In women, physical changes resulting from pregnancy, childbirth, and menopause often contribute to stress incontinence. Stress incontinence can worsen during the week before the menstrual period. At that time, lowered estrogen levels may lead to lower muscular pressure around the urethra, increasing chances of leakage. The incidence of stress incontinence increases following menopause, similarly because of lowered estrogen levels. In female high-level athletes, effort incontinence occurs in all sports involving abrupt repeated increases in intra-abdominal pressure that may exceed perineal floor resistance.

In addition to weight loss and exercise there are some behavioral changes that can improve stress incontinence. First decrease the amount of liquid that you are ingesting, and avoid drinking caffeinated beverages because they irritate the bladder. Spicy foods, carbonated beverages, alcohol and citrus also irritate the bladder and should be avoided. Quitting smoking can also improve stress incontinence because smoking irritates the bladder and can make you cough (putting stress on the bladder).

Several definitions have been offered:

- "Absence of normal relaxation of pelvic floor muscles during defecation, resulting in rectal outlet obstruction".

- "Malfunction (a focal dystonia) of the external anal sphincter and puborectalis muscle during defecation".

- "[...] failure of [the external anal sphincter and puborectalis] muscle[s] to relax, resulting in maintenance of the anorectal angle and the difficulty with initiating and completing bowel movements".

- "[...] failure of relaxation (or paradoxic contraction) of the puborectalis muscle sling during defaecation, attempted defaecation or straining."

Without diagnostic evaluation, the cause of UAB is unclear, as there are multiple possible causes. UAB symptoms can accurately reflect impaired bladder emptying due either to DU or obstruction (normal or large storage volumes, elevated post-void residual volume), or can result from a sense of incomplete emptying of a hypersensitive bladder (small storage volumes, normal or elevated postvoid residual volume). UAB potentially might also result from inaccurate perceptions of bladder function, such as in neurologic or psychiatric disease. DU itself is often linked to a weak detrusor muscle (impaired contractility), however this association is weak. Both UAB and DU have been associated with diminished sensitivity to bladder volumes rather than objective detrusor weakness, suggesting both symptoms (UAB) and function (DU) have a significant component of sensory dysfunction, leading to impaired bladder sensations and control (Smith et al., 2015).

The underlying contributors to UAB include neurologic disease, metabolic disease (e.g. diabetes), chronic bladder outlet obstruction (e.g. obstructive BPH or complications of anterior vaginal surgery), cognitive decline (such as with aging), psychiatric disorders, and adverse effects of medications. Additionally, structural abnormalities expanding the urinary reservoir beyond the bladder, such as massive vesicoureteral reflux or large bladder diverticulae, can result in UAB. While aging itself is often associated with UAB (and DU), there is scant evidence to support this claim.

Globally, up to 35% of the population over the age of 60 years is estimated to be incontinent.

In 2014, urinary leakage affected between 30% and 40% of people over 65 years of age living in their own homes or apartments in the U.S. Twenty-four percent of older adults in the U.S. have moderate or severe urinary incontinence that should be treated medically.

Bladder control problems have been found to be associated with higher incidence of many other health problems such as obesity and diabetes. Difficulty with bladder control results in higher rates of depression and limited activity levels.

Incontinence is expensive both to individuals in the form of bladder control products and to the health care system and nursing home industry. Injury related to incontinence is a leading cause of admission to assisted living and nursing care facilities. More than 50% of nursing facility admissions are related to incontinence.

Anismus is classified as a functional defecation disorder. It is also a type of rectal outlet obstruction (a functional outlet obstruction). Where anismus causes constipation, it is an example of functional constipation. Some authors describe an "obstructed defecation syndrome", of which anismus is a cause.

The Rome classification subdivides functional defecation disorders into 3 types, however the symptoms the patient experiences are identical.

- Type I: paradoxical contraction of the pelvic floor muscles during attempted defecation

- Type II: inadequate propulsive forces during attempted defecation (inadequate defecatory propulsion)

- Type III: impaired relaxation with adequate propulsion

It can be seen from the above classification that many of the terms that have been used interchangeably with anismus are inappropriately specific and neglect the concept of impaired propulsion. Similarly, some of the definitions that have been offered are also too restrictive.

Liquid stool is more difficult to control than formed, solid stool. Hence, FI can be exacerbated by diarrhea. Some consider diarrhea to be the most common aggravating factor. Orlistat is an anti-obesity (weight loss) drug that blocks the absorption of fats. This may give side effects of FI, diarrhea and steatorrhea.

Continence requires conscious and subconscious networking of information from and to the anorectum. Defects/brain damage may affect the central nervous system focally (e.g. stroke, tumor e.g. spinal cord lesions, trauma, multiple sclerosis) or diffusely (e.g. dementia, multiple sclerosis, infection, Parkinson's disease or drug-induced). FI (and urinary incontinence) may also occur during epileptic seizures. Dural ectasia is an example of a spinal cord lesion that may affect continence.

Lesions affecting sacral segments or peripheral autonomic fibres result in atonic bladder with loss of sphincteric coordination. This results in loss of detrusor contraction, difficulty in initiating micturition and overflow incontinence. Anticholinergic side effects of certain medications (for example, certain antipsychotics and antidepressants) may cause urinary retention which may lead to overflow incontinence. Alpha-adrenergic agonists may cause urinary retention by stimulating the contraction of the urethral sphincter. Calcium channel blockers may decrease the contractility of the smooth muscle tissue in the urinary bladder, causing urinary retention with overflow incontinence.

Epidural anesthesia and delivery also can cause the overflow incontinence.

Botulinum A toxin is a valuable alternative for patients who do not want surgical methods.

The most common types of urinary incontinence in women are stress urinary incontinence and urge urinary incontinence. Women with both problems have mixed urinary incontinence. After menopause, estrogen production decreases and in some women urethral tissue will demonstrate atrophy with the tissue of the urethra becoming weaker and thinner. Stress urinary incontinence is caused by loss of support of the urethra which is usually a consequence of damage to pelvic support structures as a result of childbirth. It is characterized by leaking of small amounts of urine with activities which increase abdominal pressure such as coughing, sneezing and lifting. Additionally, frequent exercise in high-impact activities can cause athletic incontinence to develop. Urge urinary incontinence is caused by uninhibited contractions of the detrusor muscle . It is characterized by leaking of large amounts of urine in association with insufficient warning to get to the bathroom in time.

- Polyuria (excessive urine production) of which, in turn, the most frequent causes are: uncontrolled diabetes mellitus, primary polydipsia (excessive fluid drinking), central diabetes insipidus and nephrogenic diabetes insipidus. Polyuria generally causes urinary urgency and frequency, but doesn't necessarily lead to incontinence.

- Enlarged prostate is the most common cause of incontinence in men after the age of 40; sometimes prostate cancer may also be associated with urinary incontinence. Moreover, drugs or radiation used to treat prostate cancer can also cause incontinence.

- Disorders like multiple sclerosis, spina bifida, Parkinson's disease, strokes and spinal cord injury can all interfere with nerve function of the bladder.

- Urinary incontinence is a likely outcome following a radical prostatectomy procedure.

- About 33% of all women experience UI after giving birth; women who deliver vaginally are about twice as likely to have urinary incontinence as women who give birth via a Caesarean section.

Overflow incontinence occurs when the patient's bladder is always full so that it frequently leaks urine. Weak bladder muscles, resulting in incomplete emptying of the bladder, or a blocked urethra can cause this type of incontinence. Autonomic neuropathy from diabetes or other diseases (e.g. Multiple sclerosis) can decrease neural signals from the bladder (allowing for overfilling) and may also decrease the expulsion of urine by the detrusor muscle (allowing for urinary retention). Additionally, tumors and kidney stones can block the urethra. Spinal cord injuries or nervous system disorders are additional causes of overflow incontinence. In men, benign prostatic hyperplasia (BPH) may also restrict the flow of urine. Overflow incontinence is rare in women, although sometimes it is caused by fibroid or ovarian tumors. Also overflow incontinence can be from increased outlet resistance from advanced vaginal prolapse causing a "kink" in the urethra or after an anti-incontinence procedure which has overcorrected the problem. Early symptoms include a hesitant or slow stream of urine during voluntary urination. Anticholinergic medications may worsen overflow incontinence. NSAIDs medications may worsen overflow incontinence.

Many people with OAB symptoms had those symptoms subside within a year, with estimates as high as 39%, but most have symptoms for several years.

One review stated that the most common causes of disruption to the defecation cycle are associated with pregnancy and childbirth, gynaecological descent or neurogenic disturbances of the brain-bowel axis. Patients with obstructed defecation appear to have impaired pelvic floor function.

Specific causes include:

- Anismus and pelvic floor dysfunction

- Rectocele

- "Rectal invagination" (likely refers to rectal intussusception)

- Internal anal sphincter hypertonia

- Anal stenosis

- Fecal impaction

- Rectal or anal cancer

- Descending perineum syndrome

For adults, the following may help prevent anal fissures:

- Avoiding straining when defecating. This includes treating and preventing constipation by eating food rich in dietary fiber, drinking enough water, occasional use of a stool softener, and avoiding constipating agents. Similarly, prompt treatment of diarrhea may reduce anal strain.

- Careful anal hygiene after defecation, including using soft toilet paper and cleaning with water, plus the use of sanitary wipes.

- In cases of pre-existing or suspected fissure, use of a lubricating ointment (It is important to note that hemorrhoid ointment is contraindicated because it constricts small blood vessels, thus causes a decrease in blood flow, which prevents healing.)

In infants, frequent diaper change can prevent anal fissure. As constipation can be a cause, making sure the infant is drinking enough fluids (i.e. breastmilk, proper ratios when mixing formulas) is beneficial. In infants, once an anal fissure has occurred, addressing underlying causes is usually enough to ensure healing occurs.

The pathophysiology of the condition results from neuronal plasticity associated with bladder afferents and motor neurons innervating the external urethral sphincter. People with this condition generally experience daytime and night time wetting, urinary retention, and often have a history of urinary tract and bladder infections. Constipation and encopresis are often associated with this condition.

Underactive Bladder Syndrome (UAB) describes symptoms of difficulty with bladder emptying, such as hesitancy to start the stream, a poor or intermittent stream, or sensations of incomplete bladder emptying. The physical finding of detrusor pressurization of insufficient strength or duration to ensure timely and efficient bladder emptying is properly termed "detrusor underactivity" (DU) (Abrams et al., 2002). Historically, UAB and DU (as well as others such as 'bladder underactivity') have been often used interchangeably (Rigby D, 2005), leading to both terminologic and pathophysiologic confusion.

Patients with UAB have a diminished sense of bladder filling and consequently are often found to have DU as an underlying finding, however bladder outlet obstruction and less frequently volume hypersensitivity ("OAB") can be associated with UAB symptoms (Chapple et al., 2015).

If bladder spasms occur or there is no urine in the drainage bag when a catheter is in place, the catheter may be blocked by blood, thick sediment, or a kink in the catheter or drainage tubing. Sometimes spasms are caused by the catheter irritating the bladder, prostate or penis. Such spasms can be controlled with medication such as butylscopolamine, although most patients eventually adjust to the irritation and the spasms go away.

Obstructed defecation has many causes, so the management in any individual case is specific to the cause of the symptom. For rectal internal intususception treatment is surgical, either STARR or rectopexy. For rectocele STARR or mesh implantation. For anismus/ pelvic floor dessynergia: biofeedback exercise.

The incidence of anal fissures is around 1 in 350 adults. They occur equally commonly in men and women and most often occur in adults aged 15 to 40.

Incidence of achalasia has risen to approximately 1.6 per 100,000 in some populations. Disease affects mostly adults between ages 30s and 50s.

Gastroesophageal reflux disease (GERD) affects approximately 40% of adults. Strictures occur in 7 to 23% of patients with GERD who are untreated.

There are two types of prostatic stent: temporary and permanent.

Although a permanent prostatic stent is not a medical treatment, it falls under the classification of a surgical procedure. Placement of a permanent prostatic stent is carried out as an outpatient treatment under local, topical or spinal anesthesia and usually takes about 15–30 minutes.

A temporary prostatic stent can be inserted in a similar manner to a Foley catheter, requiring only topical anesthesia.

It is not clear exactly what causes esophageal spasms. Sometimes esophageal spasms start when someone eats hot or cold foods or drinks. However, they can also occur with eating or drinking. The increased release of acetylcholine may also be a factor, but the triggering event is not known.

The precise cause is unknown, and has been much debated. In 1912 Moschcowitzl proposed that rectal prolapse was a sliding hernia through a pelvic fascial defect.

This theory was based on the observation that rectal prolapse patients have a mobile and unsupported pelvic floor, and a hernia sac of peritoneum from the Pouch of Douglas and rectal wall can be seen. Other adjacent structures can sometimes be seen in addition to the rectal prolapse. Although a pouch of Douglas hernia, originating in the cul de sac of Douglas, may protrude from the anus (via the anterior rectal wall), this is a different situation from rectal prolapse.

Shortly after the invention of defecography, In 1968 Broden and Snellman used cinedefecography to show that rectal prolapse begins as a circumferential intussusception of the rectum, which slowly increases over time. The leading edge of the intussusceptum may be located at 6–8 cm or at 15–18 cm from the anal verge. This proved an older theory from the 18th century by John Hunter and Albrecht von Haller that this condition is essentially a full-thickness rectal intussusception, beginning about 3 inches above the dentate line and protruding externally.

Since most patients with rectal prolapse have a long history of constipation, it is thought that prolonged, excessive and repetitive straining during defecation may predispose to rectal prolapse. Since rectal prolapse itself causes functional obstruction, more straining may result from a small prolapse, with increasing damage to the anatomy. This excessive straining may be due to predisposing pelvic floor dysfunction (e.g. obstructed defecation) and anatomical factors:

- Abnormally low descent of the peritoneum covering the anterior rectal wall

- poor posterior rectal fixation, resulting in loss of posterior fixation of the rectum to the sacral curve

- loss of the normal horizontal position of the rectum with lengthening (redundant rectosigmoid) and downward displacement of the sigmoid and rectum

- long rectal mesentery

- a deep cul-de-sac

- levator diastasis

- a patulous, weak anal sphincter

Some authors question whether these abnormalities are the cause, or secondary to the prolapse. Other predisposing factors/associated conditions include:

- pregnancy (although 35% of women who develop rectal prolapse are nulliparous (have never given birth)

- previous surgery (30-50% of females with the condition underwent previous gynecological surgery)

- pelvic neuropathies and neurological disease

- high gastrointestinal helminth loads (e.g. Whipworm)

- COPD

- cystic fibrosis

The association with uterine prolapse (10-25%) and cystocele (35%) may suggest that there is some underlying abnormality of the pelvic floor that affects multiple pelvic organs. Proximal bilateral pudendal neuropathy has been demonstrated in patients with rectal prolapse who have fecal incontinence. This finding was shown to be absent in healthy subjects, and may be the cause of denervation-related atrophy of the external anal sphincter. Some authors suggest that pudendal nerve damage is the cause for pelvic floor and anal sphincter weakening, and may be the underlying cause of a spectrum of pelvic floor disorders.

Sphincter function in rectal prolapse is almost always reduced. This may be the result of direct sphincter injury by chronic stretching of the prolapsing rectum. Alternatively, the intussuscepting rectum may lead to chronic stimulation of the rectoanal inhibitory reflex (RAIR - contraction of the external anal sphincter in response to stool in the rectum). The RAIR was shown to be absent or blunted. Squeeze (maximum voluntary contraction) pressures may be effected as well as the resting tone. This is most likely a denervation injury to the external anal sphincter.

The assumed mechanism of fecal incontinence in rectal prolapse is by the chronic stretch and trauma to the anal sphincters and the presence of a direct conduit (the intussusceptum) connecting rectum to the external environment which is not guarded by the sphincters.

The assumed mechanism of obstructed defecation is by disruption to the rectum and anal canal's ability to contract and fully evacuate rectal contents. The intussusceptum itself may mechanically obstruct the rectoanal lumen, creating a blockage that straining, anismus and colonic dysmotility exacerbate.

Some believe that internal rectal intussusception represents the initial form of a progressive spectrum of disorders the extreme of which is external rectal prolapse. The intermediary stages would be gradually increasing sizes of intussusception. However, internal intussusception rarely progresses to external rectal prolapse. The factors that result in a patient progressing from internal intussusception to a full thickness rectal prolapse remain unknown. Defecography studies demonstrated that degrees of internal intussusception are present in 40% of asymptomatic subjects, raising the possibility that it represents a normal variant in some, and may predispose patients to develop symptoms, or exacerbate other problems.