Pathoma Male Genital System Pathology 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 inflammation is seen in Lymphogranuloma venereum?

A

Vesicle at site ofinfection ulcers and has purulent exudate.

base will have granulomatous inflammation
-> both suppurative and granulomatous inflammation

Swollen inguinal, pelvic, and rectal nodes will be seen

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3
Q

What is PeIN and what causes it?

A

Penile intraepithelial neoplasia

  • > precursor lesion of invasive squamous cell carcinoma
  • > usually associated with HPV 16
  • > also associated with a lack of circumcision - foreskin acts as a nidus for inflammation / irritation
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4
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 -> think of it being on the side like how hairy oral leukoplakia is on the side of the tongue

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

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5
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-“oid”

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

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6
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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7
Q

When should orchiplexy be done for cryptorchidism 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 chances of fertility, and risk of seminoma is higher in an undescended testes.

Undescended testes = higher risk of infertility / atrophy.

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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8
Q

What is the DDx of granulomas in the testes?

A
  1. TB - necrotizing granulomas

2. Autoimmune orchitis - nonnecrotizing granulomas

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9
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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10
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

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11
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 (nut-cracker). Also blocked by thrombosis in left-sided RCC.

Common complication: infertility (due to increased temperature)

Feels like “a bag of worms”

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12
Q

What causes congenital hydrocele vs acquired hydrocele?

A

Congenital:
Incomplete obliteration of processus vaginalis, most resolving spontaneously by 1 year

Acquired: (adults)
Fluid collection in tunica vaginalis due to infection, trauma, or tumor -> blockage of lymphatic drainage.

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13
Q

How should you biopsy a testicular mass?

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

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14
Q

What is the most common testicular tumor overall and who tends to get it?

A

Seminoma

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

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15
Q

How does seminoma appear grossly? Tumor marker?

A

Homogenous, lobulated gray-white mass with no hemorrhage or necrosis.

Placental alkaline phosphatase (Placental ALP) is a common tumor marker

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16
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

Contrast this to non-seminoma germ cell tumors which all have a poorer response and often metastasize early.

17
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

18
Q

What are embryonal carcinomas commonly mixed with / how does this affect their markers which are elevated in serum? Do they remain static with chemotherapy?

A

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.

With chemotherapy, since they are primitive fetal cells, they can actually differentiate into other germ cell structures i.e. teratomas, so don’t be surprised by this.

19
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).

20
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. (no villi)

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)

21
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

22
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
-> mature ones in children can be benign

23
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)

24
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

25
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)
26
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, usually bilateral
27
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

28
Q

What symptoms characterize prostatitis?

A

Dysuria, fever, and chills.

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

29
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.

30
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 (despite being hyperplasia)

31
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)

32
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

33
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 -> osteoBLAST metastasis which presents as lower back pain.

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

34
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.

35
Q

What is the growth pattern of prostate adenocarcinoma?

A

Small, invasive glands with PROMINENT NUCLEOLI Basal cell layer is lost.

36
Q

Is nuclear atypia considered in the Gleason grading system?

A

No, only glandular architecture -> very high yield to know for the purposes of board examinations

37
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.

38
Q

What are some anti-androgens used in prostate cancer?

A

Leuprolide - continuous GnRH analog

Flutamide - competitive inhibitor at the androgen receptor
Flutes are anti-manly