Download MBBS Pathology PPT 5 Male Genital Lecture Notes

Diseases of Male Genital Tract

Penile Diseases

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Testicular Diseases

Prostatic Diseases

Penile Diseases

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?Congenital Anomalies
?Inflammation
? Tumors
? Benign Tumors

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? Premalignant lesion(carcinoma in situ)
? Malignant Tumors
?WHO histological classification

of tumours of the penis

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?

__________

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Malignant epithelial tumours of the penis

? Squamous cell carcinoma 8070/31

? Basaloid carcinoma 8083/3

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? Warty (condylomatous) carcinoma 8051/3

? Verrucous carcinoma 8051/3

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? Papillary carcinoma, NOS 8050/3

? Sarcomatous carcinoma 8074/3
? Mixed carcinomas
? Adenosquamous carcinoma 8560/3

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? Merkel cell carcinoma 8247/3
? Small cell carcinoma of neuroendocrine type 8041/3
? Sebaceous carcinoma 8410/3
? Clear cell carcinoma 8310/3
? Basal cell carcinoma 8090/3

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Precursor lesions

? Intraepithelial neoplasia grade I I Bowen disease 8081/2

? Erythroplasia of Queyrat 8080/2

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? Paget disease 8542/3

? Melanocytic tumours

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? Melanocytic nevi 8720/0

? Melanoma 8720/3

? Mesenchymal tumours

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? Haematopoietic tumours

? Secondary tumours

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Benign Tumors

1-Condyloma Acuminatum-
? Wart
? STD

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? HPV


Morphology-
? coronal sulcus and inner surface of the prepuce

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? single or multiple sessile or pedunculated, red papillary excrescences
Histologically-
? Acanthosis
? koilocytosis
2-Peyronie Disease-(Idiopathic Fibrous Induration )

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? fibromatosis
? fibrous bands involving the corpus cavernosum of the penis
? Microscopically, dense fibrosis is associated with sparse, nonspecific,

chronic inflammatory infiltration

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Precursor lesions-
? Intraepithelial neoplasia Grade II
qClinical Variant
?Bowenoid papulosis

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?Bowen disease
?Erythroplasia of Queyrat
? Paget disease
Bowenoid papulosis ?
? younger age

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? multiple reddish brown papular lesions
? histologically indistinguishable from Bowen disease
? HPV type 16

Bowen disease-

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? >35Yr
? shaft of the penis and the scrotum
? solitary, thickened, gray-white, opaque plaque
? turn in to 10% scc (5-33% WHO)

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Normal Skin histology
Invasive Carcinoma-
squamous cell carcinomas
Etiology-

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? phimosis
? chronic inflammatory conditions, especially lichen sclerosus
? smoking
? ultraviolet irradiation
? history of warts, or condylomas

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Clinical features
? 40 -60 years
? glans or inner surface of the prepuce
MORPHOLOGY-

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? papillary
? flat
? Ulcerated
? Exophytic

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Histopathology-
? spectrum of differentiation from well to poorly differentiated.
? Superficial ?WD
? Deep-PD

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Verrucous carcinoma-
? variant of squamous cell carcinoma
? exophytic well-differentiated
? locally invasive, but rarely metastasize

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Other variants
? basaloid, warty, and papillary variants


? acanthosis and hyperkeratosis

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? into the underlying stroma with a broad based, pushing border
? No koilocytotic changes
? Not HPV related
? D/D Condyloma acuminatum

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Tumour spread-
? superficial inguinal lymph node
? deep groin and pelvic nodes

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Three most important pathological factors to predict final outcome are
? histological grade
? depth of invasion
? vascular invasion

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Diseases of Prostate

? Inflammation
? Benign Enlargement
? Tumors

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q Inflammation
?Acute bacterial prostatitis
?Chronic bacterial prostatitis
?Chronic abacterial prostatitis

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?Granulomatous prostatitis
1. Acute bacterial prostatitis
Etiology-
? bacteria ,E. coli,
? from the urethra

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? Diagnosis-culture

MORPHOLOGY-
Gross- enlarged, swollen and tense
Cut section- abscesses and foci of necrosis

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M/E-
? Necrosis
? Or as diffuse edema
? Congestion
?biopsy is contraindicated

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2-Chronic Prostatitis-
?Chronic bacterial prostatitis-
? consequence of recurrent UTI
? E coli
? 10-12 wbc/hpf

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?Chronic abacterial prostatitis-
? more common
? No h/o Reccurent UTI
? Wbc in prostatic secretion

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? culture of urine and prostatic secretions is always negative
? Chlamydia trachomatis and Ureaplasma urealyticum
MORPHOLOGY-
? Grossly, enlarged, fibrosed and shrunken
? Histologically-lymphocytes, plasma cells, macrophages and

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neutrophils within the prostatic tissue

3-Granulomatous Prostatitis-

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? variety of chronic prostatitis
?Etiology-

? Tubercular

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? Fungal

? autoimmune origin
?MORPHOLOGY-

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? Grossly-firm to hard

? Histology-macrophages, lymphocytes, plasma cel s and some multinucleate

giant cel s

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qBenign Prostatic Hyperplasia or Nodular Hyperplasia-
? most common benign prostatic disease
? Incidence increases >50yrs

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? 70% >60yrs

ETIOLOGY-
? endocrinologic, racial, inflammation and arteriosclerosis
? advancing age,--androgen-- oestrogen-periurethral inner prostatsensitive to

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estrogen oestrogen--

Nod hyprplasia

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? Stromal cell produce type 2 5-reductase enzyme
? epithelial cells do not express type 2 5-reductase

? DHT-induced growth factors-- increasing the proliferation of

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stromal cells and decreasing the death of epithelial cells


? MORPHOLOGY-

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? Gross- nodular, smooth and firm and weighs 2-4 times its normal

weight

Cut surface-

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?pale gray and tough-fibromuscular stroma-EARLY
?yellow-pink and soft- gland-LATER

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Microscopy- hyperplasia of all three tissue elements in varying

proportions--
? glandular

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? fibrous
? Muscular
called as fibromyoadenomatous nodules- well developed satge
Variable histological features-
? lymphocytic aggregates

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? small areas of infarction
? corpora amylacea
? foci of squamous metaplasia

CLINICAL FEATURES-

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? frequency, nocturia
? difficulty in micturition
? pain
? haematuria

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Complications of NPH

CARCINOMA OF PROSTATE

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? men older than age 50 years
? ETIOLOGY-
?Endocrinologic factors
?Racial and geographic influences-
? uncommon in Japanese and Chinese, while the prevalence is high in

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Americans

?Environmental influences-
? high dietary fat, and exposure to polycyclic aromatic hydrocarbons

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?Nodular hyperplasia
?Heredity-
?2-fold higher frequency in first-degree relatives

Molecular Pathogeneis

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? Most common-TPRSS2-ETS fusion genes and mutations or deletions

that activate the PI3K/AKT signalling pathway

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Others

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? PTEN
? BRCA2
? HOXB13
? 8q24 amplification
? Loss of P53, in last stage

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? Glutathione S-transferase P1 gene,hypermethylation
? Epigenetic modification ?RB,CDKN2A

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MORPHOLOGIC FEATURES.
? Grossly, enlarged, normal in size or smaller than normal
? Cut section- gritty and firm,homogeneous and contains irregular

yellowish areas

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Microscopically-
? Adenocarcinoma ,96%
? transitional cell carcinoma
? squamous cell carcinoma
? undifferentiated carcinoma

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Histologic characteristics-
? Architectural disturbance-closely packed in back-to-back arrangement

without intervening stroma

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? Gland pattern
? Stroma- scant , tumour cells may penetrate and replace the

fibromuscular stroma

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High-grade prostatic intraepithelial neoplasia (PIN)
? Gleason's microscopic grading system- based on two features:
i) Degree of glandular differentiation

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ii) Growth pattern of the tumour in relation to the stroma
These features are assessed by low-power examination

? Only one pattern- double the number
? Two pattern- predominant p+ secondary p

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? Three pattern- pred p+ higher pattern
3 (70%)+4(20%)+5(10%)3+5=8

? 2 (1 + 1)- well-differentiated
? 10 (5 + 5)-and the least-differentiated tumors

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closely packed uniform

glands

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loosely packed slightly

variable glands

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Single glands of variable size

and density, with an

infiltrative pattern

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Ragged infiltration with poorly

formed glands or sheets and

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cords of fused glands

Single cel s,Solid

sheet,comedonecrosis

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3+3

3+4

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4+4

4+4

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4+4

4+4
GS-5+5

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Biomarkers of prostate cancer

1-PSA
?PSA density
?PSA velocity

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?age-specific reference ranges
?ratio of free and bound PSA (free psa low in cancer)
2-PCA3
3-combination of urinary PCA3 with screening of urine for TMPRSS2-

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ERG fusion DNA>psa alone
Testis

Must know

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1-Classification of testicular tumor
2-Tumor markers in diagnosis
3-Morphology of
a)

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Seminoma

b)

Embryonal carcinoma

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c)

Yolk sac tumor

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4-Cryptorchidism


Testicular lesion

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? CongenitalAnomalies
? RegressiveChanges
? Inflammation (Nonspecific , Specific Inflammations, Granulomatous

(Autoimmune) Orchitis)

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? VascularDisorders(torsion)
? SpermaticCordandParatesticularTumors
? TesticularTumors
INFLAMMATIONS-

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? Inflammation of the testis is termed as orchitis and of epididymis is

called as epididymitis; the latter being more common

1-Non-specific Epididymitis and Orchitis-

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? may be acute or chronic
? common routes of spread are via the vas deferens, or lymphatic and

haematogenous routes

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? caused by urethritis, cystitis, prostatitis and seminal vesiculitis
? common infecting organisms in Neisseria gonorrhoeae and Chlamydia

trachomatis
Grossly,

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? acute stage- firm, tense, swollen and congested
may be multiple abscesses, especially in gonorrhoeal

infection

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? chronic stage- variable degree of atrophy and fibrosis

Histological y,
? acute- congestion, oedema and diffuse infiltration by neutrophils, or formation of

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neutrophilic abscesses

? Chronic- focal or diffuse chronic inflammation, disappearance of seminiferous

tubules, fibrous scarring and destruction of interstitial Leydig cells

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2-Granulomatous (Autoimmune) Orchitis -
Non-tuberculous granulomatous orchitis-
? unilateral, painless testicular enlargement
? may resemble a testicular tumour clinically
? autoimmune basis is suspected

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Gross- enlarged
? Cut section of the testicle is greyish-white to tan-brown
? Histological y, granulomatous reaction(non caseating) is present diffusely

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throughout the testis and is confined to the seminiferous tubules

? Peritubular fibrosis
? interstitial lymphocytes and plasma cells
3-Tuberculous Epididymo-orchitis-

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? invariably begins in the epididymis and spreads to the testis

? May spread via -tuberculous seminal vesiculitis, prostatitis and renal tuberculosis
? haematogenous spread- from tuberculosis of the lungs

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Grossly, discrete, yellowish, caseous necrotic areas
? Microscopical y, numerous tubercles which may coalesce to form large caseous

mass

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? Characteristics of typical tubercles such as epithelioid cells, peripheral mantle of

lymphocytes, occasional multinucleate giant cells and central areas of caseation

necrosis are seen

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? AFB positive


4-Spermatic Granuloma(epididymitis nodosa)

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? inflammatory lesions due to invasion of spermatozoa into the stroma
MORPHOLOGIC FEATURES-
Grossly,
? a small nodule, 3 mm to 3 cm in diameter in head of epididymis

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? firm, white to yellowish-brown

? Histological y,
? Characteristical y, the centre of spermatic granuloma contains

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spermatozoa and necrotic debris+epethelioid cell granuloma
Vascular disorder

Torsion of Testis
? usually followed by sudden muscular effort or physical trauma

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? Twisting of the spermatic cord
? sudden cessation of venous drainage and arterial supply
? Trauma may occure in either in a fully-descended testis or in an

undescended testis

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1-Neonatal torsion-
? occurs either in utero or shortly after birth

? It lacks any associated anatomic defect in testis

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2-"Adult" torsion-
? is typically seen in adolescence and presents with the sudden onset of

testicular pain

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? Viable- manually untwisted within approximately 6 hours of the

onset of torsion

MORPHOLOGIC FEATURES-

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duration and severity of vascular occlusion
? may be coagulative necrosis of the testis and epididymis
? may be haemorrhagic infarction
Spermatic Cord and Paratesticular Tumors

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1-Lipomas
? common lesions involving the proximal spermatic cord, identified at

the time of inguinal hernia repair

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? represent retroperitoneal adipose tissue that has been pulled into the

inguinal canal along with the hernia sac, rather than a true neoplasm

2-Adenomatoid tumor-

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? most common benign paratesticular tumor

? upper pole of the epididymis
? grossly , well circumscribed small nodules
? Microscopically- Proliferation of glandular structures, irregularly lined by cuboidal

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to flattened epithelial cell

? Treatmet- local excision

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Malignant tumor

? rhabdomyosarcomas -children
? liposarcomas- adults

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CLASSIFICATION OF TESTICULAR TUMOR

? most useful classification of tumors is histogenetic
? Named according to from which tissue they arise and of which they consist

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WHO histological classification of testis tumours

? Germ cell tumours

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? Tumours of one histological type (pure forms)
? Tumours of more than one histological type (mixed forms)
? Sex cord/gonadal stromal tumours Pure forms
? Miscellaneous tumours of the testis
? Haematopoietic tumours

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? Tumours of collecting ducts and rete
? Tumours of paratesticular structures
? Mesenchymal tumours of the spermatic cord and testicular adnexae
? Secondary tumours of the testis

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Testicular cancer is staged using the TNM system created by the American Joint

Committee on Cancer (AJCC)
It's based on 4 key pieces of information:
? T refers to how much the main (primary) tumor has spread to tissues next to the

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testicle

? N describes how much the cancer has spread to regional (nearby) lymph nodes
? M indicates whether the cancer has metastasized (spread to distant lymph nodes

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or other organs of the body)

? S indicates the serum (blood) levels of tumor markers that are made by some

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testicular cancers
? Letters or numbers appear after T, N, M, and S to provide more details about

each piece of information.

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? The numbers 0 through 4 indicate increasing severity
? The letters "IS" after the T stand for in situ, which means the tumor is contained

in one place and has not yet penetrated to a deeper layer of tissue.

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? The letter X after T, N, M, or S means "cannot be assessed" because the

information is not known

TNM classification of germ cel tumours of the testis

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pTNM pathological classification
? pTx ?Primary tumour cannot be assessed
? pT0 No evidence of primary tumour pTis Intratubular germ cell neoplasia

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(carcinoma in situ)

? pT1 Tumour limited to testis and epididymis without vascular/lymphatic

invasion; tumour may invade tunica albuginea but not tunica vaginalis

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? pT2 Tumour pT1+v/L + involvement of tunica vaginalis
? pT3 Tumour invades spermatic cord with or without vascular/lymphatic invasion
? pT4 Tumour invades scrotum with or without vascular/lymphatic invasion
pN ? Regional lymph nodes

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? pNX Regional lymph nodes cannot be assessed
? N0 No regional lymph node metastasis
? pN1 <2 cm or </=5 or fewer positive nodes
? pN2 2 to 5 cm in greatest dimension; or more than 5 nodes positive, none more

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than 5 cm; or evidence of extranodal extension of tumour

? pN3 Metastasis with a lymph node mass more than 5 cm in greatest dimension

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S ? Serum tumour markers
? SX Serum marker studies not available or not performed
? S0 Serum marker study levels within normal limits
? LDH, hCG (mIU/ml) ,AFP (ng/ml)
Cryptorchidism

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? Cryptorchidism is a complete or partial failure of the intra-abdominal testes to

descend into the scrotal sac

associated with

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? testicular dysfunction
? an increased risk of testicular cancer

? In 70% of cases, the undescended testis lies in the inguinal ring
? in 25% in the abdomen

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ETIOLOGY. exact etiology is not known in majority of cases
1. Mechanical factors-
? short spermatic cord
? narrow inguinal canal
? adhesions to the peritoneum

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? problems with development of the gubernaculum
? a patent processus vaginalis, or impaired intra-abdominal pressure have also

been hypothesized to contribute to cryptorchidism

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2. Genetic factors-
? up to 23% of cases
? Mutations in insulin-like factor 3 and its receptor, LGR8, have been

demonstrated in a small number of cases

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? trisomy 13
3. Hormonal factor- rarely associated
? deficient androgenic secretions
? mullerian inhibiting substance

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? insulin-like 3 hormone
4. Neuromuscular- abnormalities of the genitofemoral nerve's calcitonin gene-

related peptide

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Miscellaneous-
? Maternal alcohol consumption
? analgesic consumption
? smoking
? Gestational diabetes

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MORPHOLOGIC FEATURES. Cryptorchidism is unilateral in 80% cases

Grossly, small in size, firm and fibrotic

Histology-

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1-Seminiferous tubules
? tubular basement membrane is thickened
? hyalinised tubules with a few Sertoli cells
? foci of spermatogenesis are discernible in 10% of cases
2. Interstitial stroma: usually increase in the

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?interstitial fibrovascular stroma
? Leydig cells,

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? CLINICAL FEATURES. asymptomatic and is discovered only on physical

examination

1. Sterility-infertility. Bilateral cryptorchidism is associated with sterility while

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unilateral disease may result in infertility
2. Inguinal hernia. A concomitant inguinal hernia is frequently present along with

cryptorchidism

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3-Malignancy. Cryptorchid testis is at 30-50 times increased risk of developing

testicular malignancy
? most commonly seminoma and embryonal carcinoma, than a normally

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descended testis

? risk of malignancy is greater in intraabdominal testis than in testis in the inguinal

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canal
? current recommendations are for correction at 6 to 12 months of age
? carcinoma arises from foci of intratubular germ cell neoplasia within the

atrophic tubules

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? Orchiopexy reduces the risk of sterility and cancer

Tumour marker

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Tumour markers- Germ cell tumours of the testis secrete polypeptide hormones

and certain enzymes which can be detected in the blood
There are two principal serum tumour markers
? alpha fetoprotein (AFP) and

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? beta subunit of human chorionic gonadotropin (shCG)

? In addition, carcinoembryonic antigen (CEA), human placental lactogen (HPL),

placental alkaline phosphatase, testosterone, oestrogen and luteinising hormone

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may also be elevated
AFP-
? synthesized by fetal yolk sac and also the liver and intestine
? elevated in 50-70% of testicular germ cell tumours

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? Markedly elevated in yolk sac tumor
? a serum half life of 4.5 days
? However, elevated serum AFP levels are also found in liver cell carcinoma

hCG-

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? secreted by placental trophoblastic cells
? elevated in non-seminomatous germ cell tumours of the testis (e.g. in

choriocarcinoma, yolk sac tumour and embryonal carcinoma)

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? elevated in 50% of patients with germ cell tumours
? elevation in seminoma in 10-25% of cases

Lactate dehydrogenase (LDH)-
? may also be elevated

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? direct relationship between LDH and tumour burden
? However, this test is nonspecific although its degree of elevation correlates with

bulk of disease
Applications-

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? In the evaluation of testicular masses
? In the staging of testicular germ cell tumors. For example, after orchiectomy,

persistent elevation of HCG or AFP concentrations indicates stage II disease even

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if the lymph nodes appear of normal size by imaging studies

? In assessing tumor burden
? In monitoring the respons to therapy. After eradication of tumors there is a

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rapid fall in serum AFP and HCG. With serial measurements it is often possible to

predict recurrence before the patients become symptomatic or develop any other

clinical signs of relapse

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TESTICULAR TUMOR
Testicular tumor

? Most germ cell tumours occur between the ages of 20 and 50 years

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? usual germ cell tumours , yolk sac tumour and the better differentiated types of

teratoma

? older patients-Spermatocytic seminoma and malignant lymphoma

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? Before puberty, seminoma is extremely uncommon

ETIOLOGIC FACTORS
? Cryptorchidism
? Other developmental disorders- androgen insensitivity syndrome

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? Genetic factors-high incidence in first-degree family members, twins
? Other factors. A few less common factors
?Orchitis
?Trauma
?Carcinogens. LSD, hormonal therapy for sterility, copper, zinc etc

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Prenatal risk factors ?
? consistent associations of testicular cancer with low birth weight
Exposures in adulthood
? Possible etiological clues, however, include a low level of physical activity

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qPATHOGENESIS-vast majority of these tumours originate from germ cells
1-Developmental disorders- contribute to the pathogenesis
2-Molecular genetic features-common molecular pathogenesis of all germ cell

tumours:

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? Hyperdiploidy is almost a constant feature
? isochromosome of short arm of chromosome 12
? Telomerase activity is present in all germ cell tumours of the testis
? Other mutations include p53, cyclin E and FAS gene
3-Intratubular germ cel neoplasia (ITGCN) or carcinoma insitu-

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Most testicular germ cel tumors originate from a precursor lesion called

intratubular germ cell neoplasia (ITGCN)exceptions to this rule are
? pediatric yolk sac tumors
? Teratomas

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? adult spermatocytic seminoma

4-Three hit' process. Germ cells in seminiferous tubules undergo
a. first hit-activate the cell
b. second hit- occure in CIS cell and further activate

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c. third hit- via some epigenetic phenomena cell become invasive
this sequential tumorigenesis explains the development of seminomatous tumours


CLINICAL FEATURES AND DIAGNOSIS

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? gradual gonadal enlargement and a dragging sensation in the testis
? secondary symptoms such as pain, lymphadenopathy, and urinary obstruction

(Metastatic involvement )

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SPREAD-
? Lymphatic spread- retroperitoneal para-aortic lymph nodes, mediastinal lymph

nodes and supraclavicular lymph nodes

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? Haematogenous spread -lungs, liver, brain and bones
1-Intratubular germ cel neoplasia, unclassified type (IGCNU)
? Also called carcinoma in situ (CIS) stage of germ cell tumours
? preinvasive stage of germ cell tumours

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? intratubular seminoma and intratubular embryonal carcinoma are common
? 2-4% of cryptorchidism pt show
? Clinical features - atrophic testis, infertility, maldescended testis, and intersex

features

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? gross- no grossly visible lesion
? Histopathology - Germ cells with abundant vacuolated cytoplasm, large, irregular

nuclei and prominent nucleoli located within the seminiferous tubules

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? restricted to the seminiferous tubules without evident invasion into the

interstitium

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? Immunoprofile- PLAP can be demonstrated in 83-99% of intratubular germ cell

neoplasia of the unclassified type (IGCNU) cases and is widely used for diagnosis

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Comparison of morphological features of normal seminiferous tubules (left part) and intratubular

germ cel neoplasia (IGCNU) in seminiferous tubules (right part).

Seminoma

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? Seminomas are the most common type of germ cell tumor, making up about

(50%)

? peak incidence is the third decade

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? it is called dysgerminoma in ovary


.

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MORPHOLOGY- cut surface has a homogeneous, graywhite, lobulated, usually

devoid of hemorrhage or necrosis
Generally the tunica albuginea is not penetrated
but occasionally extension to the epididymis, spermatic cord, or scrotal sac occurs

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Microscopy- typical seminoma is composed of sheets of uniform cells divided

into poorly demarcated lobules by delicate fibrous septa containing a lymphocytic

infiltrate

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Tumor cell-
cell is large and round to polyhedral and has a distinct cell membrane; clear or

watery-appearing cytoplasm; and a large, central nucleus with one or two

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prominent nucleoli

Stroma-
? delicate fibrous tissue which divides the tumour into lobules
? characteristic lymphocytic infiltration, indicative of immunologic response of the

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host to the tumour

Variable features-
? tumor giant cells and greater mitotic activity

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? 15% of seminomas contain syncytiotrophoblasts
? ill-defined granulomatous reaction (20%)


Special stain-Cytoplasm contains variable amount of glycogen that stains positively

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with PAS reaction

IHC- seminoma cells stain positively for KIT, (regardless of KIT mutational status),

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OCT4, and placental alkaline phosphatase (PLAP)
Prognosis-
? better than other germ cell tumours
? tumour is highly radiosensitive

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Spermatocytic Seminoma-
? Spermatocytic seminoma is both clinically and morphologically a distinctive

tumour from classic seminoma

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? Incidence of about 5% of all germ cell tumours
? older patients
? generally in 6th decade of life
? bilateral in 10% of patients
? Grossly, spermatocytic seminoma is homogeneous, larger, softer and

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more yellowish and gelatinous than the classic seminoma

? Histological y, the distinctive features are as under:
1. Tumour cells. lymphocyte-like to huge mononucleate or multinucleate giant

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cells. Majority of cells are, however, of intermediate size. Mitoses are often

frequent.
2. Stroma. stroma lacks lymphocytic and granulomatous reaction seen in classic

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seminoma.
? prognosis of spermatocytic seminoma is excellent
? slow-growing and rarely metastasises
? tumour is radiosensitive

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Embryonal Carcinoma-
? 30% of germ cell tumours more common
? 2nd to 3rd decades of life
? 90% cases are associated with elevation of AFP or hCG or both

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Grossly,- a small tumour in the testis
? distorts the contour of the testis as it frequently invades the tunica and the

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epididymis

? Cut surface- grey white, soft with areas of haemorrhages and necrosis

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Microscopy-
1. tumour cells are arranged in a variety of patterns-- glandular, tubular, papillary

and solid
2.tumour cells are highly anaplastic carcinomatous cells having large size,

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amphophilic cytoplasm and prominent hyperchromatic nucleoli
Yolk Sac Tumour (Synonyms: Endodermal Sinus Tumour,

Orchioblastoma, Infantile Embryonal Carcinoma)

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? most common testicular tumour of infants and young children upto the age of 4

year

? may be present as the major component in 40% of germ cell tumours

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? AFP levels are elevated in 100% cases of yolk sac tumours

? Grossly, the tumour is generally soft, yellow-white, mucoid with areas of necrosis

and haemorrhages

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Microscopical y, yolk sac tumour has the following features
1. patterns--loose reticular network, papil ary, tubular and solid arrangement
2. flattened to cuboid epithelial cells with clear vacuolated cytoplasm
3.A pathognomonic feature is Schil er -Duvel body

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a central vessel surrounded by tumor cells in a cystic space often lined by flattened

tumor cells
4. presence of both intracellular and extracellular PAS-positive hyaline globules

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Choriocarcinoma
? highly malignant tumour composed of syncytiotrophoblast and cytotrophoblast
? 2nd decade of life
? serum and urinary levels of hCG are greatly elevated in 100% cases

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? Grossly, the tumour is usually small and may appear as a soft, haemorrhagic

and necrotic mass

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? Microscopical y, the characteristic feature is syncytiotrophoblast and

cytotrophoblast without formation of definite placental-type vil i

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Teratoma-
? Teratomas are complex tumours composed of tissues derived from more than

one of the three germ cell layers--endoderm, mesoderm and ectoderm

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? more common in infants and children and constitute ( 40%)
? in adults they comprise 5% of all germ cell tumours
MORPHOLOGIC FEATURES. Testicular teratomas are classified into 3 types:
1. Mature (differentiated) teratoma

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2. Immature teratoma
3. Teratoma with malignant transformation

Gross-
? large, grey-white masses enlarging testis

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? Cut surface shows characteristic variegated appearance--grey-white solid areas,

cystic and honey-combed areas, and foci of cartilage and bone

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Microscopicy-
? three categories of teratomas show different appearances:
1-Mature (differentiated) teratoma. Well differentiated structures such as

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cartilage, smooth muscle, intestinal and respiratory epithelium, mucus glands, cysts

lined by squamous and transitional epithelium, neural tissue, fat and bone

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2-Immature teratoma.
? incompletely differentiated and primitive or embryonic tissues
? Mature+poorly-formed tissue (cartilage, mesenchyme, neural tissues, abortive

eye, intestinal and respiratory tissue elements) etc

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? Mitoses are usual y frequent


Immature stroma

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3-Teratoma with malignant transformation-
? extremely rare form of teratoma
? one or more of the tissue elements show malignant transformation
?squamous cell carcinoma

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?mucin-secreting adenocarcinoma,
?sarcoma, or other cancers
? importance of recognizing a non?germ cell malignancy arising in a teratoma is

that these secondary tumors are chemoresistant

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Mixed Germ Cell Tumours
? About 60% of germ cel tumours have more than one of the above

histologic types (except spermatocytic seminoma) and are cal ed mixed

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germ cel tumours

most common combinations of mixed germ cel tumours are as under:
1. Teratoma, embryonal carcinoma, yolk sac tumour and syncytiotrophoblast
2. Embryonal carcinoma and teratoma (teratocarcinoma)

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3. Seminoma and embryonal carcinoma

? SEX CORD-STROMAL TUMOURS-Tumours arising from specialised gonadal

stroma

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source of tumor-
? theca, granulosa and lutein cells in the female
? Sertoli and interstitial Leydig cells in the male
Must know

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1-classification
2-Tumor markers in diagnosis
3-Morphology of
a)

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Seminoma

b)

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Embryonal carcinoma

c)

Yolk sac tumor

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4-Cryporchidism