Micturition disorders

Question 1

Outline the parasypathetic involvement with micturition

Answer 1

Controls Bladder body (detrusor)
Pelvic nerve (S1–S3)
Causes Contraction and bladder emptying When blocked - Detrusor relaxation and bladder filling When inappropriately stimulated - Overactive bladder
When inappropriately blocked - Bladder atony, urine retention

Question 2

outline the b3 adrenergic sympathetic involvement with micturition

Answer 2

Controls Bladder body (detrusor)
Hypogastric nerve (L1–L4)
Causes Detrusor relaxation and filling when stimulated
When blocked - Detrusor contraction and bladder emptying
When inappropriately stimulated - Urine retention
When inappropriately blocked - Decreased bladder compliance and increased filling pressure

Question 3

Outline the Sympathetic (alpha1-adrenergic) involvement with micturition

Answer 3

Controls Bladder neck/urethra
Hypogastric nerve (L1-l4)
Causes Contraction and continence when stimulated
Causes Urination when blocked
When inappropriately stimulated - Urine retention
When inappropriately blocked - Open urethra, incontinence

Question 4

Outline the somatic involvement with micturition (nicotinitic)

Answer 4

Controls distal urethra/ pelvic floor
Pudendal nerve (S1–S2)
Causes Conscious/reflex contraction and continence
When blocked - urination
When inappropriately stimulated - Urine retention
When inappropriately blocked - Open urethra, incontinence

Question 5

What occurs during filling and storage?

Answer 5

stretch receptors in the bladder wall send afferent signals along the pelvic nerve, which activate a reflex arc through the hypogastric nerve to the urethra
Norepinephrine is released by postganglionic neurons to activate beta3-adrenergic receptors in the bladder wall, allowing relaxation and continued filling. Norepinephrine also stimulates alpha1-adrenergic receptors in the urethra and causes contraction of the urethral smooth muscle, thus preventing urine leakage.

Question 6

/What happens during the initiation of micturition

Answer 6

stretch receptors send afferent signals along myelinated fibers of the pelvic nerve to the lumbar spinal cord and cranial to the pontine micturition center in the brain. Signals from the cerebral cortex and the hypothalamus are processed to determine whether the situation is appropriate for urination. If so, signals are sent down the pelvic nerve, which leads to acetylcholine release at the postganglionic parasympathetic neurons. Acetylcholine binds to M3 receptors and stimulates bladder smooth muscle contraction. At the same time, inhibitory signals are sent to the sympathetic reflexes and the urethra relaxes, allowing normal emptying.

Question 7

What are disorders of storage?

Answer 7

occur because of an inability to maintain adequate urethral tone if there are normal or increased bladder pressures.
may result from an anatomic or developmental abnormality or acquired dysfunction in the spinal cord, urinary bladder, or urethra and surrounding tissues. Disorders of storage generally result in the unconscious loss of urine: urinary incontinence. These disorders include USMI, lower motor neuron bladder (LMB), and overactive bladder (OAB).

Question 8

Outline USMI

Answer 8

common storage disorder in dogs.
The urethral sphincter mechanism involves the smooth muscle of the urethra, surrounding support tissues, submucosal vasculature, and urothelium.
thought to result from the breakdown in this complex through reduced muscular responsiveness and tone, and structural changes in the periurethral tissues.
In female dogs seem to be associated with a reduction in estrogen and alterations in follicle-stimulating hormone and luteinizing hormone after neutering;

Question 9

Who is most at risk of USMI?

Answer 9

Approx 30% female neutered dogs >30kg
Doberman pinscher, giant schnauzer, Old English sheepdog, rottweiler, Weimaraner, and boxer
Those with pelvic bladder, short urethra, or recessed vulva

Question 10

What are the signs of USMI?

Answer 10

Unconcious dribbles of u+ sleeping/ after exertion etc
Urination is observed to be normal and complete, with little or no residual volume. The assessment of residual urine is essential in male dogs to differentiate USMI from detrusor urethral dyssynergia, which is a disorder of incomplete bladder emptying (discussed later).

Question 11

What is the theory behind USMI treatment?

Answer 11

Medical treatment of USMI in neutered female dogs consists of increasing the number and sensitivity to estrogen of alpha receptors in the urethral sphincter, or stimulating those receptors with an alpha-agonist

Question 12

Outline phenylpropanolamine

Answer 12

For USMI
Alpha agonist
cause cause Hypertension, aggression, restlessness, gastrointestinal upset, anxiety
Caution in animals with Hypertension, hyperadrenocorticism, renal disease
Does needed is varied between animals and may need trial and error

Question 13

Outline oestriol

Answer 13

For USMI
An oestrogen
Can cause Myelosuppression (rare at these doses), attractiveness to males, mammary/vulvar swelling, behavior changes
Caution in males as can cause prostate metaplasia

Question 14

Outline surgical treatment of USMI

Answer 14

Only when medical treatment has failed
Most aim to increase abdominal pressure to the urethra
colposuspension, transobturator vaginal tape, and urethropexy. These procedures have had variable outcomes and are considered to have poor long-term efficacy, particularly in animals with normal bladder position.
The most promising surgical procedure for USMI is placement of an artificial urethral sphincter that may be adjusted via a subcutaneous port.

Question 15

Whaat would you see with lesions to S1-S2

Answer 15

weakness of the striated muscular sphincter (weakened urethral tone)
easily expressible bladder that may empty with minor increases in abdominal pressure. These animals are identified by decreased anal tone and a poor perineal reflex as well as their easily expressible bladder. Most of these animals are unable to voluntarily void and require intermittent catheterization or manual expression by the owner
At high risk of uti
The muscarinic agonist bethanechol has been used in these patients to increase detrusor contraction; however, the evidence for its efficacy remains controversial

Question 16

What is detrusor hyperreflexia/ an overactive bladder?

Answer 16

characterized by sudden urgency to urinate and involuntary loss of urine associated with bursts of detrusor contractions at bladder volumes far less than capacity.
manifest as an animal that loses bladder compliance and capacity and thus may need to urinate more often than before without an increase in urine production or inflammation of the lower urinary tract.
OAB may be a cause of treatment failure in some dogs treated for USMI, and should be considered in these cases. Diagnosis of OAB in animals can be challenging and is only definitively made using urodynamic studies

Question 17

How can you treat an overactive bladder (trial treatment is normally how you diagnose)

Answer 17

oxybutynin and imipramine, the latter of which also has alpha-agonist effects, potentially increasing urethral sphincter tone. Adverse effects of these medications include gastrointestinal abnormalities such as diarrhea and constipation, as well as parasympatholytic signs like tachycardia and hyposalivation.

Question 18

Outline disorders of emptying

Answer 18

either a functional or mechanical obstruction of the outflow tract and urethra, or an abnormality of the detrusor muscle that impairs its complete contraction. Overflow incontinence can result from the lack of complete emptying, often when the animal is at rest

Question 19

How can you manage damage to the detrusor muscle?

Answer 19

Keep the bladder small for 2 weeks to allow healing
Can trial bethanacol
Some animals will repsond to cisapride and metoclopramide

Question 20

What causes funtional urethral obstruction/ detrusor urethral dyssyndergy?

Answer 20

arises from an abnormality in the reflex arc that allows the urethral sphincter to relax at the initiation of detrusor contraction and urination.
Typically have a normal neuro exam

Question 21

What happens in DUD?

Answer 21

primarily middle-aged large and giant-breed male dogs, although female dogs and cats can be affected.
Clinical signs are similar to those of mechanical obstruction. The animal often postures to urinate and is able to produce a urine stream that quickly becomes attenuated or stops completely. The animal may continue to posture to urinate or make several attempts without fully emptying the bladder
The presence of large amounts of residual urine typically leads to overflow incontinence and may be mistaken for USMI.
leakage can occur because the hypertonicity of the involved sphincter is often dynamic and is triggered by the act of voiding. In chronic cases, bladder overdistension and subsequent atony may develop. Unlike animals with mechanical obstruction, these dogs are typically easy to catheterize

Question 22

How do you presumptively diagnose DUD?

Answer 22

made by observing the dog urinate with a typical interrupted pattern, documentation of a large residual urine volume, easy passage of a urinary catheter, and ruling out of a mechanical obstruction

Question 23

How can you treat DUD?

Answer 23

Start with prazosin - Alpha1-antagonism, smooth muscle relaxant
If not enough, Diazepam 30 mins beofre u+ or ACP can be useful

Question 24

How do you tx an UMN bladder?

Answer 24

Treat underlying spinal cord disease
Until normal voiding resumes, the patients are managed as for DUD with alpha-adrenergic blockade and manual expression or catheterization.

Question 25

What is dyautonomia?

Answer 25

degeneration of the neurons of the autonomic nervous ganglia, leading to sympathetic and parasympathetic dysfunction
Thought to be associated with a neurotoxin
classic findings of unresponsive mydriasis and prolapsed nictitans, the abnormalities seen with dysautonomia can range from ileus and constipation to decreased systolic function of the heart. These dogs and cats often have significant voiding dysfunction and urine retention caused by bladder atony and overflow incontinence secondary to urethral sphincter incompetence. There is no specific treatment of dysautonomia and spontaneous remission is uncommon.