed that the more effective the α-blocker (improvement in urinary symptoms
and flow rate) the greater the incidence of ejaculatory disorders.

73. • Practical consideration:
• α1-blockers should be considered the first line treatment for
LUTS due to rapid onset of action, good efficacy and better
tolerability.
• In young age better to start with α1-blockers that do not
increase EJD like Alfuzosin.
• α1-blockers do not reduce risk of AUR or need for surgery.

75. 5α-reductase inhibitors
• MOA:
• Finasteride and Dutasteride.
• Have similar potency.
• Reduce prostate size by 20% over a period of 6 months by
inducing apoptosis of epithelial calls.
• It decreases PSA levels of about 50%.
• It causes VC of prostatic BVs

76. • Efficacy:
• Clinical effect seen after a minimum treatment duration of 6-12 mo.
• It reduce prostate size by 25%, reduce IPPS by 30%and increase Q-max 2ml/s in pt with LUTS
dt PE. (after 2-4 years.
• Finasteride may not be effective than placebo in Prostate<40cc.
• Dutasteride reduce prostate size, IPPS, risk of AUR & increase Q-max.
• In a study comparing Dutasteride to Tamsulosin in prostate >30cc showed that Dutasteride
reduce LUTS as or even more than Tamsulosin, the greater the prostate size the more
pronounced the benefit of Dutasteride over Tamsulosin
• In another study It reduce the risk of AUR and need for surgery after 1 year over Tamsulosin.
• In MTOPS study Finasteride reduces the risk of AUR and need for surgery by 68%, 65% over
placebo.
• Finasteride might reduce risk of bleeding during TURP dt its prostatic VC effect.

77. • Results:
• Combination therapy was significantly superior to tamsulosin
monotherapy but not dutasteride monotherapy at reducing the relative
risk of AUR or BPH-related surgery.
• Combination therapy was also significantly superior to both
monotherapies at reducing the relative risk of BPH clinical progression.
• Combination therapy provided significantly greater symptom benefit than
either monotherapy at 4 yr.

78. Medical Therapy of Prostatic Symptoms
(MTOPS)

79. • Tolerability and safety:
• ED
• Reduce libido
• Less frequently EJD
• Gynecomastia.

80. • Practical consideration
• 5α-reductase inhibitors should be considered in patients
with moderate to sever LUTS and EP >40 cc and or
elevated PSA >1.5ng/ml.
• Due to slow onset of action it is suitable for long term
treatment (years) so patient should be counseled.
• Their effect on PSA needs to be considered for PCa
screening.

82. Muscarinic receptor antagonit
• MAO:
• 5 muscarinic receptors subtypes have been described.
• M2&M3 are present in UB, M2 are numerous but M3 are
important for contraction.
• Used for treatment of OAB / storage symptoms.
• Types of licensed muscarinic antagonist (Darifenacin,
Fesoterodin, oxybutynin, propiverin, solifenacin,
tolterodine, trospium chloride, transdermal oxybutynin)

83. • Efficacy:
• They significantly improve urge incontinence, urgency and
day time frequency (IPPS storage score).
• Theoretically they might decrease bladder strength and
hence might be associated with increased PVR and urine
retention.( a 12 week safety study on men with mild to
moderate BOO showed that Tolterodine increased the PVR
(49ml vs 16 ml) but not AUR (3% in both arms)

84. • Tolerability & safety:
• Withdrawal 3-10%
• Dry mouth 16%
• Constipation 4%
• Micturition difficulties 2%
• Nasopharyngities3%
• Dizziness 5%

85. • Practical consideration:
• It should prescribed with caution in elderly and PVR should
be regularly re-evaluated.
• It should be stopped if worsening urinary stream or voiding
LUTS is noted

87. Phosphodiesterase 5 inhibitors
• MOA:
• Increase intracellular cyclic guanosine monophosphate
leading to reduction in smooth muscle tone of the detrusor,
prostate and urethra.
• Increase blood perfusion and oxygenation in the LUT.
• Reduce chronic inflammation of prostate and bladder.
• Available drug Tadalafil 5 mg

88. • Efficacy:
• Several RCTs have demonstrated that PDE5I reduce IPPS ” by
30%”, storage, voiding LUTS, IIEF and improve QOL however Q-
max did not significantly differ from placebo ” in another placebo
controlled clinical studies there was a small but significant increase
in Q-max)
• Combination with alpha blockers  significant improvement in
IPPS, IIEF and Q-max.
• Combination with 5α-reductase (Finasteride)  early improvement
of IPPS, IIEF and QOL

89. • Tolerability and safety:
• It is CI in patient taking Nitrates, Doxazocin, Terazosin,
potassium channel opener Nicorandil, unstable angina,
recent MI, recent stroke, CHF, hypotension, uncontrolled
BP, significant hepatic or renal insufficiency, and known
optic neuropathy with sudden loss of vision from previous
PDF5I
• SE: flashing, GIT upset, headache, back pain and nasal
congestion.

90. • Practical consideration:
• Only Tadalafil 5 mg is the officially licensed for LUTS with
or without ED.
• Younger men with low body mass index and more sever
LUTS benefits more from PDE5I

92. Beta3 agonist
• MOA:
• Stimulation produce detrusor relaxation.
• Efficacy:
• It improved Urgency, UI, and micturition frequency.
• SE:
• HTN (BP to be measured before starting and monitored regularly
during treatment), UTI, headache and nasopharyngitis.
• Dry mouth and constipation were notably lower than reported with
other antimuscarinic.
• Overall change in PVR is small

93. • Practical consideration:
• Used in patient with storage LUTS.
• In patients aged > 65 years, a more favorable tolerability
profile for mirabegron than antimuscarinics

95. Combination therapy
• α1- blocker with 5 α-reductase inhibitors.
• α1- blocker with muscarinic receptor antagonist.
• Tadalafil 5 mg with α1- blocker.
• Tadalafil 5 mg with finasteride.

96. Alpha-
Blockers:
Relieve
Symptoms
Rapidly
5-Reductase
Inhibitors:
Arrest Disease
Progression
Combination Therapy: Arrest Disease Progression
and Rapidly Relieve Symptoms
α1- blocker with 5 α-reductase inhibitors.
Rationale for
Combination Therapy

98. α1- blocker with muscarinic receptor antagonist
• Use this combination in patient with moderate to sever
LUTS if relieve of storage symptoms has been insufficient
with monotherapy of either drug.
• Do not prescribe in men with PVR>150ml as there is a low
risk of AUR.
• Measuring PVR is recommended during combination
therapy.

99. • In a meta-analysis of sixteen studies with 3,548 patients with
BPH/OAB, initial combination treatment of an α1-blocker with
anticholinergic medication improved storage symptoms and QoL
compared to α1-blocker monotherapy without causing significant
deterioration of voiding function.

101. Tadalafil 5 mg with α1- blocker.
• Significantly improve IPPS and IIEF score and Q-max
compared to α1- blocker alone.

102. Tadalafil 5 mg with finasteride.
• This combination provides an early improvement in urinary
symptoms with significant improvement of storage and
voiding symptoms and QOL.

103. Phytotherapy(plant extract)
• Harpal drugs(pumpkin seeds, saw palmetto)
• Mechanism remains unclear
• anti-inflammatory, antiandrogenic, or oestrogenic effects
• Decrease sexual hormone binding globulin (SHBG)
• Inhibit aromatase, lipoxygenase, growth-factor stimulated proliferation of
prostatic cells, Α-adrenoceptors, 5α-reductase, muscarinic cholinoceptors,
dihydropyridine receptors, or vanilloid receptors
• Improve detrusor function
• Neutralize free radicals .

104. • Almost has no SE (GIT upset)
• In a short term study Combining (Serenoe Repens, lycopenes and
selenium with Tamsulosin has a promising results as it improved
IPPS and increased Q-max in patient with LUTS at 12 months in the
combination group compared to Tamsulosin alone.
• There is no guidelines on its use due to product heterogenicity
(different concentrations of active ingredients); therefore, meta-
analyses should be interpreted with caution.

105. F/U
• F/U visits : history, IPPS, FVC, uroflow, PVR, PSA” 5ARI,
life expectancy>10 years, diagnosis of PCa could alter
management”.
• 4-6 weeks after drug initiation to determine the treatment
response and SE.
• 6 months.
• Annually.

106. Thank you