Benign prostatic hyperplasia by Sayed Eleweedy

1. Benign Prostatic Hyperplasia Sayed M Eleweedy Prof. Of Urology Urology Department Alazhar University

2. Benign Prostatic Hyperplasia Definition A regional nodular prostatic growth of varying combination of glandular and stromal (fibromuscular) proliferation that occurs in almost men who have testes and who live long enough Hyperplasia not hypertrophy

3. Benign Prostatic Hyperplasia Definition and terminology • Microscopic BPH • Histological evidence of cellular proliferation • Macroscopic BPH • Organ enlargement due to cellular proliferation • Clinical BPH • LUTS thought to be due to BPH

4. Benign Prostatic Hyperplasia Definition and terminology BPH (benign prostatic hyperplasia) – for histological diagnosis only BPE (benign prostatic enlargement) – for anatomical diagnosis only BOO (bladder outlet obstruction) – for functional diagnosis only BPO (benign prostatic obstruction) – functional diagnosis when the prostate is the cause. LUTS – Instead of prostatism

5. Prevalence of pathological BPH with age 48% 29% 11% 92% 87% 77% 31-40 41-50 51-60 61-70 71-80 81+ Age (years)

6. Benign Prostatic Hyperplasia Prevalence Clinical BPH develop in 20-50% of men with microscopic or macroscopic BPH Clinical BPH in 5-30% of men ages 55-74 years. Only 40% of them complain of LUTS. Only 20% of them seek medical advice.

7. Prostatic Configuration  LOBAR CONFIGURATION (LOWSLY) Anterior, Posterior, Middle and 2 Lateral Lobes  ZONAL CONFIGURATION( McNEAL, 1972, 1968, 1980) Anterior fibromuscular stroma (30% of the prostatic volume) Glandular part (70% of the prostatic volume) Peripheral zone Central zone Transition zone

8. Prostatic Configuration Fibromuscular stroma 30% of the prostatic bulk Has no specific pathology Peripheral zone 75% of the glandular tissue Site of cancer Central zone – Between peripheral and transition zone Has no specific pathology Transition zone Periurethral zone Site of BPH

9. Schematic coronal section of normal prostate

10. Schematic coronal section of enlarged prostate

11. Schematic transverse section of normal prostate

12. Schematic transverse section of enlarged prostate Typical location of benign nodular hyperplasia. Posterior displacement of both peripheral and central zones.

13. Prostate Growth

14. DHT- a determinant of prostate growth DHT thought to exert influence over prostate cells via cascade of molecular interactions Androgenic action of DHT dependent upon the binding to the high affinity nuclear androgen receptor (AR) protein Androgen receptor proteins contain both DHT and DNA binding domains Affinity of binding of DHT to AR complex is 5 times higher than with Testosterone

15. DHT formation Testosterone (T) is the principal androgen secreted by the testis T is converted to DHT by the enzyme 5 a-reductase (5-AR) DHT is the active intracellular androgen that has the major androgenic effect This provides the scientific basis for the advent of 5-AR inhibitors for the management of BPH

16. Type 1 Type 2 Size 259 amino-acids 254 amino acids Gene location Chromosome 5 Chromosome 2 Enzyme location Liver Non-genital skin Scalp Genital tissue Seminal vesicles 5-alpha reductase enzymes Occurs as two isoenzymes type 1 and type 2

17. Growth factors and prostate development A number of growth factors, expressed by mesenchymal or epithelial components of the prostate have been identified: –Stimulatory growth factors : Epidermal growth factor EGF, Fibroblast growth factor FGF Insulin-like growth factor IGF Transforming growth factor TGF a – Inhibitory growth factors : Transforming growth factor TGF- b

18. Growth factors and prostate development + Androgen ― Androgen TGFb1 EGF bFGF1/FGF2 TGFb1 Apoptosis Cell Proliferation Apoptosis Cell Proliferation An almost homeostatic relationship between TGFb1 (growth suppressing) and the Stromal growth promoter bFGF/FGF2 This suggests a degree of resilience to variation in androgen level which may explain the comparatively slow normal growth of the prostate in response to continuous exposure to DHT

19. BPH Development & Aetiology

20. BPH Development BPH develops in various stages; Induction of microscopic hyperplasia Development of microscopic nodules Manifestation of clinical BPH : – Prostatic enlargement – Bladder outlet obstruction – LUTS

21. BPH Development Microscopic Stromal nodules begin to grow within the prostate around the age of 30 - 40 years The nodules occur around the transition zone in the Periurethral area and glandular hyperplasia then develops around them Nodules vary in size from a few mm to a few cm and contain either: – Glandular elements – Fibromuscular elements (Stromal generally the larger component) – Mixture of both The nodules will continue to grow in most men when they age

22. BPH Development As the amount of glandular tissue grows, the outer layer of prostate tissue becomes compressed A tough capsule is created which forces the gland to form lobes The size and position of the lobes relative to the bladder and urethra can impact the type and severity of LUTS If the enlarged prostate encroaches on the urethra obstruction can occur, but this can also result from an alteration of prostate smooth muscle contractility or by the prominent median lobe of the prostate behaving as a ball valve

23. Development of BPH : Early

24. Development of BPH : Intermediate

25. Development of BPH : Late

26. Normal bladder and prostate BPH is the most common neoplasm in man Pathological changes of this disorder can be found in 50% of men in their 5th decade and in 90% of men in their ninth decade The aetiology of BPH is multifactorial but there are two essential prerequisites: the presence of testes and ageing

27. Pathophysiology Prostatic hyperplasia increases urethral resistance, resulting in compensatory changes in bladder function.

28. The median lobe projects into the base of the bladder The prostatic urethra narrows The bladder shows trabeculation and thickening of the wall Benign prostatic enlargement

29. Thickening of the bladder wall Recurrent hematuria Bladder diverticulum formation Urinary tract infections Bladder stone formation Upper tract dilation Effects of Benign prostatic obstruction

30. Renal damage Renal damage from obstructive uropathy due to BOO (bladder outlet obstruction) is a feared complication It can happen in men with minimal symptoms and the renal impairment is not always reversible The risk of a man with symptoms of BOO developing renal failure whilst under follow up is not known for certain but is minimal

31. Bladder Changes Flow is maintained in the early phases of outflow obstruction, as a result of hypertrophy of the detrusor muscle allows an increase in detrusor pressure As outflow obstruction progresses, smooth muscle hypertrophy occurs followed by connective tissue infiltration and reduced parasympathetic innervations Impaired emptying results, caused by decreased compliance in the bladder wall and secondary detrusor instability, due to the previous events Ultimately these changes translate into the persistent symptoms of frequency, urgency and urge incontinence

32. Aetiology of BPH – principal hypotheses The molecular processes underlying the development of BPH are not completely understood, but androgens and age play a central role Several hypotheses have been proposed – Dihydrotestosterone (DHT) hypothesis – Oestrogen-testosterone imbalance – Stromal-epithelial interactions – Reduced cell death – Stem cell theory

33. Aetiology of BPH – Dihydrotestosterone hypothesis Adapted from Kirby et al. 199 Dihydrotestosterone (DHT) is the main androgen responsible for prostate growth. two isoenzymes of 5-alpha-reductase have been identified 5-alpha- reductase inhibitors suppress DHT formation.

34. BPH Appearance A characteristic of the gross appearance of BPH are rubbery yellow/grey nodules of variable size within the prostate gland The nodules are composed of epithelium, smooth muscle and fibrous tissue in varying amounts Ratio of Stromal tissue to epithelium in BPH varies and has been suggested to determine the symptomatology of a BPH patient

35. Pathologic phase of BPH Histological changes occur within the prostate but no symptoms Changes result as a consequence of a neoplastic transformation of prostatic cells The prostatic cells begin to behave like embryonic cells, budding off existing ducts These later organise to form modules of stroma and glandular epithelium

36. Macroscopic phase of BPH Not all men with histological BPH progress to the macroscopic phase The prostate becomes grossly enlarged and symptoms become apparent in some men As the amount of glandular tissue grows, the outer layer of prostate tissue is compressed This creates a tough capsule that forces the growing gland to form lobes The type of severity of symptoms appears to be related to the size and position of the lobes relative to the bladder and urethra

37. Benign Prostatic Hyperplasia Etiologic Theories Unclear Factors association Androgens, estrogens, Stromal-epithelial interactions, growth factors, and neurotransmitters may play a role, either singly or in combination, in the etiology of the Multiple factors – HORMONES Functioning testes (ANDROGEN INFLUENCE) DHT Prostate growth, maintenance of size and function Abnormal accumulation of DHT is the primary cause of BPH Estrogen/Androgen synergism

38. Benign Prostatic Hyperplasia Correlated Factors AGE TESTES – Smoking – Race – Diet – Body habitus – Sexual history – Vasectomy – Medications – Diseases

39. Benign Prostatic Hyperplasia Etiologic Theories Stromal-epithelial Interaction Theory – The stroma may mediate the effect of androgen on the epithelial components by production various growth factors

40. Benign Prostatic Hyperplasia Etiologic Theories STEM CELL THEORY – Abnormal maturation and regulation of the cell renewal process may result into BPH. – Hormones, growth factors and oncogens may affect this abnormalities.

41. Benign Prostatic Hyperplasia Etiologic Theories Static And Dynamic Components – STATIC: Prostatic bulk Stromal, epithelial and extracellular matrix – Androgen ablation affect epithelial volume – Therapeutic modalities to reduce the size of the prostate – DYNAMIC COMPONENT Alpha adrenergic receptors Obstruction by prostatic smooth muscle – Responsible for variation of symptoms – Therapeutic modalities that interact with receptors

42. Stromoglandular hyperplasia of the prostate showing glandular (upper left) and Stromal (lower right) tissue

43. Benign Prostatic Hyperplasia Etiologic Theories Aging, perhaps through vascular mechanisms, leads to further alteration in bladder biology that in all likelihood amplifies the effects of obstruction. Prostate growth is only one component of LUTS in aging men. Physicians tend to overlook the significant contribution of aging, bladder dysfunction, nervous system changes, and systemic disease that in many cases has more impact on symptoms than the size of the prostate.

44. Natural history The natural history of a disease process refers to the prognosis of the disease over time BPH Is slowly progressive disease Spontaneous improvement within(1-5y) – 18-32% subjective improvement – 15-32% no change – 16-60% worsening – Placebo response 20-40% – Watchful waiting: 42% improvement – Placebo/sham studies: 30% improvement

45. Complications Bladder stones UTI Bladder decompensation Urinary incontinence – Overflow – Detrusor overactivity Upper urinary tract deterioration and Azotemia – 0.3-30 % of patients with BPH Hematuria – Microvessel density is high in patients with gross hematuria – Finatstride and treatment of hematuria associated with BPH Acute urine retention Mortality

46. Benign Prostatic Hyperplasia Clinical Picture Symptoms Prostatism LUTS (not symptom specific for BPH) Irritative Obstructive

47. Benign Prostatic Hyperplasia Clinical Picture Symptoms OBSTRUCTIVE – Impairment in the size and force of stream – Hesitancy – Intermittency – Incomplete voiding – Abdominal straining – Terminal dribbling

48. Benign Prostatic Hyperplasia Clinical Picture Symptoms IRRITATIVE – Nocturia – Daytime frequency – Urgency – Urge incontinence – Dysuria

49. Benign Prostatic Hyperplasia Clinical Picture Symptoms The primary focus of initial evaluation and diagnostic testing is to establish that the symptoms are, in fact, a result of BPH. Nonprostatic causes of symptoms can be excluded in a significant majority of patients on the basis of history, physical examination, and urinalysis. Additional diagnostic testing is necessary in patients in whom the diagnosis is still unclear after initial evaluation

50. Benign Prostatic Hyperplasia Clinical Picture Signs Anatomic Enlargement Of The Prostate (Examination Or Imaging)

51. Benign Prostatic Hyperplasia Clinical Picture Signs BLADDER CHANGES – Wall thickening – Trabeculation – Diverticular formation – Calculi – Chronic distention – Large residual urine – Acute retention – UTI – Hematuria

52. Benign Prostatic Hyperplasia Clinical Picture Signs Upper Urinary Tract – Ureterctasis – Hydroureter – Hydronephrosis – Azotemia

53. Benign Prostatic Hyperplasia Clinical Picture Signs Urodynamic Signs – Decreased Peak flow rate – Elevated detrusor pressure – Increase residual urine – Bladder hyperactivity

54. Benign Prostatic Hyperplasia Clinical Picture Signs Residual Urine – Measurement Ultrasonography Catheter – 50-100 ml is significant

55. Benign Prostatic Hyperplasia Clinical Picture Signs UROFLOWMETRY – Least controversy – Diminished flow Obstruction Hypoactive bladder – Peak flow <10 ml/sec >15 ml/sec 10-15 ml/sec

56. Benign Prostatic Hyperplasia Clinical Picture Signs CMG and Pressure Flow Studies – Filling Cystometry information Sensation Compliance Involuntary bladder contraction Bladder capacity – Relationship between flow rate and detrusor contractility

57. Differential diagnosis ImagingLabExaminationPast history Symptoms ++ Cystitis ++ Prostatitis +++Urethral stricture +++ Prostatic cancer +++ Neurogenic bladder +Bladder stone

58. Benign Prostatic Hyperplasia Clinical Picture Initial evaluation Medical History – A detailed medical history should be obtained to identify other causes of voiding dysfunction or co morbidities that may complicate treatment. – Assessment of LUTS symptom severity and bother Physical examination – DRE – Focused neurological assessment Urinalysis Serum creatinine and imaging of UUT PSA (if life expectancy>10years, if the diagnosis of prostate cancer can modify the management and before treatment with 5α-reductase inhibitors)

59. Symptom Assessment The International Prostate Symptom Score (IPSS) is recommended as the symptom scoring instrument When the IPSS system is used, symptoms classified as: – Mild (0 to 7) – Moderate (8 to 19) – Severe (20 to 35). IPSS is the ideal instrument to; – Grade baseline symptom severity – Assess the response to therapy – Detect symptom progression in those men managed by watchful waiting. IPSS cannot be used to establish the diagnosis of BPH.

60. Additional Diagnostic Tests Additional testing should be considered after the initial evaluation if there is a significant chance the patient’s LUTS may not be due to BPH. 1. Urinary flowrate 2. Postvoid residual (PVR) urine volume 3. Pressure-flow urodynamic studies 4. Cystourethroscopy 5. Imaging of the UUT: – Hematuria – UTI – Renal insufficiency – History of Urolithiasis – History of urinary tract surgery

61. Benign Prostatic Hyperplasia Evaluation Men with Symptom score <7 – No absolute or near-absolute indication for treatment – No further investigation – WATCHFUL WAITING

62. Benign Prostatic Hyperplasia Evaluation Patient with severe symptoms Candidate for active treatment – Urodynamic Flowmetry Residual urine – Cystoscopy Other LUT pathology Prior to treatment

63. Voiding time T100 13.5 s Flow time TQ 12.5 s Time to max. flow TQmax 4.8 s Max. flow rate Qmax 18.5 ml/s Average flow rate Qave 12.2 ml/s Voided volume Vcomp 158.0 ml 70 year old man normal flow trace Uroflowmetry: Unobstructed

64. Uroflowmetry: Obstructed Voiding time T100 68.0 s Flow time TQ 48.5 s Time to max. flow TQmax 6.2 s Max. flow rate Qmax 7.0 ml/s Average flow rate Qave 2.7 ml/s Voided volume Vcomp 133.0 ml 70 year old man moderate obstruction due to BPH reduced average and peak flow prolonged duration

65. :Uroflowmetry Urethral stricture Voiding time T100 117.0 s Flow time TQ 115.0 s Time to max. flow TQmax 0.5 s Max. flow rate Qmax 5.5 ml/s Average flow rate Q ave 4.9 ml/s Voided volume Vcomp 567 ml 50 year old man plateau shaped trace similar Qmax and Qave long duration

66. Post-void Residual UrineVol (PVRV) PVRV measurement is performed non-invasively using Transabdominal U/S It can be useful in assisting with treatment decisions It should not be used alone to diagnose BPH Patients found to have a large PVRV should receive active treatment Otherwise they may be more likely to develop AUR or fail conservative therapy Although an increased PVRV may be indicative of obstruction More than one measurement should be made Variation has been known to occur between voids PVRV measurement can also be useful for monitoring: • improvement or worsening of BPH in non-treated patients

67. Benign Prostatic Hyperplasia Indication Of Treatment Absolute Or Near-absolute  Refractory or repeated retention  Renal insufficiency  Recurrent significant hematuria  Recurrent UTI  Bladder calculi  Large residual urine  Overflow incontinence  Large bladder diverticulae

68. Benign Prostatic Hyperplasia Treatment Options Watchful waiting Pharmacologic Mechanical Endoscopic Surgical

69. Benign Prostatic Hyperplasia Treatment Options Watchful waiting Reassured that the symptoms are not caused by cancer or other serious genitourinary pathology, or that the delay in treatment will not have irreversible consequences Decreasing total fluid intake especially before bedtime Moderating the intake of alcohol- and caffeine-containing products Maintaining timed voiding schedules.

70. Benign Prostatic Hyperplasia Treatment Options Medical treatment Medical therapy is currently considered the preferred treatment Alternative for those individuals who lack absolute indications for surgery. – α-adrenergic blockers – 5α-reductase inhibitors, – Aromatase inhibitors (decreasing the estrogen) – Plant extracts. – Newer therapies: Antimuscarinic drugs Phosphodiesterase inhibitors (PDEIs)

71. Benign Prostatic Hyperplasia Treatment Options Pharmacologic Reduce Prostate smooth Muscle tone – Alpha adrenergic antagonists Reduce Prostate Bulk – 5 alpha reductase inhibitors (androgen suppression) Unknown – Phytotherapy – Others

72. Medical treatment Alpha blockers: – Non-selective – Selective short acting – Selective long acting (alfuzosin, doxazosin, terazosin) – Selective alpha 1a blockers (tamsulosin) 5 alpha reductase inhibitors – Finasteride – Dutasteride Combination Phytotherapy

73. Benign Prostatic Hyperplasia Treatment Options Mechanical Prostatic urethral stent Balloon dilator Transurethral thermotherapy – TUMT – TUNA LASER HIFU

74. Benign Prostatic Hyperplasia Treatment Options Endoscopic Transurethral resection Transurethral incision – Electrosurgery – Laser – Electrovaporization

75. Benign Prostatic Hyperplasia Treatment Options Surgical Transvesical Retropubic Perineal

76. Minimally Invasive Treatment For Benign Prostatic Hyperplasia

77. INTRODUCTION TURP • Gold Standard For Decades • Last Decades Challenges : • Medical Therapy • Minimally Invasive Treatments

78. Minimally Invasive Treatments  Thermal-based Therapy  Laser Therapies  TUVP  Balloons And Stents  Chemoablation

79. Thermal-based Therapy  Use of high temperature  Within the prostate  Coagulative necrosis

80. Thermal-based Therapy Hyperthermia Temperature < 45 Thermotherapy (TUMT) Temperature < 45 Low-energy TUMT High-energy TUMT

81. Thermal-based Therapy Hyperthermia  Temperature Below 45  Transurethral  Transrectal

82. Thermal-based Therapy Hyperthermia  Temperature < 45  Microwave  Randomized Clinical Trials:  Transient Improvement  No Proof Of Long Term Efficacy  Not Recommended By AUA And EUA  Obsolete

83. Thermal-based Therapy Thermotherapy LOW-ENERGGY TUMT  Temperature 45-60  Short Term Results Good  Long Term Results Disappointing  Failure Rate 25-70%  Abandoned

84. Thermal-based Therapy Thermotherapy HIGH-ENERGGY TUMT  Temperature >60  Short term results good  Long term results comparable  Local anesthesia  Prolonged catheterization (2-4 w)  At one year retreatment rate 5-15%  Reserved for  Patients who prefer to avoid surgery  Failed medical therapy

85. Thermal-based Therapy Water-induced Thermotherapy(WIT) • Device consists of:  Treatment balloon catheter  18 Fr Catheter Inflatable To 50 Fr  Heated water circulates within  Positioning balloon • Treatment under local anesthesia • Investigational procedure

86. Thermal-based Therapy High Intensity Focused Ultrasound Spinal or general anesthesia Transrectal ultrasound transducer Temperature of 80-200 Coagulative necrosis Investigational procedure

87. Thermal-based Therapy Transurethral Needle Ablation(TUNA) Low radiofrequency energy  Delivered through catheter equipped with adjustable needles to selected areas of the prostate  Producing coagulative necrosis with sparing the mucosa Temperature 80-100 Local anesthesia Higher analgesia and sedation Not recommended as first line treatment

88. Laser Therapy Coagulation Necrosis Tissue Vaporization Tissue Resection Tissue Enucleation

89. Laser Therapy Visual Laser ablation(VLAP) Nd YAG •Nonconduct technique • Coagulative necrosis •Conduct technique • Tissue vaporization • Tissue resection • Tissue enucleation •Advantages • Less bleeding • Less TUR syndrome •Disadvantage • Prolonged period of catheterization • No pathological specimen • Not recommended as first line treatment • May have a role in high risk patient

90. Laser Therapy Interstitial Laser Coagulation •Cystoscopic control •Laser fibers directly introduced into the prostate •Spared mucosa •Few Irritative symptoms •Retreatment rate 5-15% •Not recommended as first line treatment •May have a role in high risk patient

91. Laser Therapy Holmium-laser Resection Prostatic adenoma is mobilizes Morcellated Resected It is an optional treatment

92. Transurethral Vaporization of The Prostate Modified electrode Uninterrupted high electrical energy Vaporization Disadvantages Electrode efficacy decreases as tissue desiccate Electrode must be reactivated

93. Balloons And Stents Balloon dilation Obsolete

94. Balloons And Stents Prostatic Stents Has Significant associated complications May be indicated only for:  high risk patients with short life expectancy suffering from urinary retention

95. Chemo ablation • Transurethral injection of absolute alcohol • Coagulative necrosis • Investigational treatment

96. MITs VS TURP INTRAOPERATIVE COMPLICATIONS Less bleeding TUR syndrome free Offerred for patients with bleeding disorders Under anticoagulant therapy

97. MITs VS TURP POSTOPERATIVECOMPLICATIONS Significantly higher Nonablative techniques Prolonged catheter time Postoperative dysuria

98. MITs VS TURP Sexual Dysfunction ED Not observed after MITs Retrograde ejaculation 30% AFTER TUMT TUNA ILC WIT >60% TUVP VLAP HOLR

99. MITs VS TURP CLINICAL EFFICACY There is a close correlation between the degree of invasiveness and the clinical efficacy  MODERATE IMPROVEMENT TUMT TUNA ILC  COMPARAPLE IMROVEMENT TO TURP TUVP HOLR

100. MITs VS TURP Durability of response Rate of secondary intervention After MITs 14-44% After TURP 2.6%

101. MITs VS TURP ANATOMICAL LIMITATIONS PROSTATE VOLUME AND SHAPE AFFECT MITs LARGE PROSTATE IS NOT RELIABLE FOR VLAP HIFU TUVP LARGE MEDIAN LOPE IS NOT A CANDIDATE FOR TUMT TUNA HIFU PROSTATIC CALCIFICATION IS CONTRAINDICATED FOR HIFU

102. Surgical Treatment Of Benign Prostatic Hyperplasia

103. INTRODUCTION Absolute indications for prostatectomy  Refractory urinary retention  Recurrent urinary tract infection  Recurrent hematuria refractory to medical treatment  Renal insufficiency  Bladder stones

104. INTRODUCTION STANDARD SURGICAL TREATMENT TURP TUIP OPEN PROSTATECTOMY

105. Transurethral Incision Of The Prostate Candidate • Small prostate <20-30 grams • No middle lobe enlargement

106. Transurethral Incision Of The Prostate Technique  Electrical knife  Bladder neck down to the vero  At 6 oclock  5 and/ or 7  Deep incision down to the capsule  Fat tissue at the bottom

107. Transurethral Incision Of The Prostate Advantages  Similar improvement to TURP  In patient with small prostate  Without middle lobe enlargement  Fast  Easy  Less expensive

108. Transurethral Resection Of The Prostate • Most frequently used method • Prostate 80-100 grams • Time limit <60 minutes

109. Transurethral Resection Of The Prostate TECHNIQUE 1. Preliminary cystourethroscopy Urethral caliber Unexpected stricture urethra Other unexpected abnormalities Identifying landmarks

110. Transurethral Resection Of The Prostate TECHNIQUE 2. Checking resectoscope assembly • Cutting loop and Coagulation loop and working element • Position • Fully backwards withdrawal • Thickness • Telescope 30 or 0 • Light source • Spare lamp • Light cable • Screw connection • Diathermy • Irrigation • Tubing connection • Irrigating fluid

111. Transurethral Resection Of The Prostate TECHNIQUE 3. Passing the resectoscope  Size of the resectoscope according to the size of the urethra  Preliminary OTIS urethrotomy  Resectoscope sheath with blind obturator  Resectoscope sheath with visualizing obturator  Free mobility after insertion

112. Transurethral Resection Of The Prostate TECHNIQUE 4. CUTTING A CHIP Extending the loop Levering the shaft of the telescope in the penis Direct the tip Depress the loop into the tissue Continuing cutting with scalloping action TUR technique for anterior aspect

113. Transurethral Resection Of The Prostate TECHNIQUE 4. CUTTING A CHIP Tow techniques for cut finishing  Elevating the beak of the resectoscope before the cutting loop enters the sheath  The loop is taken fully inside the sheath (The beak is not distal to the Vero)

114. Transurethral Resection Of The Prostate TECHNIQUE 4. CUTTING A CHIP • Length of the ships depends on • Outside distance of loop from the sheath • Mobility of the sheath within the urethra

115. Transurethral Resection Of The Prostate TECHNIQUE 4. BLADDER NECK RESECTION  Trilobar hypertrophy  Allows floating back of the ships into bladder  Depth of two cuts is sufficient  Extra care in case of large middle lobe Undermining of the bladder neck Resection of the ureteric orifices  Hemostasis  Evacuation of the ships  Recheck the hemostasis

116. Transurethral Resection Of The Prostate TECHNIQUE 5. LATERAL LOBE RESECTION  Visibility is clear if not further hemostasis  Orientation of the landmarks  Left or right lobe first  Start at 3 oclock  Up and down order fashion  Layer by layer  Hemostasis for profuse bleeding  Stoppage at the level of the capsule  Hemostasis  Systemic check, 1,3,5 oclock  Evacuation of the ships

117. Transurethral Resection Of The Prostate TECHNIQUE 6. Tissue In The Roof Of The Prostatic Urethra Sometimes bulky tissue at the roof Usually thin and veins are easily breached Little hypertrophy y in this area Holding the resectoscope straight to visualize hanging tissue Better to leave a strip of mucosa at 12 o'clock to reduce incidence of stricture

118. Transurethral Resection Of The Prostate TECHNIQUE 7. APICAL TISSUE RESECTION – Require great care – Incontinence – Back-cutting is safe – Clean cut and not to prolong the diathermy – Hemostasis is short and accurate – Reduce the thermal injury – Leave minor bleeding at the apex rather than causing incontinence – Withdrawing the resectoscope distal to the Veru and held straight to visualize protruding tissue

119. Transurethral Resection Of The Prostate TECHNIQUE 7. FINAL HEMOSTASIS  Systemic hemostasis  Bladder neck  mucosal edge  5 and 7 o'clock  Lateral lobes  1, 3, 7, 9, and 11 o'clock  Apex and either sides of the veru  Washing out of the remaining ships  Inspecting diverticulum to remove ships  Running some irrigant into the bladder before removal of the instrument

120. Transurethral Resection Of The Prostate TECHNIQUE 8. CATHETERIZATION  20 or 22 Ch three way  Check the balloon 300 ml Completely filled to prevent sliding into fossa  Catheter introducer  Check the correct position by irrigation with a syring

121. Transurethral Resection Of The Prostate PROPLEMS DURING RESECTION I. PROBLEMS WITH HEMOSTASIS CAUSES A. TOO MUCH RESECTION WITH LITTLE ATTENTION TO HEMOSTASIS AT EACH STAGE B. TOO DEEP RESECTION WITH VENOU BREACHING C. RESECTION INSPITE POOR VISIBLITY

122. Transurethral Resection Of The Prostate PROPLEMS DURING RESECTION I. PROBLEMS WITH HEMOSTASIS Management of profuse bleeding  Stop resection  Efforts to stop bleeding  Warning the anesthetic  Order blood  Plasma may be given  Help if the resectionest is inexperienced

123. Transurethral Resection Of The Prostate PROPLEMS DURING RESECTION I. PROBLEMS WITH HEMOSTASIS MANAGEMENT OF PROFUSE BLEEDING  Washing out the bladder  Attempt to localize the site of bleeding  Changing into the continuous flow resectoscope  Chang the electrode to rolley ball type  Large or atheromatous artery Compressing the arterial wall  Opposite side of area of poor visibility  Venous bleeding coagulation  Catheter insertion and gentle traction on the bladder neck  Open surgery

124. Transurethral Resection Of The Prostate PROPLEMS DURING RESECTION II. PROBLEMS WITH CUTTING Failure to cut check the following  Diathermy unit plugging to the main electric supply  Diathermy unit switching on  Foot pedal connection to diathermy  Correct positioning of the diathermy plate under the patient  Connection between the diathermy and resectoscope  Correct irrigant  Diathermy loop  Broken  Properly pushed into the resectoscope ( commonest)  Thin  Complete drawing back of the loop during resection without interring cables

125. Transurethral Resection Of The Prostate PROPLEMS DURING RESECTION III. PROBLEMS WITH POOR VISIBILITY Check the following  Bladder fullness  Light source  Light cable  Old with light emerging from its side  Fully screwed on  Clean telescope  Flowing irrigant  Clear irrigant  Adequate hemostasis  Bladder perforation

126. Transurethral Resection Of The Prostate PROPLEMS DURING RESECTION IV. PROBLEMS WITH CATHETERIZATION  Catheter introducer  Recheck the urethra with direct vision  Ureteric catheter guide the insertion of the catheter

127. Transurethral Resection Of The Prostate POSTOPERATIVE CARE IRRIGATION  Continuous irrigation or forced Diuresis  Routine set irrigation  Irrigation for 24-48 hours  Normal saline  Speed of irrigation adjustment

128. Transurethral Resection Of The Prostate POSTOPERATIVE CARE CONSTIPATION – Elderly, immobile patient – Straining causing bleeding – Adequate hydration – Mobilization – Laxatives

129. Transurethral Resection Of The Prostate POSTOPERATIVE CARE METORISM • Abdominal distention with active bowel sounds • Conservative treatment

130. Transurethral Resection Of The Prostate POSTOPERATIVE CARE PATHOLOGY • Abnormal tissues sent in a separate specimen

131. Transurethral Resection Of The Prostate POSTOPERATIVE IMMEDIATE COPLICATIONS BLOOD LOSS Bladder lavage Transfusion Endoscopic inspection Open surgery

132. Transurethral Resection Of The Prostate POSTOPERATIVE IMMEDIATE COPLICATIONS Catheter Blockage Blood clots or prostatic ships Catheter tip syringe suction Washing out with saline Catheter change (may be difficult) Caude catheter or introducer

133. Transurethral Resection Of The Prostate POSTOPERATIVE COPLICATIONS CLOT RETENTION  Restlessness  Abdominal pain  Tachycardia  Low blood pressure  Distended bladder  Evacuation of the clots  Blood replacement  General anaesthesia may be required

134. Transurethral Resection Of The Prostate POSTOPERATIVE COPLICATIONS HEMOLYSIS • Hemolytic irrigant (water) • Resection time more than three quarters hour • Intravascular hemolysis • Water is not used for TURP

135. Transurethral Resection Of The Prostate POSTOPERATIVE COPLICATIONS SEPTECAEMIA Prophylactic antibiotic not given Preexisting unrecognized urinary infection Rapid pulse Low blood pressure Looking ill No evidence of bleeding

136. Transurethral Resection Of The Prostate POSTOPERATIVE COPLICATIONS POS-TUR SYNDROME  Irrigant absorption  Unrecognized prostatic perforation  Tachycardia  Hypertension  Muscle paralysis  Confusion  Local anesthesia rather than general  Serum sodium  Diuretics  Hypertonic saline

137. Transurethral Resection Of The Prostate POSTOPERATIVE COPLICATIONS POS-TUR SYNDROME Preventative measures  Do not use too high pressure during resection  Use continuous-flow resectoscope  Saline irrigation postoperatively

138. Transurethral Resection Of The Prostate POSTOPERATIVE COPLICATIONS POS-TUR HYPEROXALLURIA  Rare  Acute renal failure after TURP  Massive oxalate crystalluria  Metabolism of absorbed glycine  Prolonged resection with capsular perforation

139. Transurethral Resection Of The Prostate POSTOPERATIVE LATER COPLICATIONS INCONTINENCE Stress or total Temporary or perminant Infection Bladder instability Residal obstructing tissue with overflow Sphincter damage

140. Transurethral Resection Of The Prostate POSTOPERATIVE LATER COPLICATIONS STRICTURE  Sites  Fossa navicularis  Distal to external sphincter  Prevention is better than cure  Use of correct adequate size of resectoscope  Adequate lubrication  Otis urethrotomy  Gentle handling of the instruments

141. Transurethral Resection Of The Prostate POSTOPERATIVE LATER COPLICATIONS RETENTION Immediate after catheter removal Residual tissues Atonic bladder External sphincter spasm(Parkinson disease) Reinsertion of the catheter for couple of days Recurrent retention do cystourethroscopy If no residual tissue do urodynamic assessment

142. Transurethral Resection Of The Prostate PREOPERATIVE ADVANCES Preoperative Use Of Finasteride  Goal to reduce significant intraoperative bleeding  3 months preoperatively  Large prostate (transition zone >30 g)

143. Transurethral Resection Of The Prostate INTRAOPERATIVE ADVANCES Coagulating Intermitted Cutting Device  Cutting phase alternating with coagulating phase during each cut  Produce efficient coagulation zone with excellent cutting quality  Decrease bleeding  Decrease TUR syndrome

144. Transurethral Resection Of The Prostate INTRAOPERATIVE ADVANCES Transurethral Vaporization • A modification of TURP • Thick loop • Increased electrosurgical settings

145. Transurethral Resection Of The Prostate INTRAOPERATIVE ADVANCES Transurethral Vaporization • Comparable results to TURP • Less bleeding • Less TUR syndrome • Shorter period of catheterization • Longer time of operation

146. Transurethral Resection Of The Prostate INTRAOPERATIVE ADVANCES Holmium Laser Resection Advantages  Shorter catheter time  Shorter hospital stay  Reduced risk of bleeding  Rapid relief of urinary symptoms Disadvantages Longer operative time

147. Transurethral Resection Of The Prostate INTRAOPERATIVE ADVANCES Ethanol-glycine Irrigation Adverse effect of glycine  TUR syndrome 2-10%  Cardiac injury Adding of 1% ethanol to 1.5% glycine  Early detection of fluid absorption  Early detection of ethanol in air  No adverse effect

148. Transurethral Resection Of The Prostate POSTOPERATIVE ADVANCES USE OF PELVIC MUSCLE EXERCISES PMEs PMEs For 15 minutes 3 times daily 4 weeks Advantages Early improvement in Less incontinence Less frequency More improvement of quality of life

149. Transurethral Resection Of The Prostate POSTOPERATIVE ADVANCES Use of bladder infusion prior to trial voiding • Filling of the bladder before removing the catheter • Lessens the hospital stay

150. OPEN PROSTATECTOMY • Suprapubic Transvesical • Retropubic

151. OPEN PROSTATECTOMY SUPRAPUPIC • Freyer 1900 • Indications • Large prostate >80-100 gm • Large median lobe • Symptomatic bladder diverticulum • Large bladder stones • Obese patient • Advantage • Greater visualization of bladder neck and bladder

152. OPEN PROSTATECTOMY RETROPUPIC • Millin 1945 • Indications • Large prostate >80-100 gm • Without median lobe • Thin patients • Advantages  Excellent anatomic exposure of the prostate  Direct visualization of the adenoma during enucleation  Precise transection of the urethra to preserve urinary continence  Control bleeding points in the fossa  Minimal trauma to bladder

153. In the development of BPH which of the following is not a growth stimulating factor? A ) KGF B ) TGFb C ) IGF D ) EGF E ) bFGF

154. In the development of BPH which of the following is not a growth stimulating factor? A ) KGF B ) TGFb C ) IGF D ) EGF E ) bFGF Transforming growth factor beta inhibits epithelial cell proliferation, the other growth factors stimulate cell division and differentiation

155. What is the risk of retention in a 70-79 year old with moderate lower urinary tract symptoms? A) 3 per 1000 person years B )9 per 1000 person years C )18 per 1000 person years D )26 per 1000 person years E )34 per 1000 person years

156. What is the risk of retention in a 70-79 year old with moderate lower urinary tract symptoms? A) 3 per 1000 person years B )9 per 1000 person years C )18 per 1000 person years D )26 per 1000 person years E )34 per 1000 person years Data comes from the Olmstead County Study (required reading) which showed that men aged 70-79 with moderate/severe symptoms had a retention risk of 34.7 /1000 person years

157. Regarding the natural history of BPH, what is the average decline in peak urinary flow rate? A 0.1mls/sec/year B 0.2mls/sec/year C 0.3mls/sec/year D 0.4mls/sec/year E 0.5mls/sec/year

158. Regarding the natural history of BPH, what is the average decline in peak urinary flow rate? A 0.1mls/sec/year B 0.2mls/sec/year C 0.3mls/sec/year D 0.4mls/sec/year E 0.5mls/sec/year You are required to be aware of the natural history of BPH and the Olmstead study showed an average decline of 0.2mls/sec/year in patients with BPH

159. What proportion of men age 61-70 have pathological evidence of BPH? A 70% B 65% C 60% D 55% E 50%

160. What proportion of men age 61-70 have pathological evidence of BPH? A 70% B 65% C 60% D 55% E 50% answer: This figure comes from Barry et al J Urol 1984 which is a useful paper

161. What proportion of men aged 50-59 with BPH have clinical symptoms? A 15% B 20% C 25% D 30% E 35%

162. What proportion of men aged 50-59 with BPH have clinical symptoms? A 15% B 20% C 25% D 30% E 35% answer: Garraway et al Lancet 1991 found that 25% of men with a TRUSS volume of >20mls had an IPSS of >11

163. What is the most important predictor of clinical progression in BPH A Gland size B Symptom severity C PSA D Age E High post-void residual

164. What is the most important predictor of clinical progression in BPH A Gland size B Symptom severity C PSA D Age E High post-void residual A PSA of >1.4ng/ml is the most important predictor of progression

165. What is the risk of erectile dysfunction after TURP? A 36% B 30% C 20% D 16% E 6%

166. What is the risk of erectile dysfunction after TURP? A 36% B 30% C 20% D 16% E 6% The national prostatectomy audit quotes a rate of 31% however it appears the risk is much lower. Wasson's TURP vs watchful waiting study found no difference in the rates of ED between the 2 groups and Marberger's BJU 1999 meta-analysis indicated a rate of 6.5%

167. What is the arterial supply of the prostate? A Superior vesical artery B Obturator artery C Inferior vesical artery D Inferior epigastric artery E External iliac artery

168. What is the arterial supply of the prostate? A Superior vesical artery B Obturator artery C Inferior vesical artery D Inferior epigastric artery E External iliac artery The inferior vesical artery supplies the prostate-as it approaches the gland it divides into urethral and capsular branches

169. What are the arteries seen after middle lobe resection during a TURP? A Capsular arteries B Badenoch's arteries C Floch's arteries D Branches of the internal pudendal artery E Branches of the superior vesical artery

170. What are the arteries seen after middle lobe resection during a TURP? A Capsular arteries B Badenoch's arteries C Floch's arteries D Branches of the internal pudendal artery E Branches of the superior vesical artery The arteries seen at 5 and 7 o clock after middle lobe resection are urethral branches of the inferior vesical artery known as Badenoch's arteries. The smaller arteries seen at 2 and 10 clock are known as Floch's arteries

171. What is the embryological origin of the transition zone? A Mesoderm B Ectoderm C Endoderm D Mullerian duct E Mesonephric duct

172. What is the embryological origin of the transition zone? A Mesoderm B Ectoderm C Endoderm D Mullerian duct E Mesonephric duct Transition zone arises from mesoderm, peripheral zone arises from endoderm and central zone appears to be embryologically distinct possibly mullerian in origin

173. Which alpha-blocker has the strongest association with floppy iris syndrome? A Alfuzosin B Indoramin C Prazosin D Tamsulosin E Doxasosin

174. Which alpha-blocker has the strongest association with floppy iris syndrome? A Alfuzosin B Indoramin C Prazosin D Tamsulosin E Doxasosin Although described as a class effect, the incidence of floppy iris syndrome with tamsulosin is approx 85%-90%

175. How much is serum dihydrotestosterone does reduced by dutasteride? A 50% B 60% C 70% D 80% E 90%

176. How much is serum dihydrotestosterone does reduced by dutasteride? A 50% B 60% C 70% D 80% E 90% The dual 5ARI reduces serum DHT levels by 90%, the reduction achieved by finasteride is less but this does not appear to translate into an increased clinical effect

177. Which adrenoreceptor subtype mediates prostatic smooth muscle contraction? A alpha1-a B alpha1-b C alpha2 D alpha1 E alpha1-L

178. Which adrenoreceptor subtype mediates prostatic smooth muscle contraction? A alpha1-a B alpha1-b C alpha2 D alpha1 E alpha1-L The alpha1-a subtype predominates in human stroma and therefore mediates prostatic smooth muscle contraction

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