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.