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CPR Exam 2 > Chapter 21: Penis and Prostate > Flashcards

Chapter 21: Penis and Prostate Flashcards

1
Q

_________ are the most important penile lesions and may be associated with ______.

A
  • Squamous cell carcinoma
  • HPV and poor genital hygeine.
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2
Q
  • Squamous cell carcinoma of the penis occurs most often in _________ males.
  • Occurs on the ________ on the penis, as an __________.
  • Does it spread?
A
  • Uncircumcized
  • Glans or shaft, as an ulcerative infiltrative lesion.
  • Can spread to inguinal nodes or infrequently to distal sites.
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3
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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4
Q
A
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5
Q

Complications with Hypospadias or Epispadias of the penis include:

A
    1. Urinary tract obstruction and ↑ risk of ascending infection
    1. Sterility
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6
Q

Phimosis (cannot pull foreskin back) has what complications?

A

1. Hard to clean

2. Infection and cancer

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7
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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8
Q

What is the cellular manifestation of HPV?

A
  • Koliocytosis: Cytoplasmic vacuolization of squamous cells
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9
Q

Squamous cell carcinoma of the penis is most common in whom?

A

People who are not circumsized: jews and muslims

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10
Q

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

A
  • HPV types 16 and 18
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11
Q

With the exception of the ___________, congenital anomalies of the testes are RARE and include _______.

A

Cryptochidism (undescended testes)

Absence of one or both testes or fusion

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12
Q

What is cryptochidism?

Cryptochidism is associated with _________.

A
  • Complete or partial failure of the intra-abdominal testes to descend into the scrotal sac
  • Testicular dysfunction & increased risk of testicular cancer.
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13
Q

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

A

Inguinal canal

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14
Q

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

A
  • Marked hyalinization + thickening of the BM of spermatic tubules
  • Progressive tubular atrophy: spermatic tubules become hyalinzed CT
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15
Q

Cryptochidism is associaged with ___% of 1 YO and may be accompanied by what?

A
  • 1%
  • Other malformations of the GU tract, such as hypospadias.
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16
Q

During the histological changes occuring in Cryptochidism _______ cells are spared and are most prominent.

A

Leydig cells

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17
Q

Bilateral, or in some cases, even unilateral cryptochidism is associated with _________

A

Tubular atrophy and sterility

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18
Q

Cryptorchid testis has a 3-5 fold risk higher of _____, which arises from _____

A
  • Testicular cancer, even in the NL undescended teste
  • Foci of intratubular germ cell neoplasia in the atrophic tubules
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19
Q

Treatment for cryptorchid testicle?

Reduces risk of?

Should be done when?

A
  • Orchiopexy (placement in the sac) –> reduces risk of sterility and cancer
  • Between 6-12 mo., before histologic deterioration begins
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20
Q

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

A

Epididymis

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21
Q

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

A

1) Gonorrhea
2) Tuberculosis

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22
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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23
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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24
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

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25
Q

Severe cases of gonococcal infection cause what in the epididymis?

A

Epididymal abscesses —> extensive destruction and scarring

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26
Q

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

A

Bell-clapper abnormality –> ↑ mobility of testes

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27
Q

Testicular neoplasms can be divided into 2 categories: ______ and ___

A
    1. Germ cell tumors (seminomas or nonseminomatous)
      * *95%
    1. Sex cord stromal tumors.
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28
Q

Men 15-34, what is the most common tumor?

A

Testicular germ cell tumor.

Most common in WHITES.

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29
Q

Describe MOST germ cell tumors in contrast to sex-cord, stromal tumors.

A
  • Germ cell tumors: aggressive, rapidly spread but most can be cured.
  • Sex-cord stromal tumors: generally benign.
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30
Q

Germ cell tumors can be seminomas or non-seminomas.

What are the difference between the two?

A
  • Seminomas tumors are made up of cells that resemeble primordial germ cells or early gonocytes.
  • Nonseminantous tumors are made up of undifferentied cells that resemble embroyonci stem cells, but malignant can differentiate along other lineages.
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31
Q

What are the two 2 types of seminomatous tumors?

A
  1. Seminoma
  2. Spermatocytic seminoma
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32
Q

What are the 3 nonseminomatous tumors?

A
  • 1. Embryonal carcinoma
  • 2. Yolk sac tumor
  • 3. Choriocarcinomas
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33
Q

What are the 2 sex cord stromal tumors?

A

1. Leydig cell tumor

2. Sertoli cell tumor

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34
Q

Germ cell tumors can be seminomas or non-seminomas.

How do they spread?

A
  • Seminomas remain in the testis for a long time and spread to via LN to [para-aortic LNs]. It is rare to spread further.
    • Spread by blood in advanced courses
  • Nonseminomas rumors spread earlier by and use hematongeous route more (and LN)
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35
Q

_______ are the most common cause of painless testicular enlargement.

A

Testicular tumors.

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36
Q

Testicular tumors occur with increased frequency in ____________.

A
  • Undescended testis.
  • Testicular dysgenesis.
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37
Q

Germ cell tumors can have which two histological patterns?

Which is most common

A

1. Single histologic pattern (*)

2. Mixed pattern

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38
Q

What are the most common “pure” histologic patterns of germ cell tumors?

A

1. Seminoma

2. Embryonal carcinoma

3. Yolk sac tumors

4. Choriocarcinomas

5. Teratoma

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39
Q

Mixed germ cell tumors contain more than 1 element and are more commonly:

A

1. Embryonal carcinoma

2. Teratoma

3. Yolk sac tumor

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40
Q

Most testicular germ cell tumors arise from which precursor lesion?

Exceptions?

A

- Intratubular germ cell neoplasia(ITGCN)

  • Exceptions =
  1. pediatric yolk sac tumors and terotoma
  2. adult spermatocytic seminomas
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41
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
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42
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
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43
Q

How does the precursor lesion (ITGCN) progress?

A
  • Arises in utero
  • Stays dormant until puberty, where it can become seminomatous or nonseminatous.
44
Q

What kind of cells make up ITGCN?

A
  • Atypical primordial cells germ cells that are 2x the size of NL germ cells with large nuclei and clear cytoplasms.
  • -Retain expression of OTC3/4 and NANOG TF.
  • -Reduplication of chromosome 12p, which is also found in all invasive germ cel ltumors.
45
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
46
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
47
Q

Seminomas alter the testis how?

A

-Enlarge testis, homogenous grey, lobulated surface that does not have hemorrage or necrosis.

48
Q

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

A

Produce ↑ HCG levels

49
Q

In contrast to TB, seminomas may be accompanied by ______

A

Poorly defined granulomas reactions

50
Q

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

A

- KIT

- OCT4

  • Placental alkaline phosphatase (PLAP)
51
Q

Embryonal carcinomas of the testis typically occur in ____ YO.

Differ from seminomas how?

A

- 20-30 YO

- MORE aggressive

52
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)
53
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)
  • (-) for KIT (seminomas are +)
54
Q

Yolk sac tumors are also called what?

Why do researchers find it so interesting?

A
  • Endodermal sinus tumors
  • Most common testicular tumors in infants and children up to 3, with good prognosis.
55
Q

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

A
    • α-fetoprotein (AFP) = characterisitc******
  • - α1-antitrypsin
56
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

57
Q

Choroicarinomas are a HIGHLY _______ type of testicular tumor.

A

MALIGNANT

58
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, but may outgrow BS and metastsize, even though primary site is hard to find.

59
Q

Histologically, choriocarcinomas contain what 2 cells types?

A
  1. Syncytiotrophoblasts = large,
  • Many nuclei
  • Cytoplasm has a bunch of abundant eosinophillic vacoules that contain hCG
  1. Cytotrophoblasts = regular and polygonal, clear cytoplasm, grow in cords or masses w/ single uniform nucleus
60
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?

Who is it more comon in?

A
  • Teratoma
  • Pure forms are common in infants andkids
  • In adults: pure forms are rare but can occur with OTHER germ cell tumors in 45% of cases.
61
Q

How do mature, differentiated teratomas found in children differ from post-pubertal males

A
  • If found in child: usually benign
  • In post-pubertal male: all are malignant, no matter if mature or immature.
    • ​So not important to determine maturity in adults .
62
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

63
Q

What is the standard treatment for a solid testicular mass?

A

Radical orchiectomy

64
Q

Where do testicular tumors spread first via lymphatics?

A
  • Retroperitoneal para-aortic nodes = 1st
  • Mediastinal and supraclavicular nodes = 2nd
65
Q

Hematogenous spread of testicular tumors is mainly to where?

A
  • Mainly to the lungs
66
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
67
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
68
Q

What is useful to assess the mass/burdern of a germ cell tumor?

A

High lactate DH

69
Q

Which biomarker is elevated with a Yolk Sac Tumor?

Which biomarker is elevated with a Choriocarcinoma?

A
  1. AFP
  2. HCG
70
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.

71
Q

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

A

Leydig Cell Tumors

72
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)
73
Q

What is characteristic of cytoplasm of Leydig cell tumors

A

Crystalloids of Reinke rods

74
Q

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

A

Testicular lymphoma (non-Hodgkin lymphoma)

75
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

76
Q

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

A

CNS

77
Q

In which anatomic zone of the prostate do most hyperplasias arise?

Where do most carcinomas arise?

A
  • Hyperplasias: transitional zone (TZ)
  • Carcinomas: peripheral zone (PZ)
78
Q

Bacterial prostatis can be acute or chronic.

What is the most common bacteria?

A
  • 1. E.coli
  • 2. Gram (-) rods
    1. Enterococcus spp.
    1. Staphylococci
79
Q
  • How does acute bacterial prostatitis present clinically (sx’s)?
  • Diagnosed how?
A
  • Fever + chills + dysuria
  • Dx: urine culture
80
Q

Chronic bacterial prostatitis may present with what sx’s?

Pts often have a hx of what?

A

- Low back pain+ Dysuria + Suprapubic/perineal discomfort

  • May also be asymptomatic
  • Often have a hx of recurrent UTI’s (cystitis, urethritis)
81
Q

Diagnosis of chronic bacterial prostatitis is made how?

A

- (+) leukocytosis in prostatic secretions

  • (+) bacterial cultures
82
Q

What is the most common type of prostatitis?

A

Chronic abacterial prostatitis

83
Q

How does chronic abacterial prostatitis differ from chronic bacterial prostatitis based off of history and cultures?

A

No hx of recurrent UTI’s

  • (+) leukocytosis of prostatic secretions w/ negative bacterial cultures
84
Q

What is the most common cause of Granulomatous Prostatitis seen in the US?

Fungal granulomatous prostatitis seen in whom?

A
  • Instillation of BCG (attenuated mycobacterial strain) for tx of superficial bladder cancer
  • Fungal causes is typically only seen in immunocompromised pts
85
Q

Which method of diagnosis for men w/ sx’s of acute or chronic bacterial prostatitis is contraindicated as it may lead to sepsis?

A

Biopsy

86
Q

BPH is characterized by proliferation of ________.

What hormone is responsible?

A
  • Benign stromal and glandular elements
  • DHT
    *
87
Q

BPH originates almost exclusively where?

A

Inner periurethral (transition zone), making nodules that compress the prostatic urethra.

88
Q

Nodules in BPH exhibit what?

Hyperplastic glands are lined by what?

A
  • Diff amounts of stroma and glands.
  • 2 cell layers: inner columnar layer and outer layer made up of flattened basal cells
89
Q

What is the major clinical problem in those with BPH?

A

urinary obstruction

90
Q

is BPH pre-neoplastic?

A

no

91
Q

The inability to empty the bladder in BPH causes an increased risk for?

A

Infections

92
Q

Can diagnosis of BPH be made with a needle biopsy?

A

No, biopsies are too small and do not usually sample the TZ

93
Q

What is the most common form of cancer in men?

A

Adenocarcinoma of the Prostate

94
Q

Cancer of the prostate is typically a disease in men of what age?

Which race has a high incidence of prostate cancer and which race has a low incidence?

A

Older than 50 yo –> 65-75 yo

Most frequently in blacks

  • Uncommon in Asians
95
Q

What are the most commonly acquired genetic lesions in prostatic carcinomas?

A
  • 1. TPRSS2-ETS fusion gene
    1. Mutations or deletions that activate PI3K/AKT signaling
96
Q

Prostate cancer arises most commonly where?

A

Outer peripheral gland and can be palpated by rectal exam

97
Q

Where does lymphatic spread and hematogenous spread of prostate cancer go?

A
  • Lymphatic —> Obturator nodes and then para-aortic
  • Hematogenous –> Axial skeleton
98
Q

What are the 2 best prognostic predictors for prostate cancer?

A

Grade via the Gleason system; correalted with stage and prognosis.

99
Q

Which factors indicate that prostatic intraepithelial neoplasia (PIN) is a precursor lesion for prostate cancer?

Is PIN considered CIS?

A
  • Both PIN and cancer predominate in peripheral zone and are uncommon in other zones
  • Prostate cancers have high frequency of PIN
  • Share many of the molecular changes

*NOT considered CIS!*

100
Q

What maintains growth and survival aof prostate cells?

What may set te stage for development of prostate cancer?

A

Androgens

Inflammation

101
Q

Which histological finding on biopsy is specific for prostate cancer?

A

Perineural invasion

102
Q
  • DRE and detection of PSA levels are useful in detection of prostate cancer, but lack what 2 things?
A

Sensitivity and specificity

103
Q

The real value of PSA for prostate cancer comes in its utility for assessing what?

A

PSA = best for monitoring response to therapy

104
Q

Which 2 additional genetic markers have increased sensitivity and specificity of detecting prostate cancer compared to just PSA alone?

A

Screen urine for:

  • 1) PCA3 = noncoding RNA overexpressed in 95% of pts
  • 2) TMPRSS2-ERG fusion DNA
105
Q

What is the most common treatment for clinically localized prostate cancer?

A

Radical prostatectomy

106
Q

What typifies advanced prostate cancer?

A

Bony metases, often osteoblastic.

CPR Exam 2 (29 decks)

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