Monday, December 17, 2012

Female urinary incontinence 1- Definitions, pathophysiology, etiology

Female urinary incontinence 

1- Definitions, pathophysiology, etiology

(Dr. Dark Drint)


Factors Involved in Maintaining Urethral Closure and Continence


Intrinsic Urethral Mechanism









The urethra consists largely of a rich vascular "sponge", lined by a moist mucosal layer and surrounded by a coat of smooth muscle, fibro-elastic tissue and striated muscle. The mucosa provides coaptation. The vascular submucosa creates the "washer effect" for the continence mechanism. Functionally, the surrounding smooth muscle coat contains this mechanism by directing submucosal expansile pressures inward towards the mucosa. Muscle tone is mediated by alpha-adreno receptors in the sympathetic nervous system. All three layers are under estrogen control. 

Extrinsic Factors


Levator Ani muscles (pelvic diaphragm) support all of the pelvic organs and the pubourethralis portion form the "external sphincter".
  1. The endopelvic fascia condenses to form three distinct ligaments: 
    a- pubourethral ligament - stabilises the urethra
    b- urethropelvic ligament - supports the bladder neck and the urethra
    c- pubocervical fascia - supports the bladder
    Their attachments to the side wall of the urethra and pelvic wall (arcuate tendons) form a "hammock" behind the urethra. When intra-abdominal pressure increases, (for example, when coughing, sneezing and during exercise), the urethra is forced closed against the posterior "hammock". 
  2. Urogenital diaphragm (perineal muscles and fascia).
  3. Uterus and cervix. The cardinal ligaments laterally, and the utero-sacral ligaments posteriorly provide direct and indirect support of the bladder as the endopelvic fascia (pubocervical fascia), is fixed to the cervix.  




Incidence of Subtypes of Urinary Incontinence in Women  

  1. Stress Incontinence 50%
  2. Urge Incontinence 20%
  3. Mixed 30%


Genuine Stress Incontinence

Definition:
The involuntary loss of urine when the intravesical pressure, as a result of an increase of intra-abdominal pressure, exceeds the resistance produced by the urethral closure mechanisms, in the absence of bladder activity (unasscociated with the desire to void).

Pathophysiology of Stress Incontinence



The basic pathology is urethral incompetence. This can be either due to:

A). Urethral hypermobility (80 - 90% of patients)
This results from loss of the normal pelvic support mechanism of the bladder and urethra due to:
Trauma and stretching of vaginal delivery
Hysterectomy
Hormonal changes ( Menopause)
Pelvic denervation
Congenital weakness

As the bladder neck support is weakened, the increase in intra-abdominal pressure is no longer transmitted equally to the bladder outlet, and therefore instantaneous leakage occurs.
B). Intrinsic Sphincter Dysfunction (10 - 20% of patients)
This results from damage to the sphincter due to:
Multiple prior operations
Trauma
Radiation
Neurogenic disorders including Diabetes Mellitus
Atrophic changes: lack of estrogen.

Reply:

2 Comments:

Charles Runel said...

There's a new and safer way to achieve the same results as Coaptite. Using blood-derived growth factors to treat stress incontinence avoids the risk of granuloma formation.

You can find out more by going to the following website: http://OShot.info/members/stress

Charles Runels said...

There's a new and safer way to achieve the same results as Coaptite. Using blood-derived growth factors to treat stress incontinence avoids the risk of granuloma formation.

You can find out more by going to the following website: http://www.southernbellemedicine.com/o-shot/

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