Prostate Cancer Flashcards
(33 cards)
What are the risk factors for prostate cancer
age, race (blacks have higher risk), family history
What is the histology of prostate cancer
adenocarcinoma
What is the key driver of prostate cancer, what level is considered castration to lower cancer, where is it made
Testosterone, less than or equal to 50 ng/dl, test and adrenal glands
What type of therapy will decrease testosterone
Androgen deprivation therapy (ADT)
What are common mechanisms of resistance for prostate cancer
Androgen receptor amplification increased hypersensitivity to low testosterone levels, activation of growth factor and signaling pathways, increased antiapoptic genes
T/F:5 alpha reductase inhibitors (finasteride and dutasteride) can be used to prevent prostate cancer
False: Using 5-alpha reductase inhibitors has no difference in overall survival and patients develop a more severe prostate cancer and high grade tumors
How is prostate cancer found
Digital rectal examination and PSA screening (does not reduce deaths)
What is used Prostate Specific Antigen, what should be monitored and what is the nuance
protein made in the prostate, can be elevated in non-cancerous moments but should be monitored by rate of change over time
What are the NCCN recommendations for screening
PSA less than 1ng/ml and DRE is normal: repeat in two to 4 year interval, PSA 1-3 ng/ml and DRE normal: repeat in 1-2 year interval, PSA greater than 3 ng/ml or very suspicious DRE: patient should have a biopsy
How does prostate cancer spread, what are the most common reigons for possible metastasis
Local extension via lymphatics or regional lymph nodes and hemtogenously/ BONE, liver, lung
How should glaeason scores be interpreted
Scores 2 to 4, well differentiated, slow growing/ scores 8 to 10, poorly differentiated, fast growing
T/F: 100% of patients will initially respond to ADT therapy but will become castrate resistant
True
What is the spectrum of Castrate Resistant Prostate Cancer (CRPC)
Patient with no metastasis and is asymptomatic, Patients with metastasis and debilitating cancer symptoms
What is the cornerstone of current standard of care for prostate cancer, what are the two ways to achieve this
Androgen Deprivation Therapy/ Surgical castration and Chemical castration
What are the drugs that can be used for chemical castration
Leuprolide and Goserelin (LHRH agonist), Degarelix (GnRH antagonist)
What is the MOA of the LHRH agonist, how long does it take for effect
Down regulation of pituitary receptors and decrease testosterone, 28 days
What are the problems with using LHRH agonists , how long does this to resolve
Tumor flare up along with increased bone pain or increased urinary symptoms, after 2 weeks
What should be given before LHRH agonists are given
Antiandrogen therapy should be started one week prior to LHRH agonist given
What is the MOA of GnRH agonists
Reversibly binds to GnRH receptors in the pituitary gland, blocking the receptor and decreasing the secretion of LH and FSH resulting in rapid androgen deprivation
What are the benefits of GnRH agonists, why is it no used as often
No initial surge in LH and FSH, no flare, testosterone is reduced to less than 50 ng/dl within 7 days/ the price is to high
What are the 1st generation antiandrogens, what is the reason for use
Flutamide, Bicalutamide, Nilutamide/ REDUCE TUMOR FLARE when combined with LHRH agonists
If a patient has localized prostate cancer what would be a cause for concern and what should be done after
Biochemical Recurrence (Rapid PSA velocity, short PSA doubling time), take to imaging to see if there is metastatic disease
What is used to determine a patient at high risk of metastatic disease, what should be given
PSA doubling less than or equal to 10 months, add 2nd generation antiandrogens to DELAY METASTASIS for castrate resistant prostate cancer
What are the 2nd generation antiandrogens
Apalutamide, Enzalutamide, Darolutamide
