call for help from step1 - okt3

[ArchivalUser]

A healthy 52 year-old man is evaluated during a routine physical examination. On rectal examination, he is found to have a nodule on the left apex of his prostate. His prostate specific antigen (PSA) is 6.7 ng/dL. He denies any nocturia, dysuria, hematuria, or urinary hesitancy. The patient undergoes a transrectal ultrasound with biopsy of the prostate gland. The pathology report is consistent with cancer of the prostate.

If this patient ultimately develops metastatic prostate cancer, he may be treated with an agent that cause an initial increase in testosterone ("flare phenomenon").

Such medications work by which of the following mechanisms?

A. Blocking cytochrome P450

B. Blocking testicular androgen production

C. Blocking testosterone at the target tissue level

D. Directly blocking the adrenal gland synthesis of androgens

E. Indirectly suppressing LH and FSH secretion

[ArchivalUser]

eeeeeee

[ArchivalUser]

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[ArchivalUser]

e.

[ArchivalUser]

Thanks for the answer.

E is correct.

[ArchivalUser]

ya e and the agent's name is leuprolide

[ArchivalUser]

leuprolide is the name of the agent used to treat prostate cancer by indirectly suppressing LH n FSH secretion.N given in continous n not in pulsatile fashion.

[ArchivalUser]

CAn you name 2 more as GnRH agonists beside leuprolide?

[ArchivalUser]

nafarelin,buserelin,histrelin,goserelin,deslorelin-google search results

[ArchivalUser]

Good job anuraj_81, google is the best source of info, here is the answer with explanation from kaplan.


The correct answer is E . These medications, known as GnRH agonists (e.g., leuprolide, nafarelin, goserelin, buserelin), work by activating the GnRH receptors in the pituitary gland. This creates an initial increase in the release of LH and FSH, causing an initial increase in testosterone ("flare phenomenon"). With time, there is down-regulation of the pulsatile release of LH and FSH, and ultimately, suppression of LH and FSH due to inhibition of the hypothalamic-pituitary axis. This leads to a decrease in testosterone levels. Castrate levels of testosterone are reached within 30 days.

Cytochrome P-450 (choice A) plays a role in the adrenal and gonadal synthesis of androgens. This can be inhibited by ketoconazole, which can produce castrate levels of testosterone within 8 hours.

Directly inhibiting testicular androgen production (choice B) can be accomplished via bilateral orchiectomy.

The activity of testosterone can be blocked at the tissue level by inhibiting the binding of testosterone and dihydrotestosterone to the intracellular androgen receptors (choice C) . Medications that work via this mechanism are classified as nonsteroidal antiandrogens, e.g., flutamide and bicalutimide.

The only way to directly block the production of androgens from the adrenal gland (choice D) is bilateral adrenalectomy. This is no longer necessary because pharmacological androgen deprivation is now available.


Thanks