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62 Cards in this Set
- Front
- Back
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What are the two types of androgen deprivation therapy |
Medical and surgical |
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Surgical castration consists of what? |
Bilateral ochiectomy |
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What is the recommended treatment for advanced disease with metastatic prostate cancer? |
Bilateral orchiectomy or medical castrastion |
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What is the recommended treatment for advanced disease (PCA) without distant metastasis if the patient is symptomatic? (M0) |
Start androgen deprivation therapy |
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What is the recommended treatment for advanced disease (PCA) without distant metastasis if the patient is not symptomatic? (m0) |
This is not clear. If started early, the risk of death from prostate cancer is decreased, but the risk of death from other causes is slightly increased. Overall survival is similar either way.
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What are two indications to treat asymptomatic advanced disease (PCA) without distant mets? |
psa doubling time less than 12 months or psa great than 50. |
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What is the preferred initial androgen deprivation therapy for advanced prostate cancer? |
medical or surgical castration combined with an antiandrogen |
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Which is more effective: LHRH agonists or bilateral orchiectomy? |
They have the same effectiveness |
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Which is more effective for overall survival: monotherapy with non-steroidal antiandrogens or bilateral orchiectomy? |
bilat orch |
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What are the benefits to intermittent androgen deprivation therapy? |
better sexual function less side effects during "off" periods similar survival
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What PSA value indicates high risk of recurrence after androgen deprivation therapy? |
0.2ng/dl at 8 moths after castrastion is associated with a proportionally higher risk of death |
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What PSA doubling time is associated with a higher risk of death from prostate cancer after curative therapy? |
less than three months |
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Prostate cancer responds to androgen deprivation therapy for what average time period? |
2-3 years (overall duration 3 months to 15 years) |
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Is there a benefit to continuing androgen deprivation therapy after PSA begins to rise? |
Yes, some of the cells will still respond to adt. |
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What if primary therapy is not working for your PCA patient? |
1. Switch to a different antiandrogen flutamide bicalutamide ketoconazole and steroids aminoglutethimide and steroids DES Chemo |
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What is the only 2nd line therapy for prostate cancer that has been shown to improve survival? |
Chemotherapy with docetaxel |
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How is bladder outlet obstruction caused by pCA treated? |
TURP, suprapubic tube, urethral catheter, or urethral stent |
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How is ureteral obstruction caused by PCA treated? |
Ureteral stents, nephrostomy tubes, |
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How is bone Mets pain from PCA treated? |
IV bisphosphonates decrease pain and fracture risk external beam radiation can help for focal mets diffuse mets can be treated with chemo or bone seeking radionucleotides may need ortho surgery to prevent fx |
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What is the most common neurological area affected by prostate cancer mets? |
sacral nerves and caude equina |
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what is the treatment for cauda equina syndrome caused by prostate mets? |
steroids and androgen deprivation by medical or surgical castration MRI of spine Possibly surgical decompression especially if related to loss of bone integrity If ortho tx is not possible then external beam radiation will help |
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What percentage of androgens come from the testicles? |
90-95% comes from the testicles and the rest comes from the adrenal glands in the form of androstenedione and DHEA |
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How does prolactin affect testosterone and prostatic growth? |
Prolactin decreases testosterone by inhibiting GnRH, but it can directly stimulate prostate tissue. |
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What is combined androgen blockade? |
It is the combination of medical or surgical castration with antiandrogen therapy. |
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Which is more effective LHRH agonist or bilateral orchiectomy? |
They are equally effective. |
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What are the types of pharmalogical androgen deprivation therapy? |
Estrogen Progestins LHRH agonism GnRH antagonism Androgen synthesis inhibitors Prolactin antagonists 5-alpha reductase inhibitors Nonsteroidal antiandrogens steroidal antiandrogens |
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What is the mechanism of action of estrogen for ADT? |
Estrogen inhibits the hypothalamic-pituitary axis which decreased LH secretion and therefore decreases testosterone production. |
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What are the side effects of estrogen therapy? |
stroke, dvt, pe, MI, gynecomastia |
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What is the mechanism of action of progestins? |
Prolactin inhibits the hypothalamic-pituitary axis and decreases LH production with decreases testosterone production. |
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Which increases prolactin levels? Progestins or estrogens? |
estrogens |
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What are the estrogens used for ADT? |
DES, Premarin, estradiol |
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What is the main problem with using progestins for prostate cancer, and the reason that it is not utilized? |
There is a testosterone escape phenomenon and the testosterone levels will begin to rise after treatment begins. |
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What is the name of the progestin that can be used for ADT? |
Megace (megestrol acetate |
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What is the mechanism of action of LHRH agonism for ADT? |
The LHRH agonists agonize the LHRH receptors and initially increases LH and FSH production which initially increases testosterone, but eventually decreases it. |
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What are the names of the LHRH agonist drugs used for ADT? |
luprolide, Lupron, Eligard, Viadur, histrelin, Vantas, gosrelin, Zoladex, tritorelin, Trelstar |
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What is the problem with using LHRH agonist drugs alone? |
There is initially a flare phenomenon as the testosterone increases initially and can make the tumor symptoms worse. |
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What is the mechanism of action of GnRH antagonism? |
The GnRG antagonists decrease LH secretion with decreases testosterone. |
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What is the name of the GnRH antagonist? |
Degarelix (Firmagon - brand name) |
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Which is more effective, GnRH antagonism or LHRH agonism at one year? |
They are equally effective at one year. |
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What is the mechanism of action of the androgen synthesis inhibitors? |
They reduce gonadal and adrenal androgen production by inhibiting cytochrome p-450. |
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What are the names of the androgren synthesis inhibitors? |
Ketoconazole and aminoglutethimide |
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What the big side effect of ketoconazole? |
hepatotoxicity |
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What must you do if you are going to use high dose ketoconazole? |
You must supplement corticosteroids and montior for hypoglycemia |
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What is required for ketoconazole absorption and dissolution? |
stomach acid |
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How does aminoglutethimide work? |
It inhibits the transformation of cholesterol to pregnenolone by inhibiting cytochrome p-450 and thus blocks the formation of glucocorticoids, mineralocorticoids and sex steroids. |
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What needs to be supplemented when someone is taking aminogluethimide? |
Mineralocorticoids and glucocorticoids |
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What is the use of prolactin antagonism? |
For those that are no longer responsive to standard hormone therapy, these can help relieve bone pain and some symptoms |
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What are the names of the prolatin antagonists? |
bromocriptine and levodopa |
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What is the use of the 5 alpha reductase inhibitors in ADT? |
Some clinicians add the 5ARI's to standard therapy. There is insufficient evidence to suggest this. |
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What is the mechanism of action of the nonsteroidal antiandrogens? |
The block binding of testosterone and DHT to the androgen receptor. Androgens receptors in the pituitary and the hypothalamus are also blocked which prevents androgens from participating in negative feedback and leads to increased levels of LH, thus adrenal and gonadal androgen production is increased. |
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What is the best part of steroidal and nonsteroidal antiandrogens? |
libido and potency are not affected. |
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What is the negative side effect of both steroidal and nonsteroidal antiandrogens? |
In the periphery, the excess testosterone can be converted to estrogen and this can cause weight gain and gynecomastia. |
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What are the names of the nonsteroidal antiandrogens? |
Flutamide - Eulexin bicalutamide - Casodex nilutamide - Nilandron |
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What is the Flare phenomenon? |
It is a phenomenon that is caused by LHRH agonism that results in an initially elevated testosterone that can cause symptoms and bone pain |
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How is the flare phenomenon prevented? |
1. Use a GnRH antagonist instead of a LHRH agonist. 2. Use ketoconazole before LHRH agonism. 3. Start antiandrogens before starting LHRH agonism. (must get to steady state) |
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How long does it take for each of the following to reach castrate level testosterone? orch ketoconazole LHRH agonists DES IV |
orch - 3 hours ketoconazole - 8 hours LHRH agonist - 30 days GnRH ant - 3 days DES IV - 24 hours DES oral >10 days |
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What is antiandrogen withdrawal? |
It is a decrease in the PSA after the antiandrogen is discontinued. It usually lasts 3-6 months and resease. |
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Which ADT meds cause hot flashes? |
LHRH agonists, GnRH antagonists, bilateral orchiectomy, and nonsteroidal antiandrogens |
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What can be used to prevent ADT associated hot flashes? |
Progesterone, Estrogen, clonidine, venlafaxine, SSRI's, Vitamin E, Gabapentin, and accupunture |
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ADT increases The risk of what problems? |
lipid profile abnormalities insulin resistance diabetes cardiovascular disease anemia osteoporosis periodontal disease sexual dysfunction infertility body habitus changes Fatigue Hot flashes Cognitive deficits |
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What is the risk of osteoporosis in men on ADT compared to other men. |
5x increased risk |
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How does ADT affect the pathology of the prostate gland? |
Atrophy of the gland with the basal layers closer together Decreased gland density increased fibromuscular stroma |
