Adult lower urinary tract voiding dysfunction
 R.A.S HEMAT, MB;BCh, FRCSI, DUL.
- Bladder outlet obstruction (BOO) is the commonest cause of non-neurogenic voiding dysfunction.
Female urinary continence closure mechanisms: 1- Urethral closure mechanisms, contraction of the anterior pubococcygeus muscle (PCM) closes the urethra. 2- Bladder neck closure mechanisms, the urethra is immobilised by forward contraction of the anterior portion of the pubococcygeus muscle.
The superficial trigone extends from bladder base to the external urethral meatus. Tension of the pubovesical ligament, prevents the anterior bladder wall from collapsing inwards with the contraction. Closure of the bladder neck by the downward force. It ensures that the anterior urethral wall remains semi-rigid.
Hypoxia is known to inhibit mechanical activity in a wide variety of smooth muscles and the bladder. Hypoxia impairs the ability of urethral smooth muscle to generate sustained tone in response to a-adrenergic stimulation. The urethral pressure decreases after aortic occlusion.
Hysterectomy affects the lower urinary tract function. Almost 4-62% of these patients would have symptoms before hysterectomy. Bladder trabeculation, detrusor hypertrophy and decreased compliance, VUR, hydronephrosis and eventually renal failure are the result of high-pressure storage and bladder emptying, which can be due to anatomic obstruction or physiological obstruction of the bladder neck. Stress incontinence alone occurs in 5% of post-prostatectomy patients and detrusor instability in >90%.
The overactive detrusor reveals ultrastructural features of dysjunction pattern that is characterised by: 1) moderate widening of spaces between individual muscle cells; 2) marked reduction or loss of intermediate cell junctions; and 3) abundant unique protrusion muscle cell junctions and ultraclose simple abutments, which are alien to normal detrusor.
The denervated bladder is generally flaccid and compliant, with no spontaneous detrusor activity.
Collagen content of detrusor increases with advancing age in women, resulting in reduction of its contractility (aging detrusor).
Oestrogen administration tends to cause a conversion from a relatively atrophic urethral transitional epithelium to more intermediate and superficial cell types.
Voiding disturbances in patients with HIV raise the difficult problem of aetiological diagnosis.
A stroke has a profound effect on lower urinary tract function, sometimes resulting in significant morbidity.
Peripheral axonopathies may be related to the bladder dysfunction in diabetes mellitus. Diabetes mellitus increases the intracellular Na concentration in proximal tubules. During early stages of diabetes, cellular hypertrophy, growth and remodelling are occurring concomitantly with cellular injury and programmed cell death.
Many drugs can influence bladder function, making it vulnerable to unwanted effects of pharmaceutical agents.
July, 2001
Note: The information in this article has been excerpted from the following books: urotext-ebook simplifying urology, Principles of modern urology, by Dr. R.A.S HEMAT. Permission is granted to copy and redistribute this document electronically as long as it is unmodified. This article may not be sold in any medium, including electronic, CD-ROM, or database, or published in print, without the explicit, written permission of Dr. R. A. S. Hemat.
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Dr. R.A.S HEMAT declares no conflicts of interest or financial interests in any product or service mentioned in this article, including grants, employment, stock holdings, gifts, or honoraria.
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