Prostate carcinoma 163

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D: Primary malignant neoplasm of the prostate gland. ^^

A/R: Age is the biggest risk factor. Race (Afro-Carribean > Caucasian, and the former tend to present at a younger age with more aggressive disease). Geographic distribution (higher in North America, Europe; low in Far East). Family history (a gene on chromosome 1 implicated). Dietary factors (high fat, meat and alcohol consumption associated, # with soy). Occupational exposure to cadmium and " sexual partners suggested but not proven.

E: Common, second most common cause of male cancer deaths. Incidence in the ^^ West of 50-70/100000. Microfoci of cancer are found in 80% of men over 80 on autopsy.

H: Often asymptomatic and detected on PSA testing.

Lower urinary tract obstruction: Frequency, hesitancy, poor stream, nocturia and terminal dribble.

Metastatic spread: Bone pain or spinal cord compression from bone metastases.

General symptoms of malignancy (malaise, anorexia and weight loss). Paraneoplastic syndromes (e.g. hypercalcaemia).

E: Asymmetrical hard nodular prostate gland with loss of the midline sulcus on rectal examination.

_I: Bloods: FBC, U&Es, PSA, acid phosphatase, LFT, bone profile.

Prostate-specific antigen: Debatable if this is a suitable tool for screening, as values are age-related and may be " in benign prostatic hyperplasia, prostatitis, following catheterisation. Refinements to improve sensitivity include PSA velocity (rate of change), PSA density and free and complex PSA values. CT/MRI scan: Assesses extent of local invasion and lymph node involvement. TRUS and needle biopsy: For histological diagnosis. Isotope bone scan: For bone metastases.

P: Macro: 70% of prostate carcinoma develops from the peripheral prostatic gland, 10% from the paraurethral tissue and 20% from the transition zone. 85% are diffuse multifocal tumours.

Micro: Adenocarcinoma (95%) with a variable degree of differentiation. Gleason score: Grading based on histology, two scores are given based on predominant appearance, with maximum score of 5 + 5 (10). Spread: Local growth into seminal vesicles, bladder and rectum; lymphatic spread to iliac and para-aortic nodes; blood-borne spread most commonly to bone (especially to the spine) as well as lung or liver.

Staging: TNM system: T1a: incidental < 5% on TURP; T1b: incidental > 5% on TURP; T1c: identified on needle biopsy. T2: confined to prostate (a: one lobe, b: both lobes). T3: extending through capsule. T4: fixed tumour invading adjacent structures other than seminal vesicles. N1: regional lymph nodes involved. M: metastases.

M: Multidisciplinary discussion: On tumour staging and optimal treatment modality considering patients age, comorbidity and wishes. Active surveillance: Watchful waiting and PSA monitoring may be appropriate in the more elderly, asymptomatic patient with small, well-differentiated tumours.

Medical hormone therapy: Androgen ablation SC LHRH analogues, e.g. goserelin combined initially with anti-androgen (cyproterone acetate) to prevent testosterone flare. Other therapies include anti-androgens: nonsteroidal, e.g. bicalutamide, flutamide or steroidal.

Surgical: Radical prostatectomy in tumours localised to the gland. This can be done either by retropubic (which allows pelvic lymph node sampling) or peri-^^ neal approaches. Androgen ablation by bilateral orchidectomy.

Radiological: Adjuvant radiotherapy if the surgical excision margins are inadequate or there is lymph node involvement to tumours confined to the pelvis. Brachytherapy can also be used. Neoadjuvant hormone treatment has been shown to be effective prior to external beam radiotherapy to large but localised ^^ tumours. Palliative radiotherapy can be used for bone pain and neurological complications

^^ Disease: Obstructive hydronephrosis, hypercalcaemia, spinal cord compression.

From surgery: Impotence, urinary incontinence, urethral stricture. ^^ From radiotherapy: Bowel and bladder damage.

OFrom hormone therapy: Androgen deficiency can cause impotence, # libido, gynaecomastia, hot flushes, osteoporosis. Tumour hormone escape can result

Ufrom tumours that evolve cell lineage dominance, which is independent of anti-androgen therapy and is very difficult to manage.

P: Untreated 5-year survival of 80%; radical treatment has a 10-year survival of more than 80%. Metastatic disease has a median survival of 18-24 months.

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