ERM2 -Male Repro Path

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jknell
ID:
184268
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ERM2 -Male Repro Path
Updated:
2012-11-18 22:43:35
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Endocrine Reproductive Pathology
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Endocrine and Reproductive Pathology
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  1. Testicular Cancer: epidemiology
    • -5/100,000 men per year
    • -avg 34 years
    • -highest incidence in scandanavians
  2. Testicular Cancer: Risk Factors
    • -cryptorchidism (undescended testicle)
    • -Testicular atrophy
    • -Previous testicular cancer
    • -CIS
  3. Testicular Cancer: Presentation
    • -painless swelling
    • -30-40% dull ache
    • -gynecomastia (5%)
  4. Testicular Cancer: Diagnosis
    -Scrotal U/S
  5. Testicular Germ Cell Tumors
    • 1. Seminoma
    • 2. Non-seminoma
  6. Seminoma
    • -undifferentiated
    • -most common (40-50%)
  7. Non-Seminoma
    • -10-20%
    • -present in mixed tumors (~40%)
    • -yolk sac
    • -embryonal carcinoma
    • -choriocarcinoma
    • -teratoma
  8. Testicular Cancer: Histologic Classification
    • 1. Non-Seminoma (Embryonal)
    •      -Teratoma
    •      -Choriocarcinoma
    •      -Yolk Sac Tumor

    2. Seminoma
  9. Histologic Classification of Seminoma
    • 1. Classic (85%)
    • 2. Anaplastic
    • 3. Spermatocytic (older patients, commonly bilateral)
  10. Classic Seminoma
    • -most common of all germ cell tumors
    • -men 15-35 years
    • -10% present with mets
    • -excellent prognosis: radiosensitive

    -Histology: fried egg appearance (cells with glycogen)
  11. Spermatocytic Seminoma
    • -avg age = 55 years
    • -better prognosis: 100% 5YS with orchiectomy alone

    -Histology: no glycogen, no lymphocytic infiltrate
  12. Gross Morphology of Seminoma
    • -fish flesh appearance
  13. Histologic Classification of Non-Seminoma
    • 1. Embryonal
    • 2. Teratoma
    • 3. Yolk Sac Tumor
    • 4. Choriocarcinoma
  14. Embryonal Carcinoma (NSGCT)
    • -age 15-35
    • -most commonly component of mixed GCT
    • -highly malignant (tend to metastasize early and often)
    • -often highly vascular and necrotic
    • -increased hCG
  15. Teratoma (NSGCT)
    • -tumor elements from at least 2 germ layers
    • -bimodal age distribution:
    •      1. infants (usually mature --> benign)
    •      2. Adolescents (usually mixed)
    • -clinically all cases considered malignant (contrast to ovary)

    • -Mature: benign structures, well differentiated
    •      -often coexist with NSGCT
    •      -doesn't respond well to chemo (surgical tx)

    -Immature: undifferentiated
  16. Yolk Sac Tumor (NSGCT)
    • -bimodal age distribution:
    •      1. infants and children (pure yolk sac tumor)
    •      2. post-puberty (mixed)

    • -often NOT metastatic
    • -produces AFP
    • -embryoid bodies
    • -Schiller Duval Bodies (perivascular cuffing)
  17. Choriocarcinoma (NSGCT)
    • -avg age = 20 years
    • -pure form is very rare
    • -two distinct cell types
    •      1. Syncytiotrophoblasts (large multinucleate cells that produce hCG)
    •      2. Cytotrophoblasts (intermediate sized cells)
    • -most malignant
    • -hemorrhagic tumors
    • -early hematogenous spread (classically presents with hemoptysis)
    • -elevated hCG
  18. Testicular Cancer Markers
    • b-hCG
    • AFP

    • LDH
    • placental alk phos
  19. Testicular Cancer: Risks for recurrance
    • -vascular invasion (strongest predictor)
    • -lymphatic invasion
    • -Embryonal elements
    • -Tunica or epidydymal invasion
    • -Absence of yolk sac elements
    • -MIB-1 immunostaining
  20. Treatment of Seminoma
    • -Stage I: observe (only 15% mets to RP)
    • -Stage II/III: chemo, RPLND if RP mets
  21. Treatment of non-seminoma
    • -Stage I: observe or RPLND (25% met to RP)
    • -Stage II/III: chemo, RPLND if RP masses left over
  22. Sympathetic Nerve Anatomy in the RP
    -can have normal sensation and erection but no emission due to sympathetic nerve damage
  23. Testicular Cancer: Chemo
    • 1. BEP (bleomycine, Etoposide, Cisplatin)
    • 2. Salvage (VIP)
  24. Testicular Cancer: Surgery
    • -radical orchiectomy (initial)
    • -RPLND
    • -resection of residual masses after chemo (main role)
  25. Testicular Cancer: Fertility Issues
    • -at diagnosis are often hypofertile (25% permanent impairment)
    • -XRT can decrease spermatogenesis
    • -chemo (50% permanent impairment)
    • -RPLND (nerve sparing technique can spare fertility)
  26. Prostate Cancer: Epidemiology
    • -most common malignancy in men
    • -highest risk in african americans
    • -high prevalence with age
    • -many men die with rather than of Prostate CA
    • -slow growing (usually not dangerous for 10-15 years after diagnosis)
  27. Prostate Cancer: Diagnosis
    • -PSA (also increase with BPH, age, infection)
    • -DRE
    • -confirm with bx or U/S
  28. Prostate Cancer: Treatment
    • -watchful waiting
    • -active surveillance

    • -XRT (brachytherapy)
    • -radical prostatectomy
    • -newer techniques
  29. Radical Prostatectomy (Pros and Cons)
    • Pros:
    • -saves lives
    • -provides accurate staging
    • -debulking
    • -low risk of side effects

    • Cons:
    • -risk of surgery
    • -incontinence/impotence
    • -cost
  30. Prostate Cancer: new therapeutic options
    -Docetaxel (for castartion resistance metastatic prostate cancer)
  31. Prostate Anatomy
    • -sits under bladder and surrounds prostatic urethra
    • -sits in front of rectum (can feel on DRE)
    • -Cowper's glands: produce secretions that lubricate urethra during ejaculation (can mimic cancer if sampled during histology)
  32. Prostate Gland Anatomy


    • BPH: anterior and middle lobe
    • Prostate Cancer: posterior lobe
  33. Histology of Normal Prostate
    • -glands and acini
    • -ducts lined by 2 cell layers
    •      1. basal (outer)
    •      2. Secretory (PSA)
    • -corpora amylasia (solidified secretions)
  34. Inflammatory Conditions of the Prostate
    • 1. Acute (microorganism, esp in elderly)
    • 2. Chronic
    • 3. Granulomatous (BCG tx, TB, fungal)
    • 4. Chronic Non-specific (most common form, may be asx, non-bacterial)
  35. Granulomatous Prostatitis
    • 1. Microbial
    •      -BCG vaccine (bladder cancer tx)
    •      -TB or fungi

    • 2. Non-microbial
    •      -usually idiopathic
    •      -may be rxn to concretions
    •      -may follow TURP
    •      -associated with systemic granulomatous diseases (Churg- Straus, Wegener Granulomatosis)
  36. BPH: Epidemiology
    -incidence: 50% by 50, 80% by 80
  37. BPH: Symptoms
    • Present in 50% of patients
    • -incomplete emptying
    • -frequency
    • -urgency
    • -straining
    • -Intermittency (Hesitancy)
    • -Weak Stream
    • -Nocturia
  38. BPH: Pathophysiology
    -may be due to age-related increase in estradiol with possible sensitization of the prostate to growth-promoting effects of DHT

    -nodular enlargement of periurethral prostate (compression of the urethra)

    -NOT pre-malignant
  39. BPH: Complications
    -bladder wall trabeculation (distention and hypertrophy of bladder)

    -urinary statsis with frequent UTIs/Stones

    -hydroureter and hydronephrosis

    -renal failure
  40. BPH: Histology
    • -looks like normal prostate, just hypertrophic
    • -gland have filiform folds
    • -stroma is more cellular --> nodules
  41. Prostate Carcinoma: Epidemiology
    -most common cancer in men
  42. Prostate Carcinoma: Risk Factors
    • -age
    • -race (black > white)
    • -Geography (US > Far East)
  43. Prostate Carcinoma: Screening
    • -DRE
    • -serum PSA
    • -needle core bx (if DRE or PSA is suspicious
  44. DRE
    • -most prostate cancers are in posterior or posterior-lateral location and can be felt
    • -sensitivity and specificity are low
  45. PSA
    • -enzyme produced by prostatic epithelial cells
    • -in serum is either free or complexed
    • -ratio of free:bound PSA is more sensitive
  46. Prostate Carcinoma: Clinical Course
    • -no sx in most cases
    • -obstructive sx in 30% (mostly due to coexisiting BPH)
    • -may present with sx of mets
    •      -spread: direct, lymphatic, hematogenous
    •      -cause lower back pain and elevated alk phos
  47. Gleason Score
    • -sum of two most predominant patterns
    • -2-4: well differentiated
    • -5-7: moderately differentiated
    • -8-10: poorly differentiated
  48. Prostatic Intraepithelial Neoplasia (PIN)
    • -asymptomatic lesion
    • -highly associated with carcinoma (concurrent or subsequent)
    • -close F/U
  49. Anatomy of the Testes


    -testes form in abdominal cavity (urogenital sinus) and descend into the scrotal sac
  50. Sertoli Cells
    • -secrete inhibin (inhibit FSH)
    • -have tight junctions (blood-testes barrier)
    • -support spermatozoa
    • -regulate spermatogenesis
    • -produce AMH
    • -inside seminiferous tubules

    "Support Sperm Synthesis"
  51. Leydig Cells
    -secrete testosterone

    Line seminiferous tubules
  52. Congenital Abnormalities of the Testes
    • 1. Aplasia: absent testes, anorchia, monorchia
    • 2. Hypoplasia: small, underdeveloped testes
    •      -cryptorchidism
    •      -Klinefelter's
    •      -Male pseudohermaphroditism
    •      -hypopituitarism (infantilism)
    • 3. Absent Germ Cell: sertoli cell only syndrome
  53. Klinefelter's Syndrome: Symptoms
    -male phenotype with small testes, gynecomastia, mental retardation

    -testicular atrophy, tall/long extremitites, female hair distribution
  54. Klinefelter's Syndrome: Pathophysiology
    -nondysjunction of X chromosome (47XXY)

    • -low testosterone
    • -dysgenesis of seminiferous tubules (decreased inhibin -->increased FSH)
    • -abnormal Leydig cell function (decreased inhibin --> increased LH --> increased estrogen)

    -infertility due to azospermia or low sperm count
  55. Male Pseudo-hermaphroditism: Symptoms
    • Pseudo-female phenotype
    • -short, blind vagina (maldeveloped scrotum)
    • -large clitoris (maldeveloped penis)
    • -no uterus or Fallopian tubes
    • -abdominal testes
  56. Male Pseudo-hermaphroditism: Pathophysiology
    • -male karyotype 46XY
    • -testosterone receptor abnormality (target organs fail to respond to testosterone)
    • -may have elevated T
    • -increased risk of GCT
  57. Testicular Atrophy: Causes
    • -pituitary destruction
    • -inflammation and scarring (chronic orchitis)
    • -complication of mumps
    • -irradiation
    • -chemo
    • -cirrhosis
    • -AIDs
    • -chronic alcoholism
    • -malnutrition
  58. Inflammation of the Penis and Scrotum
    • -balanoposthitis NOS
    • -plasma cell balanitis (Zoon's balanitis)
    • -Balanitis Xerotic Oblitrans (BXO)
    • -Chancre (syphilis)
    • -Herpes Simplex
    • -Lymphogranuloma venerum (chlamydia)
    • -Granuloma inguinale
  59. Plasma cell balanitis (zoon's)
    • -attenuated epidermis
    • -lots of plasma cells
  60. Balanitis Xerotica Oblitrans (BXO)
    • -some inflammatory cells
    • -sclerosis of epidermis
  61. Penile Tumors
    • Condyloma acuminatum
    • Giant condyloma
    • Squamous Carcinoma in situ
  62. Condyloma acuminatum
    • -benign tumor (due to STD)
    • -HPV 6 and 11
    • -coronal sulcus and inner side of prepuce
  63. Giant Condyloma
    • -locally aggressive and may destroy the penis and adjacent areas
    • -does not metastasize
    • -HPV 6 and 11
  64. Squamous Carcinoma in situ
    • -premalignant (potential to invade)
    • -very rare
    • -men between 40 and 70 years
    • -decreased incidence in circumcised
    • -painless
    • -27% 5YS with positive LNs

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