Steers OAB
cause
nerves
urothelium
smooth muscles
increased excitability and connectivity
growth factors
enhanced spontaneous contractile activity
obstructed bladder
supersensitivity to muscarine agonists
increased coupling
morphological changes
patchy denervation
innervated areas have increased connective tissue
complete denervation
increased contractions due to KCl
reduced electrical evoked contractions
altered response to stimuli
obstructed bladder
supersensitivity to muscarine agonists
increased contractions due to KCl
reduced electrically evoked contractions
idiopathic unstability
increased electrically evoked contractions
normal sensitivity to muscarine agents
denervated bladders have increased M3 expression
relationship with other conditions
ischemia
initiates apoptsis of smooth muscle cells
damages intrinsic nerves
can occur in conjugation with obstructed bladder as obstructed bladder->hypertrophy(afferent as well as efferent neurons)
downstream mechanism
hypertrophy
ischemia
reorganization of spinobulbal pathway to spinal pathway. lesser delay in central transmission of micturition reflex(this happens in spinal injury not sure if it happens in obstructed bladder as well
C-fibre activation
urgency causes
increased coupling
lowering of threshold for firing of afferent
molecular trigger could be NGF and other chemicals
hypertrophy of smooth muscle cells