Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
35 Cards in this Set
- Front
- Back
Describe normal reflex voiding in infants:
|
*Bladder storage “problem”
*Stops when brain and spinal cord develop further at 3-5 years old.: 1) Toilet training 2) Brain gains control over voiding through the pons 3) Applies to defecation as well *Pontine Micturition Center (PMC): -Dorsal pontine tegmentum. -Bladder storage and emptying by coordinating bladder parasympathetics (PS) and sphincter somatics. *Brain is largely inhibitory (promoting urine storage): -Detrusor control involves brain (right superior frontal gyrus, pons, and sacral spinal cord. |
|
What are the components of the sacral spinal cord involved in normal reflex voiding in infants?
|
1) Parasympathetic stretch receptors to bladder.
2) Somatic nerve bodies that innervate external sphincter (ES). *SPN= sacral PS nucleus *ON= onuf's nucleus |
|
Nervous system pathways of bladder control:
|
|
|
With toilet training, what does the nervous system do as the bladder fills?
|
*As bladder fills, brain sends inhibitory messages to pontine micturition center (PMC).
*STORAGE: -PMC sends messages to sacral spinal cord. -Inhibiting parasympathetic nerve bodies to bladder detrusor. -Stimulating somatic nerve bodies to external sphincter. *At capacity, PMC stimulates somatics to ES: -External sphincter squeezes to keep urine in (“Curtsy Sign”) *Normal voiding= No urge or reflex voiding. |
|
With toilet training, what does the nervous system do when the bladder is full?
|
*COORDINATED VOIDING WHEN BLADDER IS FULL.
*Brain then becomes aware of urge to void & when the time/place is socially acceptable. *Brain releases inhibition to PMC: -PMC sends messages to sacral spinal cord, inhibiting somatics to ES (relaxation) and stimulating PS to bladder detrusor (squeeze). -Sympathetics relax internal sphincter (at BN). -Sphincter relaxes, bladder squeezes at low pressure, quickly and to completion. |
|
Discuss Nocturnal Enuresis in the context of Development of Control:
|
*Bedwetting is a delay in the completion of toilet training.
*Sequence of development of control: 1) Daytime fecal continence 2) Nighttime fecal continence 3) Daytime urinary continence 4) Nighttime urinary continence *Nighttime control of urine usually comes last. |
|
Discuss Nocturnal Enuresis. What causes it? How do we treat it?
|
*Bladder Storage Problem.
*Unclear what is the exact cause: -Heavy sleeping, hormonal problems (lack of ADH), genetics, small bladder capacity, or psych issues (stress). *Treatments: -“Positive imagery” -Nocturnal alarm to wake up before wets bed. -DDAVP (synthetic vasopressin); increases water resorption in renal collecting duct. *Should resolve spontaneously. |
|
Describe sensory neuropathy of the bladder:
|
*Pt loses urge to void, forgets to void.
*Urinary retention, overflow incontinence. *Bladder emptying problem. *Often seen in diabetes! |
|
What's the treatment for Sensory Neuropathy?
|
*Usually there's no motor neuropathy; recommend timed voiding for these patients even if they don't feel like it.
*If there IS motor neuropathy (neurogenic bladder): -“clean intermittent cath” (CIC): patients cath themselves every 3-4 hours. Yikes! -Chronic foley. -Sacral nerve stimulator (photo). |
|
Discuss normal bladder physiology:
|
*Normal capacity is 300-400 mL comfortably without uninhibited contractions or increase in bladder pressure.
*Compliance = Δvolume/Δpressure= ∞ (normal). -Impaired compliance causes increased bladder pressure with small changes in bladder volume. *Low voiding pressures protect bladder from developing hypertrophy (trabeculation). -Normal voiding pressures: *Female- near zero voiding pressures. *Male- usually <30 cm H2O. |
|
What is bladder hypertrophy?
|
*Hypertrophy --> worsening compliance --> high pressures transmitted to kidneys --> renal failure!
*Clinical signs of “too high” pressure: hydronephrosis, VUR. |
|
|
Hydronephrosis.
Left: black stuff is extra urine in kidney. Bottom right: hydronephrosis in both kidneys. |
|
What is Neurogenic Detrusor Overactivity?
|
*Remember toilet training model. Brain normally exerts inhibitory control over bladder through pontine control of detrusor and sphincter.
*If brain is damaged or if message from pons cannot travel to sacral cord b/c of spinal cord injury, you no longer have control. Leads to urinary urgency, frequency and urge incontinence--> REFLEX VOIDING. *This is a Bladder storage problem called "NEUROGENIC DETRUSOR OVERACTIVITY." |
|
What kind of lesions cause detrusor overactivity?
|
*Cranial lesions:
-CVA, tumor, brain surgery, Multiple sclerosis (cortical plaques), Parkinson’s disease (basal ganglial lesions). *Spinal cord lesion or injury above sacral cord. |
|
What is the role of Stroke in neurogenic detrusor overactivity?
How would you treat this? |
*Particularly bad b/c usually impaired mobility which adds to urge incontinence and/or urgency.
*Can inhibit PS with anticholinergic meds. |
|
What is Neurogenic Acontractile Bladder?
|
*Compression of sacral spinal cord nerve roots from herniated lumbar disk affect:
-Parasympathetics to bladder, rectum and penis. -Somatics to perineum. *Parasympathetic sensory and motor problem: bladder can’t feel or squeeze. *Anticholinergic effect of narcotic pain meds can make this a lot worse. *May get better after spinal surgery or stopping pain meds. -If not, CIC. *Remember that sacral spinal cord ends at L1-L2 (this does vary). *Bladder emptying problem= ACUTE URINARY RETENTION. |
|
|
*Caude equina syndrome.
*This can be a cause of Neurogenic acontractile bladder (acute urinary retention). |
|
Discuss Spinal shock in regards to bladder control:
|
*General CNS functional impairment from injury; lasts weeks to months; usually around 6-8 weeks.
*It causes a bladder EMPTYING problem. *Urinary retention until spinal shock resolves: -Treatment: Foley catheter or CIC until then. |
|
|
*High grade reflux; can lead to renal failure.
|
|
What is Autonomic dysreflexia:
|
*Combination of headache and HTN.
*Seen in Spinal lesions above T6. *Unopposed sympathetic response ESPECIALLY DURING full bladder, fecal impaction, UTI’s, decubiti, other stressors. *Severe HTN and therefore headache, can cause stroke. *Often seen with DSD. *Treatment: avoid these stressors -For Urinary retention--> foley. *Rapid onset with permanent bladder and renal damage: These patients used to die from renal failure. *Biggest clinical issues: recurrent UTIs, decubitus ulcers from constant leakage and poor mobility. *This is a Bladder emptying and storage problem. |
|
Discuss BPH:
|
*Prostatic obstruction causes increased work for detrusor.
*Detrusor becomes trabeculated and thick. *Bladder capacity can decrease, leading to frequency and nocturia. *Blockage from BPH/BPE - now referred to as Bladder Outlet Obstruction (BOO). |
|
|
*BOO: trabeculated bladder.
*Middle: trabeculated bladder. *Right: normal bladder. |
|
What are the consequences of BOO?
|
*Obstruction can cause:
-Overflow incontinence. -LUTS (lower urinary tract symptoms). *This is a Bladder Emptying problem, but can also be a Bladder Storage Problem! -OVERACTIVE BLADDER (OAB) -Detrusor overactivity, “Irritable bladder” *Caused by increased PS input from bladder to brain: -Irritation from overwork (trabeculation) -Inflammation -Cancer -Neurogenic |
|
How do you treat BOO?
|
*Relief of obstructing prostate:
-Medications. -Surgery: TURP (transurethral resection of prostate). *Increased PS input may decrease if work decreases. *May need anticholinergic meds postop. |
|
|
Bladder cancer.
|
|
What are the urinary consequences of bladder cancer? How do you treat it?
|
*There is mucosal irritation from cancer.
*Increased PS input to brain--> urge and urge incontinence. *Causes a bladder storage problem = Overactive bladder (OAB). *Treatment: Surgery to resect cancer (TURBT). |
|
|
Acute bacterial cystitis
|
|
What are the urinary consequences of UTI? How do you treat it?
|
*Increased PS input to brain from bacterial inflammation.
*Bladder storage problem = OAB. *Urinalysis & urine culture. *Treatment: antibiotics. |
|
Discuss Stress urinary incontinence following surgery:
|
*Damage to external urinary sphincter from surgery (prostatectomy).
*Not a bladder emptying problem (no overflow incontinence). *Although no urgency or urge incontinence, bladder storage problem. *URINARY INCONTINENCE from incompetent sphincter. |
|
What's the treatment for Post prostatectomy incontinence?
|
-Kegels.
-Male sling (shown). -Artificial urinary sphincter if it's really bad. |
|
|
Artificial urinary sphincter.
|
|
Discuss Stress urinary incontinence (SUI) from childbirth:
|
*Damage to external urinary sphincter from childbirth.
*Bladder storage problem--> STRESS URINARY INCONTINENCE. *Treatment: -Kegel exercises. -Transurethral collagen injection. -Pubovaginal sling. |
|
|
Transurethral collagen injection to increase outlet resistance. For treating stress urinary incontinence in women.
|
|
|
Pubovaginal slings for stress urinary incontinence in women.
|
|
Take home points from this lecture:
|
1) Bladder stores:
-Must store enough urine (12-15 ounces/360-450 cc) to avoid frequency, urgency and incontinence. 2) Bladder empties: *Must do at low pressures to avoid renal damage. *Must do completely to avoid retention. 3) Involves coordination of cortex, pons, spinal cord, bladder and sphincter. *Lesion above brainstem (in cerebrum/cerebellum/basal ganglia): NEUROGENIC DETRUSOR OVERACTIVITY: Lesions above lead to ‘coordinated incontinence,’ Lesions below lead to incoordination (or DSD). *Spinal cord lesion above T6 and below brainstem: 1) NEUROGENIC DETRUSOR OVERACTIVITY & DSD (also dyssynergia of internal sphincter- above T8). 2) AUTONOMIC DYSREFLEXIA *Spinal cord lesion between T6 and S2: NEUROGENIC DETRUSOR OVERACTIVITY & DSD (synergy of internal sphincter- below T8). *Lesion below sacral spinal cord (S2) or nerve root trauma--> ACUTE URINARY RETENTION. *In bladder: -Tumor, infection/inflammation, stones, trabeculation, or other injury can lead to overactive bladder (OAB). -Obstruction can cause retention. |