Urology 5th year, 2nd lecture (Dr. Sarwar)

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The lecture has been given on Dec. 22nd, 2010 by Dr. Sarwar.

Published in: Health & Medicine

Urology 5th year, 2nd lecture (Dr. Sarwar)

  1. 1. Carcinoma of prostate Prepared by Dr. sarwar N mahmood F.I.C.M.S( urology),F.E.B.U, E.A.U
  2. 2. Carcinoma of prostate <ul><li>CaP is the most common cancer diagnosed and is the second leading cause of cancer death in American men, and the prevalence of CaP increases with age. </li></ul><ul><li>60-70% of CaP originates in the peripheral zone, 10-20% in the transitional zone, 5-10 % in the central zone. </li></ul>
  3. 4. Risk factors <ul><li>Increasing age : probability of CaP developing in men under the age of 40 is 1 in 10000.and for men 60-79 it is 1 in 8. </li></ul><ul><li>Race : African American are at higher risk for CaP than whites. And tumor tends to be more aggressive than in white race also. </li></ul><ul><li>Positive family history increase the risk: and age of disease onset in the family member with the diagnosis affects a patient’s relative risks e.g. if age of onset is 70 the relative risk is 4 fold, if the age of onset is 50 the relative risk is increased 7 fold. </li></ul><ul><li>High dietary fat intake increases the relative risk by 2 fold. </li></ul><ul><li>Exposure to cadmium increases the risk, which found in cigarette smoke, alkaline batteries, and in the welding industries </li></ul>
  4. 5. Pathology <ul><li>Over 95% of the cancers are adenocarcinoma, others e.g. </li></ul><ul><ul><li>transitional cell carcinoma </li></ul></ul><ul><ul><li>small cell carcinoma </li></ul></ul><ul><ul><li>sarcoma. </li></ul></ul><ul><li>Histological classification commonly used is ( Gleason ) </li></ul><ul><li>(Relies upon the lower power appearance of the glandular architecture under the microscope). In which we have 5 grades. </li></ul>
  5. 7. Spread <ul><li>Local spread : </li></ul><ul><li>seminal vesicles, bladder neck, trigon, and distal urethral sphincter, involving the trigon may obstruct of one or both ureter may result in anuria if bilateral. </li></ul><ul><li>Rectal involvement is rare as denonvillier’fascia represent a strong barrier. But may become stenosed by tumor infiltrating around it. </li></ul><ul><li>Spread by the bloodstream : </li></ul><ul><li>Particularly to bones (most common site of origin for skeletal metastasis is CaP ),most frequently the pelvic bones and the lower lumbar vertebrae , femoral head ,rib cage and the skull. </li></ul><ul><li>Lymphatic spread : </li></ul><ul><li>spreads to obturator lymph nodes and internal iliac and external iliac and common iliac lymph nodes and to the presacral lymph nodes. And periaortal lymphnodes. </li></ul>
  6. 9. Types of prostate cancer <ul><li>Microscopic latent cancer found on autopsy or at cystoprostatectomy. </li></ul><ul><li>Tumors found incidentally during TURP or following screening by PSA (T1a and T1b) </li></ul><ul><li>Early, localized prostate cancer (T2). </li></ul><ul><li>Advanced local prostate cancer (T3-T4) </li></ul><ul><li>Metastatic disease either originate from apparent tumor or from occult prostate cancer (apparently benign gland)(T0-T1) </li></ul>
  7. 10. Clinical features <ul><li>Most patients with early stage CaP are asymptomatic. The presence of symptoms often suggests locally advanced or metastatic disease. </li></ul><ul><li>Symptoms of advanced disease include : </li></ul><ul><li>BOO (IVS and OVS), pelvic pain and hematuria, bone pain malaise, anemia, renal failure (uremia), urinary and fecal incontinence. </li></ul><ul><li>Early disease usually found incidentally following </li></ul><ul><li>TURP for BPH, or by DRE </li></ul>
  8. 12. <ul><li>suspicion of prostate cancer : </li></ul><ul><ul><li>because of either local findings (DRE) </li></ul></ul><ul><ul><ul><li>nodule </li></ul></ul></ul><ul><ul><ul><li>indurations </li></ul></ul></ul><ul><ul><ul><li>diffuse hardness of the prostate). </li></ul></ul></ul><ul><ul><li>raised PSA (>10ng/ml highly suspicious ), </li></ul></ul><ul><ul><ul><li>4-10 ng/ml suspicious </li></ul></ul></ul><ul><ul><ul><li>below 4 ng/ml regard as normal ), </li></ul></ul></ul><ul><ul><li>then transrectal ultrasound guide sextant biopsy taken </li></ul></ul>
  9. 17. Lab findings <ul><li>Uremia can result from bilateral ureteral obstruction either from direct extension into the trigon or from retroperitoneal adenopathy. </li></ul><ul><li>Anemia may be present in metastatic diseas. </li></ul><ul><li>Alkaline phosphatase may be elevated in the presence of bone metastasis, or extensive liver metastasis. </li></ul><ul><li>Serum acid phosphatase may be elevated with disease outside the confines of the prostate. </li></ul>
  10. 18. <ul><li>PSA is a useful as tumor marker for </li></ul><ul><ul><li>screening, </li></ul></ul><ul><ul><li>Staging e.g. >20ng/ml go with advanced disease <10ng/ml most of the case localized tumor </li></ul></ul><ul><ul><li>evaluate respond to the treatment (follow up). </li></ul></ul><ul><li>CXR for lung, or ribs metastasis, abdominal X-ray for lumbar and pelvic bone metastasis which is commonly osteoblastic. </li></ul><ul><li>Ultrasound and IVP for evaluation of the upper urinary tract. </li></ul><ul><li>Bone scan if PSA >20ng/ml in which performed by injection of technetium-99m which is then monitored using gamma camera. </li></ul>staging the tumor
  11. 19. staging <ul><li>TRUS is useful in performing prostatic biopsy and in providing some useful local staging information if cancer is detected. If visible CaP tends to appear as a hypoechoic lesion in the peripheral zone. </li></ul><ul><li>Endorectal MRI used for local staging also has high accuracy. </li></ul><ul><li>CT, MRI of the pelvis in patients with CaP is selectively performed to exclude lymph node metastasis in high risk. </li></ul><ul><ul><li>CT-guided fine-needle aspiration. </li></ul></ul><ul><ul><li>Antibody imaging— ProstaScint is a murine monoclonal antibody to an intracellular component of the prostate-specific membrane antigen (PSMA), which is conjugated to 111 indium. </li></ul></ul><ul><ul><li>However, this antibody recognizes the intracellular domain of PSMA; only soft tissues are imaged </li></ul></ul>
  12. 26. DDX <ul><li>Factors leads to elevation of PSA include </li></ul><ul><ul><li>(BPH </li></ul></ul><ul><ul><li>urethral instrumentation </li></ul></ul><ul><ul><li>prostatitis, prostatic infarction </li></ul></ul><ul><ul><li>vigorous prostatic massage). </li></ul></ul><ul><li>indurations of prostate others as </li></ul><ul><ul><li>(chronic granulomatous prostatitis </li></ul></ul><ul><ul><li>previous TURP </li></ul></ul><ul><ul><li>previous needle biopsy </li></ul></ul><ul><ul><li>prostatic calculi </li></ul></ul>
  13. 27. <ul><li>Treatment decision are based on </li></ul><ul><li>Grade </li></ul><ul><li>Stage </li></ul><ul><li>Life expectancy </li></ul><ul><li>Ability of each therapy to ensure </li></ul><ul><ul><li>disease free survival </li></ul></ul><ul><ul><li>Associated morbidity </li></ul></ul><ul><ul><li>Patient and physician preferences </li></ul></ul>
  14. 28. Treatment <ul><li>A. localized disese(T1-T2): </li></ul><ul><li>1.watchful waiting (surveillance): </li></ul><ul><li>For highly selected patients with CaP, old age with limited life expectancy, concomitant illnesses, small, well differentiated tumor.(cancer death rate 10%) </li></ul><ul><li>2. Radical prostatectomy (RP): </li></ul><ul><li>Includes removal of prostate+seminal vesicles +pelvic lymphadenectomy and anastomosis of bladder to the membranous urethra can be performed </li></ul><ul><ul><li>Retropubically </li></ul></ul><ul><ul><li>Perinealy </li></ul></ul><ul><ul><li>Laparoscopically. </li></ul></ul>
  15. 42. Complications of RP <ul><li>Immediate includes </li></ul><ul><ul><li>blood loss </li></ul></ul><ul><ul><li>rectal injury </li></ul></ul><ul><ul><li>ureteral injury </li></ul></ul><ul><ul><li>and perioperative complications include </li></ul></ul><ul><ul><ul><li>DVT </li></ul></ul></ul><ul><ul><ul><li>pulmonary embolism </li></ul></ul></ul><ul><ul><ul><li>lymphocele formation </li></ul></ul></ul><ul><ul><ul><li>wound infection. </li></ul></ul></ul><ul><li>Late complications include </li></ul><ul><ul><li>urinary incontinence </li></ul></ul><ul><ul><li>impotence </li></ul></ul>
  16. 43. Localized disease <ul><li>3. Radiation therapy –external beam therapy </li></ul><ul><li>By 3 dimensional conformal radiotherapy (CT guided), in which use 3 dimensional treatment planning software. In which treatment field accurately placed allow higher dose of radiation to be given without exceeding the tolerance of surrounding normal tissue </li></ul><ul><li>4. Radiation therapy- brachytherapy : </li></ul><ul><li>Deliver a very high dose of radiation to a localized area . and this by placing radioactive seeds under TRUS guidance. </li></ul>
  17. 46. Localized disease <ul><li>5. Cryosurgery: </li></ul><ul><li>By freezing of the prostate by using a multiprobe cryosurgical device, percutaneously under TRUS guide , </li></ul>
  18. 50. B. locally advanced disease <ul><li>Most patients with T3 cap are treated with neoadjuvant hormonal therapy followed by XRT. </li></ul>
  19. 51. D.metastatic disease <ul><li>Endocrine therapy: </li></ul><ul><li>Most of the prostatic carcinoma are hormone dependant and 70-80% of men with metastatic cap respond to various forms of androgen deprivation. </li></ul><ul><li>Androgen deprivation may be induced at several levels along the pituitary-gonadal axis using variety of methods or agents: </li></ul>
  20. 54. Level Agent route Dose(mg) Frequency Pituitary Diethylstilbesterol Goserlin Goserlin Leuprolide Leuprolide Oral SC SC IM IM 1-3 10.8 3.6 22.5 7.5 Daily Every 3 month Every month Every 3month Every month Adrenal Ketoconazole Oral 400 Daily Testicle Orchiectomy Prostate cell Bicalutamide Flutamide Nilutamide Oral Oral Oral 50 250 150 Daily 3 times a day daily
  21. 55. <ul><li>Current administration of LHRH agonists and orchiectomy are the most common form of primary androgen blockade used. </li></ul><ul><li>Suppression of both testicular and adrenal androgens (complete androgen blockade. And this can be achieved by LHRH agonist+ antiandrogen. </li></ul><ul><li>Antiandrogen appear to act by competitively binding the receptor for DHT the intratesticular androgen responsible for prostate cell growth and development. </li></ul>

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