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

– 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

HYPOSPADIAS AND EPISPADIAS

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

• 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

INFLAMMATORY LESIONS OF THE PENIS

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

• 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

SCC OF THE PENIS

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

• SCROTAL ENLARGEMENT– HYDROCELE - MOST COMMON CAUSE

• ACCUMULATION OF SEROUS FLUID WITHIN TUNICA VAGINALIS

• INFECTIONS, TUMOR, IDIOPATHIC

– HEMATOCELE– CHYLOCELE

• FILIARIASIS - ELEPHANTIASIS

– TESTICULAR DISEASE

LESIONS INVOLVING THE SCROTUM

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

• 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

CRYPTORCHIDISM AND TESTICULAR ATROPHY

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

• 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

INFLAMMATORY LESIONS OF THE TESTIS

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)

• 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

TESTICULAR NEOPLASMS

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

SEMINOMA(40-50 Y)

GONADALDIFFERENTIATION

EMBRYONAL CA(UNDIFFERENTIATED)

(20-30 Y)

TOTIPOTENTIALDIFFERENTIATION(NONSEMINOMA)

CHORIOCARCINOMA(20-30 Y)

hCG +

TROPHOBLASTICDIFFERENTIATION

YOLK SAC TUMOR(< 3 Y)AFP +

YOLK SACDIFF

TERATOMA(ALL AGES)

MATURE

IMMATURE

MALIGNANT TX

SOMATICDIFFERENTIATION

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

• 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

ACUTE BACTERIAL PROSTATITIS

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

• 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

CHRONIC PROSTATITIS

PROLIFERATIVE LESIONS OF THE PROSTATE

URETHRAPERIURETHRAL AND 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

• 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 NODULAR HYPERPLASIA

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

• 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

CARCINOMA OF THE PROSTATE

Needle bx of prostate

• STAGINGA (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

CARCINOMA OF THE PROSTATE

Hydronephrosis