Lecture 3 - Micturition Flashcards
internal urethral sphincter
not an actual structure toward the neck of the bladder/urethra
external urethral sphincter
striated skeletal muscle structure
hypogastric n.
- sympathetic
- beta fibers @ bladder which relax detrussor allowing bladder to distend
- alpha fibers @ neck of bladder or internal sphincter which increase tone, prevent urine from leaking out
pudendal n.
- somatic efferent @ external sphincter allows for voluntary control of urination
- alpha receptors @ neck of bladder or internal sphincter to increase tone
pelvic n.
- parasympathetic
- ACh receptors @ bladder which causes detrussor contraction
storage phase = ______ dominance
explain the role of each nerve
sympathetic dominance
hypogastric n.
- beta receptors relax bladder wall for distention
- alpha receptors increase tone of internal sphincter to prevent leaks
pudendal n.
- alpha receptors increase tone and conscious holding of pee
voiding phase = _________ dominance
parasympathetic
explain the 3 processes of the voiding phase: sensory, voluntary voiding and the motor voiding phase
sensory
- distention via stretch receptors –> pelvic n. –> brain
- pain –> hypogastric n. –> brain
voluntary voiding: signal of distention reaches brain and brain says its an appropriate time to pee
- pons –> reticulospinal tract –> pelvic n. and pudendal n.
- the bladder must contract and the urethra must relax at the same time!!
voiding phase: motor
- inhibit hypogastric n.: prevents detrustor m. relaxation and allow bladder contraction
- inhibit pudendal n.: prevent contraction of external sphincter and allow urethral relaxation
- stimulate pelvic n.: ACh contracts bladder
what are the 3 storage disorders?
- urethral incompetence (USMI)
- bladder dysfunction (detrusor spasticity)
- urethral malposition (ectopic ureters)
what are the clinical signs of a storage disease?
involuntary leakage: continuous or intermittent
actual urination is normal
bladder empties
no stranguria
what is USMI? what are the clinical features? what is the cause?
USMI = urethral sphincter mechanism incompetence
- usually young-middle aged spayed female, usually large breed
clinical features:
- incontinence
- months-years post spay
+/- recurrent UTIs
cause:
- decreased estrogen causing decreased alpha receptor numbers
- increased collagen/decreased muscle in internal sphincter
how is USMI treated?
by increasing uretheral sphincter tone
- phenylpropanolamine (PPA) - alpha agonist
- DES (estrogenic compound) - increases alpha receptor sensitivity
what are the clinical features of detrussor spasiticity? how is it dx? how is it treated?
- bladder doesn’t relax appropriately to allow for distention
- sudden voiding of small bladder
- +/- inflammation
- dx is often presumptive; look for inflammation
Tx:
- look for underlying cause
- enhance relaxation via anticholinergics to inhibit the pelvic n. like propantheline
what are the clinical features of ectopic ureters? how are they dx? tx?
clinical features:
females - constant dribbling
males - intermittent dribbling
dx:
- contrast rads or CT
- cystoscopy
what are the 3 voiding disorders?
detrussor contraction (detrussor atony or upper motor neuron lesion) urethral relaxation (urethrospasm) physical obstruction
in a voiding disorder, residual volume is _________
increased
in a storage disorder, residual volume is _______
normal
what are the clinical signs of a voiding disorder?
posturing to urinate stranguria, pollakiuria urine passage is decreased residual volume is increased \+/- hematuria
urethrospasm - how is it acquired? CS? Dx and tx?
relatively common post-catheterization - especially cats
CS: stranguria, pollakiuria, large and firm bladder
dx: looks similar to obstruction but catheterization is easy, rads
tx:
internal sphincter relaxation = alpha antagonist like phenoxybenzamine, prazosin, tamsulosin (in dogs only)
external sphincter = somatic muscle relaxant like benzodiazepam, diazepam, alprazolam, midazolam, ace (all cause sedation)
upper motor neuron lesion - what happens? CS? ddx? what can happen over time?
affects urethral relaxation - VOLUNTARY bladder function is lost but sphincter is still intact due to pudendal nerve therefore its difficult to express bladder
CS: paresis or paralysis, hyperreflexia, CP deficts
DDX: IVDD, trauma, neoplasia
over time, can develop ability to empty bladder to degree but cant fully empty
physical obstruction: clincal features
stranguria, pollakiuria, +/- hematuria
- large, firm, painful bladder
- +/- systemic signs
emergency! check electrolytes for hyper K!
detrussor atony - how is it acquired? clinical features? dx? tx?
acquired via post-obstruction or lower motor neuron disease
CS = general
- large, soft bladder
- easy to express
- stranguria with a weak stream
- increased residual volume after urination
CS = LMN disease
- sacral lesion takes out pudendal and pelvic n. = no anal tone
- distended / flaccid bladder, easily expressed
- decreased anal tone, decreased perineal reflex
dx:
neurogenic = complete neuro exam, imaging: rads, CT/MRI
non-neurogenic = neuro exam, rectal exam, imaging: cysto
tx:
neurogenic = fix underlying problem
non neurogenic - relieve obstruction
- restablish tight junction by keeping bladder small
- leave in-dwelling catheter and stimulate detrusor contraction with ACh agonist (Bethanechol) AFTER obstruction is addressed
detrussor muscle
meshwork of fibers in different planes of the bladder that allow it to expand and contract