21 Lower Urinary Tract and Male Genital System Flashcards Preview

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Flashcards in 21 Lower Urinary Tract and Male Genital System Deck (28):
1

What are the four zones of the prostate?

1) peripheral zone
2) central zone
3) transitional zone
4) region of the anterior fibromuscular stroma

2

From which zone do the most hyperplasias arise?

Transitional zone

3

From which zone do the most carcinomas arise?

Peripheral zone

4

What are the two histological layers of the prostate gland?

1) Basal layer
2) Columnar secretory cells

5

What hormone controls growth and survival of prostatic cells and what occurs in its withdrawal?

Testicular androgens; castration results in atrophy caused by widespread apoptosis

6

Classify types of prostatitis

Acute
Chronic bacterial
Chronic abacterial
Granulomatous

7

What are the typical sources for acute prostatitis?

1) ascending - intraprostatic reflux of urine
2) lymphohematogenous routes from distant foci
3) surgical manipulation of urethra or prostate - catheterisation, cystoscopy, urethal dilation or resection

8

What are the typical organisms of acute prostatitis?

E. coli, Gram negative rods, enterococci and staphylococci; typically similar to UTI

9

What is the pathogenesis of chronic bacterial prostatitis?

-recurrent urinary tract infections by organisms identical to those that cause acute prostatitis
-poor antibiotic penetration of prostate
-bacterial organisms colonise and then seed recurrent infections

10

What is the most common form of prostatitis?

Chronic abacterial prostatitis

11

What are causes of granulmoatous prostatitis?

1) BCG (most common)
2) Fungal (immunocompromised pt)
3) reaction to ruptured prostatic ducts and acini

12

What is the main androgen active in the prostate?

Dihydrotestosterone

13

What is the mechanism for benign prostatic hyperplasia?

- Impaired cell death of epithelial cells
- there is no clear evidence of increased epithelial cellular proliferation
- increased stromal proliferation leading to increased DHT conversion
-DHT binds to nuclear androgen receptors to increase transcription of growth factors and their receptors leading ultimately to stromal growth and impaired epithelial cell death

14

How are stromal cells of the prostate responsible for androgen-dependent prostatic growth?

- only stromal cells contain type 2 5-alpha-reductase which converts testosterone to the more potent dihydrotestosterone (higher receptor affinity, greater ligand-receptor complex stability). (Type 1 5-alpha-reductase is found in the skin and liver.)
- DHT binds nuclear androgen receptor in stromal and epithelial prostate cells
- increased transcription of genes for small growth factors and receptors (DHT is not a direct mitogen)
- these growth factors include: FGF-7, FGF1, FGF2 and TGFbeta
- FGF7 most important

15

What is median lobe hypertrophy

Nodular enlargement projecting into the floor of the urethra as a hemispheric mass beneath the mucosa

16

What is the pathophysiology of benign prostatic hyperplasia to symptoms of prostatism?

- increased size of gland due to increased DHT levels causing impaired epithelial death and stromal proliferation
-smooth muscle-mediated contraction of prostate leads to urethral obstruction
-increased resistance to urinary outflow --> bladder hypertrophy, distention and urinary retention
-increased risk of infection

17

What are the main therapies used for BPH?

Conservative: decreasing evening fluid intake, moderating alcohol and caffeine, timed voiding schedules
Medical: alpha-blockers, 5-alpha reductase inhibitors
Surgical: TURP

18

What are the approximate incidences of prostate cancer in their 50s and then between 70-80?

50s - 20%
70-80 - 70%

19

What are risk factors for prostate cancer?

Non-modifiable: age, race, family history, hormone levels
Environmental: consumption of fats
Protective (putative): lycopenes, selenium, soy products, vitamin D

20

What are the heritable risk factors that play a role in prostate cancer?

- AR gene polymorphism (CAG repeats, short sensitive, long resistant)
- resistance to androgen blockade: AR gene amplification, mutations in AR giving rise to non-androgen ligand binding, activating P13 kinase /AKT signalling
-BRCA2: 20X risk
-locus at 8q24: only increased risk in men of African origin
-tumour-specific:ETS family transcription factor (ERG, ETV1) rearrangements with TMPRSS2 promoter (androgen-sensitive); hypermethylation of GSTP1
-epigenetic changes in tmour suppressor genes: PTEN, RB, p16/INK4a, MLH1, MSH2, APC

21

What are some of the characteristic features of ETS family transcription factor gene rearranged tumours?

-increased invasiveness, possible through matrix metalloproteinases
-morphologic features

22

What are some of the molecular characteristics of prostate carcinoma?

-ETS family transcription factor (ERG, ETV1) rearrangements with TMPRSS2 promoter (androgen-sensitive)
-hypermethylation of GSTP1
-epigenetic changes in tmour suppressor genes: PTEN, RB, p16/INK4a, MLH1, MSH2, APC
-loss of E-cadherin (associated with high EXH2)
-increased AMACR
-increased PCA3

23

What is the actual variant which comprises the most common prostate carcinoma?

Prostate adenocarcinoma, acinar variant

24

Where does prostate carcinoma usually spread?

Local extension: Periprostatic tissue, seminal vesicles, base of urinary bladder
LN: obturatory nodes, then paraaortic nodes
Hematogenous: bones of axial skeleton > femur>ribs

25

Name benign mimics of prostatic carcinoma.

Adenosis (atypical adenomatous hyperplasia)
Atrophy and variants (partial, PAH)
Basal cell hyperplasia
Seminal vesicle / ejaculatory duct epithelium
Mucinous metaplasia
Nephrogenic metaplasia (adenoma)
Cowper’s glands
Paraganglion
Xanthoma

26

Name prostatic carcinomas which mimic benign lesions.

Atrophic cancer
Foamy cancer
Pseudohyperplastic cancer

27

What lines of evidence show the relation between PIN and prostate carcinoma?

-PIN and PCA both predominant in the peripheral zone
-prostates with cancer have higher PIN frequency and extent
-PIN is seen in proximity to PCA
-molecular changes seen in invasive cancers are present in PIN

28

What are the most common subtypes of acinar adenocarcinoma?

Atrophic
Pseudohypertrophic
PIN-like
Stratified/double cell layer
Foamy gland (xantomatous)
With Paneth cell-like differentiation
Oncocytic