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Human Reproduction > Week 4: Male genital system pathology > Flashcards

Week 4: Male genital system pathology Flashcards

1
Q

What is Hypospadias?

A

Opening of the urethra on the inferior surface of the penis

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2
Q

Etiology/Pathophysiology of hypospadias

A

Due to failure of the urethral folds to close

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3
Q

What is epispadias?

A

Opening of the urethra on the superior surface of the penis

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4
Q

Etiology/Pathophysiology of epispadias

A

due to abnormal positioning of the genital tubercle

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5
Q

Epispadias associations

A

Associated with bladder exstrophy

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6
Q

What is Condyloma acuminatum?

A

Benign warty growth on genital skin

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7
Q

Etiology of Condyloma acuminatum

A

Due to HPV 6 or 11

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8
Q

Histological features of Condyloma acuminatum

A

Characterized by Koilocytic change

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9
Q

What is Lymphogranuloma venerum?

A

Necrotizing granulomatous inflammation of the inguinal lymphatics and lymph nodes

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10
Q

Lymphogranuloma venerum etiology

A

Sexually transmitted disease caused by Chlamydia trachomatis (serotypes L1-L3)

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11
Q

Prognosis of Lymphogranuloma venerum

A
  • Eventually heals with fibrosis
  • perianal involvement may result in rectal stricture
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12
Q

What is male genital squamous cell carcinoma?

A

Malignant proliferation of squamous cells of penile skin

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13
Q

Risk factors for male genital squamous cell carcinoma

A
  • High risk HPV (2/3 cases)
  • Lack oof circumcision - foreskin acts as a nidus for inflammation and irritation if not properly maintained
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14
Q

Precursor lesions of male genital squamous cell carcinoma

A
  • Bowen disease - in situ carcinoma of the penile shaft or scrotum that presents as leukoplakia
  • Erythroplasia of Queyrat - in situ carcinoma of the glans that presents as erythroplakia
  • Bowenoid papulosis - in situ carcinoma that presents as multiple reddish papules
    • seen in younger patients (40s) relative to Bowen disease or Erythroplasia of Queyrat
    • Does NOT progress to invasive carcinoma
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15
Q

Some forms of testicular pathology

A
  • Cryptorchidism
  • Orchitis
  • Testicular torsion
  • Variocele
  • Hydrocele
  • Testicular tumors
    • Germ cell tumors
    • sex cord-stromal tumors
    • Lymphoma
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16
Q

What is Cryptorchidism?

A
  • Failure of the testicle to descend into the scrotal sac
    • testicles normally develop in the abdomen and then “descend” into the scrotal sac as the fetus grows
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17
Q

Epidemiology of Cryptorchidism

A

The most common congenital male reproductive abnormality (1% of male infants)

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18
Q

Prognosis of Cryptorchidism

A
  • Most cases resolve spontaneously
    • otherwise: Orchiopexy is performed before 2 years of age
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19
Q

Complications of Cryptorchidism

A
  • testicular atrophy with infertility
  • increased risk for seminoma
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20
Q

What is Orchitis?

A

Inflammation of the testicle

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21
Q

Common etiologies of Orchitis

A
  • Chlamydia trachomatis (serotypes D-K)
  • Neisseria gonorrhoeae
  • Escherichia coli
  • Pseudomonas
  • Mumps virus
  • Autoimmune orchitis
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22
Q

Features of orchitis caused by Chlamydia trachomatis or Neisseria gonorrhoeae

A
  • seen in young adults
  • increased risk of sterility
  • Libido not affected because Leydig cells are spared
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23
Q

Features of orchitis caused by Escherichia coli and Pseudomonas

A
  • seen in older adults
  • urinary tract infection pathogens spread into the reproductive tract
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24
Q

Features of orchitis caused by mumps virus

A
  • occurs in teenage males
  • increased risk for infertility
  • testicular inflammation is usually not seen in children < 10 years old
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25
Q

Features of orchitis caused by Autoimmunity

A
  • Characterized by granulomas involving the seminiferous tubules
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26
Q

What is testicular torsion?

A
  • Twisting of the spermatic cord
    • thin-walled veins become obstructted leading to congestion and hemorrhagic infarction
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27
Q

testicular torsion etiology

A

Usually due to congenital failure of testes to attach to the inner lining of the scrotum (via the processus vaginalis)

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28
Q

testicular torsion clinical presentation

A

presents in adolescents with sudden testicular pain and absent cremasteric reflex

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29
Q

What is Varicocele?

A

Dilation of the spermatic vein due to impaired drainage

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30
Q

Varicocele clinical presentation

A
  • presents as scrotal swelling with a “bag of worms” appearance
  • Usually left-sided
  • Left testicular vein drains into the left renal vein while the right testicular vein drains directly to the IVC
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31
Q

Varicocele risk factors

A

Seen in a large percentage of infertile males

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32
Q

Varicocele which side and why?

A
  • Usually left-sided
  • Left testicular vein drains into the left renal vein while the right testicular vein drains directly to the IVC
33
Q

Varicocele associations

A

Associated with left-sided renal cell carcinoma, RCC often invades the renal vein

34
Q

What is Hydrocele?

A
  • Fluid collection within the tunica vaginalis
    • the tunica vaginalis is a serous membrane that covers the testicle as well as the internal surface of the scrotum
35
Q

Hydrocele etiologies

A

Associated with incomplete closure of the processus vaginalis leading to communication with the peritoneal cavity (infants) or blockage of lymphatic drainage in adults

36
Q

Types of Testicular tumors

A
  • germ cell tumors
  • Sex-cord stroma tumors
  • lymphomas
37
Q

Basic presentation of testicular tumors

A
  • Presents as a firm, painless testicular mass that cannot be transilluminated
  • Usually not biopsied due to risk of seeding the scrotum
  • Removed via radical orchiectomy
  • Most testicular tumors are malignant germ cell tumors
38
Q

Epidemiology of germ cell tumors

A
  • The most common type of testicular tumor ( >95% of cases)
  • usually occur between 15-40 years of age
39
Q

Risk factors for germ cell tumors

A
  • Cryptorchidism
  • Kleinfelter syndrome
40
Q

Types of germ cell tumors

A
  • Seminoma
  • Nonseminoma
41
Q

Features of seminoma germ cell tumors

A
  • 55% of cases (most common testicular tumor)
  • Often resembles ovarian dysgerminoma
  • highly responsive to radiotherapy
  • metastasize late
  • excellent prognosis
  • Rare cases may produce β-hCG
42
Q

Features of nonseminoma germ cell tumors

A
  • 45% of cases
  • show variable response to treatment and often metastasize early
43
Q

Histological features of seminoma germ cell tumors

A

a malignant tumor comprised of large cells with clear cytoplasm and central nuclei (resemble spermatogonia) forms a hemogeneous mass with no hemorrhage or necrosis

44
Q

Histological features of Embryonal carcinoma

A
  • malignant tumor comprised of immature, primtive cells that may produce glands
  • forms a hemorrhagic mass with necrosis
45
Q

Types of nonseminiferous germ cell tumors

A
  • Embryonal carcinoma
  • Yolk sac tumor
  • Choriocarcinoma
  • Teratoma
  • mixed germ cell tumors
46
Q

Features of Embryonal carcinoma

A
  • a malignant nonseminiferous germ cell tumor
  • aggressive with early hematogenous spread
  • chemotherapy may result in differentiation into another type of germ cell tumor (eg teratoma)
  • Increased AFP or β-hCG may be present
47
Q

What is the most common testicular tumor in children

A

Yolk sac tumor

48
Q

Histological features of Yolk sac tumor

A
  • malignant tumor that resembles yolk sac elements
  • Schiller-Duval bodies (glomerulus-like structures)
49
Q

Features of Yolk Sac tumor

A
  • Most common testicular tumor in children
  • Schiller-Duval bodies (glomerulus-like structures) seen on histology
  • AFP is characteristically elevated
50
Q

What is AFP?

A

Alpha-fetoprotein is a protein that in humans is encoded by the AFP gene. The AFP gene is located on the q arm of chromosome 4. AFP is a major plasma protein produced by the yolk sac and the fetal liver during fetal development. It is thought to be the fetal analog of serum albumin.

51
Q

Histological features of Choriocarcinoma

A
  • malignant tumor of syncytiotrophoblasts and cytotrophoblasts (placenta-like tissue but villi are absent)
52
Q

Features of Choriocarcinoma

A
  • malignant nonseminiferous germ cell tumor composed of syncytiotrophoblasts and cytotrophoblasts (placenta-like tissue but villi are absent)
  • early hematogenous spread
  • β-hCG is characteristically elevated
    • may lead to hyperthyroidism or gynecomastia (α-subunit of hCG is similar to that of FSH, LH and TSH)
53
Q

Testicular tumor that can produce β-hCG

A
  • Rare cases of Seminoma germ cell testicular tumor
  • Embryonal carcinoma
  • Choriocarcinoma
  • Teratoma
54
Q

Histological features of Teratoma

A

tumor composed of mature fetal tissue derived from two or three embryonic layers

55
Q

Features of Teratoma

A
  • malignant germ cell tumor that is composed of mature fetal tissue derived from two or three embryonic layers
  • Malignant in males (not in females)
  • AFP or β-hCG may be increased
56
Q

Features of mixed-germ cell tumors

A
  • Germ cell tumors are usually mixed
  • Prognosis is based on the worst component
57
Q

Describe Sex cord-stromal tumors

A
  • Tumors that resemble sex cord-stromal tissues of the testicle
  • Usually benign
  • Leydig cell tumor usually produces androgen, causing precocious puberty in children or gynecomastia in adults
  • Sertoli cell tumor is comprised of tubules and is usually clinically silent
58
Q

Sex-cord stromal tumors histological features

A

Leydig cell tumor - Reinke crystals may be seen on histology

59
Q

What is the most common cause of testicular mass in males > 60 years old?

A

Lymphoma

60
Q

Features of Lymphoma testicular tumors

A
  • often bilateral
  • most common cause of testicular mass in men > 60 years old
  • Usually of diffuse large B-cell type
61
Q

Basic description of the prostate

A
  • small round organ that lies at the base of the bladder encircling the urethra
  • Sits anterior to the rectum; posterior aspect of prostate is palpable by digital rectal exam (DRE)
  • Consists of glands and stroma
    • glands are composed of an inner-layer of luminal cells and an outer layer of basal cells; secrete alkaline, milky fluid that is added to sperm and seminal vescile fluid to make semen
    • Glands and stroma are maintained by androgens
62
Q

What is acute prostatitis?

A

Acute inflammation of the prostate, usually due to bacteria

63
Q

Etiology of acute prostatitis

A
  • Chlamydia trachomatis (young adults)
  • Neisseria gonorrhoeae (young adults)
  • Escherichia coli (older adults)
  • Pseudomonas (older adults)
64
Q

Clinical presentation of Acute prostatitis

A
  • Presents as dysuria with fever and chills
  • prostate is tender and boggy on DRE
  • prostatic secretions show WBCs, culture reveals bacteria
65
Q

What is chronic prostatitis?

A

Chronic inflammation of the prostate

66
Q

Clinical presentation of Chronic prostatitis

A
  • dysuria with low back or pelvic pain
  • prostatic secretions show WBCs, cultures are negative
67
Q

What is BPH?

A

Benign prostatic hyperplasia

  • Hyperplasia of the stroma and glands
  • Age-related change (present in most men by the age of 60)
  • no increased risk for cancer
68
Q

BPH etiology

A
  • BPH is related to dihydrotestosterone (DHT)
    • Testosterone is converted to DHT by 5α-reductase in stromal cells
    • DHT acts on the androgen receptor of stromal and epithelial cells resulting in hyperplastic nodules
69
Q

Clinical features of BPH

A
  • Occurs in the central periurethral zone of the prostate
  • problems starting and stopping urine stream
  • Impaired bladder emptying with increased risk for infection and hydronephrosis
  • Dribbling
  • Hypertrophy of bladder wall smooth muscle (increased risk for bladder diverticula)
  • microscopic hematuria may be present
  • PSA is often slightly elevated (usually less than 10 ng/mL) due to the increased number of glands
    • PSA is made by prostate glands and liquefies semen
70
Q

Treatment of BPH

A
  • α1-antagonists (eg Terazosin) to relax smooth muscle
    • also relaxes vascular smooth muscle lowering blood pressure
    • Selective α1A-antagonists (eg tamsulosin) are used in normotensive individuals to avoid α1B effects on blood vessels
  • 5α-reductase inhibitor (eg finasteride)
    • blocks conversion of testosterone to DHT
    • takes months to produce results
    • also useful for male pattern baldness
    • side effects are gynecomastia and sexual dysfunction
71
Q

What is Prostate adenocarcinoma?

A

Abnormal proliferation of prostatic glands

72
Q

Prostate adenocarcinoma epidemiology

A
  • Most common cancer in men
  • 2nd most common cause of cancer-related death
73
Q

Risk factors of Prostate adenocarcinoma

A
  • Age > 50 years
  • African American > Caucasians > Asians
  • diet high in saturated fats
74
Q

Clinical presentation of Prostate adenocarcinoma

A

Prostatic carcinoma is often clinically silent

  • usually arises in the peripheral, posterior region of the prostate and, hence, does not produce urinary symptoms early on
  • Screening begins at the age of 50 with DRE and PSA
    • normal PSA levels increase with age due to BPH (2.5 ng/mL for ages 40-49 vs 7.5 ng.mL for 70-79 years)
    • PSA > 10 ng/mL is worrisome at any age
    • Decreased % free PSA is suggestive on cancer (cancer makes bound PSA)
75
Q

Diagnosis of Prostate adenocarcinoma

A
  • Biopsy is required to confirm the presence of carcinoma
76
Q

Histological features of Prostate adenocarcinoma

A
  • small invasive glands with prominent nucleoli
77
Q

Gleason score of Prostate adenocarcinoma

A

Gleason grading is based on architecture alone (not nuclear atypia)

  • Multiple regions of the tumor are assessed because architecture can vary from area to area
  • A score of (1-5) is assigned for two distinct areas then added to produce a final score of (2-10)
  • The higher the score, the worse the prognosis
78
Q

Prostate adenocarcinoma common spread sites

A
  • Spread to bone of lumbar or pelvis is common
  • Results in osteoblastic metastases that present as low back pain and increased serum alkaline phosphatase, PSA and prostatic acid phosphatase (PAP)
79
Q

Prostate adenocarcinoma treatment

A
  • Prostatectomy is performed for localized disease
  • Advanced disease is treated with hormone suppression to reduce testosterone and DHT
    • continuous GnRH analogs (eg Leuprolide) shit down anterior pituitary gonadotrophs (LH and FSH are reduced)
    • Flutamide acts as a competitive inhibitor at the androgen receptor

Human Reproduction (40 decks)

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