1. Carcinoma of the Prostate
الدكتور
حارث محمد قنبر السعداوي
اختصاص جراحة الكلى والمسالك البولية والتناسلية والعقم
كلية طب الكندي - جامعة بغداد

2. Carcinoma of the prostate
Epidemiology
Histology
Etiology
Clinical Feature
Spread
Investigations
Staging
Treatment

3. Epidemiology:
Ca. prostate is the most common malignant tumour in men over the age of 65 y. It is rare below the age of 40 y.
Peak incidence is at 70 y. While in testicular ca. the peak incidence is between y.
Histology:
>95% of prostatic neoplasms are adenocarcinomas arising from prostatic acinar cells at the periphery of the gland.
Squamous cell carcinoma & transitional cell carcinoma of the prostate occur only rarely.
Ca. prostate usually originates in in the peripheral zone of the prostate, so prostatectomy for benign enlargement of the gland confers no protection from subsequent carcinoma.

4. Etiology:
the cause is unknown, but several factors have been noted to play a role in its development
Genetic influences: The risk for development of prostate cancer is increased two to three times if a father or brother has had the disease.
Hormonal factors: All prostate cancer cells exhibit some degree of androgen dependence. This is supported by the observation that prostate cancer does not occur in castrated persons.
Chemical factors: Workers in the rubber, fertilizer, textile, and batteries industries have increased rates of prostate cancer.
Diet: A diet high in saturated fat and cigarette smoking have also been suggested to have an association with prostate cancer.

5. Clinical features:
Symptoms of obstruction ( like BPH); patient presented with frequency, acute retention, haematuria, & may had hydronephrosis
Symptoms of local invasion like pelvic pain & infiltration of the ureters back pressure with hydroureter & later hydronephrosis  uremia & renal insufficiency
Symptoms of distant metastasis into bones ( sacrum, spines, femur, ribs)
DRE → hard nodule in one lobe or the whole prostate is hard

6. Route of spread:
Haematogenous: usually to the bones, lungs, liver, and kidneys.
Lymphatic: First to external iliac (obturator group), internal iliac, presacral nodes.
Local spread: Extra-capsular spread to the surrounding tissues
note: Prostate Ca. differs from other types of carcinoma because it is osteoblastic (osteosclerotic type) i.e. Bone forming carcinoma. So we will notice high density areas on X-ray.

7. Investigation:
GUE, HB, blood urea, S.creatinine
Liver function tests: these will be abnormal if there is extensive metastatic invasion of the liver . Alkaline phosphetase may be increase either from hepatic involvement or from secondaries in the bone
PSA (prostatic specific antigen):
secreted by prostatic cells which is a tumor marker that increase in carcinoma.
Normal level is ng/ml.
PSA may increase in some conditions such as carcinoma, infection, BPH, and instrumentation like catheterization but in the last 3 the level is increased less than in carcinoma.
It is related to the size of prostate gland, where the bigger the size the more the secretion of PSA.
It is normally secreted to the semen but some goes to blood & this is the measured one.

8. Prostatic acid phosphatase (PAP):
It is elevated in 75% to 80% of patients with metastatic prostate cancer & in 10% to 30% of patients with local disease.
It lacks the specificity & sensitivity needed to be a reliable screening test for prostate cancer.
It remains occasionally useful in detecting metastatic disease & in monitoring therapy.
Transrectal ultrasonograply (TRUS):
It is more accurate than abdominal US in assessing the presence and extent of prostate cancer.
It is very accurate in the assessment of capsular invasion, especially into the seminal vesicles.
Also we can do transrectal needle biopsy under local anesthesia.

9. X-ray:
chest X-ray may reveal metastases either in the lung fields or the ribs
Abdominal X-ray may show the characteristic sclerotic metastases that occurs commonly in the lumber vertebrae & pelvic bones
Bone scanning:
this is achieved by injection of TC- 99m, which is then monitored using a gamma camera.
It is more sensitive in the diagnosis of metastases than a skeletal survey, but false positives occur in areas of arthritis, osteomyelitis or a healing fracture.
CT scan & MRI: to detect L.N. involvement.
Bone marrow biopsy :- when there is metastases.

10. Staging of the disease Primary tumor: T1 (non-palpable tumor)
T1a (A1): Tumor found incidentally at TURP (<5% of resected tissue)
T1b (A2): Tumor found incidentally at TURP (>5% of resected tissue)
T1c (B0): Non palpable tumor identified because of an elevated PSA
T2 (palpable tumor)
T2a ( B1): Tumor involves one lobe
T2b (B2): Tumor involves both lobes
T3 (locally advanced)
T3a (C1): Extra capsular extension (unilateral or bilateral)
T3b (C2): Seminal vesicle involvement
T4 (locally advanced)
T4 (C2): Tumor invades adjacent structures other than seminal vesicle
like bladder neck, external sphincter, rectum, or pelvic side wall
Lymph nodes:
N0: No regional L.N. metastases
N1 (D1): Metastases to regional ( pelvic) L.N.
Metastases:
M1a (D2): Metastases to nonregional L.N.
M1b (D2): Metastases to bone
M1c (D2): Metastases to other sites
(D3): Hormone-refractory metastatic disease

12. Grading Of Prostatic Adenocarcinoma:
Microscopically, adenocarcinoma is graded as a pattern 1 to 5.
Adenocarcinoma of the prostate is graded using the Gleason system, Since most prostatic Carcinoma are multifocal, an allowance is made by adding the two dominant grades to give a sum score between 2 and 10. If only one pattern is observed, the grade is simply doubled. The system is used with needle biopsies, TURP, and radical prostatectomy specimens

13. Treatment:
The following factors should be considered:
Patient’s life expectancy and overall health status.
Tumor characteristics, including Gleason score, tumor stage, PSA levels, PSA velocity and PSA doubling times.
Risk stratification.
Outcome tools such as nomograms.

14. Treatment Options Include:
Watchful waiting and active Surveillance.
Radical prostatectomy.
Radiotherapy (External Beam Radiotherapy).
Brachytherapy (BT).
Cryotherapy & High Intansity Focused Ultrasound (HIFU).
Hormonal Therapy.
Chemotherapy.
Immunotherapy.

15. Radical Prostatectomy:
Open Radical Prostatectomy
Abdominal
Perineal
Laparoscopic Radical Prostatectomy.
Robotically Assisted Laparoscopic Radical Prostatectomy.

16. Hormonal Therapy:
Surgical Castration (Bilateral Orchidectomy): Bilateral orchidectomy, whether total or sub capsular, will eliminate the major source of testosterone production.
Medical castration
Luteinizing hormone-releasing hormone agonists: as effectively as surgically removing the testicles. E.g. goserelin (Zoladex).
Nonsteroidal antiandrogens: such as flutamide, and bicalutamide.
Combination hormone therapy: or total androgen blockade.
Estrogenic compounds: such as diethylstilbestrol, for the negative feedback effect of testosterone and suppress the secretion of LH. this results in lowering of serum testosterone to castrate levels.
Steroidal antiandrogens: such as cyproterone acetate.