Voiding Dysfunction Flashcards
Understand LUT antatomy
There are three pathways of urine
What is the pontine micturition centers role in normal voiding
to coordinate contraction of the detrusor and relaxation of the sphincters; talks to PNS and SNS from lumbar and sacral area which innervates the bladder and the urethral spincter
Role of CNS in the micturition
– Voluntary control over micturition
– Inhibition of reflex detrusor contraction
Parasympathetic – facilitates micturition, how?
– Direct motor activation of detrusor contraction (acetylcholine; muscarinic receptors)
– Indirect facilitation of detruso rcontraction via stretch receptors
Sympathetic – facilitates urine storage
– Inhibition of detrusor
» Direct (β3- adrenergic receptors)
» Indirect (via inhibition of parasympathetic stimulation)
– Contraction of “internal sphincter”/bladder neck (α adrenergic receptors)
– Inhibition of detrusor
» Direct (β3- adrenergic receptors)
» Indirect (via inhibition of parasympathetic stimulation)
– Contraction of “internal sphincter”/bladder neck (α adrenergic receptors)
Sympathetic – facilitates urine storage
– Direct motor activation of detrusor contraction (acetylcholine; muscarinic receptors)
– Indirect facilitation of detrusor contraction via stretch receptors
Parasympathetic – facilitates micturition
Which part of the nervous system is under voluntary control?
Somatic – voluntary control
• Innervation of external urethral sphincter
responsible for smooth muscle sphincter contraction and relaxation
sympathetic nervous system; alpha-adrenergic fibers
Responsible for detrusor contraction and relaxation
cholinergic fibers; Parasympathetic Nervous System
Striated muscle sphincter contraction and relaxation
Somatic nervous system
Autonomic reflex between bladder and spinal cord promoting bladder emptying
Micturition Reflex
Bladder fills with urine causing stretching of bladder wall
Stretch receptors activated and send signals back to spinal cord that :
Further activation of stretch receptors with :
promote detrusor contraction
further promotion of detrusor contraction
CNS (cortex) sends inhibitory signals to __________micturition reflex in cognitively intact people (otherwise we’d peeing all the time like a baby)
“turn off”
Micturition reflex can also be abolished by
external sphincter contraction (guarding reflex, voluntary/involuntary contraction of sphincter)
When decision to urinate is made,______ removes the inhibitory signals and external sphincter relaxes to allow for micturition reflex to occur
CNS
Detrusor contraction via:
Internal sphincter relaxation via:
– Parasympathetic innervation
– Sympathetic innervation
have the potential to cause discoordination of these phenomena
• Damage to the brainstem/pons or spinal cord lesions below the brainstem
Detrusor contracts simultaneously with external sphincter (detrusor-sphincter dyssynergia)
Excessively high bladder pressures and trouble emptying bladder
What promotes urine emptying?
Release of central inhibition of detrusor (brain decides “it’s time to pee”)
External sphincter relaxes
Detrusor contracts
Bladder neck/internal sphincter relaxes
What promotes urine storage?
Descending signals from CNS inhibit detrusor
Detrusor at rest
Sphincters contracted
= Gas pedal of car
= Brakes
- Detrusor
- Urethral sphincters
________ = Car moving forward
________ ≈ detrusor contraction
________ ≈ relax urethral sphincters
• Voiding
– Foot on gas
– Take foot off brake
_______ = Car stopping/stopped
_________ ≈ detrusor relaxed
_________ ≈ sphincter muscles active
Urine storage
– Foot off accelerator
– Foot on brake
Failure to store urine
– Bladder (detrusor) – overactive (OAB) vs underactive
OAB/detrusor overactivity–>_________
Underactive detrusor with chronic urinary retention and bladder
overdistension–> _________
urge incontinence
overflow incontinence
– Urethral sphincter–>stress incontinence
• Incompetent/weakness
This is what type of voiding dysfunction
voiding dysfunction; social or anxiety with extrinsic force on the bladder from raising abdrominal pressure
– Urethral obstruction: Anatomic causes
– Prostatic enlargement
– Urethral stricture
– Prior incontinence surgery
Failure to empty urine
– Bladder (detrusor)
- weak/underactive/atonic/areflexic
Functional (hyperactive sphincter)
– Neurogenic =
– Non-neurogenic =
Functional (hyperactive sphincter)
– Neurogenic = detrusor-sphincter dyssynergia
– Non-neurogenic = dysfunctional voiding
Failure to store urine (car keeps moving when you want it to stop) – Intermittent stepping on accelerator ≈
*Urge Incontinence
– Brake malfunction ≈
*Stress Incontinence
detrusor overactivity
urethral sphincter dysfunction
Failure to empty urine (car won’t move forward)
– Engine malfunction/failure to step on accelerator ≈ ______
– Something blocking the front of car ≈ __________
– Intermittent/continuous stepping on brakes ≈ __________
bladder dysfunction
anatomic urethral obstruction
hyperactive urethral sphincter (e.g. detrusor-sphincter dyssynergia)
Urinary Incontinence =
Failure to Store Urine
Two causes of urinary incontinence
• Due to Detrusor – Overactive bladder/Urge urinary incontinence (UUI) • Due to sphincter – stress urinary incontinence (SUI)
≈ Hyperactive/Irritable detrusor
“Bladder spasms”
Bladder decides “to go” independent of the brain’s control
Urinary Urgency (gotta go in a hurry)
Urinary Frequency (>8 voids/24 hr)
Nocturia (night time voiding)
Urge incontinence (have to go so bad that you start leaking/voiding before reaching toilet)
Overactive Bladder
Causes of overactive bladders
- Inflammation/infection (e.g. UTI)
- Bladder Irritants
- Neurologic conditions – Spinal cord injury, stroke, multiple sclerosis • Metabolic conditions – Diabetes
- Urethral obstruction – Enlarged prostate, prior surgery for incontinence
Etiology of overactive bladder
- 16.5% of Americans met the criteria for OAB – Telephone survey of >5200 American adults
- Estimated that 29.8 million adults aged ≥40 years in the United States have bothersome OAB symptoms
– Internet survey of 20,000 American adults
• Prevalence increases with age (not normal part of aging) – Age <70: female > male – Age >70: female ≈ male
Behavioral therapies for OAB
Behavioral therapies – Fluid management – Pelvic floor exercises (Kegels)
• Inhibit detrusor contraction by contracting urinary sphincter/pelvic floor
Why are anticholinergics such as oxybutynin and **tolterodine **recommend to tx overactive bladder?
• Block acetylcholine receptor in detrusor
Inhibit overactive detrusor contractions
Why do B-3 Adrenergic agonists work to treat OAB: Myrbetriq
Activates β-3 receptor in detrusor
–> Relaxation of detrusor
Cause of stress urinary incotinence
(Incontinence with coughing, sneezing, exercise, heavy lifting (ie anything that increases intra-abdominal pressure)
Due to weakness of urinary sphincter and support structures of urethra and bladder neck
– Vaginal/pevic trauma:
- Multiple vaginal deliveries
- Pelvic surgery (incl prior incontinence surgery)
- External trauma (e.g. car accident)
- Often associated with vaginal prolapse – Lack of estrogen (i.e. menopause) – Neurologic (e.g spina bifida) – Radiation therapy scarring – Obesity
All can cause or risk factor for stress urinary incontinence
How common is stress incontinence
- Approx 40% of healthy females aged 30-49 have experienced some degree of incontinence with exercise
- Up to 25% of women may experience incontinence 3 months following their first vaginal delivery
Risk of incontinence increases with:
– Number of children (vaginally > C-section)
– Age older than 45 yrs
A 50 yr old with 3 children delivered vaginally has an almost _____risk of being incontinent
40%
Behavorial therapies for Stress incontinence
• Behavioral therapies
– Pelvic floor exercises (Kegels)
• Learn to contract pelvic floor/sphincter prior to activity (the knack) – Weight loss
What is duloxetine and why is it recommended for tx of stress incontinence
• Medication (technically no approved drug for SUI)
– Duloxetine (selective serotonin and norepinephrine reuptake inhibitor)
Increases neural output from spinal cord to external urinary sphincter
Contraction of sphincter muscle
What are some causes of “failure to empty” that involved the detrusor
Due to Detrusor
– Neurogenic
– Myogenic
– Psychogenic
– Medication
What medications can affect the detrusor muscle and prevent it from emptying
- Anticholinergics
- α-agonists
- Narcotics
Urinary retention; what are some anotomic causes
– Anatomic • Prostate enlargement
- Urethral stricture
- Prior incontinence surgery
Urinary retention or failure to empty can be caused by spincter hyperactivity, what are two causes?
– Functional (sphincter hyperactivity)
- Neurogenic (detrusor-sphincter dyssynergia)
- Non-neurogenic (dysfunctional voiding)
Post-operative state: – Anesthetics (anticholinergic activity) still on board will:
Inhibit detrusor thus get retention of urine
Post Op – Increased sympathetic tone results in:
Inhibit detrusor
Internal sphincter/bladder neck contraction
What are some signs and symptoms of urinary retention
Voiding difficulty/inability to urinate • Straining to urinate • Hesitancy • Intermittent stream • Weak urinary stream – Urinary frequency (from lack of bladder emptying) – Lower abdominal/suprapubic pain (acute) – “Overflow” urinary incontinence (chronic) – Suprapubic fullness/mass (distended bladder) – Hydronephrosis/renal failure
Management of Urinary retention:
Catheter drainage of bladder – Indwelling – Intermittent (ideal)
- Treat UTI
- Stop aggravating meds (e.g. anticholinergics)
- Relieve any obstruction – α-blocker medication (reduce internal sphincter tone) – Surgery on prostate
- Neuromodulation (for non-obstructive retention)
Parasympathetic nervous system activates the _____for micturition
detrusor muscle (via acetylcholine)
inhibits the detrusor (β3 -receptor activation, inhibition of parasympathetics) and activates the bladder neck/internal sphincter for urine storage
Sympathetic nervous system
Somatic nervous system controls the
external sphincter (voluntary control)
CNS tonically inhibits the micturition reflex; __________ initiates micturition
release of this inhibition
Failure to store (urinary incontinence)
Due to hyperactive/overactive bladder
Urge incontinence
Due to weak overdistended bladder (ie urinary retention) Overflow incontinence
Due to sphincter (weak/damaged)
Stress incontinence
Failure to empty (urinary retention)
Due to bladder (weak/underactive)
Due to sphincter (hyperactive)
Neurologic disorder
Detrusor-sphincter dyssynergy
Non-neurologic
Dysfunctional voiding
