Male GU Pathology Flashcards
Penis - congenital anomalies
Hypospadias - more common
- urethral opening on the ventral surface of the penis
Epispadias = uretrhal opening on the dorsal surface of the penis
- -> Both malformations may leads to:
- urinary tract obstruction and infections
- ejaculation disturbance - sterility
Phimosis = orifice of the prepuce is too small to permit its retraction
- secondary to repeated infections and scarring
- interferes with cleanliness leading to infections
- paraphimosis = forcible retraction - unable to replace the prepuce
Penis - inflammation
Sexually transmitted - gonorrhea, syphillis, chancroid, genital herpes, etc
Non-specific
- balanoposthitis = infection of the glans and prepuce
- most cases due to poor local hygiene in uncircumcised men
Penis - neoplasms
Benign = condyloma acuminatum
Malignant
- carcinoma in situ
- squamous cell carcinoma
Condyloma acuminatum
Genital warts - caused by HPV types 6 +11
- may recur but do not evolve into cancers
Histology - hyperchromatic nuclei with irregular nuclear membranes and with a halo around the nucleus = koilocytes (cells are infected by hpv)
Squamous carcinoma in situ (CIS)
Malignant changes are confined to the epithelium
- no evidence of local invasion
- no possibility of distant mets
Synonyms
- Bowen’s disease
- Bowenoid papulosis
- erythroplasia of Querat
Associated with HPV - esp HPV 16
Squamous cell carcinoma
Uncommon in US, <1% of male cancers
- occurs in 40-70 year olds
- increased incidence in uncircumcised
- HPV 16/18 implicated in 50% of cases
Histology - irregular nests of squamous carcinoma invading connective tissue;
- keratinization and keratin pearl formation
Slow growing, locally invasive, metastasize to inguinal and iliac lymph nodes
- prognosis related to stage
Verrucous carcinoma
Variant of SCC
- very rare
- very well differentiated - difficult to differentiate from condyloma
- local invasion, no mets
Prostate - inflammation
Acute and chronic bacterial prostatitis
Chronic abacterial prostatitis
Granulomatous prostatitis
- BCG therapy
- fungal - in immunosuppressed
- non-specific granulomatous prostatitis
Benign prostatic hyperplasia
Extremely common in men >50 years
- hyperplasia of prostatic stroma and epithelial cells, forming large discrete nodules
- predominantly involves periurethral region and compresses the urethra –> difficulty in urination, retention of urine, distension and hypertrophy or bladder + infections
Treatment
- medical - alpha blockers + DHT inhibitors
Prostate cancer = adenocarcinoma
Most common form of male cancer - second leading cause of cancer death
- older age >50 years
Etiology = multifactorial
- environmental factors - red meat, fat
- androgens
- genetics –> one first degree relative = 2x risk; 2 first degree relatives = 5x risk
Prostate cancer
- gross
- histology
Gross
- subtle gross findings, sometimes invisible
- 70% arise in peripheral zone
Histology
- most are bland - difficult to distinguish from normal prostate glands
- small glands infiltrating through normal tissue
- composed exclusively of malignant epithelial cells - LACK BASAL CELLS
- cells have enlarged nuclei with large, prominent nucleoli
Prostate intraepithelial neoplasia
Presumed precursor of adenocarcinoma
- cells have features of adenocarcinoma, but still in normal glands with basal cells
- increased likelihood of invasive carcinoma elsewhere in prostate or in the future (1/3 in 10 years)
- generally followed by repeat biopsy
Gleason grading
Best marker along with the stage for predicting prognosis and impacts treatment
- stratified into 5 patterns on the basis of ARCHITECTURE (most grades are based on nuclei)
- gleason score = sum of the 2 most predominant patterns
TNM staging of prostate cancer
T1 - clinically unapparent, non-palpable tumor
T2 - tumor confined within prostate
T3 - tumor extends beyond the prostate
T4 - tumor invades adjacent organs
N0 - no lymph node mets
N1 - regional lymph node mets
M1 - distant mets
Testis - congenital
Cryptocordism
- 10% undescended at birth, 1% by 1 year old
- most often unilateral, 25% bilateral
- irreversible injury begins around 2 years of age
Complications
- trauma
- infertility
- testicular cancer - 30-50x risk
Treatment = surgical by age 2
Testis - regressive changes
Atrophy - causes
- progressive atherosclerosis
- end stage inflammatory orchitis
- cryptochidism
- hypopituitarism
- irradiation
- prolonged administration of female sex hormones
Decreased fertility - various causes
- hypospermatogenesis
- maturation arrest
- vas deferens obstruction
Testis - inflammatory
- non-specific epididymitis and orchitis
- granulomatous/autoimmune orchitis
- specific inflammation - gonorrhea, mumps, TB, syphillis
Testicular torsion
Twisting of testis around spermatic cord - blocks venous outflow
- surgical emergency - testicular infarction
- most cases in first year of life, another peak around puberty
Testicular neoplasms - classification
Germ cell tumors = 95%
- Seminoma = 33%
- - classic
- - spermatocytic - Non-seminomatous = 62%
- - mixed (most common)
- - pure
- –> teratoma
- –> embryonal carcinoma
- –> yolk sac tumor
- –> choriocarcinoma
Sex cord stromal tumors (<1%)
Secondary - particularly lymphoma (5%)
Germ cell tumors
About 8000 cases/year - 400 deaths/year
- affect predominantly young patients - 15-34 most common
- whites 5:1 vs. AA
- presents as painless testicular enlargement
Seminoma (classic)
Most common pure germ cell tumor
- peak in 30s
Gross = bulky, lobulated, homogenous, gray-white mass
Histology = recapitulates primitive germ cells
- large polygonal cells with clear cytoplasma dn distinct cell membranes
- large central nucleus with prominent nucleoli
- CORDS OF CELLS DIVIDED BY FIBROUS STROMA WITH LYMPHOCYTIC INFILRATE
placental alkaline phosphatase (PLAP) positive
70% confined to testis (stage 1) at presentation
- highly sensitive to radiation and chemo
- 95% cure rate even if metastatic
Spermatocytic seminoma
Very different from classic seminoma
- older men - usually 55+
- different morphology - no lymphocytes, 3 cell types
- PLAP negative
- much better natural history, so different treatment = orchiectomy is curative, no chemo needed
Non-seminomatous germ cell tumors - overview (NSGCT)
Cell types mimic different parts/stages of embryonic development
- most are mixed; pure are rare
- prognosis and treatment are basically the same for all of them, but different from pure classical seminoma
- mixed tumors may have seminoma component; still treated as NSGCT
- mets and recurrences may have different cell types than primary tumor
Teratoma
Components reminiscent of normal derivatives from more than one germ layer
- mature - fetal/adult type tissues
- immature - primitive embryonal tissues
Pure teratoma common in infants and children
Prognosis depends on age
- kids - teratomas are benign
- postpubertal males - all teratomas are malignant –> DIFFERENT THAN IN OVARY!
Teratoma - gross and micro
Gross - large tumors with heterogeneous appearance
Micro - mixture of tissues from various organs
- skin, GI ,resp epithelium, thyroid, bone, muscle, etc
Embryonal carcinoma
Recapitulates most primitive embryonal tissue
- 20-30 year old
- usually smaller than seminoma
Forms epithelial structures = alveolar or tubular pattern or sheet like growth
- epithelial appearing large anaplastic cells - looks like a really bad carcinoma
Stains with cytokeratin
Yolk sac tumor
AKA endodermal sinus tumor
- most common testicular tumor in infants and kids up to 3 yo (pure)
- non-encapsulated, homogenous, yellow white, mucinous appearance
- AFP useful marker in blood and on tissue
Recapitulates yolk sac
- lace like reticular pattern
- med sized cuboidal or elongated cells
- 50% have schiller-duval bodies = endodermal sinuses ***
- eosinophilic hyaline globules
Choriocarcinoma
1% pure form, highly malignant, usually small
Gross = hemorrhage and necrosis common
Micro - recapitulates placental trophoblast
- composed of both…
1. cytotrophoblasts - polygonal cells with clear cytoplasm
2. syncyttiotrophoblast - large multinucleated cells
HCG = useful marker in blood and tissue
Intratubular germ cell neoplasia
Presumed origin of germ cell tumors
- large, atypical cells in base of sertoli tubules
- look like seminoma cells
- seen adjacent to many germ cell tumors - not spermatocytic seminoma
Germ cell tumors - mets
lymphocytic spread is common to
- retroperitoneal para aortic lymph nodes
- mediastinal lymph nodes
- supraclavicular lymph nodes
Hematogenous spread is to lungs primarily
- also liver, brain and bones
NSGCT mets earlier, more commonly via hematogenous route than seminoma
Stages of testicular tumors
Stage 1 - tumor confined to testis, epididymus, or spermatic cord
Stage 2 - distant spread confined to retroperitoneal nodes below the diaphragm
Stage 3 - mets outside the retroperitoneal nodes or above the diaphragm
Germ cell tumors - tx
Standard management of solid testicular mass is radical orchiectomy
Adjuvant chemo and/or radiation
- Seminoma particularly radiosensitive
- Exceptions spermatocytic seminoma, teratoma in children – no adjuvant therapy
Natural history of germ cell tumors is mostly very bad – rapidly fatal
BUT they are very sensitive to therapy
- NSGCT >90% long-term remission, most cured
- Seminoma >95% cure
Key points about testicular tumors
- Key clinical distinction is seminoma vs other
- Spermatocytic seminoma is totally different from classic seminoma
- Testicular teratomas prognosis is defined by AGE. Any teratoma in a postpubertal male has malignant potential.
- Most NSGCTs are mixed. All treated the same.
- Mixed germ cell tumors may show different components in metastases and recurrences than in the original tumor
