Bladder Over Active Bladder(OAB)- pathophysiolog

1. Dept of Urology
Govt Royapettah Hospital and Kilpauk Medical College
Chennai
1

2. Professors:
 Prof. Dr. G. Sivasankar, M.S., M.Ch.,
 Prof. Dr. A. Senthilvel, M.S., M.Ch.,
Asst Professors:
 Dr. J. Sivabalan, M.S., M.Ch.,
 Dr. R. Bhargavi, M.S., M.Ch.,
 Dr. S. Raju, M.S., M.Ch.,
 Dr. K. Muthurathinam, M.S., M.Ch.,
 Dr. D. Tamilselvan, M.S., M.Ch.,
 Dr. K. Senthilkumar, M.S., M.Ch.
Dept of Urology, GRH and KMC,
Chennai. 2

3.  Overactive bladder (OAB) - syndrome,
defined by the International Continence
Society (ICS),
- Urgency, with or without urgency urinary
incontinence,
- Usually with frequency and nocturia,
- In the absence of causative infection or
pathologic conditions
3
Dept of Urology, GRH and KMC,
Chennai.

4.  - Overall prevalence rate about 11.8%
- Increases with age
- Similar in men and women
- MEN – higher prevalence of OAB wet
- WOMEN –higher prevalence of OAB dry
4
Dept of Urology, GRH and KMC,
Chennai.

5. ETIOLOGY:
Neurological causes:
Neurologic injuries
Spinal cord injury
Stroke
Neurologic diseases
Multiple sclerosis
Dementia
Parkinson disease
Medullary lesions
Diabetic neuropathy
5
Dept of Urology, GRH and KMC,
Chennai.

6.  MEDICATIONS
Diuretics - cause symptoms of urge
incontinence because of increased bladder
filling, stimulating the detrusor
Bethanechol - cause urge incontinence
through its stimulation of bladder smooth-
muscle contraction.
 Idiopathic
6
Dept of Urology, GRH and KMC,
Chennai.

7. Cardiologic
❖ Heart failure or peripheral venous and
vascular disease - contribute to OAB
❖ During the day, individuals have excess
fluid collect in dependent positions
❖ When they go to sleep, much of this fluid
becomes mobilized and increases renal
output, thereby increasing urine output ->
increased nocturia that manifests as OAB.
7
Dept of Urology, GRH and KMC,
Chennai.

8.  Non Neurogenic ;
-urinary tract infection
- bladder cancer
- bladder stones
- bladder inflammation
- bladder outlet obstruction can mimic
OAB
8
Dept of Urology, GRH and KMC,
Chennai.

9.  Three main theories - prosposed regarding
cause of OAB
NEUROGENIC
MYOGENIC
AUTONOMOUS BLADDER
9
Dept of Urology, GRH and KMC,
Chennai.

10.  States that DO arises from generalized,
nerve-mediated excitation of the detrusor
muscle
Several interdependent mechanisms.
 Damage to the brain can induce DO by
reducing suprapontine inhibition.
 Damage to axonal pathways in the spinal
cord allows the expression of primitive
spinal bladder reflexes
10
Dept of Urology, GRH and KMC,
Chennai.

11.  Synaptic plasticity leads to reorganization of
sacral activity, triggered by C-fiber bladder
afferent neurons
 Finally, sensitization of peripheral afferent
terminals in the bladder can trigger DO
11
Dept of Urology, GRH and KMC,
Chennai.

12.  Alterations in properties of detrusor myocytes
necessary prerequites for production of
involuntary detrusor contraction
 Increases in intravesical pressure during
voiding results in damage to intrinsic neurons
in bladder wall & secondary changes in
smooth muscle properties
 Local contractions in any part of detrusor
spread throughout bladder wall results in
coordinated myogenic contraction of entire
bladder
12
Dept of Urology, GRH and KMC,
Chennai.

13.  Suggests that detrusor muscle is arranged
into modules active during filling phase of
micturition cycle
 Controlled by a peripheral myovesical plexus
units of intramural ganglia & interstial cells
 Synchronization of activity between modules
which could propagate through intramural
nerve or by direct communication between
muscle cells
13
Dept of Urology, GRH and KMC,
Chennai.

14.  Detrusor overactivity results from
exaggerated sympotamatic expression of
peripheral automous activity , results from
shift in balance of excitation & inhibition
smooth muscles modules
14
Dept of Urology, GRH and KMC,
Chennai.

15.  The afferent nerve endings are widely
distributed in the bladder wall , particularly
dense in the connective tissue underneath
the urothelium.
 Urothelial cells possess sensory and
signaling properties that allow them to
respond to their chemical and physical
environments
15
Dept of Urology, GRH and KMC,
Chennai.

16.  Suburothelial interstitial cells lie in close
physical proximity to nerve fibers, suggesting
a role in sensory transduction or regulation.
 OAB - arises if the level of sensory activity
is inappropriately high for any given degree
of bladder distention, resulting from
pathologically sensitized or abnormally
numerous afferent nerve
16
Dept of Urology, GRH and KMC,
Chennai.

17.  Impulses fire by an afferent ending at any
level of distention can be varied
physiologically
(afferent sensitivity )
 Release of substances from the urothelium
& direct interaction between afferent nerve
endings contribute pathophysiology of
bladder
17
Dept of Urology, GRH and KMC,
Chennai.

18.  Important role in pathophysiology in OAB
 Not only passive barrier also responsive
structure capable of detect thermal,
mechanical & chemical stimuli
 Factors release from urothelium alter the
excitability of afferent neurons & affect
detrusor muscle contractions
 Chronic urothelial injury leads to increase in
urinary frequency & decrease in voided
volume
18
Dept of Urology, GRH and KMC,
Chennai.

19.  Located in detrusor layer orginates from
smooth muscle act as pacemaker of
spontaneous activity in detrusor
 Sub urothelial ICs form a network of gap
junctions - role in amplify sensory
response to bladder wall stretch through
physical interactions
 Responds to cholinergic stimulation - Ca 2+
transients
19
Dept of Urology, GRH and KMC,
Chennai.

20.  Imatinib mesylate ( c-kit antagonist)
ability to affect spontaneous electrical
activity
inhibits the spontaneous activity of evoked
smooth muscle contractions in OAB
 Enhanced activity of ICS cause detrusor
activity
20
Dept of Urology, GRH and KMC,
Chennai.

21.  Damage to intrinsic neurons results in altered
properties of smooth muscle cells
 Decreased suppression of suprapontine
inhibition
 Abnormal peripheral neurotransmission
 Increased afferent activity
 Changes in urothelial signaling
 Enhanced activity of interstial cells
21
Dept of Urology, GRH and KMC,
Chennai.

22. 22
Dept of Urology, GRH and KMC,
Chennai.