Prostatako minbiziaren patofisiologiak gaixotasunaren garapena eta progresioa eragiten dituzten oinarrizko mekanismoak eta prozesuak aipatzen ditu.
Prostatako minbizia tumore gaizto bat da, prostatako zeluletatik sortzen dena, gizonen maskuria azpian dagoen intxaur itxurako organo txiki bat dena.
Prostatak semena ekoizten du, espermatozoideak elikatzen eta garraiatzen dituena.
Prostatako minbiziaren kausa zehatza ez da guztiz ulertzen, baina hainbat faktore ezagutzen dira gaixotasuna garatzeko arriskua handitzen dutenak.
Adina, familia-historia, arraza eta zenbait mutazio genetiko.
Prostatako minbizia ohikoagoa da adineko gizonengan, kasu gehienak 65 urtetik gorako gizonengan gertatzen direlarik.
Gainera, familian prostatako minbizia duten gizonak arrisku handiagoa dute, baita afroamerikar gizonak eta Karibeko jatorriko gizonak ere.
Prostatako minbiziaren fisiologia prostatako guruinaren barruko zelulen hazkunde eta zatiketa kontrolatu gabeak barne hartzen ditu.
Hau mutazio genetikoen ondorioz gerta daiteke, hazkunde-faktore batzuen gehiegizko adierazpena edo tumore-supresore-genen desaktibazioa dakartzanak.
Mutazio horiek zelulen hazkunde desregulatua eragin dezakete, tumore baten sorrera eraginez.
Tumorea handitzen doan heinean, inguruko ehunak eta organoak inbaditu ditzake, hala nola, maskuria, ondestuna eta inguruko linfa-korapiloak.
Kasu batzuetan, minbizi-zelulak tumore primariotik bereiz daitezke eta gorputzeko beste zati batzuetara hedatzen dira odol-fluxuaren edo sistema linfatikoaren bidez, metastasia bezala ezagutzen den prozesuan.
Behin minbizia hedatu denean, zailagoa da tratatzea.
Prostatako minbizia faktore hormonalek ere eragin dezakete, batez ere testosterona hormona androgenoak.
Testosteronak prostatako minbiziaren zelulen hazkundea estimulatu dezake, eta prostatako minbiziaren tratamendu askok hormona honen mailak murriztea edo bere efektuak blokeatzea dute helburu.
Laburbilduz, prostatako minbiziaren fisiologia zelulen hazkunde eta zatiketa kontrolatu gabeak dira prostatako guruinaren barruan, faktore genetikoek, hormonalek eta ingurumenek eragin ditzaketenak.
Gaixotasunaren oinarrizko mekanismoak ulertzea funtsezkoa da tratamendu eraginkorrak garatzeko eta prostatako minbizia duten gaixoen emaitzak hobetzeko.
Zobniw CM, Causebrook A, Fong MK: Clinical use of abiraterone in the treatment of metastatic castration-resistant prostate cancer. Res Rep Urol. 2014, 6 (): 97-105.
Lim HY, Agarwal AM, Agarwal N, Ward JH: Recurrent epistaxis as a presenting sign of androgen-sensitive metastatic prostate cancer. Singapore Med J. 2009, 50 (5): e178-80.
Kohli M, Qin R, Jimenez R, Dehm SM: Biomarker-based targeting of the androgen-androgen receptor axis in advanced prostate cancer. Adv Urol. 2012, 2012 (): 781459.
Nelson JB, Hedican SP, George DJ, Reddi AH, Piantadosi S, Eisenberger MA, Simons JW: Identification of endothelin-1 in the pathophysiology of metastatic adenocarcinoma of the prostate. Nat Med. 1995, 1 (9): 944-9.
Msaouel P, Nandikolla G, Pneumaticos SG, Koutsilieris M: Bone microenvironment-targeted manipulations for the treatment of osteoblastic metastasis in castration-resistant prostate cancer. Expert Opin Investig Drugs. 2013, 22 (11): 1385-400.
Kotani K, Sekine Y, Ishikawa S, Ikpot IZ, Suzuki K, Remaley AT: High-density lipoprotein and prostate cancer: an overview. J Epidemiol. 2013, 23 (5): 313-9.
Jadvar H: Molecular imaging of prostate cancer: a concise synopsis. Mol Imaging. , 8 (2): 56-64.
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What is pathophysiology of prostate cancer?
The pathophysiology of prostate cancer refers to the underlying mechanisms and processes that lead to the development and progression of the disease.
Prostate cancer is a malignant tumor that arises from the cells of the prostate gland, which is a small, walnut-shaped organ located below the bladder in men.
The prostate gland produces seminal fluid, which nourishes and transports sperm.
The exact cause of prostate cancer is not fully understood, but several factors are known to increase the risk of developing the disease.
These include age, family history, race, and certain genetic mutations.
Prostate cancer is more common in older men, with the majority of cases occurring in men over the age of 65.
Additionally, men with a family history of prostate cancer are at an increased risk, as are African American men and men of Caribbean descent.
The pathophysiology of prostate cancer involves the uncontrolled growth and division of cells within the prostate gland.
This can occur due to genetic mutations that lead to the overexpression of certain growth factors or the inactivation of tumor suppressor genes.
These mutations can result in the unregulated growth of cells, leading to the formation of a tumor.
As the tumor grows, it can invade nearby tissues and organs, such as the bladder, rectum, and nearby lymph nodes.
In some cases, cancer cells can break away from the primary tumor and spread to other parts of the body through the bloodstream or lymphatic system, a process known as metastasis.
Once the cancer has spread, it can be more difficult to treat.
Prostate cancer can also be influenced by hormonal factors, particularly the androgen hormone testosterone.
Testosterone can stimulate the growth of prostate cancer cells, and many treatments for prostate cancer aim to reduce the levels of this hormone or block its effects.
In summary, the pathophysiology of prostate cancer involves the uncontrolled growth and division of cells within the prostate gland, which can be influenced by genetic, hormonal, and environmental factors.
Understanding the underlying mechanisms of the disease is crucial for developing effective treatments and improving outcomes for patients with prostate cancer.
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