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Phar 509 > Prostate Cancer > Flashcards

Prostate Cancer Flashcards

1
Q

What are the risk factors for prostate cancer

A

age, race (blacks have higher risk), family history

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2
Q

What is the histology of prostate cancer

A

adenocarcinoma

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3
Q

What is the key driver of prostate cancer, what level is considered castration to lower cancer, where is it made

A

Testosterone, less than or equal to 50 ng/dl, test and adrenal glands

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4
Q

What type of therapy will decrease testosterone

A

Androgen deprivation therapy (ADT)

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5
Q

What are common mechanisms of resistance for prostate cancer

A

Androgen receptor amplification increased hypersensitivity to low testosterone levels, activation of growth factor and signaling pathways, increased antiapoptic genes

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6
Q

T/F:5 alpha reductase inhibitors (finasteride and dutasteride) can be used to prevent prostate cancer

A

False: Using 5-alpha reductase inhibitors has no difference in overall survival and patients develop a more severe prostate cancer and high grade tumors

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7
Q

How is prostate cancer found

A

Digital rectal examination and PSA screening (does not reduce deaths)

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8
Q

What is used Prostate Specific Antigen, what should be monitored and what is the nuance

A

protein made in the prostate, can be elevated in non-cancerous moments but should be monitored by rate of change over time

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9
Q

What are the NCCN recommendations for screening

A

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

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10
Q

How does prostate cancer spread, what are the most common reigons for possible metastasis

A

Local extension via lymphatics or regional lymph nodes and hemtogenously/ BONE, liver, lung

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11
Q

How should glaeason scores be interpreted

A

Scores 2 to 4, well differentiated, slow growing/ scores 8 to 10, poorly differentiated, fast growing

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12
Q

T/F: 100% of patients will initially respond to ADT therapy but will become castrate resistant

A

True

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13
Q

What is the spectrum of Castrate Resistant Prostate Cancer (CRPC)

A

Patient with no metastasis and is asymptomatic, Patients with metastasis and debilitating cancer symptoms

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14
Q

What is the cornerstone of current standard of care for prostate cancer, what are the two ways to achieve this

A

Androgen Deprivation Therapy/ Surgical castration and Chemical castration

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15
Q

What are the drugs that can be used for chemical castration

A

Leuprolide and Goserelin (LHRH agonist), Degarelix (GnRH antagonist)

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16
Q

What is the MOA of the LHRH agonist, how long does it take for effect

A

Down regulation of pituitary receptors and decrease testosterone, 28 days

17
Q

What are the problems with using LHRH agonists , how long does this to resolve

A

Tumor flare up along with increased bone pain or increased urinary symptoms, after 2 weeks

18
Q

What should be given before LHRH agonists are given

A

Antiandrogen therapy should be started one week prior to LHRH agonist given

19
Q

What is the MOA of GnRH agonists

A

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

20
Q

What are the benefits of GnRH agonists, why is it no used as often

A

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

21
Q

What are the 1st generation antiandrogens, what is the reason for use

A

Flutamide, Bicalutamide, Nilutamide/ REDUCE TUMOR FLARE when combined with LHRH agonists

22
Q

If a patient has localized prostate cancer what would be a cause for concern and what should be done after

A

Biochemical Recurrence (Rapid PSA velocity, short PSA doubling time), take to imaging to see if there is metastatic disease

23
Q

What is used to determine a patient at high risk of metastatic disease, what should be given

A

PSA doubling less than or equal to 10 months, add 2nd generation antiandrogens to DELAY METASTASIS for castrate resistant prostate cancer

24
Q

What are the 2nd generation antiandrogens

A

Apalutamide, Enzalutamide, Darolutamide

25
Q

If a patient has Metastatic disease what must be determined

A

Whether the patient is hormone sensitive or hormone resistant

26
Q

What is the first line therapy in patients with metastatic prostate cancer and is also HORMONE SENSITIVE, high risk (4 or more bone mets or visceral organs)

A

LHRH agonist/GnRH antagonist plus antiandrogen for 7 days/ Docetaxel 75mg/m2 for six cycles OR Abiraterone PLUS prednisone

27
Q

What is the MOA of abiraterone, why is predisone given with abrir

A

Inhibits intratumoral sysnthesis of testosterone/ avoid the adverse effects of abiraterone including hypertension, fluid retention, and hypokalemia

28
Q

What is the first line therapy for patients with metastatic prostate cancer that are CPRC with NO visceral metastasis (lung,liver, brain, adrenal, and peritoneal)

A

Abiraterone plus prednisone, docetaxel with prednisone, enzalutamide

29
Q

What is the first line therapy for patients with metastatic prostate cancer that are CPRC with VISCERAL metastasis, 2nd line

A

Docetaxel plus prednisone, enzalutamide, or abiraterone plus prednisone/ cabitaxel plus predinisone

30
Q

What are the premeds for taxels

A

H1 and H2 blockers plus dexamethasone

31
Q

T/F: Prednisone is used for the same reason in these regimens

A

False: Prednisone is used to counteract the side effects of Abiraterone while in the other regimens it is used to shut down the adrenals

32
Q

What 2nd generation antiandrogen should not be given if a patient has a history of seizures

A

Enzalutamide

33
Q

What should be given if bone metastasis is present

A

Denosumab and Zoldronic Acid

Phar 509 (22 decks)

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