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29 Cards in this Set

  • Front
  • Back
What is stress urinary incontinence?
The symptom is the complaint of involuntary leakage on exertion or on sneezing or coughing. The sign is the observation of involuntary urinary loss from the urethra synchronous with exertion, sneezing, or coughing. Urodynamic stress incontinence is noted during urodynamic testing (filling cystometry) and is defined as the involuntary leakage of urine during increases in abdominal pressure in the absence of a detrusor contraction
What is urge urinary incontinence?
The symptom is the complaint of an involuntary leakage accompanied by or immediately preceded by urgency. The sign is the observation of involuntary urinary loss from the urethra that is accompanied by or immediately preceded by urgency. Detrusor overactivity incontinence is incontinence related to an involuntary detrusor contraction during urodynamics
What is accomodation, in regards to the bladder? How does this translate into what we see during filling on vuds?
During bladder filling at physiologic rates, detrusor pressure remains nearly constant because of a special property of the bladder known as accommodation.

Accommodation accounts for the nearly flat cystometric curve that is seen during normal bladder filling
Is the micturition reflex under voluntary control? Where is it organized?
The micturition reflex is normally under voluntary control and is organized in the rostral brain stem (the pontine micturition center).
What are the gaurding reflexes?
Normal storage of urine is dependent on (1) spinal reflex mechanisms that activate sympathetic and somatic pathways to the bladder outlet and (2) tonic inhibitory systems in the brain that suppress parasympathetic excitatory outflow to the bladder (Morrison et al, 2005). Distention of the bladder walls during filling leads to sympathetic stimulation of the bladder outlet smooth musculature and pudendal outflow to the external urethral sphincter. Sympathetic stimulation also inhibits the bladder body musculature and transmission in the bladder parasympathetic ganglia (de Groat, 1997; Yoshimura and de Groat, 1997). These responses occur by spinal reflex pathways and represent the guarding reflexes
What are the neurologic steps of micturition? How does voiding stop midstream if a patient desires?
At the initiation of micturition, intense bladder afferent activity activates the pontine micturition center, which inhibits the spinal guarding reflexes (de Groat, 1997). Relaxation of the urethral muscles is mediated in some species by activation of a parasympathetic pathway to the urethra that triggers the release of the inhibitory neurotransmitter nitric oxide (Anderson, 1993; Bennett et al, 1995) and by removal of adrenergic and somatic cholinergic excitatory inputs (Yoshimura and de Groat, 1997; de Groat et al, 2001). Thus, the first recorded event is sudden and complete relaxation of the striated sphincteric muscles, characterized by complete electrical silence of the sphincter electromyogram (Tanagho and Miller, 1970; Blaivas, 1982). This is followed almost immediately by a rise in detrusor pressure and concomitant fall in urethral pressure as the bladder and proximal urethra become isobaric (Yalla et al, 1980; Blaivas, 1988a). The bladder neck and urethra open, and voiding ensues. Voluntary interruption of the stream is accomplished by a sudden contraction of the striated periurethral musculature, which, through a reflex mechanism, shuts off the detrusor contraction, aborting micturition. The sphincteric system is also designed to resist physiologic increases in abdominal pressure.
What are the underlying principles of a sound urinary sphincter?
The principles underlying the function of a sphincter are (1) watertight apposition of the urethral lumen, (2) compression of the wall around the lumen, (3) structural support to keep the proximal urethra from moving during increases in pressure, (4) a means of compensating for abdominal pressure changes (pressure transmission), and (5) neural control. Thus, normal sphincteric function is the result of an integrated interaction among all these factors.
Urethral hypermobility is proposed to cause incontinence by what mechanism? Can a woman have severe urethral hypermobility and not leak urine?
It was also thought that the normally supported bladder neck and proximal urethra sit in a high retropubic position and that increased intra-abdominal pressure is transmitted equally to both bladder and urethra. In cases of stress-induced urethral descent, the urethra attains a low, dependent position. Increased intra-abdominal pressure is then transmitted unequally to the urethra and bladder; and when bladder pressure exceeds urethral pressure, SUI ensues.

However, the fact that many women are totally continent despite clinical evidence of urethral hypermobility somewhat refutes that theory. This implies that the normal urethra remains closed even during stress-induced descent.
What is DeLancy's theory of urethral support or the so called Hammock theory?
In anatomic specimens in which increases in abdominal pressure were simulated, he found that the urethra lies in a position where it can be compressed against a hammock-like musculofascial layer on which the bladder and urethra rest (DeLancey, 1994). In this model, it is the stability of this supporting layer rather than the position of the urethra that determines stress continence. Urethral support is supplied by connective tissue and muscle arranged to resist the downward pressure created by increases in abdominal pressure. The urethra is intimately connected to the anterior vaginal wall, and the connections of these two structures to the levator ani muscle complex and arcus tendineus fascia pelvis (ATFP) determine the stability of the urethra. The ATFP is a fibrous fascial band that stretches from the pubic bone anteriorly to the ischial spine. The fascial covering of the levator ani consists of two leaves: the endopelvic fascia (abdominal side) and the pubocervical fascia (vaginal side). The two leaves fuse laterally to insert ATFP, creating a hammock of support under the urethra and bladder neck Normally, with rises in intra-abdominal pressure, the urethra is compressed against the supporting structures, which act like a backboard and prevent loss of urine
What is ISD? Who coined the term and how was it discovered?
McGuire and colleagues first introduced the concept of intrinsic sphincteric deficiency (ISD) when, in a retrospective analysis of the results of anti-incontinence surgery, they noted that some women who had undergone multiple retropubic operations had a deficient sphincteric mechanism characterized by an open bladder neck and proximal urethra at rest with minimal or no urethral descent during stress. They stated that ISD denotes an intrinsic malfunction of the urethral sphincter, regardless of its anatomic position. Contemporary theories suggest that all patients with sphincteric incontinence have some degree of ISD. Considerations that support this theory include the fact that the normal urethra is intended to remain closed no matter what the degree of stress or rotational descent.
What portion of the urinary sphincter complex in men is removed during prostatectomy?
The PUS consists of the bladder neck, prostate, and prostatic urethra to the level of the verumontanum. It is innervated by autonomic parasympathetic fibers from the pelvic nerve. This portion of the continence mechanism is removed during prostatectomy, leaving only the DUS to prevent urinary leakage.
What makes up the distal urethral complex in males?
The male DUS complex is composed of the prostatomembranous urethra, cylindrical rhabdosphincter (external sphincter muscle) surrounding the prostatomembranous urethra, and extrinsic paraurethral musculature and connective tissue structures of the pelvis
What are two bladder abnormalities that can lead to urinary incontinence?
Bladder abnormalities that cause urinary incontinence include detrusor overactivity and low bladder compliance.
When talking about impaired compliance is it more important to discuss a number in terms of what is poor compliance or the detrusor pressure during filling?
The calculated value of compliance is probably less important then the actual bladder pressure during filling. This is because the compliance value can change depending on the volume over which it is calculated. For this reason, numeric values of compliance are rarely reported. For example, absolute sustained detrusor pressures of 35 to 40 cm H2O or greater during storage, regardless of the bladder volume, can lead to upper tract damage (McGuire et al, 1981; Churchill et al, 1987). When the detrusor pressure exceeds the pressure capacity of the sphincter to resist that pressure, incontinence results
What is a differential diagnosis for the etiology of detrusor overactivity in a patient?
*Idiopathic

*Neurogenic - can be subclassified into,
Supraspinal - stroke, parkinson's, hydrocephalus, brain tumor, traumatic brain injury, MS.
Spinal Lesion - spinal cord injury, tumor, MS, transverse myelitis, myelodysplasia.
DM

Non-neurogenic detrusor overactivity: infection, obstruction from stricture or BPH, cancer, women with POP, stricture, bladder stones, foreign body, etc.
What is the typical picture of a patient with a lesion above the pons, in other words a patient say with a stroke as far as urinary incotinence and voiding dysfunction?
Neurologic lesions above the pons (e.g., cerebrovascular accident, brain trauma) usually leave the micturition reflex intact. Many affected patients have no voiding phase dysfunction at all. When micturition is affected, there is generally a loss of voluntary control of the micturition. In these patients, micturition is physiologically normal-there is a coordinated relaxation of the sphincter during detrusor contraction, but the patient has simply lost the ability either to initiate or to prevent voiding (Blaivas, 1982; Morrison, 1987a; Khan et al, 1990). There is great variability in the degree of the patient's awareness of, control of, and concern about micturition. Some patients have either no awareness or no concern and simply void involuntarily. Some patients can sense the impending onset of an involuntary detrusor contraction and are able to contract the sphincter voluntarily and abort the detrusor contraction before it starts. Such patients usually complain of urgency but not urge incontinence. Others are aware of the involuntary detrusor contraction and can contract the striated sphincter, but this does not abort the detrusor contraction and incontinence ensues. In addition to urinary urgency, these patients complain of urge incontinence. Still others can contract the sphincter during an involuntary detrusor contraction and abort the stream but not the detrusor contraction. As soon as they relax the sphincter, incontinence occurs. Some patients with supraspinal neurologic lesions develop detrusor areflexia or an acontractile detrusor, but the neurophysiologic pathways responsible for this have not been well described
What is typically the result of a patient with a lesion somewhere in the cord between the pons and the sacral cord?
Interruption of the neural pathways connecting the "pontine micturition center" to the "sacral micturition center" also results in detrusor overactivity, which is often accompanied by detrusor external sphincter dyssynergia (DESD) or other manifestations of poor coordination of the micturition reflex, such as weak, poorly sustained detrusor contractions (McGuire and Brady, 1979; Blaivas, 1982; Rudy et al, 1988). DESD is characterized by involuntary contractions of the striated musculature of the urethral sphincter during an involuntary detrusor contraction. It is seen exclusively in patients with neurologic lesions between the brain stem (pontine micturition center) and the sacral spinal cord (sacral micturition center). DESD often results in high-pressure involuntary contractions because of the high outlet resistance. These lesions include traumatic spinal cord injury, multiple sclerosis, myelodysplasia, and other forms of transverse myelitis
What are the four types of OAB?
four types of OAB. In type 1, the patient complains of OAB symptoms, but no involuntary detrusor contractions are demonstrated (Fig. 60-8). In type 2, there are involuntary detrusor contractions, but the patient is aware of them and can voluntarily contract the sphincter, prevent incontinence, and abort the detrusor contraction (Fig. 60-9). In type 3, there are involuntary detrusor contractions, the patient is aware of them and can voluntarily contract the sphincter and momentarily prevent incontinence, but the patient is unable to abort the detrusor contraction and when the sphincter fatigues, incontinence ensues (Fig. 60-10) In type 4, there are involuntary detrusor contractions, but the patient is not able to contract the sphincter voluntarily or abort the detrusor contraction and simply voids involuntarily.

For example, a patient with type 1 and 2 OAB exhibits normal neural control mechanisms and, at least theoretically, is an excellent candidate for behavioral therapy. It is likely that over time (with or without treatment), an individual patient can change from one type to another. Further, this classification relates only to the storage stage and can coexist with normal voiding, bladder outlet obstruction, or impaired detrusor contractility
Can obstruction cause decreased compliance and can relief of obstruction improve bladder compliance?
Yes

Leng and McGuire (2003) showed that relief of obstruction by transurethral incision or resection of the prostate can improve compliance.
What are conditions associated with increased risk of ISD in women?
Previous urethral or periurethral surgery (e.g., anti-incontinence surgery, urethral diverticulectomy) may result in postoperative ISD from periurethral fibrosis, scarring, or denervation (Haab et al, 1996). Prevalence of ISD after two or more failed anti-incontinence operations was found to be as high as 75% (McGuire, 1980).
Neurologic insult may cause ISD. Sacral neurologic lesions have a variable effect on micturition, depending on the extent to which the neurologic injury affects the parasympathetic, sympathetic, and somatic systems (Gerstenberg et al, 1980; Blaivas and Barbalias, 1983; Wheeler et al, 1986; McGuire et al, 1988). In complete parasympathetic lesions, the bladder is areflexic and the patient is in urinary retention. When, in addition to a parasympathetic lesion, there is a sympathetic lesion, the proximal urethra loses its sphincteric function. Clinically, this results in incomplete bladder emptying, caused by the acontractile detrusor, and sphincteric incontinence, caused by the nonfunctioning proximal urethra (Gerstenberg et al, 1980; Blaivas and Barbalias, 1983). Somatic neurologic lesions affect pudendal afferent and efferent nerves (Blaivas, 1982). In addition to loss of perineal and perianal sensation, these lesions abolish the bulbocavernosus reflex and impair the ability to contract the urethral and anal sphincters voluntarily. Sacral neurologic lesions are caused by herniated disks, diabetic neuropathy, multiple sclerosis, and spinal cord tumors. They are also commonly encountered after extensive pelvic surgery such as abdominoperineal resection of the rectum and radical hysterectomy (Gerstenberg et al, 1980; Blaivas and Barbalias, 1983; Chang and Fan, 1983; McGuire et al, 1988).
Pelvic radiation therapy has been associated with damage to the mucosal seal coaptation of the urethra as well as local neurologic damage (Haab et al, 1996).
What are some causes of transient incontinence?
Conditions causing transient incontinence are more common in elderly persons and can be recalled using the mnemonic DIAPPERS

D - delirium
I - infection
A - atrophic vaginitis/urethritis
P - psychological
P - pharmacological
E - excess urine production
R - restricted mobility
S - stool impaction
What is the bulbocavernosus reflex? Is that reflex always present in men or women?
The bulbocavernosus reflex is checked by suddenly squeezing the glans penis or clitoris and feeling (or seeing) the anal sphincter and perineal muscles contract. Alternatively, the reflex may be initiated by suddenly pulling the balloon of the Foley catheter against the bladder neck.

The absence of this reflex in men is almost always associated with a neurologic lesion, but the reflex is not detectable in up to 30% of otherwise normal women
What does a well-estrogenized vaginal epithelium look like? A poorly estrogenized epithelium looks like what?
The well-estrogenized vagina has thick, pink epithelium with transverse rugae. The poorly estrogenized vagina has a paler, thinner epithelium with loss of rugae.
What is the Q tip test?
The Q-tip test is performed by inserting a well-lubricated sterile cotton-tipped applicator gently through the urethra into the bladder. Once in the bladder, the applicator is withdrawn to the point of resistance, which is at the level of the bladder neck. The resting angle from the horizontal is recorded. The patient is then asked to strain and the degree of rotation is assessed. Hypermobility is defined as a resting or straining angle greater than 30 degrees from the horizontal.
What does the term occult stress incontinence in a woman refer to?
Stress incontinence that is not present clinically or with a prolapse unreduced but is present after reduction of prolapse is termed occult stress incontinence
What are some ways to distinguish a rectocele from an enterocele?
The posterior vaginal wall and vault are examined for the presence of posterior prolapse (rectocele or enterocele). As the speculum is slowly withdrawn, a transverse groove separating an enterocele from a rectocele below may be visible. A finger inserted into the rectum can "tent up" a rectocele but not an enterocele.
What are the two systems for assessing severity of pelvic organ prolapse?
Baden-Walker system (grade 1 to 4) (Baden and Walker, 1992) or the pelvic organ prolapse quantification system (POP-Q), which assesses each compartment separately (Bump et al, 1996).
Should you do a u/a in patients with incontinence?
yes
What are the negative and positive aspects of PVR?
nonrepresentative PVR is common when the patient's bladder is not sufficiently full to yield a normal urge to void. In interpreting the results, consideration should be given to the fact that voiding in unfamiliar surroundings may lead to unrepresentative results and an isolated finding of residual urine requires confirmation before being considered significant (Abrams et al, 1988). Furthermore, if results are "abnormal," tests should be repeated because the test-retest reliability of PVR measurements is poor

There is no evidenced-based specific maximum PVR that is considered normal, nor is there a minimal PVR that is considered abnormal The Agency for Health Care Policy and Research (AHCPR) guidelines state that, in general, a PVR less than 50 mL is adequate bladder empting and a PVR more than 200 mL is inadequate emptying.

third International Consultation on Incontinence recommends that PVR be determined in the initial assessment