(genitourinary) 4-16-15 disorders of the prostate gland

Prostate gland
Click the card to flip 👆
1 / 27
Terms in this set (27)
Acts as a valve that permits both sperm and urine to flow in the proper direction.
It produces a thin, milky white fluid containing calcium, citrate, and phosphate ions; a clotting enzyme; and a protein-hydrolyzing enzyme called serine protease (prostate specific antigen, PSA).
Empty through pores in the urethral wall
The stroma of the prostate consist of connective tissue and smooth muscle
Noncancerous enlargement of the glad
Major complication: compresses the urethra, obstructs the flow of urine, and may promote bladder and kidney infectionsStatistics:
By age 50 - 30% of males begin to experience BPH
By age 60 - 50%
By age 70 - over 90%.
20% of men with BPH will develop prostate cancer.
Benign Prostatic Hyperplasia

NOTE --- pro tip: Bc the major prostatic changes are caused by hyperplasia and not hypertrophy, the preferred term is benign prostatic hyperplasia
Become problematic when prostatic tissue compresses the urethra, where it passes through the prostate, resulting in frequency of lower urinary tract symptoms
Also called benign prostatic hypertrophy
Is an enlargement of the prostate gland.
Has a relationship to aging.
BPH is part of the natural aging process
Prostate grows with age
Dihydrotestosterone (DHT) may play a role
BPH cannot be prevented
BPH can be treated
The precise cause is not known but probably involves changes induced by hormones, especially testosterone
Is an enlargement of the prostate gland.
Symptoms associated with urethral compression
Urge to urinate often
Some delay in starting urination
Decreased force of the urinary stream.
Feeling of incomplete bladder emptying
Common complications:
Bladder or kidney infection
Bladder calculi, hydronephrosis and renal insufficiency
Inflammation of the prostate
Acute bacterial infection: Ascending infection of the
urinary tract
Symptoms: Signs of infection
Treatment: Antibiotics, analgesics, antipyretics, bedrest,
adequate hydration; Foley catheter contraindicated
Chronic bacterial infection: Recurrent urinary tract symptoms and persistence of pathogenic bacteria
Treatment: Surgery
Nonbacterial infection
Chronic prostatitis or chronic pelvic pain syndrome: No pathogenic bacteria is localized to the prostate.
Nonbacterial infection: Complaint of pain or a dull ache that is continuous or spasmodic in the suprapubic, infrapubic, scrotal, penile, or inguinal area
Treatment: Hot sitz baths, bedrest, alpha-blockers, anticholinergics, and antiinflammatory drugs
PROSTATE CANCERprostate cancer (key points)Mostly adenomas, in the periphery of the prostate Grows very slowly. Make take decades to produce symptoms. Symptoms develop only after the cancer has enlarged enough to be more difficult to cure. Complications due to bone metastases are common and consequential. The exact mechanism of carcinogenesis is unknown- likely a combination of dietary, environmental, genetic, lifestyle and hormonal causes. Hereditary factors account for a relatively small percentage (∼10%) of prostate cancers and are generally associated with early onset diseaseprostate cancer screeningDigital Rectal Exam- DRE abnormal in 6%-15% of men * About 25% of cancers found with DRE alone * Still plays a role PSA- Most significant test used in diagnosis * 25% positive predictive value to detect disease * predictive of tumor stage * Most predictive factor for biochemical recurrence * Excellent tumor marker for detecting recurrent diseaseadvantages/disadvantages of PSAOverdetection Delay in diagnosis since cut-off is 4ng/ml 20 to 40% of men with PSA of <4 ng/ml have prostate cancer PSA levels normally increase with age. PSA levels can be elevated due to other causesGleason Grading Systempreferred system for grading tumors and has been incorporated as a key prognostic factor in the 2010 TNM staging system for prostate cancerProstate Cancer- TreatmentNo treatment Watchful waiting Surgical treatments Total prostatectomy Transurethral resection of the prostate (TURP) Cryotherapy Nonsurgical treatments Radiation therapy Hormone therapy Chemotherapy Immunotherapy5 year survival rate for prostate cancer5-year survival rate of men with localized cancer is 100% with or without treatmentPathway for PCa initiation and progressionInfiltration of lymphocytes, macrophages, and neutrophils caused by repeated infections dietary factors Hormomes Epigenetic alterations mediate telomere shortening Altered cell-cycle regulatory genes Altered apoptotic regulatory genes Genetic instability and accumulation of genetic alterations Continued proliferation of genetically unstable cells leading to cancer progression. PIN, Prostatic intraepithelial neoplasia.dietary factors in development of prostate cancerHigh intake of fat is a risk factor for prostate cancer- possibly due to role in enhancing carcinogenesis, hormonal-like properties and generation of free radicals. High fat is been shown to decrease levels of dihydroxyvitamin D High-energy intake linked to high insulin and IGF-1, a powerful carcinogenic agent. Change in diet from animal products to vegetables and fruits may decrease the incidence of prostate cancer.Prostate cancer: hormones*Prostate is the equivalent to the uterus. *Hormones: Testosterone, Dihydroxytestosterone (DHT) and EstradiolAndrogensTestosterone and DHT are the most important androgens in the adult male Testosterone is the major circulating androgen DHT predominates in prostate tissue. Higher affinity for the androgen receptorPCa (prostate cancer) fun factsThe first advance in the history of studies on PCa and androgens was the development of treatment with castration and administration of estrogen by Charles B. Huggins, who won the Nobel Prize in Physiology and Medicine Androgen deprivation therapy has been standard of care for management of metastatic prostate cancer for the past 60 years John Hunter, the Scot known as the father of scientific surgery, observed in 1786 that castrated bulls had small prostates: "The prostate gland, Cowper's glands, and the glands along the urethra in the perfect male are large and pulpy...while in the castrated animal they are small, flabby, tough and ligamentous, and have little secretion...."AndrogensBenign and malignant prostate tissue is heavily dependent on androgen receptor (AR) signaling for growth and proliferation. Androgen production occurs primarily in the testes, which account for 90 to 95 percent of total circulating testosterone; testicular production of androgen is regulated by the hypothalamic pituitary axis. The adrenal glands produce the remainder of the circulating androgens. In the prostate, testosterone is converted into dihydrotestosterone (DHT) by the enzyme 5-alpha-reductase. DHT is the primary androgen that stimulates the growth of both benign and malignant prostate tissues.physiological role of androgens and estrogensThe normal development and maintenance of the prostate is dependent on androgen acting through the androgen receptor Recently, estrogens have been shown to contribute to PCa carcinogenesis Androgens and estrogens participate in the pathogenesis and development of benign prostatic hyperplasia and prostate cancer by activating androgen receptor and estrogen-receptor α.prostate cancerAndrogen-receptor signaling * Stromal androgen receptors are the priority. Prostatic epithelial neoplasia Vasectomy * Circulating free testosterone is elevated. Chronic inflammation * Risk for prostate cancer is increased. Genetic and epigenetic factors * Has a strong familial tendency; BRCA2 mutations.prostate cancer (cont)Stromal environment Multifactorial hypothesis of prostate carcinogenesis * Androgens act as strong tumor promoters to enhance DNA toxic carcinogens (reactive estrogen metabolites and estrogen, and prostate-generated reactive oxygen species). * Alterations in autocrine/paracrine growth-stimulating and growth-inhibiting factors between the prostate tumor cells and the microenvironment influence cancer pathogenesis. * Possibly unknown environmental-lifestyle carcinogens may contribute to prostate cancer.prostate cancerCellular and Molecular Model of Early Prostate Neoplasia Progression. A, This stage includes infiltration of lymphocytes, macrophages, and neutrophils caused by repeated infections, dietary factors, urine reflux, injury, onset of autoimmunity (which triggers inflammation), and wound healing. B, Epigenetic alterations mediate telomere shortening. C, Genetic instability and accumulation of genetic alterations. D, Continued proliferation of genetically unstable cells leading to cancer progression. PIN, Prostatic intraepithelial neoplasia.