restage with radiographs and scans, evaluate serum testosterone level if less than 50 ng/mL, and discontinue all hormonal therapy (LH-RH analogue and antiandrogen) for 4 to 8 weeks before planning the next therapeutic step.
if the patient is on an antiandrogen in addition to a luteinizing hormone–releasing hormone (LH-RH) analogue, discontinue this for 4 weeks in the case of flutamide/nilutamide and for 8 weeks in the case of bicalutamide.
if the patient has no symptoms, the workup shows that he has adequate gonadal suppression (serum testosterone <50 ng/mL), and the only evidence of disease progression is a rising prostate-specific antigen (PSA) and scans are unchanged, try a second-line hormonal therapy before chemotherapy is offered.
if the patient experiences severe focal bone pain that requires regular use of narcotic analgesics, consider palliative radiation therapy.
obtain a serum testosterone level to evaluate adequate gonadal suppression, restage the disease with radiographs and scans, maintain gonadal suppression, and plan the next therapeutic step.
Radiate the prostatic bed and the pelvis.
Send the patient to an oncologist for initiation of chemotherapy.
Continue follow-up with regular PSA tests and restage when the patient becomes symptomatic.
Assess the PSA doubling time (PSADT): if less than 6 months, consider treatment as soon as possible; otherwise, observation may be reasonable.
Evaluate the adequacy of gonadal suppression (check serum testosterone level) and plan for second-line endocrine manipulations.
Wait until he becomes symptomatic.
Administer docetaxel, 75 mg/m2 every 3 weeks, and zoledronate, 4 mg monthly.
Administer a radiopharmaceutical.
Treat aggressively with high-dose bicalutamide, calcium, and vitamin
Plan for next endocrine treatment approach, including the infusion of zoledronate given 3 times yearly.
order radiation therapy followed by docetaxel.
give analgesics as needed and consider a workup when the PSA value rises.
add zoledronate to management.
order magnetic resonance imaging (MRI) of the spine to rule out cord compression.
consider radiation therapy.
treat with bicalutamide because the PSA level is still low.
send him for a colonoscopy because he probably has another cancer because the PSA value is negative.
perform a biopsy of the pelvic mass to rule out the neuroendocrine/anaplastic subtype.
administer radiation to the pelvis followed by docetaxel.
begin docetaxel because he has castration-resistant prostate cancer (CRPC).
docetaxel combined with zoledronate.
a bronchoscopy, because of the histology (small cell carcinoma).
radiation to the pelvis followed by ketoconazole and hydrocortisone.
radiation therapy followed by second-line hormonal therapy until progression; then offer chemotherapy.
chemotherapy with carboplatin and etoposide preceded or followed by irradiation.
Quality of life
All of the above
It has no activity at all in CRPC.
Thromboembolic events are usually prevented by prophylactic anticoagulation.
It is critical to use it combined with docetaxel.
It adds significant toxicity to docetaxel without an apparent survival benefit.
It has significant single-agent activity in CRPC.
toxicity overrides quality of life benefits.
it may cause fatigue and neurotoxicity.
it may cause modest elevation of liver function test results.
it may cause myelosuppression.
it may cause edema.
increased osteoclastic activity.
proliferation of osteoblasts.
depletion of osteoclasts.
They are always osteoblastic, because of growth factor effects.
They are mostly lytic, associated with a predominant osteoclastic effect associated with treatment.
Pathologic fractures are common.
Hypercalcemia is common.
There is increasing evidence that growth factors, cytokines, and other proteins may play a role in the development of bone metastases.
It rarely may cause osteonecrosis of the jaw in patients who are undergoing dental work.
Side effects include anemia and renal dysfunction.
It is approved for the treatment of hypercalcemia.
It reduces the increase in osteoclastic activity associated with androgen deprivation.
is usually seen in the first 3 months of treatment.
None of the above
is seen in about 50% of patients receiving docetaxel treatment.
represents evidence of therapeutic benefit but not necessarily longer survival.
Brain metastasis associated with small cell histology should be treated surgically.
Routine MRI of the brain should be considered in all CRPC patients.
It is common in patients progressing rapidly on hormonal therapy.
It is seen in about 25% of patients with CRPC.
It is seen in less than 1% of patients, except when they demonstrate the neuroendocrine phenotype.
They are associated with an increased accumulation of cells in the G2M phase of the cell cycle.
They cause radiosensitization in vitro.
They are antimitotic agents.
They induce BCL2 phosphorylation.
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