Urinary Incontinence Flashcards
How does the CNS affect bladder control?
Pons = facilitates voiding of the bladder
- promotes micturition cycle but can also override it with help of the cerebral cortex
Cerebral cortex = inhibts voiding of the bladder
- can override the micturation reflex if the person consciously decides its not time to void
**voiding centers around the detrusor muscle action
Difference between transient/acute and chronic urinary incontinence
Transient
- < 6 months
- has a reversible underlying cause always
Chronic
- > 6 months
- differs into subset types
- usually reversible but not always
Stress incontinence
- *Damage/weakness to the pelvic floor, urethral hyper mobility and/or intrinsic sphincter deficiencies are the causes of this.
- vaginal delivery and surgical complications are the top 2 mechanical causes of this!
Is triggered by anything that causes increased intra-abdominal pressures
- laughing, sneezing, coughing, exercise, etc.
When intra-abdominal pressure increases, patients with stress incontinence either dont have the pelvic muscle strength to push back and therefore the pressures forces the urine out, or they just straight up have weak sphincters which allows for easily pushed out urgency (outlet incompetence)
Risk factors:
**Highly associated with obesity, repeated vaginal delivery, menopause, injury to the urethra and prostate surgeries
**Diagnosis = bladder stress test under valsalva maneuver/ increased abdominal pressure
Treatment = kegal exercises, alphas agonists weight loss and pressaries (prosthetic device that is inserted into the vagina to support internal structure)
- DONT GIVE ORAL ESTOGEN
Urgency incontinence
Caused by detrusor overactivity (uninhibited contractions/ decreased sympathetics or increased parasympathetics ((almost always parasympathetics))
- causes extreme urge to urinate and involuntary urination
**Highly associated with UTIs (can cause over sensitivity to parasympathetics and subsequent involuntary contractions fo the detrussor), neurological disorders, any cause of bladder outlet obstruction and tumors
- *patients will often say “ i cant get to the bathroom fast enough”
- also patients often experience nocturia often
diagnosis = detrusor overactivity tests
Treatment = #1 = (kegel exercises, bladder training, and distraction relaxation techniques)
- #2 = antimuscarinics (oxybutynin is #)
Red flag symptoms for urinary incontinence
Rapid onset urinary incontinence
Pelvic pain
Hematuria
Overall risk factors for urinary incontinence
Obesity
Functional impairments
Dementia
Medications
High levels of vaginal deliveries
High impact exercise
Overflow incontinence
Incomplete emptying due to detrusor underactivity (decreased parasympathetics) or outlet obstruction
- causes weakened/intermittent streams and hesitancy. Leads a to leakage with overfilling of bladder
Has high levels of post-void residues on catheterization or ultrasound
**Highly associated with diabetes (will show polyuria), bladder outlet obstruction (especially benign prostate hyperplasia (BPH)) and neurogenic bladder issues (especially MS)
Diagnosis = PVR test (volume left will be >200 cc)
Treatment = catheterization, release the obstruction if present, alpha blockers if BPH.
Mixed incontinence
Features of both stress and urgency incontinence
- very often seen in pregnant patients who get UTIs during pregnancy
How does aging affect urinary incontinence?
Decreased:
- bladder contractility
- bladder capacity
- attenuated striated muscles
- vaginal mucosal activity and urethral closure pressure in females
Increased:
- post-void residual volume (PVR)
- prostate hypertrophy (males)
- uninhibited bladder contractions
What is always done in urine diagnostics and urinary incontinence
Urinalysis
rarely ever need urodynamic testing and almost nerve used in initial work ups
Should you perform cystoscope/urodynamic or renal/bladder ultrasounds of an uncomplicated overactive bladder patient in the initial work up?
NO
Only do this if you cant solve it on initial work up or if it is a complicated case
Mnemonics for causes of transient incontinence
1) “DIAPPERS”
Delirium Infection Atrophic vaginitis Urethritis Pharmaceuticals Psychological disorders Endocrine disorders Restricted mobility Stool impaction
2) “TOILETED”
Thin, dry vaginal and urethral epithelium Obstruction Infection Limited mobility Emotional/psychological disorders Therapeutic medications Endocrine disorders Delirium
Common medications that cause incontinence
Diuretics
Anticholinergics/antihistamines
Antipsychotics/antidepressants
Sedatives/hypnotics
Alcohol
Narcotics
A-adrenergic agonists/antagonists
CCBs
How does the angle of the urethra change with the valsalva maneuver in normal patients and stress incontinence patients?
Normal = <30 degrees
Stress = > 30 degrees
Extra strategies for making Urinary incontinence
Be aware of fluid intake
Avoid bladder stimulants (such as caffeine)
Avoid taking diuretics after 4pm
Reduce physical barriers to the toilet
Avoid constipation
Perform pelvic floor exercises
Cease smoking
Broad physiology of micturation in males and females
1) both have parasympathetics from pelvic nerves to innervate the detrusor muscle in the bladder
- contraction of this muscle voids bladder
2) both have sympathetic nerves that use a1 receptors to control the internal urethral sphincter. B3 receptors are used by both to inhibit the detrusor muscles in the bladder as well
3) both have somatic innervation provided by the pudendal nerve to consciously control external urethral sphincter
First line treatment of all urinary incontinence issues
Lifestyle modifications
- weight loss
- pelvic flood exercises
- bladder training
Decrease water intake if >64oz a day
- also decrease caffeine, carbonated beverages and alcoholic beverages
2nd line treatment for all urinary incontinence
Drug therapies for specific incontinence types
- MUST do lifestyle changes first since even if they dont work alone, studies have shown increased efficacy of medications when these lifestyle changes have been in place
Common drug therapies
- anti-muscarinic = urge and overactive
- B3 agonists = urge
- topical estrogen = stress
third and last line is surgery
Which receptors in the micturation tract are G-protein coupled?
Muscarinic receptors = Gq -> PLC/IP3/DAG/Ca2+ increases
B3 receptors = Gs -> AC/cAMP increases
General physiological background of urinary process
Filling phase
- sympathetics predominant by inhibiting the detrusor (B2) and tonic contraction of the internal sphincter (a1)
- umbrella (dome) cells of the urothelium will flatten and expand allowing for the bladder to stretch and fill with urine
Voiding phase
- parasympathetic predominant by both inhibiting tonic sympathetic tone oft he detrusor and by M receptor activation. Also induces tonic inhibition of the internal sphincter via M receptors also
- umbrella cells straighten up as bladder voids
- pudendal nerve is required to consciously void urine
difference between external and internal urethral sphincters
External:
- voluntary control via the pudendal nerve
- is made up of skeletal muscle
Internal:
- involuntary control via sympathetics (a1) and parasympathetics (M1)
- is made up of smooth muscle
What is the micturation center of the spine?
S2 and 3
Receives tonic information from the urinary bladder and signals to the pons when it is time to void.
- **the pons can choose to override the micturation reflex if the person decides it is not a good time to urinate
- activates micturation reflex which disables tonic sympathetic activity and signals parasympathetics to function.
