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Pathology Post Midterm > Module 4: Male Genital Pathologies > Flashcards

Module 4: Male Genital Pathologies Flashcards

1
Q

Starting off with male pathology, what is prostatitis?

A
  • -Dysuria, frequency and urgency
  • -low back/pelvic or genital pain
  • -loss of sex drive
  • –painful erections/ejaculation
  • -DRE= enlarged tender prostate
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2
Q

Moving on to Benign Prostate Hyperplasia, what is the etiology?

A

Most commonly seen in older men
Etiology: Testosterone —- DHT by 5 alpha reductase causes hyperplasia of stroma and glands
–affects central/periurethral and transitional zones
—does NOT affect peripheral zone (prostate cancer) only

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3
Q

What are the pre-disposing factors to BPH?

A

Testosterone
Age
–importantly not seen in castrated men

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4
Q

Describe the cut section seen on lab slide 2 of BPH as well as histology

A

Nodular on cut section
–compresses urethra into a slit
Hyperplasia of stoma and glands (tortuous-distended/dilated) due to proliferation
–see two layers: inner columnar and outer basal flat cells

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5
Q

What do patients who have BPH present with?

A 
Increased frequency of urination 
Increased urgency 
Nocturia 
Intermittency 
Hesitancy 
Slow flow 
Terminal Dribbling 
Compression of urethra to a slit ---- presents with difficulty starting/stopping urination, frequency/dribbling, nocturia and dysuria
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6
Q

On DRE examination what do you find in patients with BPH?

A

Normal: dont feel anything
–uniform enlargement, firm, smooth and non tender (NOT NODULAR)
(remember that cancer is hard and nodular) and infection would be soft

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7
Q

What are the complications of BPH?

A

Back up of urine — bilateral hydroureters/hydronephrosis — chronic renal failure —- increased serum calcium —- recurrent kidney and bladder stones/infections
–Trabeculae (diverticuli in the bladder) due to chronic urinary retention
BPH can indirectly lead to bladder cancer :stones can lead to squamous and diverticulum can lead to adeno

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8
Q

Does BPH transition to cancer?

A

nope never
–patients die from obstructive complications
(again can indirectly lead to bladder cancer)

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9
Q

What is the treatment for BPH?

A

TURP: transurethral resection of prostate – may lead to impotence
5 alpha reductase inhibitors

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10
Q

Next is adenocarcinoma of the prostate, what are some features?

A

Most common cancer in men
2nd most common cancer related COD in men
men greater than 50 years old

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11
Q

What are the pre-disposing factors for prostate cancer?

A

Genetics (KRAS)
Age (over 65)
Blacks (not common in whites or asians)
High fat diet

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12
Q

How does prostate cancer arise?

A

Arises de novo due to increased sensitivity to dihydrotestosterone – not caused by BPH

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13
Q

Prostate cancer affects which part of the prostate?

A

Peripheral zone – presents later b/c further away from the urethra and metastasis to CNS via plexus of Batson (Causes back pain)

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14
Q

What is the presentation of prostate cancer?

A

50% are asymptomatic

  • -microscopic hematuria, lower back pain due to osteoblastic (bone forming) lesions (not lytic), weight loss, urinary symptoms
  • -urethra obstruction
  • -spread by the time they present though (pulmonary symptoms, neuro symptoms and bone pain)
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15
Q

What is felt on DRE in a patient with prostate cancer?

A 
Hard 
Nodular 
Irregular 
Non tender 
(remember prostatitis is tender)
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16
Q

What is seen on transrectal biopsy in patients with Prostate Cancer?

A

Malignant glands back to back with little stroma - lined by single layer of cuboidal epithelial cells with atypica

  • -columnar — cuboidal with atypica and no basal flat cells
  • -positive for cytokeratin
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17
Q

When should men start getting DRE for screening of both prostate and BPH?

A

over 50

18
Q

What is the treatment for prostate cancer?

A

Radical prostatectomy, radiotherapy, hormonal therapy, cryosurgery

19
Q

What are the complications of prostate cancer?

A

Mets
lymph — blood – liver, lungs, brain, bones
Urethra obstruction problems (Stricture)
–infection, etc.

20
Q

Finally what is the Gleason grading for prostate cancer?

A

Gleason grading:
grade 1 = well differentiated (good)
Grade 5 = poorly differentiated (Bad)
looks at the architecture but remember staging is always better!

21
Q

PSH is organ, not cancer specific, antigen. What conditions is it falsely increased levels in?

A 
Cancer 
BPH
Prostatitis, infection 
Ejaculation 
Extensive Exercise
22
Q

What is the normal PSH range?

A

less than 4ng/ml

greater than 10ng/ml = high

23
Q

PSH results do not provide diagnosis, describe the free PSA, PSA density and PSA velocity

A

Low percent free PSA (less than 10%) = 50% risk of prostate cancer
–biopsy would be recommended
PAS density (PSAd) = not as accurate as fPSA
–greater than 0.125 = 80% likelihood of detecting caner
PSA velocity= change in serum PSA over time
–high degree of suspicion when the serum PSA increases to greater than 0.75ng/ml/yr

24
Q

Moving on to Cryptorchidism, first describe spermatogenesis in the seminiferous tubules

A

Spermatogenesis: sperm cells mature as they migrate towards the center of the lumen
–spermatogonia — spermatocytes — spermatids (in the middle)

25
Q

What is between two seminiferous tubules?

A

Basement membrane

–interstitial cells of Leydig (make testosterone under the influence of LH)

26
Q

What are the job of sertoli cells?

A

maintain the blood-testes barrier and support spermatogenesis (Secrete inhibin under the influence of FSH)

27
Q

What is the path of sperm? Hint SEVEN UP

A 
SEVEN UP
Seminiferous Tubules 
Epididymis 
Vas Deferens 
Ejaculatory Duct 
Nothing 
Urethra 
Penis
28
Q

So now that the basic pathology of the seminiferous tubules is known,what is cryptorchidism?

A

Undescended testes; usually unilateral (on right side)

29
Q

What are some general features of cryptorchidism?

A

Most common location: upper scrotal (more common), inguinal canal and abdominal (most dangerous)

  • -usually descend in the first year of life
  • -higher you go up the more likely the patient is to get cancer
30
Q

When would you do an orchiopexy (Fixation of the tests in the scrotum) on a patient?

A

Age 2: to reduce infertility

Age 5: reduce testicular cancer/germ cell tumors

31
Q

What do you see on histology for a patient with cryptorchidism?

A

Atrophied seminiferous tubules due to increased temperature outside of the scrotum — affects sertoli cells — no spermatogenesis

  • -hyperplasia of Leydig cells due to atrophy of seminiferous tubules
  • -similar histology is seen with atherosclerotic narrowing of testicular artery
32
Q

What is seen on hormone profile in patient with cryptorchidism?

A

LH and testosterone are both normal because Leydig cells are unaffected

  • -but still infertile because no sertoli cells
  • -decreased inhibin and increased FSH because sertoli cells are affected
33
Q

What are complications of cryptorchidism?

A 
Infertility 
Testicular Cancer (increases as you go higher) -- germ cell tumors
34
Q

Explain very briefly what epididymo-orchitis is?

A

Purulent urethral discharge with swollen/tender testes
–Etiology varies with age: children is gram negative bacilli; less than 35 years old STD and greater than 35 years old is UTI

35
Q

What are the three reasons for male infertility?

A

Pre-testicular: hypopituitarism, estrogen excess
Testicular: agonadism, atrophy, germ cell aplasia and maturation arrest
Post-Testicular: bilateral obstruction, infections, and immotile cilia syndrome

36
Q

What is a hematocele?

A

Blood in tunica vaginalis due to trauma

37
Q

What is a hydrocele?

A

Accumulation of fluid in the tunica

38
Q

What is a chylocele?

A

Accumulation of lymph in the tunica

39
Q

What is varicocele?

A

Dilatation of congested blood vessels in spermatic cord

40
Q

What is spermatocele?

A

Dilation of epididymis with semen (Sperm)

41
Q

What is the major risk factor for scrotal carcinoma?

A

Chimney sweeps

42
Q

Finally what is seen in the urogential area of men with herpes simplex virus?

A

Painful vesicular perianal lesions (multinucleated syncytial cells with intranuclear inclusion bodies and perinuclear halo)

Pathology Post Midterm (50 decks)

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