MALE GENITAL SYSTEM - PowerPoint by hcj

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									MALE GENITAL SYSTEM
    Dr Ismail Matalka ,MRCPath
        Department of pathology
    School of medicine & KAUH
  Jordan University of Science &
                     Technology
MALE GENITAL SYSTEM
   PENIS
   SCROTUM, TESTIS, & EPIDIDYMIS
   PROSTATE
   SEXUALLY TRANSMITTED DISEASES

KUMAR, COTRAN, AND ROBBINS, CH 18
PENIS
   MALFORMATIONS
   INFLAMMATORY LESIONS
   NEOPLASMS
MALFORMATIONS OF THE
PENIS
   ABNORMAL LOCATION OF URETHRAL ORIFICE
    ALONG PENILE SHAFT
       HYPOSPADIAS (VENTRAL ASPECT)
           MOST COMMON (1/300 LIVE MALE BIRTHS)
       EPISPADIAS (DORSAL ASPECT)
       MAY BE ASSOCIATED WITH OTHER GENITAL
        ABNORMALITIES
           INGUINAL HERNIAS
           UNDESCENDED TESTES
       CLINICAL CONSEQUENCES
           CONSTRICTION OF ORIFICE
           URINARY TRACT OBSTRUCTION
           URINARY TRACT INFECTION
           IMPAIRED REPRODUCTIVE FUNCTION
INFLAMMATORY LESIONS
OF THE PENIS
   SEXUALLY TRANSMITTED DISEASES
   BALANITIS (BALANOPOSTHITIS)
       INFLAMMATION OF THE GLANS (PLUS
        PREPUCE)
       ASSOCIATED WITH POOR LOCAL HYGIENE IN
        UNCIRCUMCISED MEN
           SMEGMA (accumulation of desquamated epithelial cells,
            sweat , and debris ).
       DISTAL PENIS IS RED, SWOLLEN, TENDER
           +/- PURULENT DISCHARGE
INFLAMMATORY LESIONS OF
THE PENIS
   PHIMOSIS
       PREPUCE CANNOT BE EASILY
        RETRACTED OVER GLANS
       MAY BE CONGENITAL
       USUALLY ASSOCIATED WITH
        BALANOPOSTHITIS AND SCARRING
       PARAPHIMOSIS (TRAPPED GLANS)
           Congestion, swelling, and pain of the distal penis
INFLAMMATORY LESIONS
OF THE PENIS
   FUNGAL INFECTIONS
       CANDIDIASIS
           ESPECIALLY IN DIABETICS
           warm moist conditions and poor local hygiene
           EROSIVE, PAINFUL, PRURITIC
           CAN INVOLVE ENTIRE MALE EXTERNAL GENITALIA
           Scrapings or biopsy:budding yeast and
            pseudohyphae
Condyloma acuminatum
Condyloma acuminatum
Penile Carcinoma in Situ
   Three variants;all are strongly associated with
    HPV infection .
    1.Bowen Disease – Solitary ,plaque-like lesion on
                              the shaft of penis .

    2.Erythroplasia of Queyrat –Erythematous patch
                                  on the glans penis

    3. Bowenoid Papulosis – Venereally transmitted viral
                           lesion involving the penile shaft
    .
Bowen’s Disease ( carcinoma in situ )
   Malignant cells within the epidermis with no
    invasion of the underlying stroma.
   Can occur in:
       Penis
       Vulva
       Oral mucosa
       Skin
   Can transform to invasive carcinoma (~10%).
   Associated with an increased incidence of
    visceral malignanccies
Bowenoid Papulosis
   Sexually active young adults
   Multiple pigmented (reddish brown)
    papular lesions
   Virtually never develops into an invasive
    carcinoma, and in many cases, it
    spontaneously regresses.
   Histologically, bowenoid papulosis is
    indistinguishable from Bowen disease
Bowen Disease (carcinoma in situ )
NEOPLASMS OF THE PENIS
   SQUAMOUS CELL CARCINOMA (SCC)
       EPIDEMIOLOGY
           UNCOMMON - ABOUT 0.25 % OF CA IN US MEN
           UNCIRCUMCISED MEN BETWEEN 40 AND 70
         Glans penis and prepuce affected most
         Circumcision confers protection



       PATHOGENESIS
           POOR HYGIENE, SMEGMA(exposure to potential carcinogens)
           HUMAN PAPILLOMA VIRUS (16 AND 18) in 50%
           SMOKING ELEVATE RISK
           CIS FIRST, THEN PROGRESSION TO INVASIVE
            SQUAMOUS CELL CARCINOMA
Carcinoma of Penis
SCC OF THE PENIS

   CLINICAL COURSE
       USUALLY INDOLENT
       LOCALLY INVASIVE
       HAS SPREAD TO INGUINAL LYMPH
        NODES IN 25% OF CASES AT
        PRESENTATION
       DISTANT METS RARE
       5 YR SURVIVAL
         70% WITHOUT LN METS
         27% WITH LN METS
SCROTUM, TESTIS, AND
          EPIDIDYMIS
LESIONS INVOLVING THE
SCROTUM
   INFLAMMATION
       TINEA CRURIS (JOCK ITCH)
            SUPERFICIAL DERMATOPHYTE INFECTION
            SCALY, RED, ANNULAR PLAQUES, PRURITIC
            INGUINAL CREASE TO UPPER THIGH
   SQUAMOUS CELL CARCINOMA
       HISTORICAL SIGNIFICANCE
       SIR PERCIVAL POTT, 18TH CENTURY
        ENGLISH PHYSICIAN
       CHIMNEY SWEEPS
LESIONS INVOLVING THE
SCROTUM
   SCROTAL ENLARGEMENT
       HYDROCELE - MOST COMMON CAUSE
            ACCUMULATION OF SEROUS FLUID WITHIN TUNICA
             VAGINALIS
            INFECTIONS, TUMOR, IDIOPATHIC
       HEMATOCELE :accumulation of blood due to trauma
                    or bleeding disorders.
       CHYLOCELE : accumulation of lymphatic fluid
            FILIARIASIS - ELEPHANTIASIS
       TESTICULAR DISEASE
Testicular Diseases
   Congenital
   Inflammatory
   Neoplastic
         Manifestations
              Infertility
              Enlargement

              Atrophy

              Pain
Normal   Atrophy
Cryptorchidism
(Failure of Testicular Descent Into the Scrotum)

   Testis descends to pelvis at the 3rd gestational month,
    into the scrotum in the last 2 months of gestation.
   Incidence: 0.7%-0.8% of the male population.
   RIGHT > LEFT, 25% BILATERAL
   Etiology:
       Hormonal: deficiency of LHRF
       Mechanical:
         Short spermatic cord        blocked inguinal canal
       Intrinsic testicular abnormalities.
        Unknown ( vast majority )
       A feature of some congenital syndromes (Prader-willi syndrome)
Cryptorchidism

Morphology:
   Smaller than normal testes, the higher the testis
    the smaller its size.
   Hypoplastic or atrophic germinal layer of tubules
   Leydig cell hyperplasia.
   Thickened basement membrane
   Intratubular germ cell neoplasia (ITGCN)
Cryptorchidism
   Complications
                Infertility
                Four-fold increased risk of testicular malignancy in both
                 testes,even if unilateral cryptorchidism
                Trauma
   Management
    - Orchiopexy (surgical placement of undescended
                      testis into scrotum before puberty )

    - This will decrease atrophy but does not guarantee
      fertility . Patients remain at same increased risk of testicular
      cancer. Controversial !!!!.
                           Cryptorchidism
        •   Location of undescended testis
            – Abdominal      10%.
            – Inguinal canal 42%.
            – Upper scrotum 48%.
    100%                             40x
Germ
                                                             Risk of
cells                                                        germ cell
        50%                          20x
                                                             tumors



               1   2   3    4    5             5   10   15
                                Age in years
OTHER CAUSES OF
TESTICULAR ATROPHY
   CHRONIC ISCHEMIA
   INFLAMMATION OR TRAUMA
   HYPOPITUITARISM
   EXCESS FEMALE SEX HORMONES
       THERAPEUTIC ADMINISTRATION
       CIRRHOSIS
   MALNUTRITION
   IRRADIATION
   CHEMOTHERAPY
INFLAMMATORY LESIONS
OF THE TESTIS
   USUALLY INVOLVE THE EPIDIDYMIS
    FIRST
   SEXUALLY TRANSMITTED DISEASES
   NONSPECIFIC EPIDIDYMITIS AND
    ORCHITIS
       SECONDARY TO UTI
           BACTERIAL AND NON-BACTERIAL
       SWELLING, TENDERNESS
       ACUTE INFLAMMATORY INFILTRATE
INFLAMMATORY LESIONS OF
THE TESTIS
   MUMPS
       20% OF ADULT MALES WITH MUMPS
       EDEMA AND CONGESTION
       CHRONIC INFLAMMATORY INFILTRATE
       MAY CAUSE ATROPHY AND STERILITY
   TUBERCULOSIS
       GRANULOMATOUS INFLAMMATION
       CASEOUS NECROSIS
   AUTOIMMUNE GRANULOMATOUS
    ORCHITIS
       RARE FINDING IN MIDDLE AGED MEN
Acute epididymitis
Torsion of testis
     Testicular Tumors
   Firm painless enlargement of testis.
   Peak incidence age is between 15-34 years
   95% are germ cell tumors; almost all are malignant.
   Non germ cell tumors may synthesize and result in
    endocrine abnormalities.
   Risk factors:
       Cryptorchidism ; four-fold increased risk
       Testicular feminization syndrome
       Klinefelter’s syndrome
       Siblings of patients with germ cell tumors
       Cytogenetic abnormalities; isochromosome i(12p)
       Unknown
TESTICULAR NEOPLASMS
   EPIDEMIOLOGY
       MOST IMPORTANT CAUSE OF PAINLESS
        ENLARGEMENT OF TESTIS
       2/100,000 MALES, WHITES > BLACKS (US)
       INCREASED FREQUENCY IN SIBLINGS
       PEAK INCIDENCE 15-34 YRS
       MOST ARE MALIGNANT
       ASSOCIATED WITH GERM CELL
        MALDEVELOPMENT
            CRYPTORCHIDISM
            TESTICULAR DYSGENESIS(XXY)
TESTICULAR NEOPLASMS
   PATHOGENESIS
       95% ARISE FROM GERM CELLS
           ISOCHROMOSOME 12, i(12p), IS A COMMON
            FINDING
       RARELY ARISE FROM SERTOLI CELLS OR
        LEYDIG CELLS
           THESE ARE OFTEN BENIGN
       Lymphoma
           men > 60 years
WHO CLASSIFICATION OF Germ
Cell TESTICULAR TUMORS
    ONE HISTOLOGIC PATTERN (40%)
        SEMINOMAS (30%)
        EMBRYONAL CARCINOMA
        YOLK SAC TUMOR
        CHORIOCARCINOMA
        TERATOMA (mature , immature , with malignancy in
         somatic elements )
    MULTIPLE HISTOLOGIC PATTERNS (60%)
        EMBRYONAL CA + TERATOMA
        CHORIOCARCINOMA + OTHER
        OTHER COMBINATIONS
     HISTOGENESIS OF TESTICULAR
     NEOPLASMS (PEAK INCIDENCE)
                   GERM CELL PRECURSOR

   GONADAL                                TOTIPOTENTIAL
DIFFERENTIATION                          DIFFERENTIATION
                                     (NONSEMINOMA)
      SEMINOMA                EMBRYONAL CA
       (40-50 Y)            (UNDIFFERENTIATED)                 SOMATIC
                                  (20-30 Y)                DIFFERENTIATION

          TROPHOBLASTIC                  YOLK SAC            TERATOMA
          DIFFERENTIATION                  DIFF               (20-30 Y)


  CHORIOCARCINOMA            YOLK SAC TUMOR                 MATURE
       (20-30 Y)                  (< 3 Y)
         hCG +                    AFP +                     IMMATURE
                                                            MALIGNANT TX
Testicular Germ Cell Tumors
Tumor             Peak age (yr)           Tumor Markers
Seminoma              40-50       ~10% have elevated hCG

Embryonal Ca.         20-30       90% have elevated hCG and/or
                                  AFP
Yolk sac tumor          3         100% have elevated AFP

Choriocarcinoma       20-30       100% have elevated hCG

Teratoma             all ages     50% have elevated hCG and/or
                                  AFP
Mixed tumors          15-30       90% have elevated hCG and AFP
      Seminoma

   35-50% of all testicular germ cell tumors.
   Malignant germ cell tumour.
   Analogous to Dysgerminoma of ovary
   Large well demarcated soft homogenous
    white/gray masses without hemorrhage.
   Cells are large with distinct cell borders, round
    nuclei and conspicuous nucleoli.
   Lymphocytic infiltrate and granulomas are
    common.
Seminoma

   10-15% have giant cells containing hCG.
   Metastases are predominantly lymphatic
    and involve iliac and para-aortic lymph
    nodes.
   Very radiosensitive
Seminoma
Seminoma
 Spermatocytic VS. Classic Seminoma
                         Spermatocytic        Classic Seminoma
Frequency                2-3%                 35-40%
Age (Y)                  >40                  25-50
Sites                    Testis only          Midline structures
Cryptorchidism           Unrelated            10%
Intratubular component   None                 95%
Cell types               3                    1, and STGC
PLAP                     Negative             Positive
Intercellular edema      Prominent            Absent
Stroma                   Scanty               Prominent septa
Lymphocytes              Absent               Present, almost always
Granulomas               Absent               Often present
Metastases               Exceptionally rare   5-10%
Embryonal Carcinoma
   The second most common germ cell
    tumour (20-30% )
   Often presents with pain or metastasis
   Admixed with other germ cell tumour in
    most cases.Pure forms comprises 2-3%.
     Embryonal Carcinoma

   Invasive hemorrhagic masses with necrosis.
   Cells are large with indistinct cell borders,
    basophilic cytoplasm large nuclei and
    conspicuous nucleoli.
   Cells form solid nests or gland like structures.
   Metastases by hematogenous and lymphatic
    routes are common even in small tumors.
Embryonal carcinoma
Embryonal carcinoma
     Yolk Sac Tumor
   Most common testicular tumor below the age of 3
    years.
   Large well demarcated masses.
   Cuboidal and columnar cells forming sheets,
    glands, papillae and microcysts.
   Schiller Duval bodies are common (resembe primitive
    glomeruli ).

   Hyaline globules are also common.
   Alpha fetoprotein in the serum and in tumor cells
    can be identified in all cases.
Yolk sac tumour
       Teratoma

   Firm masses with cystic structures.
   Mature teratomas contain differentiated tissue from
    one or more germ cell layers.
   Immature teratomas contain immature somatic
    elements.
   Teratomas with malignant transformation contain
    malignancy arising in a teratomatous element (SCC &
    adenocarcinoma ).
   Most frequently malignant
   Prepubertal pure teratoma are benign.
   Teratomas in adults are malignant and often contain
    other germ cell elements.
Teratoma of Testis
Teratoma of Testis
Choriocarcinoma

    Often small non palpable tumor with wide
     spread metastases.
    Aggressive malignant germ cell tumor
    Has the worst prognosis of germ cell tumor
    Pure forms are rare representing only 1% of
     GCT.
    Similar tumors may arise in
     placenta,ovary,mediastinum, or abdomen.
Choriocarcinoma
   Tumor contains cytotrophoblasts and
    syncytiotrophoblasts in a hemorrhagic
    background.
   hCG can be identified in tumor cells and in
    the serum.
Choriocarcinoma
    Staging of Testicular Germ
    Cell Tumors
   Stage I:     tumor confined to testis,
                 epididymis ,or spermatic cord.

   Stage II:    metastases confined to
                 retroperitoneal nodes
                 below diaphragm.

   Stage III:   metastases beyond
                 retroperitoneal nodes.
CLINICAL COURSE OF
TESTICULAR TUMORS
   USUALLY PRESENT WITH PAINLESS
    ENLARGEMENT OF TESTIS
   MAY PRESENT WITH METASTASES
       NONSEMINOMAS (MORE COMMON)
           LYMPH NODES, LIVER AND LUNGS
       SEMINOMAS
           USUALLY JUST REGIONAL LYMPH NODES
   TUMOR MARKERS (hCG AND AFP)
   TREATMENT SUCCESS DEPENDS ON
    HISTOLOGY AND STAGE
       SEMINOMAS VERY SENSITIVE TO BOTH
        RADIO- AND CHEMOTHERAPY
Testicular Stromal/sex Cord
Tumors
    5% of testicular tumors.
    Most are benign ; 10 % are invasive or
     malignant.
    Leydig cell tumors may produce testosterone
     leading to precocious puberty. In adults, they
     may cause feminization.(intracytoplasmic Reinke
     crystals)
    Sertoli cell tumors form tubular
     arrangements.No significant endocrine
     effects
Leydig (interstitial) cell tumor
DISEASES OF THE PROSTATE

           PROSTATITIS
       NODULAR HYPERPLASIA
             CANCER
Adult Prostate
Benign prostate gland
PROSTATITIS
   ACUTE BACTERIAL PROSTATITIS
  CHRONIC BACTERIAL PROSTATITIS

 CHRONIC ABACTERIAL PROSTATITIS
ACUTE BACTERIAL
PROSTATITIS
   ETIOLOGY
       SAME ORGANISMS THAT CAUSE UTI
           E COLI , PROTEUS, OTHER GNR
   PATHOGENESIS
       ORGANISMS ASCEND FROM URETHRA
        AND URINARY BLADDER
       RARELY, HEMATOGENOUS SPREAD
ACUTE BACTERIAL
PROSTATITIS
   MORPHOLOGY
       ACUTE INFLAMMATION, ESPECIALLY IN THE
        GLANDS, WITH MICROABSESSES
       CONGESTION, EDEMA
   CLINICAL COURSE
       DYSURIA, FREQUENCY, LOW BACK PAIN,
        PELVIC PAIN
       ENLARGED, EXQUISITELY TENDER
       +/- FEVER ,CHILLS OR LEUKOCYTOSIS
       USUALLY RESOLVES WITH AB RX
CHRONIC PROSTATITIS
   ETIOLOGY
       MAY FOLLOW ACUTE PROSTATITIS
       MAY DEVELOP INSIDIOUSLY
       CULTURE POSITIVE (BACTERIAL)
           SAME ORGANISMS THAT CAUSE AP
       CULTURE NEGATIVE (ABACTERIAL)
           MAY BE RELATED TO
                CHLAMYDIA TRACHOMATIS
                UREAPLASMA UREALYTICUM
                TRICHOMONAS
           MOST COMMON FORM OF CP
CHRONIC PROSTATITIS

   MORPHOLOGY
       LYMPHOCYTIC INFILTRATE
       NEUTROPHILS AND MACROPHAGES
       SOME EVIDENCE OF TISSUE DESTRUCTION
   CLINICAL COURSE
       SIMILAR TO AP
            LESS ACUTE SYMPTOMS
            MORE RESISTANT TO AB RX
       CBP OFTEN ASSOCIATED WITH RECURRENT
        UTI
PROLIFERATIVE LESIONS OF THE
PROSTATE
 PERIURETHRAL
 AND                              URETHRA
 TRANSITIONAL
 ZONES                            PERIPHERAL
                                  ZONE
                NORMAL PROSTATE




NODULAR HYPERPLASIA           CARCINOMA
NODULAR HYPERPLASIA
   OTHER TERMS USED
       GLANDULAR AND STROMAL HYPERPLASIA
       BENIGN PROSTATIC HYPERTROPHY
        (HYPERPLASIA)
   EPIDEMIOLOGY
       OCCURS IN 20% OF MEN OVER 40
       OCCURS IN 70% OF MEN OVER 60
       OCCURS IN 90% OF MEN OVER 70
PATHOGENESIS OF
NODULAR HYPERPLASIA
   PROLIFERATION OF BOTH EPITHELIAL
    AND STROMAL ELEMENTS
   BOTH ANDROGENS AND ESTROGENS
    MAY PLAY A ROLE
       NOT SEEN IN MALES CASTRATED BEFORE
        PUBERTY
       INHIBITORS OF TESTOSTERONE
        METABOLISM USEFUL IN TREATMENT
       RELATIVE INCREASE IN ESTROGENS IN
        OLDER MEN MAY INCREASE DHT
        RECEPTORS IN PROSTATE
Pathogenesis of prostatic hyperplasia
Nodular prostatic hyperplasia
Periurethral nodules
    CLINICAL COURSE OF
    NODULAR HYPERPLASIA
   SYMPTOMS OCCUR IN ONLY 10% OF MEN
    WITH NODULAR HYPERPLASIA(URETHRAL
    OBSTRUCTION & NARROWING   )
   HESITANCY
   URINARY RETENTION
       URGENCY, FREQUENCY, NOCTURIA, UTI
   TREATMENT
       MEDICAL
       SURGICAL
   COMMON CAUSE FOR ELEVATED
    PROSTATE SPECIFIC ANTIGEN (PSA)
    Association of NH and
    Prostate Carcinoma
   Both are related to advanced age and
    androgens.
   Both may respond to androgen deprivation.
   Carcinoma occurs 10-15 yr after NH.
   10% of NH cases contain incidental
    carcinoma.
   NH is not a premalignant condition and is not
    precursor of carcinoma.
CARCINOMA OF THE
PROSTATE
   EPIDEMIOLOGY
       MOST COMMON VISCERAL CANCER IN
        MALE
         ABOUT 70/100,000 MEN IN US
         200,000 NEW CASES/YR IN US

         20% ARE LETHAL

       SECOND MOST COMMON CAUSE OF
        CANCER DEATH IN MEN
       PEAK INCIDENCE OF CLINICAL
        CANCER IS 65-75 YO
CARCINOMA OF THE
PROSTATE
    PEAK INCIDENCE OF CLINICAL CANCER
     IS 65-75 YO
    IT IS DISEAE OF ELDERLY MEN
      10% at 50 yr of age (autopsy studies )
      80% at 80 yr of age (autopsy studies )

      5 per 100,000 (45-49yr)

      500 per 100,000 (70-75yr)

    LATENT CA IS EVEN MORE PREVALENT
        >50% IN MEN > 80 YO
CARCINOMA OF THE
PROSTATE

   PATHOGENESIS
       HORMONAL FACTORS
           DOES NOT OCCUR IN CASTRATED MEN
           ORCHIECTOMY AND/OR ESTROGEN TREATMENT
            INHIBITS GROWTH
       GENETIC FACTORS
           INCREASED RISK IN FIRST ORDER RELATIVES
           BLACKS > WHITES (SYMPTOMATIC CA)
       ENVIRONMENTAL FACTORS
           GEOGRAPHIC DIFFERENCES IN INCIDENCE OF
            CLINICAL CANCER (NOT OF LATENT CA)
           CHANGE IN INCIDENCE WITH MIGRATION
     Prostatic Carcinoma
   Clinical features:
       Often clinically silent.
       Urinary obstructive symptoms.
       75% present in stages C and D.
   Diagnosis is made in one of the following
    instances:
       Routine surveillance in men over 40 yr.
       Incidental finding in TURP.
       Adenocarcinoma with unknown primary.
       Rarely, rectal or perirectal mass.
CARCINOMA OF THE PROSTATE


   CLINICAL COURSE
       DIGITAL RECTAL EXAM (DRE)
       PROSTATE SPECIFIC ANTIGEN (PSA)
           > 4 ng/ml IN PERIPHERAL BLOOD
           FREE PSA < 25%
       TRANSRECTAL ULTRASOUND
       NEEDLE BIOPSY
       PROSTATISM (LIKE NH)
       METASTASES
           OSTEOBLASTIC
       TREATMENT- SURGERY, RADIATION,
        HORMONES, CHEMO
 Prostatic Carcinoma

Pathology
   Yellow-white hard multifocal foci with
    predilection for peripheral zones.
   Haphazard small irregularly shaped
    invasive glands with abortive lumens.
   Glands lack basal cell layer.

   Cells contain prominent nucleoli.

   Perineural invasion.
Prostatic Intraepithelial Neoplasia
PIN
Adenocarcinoma of prostate
Metastatic osteoblastic prostatic
carcinoma
Prostatic adenocarcinoma
Perineural invasion
Gleason Scoring
Low grade carcinoma
Gleason Scoring
High grade carcinoma
CARCINOMA OF THE
PROSTATE
   STAGING
    A MICROSCOPIC NON-PALPABLE
    B MACROSCOPIC (PALPABLE & CONFINED TO
                   PROSTATE)
    C EXTRACAPSULAR EXTENSION
    D METASTATIC
   PROGNOSIS DEPENDENT ON STAGE AND
    HISTOLOGIC GRADE
       90% 10 YR SURVIVAL FOR A AND B
       10-40% 10 YR SURVIVAL FOR C AND D
Prostate Specific Antigen (PSA)
   34 kd serine protease       For screening: PSA
   Specific for prostate        should be used in
    tissue. Not cancer           combination with digital
    specific.                    or ultrasound exam.
   Normal level < 4ng/ml.       PSA can be used for :
   Elevated in                     Monitoring success of
                                     prostatectomy.
       Carcinoma
                                    Detecting early relapses
       NH
                                    Differential diagnosis of
       Prostatitis                  other malignancies.
       After bx.
                                PSA velocity & density.

								
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