1887

Urinary incontinence and urine retention

image of Urinary incontinence and urine retention
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Abstract

Urine storage disorders usually manifest as urine retention. Successful management of incontinence and urine retention depends foremost on accurate description of the problem and localization of the disorder, augmented by a clear understanding of the neurophysiology, as covered in this chapter.

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/content/chapter/10.22233/9781910443354.chap3

Figures

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3.1 Basic anatomy of the (a) female and (b) male lower urinary tract.
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3.2 The urine storage phase of micturition. Sympathetic input to the beta (β) adrenoceptors in the bladder stimulates detrusor muscle relaxation; sympathetic input to the alpha (α) adrenoceptors in the IUS stimulates smooth muscle contraction. Voluntary input to the nicotinic cholinergic receptors (Ach-n) in the EUS stimulates striated muscle contraction. During the storage phase, outlet resistance must exceed intravesicular pressure to maintain continence.
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3.3 Central nervous system input to the lower urinary tract. Sympathetic input is supplied to the bladder and proximal urethra via the hypogastric nerve (green); parasympathetic input is supplied via the afferent pelvic nerve (red) and sensation of stretch is relayed to higher centres via the efferent pelvic nerve (blue). The afferent (red) and efferent (blue) branches of the pudendal nerve relay somatic input to and from the external urethral sphincter. Voiding is coordinated in the pontine micturition centre, with input from cerebrocortical centres.
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3.4 The urine voiding phase of micturition. Parasympathetic stimulation of muscarinic cholinergic receptors (Ach-m) causes contraction of the detrusor muscle. Parasympathetic inhibition of sympathetic input to the IUS ( ) and voluntary inhibition of EUS contraction ( ) cause passive relaxation of the outflow tract and intravesicular pressure to exceed outlet pressure, permitting urine voiding.

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