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what is urinary incontinence?
Loss of bladder control with involuntary loss of urine frequently accompanied by bothersome lower urinary tract symptoms (LUTS)
what 3 factors are used for LUTS
urgency
sudden desire, often painful
frequency
increased micturition (Urination)
nocturia
interruption of sleep to pee
T/F: urinary incontinence is more common in men
false
more common in women
what is the most common type of urinary incontinence?
stress incontinence
what organs are a part of the upper urinary tract system?
kidneys
ureter
hollow muscular tube channeling urine out of the bladder is what organ?
urethra
internal sphincter
smooth muscle
involuntary
CLOSED at rest
external sphincter
striated muscle
voluntary
relaxation = urination
to urinate, the internal sphincter is (open/closed) and the external sphincter is (open/closed)
internal = open
external = open
what type of receptors are in the detrusor muscle? which one is there more of? Which one causes the contractions?
M2
M3
more M3
M3 causes contractions
B3 receptors
what NT activates detrusor muscle ?
ACh → M3
NE → B3
what is the main type of receptor in the urothelium?
B3
what is the main type of receptor in the internal sphincter? what NT activates it? What happens when it is activated?
alpha1
use NE → cause contraction → continence/ maintain storage
what is the main type of receptor in the external urethral sphincter? what is the NT used? What is the effect?
nicotinic
ACh → voluntary contraction (Continence)
what is the b3 agonists mechanism of action in urge incontinence?
a) increases bladder storage by relaxing detrusor smooth muscle
b) Blocks smooth muscle contraction by binding to muscarinic receptors
c) Blocks alpha receptors to promote urethral relaxation
d) increases urination by blocking sodium and chloride absorption in the nephron
b) Blocks smooth muscle contraction by binding to muscarinic receptors
what happens during the storage phase?
detrusor relaxation (B3 stimulation)
urethral internal sphincter contraction (A1 activation, external sphincter active)
what happens during the voiding phase?
aparasympathetic ACh release → M3 receptor activation → detrusor contraction
internal sphincter relaxation (reduced alpha1 stimulation + voluntary relaxation of external sphincter)
which of the following stimulates bladder smooth muscle contraction?
a) ACh
b) beta-3 agonists
c) alpha-1 agonists
a) ACh
what are not modifiable risk factors for urinary incontinence?
age
gender
what are the modifiable urinary incontinence risk factors?
DIPPERS
delirium, infection, pharmaceuticals, psychological, excess urine output, restricted mobility, stool impaction/constipation
Caffeine
Smoking
what are the 3 types of urinary incontinence?
stress urinary incontinence
urge urinary incontinence / overactive bladder
overflow urinary incontinence
mixed incontinence
functional incontinence
what are symptoms of stress urinary incontinence?
involuntary loss of urine on effort or physical exertion (sneezing, physical activity)
not complete void
minimal nocturia
what causes stress urinary incontinence/
abnormalities with urethra and/or urinary sphincter
decreases/inadequate urethral closure forces → unintentional micturition
SUI risk factors for women
pregnancy
vaginal childbirth
menopause
obesity
chronic conditions (Ex. COPD → constant coughing)
aging
list the medications that worsen SUI
alpha1-blockers
estrogen depletion therapies
angiotensin converting enzyme (ACE) inhibitors
diuretics
sedatives / CNS depressants
why do alpha-1 blockers worsen stress urinary incontinence?
relax smooth muscle of urethra; sphincter → easier leakage
why do estrogen depletion therapies worsen stress urinary incontinence?
decrease estrogen = atrophy of urethra mucosa and pelvic tissue
why do ACE inhibitors worsen stress urinary incontinence?
ADR: chronic cough → repeated rises in abdominal pressure
why do diuretics worsen stress urinary incontinence?
indirect
more urine = more opportunities for leakage
why do sedatives/CNS depressants worsen stress urinary incontinence?
indirect
decreases voluntary pelvic floor control
UUI/OAB symptoms
urinary urgency
urinary frequency
nocturia
not complete voiding, but high volume loss
what causes UUI/OAB
abnormalities with bladder
detrusor muscle contracts inappropriately during urine storage → urge to urinate → voids before bladder is completely full
what are the risk factors for UUI/OAB
considered idiopathic
aging
neurological diseases (ex. spinal cord injury, MS, etc)
bladder outlet obstruction (BPH, prostate cancer)
Cystitis
obesity
what medications worsen UUI/OAB
diuretics
cholinesterase inhibitors
alcohol/caffeine
why do a diuretics worsen UUI/OAB?
promotes increased urine production
why do a diuretics worsen cholinesterase inhibitors?
increase in circu
what are overflow urinary incontinence symptoms?
frequent or constant dribbling or urine “weak stream”
feeling of incomplete bladder emptying
nocturia
obstructive urinary symptoms
- abnormahesitancy
straining to void
what causes overflow urinary incontinence?
abnormalities with urethra and/or urinary sphincter (overactivity)
abnormalities with bladder (Underactivity)
what are risk factors for OUI
bladder obstruction
detrusor underactivity
neurological disorders, age, chronic bladder overdistension
what medications can worsen OUI?
alpha-1 agonists
tricyclic antidepressants
antihistamines
why do a alpha-1 agonists worsen OUI?
increase urethral resistance or closure pressure
why do tricyclic antidepressants worsen OUI?
increase urethral resistance or closure pressure
why do antihistamines worsen OUI?
promotes urinary retention
“pressure problem”; urethral closure failure is
a) stress UI
b) urge UI
c) overflow UI
d) functional UI
a) stress UI
bladder overactivity; “Can’t hold it” is
a) stress UI
b) urge UI
c) overflow UI
d) functional UI
b) urge UI
bladder underactivity or outlet obstruction; “Can’t empty it” is
a) stress UI
b) urge UI
c) overflow UI
d) functional UI
c) overflow UI
bladder underactivity or outlet obstruction; “Can’t empty it” is
a) stress UI
b) urge UI
c) overflow UI
d) functional UI
c) overflow UI
external (Non-urinary) cause is
a) stress UI
b) urge UI
c) overflow UI
d) functional UI
d) functional UI
what is 1st line treatment?
NON-pharmacological treatment
behavioral therapy
T/F: surgery is usually last line option and is more common with stress incontinence
true
what are behavioral therapy examples
dietary fluid management (<2 L per day)
weight loss
timed voiding/bladder training
pelvic floor muscle training
T/F: guidelines recommend pharmacological treatment for stress incontinence
false
NOT recommended
use vaginal estrogen (cream/ring) or off-label Duloxetine (Off label)
what pharmacological classes are recommended for the treatment of urge/OAB?
antimuscarinics
beta-3 agonists
combination
desmopressin (Nocturia-limited use)
what pharmacological classes are recommended for the treatment of overflow?
due to BPH = BPH treatment
bethanechol (urinary retention)
antimuscarinic agents MOA
antagonists at M2 + M3 bladder receptors → inhibiting involuntary detrusor contractions → bladder storage
ADR Of antimuscarinic agents
dry mouth
constipation
blurry vision
fatigue cognitive dysfunction
contraindications for antimuscarinics
narrow-angle glaucoma
urinary retention
extreme caution for antimuscarinic agents
dementia
cognitive impairment
rank oxybutynin dosage forms from least tolerable to most
IR < ER < patch < gel
oxybutynin dosing for gel
apply contents of 1 sachet once daily
oxybutynin IR dosing
5 mg 2-3 times a day, increase at 5 mg increments every 2 weeks, max 5 mg 4 times a day
T/F: you can switch a patient from fesoterodine to tolterodine if theyr are hypersensitive to fesoterodine
false
should NOT, both agents have a similar metabolite
fesoterodine dose
- initiate at 4 mg daily, increase to max 8 mg daily
trospium dose
IR: @0 mg BID
ER: 60 mg daily
take without food
solifenacin dose
initiate at 5 mg daily; increase to max of 10 mg/day
solifenacin risk
prolonged QTc w/ 10 mg dose
darifenacin dose
initiate at 7.5 mg daily; can increase to 15 mg daily
which antimuscarinics negatively impairs cognition in elderly?
oxybutynin
tolterodine
which antimuscarinics don’t impair cognition in elderly?
fesoterodine
trospium
beta 3 agonist MOA
stimulate B3 receptors in detrusor muscle → Relaxation during filling phase → increase bladder capacity + decrease urgency
mirabegron should be avoided in what patients
severe uncontrolled hypertension (>180/110 mmHg)
T/F: VIbegron can be used in patients with elevated BP
true
MIrabegron dosing
25 mg daily ; can be increased to 50 mg daily after 4-8 weeks (If tolerated)
vibegron dosing
75 mg oral daily (no titration needed)
can be taken with or without food
what drug is typically started for a patient with UUI
oxybutynin
as long as no CI
can add Beta-3 agonist if symptoms still not relieved ith antimuscarinic
T/F: you can use 2 antimuscarinics together
-false
do not use them together
if there are ADRs, what can be done?
decrease dose
what is the preferred option for geriatrics?
solifenacin or trospium = preferred
darifenacin and fesoterodine = no short-term cognitive changes
oxybutynin = worst offender
what is the most common dose limiting reason for antimuscarinics?
anticholinergic ADRs
what is the last line in stress incontinence?
pharmacotherapy