Download eL BPH+PCa - UMF IASI 2015

PROSTATE TUMORS
DEPARTMENT OF UROLOGY IAŞI – 2013
PROSTATE TUMORS
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prostate gland – the male organ most commonly afflicted with
benign (BPH) or malignant (CaP) neoplasms
zonal anatomy of the
prostate (McNeal, 1988)
 peripheral zone
(70%) – 60-70% CaP
 central zone (25%)
– 5-10% CaP
 transition zone (5%)
– 10-20% CaP, BPH
BPH
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INCIDENCE & EPIDEMIOLOGY
most common benign tumor in men
incidence – age-related
 histologic BPH: 41-50 – 20%, 51-60 – 50%, > 80 – > 90%
 clinical BPH (prostatic obstruction): 55 – 25%, 75 – 50%
genetic predisposition: autosomal dominant – first-degree
relatives (4×)
racial differences ?
ETIOLOGY
multifactorial and endocrine controlled
levels of free testosterone and estrogen  volume of BPH
aging   estrogen levels  induction of the androgen receptor
 sensitization of the prostate to free testosterone
BPH
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PATHOLOGY
transition zone – hyperplasia
histologic components
 stroma – collagen and smooth
muscle  alpha-blockers
 epithelium  reductase inhibitors
formation of ‘surgical capsule’
PATHOPHYSIOLOGY
obstructive component (prostate) +
secondary response to outlet resistance
(bladder)  symptoms of BPH
BPH
obstructive component (prostate)
 mechanical – intrusion into the urethral lumen or bladder
neck (median lobe !)
 dynamic – smooth muscle, rich in adrenergic nerve supply;
autonomic stimulation  tone to the prostatic urethra
 secondary response (bladder)  detrusor muscle hypertrophy and
hyperplasia + collagen deposition   bladder compliance,
detrusor instability  irritative voiding complaints
CLINICAL FINDINGS
Symptoms
 obstructive
 irritative
 IPSS
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BPH
Signs
 physical examination
 DRE – size and consistency of the prostate – smooth, firm, elastic
enlargement of the prostate
 focused neurologic examination
Laboratory Findings
 urinalysis, serum creatinine, serum PSA
Imaging
 US
 IVU – only with concomitant urinary tract disease or
complications from BPH (hematuria, history of stone disease)
Cystometrograms and urodynamic profiles
BPH
Differential Diagnosis
 urethral stricture, bladder neck contracture, bladder stone, CaP,
urinary tract infection, carcinoma of the bladder, neurogenic
bladder disorders (neurologic disease, stroke, diabetes mellitus,
back injury)
Treatment
 watchful waiting
 medical therapy
 alpha blockers
 5α-reductase inhibitors
 phytotherapy
BPH
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conventional surgical therapy
 transurethral resection of the prostate (TURP)
 transurethral incision of the prostate (TUIP)
 open simple prostatectomy
minimally invasive therapy
 laser therapy
 transurethral electrovaporization of the prostate
 hyperthermia
 transurethral needle ablation of the prostate
 high-intensity focused ultrasound
 intraurethral stents
 transurethral balloon dilation of the prostate
PROSTATE CANCER
the most common cancer diagnosed and the second leading cause
of cancer death in men
 risk factors
 increasing age
 race
 family history of CaP
 high dietary fat intake
 exposure to cadmium (cigarette smoke, alkaline batteries,
welding industry)
Etiology
 gene for familial CaP – chromosome 1
 suppressor genes – chromosomes 8p, 10q, 13q, 16q, 17p, 18q
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PROSTATE CANCER
epithelial-stromal interactions under the influence of growth
factors (transforming growth factor-β, platelet-derived growth
factor and neuroendocrine peptides) modulate prostate cell
development, differentiation and metastasis
Pathology
 adenocarcinoma (95%)
Grading & Staging
 grade (1-5)
 Gleason score (2-10) = primary grade + secondary grade
 TNM staging system: T1a – ≤ 5% of tissue (TURP) has cancer, T1b –
> 5% of tissue (TURP) has cancer, T1c – elevated PSA alone, T2a –
tumor palpable by DRE or visible by TRUS on one side, confined to
prostate, T2b – tumor palpable by DRE or visible by TRUS on both
sides, confined to prostate
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PROSTATE CANCER
T3a – extracapsular extension, T3b – seminal vesicle involvement,
T4 – extention into bladder neck, sphincter, rectum, levator
muscles or into pelvic sidewall
 N1 – metastasis in a regional lymph node or nodes (obturator,
internal iliac, external iliac and presacral); M1a – distant
metastasis in nonregional lymph nodes, M1b – distant metastasis
to bone, M1c – distant metastasis to other sites
Patterns of Progression
 risk of extracapsular extension, seminal vesicle invasion and
distant metastases raises with increasing tumor volume and more
poorly differentiated cancers
 locally advanced CaP may invade the bladder trigone  ureteral
obstruction
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PROSTATE CANCER
distant metastases – bones (lumbar spine, proximal femur, pelvis,
thoracic spine, ribs, sternum, skul and humerus)  pathologic
fractures, cord compression; lesions are typically osteoblastic
 visceral metastases – lung, liver and adrenal gland
Clinical Findings
 most patients with early-stage CaP are asymptomatic; presence of
symptoms often suggests locally advanced or metastatic disease
 local growth into the urethra or bladder neck or direct extension
into the trigone  obstructive or irritative voiding complaints
 metastatic disease  bone pain and symptoms of cord
compression (paresthesias and weakness of the lower
extremities, urinary or fecal incontinence)
 DRE – induration
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PROSTATE CANCER
bulky regional lymphadenopathy  lymphedema of the lower
extremities
Investigations
 bilateral ureteral obstruction  azotemia
 bone metastases  elevated alkaline phosphatase
 disease outside the prostate  raised serum acid phosphatase
 serum PSA has increased the ability to detect CaP; other factors
(BPH, urethral instrumentation and infection)  PSA
 PSA velocity – increases > 0.75 ng/mL/y
 PSA density – prostate biopsy if > 0.1 or 0.15
 free-to-total PSA ratio < 25% would detect 95% of cancers,
because prostate cancer patients demonstrate a lower
percentage of free PSA (not protein-bound)
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PROSTATE CANCER
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systematic sextant prostatic biopsy – under TRUS guidance
TRUS – useful in performing prostatic biopsies and in local staging
information – hypoechoic lesion in the peripheral zone
CT and MRI of the pelvis – exclude lymph node metastases in
high-risk patients who are thought to be candidates for definitive
local therapy (surgery or irradiation); cases identified as having
lymphadenopathy may undergo CT-guided fine-needle aspiration;
if lymph node metastases are confirmed, such patients may be
candidates for alternative treatment regimens
the risk of disemination, in clinically localized prostate cancer, can
be quantified, on the basis of serum PSA, tumor stage and grade
(nomograms and probability curves) – Partin tables
bone scan can be excluded on the basis of serum PSA
PROSTATE CANCER
Differential Diagnosis
  serum PSA – BPH, urethral instrumentation, infection, prostatic
infarction, prostate massage or even DRE
 induration of the prostate – chronic granulomatous prostatitis,
prostatic calculi, previous TURP or needle biopsy
 sclerotic lesions on plain x-ray films and  alkaline phosphatase –
Paget disease (normal PSA, subperiosteal cortical thickening)
Treatment
 localized disease
 watchful waiting
 radical prostatectomy
 external beam radiotherapy
 brachytherapy
PROSTATE CANCER
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locally advanced disease (T3)
 neoadjuvant hormonal therapy followed by XRT
recurrent disease
 following radical prostatectomy  radiation therapy
(documented, isolated local recurrence)
 following radiation therapy  androgen ablation therapy;
only local recurrence  salvage radical prostatectomy
metastatic disease – androgen deprivation
 primary androgen blockade – LHRH agonists (Goserelin,
Leuprolide) or orchiectomy
 estrogens (diethylstilbestrol)
 complete androgen blockade – antiandrogen (Ketoconazole,
Aminoglutethimide, Bicalutamide, Flutamide, Nilutamide) +
LHRH agonist or orchiectomy