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Robbins et al. > 21 Lower Urinary Tract and Male Genital System > Flashcards

21 Lower Urinary Tract and Male Genital System Flashcards

1
Q

What are the four zones of the prostate?

A

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

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2
Q

From which zone do the most hyperplasias arise?

A

Transitional zone

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3
Q

From which zone do the most carcinomas arise?

A

Peripheral zone

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4
Q

What are the two histological layers of the prostate gland?

A

1) Basal layer

2) Columnar secretory cells

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5
Q

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

A

Testicular androgens; castration results in atrophy caused by widespread apoptosis

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6
Q

Classify types of prostatitis

A

Acute
Chronic bacterial
Chronic abacterial
Granulomatous

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7
Q

What are the typical sources for acute prostatitis?

A

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

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8
Q

What are the typical organisms of acute prostatitis?

A

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

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9
Q

What is the pathogenesis of chronic bacterial prostatitis?

A
  • 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
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10
Q

What is the most common form of prostatitis?

A

Chronic abacterial prostatitis

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11
Q

What are causes of granulmoatous prostatitis?

A

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

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12
Q

What is the main androgen active in the prostate?

A

Dihydrotestosterone

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13
Q

What is the mechanism for benign prostatic hyperplasia?

A
  • 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
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14
Q

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

A
  • 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
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15
Q

What is median lobe hypertrophy

A

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

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16
Q

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

A
  • 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
Q

What are the main therapies used for BPH?

A

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

18
Q

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

A

50s - 20%

70-80 - 70%

19
Q

What are risk factors for prostate cancer?

A

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

20
Q

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

A
  • 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
Q

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

A
  • increased invasiveness, possible through matrix metalloproteinases
  • morphologic features
22
Q

What are some of the molecular characteristics of prostate carcinoma?

A
  • 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
Q

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

A

Prostate adenocarcinoma, acinar variant

24
Q

Where does prostate carcinoma usually spread?

A

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

25
Q

Name benign mimics of prostatic carcinoma.

A 
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
Q

Name prostatic carcinomas which mimic benign lesions.

A

Atrophic cancer
Foamy cancer
Pseudohyperplastic cancer

27
Q

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

A
  • 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
Q

What are the most common subtypes of acinar adenocarcinoma?

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

Robbins et al. (4 decks)

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