Prostata rakynyň patofiziologiyasy keselçiligiň ösüşine we ilerlemesine getirýän esas mexanizmleri we proseslerini aňladýar.
Prostat raky erkeklerde mesanäniň aşagynda ýerleşýän kiçijik, ceviz şekilli organ bolan prostata beziniň öýjüklerinden dörän erbet rak.
Prostat beziniň spermany iýmitlendirýän we göterýän tohumly suwuny emele getirýär.
Prostata rakynyň anyk sebäbi doly düşünilmeýär, ýöne keselçilik döremegiň howplulygyny artdyrýan birnäçe faktorlar belli.
Bular ýaş, maşgala taryhy, millet we käbir genetik mutasiýalary öz içine alýar.
Prostata raky gartaşan erkeklerde has köp bolýar, köplenç 65 ýaşdan geçen erkeklerde bolýar.
Şeýle - de maşgalada prostat raky bolan erkek adamlar, afroamerikalı we karib taýpasyndan bolan erkek adamlar hem rakdan ejir çekýärler.
Prostata rakynyň patofiziologiyasy prostata bezindäki öýjükleriň kontrolsuz ösüşini we bölünmegini öz içine alýar.
Bu käbir ösüş faktorlarynyň artykmaç görkezilmegine ýa-da tümor süpresor genleriniň inaktivatsiýasyna eltýän genetik mutasiyalar sebäpli bolup biler.
Bu mutasiýalar hüceyreleriň tertipsiz ösüşine we tümör döremegine eltýär.
Ösümlik ösüp barýarka, ol garynja, garynja we garynja limfa tohumlary ýaly golaýdaky dokulary we organlary basyp alýar.
Käbir ýagdaýlarda rak öýjükleri esasy tümordan aýrylyp, gan ýa-da limfa sistemasy arkaly bedeniň başga böleklerine ýaýrap biler.
Kanser ýaýransoň, bejermek kyn bolýar.
Prostata raky gormonal faktorlar, esasanam, testosteron gormony täsir edip biler.
Testosteron prostat rak öýjükleriniň ösüşini oýarýar we prostat rak üçin köp bejergiler bu gormonyň derejesini azaltmagy ýa-da onuň täsirini togtatmagy maksat edinýär.
Gysgaça aýtmak üçin, prostata rakynyň patofiziologiyasy genetik, gormonal we daşky şertlerden täsirlenýän prostata bezindäki öýjükleriň kontrolsuz ösüşini we bölünmegini öz içine alýar.
Keselligiň esasy mehanizmlerini bilmek netijeli bejergi we prostat raky bilen keselleriň netijesini gowulandyrmak üçin örän wajypdyr.
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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