W1 Non-Obstructive Lower Urinary Tract Uropathies Flashcards
Urinary incontinence
What is urge, stress, mixed and overflow?
Urge Incontinence (UUI):
—UUI is a urinary incontinence as a direct result of excessive urinary urgency (can’t hold long enough)
—This may be d/t bladder hypersensitivity / overactivity, or may be d/t excessive storage
Stress Incontinence (SUI):
—SUI is an incontinence primarily as a result of a poorly compliant bladder neck, typically 2/2 either Intrinsic Sphincter Deficiency (ISD) or Urethral Hypermobility (often the bladder itself is function ok - the PF is not)
Mixed Incontinence (MUI):
—A combination of UUI and SUI, often this starts as pt having UUI, then pt subsequently develops a component of pelvic floor laxity (either 2/2 age, pelvic floor injury, among others)
Overflow Incontinence (OUI):
—An incontinence type that is a sequelae of storage problems, either 2/2 bladder outlet obstruction or UAB
Overactive bladder (OAB)
What is it?
What are 3 intrinsic factors?
What are some extrinsic factors?
Overactive Bladder is a voiding dysfunction syndrome that comprises of persistent and chronic bothersome urinary urgency that leads to significant impact on pt’s quality of life
Causes:
Intrinsic Factors that may contribute:
○ Bladder lining hypersensitivity
○ Excessive bladder contractions
○ Decreased bladder compliance, not as stretchy
Extrinsic Factors
○ Excessive PO fluid intake, or excessive intake of spicy or acidic food or beverages
○ Caffeine and sugar intake
○ Meds that make you urinate more (like diuretics)
○ Anxiety
Overactive Bladder - Presentation, Signs, Symptoms
What is the key to the patients symptoms?
Symptoms:
—Urgency
—Frequency
—Incontinence (UUI, MUI)
—Nocturnal
—Polyuria (subjective)
⭐️Bothersome all day long and night, not just daytime or nighttime
DDX:
—pregnancy
—UTI
—GI issues
Overactive bladder — PE
Overactive bladder — work up 2
What tests would you order?
What do you need to rule out? 4
What can you use to definitely diagnose OAB but probably wouldn’t because it is so invasive?
CMP: assess kidney function
UA: rule out UTI if leuks, esterase and nitrites present
Renal bladder U/S to rule out hydronephrosis
Post void residual (PVR — to see if the bladder is emptying correctly/fully) to rule out urinary retention/ incomplete bladder emptying as contributory to sx <50cc
Rule out
—infection
—malignancy
—kidney injury
—hematuria
Urodynamic studies: definitive but invasive
Overactive bladder
Treatment — 1st approach?
Pharm agents?
Which class and an example of each
—conservative approach first, avoid triggers
—keep a bladder diary
Pharm:
Anticholinergics:
—Affordable but have a lot of side effects
—oxybutynin
(cholinergic, ACh, parasympathetic, effect is to contract the detrusor so you can pee, if you take an anti-cholinergic, you block this and don’t pee as much)
Beta-3 agonists:
—T10 SNS trunk: norepi agonism of beta-3 receptors, relaxation of the bladder to balloon and store urine = no pee.
⭐️mirabegron ⭐️
(think: beta: balloons out to hold the pee. Or sympathetic = store)
Anti-cholinergic side effects, list 6
Avoid in which cases?
They are not specific and selective to the bladder. They can hit receptors all over the body.
Remember: MR. T BF HD
tachycardia earliest and most reliable sign!!
Dry mouth
Bronchial secretions
Decrease sweating
Increase pupil size
Increased HR
Difficulty urinating
Avoid:
—elderly
—narrow/closed angle glaucoma
—arrhythmia
—fall risk
Oxybutynin vs Trospium
Which crosses the BBB?
Oxybutynin:
—net neutral charge
—lipophilic
—higher BBB penetration
—a/w neuro side effects
Trospium
—slight + charge in solution
—more hydrophilic
—lower BBB penetration
—less neuro s/e
⭐️Mirabegron side effect
Route?
Mirabegron, selective for B3 but not specific, as you increase the dose, 50mg and above, can hit B1 and B2 receptors, when this happens, it can exacerbate HTN
Mirabegron 25 - 50 mg PO daily (usually lasts 12- 24 hours)
Overactive bladder — other procedural treatments
5
● Botox:
—into the detrusor muscle = decreased muscle contractility
—several weeks effect to take place
—repeat dosing q 3 - 12 months
—Risk: UTI, Urinary Retention
—Costly $$$, insurance wants you to try others first
● Neuromodulation:
—Peripheral: PTNS (posterior tibial nerve stimulation)
—Sacral Neuromodulation (ex: interstim)
Urinary Diversion:
● Foley catheter placement
● Suprapubic Tube Placement
● Cystectomy & urinary diversion via ileal conduit (far more rare, a very aggressive approach for OAB)
Interstitial cystitis
A syndrome defined as….
It presents like ________ but more like to have _______
A lot of patients have concomitant _________
Affects _____ more than _______ (gender)
IC is (simply) defined as a syndrome of chronic, persistent suprapubic & pelvic pain a/w irritative voiding sx like urinary urgency, frequency, & dysuria
Presents like overactive bladder but may have pelvic pain and pain w/ urination
A lot of patients have concomitant auto immune diseases (atopy, IBS), lining dysfunction, hypersensitivity pain syndrome, viral syndrome
More common in females
Correlated to mental health issues as well
Interstitial cystitis (diagnosis of exclusion)
HPI and work up same as overactive bladder
When would you consider interstitial cystitis?
Which study is warranted in pats w/ persistent urgency?
⭐️ What might you see with this study?
Histopathology might also have ______
Often pts present as classic OAB, frequent UTI, pelvic pain, tried all 1st line therapies but still having symptoms
Cystoscopy often warranted in pts w/ persistent urgency
5-10% of patients have ⭐️ ulcerative, erythematous lesions, called Hunner’s lesions
Histopathology might also have high mast cell concentrations
Interstitial cystitis treatment
The goal is to provide _________ and _________
Pain relief is often w/ _________ , _________ and _________
_________ , _________ and _________ are usually NOT helpful
Some other treatments include
1.
2.
3.
4. Last line:
The goal is to provide relief of voiding symptoms and pain relief
Pain relief is often w/ NSAIDs, Pentosan and tricyclics
Kegels, myofasical release and antibiotics are usually NOT helpful
Some other treatments include
1. High pressure hydro distention: goal to stretch bladder lining, repeat Q3-6months
2. Installing: lidocaine, pentosan, heparin, DMSO
3. Botox, PTNS
4. Last line: cystectomy and urinary diversion
Underactive Bladder
What is it?
May be a result of what 3 things?
2 associated populations / 2 causes
Underactive Bladder (UAB) is an umbrella term for a syndrome of chronic increased urinary storage, weakened bladder contractility, and delayed / prolonged emptying, all as a sequela of impaired detrusor / bladder function
Typically as a result of:
1. Decreased perception of urinary urgency
2. Decreased detrusor muscle contractility
3. Excessive detrusor compliance
Most commonly found in
1. elderly populations
2. DM patients
3. neurologic injury pts (stroke, spinal cord injury, etc)
4. Chronic Bladder Outlet Obstruction (BOO) → chronic detrusor distention → increased bladder compliance
(“floppy bladder syndrome”) r/t both chronic nerve injury (sensory & motor) and chronic muscle fiber injury
Underactive Bladder 2/2 Diabetes
How does this pathogenesis start? Presenting symptoms?
As it progresses, what happens?
What is the late phase presentation?
DM Cystopathy commonly starts with symptoms of OAB and polyuria
Diabetics pee out a lot of glucose, can have a lot of acidity, impaired blood flow can cause peripheral nerve injury (like diabetics get in their feet) — can happen in the bladder as well.
Regenerating nerves are hyperactive, takes years for regeneration to occur. So diabetics have a lot of sensory issues, feel like they need to pee a lot.
After a while, goes numb, so can’t perceive it. So then become underactive
DM cystopathy ends as underactive bladder