Prostate cancer
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131 terms
Terms | Definitions |
|---|---|
 What populations are at an increased risk of prostate cancer? | First degree relative (particularly diagnosed at a younger age or multiple relatives), AA race, age >65yo |
| What are the most to least common site of mets for CaP? | Pelvic lymph nodes (hypogastric and obturator), bone, lung, liver |
| What is the most common histologic type of CaP? | Adenocarcinoma (>95%) |
| What is the most common non-adeno type of CaP? | Urothelial carcinoma, then ductal adenocarcinoma, mucinous adenocarcinoma, neuroendocrine (small-cell) tumors, signet-ring tumors |
| What cells does prostatic adenocarcinoma originate from? | Epithelial cells Stains positive for prostatic acid phosphatase (PAP) and PSA |
| What do prostate adenocarcinoma cells NEVER have histologically? | A basal cell layer. |
| What do basal cells stain positive for? | High molecular weight keratin (HMWK) and negative for PSA and PAP. So cancer cells are neg for HMWK and pos for PAP and PSA |
| What zone is the most common location for prostate cancer? | Peripheral zone |
| Where is capsular penetration most common? | Near the NVB |
| What percentage of men with ASAP on prostate biopsy will develop prostate cancer? | 40-60% therefore these men should undergo repeat prostate biopsy within 3 months with increased sampling from atypical region. |
| What % of men with HG PIN after a 10-12 core biopsy develop prostate cancer? | 10-20% |
| Describe the inclusion criteria of the PCPT | 18,000 men, age >=55, nl DRE, PSA <=3.0 randomized to placebo for finasteride 5mg daily and followed for 7 yrs |
| What were the results of PCPT? | Finasteride decreased the risk of developing prostate cancer by 25%. There is uncertainty surrounding its effect on high grade cancer. Likely detection bias |
| Describe inclusion criteria for REDUCE | 8,000 men, age >50, neg PBx, prostate vol <80cc, and PSA 2.5-10 randomized to placebo or dutasteride 0.5mg daily and followed for 4 yrs |
| What were the results of REDUCE? | Dutasteride decreased the risk of Gl 5-6 prostate cancer by 27% but did not reduce Gl 7-10. Did not increase risk of high grade. Did reduce HG PIN and ASAP. |
| What were the results of REDEEM? | Reduced risk of progression for AS on Dutasteride |
| What substances should not be recommended for patients with CaP? | Vit E, selenium, and Vit C |
| Describe the PLCO trial? | 76,693 US men, age 55-74 randomized to annual PSA/DRE or "usual care" (could include screening). After 7-10yrs detection was higher in screened group but risk of death from CaP was similar. The problem was contamination in control group |
| Describe ERSPC trial? | 182,000 european men, age 50-74 randomized to routine PSA screening (q4yrs) or none. After 9 yrs screening reduced risk of death by 20%. 1410 men would have to screened and 48 men treated to prevent 1 death |
| CaP is found in what % of men with abnormal DRE? | 30% |
| What are the age adjusted PSA norms? | W AA Asian 40-49 0-2.5 0-2.0 0-2.0 50-59 0-3.5 0-4.0 0-3.0 60-69 0-4.5 0-4.5 0-4.0 70-79 0-6.5 0-5.5 0-5.0 |
| What is abnormal PSA velocity if PSA <4? | >0.35 ng/ml/yr |
| What is abnormal PSA velocity if PSA >4? | >0.75 ng/ml/yr |
| What PSA density suggests CaP? | >=0.15 |
| What is % free PSA valid to use? | When PSA is 4-10ng/ml |
| What is an alternate regimen for abx prophylaxis during PBx other than fluroquinolone? | Aminoglycoside with metronidazole or with clinda |
| What is prostate innervation? | Sympathetics and parasympathetics from inf hypogastric plexus |
| Why do apical biospies hurt? | Above dentate line (anatomic division of anus and rectum) innervated by inf hypogastric plexus. Below innervated by inf rectal nerve and these aren't anesthetized in usual block |
| When cancer is missed on prostate biopsy where is it usually hiding? | Anterior-apical PZ Midline PZ Anterior TZ |
| Men considering salvage cryo should undergo sampling of what? | SV's Cancer in SV occurs in 42% of men who recur after radiation |
| What should repeat biopsies consist of? | 12 cores plus lateral peripheral zones and apical ant prostate. +/- TZ |
| Who should get a bone scan in w/u of CaP? | PSA>20, Gl 8/>, cT3-4, elevated alk phos, elevated serum Ca. Similar criteria for CT pelvis |
| What is cT1b CaP? | More than 5% of histologically incidental cancer on resected prostate |
| In the TNM staging system how are positive surgical margins described? | R1 |
| What factors increase risk of death from CaP? | PSA velocity >2.0 ng/ml/year High PSA at diagnosis Biospy Gl 8-10 Palpable nodes |
| What is low risk CaP? | PSA <10 Gl <=6 cT1 or T2a |
| What is intermediate risk CaP? | PSA 10-20 Gl 7 cT2b or T2c |
| What is high risk CaP? | PSA >20 Gl 8-10 cT3 |
| What is PCA-3? | Voided urine test based on reverse transciptase-polymerase chain reaction assay for prostate-specific gene (DD3) |
| What is EPCA-2? | Blood based test which detects nuclear matrix protein linked to prostate cancer. More sensitive and specific for CaP even if normal PSA and BPH. Predicted ECE as well |
| What is the treatment of choice for men with CaP <50yo? | RP based on a retrospective report by Pokala and Menon 2009 |
| What are treatment option for men >50yo with low risk prostate cancer? | RP, XRT, permanent brachy and cryo appear to have similar cure rates |
| Name three trials looking at AS? | PIVOT, ProTeCT, and START |
| What is the ASTRO definition of PSA failure after XRT? | 3 consecutive rises in PSA above post-tx nadir. Now outdated? More recently use an absolute PSA rise of 2ng/ml above the post-treatment nadir PSA level |
| Regarding CaP the beneficial effects of soy protein are thought to arise from? | Isoflavones |
| Regarding CaP the beneficial effects of green tea are thought to arise from? | Polyphenols |
| How does cryotherapy work? | It freezes which creates a region of coagulative necrosis. It achieves cell kill by cell rupture (during freezing), apoptosis (6-12 hrs p freeze), and ischemia (24-48 hrs p freeze) |
| In what direction is the prostate frozen during cryosurgery? | Anterior to posterior |
| To ensure cell death how do urologists freeze the prostate? | At a temp of -40C with 2 freeze-thaw cycles |
| What is the patient population for cryo? | Stage T1-2 N0 M0, impotent, relatively small prostate, no previous TURP |
| Where does the NVB course and what is it composed of? | Posterior-lateral to prostate and is composed of cavernous blood vessels and nerves |
| What does BN preservation do? | Allows continence to return sooner and results in lower rate of BNC. Does NOT improve final degree of continence |
| What area should be avoided during PLND for CaP? | Anterior and lateral to prostate as this increases risk of lymphedema |
| What medication can be used as a sclerosing agent if lymphocele occurs? | Doxycycline |
| What % of men with + surgical margins recur? | 50% |
| What is the most common site of positive margin? | Apex for RRP and anterior for perineal |
| What increased risk is associated with ECE? | 14 fold higher risk of dying from prostate cancer than men with cancer confined to the prostate |
| What is SV invasion associated with? | Higher risk of recurrence, mets, and death |
| What did the "Messing Trial" show? | Immediate androgen dep improves survival in men who did undergo RP and who have micromets to PLN |
| Should men with poor pathologic features undergo adjuvant or salvage XRT? | Still unknown which is better. But if the path is really bad consider whole pelvis rads and ADT |
| What percentage of men progress on AS and require definitive treatment? | 25-30% |
| Outcomes of RRP are better at centers that perform how many per year? | 40 or more |
| Most urologists wait until a PSA of what post-prostatectomy to say its a meaningful rise? | >0.4ng/ml |
| After recurrence men with a PSA doubling time of less than what may be more likely to die of CaP? | 15 months |
| What is the XRT dose for low risk prostate cancer? | Prostate +/- SV 70-79Gy with no ADT |
| What is the XRT dose for intermediate risk CaP? | Prostate + SV +/- PLN at 75-80Gy with optional 4-6mo ADT (LHRH agonist +/- antiandrogen) |
| What is the XRT dose for high risk CaP? | Prostate + SV + PNL at 75-80Gy with 2-3 yrs ADT (LHRH agonist +/- antiandrogen) |
| What is high dose rate brachy? | Delivered using Ir-192, over 1-2 days several sessions are conducted. Usually combined with 4-5 weeks of XRT |
| What is the half life, time to deliver 90% of radiation, and dose for elements used for brachy? | 1/2 life 90% Dose I-125 60d 204d 145Gy Pd-103 17d 58d 125Gy Cs-131 9.7d 33d 115Gy |
| Who is brachy avoided in? | Intermediate or high risk patients, gland >60gm, previous TURP, and significant voiding symptoms |
| What is PSA bounce? | Temporary rise in PSA in 20-30% of men not receiving ADT that occurs 1-3 years after radiation and lasts 6-18 months |
| How does EBRT work? | Utilizes high-energy photons to destroy cancer by damaging cellular DNA |
| What dose of radiation is now administered with 3D conformational EBRT? | >75Gy |
| What is IMRT? | It is photon based. It is quickly becoming the standard of care. Give doses between 81-86.4Gy |
| What is sterotactic body radiotherapy (SBRT)? | Employs high-dose (700cGy) for several fractions delivered with linear accelerator or cyberknife |
| What must be done before administering curative salvage therapy for radiation failure? | Document local recurrence with a prostate biopsy |
| From the time of PSA recurrence after prostatectomy what is the median time to detectable mets? Median time to death? | 8 years 13 years |
| What is the XRT dose for salvage radiation after prostatectomy? | At least 64Gy |
| What must be done before administering salvage therapy for cryotherapy failure? | Local recurrence must be confirmed with biospy |
| T/F LHRH agonists and bilateral orchiectomy are equally as effective? | True |
| What PSA at 7-8 months post-castration is associated with a higher risk of death from CaP? | PSA >0.2ng/dl Also a PSA DT of <3 months |
| When does prostate cancer typically stop responding to castration? | Usually after 2-3 years but can range from months to 15 years |
| Should ADT be stopped when a man becomes "hormone refractory"? | No |
| What is the algorithm for BCR after ADT? | Obtain a serum T. If <50 they are castrate. If taking an antiandrogen stop it (antiandrogen withdrawal) and recheck PSA. If not taking antiandrogen start one and recheck PSA. If T is >50 then either incomplete orchiectomy or non-compliance/error with LHRH agonist |
| What are second line therapies for mCaP? | Change to different antiandrogen Ketoconazole and steroids Aminoglutethimide and sterioid Diethylstilbestrol Docetaxol |
| Who should IV bisphosphonates be started on with CaP? | Hormone refractory with bone mets should receive IV bisphosphonates. Zometa 4mg IV q3wks for 20 cycles |
| What should be done for acute spinal compression from mets? | IV steroids (dex 100 IV bolus then 25mg PO QID) Ketoconazole 400mg PO q8h GnRH antagonists (Degarelix) Diethylstilbestrol 1g IV q24hr MRI spine Surgery or rads |
| What is the MOA of GnRH antagonists? | Reversibly binds to GnRH receptor in the pituitary gland and suppresses secretion of LH, FSH, and T Castrate level in 3 days Ex: degarelix |
| What is the MOA of antiandrogens? | Block binding of DHT to androgen receptor blocking the translocation of DHT-androgen receptor complex into the nuclei of cells |
| What should be considered if a patient is going to have prolonged monotherapy with antiandrogen? | Breast radiation prophylactically prior to initiation of med because of high risk of gynacomastia |
| What does CAB imply and how is it administered? | Elimination of testicular androgen and blockade of adrenal androgen generally with LHRH analog and antiandrogen agent |
| What is the MOA of abiraterone or Zytiga? | Inhibits CYP17A1 and enzyme expressed in testicular, adrenal, and prostate tissue. It is an adrenal androgen synthesis inhibitor |
| What is the MOA of Provenge? | It is sipuleucel-T immunotherapy vaccination. It is an autologus dendritic cell therapy vaccine that utilizes a PAP-GMCSF fusion protein to stimulate immune cells |
| Who is it approved for? | Men with presymptomatic metastatic castrate resistent prostate cancer. Survival advantage of 4.1-5 months over sham |
| Who is not eligible for Provenge? | Men that require narcotics, visceral mets, and life expectancy <6 months |
| What is MDV3100? | An experimental androgen receptor antagonist with a higher binding affinity for AR than biclutamide |
| What agents are under Phase III trials in post docetaxel castrate resistant setting? | Cabazitaxel - antimicrotubule agent Ipilimumab - CTLA-4 blocker combined with XRT MDV3100 - novel antiandrogen Abiraterone - adrenal/autocrine androgen synthesis inhibitor Sunitinib - Oral VEGF/PDGF inhibitor |
| T/F docetaxel has been shown to have advantage over mitoxantrone? | True |
| What is the toxicity of mitoxantrone? | Cardiac - should get pretreatment and serial EF measurements during treatment |
| What are the toxicities of docetaxel? | Myelosuppression and peripheral neuropathy |
| What are the toxicities of bisphosphonates? | Renal failure and osteonecrosis of the jaw |
| What is Denosumab | A RANKL anagonist which has shown improvment in prevention of skeletal related events in men with met castration resistant CaP compared to Zoledronic acid. Side effect is osteonecrosis of the jaw |
| What is the treatment regimen for radiation therapy to palliate bone mets? | 30Gy over 10 treatments. Single dose palliative radiation may also be equally as good. |
| What is the radiation regimen for more extensive disease? | Wide field radiation or administration of radioactive bone-seeking isotopes like stontium-89 Cl or samarium 153 lexidronam |
| What are sources of androgens in men? | Testis - 90-95% Adrenal glands - <5% |
| What does prolactin do to testosterone? | Decreases it by inhibiting GnRH secretion from hypothalamus. It may stimulate prostate cancer by directly stimulating prostate tissue |
| What conditions cause increase prolactin? | Prolactinoma, hypothyroidism, stress, CRF, antipsychotic drugs |
| Castrate levels of T occur how soon after b/l orchiectomy? | 2-12 hrs |
| What is the MOA of estrogen in ADT? | Inhibits hypothalamic-pituitary axis - decreases LH and therefore T. This increases prolactin Castrate levels in 10-14 days Ex: diethylstilbestrol, premarin, estradiol |
| What is the big side effect of estrogen therapy? | Emboli |
| What is the MOA of progestins? | Inhibits hypothalamic-pituitary axis - decreases LH and therefore T. This DOES NOT increases prolactin Ex: Megace |
| What is the MOA of LHRH agonists? | Stimulation of LHRH receptors that causes an initial flare then suppresses secretion Castrate levels in 30 days Ex: leuprolide, histrelin, goserelin, and triptorelin |
| What is the MOA of Ketoconazole in ADT? | Reduces gonadal and adrenal synthesis by inhibiting cytochrome P-450 Castrate levels in 8hrs Administer with steroid b/c lowers glucocorticoid as well |
| What is the toxicity of Ketoconazole? | Hepatotoxicity, dose limiter is N/V |
| What ist he MOA of aminoglutethimide in ADT? | Blocks the transformation of cholesterol to pregnenolone by inhibiting cytochrome P-450. Blocks glucocorticoid and mineralocorticoid as well as sex steroids. Must supplement the first two to avoid Addisonian crisis |
| What are the side effects of antiandrogens? | Hepatotoxicity, gynecomastia, N/V Nilutamide has visual disturbances |
| When does the flare phenomenon peak and how long does it last? | 3-4 days, 7 days |
| What can be done to prevent flare phenomenon? | Usa a GnRH antagonist or orchiectomy instead Use ketoconazole before LHRH agonist Antiandrogen (4 1/2 livees) b/f LHRH agonist Flutamide >32 hrs before Nilutamide >8 days before Bicalutamide >24 days before |
| What is antiandrogen withdrawl? | Decline in PSA (usually by 50%) after stopping antiandrogen. Occurs in 30% of patients and lasts 3-6 months Flutamide decline begins within few days Bicalutamide begins 4-8 weeks |
| What agents cause hot flashes? | LHRH agonists, GnRH antagonists, bilateral orch, and nonsteroidal antiandrogens |
| What prevents hot flashes? | Progesterone, estrogen, clonidine, venlafaxine, Vit E, gabapentin, and acupuncture |
| What are the risks of long-term ADT? | Adverse lipids, insulin resistance, DM, CAD, anemia, ostoporosis, peridontal disease, sexual dysfuntion, infertility, fatigue, hot flashes, cognitive deficits |
| What pathologic changes are seen in the prostate after ADT? | atrophy of gland, decreased gland density, increased fibromuscular stoma, apoptosis, nuclear pyknosis. Necrosis is rarely seen |
| What is PSA? | Serum protease human kallikrein gene on Ch 19 Cleaves spermatogelin Half life of 3.4 days |
| T/F there is evidence that enemas reduce risk of infection after PBx | False |
| T/F a PSA velocity >2 years prior to dx portends a worse outcome? | True |
| Describe the scores for a bone scan? | Z score: compares to age matched population T score: compares to 25 yr old |
| What is the MOA of docetaxol? | Interferes with microtubules |
| What is the survival benefit of docetaxol over mitozantrone + prednisone? | 2 months |
| What is mitoxantrone? | Interferes with DNA synthesis and repair Improves pain but not survival |
| What is the treatment of neuroendocrine tumor of the prostate? | Cisplatin and etoposide |
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