- •Preface
- •Acknowledgments
- •Contents
- •1.1 Introduction
- •1.2 Normal Embryology
- •1.3 Abnormalities of the Kidney
- •1.3.1 Renal Agenesis
- •1.3.2 Renal Hypoplasia
- •1.3.3 Supernumerary Kidneys
- •1.3.5 Polycystic Kidney Disease
- •1.3.6 Simple (Solitary) Renal Cyst
- •1.3.7 Renal Fusion and Renal Ectopia
- •1.3.8 Horseshoe Kidney
- •1.3.9 Crossed Fused Renal Ectopia
- •1.4 Abnormalities of the Ureter
- •1.5 Abnormalities of the Bladder
- •1.6 Abnormalities of the Penis and Urethra in Males
- •1.7 Abnormalities of Female External Genitalia
- •Further Reading
- •2.1 Introduction
- •2.2 Pathophysiology
- •2.3 Etiology of Hydronephrosis
- •2.5 Clinical Features
- •2.6 Investigations and Diagnosis
- •2.7 Treatment
- •2.8 Antenatal Hydronephrosis
- •Further Reading
- •3.1 Introduction
- •3.2 Embryology
- •3.3 Pathophysiology
- •3.4 Etiology of PUJ Obstruction
- •3.5 Clinical Features
- •3.6 Diagnosis and Investigations
- •3.7 Management of Newborns with PUJ Obstruction
- •3.8 Treatment
- •3.9 Post-operative Complications and Follow-Up
- •Further Reading
- •4: Renal Tumors in Children
- •4.1 Introduction
- •4.2 Wilms’ Tumor
- •4.2.1 Introduction
- •4.2.2 Etiology
- •4.2.3 Histopathology
- •4.2.4 Nephroblastomatosis
- •4.2.5 Clinical Features
- •4.2.6 Risk Factors for Wilms’ Tumor
- •4.2.7 Staging of Wilms Tumor
- •4.2.8 Investigations
- •4.2.9 Prognosis and Complications of Wilms Tumor
- •4.2.10 Surgical Considerations
- •4.2.11 Surgical Complications
- •4.2.12 Prognosis and Outcome
- •4.2.13 Extrarenal Wilms’ Tumors
- •4.3 Mesoblastic Nephroma
- •4.3.1 Introduction
- •4.3.3 Epidemiology
- •4.3.5 Clinical Features
- •4.3.6 Investigations
- •4.3.7 Treatment and Prognosis
- •4.4 Clear Cell Sarcoma of the Kidney (CCSK)
- •4.4.1 Introduction
- •4.4.2 Pathophysiology
- •4.4.3 Clinical Features
- •4.4.4 Investigations
- •4.4.5 Histopathology
- •4.4.6 Treatment
- •4.4.7 Prognosis
- •4.5 Malignant Rhabdoid Tumor of the Kidney
- •4.5.1 Introduction
- •4.5.2 Etiology and Pathophysiology
- •4.5.3 Histologic Findings
- •4.5.4 Clinical Features
- •4.5.5 Investigations and Diagnosis
- •4.5.6 Treatment and Outcome
- •4.5.7 Mortality/Morbidity
- •4.6 Renal Cell Carcinoma in Children
- •4.6.1 Introduction
- •4.6.2 Histopathology
- •4.6.4 Staging
- •4.6.5 Clinical Features
- •4.6.6 Investigations
- •4.6.7 Management
- •4.6.8 Prognosis
- •4.7 Angiomyolipoma of the Kidney
- •4.7.1 Introduction
- •4.7.2 Histopathology
- •4.7.4 Clinical Features
- •4.7.5 Investigations
- •4.7.6 Treatment and Prognosis
- •4.8 Renal Lymphoma
- •4.8.1 Introduction
- •4.8.2 Etiology and Pathogenesis
- •4.8.3 Diagnosis
- •4.8.4 Clinical Features
- •4.8.5 Treatment and Prognosis
- •4.9 Ossifying Renal Tumor of Infancy
- •4.10 Metanephric Adenoma
- •4.10.1 Introduction
- •4.10.2 Histopathology
- •4.10.3 Diagnosis
- •4.10.4 Clinical Features
- •4.10.5 Treatment
- •4.11 Multilocular Cystic Renal Tumor
- •Further Reading
- •Wilms’ Tumor
- •Mesoblastic Nephroma
- •Renal Cell Carcinoma in Children
- •Angiomyolipoma of the Kidney
- •Renal Lymphoma
- •Ossifying Renal Tumor of Infancy
- •Metanephric Adenoma
- •Multilocular Cystic Renal Tumor
- •5.1 Introduction
- •5.2 Embryology
- •5.4 Histologic Findings
- •5.7 Associated Anomalies
- •5.8 Clinical Features
- •5.9 Investigations
- •5.10 Treatment
- •Further Reading
- •6: Congenital Ureteral Anomalies
- •6.1 Etiology
- •6.2 Clinical Features
- •6.3 Investigations and Diagnosis
- •6.4 Duplex (Duplicated) System
- •6.4.1 Introduction
- •6.4.3 Clinical Features
- •6.4.4 Investigations
- •6.4.5 Treatment and Prognosis
- •6.5 Ectopic Ureter
- •6.5.1 Introduction
- •6.5.3 Clinical Features
- •6.5.4 Diagnosis
- •6.5.5 Surgical Treatment
- •6.6 Ureterocele
- •6.6.1 Introduction
- •6.6.3 Clinical Features
- •6.6.4 Investigations and Diagnosis
- •6.6.5 Treatment
- •6.6.5.1 Surgical Interventions
- •6.8 Mega Ureter
- •Further Reading
- •7: Congenital Megaureter
- •7.1 Introduction
- •7.3 Etiology and Pathophysiology
- •7.4 Clinical Presentation
- •7.5 Investigations and Diagnosis
- •7.6 Treatment and Prognosis
- •7.7 Complications
- •Further Reading
- •8.1 Introduction
- •8.2 Pathophysiology
- •8.4 Etiology of VUR
- •8.5 Clinical Features
- •8.6 Investigations
- •8.7 Management
- •8.7.1 Medical Treatment of VUR
- •8.7.2 Antibiotics Used for Prophylaxis
- •8.7.3 Anticholinergics
- •8.7.4 Surveillance
- •8.8 Surgical Therapy of VUR
- •8.8.1 Indications for Surgical Interventions
- •8.8.2 Indications for Surgical Interventions Based on Age at Diagnosis and the Presence or Absence of Renal Lesions
- •8.8.3 Endoscopic Injection
- •8.8.4 Surgical Management
- •8.9 Mortality/Morbidity
- •Further Reading
- •9: Pediatric Urolithiasis
- •9.1 Introduction
- •9.2 Etiology
- •9.4 Clinical Features
- •9.5 Investigations
- •9.6 Complications of Urolithiasis
- •9.7 Management
- •Further Reading
- •10.1 Introduction
- •10.2 Embryology of Persistent Müllerian Duct Syndrome
- •10.3 Etiology and Inheritance of PMDS
- •10.5 Clinical Features
- •10.6 Treatment
- •10.7 Prognosis
- •Further Reading
- •11.1 Introduction
- •11.2 Physiology and Bladder Function
- •11.2.1 Micturition
- •11.3 Pathophysiological Changes of NBSD
- •11.4 Etiology and Clinical Features
- •11.5 Investigations and Diagnosis
- •11.7 Management
- •11.8 Clean Intermittent Catheterization
- •11.9 Anticholinergics
- •11.10 Botulinum Toxin Type A
- •11.11 Tricyclic Antidepressant Drugs
- •11.12 Surgical Management
- •Further Reading
- •12.1 Introduction
- •12.2 Etiology
- •12.3 Pathophysiology
- •12.4 Clinical Features
- •12.5 Investigations and Diagnosis
- •12.6 Management
- •Further Reading
- •13.1 Introduction
- •13.2 Embryology
- •13.3 Epispadias
- •13.3.1 Introduction
- •13.3.2 Etiology
- •13.3.4 Treatment
- •13.3.6 Female Epispadias
- •13.3.7 Surgical Repair of Female Epispadias
- •13.3.8 Prognosis
- •13.4 Bladder Exstrophy
- •13.4.1 Introduction
- •13.4.2 Associated Anomalies
- •13.4.3 Principles of Surgical Management of Bladder Exstrophy
- •13.4.4 Evaluation and Management
- •13.5 Cloacal Exstrophy
- •13.5.1 Introduction
- •13.5.2 Skeletal Changes in Cloacal Exstrophy
- •13.5.3 Etiology and Pathogenesis
- •13.5.4 Prenatal Diagnosis
- •13.5.5 Associated Anomalies
- •13.5.8 Surgical Reconstruction
- •13.5.9 Management of Urinary Incontinence
- •13.5.10 Prognosis
- •13.5.11 Complications
- •Further Reading
- •14.1 Introduction
- •14.2 Etiology
- •14.3 Clinical Features
- •14.4 Associated Anomalies
- •14.5 Diagnosis
- •14.6 Treatment and Prognosis
- •Further Reading
- •15: Cloacal Anomalies
- •15.1 Introduction
- •15.2 Associated Anomalies
- •15.4 Clinical Features
- •15.5 Investigations
- •Further Reading
- •16: Urachal Remnants
- •16.1 Introduction
- •16.2 Embryology
- •16.4 Clinical Features
- •16.5 Tumors and Urachal Remnants
- •16.6 Management
- •Further Reading
- •17: Inguinal Hernias and Hydroceles
- •17.1 Introduction
- •17.2 Inguinal Hernia
- •17.2.1 Incidence
- •17.2.2 Etiology
- •17.2.3 Clinical Features
- •17.2.4 Variants of Hernia
- •17.2.6 Treatment
- •17.2.7 Complications of Inguinal Herniotomy
- •17.3 Hydrocele
- •17.3.1 Embryology
- •17.3.3 Treatment
- •Further Reading
- •18: Cloacal Exstrophy
- •18.1 Introduction
- •18.2 Etiology and Pathogenesis
- •18.3 Associated Anomalies
- •18.4 Clinical Features and Management
- •Further Reading
- •19: Posterior Urethral Valve
- •19.1 Introduction
- •19.2 Embryology
- •19.3 Pathophysiology
- •19.5 Clinical Features
- •19.6 Investigations and Diagnosis
- •19.7 Management
- •19.8 Medications Used in Patients with PUV
- •19.10 Long-Term Outcomes
- •19.10.3 Bladder Dysfunction
- •19.10.4 Renal Transplantation
- •19.10.5 Fertility
- •Further Reading
- •20.1 Introduction
- •20.2 Embryology
- •20.4 Clinical Features
- •20.5 Investigations
- •20.6 Treatment
- •20.7 The Müllerian Duct Cyst
- •Further Reading
- •21: Hypospadias
- •21.1 Introduction
- •21.2 Effects of Hypospadias
- •21.3 Embryology
- •21.4 Etiology of Hypospadias
- •21.5 Associated Anomalies
- •21.7 Clinical Features of Hypospadias
- •21.8 Treatment
- •21.9 Urinary Diversion
- •21.10 Postoperative Complications
- •Further Reading
- •22: Male Circumcision
- •22.1 Introduction
- •22.2 Anatomy and Pathophysiology
- •22.3 History of Circumcision
- •22.4 Pain Management
- •22.5 Indications for Circumcision
- •22.6 Contraindications to Circumcision
- •22.7 Surgical Procedure
- •22.8 Complications of Circumcision
- •Further Reading
- •23: Priapism in Children
- •23.1 Introduction
- •23.2 Pathophysiology
- •23.3 Etiology
- •23.5 Clinical Features
- •23.6 Investigations
- •23.7 Management
- •23.8 Prognosis
- •23.9 Priapism and Sickle Cell Disease
- •23.9.1 Introduction
- •23.9.2 Epidemiology
- •23.9.4 Pathophysiology
- •23.9.5 Clinical Features
- •23.9.6 Treatment
- •23.9.7 Prevention of Stuttering Priapism
- •23.9.8 Complications of Priapism and Prognosis
- •Further Reading
- •24.1 Introduction
- •24.2 Embryology and Normal Testicular Development and Descent
- •24.4 Causes of Undescended Testes and Risk Factors
- •24.5 Histopathology
- •24.7 Clinical Features and Diagnosis
- •24.8 Treatment
- •24.8.1 Success of Surgical Treatment
- •24.9 Complications of Orchidopexy
- •24.10 Infertility and Undescended Testes
- •24.11 Undescended Testes and the Risk of Cancer
- •Further Reading
- •25: Varicocele
- •25.1 Introduction
- •25.2 Etiology
- •25.3 Pathophysiology
- •25.4 Grading of Varicoceles
- •25.5 Clinical Features
- •25.6 Diagnosis
- •25.7 Treatment
- •25.8 Postoperative Complications
- •25.9 Prognosis
- •Further Reading
- •26.1 Introduction
- •26.2 Etiology and Risk Factors
- •26.3 Diagnosis
- •26.4 Intermittent Testicular Torsion
- •26.6 Effects of Testicular Torsion
- •26.7 Clinical Features
- •26.8 Treatment
- •26.9.1 Introduction
- •26.9.2 Etiology of Extravaginal Torsion
- •26.9.3 Clinical Features
- •26.9.4 Treatment
- •26.10 Torsion of the Testicular or Epididymal Appendage
- •26.10.1 Introduction
- •26.10.2 Embryology
- •26.10.3 Clinical Features
- •26.10.4 Investigations and Treatment
- •Further Reading
- •27: Testicular Tumors in Children
- •27.1 Introduction
- •27.4 Etiology of Testicular Tumors
- •27.5 Clinical Features
- •27.6 Staging
- •27.6.1 Regional Lymph Node Staging
- •27.7 Investigations
- •27.8 Treatment
- •27.9 Yolk Sac Tumor
- •27.10 Teratoma
- •27.11 Mixed Germ Cell Tumor
- •27.12 Stromal Tumors
- •27.13 Simple Testicular Cyst
- •27.14 Epidermoid Cysts
- •27.15 Testicular Microlithiasis (TM)
- •27.16 Gonadoblastoma
- •27.17 Cystic Dysplasia of the Testes
- •27.18 Leukemia and Lymphoma
- •27.19 Paratesticular Rhabdomyosarcoma
- •27.20 Prognosis and Outcome
- •Further Reading
- •28: Splenogonadal Fusion
- •28.1 Introduction
- •28.2 Etiology
- •28.4 Associated Anomalies
- •28.5 Clinical Features
- •28.6 Investigations
- •28.7 Treatment
- •Further Reading
- •29: Acute Scrotum
- •29.1 Introduction
- •29.2 Torsion of Testes
- •29.2.1 Introduction
- •29.2.3 Etiology
- •29.2.4 Clinical Features
- •29.2.5 Effects of Torsion of Testes
- •29.2.6 Investigations
- •29.2.7 Treatment
- •29.3 Torsion of the Testicular or Epididymal Appendage
- •29.3.1 Introduction
- •29.3.2 Embryology
- •29.3.3 Clinical Features
- •29.3.4 Investigations and Treatment
- •29.4.1 Introduction
- •29.4.2 Etiology
- •29.4.3 Clinical Features
- •29.4.4 Investigations and Treatment
- •29.5 Idiopathic Scrotal Edema
- •29.6 Testicular Trauma
- •29.7 Other Causes of Acute Scrotum
- •29.8 Splenogonadal Fusion
- •Further Reading
- •30.1 Introduction
- •30.2 Imperforate Hymen
- •30.3 Vaginal Atresia
- •30.5 Associated Anomalies
- •30.6 Embryology
- •30.7 Clinical Features
- •30.8 Investigations
- •30.9 Management
- •Further Reading
- •31: Disorders of Sexual Development
- •31.1 Introduction
- •31.2 Embryology
- •31.3 Sexual and Gonadal Differentiation
- •31.5 Evaluation of a Newborn with DSD
- •31.6 Diagnosis and Investigations
- •31.7 Management of Patients with DSD
- •31.8 Surgical Corrections of DSD
- •31.9 Congenital Adrenal Hyperplasia (CAH)
- •31.10 Androgen Insensitivity Syndrome (Testicular Feminization Syndrome)
- •31.13 Gonadal Dysgenesis
- •31.15 Ovotestis Disorders of Sexual Development
- •31.16 Other Rare Disorders of Sexual Development
- •Further Reading
- •Index
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11 Neurogenic Bladder Sphincter Dysfunction |
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•Urodynamic studies can be simple and noninvasive (bladder diary and flow rate) or invasive (cystometrogram and videourodynamics).
•A cystometrogram measures the relationship between bladder filling and pressure. Parameters used to characterize the bladder are capacity, compliance, detrusor activity and sphincter activity.
•On the other hand, invasive urodynamic studies are indicated to evaluate and characterize the neuropathic bladder.
•Risk factors indicative of a poor prognosis include:
–Reduced bladder capacity for age
–Poor compliance
–Elevated detrusor leak point pressure (>40 cm H2O)
–Features of functional bladder outlet obstruction on electromyography, such as detrusor sphincter dyssynergia.
•The urodynamic studies allows each child to be categorized into one of four subtypes of neuropathic bladder dysfunction based on sphincter and detrusor muscle activity. Although these categories may overlap, they assist in patient management.
–Type A: Sphincter overactivity combined with detrusor underactivity
–Type B: Sphincter overactivity combined with detrusor overactivity
–Type C: Sphincter underactivity combined with detrusor underactivity
–Type D: Sphincter underactivity combined with detrusor overactivity
•Despite the etiology, the principles for management are similar:
–To insure and maintaining an adequate sized, normally compliant, urinary bladder
–To evacuates urine completely, at a relatively low pressure
•Early diagnosis and treatment can prevent both renal damage and secondary bladderwall changes, thereby improving long-term outcomes.
•Medical management with CIC and anticholinergics is effective in preserving renal
function and providing safe urinary continence in more than 90 % of patients with a neurogenic bladder.
11.2Physiology and Bladder Function
•The urinary bladder has two functions:
–To store urine (A storage function)
–To expel urine (A micturition function)
•Both of these functions are well coordinated and this coordinated function is regulated by the central and peripheral nervous systems.
•During the storage phase, the urinary bladder acts as a low-pressure reservoir, while the urinary sphincter maintains high resistance to urinary flow to keep the bladder outlet closed.
•During this phase, the pressure inside the urinary bladder remains low.
•This phase depends on:
–The intrinsic viscoelastic properties of the bladder
–Inhibition of the parasympathetic nerves
–Sympathetic nerves also facilitate urine storage in the following ways:
•Sympathetic nerves inhibit the parasympathetic nerves from triggering bladder contractions.
•Sympathetic nerves directly cause relaxation and expansion of the detrusor muscle.
•Sympathetic nerves close the bladder neck by constricting the internal urethral sphincter.
•During micturition, the urinary bladder contracts to expel urine while the urinary sphincter relaxes and opens to allow unobstructed urinary flow and bladder emptying.
•As the bladder fills, the pudendal nerve becomes excited.
•Stimulation of the pudendal nerve results in contraction of the external urethral sphincter.
•Contraction of the external sphincter, coupled with that of the internal sphincter, maintains
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urethral pressure higher than normal bladder pressure.
•The combination of both urinary sphincters is known as the continence mechanism.
•The pressure gradients within the bladder and urethra play an important functional role in normal micturition.
•As long as the intraurethral pressure is higher than that of the intravesical, patients will remain continent.
•If the urethral pressure is abnormally low or if the intravesical pressure is abnormally high, urinary incontinence will result.
•The bladder and urethra are innervated by three sets of peripheral nerves arising from the autonomic nervous system (ANS) and somatic nervous system.
–Autonomic nervous system
•Parasympathetic (S2, S3, S4)
–This is motor to detrusor muscles of urinary bladder
–This is inhibitory to internal urethral sphincter
•Sympathetic (T10 to L2)
–This is motor to internal urethral sphincter
–This is inhibitory to detrusor muscle of urinary bladder
–Somatic nerve (S2, S3, S4)
•Pudendal nerves
•Micturition is a spinal reflux facilitated and inhibited by higher brain center and subject to voluntary facilitation and inhibition.
•The brain is the master control of the entire urinary system and this is done through the micturition control center which is located in the frontal lobe of the brain.
•The micturition control center send inhibitory signals to the detrusor muscle of the urinary bladder to prevent the bladder from contracting and emptying until a socially acceptable time and place to urinate is available.
•The signal transmitted by the brain reach the urinary bladder through the brainstem and the sacral spinal cord.
•The pons part of the brainstem is responsible for coordinating the activities of the urinary sphincters and the bladder so that they work in synergy.
•This is done through the pontine micturition center (PMC).
•The PMC coordinates the urethral sphincter relaxation and detrusor contraction to facilitate urination.
•Stimulation of the PMC causes the urethral sphincters to open while facilitating the detrusor muscle to contract and expel the urine.
•The PMC is also affected by emotions, which is why some people may experience incontinence when they are excited or scared.
•The ability of the brain to control the PMC is part of the social training that children experience during growth and development.
•Usually the brain takes over the control of the pons at age 3–4 years, which is why most children undergo toilet training at this age.
•When the bladder becomes full, the stretch receptors of the detrusor muscle send a signal to the PMC, which in turn notifies the brain that there is a sudden desire to go to the bathroom and empty the urinary bladder.
•Under normal situations, the brain sends an inhibitory signal to the pons to inhibit the bladder from contracting until it is socially acceptable to micturate.
•When the PMC is deactivated, the urge to urinate disappears, allowing the patient to delay urination until finding a socially acceptable time and place.
•When urination is appropriate, the brain sends excitatory signals to the PMC, allowing the urinary sphincters to open and the detrusor muscle to contract and empty the urinary bladder.
•All these excitatory and inhibitory signals pass via the spinal cord (the sacral reflex center).
•The information (signals) from the urinary bladder travels up the spinal cord via the sacral cord to the PMC and then to the brain.
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11 Neurogenic Bladder Sphincter Dysfunction |
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•The brain interprets this signal and sends a reply via the PMC that travels down the spinal cord to the sacral cord and, subsequently, to the urinary bladder.
•An intact spinal cord is critical for normal micturition.
•In the event of spinal cord injury, the patient will develop detrusor sphincter dyssynergia with detrusor hyperreflexia (DSD-DH). The patient will have urinary frequency, urgency, and urge incontinence but cannot empty the bladder completely.
•In infants, the spinal reflex center is responsible for controlling the act of micturition which happens involuntary once the bladder is full. When the bladder is full, an excitatory signal is sent to the sacral cord (the sacral reflex center) which automatically triggers the detrusor to contract leading to involuntary detrusor contractions and bladder emptying. This is temporary and once the higher center of voiding control (the brain) is mature enough it will control and command the bladder. Voluntary continence usually is attained by age 3–4 years.
•Another important component of the act of micturition is the autonomic nervous system which is divided into the sympathetic and the parasympathetic nervous system.
•Under normal conditions, the bladder and the internal urethral sphincter primarily are under sympathetic nervous system control. When the sympathetic nervous system is active:
–It causes the bladder to relax and increase its capacity without increasing detrusor resting pressure
–It stimulates the internal urinary sphincter to remain tightly closed.
–It also inhibits parasympathetic stimulation
–As a result the micturition reflex is inhibited
Effects of the Sympathetic System on the Urinary Bladder
•It causes bladder relaxation
•It stimulates the internal urinary sphincter to remain closed
•It inhibit the effect of the parasympathetic system
•The end result is inhibition of micturition
•The parasympathetic nervous system functions in a manner opposite to that of the sympathetic nervous system.
–The parasympathetic nerves stimulate the detrusor to contract.
–The sympathetic influence on the internal urethral sphincter becomes suppressed so that the internal sphincter relaxes and opens.
–The activity of the pudendal nerve is inhibited and this causes the external urethral sphincter to open.
–The end result is voluntary urination.
Effects of the Parasympathetic System on the Urinary Bladder
•It stimulates the detrusor muscles to contract
•It stimulates the internal urinary sphincter to relax and open by suppression of the sympathetic effect
•It inhibit the effect of the pudendal nerve which causes relaxation of the external urethral sphincter
•The end result is voluntary micturition
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Somatic Nerve (S2, S3, S4) Supply to the Urinary Bladder
•Stimulation leads to contractions of the skeletal muscle fibers of the external urinary sphincter
•During micturition, this nerve is inhibited leading to relaxation of the external urinary sphincter which allows urination
Control of Urinary Bladder Function
•The storage function of the urinary bladder is enabled by:
–Inhibition of detrusor muscles (sympathetic innervation)
–Contraction of the striated external urinary sphincter (somatic innervation)
–Contraction of smooth muscle internal sphincter (sympathetic innervation)
•The micturition function of the urinary bladder is enabled by:
–Relaxation of the striated external sphincter (somatic innervation)
–Relaxation of the smooth muscle internal sphincter and opening of the bladder neck (sympathetic innervation)
–Detrusor muscle contraction (parasympathetic innervation)
•The somatic nervous system regulates the actions of the muscles under voluntary control. The pudendal nerve originates from the nucleus of Onuf and regulates the voluntary actions of the external urinary sphincter and the pelvic diaphragm.
–Activation of the pudendal nerve causes contraction of the external sphincter and the pelvic floor muscles and prevent micturition.
–Inhibition of the activity of the pudendal nerve causes the external urethral sphincter to relax and open to allow micturition
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11 Neurogenic Bladder Sphincter Dysfunction |
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