Ask family, friends, neighbors and/or co-workers.
		Contact your local Chamber of Commerce or Better Business Bureau for reputable Physicians that specialize in the area of medicine that you have a need for.
		Contact your city, county or state medical agencies for names of qualified Urologists. Contact and ask for referrals from medical associations. Many are listed in this publication.
		Ask your family doctor. They are in constant contact with all kinds of health care professionals and will be able to provide you with recommendations.

The Prostate
From Wikipedia

The prostate is a male reproductive organ which helps make and store seminal fluid. In adult men a typical prostate is about three centimeters long and weighs about twenty grams. It is located in the pelvis, under the urinary bladder and in front of the rectum. The prostate surrounds part of the urethra, the tube that carries urine from the bladder during urination and semen during ejaculation. Because of its location, prostate diseases often affect urination, ejaculation, or defecation. The prostate contains many small glands which make about twenty percent of the fluid comprising semen. In prostate cancer the cells of these prostate glands mutate into cancer cells. The prostate glands require male hormones, known as androgens, to work properly. Androgens include testosterone, which is made in the testes; dehydroepiandrosterone, made in the adrenal glands; and dihydrotestosterone, made in the prostate itself. Androgens are also responsible for secondary sex characteristics such as facial hair and increased muscle mass.

Prostatitis

Prostatitis is any form of inflammation of the prostate gland. Because women do not have a prostate gland, it is a condition only found in men, although women do have microscopic paraurethral Skene's glands connected to the distal third of the urethra in the prevaginal space that are homologous to the prostate, and may cause symptoms.

A prostatitis diagnosis is assigned at 8% of all urologist and 1% of all primary care physician visits in the USA.

Nomenclature

The term prostatitis refers in its strictest sense to histological (microscopic) inflammation of the tissue of the prostate gland, although historically the term has loosely been used as a rubric to describe a set of quite different conditions. To try to remedy this, the NIH devised a new classification system in 1999.

Classification

According to the 1999 National Institute of Health (NIH) Classification, there are four categories of prostatitis:

Category I: Acute prostatitis (bacterial)

Signs and symptoms

Men with this disease often have chills, fever, pain in the lower back and genital area, urinary frequency and urgency often at night, burning or painful urination, body aches, and a demonstrable infection of the urinary tract, as evidenced by white blood cells and bacteria in the urine. There may be discharge from the penis.

Diagnosis

Acute prostatitis is relatively easy to diagnose due to its symptoms that suggest infection. Common bacteria are E. Coli, Klebsiella, Proteus, Pseudomonas, Enterobacter, Enterococcus, Serratia, and Staphylococcus aureus. This can be a medical emergency in some patients and hospitalization with intravenous antibiotics may be required. A full blood count reveals increased white blood cells. Sepsis from prostatitis is very rare, but may occur in immunocompromised patients; high fever and malaise generally prompt blood cultures, which are often positive in sepsis.

Treatment

Antibiotics are the first line of treatment in acute prostatitis (Cat. I). Antibiotics usually resolve acute prostatitis infections in a very short period of time. Appropriate antibiotics should be used, based on the microbe causing the infection. Some antibiotics have very poor penetration of the prostatic capsule, others, such as Ciprofloxacin, penetrate well. Severely ill patients may need hospitalization, while nontoxic patients can be treated at home with bed rest, analgesics, stool softeners, and hydration.

Prognosis

Full recovery without sequelae is usual.

Category II: Chronic bacterial prostatitis

Signs and symptoms

Chronic bacterial prostatitis is a relatively rare condition (<5% of patients with prostate-related non-BPH LUTS) that usually presents with an intermittent UTI-type picture and that is defined as recurrent urinary tract infections in men originating from a chronic infection in the prostate. Dr. Weidner, Professor of Medicine, Department of Urology, University of Giessen, has stated: "In studies of 656 men, we seldom found chronic bacterial prostatitis. It is truly a rare disease. Most of those were E-coli." Symptoms may be completely absent until there is also bladder infection, and the most troublesome problem is usually recurrent cystitis.

Diagnosis

In chronic bacterial prostatitis there are bacteria in the prostate but usually no symptoms. The prostate infection is diagnosed by culturing urine as well as prostate fluid (expressed prostatic secretions or EPS) which are obtained by the doctor doing a rectal exam and putting pressure on the prostate. If no fluid is recovered after this prostatic massage, a post massage urine should also contain any prostatic bacteria. Prostate specific antigen levels may be elevated, although there is no malignancy.

Treatment

Treatment requires prolonged courses (4-8 weeks) of antibiotics that penetrate the prostate well (?-lactams and nitrofurantoin are ineffective). These include quinolones (ciprofloxacin, levofloxacin), sulfas (Bactrim, Septra) and macrolides (erythromycin, clarithromycin). Persistent infections may be helped in 80% of patients by the use of alpha blockers (tamsulosin (Flomax), alfuzosin), or long term low dose antibiotic therapy. Recurrent infections may be caused by inefficient urination (benign prostatic hypertrophy, neurogenic bladder), prostatic stones or a structural abnormality that acts as a reservoir for infection.

The addition of prostate massage to courses of antibiotics was previously proposed as being beneficial. It is though not without some risk, and has not been shown in more recent trials to improve outcome compared to antibiotics alone.

Prognosis

Over time, the relapse rate is high, exceeding 50%.

Category III: CP/CPPS, pelvic myoneuropathy

Signs and symptoms

In chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) there is pelvic pain of unknown cause, lasting longer than 6 months, as the key symptom. Symptoms may wax and wane. Pain can range from mild discomfort to debilitating. Pain may radiate to back and rectum, making sitting difficult. Dysuria, arthralgia, myalgia, unexplained fatigue, abdominal pain, and frequency may all be present. Frequent urination and increased urgency may suggest interstitial cystitis (inflammation centred in bladder rather than prostate). Ejaculation may be painful, as the prostate contracts during emission of semen, although nerve- and muscle-mediated post-ejaculatory pain is more common, and a classic sign of CP/CPPS. Some patients report low libido, sexual dysfunction and erectile difficulties. Pain after ejaculation is a very specific complaint that distinguishes CP/CPPS from men with BPH or normal men.

Theories of Etiology

Theories behind the disease include autoimmunity, for which there is scant evidence, neurogenic inflammation and myofascial pain syndrome. In the latter two categories, dysregulation of the local nervous system due to past traumatic experiences or an anxious disposition and chronic albeit unconscious pelvic tensing lead to inflammation that is mediated by substances released by nerve cells (such as substance P). The prostate (and other areas of the genitourinary tract: bladder, urethra, testicles) can become inflamed by the action of the chronically activated pelvic nerves on the mast cells at the end of the nerve pathways. Similar stress-induced genitourinary inflammation has been shown experimentally in other mammals.

Prostatitis researcher Dr Anthony Schaeffer commented in a 2003 editorial of The Journal of Urology that: "It is well recognized that even if pathogenic bacteria are present in the prostate, as in men with established chronic bacterial prostatitis, they do not cause chronic pelvic pain unless acute urinary tract infection develops. Taken together, these data suggest that bacteria do not have a significant role in the development of the chronic pelvic pain syndrome. The clinical observation that antimicrobial therapy reduces symptomatology in men with chronic pelvic pain syndrome is being tested in a double-blinded NIH controlled study. Since antimicrobials may have anti-inflammatory activity, it is possible that these drugs may benefit the patient by reducing inflammation rather than eradicating bacteria."

A year after making that statement, Dr Schaeffer and his colleagues published studies showing that antibiotics are essentially useless for CP/CPPS.

The bacterial infection theory that for so long had held sway in this field was again shown to be unimportant in another 2003 study from the University of Washington team led by Dr Lee and Professor Richard Berger. The study found that one third of both normal men and patients had equal counts of similar bacteria colonizing their prostates.

Since the publication of these studies, the focus has shifted from infection to neuromuscular and psychological etiologies for chronic prostatitis .

* Possible role of unculturable bacteria in CPPS: There have been some questions regarding the role of unculturable/ultra-fastidious organisms in prostatitis. Although a team led by Keith Jarvi reported the isolation of unusual bacteria at the American Urological Association's annual meeting in 2001, it was not published in any urology journals, a sign that the paper did not withstand the peer review process. An item about the study was published in Urology Times, a newsletter for urologists. However, subsequent careful PCR studies failed to replicate these findings, and medical researchers are now in general agreement that CPPS is not caused by active bacterial infection.

* Non-bacterial prostatitis as a form of interstitial cystitis (IC): Some researchers have suggested that non-bacterial prostatitis is a form of interstitial cystitis. A large multicenter prospective randomized controlled study showed that Elmiron was slightly better than placebo in treating the symptoms of chronic prostatitis. Other therapies shown more effective than Elmiron in treating interstitial cystitis, such as quercetin and Elavil (amitriptyline), can help with chronic prostatitis.

Diagnosis

There are no definitive diagnostic tests for CP/CPPS. This is a poorly understood disorder, even though it accounts for 90%-95% of prostatitis diagnoses. It is found in men of any age, with the peak onset in the early 30s. CP/CPPS may be inflammatory (category IIIa) or non-inflammatory (category IIIb). In the inflammatory form, urine, semen, and other fluids from the prostate contain pus cells (dead white blood cells or WBCs), whereas in the non-inflammatory form no pus cells are present. Recent studies have questioned the distinction between categories IIIa and IIIb, since both categories show evidence of inflammation if pus cells are ignored and other more subtle signs of inflammation, like cytokines, are measured. In 2006, Chinese researchers found that men with categories IIIa and IIIb both had significantly and similarly raised levels of anti-inflammatory cytokine TGF and pro-inflammatory cytokine IFN in their expressed prostatic secretions when compared with controls; therefore measurement of these cytokines could be used to diagnose category III prostatitis.

Normal men have slightly more bacteria in their semen than men with chronic prostatitis/pelvic myoneuropathy. The traditional Stamey 4-glass test is invalid for diagnosis of this disorder, and inflammation cannot be localized to any particular area of the lower GU tract.

Men with CP/CPPS are more likely than the general population to suffer from Chronic Fatigue Syndrome (CFS), and Irritable Bowel Syndrome (IBS). Prostate specific antigen levels may be elevated, although there is no malignancy.

Experimental tests that could be useful in the future include tests to measure semen and prostate fluid cytokine levels. Various studies have shown increases in markers for inflammation such as elevated levels of cytokines, myeloperoxidase, and chemokines.

Treatment

Physical and psychological therapy

For chronic nonbacterial prostatitis (Cat III), also known as pelvic myoneuropathy or CP/CPPS, which makes up the majority of men diagnosed with "prostatitis", a treatment called the Stanford Protocol, developed by Stanford University Professor of Urology Rodney Anderson and psychologist David Wise in 1996, has recently been published. This is a combination of medication (using tricyclic antidepressants and benzodiazepines), psychological therapy (paradoxical relaxation, an advancement and adaptation, specifically for pelvic pain, of a type of progressive relaxation technique developed by Edmund Jacobson during the early 20th century), and physical therapy (trigger point release therapy on pelvic floor and abdominal muscles, and also yoga-type exercises with the aim of relaxing pelvic floor and abdominal muscles). While these studies are encouraging, definitive proof of efficacy would require a randomized, sham controlled, blinded study, which is not as easy to do with physical therapy as with drug therapy.

Cat. III prostatitis may have no initial trigger other than anxiety, often with an element of Obsessive Compulsive Disorder or other anxiety-spectrum problem. This is theorized to leave the pelvic area in a sensitized condition resulting in a loop of muscle tension and heightened neurological feedback (neural wind-up). Current protocols largely focus on stretches to release overtensed muscles in the pelvic or anal area (commonly referred to as trigger points), physical therapy to the area, and progressive relaxation therapy to reduce causative stress. Biofeedback physical therapy to relearn how to control pelvic floor muscles may be useful.

Aerobic exercise can help those sufferers who are not also suffering from Chronic Fatigue Syndrome (CFS) or whose symptoms are not exacerbated by exercise.

Food allergies

Anecdotal evidence suggests that food allergies and intolerances may have a role in exacerbating CP/CPPS, perhaps through mast cell mediated mechanisms. Specifically patients with gluten intolerance or celiac disease report severe symptom flares after sustained gluten ingestion. Patients may therefore find an exclusion diet helpful in lessening symptoms by identifying problem foods. Studies are lacking in this area.

Pharmacological treatment

There is a substantial list of medications used to treat this disorder.

Alpha blockers (tamsulosin, alfuzosin) are moderately helpful for many men with CPPS; duration of therapy needs to be at least 3 months.

Quercetin has shown effective in a randomized, placebo-controlled trial in chronic prostatitis using 500 mg twice a day for 4 weeks. Subsequent studies showed that quercetin, a mast cell inhibitor, reduces inflammation and oxidative stress in the prostate.

Pollen extract (Cernilton) has also been shown effective in randomized placebo controlled trials.

Commonly used therapies that have not been properly evaluated in clinical trials are dietary modification, gabapentin, and amitriptyline. Therapies shown to be ineffective by randomized placebo/sham controlled trials: levaquin (antibiotics), alpha blockers for 6 weeks or less, transurethral needle ablation of the prostate (TUNA).

At least one study suggests that multi-modal therapy (aimed at different pathways such as inflammation and neuromuscular dysfunction simultaneously) is better long term than monotherapy.

Prognosis

In recent years the prognosis for CP/CPPS has improved greatly with the advent of multimodal treatment, phytotherapy and protocols aimed at quieting the pelvic nerves through myofascial trigger point release and anxiety control.

Category IV: Asymptomatic inflammatory prostatitis

Signs and symptoms

These patients have no history of genitourinary pain complaints, but leukocytosis or bacteria have been noted during evaluation for other conditions.

Diagnosis

Diagnosis is through tests of semen, EPS or urine that reveal inflammation in the absence of symptoms.

Treatment

No treatment required. It is standard practice for men with infertility and category IV prostatitis to be given a trial of antibiotics and/or anti-inflammatories however evidence for efficacy are weak. Since signs of asymptomatic prostatic inflammation may sometimes be associated with prostate cancer, this can be addressed by tests that assess the ratio of free-to-total PSA. The results of these tests were significantly different in prostate cancer and category IV prostatitis in one study.

Benign Prostatic Hyperplasia (BPH)

Benign prostatic hyperplasia (BPH) also known as Benign prostatic hypertrophy or Benign enlargement of the prostate (BEP) refers to the increase in size of the prostate in middle-aged and elderly men. To be accurate, the process is one of hyperplasia rather than hypertrophy, but the nomenclature is often interchangeable, even amongst urologists. In BPH, the prostate grows larger and presses against the urethra and bladder, interfering with the normal flow of urine. It leads to symptoms of urinary hesitancy, frequent urination, increased risk of urinary tract infections and urinary retention. There is little correlation between BPH symptoms and the presence of prostate cancer.

Symptoms

Urinary symptoms of hesitancy, sensation of incomplete voiding and frequently passing small amounts of urine are all suggestive of BPH in middle-aged and elderly men. Due to the incomplete voiding, there is stasis of bacteria in the bladder residue and an increased risk of urinary tract infections.

Incomplete voiding (emptying) of the bladder caused by BPH also provides suitable conditions for the development of urinary bladder stones. These are formed from the crystallization of waste salts in the urine. Symptoms of bladder stone include blood in the urine and moderate to severe pain which can feel as though it is located in the penis, or around the anus, as well as the bladder. As the stone (which is often spikey) develops in size it produces increased pain and gradual reduction in mobility.

A small proportion presents with urinary retention, in which inadequate amounts of urine are passed and the bladder distends greatly. Untreated, this leads to a decrease in renal function and hydronephrosis (obstructive uropathy).

Etiology

Androgens (testosterone and related hormones) are considered to play a permissive role in BPH by most experts. This means that androgens have to be present for BPH to occur, but do not necessarily directly cause the condition. This is supported by the fact that castrated boys do not develop BPH when they age, unlike intact men. Additionally, administering exogenous testosterone is not associated with a significant increase in the risk of BPH symptoms. Dihydrotestosterone (DHT), a metabolite of testosterone is a critical mediator of prostatic growth. DHT is synthesized in the prostate from circulating testosterone.

DHT is localized principally in the stromal cells. Once synthesized, DHT can act in an autocrine fashion on the stromal cells or in paracrine fashion by diffusing into nearby epithelial cells. In both of these cell types, DHT binds to nuclear androgen receptors and signals the transcription of growth factors that are mitogenic to the epithelial and stromal cells. The importance of DHT in causing nodular hyperplasia is supported by clinical observations in which an inhibitor of 5?-reductase is given to men with this condition. Therapy with 5?-reductase inhibitor markedly reduces the DHT content of the prostate and in turn reduces prostate volume and, in many cases, BPH symptoms.

There is growing evidence that estrogens play a role in the etiology of BPH. This is based on the fact that BPH occurs when men generally have elevated estrogen levels and relatively reduced free testosterone levels, and when prostate tissue becomes more sensitive to estrogens and less responsive to DHT. Cells taken from the prostates of men who have BPH have been shown to grow in response to high estradiol levels with low androgens present.

On a microscopic level, BPH can be seen in the vast majority of men as they age, particularly over the age of 70 years, around the world. However, rates of clinically significant, symptomatic BPH vary dramatically depending on lifestyle. Men who lead a western lifestyle have a much higher incidence of symptomatic BPH than men who lead a traditional or rural lifestyle. This is confirmed by research in China showing that men in rural areas have very low rates of clinical BPH, while men living in cities adopting a western lifestyle have a skyrocketing incidence of this condition, though it is still below rates seen in the West.

Much work remains to be done to completely clarify the causes of BPH.

Diagnosis

Rectal examination (palpation of the prostate through the rectum) may reveal a markedly enlarged prostate. It is dependent on the skills of the doctor.

Often, blood tests are performed to rule out prostatic malignancy: elevated prostate specific antigen (PSA) levels suggest prostate cancer. It has to be borne in mind that rectal examination can increase PSA levels in patients without malignancy.

Ultrasound examination of the testicles, prostate and kidneys is often performed, again to rule out malignancy and hydronephrosis.

Epidemiology

More than half of the men in the United States between the ages of 60 and 70 and as many as 90% between the ages of 70 and 90 have symptoms of BPH. For some men, the symptoms may be severe enough to require treatment.

Medications

Alpha blockers (adrenergic receptor antagonists) (such as doxazosin, prazosin, alfuzosin and tamsulosin) and certain antiandrogens such as the reductase inhibitors (finasteride and dutasteride) are used, often together, in suppressing the symptoms. Alpha-blockers relax smooth muscle in the prostate and bladder neck decreasing the degree of blockage of urine flow. Alpha-blockers may cause ejaculation back into the bladder (retrograde ejaculation). This is not harmful.

There is also extensive evidence of the efficacy of Serenoa repens (saw palmetto) fruit extracts in alleviating mild-to-moderate BPH symptoms. A systematic review of evidence found comparable efficacy to finasteride.  Other herbal medicines that have solid research support in systematic reviews include beta-sitosterol from Hypoxis rooperi (African star grass) and Prunus africanum (pygeum) bark, while there is less substantial support for the efficacy of Cucurbita pepo (pumpkin) seed and Urtica dioica (stinging nettle) root. At least one double-blind trial has also supported the efficacy of rye flower pollen.

Sildenafil shows some symptomatic relief, suggesting a possible common etiology with erectile disfunction. 

Surgery

If medical treatment fails, transurethral resection of prostate (TURP) surgery may need to be performed. This involves removing (part of) the prostate through the urethra. There are also a number of new methods for reducing the size of an enlarged prostate, some of which have not been around long enough to fully establish their safety or side effects. These include various methods to destroy or remove part of the excess tissue while trying to avoid damaging what's left. Transurethral electrovaporization of the prostate (TVP), laser TURP, visual laser ablation (VLAP), TransUrethral Microwave ThermoTherapy (TUMT), TransUrethral Needle Ablation (TUNA), ethanol injection, and others are studied as alternatives.

Newer techniques involving lasers in urology have emerged in the last 5-10 years. Starting with the VLAP technique involving the ND:YAG laser with contact on the prostatic tissue. A similar technology called Photoselective Vaporization of the Prostate (PVP) with the GreenLight (KTP) laser have emerged very recently. This procedure involves a high powered 80 Watt KTP laser with a 550 micrometre laser fiber inserted into the prostate. This fiber has an internal reflection with a 70 degree deflecting angle. It is used to vaporize the tissue to the prostatic capsule. KTP lasers target haemoglobin as the chromophore and have typically have a penetration depth of 2.0mm (four times deeper than holmium).

Another procedure termed Holmium Laser Ablation of the Prostate(HoLAP) has also been gaining acceptance around the world. Like KTP the delivery device for HoLAP procedures is a 550um disposable side-firing fiber that directs the beam from a high powered 100 Watt laser at a 70degree from the fiber axis. The holmium wavelength is 2,140nm, which falls within the infrared portion of the spectrum and is invisible to the naked eye. Where KTP relies on haemoglobin as a chromophore, water within the target tissue is the chromophore for Holmium lasers. The pentration depth of Holmium lasers is <0.5mm avoiding complications associated with tissue necrosis often found with the deeper penetration and lower peak powers of KTP.

Both wavelengths, KTP and Holmium, ablate approximately one to two grams of tissue per minute.

Cystitis

Cystitis is the inflammation of the bladder. The condition primarily affects women, but can affect either sex and all age groups.

Types

There are several types of cystitis:

Causes, incidence and risk factors:

Cystitis occurs when the normally sterile lower urinary tract (urethra and bladder) is infected by bacteria and becomes irritated and inflamed. It is very common.

The condition frequently affects sexually active women ages 20 to 50 but may also occur in those who are not sexually active or in young girls. Older adults are also at high risk for developing cystitis, with the incidence in the elderly being much higher than in younger people.

Cystitis is rare in males. Females are more prone to the development of cystitis because of their relatively shorter urethra -- bacteria do not have to travel as far to enter the bladder -- and because of the relatively short distance between the opening of the urethra and the anus.

More than 85% of cases of cystitis are caused by Escherichia coli, a bacterium found in the lower gastrointestinal tract. Sexual intercourse may increase the risk of cystitis because bacteria can be introduced into the bladder through the urethra during sexual activity. Once bacteria enter the bladder, they normally are removed through urination. When bacteria multiply faster than they are removed by urination, infection results.

Risks for cystitis include obstruction of the bladder or urethra with resultant stagnation of urine, insertion of instruments into the urinary tract (such as catheterization or cystoscopy), pregnancy, diabetes, HIV, and a history of analgesic nephropathy or reflux nephropathy.

The elderly of both sexes are at increased risk for developing cystitis due to incomplete emptying of the bladder associated with such conditions as benign prostatic hyperplasia (BPH), prostatitis and urethral strictures. Also, lack of adequate fluids, bowel incontinence, immobility or decreased mobility and placement in a nursing home, all put people at increased risk for cystitis.

Symptoms

Signs and Tests

Treatment

Because of the risk of the infection spreading to the kidneys (complicated UTI) and due to the high complication rate in the elderly population and in diabetics, prompt treatment is almost always recommended.

Medication

Antibiotics are used to control the bacterial infection. It is vital that you finish the entire course of prescribed antibiotics. Commonly used antibiotics include:

The choice of antibiotic should preferably be guided by the result of urine culture.

Chronic or recurrent UTI should be treated thoroughly because of the chance of kidney infection (pyelonephritis). Antibiotics control the bacterial infection. They may be required for long periods of time. Prophylactic low-dose antibiotics are sometimes recommended after acute symptoms have subsided.

Pyridium may be used to reduce the burning and urgency associated with cystitis. In addition, common substances that increase acid in the urine, such as ascorbic acid or cranberry juice, may be recommended to decrease the concentration of bacteria in the urine.

Monitoring

Follow-up may include urine cultures to ensure that bacteria are no longer present in the bladder.

Expectations

Most cases of cystitis are uncomfortable but disappear without complication after treatment.

Possible complications

Prevention

Keeping the genital area clean and remembering to wipe from front to back may reduce the chance of introducing bacteria from the rectal area to the urethra.

Increasing the intake of fluids may allow frequent urination to flush the bacteria from the bladder. Urinating immediately after sexual intercourse may help eliminate any bacteria that may have been introduced during intercourse. Refraining from urinating for long periods of time may allow bacteria time to multiply, so frequent urinating may reduce risk of cystitis in those who are prone to urinary tract infections.

Drinking cranberry juice prevents certain types of bacteria from attaching to the wall of the bladder and may lessen the chance of infection.

Prostate Cancer

Prostate cancer is a disease in which cancer develops in the prostate, a gland in the male reproductive system. Cancer occurs when cells of the prostate mutate and begin to multiply out of control. These cells may spread (metastasize) from the prostate to other parts of the body, especially the bones and lymph nodes. Prostate cancer may cause pain, difficulty in urinating, erectile dysfunction and other symptoms.

Rates of prostate cancer vary widely across the world. Although the rates vary widely between countries, it is least common in South and East Asia, more common in Europe, and most common in the United States. According to the American Cancer Society, prostate cancer is least common among Asian men and most common among black men with figures for European men in-between . However, these high rates may be affected by increasing rates of detection .

Prostate cancer develops most frequently in men over fifty. This cancer can occur only in men, as the prostate is exclusively of the male reproductive tract. It is the most common type of cancer in men in the United States, where it is responsible for more male deaths than any other cancer, except lung cancer. However, many men who develop prostate cancer never have symptoms, undergo no therapy, and eventually die of other causes. Many factors, including genetics and diet, have been implicated in the development of prostate cancer.

Prostate cancer is most often discovered by physical examination or by screening blood tests, such as the PSA (prostate specific antigen) test. There is some current concern about the accuracy of the PSA test and its usefulness. Suspected prostate cancer is typically confirmed by removing a piece of the prostate (biopsy) and examining it under a microscope. Further tests, such as X-rays and bone scans, may be performed to determine whether prostate cancer has spread.

Prostate cancer can be treated with surgery, radiation therapy, hormone therapy, occasionally chemotherapy, or some combination of these. The age and underlying health of the man as well as the extent of spread, appearance under the microscope, and response of the cancer to initial treatment are important in determining the outcome of the disease. Since prostate cancer is a disease of older men, many will die of other causes before the prostate cancer can spread or cause symptoms. This makes treatment selection difficult. The decision whether or not to treat localized prostate cancer (a tumor that is contained within the prostate) with curative intent is a patient trade-off between the expected beneficial and harmful effects in terms of patient survival and quality of life.

Symptoms

When normal cells are damaged beyond repair, they are eliminated by apoptosis. Cancer cells avoid apoptosis and continue to multiply in an unregulated manner.

Early prostate cancer usually causes no symptoms. Often it is diagnosed during the workup for an elevated PSA noticed during a routine checkup. Sometimes, however, prostate cancer does cause symptoms, often similar to those of diseases such as benign prostatic hypertrophy. These include frequent urination, increased urination at night, difficulty starting and maintaining a steady stream of urine, blood in the urine, and painful urination. Prostate cancer may also cause problems with sexual function, such as difficulty achieving erection or painful ejaculation

Advanced prostate cancer may cause additional symptoms as the disease spreads to other parts of the body. The most common symptom is bone pain, often in the vertebrae (bones of the spine), pelvis or ribs, from cancer which has spread to these bones. Prostate cancer in the spine can also compress the spinal cord, causing leg weakness and urinary and fecal incontinence.

Pathophysiology

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 the seminal 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.

Epidemiology

The specific causes of prostate cancer remain unknown 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 70. However, many men never know they have prostate cancer. Autopsy studies of Chinese, German, Israeli, Jamaican, Swedish, and Ugandan men who died of other causes have found prostate cancer in thirty percent of men in their 50s, and in eighty percent of men in their 70s. In the year 2005 in the United States, there were an estimated 230,000 new cases of prostate cancer and 30,000 deaths due to prostate cancer.

A man's genetic background contributes to his risk of developing prostate cancer. This is 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. In the United States, prostate cancer more commonly affects black men than white or Hispanic men, and is also more deadly in black men. Men who have a brother or father with prostate cancer have twice the usual risk of developing prostate cancer. Studies of twins in Scandinavia suggest that forty percent of prostate cancer risk can be explained by inherited factors. However, no single gene is responsible for prostate cancer; many different genes have been implicated. Two genes (BRCA1 and BRCA2) that are important risk factors for ovarian cancer and breast cancer in women have also been implicated in prostate cancer.

Dietary amounts of certain foods, vitamins, and minerals can contribute to prostate cancer risk. Men with higher serum levels of the short-chain fatty acid linolenic acid have higher rates of prostate cancer. However, the same series of studies showed that men with elevated levels of long-chain (EPA and DHA) had lowered incidence. A long-term study reports that "blood levels of trans fatty acids, in particular trans fats resulting from the hydrogenation of vegetable oils, are associated with an increased prostate cancer risk." Other dietary factors that may increase prostate cancer risk include low intake of vitamin E (Vitamin E is found in green, leafy vegetables), lycopene (found in tomatoes), omega-3 fatty acids (found in fatty fishes like salmon), and the mineral selenium. 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. Green tea may also be protective (due to its polyphenol content), though the data are mixed.

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. Sterilization by vasectomy may increase the risk of prostate cancer, though there are conflicting data. More frequent ejaculation also may decrease a man's risk of prostate cancer. One study showed that men who ejaculated five times a week in their 20s had a decreased rate of prostate cancer, though others have shown no benefit.

Infection or inflammation of the prostate (prostatitis) may increase the chance for prostate cancer. In particular, infection with the sexually transmitted infections chlamydia, gonorrhea, or syphilis seems to increase risk. Finally, obesity and elevated blood levels of testosterone may increase the risk for prostate cancer.

Prostate cancer risk can be decreased by modifying known risk factors for prostate cancer, such as decreasing intake of animal fat. Several medications and vitamins may also help prevent prostate cancer. Two dietary supplements, vitamin E and selenium, may help prevent prostate cancer when taken daily. Estrogens from soybeans and other plant sources (called phytoestrogens) may also help prevent prostate cancer. The selective estrogen receptor modulator drug toremifene has shown promise in early trials. Two medications which block the conversion of testosterone to dihydrotestosterone, finasteride and dutasteride, have also shown some promise. As of 2006 the use of these medications for primary prevention is still in the testing phase, and they are not widely used for this purpose.

Screening

Prostate cancer screening

Prostate cancer screening is an attempt to find unsuspected cancers. Screening tests may lead to more specific follow-up tests such as a biopsy, where small pieces of the prostate are removed for closer study. As of 2006 prostate cancer screening options include the digital rectal exam and the prostate specific antigen (PSA) blood test. Screening for prostate cancer is controversial because it is not clear if the benefits of screening outweigh the risks of follow-up diagnostic tests and cancer treatments.

Prostate cancer is a slow-growing cancer, very common among older men. In fact, most prostate cancers never grow to the point where they cause symptoms, and most men with prostate cancer die of other causes before prostate cancer has an impact on their lives. The PSA screening test may detect these small cancers that would never become life threatening. Doing the PSA test in these men may lead to overdiagnosis, including additional testing and treatment. Follow-up tests, such as prostate biopsy, may cause pain, bleeding and infection. Prostate cancer treatments may cause urinary incontinence and erectile dysfunction. Therefore, it is essential that the risks and benefits of diagnostic procedures and treatment be carefully considered before PSA screening.

Prostate cancer screening generally begins after age fifty, but may be offered earlier in black men or men with a strong family history of prostate cancer. Although there is no officially recommended cutoff, many health care providers stop monitoring PSA in men who are older than 75 years old because of concern that prostate cancer therapy may do more harm than good as age progresses and life expectancy decreases.

Digital rectal examination

Digital rectal examination (DRE) is a procedure where the examiner inserts a gloved, lubricated finger into the rectum to check the size, shape, and texture of the prostate. Areas which are irregular, hard or lumpy need further evaluation, since they may contain cancer. Although the DRE only evaluates the back of the prostate, 85% of prostate cancers arise in this part of the prostate. Prostate cancer which can be felt on DRE is generally more advanced. The use of DRE has never been shown to prevent prostate cancer deaths when used as the only screening test.

Prostate specific antigen

The PSA test measures the blood level of prostate-specific antigen, an enzyme produced by the prostate. Specifically, PSA is a serine protease similar to kallikrein. Its normal function is to liquify gelatinous semen after ejaculation, allowing spermatazoa to more easily "swim" through the uterine cervix.

PSA levels under 4 ng/mL (nanograms per milliliter) are generally considered normal, while levels over 4 ng/mL are considered abnormal (although in men over 65 levels up to 6.5 ng/mL may be acceptable, depending upon each laboratory's reference ranges). PSA levels between 4 and 10 ng/mL indicate a risk of prostate cancer higher than normal, but the risk does not seem to rise within this six-point range. When the PSA level is above 10 ng/mL, the association with cancer becomes stronger. However, PSA is not a perfect test. Some men with prostate cancer do not have an elevated PSA, and most men with an elevated PSA do not have prostate cancer.

PSA levels can change for many reasons other than cancer. Two common causes of high PSA levels are enlargement of the prostate (benign prostatic hypertrophy (BPH)) and infection in the prostate (prostatitis). It can also be raised for several weeks after ejaculation and after catheterization. PSA levels are lowered in men who use medications used to treat BPH or baldness. These medications, finasteride (marketed as Proscar or Propecia) and dutasteride (marketed as Avodart), may decrease the PSA levels by 50% or more.

Several other ways of evaluating the PSA have been developed to avoid the shortcomings of simple PSA screening. The use of age-specific reference ranges improves the sensitivity and specificity of the test. The rate of rise of the PSA over time, called the PSA velocity, has been used to evaluate men with PSA levels between 4 and 10 ng/ml, but as of 2006, it has not proven to be an effective screening test. Comparing the PSA level with the size of the prostate, as measured by ultrasound or magnetic resonance imaging, has also been studied. This comparison, called PSA density, is both costly and, as of 2006, has not proven to be an effective screening test. PSA in the blood may either be free or bound to other proteins. Measuring the amount of PSA which is free or bound may provide additional screening information, but as of 2006, questions regarding the usefulness of these measurements limit their widespread use.

Confirming the diagnosis

When a man has symptoms of prostate cancer, or a screening test indicates an increased risk for cancer, more invasive evaluation is offered. The only test which can fully confirm the diagnosis of prostate cancer is a biopsy, the removal of small pieces of the prostate for microscopic examination. However, prior to a biopsy, several other tools may be used to gather more information about the prostate and the urinary tract. Cystoscopy shows the urinary tract from inside the bladder, using a thin, flexible camera tube inserted down the urethra. Transrectal ultrasonography creates a picture of the prostate using sound waves from a probe in the rectum.

If cancer is suspected, a biopsy is offered. During a biopsy a urologist obtains tissue samples from the prostate via the rectum. A biopsy gun inserts and removes special hollow-core needles (usually three to six on each side of the prostate) in less than a second. The tissue samples are then examined under a microscope to determine whether cancer cells are present, and to evaluate the microscopic features (or Gleason score) of any cancer found. Prostate biopsies are routinely done on an outpatient basis and rarely require hospitalization. Fifty-five percent of men report discomfort during prostate biopsy.

Currently, an active area of research involves non-invasive methods of prostate tumor detection. Adenoviruses modified to transfect tumor cells with harmless yet distinct genes (such as luciferase) have proven capable of early detection. So far, though, this area of research has only been tested in animal and LNCaP models.

Staging

Prostate cancer staging

An important part of evaluating prostate cancer is determining the stage, or how far the cancer has spread. Knowing the stage helps define prognosis and is useful when selecting therapies. The most common system is the four-stage TNM system (abbreviated from Tumor/Nodes/Metastases). Its components include the size of the tumor, the number of involved lymph nodes, and the presence of any other metastases.

The most important distinction made by any staging system is whether or not the cancer is still confined to the prostate. In the TNM system, clinical T1 and T2 cancers are found only in the prostate, while T3 and T4 cancers have spread elsewhere. Several tests can be used to look for evidence of spread. These include computed tomography to evaluate spread within the pelvis, bone scans to look for spread to the bones, and endorectal coil magnetic resonance imaging to closely evaluate the prostatic capsule and the seminal vesicles.

After a prostate biopsy, a pathologist looks at the samples under a microscope. If cancer is present, the pathologist reports the grade of the tumor. The grade tells how much the tumor tissue differs from normal prostate tissue and suggests how fast the tumor is likely to grow. The Gleason system is used to grade prostate tumors from 2 to 10, where a Gleason score of 10 indicates the most abnormalities. The pathologist assigns a number from 1 to 5 for the most common pattern observed under the microscope, then does the same for the second most common pattern. The sum of these two numbers is the Gleason score. The Whitmore-Jewett stage is another method sometimes used. Proper grading of the tumor is critical, since the grade of the tumor is one of the major factors used to determine the treatment recommendation

Risk assessment

Many prostate cancers are not destined to be lethal, and most men will ultimately die from causes other than of the disease. Decisions about treatment type and timing may therefore be informed by an estimation of the risk that the tumor will ultimately recur after treatment and/or progress to metastases and mortality. Several tools are available to help predict outcomes such as pathologic stage and recurrence after surgery or radiation therapy. Most combine stage, grade, and PSA level, and some also add the number or percent of biopsy cores positive, age, and/or other information.

The D’Amico classification stratifies men to low, intermediate, or high risk based on stage, grade, and PSA. It is used widely in clinical practice and research settings. The major downside to the 3-level system is that it does not account for multiple adverse parameters (e.g., high Gleason score and high PSA) in stratifying patients.

The Partin tables predict pathologic outcomes (margin status, extraprostatic extension, and seminal vesicle invasion) based on the same 3 variables, and are published as lookup tables.

The Kattan nomograms predict recurrence after surgery and/or radiation therapy, based on data available either at time of diagnosis or after surgery. The nomograms can be calculated using paper graphs, or using software available on a website or for handheld computers. The Kattan score represents the likelihood of remaining free of disease at a given time interval following treatment.

The UCSF Cancer of the Prostate Risk Assessment (CAPRA) score predicts both pathologic status and recurrence after surgery. It offers comparable accuracy as the Kattan preoperative nomogram, and can be calculated without paper tables or a calculator. Points are assigned based on PSA, Grade, stage, age, and percent of cores positive; the sum yields a 0-10 score, with every 2 points representing roughly a doubling of risk of recurrence. The CAPRA score was derived from community-based data in the CaPSURE database.

Treatment

Treatment for prostate cancer may involve watchful waiting, surgery, radiation therapy, High Intensity Focused Ultrasound (HIFU), chemotherapy, cryosurgery, hormonal therapy, or some combination. Which option is best depends on the stage of the disease, the Gleason score, and the PSA level. Other important factors are the man's age, his general health, and his feelings about potential treatments and their possible side effects. Because all treatments can have significant side effects, such as erectile dysfunction and urinary incontinence, treatment discussions often focus on balancing the goals of therapy with the risks of lifestyle alterations.

If the cancer has spread beyond the prostate, treatment options significantly change, so most doctors who treat prostate cancer use a variety of nomograms to predict the probability of spread. Treatment by watchful waiting, HIFU, radiation therapy, cryosurgery, and surgery are generally offered to men whose cancer remains within the prostate. Hormonal therapy and chemotherapy are often reserved for disease which has spread beyond the prostate. However, there are exceptions: radiation therapy may be used for some advanced tumors, and hormonal therapy is used for some early stage tumors. Cryotherapy, hormonal therapy, and chemotherapy may also be offered if initial treatment fails and the cancer progresses.

Watchful waiting / Active Surveillance

Watchful waiting, also called "active surveillance," refers to observation and regular monitoring without invasive treatment. Watchful waiting is often used when an early stage, slow-growing prostate cancer is found in an older man. Watchful waiting may also be suggested when the risks of surgery, radiation therapy, or hormonal therapy outweigh the possible benefits. Other treatments can be started if symptoms develop, or if there are signs that the cancer growth is accelerating (e.g., rapidly rising PSA, increase in Gleason score on repeat biopsy, etc.). Most men who choose watchful waiting for early stage tumors eventually have signs of tumor progression, and they may need to begin treatment within three years. Although men who choose watchful waiting avoid the risks of surgery and radiation, the risk of metastasis (spread of the cancer) may be increased. For younger men, a trial of active surveillance may not mean avoiding treatment altogether, but may reasonably allow a delay of a few years or more, during which time the quality of life impact of active treatment can be avoided. Published data to date suggest that carefully selected men will not miss a window for cure with this approach. Additional health problems that develop with advancing age during the observation period can also make it harder to undergo surgery and radiation therapy.

Surgery

Surgical removal of the prostate, or prostatectomy, is a common treatment either for early stage prostate cancer, or for cancer which has failed to respond to radiation therapy. The most common type is radical retropubic prostatectomy, when the surgeon removes the prostate through an abdominal incision. Another type is radical perineal prostatectomy, when the surgeon removes the prostate through an incision in the perineum, the skin between the scrotum and anus. Radical prostatectomy can also be performed laparoscopically, through a series of small (1cm) incisions in the abdomen, with or without the assistance of a surgical robot.

Radical prostatectomy is highly effective for tumors which have not spread beyond the prostate; cure rates depend on risk factors such as PSA level and Gleason grade. However, it may cause nerve damage that significantly alters the quality of life of the prostate cancer survivor. The most common serious complications are loss of urinary control and impotence. Reported rates of both complications vary widely depending on how they are assessed, by whom, and how long after surgery, as well as the setting (e.g., academic series vs. community-based or population-based data). Although penile sensation and the ability to achieve orgasm usually remain intact, erection and ejaculation are often impaired. Medications such as sildenafil (Viagra), tadalafil (Cialis), or vardenafil (Levitra) may restore some degree of potency. For most men with organ-confined disease, a more limited "nerve-sparing" technique may help avoid urinary incontinence and impotence.

Radical prostatectomy has traditionally been used alone when the cancer is small. In the event of positive margins or locally advanced disease found on pathology, adjuvant radiation therapy may offer improved survival. Surgery may also be offered when a cancer is not responding to radiation therapy. However, because radiation therapy causes tissue changes, prostatectomy after radiation has a higher risk of complications.

Transurethral resection of the prostate, commonly called a "TURP," is a surgical procedure performed when the tube from the bladder to the penis (urethra) is blocked by prostate enlargement. TURP is generally for benign disease and is not meant as definitive treatment for prostate cancer. During a TURP, a small tube (cystoscope) is placed into the penis and the blocking prostate is cut away.

In metastatic disease, where cancer has spread beyond the prostate, removal of the testicles (called orchiectomy) may be done to decrease testosterone levels and control cancer growth. (See hormonal therapy, below).

Radiation therapy

External beam radiation therapy for prostate cancer is
delivered by a linear accelerator, such as this one.

External beam radiation therapy uses a linear accelerator to produce high-energy x-rays which are directed in a beam towards the prostate. A technique called Intensity Modulated Radiation Therapy (IMRT) may be used to adjust the radiation beam to conform with the shape of the tumor, allowing higher doses to be given to the prostate and seminal vesicles with less damage to the bladder and rectum. External beam radiation therapy is generally given over several weeks, with daily visits to a radiation therapy center.

Permanent implant brachytherapy is a popular treatment choice for patients with low to intermediate risk features, can be performed on an outpatient basis, and is associated with good 10-year outcomes with relatively low morbidity. It involves the placement of about 100 small "seeds" containing radioactive material (such as iodine-125 or palladium-103) with a needle through the skin of the perineum directly into the tumor while under spinal or general anesthetic. These seeds emit lower-energy X-rays which are only able to travel a short distance. Although the seeds eventually become inert, they remain in the prostate permanently. The risk of exposure to others from men with implanted seeds is generally accepted to be insignificant.

Radiation therapy is commonly used in prostate cancer treatment. It may be used instead of surgery for early cancers, and it may also be used in advanced stages of prostate cancer to treat painful bone metastases. Radiation treatments also can be combined with hormonal therapy for intermediate risk disease, when radiation therapy alone is less likely to cure the cancer. Some radiation oncologists combine external beam radiation and brachytherapy for intermediate to high risk situations. One study found that the combination of six months of androgen suppressive therapy combined with external beam radiation had improved survival compared to radiation alone in patients with localized prostate cancer. Others use a "triple modality" combination of external beam radiation therapy, brachytherapy, and hormonal therapy.

Less common applications for radiotherapy are when cancer is compressing the spinal cord, or sometimes after surgery, such as when cancer is found in the seminal vesicles, in the lymph nodes, outside the prostate capsule, or at the margins of the biopsy.

Radiation therapy is often offered to men whose medical problems make surgery more risky. Radiation therapy appears to cure small tumors that are confined to the prostate just about as well as surgery. However, as of 2006 some issues remain unresolved, such as whether radiation should be given to the rest of the pelvis, how much the absorbed dose should be, and whether hormonal therapy should be given at the same time.

Side effects of radiation therapy might occur after a few weeks into treatment. Both types of radiation therapy may cause diarrhea and rectal bleeding due to radiation proctitis, as well as urinary incontinence and impotence. Symptoms tend to improve over time. Men who have undergone external beam radiation therapy will have a higher risk of later developing colon cancer and bladder cancer.

Cryosurgery

Cryosurgery is another method of treating prostate cancer. It is less invasive than radical prostatectomy, and general anesthesia is less commonly used. Under ultrasound guidance, metal rods are inserted through the skin of the perineum into the prostate. Highly purified Argon gas is used to cool the rods, freezing the surrounding tissue at -196 °C (-320 °F). As the water within the prostate cells freeze, the cells die. The urethra is protected from freezing by a catheter filled with warm liquid. Cryosurgery generally causes fewer problems with urinary control than other treatments, but impotence occurs up to ninety percent of the time. When used as the initial treatment for prostate cancer, cryosurgery is not as effective as surgery or radiation. However, cryosurgery is potentially better than radical prostatectomy for recurrent cancer following radiation therapy.

Hormonal therapy

Hormonal therapy in prostate cancer. Diagram shows the different organs (purple text), hormones (black text and arrows), and treatments (red text and arrows) important in hormonal therapy.

Hormonal therapy for prostate cancer targets the pathways the body uses to produce DHT. A feedback loop involving the testicles, the hypothalamus, and the pituitary, adrenal, and prostate glands controls the blood levels of DHT. First, low blood levels of DHT stimulate the hypothalamus to produce gonadotropin releasing hormone (GnRH). GnRH then stimulates the pituitary gland to produce luteinizing hormone (LH), and LH stimulates the testicles to produce testosterone. Finally, testosterone from the testicles and dehydroepiandrosterone from the adrenal glands stimulate the prostate to produce more DHT. Hormonal therapy can decrease levels of DHT by interrupting this pathway at any point.

There are several forms of hormonal therapy:

	Orchiectomy is surgery to remove the testicles. Because the testicles make most of the body's testosterone, after orchiectomy testosterone levels drop. Now the prostate not only lacks the testosterone stimulus to produce DHT, but also it does not have enough testosterone to transform into DHT.
	Antiandrogens are medications such as flutamide, bicalutamide, nilutamide, and cyproterone acetate which directly block the actions of testosterone and DHT within prostate cancer cells.
	Medications which block the production of adrenal androgens such as DHEA include ketoconazole and aminoglutethimide. Because the adrenal glands only make about 5% of the body's androgens, these medications are generally used only in combination with other methods that can block the 95% of androgens made by the testicles. These combined methods are called total androgen blockade (TAB). TAB can also be achieved using antiandrogens.
	GnRH action can be interrupted in one of two ways. GnRH antagonists suppress the production of GnRH directly, while GnRH agonists suppress GnRH through the process of downregulation after an initial stimulation effect. Abarelix is an example of a GnRH antagonist, while the GnRH agonists include leuprolide, goserelin, triptorelin, and buserelin. Initially, these medications increase the production of LH. However, because the constant supply of the medication does not match the body's natural production rhythm, production of both LH and GnRH decreases after a few weeks.

As of 2006 the most successful hormonal treatments are orchiectomy and GnRH agonists. Despite their higher cost, GnRH agonists are often chosen over orchiectomy for cosmetic and emotional reasons. Eventually, total androgen blockade may prove to be better than orchiectomy or GnRH agonists used alone.

Each treatment has disadvantages which limit its use in certain circumstances. Although orchiectomy is a low-risk surgery, the psychological impact of removing the testicles can be significant. The loss of testosterone also causes hot flashes, weight gain, loss of libido, enlargement of the breasts (gynecomastia), impotence and osteoporosis. GnRH agonists eventually cause the same side effects as orchiectomy but may cause worse symptoms at the beginning of treatment. When GnRH agonists are first used, testosterone surges can lead to increased bone pain from metastatic cancer, so antiandrogens or abarelix are often added to blunt these side effects. Estrogens are not commonly used because they increase the risk for cardiovascular disease and blood clots. The antiandrogens do not generally cause impotence and usually cause less loss of bone and muscle mass. Ketoconazole can cause liver damage with prolonged use, and aminoglutethimide can cause skin rashes.

Palliative care

Palliative care for advanced stage prostate cancer focuses on extending life and relieving the symptoms of metastatic disease. Chemotherapy may be offered to slow disease progression and postpone symptoms. The most commonly used regimen combines the chemotherapeutic drug docetaxel with a corticosteroid such as prednisone. Bisphosphonates such as zoledronic acid have been shown to delay skeletal complications such as fractures or the need for radiation therapy in patients with hormone-refractory metastatic prostate cancer.

Bone pain due to metastatic disease is treated with opioid pain relievers such as morphine and oxycodone. External beam radiation therapy directed at bone metastases may provide pain relief. Injections of certain radioisotopes, such as strontium-89, phosphorus-32, or samarium-153, also target bone metastases and may help relieve pain.

Prognosis

Prostate cancer rates are higher and prognosis poorer in Western societies than the rest of the world. Many of the risk factors for prostate cancer are more prevalent in the Western world, including longer life expectancy and diets high in animal fats. Also, where there is more access to screening programs, there is a higher detection rate. Prostate cancer is the ninth most common cancer in the world, but is the number one non-skin cancer in United States men. Prostate cancer affected eighteen percent of American men and caused death in three percent in 2005. In Japan, death from prostate cancer was one-fifth to one-half the rates in the United States and Europe in the 1990s. In India in the 1990s, half of the people with prostate cancer confined to the prostate died within ten years. African-American men have 50-60 times more prostate cancer and prostate cancer deaths than men in Shanghai, China. In Nigeria, two percent of men develop prostate cancer and 64% of them are dead after two years.

In patients who undergo treatment, the most important clinical prognostic indicators of disease outcome are stage, pre-therapy PSA level and Gleason score. In general, the higher the grade and the stage, the poorer the prognosis. Nomograms can be used to calculate the estimated risk of the individual patient. The predictions are based on the experience of large groups of patients suffering from cancers at various stages.

History

Although the prostate was first described by Venetian anatomist Niccolò Massa in 1536, and illustrated by Flemish anatomist Andreas Vesalius in 1538, prostate cancer was not identified until 1853. Prostate cancer was initially considered a rare disease, probably because of shorter life expectancies and poorer detection methods in the 19th century. The first treatments of prostate cancer were surgeries to relieve urinary obstruction. Removal of the entire gland (radical perineal prostatectomy) was first performed in 1904 by Hugh Young at Johns Hopkins Hospital. Surgical removal of the testes (orchiectomy) to treat prostate cancer was first performed in the 1890s, but with limited success. Transurethral resection of the prostate (TURP) replaced radical prostatectomy for symptomatic relief of obstruction in the middle of the 20th century because it could better preserve penile erectile function. Radical retropubic prostatectomy was developed in 1983 by Patrick Walsh. This surgical approach allowed for removal of the prostate and lymph nodes with maintenance of penile function.

In 1941 Charles B. Huggins published studies in which he used estrogen to oppose testosterone production in men with metastatic prostate cancer. This discovery of "chemical castration" won Huggins the 1966 Nobel Prize in Physiology or Medicine. The role of the hormone GnRH in reproduction was determined by Andrzej W. Schally and Roger Guillemin, who both won the 1977 Nobel Prize in Physiology or Medicine for this work. Receptor agonists, such as leuprolide and goserelin, were subsequently developed and used to treat prostate cancer.

Radiation therapy for prostate cancer was first developed in the early 20th century and initially consisted of intraprostatic radium implants. External beam radiation became more popular as stronger radiation sources became available in the middle of the 20th century. Brachytherapy with implanted seeds was first described in 1983.

Systemic chemotherapy for prostate cancer was first studied in the 1970s. The initial regimen of cyclophosphamide and 5-fluorouracil was quickly joined by multiple regimens using a host of other systemic chemotherapy drugs.

Diabetes

Diabetes is a set of diseases in which the body cannot regulate the amount of glucose, or sugar, in the blood. Glucose in the blood gives your body energy. The pancreas is an organ that creates a hormone called insulin. Insulin allows glucose to move from the blood into liver, muscle, and fat cells, where it is used for fuel. When a person has diabetes, their body either doesn't make enough insulin or can't use its own insulin as well as it should. This causes sugar to build up in your blood.

Approximately, there are 20 million people in the United States, or 7% of the population, who have diabetes. While an estimated 14.6 million have been diagnosed with diabetes, 6.2 million people, or nearly one-third, are unaware that they have the disease.

Type 1

Type 1 diabetes is an autoimmune disease in which the immune system attacks the beta cells in the pancreas that make insulin. This makes the pancreas make less amount of make insulin, a hormone which helps turn blood sugar into energy. The cells become starved of energy and there is an excess of glucose in the blood. People with Type 1 diabetes must have daily injections of insulin to live. Proper diet, exercise and home blood sugar monitoring is essential to manage the disease. If your blood sugar level becomes very high, a life-threatening chemical imbalance called diabetic ketoacidosis can develop.

Type 1 diabetes can develop at any age. However, it usually develops in children and young adults, which is why it used to be called juvenile diabetes. About 5-10% of people with diabetes have type 1.

Treatment for type 1 diabetes focuses on keeping blood sugar levels within a target range. Usual treatments are:

		Taking daily insulin injections.
		Maintaining a healthy diet.
		Monitoring blood sugar levels at home.
		Getting regular exercise.

People with type 1 diabetes can live long, healthy lives if they keep their blood sugar levels as close to normal as possible.

Type 2

Type 2 diabetes is a lifelong disease that develops when the pancreas cannot produce enough insulin or when the body's tissues become resistant to insulin. Insulin helps sugar glucose enter cells, where it is used for energy. It also helps the body store extra sugar in muscle, fat, and liver cells.

When insulin is not available or is not used properly, blood sugar rises above a safe level. If blood sugar remains high for years, blood vessels and nerves throughout the body may be damaged. This puts you at increased risk for eye, heart, blood vessel, nerve, and kidney disease. Type 2 diabetes can develop at any age, although it usually develops in adults. Between 90-95% of people with diabetes have type 2.

Type 2 diabetes is caused by insulin resistance, which occurs when the body's cells and tissues do not respond properly to insulin. An individual’s weight, level of physical activity, and family history affect how your body responds to insulin. People who are overweight, get little or no exercise, or have diabetes in their family have an increased risk of developing type 2 diabetes.

Risk factors for type 2 diabetes include older age, obesity, family history, physical inactivity, and race/ethnicity. African Americans, Hispanic/Latino Americans, American Indians, and some Pacific Islanders are at particularly high risk for type 2 diabetes.

What other complications can diabetes lead to?

		Heart disease and stroke: Heart disease and stroke account for about 65% of deaths in people with diabetes.
		High blood pressure: About 73% of adults with diabetes have high blood pressure.
		Blindness: Diabetes is the leading cause of new cases of blindness among adults aged 20–74years.
		Kidney disease: Diabetes is the leading cause of kidney failure, accounting for 40% of new cases.
		Nervous system disease: About 60-70% of people with diabetes have mild to severe forms of nervous system damage.
		Amputations: More than 60% of non-traumatic leg amputations occur in people with diabetes.
		Dental disease: Almost 30% of people with diabetes have severe gum disease.

 

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About Cholesterol

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Cholesterol is a white-colored waxy substance found in cell membranes and is required for the body to help produce other cell membranes and a variety of hormones. The majority of cholesterol is produced by the liver, and the cholesterol levels found in our blood are affected by the types of foods we eat. Excessive amounts of cholesterol can build up in the arterial walls over time, thus causing hardening and narrowing of the blood vessels. When this occurs it increases the risk of heart disease by reducing the flow of blood.

Causes of high cholesterol include:

	A diet too high in saturated fats
	A genetic trait of high cholesterol
	Improper liver function
	Hormonal problems

Certain foods contain high amounts of cholesterol, and people who are concerned about reducing their cholesterol intake should avoid the following foods:

	Fatty Meats
	Full-fat dairy products
	Shrimp
	Cream, butter, cheese, ice cream, milk
	Vegetable fats, shortening and some margarines
	Sausage, salami and other similar meats
	Cakes, muffins, biscuits
	Salted nuts, crackers
	Pastry, croissants

Others can be beneficial in striving to reduce cholesterol levels. These foods include the following:

	High fiber foods
	Whole grain bread, cereals, brown rice and whole grain pasta
	Vegetable skin items, i.e.: potatoes (with skin on)
	Whole grain rolled oats, oat bran
	Fruit and vegetables
	Lean meats , skinned poultry and fish

Most people can reduce cholesterol by 10 to 20% by watching their diet. In many cases this is not enough and therefore other remedies are necessary. Medication may be required and research has shown that new drugs can be very effective in reducing cholesterol levels.

 

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Kidney Stones

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Kidney stones, also known as nephrolithiasis, urolithiasis or renal calculi, are solid concretions (crystal aggregations) of dissolved minerals in urine found inside the kidneys or ureters. They vary in size from as small as a grain of sand to as large as a grapefruit. Kidney stones typically leave the body in the urine stream; if they grow relatively large before passing (on the order of at least 2-3 millimeters), obstruction of a ureter and distention with urine can cause severe pain most commonly felt in the flank, lower abdomen and groin. Such pain, called renal colic, often comes in waves and can be particularly severe. Nausea is associated with this particular pain primarily due to the embyrological association of the kidneys and the intestinal tract. Recurrence rates are estimated at about 10% per year. Kidney stones are totally unrelated to gallstones.

An 8-mm kidney stone        

Etiology

Conventional wisdom and common sense has long held that consumption of too much calcium can aggravate the development of kidney stones, since the most common type of stone is calcium oxalate. However, strong evidence has accumulated demonstrating that low-calcium diets are associated with higher overall stone risk for the typical stone former. This is thought to be due to the binding of ingested intestinal oxalate with calcium in the gastrointestinal tract. Such oxalate binding would prevent oxalate absorption resulting in lower urinary oxalate levels. In the urine, oxalate is a very strong promotor of crystal and stone formation, about 15 times stronger than calcium.

    Star shaped bladder urolith

Other examples of kidney stones include struvite (magnesium, ammonium and phosphate), uric acid, calcium phosphate, or cystine (found only in people suffering from cystinuria). The formation of struvite stones is associated with the presence of urea-splitting bacteria, most commonly Proteus mirabilis (also Klebsiella, Serratia, Providencia species) which can split urea into ammonia, resulting in favorable conditions for the formation of struvite. Calcium phosphate is associated with metabolic disorders like hyperparathyroidism and renal tubular acidosis while uric acid stones are most common in patients with gout or other disorders of acid/base metabolism.

Renal calculi can occur due to other underlying conditions, such as renal tubular acidosis, Dent's disease and medullary sponge kidney, which are screened for in some centers in those with recurrent urinary calculi formation.

Symptoms

Kidney stones are usually asymptomatic until they obstruct the flow of urine. Symptoms can include acute flank pain (renal colic), nausea and vomiting, restlessness, dull pain, hematuria, and possibly fever if an infection is present. Acute renal colic is described as one of the worst types of pain that a patient can suffer. Note that the pain is generally due to the stone's presence in the ureter, and not—as is commonly believed—the urethra and lower genitals.

Some patients show no symptoms until their urine turns bloody—this may be the first symptom of a kidney stone. The amount of blood may not be sufficient to be seen, and thus the first warning can be microscopic hematuria, when red blood cells are found in the microscopic study of a urine sample, during a routine medical test. However, not every kidney stone patient demonstrates blood in urine, even microscopically. About 15% of proven kidney stone patients may not show even microscopic hematuria so this is not considered a definitive diagnostic sign.

Diagnosis & Investigation

Diagnosis is usually made on the basis of the location and severity of the pain, which is typically colic in nature (comes and goes in spasmodic waves). Radiological imaging is used to confirm the diagnosis and a number of other tests can be undertaken to help establish both the possible cause and consequences of the stone. Ultrasound imaging is also useful as it will give details about the presence of hydronephrosis (swelling of the kidney - suggesting the stone is blocking the outflow of urine). It can also be used to show the kidneys during pregnancy when standard x-rays are discouraged. About 10% of stones do not have enough calcium to be seen on standard x-rays (radiolucent stones) and may show up on ultrasound although they typically are seen on CT scans.

         Staghorn calculus

The relatively dense calcium renders these stones radio-opaque and they can be detected by a traditional X-ray of the abdomen that includes Kidneys, Ureters and Bladder—KUB. This may be followed by an IVP (Intravenous Pyelogram; IntraVenous Urogram (IVU) is the same test by another name) which requires about 50ml of a special dye to be injected into the bloodstream that is excreted by the kidneys and by its density helps outline any stone on a repeated X-ray. These can also be detected by a Retrograde pyelogram where similar "dye" is injected directly into the ureteral opening in the bladder by a surgeon, usually a urologist. Computed tomography (CT or CAT scan), a specialized X-ray, is considered the gold-standard diagnostic test for the detection of kidney stones, and in this setting does not require the use of intravenous contrast, which carries some risk in certain people (eg, allergy, kidney damage). All stones are detectable by CT except very rare stones composed of certain drug residues in urine. The non-contrast "renal colic study" CT scan has become the standard test for the immediate diagnosis of flank pain typical of a kidney stone. If positive for stones, a single standard x-ray of the abdomen (KUB) is recommended. This additional x-ray provides the physicians with a clearer idea of the exact size and shape of the stone as well as its surgical orientation. Further, it makes it simple to follow the progress of the stone without the need for the much more expensive CT scan just by doing another single x-ray at some point in the future.

Investigations typically carried out include:

	Microscopic study of urine, which may show proteins, red blood cells, pus cells, cellular casts and crystals.
	Culture of a urine sample to exclude urine infection (either as a differential cause of the patient's pain, or secondary to the presence of a stone)
	Blood tests: Full blood count for the presence of a raised white cell count (Neutrophilia) suggestive of infection, a check of renal function and if raised blood calcium blood levels (hypercalcaemia).
	24 hour urine collection to measure total daily urinary volume, magnesium, sodium, uric acid, calcium, citrate, oxalate and phosphate.

Treatment

90% of stones 4 mm or less in size usually will pass spontaneously, however the majority of stones greater than 6 mm will require some form of intervention. In most cases, a smaller stone that is not symptomatic is often given up to 30 days to move or pass before consideration is given to any surgical intervention as it's been found that waiting longer tends to lead to additional complications. Immediate surgery may be required in certain situations such as in people with only one working kidney, intractable pain or in the presence of an infected kidney blocked by a stone which can rapidly cause severe sepsis and toxic shock.

Management of pain from kidney stones varies from country to country and even from physician to physician, but may require intravenous medication (eg, narcotic or nonsteroidal anti-inflammatories) in acute situations. Similar classes of drugs may be effectve orally in an outpatient setting for less severe discomfort. Intravenous ketorolac (Toradol) has been found to be quite effective in many cases of acute renal colic to control the pain without the need for narcotic medications. Ketorolac is a non-steroidal anti-inflammatory that is related to aspirin and ibuprofen. Most acute kidney stone pain will last less than 24 hours and not require hospitalization. Patients are encouraged to strain their urine so they can collect the stone when it eventually passes and send it for chemical composition analysis.

In many cases non-invasive Extracorporeal Shock Wave Lithotripsy or (ESWL) may be used. Otherwise some form of invasive procedure is required; with approaches including ureteroscopic fragmentation (or simple basket extraction if feasible) using laser, ultrasonic or mechanical (pneumatic, shock-wave) forms of energy to fragment the stones. Percutaneous nephrolithotomy or open surgery may ultimately be necessary for large or complicated stones or stones which fail other less invasive attempts at treatment.

A single retrospective study in the USA, at the Mayo Clinic, has suggested that lithotripsy may increase subsequent incidence of diabetes and hypertension, but it has not been felt warranted to change clinical practice at the clinic. The study reflects early experience with the original lithotripsy machine which had a very large blast path, much larger than what is used on modern machines. Further study is believed necessary to determine how much risk this treatment actually has using modern machines and treatment regimens.

Prevention

Preventive strategies include dietary modifications and sometimes also taking drugs with the goal of reducing excretory load on the kidneys:

	Drinking enough water to make 2 to 2.5 litres of urine per day.
	A diet low in protein, nitrogen and sodium intake.
	Restriction of oxalate-rich foods and maintaining an adequate intake of dietary calcium is recommended. There is equivocal evidence that calcium supplements increase the risk of stone formation, though calcium citrate appears to carry the lowest, if any, risk.
	Taking drugs such as thiazides, potassium citrate, magnesium citrate and allopurinol depending on the cause of stone formation.
	Depending on the stone formation disease, vitamin B-6 and orthophosphate supplements may be helpful, although these treatments are generally reserved for those with Hyperoxaluria. Cellulose supplements have also shown potential for reducing kidney stones caused by hypercalciuria (excessive urinary calcium) although today other means are generally used as cellulose therapy is associated with significant side effects.

Certain foods may increase the risk of stones: spinach, rhubarb, chocolate, peanuts, cocoa, tomato juice, grapefruit juice, apple juice, soda (acidic and contains phosphorus), and berries (high levels of oxalate). In the United States, the South has the highest incidence of kidney stones, a region where sweet tea consumption is very common. Other drinks are associated with decreased risk of stones, including wine, lemonade and orange juice, the latter two of which are rich in citrate, a stone inhibitor.

Although it has been claimed that the diuretic effects of alcohol can result in dehydration, which is important for kidney stones sufferers to avoid, there are no conclusive data demonstrating any cause and effect regarding kidney stones. However, some have theorized that frequent and binge drinkers create situations that set up dehydration, (alcohol consumption, hangovers, and poor sleep and stress habits). In this view, it is not the alcohol that creates a kidney stone but it is the alcohol drinker's associated behavior that sets it up.

One of the recognized medical therapies for prevention of stones is thiazides, a class of drugs usually thought of as diuretic. These drugs prevent stones through an effect independent of their diuretic properties: they reduce urinary calcium excretion. Nonetheless, their diuretic property does not preclude their efficacy as stone preventive. Sodium restiction is necessary for clinical effect of thiazides, as sodium excess promotes calcium excretion. Though some have said that the effect probably fades after two years or so of therapy (tachyphylaxis), in fact it is only randomized controlled trials lasting 2 years or more that show the effect; there is really no good evidence from studies of calcium metabolism that the thiazide effect does not last indefinitely. Thiazides are the medical therapy of choice for most cases of hypercalciuria (excessive urinary calcium) but may not be suitable for all calcium stone formers; just those with high urinary calcium levels.

Allopurinol (Zyloprim) is another drug with proven benefits in some calcium kidney stone formers. Allopurinol interferes with the liver's production of uric acid. Hyperuricosuria, too much uric acid in the urine, is a risk factor for calcium stones. Allopurinol reduces calcium stone formation in such patients. The drug is also used in patients with gout or hyperuricemia, but hyperuricosuria is not the critical feature of uric acid stones. Uric acid stones are more often caused by low urine pH. Even relatively high uric acid excretion will not be associated with uric acid stone formation if the urine pH is alkaline. Therefore prevention of uric acid stones relies on alkalinization of the urine with citrate. Allopurinol is reserved for patients in whom alkalinization is difficult. For patients with increased uric acid levels and calcium stones, alloprinol is one of the few treatments that has been shown in double-blinded placebo controlled studies to actually reduce kidney stone recurrences. Dosage is adjusted to maintain a reduced urinary excretion of uric acid. Serum uric acid level at or below 6 mg/dL is often the goal of the drug's use in patients with gout or hyperuricemia.

Potassium citrate is also used in kidney stone prevention. This is available as both a tablet and liquid preparation. The medication will increase the urinary pH making it more alkaline as well as increasing the urinary citrate level which helps reduce calcium oxalate crystal aggregation. Optimal 24 hour urine levels of citrate are thought to be over 320 mg/liter of urine or over 600 mg per day. There are urinary dipsticks available that allow patients to monitor and measure urinary pH so patients can optimize their urinary citrate level.

Though caffeine does acutely increase urinary calcium excretion, several independent epidemiologic studies have shown that coffee intake overall is protective for stones.

Measurements of food oxalate content have been difficult and issues remain about the proportion of oxalate that is bio-available, versus a proportion that is not absorbed by the intestine. Oxalate-rich foods are usually restricted to some degree, particularly in patients with high urinary oxalate levels, but no randomized controlled trial of oxalate restriction has been performed to test that hypothesis.

A high protein diet might be partially to blame. Protein from meat and other animal products is broken down into acids, including uric acid. The most available alkaline base to balance the acid from protein is calcium phosphate (hydroxyapatite) from the bones (buffering). The kidney filters the liberated calcium which may then form insoluble crystals (ie, stones) in urine with available oxalate (partly from metabolic processes, partly from diet) or phosphate ions depending on conditions. High protein intake is therefore associated with decreased bone density as well as stones. The acid load is associated with decreased urinary citrate excretion; citrate competes with oxalate for calcium and can thereby prevent stones. One of the simplest fixes in addition to increased fluid intake is to moderate animal protein consumption. However, despite epidemiologic data showing that more protein intake is associated with more stones, randomized controlled trials of protein restriction have not shown reduced stone prevalence. In this regard, it is not just dietary calcium per se that may cause stone formation, but rather the leaching of bone calcium. Some diseases (eg, distal renal tubular acidosis) which cause a chronically acidic state also decrease urinary citrate levels; since citrates are normally present as potent inhibitors of stone formation, these patients are prone to frequent stone formation.

For those patients interested in optimizing their kidney stone prevention options, it's essential to have a 24 hour urine test performed. This should be done with the patient on his or her regular diet and activities. The results can then be analyzed for abnormalities and appropriate treatment given.

Famous Kidney Stone Sufferers

In 271 or 270 BC, the Greek Philosopher Epicurus died from a kidney stone blockage lasting a fortnight according to his successor Hermarchus and reported by his biographer Diogenes Laertius.

French Renaissance essayist Montaigne suffered from kidney stones. British statesman Samuel Pepys also suffered from kidney stones and was operated on, pre-anesthesia, to remove a large stone which he carried with him and used to try to persuade fellow sufferers to endure the painful surgery. His contemporary, John Wilkins, Bishop of Chester, could not face the prospect and died as a result.

Dutch blacksmith Jan de Doot is remembered for having his portrait painted with the large stone that he removed from himself in 1651.

Author Chuck Palahniuk wrote about his experience with a kidney stone in his nonfiction book Stranger Than Fiction: True Stories.

Author Isaac Asimov suffered from kidney stones, and wrote about how his pain was treated with morphine, saying that he feared becoming addicted to morphine if he ever needed it again.

Astronauts often get kidney stones because of an increase in the amount of calcium in their blood due to a loss of bone density in zero gravity.

In his book, "A Year At the Movies", Mystery Science Theatre 3000 writer/performer Kevin Murphy describes his ordeal with a kidney stone: "Being gut-stabbed with a dirty spoon in a prison cafeteria is less painful."

Former Speaker of the House of Representatives, Dennis Hastert, has had a number of kidney stones. Hastert had to have kidney stone removal surgery.

Lyndon B. Johnson suffered from kidney stones at various times in his life. See Woods, "LBJ: Architect of American Ambition".

While DJ'ing at a student event, British DJ John Peel passed a kidney stone, and then proceeded to auction it off for charity at the same event.

On October 19, 2005, while working on the set of Boston Legal, actor William Shatner was taken to the emergency room for lower back pain. He eventually passed a kidney stone, but recovered and soon returned to work. Shatner sold his kidney stone in 2006 for $75,000 to GoldenPalace.com. The money will go to a housing charity.

Minnesota Twins catcher Joe Mauer has also suffered from kidney stones, when asked about it he stated, "I don't wish that on anyone."

Reggaeton artist Tito El Bambino briefly suffered from kidney stones.

Karl Pilkington was diagnosed with kidney stones in late August 2006

John Hart, signer of the Declaration of Independence, died of kidney stones.

Tycho Brahe, astronomer.

Peter Baulman (Australia) had a kidney stone removed from his right kidney in December 2003 at The Gold Coast Hospital, Southport, Queensland, Australia, weighing 356 g (12.5 oz) and measuring at its widest point, 11.86 cm (4.66 in). It holds the Guinness world record for largest and heaviest kidney stone removed from a human being.

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Bladder Cancer

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Bladder cancer refers to any of several types of malignant growths of the urinary bladder. It is a disease in which abnormal cells multiply without control in the bladder. The bladder is a hollow, muscular organ that stores urine; it is located in the pelvis. The most common type of bladder cancer begins in cells lining the inside of the bladder and is called urothelial cell or transitional cell carcinoma (UCC or TCC).

Exposure to environmental carcinogens of various types is responsible for the development of most bladder cancers. Tobacco abuse (specifically cigarette smoking) is thought to cause 50% of bladder cancers discovered in male patients and 30% of those found in female patients. Thirty percent of bladder tumors probably result from occupational exposure in the workplace to carcinogens such as benzidine. Approximately 20% of bladder cancers occur in patients without predisposing risk factors. Bladder cancer is not currently believed to be heritable (i.e., does not "run in families" as a consequence of a specific genetic abnormality).

Signs and symptoms

Bladder cancer may cause blood in the urine, pain during urination, frequent urination, or feeling the need to urinate without results. These signs and symptoms are not specific to bladder cancer, and are also caused by noncancerous conditions, including prostate infections and cystitis.

Treatment

The treatment of bladder cancer depends on how deep the tumor invades into the bladder wall. Superficial tumors (those not entering the muscle layer) can be "shaved off" using an electrocautery device attached to a cystoscope. Immunotherapy in the form of BCG instillation is also used to treat and prevent the recurrence of superficial tumors. BCG immunotherapy is effective in up to 2/3 of the cases at this stage. Instillations of chemotherapy into the bladder can also be used to treat superficial disease.

Untreated, superficial tumors may gradually begin to infiltrate the muscular wall of the bladder. Tumors that infiltrate the bladder require more radical surgery where part or all of the bladder is removed (a cystectomy) and the urinary stream is diverted. In some cases, skilled surgeons can create a substitute bladder (a neobladder) from a segment of intestinal tissue, but this largely depends upon patient preference, age of patient, renal function, and the site of the disease.

A combination of radiation and chemotherapy can also be used to treat invasive disease, and, in many cases, it is not yet known which is the better treatment - radiotherapy or radical ablative surgery.

There is weak observational evidence from one very small study (84) to suggest that the concurrent use of statins is associated with a worse outcome.

Epidemiology

In the United States, bladder cancer is the fourth most common type of cancer in men and the ninth most common cancer in women. More than 47,000 men and 16,000 women are diagnosed with bladder cancer each year.

Genetics

Bladder cancer is not linked to specific genes; however some which are more prominently studied include the FGFR3, HRAS, RB1 and TP53 genes. As with most cancers, the exact causes of bladder cancer are not known; however, many risk factors are associated with this disease. Chief among them are smoking, followed by exposure to certain chemicals. Mutations in the gene that arise in the bladder are another important risk factor for developing bladder cancer. Several genes have been identified which play a role in regulating the cycle of cell division, preventing cells from dividing too rapidly or in an uncontrolled way. Alterations in these genes may help explain why some bladder cancers grow and spread more rapidly than others.

Bladder cancer is generally not inherited; tumors usually result from genetic mutations that occur in certain bladder cells during a person's lifetime. These noninherited genetic changes are called somatic mutations. A family history of bladder cancer is, however, a risk factor for the disease. Along these lines, some people appear to inherit a reduced ability to break down certain chemicals, which makes them more sensitive to the cancer-causing effects of tobacco smoke and certain industrial chemicals.

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Development of the Urinary and
Reproductive Organs

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Note: this article is taken from the public domain 1918 Gray's Anatomy. As such, it may be in need of updating to reflect modern medical knowledge and modern writing style.

In human fetal development, the urinary and reproductive organs are developed from the intermediate cell-mass which is situated between the primitive segments and the lateral plates of mesoderm. The permanent organs of the adult are preceded by a set of structures which are purely embryonic, and which with the exception of the ducts disappear almost entirely before the end of fetal life. These embryonic structures are on either side; the pronephros, the mesonephros, the metanephros, and the Wolffian and Müllerian ducts. The pronephros disappears very early; the structural elements of the mesonephros mostly degenerate, but in their place is developed the genital gland in association with which the Wolffian duct remains as the duct of the male genital gland, the Müllerian as that of the female; some of the tubules of the metanephros form part of the permanent kidney.

The Pronephros and Wolffian Duct

In the outer part of the intermediate cell-mass, immediately under the ectoderm, in the region from the fifth cervical to the third thoracic segments, a series of short evaginations from each segment grows dorsalward and extends caudalward, fusing successively from before backward to form the pronephric duct. This continues to grow caudalward until it opens into the ventral part of the cloaca; beyond the pronephros it is termed the Wolffian duct.

The original evaginations form a series of transverse tubules each of which communicates by means of a funnel-shaped ciliated opening with the celomic cavity, and in the course of each duct a glomerulus also is developed. A secondary glomerulus is formed ventral to each of these, and the complete group constitutes the pronephros. The pronephros undergoes rapid atrophy and disappears.

The Mesonephros, Müllerian Duct, and Genital Gland

On the medial side of the Wolffian duct, from the sixth cervical to the third lumbar segments, a series of tubules, the Wolffian tubules, is developed; at a later stage in development they increase in number by outgrowths from the original tubules. These tubules first appear as solid masses of cells, which later become hollowed in the center; one end grows toward and finally opens into the Wolffian duct, the other dilates and is invaginated by a tuft of capillary bloodvessels to form a glomerulus. The tubules collectively constitute the mesonephros or Wolffian body

By the fifth or sixth week this body forms an elongated spindle-shaped structure, termed the urogenital fold (Fig. 1106), which projects into the celomic cavity at the side of the dorsal mesentery, reaching from the septum transversum in front to the fifth lumbar segment behind; in this fold the reproductive glands are developed. The Wolffian bodies persist and form the permanent kidneys in fishes and amphibians, but in reptiles, birds, and mammals, they atrophy and for the most part disappear coincidently with the development of the permanent kidneys. The atrophy begins during the sixth or seventh week and rapidly proceeds, so that by the beginning of the fifth month only the ducts and a few of the tubules remain.

In the male the Wolffian duct persists, and forms the tube of the epididymis, the ductus deferens and the ejaculatory duct, while the seminal vesicle arises during the third month as a lateral diverticulum from its hinder end. A large part of the head end of the mesonephros atrophies and disappears; of the remainder the anterior tubules form the efferent ducts of the testis; while the posterior tubules are represented by the ductuli aberrantes, and by the paradidymis, which is sometimes found in front of the spermatic cord above the head of the epididymis.

In the female the Wolffian bodies and ducts atrophy. The remains of the Wolffian tubules are represented by the epoöphoron or organ of Rosenmüller, and the paroöphoron, two small collections of rudimentary blind tubules which are situated in the mesosalpinx. The lower part of the Wolffian duct disappears, while the upper part persists as the longitudinal duct of the epoöphoron or duct of Gärtner.

The Müllerian Ducts

Shortly after the formation of the Wolffian ducts a second pair of ducts is developed; these are named the Müllerian ducts. Each arises on the lateral aspect of the corresponding Wolffian duct as a tubular invagination of the cells lining the celom. The orifice of the invagination remains patent, and undergoes enlargement and modification to form the abdominal ostium of the uterine tube. The ducts pass backward lateral to the Wolffian ducts, but toward the posterior end of the embryo they cross to the medial side of these ducts, and thus come to lie side by side between and behind the latter—the four ducts forming what is termed the genital cord. The Müllerian ducts end in an epithelial elevation, the Müllerian eminence, on the ventral part of the cloaca between the orifices of the Wolffian ducts; at a later date they open into the cloaca in this situation.

In the male the Müllerian ducts atrophy, but traces of their anterior ends are represented by the appendices testis (hydatids of Morgagni), while their terminal fused portions form the utriculus in the floor of the prostatic portion of the urethra.

In the female the Müllerian ducts persist and undergo further development. The portions which lie in the genital core fuse to form the uterus and vagina; the parts in front of this cord remain separate, and each forms the corresponding uterine tube—the abdominal ostium of which is developed from the anterior extremity of the original tubular invagination from the coelom. The fusion of the Müllerian ducts begins in the third month, and the septum formed by their fused medial walls disappears from below upward, and thus the cavities of the vagina and uterus are produced. About the fifth month an annular constriction marks the position of the neck of the uterus, and after the sixth month the walls of the uterus begin to thicken. For a time the vagina is represented by a solid rod of epithelial cells. A ring-like outgrowth of this epithelium occurs at the lower end of the uterus and marks the future vaginal fornices; about the fifth or sixth month the lumen of the vagina is produced by the breaking down of the central cells of the epithelium. The hymen represents the remains of the Müllerian eminence.

Genital Glands

The first appearance of the genital gland is essentially the same in the two sexes, and consists in a thickening of the epithelial layer which lines the peritoneal cavity on the medial side of the urogenital fold. The thick plate of epithelium extends deeply, pushing before it the mesoderm and forming a distinct projection. This is termed the genital ridge, and from it the testis in the male and the ovary in the female are developed. At first the mesonephros and genital ridge are suspended by a common mesentery, but as the embryo grows the genital ridge gradually becomes pinched off from the mesonephros, with which it is at first continuous, though it still remains connected to the remnant of this body by a fold of peritoneum, the mesorchium or mesovarium. About the seventh week the distinction of sex in the genital ridge begins to be perceptible.

The Ovary

The ovary, thus formed from the genital ridge, is at first a mass of cells derived from the celomic epithelium; later the mass is differentiated into a central part or medulla covered by a surface layer, the germinal epithelium. Between the cells of the germinal epithelium a number of larger cells, the primitive ova, are found, and these are carried into the subjacent stroma by bud-like ingrowths (genital cords) of the germinal epithelium. The surface epithelium ultimately forms the permanent epithelial covering of this organ; it soon loses its connection with the central mass, and a tunica albuginea develops between them. The ova are chiefly derived from the cells of the central mass; these are separated from one another by the growth of connective tissue in an irregular manner; each ovum assumes a covering of connective tissue (follicle) cells, and in this way the rudiments of the ovarian follicles are formed. According to Beard the primitive ova are early set apart during the segmentation of the ovum and migrate into the germinal ridge.

The Testis

The testis is developed in much the same way as the ovary. Like the ovary, in its earliest stages it consists of a central mass of epithelium covered by a surface epithelium. In the central mass a series of cords appear, and the periphery of the mass is converted into the tunica albuginea, thus excluding the surface epithelium from any part in the formation of the tissue of the testis. The cords of the central mass run together toward the future hilus and form a network which ultimately becomes the rete testis. From the cords the seminiferous tubules are developed, and between them connective-tissue septa extend. The seminiferous tubules become connected with outgrowths from the Wolffian body, which, as before mentioned, form the efferent ducts of the testis.

Descent of the Testes

The testes, at an early period of fetal life, are placed at the back part of the abdominal cavity, behind the peritoneum, and each is attached by a peritoneal fold, the mesorchium, to the mesonephros. From the front of the mesonephros a fold of peritoneum termed the inguinal fold grows forward to meet and fuse with a peritoneal fold, the inguinal crest, which grows backward from the antero-lateral abdominal wall. The testis thus acquires an indirect connection with the anterior abdominal wall; and at the same time a portion of the peritoneal cavity lateral to these fused folds is marked off as the future saccus vaginalis. In the inguinal crest a peculiar structure, the gubernaculum testis, makes its appearance. This is at first a slender band, extending from that part of the skin of the groin which afterward forms the scrotum through the inguinal canal to the body and epididymis of the testis. As development advances, the peritoneum enclosing the gubernaculum forms two folds, one above the testis and the other below it. The one above the testis is the plica vascularis, and contains ultimately the internal spermatic vessels; the one below, the plica gubernatrix, contains the lower part of the gubernaculum, which has now grown into a thick cord; it ends below at the abdominal inguinal ring in a tube of peritoneum, the saccus vaginalis, which protrudes itself down the inguinal canal. By the fifth month the lower part of the gubernaculum has become a thick cord, while the upper part has disappeared. The lower part now consists of a central core of unstriped muscle fiber, and outside this of a firm layer of striped elements, connected, behind the peritoneum, with the abdominal wall. As the scrotum develops, the main portion of the lower end of the gubernaculum is carried, with the skin to which it is attached, to the bottom of this pouch; other bands are carried to the medial side of the thigh and to the perineum. The tube of peritoneum constituting the saccus vaginalis projects itself downward into the inguinal canal, and emerges at the cutaneous inguinal ring, pushing before it a part of the Obliquus internus and the aponeurosis of the Obliquus externus, which form respectively the Cremaster muscle and the intercrural fascia. It forms a gradually elongating pouch, which eventually reaches the bottom of the scrotum, and behind this pouch the testis is drawn by the growth of the body of the fetus, for the gubernaculum does not grow commensurately with the growth of other parts, and therefore the testis, being attached by the gubernaculum to the bottom of the scrotum, is prevented from rising as the body grows, and is drawn first into the inguinal canal and eventually into the scrotum. It seems certain also that the gubernacular cord becomes shortened as development proceeds, and this assists in causing the testis to reach the bottom of the scrotum. By the end of the eighth month the testis has reached the scrotum, preceded by the saccus vaginalis, which communicates by its upper extremity with the peritoneal cavity. Just before birth the upper part of the saccus vaginalis usually becomes closed, and this obliteration extends gradually downward to within a short distance of the testis. The process of peritoneum surrounding the testis is now entirely cut off from the general peritoneal cavity and constitutes the tunica vaginalis.

Descent of the Ovaries

In the female there is also a gubernaculum, which effects a considerable change in the position of the ovary, though not so extensive a change as in that of the testis. The gubernaculum in the female lies in contact with the fundus of the uterus and contracts adhesions to this organ, and thus the ovary is prevented from descending below this level. The part of the gubernaculum between the ovary and the uterus becomes ultimately the proper ligament of the ovary, while the part between the uterus and the labium majus forms the round ligament of the uterus. A pouch of peritoneum analogous to the saccus vaginalis in the male accompanies it along the inguinal canal: it is called the canal of Nuck. In rare cases the gubernaculum may fail to contract adhesions to the uterus, and then the ovary descends through the inguinal canal into the labium majus, and under these circumstances its position resembles that of the testis.

The Metanephros and the Permanent Kidney

The rudiments of the permanent kidneys make their appearance about the end of the first or the beginning of the second month. Each kidney has a two-fold origin, part arising from the metanephros, and part as a diverticulum from the hind-end of the Wolffian duct, close to where the latter opens into the cloaca. The metanephros arises in the intermediate cell mass, caudal to the mesonephros, which it resembles in structure. The diverticulum from the Wolffian duct grows dorsalward and forward along the posterior abdominal wall, where its blind extremity expands and subsequently divides into several buds, which form the rudiments of the pelvis and calyces of the kidney; by continued growth and subdivision it gives rise to the collecting tubules of the kidney. The proximal portion of the diverticulum becomes the ureter. The secretory tubules are developed from the metanephros, which is moulded over the growing end of the diverticulum from the Wolffian duct. The tubules of the metanephros, unlike those of the pronephros and mesonephros, do not open into the Wolffian duct. One end expands to form a glomerulus, while the rest of the tubule rapidly elongates to form the convoluted and straight tubules, the loops of Henle, and the connecting tubules; these last join and establish communications with the collecting tubules derived from the ultimate ramifications of the diverticulum from the Wolffian duct. The mesoderm around the tubules becomes condensed to form the connective tissue of the kidney. The ureter opens at first into the hind-end of the Wolffian duct; after the sixth week it separates from the Wolffian duct, and opens independently into the part of the cloaca which ultimately becomes the bladder. The secretory tubules of the kidney become arranged into pyramidal masses or lobules, and the lobulated condition of the kidneys exists for some time after birth, while traces of it may be found even in the adult. The kidney of the ox and many other animals remains lobulated throughout life.

The Urinary Bladder

The bladder is formed partly from the entodermal cloaca and partly from the ends of the Wolffian ducts; the allantois takes no share in its formation. After the separation of the rectum from the dorsal part of the cloaca, the ventral part becomes subdivided into three portions:

	1.	an anterior vesico-urethral portion, continuous with the allantois—into this portion the Wolffian ducts open;
	2.	an intermediate narrow channel, the pelvic portion; and
	3.	a posterior phallic portion, closed externally by the urogenital membrane.

The second and third parts together constitute the urogenital sinus. The vesico-urethral portion absorbs the ends of the Wolffian ducts and the associated ends of the renal diverticula, and these give rise to the trigone of the bladder and part of the prostatic urethra. The remainder of the vesico-urethral portion forms the body of the bladder and part of the prostatic urethra; its apex is prolonged to the umbilicus as a narrow canal, which later is obliterated and becomes the median umbilical ligament (urachus).

The Prostate

The prostate originally consists of two separate portions, each of which arises as a series of diverticular buds from the epithelial lining of the urogenital sinus and vesico-urethral part of the cloaca, between the third and fourth months. These buds become tubular, and form the glandular substance of the two lobes, which ultimately meet and fuse behind the urethra and also extend on to its ventral aspect. The isthmus or middle lobe is formed as an extension of the lateral lobes between the common ejaculatory ducts and the bladder. Skene’s ducts in the female urethra are regarded as the homologues of the prostatic glands.

The bulbourethral glands of Cowper in the male, and greater vestibular glands of Bartholin in the female, also arise as diverticula from the epithelial lining of the urogenital sinus.

The External Organs of Generation

As already stated, the cloacal membrane, composed of ectoderm and entoderm, originally reaches from the umbilicus to the tail. The mesoderm extends to the midventral line for some distance behind the umbilicus, and forms the lower part of the abdominal wall; it ends below in a prominent swelling, the cloacal tubercle. Behind this tubercle the urogenital part of the cloacal membrane separates the ingrowing sheets of mesoderm.

The first rudiment of the penis (or clitoris) is a structure termed the phallus; it is derived from the phallic portion of the cloaca which has extended on to the end and sides of the under surface of the cloacal tubercle. The terminal part of the phallus representing the future glans becomes solid; the remainder, which is hollow, is converted into a longitudinal groove by the absorption of the urogenital membrane.

In the female a deep groove forms around the phallus and separates it from the rest of the cloacal tubercle, which is now termed the genital tubercle. The sides of the genital tubercle grow backward as the genital swellings, which ultimately form the labia majora; the tubercle itself becomes the mons pubis. The labia minora arise by the continued growth of the lips of the groove on the under surface of the phallus; the remainder of the phallus forms the clitoris.

In the male the early changes are similar, but the pelvic portion of the cloaca undergoes much greater development, pushing before it the phallic portion. The genital swellings extend around between the pelvic portion and the anus, and form a scrotal area; during the changes associated with the descent of the testes this area is drawn out to form the scrotal sacs. The penis is developed from the phallus. As in the female, the urogenital membrane undergoes absorption, forming a channel on the under surface of the phallus; this channel extends only as far forward as the corona glandis.

The corpora cavernosa of the penis (or clitoris) and of the urethra arise from the mesodermal tissue in the phallus; they are at first dense structures, but later vascular spaces appear in them, and they gradually become cavernous.

The prepuce in both sexes is formed by the growth of a solid plate of ectoderm into the superficial part of the phallus; on coronal section this plate presents the shape of a horseshoe. By the breaking down of its more centrally situated cells the plate is split into two lamellæ, and a cutaneous fold, the prepuce, is liberated and forms a hood over the glans. "Adherent prepuce is not an adhesion really, but a hindered central desquamation" (Berry Hart, op. cit.).

The Urethra

As already described, in both sexes the phallic portion of the cloaca extends on to the under surface of the cloacal tubercle as far forward as the apex. At the apex the walls of the phallic portion come together and fuse, the lumen is obliterated, and a solid plate, the urethral plate, is formed. The remainder of the phallic portion is for a time tubular, and then, by the absorption of the urogenital membrane, it establishes a communication with the exterior; this opening is the primitive urogenital ostium, and it extends forward to the corona glandis.

In the female this condition is largely retained; the portion of the groove on the clitoris broadens out while the body of the clitoris enlarges, and thus the adult urethral opening is situated behind the base of the clitoris.

In the male, by the greater growth of the pelvic portion of the cloaca a longer urethra is formed, and the primitive ostium is carried forward with the phallus, but it still ends at the corona glandis. Later it closes from behind forward. Meanwhile the urethral plate of the glans breaks down centrally to form a median groove continuous with the primitive ostium. This groove also closes from behind forward, so that the external urethral opening is shifted forward to the end of the glans.

Retrograde pyelogram

Retrograde Pyelogram is a urologic procedure where the physician injects contrast into the ureter in order to visualize the ureter and kidney. The flow of contrast (up from the bladder to the kidney) is opposite the usual flow of urine, hence the retrograde name.

Reasons for performing a retrograde pyelogram include identification of filling defects (e.g. stones or tumors), as an adjunct during the placement of ureteral stents or ureteroscopy, or to delineate renal anatomy in preparation for surgery. Retrograde pyelography is generally done when an intravenous excretory study (IVP or contrast CT scan) cannot be done because of renal disease or allergy to intravenous contrast. Relative contraindications include the presence of infected urine, pregnancy and contrast allergy.

The procedure requires cystoscopy and the placement of a small tube into the lower part of the ureter to inject contrast and opacify the ureter and renal pelvis. Fluoroscopy, or dynamic X-Rays, is typically used for visualization. The procedure is usually done under general or regional anesthesia.

It is the historic medical practice of visually examining a patient's urine for pus, blood, or other symptoms of disease. It dates back to ancient Egypt, Babylon, and India. It was particularly emphasized in Byzantine medicine.

By modern medical standards, Uroscopy is considered to be a very limited means of obtaining evidence for the correct diagnosis of a patient's condition. In addition, many of the assumptions made by ancient physicians regarding uroscopy have proved to be quite incorrect and unscientific. However, visual examination of a patient's urine may provide preliminary evidence for a diagnosis, but is generally limited to conditions that affect the urinary system (such as infection (turbidity) or blood (infection or haemorrhage).

The procedure

How Uroscopy Flask is Used

A uroscopy flask is a piece of glass that is circular at the bottom, while there is a thin neck at the top, and on top of that neck there is an opening for urine. In order for a doctor to examine a patient's urine one would have to urinate into a uroscopy flask. A uroscopy flask is a glass bottle that must be transparent. If there is any color to the uroscopy flask, diagnosis could be wrong. In the process of uroscopy, color is very crucial to find diseases. If the uroscopy flask has a tint of color, the doctor may not be able effectively diagnose the patient. The glass must also have an even thickness throughout the flask. If the top is very thin glass and the bottom is thick glass, then the impurities in the top may look different from the top and bottom. While in all actuality they could be the very same impurities. The impurities in urine have varying shapes, uneven glass will corrupt the diagnosis

The uroscopy wheel is a diagram that linked the color of urine to a particular disease. 

Uroscopy Wheel

It usually has twenty different uroscopy flasks with urine of different colors aligned around the boarder of the circle. Each flask has a line that connects it to a summary of a particular disease. This allowed doctors to have a quick reference guide to twenty different types of urine.

Temperatue When Testing

The temperature at which the urine is examined is a very important factor to consider in the process of uroscopy. When a patient urinates, the urine will be warm, so it is necessary for it to stay warm for proper evaluation. The external temperature should be the same as the internal temperature. When the temperature of urine goes down the bubbles in it will change. Some of them will disappear, but some will remain. With the temperature decrease particles and impurities will be more difficult to evaluate. They will toward the middle of the flask, then sink to the bottom. They will all mix together, making it more difficult to see the impurities.

Another problem with urine cooling is that it would become thicker. The longer that it had to cool down the more likely it was that the crystals in the it would bond together, causing it to thicken. This could lead to a false diagnosis, that is why doctors usually inspected the urine quickly.

Richard Bright in the 19th century A.D. invented a technique that allowed doctors to examine a patients urine effectively after the temperature had dropped. The process involved heating water, then inserting the uroscopy flask containing cooled urine. This would heat the urine causing the crystals that formed during loss of temperature to break down. As a result the urine will become thin again. This process is very effective, but it should be noted that a doctor should, "also be careful not to shake them much before you inspect them for you will move the particles and destroy the bubbles and dilute the deposits and confuse the situation," (The Late Greco-Roman and Byzantine Contribution to the Evolution of Laboratory Examinations of Bodily Excrement. Part1: Urine, Sperm, Menses and Stools, Pavlos C. Goudas).

Lighting When Testing

Since the identifying the color of the urine is essential for a proper diagnosis, the lighting is crucial. This is a very complicated step in the uroscopy test. The doctor must can not visualy examine the urine in an overly lit location, because it will make the urine seem too bright. He can not examine the urine in a poorly lit location, because he will not be able to properly see the urine. So, he must examine the urine in both conditions. This is done to offset the effects of not enough light and too much light. After he examines in both conditions the doctor must use his best judgment, to make a diagnosis.

 

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Common Urological Diseases

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Diabetes mellitus

Disease in which the pancreas does not function properly. Victims of this disease will have high glucose blood sugar. Victims may suffer from: cardiovascular disease (doubled risk), chronic renal failure (it is the main cause for dialysis in developed world adults), retinal damage which can lead to blindness and is the most significant cause of adult blindness in the non-elderly in the developed world, nerve damage, erectile dysfunction (impotence), to gangrene with risk of amputation of toes, feet, and even legs. Doctors would test by tasting the urine. If it was sweet tasting then it meant the patient had diabetes.

Jaundice

Yellowish discoloration of the whites of the eyes, skin, and mucous membranes caused by deposition of bile salts in these tissues. It occurs as a symptom of various diseases, such as hepatitis, that affect the processing of bile. Also called icterus.

Doctors would test by using their vision. If the urine had a brownish tint then the patient would most likely have jaundice.

Kidney Disease

The kidneys are supposed to filter wastes (especially urea) from the blood and excrete them, along with water, as urine. When they are not performing this task they patient is suffering from kidney disease. The medical field that studies the kidneys and diseases affecting the kidney is called nephrology, from the Ancient Greek name for kidney.

Doctors would test urine using a visual examination. If the urine was red and/or foamy the patient was suffering from kidney disease.

Kidney Stones

"...and I also suffer chronic disease from my kidneys for there are stones that come through the glands of my penis, sometimes big like grams, only heavier, and have many shapes. And they are polygonal and like pyramids or cubes. And because of the different shapes they hurt the lumen of the urethra and cause extreme pains and sufferings. And some other times when they are big enough they completely block my urethra and I'm completely filled with liquids. And by tearing the lumen it causes such pain, bringing death before my eyes..." (Johannes Apokaukos, metropolitan of Naupaktos and Arta 1219AD)

Tumors of Urinary Tract

When a patient develops an uncontrolled, abnormal, circumscribed growth of cells in the urinary tract.

Doctors would test urine by using a visual examination. If the urine had blood in it the patient was suffering from tumors in the urinary track.

Importance of Uroscopy

Uroscopy was important to the Roman and Byzantine eras, because it allowed doctors to diagnose patients without technology. This was an era in which there was no microscope, stethoscope, or even thermometers. All that was needed was a uroscopy wheel, uroscopy flask, and an experienced doctor to be able to give a diagnosis. It was a very simple procedure that a doctor could determine a patients problem by simply tasting and/or looking at their urine.

Uroscopy was also necessary, because the Hippocratic Oath did not allow doctors to perform any type of surgery. It stated "I will not cut for stone, even for patients in whom the disease is manifest . . ." Doctors needed a different way to find out the problems with their patients. That is when the uroscopy test became involved. It followed the Hippocratic Oath and was a very effective test for that particular time period.

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Vasectomy

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Vasectomy is a permanent birth control method. In some conventional clinics all or part of the vasa deferentia are surgically removed, thus sterilizing the patient. In more modern clinics and in no-scalpel (keyhole) vasectomies none of the vas is removed, but is instead cut and sealed.

Vasectomy should not be confused with castration: vasectomy does not involve removal of the testicles and it affects neither the production of male sex hormones (mainly testosterone) nor their secretion into the bloodstream. Therefore sexual desire (libido) and the ability to have an erection and an orgasm with an ejaculation are not affected. Because the sperm itself makes up a very small proportion of an ejaculation, vasectomy does not significantly affect the volume, appearance, texture or flavor of the ejaculate. Similarly, in females, hormone production, libido, and the menstrual cycle are not affected by a tubal ligation.

When the vasectomy is complete, sperm can no longer exit the body through the penis. They are broken down and absorbed by the body. Much fluid content is absorbed by membranes in the epididymis, and much solid content is broken down by macrophages and re-absorbed via the blood stream. Sperm is matured in the epididymis for about a month once it leaves the testicles, and approximately 50% of the sperm produced never make it to ejaculation in a non-vasectomized man. After vasectomy, the membranes increase in size to absorb more fluid, and more macrophages are recruited to break down and re-absorb more of the solid content.

Early failure rates of vasectomy are below 1%, but the effectiveness of the operation and rates of complications vary with the level of experience of the surgeon performing the operation and the surgical technique used. Most men will experience minor bruising in the scrotum for three to five days following the operation. Animal and human data indicate that vasectomy does not increase atherosclerosis and that increases in circulating immune complexes after vasectomy are transient. The weight of the evidence regarding prostate and testicular cancer suggests that men with vasectomy are not at increased risk of these cancers.

Although late failure (caused by recanalization of the vasa deferentia) is very rare, it has been documented. Some sources recommend yearly prostate examinations starting at an earlier age,.

Vasectomy is the most effective long-term contraceptive method, and is among the safest options for family planning. How popular sterilization is as a birth control method varies by age, with men in their mid 30's to mid 40's being most likely to have a vasectomy. The rate of vasectomies to tubal ligations worldwide is extremely variable, and the statistics are mostly based on questionnaire studies rather than actual counts of procedures performed. In the U.S. in 2005, the CDC published state by state details of birth control usage by method and age group. Overall, tubal ligation is ahead of vasectomy but not by a large factor. In Britain vasectomy is more popular than tubal ligation, though this statistic may be as a result of the data-gathering methodology.

Couples who opt for tubal ligation do so for a number of reasons, including:

	Convenience of coupling the procedure with delivery at a hospital.
	Refusal of the man to undergo vasectomy due to fear of possible side effects.

Couples who choose vasectomy are motivated by, among other factors:

	The lower cost and simplicity of vasectomy
	Fewer complications
	The lower mortality of vasectomy
	Fear of surgery in the woman
	Knowing men who have had the procedure and are satisfied with the results
	A stronger motivation for sterilization in the man

Recovery

Dependant on the clinic, patients may be offered/given anti-anxiety medication (such as Xanax) approximately one hour prior to the procedure. After the procedure, the patient may rest for a short time, about 15-30 minutes. It is recommended that the patient be driven home, mainly due to effects caused by the anti-anxiety medication including sedation.

Ice should be placed over the dressing or gauze, at the area of incision for 20 minutes each hour for the first 12 hours, helping to reduce swelling and pain. The dressing or gauze should be kept in place for several days to absorb any minor bleeding (bleeding should be minimal). Anecdotal evidence highly supports faster recoveries for those who follow the strict advice regarding rest and icing of the incision.

For the next 24-72 hours, the patient should remain at home, sitting or lying for most of the time. Patients should not shower, bathe, or wet the incision for 24 hours after the procedure. Patients are typically advised not to operate a motor vehicle or engage in moderate activity (such as climbing stairs more than necessary) for 72 hours. Patients may usually resume normal day-to-day activity after 72 hours but it is recommended that they wear scrotal support (can be found in sporting goods stores) or normal supportive underwear (such as briefs rather than boxer shorts) for one week. A light dressing is to be held in place for up to one week. Sexual activity should be avoided for approximately one week, but some physicians recommend resumption when "comfortable". Of course, this varies from patient to patient and their respective recovery rate. Vigorous exercise (especially bicycle riding) should be avoided for two to four weeks. After four weeks, the patient is typically clear to resume all normal activities. In some cases pain in the testicles can last past four weeks, maybe even years. This side effect is not well understood. Some men have to undergo further surgery to reduce the pain. Typically removal of the epididymis, removal of the testicle(s) or in some cases reversal of the vasectomy is employed to lessen the pain.

Reversal

Although men considering vasectomies should not think of them as reversible, and most men and their spouses are satisfied with the operation, there is a procedure to reverse vasectomies using  vasovasostomy (a form of microsurgery). It is, however, not effective in all cases, with the success rate depending on such factors as the method used for the vasectomy and the length of time that has passed since the vasectomy was performed. There is evidence that men who have had a vasectomy produce abnormal sperm, which would explain why even a mechanically successful reversal does not always restore fertility.

In one study, vasectomy reversal was found to be 75% effective for reducing the symptoms of chronic post-vasectomy pain.

In order to allow a possibility of reproduction (via artificial insemination) after vasectomy, some men opt for cryostorage of sperm before sterilization, and although the long term viability of spermatozoa in cryostorage is questionable, some experts advise that this be done before vasectomy.

Various temporary male contraceptives are being researched but not yet available, such as male hormonal contraceptives and the intra vas device. There has been at least one documented case of a vasectomy being reversed on a dog, which then fathered puppies after the reversal.

Availability

In the UK, Vasectomy is often available free of charge through the National Health Service upon referral by one's GP. However, some PCTs do not fund the procedure and patients may have to obtain a vasectomy privately. There are also private clinics (such as Marie Stopes International) who perform the operation with shorter waiting times.

Chronic Post-Vasectomy Pain

The incidence of chronic post-vasectomy pain is estimated to be less than 10% depending on the severity of pain that qualifies for the particular study. While the evidence of post vasectomy pain (PVP) is strong, it should not currently be made a major consideration when choosing to have a vasectomy.

A recent study by John Guillebaud on 5000 patients studying the effects of PVP confirmed the evidence quoted above. However, it also showed that the background risk of testicular pain in the general (non vasectomized) population is 10%. All 5000 patients when asked in questionnaires following the procedure said they would have a vasectomy again as benefits outweighed the risks.

 

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