Prostate Cancer PJ Articles Flashcards
The most important risk factor for developing PC is
Age
Why is early stage PC generally asymptomatic?
Many PC start in the posterior peripheral zone (the outer part of the prostate away from the urethra). It is not until the tumour has grown large enough to put pressure on the urethra that symptoms are noticeable.
Patients presenting to the GP with signs of prostate cancer, such as ______,______,______,______,______,__ or _____ ______ are given a ___ and a ___ blood test.
Nocturia, Urinary freq, Hesitancy, Urgency, Retention ED Visible Haematuria DRE PSA
PSA levels of below _ng/mL are not indicative of PC.
5ng/mL
10ng/mL can be an indication of a non-cancerous (benign)enlargement of the prostate gland..
Higher the level….
What is the Gleason grading system?
The Gleason grading system is used to provide the pathological prognostic information based on the microscopic appearance of the cancer cells in addition to clinical stage
Treatment of early stage prostate cancer and locally advanced disease can involve _______, _______ or __________ _______- therapy; however, as the disease progresses, these options change.
Treatment of early stage prostate cancer and locally advanced disease can involve surveillance, radical treatment or androgen deprivation therapy; however, as the disease progresses, these options change.
_______ _________or radical ________ are recommended for men with intermediate- and high-risk localised prostate cancer, where there is a prospect of long-term disease control. However, both options are associated with complications, including impaired sexual function.
Radical prostatectomy or radical radiotherapy are recommended for men with intermediate- and high-risk localised prostate cancer, where there is a prospect of long-term disease control. However, both options are associated with complications, including impaired sexual function.
What is the advantage of brachytherapy to radical radiotherapy?
The advantage of brachytherapy is that a substantial dose can be delivered to the prostate with minimal effect on the surrounding tissue.
The gold standard androgen deprivation therapy is
castration - bad psychological effects.
ADT is based on luteinising hormone-releasing hormone (LHRH) agonists, why?
ADT has been based on luteinising hormone-releasing hormone (LHRH) agonists, which act to reduce testosterone levels by blocking the production and release of gonadotrophins, exerting a negative feedback control on hypothalamic luteinising hormone (LH) secretion and reducing follicle-stimulating hormone (FSH) in the medium- to long-term. If prostate cells are deprived of androgenic stimulation, they undergo apoptosis.
LHRH agonists include goserelin[3], triptorelin[4] and buserelin, with the choice of treatment based on local formulary and cost, rather than any significant differences in clinical effectiveness
LHRH agonists include
LHRH agonists include goserelin[3], triptorelin[4] and buserelin, with the choice of treatment based on local formulary and cost, rather than any significant differences in clinical effectiveness
What are the side effects of ADT?
Hot flushes Weight gain Loss of libido Loss of peripheral hair growth Gynaecomastia Elevated risk of diabetes Loss of bone mineral density Raised risk of fracture Increased cardiovascular complication risk.
Why can tumour flare occur initially with ADT?
ADT initially results in an increase in testosterone levels, producing a testosterone surge, prior to down-regulation of testosterone production. This elevation in testosterone levels can result in a ‘tumour flare’ in some patients, who experience a temporary deterioration in their condition. It is common practice to pre-treat patients with anti-androgen therapy prior to starting LHRH therapy and for the first two weeks of LHRH therapy. Anti-androgen therapy reduces the testosterone surge symptoms by blocking the action of testosterone, rather than lowering serum testosterone levels. The most commonly used anti-androgens include nonsteroidal agents (e.g. flutamide, bicalutamide) and steroidal agents (e.g. cyproterone, megestrol).
Why might a patient about to begin ADT be given flutamide?
ADT initially results in an increase in testosterone levels, producing a testosterone surge, prior to down-regulation of testosterone production. This elevation in testosterone levels can result in a ‘tumour flare’ in some patients, who experience a temporary deterioration in their condition. It is common practice to pre-treat patients with anti-androgen therapy prior to starting LHRH therapy and for the first two weeks of LHRH therapy. Anti-androgen therapy reduces the testosterone surge symptoms by blocking the action of testosterone, rather than lowering serum testosterone levels. The most commonly used anti-androgens include nonsteroidal agents (e.g. flutamide, bicalutamide) and steroidal agents (e.g. cyproterone, megestrol).
What are the benefits of LHRH antagonists over LHRH agonists? Why do they have this benefit?
They do not cause tumour flare.
LHRH antagonists (e.g. cetrorelix, ganirelix, degaralix), in contrast to LHRH agonists, bind immediately and competitively to LHRH receptors in the pituitary gland. The effect is a rapid decrease in LH, FSH and testosterone levels without tumour flare. This seemingly more desirable mechanism of action has made LHRH antagonists appear to have an advantage over LHRH agonists, but so far they remain in limited use. Degaralix is currently being reviewed by NICE; draft guidance recommends it as an option only for advanced hormone-dependent prostate cancer patients with spinal metastases who present with signs or symptoms of spinal cord compression (because the tumour flare when starting an LHRH agonist would be dangerous for these patients)
LHRH antagonists are more expensive than LHRH agonists and less cost-effective for all patients; NICE reported it costs £12,306 (excluding VAT) per course of treatment. Clinical trials have compared degarelix with leuprorelin or goserelin with or without bicalutamide, with the primary outcome being prostate-specific antigen (PSA) suppression.
