Genitourinary disorders are illnesses that occur when the urinary organs and genital organs are not

functioning properly. These disorders may be the result of aging, illness, or injury.

EXAMPLES OF GUT DISORDERS

1. Acquired Platelet Function Disorder

Overview, Causes, & Risk Factors An acquired platelet function disorder refers to an abnormality in the clotting ability of the platelets that develops sometime after birth. Platelets are a type of cell found in the blood that help the blood to clot. A number of disorders can affect the function of platelets. What is going on in the body? Platelets, along with a number of other substances in the blood, help blood to clot. When a person cuts him- or herself, blood must clot, or turn solid, to stop the bleeding. When platelets lose their ability to function for any reason, abnormal bleeding and bruising may occur. What are the causes and risks of the condition? There are many possible causes of acquired platelet function defect. Common causes are as follows: certain cancers of the blood, such as multiple myeloma and polycythemia vera long-standing kidney failure, known as chronic renal failure medicines, including aspirin, penicillin, and nonsteroidal anti-inflammatory drugs, which are called NSAIDs open heart surgery severe liver disease, such as cirrhosis systemic lupus erythematosus, which is an autoimmune disorder where a person's immune system attacks his or her own body for unknown reasons

Symptoms & Signs

What are the signs and symptoms of the condition? An acquired platelet function disorder may cause no symptoms at all. When symptoms do occur, they are usually mild, unless the person has another bloodclotting problem. Some of the symptoms include: abnormally heavy bleeding from cuts or other injuries easy bruising nosebleeds petechiae, which are small red dots on the skin that signal tiny areas of bleeding

Diagnosis & Tests How is the condition diagnosed? Diagnosis of acquired platelet function defect begins with a medical history and physical exam. A blood test called a complete blood count, or CBC, is often done first. This test counts the number and types of cells in the blood. If the platelet count is in a healthy range, a test called the bleeding time can help confirm the diagnosis. In this test, the forearm is scratched to cause a small area of bleeding. The amount of time it takes for the scratch to stop bleeding is then measured. When the platelets are not working properly, this time will be longer than normal. More specialized tests of platelet function may also be done. These tests can help detect the exact type and severity of the problem. Prevention & Expectations What can be done to prevent the condition? Most cases of acquired platelet function defect cannot be prevented. Avoiding alcohol abuse, which is the most common cause of cirrhosis, could prevent many cases due to liver disease. What are the long-term effects of the condition? Most long-term effects are related to the cause of the acquired platelet function defect. For example, cases due to medicines usually go away when the medicine is stopped. These cases may cause no long-term effects. If the cause is cancer or liver disease, death may result. In rare cases, platelet function problems can cause serious abnormal bleeding in certain areas, such as the brain.

What are the risks to others? Acquired platelet function disorders pose no risk to others.

Treatment & Monitoring What are the treatments for the condition? If the cause is a medicine, the medicine can be stopped, and the problem usually goes away. In cases due to other causes, treatment is directed at the cause when possible. Someone who has blood cancer may need chemotherapy. An individual with systemic lupus erythematosus may need medicines such as prednisone to suppress the immune system. Regardless of the cause, a platelet transfusion, which is similar to a blood transfusion, can be given if severe bleeding occurs. Rarely, a drug called DDAVP is used when platelet bleeding problems occur in a person with kidney failure. What are the side effects of the treatments? A platelet transfusion may cause an allergic reaction or infection. DDAVP may cause fluid retention and high blood pressure. What happens after treatment for the condition? If the condition is caused by a medicine, it will go away after the medicine is stopped. No further treatment may be needed in these cases. Those with more serious causes, such as cancer or liver failure, often need further treatment for these conditions. How is the condition monitored? Any new or worsening symptoms should be reported to the doctor. Tests of platelet function may also be repeated in some cases.

2. Reactive Arthritis - Reiter's Syndrome

Overview, Causes, & Risk Factors Reiter's syndrome is a condition that causes arthritis in people who are genetically susceptible. It may also affect the eyes and the urethra, the tube that drains urine from the bladder.

What is going on in the body? Reiter's syndrome refers to a condition in which a person develops acute arthritis in response to an infection. The affected joints involved in the arthritis do not contain infection. The immune system causes inflammation of the joints in response to an infection in a person with Reiter's syndrome. Reiter's syndrome may be seen following many different infections, including: sexually transmitted disease, such as Chlamydia trachomatis\. Sexually transmitted disease refers to any contagious disease transmitted from one person to another during sexual contact. ',CAPTION,'Chlamydia');" onmouseout="return nd();">chlamydia infection or HIV urinary tract infection intestinal infection, such as food poisoning known as salmonellosis What are the causes and risks of the condition?

For unknown reasons, certain people are genetically susceptible to Reiter's syndrome. Eighty percent of the people with Reiter's syndrome have a gene known as HLA-B27. These individuals are at risk for Reiter's syndrome following an infection with certain bacteria or viruses, including: campylobacter chlamydia HIV salmonella shigella Reiter's syndrome is most commonly seen in men between the ages of 20 and 40 years. While women can develop the condition, they usually have milder symptoms than the men do.

Symptoms & Signs What are the signs and symptoms of the condition? Typically the symptoms of Reiter's syndrome begin 7 to 14 days after the initial infection. The first symptom is often inflammation of the urethra.

 There may be a discharge from the penis or vagina. The person may experience pain or burning when urinating. The conjunctiva, or membrane that covers the eyeball, can become red and inflamed. This causes itching and excessive tearing. Several joints are usually affected at once. The toes, legs, hips, and back are generally involved. There is inflammation, redness, and pain in the affected joints. Small, painless sores develop in the mouth, on the tongue, and on the end of the penis. Occasionally, a distinctive rash of hard, thickened spots may develop on the skin on the palms and the soles of the feet. Yellow deposits may develop under the fingernails and toenails.

Diagnosis & Tests How is the condition diagnosed? Reiter's syndrome may be suspected when someone develops arthritis following an infection. The organism may be cultured from the throat, intestinal tract, or genitourinary tract. Blood tests can help confirm the diagnosis. In some cases, a joint aspiration is done to remove fluid from the joints by a needle. The fluid is then examined under a microscope in the laboratory. Prevention & Expectations What can be done to prevent the condition? Practicing safer sex can eliminate some cases of Reiter's syndrome caused by a sexually-transmitted disease. Reiter's syndrome that follows food poisoning can be avoided by using good food-handling techniques. What are the long-term effects of the condition? Although most people recover completely from Reiter's syndrome, about 20% may be left with ongoing joint pain. Some individuals may develop chronic eye irritation known as uveitis,. Ten percent of the people who have Reiter's syndrome will develop heart valve problems, including aortic regurgitation. Rarely, the syndrome may cause severe arthritis and disability. What are the risks to others?

The original infection, which triggers Reiter's syndrome, can be spread to others. However, not all people will develop Reiter's syndrome as a result of the infection. Treatment & Monitoring What are the treatments for the condition? When Reiter's syndrome is first diagnosed, a short period of bed rest may be recommended to reduce pain and inflammation in the joints. The healthcare provider may then recommend strengthening and range-of-motion exercises . Following are some of the medications used to treat Reiter's syndrome: antibiotics to treat the underlying infection that triggered Reiter's syndrome nonsteroidal anti-inflammatory drugs, or NSAIDs, such as ibuprofen and aspirin, to help control joint pain corticosteroids injected into the joints to control the swelling and pain corticosteroid ointments applied to skin lesions medications, such as methotrexate or sulfasalazine, to suppress the immune system response What are the side effects of the treatments? Antibiotics may cause stomach upset, diarrhea, and allergic reaction. NSAIDs can cause stomach upset and allergic reactions. Steroids may cause weight gain, high blood pressure, and an increased risk of infection. What happens after treatment for the condition? Arthritis symptoms may continue for up to six months. Most people recover in 2 to 16 weeks, but some have recurrent flare-ups and remissions. How is the condition monitored? Repeated physical examinations and blood tests help monitor Reiter's syndrome. Any new or worsening symptoms should be reported to the healthcare provider.

3. Liddle Syndrome

A rare hereditary disorder in which the kidneys excrete K but retain too much Na and water, leading to hypertension. Symptoms are of hypertension, fluid retention, and metabolic alkalosis. Diagnosis is through measurement of urinary electrolytes. K-sparing diuretics provide the best treatment. Liddle syndrome is a rare autosomal dominant disorder of renal epithelial transport that clinically resembles primary aldosteronism with hypertension and hypokalemic metabolic alkalosis but without elevated plasma renin or aldosterone levels. The syndrome results from an inherently increased activity of the luminal membrane Na channels, which accelerates Na resorption and K secretion in the collecting tubule. Patients with Liddle syndrome present at age < 35 yr. Hypertension and symptoms and signs of hypokalemia and metabolic alkalosis occur. Diagnosis Urine Na level Plasma renin and aldosterone levels

Diagnosis is suggested by the presence of hypertension in a young patient, particularly one with a positive family history. Low urine Na (< 20 mEq), normal plasma renin and aldosterone levels, and response to empiric treatment usually are considered sufficient to confirm the diagnosis. Definitive diagnosis can be achieved through genetic testing (see www.genetests.org for more information).

Treatment Triamterene 100 to 200 mg po bid and amiloride 5 to 20 mg po once/day are both effective because they close Na channels. Spironolactone is ineffective.

4. Fanconi Syndrome
consists of multiple defects in renal proximal tubular reabsorption, causing glucosuria, phosphaturia, generalized aminoaciduria, and HCO3 wasting. Symptoms in children are failure to thrive, growth retardation, and rickets. Symptoms in adults are osteomalacia and muscle weakness. Diagnosis is by showing glucosuria, phosphaturia, and aminoaciduria. Treatment is HCO3 replacement and measures directed at renal failure. Etiology

Hereditary Acquired

Hereditary Fanconi syndrome: This disorder usually accompanies another genetic disorder, particularly cystinosis. Cystinosis is an inherited (autosomal recessive) metabolic disorder in which cystine accumulates within cells and tissues (and is not excreted to excess in the urine as occurs in cystinuriasee Congenital Renal Transport Abnormalities: Cystinuria). Besides renal tubular dysfunction, other complications of cystinosis include eye disorders, hepatomegaly, hypothyroidism, and other manifestations. Fanconi syndrome may also accompany Wilson's disease, hereditary fructose intolerance, galactosemia, glycogen storage disease, oculocerebrorenal syndrome (Lowe syndrome), mitochondrial cytopathies, and tyrosinemia. Inheritance patterns vary with the associated disorder. Acquired Fanconi syndrome: This disorder may be caused by various drugs, including certain cancer chemotherapy drugs (eg, ifosfamide, streptozocin), antiretrovirals (eg, didanosine, cidofovir), and outdated tetracycline. All of these drugs are nephrotoxic. Acquired Fanconi syndrome also may occur after renal transplantation and in patients with multiple myeloma, amyloidosis, intoxication with heavy metals or other chemicals, or vitamin D deficiency. Pathophysiology Various defects of proximal tubular transport function occur, including impaired resorption of glucose, phosphate, amino acids, HCO3, uric acid, water, K, and Na. The aminoaciduria is generalized, and, unlike that in cystinuria, increased cystine excretion is a minor component. The basic pathophysiologic abnormality is unknown but may involve a mitochondrial disturbance. Low levels of serum phosphate cause rickets, which is worsened by decreased proximal tubular conversion of vitamin D to its active form. Symptoms and Signs In hereditary Fanconi syndrome, the chief clinical featuresproximal tubular acidosis, hypophosphatemic rickets, hypokalemia, polyuria, and polydipsiausually appear in infancy. When Fanconi syndrome occurs because of cystinosis, failure to thrive and growth retardation are common. The retinas show patchy depigmentation. Interstitial nephritis develops, leading to progressive renal failure that may be fatal before adolescence. In acquired Fanconi syndrome, adults present with the laboratory abnormalities of renal tubular acidosis (proximal type 2), hypophosphatemia, and hypokalemia.

They may present with symptoms of bone disease (osteomalacia) and muscle weakness. Diagnosis Urine testing for glucose, phosphates, and amino acids

Diagnosis is made by showing the abnormalities of renal function, particularly glucosuria (in the presence of normal serum glucose), phosphaturia, and aminoaciduria. In cystinosis, slit-lamp examination may show cystine crystals in the cornea. Treatment Sometimes NaHCO3 or KHCO3 or Na citrate or K citrate Sometimes K supplementation

Other than removing the offending nephrotoxin, there is no specific treatment. Acidosis may be lessened by giving tablets or solutions of Na or K HCO3 or citrate, eg, Shohl's solution (Na citrate and citric acid; 1 mL is equivalent to 1 mmol of HCO3) given 1 mEq/kg bid to tid or 5 to 15 mL after meals and at bedtime. K depletion may require replacement therapy with a K-containing salt. Hypophosphatemic rickets can be treated (see Congenital Renal Transport Abnormalities: Hypophosphatemic Rickets). Renal transplantation has been successful in treating renal failure. However, when cystinosis is the underlying disease, progressive damage may continue in other organs and eventually result in death.

5. Erectile Dysfunction/Impotence
The inability to attain or sustain an erection satisfactory for sexual intercourse. Most erectile dysfunction is related to vascular, neurologic, psychologic, and hormonal disorders; drug use can also be a cause. Evaluation typically includes screening for underlying disorders and measuring testosterone levels. Treatment options include oral phosphodiesterase inhibitors or apomorphine, intraurethral or intracavernosal prostaglandins, mechanical pump devices, and surgical implants. The term impotence has been replaced by the term erectile dysfunction. In the US, at least 10 to 20 million men > 18 are affected. The prevalence of partial or complete ED is about 50% in men 40 to 70 and increases with aging. However, many men can be successfully treated. Etiology

Primary ED (ie, the man has never been able to attain or sustain erections) is rare and is almost always due to psychologic factors (guilt, fear of intimacy, depression, severe anxiety) or clinically obvious anatomic abnormalities. Most often, ED is secondary (ie, a man who previously could attain and sustain erections no longer can). Over 80% of secondary ED cases have an organic etiology. However, in many men with organic disease, ED leads to secondary psychologic difficulties that compound the problem. Psychologic factors must be considered in every case. Psychologic causes may relate to performance anxiety, stress, or a mood disorder (particularly depression). ED may be situational, involving a particular place, time, or partner. The major organic causes of ED are vascular and neurologic disorders, often stemming from atherosclerosis and diabetes. Complications of surgery, usually prostate surgery, are another common cause. Other causes include hormonal disorders, drugs, and structural disorders of the penis (eg, Peyronie's disease). The most common vascular cause is atherosclerosis of penile arteries, often secondary to diabetes. Atherosclerosis and aging decrease the capacity for dilation of arterial blood vessels and smooth muscle relaxation, limiting the amount of blood that can enter the penis. Inadequate impedance of venous outflow (venous leaks) may cause ED or, more commonly, failure to maintain tumescence as long as desired. Venous leaks make it difficult for blood to remain in the penis during erection, so erections occur but cannot be sustained. Priapism, particularly as in sickle cell disease, may damage penile vasculature and lead to ED. Stroke, partial complex seizures, multiple sclerosis, peripheral and autonomic neuropathies, and spinal cord injuries are among the neurologic causes. Diabetic neuropathy and surgical injury are particularly common causes. Any endocrinopathy associated with testosterone deficiency (hypogonadism) may decrease libido and cause ED. However, erectile function only rarely improves with normalization of serum testosterone levels. Of men who have undergone transurethral resection of the prostate, up to 40% can experience problems with erections for reasons that are not clear. ED is more common after more extensive prostatic resection (eg, radical prostatectomy). Prolonged perineal pressure (as occurs during bicycle riding) can cause temporary ED.

Diagnosis Clinical evaluation Screening for depression

Testosterone level

Evaluation should include history of drug and alcohol use, smoking, diabetes, hypertension, and atherosclerosis and symptoms of vascular, hormonal, neurologic, and psychologic disorders. It is vital to screen for depression, which may not always be apparent. The Beck Depression Scale or, in older men, the Yesavage Geriatric Depression Scale is easy to administer and may be useful. Satisfaction with sexual relationships should also be explored. Partner sexual dysfunction (eg, atrophic vaginitis, depression) must be considered and evaluated. Examination is focused on the genitals and extragenital signs of hormonal, neurologic, and vascular disorders. Genitals are examined for anomalies, signs of hypogonadism, and fibrous bands or plaques (Peyronie's disease). Poor rectal tone, perineal sensation, or abnormal anal wink or bulbocavernosus reflexes may indicate neurologic dysfunction. Diminished peripheral pulses suggest vascular dysfunction. A psychologic cause should be suspected in young healthy men with abrupt onset of ED, particularly if onset is associated with a specific emotional event or if the dysfunction occurs only in certain settings. A history of ED with spontaneous improvement also suggests psychologic origin (psychogenic ED). Men with psychogenic ED usually have normal nocturnal erections and erections upon awakening, whereas men with organic ED often do not. Laboratory assessment should include measurement of testosterone level; if the level is low or low-normal, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) should be measured (see Male Reproductive Endocrinology and Related Disorders: Diagnosis of primary and secondary hypogonadism). Evaluation for occult diabetes, dyslipidemias, hyperprolactinemia, thyroid disease, and Cushing's syndrome should be done based on clinical suspicion. A penile pressurebrachial pressure index (systolic BP in the penis divided by systolic BP in the arm) < 0.6 indicates impaired blood flow to the penis, but this test is seldom done in general clinical practice. Additional invasive or provocative penile tests include duplex ultrasonography before and after injection of a vasoactive drug and cavernosography or cavernosometry; these tests can be considered in some patients, such as those with posttraumatic erectile dysfunction or before penile reconstructive surgery (eg, for Peyronie's disease). Treatment Treatment of cause Usually an oral phosphodiesterase inhibitor Sometimes a mechanical device or an intracavernosal or intraurethral prostaglandin

Underlying organic disorders require appropriate treatment. Drugs that are temporally related to onset of ED should be stopped or switched. Depression may require treatment. For all patients, reassurance and education (including of the patient's partner whenever possible) are important. For further therapy, noninvasive methods (mechanical devices and drugs) are tried first. All drugs and devices should be tried 5 times before being considered ineffective. Mechanical devices: Men who can develop but not sustain an erection may use a constriction ring. As soon as erection occurs, a metal or elastic ring or a leather band with snaps (sold by prescription in pharmacies or OTC in sex paraphernalia stores as a cock ring) is placed around the base of the penis, preventing venous outflow. If the man cannot develop an erection, a vacuum device can draw blood into the penis, after which the band or ring is placed at the base of the penis to retain the erection. Bruising of the penis, coldness of the tip of the penis, and lack of spontaneity are some drawbacks to this modality. A constriction ring and vacuum devices might also be useful adjuncts for patients who do not respond satisfactorily to drug therapy. Drugs: The primary drugs for ED are oral phosphodiesterase inhibitors, oral apomorphine(not available in the US), and intracavernosal or intraurethral prostaglandins. Almost all patients prefer oral drug therapy to other methods for treating ED.Oral phosphodiesterase inhibitors selectively inhibit cyclic guanosine monophosphate (cGMP)specific phosphodiesterase type 5 (PDE5), the predominant phosphodiesterase isoform in the penis. These drugs include sildenafil, vardenafil, and tadalafil. By increasing cGMP, these drugs enhance the nitric oxide release essential for normal erection. Although vardenafil and tadalafil are more selective for the penile vasculature than sildenafil, adverse effects of these drugs are similar. Although no clinical trials directly compare the drugs, all 3 appear to be equally effective (60 to 75%). Sildenafil dose is 50 mg, although most men respond best to 100 mg. Tadalafil has a significantly longer duration of action (24 to 48 h) than sildenafil and vardenafil(about 4 to 6 h), which might lead to more convenient dosing. The usual dosage for tadalafil and vardenafil is 5 to 20 mg. All PDE5 inhibitors are generally taken at least 1 h before sexual intercourse. Dosing frequency should not be 24 h for sildenafil and vardenafil and not 48 h for tadalafil. All PDE5 inhibitors cause direct coronary vasodilation and potentiate the hypotensive effects of other nitrates, including those used to treat cardiovascular disease as well as recreational amyl nitrate (poppers). Thus, all nitrates are contraindicated for 24 h after the administration of any PDE5 inhibitor. Other adverse effects of PDE5 inhibitors include flushing, visual abnormalities, and headache. Sildenafil and vardenafil may cause abnormal color perception. Tadalafil use has been linked with myalgias. Some users of PDE5 inhibitors have rarely developed anterior ischemic optic neuropathy, but whether there is a causal relationship is unclear. Vardenafil should be administered cautiously and at lower

initial dosages to patients receiving -blockers, such as prazosin, doxazosin, and tamsulosin, because of the risk of prolonged hypotension. One study showed that sildenafil may be safely administered with doxazosin Apomorphine increases erectile neurogenic signals by CNS mechanisms. It appears to be only moderately effective and can cause nausea, somnolence, and hypotension.

Alprostadil (the prostaglandin PGE1), given via intraurethral insertion or intracavernosal injection, can produce erections with a mean duration of about 60 min. It causes priapism (see Symptoms of Genitourinary Disorders: Priapism) in 1% and penile pain in about 10%. The intracavernosal dose is adjusted by the physician to minimize priapism; the patient can then self-inject at home. Priapism is less common with intraurethral therapy, but intraurethral therapy is much less effective (50 to 60%) than intracavernosal injection, the most effective pharmacotherapy for erectile dysfunction (80 to 90%). Combination therapy with a PDE5 inhibitor and alprostadil may be useful for some patients who fail to respond to oral PDE5 inhibitors alone. Surgery: For patients who do not respond to drug therapy, invasive treatment options include implantation of a penile prosthesis. Prostheses can be rigid plastic rods or hydraulically operated devices. Both involve the risks of general anesthesia, infection, and prosthetic malfunction.