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					  MALE GENITAL SYSTEM
• PENIS
• SCROTUM, TESTIS, & EPIDIDYMIS
• PROSTATE

  KUMAR, COTRAN, AND ROBBINS
           7th Edition
             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)
Hypospadias
Epispadias
HYPOSPADIAS AND EPISPADIAS
 – 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
 – 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)
   • URETHRAL CONSTRICTION
 INFLAMMATORY LESIONS
      OF THE PENIS
• FUNGAL INFECTIONS
 – CANDIDIASIS
   • ESPECIALLY IN DIABETICS
   • EROSIVE, PAINFUL, PRURITIC
   • CAN INVOLVE ENTIRE MALE
     EXTERNAL GENITALIA
  NEOPLASMS OF THE PENIS
• SQUAMOUS CELL CARCINOMA (SCC)
 – EPIDEMIOLOGY
   • UNCOMMON – LESS THAN 1 % OF CA IN US MEN
   • UNCIRCUMCISED MEN BETWEEN 40 AND 70
 – PATHOGENESIS
   • POOR HYGIENE, SMEGMA
   • HUMAN PAPILLOMA VIRUS (16 AND 18)
   • CIS FIRST, THEN PROGRESSION TO INVASIVE
     SQUAMOUS CELL CARCINOMA
Squamous Cell Carcinoma
      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
 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
 – CHYLOCELE
   • FILIARIASIS - ELEPHANTIASIS
 – TESTICULAR DISEASE
Hydrocele
LESIONS OF THE TESTES

      • CONGENITAL
   • INFLAMMATORY
      • NEOPLASTIC
  CRYPTORCHIDISM AND
  TESTICULAR ATROPHY
• FAILURE OF TESTICULAR
  DESCENT
• EPIDEMIOLOGY
 – ABOUT 1% OF MALES
 – RIGHT > LEFT, 25% BILATERAL
• PATHOGENESIS
 – HORMONAL ABNORMALITIES
 – TESTICULAR ABNORMALITIES
 – MECHANICAL PROBLEMS
Atrophic testes
secondary to
cryporchidism
    CRYPTORCHIDISM AND
    TESTICULAR ATROPHY
• CLINICAL COURSE
 – WHEN UNILATERAL, MAY SEE ATROPHY IN
   CONTRALATERAL TESTIS
 – STERILITY
 – INCREASED RISK OF MALIGNANCY (4-10X)
 – ORCHIOPEXY
   • MAY HELP PREVENT ATROPHY
   • MAY NOT DECREASE RISK OF MALIGNANCY
       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
 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
   • INTRATUBULAR GERM CELL NEOPLASMS
 – RARELY ARISE FROM SERTOLI CELLS
   OR LEYDIG CELLS
   • THESE ARE OFTEN BENIGN
 – Lymphoma
   • men > 60 yo
      WHO CLASSIFICATION OF
       TESTICULAR TUMORS
• ONE HISTOLOGIC PATTERN (40%)
  –   SEMINOMAS (30%)
  –   EMBRYONAL CARCINOMA
  –   YOLK SAC TUMOR
  –   CHORIOCARCINOMA
  –   TERATOMA
• 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              (ALL AGES)


  CHORIOCARCINOMA            YOLK SAC TUMOR                 MATURE
       (20-30 Y)                  (< 3 Y)
         hCG +                    AFP +                     IMMATURE
                                                            MALIGNANT TX
Seminoma, with focal hemorrhage and necrosis
Normal testicular tissue
Seminoma
Seminoma




           Syncytiotrophoblast
Dermoid Cyst
Immature Teratoma




            With Embryonal Carcinoma
    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
   DISEASES OF THE
      PROSTATE

     • PROSTATITIS
• NODULAR HYPERPLASIA
        • CANCER
        PROSTATITIS
  • ACUTE BACTERIAL PROSTATITIS
 • CHRONIC BACTERIAL PROSTATITIS
• CHRONIC ABACTERIAL PROSTATITIS
     ACUTE BACTERIAL
       PROSTATITIS
• ETIOLOGY
 – SAME ORGANISMS THAT CAUSE UTI
   • E coli, 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 OR LEUKOCYTOSIS
 – USUALLY RESOLVES WITH 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
   • 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 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
   CLINICAL COURSE OF
  NODULAR HYPERPLASIA
• SYMPTOMS OCCUR IN ONLY 10% OF MEN
  WITH NODULAR HYPERPLASIA
• HESITANCY
• URINARY RETENTION
  – URGENCY, FREQUENCY, NOCTURIA, UTI
• TREATMENT
  – MEDICAL
  – SURGICAL
• COMMON CAUSE FOR ELEVATED
  PROSTATE SPECIFIC ANTIGEN (PSA)
    CARCINOMA OF THE
       PROSTATE
• EPIDEMIOLOGY
 – MOST COMMON VISCERAL CANCER
   • 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
 – LATENT CA IS EVEN MORE PREVALENT
   • >50% IN MEN > 80 YO
CARCINOMA OF THE PROSTATE
 • PATHOGENESIS
  – HORMONAL FACTORS
    • DOES NOT OCCUR IN EUNUCHS
    • 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
 CARCINOMA OF THE PROSTATE
• CLINICAL COURSE
 – OFTEN CLINICALLY SILENT
 – DIGITAL RECTAL EXAM (DRE)
 – PROSTATE SPECIFIC ANTIGEN (PSA)
     • > 4 ng/ml IN PERIPHERAL BLOOD
     • FREE PSA < 25%
 –   TRANSRECTAL ULTRASOUND
 –   NEEDLE BIOPSY
 –   PROSTATISM (LIKE BPH)
 –   METASTASES
     • OSTEOBLASTIC
 – TREATMENT- SURGERY, RADIATION,
   HORMONES, CHEMO
Needle bx of prostate
CARCINOMA OF THE PROSTATE
 • STAGING
   A (T1)       MICROSCOPIC ONLY
   B(T2)        MACROSCOPIC (PALPABLE)
   C(T3 &T4)    EXTRACAPSULAR
   D(N1-3,M1)   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
Hydronephrosis

				
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posted:12/3/2011
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