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Oncology Exam 3
Frei Prostate Cancer (Curable non-metastatic) C
| Question | Answer |
|---|---|
| Historical Background Prostate Cancer? | 1980-90’s, number of newly diagnosed Prostate Cancer (PC) increased dramatically Changes most likely due to emergence of prostate specific antigen (PSA) Most commonly diagnosed cancer in US |
| (T/F) Prostate cancer is the most commonly diagnosed form of cancer | True |
| Prostate cancer is the ___ most common cause of cancer related deaths | 2nd |
| Prostate cancer Incidence and Survival? | #1 for incidence; #2 for mortality |
| Anatomy of the prostate | -Male sex gland -Size of a walnut -Helps control urine flow -Produces fluid component of semen -Produces Prostate Specific Antigen (PSA) and Acid Phosphatase |
| Prostate Cancer Pathogenesis? | Semen-secreting prostate gland cells mutate into cancer cells *where prostate cancer develops from *in situ (in the place but hasn’t started invasion) -Most prostate cancer is adenocarcimona--> Located in peripheral zone; Initially, small clumps of cancer cells remain confined within normal prostate glands, a condition known as carcinoma in situ (CIS) |
| Prostate Cancer Risk Factors? | -Age (increases with age usually after 50 yo) -Gender *NO PSA for women only MALE -Ethnicity: ↑ risk of incidence and death in African American males -Family history of prostate cancer -Life time risk of prostate cancer is inc by 8% if one first degree relative -Agent Orange exposure |
| Prostate Cancer Screening? | ⭐️ *risk/benefits (used to be overdiagnosed and aggressive) but no health problems… idea that you have cancer morbidity and changes in indiv. lives -digital rectal exam (feel for nodules) -PSA (blood test)⭐️ before physical exam -Biopsy (determines yes or no) First two tests are convenient and inexpensive *NEAT (no tissue or biopsy as a neat sample? no neat, no treat unless you have a tissue biopsy. |
| PSA Confounders: what increases PSA? | -BPH -Age: older you are, the higher your PSA is (prostatic hypertrophy and large the prostate, the more PSA -Prostatitis: inflammation of the prostate -Ejaculation -DRE *must do the blood test first before you palpate, poke the prostate otherwise will cause an increase in the PSA and have a falsely elevated # |
| PSA Confounders: what decreases PSA? | Drugs: finasteride, dutasteride, herbs Obesity |
| S & Sx of Prostate cancer include? (first 4 are hallmark for metastatic PC) | -Hematuria -Bone pain -Lower extremity numbness or weakness -Bladder/bowel incontinence *effects on the spine *Decreased urinary stream and urinary frequency may be only BPH or getting older |
| PCPT trial Shows ⬇️ in prostate cancer--> Comparison of Finasteride 5 mg daily vs Placebo. MOA of Finasteride? Results? | -blocks conversion of testosterone to dihydrotestosterone (DHT); -24.4% decrease in PC in finasteride arm Effect occurs in less aggressive tumors (≤ Gleason 6) men who developed prostate cancer who received prostate developed prostate cancer in a more aggressive manner and required more aggressive treatment. Overall survival – no difference (hard to determine if cancer was cause of death since death can come from other causes) |
| PCPT trial Shows ⬇️ in prostate cancer--> Comparison of Finasteride 5 mg daily vs Placebo. AE of Finasteride? | -Patients on finasteride reported increase sexual side effects, but decreased urinary symptoms -⭐️Increased high grade PC (Gleason 7-10) in finasteride group |
| REDUCE Trial (the other 5AR inhibitor "Dutasteride") shows Decrease in prostate cancer: Takeaways? | Reduced prostate cancer incidence and similar reduction to Finasteride. But different Dutasteride didn't cause those aggressive types like Finasteride caused *both 5ARI (neither show a difference similar trial but dutasteride was a better choice since the aggressive tyepes of cancers wouldn’t be formed. Guidelines: either or. *Dutasteride would be a safer option due to risk of aggressive prostate cancer |
| COMBAT Trial: Dutasteride + Tamsulosin vs Tamsulosin alone: Takeaways? | -40% lower incidence of prostate cancer with dutasteride plus tamsulosin (another BPH drug) compared to tamsulosin alone |
| ASCO (American society of clinical oncology) Recommendations for Prevention of Prostate Cancer | Decreased incidence of PC: 5-AR inhibitors decrease, but do not eliminate risk for PC; Elevated rate of high-grade PC in those taking finasteride Overall survival: No diff in overall survival for finasteride; Unknown for dutasteride (data to immature) ADEs 5ARIs *sexual dysfunctions gynecomastia, decreased libido, erectile dysfunction, nausea, abdominal pain, asthenia, dizziness, flatulence, headache, rash, muscle weakness, teratogenicity |
| OTC Antioxidants Do Not Prevent Prostate Cancer as proven by the SELECT trial: Takeaways? | Selenium and Vitamin E -⭐️Men only taking HIGH DOSE vitamin E had 17% increase risk for development of prostate cancer (p=0.008) High dose Vitamin E has been shown to increase risk of prostate cancer. NOT RECOMMENDED |
| Establishing Diagnosis for Prostate Cancer: *until you have the biopsy, you can't diagnose | -Digital rectal exam (DRE) -PSA (70 yo and older, higher PSA)⭐️ -Transrectal ultrasound -Ultrasound guided biopsy-diagnostic |
| Establish diagnosis of Prostate cancer by looking at PSA. Normal ranges are? 10 ng/mL? | 0-3 ng/mL (>3 ng/mL--> requires further evaluation) *10 ng/mL--> highly suspicious for malignancy *just bc its over 10, still need biopsy |
| Biopsy Gives Tumor Grade Gleason Score--> Grading system evaluating architectural details of individual cancer glands: 2-4? 5-6? 7-10? | 2-4--> Best prognosis; predicts risk of spread (12%) 5-6--> Intermed. prognosis; predicts risk of spread (33%) 7-10--> Worse prognosis; predicts risk of spread (61%) *the more aggressive, the worse the spread and outcomes |
| Gleason Grading system: Must know? | know 2 (least aggressive) and 10 is (most aggressive form of prostate cancer). more aggressive, the worse the spread. *Gleason score used in staging |
| History of Prostate cancer: Histology: _________ 99% ⭐️. Indolent (slow) growth is common in early stages. Spreads by local _____ via lymphocytes or regional lymph nodes and ________ to other organs. | Adenocarcinoma; extension; Hematogenously |
| Prostate cancer metastasizes where? | Bone most commonly⭐ Lungs, liver, lymph nodes are possible *usually bones first ⭐️ |
| How do we stage for prostate cancer? | TNM (Tumor (size) Node (# involved) Metastasis(usually Y/N) staging system + Gleason *incorporate in order to determine aggressiveness ⭐️ |
| Prognostic factors of prostate cancer staging? | -Gleason score (lower the better prognostic factor -Tumor grade (more aggressive the worse the outcome) -DNA analysis by flow cytometry (determine aggressiveness and course of outcome) -PSA level (above 20? Likley to have metastasis; higher PSA level, the worse the prognosis) -Predictive models for organ-confined versus non-organ confined disease |
| Staging of Prostate cancer (looking at physical exam and labs)? | -Abdominal and pelvic CT scans -Chest x-ray (lungs) -Bone scan (signs for mets) -LFT’s -Serum PSA and acid phosphatase |
| Treatment of Prostate Cancer: Localized (curable) stage 1-3? | Active surveillance Surgery Radiation +/- ADT# (Abiraterone and prednisone is added to radiation and ADT in high risk pts *remember that stage 4 is incurable |
| Local therapies for Curable Prostate Cancer include? | -Active surveillance -Radiation: External beam, Brachytherapy -Radical prostatectomy (removal of prostate) -Hormone deprivation therapy/ Androgen deprivation therapy (local + spread) |
| SUMMARY for CURABLE PROSTATE CANCER: ______ (radical prostatectomy) OR ______ (external beam or branchytherapy). Then maybe ⭐️? | Surgery; Radiation; -*ADT (LHRH agonist +/- anti-androgen Short term 3-6 months; Usually 1 -2 years; Long term 2 – 3 years) -GnRH Antagonists -Abiraterone (very high risk) -Can be combination if high risk or local recurrence |
| What is Active surveillance? | A.K.A. observation, expectant therapy or deferred therapy Early-stage (T1-T2), low-grade tumors⭐️ Appropriate for men with < 10 year life expectancy⭐️ No medical treatment is provided Patient receives regular follow-up ⭐️ to monitor tumor |
| Radiation Therapy in Prostate cancer appears equivalent to surgery in outcome. This is an option for pts who are not surgical candidates. What are some complications to consider? | -impotence (30%), rectal, bladder symptoms *damage to the bladder, colon, and urethra (damage to tissue around). Radiation (machine and gets shot to minimize damage of surrounding tissue; will see urinary, ED, and bladder symptoms); drink water and fill bladder, lifts (floats) it off the prostate so you aren’t hitting the bladder |
| Radiation therapy uses External beam or Brachytherapy which are ______. Define External beam radiation? Brachytherapy? | Equivalent; - radiation therapy that uses a machine to aim high-energy rays at the cancer from outside of the body but have to go back daily (for 4-5 weeks) -1 time procedure*gold pellets embedded into prostate and less toxicity from the outside but invasiveness to the procedure |
| ADT stands for Androgen Deprivation Therapy. What is the goal? | Goal - Serum testosterone < 50ng/dL in 1 month -Surgical castration: Orchiectomy *removal of testes |
| ADT stands for Androgen Deprivation Therapy. Aside from surgical castration, Medical castration is also an option. What are the agents involved in this procedure? | -LHRH agonists= GnRH agonist (increases Testosterone and shuts off via feedback +/- antiandrogen (shuts down testosterone cascade immediately) -LHRH antagonist=GnRH antagonists – degarelix or relugolix Equivalent to leuprolide in lowering testosterone levels Major advantage - immediate down regulation of testosterone ⭐️KEY POINT - LHRH agonist alone or GnRH antagonist = standard of care |
| Androgen Deprivation Therapy can use LHRH agonists for medical castration what are the agents involved and SE? | ⭐️Goserelin, Histerelin, ⭐️Leuprolide, Triptorelin SE: Acute Tumor flare (surge of testosterone can cause bone pain), gynecomastia, hot flashes, erectile dysfunction, edema, hyperglycemia, QTc prolongation Long SE: osteoporosis, obesity, insulin resistance, alteration in lipids, cardiovascular disease (Inc MI) *all injectable |
| Androgen Deprivation therapy: uses Anti-androgens: Key points? | Combined androgen blockade not superior to LHRH therapy alone Increased cost and ADEs vs. LHRH alone Primary value of Anti-androgens comes from adding it to LHRH therapy and will decrease the flare reaction ⭐️ (block the tumor flare, since anti-androgens block the receptor. LHRH (tumor flare, don’t get tumor flare). |
| Androgen Deprivation therapy: uses Anti-androgens: Drug agents and AE? | *1st gen: Flutamide (TID), Bicalutamide (Daily), Nilutamide (daily) ⭐️F: severe hepatic impairment; BBW of Liver Failure B: no major BBW (used commonly in practice) N: ⭐️disulfiram rxn; BBW: intestinal pneumonitis NAPLEX ⭐️ daily 300 mg then 1 month 150 mg daily *added for symptom control to block the tumor flare |
| ADT: GnRH antagonists key point in figure? | Figure--> Key point--> GRH antagonists have immediate down regulation of testosterone compared to a drug like Luprolide (you would have an increase in testosterone initially) |
| ADT: GnRH antagonists: Similar to LHRH agonists in lowering testosterone levels; Immediate downregulation of testosterone. Degarelix acetate: Dosing? ADRs? DI? | SubQ; ADR: Hot flashes, weight gain, injection site discomfort (degarelix only), QTc prolongation, increase in liver enzymes DI: None *less CV toxicity compared to LHRH antagonists |
| ADT: GnRH antagonists: Similar to LHRH agonists in lowering testosterone levels; Immediate downregulation of testosterone. Relugolix: Dosing? ADRs? DI? | PO; Hot flashes, weight gain, injection site discomfort (degarelix only), QTc prolongation, increase in liver enzymes DI: Relugolix is CYP3A and Pgp substrate (Avoid any CYP 3A and Pgp inducers) *less CV toxicity compared to LHRH antagonists |
| Abiraterone is given with prednisone due to its effect on? | *Androgen biosynthesis inhibitor - 17 alpha 1 inhibitor. -Suppresses testosterone and cortisol production; Added to early prostate cancer treatment if node positive disease Key toxicities to remember: HTN, Cardiac disorders (AFib) Frei: *main point (decreases testosterone production and its main SE (will be it causes Cardiac disorders, still low rate of causing AFIB⭐ and also causes HBP and Diarrhea |
| TREATMENT OF PROSTATE CANCER (PC): Non-metastatic Castration Resistant Prostate Cancer uses ADT therapy along with what agents? | Apalutamide, Darolutamide, Enzalutamide *Continue leuprolide and add on 2nd gen. watch for seizure and CV risk. Apalutamide (monitor thyroid *continue to suppress ADT to keep testosterone low (some cells are still sensitive due to heterogeneity |
| TREATMENT OF PROSTATE CANCER (PC) check for? | -Check for growth--> lab work--> PSA--> check testosterone levels (still low? But cancer still growing) Castration resistant means that you suppressed their testosterone but cancer is still growing. Add more aggressive therapy. -Even when pt starts entering non-metastatic or castration resistant--> we still restrict testosterone throughout the process so ADT therapy is for all. Except curable. Keep testosterone suppressing therapy throughout the process. Due to a lot of heterogeneitiy |
| TREATMENT OF PROSTATE CANCER (PC): Figure from guidelines, know? | shows that imaging studies, continue ADT therapy (androgen deprivation therapy) and make sure testosterone levels stay below 50. Doubling time occurs--> if growing fast (we start any of these 3 drugs (category 1 all receommended) Apulatamide; darolutamide; enzalutamide all for non-metastatic |
| TREATMENT OF PROSTATE CANCER: Apalutamide Drug information: | -MOA: 2nd generation anti-androgen (more effective than 1st gen) (PO) ⭐️ -⭐️Key Toxicities: CV toxicities are uncommon (ischemic heart disease, HTN, HF),⭐️Hypothyroidism, Seizures - rare ⭐️ -DI: Avoid strong CYP2C8 and CYP 3A4 inhibitors |
| TREATMENT OF PROSTATE CANCER: Darolutamide Drug information: | MOA: 2nd gen anti-androgen -PO BID with food -Key toxicities: rash, fatigue, hot flashes, CV toxicities are uncommon (ischemic heart disease, HTN, HF), Seizures: rare (least risk) ⭐️ -DI: Avoid PgP and CYP 3A4 inducers and inhibitors |
| TREATMENT OF PROSTATE CANCER: Enzalutamide Drug Information | -PO Daily -Key toxicities: Fatigue, Diarrhea, HA, Hot flashes, Seizures (1-2% HIGHEST RISK of 2nd gen Antiandrogens) TEST QUESTION ⭐️ -DI: Avoid CYP 3A4 inducers and 2C8 inducers; Avoid warfarin – may result in decreased exposure to warfarin |
| Pt is a 74 yo male with metastatic hormone resistant prostate cancer with METS in lungs and bones. Which of the following is the best answer in addition to ADT therapy? | Enzalutamide |
| Most common site of Mets for prostate cancer? | Bone |
| Pt has a curable prostate cancer. Which of the following is the best description of brachytherapy? | Tx that involves placing radioactive material inside or near a tumor to destroy cancer cells |
| Which of the following is preferred for ADT therapy in curable prostate cancer? | Relugolix *Bicalutamide is incorrect bc its an anti-androgen and so it would never be used by itself (combined with LHRH or GNRH agonist) *Docetaxel + prednisone (for metastatic) *Nilutamide (anti-androgen) only be used in combination with LHRH or GNRH agonist |
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Xander635
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