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Pathology of the Male Genital Tract: Penis, Testis, and Epididymis

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Title: Pathology of the Male Genital Tract: Penis, Testis, and Epididymis


1
Pathology of the Male Genital Tract
Penis, Testis, and Epididymis
Scott Arnold, M.D. Assistant Clinical Professor
of Pathology, Boonshoft SOM Department of
Pathology, Greene Memorial Hospital sarnold_at_med-he
alth-system.org
2
Outline Penis,Testis, Epididymis
  • I. Penis
  • A) Congenital Anomalies
  • B) Inflammations
  • C) Neoplasms
  • II. Testis and Epididymis
  • A) Inflammations
  • B) Torsion
  • C) Cryptorchidism and Atrophy
  • D) Germ Cell Tumors (GCT) of Testis
  • E) Clinical Features of GCT
  • F) Sex Cord-Stromal Tumors of Testis
  • G) Malignant Lymphoma of Testis

3
Congenital Anomalies 1 Hypospadias and Epispadias
  • Malformations of urethral groove and/or urethral
    canal
  • Abnormal opening on ventral surface hypospadias
    (1/300 live male births)
  • Abnormal opening on dorsal surface epispadias
    (less common than hypospadias)
  • Associated with
  • Failure of normal descent of testes
  • Other malformations of urinary tract
  • Clinical sequelae urinary tract obstructions,
    infections, sterility

4
Congenital Anomalies 2 Phimosis
phimosis inflammation
  • Phimosis orifice of the prepuce is too small to
    permit its normal retraction
  • May be congenital or acquired from repeated
    infections with secondary fibrosis (scarring)
  • Complications
  • Secondary infections
  • Carcinoma of penis
  • Paraphimosis constriction of prepuce around
    penis with swelling and edema, preventing its
    replacement over the glans

phimosis
scarring
Paraphimosis with edema
5
Inflammation Balanoposthitis
simple
  • Balanoposthitis inflammation of the glans penis
    prepuce
  • Caused by a wide variety of organisms
  • Predisposing factors
  • Lack of circumcision
  • Poor hygiene
  • Phimosis

erosive
gangrenous
Herpes simplex
Atrophic leukoplakic
6
Balanoposthitis Histopathology
Reactive epidermal hyperplasia
Lymphocytes and plasma cells infiltrating the
dermis
7
Benign neoplasm condyloma acuminatum
  • Sexually transmitted
  • Located on mucocutaneous surfaces of external
    genitalia
  • human papillomavirus HPV 6 most frequently
  • Gross exophytic papillary lesion

Anal lesions
8
Condyloma acuminatum histopathology
  • Exophytic lesion with papillary architecture
    does not invade the underlying dermis
  • Distinctive features
  • Hyperplastic epithelium with hyperkeratosis and
    acanthosis
  • Branching connective tissue stroma
  • Koilocytotic changes in squamous cell nuclei

Fig. 23-2, Pathologic Basis of Disease, 6th ed,
WB Saunders
9
Condyloma acuminatum histopathology
  • Koilocytosis HPV-related cytologic changes
  • Perinuclear vacuoles (clear spaces)
  • Enlarged and hyperchromatic nuclei with irregular
    membranes raisinoid

Upper photo fig. 23-3, Pathologic Basis of
Disease, 6th ed, WB Saunders, 1999.
10
Squamous carcinoma-in-situ (CIS)
  • Definition malignant cytologic changes confined
    within epithelium, with no invasion through
    basement membrane
  • Three terms describe clinically distinctive
    lesions with different gross appearances, but all
    three share histopathologic features of CIS
  • Bowen disease
  • erythroplasia of Queyrat
  • bowenoid papulosis
  • HPV DNA identified in 80 of CIS
    (usually HPV type 16)

11
Carcinoma-in-situ (clinically Bowen disease)
  • Bowen disease solitary gray-white plaque
    involving skin of penis or scrotum
  • Untreated lesions may evolve (over years) into
    invasive squamous cell carcinoma
  • HPV-associated, most commonly HPV-16
  • Microscopic features full thickness dysplasia,
    nuclear pleomorphism, mitoses basement membrane
    intact

Fig. 21-18, PBD, 8th ed, 2010
12
CIS erythroplasia of Queyrat and bowenoid
papulosis
  • erythroplasia of Queyrat
  • Shiny, red velvety plaques involving glans and
    prepuce
  • Histopathology same as Bowen disease
  • bowenoid papulosis
  • Multiple red-brown papules, some verrucous
    (wart-like)
  • Seen in sexually active young adults
  • Histopathology same as Bowen disease

13
Invasive Squamous Carcinoma of Penis (1)
  • Penile carcinoma is 1 of male carcinomas in U.S.
  • Begins on glans or inner surface of prepuce
  • Risk factors
  • Lack of circumcision (rarely seen in circumcised
    men)
  • Circumcision improves genital hygiene by reducing
    exposure to carcinogens
  • Human papillomavirus DNA identified in cells of
    50 of carcinomas (HPV-16 and 18 most frequent)

Fig. 23-5, Pathologic Basis of Disease, 6th ed,
WB Saunders, 1999.
14
Invasive Carcinoma of Penis (2)
  • Gross Features
  • Ulcerated flat lesion or exophytic papillary
    lesion
  • Microscopic Features
  • Squamous cell carcinoma
  • Prognosis
  • Slow-growing, metastasizes to inguinal and iliac
    lymph nodes
  • Negative lymph nodes 66 5-year survival
  • Positive lymph nodes 27 5-year survival

15
Epididymitis
Fig 21-21, Pathologic Basis of Disease, 8th ed,
2010
  • Causes vary with age
  • Children assoc. with congenital anomalies,
    gram-negative bacilli
  • Sexually active men Chlamydia trachomatis and
    N. gonorrhoeae
  • Older men urinary tract pathogens (E.
    coli, Pseudomonas)

Epididymis replaced by abscess
Normal testis
Histopathology acute chronic inflammation
with variable fibrosis N. gonorrhoeae
suppurative inflammation extends from posterior
urethra to prostate, seminal vesicles, and
epididymis M. tuberculosis granulomatous
inflammation originates in epididymis/prostate/se
minal vesicles and may spread to testis
Sequelae abscess formation, sterility
16
Orchitis
  • Orchitis inflammation of the testis, commonly
    related to urinary tract or prostatic infections
    that reach testis through vas deferens or
    spermatic cord
  • Causes
  • Mumps systemic viral disease common in
    school-aged children and rarely affects testis in
    prepubertal boys, but 20-30 postpubertal men
    with mumps develop orchitis, usually about one
    week after parotid gland swelling infertility or
    sterility may result
  • Syphilis almost always affects testis first,
    later epididymis
  • Tuberculosis usually affects epididymis first,
    later testis
  • Gonorrhea orchitis only in untreated or
    neglected cases (typically limited to urethritis
    and epididymitis)

17
Torsion of Testis
  • Definition twisting of testis on spermatic
    cord, presenting as sudden onset testicular pain
  • Often without trauma or injury
  • Predisposing Factor
  • Bilateral anatomic defect allowing increased
    mobility of testis in scrotum
  • Pathogenesis
  • Arterial inflow remains patent
  • Venous outflow cut off
  • Marked congestion leading to hemorrhage and
    possibly infarction (if not treated)
  • Surgical untwisting of testis usually prevents
    infarction if within 6 hours after onset pain

Lower photo fig. 21-22, PBD, 8th ed, 2010.
18
Cryptorchidism
  • Definition undescended testis or testes
  • Incidence 1 of 1-year-old boys 0.3-0.8 of
    adult males
  • Diagnosis by clinical exam revealing scrotal
    sac with no testis (asymptomatic) testis often
    palpable within inguinal canal
  • 75 cases unilateral 25 cases bilateral
  • Pathogenesis
  • Failure of intra-abdominal testis to descend into
    scrotum
  • Hormonal factors control descent
    trans-abdominal to pelvic brim by
    mullerian-inhibiting substance through inguinal
    canal to scrotum androgen dependent
  • May be associated with other genitourinary
    anomalies

19
Cryptorchidism Sequelae
Normal active spermatogenesis
  • Progressive tubular atrophy
  • Begins around age 2
  • Decreased number of germ cells (absence of germ
    cells leaves only Sertoli cells)
  • Infertility or sterility
  • Increased risk of neoplasm
  • 5-10 fold increase in tumors within undescended
    testis
  • Earlier surgical placement of testis in scrotum
    (orchiopexy) decreases risk of neoplasia
  • Risk of neoplasm also increased in contralateral
    normally descended testis

Fig. 21-20, Pathologic Basis of Disease, 8th ed,
2010.
Atrophy Sertoli cells only, with thickened
basement membranes
20
Neoplasms of Testis Overview
  • Two major types of neoplasms

Type Usual behavior Comments
Germ Cell 95 Malignant aggressive with rapid dissemination Most are cured with surgery multiagent chemotherapy
Sex Cord- Stromal (non-germ cell) 5 Usually benign generally cured by excision May elaborate steroid hormones and produce endocrinologic syndromes
21
Testis Germ Cell Neoplasms
  • Epidemiology
  • Annual incidence 6 per 100,000 males peak
    incidence ages 15-34 (most common neoplasm in
    young males)
  • Incidence 5x higher in whites compared to blacks
  • Predisposing Factors
  • Cryptorchidism most important, in 10 germ cell
    tumors
  • Genetic
  • sons of father with GCT at 4x higher risk than
    population
  • brothers at 8-10x higher risk than population
  • Testicular dysgenesis syndromes (spectrum)
  • Includes cryptorchidism, hypospadias, poor sperm
    quality
  • Klinefelter syndrome (47XXY) 50x higher risk of
    mediastinal GCT (not testicular GCT)

22
Classification and Pathogenesis of Germ Cell
Tumor (GCT)
  • Origin normal intratubular multipotential germ
    cells transform into larger atypical cells
    intratubular germ cell neoplasia (ITGCN)
    precursor lesion of invasive germ cell tumors.
  • 50 persons with ITGCN develop invasive GCT in 5
    yrs.
  • Transformation may occur in utero remain
    dormant until puberty, after which tumors develop
  • Genomic pathogenesis invasive GCTs (and many
    ITGCN) gain extra copy (isochromosome) of short
    arm of 12 i(12p)
  • Pathologic classification identifies all
    histologic types of GCT present 40 single
    type 60 mixed types
  • Clinical classification 2 groups
  • Seminomatous resemble primordial germ cells
  • Non-seminomatous differentiated or
    undifferentiated cells

23
Germ Cell Neoplasm Seminoma
  • Most common germ cell neoplasm (50 of all)
  • Postpubertal males incidence peaks in 30s
  • Histologically identical to ovarian dysgerminoma
  • Seminoma cells contain isochromosome 12p
  • Immunohistochemistry
  • positive for overexpression c-KIT (CD 117) and
    placental alkaline phosphatase
  • Seminoma cells negative for ?-fetoprotein (AFP)
    and human chorionic gonadotropin (HCG) minority
    of seminomas contain syncytiotrophoblasts ?
    elevated serum HCG.
  • Two histologic subtypes
  • Typical (85-90) classic uniform cells, low
    mitotic rate
  • Spermatocytic (5-10) three intermixed cell
    populations

24
Seminoma Gross Features
Bulky mass, 2-10x normal testis Often
replaces entire testis Usually confined within
tunica albuginea (AJCC stage T1) Tan-white,
lobulated surface Little hemorrhage or necrosis
25
Typical Seminoma Histopathology
  • Sheets of uniform cells divided by thin septae of
    fibrous tissue
  • Classic seminoma cell
  • Large, distinct cell borders, with clear or
    pale-staining cytoplasm (much glycogen)
  • 1-2 prominent nucleoli
  • Scattered reactive lymphocytes
  • Mitoses infrequent

Fig. 21-24, Pathologic Basis of Disease, 8th ed,
2010.
26
Spermatocytic Seminoma
  • Only 1-2 of germ cell neoplasms
  • Older men (usually gt65)
  • Slow-growing, rarely metastasizes (good
    prognosis)
  • 3 intermixed cell populations showing features of
    spermatocytes by electron microscopy
  • Medium-sized (15-18 microns) with round
    nucleus/pink cytoplasm
  • Small (6-8 microns) with minimal cytoplasm, like
    secondary spermatocytes
  • Scattered giant cells (50-100 microns)

27
Embryonal Carcinoma
Clinical ages 20-30 more aggressive than
seminomas Gross features variegated color,
poorly demarcated, zones of hemorrhage
necrosis Mixed germ cell tumors 45 have
embryonal component Pure embryonal CA only 3
of GCTs
28
Embryonal Carcinoma
Microscopic --solid syncytial sheets, glandular,
or tubular patterns --large anaplastic cells with
scattered tumor giant cells --indistinct cell
borders --frequent mitoses --IHC positive PLAP,
cytokeratin, neg. c-KIT
29
Yolk Sac Tumor (Endodermal Sinus Tumor)
Most common testicular tumor in children lt3
years age very good prognosis Pure form is
rare in adults usually seen as component of
mixed germ cell tumor Microscopic lacy
network of cuboidal or elongated cells
pathognomonic feature endodermal sinuses (core
with central capillary, covered by visceral
parietal cells, resembling primitive
glomerulus) --eosinophilic globules in cytoplasm
positive for ?-fetoprotein
30
Choriocarcinoma
Pure form rare more commonly in mixed GCTs
Composed of 2 cell types BOTH cytotrophoblasts
and syncytiotrophoblasts Most aggressive of all
GCTs, rapidly growing lesions, early metastasis
outgrow blood supply ? hemorrhage and necrosis
HCG positive in syncytiotrophoblastic cells
Arrowhead cytotrophoblastic cells (single
nucleus) Arrow synctyiotrophoblastic cells
(mulitple nuclei
Fig. 21-27, PBD 8th ed. 2010
31
Teratoma
Germ cell tumor containing elements from more
than one embryonic layer Pure form infants and
children benign behavior Adults pure form
rare usually mixed with other types of GCT
always considered malignant Gross
heterogeneous texture with solid and cystic
areas may have grossly apparent cartilage
Fig. 21-28, PBD, 8th ed, 2010
32
Teratoma
  • MICROSCOPIC 3 variants
  • Mature teratoma all elements
    differentiated (mature epithelial, connective,
    neural, etc.)
  • Immature teratoma incomplete differentiation,
    fetal-type mesenchymal cells, neuroblasts, etc.
  • Teratoma with malignant transformation definite
    histologic criteria for malignancy (squamous
    carcinoma, sarcoma, etc.)

MATURE
IMMATURE
MALIGNANT TRANSFORMATION
33
Seminoma Clinical Features
  • 70 localized at time of diagnosis (Stage I)
  • Metastasis via lymphatics typical
  • para-aortic retroperitoneal lymph nodes involved
    first
  • hematogenous spread later in course
  • Radiosensitive (responds well to radiation)
  • Best prognosis of adult testicular GCTs
  • 95 cure rate in men with Stage I and II pure
    seminomas

34
Non-seminomatous germ cell tumors (NSGCT)
  • More aggressive than seminomas
  • 60 advanced stage (II III) at time of
    diagnosis
  • Metastases by hematogenous routes more often
    than seminomas
  • Hematogenous lungs most likely (receives all
    venous drainage) liver, brain, bones
  • Radioresistant (poor response to radiation)
  • 90 complete remission after orchiectomy and
    multiagent chemotherapy most of these are cured

35
Clinicopathologic Correlations Neoplasms of
Testis
  • Painless mass in testis (usual presentation)
  • Modes of metastasis
  • Lymphatic para-aortic lymph nodes first
  • Supraclavicular and mediastinal nodes later
  • Hematogenous spread to lungs, liver, bones, brain
  • Metastases may be histologically different than
    primary testicular tumor
  • Derivation from pluripotent germ cells allows
    forward differentiation (more mature) or
    backward differentiation into more immature
    cells
  • Components of tumor that are chemotherapy-resistan
    t survive
  • Quantitatively minor components not detected by
    surgical pathologist at time of diagnosis

36
Staging of Testicular Cancer
  • Stage I tumor confined to testis, epididymis,
    or spermatic cord
  • Stage II metastases confined to retroperitoneal
    nodes below the diaphragm
  • Stage III metastases outside the
    retroperitoneal nodes OR above the diaphragm

37
Biologic Tumor Markers in Serum
Used for diagnosis and management of germ cell
tumors Staging a
persistently elevated serum tumor marker after
orchiectomy indicates at least stage II disease,
even if lymph nodes appear negative by imaging or
pathologic examination
Response to Therapy persistently elevated serum
tumor marker indicates residual or recurrent
disease decreasing or undetectable level
indicates response to therapy
Marker Source Associated Tumor(s)
HCG Syncytiotrophoblast (SCT) Choriocarcinoma (pure or mixed) or SCT within a seminoma
AFP Fetal gut, liver, yolk sac Yolk sac tumor (pure or mixed) --also hepatocellular carcinoma
LDH Multiple tissues Non-specific, but level correlates with proliferating tumor burden
38
Sex Cord-Stromal Tumors of Testis
Only 5 testicular neoplasms usually benign
behavior
LEYDIG CELL TUMOR derived from interstitial
stromal cells of Leydig may secrete androgens
or estrogens, producing sexual precocity (kids)
or gynecomastia (adults) Gross homogeneous,
well-demarcated brown nodule Micro polygonal
cells with dense granular red cytoplasm
containing rod-like crystalloids of Reinke in
25 Prognosis 90 benign 10 invasive
(malignant)
39
Sex Cord-Stromal Tumors of Testis
SERTOLI CELL TUMOR (ANDROBLASTOMA) most
hormonally silent, presenting as mass in testis
Microscopic trabeculae and cords with tendency
to form immature seminiferous tubules 90
benign 10 malignant
40
Malignant Lymphoma of Testis
Most common testicular neoplasm in men gtage
60 5 of all testicular tumors Gross
fleshy, tan, solid Micro usually diffuse
large B-cell lymphoma Most men have
disseminated lymphoma at time of diagnosis
(rarely confined only to testis) Treatment
multi-agent chemotherapy (for systemic disease)
Prognosis previously poor, now improving due to
more effective chemotherapy
41
Lesions of Tunica Vaginalis
  • Tunica vaginalis mesothelial-lined sac proximal
    to testis and epididymis
  • Lesions present with scrotal enlargement
    delineated from testis by physical exam or
    imaging corrected surgically
  • Hydrocele clear serous fluid in sac

hypoechoic fluid in scrotal sac
testis displaced medially
42
Lesions of tunica vaginalis, cont.
spermatocele
  • Hematocele post-trauma or torsion
  • Spermatocele cystic accumulation of semen in
    dilated efferent ducts of testis
  • Varicocele dilated veins of pampiniform plexus
    within spermatic cord may cause infertility

testis
rope-like mass of dilated veins
43
References (textbooks only)
  • Kumar, Abbas, Fausto, Aster Robbins and Cotran
    Pathologic Basis of Disease, 8th edition,
    Elsevier 2010.
  • Photos from previous editions of Pathologic Basis
    of Disease 6th (1999) 7th (2004)
  • Bostwick and Eble Urologic Surgical Pathology,
    C.V. Mosby, 1997.
  • Fletcher Diagnostic Histopathology of Tumors,
    2nd edition, Churchill-Livingstone 2000.
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