IDEAL PATHOPHYSIOLOGY
PREDISPOSING FACTORS PRECIPITATING FACTORS
FAMILY HISTORY
GENDER: MALE HORMONAL IMBALANCE AGE: 65 YEARS AND UP LEAST FREQUENCY OF EJACULATION
ENVIRONMENTAL AND OCCUPATIONAL FACTORS: URBAN AREAS; EXPOSURE TO FERTILIZER, TEXTILE, RUBBER INDUSTRIES, AND BATTERIES
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NECROTIC CELLS REACHED THE PROSTATE GLAND INFECTION IN THE PERIPHERAL ZONE OF PROSTATE NORMAL SEMEN-SECRETING GLAND MUTATES CANCER CELLS IN THE PROSTATE GLAND DEVELOP CANCER CELLS CAN AVOID APOPTOSIS
TUMOR FORMATION
COMPRESSION OF URETHRA
HEMATURIA 38
DYSURIA
HEMATUSPERMIA
POLYURIA
INABILITY TO URINATE
NOCTURIA
INVADES SEMINAL VESICLES DEEP PAIN IN LOWER ABDOMEN AND PELVIS DEEP PAIN IN LOWER BACK
PROSTATE CANCER
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TEXTUAL EXPLANATION
A man's risk of developing prostate cancer is related to his age, genetics, race, diet, lifestyle, medications, and other factors. The primary risk factor is age. Prostate cancer is uncommon in men less than 45, but becomes more common with advancing age. The average age at the time of diagnosis is 65. A man's genetic background contributes to his risk of developing prostate cancer. This was suggested by an increased incidence of prostate cancer found in certain racial groups, in identical twins of men with prostate cancer, and in men with certain genes. Dietary amounts of certain foods, vitamins, and minerals can contribute to prostate cancer risk. Dietary factors that may increase prostate cancer risk include low intake of vitamin E and the mineral selenium. A study in 2007 cast doubt on the effectiveness of lycopene (found in tomatoes) in reducing the risk of prostate cancer. Lower blood levels of vitamin D also may increase the risk of developing prostate cancer. This may be linked to lower exposure to ultraviolet (UV) light, since UV light exposure can increase vitamin D in the body. A large study has implicated dairy, specifically low-fat milk and other dairy products to which vitamin A palmitate has been added. This form of synthetic vitamin A has been linked to prostate cancer because it reacts with zinc and protein to form an unabsorbable complex. There are also some links between prostate cancer and medications, medical procedures, and medical conditions. Daily use of anti-inflammatory medicines such as aspirin, ibuprofen, or naproxen may decrease prostate cancer risk. Use of the cholesterol-lowering drugs known as the statins may also decrease prostate cancer risk. Infection or inflammation of the prostate (prostatitis) may increase the chance for prostate cancer. In particular, infection with the sexually transmitted infections chlamydia, gonorrhea,
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or syphilis seems to increase risk. Finally, obesity and elevated blood levels of testosterone may increase the risk for prostate cancer. When normal cells are damaged beyond repair, they are eliminated by apoptosis. Cancer cells avoid apoptosis and continue to multiply in an unregulated manner. Prostate cancer is classified as an adenocarcinoma, or glandular cancer, that begins when normal semen-secreting prostate gland cells mutate into cancer cells. The region of prostate gland where the adenocarcinoma is most common is the peripheral zone. Initially, small clumps of cancer cells remain confined to otherwise normal prostate glands, a condition known as carcinoma in situ or prostatic intraepithelial neoplasia(PIN). Although there is no proof that PIN is a cancer precursor, it is closely associated with cancer. Over time these cancer cells begin to multiply and spread to the surrounding prostate tissue (the stroma) forming a tumor .Eventually, the tumor may grow large enough to invade nearby organs such as these minal vesicles or the rectum, or the tumor cells may develop the ability to travel in the bloodstream and lymphatic system. Prostate cancer is considered a malignant tumor because it is a mass of cells which can invade other parts of the body. This invasion of other organs is called metastasis. Prostate cancer most commonly metastasizes to the bones, lymph nodes, rectum, and bladder.
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ACTUAL PATHOPHYSIOLOGY
PREDISPOSING FACTORS PRECIPITATING FACTORS
FAMILY HISTORY
HORMONAL IMBALANCE
GENDER: MALE
ENVIRONMENTAL AND OCCUPATIONAL FACTORS: RURAL AREAS; EXPOSURE TO FERTILIZER AND PESTICIDE; FARMING
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NECROTIC CELLS REACHED THE PROSTATE GLAND INFECTION IN THE PERIPHERAL ZONE OF PROSTATE NORMAL SEMEN-SECRETING GLAND MUTATES CANCER CELLS IN THE PROSTATE GLAND DEVELOP CANCER CELLS CAN AVOID APOPTOSIS
TUMOR FORMATION
COMPRESSION OF URETHRA
HEMATURIA
DYSURIA
HEMATUSPERMIA
POLYURIA
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INABILITY TO URINATE
NOCTURIA
INVADES SEMINAL VESICLES DEEP PAIN IN LOWER ABDOMEN AND PELVIS DEEP PAIN IN LOWER BACK
PROSTATE CANCER
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TEXTUAL EXPLANATION
The patient developed prostate cancer in relation to his age, family history, lifestyle, and exposure to environmental and occupational factors. The primary risk factor is age, because he is 65 years old. Prostate cancer is uncommon in men less than 45, but becomes more common with advancing age. The average age at the time of diagnosis is 65. A man's genetic background contributes to his risk of developing prostate cancer. Finally, elevated blood levels of testosterone may increase the risk for prostate cancer. Testicular cells are damaged due to exposure to excessive heat, chemical agents like pesticides and fertilizer. Remember that this agents are toxins. As they go through with systemic circulation, seminal vesicles are reached. These seminal vesicles are the ones responsible in producing fructose in the production of semen in order to sustain energy needed by the sperm to travel during ejaculation. In the progression of testicular cell necrosis, the seminal vesicles are totally being damaged. The necrotic cells are being absorbed by the seminal vesicles as a response. As a result, necrotic cells reached the prostate gland causing infection in the peripheral zone of the prostate gland. The normal semensecreting gland mutates. Cancer cells in the gland then develops. When normal cells are damaged beyond repair, they are eliminated by apoptosis. Cancer cells avoid apoptosis and continue to multiply in an unregulated manner. Prostate cancer is classified as anadenocarcinoma, or glandular cancer, that begins when normal semen-secreting prostate gland cells mutate into cancer cells. The region of prostate gland where the adenocarcinoma is most common is the peripheral zone. Initially, small clumps of cancer cells remain confined to otherwise normal prostate glands, a condition known as
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carcinoma in situ or prostatic intraepithelial neoplasia (PIN). Although there is no proof that PIN is a cancer precursor, it is closely associated with cancer. Over time these cancer cells begin to multiply and spread to the surrounding prostate tissue (the stroma) forming a tumor . The development of tumor produces causes compression of urethra. As a response, the
patient experienced hematuria, dysuria, weakened urine stream, hematuspermia and polyuria. In the early stage of prostate cancer, polyuria is evident. In the later part, urine output will be affected due to compression of urethra. Eventually, the tumor may grow
large enough to invade nearby organs such as these minal vesicles or therectum, or the tumor cells may develop the ability to travel in the bloodstream and lymphatic system. Prostate cancer is considered a malignant tumor because it is a mass of cells, which can invade other parts of the body. This invasion of other organs is called metastasis. Prostate cancer most commonly metastasizes to the bones, lymph nodes, rectum, and bladder.
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