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Endocrine and Reproductive Systems > P- Male GU System > Flashcards

P- Male GU System Flashcards

1
Q

What are the 2 congenital anomalies associated with the penis?

A
  1. hypospadias - urethra opens ventrally

2. epispadias- urethra opens dorsally

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2
Q

What is phimosis?
What is the etiology?
What are the sequelae?

A

It is when the orifice of the prepuce [foreskin] is too small to retract over the glans.
It occurs because of inflammatory scarring or anomalous development.

Sequelae:

  1. interfere with hygiene
  2. accumulation of smegma [sebaceous secretion]
  3. infections
  4. carcinoma [not likely]
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3
Q

What is condyloma accuminatum?

What is the likely cause?

A

It is a genital wart most likely caused by HPV 6, 11

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4
Q

What is the likely etiological agent of carcinoma in situ in the penis?
What are the 3 clinical variants of penile CIS?

A

Penile CIS is likely caused by HPV 16

Clinical variants:

  1. Bowen disease
  2. erythroplasia of Queyrat
  3. Bowenoid papulosis
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5
Q

A 60 year old man presents with a scaly erythematous plaque on the penile shaft and scrotum. On histology you note features of squamous cell carcinoma but without invasion. What is the likely diagnosis?

A

Bowen disease

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6
Q

A man presents with a growing red plaque on the glans of his penis. Histology shows what looks like squamous cell carcinoma in situ. What is the likely diagnosis?

A

Erythroplasia of Queyrat

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7
Q

A 30 year old presents with multiple papular lesions on the body of the penis. Histology shows squamous cell CIS. What is the likely diagnosis?

A

Bowenoid papulosis

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8
Q

What is the etiology of penile invasive carcinoma?
What confers protection from getting it?
Who is most likely to get penile carcinoma?
Does it metastasize? If so, where?
What is the prognosis?

A

Penile invasive carcinoma is a squamous cell carcinoma caused by HPV 16, 18.

Circumcision confers protection so the most frequent patient is a 40-70 yr old uncircumcised man.

It metastasizes to the inguinal and iliac lymph nodes

66% 5YSR if confined to penis, 27% if mets

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9
Q

What is testicular torsion?
What is the cause?
What is the treatment?
How does it look grossly and histologically?

A

It is when the spermatic cords twists and leads to hemorrhagic infarction of the testes.

It is caused by trauma and the predisposing factor of increased mobility due to the absence of gubernaculum or atrophy.

Treatment: untwist the cord w/in 6 hours or give orchiectomy

Gross: red, hemorrhagic
Microscopic: coagulative necrosis

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10
Q

What is cryptochidism?
What are the two most important sequelae?
What is treatment?

A

It is when the testes fail to descend into the scrotum.

Sequelae:

  1. atrophy and sterility
  2. 10x increased risk of germ cell tumor development [risk is bilateral even if only one teste is not descended]

Treatment: orchiplexy [drop the balls down and fix them into the scrotum] by 2-3 months to preserve fertility

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11
Q

What type of tumor compose 95% of all testicular tumors? How does this compare to ovarian tumors?

A

Majority of testicular tumors are germ cell tumors.

The majority of ovarian tumors are from surface epithelial cell origin

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12
Q

95% of testicular tumors are germ cell tumors. The other 5% are what?

A
  1. Sex chord tumors - stromal tumors of leydig and sertoli cells
  2. surface epithelium tumors [so rare they basically don’t occur]
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13
Q

What is the most important distinction to make when classifying germ cell tumors of the testes?

A
  1. classic seminoma

2. non-seminomatous germ cell tumors

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14
Q

For a classic seminoma

  1. age of presentation
  2. histology
  3. Rx
  4. serum markers
  5. spread?
  6. stage at presentation
  7. prognosis
A
  1. 30s
  2. pure [not a mixed germ cell tumor] sheets of polygonal cells
  3. orchiectomy or radiotherapy
  4. none
  5. to the lymphatics
  6. low, 70% are in stage 1
  7. 95% cure with stage 1 or 2
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15
Q

What are the 4 types of non-seminomatous germ cell tumors of the testes?

A
  1. embryonal carcinoma
  2. yolk sac tumor [endodermal sinus tumor]
  3. teratoma
  4. choriocarcinoma
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16
Q

For non-seminomatous carcinoma of the testes:

  1. age
  2. histology
  3. treatment
  4. serum markers
  5. spread?
  6. stage at presentation
  7. prognosis
A
  1. infant to 30
  2. mixed
  3. ochiectomy and chemotherapy
  4. choriocarcinoma =hCG, yolk sac = AFP
  5. lymphatics and hematogenous
  6. late, 40% stage 1
  7. 90% with chemo
17
Q

You do histology of a germ cell tumor and note:

  1. sheets of polygonal cells
  2. clear cytoplasm with prominent nucleoli
  3. fibrous bands infiltrated with lymphocytes

There are no glands, keratin pearls, or cartilage. What type of tumor is this suggestive of?

A

Classic Seminona

18
Q

You do histology of a testicular germ cell tumor and note:

  1. pleomorphic epithelioid malignant cells
  2. formation of gland-like structures

What is the likely tumor type?

A

Embryonal carcinoma

19
Q

You do histology of a testicular germ cell tumor and note:

perivascular rosettes of cells [Schiller-Duval bodies]

What is the likely tumor and what is the serum marker?

A

Endodermal sinus tumor [yolk sac] and the serum marker is AFP

20
Q

You do a biopsy of a testicular germ cell tumor and note syncytiotrophoblast surrounding cytotrophoblasts. What serum marker is bound to be elevated and what is the suspected tumor?

A

HCG will be high because this histology is associated with choriocarcinoma

21
Q

What is the likely cause of:

  1. acute bacterial prostatitis
  2. chronic bacterial prostatitis
  3. chronic abacterial prostatitis

Which of the 3 is most common?

A
  1. E. coli
  2. E. coli
  3. culture neg and etiology unknown [possibly chlamydia, ureaplasma]

chronic abacterial prostatitis is the most common

22
Q

How does the pathology of BPH compare to prostate carcinoma?

How does the feeling differ for DRE?

A

BPH is periurethral and symmetrical nodules of hyperplastic glands and/or stroma.

On DRE, you would feel large rubbery symmetrical masses

Carcinoma is peripheral and would feel rock hard on DRE palpation

23
Q

What is the incidence of prostatic nodular hyperplasia [BPH]?
What is the etiology?
What is the chance it progresses to carcinoma?

A

90% of men will have BPH by the age of 70.

It is caused by DHT and estogens

It does NOT progress to carcinoma

24
Q

A patient presents with urinary frequency, nocturia, hesitancy, dribbling and history of UTIs. What is the likely cause and what are possible treatments?

A

BPH

Treatments:

  1. TURP - [transurethral resection of the prostate-scrape a bigger urethra opening]
  2. 5a-reductase inhibitor so testosteroneue can’t go to DHT [finasteride]
  3. a1 adrenergic inhibitor to relax the urethra to open more [doxazosin]
25
Q

What age does prostate carcinoma usually present?

A

Most patients are over 50, but we are seeing more patients in their 40s due to more PSA screenings

26
Q

What are the 3 ways a person with prostate cancer can present?

A
  1. asymptomatic
  2. symptoms similar to BPH [obstructive symptoms like hesitancy, dribbling, nocturia, and frequency
  3. bone pain from the osteoblastic mets
27
Q

You are doing a DRE and note a rock hard, irregular gland for the prostate. What is the concern?
What would you see on ultrasound?

A

Prostate carcinoma and it would be hypoechoic [black] on US

28
Q

What is PSA? What is the normal range?
Why is it not the most useful marker of carcinoma?
What 3 things are used to improve utility for diagnosing prostate carcinoma?

A

PSA is a seirne protease that liquified seminal coagulum
<4 is normal above 10 is bad, but still not 100% specific for carcinoma. Biopsy is necessary for diagnosis prior to therapy

  1. PSA density - PSA/prostate volume on US
  2. PSA velocity- follow it over years to chart changes
  3. Percent free PSA- LOWER percent free with cancer
29
Q

What is the most helpful use of PSA ?

A

To assess response to therapy

ex. after prostatectomy PSA drops to 0, if it rises again it means there is recurrence

30
Q

What are 3 etiologies that increase prostate cancer risk?

A
  1. african american&raquo_space;»asians
  2. 1st degree relatives
  3. fatty diet
31
Q

How does the histology of prostatic carcinoma differ from penile carcinoma?

A

Penile is squamous cell carcinoma

Prostate is adenocarcinoma

32
Q

How does prostate cancer spread? What are the most likely places to find mets?

A

IT spreads lymphatically via pelvic nodes and hematogenously primarily to the skeleton [osteoblastic mets]

33
Q

What is the Gleason system for grading prostate cancers?

A

It looks at architecture and grades it 1- 5 with one looking decently normal and 5 being really bad.
After looking at the histology of your sample, you add the numbers of the 2 most common architectural patterns and get the score. The most common score is 7 [3+4]

34
Q

Describe the pathology of prostatic adenocarcinoma.

A
  1. back-to-back infiltrative gland proliferation
  2. enlarged nucleus with cherry red nucleoli
  3. pink amorphous secretions
  4. nerve invasion in perineural areas
35
Q

What is the treatment for localized prostatic adenocarcinoma?
What is the prognosis?
What are side effects?

A

surgery or radiotherapy each have a 90% 15YSR

side effects are the same for both: impotence, incontinence

Arguement is usually for surgery because if there is recurrence, then radiation can fix it.
If you radiate first, there will be scarring making it difficult to surgically remove recurrence

36
Q

What is the treatment for disseminated prostatic adenocarcinoma?
What is the prognosis?

A

endocrine therapy- 10-40% 10YSR

Tumors are dependent on androgens in early stages so you can use endocrinology to perform “chemical castration”

Orchiectomy- remove main source of androgens

Pharmacological orchiectomy: LHRH agonist + non steroidal anti-androgen

37
Q

What is PIN?

A

Prostatic intraepithelial neoplasia: it is the CIS of the prostate [premalignant lesion]
High grade is seen with basal cell layer remaining but prostatic adenocarcinoma looking cells {large nuclei with cherry red nuceoli etc]

Endocrine and Reproductive Systems (27 decks)

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