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Pathophysiology - Endocrine and Reproductive > Diseases of the Male Genital Tract > Flashcards

Diseases of the Male Genital Tract Flashcards

1
Q

What is hypospadias and what condition is it associated with? Is it more or less common than epispadias?

A

Abnormal opening of penile urethra on ventral (downward) surface of penis due to failure of urethral folds to fuse.

Associated with poorly developed penis which is hook shaped (chordee) + inguinal hernia + cryptorchidism.

More common than epispadias

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2
Q

What is epispadias and what condition is it associated with?

A

Abnormal opening of penile urethra on dorsal surface of penis due to faulty growth of the genital tubercle downward instead of upwards.

Associated with exstrophy of the bladder -> bladder sticks out through abdominal wall

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3
Q

What is phimosis and what can cause it?

A

Condition in which orifice of the prepuce (foreskin) is too small so the gland penis cannot push through it
-> may be due to a primary developmental defect or occur secondary to inflammation

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4
Q

What is balanoposthitis and how can it be prevented?

A

Infection of glans penis + prepuce
-> can be prevented with circumcision, since it is generally due to poor local hygiene in uncircumcised penis getting infected

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5
Q

What is Peyronie disease and what is it caused by? Symptoms?

A

“Bent penis” caused by fibroblast proliferation forming fibrous bands within the corpus cavernosa
-> penile curvature with pain during intercourse, may need surgical correction

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6
Q

What is acanthosis / hyperkeratosis and when might they be seen on the penis?

A

Hyperkeratosis - increased thickness of the stratum corneum

Acanthosis - Increased epidermal thickness due to epidermal hyperplasia (increased spinosum thickness)

Can be seen in condyloma acuminatum in HPV types 6&11

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7
Q

What is PeIN and what causes it?

A

Penile intraepithelial neoplasia

  • > precursor lesion of invasive squamous cell carcinoma
  • > usually associated with HPV 16
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8
Q

What is Bowen disease vs erythroplasia of Queyrat?

A

Both are forms of squamous cell carcinoma in situ

Bowen disease - occurs on penile shaft or scrotum and appears as leukoplakia

erythroplasia of Queyrat - occurs on glands penis as shiny red or velvety plaques

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9
Q

What is Bowenoid papulosis and how is it different from Bowen disease?

A

Bowenoid papulosis is SqCC in situ which occurs in younger patients (<40 years) and presents as multiple pigmented reddish papules.
-> will NOT progress to invasive carcinoma

Bowen disease - happens in older patients, more frequently progresses to invasion

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10
Q

What can be done to prevent squamous cell carcinoma of the penis?

A

Circumcision is protective. Also, getting the HPV vaccine since most are related to HPV

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11
Q

What are the tunica vaginalis and tunica albuginea?

A

Tunica vaginalis - embryonic remnant of peritoneum which covers most of the anterior and lateral surfaces of the testes, but typically not the back

Tunica albuginea - white, smooth fibrous capsule wrapping around the testicle

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12
Q

What is the function of the Sertoli cells in development of male gonads?

A

In addition to nourishing the developing sperm, they also secrete Mullerian inhibiting factor (MIF) which suppresses formation of the Mullerian duct (paramesonephric duct, which develops female internal structures)

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13
Q

What controls the descent of the testes / what are the two phases? What happens if this fails and where does this usually occur?

A
  1. Transabdominal phase - controlled by Mullerian-inhibiting factor of Sertoli cells
  2. Inguinoscrotal phase - through inguinal canal, controlled by androgens

If this fails -> Cryptorchidism. Usually the testes are found in the inguinal canal.

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14
Q

Can cryptorchidism be bilateral? What will the tubules look like on histology?

A

Bilateral about 25% of the time

On histology -> Sertoli cells in tubules with thickened basic membrane, but no germ cells are seen. Associated with testicular atrophy and infertility

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15
Q

When should orchiplexy be done and why? If cryptorchidism is unilateral, is the other testicle okay?

A

Should be done around 6 to 12 months of age since it increases changes of fertility, and risk of seminoma is higher in an undescended testes.

Contralateral testis which has descended also has a paucity of germ cells and an increased risk of cancer -> indicates cryptorchidism is a general developmental problem.

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16
Q

What are the two age groups which get testicular torsions and why do they occur (defect?)?

A
  1. Neonates - in utero or shortly after birth, not associated with any developmental abnormality
  2. Adolescents - occur due to bell-clapper abnormality -> tunica vaginalis does not stop posteriorly but entirely wraps around testes, allowing for increase mobility of testicle.

Abnormality is often bilateral and needs to be fixed surgical when one presents

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17
Q

What are the presenting symptoms of testicular torsion and how quickly must it be corrected?

A

Acute, severe pain in testes without any inciting event, as well as absent cremasteric reflex

Must be corrected within 6 hours to preserve fertility

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18
Q

What causes testicular torsion mechanically and how will they appear on histology if not corrected quickly enough?

A

Occurs due to twisting of spermatic cord, strangling blood supply and venous return

Appear as coagulative necrosis if not fixed

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19
Q

Is inflammation of the testis (what is this called?) or epididymis more common? What does syphilis affect first?

A

Inflammation of the epididymis is more common -> it is closer to the inlet tract

Note: inflammation of the testis is called orchitis!

Syphilis tends to cause orchitis before it does epididymitis

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20
Q

What tends to cause orchitis is young adults vs older adults?

A

Young adults - Chlamydia trachomatis, Neisseria gonorrhoeae

Older adults - E. coli and Pseudomonas -> as a result of ascending UTIs

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21
Q

Who does mumps cause orchitis in?

A

Mostly post-pubertal males. It generally does not cause orchitis if it infects children <10 years old.

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22
Q

What is the most common category of all testicular tumors and how does this relate to how we tend to treat testicular tumors? Who tends to get them?

A

Germ cell tumors -> represent 95% of all testicular tumors. These are usually malignant and as a result we tend to resort to radical orchiectomy as empiric treatment

These commonly occur in young men (15-40)

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23
Q

What are the two subgroups of germ cell tumors and what does this mean?

A
  1. Germ cell neoplasia in situ (GCNIS)-derived
    and
  2. non-GCNIS

These are seminoma-like cells (germ cells) with large nuclei, clumped chromatin, and prominent nucleioli along the basememnt membrane of seminiferous tubules. These cells are positive for embryonic stem cell marker OCT3/4

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24
Q

What tumors fall into GCNIS derived?

A
  1. Seminoma
  2. Embryonal carcinoma
  3. Yolk sac tumor
  4. Trophoblastic tumors (i.e. choriocarcinoma)
  5. Teratoma, post-pubertal type
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25
Q

What tumors fall into non-GCNIS derived?

A
  1. Spermatocytic tumor
  2. Prepubertal Yolk sac tumor
  3. Prepubertal teratoma
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26
Q

What is the most common testicular tumor overall, who tends to get it, and what female tumor is it similar to?

A

Seminoma

Tends to occur in men in their 30s, and NEVER occurs in infants

Similar to dysgerminoma in females

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27
Q

How does seminoma appear grossly?

A

Homogenous, lobulated gray-white mass with no hemorrhage or necrosis. Lobules are made via delicate fibrous stroma infiltrated by T cells.

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28
Q

What does a seminoma look like histologically?

A

Comprised of large cells with clear cytoplasm and central nuclei (resembling spermatogonia) -> fried egg appearance.

There may be lymphocytic infiltrate (usually T cells) within the fibrous stroma which separates the irregular lobules

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29
Q

What marker might seminomas rarely express and what is the prognosis?

A

Rarely express beta-HCG because they can contain syncytiotrophoblast cells which produce it

Prognosis is good because it metastasizes late and is highly radiosensitive

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30
Q

How does embryonal carcinoma differ from seminoma grossly and prognostically?

A

It is grossly much more poorly demarcated and punctuated by foci of hemorrhage and/or necrosis, more painful than seminoma.

It is composed of primitive epithelial cells forming sheets, glands, and papillary structures

It has a much worse prognosis than seminoma because it can rapidly hematogenously disseminate

31
Q

What marker do embryonal carcinoma stain positive for, and what are they commonly mixed with / how does this affect their markers which are elevated in serum?

A

EC is positive for CD30

Commonly mixed with yolk sac tumors, so can also cause elevated alpha-fetoprotein (AFP levels)

Also, like seminomas they can have syncytiotrophoblasts and have elevated hCG.

32
Q

What are yolk sac tumors also called and who tends to get them? What is the prognosis in this group?

A

Also called endodermal sinus tumors

Tends to occur in children. It is the most common testicular tumor in children <3 years. In this age group, it is a pre-pubertal YST which is non-GCNIS derived and has an excellent prognosis (pure form of yolk sac tumor).

33
Q

What form of yolk sac tumor appears in adults?

A

GCNIS derived, most commonly mixed with embryonal carcinoma, shitty prognosis.

34
Q

How do yolk sac tumors appear grossly and microscopically?

A

Grossly - yellow, mucinous appearance which is infiltrative

Microscopically - Cuboidal cells in a trabecular network, with Schiller-Duval bodies

35
Q

What are Schiller-Duval bodies? And what marker do YSTs characteristically express?

A 
Central vascular (mesodermal) core surrounded by some cells which looks like which makes it look like a primitive glomerulus
-> "endodermal sinus"

YSTs characteristically express alpha-fetoprotein

36
Q

Are pure choriocarcinomas common? And what is their pattern of infiltration? What cell types make them up?

A

Made of syncytiotrophoblasts and cytotrophoblasts which produce beta-HCG.

Pattern of infiltration is formation of small tumors with rapid hematogenous spread around the body (since trophoblast cells have a tropism towards blood cells)

They are rare in their pure form, tend to be expressed in another form of germ cell tumor (i.e. seminoma, embryonal carcinoma)

37
Q

What symptoms do patients with choriocarcinoma often have and why?

A

Often have symptoms of hyperthyroidism or gynecomastia

-> alpha subunit of hCG is structurally similar to LH, FSH, and TSH

38
Q

What does choriocarcoma look like histologically?

A

Syncytiotrophoblasts - large cells with many irregular hyperchromatic nuclei + abundant eosinophilic cytoplasm (make HCG)

Cytotrophoblasts - polygonal cells with distinct borders, form uniform nuclei

NO chorionic villi will be present

39
Q

What is a teratoma?

A

A tumor composed of elements derived from 2+ germ layers

May be mature or immature, depending on degree of differentiation of elements

40
Q

What would you call it if a squamous cell carcinoma of adenocarcinoma arose within a teratoma? What is the most common tumor to do this?

A

Teratoma with malignant transformation
-> most commonly occurs as rhabdomyosarcoma (beware of this, pathoma says it’s squamous cell carcinoma, but may that’s just for women. Change this card later to reflect the truth)

41
Q

How does the prognosis of prepubertal and postpubertal teratoma differ?

A

Prepubertal - (in children) -> always a MATURE teratoma, non GCNIS-derived = BENIGN

Postpubertal - GCNIS derived, ALL teratomas are malignant, regardless of mature or immature

42
Q

How do teratomas differ between males and females?

A

Females - mature teratomas are often benign, and the distinction between mature / immature is useful

(Adult) Males - whether mature or immature, teratomas are ALWAYS malignant

43
Q

What is a spermatocytic tumor, who tends to get it, and how is it different than a seminoma?

A

Tumor occurring in older patients (>65 years), has morphologically three distinct cell populations.

Difference from seminoma -> NOT GCNIS-derived, virtually no ability to metastasize.

44
Q

How should you biopsy a testicular mass, and in what tumor type does the tumor metastasis looks different than the original tumor?

A

I trick you! You should never biopsy a testicular mass due to risk of tumor spillage
-> standard management is radical orchiectomy on presumption of malignancy

Commonly embryonal carcinoma appears different than original testicular lesion, but can occur in all.

45
Q

How do testicular cancers tend to spread?

A

Seminomas tend to spread via para-aortic lymph nodes before hematogenous.

Non-seminoma GCNIS derived tend to present at a later stage via metastasis with hematogenous routes very early.

46
Q

What are the sex cord stromal tumors and are they common?

A
  1. Leydig cell tumors
  2. Sertoli cell tumors

Keep in mind they are very uncommon, germ cell tumors make up 95% of tumors, so these make up less than 5%

47
Q

How does a Leydig cell tumor present?

A

Produces androgens so:
Prepubertal boys -> presents as precocious puberty
Adults -> Presents as gynecomastia (excess testosterone gets converted to estrogen)

48
Q

What does a Leydig cell tumor look like histologically and grossly?

A

Gross - Golden brown tumor due to high degree of lipid granules + vacuoles for androgen production

-> Appears with areas of vacuolization where lipid is stored + large cells with granular, eosinophilic cytoplasm.

Pathognomonic finding:

Reinke crystals - rod-shaped eosinophilic cytoplasmic inclusions with unknown function

49
Q

What is a Sertoli cell tumor also called? What does it look like microscopically and what is its clinical behavior?

A

Androblastoma

  • > looks like tall columnar cells forming cords -> immature seminiferous tubules
  • > Usually benign and clinically silent (does not produce enough androgen to be significant)
50
Q

What is the most common form of testicular tumor in men over the age of 60 and what is its behavior? Is it a primary tumor?

A

Testicular lymphoma - usually a diffuse B cell lymphoma

  • > very aggressive with a poor prognosis
  • > It is a secondary tumor arising elsewhere
51
Q

How is a solid testicular tumor differentiated from benign scrotal lesions?

A

Benign - lesion can be transilluminated

Tumor mass - mass does not transilluminate

52
Q

What is a hydrocele vs a varicocele?

A

Hydrocele - Fluid collection within the tunica vaginalis

Varicocele - Dilation of spermatic vein within the pampiniform plexus

53
Q

Where do varicoceles tend to arise and what is the complication? What does it feel like on palpation?

A

Tend to arise on the left side due to the left gonadal vein draining into the left renal vein which gets compressed via the SMA on its way to the IVC

Common complication: infertility (due to increased temperature)

Feels like “a bag of worms”

54
Q

What causes congenital hydrocele? When does it get better?

A

Incomplete obliteration of processus vaginalis, which allows communication of tunica vaginalis with the abdominal cavity

Most resolve spontaneously by 1 year

55
Q

What causes hydrocele in adults? What is it called when it’s bloody?

A

Fluid collection in tunica vaginalis due to infection, trauma, or tumor -> blockage of lymphatic drainage.

Bloody = hematocele

56
Q

What zone typically give rise to benign prostatic hyperplasia?

A

Transitional zone -> zone surrounding the urethra, including the middle lobe / periurethral zone

57
Q

What are the cell layers of the prostate gland and why are these important?

A
  1. Inner layer of luminal cells
  2. Outer layer of basal cells

Basal cell layer will be lost in prostate adenocarcinoma -> can be highlighted via immunohistochemical stain

58
Q

What symptoms characterize prostatitis?

A

Dysuria, fever, and chills.

Prostate will be tender and boggy on digital rectal exam (filled with PMNs).

59
Q

What are the causes of acute bacterial prostatitis?

A

Same causes of orchitis - UTI things.

Younger men - Chlamydia and Neisseria

Older men - E. coli, Pseudomonas

60
Q

What causes chronic prostatitis and how will the symptoms differ?

A

May or may not be UTI related, but often cultures of prostatic secretions are negative despite showing lymphocytic inflammatory infiltrate.

More likely to peresent with lower back pain.

61
Q

What is the most common cause of granulomatous prostatitis?

A

BCG treatment of superficial bladder cancer

-> BCG vaccine used as an immunotherapy directly into bladder wall

62
Q

What is the cause of benign prostatic hyperplasia? Will it lead to cancer?

A

An age-related change in androgens -> more testosterone being converted to dihydrotestosterone -> hyperplastic nodules in transitional zone, narrowing urethra

Condition is benign with no increased risk of malignancy

63
Q

What are the symptoms of BPH? What marker will be elevated and what is its function?

A

Increased urinary frequency, nocturia, dysuria, difficulty starting and stopping, dribbling

Prostate-specific antigen (PSA) will be elevated - functions to liquefy semen

64
Q

What are the secondary complications which may occur due to BPH? What can be done to surgically correct this problem?

A

Distention and hypertrophy of bladder (Due to increased resistance), hydronephrosis (due to backflow of urine), recurrent UTIs

Surgically correct with TURP - transurethral resection of the prostate

65
Q

What is the medical management of BPH and how does it work?

A

alpha1-antagonists - terazosin, tamsulosin -> relax vascular smooth muscle to lower blood pressure. Tamsulosin is more selective for bladder (avoids alpha-1b), and should be used in normotensive individuals

5alpha reductase inhibitors - finasteride (not gonna have an ass to ride cuz it causes gynecomastia and sexual dysfunction)

66
Q

What races are more susceptible to prostate adenocarcinoma and what is its relative frequency?

A

Blacks > whites > asians

Most common cancer in men, second most common cause of cancer death

67
Q

Where does prostate cancer arise? Why is this useful?

A

Typically in the peripheral, posterior region of the prostate -> not associated with urinary symptoms early, but may be easily palpable by prostate exam

68
Q

What is the growth pattern of prostate adenocarcinoma?

A

Small, invasive glands with prominent nucleoli. Basal cell layer is lost.

Tends to show perineural invasion

69
Q

What is the most common site of metastasis for prostate cancer and how does this show up on labs?

A

Lumbar spine or pelvis -> osteoblastic metastasis which presents as lower back pain.

Serum alkaline phosphatase will go up (osteoblastic activity marker) as well as prostatic acid phosphatase (PAP)

70
Q

How is the Gleason score calculated and what is the lowest one you can have? How is sampling done?

A

Sampling should be done via multiple needle core biopsy

Grade 1: Normal glandular differnetiation
Grade 5: Ugly as shit solid cell mass

Add together the two most predominant grades to get the gleason score.

Lowest one you can have: Gleason score of 6, assigned to scores 2-5 since urologists basically think that gleason grades 1-2 do not really happen in isolation for diagnosis.

71
Q

What are Gleason groups and what are they used for? What is the most useful prognosticator?

A

Groups of Gleason scores to indicate prognosis. There are groups 1-5 (probs don’t memorize):

Group 1: Score 6
Group 2: Score 7 (3+4)
Group 3: Score 7 (4+3)
Group 4: Score 8
Group 5: Scores 9-10

Most useful prognosticator is the Gleason score associated with the stage

72
Q

What is the PSA tumor marker / how should it be monitored? What is its use in screening?

A

Total PSA will be increased as cancer grows, and % free PSA will be down (cancer secretes PSA bound to protein)

Can be monitored on a patient to patient basis based on doubling time, and is useful as a screen (>10 ng/mL is worrisome at any age). Generally increases with age due to it being age-specific.

73
Q

What is the management of prostate cancer?

A

Generally hormonal treatment with anti-androgens will decrease glandular growth (androgen dependent) until the tumor mutates.

Radical prostatectomy and radiation are also an option.

74
Q

What are some anti-androgens used in prostate cancer?

A

Leuprolide - continuous GnRH analog

Flutamide - competitive inhibitor at the androgen receptor

Pathophysiology - Endocrine and Reproductive (27 decks)

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