1. KUMAR, COTRAN, AND ROBBINS
MALE GENITAL SYSTEM
PENIS
SCROTUM, TESTIS, & EPIDIDYMIS
PROSTATE
KUMAR, COTRAN, AND ROBBINS
7th Edition
CH 18

2. PENIS
MALFORMATIONS
INFLAMMATORY LESIONS
NEOPLASMS

3. 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)

4. Hypospadias
Hypospadias

5. Epispadias
Epispadias

6. 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

7. 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

8. 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

9. INFLAMMATORY LESIONS OF THE PENIS
FUNGAL INFECTIONS
CANDIDIASIS
ESPECIALLY IN DIABETICS
EROSIVE, PAINFUL, PRURITIC
CAN INVOLVE ENTIRE MALE EXTERNAL GENITALIA

10. 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

11. Squamous Cell Carcinoma

14. 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

15. 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

16. 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

17. Hydrocele

18. LESIONS OF THE TESTES
CONGENITAL
INFLAMMATORY
NEOPLASTIC

19. CRYPTORCHIDISM AND TESTICULAR ATROPHY
FAILURE OF TESTICULAR DESCENT
EPIDEMIOLOGY
ABOUT 1% OF MALES
RIGHT > LEFT, 25% BILATERAL
PATHOGENESIS
HORMONAL ABNORMALITIES
TESTICULAR ABNORMALITIES
MECHANICAL PROBLEMS

20. Atrophic testes secondary to cryporchidism

21. 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

22. OTHER CAUSES OF TESTICULAR ATROPHY
CHRONIC ISCHEMIA
INFLAMMATION OR TRAUMA
HYPOPITUITARISM
EXCESS FEMALE SEX HORMONES
THERAPEUTIC ADMINISTRATION
CIRRHOSIS
MALNUTRITION
IRRADIATION
CHEMOTHERAPY

23. 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

24. 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

25. TESTICULAR NEOPLASMS EPIDEMIOLOGY
MOST IMPORTANT CAUSE OF PAINLESS ENLARGEMENT OF TESTIS
2/100,000 MALES, WHITES > BLACKS (US)
INCREASED FREQUENCY IN SIBLINGS
PEAK INCIDENCE YRS
MOST ARE MALIGNANT
ASSOCIATED WITH GERM CELL MALDEVELOPMENT
CRYPTORCHIDISM
TESTICULAR DYSGENESIS(XXY)

26. 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

27. 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

28. 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

29. 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.

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

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

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

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

34. Dermoid Cyst
Dermoid cyst.

35. Immature Teratoma With Embryonal Carcinoma

36. 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

37. DISEASES OF THE PROSTATE
PROSTATITIS
NODULAR HYPERPLASIA
CANCER

38. PROSTATITIS ACUTE BACTERIAL PROSTATITIS CHRONIC BACTERIAL PROSTATITIS
CHRONIC ABACTERIAL PROSTATITIS

39. ACUTE BACTERIAL PROSTATITIS
ETIOLOGY
SAME ORGANISMS THAT CAUSE UTI
E coli, OTHER GNR
PATHOGENESIS
ORGANISMS ASCEND FROM URETHRA AND URINARY BLADDER
RARELY, HEMATOGENOUS SPREAD

40. 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

41. 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

42. 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

43. PROLIFERATIVE LESIONS OF THE PROSTATE
PERIURETHRAL AND TRANSITIONAL ZONES
URETHRA
PERIPHERAL
ZONE
NORMAL PROSTATE
NODULAR HYPERPLASIA
CARCINOMA

44. 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

45. 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

46. 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)

47. 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 YO
LATENT CA IS EVEN MORE PREVALENT
>50% IN MEN > 80 YO

48. 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

49. 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

51. Needle bx of prostate

55. 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

56. Carcinoma of prostate. Dilated bladder and urethra.

60. Hydronephrosis
Hydronephrosis.