Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Pathology PPT 5 Male Genital Lecture Notes
Diseases of Male Genital Tract
Penile Diseases
Testicular Diseases
Prostatic Diseases
Penile Diseases
?Congenital Anomalies
?Inflammation
? Tumors
? Benign Tumors
? Premalignant lesion(carcinoma in situ)
? Malignant Tumors
?WHO histological classification
of tumours of the penis
?
__________
Malignant epithelial tumours of the penis
? Squamous cell carcinoma 8070/31
? Basaloid carcinoma 8083/3
? Warty (condylomatous) carcinoma 8051/3
? Verrucous carcinoma 8051/3
? Papillary carcinoma, NOS 8050/3
? Sarcomatous carcinoma 8074/3
? Mixed carcinomas
? Adenosquamous carcinoma 8560/3
? 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
Precursor lesions
? Intraepithelial neoplasia grade I I Bowen disease 8081/2
? Erythroplasia of Queyrat 8080/2
? Paget disease 8542/3
? Melanocytic tumours
? Melanocytic nevi 8720/0
? Melanoma 8720/3
? Mesenchymal tumours
? Haematopoietic tumours
? Secondary tumours
Benign Tumors
1-Condyloma Acuminatum-
? Wart
? STD
? HPV
Morphology-
? coronal sulcus and inner surface of the prepuce
? single or multiple sessile or pedunculated, red papillary excrescences
Histologically-
? Acanthosis
? koilocytosis
2-Peyronie Disease-(Idiopathic Fibrous Induration )
? fibromatosis
? fibrous bands involving the corpus cavernosum of the penis
? Microscopically, dense fibrosis is associated with sparse, nonspecific,
chronic inflammatory infiltration
Precursor lesions-
? Intraepithelial neoplasia Grade II
qClinical Variant
?Bowenoid papulosis
?Bowen disease
?Erythroplasia of Queyrat
? Paget disease
Bowenoid papulosis ?
? younger age
? multiple reddish brown papular lesions
? histologically indistinguishable from Bowen disease
? HPV type 16
Bowen disease-
? >35Yr
? shaft of the penis and the scrotum
? solitary, thickened, gray-white, opaque plaque
? turn in to 10% scc (5-33% WHO)
Normal Skin histology
Invasive Carcinoma-
squamous cell carcinomas
Etiology-
? phimosis
? chronic inflammatory conditions, especially lichen sclerosus
? smoking
? ultraviolet irradiation
? history of warts, or condylomas
Clinical features
? 40 -60 years
? glans or inner surface of the prepuce
MORPHOLOGY-
? papillary
? flat
? Ulcerated
? Exophytic
Histopathology-
? spectrum of differentiation from well to poorly differentiated.
? Superficial ?WD
? Deep-PD
Verrucous carcinoma-
? variant of squamous cell carcinoma
? exophytic well-differentiated
? locally invasive, but rarely metastasize
Other variants
? basaloid, warty, and papillary variants
? acanthosis and hyperkeratosis
? into the underlying stroma with a broad based, pushing border
? No koilocytotic changes
? Not HPV related
? D/D Condyloma acuminatum
Tumour spread-
? superficial inguinal lymph node
? deep groin and pelvic nodes
Three most important pathological factors to predict final outcome are
? histological grade
? depth of invasion
? vascular invasion
Diseases of Prostate
? Inflammation
? Benign Enlargement
? Tumors
q Inflammation
?Acute bacterial prostatitis
?Chronic bacterial prostatitis
?Chronic abacterial prostatitis
?Granulomatous prostatitis
1. Acute bacterial prostatitis
Etiology-
? bacteria ,E. coli,
? from the urethra
? Diagnosis-culture
MORPHOLOGY-
Gross- enlarged, swollen and tense
Cut section- abscesses and foci of necrosis
M/E-
? Necrosis
? Or as diffuse edema
? Congestion
?biopsy is contraindicated
2-Chronic Prostatitis-
?Chronic bacterial prostatitis-
? consequence of recurrent UTI
? E coli
? 10-12 wbc/hpf
?Chronic abacterial prostatitis-
? more common
? No h/o Reccurent UTI
? Wbc in prostatic secretion
? 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
neutrophils within the prostatic tissue
3-Granulomatous Prostatitis-
? variety of chronic prostatitis
?Etiology-
? Tubercular
? Fungal
? autoimmune origin
?MORPHOLOGY-
? Grossly-firm to hard
? Histology-macrophages, lymphocytes, plasma cel s and some multinucleate
giant cel s
qBenign Prostatic Hyperplasia or Nodular Hyperplasia-
? most common benign prostatic disease
? Incidence increases >50yrs
? 70% >60yrs
ETIOLOGY-
? endocrinologic, racial, inflammation and arteriosclerosis
? advancing age,--androgen-- oestrogen-periurethral inner prostatsensitive to
estrogen oestrogen--
Nod hyprplasia
? 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
stromal cells and decreasing the death of epithelial cells
? MORPHOLOGY-
? Gross- nodular, smooth and firm and weighs 2-4 times its normal
weight
Cut surface-
?pale gray and tough-fibromuscular stroma-EARLY
?yellow-pink and soft- gland-LATER
Microscopy- hyperplasia of all three tissue elements in varying
proportions--
? glandular
? fibrous
? Muscular
called as fibromyoadenomatous nodules- well developed satge
Variable histological features-
? lymphocytic aggregates
? small areas of infarction
? corpora amylacea
? foci of squamous metaplasia
CLINICAL FEATURES-
? frequency, nocturia
? difficulty in micturition
? pain
? haematuria
Complications of NPH
CARCINOMA OF PROSTATE
? men older than age 50 years
? ETIOLOGY-
?Endocrinologic factors
?Racial and geographic influences-
? uncommon in Japanese and Chinese, while the prevalence is high in
Americans
?Environmental influences-
? high dietary fat, and exposure to polycyclic aromatic hydrocarbons
?Nodular hyperplasia
?Heredity-
?2-fold higher frequency in first-degree relatives
Molecular Pathogeneis
? Most common-TPRSS2-ETS fusion genes and mutations or deletions
that activate the PI3K/AKT signalling pathway
Others
? PTEN
? BRCA2
? HOXB13
? 8q24 amplification
? Loss of P53, in last stage
? Glutathione S-transferase P1 gene,hypermethylation
? Epigenetic modification ?RB,CDKN2A
MORPHOLOGIC FEATURES.
? Grossly, enlarged, normal in size or smaller than normal
? Cut section- gritty and firm,homogeneous and contains irregular
yellowish areas
Microscopically-
? Adenocarcinoma ,96%
? transitional cell carcinoma
? squamous cell carcinoma
? undifferentiated carcinoma
Histologic characteristics-
? Architectural disturbance-closely packed in back-to-back arrangement
without intervening stroma
? Gland pattern
? Stroma- scant , tumour cells may penetrate and replace the
fibromuscular stroma
High-grade prostatic intraepithelial neoplasia (PIN)
? Gleason's microscopic grading system- based on two features:
i) Degree of glandular differentiation
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
? 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
closely packed uniform
glands
loosely packed slightly
variable glands
Single glands of variable size
and density, with an
infiltrative pattern
Ragged infiltration with poorly
formed glands or sheets and
cords of fused glands
Single cel s,Solid
sheet,comedonecrosis
3+3
3+4
4+4
4+4
4+4
4+4
GS-5+5
Biomarkers of prostate cancer
1-PSA
?PSA density
?PSA velocity
?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-
ERG fusion DNA>psa alone
Testis
Must know
1-Classification of testicular tumor
2-Tumor markers in diagnosis
3-Morphology of
a)
Seminoma
b)
Embryonal carcinoma
c)
Yolk sac tumor
4-Cryptorchidism
Testicular lesion
? CongenitalAnomalies
? RegressiveChanges
? Inflammation (Nonspecific , Specific Inflammations, Granulomatous
(Autoimmune) Orchitis)
? VascularDisorders(torsion)
? SpermaticCordandParatesticularTumors
? TesticularTumors
INFLAMMATIONS-
? 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-
? may be acute or chronic
? common routes of spread are via the vas deferens, or lymphatic and
haematogenous routes
? caused by urethritis, cystitis, prostatitis and seminal vesiculitis
? common infecting organisms in Neisseria gonorrhoeae and Chlamydia
trachomatis
Grossly,
? acute stage- firm, tense, swollen and congested
may be multiple abscesses, especially in gonorrhoeal
infection
? chronic stage- variable degree of atrophy and fibrosis
Histological y,
? acute- congestion, oedema and diffuse infiltration by neutrophils, or formation of
neutrophilic abscesses
? Chronic- focal or diffuse chronic inflammation, disappearance of seminiferous
tubules, fibrous scarring and destruction of interstitial Leydig cells
2-Granulomatous (Autoimmune) Orchitis -
Non-tuberculous granulomatous orchitis-
? unilateral, painless testicular enlargement
? may resemble a testicular tumour clinically
? autoimmune basis is suspected
Gross- enlarged
? Cut section of the testicle is greyish-white to tan-brown
? Histological y, granulomatous reaction(non caseating) is present diffusely
throughout the testis and is confined to the seminiferous tubules
? Peritubular fibrosis
? interstitial lymphocytes and plasma cells
3-Tuberculous Epididymo-orchitis-
? 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
Grossly, discrete, yellowish, caseous necrotic areas
? Microscopical y, numerous tubercles which may coalesce to form large caseous
mass
? Characteristics of typical tubercles such as epithelioid cells, peripheral mantle of
lymphocytes, occasional multinucleate giant cells and central areas of caseation
necrosis are seen
? AFB positive
4-Spermatic Granuloma(epididymitis nodosa)
? 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
? firm, white to yellowish-brown
? Histological y,
? Characteristical y, the centre of spermatic granuloma contains
spermatozoa and necrotic debris+epethelioid cell granuloma
Vascular disorder
Torsion of Testis
? usually followed by sudden muscular effort or physical trauma
? 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
1-Neonatal torsion-
? occurs either in utero or shortly after birth
? It lacks any associated anatomic defect in testis
2-"Adult" torsion-
? is typically seen in adolescence and presents with the sudden onset of
testicular pain
? Viable- manually untwisted within approximately 6 hours of the
onset of torsion
MORPHOLOGIC FEATURES-
duration and severity of vascular occlusion
? may be coagulative necrosis of the testis and epididymis
? may be haemorrhagic infarction
Spermatic Cord and Paratesticular Tumors
1-Lipomas
? common lesions involving the proximal spermatic cord, identified at
the time of inguinal hernia repair
? 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-
? most common benign paratesticular tumor
? upper pole of the epididymis
? grossly , well circumscribed small nodules
? Microscopically- Proliferation of glandular structures, irregularly lined by cuboidal
to flattened epithelial cell
? Treatmet- local excision
Malignant tumor
? rhabdomyosarcomas -children
? liposarcomas- adults
CLASSIFICATION OF TESTICULAR TUMOR
? most useful classification of tumors is histogenetic
? Named according to from which tissue they arise and of which they consist
WHO histological classification of testis tumours
? Germ cell tumours
? 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
? Tumours of collecting ducts and rete
? Tumours of paratesticular structures
? Mesenchymal tumours of the spermatic cord and testicular adnexae
? Secondary tumours of the testis
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
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
or other organs of the body)
? S indicates the serum (blood) levels of tumor markers that are made by some
testicular cancers
? Letters or numbers appear after T, N, M, and S to provide more details about
each piece of information.
? 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.
? 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
pTNM pathological classification
? pTx ?Primary tumour cannot be assessed
? pT0 No evidence of primary tumour pTis Intratubular germ cell neoplasia
(carcinoma in situ)
? pT1 Tumour limited to testis and epididymis without vascular/lymphatic
invasion; tumour may invade tunica albuginea but not tunica vaginalis
? 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
? 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
than 5 cm; or evidence of extranodal extension of tumour
? pN3 Metastasis with a lymph node mass more than 5 cm in greatest dimension
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
? Cryptorchidism is a complete or partial failure of the intra-abdominal testes to
descend into the scrotal sac
associated with
? 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
ETIOLOGY. exact etiology is not known in majority of cases
1. Mechanical factors-
? short spermatic cord
? narrow inguinal canal
? adhesions to the peritoneum
? problems with development of the gubernaculum
? a patent processus vaginalis, or impaired intra-abdominal pressure have also
been hypothesized to contribute to cryptorchidism
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
? trisomy 13
3. Hormonal factor- rarely associated
? deficient androgenic secretions
? mullerian inhibiting substance
? insulin-like 3 hormone
4. Neuromuscular- abnormalities of the genitofemoral nerve's calcitonin gene-
related peptide
Miscellaneous-
? Maternal alcohol consumption
? analgesic consumption
? smoking
? Gestational diabetes
MORPHOLOGIC FEATURES. Cryptorchidism is unilateral in 80% cases
Grossly, small in size, firm and fibrotic
Histology-
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
?interstitial fibrovascular stroma
? Leydig cells,
? CLINICAL FEATURES. asymptomatic and is discovered only on physical
examination
1. Sterility-infertility. Bilateral cryptorchidism is associated with sterility while
unilateral disease may result in infertility
2. Inguinal hernia. A concomitant inguinal hernia is frequently present along with
cryptorchidism
3-Malignancy. Cryptorchid testis is at 30-50 times increased risk of developing
testicular malignancy
? most commonly seminoma and embryonal carcinoma, than a normally
descended testis
? risk of malignancy is greater in intraabdominal testis than in testis in the inguinal
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
? Orchiopexy reduces the risk of sterility and cancer
Tumour marker
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
? beta subunit of human chorionic gonadotropin (shCG)
? In addition, carcinoembryonic antigen (CEA), human placental lactogen (HPL),
placental alkaline phosphatase, testosterone, oestrogen and luteinising hormone
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
? 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-
? 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)
? elevated in 50% of patients with germ cell tumours
? elevation in seminoma in 10-25% of cases
Lactate dehydrogenase (LDH)-
? may also be elevated
? direct relationship between LDH and tumour burden
? However, this test is nonspecific although its degree of elevation correlates with
bulk of disease
Applications-
? 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
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
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
TESTICULAR TUMOR
Testicular tumor
? Most germ cell tumours occur between the ages of 20 and 50 years
? usual germ cell tumours , yolk sac tumour and the better differentiated types of
teratoma
? older patients-Spermatocytic seminoma and malignant lymphoma
? Before puberty, seminoma is extremely uncommon
ETIOLOGIC FACTORS
? Cryptorchidism
? Other developmental disorders- androgen insensitivity syndrome
? 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
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
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:
? 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-
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
? 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
c. third hit- via some epigenetic phenomena cell become invasive
this sequential tumorigenesis explains the development of seminomatous tumours
CLINICAL FEATURES AND DIAGNOSIS
? gradual gonadal enlargement and a dragging sensation in the testis
? secondary symptoms such as pain, lymphadenopathy, and urinary obstruction
(Metastatic involvement )
SPREAD-
? Lymphatic spread- retroperitoneal para-aortic lymph nodes, mediastinal lymph
nodes and supraclavicular lymph nodes
? 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
? intratubular seminoma and intratubular embryonal carcinoma are common
? 2-4% of cryptorchidism pt show
? Clinical features - atrophic testis, infertility, maldescended testis, and intersex
features
? gross- no grossly visible lesion
? Histopathology - Germ cells with abundant vacuolated cytoplasm, large, irregular
nuclei and prominent nucleoli located within the seminiferous tubules
? restricted to the seminiferous tubules without evident invasion into the
interstitium
? 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
Comparison of morphological features of normal seminiferous tubules (left part) and intratubular
germ cel neoplasia (IGCNU) in seminiferous tubules (right part).
Seminoma
? Seminomas are the most common type of germ cell tumor, making up about
(50%)
? peak incidence is the third decade
? it is called dysgerminoma in ovary
.
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
Microscopy- typical seminoma is composed of sheets of uniform cells divided
into poorly demarcated lobules by delicate fibrous septa containing a lymphocytic
infiltrate
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
prominent nucleoli
Stroma-
? delicate fibrous tissue which divides the tumour into lobules
? characteristic lymphocytic infiltration, indicative of immunologic response of the
host to the tumour
Variable features-
? tumor giant cells and greater mitotic activity
? 15% of seminomas contain syncytiotrophoblasts
? ill-defined granulomatous reaction (20%)
Special stain-Cytoplasm contains variable amount of glycogen that stains positively
with PAS reaction
IHC- seminoma cells stain positively for KIT, (regardless of KIT mutational status),
OCT4, and placental alkaline phosphatase (PLAP)
Prognosis-
? better than other germ cell tumours
? tumour is highly radiosensitive
Spermatocytic Seminoma-
? Spermatocytic seminoma is both clinically and morphologically a distinctive
tumour from classic seminoma
? 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
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
cells. Majority of cells are, however, of intermediate size. Mitoses are often
frequent.
2. Stroma. stroma lacks lymphocytic and granulomatous reaction seen in classic
seminoma.
? prognosis of spermatocytic seminoma is excellent
? slow-growing and rarely metastasises
? tumour is radiosensitive
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
Grossly,- a small tumour in the testis
? distorts the contour of the testis as it frequently invades the tunica and the
epididymis
? Cut surface- grey white, soft with areas of haemorrhages and necrosis
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,
amphophilic cytoplasm and prominent hyperchromatic nucleoli
Yolk Sac Tumour (Synonyms: Endodermal Sinus Tumour,
Orchioblastoma, Infantile Embryonal Carcinoma)
? 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
? 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
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
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
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
? Grossly, the tumour is usually small and may appear as a soft, haemorrhagic
and necrotic mass
? Microscopical y, the characteristic feature is syncytiotrophoblast and
cytotrophoblast without formation of definite placental-type vil i
Teratoma-
? Teratomas are complex tumours composed of tissues derived from more than
one of the three germ cell layers--endoderm, mesoderm and ectoderm
? 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
2. Immature teratoma
3. Teratoma with malignant transformation
Gross-
? large, grey-white masses enlarging testis
? Cut surface shows characteristic variegated appearance--grey-white solid areas,
cystic and honey-combed areas, and foci of cartilage and bone
Microscopicy-
? three categories of teratomas show different appearances:
1-Mature (differentiated) teratoma. Well differentiated structures such as
cartilage, smooth muscle, intestinal and respiratory epithelium, mucus glands, cysts
lined by squamous and transitional epithelium, neural tissue, fat and bone
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
? Mitoses are usual y frequent
Immature stroma
3-Teratoma with malignant transformation-
? extremely rare form of teratoma
? one or more of the tissue elements show malignant transformation
?squamous cell carcinoma
?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
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
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)
3. Seminoma and embryonal carcinoma
? SEX CORD-STROMAL TUMOURS-Tumours arising from specialised gonadal
stroma
source of tumor-
? theca, granulosa and lutein cells in the female
? Sertoli and interstitial Leydig cells in the male
Must know
1-classification
2-Tumor markers in diagnosis
3-Morphology of
a)
Seminoma
b)
Embryonal carcinoma
c)
Yolk sac tumor
4-Cryporchidism
This post was last modified on 07 April 2022