Systemic Pathology - Male genital - Galan

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  1. Spermatogenesis starts in the testes, and goes through or pass by the epididymis, the prostate, urethra, ejaculatory ducts, merge, go to the penis.
  2. Anatomy
    • Three corpora - bilateral corpus cavernosas and ventrally the corpus spongiosa
    • - Cavernosa is highly vascular
    • - Spongiosa has the urethra passing through, surrounded by dense fibrous tissue
    • Squamous epithelium covers the surface, don’t need to be metabolically active, HPV problems can occur here
    • Basal layer under the squamous epithelium
  3. Congenital Anomalies
    • Hypospadias (ventral) - urethral meatus forms ventral to where it should, 50% in the glans, less in the posterior, but more difficult to repair
    • Epispadias (dorsal)
  4. Genital warts (Condyloma Acuminatum)
    • Caused by human Papillomavirus; Transmission via contact, usually sexual
    • Types 6, 11, 42 and 44 most often cause visible external genital warts, Low grade dysplasia.
    • Types 16, 18, 31, 33, and 35, have been strongly associated with cervical dysplasia in women and the development of cervical carcinoma.
    • Both men and women have a high prevalence of asymptomatic HPV infection.
  5. Pathology of genital warts
    • Exophytic and papillary, Around the coronal surface, also around meatus
    • The types of cells generated by HPV infection are called koilocytes, in which nucleus is taken over by HPV, surrounded by nuclear clearing, halo-look, hallmark. Can be binucleated and look like raisins. Jumbled, lacking layered appearance. This is considered to be low-grade dysplasia.
    • Viruses causing low grade dysplasia will be cleared out eventually.
    • Viruses causing high grade dysplasia cause the dysplasia to grow from low grade to high grade, carcinoma in situ before becoming invasive.
  6. Carcinoma in situ of penis
    • The papillary appearance
    • There are many manifestations
    • Bowen’s disease - flattened irregular plaque anywhere in the genital area
    • Bowenoid papilloma - multiple lesions
    • No koilocytes; Mitotic figures more than 50%, increased Nucleus-to-Cytoplasm ratio, irregular nuclear contours.
  7. Squamous Cell Carcinoma of the Penis - Causes and risk factors
    • <1% of cancers in males.
    • High-risk HPV types - 16, 18, 31, and 33 (16 is the most important, most frequently detected type in primary carcinomas and has been detected in metastatic lesions), associated with in-situ and invasive carcinomas.
    • Increased risks - Smoking, Ages between 40 and 70
    • Circumcision confers protection
  8. Squamous Cell Carcinoma of the Penis - Micro pathology
    • A nest of squamous cells
    • Over-produced keratin - used to identify squamous cell origin
  9. Prostate - anatomy
    • Fibromuscular stroma with branching glands
    • Two layers of epithelium - inner secretory, outer flattened basal, myoepithelial
    • Secretions contain hydrolytic enzymes which liquefy coagulated semen in female genital tract.
  10. Geographic zones of prostate
    • Transitional Zone (5%) - surrounds urethra
    • Central Zone (20%) - most posterior, surrounds ejaculatory ducts
    • Peripheral Zone (70%) - surrounds central zone
  11. Benign Prostatic Hypertrophy (B.P.H.)
    • Histological evidence seen in:
    • – 20% of men above 40 years
    • – 90% of men above 90 years
    • Almost physiologic, rather than pathologic.
    • Clinically detectable in about 50% of those with microscopic evidence.
    • Most commonly occurs in transitional and central zones (affecting urination), but can occur in peripheral zone
    • Is it a risk factor for prostate cancer??? - generally not; cancer usually happens in the peripheral zone, no urinary symptoms until very late
  12. B.P.H. - Therapy
    • Medical - Drugs to shrink the prostate
    • Surgical - Transurethral Resection of Prostate (TURP) - prostate chips
  13. Prostate Cancer
    • Most common carcinoma in men
    • Second-leading cause of cancer death in men
  14. Risk factors of Prostate Cancer
    • Age (especially >50)
    • Race (AA > white)
    • Family history
    • Hormone levels (androgen, can be treated by androgen deprivation)
    • Environmental influences
  15. Diagnosis of Prostate Cancer
    • Prostate-Specific Antigen (P.S.A.): very bad screening too; many cases end up needing biopsies with false positive.
    • Digital Rectal Exam (D.R.E.) - peripheral zone, not sensitive, late diagnosis.
    • Transrectal needle biopsy
  16. Prostate cancer - Micro
    • myoepithelial layer (basal cells) disappear, doesn't show in immunohistological stain
    • Perineural invasion is an adverse feature
  17. After grading
    • Staging - Assessing potential metastases
    • Prostate cancer has propensity to metastasize to the axial skeleton, shoulder, hips, ribs
  18. Gleason grading of prostate cancer
    • Based on the architecture
    • 1 and 2 - simple individual glands, round uniform in 1. 2 is looser.
    • 3 - most common. variation in size and complexity.
    • 4 - gland fusion
    • 5 - no architectural design, haphazard sheet
  19. The Testis
    • Typical weight is 15-19 gm; the right one is usually heavier.
    • Spermatogenesis begins inside seminiferous tubules, then go through epididymis, vas deferens.
  20. Seminiferous tubules
    • Spermatogenesis works from the outermost layer to the innermost layer
    • Germ cell -> spermatid -> spermatozoon
    • Surrounding sertoli cells provide nourishment.
  21. Sperm contains paternal mitochondria in the mid (connecting) piece. However, when sperm enters the egg, only the head gets into the egg and the remaining part breaks down. That is why only maternal mitochondrial DNA is passed on.
  22. Cryptorchidism
    • Congenital abnormalities in which the testis has not descended down the inguinal canal by birth.
    • ~3% of full-term and 30% of premature infant boys
    • 80% of the time, the testis will descend on its own in the first year (leaving an incidence of ~1% after 1 year)
    • ~2/3 unilateral, 1/3 bilateral
    • Two types:
    • - True: somewhere around the inguinal canal, in abdomen, inguinal canal, or suprascrotal, more likely to descend on its own
    • - Ectopic: located outside the inguinal canal.
    • Pathology - atrophy, no germ cell, sertoli cell only
  23. Cryptorchidism
    • Can impair spermatogenesis (inappropriate environmental temperature)
    • Can be a predisposing factor to testicular cancers (particularly seminomas)
    • Treatment - watchful waiting since most will descend on their own; if necessary, by orchipexy.
  24. Testicular Torsion
    • 90% of cases are due to congenital malformations - testis insufficiently anchored to the inner scrotal wall (“bell-clapper deformity”)
    • The free-floating testis can then rotate around the spermatic cord, causing ischemia
    • A surgical emergency
    • – 90% chance of preserving the testis after 6h
    • – 50% after 12h
    • – 10% after 24h
  25. Testicular Tumors
    • Most common cancer in men between 15 and 34.
    • Testicular masses are assumed to be cancer unless
    • proven otherwise.
    • Overall five-year survival rate has increased from ~63% in 1963 to ~95% today.
    • Delay in diagnosis is associated with worse prognosis.
    • Can metastasize by lymphatic spread (retroperitoneal
    • lymph nodes and beyond), or by hematologic spread.
    • The most common presentation is painless mass.
    • In advanced cases, palpable abdominal masses can be found.
    • Imaging may also show enlarged retroperitoneal lymph nodes.
    • Biochemical markers may also be elevated (e.g. Placental alkaline phosphatase, LDH).
  26. Two Major Types of Testicular Tumors
    • Germ Cell Tumors
    • - 95% of all testicular tumors
    • - Most common tumor between the ages of 15-34
    • - White/AA ratio is about 5:1
    • - Aggressive (but treatable)
    • - 1-2% bilateral (higher if there was cryptorchidism)
    • - Predisposing factors: Cryptorchidism (the higher the testis, the greater the risk), Genetic factors (p53), Testicular dysgenesis
    • Non-Germ Cell Tumors
    • - ~5% of all testicular tumors
  27. Germ Cell Tumors
    • Seminoma (the most common type; various subtypes)
    • Embryonal
    • Yolk sac tumor
    • Choriocarcinoma
    • Teratoma
    • Mixed germ cell tumors – combination of two or more types; Very frequently seen.
    • The main distinction - Seminoma vs. Non-seminoma
  28. Seminoma
    • The most common type of GCT - 30-50% of all GCTs.
    • Peak incidence in 30s (4th decade)
    • There are a few histologic variants, only talk about the “classic” type.
  29. Gross appearance of classic seminoma
    • Gray/white/tan.
    • Solid, well demarcated, lobulated mass.
    • No hemorrhage.
    • No cystic change.
  30. Micro appearance of classic seminoma
    • Tumor cells are uniformly large and polygonal with dark large nuclei.
    • Uniform nest of cells surrounded by lymphocytes.
    • Very frequently see nests of seminomas that are benign and non-reactive.
  31. Non-seminomatous G C T (a.k.a. all the rest)
    • Embryonal carcinoma
    • Yolk sac tumor
    • Choriocarcinoma
    • Teratoma
    • Mixed tumors - The most common type; it is far rarer to have a “pure” tumor comprised of just one of the above types.
  32. Embryonal Carcinoma
    • Pure embryonal carcinomas are rare (~2% of all testicular tumors), but ~85% of all NSCGTs contain an
    • embryonal component.
    • ~65% people with embryonal carcinomas have mets at presentation
    • Gross appearance:
    • - Variegated, white/gray/tan/red
    • - Poorly-demarcated
    • - Hemorrhagic (causing infarction) and necrotic
    • Micro appearance:
    • - large and irregular looking cancer cells
    • - No coherent architectures
    • - hemorrhage
    • - haphazard sheets of cells
  33. Yolk Sac Tumor
    • Very rare to see pure (except for children <=3), but very common in mixed GCTs.
    • Cells are trying to recapitulate the yolk sac.
    • Gross - look like embryonal, but often have a microcystic look
    • Microcystic histology ("Swiss cheese pattern") is common, indicative.
    • Schiller-Duval bodies (vascular core surrounded by ring of cells) are classic, but not as common.
  34. Choriocarcinoma
    • Pure is very rare (1%), but usually fatal.
    • Much more common as a component of a mixed GCT, where it has no effect on prognosis.
    • The tumor mimics immature placental villi. Can present with elevated serum hCG.
    • Gross - poorly demarcated, hemorrhagic mass.
    • Micro- cytotrophoblasts and syncytiotrophoblasts, both stain for hCG.
  35. Teratoma
    • ~5% of GCTs.
    • Contains elements of ectoderm, endoderm, and mesoderm.
    • In children:
    • – Usually pure.
    • – Associated with trisomy 21, Klinefelter, and other genetic issues.
    • – Assumed to be benign.
    • In adults:
    • – Assumed to be malignant, even if well-differentiated.
    • – Rare to be pure; most commonly part of a mixed GCT.
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Systemic Pathology - Male genital - Galan
2016-11-20 05:32:38
Systemic Pathology - Male genital - Galan
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