MICTURITION
The bladder is composed of bands of interlaced smooth muscle( detrusor). The innervation of
the body of the bladder is different from that of the bladder neck. The body is rich in beta adrenergic
receptors. These receptors are stimulated by the sympathetic component of the autonomic nervous
system (ANS). Beta stimulation, via fibers of the hypogastric nerve, suppress contraction of the
detrusor. Conversely, parasympathetic stimulation, by fibers in the pelvic nerve, cause the detrusor
to contract. Sympathetic stimulation is predominant during bladder filling, and
the parasympathetic causes emptying.
IN SHORT, The sympathetic nervous system predominates during the storage phase. Alpha adrenergic
receptors in the base and neck of the bladder increase muscle tone. Simultaneously beta-adrenergic receptors
in the body of the bladder depress detrusor tone.
Two sphincters control the bladder outlet. The internal sphincter is composed of smooth
muscle like the detrusor and extends into the bladder neck. Like the detrusor, the internal sphincter is
controlled by the ANS and is normally closed. The primary receptors in the bladder neck are alphaadrenergic. Sympathetic stimulation of these alpha receptors, via fibers in the hypogastric nerve,
contributes to urinary continence.
Effect of sympathetic stimulation: relaxation of detrusor muscle; contraction of trigone and
internal sphincter resulting in retention of urine.
The external sphincter is histologically different from the detrusor and internal sphincter. It is
striated muscle. Like skeletal muscle, it's under voluntary control. It receives its innervation from
the pudendal nerve, arising from the ventral horns of the sacral cord. During micturition, supraspinal
centers block stimulation by the hypogastric and pudendal nerves. This relaxes the internal and
external sphincters and removes the sympathetic inhibition of the parasympathetic receptors. The
result is unobstructed passage of urine when the detrusor contracts.
The ureters pass between the layers of the detrusor and enter the bladder through the trigone.
The ureters propel urine into the bladder. The bladder passively expands to accept urine. As the
bladder expands and intravesicular pressure increases, the ureters are compressed between the
layers of muscle, creating a valve mechanism. This valve mechanism limits the backflow of urine.
The normal adult bladder can hold about 500 cc of urine. After emptying, the bladder may still
retain about 50 cc residual volume. At about 150 cc of volume, stretch receptors in the detrusor begin
signaling the CNS via afferent nerves; at 400 cc we are "seeking" an appropriate toilet. Healthy
subjects usually experience the first need to void at a bladder volume of 150 ml and the urge to void
at 300 ml.
Summary: Normally, we are able to control where and when we void. This is largely because the
cerebrum is able to suppress the sacral micturition reflex. If the sacral reflex is unrestrained,
parasympathetic stimulation via the pelvic nerve causes detrusor contraction. Detrusor contraction is
suppressed by alpha and beta sympathetic stimulation via the hypogastric nerve. In response
to afferent stimulation, the cerebrum becomes aware of the need to void. If it is appropriate, the
cerebrum relaxes the external sphincter, blocks sympathetic inhibition, the bladder contracts and urine
is expelled.
CONSCIOUS CONTROL
The ability to control urination is dependent upon intact communication between the cerebrum,
pons, sacral cord and peripheral nerves. We become aware of the need to void when the urine
volume is about 150cc. Ascending afferent fibers relay sensation to the pons and then to the
cerebrum. The cerebrum determines if the surroundings and social conditions are appropriate to void.
If it is appropriate to void, the cerebrum switches the pons to emptying mode, which inhibits
sympathetic output and pudendal nerve stimulation of the external sphincter.
When the sympathetic system is no longer stimulated the parasympathetic system is activated to
have maximum effect. Detrusor contraction ensues.
AUTONOMIC INNERVATION
Sympathetic: hypogastric nerve L1, L2.
Effect of stimulation:
1. Relaxation of detrusor muscle; contraction of
2. trigone and internal sphincter resulting in retention
3. of urine.
Parasympathetic: nervi erigentes aka pelvic splanchnic nerves, aka pelvic nerves
synapse
Effect of stimulation:
1. Contraction of detrusor muscle;
2. relaxation of trigone and internal
3. sphincter resulting in emptying of
4. bladder. at inferior hypogastric ganglion
SOMATIC INNERVATION
Anterior horn cells S2,S3,S4. Pudendal nerve(pubic nerve).
Parts innervated
Prostatic urethra and external sphincter.
Effect of stimulation
Parts innervated are under higher control .
NEUROGENIC BLADDER
Neurogenic bladder is a urinary problem in which the bladder does not empty properly.
Depending on the type of neurological disorder causing the problem, the bladder may empty
spontaneously (incontinence) or may not empty at all (retention with overflow leakage).
DIFFERENT CLASSIFICATIONS OF NEUROGENIC BLADDER DYSFUNCTION
I. ABOVE OR BELOW PONTINE MICTURITION CENTER / SACRAL CORD LESIONS WITH OR WITHOUT
DAMAGE TO DETRUSOR NUCLEUS / LOWER MOTOR NEURON BLADDER
1. lesions above the pontine micturition center (e.g., stroke or brain tumor) producing an
uninhibited bladder,
2.
lesions between the pontine micturition center and sacral spinal cord (e.g., traumatic spinal
cord injury or multiple sclerosis involving cervicothoracic spinal cord) producing an upper
motor neuron bladder,
3. sacral cord lesions that damage the detrusor nucleus but spare the pudendal nucleus
producing a mixed type A bladder,
4. sacral cord lesions that spare the detrusor nucleus but damage the pudendal nucleus
producing a mixed type B bladder,
5. lower motor neuron bladder from sacral cord or sacral nerve root injuries.
UNINHIBITED NEUROGENIC BLADDER DYSFUNCTION
 reduced awareness of bladder fullness and a low capacity bladder due to reduction of inhibition of the pontine
micturition center (PMC) by cortical and subcortical structure damage.
 Urinary incontinence may occur with brain lesions occurring above the pontine micturition center, especially with
bilateral lesions. Since the PMC is intact, the normal opposition of detrusor and internal/external sphincter tonus is
maintained so there are no high bladder pressures developed that can lead to upper urinary tract damage.
UPPER MOTOR NEURON NEUROGENIC BLADDER
 characterized by detrusor-sphincter dyssynergia (DSD) - simultaneous detrusor and urinary sphincter contraction
producing high pressures in the bladder leading to vesicoureteral reflux that can produce renal damage.
 bladder and sphincters spastic, especially if lesions are above T10 level (above the sympathetic autonomic nervous
system innervation of the bladder).
 bladder capacity is usually reduced due to the high detrusor tonus
 If detrusor pressure exceeds internal/external urinary sphincter pressure in the proximal urethra, then incontinence may
occur.
MIXED TYPE A NEUROGENIC BLADDER
 (the more common of the mixed type bladders)
 detrusor nucleus damage renders the detrusor flaccid (also referred to as detrusor areflexia
 intact pudendal nucleus is spastic producing a hypertonic external urinary sphincter.
 bladder is large and has low pressure, so the spastic external sphincter produces urinary retention.
 detrusor pressure is low so upper urinary tract damage from vesicoureteral reflux does not occur, and incontinence is
uncommon.
MIXED TYPE B NEUROGENIC BLADDER
 characterized by a flaccid external urinary sphincter due to the pudendal nucleus lesion
 bladder is spastic due to the disinhibited detrusor nucleus.
 bladder capacity is low but vesicular pressures are usually not elevated since there is little outflow resistance. This
leads to problems with incontinence, however.
LOWER MOTOR NEURON NEUROGENIC BLADDER
 the sacral micturition centers or related peripheral nerves are damaged though the thoracic sympathetic nervous
system outflow to the lower urinary tract is intact.
 bladder capacity is large since detrusor tone is low (detrusor areflexia) and internal urinary sphincter innervation is
intact. Despite the low detrusor pressure, overflow urinary incontinence and urinary tract infections are not uncommon.
II. SPASTIC / FLACCID / UNINHIBITED
III. FLACCID OR SPASTIC BLADDER (based on above or below T12)
Spinal cord injury T12 or above- reflex, automatic or spastic bladder
- automatic, involuntary control of the bladder so when the bladder fills above a certain level it
contracts and urine flows out automatically
Spinal cord injury below T12- atonic, flaccid bladder
- bladder has no muscle tone and doesn't contract to empty automatically. Instead, it continues to fill
and small amounts of urine may eventually dribble out.
MICTURITION
-
storage of urine to micturition depends on intensity of afferent input (stretching of
bladder wall, increased intravesical pressure)
DURING URINE STORAGE (no micturition occurs)
low level of afferent activity causes
-
efferent input via somatic pudendal nerve (S2-4) to urethral sphincter – contraction
efferent input via hypogastric nerve (sympathetics T11-L1) to bladder neck – contraction
inhibition of detrusor muscle via hypogastric nerve --- relaxation
MICTURITION: (events)
-
high level of afferent activity causes signals via pelvic nerve up to brainstem and
cortex, initiating the voiding mechanism
pontine micturition center causes
inhibition of pudendal nerve – relaxation of urethral sphincter
inhibition of hypogastric nerve --- relaxation of bladder neck
efferent input to pelvic nerve (parasympathetics) – detrusor contraction
summary:
MICTURITION REFLEX
1. Stretch of bladder wall
2. Increase afferent activity in sensory neurons
3. Increase parasympathetic activity
4. Increase detrusor muscle contraction
5. Inhibition of pudendal nerve
6. Results in skeletal muscle relaxing
7. Urine voided
Detrusor External Sphincter Dyssynergia
- contraction of bladder and external sphincter at the same time
- caused by injury between brainstem and sacral cord
Autonomic Dysreflexia, sweating and vasoconstriction below lesion
- syndrome of exaggerated sympathetic activity in response to a noxious stimuli
(distended bladder in a para or quadriplegic) below the lesion usually above T6, 7
- hypertension, reflex bradycardia
- treatment: remove noxious stimulus (insert a catheter), parenteral ganglionic or alphablockers or chlorpromazine
INCONTINENCE the involuntary passage of urine sufficiently severe to cause social or hygiene problems
most frequent in the elderly
Classification
1. Total: constant or periodic loss of urine without warning
exstrophy of bladder
epispadias
vesico-vaginal fistulas
ectopic ureteral orificas
2. Stress: urine loss with sudden increase in intra-abdominal pressure (e,g, coughing
or sneezing)
weakness of pelvic floor musculature (child bearing, (previous
abdominal pelvic surgery)
damage weakness of urethra or sphincter
3. Urge: urine loss due to uninhibited bladder contractions
local bladder irritation (eg cystitis, stone, tumor)
CNS disorder
4. Overflow: urine loss when intravesical pressure exceeds urethral pressure
obstructive (eg Benign Prostatic Hypertrophy)
hypotonic bladder
detrusor –sphincter dyssynergia
5. Functional: urine loss caused by inability to reach toilet in time
physical immobility
MICTURITION REFLEX
1. as the bladder fills with urine, increased pressure stimulates the stretch receptors
which stimulates the parasympathetic nerves
2. high level of afferent activity causes signals via pelvic nerve up to brainstem and
cortex...
3. pontine micturition center causes inhibition of pudendal nerve – relaxation of urethral
sphincter
4. inhibition of hypogastric nerve (sympathetic) --- relaxation of bladder neck
5. efferent input to pelvic nerve (parasympathetics) – detrusor contraction
6. When the detrusor muscle contracts, it pulls open the internal urethral sphincter (the
muscle at the base of the bladder).
(The internal urethral sphincter is closed when the detrusor muscle is relaxed. )
. ...message is sent to the brain that the bladder is becoming full, resulting in the urge to
void.
This initiates the voiding mechanism.
7. contraction of the detrusor muscle produces a change in the shape in this muscle,
which opens this sphincter... Urine is released through the urethra
summary:
MICTURITION REFLEX
1. Stretch of bladder wall
2. Increase afferent activity in sensory neurons
3. Increase parasympathetic activity
4. Increase detrusor muscle contraction
5. Inhibition of pudendal nerve
6. Results in skeletal muscle relaxing
7. Urine voided
INCONTINENCE
the involuntary passage of urine sufficiently severe to cause social or hygiene problems
most frequent in the elderly
Classification : TOTAL, STRESS, URGE, OVERFLOW, FUNCTIONAL
TOTAL: constant or periodic loss of urine without warning
exstrophy of bladder
epispadias
vesico-vaginal fistulas
ectopic ureteral orificas
STRESS: urine loss with sudden increase in intra-abdominal pressure (e,g, coughing or
sneezing) weakness of pelvic floor musculature (child bearing, (previous abdominal
pelvic surgery) damage weakness of urethra or sphincter
URGE: urine loss due to uninhibited bladder contractions local bladder irritation (eg
cystitis, stone, tumor) CNS disorder
OVERFLOW: urine loss when intravesical pressure exceeds urethral pressure
obstructive (eg Benign Prostatic Hypertrophy) hypotonic bladder
detrusor –sphincter dyssynergia
FUNCTIONAL: urine loss caused by inability to reach toilet in time
physical immobility
PELVIC FLOOR
Kegel exercise, consists of repeatedly contracting and relaxing the muscles that form
part of the pelvic floor
done to reduce urinary incontinence, reduce premature ejaculation as well as to increase
the size and intensity of erections.
RENAL FAILURE
EFFECTS OF COMPLETE RENAL FAILURE ON THE BODY:
1. Effects of complete renal failure on the body:
2. Generalized edema resulting from water and salt retention
3. Hypertension resulting from water and salt retention
4. Uremia due to increase in urea and other nonprotein nitrogens (azotemia)
5. Acidosis resulting from failure to excrete normal acidic products
6. Anemia caused by decreased erythropoietin
7. Osteomalacia caused by decreased production of active vitamin D and by phosphate
retention
Treatment of Renal Failure by Dialysis with an Artificial Kidney
Severe loss of kidney function - renal failure
 a threat to life and requires removal of toxic waste products and restoration of body
fluid volume and composition toward normal.
 accomplished by dialysis with an artificial kidney.
BASIC PRINCIPLES OF DIALYSIS
 Blood flows continually between two thin membranes of cellophane
 Outside the membrane is a dialyzing fluid
 membranes of cellophane - porous to allow constituents of plasma, except the
plasma proteins, to diffuse in both directions—from plasma into the dialyzing fluid
or from the dialyzing fluid back into the plasma.
 If a substance is greater in the plasma than in the dialyzing fluid, there will be
transfer of the substance from the plasma to the dialyzing fluid.