Endocrine Related Cancer: Prostate Flashcards

1
Q

how many men show incidence of benign prostatic hyperplasia (BPH)?

A

70% of men > 50 and prob. 100% of men >80

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2
Q

what is the pathological description of pT2 on the Gleasons scores?

A

Tumor confined to the prostate

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3
Q

what is the pathological description of pT2a on the Gleasons scores?

A

Tumor affects one-half of one lobe or less

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4
Q

what is the pathological description of pT2b on the Gleasons scores?

A

Tumor affects more than one-half of one lobe but not both lobes

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5
Q

what is the pathological description of pT2c on the Gleasons scores?

A

Tumor affects both lobes

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6
Q

what is the pathological description of pT3 on the Gleasons scores?

A

Tumor extends beyond the prostate

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7
Q

what is the pathological description of pT3a on the Gleasons scores?

A

Tumor extends beyond the prostate

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8
Q

what is the pathological description of pT3b on the Gleasons scores?

A

Tumor invades seminal vesicle(s)

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9
Q

what is the pathological description of pT4 on the Gleasons scores?

A

Tumor invades the bladder, rectum

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10
Q

what is the link between fat and prostate cancer?

A

strong association but no specific fat components identified.

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11
Q

what is the link between fibre and prostate cancer?

A

decreased fibre in diet associated with prostate cancer.

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12
Q

what is the link between phytoestrogens and prostate cancer?

A

very high in oriental diet. May disturb androgen-oestrogen balance

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13
Q

what are the risk factors associated with prostate cancer?

A

fat

fibre

phytoestrogens

oestrogens

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14
Q

what is the prostate highly dependent on?

A

androgen

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15
Q

which is more important in the mechanism of disease - testosterone or dihydrotestosterone?

A

Dihydrotestosterone

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16
Q

how is testosterone converted to dihydrotestosterone?

A

Conversion (via 5a-reductase) occurs in prostate –> maintenance & growth of glandular epithelium.

17
Q

how are the effects of dihydrotestosterone and testosterone mediated?

A

androgen receptors

Also a ligand-dependent transcription factor

18
Q

how can prostate cancer progress to hormone independent form?

A

mutation of androgen rec. (AR) gene –>
responds to other steroids or to growth factors or cytokines;
amplification of rec. or cofactors;

or bypass of AR pathway.

19
Q

what is the treatment for prostate cancer?

A
  • Prevention/early management (BPH): finasteride (antiandrogens); vitamin E/Se supplements
  • Early stages may respond to local treatment e.g., radiation therapy, surgery (prostate reduction)
  • Removal of androgens induces apoptosis in epithelium –> involution of tissue. Effective even in metastatic stage.
20
Q

how is removal of androgens achieved?

A

Castration - radical & now rel. uncommon in UK & USA.

Inhibition of 5DHT reductase e.g. by finasteride.

GnRH (ant)agonists to reduce LH & FSH & hence T and thus DHT.

Cyproterone acetate: both anti-androgenic in prostate & inhibits LH release.

Combination of local anti-androgen with anti-GnRH treatment seems promising.

21
Q

what happens if prostate cancer is further advanced?

A

chemo/radiotherapy required

22
Q

what is prostate-specific antigen used for?

A

marker for progress of the disease

23
Q

what level is the threshold indicator of disease?

A

4ng/ml