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Slide 2 - PROSTATE ANATOMY Ant. Fibromuscular tissue peripheral zone (PIN,ASAP,CA) central zone transition zone (BPH,low grade cancers) Peri-urethral zone
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Slide 4 - BENIGN PROSTATIC HYPERPLASIA 17% of men age 50-59 (require Rx) 27% of men age 60-69 (require Rx) 35% of men age 70-79 (require Rx) Some genetic and racial susceptibility to symptom severity (autosomal dominant) Diet high in saturated fats, zinc and low in fruits and vegetables. Sedentary life style.
Slide 5 - BPHProposed Etiologies Reawakening of the urogenital sinus(mullerian duct) Alterations in the testosterone/estrogen balance Induction of prostatic growth factors Increased stem cells/decreased stromal cell death
Slide 6 - BPHPathophysiology Slow and insidious changes over time Complex interactions between prostatic urethral resistance, intra-vesical pressure, detrusor function, nerves damage.
Slide 7 - BPH Pathophysiologyearly/late Initial hypertrophydetrusor decompensationpoor tonediverticula formation increasing urine volume hydronephrosis upper tract dysfunction, renal failure .
Slide 8 - BPH SYMPTOMSObstructive and Irritative Hesitancy Intermittency Weak stream straining Terminal dribbling Incomplete emptying Nocturia Frequency Urgency Urge incontinence Dysuria
Slide 9 - Other late presenting signs/symptoms Abdominal/flank pain with voiding Uremiafatigue,anorexia,somnolence Hernias, hemorroids, bowel habit change UTI’s Bladder calculi Hematuria
Slide 10 - Other Relevant History GU History (trauma,STD, PSHx) Other disorders ( diabetes,parkinson dx) Medications (anti-cholinergics) Clinical performance status
Slide 11 - BPHClinical Findings Late signs of renal failure ( eg. anemia, HTN) Abdominal examhydronephrosis/pyelonephritis GU exam hernia, stricture, phimosis ? DRE a smooth enlargement, “non-palpable” nodularity with a loss of distinction between the lobes. A soft/firm consistency,underestimates enlargement .
Slide 12 - BPH Prostate : size , firm Surface ,irregular , unequal lobes Consistency , induration ? Tenderness ? Stony hard prostate Any palpable nodular abnormality suggests cancer and warrants investigation
Slide 13 - BPHClinical Evaluation: summary IPSS Score to assess sx severity but NOT for DDX DRE for prostate size, Surface , consistency, nodules, asymmetry, rectal tone and focused neuro exam Abdominal/GU exam Urea,Creat,Electrolytes , PSA(interpret carefully) Uroflowmetry/residual urine measure Upper tract evaluation if hematuria, increased creatinine Ultrasound Cystoscopy ? Urine cytology?
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Slide 15 - BPH SYMPTOMSDifferential Diagnosis Carcinoma of the prostate Prostatitis Urethral stricture Carcinoma of the bladder Bladder calculi Neurogenic bladder
Slide 16 - BPHNatural History A progressive condition (usually) with histological onset in the 30’s and worse with age A 50 yo has a 20-25% lifetime chance of needing a prostatectomy A 40 yo who lives to 80 has a 30-40% chance of prostatectomy But these numbers will change with new medical Rx and one third of patients improve on their own Higher initial PSA’s predict faster growth and higher risk of acute urinary retention
Slide 17 - BPH TREATMENT INDICATIONSAbsolute vs Relative Severe obstruction Urinary retention Signs of upper tract dilatation and renal insufficiency Moderate symptoms of prostatism Recurrent UTI’s Hematuria Quality of life issues
Slide 18 - ONE POSSIBLE APPROACH(use cautiously)
Slide 19 - BPH TREATMENTNON-SURGICAL Watchful waiting, AUA score < 7, 1/3 improve on own. Herbal Phytotherapy (eg. Saw Palmetto) Alpha-1-adrenergic antagonists (terazosin,doxazosin,tamsulosin,alfuzosin) 5-Alpha-reductase inhibitors (finasteride,dutasteride) Combination Rx most effective for most severe. Medical Rx has likely reduced Medicare claims for BPH surgery by 50%.
Slide 20 - BPH TREATMENTSurgical Indicated for AUA/IPSS score >16 Transurethral Prostatectomy(TURP): 18% morbidity with .2% mortality. 80-90% improvement at 1 year but 60-75% at 5 years and 5% require repeat TURP. Transurethral Incision of Prostate (TUIP): less morbidity with similar efficacy indicated for smaller prostates. Open Prostatectomy: indicated for glands > 60 grams or when additional procedure needed : stones ,diverticulum .
Slide 21 - BPH TREATMENTNew Modalities Minimally invasive: (Prostatic Stents,TUNA,TUMT, HIFU,Water-induced Thermotherapy) Laser prostatectomy (VLAP ,HoLRP) Electrovaporization (TUVP )
Slide 23 - 23 Prostatitis Inflammation of prostate gland and surrounding tissue due to infection Acute or chronic Rare in young males Commonly associated with recurrent infections in persons >30 years of age Up to 50% of males develop some form of prostatitis
Slide 24 - 24 Prostatitis Acute prostatitis acute infectious disease sudden onset fever, tenderness, urinary symptoms, constitutional symptoms Chronic prostatitis recurring infection with same organism incomplete eradication of bacteria few prostate related symptoms difficulty urinating, low back pain, perineal pressure
Slide 25 - 25 Pathogenesis and Etiology Mechanism of prostate bacterial infection not well understood Possible causes of prostate gland infection intraprostatic reflux of urine sexual intercourse indwelling urethral and condom catheterization urethral instrumentation transurethral prostatectomy
Slide 26 - 26 Pathogenesis and Etiology Functional abnormalities in bacterial prostatitis  altered prostate secretory functions normal prostatic fluid contains prostatic antibacterial factor heat-stable, low-molecular-weight cation zinc-complexed polypeptide bactericidal to most urinary tract pathogens antibacterial activity related to prostatic fluid zinc content prostate fluid zinc levels and antibacterial factor activity diminished in prostatitis and elderly patients; not known whether changes are cause or effect of prostatitis
Slide 27 - 27 Pathogenesis and Etiology Prostatic secretion pH altered in prostatitis normal pH 6.6 to 7.6 more alkaline with increasing age alkaline pH of 7 to 9 with prostate inflammation Changes suggest generalized prostate secretory dysfunction can affect pathogenesis can influence mode of therapy
Slide 28 - 28 Pathogenesis and Etiology Gram-negative enteric organisms most frequent pathogens in acute bacterial prostatitis E. coli predominant in 75% of cases other frequently isolated gram-negative organisms K. pneumoniae P. mirabilis less frequently P. aeruginosa Enterobacter spp. Serratia spp. gonococcal and staphylococcal prostatitis uncommon
Slide 29 - 29 Pathogenesis and Etiology E. coli most common cause of chronic bacterial prostatitis Other gram-negative organisms less common Importance of gram-positive organisms in chronic bacterial prostatitis controversial; isolated in some studies S. epidermidis S. aureus CMV, TB, CANDIDA
Slide 30 - 30 Prostatitis Clinical Presentation
Slide 31 - 31 Prostatitis: Clinical Presentation Physical examination often normal Acute bacterial prostatitis: diagnosis made from clinical presentation and significant bacteriuria Chronic bacterial prostatitis: more difficult to diagnose and treat typically recurrent UTI with same pathogen  most common cause of recurrent UTI in males clinical presentation varies widely many adults asymptomatic
Slide 32 - 32 Prostatitis: Clinical Presentation Quantitative localization culture is diagnostic standard for chronic bacterial prostatitis diagnosis compare bacteria in sequential urine and prostatic fluid cultures collect 1st 10 mL of voided urine (voiding bladder 1, or VB1): constitutes urethral urine after ~200 mL of urine voided, collect 10-mL midstream sample (VB2): represents bladder urine after voiding, massage prostate and collect expressed prostatic secretions (EPS) void after prostatic massage; collect 10 mL of urine (VB3)
Slide 33 - 33
Slide 34 - NIDDK Classification • Category 1: Acute bacterial prostatitis • Category 2: Chronic bacterial prostatitis • Category 3: Chronic abacterial prostatitis – chronic pelvic pain syndrome – 3A leukocytes in prostatic secretion or semen – 3B absence of inflammatory cells in prostate secretion or semen • Category 4: Asymptomatic patients with inflammation in the expressed prostatic secretion, semen, or in biopsied prostate tissue Class 4 patients require no treatment
Slide 35 - 35 Prostatitis: Clinical Presentation Bacterial prostatitis diagnosis number of EPS bacteria 10 times that of urethral sample (VB1) and midstream sample (VB2) if no EPS available, urine sample following massage (VB3) should contain bacterial count 10-fold greater than VB1 or VB2 If significant bacteriuria; ampicillin, cephalexin, or nitrofurantoin for 2 to 3 days to sterilize urine prior to study
Slide 36 - Prostatitis Treatment
Slide 37 - 37 Prostatitis Treatment Treatment goals same as for UTIs Acute bacterial prostatitis responds well to empirical antimicrobial therapy Antimicrobials penetrate the prostate: acute inflammatory reaction alters cellular membrane barrier between the bloodstream and prostate Most patients managed with Per os antimicrobials trimethoprim-sulfamethoxazole fluoroquinolones (e.g., ciprofloxacin, levofloxacin)
Slide 38 - 38 Prostatitis Treatment Other effective agents cephalosporins β-lactam–β-lactamase combinations IV therapy rarely necessary for total treatment IV to PO sequential therapy with trimethoprim-sulfamethoxazole or fluoroquinolones appropriate consider PO conversion after patient afebrile for 48 hours or after 3 to 5 days of IV therapy
Slide 39 - 39 Prostatitis Treatment 4 weeks of antibiotic therapy to reduce chronic prostatitis risk May treat chronic prostatitis for 6 to 12 weeks Initiate long-term suppressive therapy for recurrent infections ciprofloxacin three times weekly trimethoprim-sulfamethoxazole regular-strength daily nitrofurantoin 100 mg daily
Slide 40 - 40 Prostatitis Treatment Chronic bacterial prostatitis rarely cured Bacteria persist in prostatic fluid despite antibiotic serum concentrations greater than minimal inhibitory concentrations inability of antibiotics to reach sufficient concentrations in prostatic fluid inability of antimicrobials to cross prostatic epithelium
Slide 41 - 41 Prostatitis Treatment Factors that determine antibiotic diffusion into prostatic secretions lipid solubility degree of ionization in plasma only unionized molecules cross prostatic cell lipid barrier drug pKa determines fraction of unchanged drug gradient of > 1 pH unit between separate compartments allows ion trapping as unionized drug crosses into prostatic fluid, it becomes ionized allows less drug to diffuse back across lipid barrier
Slide 42 - 42 Prostatitis Treatment Fluoroquinolones best options for chronic bacterial prostatitis Trimethoprim-sulfamethoxazole also effective sulfamethoxazole penetrates poorly; contributes little to trimethoprim efficacy Initial therapy 4 to 6 weeks longer treatment in some cases if therapy fails, consider chronic suppressive therapy or surgery
Slide 43 - 43 Prostatitis Summary Acute bacterial prostatitis responds well to 4 to 6 weeks of empirical antimicrobial therapy Chronic bacterial prostatitis rarely cured Best option for chronic bacterial prostatitis: fluoroquinolones Long-term suppressive therapy needed for recurrent infections