Urinary system is composed of kidney, ureters, urinary bladder, and urethra. Infection of any part or the urinary system is known as urinary tract infection. 95% women are at the risk of developing a urinary tract infection. Latest research shows that almost all women will develop a urinary tract infection at some point during their lives, and many will experience more than one.

Urinary tract infection may be classified as uncomplicated (normal urinary tract and function), or complicated (male patients, abnormal renal tract, impaired renal function).A recurrent UTI is further infection with a new organism and a replace with the same organism.

What are the risk factors for UTI?

Some people appear to be more likely than are others to develop urinary tract infections. Risk factors include:

1. Female sex
2. Sexual active
3. using diaphragm contraceptive
4. vaginal spermicidal
5. Diabetes mellitus
6. Immunosuppressant people
7. During pregnancy ,
8. during menopause
9. Urinary tract obstruction ( kidney stone , or tumor)
10. instrumentation of urinary tract
11. malformation of urinary tract
12. unhygienic

What are the organisms that cause the urinary tract infection?

Bacteria are the main causes of UTI.

• Bacteria includes: E.coli is the most common (>70% in the community), staphylococcus saprophyticus, Enterococcus faecalis, proteus mirabilis, Klebsiella, Pseudomonas aeruginosa and serratia marascens.
• Virus : Simplex herpes virus type 2
• Fungal : yeast infections
• Parasites :   chistosomiasis

What are the symptoms of UTI?

Symptoms depend on which part of the urinary tract is infected.

1. Cystitis (infection of Urinary bladder): Frequency, dysuria (painful urination), urgency, strangury, haematuria, lower abdominal pain, low grade fever.
2. Acute pyelonephritis (infection of kidney): high grade fever, rigors, chills, nausea, vomiting, loin pain.
3. urethritis( infection of urethra) : Burning urination
4. Prostatitis (infection of prostate gland, only in man): flu like symptoms, lower back pain, swollen, low grade fever.

How UTI is  diagnosed?

Diagnosis relies on patient’s history, normal urinary analysis (a pure growth of >108 colony forming units (CFU/L) is diagnostic) , and urine culture .some complicated cases Total blood count, blood culture , CRP , X-ray KUB and ultrasound may required.

How is UTI treated?

Patient is advice to drink plenty of water, urinate frequently, maintain hygiene, and post intercourse urination. In simple urinary tract infections antibiotic like Amoxicillin, Nitrofurantion, ofloxiacin, Co-trimoxazole is giving for 7-11 days. Severely ill patients with kidney infections may be hospitalized and give intravenous antibiotic according urine culture and sensitivity until they can take fluids and needed drugs on their own.

What is the prevention?

Antibiotic prophylaxis, either continuous or post coital, decreases infection rates in women with recurrent UTIs. Self treatment with a single antibiotic dose as symptoms start is an option. Effects of cranberry juice have not been fully assessed but this long term established alternative remedy may inhibit adherent of E.coli to bladder cells.

What to prevent UTI?

In the simple urinary traction infection prognosis is excellent.

References:

• Sabiston textbook of surgery 18th edition
• Bailey and love, surgery 25th edition
• The Washington manual of surgery, 5th edition.
• emedicine.medscape.com

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Micturition syncope is described as fainting attack during mostly immediately after urination due to reduction of cerebral blood flow.

Epidemiology
More common in male but female also suffer from this condition .furthermore about 61% with micturition syndrome also suffered from other kinds of syncope.

Pathophysiolgy
The mechanism of micturition syncope is still unknown but believed that it is related to vasovagal syncope.
During micturition there is increased vagal tone as a result from straining (Valsalva maneuver) which results in bradycardia leads to syncope due to decreased cerebral blood flow. However the trigger of the vasovagal response is unclear but though to be that the bladder becomes hyper-reflexic.

Symptoms
1. Dizziness
2. lightheaded or short lived loss of consciousness when passing urine
3. Pale appearance to your skin
4. Nausea

Triggers for micturition syncope
1. Standing long periods of time
2. Heat exposure
3. Having blood drawn
4. Fear of bodily injury

Diagnosis
Diagnosis mainly relies on patient history but other investigation like ECG, echocardiogram, exercise stress test and blood tests need to rule out other diseases.

Management
Usually no treatment is required. If it enough to interfere the quality of life treatment is required like.
1. Life style changes: If felling of faint, lie down and lift the legs, this allows gravity to keep blood flowing to brain.
2. Medical treatment:

• Beta blocker, it is not only used in hypertensive patient but it also used to prevent vasovagal syncope.
• Antidepressants: selective serotonin reuptake inhibitor like paroxetine ,fluoxetine and sertraline is used to prevent micturition syncope.

3. Surgery: Insertion of pacemaker may help in some patient.

References:
1. www.medterms.com
2. www.mayoclinic.com
3. www.patient.co.uk
4. cat.inist.fr
5. en.wikipedia.org

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A kidney stone is hard mass that forms in the urinary tract. Nephrolithiasis or kidney stone disease occurs more commonly in men than in women and usually strikes men between the ages of 30 and 60. A stone lodged in the ureter will cause bleeding and intense pain. Kidney stone diseases causes’ considerable suffering and loss of time from work, and it may lead to kidney damage. Once a stone forma in a person, stone formation often occur.

Stones form when poorly soluble substances in the urine precipitate out of solution, causing crystal to form aggregate, and grow. Most kidney stones (75-85%) are made up of insoluble Ca2+ salts of oxalate and phosphate. There may be excessive amount of Ca2+or oxalate in urine as a result of diet, a genetic defect, or unknown cause. Stones may also form from precipitated ammonium magnesium phosphate (struvite), uric acid and cystine. Struvite stones (10 to 15%of all stones) are the result of infection with bacteria, usually proteus species. Uric acid stones (5-8%) may form in patients with excessive uric acid production and excretion, as occur in some patients with gout. Defective tubular reabsorption of cystine (in patients with cystinuria) leads to cystine stones (1% of stones). The rather insoluble amino acid cystine was first isolated from a urinary bladder stone by Wollaston in 1810, hence, its name. Because low urine flow rate raise the concentration of all poorly soluble substances in the urine, favoring precipitation, a key to prevention of kidney stones is to drink plenty of water and maintain a high urine output day and night.

Fortunately, most stones are small enough to be passed down the urinary tract and spontaneously eliminated. Microscopic and chemical examination of the eliminated stones is used to determine the nature of the stone and help guide treatment. Sometimes achange in diet is recommended to reduce the amount of potential stone-forming-material in the urine. Thiazide diuretics are useful in reducing in treating most stone disease because citrate complexes Ca2+ salts. It also makes the urine more alkaline (since citrate is oxidized to HCO3- in the body). This is helpful in reducing the risk of uric acid stones because urates (favored in alkaline urine) are more soluble than uric acid (the form favored in acidic urine). Administering an inhibitor of uric acid synthesis, such as allopurinol, can help reduce the amount of uric acid in the urine.

If the stone is not passed, several options are available. Surgery to remove the stone can be done, but extracorporeal shock wave lithotripsy is more common, using a device called a lithotriptor. The patient is placed in a tub of water, and the stone is localized by X-ray imaging. Shock waves are generated in the water by high-voltage electric discharges and are focused on the stone through the body wall. The shock waves fragment the stone so that it can passed down the urinary tract and eliminated. As some renal injury is produced by this procedure, it may not be entirely innocuous. Other procedure includes passing a tube with an ultrasound transducer through the skin into the renal pelvis; stone fragments can be removed directly. A ureteroscope with a laser can also be used to break up stones.

Frequently asked question.

Does eating stone cause renal stone?

Answer: There is no relation between eating stone and formation of renal stone.

References:

1. Short practice of surgery, bailey and love, 25^th edi.
2. Harrison’s Principles of Internal Medicine, 17th edition.
3. Davidson’s Principles and Practice of Medicine, 20th Edition
4. The Washington Manual of surgery, 5th edition.
5. Medical physiology, Lippincott Williams & Wilkins 3rd edi.

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A 60-year-old woman is referred to the emergency department (ED) because of a recent event of painless macroscopic hematuria. She reports having experienced several similar episodes during the past year, all of which resolved spontaneously. She regards these episodes as being of gynecologic origin because she is 5 years postmenopausal. She describes a general feeling of malaise in the days preceding the current episode, but she denies having any fever, dysuria, or increased frequency or urgency of urination. The patient also describes an unintentional weight loss of 11 lb (5 kg) during the past 2 years. The patient’s previous medical history includes hypothyroidism that was treated medically with thyroxine, and her surgical history includes 2 treatments of dilatation and curettage (D&C) and a tonsillectomy. She has no known drug or food allergies, and she denies smoking, drug use, or alcohol consumption. She has no previous history of kidney stones or recurrent urinary tract infections.

On physical examination, the patient appears well. She has a temperature of 98.8°F (37.1°C), a pulse rate of 71 bpm, and a blood pressure of 150/86 mm Hg. The head and neck examination is normal. Lung auscultation reveals normal breath sounds bilaterally, without wheezing or crackles. Her heart sounds are regular, with a 2/6 systolic murmur maximally auscultated over the right second intercostal space. The abdomen is nondistended and nontender, no masses are palpated, and there are no signs of peritoneal irritation. No peripheral edema is noticed, peripheral pulses are palpated, and the neurologic examination is normal. A gynecologic evaluation that includes a speculum examination and transvaginal ultrasonography is performed, which reveals no pathologic findings.

A laboratory analysis, including a complete blood cell (CBC) count, coagulation studies, and a basic metabolic panel, shows a normal hemoglobin level, normal platelet count, and no coagulopathy. No electrolyte abnormalities are present. A urine dipstick test shows no signs of hematuria, and a urine culture is negative. Urine cytology is positive for malignant cells. Cystoscopy is performed, which demonstrates a normal urethra leading to a urinary bladder covered by normal mucosa, with no exophytic lesions and no active bleeding. A computed tomography (CT) examination of the abdomen and pelvis with intravenous contrast is obtained

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“This Guideline advises physicians to counsel their patients and set expectations prior to undergoing treatment,” AUA Guideline Panel Chair Roger Dmochowski, MD, said in a news release. “This is very important because often the patient thinks that surgery will completely cure their incontinence, when in reality, it may only make modest improvements.”

The new recommendations update the previous 1997 AUA guideline discussing surgery to treat SUI, based on articles retrieved for the previous guideline and those resulting from 4 MEDLINE searches beginning in December 2002 and ending in June 2005. There were 436 articles included in the meta-analysis and 155 articles considered to be suitable only for their complications data because follow-up duration was insufficient for efficacy outcomes analysis.

When considering surgery to treat female SUI, clinicians should perform a complete evaluation, including measurement of postvoid residual volume.

The updated guidelines also recommend counseling patients regarding the benefits and risks of both surgical and nonsurgical options for SUI. Potential treatment choices may include injectable agents, laparoscopic and retropubic suspension procedures, and midurethral and pubovaginal slings. The surgeon and patient should collaborate on formulating the treatment plan, considering the patient’s preferences as well as the surgeon’s judgment and expertise. The updated guideline also highlights issues involved in surgical correction of pelvic prolapse at the same time as SUI surgery.

Determining postvoid residual urine volume is a key feature of complete assessment of the patient with SUI. Surgical techniques should be tailored to specific patient needs based on detrusor contractility, urinary retention, or other comorbitities.

Other important features of the diagnostic workup of SUI are focused history, physical examination, looking for evidence of leakage with increasing abdominal pressure, urinalysis, and cultures. In some patients, urinary tract imaging, voiding diaries, cystoscopy, and urodynamics may also be indicated. Further testing to confirm the diagnosis of SUI may also be helpful in patients with known or suspected neurogenic bladder, concurrent symptoms of overactive bladder, excessive residual volume, dysfunctional voiding, or history of previous lower urinary tract surgery.

An important caveat is that patients who have urge incontinence in the absence of SUI should not be offered a surgical procedure for SUI. However, surgery may be helpful in patients who have mixed incontinence, involving urge incontinence and a significant stress component.

For long-term success measured in cure/dry rates, retropubic suspensions are still thought to be one of the most effective options, even though they have been largely supplanted by sling procedures. Patients should be counseled preoperatively regarding the slightly higher complication rates associated with retropubic suspensions, such as postoperative voiding dysfunction and longer postoperative recovery. These recommendations have not changed since the 1997 guideline.

For patients declining invasive surgery, collagen and other nondegradable synthetic injectable agents may be considered. However, efficacy and duration of treatment response seen with injectable agents are inferior to those achieved with surgery.

The updated guidelines recommend that artificial urinary sphincters be used only in patients with nonfunctioning urethras; for example, those with spina bifida, men with postprostatectomy incontinence, and patients with pelvic nerve trauma. Patients with severe intrinsic sphincteric deficiency who have failed other surgical procedures may benefit from the use of artificial urinary sphincters.

Synthetic slings should not be used in patients with SUI who have a concurrent urethrovaginal fistula, urethral erosion, intraoperative urethral injury, and/or urethral diverticulum, because use of synthetic material in these patients may increase risk for adverse effects. The guidelines panel suggests that use of autologous fascial and alternative biologic slings may be considered in these patients, but notes that data are severely limited regarding the use of cadaveric slings.

Specific guidelines recommendations for sling surgery are as follows:

• Patients should be instructed about the benefits and risks of both biological and synthetic sling materials. In particular, the US Food and Drug Administration recently issued an alert regarding surgical mesh.
• Before the conclusion of sling surgery, the bladder and urethra must be inspected with either a rigid or flexible cystoscope to identify potential intraoperative complications.
• When prolapse repair is performed at the same time as SUI surgery, the prolapse surgery should be fully completed before the sling is tensioned.

“The profession at large and the individual physician should insure the safety and efficacy of any new device or sling,” the guidelines authors conclude. “If safety and efficacy has not been shown with reasonable certainty, the new treatment should only be performed as part of clinical research studies and/or with informed consent recognizing that safety and/or efficacy has not been demonstrated.”

In collaboration with the American College of Obstetricians and Gynecologists, the AUA is developing physician performance measures reflecting all changes made in the 2009 SUI Guideline update. These measures, which will eventually be submitted to the National Quality Forum for endorsement, are being developed under the independent measure development process of the American Medical Association’s Physician Consortium for Performance Improvement.

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Benign prostatic hypertrophy (BPH) is known as Benign Prostatic Hyperplasia is a enlargement of prostate in older males. As a size of the prostate increases, it can put pressure on the urethra, causing a slowdown in the urine stream, hesitancy in urinating, and urgency.

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.Some researches suggest that diet has an effect on the likelihood of developing BPH,A diet rich in cereals, bread, eggs, and poultry should be avoided, and replaced by one with plenty of soups, vegetables, pulses (peas, beans, lentils) and citrus fruits, if one wishes to lower the chance of developing prostatism.

References

1. Food groups and risk of benign prostatic hypertrophy. BF. Bravi, C. Bosetti, L. Dal Maso,  et al., Urology, 2006, vol. 67, pp. 73–79

2. MacDonald R; Wilt TJ; Howe RW (December 2004). “Doxazosin for treating lower urinary tract symptoms compatible with benign prostatic obstruction: a systematic review of efficacy and adverse effects”. BJU International 94 (9): 1263–70. PMID 15610102.

3 .MacDonald R; Wilt TJ (October 2005). “Alfuzosin for treatment of lower urinary tract symptoms compatible with benign prostatic hyperplasia: a systematic review of efficacy and adverse effects”. Urology 66 (4): 780–8 PMID = 16230138.

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