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Flashcards in male GU path Deck (48):
1

hypospadias

urethral opening on the inferior

2

epispadias

(dorsal [superior] urethral opening)
• Less common, but ↑assoc. with other GU anomalies
• Both associated with constriction…UTIs
• almost ALWAYS occurs with extrophy of the bladder!!

3

phimosis

inability to retract the foreskin
• Congenital (normal during infancy, for prepuce and glans to be adherent)
• acquired (recurrent infection in uncircumcised adults males), secondary changes microbiome-type infection
• May lead to paraphimosis (strangulation of venous flow)
o foreskin has become retracted back, and can not longer be pulled back over

4

Patent Urachus

- Failure of urachus to obliterate, giving vesico -umbilical fistula or urachal cyst

5

Extrophy of bladder

- Failure of cloacal membrane development
- occurs at the same time as lower abdominal
- wall formation → bladder connects to surface
- Associated with epispadias of penis
- Requires surgical repair

6

testicular descent

testes appear on urogenital ridge

coelomic cavity evaginates into the scrotal swelling forming the processus vaginalis

testes begin descent into the scrotum through the processes and guided by the gubernaculum

testical mvmt down processus creates the inguinal canal

processus obliterates shortly after birth

7

Hydrocele:

- Communicating hydrocele: the sac that is down in the scrotum continues to communicate w/ the abdomen and fills w/ peritoneal fluid – this communication can be narrow or wide
o as a clinician you can usually reduce the sac created in the scrotum through pushing fluid back into the abdominal cavity through the patent processus vaginalis
o these are common and normal in first 6-12 months of infancy
o present as bulging scrotal enlargement – esp. w/ increased intra-abdominal pressure (w/ valsalva maneuver) → pushes fluid through patent processus vaginalis
o this is usually seen on right hand side – d/t descent of right testicle occurring later

- Noncommunicating hydrocele: Processus vaginalis partially obliterates, but not completely in the middle
o cysts can occur in inguinal canal but don’t communicate w/ abdominal cavity

- A hydrocele must be distinguished from a true testicular mass, and transillumination may help, because the hydrocele will transilluminate but a testicular mass will be opaque.

8

spermatocele

: “Epididymal cyst”
- masses in testes that DO contain sperm
- cyst is painless and filled with fluid – usually doesn’t cause sx, unless there is extravasation of sperm into the surrounding tissues
- no effect on fertility

9

varicocele

- collection of dilated and tortuous veins
- clinically may present w/ sense of heaviness on one side of scrotum
- when palpated fells like “bag of worms”
- presence of varicocele on one side may reduce the fertility of the individual

** note: increases with valsalva maneuver

10

indirect inguinal hernia

occurs more laterally
o majority are indirect
o herniation through internal ring : formed through internal oblique and transversus abdominis
o results from patent processus vaginalis

- clinical features: increased intraabdominal pressure results in increased scrotal size. If there is no vascular compromise there are usually no clinical sx
- when the intestine becomes compromised and not enough O2 is getting to the intestine, can result in reddened scrotum, painful to the touch, and intestine cannot be reduced and pushed back up through inguinal canal d/t being swollen


11

direct inguinal hernia

- Direct hernia: more medial to major vessels
o herniation through external ring: formed by external oblique aponeurosis

- clinical features: increased intraabdominal pressure results in increased scrotal size. If there is no vascular compromise there are usually no clinical sx
- when the intestine becomes compromised and not enough O2 is getting to the intestine, can result in reddened scrotum, painful to the touch, and intestine cannot be reduced and pushed back up through inguinal canal d/t being swollen


12


Balanoposthitis

(balanitis-glans; posthitis- prepuce)
• foreskin (prepuce) AND glans are inflamed together
• Inflammation from poor hygiene in the uncircumcised
• Caused by multiple organisms
• Smegma: accumulation of desquamated epithelial cells, sweat and inflammatory debris
• May lead to phimosis, etc.

13

Condyloma Accuminata:

- Benign sexually transmitted disease of HPV types 6 and 11
- Most often in coronal sulcus and inner surface of prepuce (check under foreskin)
- 2/3 of partners will develop infection
• Condylomata of the meatus and glans tend to have cauliflower morphology (left)
• Condylomata of the shaft tend to be flat (right)
• if remove the lesion – need to know you’re not removing the virus and partner has also been infected
Morphology: papillary architecture w/ koilocytic atypia

14

bowen disease

red or gray plaque on the shaft = CIS of the penis
o must be excised completely w/ clean margins and w/ careful follow up

** pre cancerous CIS of HPV (type 16)
- on exam see erythroplakia and leukoplakia

15

bowenoid papulosis

multiple reddish-tan papules in young adults. Do not go onto invasive SCC
o These NEVER invade – though looks like CIS
o looks like SCC in situ – though dermatologist will recognize the gross pattern of distribution and conclude that it will not be invasive, regress on its own

** DOES NOT EVER INVADE
- CIS lesion of HPV 16
- on exam see multiple papules that regress on their own

16

Invasive Squamous Cell Carcinoma of the penis:

• Rare Tumor in US: < 1% of tumors in males
– 10-20% tumors of males in parts of 3rd world
• Risk factors
– lack of circumcision
– Association with HPV 16 & 18, etc. (About 50% associated with HPV)
– Occurs between ages 40 & 70
– Association with smoking
• Slow-growing, painless tumor that presents late
• Prognosis depends on spread to regional lymph nodes
– Inguinal lymph nodes (-): 66% 5 year survival
– Inguinal lymph nodes (+): 27% 5 year survival

morphology: see squamous pearls!

17


Pearly Penile Papules:

• not HPV/genital wart
• normal variant - cause is unknown
• not sexually transmitted
• appears in 2nd/3rd decade
• no tx necessary
• relatively common – no viral
changes

18

Cryptorchidism:

• The failure of the testicle to descend into the scrotum
– sertoli cells produce MIS (AMH) → causes initial descent of testicle
– most likely d/t imbalance of androgen and improper guidance of testicle
• Two embryologic phases
– Transabdominal: at 6 weeks, Sertoli cells → MIS (Mullerian inhibition substance) → regression female organs. At 9 weeks, Leydig cells produce testosterone → Wolffian duct develops into male genitalia, testis up in lower abdomen. "Differential Growth"
– Inguinal-scrotal (Androgen driven): craniosuspensory ligament dissolves and gubernaculum guides testis into scrotum
• Present in 1% at 1 year; 25% are bilateral
– Associated with Klinefelter syndrome, premature birth and family history
• At risk for: testicular cancer, trauma, torsion and infertility
• Surgical correction is necessary (orchiopexy)
– when identified it has to be corrected: bringing into scrotum or removal

19

Prune Belly Syndrome:

• Abdominal muscle deficiency
• Severe urinary tract abnormalities
• Bilateral cryptorchidism in males

20

testicular torsion


o if this occurs in uterus there are no clinical sx – it may be discolored, or hard
• Color Doppler Ultra sound: see that there is no blood flow present
• Nuclear scan: shows no blood flow – avascular necrosis

Clinical presentation:
• typically presents as scrotal pain in an adolescent male
• true urologic emergency: surgical salvage if within 6-8 hours
• 2/3 rotate medially, 1/3 rotate laterally
• often as it is torsed it moves up in the sac – shorter testicle will be the one that is torsed
• if there is a torsed testicle and ischemia – there is a
breakdown of blood and sperm barrier – immune system
will recognize the germ cells as foreign – thus many will develop infertility b/c antibodies directed against the sperm in affected testicle will also affect the unaffected testicle

Morphology:
• early torsion = dusky red discoloration (left)
• late torsion = shows infarct (right)

21

epididymitis

inflammation of epididymis

• Bacteria
– Young men: gonorrhea, chlamydia, may form abscesses
– Old men: E. coli from urinary tract infections (prostatic obstruction)
• Tuberculosis
– Palpable enlargement in pre-established disease

22

orchitis

inflammation of testicle

• Gram (-) bacteria: part of epididymal involvement
• Syphilis: testis affected first and may spare epididymis
• Mumps: pressure atrophy due to tunica albuginea (very unusual in kids)

Granulomatous (?Autoimmune) Orchitis:
– when male has vasectomy the sperm sometimes can get past the ligation and go into the surrounding tissue → inducing a granulomatous response
– most common cause is secondary to BCG therapy for transitional cell carcinoma of bladder
• usually secondary to infection that is in the epididymis
– may think that it is d/ t a reflux of urine from bladder → epididymis → testicle
• test? do urine cultures!

23

Testicular Dysgenesis Syndrome

- Cryptorchidism
- Hypospadius
- Poor sperm quality

associataed with germ cell tumors: both seminomatous and non-seminomatous

24

abnormal chromosome seen in in GCT?

– Precursor malignant cell develops in fetus and is activated at puberty; called IntraTubular Germ Cell Neoplasia (ITGCN ≡ CIS). These have the abnormal chromosome 12 i(12p) seen in most GCT → progression
• Child is born with germ cell CIS! these carcinoma in situ cells are common in testicles of cryptorchid testes
• classic marker is i(12p) seen in genetic marker of tumors

25

origin of seminomas?

GCT seminoma seen in young men w/ i(12)p mutation

spermatocytic seminoma is seen in older men

origin is spermatagonia

26

origin of embryonal carcinoma (NSGCT)?

origin is primitive germ cells

27

GCT?

Germ Cell Tumors of the Testis (GCT):
• Commonest neoplasm of young adult males; ↑ incidence
• Risk factors
– Abnormal testis: cryptorchidism, prior GCT
– General: family history (linked to KIT and BAK), environmental,
whites > blacks (5:1)
brothers have 8-10 Xs relative risk

pathogenesis:
– Precursor malignant cell develops in fetus and is activated at puberty; called IntraTubular Germ Cell Neoplasia (ITGCN ≡ CIS). These have the abnormal chromosome 12 i(12p) seen in most GCT → progression
• Child is born with germ cell CIS! these carcinoma in situ cells are common in testicles of cryptorchid testes
• classic marker is i(12p) seen in genetic marker of tumors

– Develop along two phenotypic cells lines:
1. Spermatogonia → Seminoma
2. Primitive germ cells → Embryonal carcinoma → differentiation

65% have serum markers (HCG, LDH, αFP)
– elevated HCG = mixed tumor

Clinical Presentation:
• painless nodule/swelling of one testicle- may be found incidentally
• dull ache or heavy sensation in the lower abdomen
• pulmonary mets are the most common (other than abdominal LNs)


28

Semioma

most common GCT
• Slow growing; late spread ( 75% stage I at time of diagnosis)

Testicular seminoma originates in the germinal epithelium of the seminiferous tubules.

• Serum markers:
– LDH: nonspecific general marker of tumor burden
– HCG: denotes presence of syncytiotrophoblasts ( ≠ choriocarcinoma)
– AFP: never seen in pure seminoma (must reclassify as NSGCT)

• Staging:
– Good risk – no metastases
– Intermediate risk - metastases

• Treatment:
– Sperm preserved → stage (serum markers, CT) → radical orchiectomy ± retroperitoneal lymph node dissection (? Pre-op info; F/S)
• Low risk: radiotherapy (seminomas are very radiosensitive)
• Intermediate risk: platinum-based chemo (NO high risk category)

Morphology:
• microscopically = fried egg appearance (high power) in nested pattern surrounded by lymphocytes (low power)
• gross: fleshy tan cut surface

29

spermatocytic seminoma

• Rare tumor of men > 65 years, slow growing, non-metastatic
• Important to know only because it looks like seminoma histologically, but is NOT and doesn't behave like one

Morphology:
• microscopically = fried egg appearance (high power) in nested pattern surrounded by lymphocytes (low power)
• gross: fleshy tan cut surface

Testicular seminoma originates in the germinal epithelium of the seminiferous tubules.

30

non-seminomatous germ cell tumors (NSGCT)

• "all the rest" usually referred to as mixed germ cell tumors
• Mixed (≥2 cell types) GCT make up 50-60% of testicular tumors; Pure (1 cell type) make up only 5-10%
• More aggressive than seminoma with worse prognosis
– May have hematogenous spread before lymphatic spread
– Behave according to the sub-types composing the tumor

Differences from seminomas:
- often seen at earlier age of presentation
- more agressive
-decreased 5 year

types:
- embryonal caricnoma
- teratoma
- yolk sac tumor
- choriocarcinoma

31

elevated HCG

most often seen with chorciocarcinoma

though can be seen in 10% of seminomas as well

32

elevated hCG and AFP

embryonal carcinoma

33

elevated AFP

yolk sak tumor

34

teratoma

NSGCT that shows all three germ layers, most chemoresistant which leaves residual tumor after treatment
• rarely pure in men, don’t respond as well to chemo

no elevation of hCG or AFP

35

yolk sac tumor

NSGCT -

endodermal sinus tumor: produces AFP. Most common GCT in children (<3 years)…Schiller-Duval bodies

36

choriocarcinoma

secretes hCG!!!

hemorrhagic, most aggressive, produces HCG, hematogenous spread first
• Risk Classification
– Low risk: confined to testicle, good serum markers
– Intermediate risk: confined to testicle, higher serum markers
– High risk: metastases, very high serum markers
• Treatment: radical orchiectomy, then chemotherapy (?sperm)
• Prognosis(5 year survival):
– Low risk: 90%; Intermediate risk: 80%; high risk: 50%
– respond super well!!!

37

sex cord stromal tumors?

Sex Cord-Stromal (Gonadal) Tumors: just need to know that these exist and are stromal
LEYDIG CELL TUMORS
- Present as testicular masses in younger adults
- Produce sex hormones (Reinke crystals)
- usually androgens (early puberty in boys; asymptomatic adults)
- may produce estrogens: feminization in males
- Most are benign, 10% invasive

SERTOLI CELL TUMOR
- Present as scrotal masses in young adult (1/3 will have gynecomastia); benign


38

TZ

Transition zone: comes into contact with the urethra – this is most important portion in hyperplasia

39

PZ

Peripheral zone: area where most of cancers arise (posterior PZ is most common – can be felt in palpation)

40

prostatitis

- see that PSA levels are REALLY high in these patients

41

Acute Prostatitis:

not very common
- same bacteria as acute ITI's (E. coli, Gm (-) rods, enterococci ...)
- thought to arise from reflux of urine or iatrogenic implant
- present as fever & chills, dysuria; Treat with antibiotics

42


Chronic Bacterial prostatitis

- patients often have history of recurrent UTI's, dysuria, localized pain
- diagnose with PMN's in urine, + culture (same organism as acute)

43

Granulomatous prostatitis:

- most are secondary to ruptured acini (foreign body granuloma)
- commonest known cause is BCG for TCC

44

BPH

Benign Prostatic Hyperplasia: (BPH)
- epidemiology: not completely sure
- both stromal and glandular cells in the transition zone are becoming hyperplastic – significantly androgen dependent – the hormones making BPH are both systemic and local
- Enlargement of prostate in transition zone
- Stromal cells make 5hydroxy-reductase:
o testosterone → DHT → ↑growth factors

Clinical Features:
- poor flow; incomplete emptying
- 2° infection: cystitis, pyelonephritis

RX:
- α-blockers (↓smooth muscle tone)
- 5 α-reductase inhibitors (↓ DHT)
- Tissue destruction - TURP, heat, US, laser ...

Morphology:
- see that near the slit, the abnormal tissue is hyperplastic
- the internal prostatic urethra is narrowed and thinned d/t hyperplasia and growth of benign tissue w/in the prostate
- glans and stroma are both proliferating and look completely benign

45

signs/complications of BPH

Signs/effects of BPH:
- rectal exam may show an enlarged prostate
- hesitancy, nocturia, difficulty urinating
- often will push up into the urinary bladder, when the bladder contracts during micturition the bulging portion of BPH will completely cover the orifice of the urethra and impede the flow of urine through the prostatic urethra
- bladder becomes distended and trabeculated d/t long persistence of BPH
- BPH → prostatitis → sepsis → death

Complications of BPH:
1. obstruction of bladder
- cystitis
- pyelonephritis
- obstructive nephropathy
2. infection of internal genitalia
- prostatitis
- epididymitis
3. Urosepsis

46

ADCA of prostate

- lesion involving prostatic tissue in the periphery of the posterior wall
- Most commonly diagnosed non-cutaneous malignancy in men; 2nd leading cause of cancer death

Risk Factors
o age > 50 years; African American; (+) family member

Pathogenesis
o Androgen dependent
o Multiplicity of genetic mutations (i.e. no established pattern)
o Prostatic Intraepithelial Neoplasm (PIN) is the precursor lesion

Screening (the way most are discovered now)
o Digital Rectal Exam (DRE)
• 70% of tumors arise in posterior lobe- feel thru' rectum
• Nodules, asymmetry, texture
o Prostatic Specific Antigen (PSA) - see next page

Treatment: options include watchful waiting, surgery, radiation
- while prevalence at autopsy is often quite high, less than half of men will have clinical sx (thus they will die with, but not of their cancer)

morphology:
- see glands that are packed together on histology that is very light pink

normal prostat: see + basal layer stain, - racemose

ADCA: see - basal layer, + racemose (marker for ADCA of prostate)

47

PSA

Prostatic Specific Antigen (PSA) – best used for monitoring disease
• There is no single cut-off level that rules in or rules out cancer

– 4 ng/mL is traditional cut-off (50% sensitivity)
Because PSA is organ-specific, but not cancer-specific:

PSA density: ratio of serum PSA to prostate volume
– ↑PSA with size of prostate. Corrects for ↑prostate size with age

PSA velocity: rate of change of PSA over time
– If PSA rises significantly in <18 moths, more likely cancer

Free PSA: PSA from cancer binds more to serum proteins
– The greater the % free PSA, the more likely to be benign

***Recurrence and rising PSA post-treatment means return of neoplasm

48

grading/staging of prostate cancer

Grading: Gleason grading system
• Tumor is classified into one of 5 patterns: 1 is best and 5 is worst
• Commonest pattern and 2nd commonest scores are added together
• Typical score: 3 + 3 =6; Worst score: 5 + 5 = 10
• Lower score correlate with better prognosis

Staging: TNM system
• T score: most important is extracapsular extension
– T2 (confined): 90%; T3: (extracapsular): 40%; T4 (adjacent organs): 10% 5 year
• N score: cure is no longer possible; palliative care
• M score: widespread dissemination, especially bone (osteoblastic)


T1 = no detectable tumor

T2 = confined to prostate

T3 = tumor extends through capsule

T4 = tumor invades adjacent structures


– Treated with androgen deprivation with eventual tumor break-through

More than 90% of treated patients live 15 years
• Highly variable disease with many indolent tumors