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CPR Exam 2 > Chapter 21: The Male Genital Tract > Flashcards

Chapter 21: The Male Genital Tract Flashcards

1
Q

What is the most common benign paratesticular tumor?

Typically occur where?

A
  • Adenomatoid tumor (mesothelial in nature)
  • Typically occurring near upper pole of epididymis
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2
Q

Malformation of the urethral groove and urethral canal of the male penis may produce what congenital anomalies?

A
  • Hypospadias = urethral opening on ventral surface (more common)
  • Epispadias = urethral opening on dorsal surface
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3
Q

Which complications may arise in a pt with Hypospadias or Epispadias of the penis?

A
  • Urinary tract obstruction and ↑ risk of ascending infection
  • Sterility
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4
Q

Which complications may arise due to Phimosis?

A
  • Difficult to clean –> accumulates secretion under prepuce
  • 2’ infection and possible carcinoma
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5
Q

Balanoposthitis refers to infection of which penile structures?

A

Glans and prepuce

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6
Q

What are the most common organisms responsible for Balanoposthitis?

A
  • Candida albicans
  • Anaerobic bacteria
  • Gardnerella
  • Pyogenic bacteria
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7
Q

Persistence of the infection in balanoposthitis is a common cause of?

A

Phimosis = orifice of prepuce too small to permit normal retraction

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8
Q

What is Condyloma Acuminatum and is caused by what?

A

Benign sexually transmitted wart caused by HPV (type 6; or 11)

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9
Q

Most cases of balanoposthitis occur as a consequence of what?

A

Poor local hygiene in uncircumscirbed males –> accumulation of desquamated epithelial cells, sweat, and debris = smegma acts as local irritant

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10
Q

What is the histology of Condyloma Acuminatum?

A
  • Branching, villous, papillary CT stroma covered w/ superficial hyperkeratotic epithelium
  • Thickening of the underlying epidermins (acanthosis)
  • Cytoplasmic vacuolization of squamous cells (koilocytosis), characteristic of HPV infection is present
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11
Q

Where on the penis does Condyloma Acuminatum most often occur?

Appears how?

A
  • About the coronal sulcus and inner surface of the prepuce
  • Consist of single or multiple SESSILE or PEDUNCULATED, red papillary excrescences
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12
Q

What are the 2 distinct lesions of the male genitalia that display histologic features of CIS?

Both have strong association with what?

A
  1. Bowen disease
  2. Bowenoid papulosis

*Strong association w/ HPV 16

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13
Q

Bowen disease occurs in most often where in men?

How does it appear grossly?

A
  • Skin of shaft of penis and the scrotum –> appears as solitary, thickened, gray-white, opaque plaque
  • May also manifest on glans and prepuce as single or multiple shiny red, sometimes velvety plaques
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14
Q

Bowen disease is most often seen in what age group vs. Bowenoid Papulosis?

A

- Bowen disease = both men and women, older than age 35 years

  • Bowenoid papulosis = sexually active adults (younger)
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15
Q

What is the dermal-epidermal border like in Bowen Disease?

A

Sharply delineated by intact BM

*Hence is carcinoma in situ

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16
Q

How is Bowenoid Papulosis distinguished from Bowen disease?

A
  • Younger age of affected pts
  • Presence of multiple (rather than solitary) reddish brown papular lesions
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17
Q

How is Bowenoid Papulosis and Bowen Disease different in terms of transformation into invasive carcinoma?

A
  • Bowen disease transforms into infiltrative SCC in 10% of pts
  • Bowenoid papulosis virtually NEVER becomes invasive carcinoma
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18
Q

Where is invasive SCC of the penis more commonly seen?

A

Africa, Asia, South Americ

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19
Q

Which types of HPV are strongly associated with SCC of the penis?

A

HPV types 16 and 18

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20
Q

Risk factors for SCC of the penis?

A
  • Uncircumscribed males
  • Cigarette smoking
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21
Q

Where on the penis does SCC begin?

What are the 2 macroscopic patterns of growth that may be seen?

A
  • Begins on glans or inner surface of the prepuce near coronal sulcus
  • Patterns = papillary or flat
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22
Q

What does the papillary pattern of penile SCC simulate?

Appears how?

A
  • Simulates condyloma acuminata
  • May produce cauliflower-like fungating mass
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23
Q

What is an exophytic well-differentiated variant of penile SCC that are locally invasive, but rarely metastasize?

A

Verrucous carcinoma

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24
Q

Where is the most common site of spread for penile SCC?

A

Inguinal lymph nodes

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25
Q

Prognosis of penile SCC is related to what?

A

Stage of the tumor

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26
Q

Invasive SCC of the penis most commonly occurs between what age?

Typical presenation and characterization of this cancer?

A
  • Between 40-70 yo
  • Slow growing, locally invasive lesion that is often present for a year before brought to medical attention
  • Nonpainful until they undergo 2’ ulceration and infection
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27
Q

Where is the most common site for the arrest of the testes during descent?

A

Inguinal canal

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28
Q

What are the histological changes that occur to the tests in Cryptorchidism?

A

- Marked hyalinization+thickeningof theBM of spermatic tubules

  • Progressive tubular atrophy: spermatic tubules become hyalinzed CT
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29
Q

During the histological changes occuring in Cryptochidism which cells are spared and appear to be prominent?

A

Leydig Cells

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30
Q

When the undescended tests lie in the inguinal canal they are prone to?

A
  • Trauma and crushing injuries
  • Concomitant inguinal hernia may develop
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31
Q

What is a serious consequence that may arise in cryptorchidism?

A
  • Germ cell tumor of undescended testicle
  • Cancer may also arise in contralateral, normally descended testicle
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32
Q

Treatment for cryptorchid testicle?

Reduces risk of?

Should be done when?

A
  • Orchiopexy –> reduces risk of sterility and cancer
  • Correction btw 6-12 mo., before histologic deterioration begins
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33
Q

Inflammation is distinctly more common where (testes/epididymis)?

A

Epididymis

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34
Q

Which 2 infections almost invariably arise in the epididymis first before spread to testis?

A

1) Gonorrhea
2) Tuberculosis

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35
Q

Which infection is disinct in the fact that it arises in the testis first and in many cases spares the epididymis?

A

Syphilis

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36
Q

Although not as common in children, the most common causes of Epididymitis are what?

A
  • Congenital genitourinary abnormality
  • Infection w/ gram-negative rods
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37
Q

What are the 2 most common causes of Epididymitis in sexually active men <35 yo?

A

1) C. trachomatis (D-K)
2) N. gonorrhoeae

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38
Q

What are the 2 most common causes of Epididymitis in men > 35 yo?

A
  1. E. coli
  2. Pseudomonas
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39
Q

Granulomatous (autoimmune) Orchitis most often presents in whom and how?

A

Middle age as tender testicular mass of sudden onset sometimes w/ fever

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40
Q

How is granulomatous (autoimmune) orchitis distinguished histologically?

A

Granulomas restricted to spermatic tubules

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41
Q

What is the most common route of spread of a neglected gonococcal infection starting at the posterior urethra?

A

Posterior urethra –> prostate –> seminal vesicles –> epididymis

42
Q

Severe cases of gonococcal infection cause what in the epididymis?

A

Epididymal abscesses —> extensive destruction and scarring

43
Q

Acute interstitial orchitis developing 1 week after onset of swelling of the parotid glands in young adult male should raise suspicion of?

A

Mumps

44
Q

Tuberculosis of the male genital tract arises where first and invokes what characteristic finding?

A
  • Epididymis —> Testis
  • Caseating granulomatous inflammation
45
Q

What are the 2 distinct morphological patterns of inflammation that may occur in the testis in association with Syphillis?

A

1) Production of gummas
2) Diffuse interstital inflammation –> obliterative endarteritis assoc. w/ perivascular cuffs or lymphocytes + plasma cells

46
Q

In contrast to neonatal testicular torsion, adult torsion results from what bilateral anatomic defect?

A

Bell-clapper abnormality –> ↑ mobility of testes

47
Q

What is the prophylactic treatment for testicular torsion?

A

Testis unaffected by torsion is surgically fixed to scrotum (orchiopexy)

48
Q

Which germ cell tumor is composed of cells that resemble primordial germ cells or early gonocytes?

A

Seminomatous tumor

49
Q

What are the most common malignant paratesticular tumors in children and adults?

A
  • Children = rhabdomyosarcoma
  • Adults = liposarcomas
50
Q

What are the 2 major categories of testicular tumors?

Which are aggressive and which are benign?

A
  1. Germ cell tumors (95%) = Seminomas and Nonseminomas = aggressive
  2. Sex-cord stromal tumors = generally benign
51
Q

What is the most common solid tumor in men aged 15-34 yo?

A

Testicular germ cell tumors

52
Q

Which ethnicity are at an increased risk of testicular germ cell tumors in the US?

A

Much more common in whites than in blacks (5:1 ratio)

53
Q

Klinefelter syndrome is associated w/ a 50x increased risk for development of what kind of germ cell tumor?

A

Mediastinal germ cell tumor, but NOT testicular tumors

54
Q

Most testicular germ cell tumors arise from which precursor lesion?

Exceptions?

A
  • Intratubular germ cell neoplasia (ITGCN)
  • Exceptions = pediatric yolk sac tumors and adult spermatocytic seminomas
55
Q

What are the genetic factors (i.e., familial and genes) associated with development of testicular germ cell tumors?

A
  • Strong familial predisposition –> 4x ↑ in fathers/sons of affected pts and 8-10x ↑ risk in brothers
  • Genes encoding the ligand for RTK - KIT and BAK
56
Q

Testicular germ cell tumors are associated with a spectrum of disorders collectively known as what?

Includes which disorders and which is most important?

A
  • Testicular dysgenesis syndrome (TDS)
  • Cryptorchidism = most important
  • Hypospadias
  • Poor sperm quality
57
Q

In contrast to typical seminomas, spermatocytic seminomas lack which 6 features?

A
  • Lymphocytes
  • Granulomas
  • Syncytiotrophoblasts
  • Extra-testicular sites of origin
  • Admixture w/ other germ cell tumors
  • Association w/ ITGCN
58
Q

What is the most common type of testicular germ cell tumor?

Peak incidence when?

A
  • Seminomas
  • Peak incidence in third decade (20’s)
59
Q

Seminomas contain which genetic mutations (i.e., genes and chromosome)?

A
  • Isochromosome 12p (i12p)
  • Express OCT3/4 and NANOG
  • 25% have KIT activating mutations
60
Q

How are the spermatic seminomas different from the classic seminoma as far as onset, growth, and prognosis go?

A
  • Rare, slow-growing germ cell tumor
  • Predominantly affect older men (>65 yo)
  • Prognosis is excellent
61
Q

What is the most common testicular tumor in infants and children up to 3 years of age?

Prognosis?

A

- Yolk Sac Tumor (AKA endodermal sinus tumor)

- Prognosis = good

62
Q

Germ cell tumors may have a single tissue component, but are most often found containing?

A

Mixtures of seminomatous and nonseminomatous components + mutiple tissues

63
Q

What 3 tumors of the testicle are classified as nonseminomatous tumors?

A

1) Embryonal carcinoma
2) Yolk sac (endodermal sinus) tumor
3) Choriocarcinoma

64
Q

Which genetic alteration seen in ITGCN is invariably found in invasive germ cell tumors regardless of histological type?

A

Reduplication of the short arm of chromosome 12 (12p) in form of isochromosome i(12p)

65
Q

What is the classic histology of the seminoma cells?

A
  • Large and round to polyhedral w/ distinct cell membrane
  • Clear or watery-appearing cytoplasm
  • Large, central nucleus w/ 1-2 prominent nucleoli
66
Q

Which testicular germ cell tumor presents as a bulk homogenous, gray-white mass with a lobulated cut surface, usually devoid of hemorrhage or necrosis?

A

Seminoma

67
Q

15% of seminomas contain syncytiotrophoblasts, why is this relevant?

A

Produce ↑ HCG levels

68
Q

Immunohistochemical stains of seminoma cells will be positive for what markers?

A
  • KIT
  • OCT4
  • Placental alkaline phosphatase (PLAP)
69
Q

Embryonal carcinomas of the testis typically occur in which age group?

Differ from seminomas how?

A
  • Occur mostly in 20- to 30-year age group
  • MORE aggressive than seminomas
70
Q

What is the gross morphology of embryonal carcinoma of the testis?

Extension through what?

A
  • Smaller than seminomas
  • Extend thru tunica albuginea into epididymis or cord (unlike seminomas)
71
Q

Which germ cell tumor often produces no testicular enlargement and are detected only as a small palpable nodule w/ hemorrhage and necrosis being extemely common?

A

Choriocarcinomas

72
Q

What is the histology of embryonal carcinomas, especially how are they different from seminomas?

A
  • Poorly demarcated and contain foci of hemorrhage and necrosis (seminomas have no hemorrhage or necrosis)
  • Cells grow in alveolar or tubular patterns, sometimes w/ papillary convolutions
73
Q

Immunohistochemical staining of embryonal carcinoma is positive for what markers, differs from seminomas how?

A
  • (+) OCT 3/4
  • (+) PLAP
  • (+) for cytokeratin and CD30 (unlike seminomas)
  • Negative for KIT (seminomas are +)
74
Q

Schiller-Duval bodies consisting of mesodermal core w/ central capillary + visceral and parietal layer of cells resembling primitive glomeruli are found in what type of testicular germ cell tumor?

A

Yolk sac tumor

75
Q

Immunocytochemical staining of testicular Yolk Sac Tumors is positive for what?

A
  • α-fetoprotein (AFP) = characterisitc
  • α1-antitrypsin
76
Q

Histologically, choriocarcinomas contain what 2 cells types?

A
  1. Syncytiotrophoblasts = large, multinucleated cells w/ abundant eosinophilic vacuolated cytoplasm containing hCG
  2. Cytotrophoblasts = regular and polygonal, clear cytoplasm, grow in cords or masses w/ single uniform nucleus
77
Q

Who are pure teratomas most commonly seen in and who are mixed teratoma/germ cell tumors most commonly seen in?

A
  • Pure teratomas = more common in infants and children (2nd only to yolk sac tumors)
  • Teratomas mixed w/ other germ cell tumors are more common in adults
78
Q

Which type of tumor may be a mix of neural tissue, muscle bundles, islands of cartilage, clusters of squamous epi, thyroid gland-like structures, bronchial epi, and bits of intestinal wall/brain substance?

A

Teratomas

79
Q

What is the clinical importance of recognizing a non-germ cell malignancy arising within a teratoma?

A

Secondary tumors are chemoresistant; thus only hope for cure = resection

80
Q

How does the classification of a teratoma differ if found in a child vs. postpubertal male?

A
  • Children = usually follow a benign course
  • Postpubertal male = all teratomas regarded as malignant
81
Q

What is the standard treatment for a solid testicular mass?

A

Radical orchiectomy

82
Q

Where do testicular tumors spread first via lymphatics?

A
  • Retroperitoneal para-aortic nodes = 1st
  • Mediastinal and supraclavicular nodes = 2nd
83
Q

Hematogenous spread of testicular tumors is mainly to where?

May also spread to which sites?

A
  • Mainly to the lungs
  • May also spread to liver, bones, and brain
84
Q

How does the behavior/spread of Seminoma GCT’s differ from NSGCT’s?

Each typically presents clinically in which stage?

A
  • Seminomas tend to stay localized to testis, present clinically in stage 1
  • NSGCT’s tend to spread to distant sites and present in stages 2 and 3
85
Q

How does the mode of spreading differ between seminoma GCT’s and NSGCT’s?

A
  • Seminomas tend to spread via LN’s w/ hematogenous spread late
  • NSGCT’s metastasize earlier and use hematogenous route more frequently
86
Q

What is the most aggressive NSGCT and via which route and to where does it rapidly spread?

A
  • Pure choriocarcinoma
  • Spreads rapidly and predominantly via blood to the lungs and liver
87
Q

Elevation of lactate dehydrogenase associated with germ cell tumors is a useful biomarker to assess what aspects?

A
  • Mass of tumor cells
  • Tool to asses tumor burdern
88
Q

Which biomarker is elevated with a Yolk Sac Tumor?

A

AFP

89
Q

Which biomarker is elevated with a Choriocarcinoma?

A

HCG

90
Q

What is the prognosis of Seminomas and NSGCT’s?

A
  • Seminomas = radiosensitive = remains localized = best prognosis
  • NSGCT’s = can be cured w/ aggressive chem

*Pure choriocarcinoma has poor prognosis, but better if minor component of mixed GCT.

91
Q

When do most Leydig Cell Tumors arise (age)?

A

20-60 yo

92
Q

Which testicular tumor elaborates androgens and in some cased both androgens and estrogen, and even corticosteroids?

A

Leydig Cell Tumors

93
Q

How may a pt with Leydig Cell Tumor present clinically?

Most common manifestation in children?

A
  • Testicular swelling
  • Gynecomastia may be 1st sx in some cases
  • In children, manifested primarily as sexual precocity (advanced for age)
94
Q

How do Leydig Cell Tumors appear grossly?

Distinctive feature.

A
  • Circumscribed nodules, usually <5cm
  • Distinctive GOLDEN brown, homogenous cut surface
95
Q

Cells w/ cytoplasm containing lipid droplets, vacuoles, or lipofuscin pigment + rod-shaped crystalloids of Reinke are characteristic of what type of testicular tumor?

A

Leydig Cell Tumor

96
Q

If after orchiectomy of testicular germ cell tumor, there is persistent elevations of HCG or AFP concentration this indicates which stage of disease, even if LN’s are normal size?

A

Stage II

97
Q

Sertoli Cell Tumors have cells arranged in what distinct pattern?

A

Arranged in trabeculae that tend to form cordlike structures and tubules

98
Q

Gonadoblastomas are composed of a mixture of what?

Arise where and in association with what?

Can they become malignant?

A
  • Germ cells + Gonadal stromal elements
  • Always arise in gonads w/ some form of testicular dysgenesis
  • Germ cell component may become malignant –> seminoma
99
Q

What is the most common form of testicular neoplasm in men >60 yo?

A

Testicular lymphoma (non-Hodgkin lymphoma)

100
Q

What are the 3 most common testicular lymphomas in decreasing order of frequency?

A

Diffuse large B-cell lymphoma > Burkitt lymphoma > EBV-(+) extranodal NK/T cell lymphoma

101
Q

Testicular lymphomas have a higher propensity for involvement of what system than do similar tumors arising at other sites?

A

CNS

CPR Exam 2 (21 decks)

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