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BENIGN PROSTATIC HYPERPLASIA

BENIGN PROSTATIC HYPERPLASIA. Assoc . Prof .Hakan KOYUNCU Yeditepe University Medical Faculty Urology. BPH is the benign enlargement of prostate due to glandular & stromal hyperplasia. Presence of BPH 4 th decade % 8 51 - 60 years % 40

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BENIGN PROSTATIC HYPERPLASIA

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  1. BENIGN PROSTATIC HYPERPLASIA Assoc.Prof.Hakan KOYUNCU Yeditepe UniversityMedical Faculty Urology

  2. BPHis the benign enlargement of prostate due to glandular& stromal hyperplasia

  3. Presence of BPH • 4th decade % 8 • 51 - 60 years % 40 • 61 - 70 years % 60 • + 80 years% 90

  4. BPH Prevelance-1 • 40–49 age group % 13.8 • 50–59 age group % 24 • 60–69 age group % 43 As life expectancy rises, 30% BPH is being operated on

  5. BPH Prevelance-2 • Hystologic BPH is seen after the 3rd decade • Incidence increases with age, peaks at 9th decade • Palpableprostate enlargement in 20% of 60 year olds and 43% of 80 year olds • Prostate enlargment does not always present symptoms

  6. Hystologic structure • Composed of fibromuscular stroma,consists of 30 - 50 tubulo-alveoler glands • Glands open to Verumontanum via 16 - 32 excretory channels to prostatic urethra • Average weight is around 18 -20 gr

  7. Epithelial cells consist of 4 main types: • Prostatik acineror secretorycells • Basal cells • Transitional cells • Endocrine-paracrine cells

  8. Prostat hiperplasiais the benign growth of prostate due to changes in glandular and/or fibromuscular elements • All cell types may increase, mostly SECRETORY HYPERPLASIA is observed

  9. The enlarged prostate causes infravesical obstructions, which affects bladder stability and contractility. • Changes can be due to above mentioned obstructions or due to the age of the patient • BPH is a lower urinary tract dysfunction

  10. ETIOLOGY • Histopathologically characterized by increased number of epithelial and stromal cells in periurethral prostate • The mechanism is still unknown but it is known that many factors play a role in BPH

  11. ETIOLOGY Aging Having functional testis

  12. ETIOLOGICAL FACTORS • Aging -Testosteron (leydig cells)production↓ - Sex hormone binding proteins↑serum testosteron level ↓. -Intraprostatic DHT and androgen receptor level↑ -Free estrogen / free testosteron↑

  13. ETIOLOGIC FACTORS CONT‘ • Role of Androgens Major trigger of BPH 5α reductase Testosteron Dihidrotestosteron (DHT) DHT is the major intraprostatic testosteron, affinity of androgen receptors are increased

  14. Role of Estrogens Is believed to show synergistic effect together with androgens in BPH Increases count of androgen receptors (?) Increases transformation of testosteron to DHT, thus increases prostatic DHT level (?)

  15. Stromal/Epithelial reaction, supported by androgens, is known to have an effect in prostate formation in an embryo • Mitotic effect of androgens is only possible if stromal cells are present

  16. 5α reductase enzyme is mostly found in the stromabut tissue culutures have androgens to cause growth of epithelias cells only in presence of stromal cells • This supports the action-reaction of stromal/epithelial cells

  17. Stromal cells‘ regulatory effect on epithelial growth is supported by studies showing paracrine mechanism and several growth factors effecting proto-oncogenes

  18. GROWTH FACTORS IN BPH • Keratinocytegrowth factor (KGF) • Epidermal growth factor (EGF) • Insulin likegrowth factor (IGF-1/2) • Fibroblast growth factor (FGF) • Transforming growth factor (TGF)

  19. RESULTS • BPH occurs with increasing age related hormonal changes, effect of GF within peptide structure and the reactivation of embryonic growth potential of stroma

  20. GENETICS • Genetic predisposition BPH Familial Sporadic 1-Family history of 3 or more 1-Prostate Volume affected family members (mean age 55.5) 2- Early onset ( surgery under 60 y/a) 3-Increased prostatic volume (average 82.7)

  21. OBSTRUCTION CAUSES • 3 steps • Anatomic obstruction • Prim. pathophysiologic obstruction (high pressure proximal to obstruction) • Second. pathophysiologicobstruction (retention - infection – hydronephrosis)

  22. BPH’da Üretradaki Değişiklikler DEFORMATION ELONGATION DEVIATION

  23. BLADDER RESPONSE TO OBSTRUCTION • Early stage • Compensatorystage • Decompensatorystage

  24. Compensatory Stage • Trabeculation • Cellule • Diverticule

  25. Decompensatory stage • Muscle tissue is replaced by connective tissue • Emptying function progressively decreases • Compliance decreases • Increased pressure • Detrusor instability

  26. Advanced stage upper urinary system • Bilateral ureterectasia • Ureterohydronephrosis • Chronic kidney failure

  27. CLINIC As the prostate grows, symptoms and urine flow rate deteriorate. Some patients present with acute urinary retention, needing emergency surgery !!!!BPH IS MOSTLY PROGRESSIVE!!!!

  28. COMPLICATIONS • Acute urinary retention • Urinary system infection • Bladder stones • Bladder damage • Renal failure • Hematuria

  29. DIAGNOSIS • History • Score of symptoms • Physical examination • Digital rectal exam,neurologic examination • Urinary diary • Complete urinanalysis • Creatinin • PSA ?? • Urine stream speed • PMR

  30. SYMPTOMS OF BPH Irritative • Nocturia • Pollakuri • Disuria • Urgency Obstructive • ↓ urinary stream speed • Difficulty/delay starting urination • Postmictionaldrops • Sensation of not fully emptying • Urinary retention • Overflow incontinence

  31. SCORES FOR BPH • Boyarsky • AUA • I-PSS • I-PSS (turkish score)

  32. IPSS • Score rates between 0-35 • 0-7 mild, • 8-19 moderate, • 20-35 advanced lower urinary system signs

  33. LABs AND RADIOLOGIC EXAM • Urinanalysis,Creatinin • PSA • UltrasonographyUrinary Transrectal • IVP • Uroflowmetry

  34. URINANALYSIS • Show hematuria and infections if present

  35. Kreatinin • Creatinineelevation may increase risk of post-op complications • Preoperative Creatinine measurement is recommended

  36. PSA • Prostate specific antigen (PSA) is a protease (glycoprotein) excreted by epithelial • BPH may cause a moderate elevation in PSA • Normal ? 4? 2.5?

  37. PSA • Between 50-70y, annual PSA&DRE check • If family history, PSA&DRE at 4th decade

  38. USG or IVP • Hematuria, history of renal stones, history of UTI,history ofurogenital surgery ve kidney function deterioration requires USG or IVP

  39. IVP Prostatic indentation - fishing hook sign - bladder stone - increased trabeculation, cellules and diverticules - Post- voiding imaging showing residual urine

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