Urine Incontinence

Scenario A 79 years old man was taken to PUSKESMAS with frequent urinate but less in quantity. Even though the process took a long time, most of the time he felt unsatisfied. This condition started 7 days ago. He also complained about knee pain that he had been having for some times. According to the family, the man was always in a bad temper, easy forgetting lots of things which he just did. He was in medication for diabetes, hypertension, heart disease and rheumatic for about 7 years now. Three years ago, he had stroke attack. Keywords 79 years old man Micturition Frequent Less in quantity Process took long time Unsatisfied Started 7 days ago Sometimes having knee pain Alloanamnesis: Always in a bad temper Easy forgetting lots of things which he just did 7 years medication: Diabetes Hypertension Heart disease Rheumatic Stroke attack 3 years ago

Clarification of Terms 1. Incontinence: Urinary incontinence (UI) is any involuntary leakage of urine. It is a common and distressing problem, which may have a profound impact on quality of life. Urinary incontinence is loss of bladder control. Symptoms can range from mild leaking to uncontrollable wetting. Questions & Answers 1.Physiology of micturition Micturation is the process where the urinary bladder empties when it becom fully filled. Urinar bladder usually can be fill until 400-500mL of urine, but first sensation of the micturation occur when the volume reach 150-350mL.

First, the bladder fills progressively until the tension in its walls rises above a threshold level. This elicits the second step, which is a nervous reflex called the micturition reflex that empties the bladder or, if this fails, at least causes a conscious desire to urinate. Although the micturition reflex is an autonomic spinal cord reflex, it can also be inhibited or facilitated by centers in the cerebral cortex or brain stem. These process controlled by both central and peripheral nervous system precisely by S2- S4. It starting to occur when the detrusir muscle starting to contract and followed by relaxation by the external and internal urethral spincther and urethra itself. The factor that contribute to the urine incontinence First factor of the urine incontinence is the aging process. As we know as we getting older all of our muscle starting to get weak. Same goes to the muscle of the urinary bladder that causes it to not fully contract and relax. It may lead to the urine incontinence. There is also infection that occur. For women, the menopause phase that they had to undergoes causes their body to be lacked of the hormone estrogen. This will make the pelvic floor muscle and urethral to be weak. This will make it more prone to the any of the infection. Otherwise, for men the obstruction especially causes by the hypertrophy of the prostate gland will cause an obstruction to be occur that will then can lead to the infection to be occur. Some of the geriatric patient consume drugs for their existing disease. For example diuretics, anti-hypertension and many other drugs, can actually make the muscle weakness of the urinary bladder that will then make the urine incontinence to happened. And also for elderly, they tend to lessen their movement as some of them that might have some problem such as obesity, rheumatic disease. As they lessen their movement, they will be to the extent where they let the micturation to occur whenever they wish. As dementia is one of the syndrome that occur among the elderly, this will actually contribute to the urine incontinence to be occur among them. It is because their behavior and logical thinking is not anymore works synergically. 2.Mechanism of aging Aging appears to be driven by the progressive accumulation through life of a variety of random molecular defects that build up within cells and tissues. These defects start to arise very early in life, probably in utero, but in the early years, both the fraction of affected cells and the average burden of damage per affected cell are low. However, over time the faults increase, resulting eventually in age-related functional impairment of tissues and organs (Figure 2-1). This concept makes clear the life-course nature of the underlying mechanisms. Aging is a continuous process, starting early and developing gradually, instead of being a distinct phase that begins in middle to late life. Since there are multiple kinds of molecular and cellular damage, and a corresponding variety of mechanisms to protect against and repair them, aging is a highly complex process involving multiple mechanisms at different levels. The clear inference is that aging is multicausal and that the various mechanisms all play their part and is likely to interact synergistically. For example, a build-up of mitochondrial DNA mutations will lead to a decline in the cells energy production, and this will reduce the capacity to carry out energydependent protein clearance.

Consequently, maintaining cell health and protecting cells from damage with good nutrition and exercise is believed to slow the aging process.

3.Theory of aging ? 1. Genetic Clock Many theories suggest that ageing results from the accumulation of damage to DNA in the cell, or organ. Since DNA is the formative basis of cell structure and function, damage to the DNA molecule, or genes, can lead to its loss of integrity and early cell death. Examples include:

Accumulative-Waste Theory: The biological theory of ageing that points to a buildup of cells of waste products that presumably interferes with metabolism. Wear-and-Tear Theory: The very general idea that changes associated with ageing are the result of chance damage that accumulates over time. Somatic Mutation Theory: The biological theory that ageing results from damage to the genetic integrity of the bodys cells. Error Accumulation Theory: The idea that ageing results from chance events that escape proof reading mechanisms, which gradually damages the genetic code.

Some have argued that ageing is programmed: that an internal clock detects a time to end investing in the organism, leading to death. This ageing-Clock Theory suggests, as in a clock, an ageing sequence is built into the operation of the nervous or endocrine system of the body. In

rapidly dividing cells the shortening of the telomeres would provide such a clock. This idea is in contradiction with the evolutionary based theory of ageing. Cross-Linkage Theory: The idea that ageing results from accumulation of crosslinked compounds that interfere with normal cell function. Free-Radical Theory: The idea that free radicals (unstable and highly reactive organic molecules), or more generally reactive oxygen species or oxidative stress create damage that gives rise to symptoms we recognize as ageing.[63][65]

Reliability theory of ageing and longevity: A general theory about systems failure. It allows researchers to predict the age-related failure kinetics for a system of given architecture (reliability structure) and given reliability of its components. Reliability theory predicts that even those systems that are entirely composed of non-ageing elements (with a constant failure rate) will nevertheless deteriorate (fail more often) with age, if these systems are redundant in irreplaceable elements. Ageing, therefore, is a direct consequence of systems redundancy. Reliability theory also predicts the late-life mortality deceleration with subsequent levelling-off, as well as the late-life mortality plateaus, as an inevitable consequence of redundancy exhaustion at extreme old ages. The theory explains why mortality rates increase exponentially with age (the Gompertz law) in many species, by taking into account the initial flaws (defects) in newly formed systems. It also explains why organisms "prefer" to die according to the Gompertz law, while technical devices usually fail according to the Weibull (power) law. Reliability theory allows to specify conditions when organisms die according to the Weibull distribution: organisms should be relatively free of initial flaws and defects. The theory makes it possible to find a general failure law applicable to all adult and extreme old ages, where the Gompertz and the Weibull laws are just special cases of this more general failure law. The theory explains why relative differences in mortality rates of compared populations (within a given species) vanish with age (compensation law of mortality), and mortality convergence is observed due to the exhaustion of initial differences in redundancy levels. Mitohormesis: It has been known since the 1930s that restricting calories while maintaining adequate amounts of other nutrients can extend lifespan in laboratory animals. Recently, Michael Ristow's group has provided evidence for the theory that this effect is due to increased formation of free radicals within the mitochondria causing a secondary induction of increased antioxidantdefence capacity. Misrepair-Accumulation Theory: Wang et al. suggest that ageing is the result of the accumulation of "Misrepair". Important in this theory is to distinguish among "damage" which means a newly emerging defect BEFORE any reparation has taken place, and "Misrepair" which describes the remaining defective structure AFTER (incorrect) repair. The key points in this theory are: 1. There is no original damage left unrepaired in a living being. If damage was left unrepaired a life threatening condition (such as bleeding, infection, or organ failure) would develop. 2. Misrepair, the repair with less accuracy, does not happen accidentally. It is a necessary measure of the reparation system to achieve sufficiently quick reparation in situations of serious or repeated damage, to maintain the integrity and basic function of a structure, which is important for the survival of the living being.

3. Hence the appearance of Misrepair increases the chance for the survival of individual, by which the individual can live at least up to the reproduction age, which is critically important for the survival of species. Therefore the Misrepair mechanism was selected by nature due to its evolutionary advantage. 4. However, since Misrepair as a defective structure is invisible for the reparation system, it accumulates with time and causes gradually the disorganisation of a structure (tissue, cell, or molecule); this is the actual source of ageing. 5. Ageing hence is the side-effect for survival, but important for species survival. Thus Misrepair might represent the mechanism by which organisms are not programmed to die but to survive (as long as possible), and ageing is just the price to be paid. 2. Somatic mutation somatic mutation theory states that random changes to the DNA of your cells can cause your cells, and eventually your body, to stop functioning correctly. A deeper understanding of this theory requires a greater biological understanding of your body. Throughout your life time, your body is constantly creating new cells. Every time one of your cells divides to create two new cells, there is a possibility that the DNA from the first cell will be copied incorrectly. This results in a mutation, a change in the copy of your DNA contained by the new cells. This mutation may be caught and corrected, but some mutations will be missed and some of these mutations will affect the way the new cell functions. All of the cells in your body are considered somatic cells, with the exception of your reproductive cells (sperm and eggs). The mutations occurring in cells other than your reproductive cells are therefore referred to as somatic mutations. These mutations will not be passed on to your children since they are not found in your reproductive cells. They do, however, accumulate in your cells as you get older. Uncorrected mutations in one cell get passed on when that cell divides and new mutations may also occur. Eventually, many of your cells have multiple mutations and these mutations begin to impact the way your body functions, causing many of the problems associated with aging. Although this theory explains one of the ways in which our bodies age, there are currently many other equally plausible theories. Many of these, including the somatic mutation theory of aging, fall into the general category of "wear-and-tear" theories. These theories state that damage accumulated over time causes the body to age. Different theories suggest different causes of this damage, including: mutations, environmental factors such as UV light, and chemical factors which affect DNA structure. Other theories suggest that aging is a pre-programmed bodily function, a function already set to occur in a specific way from the moment we're born. One such "aging-clock" theory is the telomere theory which claims that we age because our telomeres (protective caps on the end of each chromosome) wear away during cell replication. Most other theories of aging are based on the idea that certain substances build up in our bodies as we age, substances that include everything from cell waste to auto-antibodies (antibodies that attack the body's own tissues). Evidence supporting many of these theories about the biological causes of aging is plentiful and

it is likely that more than one of the theories described above are correct. Many of these theories are compatible with the somatic mutation theory of aging, a theory which is well supported, but unlikely to provide a full explanation of the reasons we age.

3. Senescence of the immune system. The immune system undergoes constant physiological changes over the human lifespan. The infant has no immunity of its own at birth; immune function develops quickly over the first few years and then builds to a complete maturation by puberty. In fertile women, immunity fluctuates cyclically in sync with the menstrual cycle; dramatic changes occur during pregnancy as well as the postpartum period. Throughout life, homeostasis is preserved in all systems through tightly regulated interactions between numerous interdependent body tissues (Figure 1). Driven by inalterable genetic factors, environmental insults, such as UV light, and lifestyle factors like nutrition and nicotine use, body tissues, with age, experience a progressive deterioration of cellular and tissue functions, largely due to genetic decay and the byproducts of metabolism. The study of aging in the immune system has revealed that immunosenescence represents a substantial remodeling of major immune functions. Immunosenescence in both genders impacts cellular, humoral and innate immunity. Significant consequences of aging include atrophy of the thymus, changes in both the total numbers and subsets of lymphocytes, changes in the function of both B and T cells, changes in the patterns of secretion of cytokines and growth factors, disruption of intracellular signaling, changes in the patterns of antibody production, loss of antibody repertoire, loss of response to antigens and mitogens and disruption of immunological tolerance Although aging affects many immune cell types, the cumulative effects of aging on T-cell function are the most consistently observed and most extensive. The human thymus decreases in both size and cellularity in a process called thymic involution; thymus tissue is replaced with fat. By 60 years, thymus-derived hormones are absent from the circulation. Involution of the thymus in humans occurs in concert with a depletion of naive T cells and a shift in the T-cell population toward memory CD4+ cells.[13] In young adulthood, the CD4+ subset is characterized by roughly equivalent numbers of memory and naive CD4+ cells but in older adults becomes predominantly memory CD4+,]a shift that reduces the potential antigenic repertoire. The shift toward memory T cells with age is largely a consequence of the imbalance in T-cell maturation produced by thymus involution paired with an age-related impairment of T-cell proliferation in concert with clonal expansion of T cells activated by specific antigens. The shift toward memory cells in the T-cell compartment affects cytokine production as well, with less IL-2 produced (primarily a product of naive T cells) but more IL-4 (primarily a product of memory T cells). The cumulative loss of T helper (Th) cells with age plays a profound role in immunosenescence, ultimately affecting both cellular and humoral immunity. Disruption of Th cells and alterations of cytokine levels that control B-cell functions compromise humoral immunity substantially, with decreased production of long-term immunoglobulin (Ig)-producing B cells as well as a reduction of Ig diversity. Although B-cell numbers do not change significantly, there is a

significant impairment of B-cell response to primary antigenic stimulation; specific immunoglobulins produced become more random, and those produced have decreased affinity for their specific antigen. With age, therefore, the B-cell repertoire poised to respond to new antigenic challenge is limited, and the predominance of memory T cells seen with thymic involution is mirrored in the B-cell compartment. IL-15, particularly, stimulates proliferation of memory T cells; IL-15 levels are nearly double in healthy adults 95 years or older (3.05 pg/ml compared with both older adults [6089 years] 1.94 pg/ml and midlife adults [3059 years] 1.73 pg/ml). Immunosenescence is compounded by the presence in the aged of a chronic low-grade inflammation characterized by increased proinflammatory cytokines, such as IL-6 and TNF-a, compounds that create oxidative stress and decrease cellular antioxidant capacity. These proinflammatory cytokines are positively associated with stress as well as salivary cortisol levels and may play a significant role in creating the degenerative changes associated with aging. Other body processes, most notably innate immunity and interactions of immunity with the neuroendocrine system, also contribute to immune system aging. Antigen-presenting cells such as dendritic cells (DCs) and macrophages serve as a bridge between the innate and the adaptive immune systems. Antigen-presenting cells interact with foreign molecules and release pathogen-specific cytokines that drive the activation of naive CD4 helper cells into either Th1 or Th2 effector cells. Production of IL-12 and IFN-g drive commitment of naive T cells to the Th1 lineage. Th1 cells produce cytokines that favor a cell-mediated response (IL-2, lymphotoxin, IFN- and TNF-), warding off intracellular pathogens, mounting delayed-type hypersensitivity responses to viral and bacterial antigens and eliminating tumor cells. Production of IL-4 and IL-10 drive commitment to the Th2 subtypes. Th2 cells release cytokines which produce an environment favoring humoral immunity (IL-4, -5, -6, -10, and -13) by stimulating Th2 cell proliferation, differentiation, and participation in humoral immunity. In the aged, however, naive cells are less likely to become effectors. In those that do, there is a documented shift towards a Th2 cytokine response. The molecular and cellular changes associated with aging have substantial clinical ramifications. The elderly have impaired ability to achieve immunization but much higher levels of circulating autoantibodies, (due to the lack of naive effectors) impaired response to viral infections, increased risk of bacterial infections, and increased risk of both neoplastic and autoimmune disease. 4. Free radicals According to the free radical theory, radicals damage cells in an organism, causing aging. Mitochondria, regions of the cell that manufacture chemical energy, produce free radicals and are the primary sites for free radical damage. By eliminating free radicals from cells through genetic means and dietary restriction, laboratories have extended the maximum age of laboratory animals. The administration of antioxidants, which eliminate radicals, to laboratory animals fails to increase maximum lifespan.

The nucleus of an atom is surrounded by a cloud of electrons. These electrons surround the nucleus in pairs, but, occasionally, an atom loses an electron, leaving the atom with an unpaired electron. The atom is then called a "free radical," or sometimes just a "radical," and is very reactive. When cells in the body encounter a radical, the reactive radical may cause destruction in the cell. According to the free radical theory of aging, cells continuously produce free radicals, and constant radical damage eventually kills the cell. When radicals kill or damage enough cells in an organism, the organism ages.1 The production of radical oxygen, the most common radical in biological systems, occurs mostly within the mitochondria of a cell. Mitochondria are small membrane-enclosed regions of a cell that produce the chemicals a cell uses for energy. Mitochondria accomplish this task through a mechanism called the "electron transport chain." In this mechanism, electrons are passed between different molecules, with each pass producing useful chemical energy. Oxygen occupies the final position in the electron transport chain. Occasionally, the passed electron incorrectly interacts with oxygen, producing oxygen in radical form.2 The primary site of radical oxygen damage is mitochondrial DNA (mtDNA). Every cell contains an enormous set of molecules called DNA which provide chemical instructions for a cell to function. This DNA is found in the nucleus of the cell, which serves as the "command center" of the cell, as well as in the mitochondria. The cell fixes much of the damage done to nuclear DNA. However, mitochondrial DNA (mtDNA) cannot be readily fixed. Therefore, extensive mtDNA damage accumulates over time and shuts down mitochondria, causing cells to die and the organism to age.4 Protection of mtDNA from radicals slows aging in laboratory animals. Some laboratories have produced fruit flies that live one-third longer than normal fruit flies. These labs genetically altered the fruit flies to produce more natural antioxidants. Antioxidants are molecules that eliminate radicals, so elevated levels of antioxidants prevent much of the mtDNA damage done by radicals.3 Other labs severely restricted the food intake of laboratory rats, causing a 50% increase in maximum lifespan compared to rats allowed to eat freely.2 The mitochondria of starved rats are not provided with enough material to function at full capacity. Therefore, the electron transport chains in mitochondria of the starved rats pass fewer electrons. With fewer electrons passed, fewer oxygen radicals are produced, so aging slows. One main problem with the free radical theory is the failure of antioxidants administered as dietary supplements, like vitamins E and C, to significantly increase maximum lifespan. Proponents of the radical theory believe that dietary antioxidants, unlike natural antioxidants produced by cells, do not reach mitochondrial DNA, leaving this site susceptible to radical attack. Interestingly, even though supplemental antioxidants fail to increase maximum lifespan, they do increase the chances of living to the maximum lifespan. This may be due to antioxidant protection of other parts of the cell, like cellular proteins and membranes, from radical damage.2 The goal of all research on the free radical theory is to slow aging and increase maximum lifespan. The achievements so far are astounding; increasing the lifespan of fruit flies and rats is an impressive feat. Despite such success, no practical applications of the theory have been perfected. Genetic alteration is both controversial and difficult for humans. Starvation, while lengthening lifespan, is an unappealing alternative. Dietary antioxidants fail to increase

maximum lifespan. However, the production of radicals and their role in aging is well understood. Further research may apply this knowledge in the development of a practical method to prevent or repair mtDNA radical damage. 4.What is urine incontinence and type of urine incontinence ? DEFINITION Urinary incontinence (UI), involuntary urination, or enuresisis any involuntary leakage of urine. It can be a common and distressing problem, which may have a profound impact on quality of life. This condition happened at unwanted times. TYPE Generally, divided into five, which are: Stress Incontinence, Urge Incontinence, Overflow Incontinence, FunctionalIncontinence, and , Mixed Incontinence 1. Stress incontinence, also known as effort incontinence, is due essentially to insufficient strength of the pelvic floor muscles. People with stress incontinence involuntarily leak urine while exercising, coughing, sneezing, laughing or lifting. During these activities, sudden pressure to the bladder causes urine to leak. Stress incontinence is the most common type of incontinence among women. It may be due to weakened pelvic muscles, weakening in the wall between the bladder and vagina, or a change in the position of the bladder. In many cases, the condition develops as a result of pregnancy and childbirth. Other causes of stress incontinence include: -Weakening of muscles that hold the bladder in place, or weakening of the bladder itself -Weakening of the urethral sphincter muscles -Damage to the nerves controlling the bladder from diseases such as diabetes, stroke, Parkinson's disease and/or multiple sclerosis, or from treatment of gynecologic or pelvic cancers with surgery, radiation or chemotherapy -In women, a hormone imbalance or a decrease in estrogen following menopause, which can weaken the sphincter muscle -In men, benign prostatic hyperplasia (a noncancerous overgrowth of the prostate gland), prostate cancer or prostate surgery

2. Urge incontinence is involuntary loss of urine occurring for no apparent reason while suddenly feeling the need or urge to urinate. A frequent, sudden urge to urinate along with little control of the bladder (especially when sleeping, drinking, or listening to running water) is known as urge incontinence. This condition is also known as spastic bladder, overactive bladder or reflex incontinence. Urge incontinence is marked by a need to urinate more than seven times daily or more than twice nightly. It is most common in older adults. It also may be a symptom of a urinary infection in the bladder or kidneys, or may result from injury, illness or surgery. Among the possible causes are:

Stroke Diseases of the nervous system, such as multiple sclerosis, Alzheimer's or Parkinson's Tumors or cancer in the uterus, bladder or prostate Interstitial cystitis (inflamed bladder wall)

Prostatitis (inflamed prostate) Prostate removal, cesarean section, hysterectomy, or surgery involving the lower intestine or rectum 3. Overflow incontinence: Sometimes people find that they cannot stop their bladders from constantly dribbling or continuing to dribble for some time after they have passed urine. It is as if their bladders were constantly overflowing, hence the general name overflow incontinence. People with overflow incontinence cannot completely empty their bladders. A constantly full bladder triggers frequent urination or a constant dribbling of urine, or both. This type of incontinence is often caused by bladder muscles weakened as a result of nerve damage from diabetes or other diseases. It can also occur when the urethra is blocked due to kidney or urinary stones, tumors, an enlarged prostate in men, female bladder surgery that is too tight, or a birth defect. 4. Functional incontinence occurs when a person recognizes the need to urinate but cannot make it to the bathroom. The loss of urine may be large. There a number of causes of functional incontinence including confusion, dementia, poor eyesight, mobility or dexterity, unwillingness to toilet because of depression or anxiety or inebriation due to alcohol.[7] Functional incontinence can also occur in certain circumstances where no biological or medical problem is present. For example a person may recognise the need to urinate but may be in a situation where there is no toilet nearby or access to a toilet is restricted. 5.Mixed incontinence is not uncommon in the elderly female population and can sometimes be complicated by urinary retention, which makes it a treatment challenge requiring staged multimodal treatment. Some people experience two types of incontinence simultaneously, typically stress incontinence and urge incontinence. 6.Structural incontinence: Rarely, structural problems can cause incontinence, usually diagnosed in childhood (for example, an ectopic ureter). Fistulas caused by obstetric and gynecologic trauma or injury are commonly known as obstetric fistulas and can lead to incontinence. These types of vaginal fistulas include, most commonly, vesicovaginal fistula and, more rarely, ureterovaginal fistula. These may be difficult to diagnose. The use of standard techniques along with a vaginogram or radiologically viewing the vaginal vault with instillation of contrast media. 7.Nocturnal enuresis is episodic UI while asleep. It is normal in young children. 8.Transient incontinence is a temporary version of incontinence. It can be triggered by medications, adrenal insufficiency, mental impairment, restricted mobility, and stool impaction (severe constipation), which can push against the urinary tract and obstruct outflow. 9.Giggle incontinence is an involuntary response to laughter. It usually affects children. 10.Double incontinence. There is also a related condition for defecation known as fecal incontinence. Due to involvement of the same muscle group (levator ani) in bladder and bowel continence, patients with urinary incontinence are more likely to have fecal incontinence in addition. This is sometimes termed "double incontinence".

5.Management of urine incontinence : There are several things patients can do to help improve continence. Avoid overconsumption of diuretics, antidepressants, antihistamines, and cough-cold preparations.

Perform Kegel exercises daily. Practice double voiding (urinate, wait a few seconds, urinate again). Eat fruits, vegetables, and whole grains daily to prevent constipation. Retrain the bladder (urinate only every 3 to 6 hours). Stop smoking (nicotine irritates the bladder).

Spicy foods may contribute to urge incontinence. Some examples of hot spices include curry, chili pepper, cayenne pepper, and dry mustard. A few medical reports have indicated that the avoidance of spicy foods may have a beneficial effect on urinary incontinence. A second food group that may worsen irritative voiding symptoms is citrus fruit. Fruits and juices that have an acidic pH worsen preexisting urge incontinence. Examples of fruits that have significant acidity include grapefruits, oranges, limes, and lemons. A third food group that may worsen urinary bladder incontinence is chocolatecontaining sweets. Chocolate snacks and treats contain caffeine, which is a bladderirritating agent. Excessive intake of chocolate confectioneries worsens irritative bladder symptoms.

A number of protective devices are available to help manage accidental urination, including the following: Bed pads

Combination pad-pant systems Disposable or reusable adult diapers Full-length absorbent undergarments Male incontinence drip collectors Underwear liners (pads, guards, shields, inserts)

Early reliance on absorbent pads may cause the wearer to accept incontinence rather than seek diagnosis and treatment. These products should be applied correctly and changed often to prevent skin irritation and urinary tract infection. In women, lower estrogen levels during menopause can cause urethral tissue to become thinner, less resilient, and less elastic, leading to reduced sphincter control. The addition of phytoestrogens (plant estrogens) to the diet can be helpful for women who experience menopause-related tissue atrophy. Phytoestrogens are compounds found in plants that produce an estrogen-like effect in the body. In most cases, adding phytoestrogens to the diet is safe and easy and the following items may be suggested: Roasted soy nuts

Soy milk

Soy protein powder Tempeh Textured soy protein Tofu

Soy isoflavones, which are the components of soy with the strongest estrogenic properties, are available in capsule form in health food stores and supermarket nutrition sections. A typical dose is 50150 mg daily. There are also several phytoestrogenic and progesterone creams that can be applied directly to the genital tissue to support the elasticity as well as reduce vaginal dryness. TREATMENT FOR URINE INCONTINENCE Treatment options for urinary incontinence depend on the type of incontinence as outlined below. Treatment is keyed to the type of incontinence. The usual approaches are as follows: Stress incontinence - Surgery, pelvic floor physiotherapy, anti-incontinence devices, and medication Urge incontinence - Changes in diet, behavioral modification, pelvic-floor exercises, and/or medications and new forms of surgical intervention Mixed incontinence - Anticholinergic drugs and surgery Overflow incontinence - Catheterization regimen or diversion Functional incontinence - Treatment of the underlying cause Stress incontinence is urine loss during physical activity that increases abdominal pressure (e.g., coughing, sneezing, laughing). Treatment options include: Injectables

Nonsurgical treatments Medications-alpha-adrenergic agonist: improve symptoms of mild stress incontinence by increasing intrinsic urethral tone due to these agents effects on the urethral sphincter. -The serotonin/norepinephrine reuptake inhibitor duloxetine is the first drug developed and marketed specifically for stress urinary incontinence.

Surgical treatments

Urge incontinence is urine loss with urgent need to void and involuntary bladder contraction (also called detrusor instability). Treatment options include: Nonsurgical treatments

Medications Anti Muscarinic Agent - Blocked the bladder abnormal contraction - Increase the bladder capacity Musculotropic relaxants depress smooth muscle activity directly but at a site distal to the cholinergic receptor. Relaxants also may work in part due to anticholinergic and local anesthetic properties at the level of the bladder. Oxybutynin is the prototype drug

in this class. The typical dosage is 5 mg 2-4 times per day. Adverse effects are related mostly to the anticholinergic effects. Lower dosages, such as 2.5 mg 2-3 times a day, may be more appropriate for elderly patients.

Surgical treatments

Mixed incontinence Tricyclic antidepressants(TCAs) TCAs have historically been used to treat major depression, but their pharmacological effects also make these drugs good choices for mixed incontinence, nocturia, and nocturnal enuresis. TCAs have also been used in the treatment of stress incontinence. TCAs have complicated direct and indirect effects on the lower genitourinary tract. They possess both a central and peripheral anticholinergic effect, as well as being alpha-adrenergic agonists and central sedatives. The resultant clinical effect is bladder muscle relaxation and increased urethral sphincter tone. Imipramine (Tofranil) is the most widely used tricyclic for urologic indications. It facilitates urine storage by decreasing bladder contractility and increasing outlet resistance. It has an alpha-adrenergic effect on the bladder neck, an antispasmodic effect on the detrusor muscle, and a local anesthetic effect on the bladder mucosa. Overflow incontinence is constant dribbling of urine; bladder never completely empties. Treatment options include: Medications

Intermittent Self-Catheterization Surgery

If other treatments aren't working, several surgical procedures have been developed to fix problems that cause urinary incontinence. Some of the commonly used procedures include:

Sling procedures. A sling procedure uses strips of your body's tissue, synthetic material or mesh to create a pelvic sling or hammock around your bladder neck and urethra. The sling helps keep the urethra closed, especially when you cough or sneeze. There are many types of slings, including tension-free, adjustable and conventional.

Bladder neck suspension. This procedure is designed to provide support to your urethra and bladder neck an area of thickened muscle where the bladder connects to the urethra. It involves an abdominal incision, so it's done using general or spinal anesthesia.

Artificial urinary sphincter. This small device is particularly helpful for men who have weakened urinary sphincters from treatment of prostate cancer or an enlarged prostate gland. Shaped like a doughnut, the device is implanted around the neck of your bladder. The fluid-filled ring keeps your urinary sphincter shut tight until you're ready to urinate. To urinate, you press a valve implanted under your skin that causes the ring to deflate and allows urine from your bladder to flow.