KUMAR, COTRAN, AND ROBBINS 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 Hypospadias

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

Seminoma, with focal hemorrhage and necrosis Seminoma, focal hemorrhage and necrosis. These features are usually not seen, and often indicate presence of other more aggressive cell types. Usually soft, well-demarcated, homogeneous, gray-white and bulge from the cut surface.

Normal testicular tissue Normal testicular tissue, showing seminiferous tubules and interstitial stroma

Seminoma Semimona. Large, well-demarcated cells with distinct borders, clear (glygocen rich) cytoplasm, round nuclei, prominent nucleoli. Lymphocytes are prominent.

Semimona. Large, well-demarcated cells with distinct borders, clear (glygocen rich) cytoplasm, round nuclei, prominent nucleoli.

Seminoma Syncytiotrophoblast Seminoma with syncytiotrophoblast, c/w trophoblastic differentiation. Syncytiotrophoblast

Dermoid Cyst 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 CLINICAL COURSE 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 TRANSITIONAL ZONES URETHRA PERIPHERAL ZONE NORMAL PROSTATE NODULAR HYPERPLASIA CARCINOMA

NODULAR HYPERPLASIA OTHER TERMS USED EPIDEMIOLOGY 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

Carcinoma of prostate. Dilated bladder and urethra.

Hydronephrosis Hydronephrosis.