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Pathology Pt. 4 > Male Reproductive System > Flashcards

Male Reproductive System Flashcards

1
Q

Name two congenital abnormalities that result in malformation of the urethral groove and urethral canal/abnormal openings. Describe each.

A
  1. Hypospadias: urethral orifice is on the ventral surface of the penis.
  2. Epispadias: urethral orifice is on the dorsal surface of the penis.
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2
Q

Which penile orifice congenital abnormality is associated with fertility issues? Which one is associated with bladder extrophy?

A

Fertility: hypospadias - semen might squirt out and not get into the vaginal canal.

Bladder extrophy: epispadias

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3
Q

Which penile abnormality is characterized by inflammation and scarring resulting in a small orifice that restricts normal retraction? What complications are associated with this condition?

A

Phimosis. Complications are: interference with cleanliness, increased risk of infection, possibly increased risk for cancer.

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4
Q

What is the name of the disease characterized by inflammation of the glans penis? What about inflammation of the glans penis + prepuce?

What can cause these?

A

Balanitis is inflammation of the glans penis.

Balanoposthitis is inflammation of the glans penis + prepuce.

Caused by bacteria or fungi.

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5
Q

Name a benign neoplasm of the penis and what it is caused by.

A

Condyloma acuminatum (genital warts) - caused by sexual transmission of HPV type 6 or, less frequently type 11.

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6
Q

Is there a vaccine for HPV?

A

Yeah, Gardasil.

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7
Q

Describe five morphological changes seen in condyloma acuminatum (genital warts).

A
  1. Sessile (not attached by a stalk) or pedunculated (attached by a stalk) red papillary outgrowth(s).
  2. 1 mm to several mm in diameter.
  3. Branching, villous, papillary connective stroma covered by epithelium with possible hyperkeratosis and thickening of the underlying epidermis (acanthosis).
  4. Orderly maturation of epithelial cells remains.
  5. Koilocytosis: clear cytoplasmic vacuolization of squamous cells (characteristic of HPV).
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8
Q

Do genital warts (condyloma acuminatum) progress to carcinoma in situ or cancer?

A

Rarely.

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9
Q

What is the cellular origin of most penile cancers?

A

From the squamous mucosa of the glans and contiguous urethral meatus or the prepuce and skin covering the penile shaft.

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10
Q

In which countries are penile cancers mostly seen? What other factors may contribute (3)?

A

Africa, Asia (more than 10% of all cancers in men). Not common in U.S.

Other factors:

  1. Most pts are uncircumcised and >40 years old.
  2. Prolonged contact between smegma and penile epithelium may be involved.
  3. HPV 16/18 may be involved.
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11
Q

What is Bowen disease? Name eight characteristics of the disease

A

Carcinoma in situ of the penis with a strong association with HPV 16:

  1. Pts are over 35 years old.
  2. Involves shaft skin and scrotum.
  3. SOLITARY, thick, gray-white opaque plaque.
  4. Epidermal proliferation with abnormal mitosis.
  5. Dysplastic cells with DISORDERLY maturation and hyperchromatic nuclei.
  6. INTACT BM between dermis and epidermis.
  7. 10% or more turn into infiltrating squamous cell cancer.
  8. Erythroplasia of Queyrat: erythematous patch on the penis.
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12
Q

Erythroplasia of Queyrat

A

Bowen disease: carcinoma in situ of the penis

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13
Q

What is the difference between Bowen disease and Bowenoid papulosis?

A

Bowen disease: pts are over 35, lesions are SINGLE, can develop into an invasive carcinoma.

Bowenoid papulosis: occurs in younger, sexually active males, lesions are MULTIPLE and reddish-brown (vs. gray-white in Bowen disease), does NOT develop into carcinoma, can spontaneously regress.

Both associated with HPV 16

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14
Q

Name the disease: gray, crusted, papular lesion of the glans or prepuce of the penis that infiltrates the underlying CT to produce an indurated, ulcerated lesion with irregular margins.

A

Squamous cell carcinoma of the penis

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15
Q

What percentage of cases of squamous cell carcinomas of the penis have metastasized to inguinal lymph nodes by the time of diagnosis? What is the 5-year survival rate?

A

25% have metastasized to the inguinal nodes by the time of Dx.

5-year survival rate is 70%

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16
Q

What is cryptorchidism?

A

Undescended testis - congenital, can be unilateral or bilateral

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17
Q

Name morphological changes seen in cryptorchidism (4).

A
  1. Progressive atrophy of testis –> small, fibrotic, firm.
  2. Germ cell development is arrested.
  3. Marked hyalinization and thickening of the BM of the seminiferous tubules.
  4. Prominent appearance of Leydig cells
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18
Q

Cryptorchidism is associated with 3-5 fold higher risk of _______ _______, even after surgical correction (bringing it down) so you should surgically remove the testis.

A

testicular cancer

19
Q

Testicular neoplasms are the most important cause of firm, painless ________ of the testis.

A

enlargement

20
Q

Peak incidence of testicular neoplasms occurs at what ages?

A

20-34 years

21
Q

What is the cellular origin of 95% of testicular neoplasms?

A

Germ cells

22
Q

Seminoma, embryonal carcinoma, yolk sac tumor, choriocarcinoma, and teratomas are all examples of _______ _______ tumors of the testis.

A

germ cell tumors of the testis

23
Q

Do tumors that arise from Leydig or Sertoli cells exist?

A

Yeah

24
Q

What is a seminoma? Describe it (6).

A

Germ cell tumor of testis - accounts for 40% of them.

  1. Tumor is solid, lumpy, rubbery and firm.
  2. Cut surface shows lobulation, homogenously tan or gray-tellow.
  3. Cellular homogeneity.
  4. Cytoplasm has lots of glycogen and lipid which stains clear.
  5. Lymphocytic infiltrate
  6. 25% stain positive for hCG.
25
Q

How do seminomas grow? How are they treated? What is the cure rate?

A

They grow as a progressive scrotal mass.

Often diagnosed while it can be cured by orchiectomy (sx removal of testicle) with or without abdominal lymph node dissection.

They are highly radiosensitive and advanced cases can be treated with chemo, cure rate is 90%.

26
Q

What are the two types of proastatitis?

A

Acute bacterial and chronic.

27
Q

What organisms can cause acute prostatitis?

A

UTI bacteria like E. coli

28
Q

Describe the morphological differences between acute bacterial and chronic prostatitis.

A

In acute bacterial, there will be NEUTROPHIL (POLY) infiltrate with congestion and edema. Neutrophils invade the glands first, then go into the stroma, leading to microabscesses.

Chronic prostatitis will have variable LYMPHOCYTE infiltrate, fibroblastic proliferation, and glandular injury. The presence of other inflammatory cells are required for a histologic diagnosis of chronic prostatitis (>10 WBCs per high field).

29
Q

What are the clinical features of prostatitis (7)?

A
  1. Dysuria
  2. Urinary frequency
  3. Low back pain
  4. Pain in the pelvic region - poorly localized.
  5. Enlarged and tender prostate (especially in acute bacterial)
  6. Chronic may be symptomatic or silent but often can cause recurrent UTI in males.
  7. PSA may be elevated.
30
Q

In which prostatic zone(s) do most hyperplastic lesions arise? In which zone(s) do prostate adenocarcinomas arise?

A

Hyperplasia happens in the transitional and central zones.

Adenocarcinoma happens in the peripheral zone (may be palpable during a digital rectal exam).

31
Q

BPH (nodular hyperplasia) begins to appear in men after the age of ______ and increases with age, affecting _____% of men in their 8th decade.

A

40 years of age; 90% of men in 8th decade

32
Q

BPH is characterized by proliferation of _______ and _______ elements, gland enlargement, and urinary ________.

A

proliferation of epithelial and stromal elements; gland enlargement and urinary obstruction (urethral compression).

33
Q

Describe six morphological changes of prostatic nodular hyperplasia (BPH).

A
  1. Cut surface contains bulging well-circumscribed nodules.
  2. Dilated glandular elements and fibromuscular stroma.
  3. Hyperplastic glands lined by tall columnar epithelial cells and peripheral basal cells.
  4. Infarcted areas seen in advanced cases.
  5. Foci of squamous metaplasia.
  6. BM is INTACT
34
Q

In which populations is prostate cancer most common?

A

Men between 65-75 years old. Blacks > caucasians > asians.

35
Q

Describe morphological features of prostate cancer (3).

A
  1. Variable differentiation and anaplasia.
  2. Neoplastic glands are lined by a single layer of cells.
  3. Basal reserve cells NOT PRESENT.
36
Q

How is prostate cancer graded? What is involved?

A

Gleason system - clinically important; includes anatomical stage and prognosis. Clinical exam, surgical exploration, imaging, tumor markers, and sometimes histologic grading is involved.

37
Q

How is prostate cancer treated?

A

Surgery, radiation, hormonal manipulations.

38
Q

What is a normal PSA level? What is suggestive of cancer?

A

4 ng/ml. Over 10 is suggestive of cancer.

39
Q

What are the clinical features of prostate cancer?

A

Most are silent!

40
Q

What is PSA? What can it indicate?

A

A serine protease made by prostatic epithelial cells. Can be an indicator of prostatitis, BPH, or cancer.

41
Q

Can histologic exam determine the aggressiveness of a prostate cancer?

A

Nope! That is one thing that sucks.

42
Q

What is the best use of PSA?

A

To monitor tumor recurrence after treatment

43
Q

What is the “wait and see” approach to treating prostate cancer.

A

Not treating the cancer because the patient (usually older) is more likely to die of something else.

44
Q

Prostate cells are heavily dependent on _______ (a hormone), which is made from testosterone with ___________ (an enzyme). Controlling activity of this enzyme may be a method of treatment of prostate hyperplasia.

A

DHT made by 5-a-reductase type 2

Pathology Pt. 4 (10 decks)

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