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RGU 3 > Pathology of the Prostate Gland > Flashcards

Pathology of the Prostate Gland Flashcards

1
Q

What is the prostate?

A
  • small, round organ that lies at the base of the bladder encircling the urethra.
  • sits anterior to the rectum; posterior aspect of prostate is palpable by digital rectal exam (DRE).
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2
Q

What does the prostate consist of?

A
  • glands= composed of an inner layer of luminal cells and an outer layer of basal cells.
  • stroma= connective tissue, maintained by androgens (glands are also maintained by androgens).
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3
Q

What do the glands of the prostate secrete?

A
  • alkaline, milky fluid that is added to sperm and seminal vesicle fluid to make semen.
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4
Q

*** What is ACUTE prostatitis?

A
  • acute inflammation of the prostate usually due to bacteria
  • Chlamydia trachomatis and Neisseria gonorrhoeae are common causes in YOUNG adults.
  • Escherichia coli and Pseudomonas are common causes in OLDER adults.
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5
Q

*** How do patients with ACUTE prostatitis present?

A
  • pain on urination (dysuria) with fever and chills.
  • prostate is TENDER and BOGGY on rectal exam.
  • prostatic secretions show WBCs and culture reveals bacteria.
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6
Q

*** How does CHRONIC prostatitis it differ from acute prostatitis?

A
  • chronic inflammation of the prostate that presents as dysuria with pelvic or low back pain. More vague.
  • prostatic secretions show WBCs, but cultures are NEGATIVE.
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7
Q

*** What is Benign Prostatic Hyperplasia (BPH)?

A
  • age-related (usually by age 60) hyperplasia of prostatic stroma and glands; specifically in the PERIURETHRAL ZONE. Driven by androgens.
  • NO increased risk for cancer :)
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8
Q

** How is BPH related to DHT?

A
  • testosterone is converted to DHT by 5 alpha-reductase in stromal cells. This DHT then acts on the androgen receptor of STROMAL cells (increasing proliferation) and EPITHELIAL cells (decreasing death), resulting in hyperplastic nodules.
  • FGF-7 is a growth factor involved.
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9
Q

*** What are the clinical features of BPH?

A
  • problems starting and stopping urine stream.
  • impaired bladder emptying with increased risk for infection and hydronephrosis.
  • dribbling
  • hypertrophy of bladder wall smooth muscle; increased risk for bladder diverticula.
  • microscopic hematuria
  • prostate-specific antigen (PSA) is often slightly elevated (usually less than 10 ng/mL) due to the increaed number of glands; PSA is made by prostatic glands and liquefies semen.
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10
Q

*** What is a normal PSA?

A
  • 0-4 ng/mL
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11
Q

What treatment options are available for BPH?

A
  • alpha 1-antagonist (terazosin) to relax smooth muscle in bladder and blood vessels (helps with HTN).
  • selective alpha 1A-antagonist (tamulosin) in normotensive individuals.
  • 5 alpha-reductase inhibitor to block converstino of testosterone to DHT. Takes months to produce results, but also useful for male pattern baldness.
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12
Q

What are the side effects of 5 alpha-reductase inhibitors?

A
  • gynecomastia and sexual dysfunction.
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13
Q

*** What is prostate adenocarcinoma?

A
  • malignant proliferation of prostatic glands.

* has wide rang of clinical types from very aggressive to clinically insignificant.

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14
Q

** What is the most common cancer in men?

A
  • prostate adenocarcinoma

* 2nd most common cause of cancer-related death.

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15
Q

*** What are the risk factors for prostate adenocarcinoma?

A
  • age
  • race (African Americans more than Caucasians, which are both more than Asians).
  • diet high in saturated fats.
  • BRCA2 gene
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16
Q

*** Where do prostatic adenocarcinomas usually arise?

A
  • in the PERIPHERAL, POSTERIOR region of the prostate and hence, does not produce urinary symptoms early on (aka clinically silent).
17
Q

When does screening begin for prostate adenocarcinoma?

A
  • age 50 with DRE and PSA.
  • PSA greater than 10 ng/mL is worrisome at any age.
  • we can also look at decreased % of free-PSA, which is suggestive of cancer bc cancer makes bound-PSA.
18
Q

What is performed to confirm prostate adenocarcinoma if clinical suspicion is high?

A
  • prostatic BIOPSY
19
Q

What will you see on biopsy of prostatic adenocarcinoma?

A
  • small, invasive gland with prominent DARK NUCLEOLI.
20
Q

*** How do we grade prostate cancer?

A
  • GLEASON GRADING system= based on ARCHITECTURE ALONE and NOT nuclear atypia.
  • multiple regions of the tumor are assessed because architecture varies from area to area.
  • 1-5 is assigned for two distinct areas and then added to produce a final score 2-10 (higher score= worse prognosis).
21
Q

*** Where does prostate adenocarcinoma like to spread?

A
  • lumbar spine or pelvis= OSTEOBLASTIC metastases. This presents as low back pain and increased serum ALK PHOS, PSA, and prostatic acid phosphatase (PAP).
22
Q

How do we treat LOCAL prostate adenocarcinoma?

A
  • prostatatectomy

- radiation

23
Q

How do we treat ADVANCED disease of prostate adenocarcinoma?

A
  • continuous GnRH analogs (LEUPROLIDE), which causes negative feedback to shut down the anterior pituitary gonadotrophs (LH and FSH reduced).
  • FLUTAMIDE= androgen receptor inhibitor
24
Q

What is GRANULOMATOUS prostatitis?

A
  • granulomas present in inflamed prostate gland.
  • usually occurs due to installation of BCG in the bladder for treatment of bladder cancer. No need to treat in this case.
  • fungi can also cause this in immunocompromised.
25
Q

What is a prostatic infarct?

A
  • seen mostly in large prostates with nodular hyperplasia.
  • may be caused from infection or indwelling catheters or trauma.
  • grayish yellow semen and streaked with blood.
  • coagulative necrosis
  • most clinically silent, but may cause urinary retention due to edema.
26
Q

Can calculi form in the prostate?

A
  • YES and can cause blood clots or bacteria may be found in some stones.
  • mainly phosphated salts, calcium carbonate, and calcium oxalate.
  • may mimic carcinoma on palpation.
27
Q

*** What is the most common epigenetic alteration in prostate cancer?

A
  • hypermethylation of glutathionine S-transferase (GSTP1), causing it’s down-regulation.
  • GTSP1 prevents a wide range of carcinogens
28
Q

*** What marker tends to be upregulated in prostate cancer?

A
  • AMACR= involved in the beta-oxidation of branched chain amino acids
29
Q

*** Is the outer basal layer seen in benign prostate glands ABSENT in malignant glands?

A

YES

*perineural invasion is another marker of malignancy

30
Q

What is prostatic intraepithelial neoplasia (PIN)?

A
  • architecturally benign glands lined by cytologically atypical cells with prominent nucleoli.
  • divided into low vs high grade based on nuclear and nucleolar changes.
  • also found in peripheral zone.
31
Q

How do we GRADE prostate cancer?

A
  • stage T1= incidentally found
  • stage T2= organ confined center
  • stage T3= extra-prostatic extension
  • stage T4= direct invasion of contiguous organs.
  • N0/N1= presence or absence of node involvement
  • M1= distant metastasis
32
Q

*** What is important to remember about PSA?

A
  • it is organ specific but NOT cancer specific.

RGU 3 (19 decks)

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