Module 4: Male Genital Pathologies Flashcards

(42 cards)

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?

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
What is between two seminiferous tubules?
Basement membrane | --interstitial cells of Leydig (make testosterone under the influence of LH)
26
What are the job of sertoli cells?
maintain the blood-testes barrier and support spermatogenesis (Secrete inhibin under the influence of FSH)
27
What is the path of sperm? Hint SEVEN UP
``` SEVEN UP Seminiferous Tubules Epididymis Vas Deferens Ejaculatory Duct Nothing Urethra Penis ```
28
So now that the basic pathology of the seminiferous tubules is known,what is cryptorchidism?
Undescended testes; usually unilateral (on right side)
29
What are some general features of cryptorchidism?
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
When would you do an orchiopexy (Fixation of the tests in the scrotum) on a patient?
Age 2: to reduce infertility | Age 5: reduce testicular cancer/germ cell tumors
31
What do you see on histology for a patient with cryptorchidism?
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
What is seen on hormone profile in patient with cryptorchidism?
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
What are complications of cryptorchidism?
``` Infertility Testicular Cancer (increases as you go higher) -- germ cell tumors ```
34
Explain very briefly what epididymo-orchitis is?
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
What are the three reasons for male infertility?
Pre-testicular: hypopituitarism, estrogen excess Testicular: agonadism, atrophy, germ cell aplasia and maturation arrest Post-Testicular: bilateral obstruction, infections, and immotile cilia syndrome
36
What is a hematocele?
Blood in tunica vaginalis due to trauma
37
What is a hydrocele?
Accumulation of fluid in the tunica
38
What is a chylocele?
Accumulation of lymph in the tunica
39
What is varicocele?
Dilatation of congested blood vessels in spermatic cord
40
What is spermatocele?
Dilation of epididymis with semen (Sperm)
41
What is the major risk factor for scrotal carcinoma?
Chimney sweeps
42
Finally what is seen in the urogential area of men with herpes simplex virus?
Painful vesicular perianal lesions (multinucleated syncytial cells with intranuclear inclusion bodies and perinuclear halo)