Male Flashcards
Histology of granulomatous prostatitis: Idiopathic type.
Giant cells, histiocytes, plasma cells, lymphocytes, and granulocytes form sheets around ruptured ducts and acini.
Histology of granulomatous prostatitis: After therapy with BCG.
Mostly histiocytes and giant cells around ducts or acini.
Histology of granulomatous prostatitis: Post-procedural type (2).
Palisade of histiocytes and giant cells around fibrinoid necrosis.
Eosinophils may be seen.
Malakoplakia:
A. Presentation.
B. Frequent cause.
A. Fever, frequency, dysuria, hematuria.
B. E. coli.
Malakoplakia: Histology.
Sheet of von Hansemann’s histiocytes, containing Michaelis-Gutmann bodies, are surrounded by chronic inflammation.
Prostatic infarct: Risk factors (3).
Nodular hyperplasia.
Hypotension.
Urinary catheter.
Histology of prostatic infarct: Acute (3).
Hemorrhage surrounding coagulative necrosis.
Reactive glands and squamous metaplasia.
Histology of prostatic infarct: Remote.
Scar containing hemosiderin and small glands that often show squamous metaplasia.
Basal-cell hyperplasia: Pitfall.
Mistaking basal-cell hyperplasia with nucleolomegaly for high-grade PIN.
Sclerosing adenosis vs. prostatic adenocarcinoma (3).
Sclerosing adenosis:
− Preserved basal-cell layer.
− Thickened basement membrane.
− Inconspicuous nucleoli.
Atypical adenomatous hyperplasia: Architecture (2).
Circumscribed but may have focally infiltrative border.
Tightly packed small glands with admixed large glands.
Atypical adenomatous hyperplasia: Cytology (2).
Basal-cell layer may be incomplete in some glands.
Some nucleoli may be large.
Urothelial metaplasia vs. normal urothelium.
The former lacks umbrella cells.
Atypical adenomatous hyperplasia vs. prostatic adenocarcinoma (2).
Atypical adenomatous hyperplasia:
− No macronucleoli (more than 3 μm).
− Often contains corpora amylacea.
Types of metaplasia of prostatic epithelium (3).
Urothelial.
Squamous.
Mucinous.
Chronic abacterial prostatitis:
A. Definition.
B. Possible causes.
A. Prostatitis with negative bacterial culture.
B. Chlamydia, Ureaplasma, Mycoplasma.
Bacterial prostatitis:
A. Organisms.
B. Complication.
A. Same as those that cause UTI.
B. Antibiotic therapy may fail because the prostate is a “safe haven” for bacteria.
Granulomatous prostatitis: Antecedents (3).
A. Therapy with BCG.
B. TURP or biopsy.
C. Infection.
Granulomatous prostatitis: Physical examination.
Prostate may be firm, raising suspicion for carcinoma.
Granulomatous prostatitis: Presentation.
Obstructive symptoms, dysuria, fever, chills.
High-grade PIN: Duration of progression to adenocarcinoma.
About 10 years.
High-grade PIN: Likelihood of adenocarcinoma on rebiopsy.
25%.
High-grade PIN: Patterns (4).
Tufted.
Cribriform.
Micropapillary.
Flat.
High-grade PIN: Nuclear features.
Large nuclei.
Large nucleoli.
High-grade PIN: Immunohistochemistry (3).
HMWCK and p63 highlight the basal cells.
AMACR: If positive, staining is less intense than that of carcinoma.
Adenocarcinoma: Typical location.
Posterior peripheral zone.
Adenocarcinoma: Activity of metastases to bone.
May be either osteoblastic or osteolytic.
Acinar adenocarcinoma: Histologic features that are pathognomonic for malignancy (4).
Glomeruloid structures.
Mucinous fibroplasia.
Circumferential perineural invasion.
Extension beyond the prostate.
Acinar adenocarcinoma: Intraluminal structures.
Blue or pink blobs and crystalloids are relatively common.
Corpora amylacea are rare.
Mucinous adenocarcinoma:
A. Definition.
B. Histology.
C. Most common pattern.
A. At least 25% of the tumor consists of extracellular lakes of mucin.
B. Malignant cells and glands in seas of snot.
C. Cribriform.
Mucinous adenocarcinoma:
A. Association.
B. Gleason’s grade.
C. Behavior.
A. Typically seen with acinar adenocarcinoma.
B. Grade 4.
C. Aggressive.
Signet-ring-cell adenocarcinoma:
A. Definition.
B. Association.
C. Gleason’s grade.
A. At least 25% of the tumor consists of signet rings.
B. Often seen with other types of adenocarcinoma.
C. Grade 5.
Ductal-type adenocarcinoma: Clinical and gross appearance.
May form polypoid mass that extends into the prostatic urethra.
Ductal-type adenocarcinoma: Origin.
Larger periurethral prostatic ducts.
Ductal-type adenocarcinoma: Histology (2).
Pseudostratified columnar cells form papillae and cribriform structures.
Mitotically active.
Ductal-type adenocarcinoma: Gleason’s grade.
Usually grade 4 (grade 5 if there is comedo necrosis).
Carcinosarcoma: Associations (2).
Previous or current high-grade prostatic adenocarcinoma.
History of radiation therapy in some cases.
Carcinosarcoma: Laboratory finding.
Serum PSA may be normal or only slightly elevated.
Carcinosarcoma: Patterns of the sarcomatous component (7).
The sarcomatous component may resemble − Fibrosarcoma. − Leiomyosarcoma. − Osteosarcoma. − Rhabdomyosarcoma. − Chondrosarcoma. − MFH. − High-grade sarcoma, NOS.
Carcinosarcoma vs. sarcomatoid carcinoma.
Carcinosarcoma: Distinct carcinomatous and sarcomatous areas.
Sarcomatoid carcinoma: There is a histologic transitional between the two elements.
Foamy-gland adenocarcinoma: Significance (2).
May be missed because of its bland nuclei.
Usually occurs with higher-grade acinar-type adenocarcinoma.
Pseudohyperplastic adenocarcinoma: Confounding features (2).
Pseudo-stratified epithelium.
Large acini in some cases.
Pseudohyperplastic adenocarcinoma: Telltale features.
Large nuclei and large nucleoli.
Histologic features of treated adenocarcinoma: Androgen deprivation (3).
Residual carcinoma: Loss of nuclear and nucleolar enlargement.
Benign glands: Stromal hyperplasia, basal-cell hyperplasia, squamous metaplasia.
Histologic features of treated adenocarcinoma: Radiation (4).
Residual carcinoma: Cytoplasmic vacuoles.
Benign glands: Atrophy, large nuclei, large nucleoli.
Types of prostatic adenocarcinoma that receive no score of Gleason (5).
Neuroendocrine.
Squamous.
Adenosquamous.
Sarcomatoid.
Treated.
Immunohistochemistry of prostatic adenocarcinoma: AMACR.
Reacts best with higher-grade, untreated, conventional acinar-type adenocarcinomas.
Immunohistochemistry of prostatic adenocarcinoma: PSA and PAP.
Both react with − Ductal type. − Mucinous type. − Signet-ring type. − Epithelial component of carcinosarcoma.
Immunohistochemistry of prostatic adenocarcinoma: CEA.
Reacts with some ductal adenocarcinomas.
Genetics of prostatic adenocarcinoma:
A. Familial locus.
B. Early molecular event.
A. 8q24.
B. Fusion of TMPRSS2 and ERG.
Prostatic adenocarcinoma: Relevance of location to clinical behavior.
Tumors of the transitional zone are less aggressive than tumors of the peripheral zone.
Proliferations of basal cells in the prostate (4).
Basal-cell hyperplasia.
Atypical basal-cell hyperplasia.
Basal-cell adenoma.
Basal-cell carcinoma.
Carcinomas of basal cells: Laboratory findings.
Usually normal serum PSA and PAP.
Basal-cell carcinoma: Histology.
Clusters of basal cells infiltrate, often with a desmoplastic response.
Basal-cell carcinoma: Clues to malignancy (3).
At least one of the following must be present:
− Necrosis.
− Perineural invasion.
− Infiltration beyond the prostatic capsule.
Adenoid-cystic carcinoma: Synonym.
Basal-cell carcinoma with cribriform spaces.
Adenoid-cystic carcinoma: Histology.
Similar to that of adenoid-cystic carcinoma of the salivary glands.
Adenoid-cystic carcinoma: Behavior (2).
Perineural invasion is rare.
Low malignant potential.
Adenoid-cystic carcinoma: Immunohistochemistry (2).
Positive: PSA, PAP.
Neuroendocrine carcinoma: Epidemiology.
Patients usually have a history of treated prostate cancer.
Neuroendocrine carcinoma: Possible paraneoplastic syndromes (4).
Cushing’s syndrome.
Malignant hypercalcemia.
SIADH.
Eaton-Lambert syndrome.
Neuroendocrine carcinoma: Route of metastasis.
Hematogenous.
Neuroendocrine carcinoma: Histopathology (2).
Resembles small-cell carcinoma of the lung.
Half of cases are accompanied by typical acinar-type adenocarcinoma.
Neuroendocrine carcinoma: Behavior.
Aggressive, but even more so if it expresses androgen receptors.
Urothelial carcinoma of the prostate: Origins (2).
Prostate: Urethra, ducts, or acini.
Bladder.
Urothelial carcinoma of the prostate: Poor prognostic factor.
Infiltration into the prostatic stroma: Makes it stage T4.
Squamous-cell carcinoma of the prostate: Clinical situations (2).
De novo.
Following treatment of adenocarcinoma.
Squamous-cell carcinoma of the prostate: Behavior of metastases.
Osteolytic.
Squamous-cell carcinoma of the prostate: Types (2).
Pure SCC.
Adenosquamous carcinoma.
Pure squamous-cell carcinoma of the prostate: Diagnostic criteria (3).
No glands.
No history of radiation or hormonal therapy.
Not a metastasis or direct spread from another organ.
Squamous-cell carcinoma of the prostate: Immunohistochemistry (2).
PSA and PAP
− Pure SCC: Usually negative.
− Adenosquamous carcinoma: Usually positive in the glandular component.
Squamous-cell carcinoma of the prostate: Prognosis.
Poor.
Phyllodes tumor of the prostate: Histologic predictors of aggressive behavior (3).
Stromal hypercellularity.
Cytologic atypia.
High mitotic rate.
Phyllodes tumor of the prostate: Sites of metastasis (2).
Lung and bone.
Postoperative spindle-cell nodule of the prostate: Histology (2).
Bland spindle cells with variable mitotic rate and no atypical mitotic figures.
Most common sarcoma of the prostate.
Rhabdomyosarcoma, particularly the embryonal type.
Rhabdomyosarcoma of the prostate: Prognosis.
Occurrence in the prostate or the urinary bladder carries a worse prognosis than usual.
Lymphoma of the prostate gland: Most common type.
DLBCL.
Lymphoma of the prostate:
A. Treatment.
B. Prognosis.
A. Surgery for relief of obstruction.
B. Death in about 2 years.
Testicles are usually descended by about what age?
3 months.
Cryptorchidism:
A. Most common site of undescended testis.
B. More common side.
C. Association of failure of descent.
A. Inguinal canal.
B. Right.
C. Inguinal hernia.
Cryptorchidism: Histology (4).
Sclerosis or atrophy of seminiferous tubules.
Increased Sertoli cells.
Hyperplasia of Leydig cells.
Contralateral, descended testis may show similar histology.
Cryptorchidism: Main causes (2).
Lack of hormonal signal.
Anatomical or mechanical impairment.
Cryptorchidism: Phases of descent.
Transabdominal.
Inguinal: Much more likely to have get disrupted.
Cryptorchidism: Rôle of orchiepexy.
Facilitates the detection of cancer but does not decrease the risk of it.
Testicular cysts: Types (3).
Albugineal.
Epidermoid.
Rete testis.
Albugineal cyst: Histology.
Lined by low-cuboidal serosal epithelium.
Epidermal cyst: Histology (2).
Similar to that of epidermal inclusion cyst.
No adnexal structures.
Rete testis cyst: Histology.
Lined by attenuated, low-cuboidal epithelium.
Hydrocele: Pathogenesis.
Serous fluid collects between the parietal and visceral tunica vaginalis.
Hydrocele: Clinical appearance.
Transilluminates unless hemorrhagic.
Hydrocele: Histology (2).
Lined by mesothelial cells that can be hyperplastic or atypical.
Tunica vaginalis may be thickened in long-standing hydroceles.
Viral orchitis: Causes (2).
Mumps virus (#1).
Coxsackie B virus.
How often is the testis involved in cases of mumps?
In about 15-30% of cases.
Viral orchitis: Histology (2).
Acute infection: Neutrophils.
Later: Atrophy and fibrosis.
Bacterial orchitis:
A. Leading cause.
B. Associations (2).
A. Escherichia coli.
B. Urinary-tract infection; bacterial epididymitis.
Bacterial orchitis: Histology (2).
Acute infection: Neutrophils and abscesses.
Chronic infection: May show granulomas.
Syphilitic orchitis: Histology (3).
Edema.
Obliterative endarteritis with perivascular lymphocytes and plasma cells.
Gummas may be present.
Infectious granulomatous orchitis: Causes (3).
Mycobacterium tuberculosis.
Fungi.
Brucella.
Noninfectious granulomatous orchitis: Causes (2).
Sarcoidosis.
Idiopathic.
Testicular malakoplakia:
A. Gross pathology.
B. Special stains.
A. Firm and tan-yellow.
B. von Kossa’s, Prussian blue, PAS.
Testicular torsion: Window for surgical salvage of the testis.
About 8 hours.
Infertility:
A. Definition.
B. Proportion of cases due to defect in the male.
A. No conception after a year of unprotected coitus.
B. 40% to 50% of infertile couples.
Male infertility: Functional types (3).
Pre-testicular (hormonal).
Testicular (75% of cases).
Post-testicular (obstructive).
Stages of normal development of spermatozoa.
Spermatogonia − primary spermatocytes − secondary spermatocytes − spermatids − spermatozoa.
Male infertility: Histologic components of testicular examination.
Seminiferous tubules.
Germ cells.
Interstitium.
Blood vessels.
Male infertility: Endocrine causes (3).
Diabetes mellitus.
Cushing’s syndrome.
Hyperprolactinemia.
Male infertility: Leydig cells.
May be hypoplastic or hyperplastic.
Factors that confer a high risk for tumors of germ cells (5).
Cryptorchidism.
Previous germ-cell tumor.
Family history.
Gonadal dysgenesis.
Androgen insensitivity.
Intratubular germ-cell neoplasia: Secondary histologic finding.
Severely diminished or absent spermatogenesis in the affected tubule.
Intratubular germ-cell neoplasia: Stains (2).
Positive: PLAP, PAS-D.
Intratubular germ-cell neoplasia vs. germinal epithelium with arrest of maturation (2).
Arrest of maturation:
− No significant nuclear pleomorphism.
− Usually negative for PLAP.
Intratubular germ-cell neoplasia: Germ-cell tumors in which it is not seen (3).
Spermatocytic seminoma.
Yolk-sac tumor.
Teratoma.
Seminoma: Age group.
Fourth decade.
Seminoma: Laboratory findings (2).
Serum hCG can be elevated.
Serum AFP is usually normal.
Seminoma: Composition of lymphoid infiltrate.
T cells.
Seminoma: Non-microscopic clues to a syncytiotrophoblastic component (2).
Elevated serum hCG.
Punctate hemorrhages on gross examination.
Note: Syncytiotrophoblasts occur without cytotrophoblasts.
Anaplastic seminoma: Histology (3).
Higher cellularity; more nuclear pleomorphism.
Three or more mitotic figures per hpf.
Many giant cells.
Seminoma: Immunohistochemistry (2,1,1).
Positive: PLAP, CD117.
Negative: EMA.
Patchy: Cytokeratin.
Seminoma: Cytogenetics.
i(12p).
Seminoma: Possibly favorable histologic feature.
Brisk lymphocytic infiltrate.
Spermatocytic seminoma: Age group.
Sixth decade.
Spermatocytic seminoma: Laboratory finding.
No elevation of serum tumor markers.
Spermatocytic seminoma: Cells.
Small: Lymphocyte-sized, smudged chromatin.
Intermediate: 15-20 μm, granular chromatin.
Giant: 50-100 μm, one or many nuclei.
Spermatocytic seminoma vs. classic seminoma (3).
Spermatocytic seminoma lacks
− Lymphocytic infiltrate.
− Granulomas.
− Intratubular germ-cell neoplasia.
Staining of spermatocytic seminoma for ___.
A. PAS.
B. Cytokeratin.
C. PLAP.
A. Negative (no glycogen).
B. May show perinuclear, dotlike positive staining.
C. May be focally positive.
Spermatocytic seminoma: Electron microscopy (2).
Intercellular bridges.
Filamentous chromosomes.
Spermatocytic seminoma: Cytogenetics.
Usually no i(12p).
Embryonal carcinoma: Presentation.
Gynecomastia or clinically evident metastasis in 40% of patients.
Embryonal carcinoma: Patterns of growth (3).
Solid.
Tubuloglandular.
Papillary.
Embryonal carcinoma: Cytology (2,3).
Cytoplasm: Ample; indistinct borders.
Nucleus: Large and vesicular; macronucleolus; mitotically active.
Embryonal carcinoma: Immunohistochemistry (3,1).
Positive: Cytokeratin, PLAP (patchy), CD30.
Negative: EMA.
Embryonal carcinoma: Cytogenetics (2).
i(12p).
Interstitial del(p13;q22).
Yolk-sac tumor: Age groups (2).
Pure yolk-sac tumor: Children.
YST as part of a mixed tumor: Adults.
Histology of yolk-sac tumor: Microcystic pattern (2).
Cytoplasmic vacuoles give lipoblastic appearance.
Cells form thin cords around cystic spaces.
Histology of yolk-sac tumor: Macrovesicular pattern.
Coalescence of microcysts forms larger cystic spaces.
Histology of yolk-sac tumor: Solid pattern (2).
Cells have well-defined borders.
Thin-walled vessels may be present.
Yolk-sac tumor, solid pattern vs. classic seminoma.
YST, solid pattern:
− No lymphocytic infiltrate.
− No fibrous septa.
Histology of yolk-sac tumor: Myxomatous pattern (2).
Spindle-shaped or epithelioid cells in abundant myxoid matrix.
Conspicuous vascular network.
Histology of yolk-sac tumor: Endodermal-sinus pattern.
Consists of Schiller-Duval (glomeruloid) bodies.
Histology of yolk-sac tumor: Papillary pattern.
Papillae with or without well-formed fibrovascular cores.
Histology of yolk-sac tumor: Tubuloalveolar pattern.
Consists of gland-like structures.
Histology of yolk-sac tumor: Polyvesicular-vitelline pattern (2).
Round, dumbbell-shaped, or irregular spaces lined by flat, bland cells.
Abundant loose, fibromyxoid stroma.
Histology of yolk-sac tumor: Hepatoid pattern (2).
Resembles hepatocellular carcinoma.
Many hyaline globules.
Hyaline globules of yolk-sac tumor:
A. Location.
B. Size.
C. Staining.
A. Intracellular.
B. 1-50 μm.
C. Positive for PAS-D; usually negative for AFP.
Yolk-sac tumor: Immunohistochemistry (3).
Positive: Cytokeratin.
Variable: PLAP, AFP, α₁-antitrypsin.
Yolk-sac tumor: Cytogenetics (2).
Adults: i(12p) may be present.
Children: No i(12p).
Pure teratoma:
A. Age group.
B. Prognosis.
A. Usually in children under 4 years of age.
B. Those in prepubertal children do not metastasize.
How many mixed germ-cell tumors of adults have a teratomatous component?
About half.
Teratoma: Cytogenetics.
There may be i(12p).
Benign teratoma: Types (3).
Epidermoid cyst: No adnexal structures.
Dermoid cyst: Yes adnexal structures.
Non-dermoid benign teratoma.
Non-dermoid benign teratoma: Incompatible histologic features (5).
Cytologic atypia.
IGCN.
Impaired spermatogenesis.
Sclerosis of seminiferous tubules.
Abnormalities of chromosome 12p.
Malignant teratoma: Histology of metastases.
May resemble the original teratoma or another germ-cell tumor.
Teratoma: Prognosis in the postpubertal male.
Any teratoma, other than non-dermoid benign teratoma, may be malignant.
Choriocarcinoma:
A. Age group.
B. Presentation.
A. Second or third decade.
B. Often with symptoms of metastatic disease.
Choriocarcinoma: Laboratory finding.
Very high serum hCG.
Choriocarcinoma: Gross pathology (3).
Testis may appear normal externally.
Tumor may be small.
Regression of the tumor may leave only a fibrous scar.
Choriocarcinoma: Cytology.
Cytotrophoblasts: Mononucleate; pale cytoplasm with discrete borders.
Syncytiotrophoblasts: Multinucleate, smudged chromatin; eosinophilic, vacuolated cytoplasm.
Choriocarcinoma:
A. Route of invasion.
B. Sites of metastases (3).
A. Hematogenous.
B. Lungs, brain, gastrointestinal tract.
Choriocarcinoma: Immunohistochemistry (3).
Positive: Cytokeratin, EMA.
hCG: Strong or absent in syncytiotrophoblasts; weak or absent in cytotrophoblasts.
Choriocarcinoma: Treatment.
Chemotherapy helps.
Radiation does not.
Leydig-cell tumor: Age groups (2).
5-10 years of age.
20-60 years of age.
Leydig-cell tumor: Presentation (2).
Boys: Precocious puberty, sometimes gynecomastia.
Men: Testicular swelling, sometimes gynecomastia.
Leydig-cell tumor: Risk factors (2).
Testicular atrophy.
Cryptorchidism.
Leydig-cell tumor: Possible cytoplasmic contents.
Lipofuscin.
Rod-shaped crystals of Reinke.
Lipid vacuoles.
Leydig-cell tumor: Histologic clue to malignancy.
At least 3 mitotic figures pet 10 hpf.
Leydig-cell tumor: Immunohistochemistry (2).
Variable: Vimentin, androgens.
Leydig-cell tumor: Electron microscopy (2).
Much smooth endoplasmic reticulum.
Hexagonal or rhomboidal crystals of Reinke.
Leydig-cell tumor vs. hyperplasia of Leydig cells (2).
Hyperplasia:
− Presevation of seminiferous tubules.
− No crystals of Reinke.
Malignant Leydig-cell tumor:
A. Frequency.
B. Relevance to age.
A. About 10% of Leydig-cell tumors.
B. Does not occur in prepubertal boys.
Sertoli-cell tumor: Age group.
Most common in middle age.
Sertoli-cell tumor: Presentation (2).
Boys: Gynecomastia sometimes.
Men: Testicular mass; impotence or gynecomastia sometimes.
Malignant Sertoli-cell tumor:
A. Frequency.
B. Relevance to age.
C. Relevance to histologic type.
A. About 10% of Sertoli-cell tumors.
B. Can occur in prepubertal boys.
C. Sclerosing Sertoli-cell tumor is always benign.
Sertoli-cell tumor: Associations with syndromes (2).
Carney’s syndrome: Large-cell calcifying.
Peutz-Jeghers: Intratubular large-cell hyalinizing Sertoli-cell neoplasia.
Sertoli-cell tumor: General histology.
Cells with clear or vacuolated cytoplasm form cords resembling immature seminiferous tubules.
Histology of variants of Sertoli-cell tumor:
A. Sclerosing.
B. Large-cell calcifying.
A. Dense collagenous stroma.
B. Myxoid or collagenous stroma that is often calcified or ossified; may show intratubular growth.
Sertoli-cell tumor: Immunohistochemistry (3).
Variable: Inhibin, S100, cytokeratin.
Sertoli-cell tumor: Electron microscopy (3).
Much smooth endoplasmic reticulum.
Mitochondria with tubular cristae.
Charcot-Böttcher (perinuclear) filaments.
Sertoli-cell tumor vs. androgen-insensitivity syndrome.
In the latter, there may be nodules of Sertoli cells, but these also contain Leydig cells.
Adult granulosa-cell tumor:
A. Presentation.
B. Behavior.
A. Testicular mass, often with gynecomastia.
B. Benign.
Adult granulosa-cell tumor: Histology.
Cells with “coffee-bean” nuclei form Call-Exner bodies.
Juvenile granulosa-cell tumor:
A. Age group.
B. Presentation.
C. Behavior.
A. Infants under 5 months of age.
B. Testicular mass; no hormonal symptoms.
C. Benign.
Juvenile granulosa-cell tumor: Patterns of growth (3).
Follicular.
Solid.
Mixed.
Juvenile granulosa-cell tumor: Cytology.
Nuclei: Hyperchromatic; visible nucleolus.
Cytoplasm: Abundant; pale or eosinophilic.
Juvenile granulosa-cell tumor: Histology of follicular pattern.
Bland tumor cells form ovarian follicle-like structures containing mucicarmine-positive matter.
Granulosa-cell tumors: Mitotic activity.
Adult type: Low.
Juvenile type: May be high.
Gonadoblastoma: Epidemiology.
Patients have abnormal gonads due to intersex syndrome or undescended testes.
Gonadoblastoma: Presentation (2).
Usually found incidentally in gonads removed for other reasons.
Gonadoblastoma: Behavior.
Benign, but 10-50% are associated with a germ-cell neoplasm.
Gonadoblastoma: Histologic components (3).
Germ cells.
Sex cord−stromal cells.
Connective-tissue stroma.
Gonadoblastoma: Histology of germ-cell component.
Resembles seminoma or immature sperm cells.
Mitotically active.
Gonadoblastoma: Histology of sex cord−stromal component (2).
Resembles immature Sertoli cells or granulosa cells.
Mitotically inactive.
Gonadoblastoma: Possible stromal features.
Calcification.
Hyalinization.
Gonadoblastoma vs. IGCN in a Sertoli-cell nodule.
The latter lesion is microscopic and occurs in a non-dysgenetic testis.
Granulosa-cell tumors: Immunohistochemistry (2).
Positive: Cytokeratins 8/18, vimentin.
Gonadoblastoma: Treatment.
Bilateral orchiectomy: Gonadoblastoma is often bilateral and may be associated with a germ-cell neoplasm.
Testicular lymphoma:
A. Most common type.
B. Versus chronic orchitis.
A. Diffuse large B-cell lymphoma.
B. Lymphoma cells typically spare the tubules.
Acute epididymitis:
A. Bacterial agents (3).
B. Viral agents (2).
A. Gram-negative bacilli, N. gonorrhoeae, C. trachomatis.
B. Mumps, CMV.
Acute epididymitis: Histology of chlamydial infection.
Minimally destructive inflammation.
Chronic epididymitis:
A. Infectious causes (3).
B. Noninfectious causes (2).
A. Tuberculosis, leprosy, fungi.
B. Sarcoidosis, sperm granuloma.
Chronic epididymitis: Histology of fungal infection.
Necrotizing granulomas and abscesses.
Spermatocele:
A. Location.
B. Wall.
A. Anywhere along the flow of spermatozoa.
B. Floppy.
Epididymal cyst: Wall.
Rubbery.
Cystic ductuli efferentes:
A. Location.
B. Structure.
A. Between the head of the epididymis and the rete testis.
B. Multilocular.
Cystic ductuli efferentes: Histology (2).
Lined by low-cuboidal epithelium.
No smooth muscle.
Adenomatoid tumor: Typical location.
Lower pole of epididymis.
Adenomatoid tumor: Gross pathology.
Firm, gray-white nodule with a solid, whorled cut surface.
Adenomatoid tumor: Histologic components (2).
Epithelioid cells.
Fibrous stroma.
Adenomatoid tumor: Patterns of growth of the epithelioid component.
Tubules, cysts, cords.
Adenomatoid tumor: Contents of fibrous stroma (2).
Hyalinized or smooth muscle.
Lymphocytes in aggregates or in patchy infiltrates.
Adenomatoid tumor: Immunohistochemistry (2).
Positive: Mesothelial markers, alcian blue.
Negative: CEA, inhibin.
Adenomatoid tumor: Electron microscopy (2).
Long, slender microvilli.
Desmosomes.
Papillary cystadenoma:
A. Frequency of bilaterality.
B. Associated syndrome.
A. 40%.
B. von Hippel-Lindau.
Papillary cystadenoma: Gross pathology.
Well circumscribed and multicystic.
Papillary cystadenoma: Histology (2).
Cysts contain papillary projections.
Densely fibrous stroma.
Papillary cystadenoma: Cytology (2).
Cuboidal or columnar and ciliated.
Clear cytoplasm due to glycogen.
Papillary cystadenoma vs. papillary carcinoma.
Carcinoma: More cells, more pleomorphism, may be solid.
Fibrous pseudotumor: Associations.
History of trauma or infection in 30% of patients.
Fibrous pseudotumor: Gross forms.
Localized: One or more nodules.
Diffuse: Diffuse thickening of tissues.
Fibrous pseudotumor: Histology (3).
Spindle cells.
Mixed inflammatory infiltrate.
Collagenous stroma.
Fibrous pseudotumor: Histologic variations (3).
Features of
− Fibroxanthoma.
− Sclerosing lipogranuloma.
− Sclerosing hemangioma.
Fibrous pseudotumor: Immunohistochemistry (3).
Negative: Cytokeratin, SMA, S100.
Paratesticular tumors of smooth muscle: Sites (2).
Leiomyoma: Epididymis.
Leimyosarcoma: Spermatic cord.
Leiomyosarcoma: Clues to malignancy (4).
Nuclear pleomorphism.
More than 1-2 mitotic figures per hpf.
Hemorrhage.
Necrosis.
Tumors of smooth muscle: Electron microscopy (2).
Thin filaments.
Pinocytotic vesicles.
Leiomyosarcoma vs. liposarcoma with smooth-muscle differentiation.
The latter shows amplification of MDM2.
Smooth-muscle hyperplasia of testicular adnexa: Histology (2).
Increased bland smooth muscle among epididymal tubules.
Tubules show secondary dilatation and squamous metaplasia.
Most common paratesticular sarcoma in ___.
A. Adults.
B. Children.
A. Liposarcoma, esp. well-differentiated.
B. Rhabdomyosarcoma.
Paratesticular liposarcoma: Sites (2).
Scrotum.
Inguinal canal.
Dedifferentiated liposarcoma: Histologic types (2).
High-grade.
Low-grade, with smooth-muscle differentiation.
Well-differentiated liposarcoma: Cytogenetics.
Ring chromosome 12.
Sclerosing lipogranuloma: Histology (3).
Granulomas and scattered giant cells.
Mixed inflammation.
Sclerotic background.
Rhabdomyosarcoma: Gross pathology.
Displaces but spares testicular parenchyma.
Paratesticular rhabdomyosarcoma: Most common subtypes.
Embryonal rhabdomyosarcoma, spindle-cell subtype (#1).
Embryonal rhabdomyosarcoma, NOS.
Embryonal rhabdomyosarcoma, spindle-cell subtype: Histology (2).
Interlacing spindle cells.
Variable numbers of strap cells and “tadpole” cells.
Embryonal rhabdomyosarcoma, NOS: Histology (2).
Alternating myxoid and cellular areas.
Spindle cells mixed with polygonal cells.
Rhabdomyosarcoma vs. leiomyosarcoma: Immunohistochemistry (2,1).
Leiomyosarcoma
− Positive: H-caldesmon.
− Negative: Myogenin, myoglobin.
Paratesticular rhabdomyosarcoma: Prognosis.
Location in this site carries a favorable prognosis.
Second most common paratesticular malignancy in adults.
Malignant mesothelioma of the tunica vaginalis.
Malignant mesothelioma of the tunica vaginalis: Associations (2).
Hydrocele.
Asbestos (sometimes).
Malignant mesothelioma of the tunica vaginalis: Gross pathology (2).
Shaggy, friable nodules
− or −
Diffuse thickening.
Malignant mesothelioma of the tunica vaginalis: Most common type and its histology (2).
Epithelial type
− Papillae, tubule, and sheets.
− Psammoma bodies sometimes.
Malignant mesothelioma: Helpful positive immunohistochemical stains (6).
CK 5/6.
EMA.
Calretinin.
GLUT1.
Telomerase.
p53.
Malignant mesothelioma vs. florid atypical mesothelial hyperplasia (3).
Atypical hyperplasia
− No true invasion of stroma.
− Positive: Desmin.
− Negative: p53, EMA.
Carcinoma of the seminal vesicle: Histologic types (3).
Papillary adenocarcinoma (most tumors).
Mucinous.
Undifferentiated.
Carcinoma of the seminal vesicle: Cytology (2).
Nuclei: Vesicular; nucleolus may be prominent.
Cytoplasm: Columnar or polygonal; clear.
Carcinoma of the seminal vesicle: Immunohistochemistry (3,3).
Positive: CEA, CA-125, CK7.
Negative: PSA, PAP, CK20.
Carcinoma of the seminal vesicle: Differential diagnosis.
Carcinomas of prostate, bladder, and colon must first be excluded.
Carcinoma of the seminal vesicle: Prognosis.
Poor.
Urethral polyp: Epidemiology (2).
Occurs only in males, usually aged 3-9 years.
Urethral polyp: Presentation (3).
Hematuria.
Urinary retention.
Infection.
Urethral polyp: Location.
Prostatic urethra next to the verumontanum.
Urethral polyp: Histology.
Urothelial lining that may show
− Squamous metaplasia.
− Ulceration.
Caruncle: Epidemiology.
Found only in women, usually later in life.
Caruncle: Clinical appearance.
Red, painful mass at the urethral meatus.
Caruncle: Histology (2).
Urothelial or squamous lining.
Fibrovascular core with extravasated red blood cells and mixed inflammation.
Nephrogenic adenoma of the urethra:
A. Typical patient.
B. Association.
A. Young adult male.
B. Chronic irritation or trauma.
Nephrogenic adenoma of the urethra: Histology (3).
Flat lesions
− Tubules, similar to renal tubules, containing pink secretions.
− Loose stroma with mixed inflammation.
Papillary lesions: Similar, but with papillae lined by cells similar to those of the tubules.
Prostatic urethral polyp: Histology.
Lined by bland prostatic acinar cells.
Thin fibrovascular core.
Urethral carcinoma: Types (4).
Squamous-cell carcinoma.
Squamous-cell carcinoma.
Spindle-cell variants of the both of the above.
Verrucous carcinoma.
Urothelial carcinoma of the urethra vs. urothelial carcinoma of the bladder involving the urethra (2).
The latter
− Much more common.
− More likely to show pagetoid growth.
Carcinoma of the urethra: Behavior.
Locally aggressive; occasional metastasis.
Adenocarcinoma of the periurethral glands: Sites (2).
Glands of Cowper: Posterior urethra or perineum.
Glands of Littre: Anterior urethra.
Adenocarcinoma of the periurethral glands: Association.
Some cases: Chronic irritation, such as from a urethral diverticulum.
Adenocarcinoma of the periurethral glands: Patterns of growth (2).
Tubular or papillary.
Penile fibromatosis: Associations.
Ten to 25% of patients also have palmar or plantar fibromatosis.
Penile fibromatosis: Histology (3).
Established lesions: Similar to that of other fibromatoses.
Early: More cells, less collagen.
Later: May be hyalinized and contain cartilage or bone.
Balanitis xerotica obliterans: Histology.
Same as that of lichen sclerosus.
Balanitis xerotica obliterans: Significance.
Can progress to SCC.
Adenocarcinoma of the periurethral glands: Cytology.
Nucleus: Large, hyperchromatic.
Cytoplasm: Cuboidal or columnar; may contain mucin or glycogen.
Plasma-cell balanitis:
A. Synonym.
B. Clinical appearance.
C. Association.
A. Zoon’s balanitis.
B. Bright red patch that resembles SCC.
C. Uncircumcisedness.
Plasma-cell balanitis: Histology (2).
Upper dermal band of plasma cells.
Telangiectasia of dermal capillaries.
Condyloma acuminatum vs. verrucous carcinoma.
Verrucous carcinoma:
− Broad, pushing growth at the deep margin.
− No association with HPV.
Condylomata acuminatum: Histologic pitfall.
Treatment with podophyllin or laser therapy can cause changes that mimic SCC.
Erythroplasia of Queyrat:
A. Location.
B. Association.
C. Significance.
A. Glans penis or prepuce.
B. Lack of circumcision.
C. About 10% of cases progress to SCC.
Erythroplasia of Queyrat: Histology.
Squamous cell carcinoma in situ.
Erythroplasia of Queyrat: Types of HPV.
16, 18.
Bowen’s disease:
A. Location.
B. Significance.
A. Shaft of penis.
B. 10% to 15% of cases progress to SCC.
Bowen’s disease: Histology.
Squamous cell carcinoma in situ.
Bowenoid papulosis:
A. Age group.
B. Clinical appearance.
A. Men 20-40 years of age (younger than those affected by SCC in situ).
B. Multiple papules on the penile shaft or the perineum.
Bowenoid papulosis:
A. Significance.
B. Treatment.
A. Does not progress to invasive SCC.
B. Topical therapy or local excision; may regress spontaneously.
Bowenoid papulosis: Histology (3).
Not as dysplastic as SCC in situ.
Scattered atypical keratinocytes.
Scattered mitotic figures.
Bowenoid papulosis: Types of HPV.
16, 18.
Squamous-cell carcinoma of the penis: Relation between growth pattern and location.
Ulcerative tumors tend to be on the glans.
Squamous-cell carcinoma of the penis: Risk factors (4).
Lack of circumcision.
Poor hygiene.
Phimosis.
HPV.
Squamous-cell carcinoma of the penis: Types of HPV.
11, 16, 18, 30.
Squamous-cell carcinoma of the penis: Prognostic factors (2).
Stage.
Depth of invasion.
Status of lymph nodes.
Squamous-cell carcinoma of the penis: Behavior (2).
Metastasis to inguinal lymph nodes is present in 40% at diagnosis.
Widespread metastasis typically occurs late.
Verrucous carcinoma of the penis:
A. Typical location.
B. Clinical appearance.
A. Coronal sulcus.
B. Often ulcerated.
Verrucous carcinoma of the penis:
A. Histologically incompatible finding.
B. Behavior.
A. True koilocytes.
B. Locally aggressive; does not metastasize.
Verrucous carcinoma of the penis: Variant.
Hybrid tumor that also includes features of well-differentiated SCC.
Epithelioid hemangioendothelioma: Behavior (2).
Low-grade: Usually indolent.
High-grade: May metastasize to lymph nodes, lung, liver, bone.
Leiomyosarcoma of the penis: Behavior (2).
Tumors of dermal smooth muscle: May recur locally after excision.
Tumors of the corpora: Poor prognosis.
Fibrosarcoma: Electron microscopy (2).
No intercellular junctions.
Rough endoplasmic reticulum, mitochondria.
Epithelioid sarcoma of the penis:
A. Age group.
B. Presentation.
A. 20-40 years.
B. Slow-growing painless mass that may ulcerate the overlying skin.
Epithelioid sarcoma of the penis: Gross pathology.
Gray-tan, firm nodules.
Epithelioid sarcoma of the penis: Pattern of growth (3).
Cellular nodules in a hyalinized stroma.
Centers of nodules may be necrotic.
Infiltrative border.
Epithelioid sarcoma of the penis: Cytology (2).
Epithelioid cells with vesicular nucleus and large nucleolus.
Many mitotic figures.
Epithelioid sarcoma of the penis: Immunohistochemistry (2).
Positive: Vimentin.
Usually positive: Cytokeratin, EMA.
Paget’s disease of the penis or scrotum: Primary sites of associated malignancies (5).
Bladder.
Prostate.
Urethra.
Rectum.
Adnexa of perineal skin.
Paget’s disease of the penis or scrotum: Stains (4,1).
Positive: CEA, PAS, mucicarmine, alcian blue.
Negative: S-100.
Scrotal calcinosis:
A. Possible etiology.
B. Gross appearance.
A. Calcification of eccrine ducts.
B. Skin is usually intact but may be ulcerated.
Squamous-cell carcinoma of the scrotum: Risk factors.
Exposure to
− Chimney dust.
− Coal.
− Petroleum.
Squamous-cell carcinoma of the scrotum: Prognosis (2).
There is ipsilateral inguinal lymphadenopathy in half of patients at presentation.
Overall poor.
Granulomatous prostatitis:
A. Bacterial causes (3).
B. Fungal causes (3).
C. Parasitic causes (2).
D. Viral cause.
A. M. tuberculosis, T. pallidum, Brucella.
B. Cryptococcus, Blastomyces, Coccidioides.
C. Schistosomes, Echinococcus.
D. Herpes viruses.
