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Repro - Pathology > Male Gential Tract > Flashcards

Male Gential Tract Flashcards

1
Q

What can result if the urethral folds fail to close

A
  1. Hypospadias - ventral side, most common congenital penile problem.
  2. Epispadias - dorsal side, occurs if genital tubercle is located more posteriorly towards the anal opening
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2
Q

What is the consequence of abnormal urethral canal?

A
  1. obstruction - impaired ejaculation – infertility, wicket dribbling
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3
Q

What else can be associated w/ congenital problems

A

undescended testes

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4
Q

What is a common cause of inflammatory penile disease

A
  1. Phismosis - inability to retract foreskin –> repeated bouts of inflammation –> scarring of preputial ring
  2. Venereal dz - syphilis, gonorrhea, chancroid, granuloma, lymphopathia venereum, herpes
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5
Q

What is balanoposthitis

A

inflammation of glans and foreskin from poor hygiene –> increased smegma, accumulation of debris, chronic inflammation – increased risk of carcinoma

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6
Q

what is a condyloma acuminatum

A

a benign sexually transmitted tumor - common wart. caused by HPV 6 and 11. It is NOT premalignant

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7
Q

What is the gross pathology of a condyloma

A

warty, cauliflower growth w/ sessile or pedunculated wart, papillary lesion, exophytic/fungating mass

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8
Q

What is the microscopic pathology of a condyloma

A

hyperkeratosis, acanthosis, koilocytes

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9
Q

What is carcinoma in situ?

A

neoplastic transformation of HPV 16; painless, nonulcerated

  • Penile skin: Bowmen’s Dz
  • Glans/Prepuce: Erythroplasia of Queyrat
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10
Q

What is the microscopic pathology of carcioma in situ?

A

Hyperchromatic, increased mitosis, increased epitherlium w/ intact basement membrane, hyperkeratosis, elevation of rete pegs,

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11
Q

What is invasive squamous cell carcinoma

A

malignant neoplasm of epithelial origin, HPV16/18

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12
Q

What are risk factors for an invasive squamous cell carcinoma

A
  • uncircumcised, cigarette smoking, poor hygiene
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13
Q

What is cryptorchidism

A

undescended testes, MC is unilateral,

-found in neonates, associated w/ inguinal hernias

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14
Q

what are the consequences of cryptochidism

A
  1. trauma - inguinal canal testicle
  2. Infertility : decreased spermatogenesis in both testicles
  3. Cancer: 5-10 x increased risk of neoplasm even in normal controlateral side
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15
Q

What are the 2 places the testes can get stuck

A
  1. transabdominal phase: testis reaches the pelvic brim – mediated bt Mullerian Inhibiting Substance; only 5-15% failure
  2. inguinoscrotal phase : testis reaches scrotum. mediated by calcitonin gene related peptide, failure here 95%
    - —> explains why most cases are found at pelvic brim or proximal to inguinal canal
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16
Q

What is the gross pathology of cryptorchidism

A

small atrophied and firm fibrotic testicles on both sides

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17
Q

What is the micro pathology of crytorchidism

A

no spermatogenesis, thickened basement membrane of spermatic tubules

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18
Q

What is the treatment of crytorchidism

A
  • orchiopexy –> before 2 y/o increased chance of spermatogenesis but does not guarantee fertility
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19
Q

What are some causes of atrophy/regression of testes

A
  1. Vascular - varioceles
  2. Endocrine
  3. Genetic/congential
  4. others: inflammatory (mumps), irradiation, malnutrition/cachexia, seminal outflow obstruction, neoplasm, agin
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20
Q

what is autoimmune granulomatous orchitis

A

rapid enlargement, unilateral testicular enlargement in middle aged men, granuloma w/out organisms present.

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21
Q

what is granulomatous orchitis

A

inflammatory process, intratubular w/ cellular infiltrate, histiocytes w/ lymphocytes and plasma cells. NO necrosis

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22
Q

What is mumps orchitis

A

mumps infection in post-pubertal males one wk post-parotid gland enlargement. causes focal atrophy of testicular tubules

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23
Q

How do GC and TB inflame the testes and epididymis

A

retrograde; from posterior urethra infxn up the tract

24
Q

how does syphilis inflame the testes and epididymis

A

antegrade; testes first then epididymis

25
Q

What is vascular torsion

A

twisting of spermatic cord – obstructed venous drainage –> venous stasis; increased risk of contralateral testicle

26
Q

What is the pathogenesis of vascular torsion

A
  1. anatomical defect - bell clapper phenomenon: bilateral, testes have increased mobility - increased torsion
  2. venous obstruction - leads to congestion and enlargement. Thick walled arteries remain open –> vascular engorgment –> hemorrhagic infarction
27
Q

why is vascular torsion a medical emergency

A
  1. surgical correction in 4-6 hours may save the testicle

2. hemorrhagic infarction post 4-6 hours + obliteration of testicle occurs otherwise

28
Q

what is the most common type of testicular tumor

A

95% are germ cell tumors - most common one is seminoma, 15-34 yr old, almost all malignant and treatable. White > AA

29
Q

what is the most common testicular tumor in infants

A

yolk sac tumor

30
Q

What testicular tumors produce hCG

A

choriocarcinoma > seminoma

31
Q

What do sex cord tumor cell produce

A

androgens, they are a minority of tumors and generally benign

32
Q

What is the pathology of a seminoma

A

Gross: Huge white homogenous mass, NO necrosis/hemorrhage
Micro: uniform cells w/ clear cytoplasm and distinct cell membranes –> fried egg appearance

33
Q

What is the pathology of embryonal carcinoma

A
  • More aggressive than seminoma
  • Gross: hemorrhagic mass
  • Micro: mixed tumor w/ sheets, tubules, alveoli, and papillary formations of ANAPLASTIC Cells
34
Q

what is the pathology of yolk sac tumor

A
  • MC germ cell in infants; Schiller Duval bodies, AFP increased
35
Q

What is the pathology of a choriocarcinoma

A

-mixed tumor, mimics normal placenta
- Increased vascularity – bleeding
Micro: mixed pattern of cyto and syncytiotrophblast –> Increased hCG

36
Q

what is the pathology of a teratoma

A
  • Malignant in males
  • Pure form in kids, mature or immature
  • presents multiple germ layers
  • cysts are common, keratin pearls may be present
37
Q

what is the prostate composed of

A

glands and stroma

38
Q

what are the divisions of the prostate

A

central, peripheral, periurethral, transitional

39
Q

Where is BPH likely to occur

A

transitional and periurethral zone (median lobe) – lots of pee b/c compresses urethra

40
Q

Where is prostate cancer likely to occur

A

peripheral zone (posterior lobe)–> palpable, urinary flow is not affected

41
Q

What is the micro anatomy of prostate

A

Luminal and basal epithelia

  • Luminal cells secrete seminal fluid and express PSA
  • Basal cells support/regulate growth of lumina cells and express P63
42
Q

What is PSA and what does it do

A

a serine protease, liquifies seminal fluid

43
Q

What causes acute bacterial prostatitis

A

UTI club – E. Coli, enterococci, staph

44
Q

what causes chronic bacterial prostatitis

A

UTI club w/ history of chronic UTI by same organism

45
Q

what causes chronic abacterial prostatitis

A

presents like chronic bacterial w/out UTI history; bugs such as mycoplasma, ureaplasma, and CT

46
Q

What is BPH

A
  • hyperplasia of glands and stroma driven by DHT

Bladder obstruction and urinary stasis – infxn

47
Q

What is the pathogenesis of BPH

A

stromal cells contain 5alpha-reductase; stromal and epithelium cells contain DHT-receptors.
** DHT + DHT-R –> increase growth factors –> increase proliferation

48
Q

What is the most common cancer in men

A

prostate carcinoma, increased risk w/ increasing age

49
Q

What is thought to be the pathogenesis of adenocarcinoma of prostate

A

unknown interplay btw androgen, genetics, and environment

50
Q

what is the gross pathology of an adenocarcinoma of the prostate

A
  • firm, yellow nodule (typical carcinoma)
51
Q

what is the micro pathology of an adenocarcinoma of the prostate

A
  • range of barely malignant to completely anaplastic glands
  • capsular invasion –> lymphatic, hematogenous, perineural
  • loss of basal layer, luminal crystals, back-back glands
52
Q

How can one dx an adenocarcionoma of the prostate

A
  • PSA is not cancer specific b/c it can increase w/ BPH and prostatitis
  • DRE
  • greatest screening benefit ages 55-69
    No routine screening needed after age 70
53
Q

What is Klinefelter syndrome

A

abnormal number of X’s, primary gondal insufficiency

54
Q

What is the clinical presentation of Klinefelter syndrome

A
  • eunuchoid appearance w/ increased stature
  • small to normal well developed testes
  • incomplete virilization
  • gynecomastia
  • mental retardation, speech difficulties
55
Q

What is the histology of Klinefelter syndrome

A
  • small hylanized seminiferous tubules; pseudoadenomatous clusters of leydig cells; increased incidence of extragonadal germ cell tumors

Repro - Pathology (5 decks)

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