Referat CARCINOMA PROSTAT

OLEH: FAJAR AL-HABIBI RAISA MAHMUDAH YENI OKTARIA

PRECEPTOR DR. MARS DWI TJAHYO, Sp.BU

SMF BEDAH RSUD ABDOEL MOELOEK BANDAR LAMPUNG MARET 2013

TINJAUAN KEPUSTAKAAN Anatomy The prostate is surrounded by the puborectal portion of the levator ani. The seminal vesicles lie superior to the prostate under the base of the bladder and are approximately 6 cm in length. Each seminal vesicle joins its corresponding ductus deferens to form the ejaculatory duct before entering the prostate. A normal prostate gland is approximately 20 g in volume, 3 cm in length, 4 cm wide, and 2 cm in depth. As men get older, the prostate gland is variable in size secondary to benign prostatic hyperplasia. The gland is located posterior to the pubic symphysis, superior to the perineal membrane, inferior to the bladder, and anterior to the rectum (see the image below). The base of the prostate is in continuity with the bladder and the prostate ends at the apex before becoming the striated external urethral sphincter. The sphincter is a vertically oriented tubular sheath that surrounds the membranous urethra and prostate. The prostate is enclosed by a capsule composed of collagen, elastin and large amounts of smooth muscle. The prostate is covered by 3 distinct layers of fascia on the anterior, lateral, and posterior aspects. The anterior and anterolateral fascia is in direct continuity of the true capsule; this is the location of the deep dorsal vein of the penis and its tributaries. Laterally, the fascia fuses with the levator fascia. The outer longitudinal fibers of the detrusor muscle fuse and blend with the fibromuscular tissue of the capsule. The posterior aspect is covered by the rectovesical (Denonvilliers) fascia. The rectovesical fascia is a connective tissue that is located between the anterior wall of the rectum and posterior aspect of the prostate. This fascial layer covers the prostate and seminal vesicles posteriorly and extends caudally to terminate as a fibrous plate just below the urethra at the level of the external urethral sphincter. This is described as a median fibrous raphe which has a distal extension to the level of the central tendon of the perineum.

The gland is supported anteriorly by the puboprostatic ligaments and inferiorly by the external urethral sphincter and perineal membrane. The puboprostatic ligaments are actually pubovesical ligaments; however, with the growth of the prostate from puberty, these ligaments have the appearance of terminating into the prostate. Arterial supply The arterial supply to the prostate is primarily from the inferior vesical artery, which originates from the anterior division of the internal iliac (hypogastric) artery. The inferior vesical artery then branches into 2 main arterial branches to feed the prostate. The prostatic vessels and the autonomic innervations run between the layers of the lateral prostatic fascia and the prostate. The inferior vesical artery supplies the base of the bladder, the distal ureters, and the prostate. The first arterial branch is the urethral artery that enters the prostatovesical junction posterolaterally and travels inward perpendicular to the urethra toward the bladder neck at approximately the 5 o'clock and 7 o'clock meridian. The urethral artery then turns caudally and parallel to the urethra to supply the transition zone. This artery is the main arterial supply for the adenomas in benign prostatic hyperplasia. The capsular artery is the second main branch of the prostate. It runs posterolateral to the prostate with the cavernous nerves. This artery enters the prostate at right angles to supply the glandular tissue. The arterial blood supply to the seminal vessels and ductus deferens comes from the deferential artery or artery of the ductus, a branch from the superior vesical artery.

Venous drainage The venous drainage of the prostate starts with the deep dorsal vein, which leaves the penis under the deep penile (Buck) fascia between the corpora cavernosa and then under the pubic arch. This vein then passes anterosuperior to the perineal membrane and divides into 3 major branches, the superficial branch and the right and left branches. The superficial branch travels between the puboprostatic ligaments and lies on top of the prostate and bladder neck. The superficial branch is outside the anterior prostatic fascia in the retropubic fat and pierces the fascia to drain into the dorsal venous complex. The common trunk of the dorsal venous complex and the lateral venous plexuses are covered by the anterior prostatic fascia and the endopelvic fascia. The lateral plexuses travel posterolaterally and communicate with the pudendal, obturator, and vesical plexus. These veins then communicate with the internal iliac vein.

Physiopathology In prostate cancer, normal cells undergo a transformation in which they not only grow and multiply without normal controls, but they also differentiate and can invade adjacent tissues. Tumors overwhelm surrounding tissue by invading their space and taking vital oxygen and nutrients. Tumors can eventually invade remote organs via the bloodstream and the lymphatic system. This process of invading and spreading to other organs is called metastasis. Common metastatic location include pelvic lymph nodes, bones, lung, and the liver. Almost all prostate cancers arise from the secretory glandular cells in the prostate. Cancer arising from a glandular cell is known as adenocarcinoma. Therefore, the most common type of prostate cancer is an adenocarcinoma and accounts for more than 95% of all prostate cancer. The most common nonadenocarcinoma is

transitional cell carcinoma. Other rare types include small cell carcinoma and sarcoma.

Epidemiology The risk factors for prostatic cancer are related to age, race, and family history. The overall risk of developing prostatic small cell carcinoma increases with age, with disease occurrence typically being in men older than 60 years. The mean age of diagnosis is 65-69 years, similar to the average age for prostatic adenocarcinoma; this finding is not surprising, since many patients actually have prostatic adenocarcinoma with a component of small cell carcinoma. (An estimated 30% of the population older than 50 years has prostatic adenocarcinoma.) In the United States, African Americans have a 1.8-fold relative risk of prostatic adenocarcinoma over white people. Black people in other countries, such as Brazil, also show an increased risk versus other populations. Prostate cancer has seemed to increase in frequency, due in part to the widespread availability of serum prostate specific antigen (PSA) testing. However, the death rate from this disease has shown a steady decline, and currently more than 2 million men in the U.S. are still alive after being diagnosed with prostate cancer at some point in their lives.

Etiology The specific cause of prostat cancer remains unknown. Hormonal, genetic, environmental, and dietary factors are thought to play roles. a. Age There is a strong correlation between increasing age and developing prostate cancer.

b. Ethnic origin Some of the ethnic differences in the incidence of prostate cancer are attributed to diets. For example, Asians have the lowest incidence of prostate cancer, while Asian immigrants who have adopted Western-style diets have an increased incidence of the disease, although still less than that of the white population. c. Diet Red meat consumption and a high-fat diet are considered possible risk factors. d. Genetics Men who have a history of prostate cancer in their family, especially if it is a first-degree relative such as a father or brither, are at an increased risk of developing prostate cancer. Some prostate cancers may have a genetic component. There is a 10-fold increased relative risk for patients with 2 or more affected first-degree relatives. A patient with a first-degree relative with prostatic adenocarcinoma has a 2-fold increased relative risk. The risk of prostate cancer decreases with distance in the family tree; eg, first versus second cousin. e. Life style Other lifestyle factors, such as sexual practices and occupation, are currently not considered important with regard to the development of prostate cancer.

Clinical Features

Most men with prostate cancer have no symptoms. This is particularly true of early prostate cancer. Symptoms usually appear when the tumor causes some degree of urinary blockage at the baldder neck or the urethra. The usual symptoms include difficultly in starting and stopping the urinary stream, increase in frequency of urination, and pain while urinating. These symptoms are commonly reffered to as irritative urinary symptoms. The urinary stream may be diminished (urinary retention), or it may simply dribble out and a feeling of bladder fullness after urination can appear as well. These symptoms are commonly reffered as obstructive urinary symptoms. If the cancer has spread to remote organs (metastasis) symptoms may include fatigue, malaise, and weight loss. Metastasis to the bones can cause deep bone pain, particularly in the hips and back or even bone fractures from weakening of the bone. Unlike patients with prostatic adenocarcinoma, in most patients with small cell carcinoma of the prostate, the serum prostate-specific antigen (PSA) level is not elevated. About 10% of prostatic small cell carcinomas secrete hormones, such as ACTH or ADH, and these patients may present with paraneoplastic syndromes.

Gross findings The tumor is not always identified on gross examination of the resected prostate. Hyperplastic nodules are commonly seen in such specimens, as most patients are older than 50 years. Prostate cancer tends to produce a subtle, yellow-white color and feels firm; it is usually identified in the peripheral zone. Small cell carcinomas have the same appearance as prostatic adenocarcinomas, but they may feel somewhat softer if significant necrosis is present. Prostate Cancer Screening

a. Elevated prostate serum antigen (PSA) b. Abnormal digital rectal exam c. Elevated prostate cancer antigen 3 (PCA 3) d. Complete Blood Cells e. BUN and Creatinin f. Liver enzyme g. Alkaline phosphatase

Treatment State-of-the-art treatment in prostate cancer provides prolonged disease-free survival for many patients with localized disease but is rarely curative in patients with locally extensive tumor. Even when the cancer appears clinically localized to the prostate gland, a substantial fraction of patients will develop disseminated tumor after local therapy with surgery or radiation therapy. This development is the result of the high incidence of clinical understaging, even with current diagnostic techniques. Metastatic tumor is currently not curable. Surgery is usually reserved for patients in good health who elect surgical intervention. Tumors in these patients should be confined to the prostate gland (stage I and stage II). Prostatectomy can be performed by the perineal or retropubic approach. The perineal approach requires a separate incision for lymph node dissection. Laparoscopic lymphadenectomy is technically possible and accomplished with much less patient morbidity. For small, well-differentiated nodules, the incidence of positive pelvic nodes is less than 20%, and pelvic node dissection may be omitted. With larger, less differentiated tumors, a pelvic lymph node dissection is more important. The value of pelvic node dissection (i.e., open surgical or laparoscopic) is not therapeutic but spares patients with positive nodes

the morbidity of prostatectomy. Radical prostatectomy is not usually performed if frozen section evaluation of pelvic nodes reveals metastases; such patients should be considered for entry into existing clinical trials or receive radiation therapy to control local symptoms. The role of preoperative (neoadjuvant) hormonal therapy is not established. Cryosurgery is a surgical technique under development that involves destruction of prostate cancer cells by intermittent freezing of the prostate tissue with cryoprobes, followed by thawing. Cryosurgery is less well established than standard prostatectomy, and long-term outcomes are not as well established as with prostatectomy or radiation therapy. Serious toxic effects include bladder outlet injury, urinary incontinence, sexual impotence, and rectal injury. Impotence is common. (Refer to the PDQ summary on Sexuality and Reproductive Issues for more information on impotence.) The frequency of other side effects and the probability of cancer control at 5 years' follow-up have varied among reporting centers, and series are small compared with surgery and radiation therapy. Candidates for definitive radiation therapy must have a confirmed pathological diagnosis of cancer that is clinically confined to the prostate and/or surrounding tissues (stage I, stage II, and stage III). Patients should have a computed tomographic scan negative for metastases, but staging laparotomy and lymph node dissection are not required. Prophylactic radiation therapy to clinically or pathologically uninvolved pelvic lymph nodes does not appear to improve overall survival (OS) or prostate cancerspecific survival. In addition, patients considered poor medical candidates for radical prostatectomy can be treated with an acceptably low complication rate if care is given to the delivery technique. Longterm results with radiation therapy are dependent on stage. A retrospective review of 999 patients treated with megavoltage radiation therapy showed cause-specific survival rates to be significantly different at 10 years by T-stage: T1 (79%), T2 (66%), T3 (55%), and T4 (22%). An initial serum prostate-specific antigen (PSA) level higher than 15 ng/mL is a predictor of probable failure with conventional radiation therapy.

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Asymptomatic patients of advanced age or with concomitant illness may warrant consideration of careful observation without immediate active treatment. One population-based study with 15 years of follow-up (mean observation time, 12.5 years) has shown excellent survival without any treatment in patients with welldifferentiated or moderately well-differentiated tumors clinically confined to the prostate, irrespective of age. None of these men were detected by PSA screening, since PSA was not available at the time. The patient cohort was followed for a mean of 21 years after initial diagnosis. The risk of prostate cancer progression and prostate cancer death persisted throughout the follow-up period. By the end of follow-up, 91% of the cohort had died; 16% had died of prostate cancer. A second, smaller population-based study of 94 patients with clinically localized prostate cancer managed by a watch and wait strategy gave very similar results at 4 to 9 years of follow-up. Although the Gleason scores at radical prostatectomy were higher in the surveillance groups than in the immediate prostatectomy group, this occurred concurrently with a national training effort in prostate tumor pathology evaluation that led to the upgrading of tumor specimens. Therefore, the investigators concluded that the delay in prostatectomy in the surveillance group artifactually led to assignment of higher tumor grades. Many men with screen-detected prostate cancer are candidates for active surveillance, with definitive therapy reserved for signs of tumor progression. In a retrospective analysis from four of the centers of the European Randomized Study of Screening for Prostate Cancer (ERSPC), 616 men (mean age 66.3 years) in the screening arm represented between 27% and 38% of the men diagnosed with prostate cancer in the trial. The 616 men met the following criteria for active surveillance:

PSA 10 ng/mL. PSA density <0.2 ng/mL. Tumor stage T1c/T2.

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Gleason score 3 + 3 = 6. 2 positive biopsy cores.

Cryotherapy is also under evaluation for the treatment of localized prostate cancer. There is limited evidence on its efficacy and safety compared to the more commonly used local therapies, and the technique is evolving in an attempt to reduce local toxicity and normal tissue damage (see below). The quality of evidence on efficacy is low, currently limited to case series of relatively small size, short follow-up, and surrogate outcomes of efficacy.