Benign diseases of male genitalia

Benign diseases of male genitalia

( Lecture )

MALE GENITAL SYSTEM

PENIS SCROTUM, TESTIS, & EPIDIDYMIS PROSTATE

PENIS

MALFORMATIONS INFLAMMATORY LESIONS NEOPLASMS

MALFORMATIONS OF THE PENIS

ABNORMAL LOCATION OF URETHRAL ORIFICE ALONG PENILE SHAFT HYPOSPADIAS (VENTRAL ASPECT) MOST COMMON (1/250 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
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)EPIDEMIOLOGYUNCOMMON – LESS THAN 1 % OF CA IN US MENUNCIRCUMCISED MEN BETWEEN 40 AND 70PATHOGENESISPOOR HYGIENE, SMEGMA, SMOKINGHUMAN 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 (AT 1 YR) RIGHT > LEFT, 10% 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 (3-5X) ORCHIOPEXY MAY HELP PREVENT ATROPHY MAY NOT ELIMINATE 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 5/100,000 MALES, WHITES > BLACKS (US) INCREASED FREQUENCY IN SIBLINGS PEAK INCIDENCE 20-34 YRS MOST ARE MALIGNANT ASSOCIATED WITH GERM CELL MALDEVELOPMENT CRYPTORCHIDISM (10%) 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 (60%) SEMINOMAS (50%) EMBRYONAL CARCINOMA YOLK SAC TUMOR CHORIOCARCINOMA TERATOMA MULTIPLE HISTOLOGIC PATTERNS (40%) EMBRYONAL CA + TERATOMA CHORIOCARCINOMA + OTHER OTHER COMBINATIONS

HISTOGENESIS OF TESTICULAR NEOPLASMS (PEAK INCIDENCE)

GERM CELL PRECURSOR
SEMINOMA (40-50 Y)
GONADAL DIFFERENTIATION
EMBRYONAL CA (UNDIFFERENTIATED) (20-30 Y)
TOTIPOTENTIAL DIFFERENTIATION (NONSEMINOMA)
CHORIOCARCINOMA (20-30 Y) hCG +
TROPHOBLASTIC DIFFERENTIATION
YOLK SAC TUMOR (< 3 Y) AFP +
YOLK SAC DIFF
TERATOMA (ALL AGES)
MATURE IMMATURE MALIGNANT TX
SOMATIC DIFFERENTIATION

Seminoma, with focal hemorrhage and necrosis

Dermoid Cyst

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

URETHRA
PERIURETHRAL 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

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
CARCINOMA OF THE PROSTATE

Hydronephrosis