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2 etiologies of UI
inability to store urine: bladder contracts too often, sphincter(s) cannot contract sufficiently to allow the bladder to store urine (cannot keep it from leaking)
result= bladder never fills to capacity and patient experiences frequent incontinent episodes of small or moderate urine volume
inability to empty/void urine: bladder unable to contract appropriately, outlet of sphincter is partially obstructed
result= bladder fills beyond capacity and overflows; patient experiences abdominal distention and frequent leakage
risk factors for UI
caffeine, fluid intake, immobility, biological sex, bowel problems, smoking, parity, UTIs, menopause, GU surgery, lack of post partum pelvic floor exercise, meds
3 types of incontinence
overflow
stress
urge
what is stress incontinence
transient loss of small amounts of urine with increased intra abdominal pressure (Coughing, laughing, sneezing, bending, lifting, posterior urethrovesicular changes- parity, surgery)
due to urethral sphincter weakness
stress incontinence risk factors
pregnancy, vaginal childbirth, obesity (abdominal)
more common in women
what is urge incontinence/overactive bladder (+ causes)
abnormal bladder contractions as a result of detrusor muscle instability:
detrusor muscle is overactive
contracts inappropriately during filling phase
detrusor instability can be the result of:
nerve damage- stroke, PD, MS, DM
spinal cord damage
unknown cause
what is overflow incontinence (+ causes)
occurs when intravesicular pressure exceeds intraurethral pressure- only at high volumes
most common type of UI seen in males with BPH
causes include:
bladder outlet obstruction (BPH, prostate cancer)
diabetic neuropathy, spinal cord lesions below T-11
drugs: muscle relaxants, CCB, anticholinergics, alpha agonists
what is functional incontinence
inability of normally continent person to reach the toilet in time to avoid an accident
MSK limitations (joint pain, arthritis, muscle weakness)
unfamilar setting, lack of conventional toilet facilities
not caused by bladder or urethral specific factors
also seen in people with dementia and cognitive deficits
causes of UI without specific urogenital pathology
D- delirium/confused state
I- infection
A- atrophic urethritis/vaginitis
P- pharmaceuticals
P- psychiatric issues
E- excessive urinary output (hyperglycemia, hypercalcemia)
R- restricted mobility
S- stool impaction
iatrogenic incontinence
incontinence related to med use
drugs contributing to incontinence
alpha agonists- urinary retention
alpha blocker- urinary leakage
anticholinergics- urinary retention and/or functional incontinence
B agonists- urinary retention
B blocker- urinary leakage, urgency
CCBs- retention
diuretics- polyuria
narcotics- urinary retention and/or functional incontinence
alcohol- polyuria and/or functional incontinence
antihistamines- urinary retention and/or functional incontinence
caffeiene- polyuria
what type of UI is inability to store urine
urge or stress
what type of UI has outlet obstruction
overflow
what type of UI has inability to reach toilet
functional
urge incontinence most common urodynamics
detrusor hyperactivity
stress incontinence most common urodynamics
sphincter incompetence
overflow incontinence most common urodynamics
outlet obstruction, detrusor hypoactivity
functional incontinence most common urodynamics
normal
possible etiologies of detrusor hyperactivity
uninhibited contractions, local irritation, CNS causes
possible etiologies of sphincter incompetence
urethral hypermobility, sphincter damage
possible etiologies of outlet obstruction
physical (BPH, tumor, stricture), neurologic lesions, meds
possible etiologies of detrusor hypoactivity
neurogenic bladder (diabetes, alcoholism)
clinical features of stress incontinence
involuntary leakage of urine when coughing, laughing, sneezing, bending or lifting
patients dry over night
clinical features of urge incontinence
urgency, frequency, nocturia, frequent small volume voiding (>8 episodes per day)
no characteristic findings on physical exam, although CNS dysfunction may be apparent
clinical features of overflow incontinence
palpable or percussable bladder
suprapubic tenderness
low urinary flow rates
post void residual volume 150-200cc
functional incontinence clinical features
accident on the way to the toilet
early morning incontinence
first line therapy for stress, urge and mixed UI
non pharm
non pharm therapies
prompted voiding
bladder training- timed voiding
pelvic floor muscle exercises
biofeedback
exercise/weight loss
pessary
**remove causative meds where appropriate
what type of meds may aggravate stress incontinence
alpha blockers
specific therapies for stress incontinence
duloxetine (off label use)
vaginal estrogens (select circumstances)
what cases of SUI may benefit from vaginal estrogens
menopausal women with mixed UI + vaginal atrophy
examples of vaginal estrogens for SUI
conjugated vaginal estrogen cream (Premarin)
estradiol-17B vaginal ring (Estring)
estradiol-17B vaginal tablet (Vagifem)
ae of vaginal estrogens
vaginal discharge
local irritation/pruritis
spotting
duloxetine ae
nausea (esp initially, reduced if taken with food)
CNS- headache, insomnia, dizziness
increased BP
constipation and dry mouth
risk of suicidal idealation (transient)
may cause hepatotoxicity
drug interactions with duloxetine
substrate and inhibitor of CYP2D6 and substrate of 1A2
increased risk of serotonin syndrome when combined with other serotonergic agents
is pseudoephedrine used for SUI
last line therapy- not recommended but some use when all else fails
ineffective and can result in serious ae
specific therapies for urge incontinence
antimuscarinics/anticholinergics (Second line)
beta 3 agonist
vaginal estrogens
TCAs
botulinum toxin
prefered treatment option for urge incontinence if fail non pharm
antimuscarinics
effectiveness of antimuscarinics
only modestly effective- may only reduce urination or incontinence by 1 episode per day
increase bladder capacity/storage
decrease urgency episodes
may decrease nocturia
available antimuscarinic agents
oxybutynin, tolterodine, fesoterodine, trospium, darifenacin, solifenacin
which muscaranic receptor blockage in the detrusor muscle results in bladder relaxation
M3, M2 (more M3)
blockade of M3 receptors in other area of body besides detrusor results in what effects
dry mouth and constipation
blockade of M1 receptors in brain results in
sleepiness and cognitive impairment
what characteristics of antimuscaranics can influence unwanted CNS effects
lipophilicity, charge or polarity and molecular size
M1 selectivity
which antimuscaranic is least likely to cross BBB and cause CNS effects
darifenacin
which antimuscarinic is most likely to cross BBB and cause CNS effects
oxybutynin
which antimuscarinic is considered gold standard
oxybutynin
dosage forms of oxybutynin
IR tab, ER tab, transdermal patch
oxybutynin ae
significant anticholinergic SE: dry mouth and eyes (mucous membranes), increased IOP (vision problems), CNS= dizziness, sleepiness, cognitive impairment, urinary retention, constipation
Is ER or IR oxybutynin tolerated better
ER
benefits of oxybutynin patch form
avoids first pass metabolism
less metabolite produced= lower side effects
how long can it take to see maximum benefit with oxybutynin
may take atleast 4wks with oral, less with patch
does tolterodine or oxybutynin have more anticholinergic SEs
oxy
dosage forms of tolterodine
IR tab, SR cap
when are dosage adjustments required with tolterodine
renal and hepatic impairment, when taking with potent 3A4i
drug interactions with tolterodine
metabolized by 3A4 abd 2D6
dose decrease required when used with potent 3A4inhibitors
no dose adjustment required when used with 2D6 inhibitors
how long does max benefit take with tolterodine
up to 8wks
solifenacin selectivity
slightly more selective for M3 than M1
drug int with solifenacin
metabolized by CYP3A4
when is dosage adjustment required in solifenacin
severe renal impairment <30mL/min, when took potent 3A4i
is solifenacin, tolterodine, or oxybutynin better tolerated
solifenacin
ae of solifenacin
primarily anticholinergic- dry mouth, constipation, tachycardia
differences between fesoterodine and tolterodine
fesoterodine is a prodrug and is not converted by 2D6
when are dosage reductions required with fesoterodine
renal and hepatic dysfxn or with use of potent 3A4 inhibitors
allergy to be aware of with fesoterodine
contains soya lecithin- avoid in patients with peanut or soybean allergy
when is dosage adjustment required with tropsium
age 75+, severe renal impairment (<30mL/min)
which antimuscarinic needs to be taken on an empty stomach
trospium
which antimuscarinic is most M3 selective
darifenacin
drug int with darafenacin
metabolized by 3A4 and 2D6
when is dose decrease required in darifenacin
elderly, potent 3A4 inhibitors
darifenacin side effects
dry mouth, constipation
contraindications for darifenacin
in patients at risk of urinary retention, gastric retention, uncontrolled narrow angle glaucoma
what is mirabegron
selective beta 3 agonists
place in therapy for mirabegron
alternative to antimuscarinics, if not tolerated/contraindicated - efficacy is similar but very expensive
better tolerated than antimuscarinics and may improve adherence
ae of mirabegron
hypertension, tachycardia, nasopharyngitis, UTIs
drug int with mirabegron
mod 2D6 inhibitor
weak inhibitor of pgp - can increase digoxin and dabigatran levels
QT prolonging
therapy of choice in overflow incontinence
surgery- in many men with chronic retention due to BPH
specific therapies for overflow incontinence
alpha blockers (first line)- faster onset
prazosin, terazosin, doxazosin, tamsulosin, alfuzosin
5 alpha reductase inhibitors (ex: finasteride, dutasteride)
non pharm functional incontinence
scheduled bathroom visits
bedside commode if needed
assist with functional disabilities
management of UI in pregnancy
preventative measures- pelvic floor muscle training
what causes UI in pregnancy
hormonal changes, weight gain
main type of UI in pregnancy
stress incontinence
who is at increased risk of UI in pregnancy
advanced maternal age and higher BMI