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RGU Exam 3 > Voiding Dysfunction > Flashcards

Voiding Dysfunction Flashcards

1
Q

Avg. Capacity of Adult Bladder

A
  • Male: 400-500cc
  • Female: 350-450cc
  • Bladder lies behind the symphysis unless overdistended
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2
Q

Bladder microstructure layers

A
  • Urothelium
  • Lamina propria
  • Muscularis propria
  • Serosa
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3
Q

Urothelium

A
  • 4-7 layers thick, attenuated to 2-3 when fully distended
  • 3 distinct layers

*basal- small cuboidal progenitor cell from which other layers arise

*intermediate- polygonal structure w/ ability to stretch and flatten

*superficial “umbrella” cell- release multiple chemical mediators which contribute to micturition signaling pathway

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4
Q

Lamina propria

A
  • Connective tissue bed supporting overlying urothelium

*seperated by basement membrane

  • Rich in capillaries, lymphatics and nerve endings
  • Contains elastin fibers, and thin poorly differentiated layer of smooth muscle fibers, muscularis mucosae

*distinct from muscularis propria

*variable position within urothelium

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5
Q

Interstitial cells of cajal

A
  • Signaling cells within lamina propria include interstitial cells of cajal (ICC)
  • ICC cells form a functional communication network thru gap junctions which facilitate communication b/w the bladder and afferent nerve pathways
  • ICC cells may also play a role in detrusor function
  • Neurologic injury is assoc. w/ changes in the urothelium which ultimately contributes to neurogenic voiding dysfunction
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6
Q

Muscularis propria

A
  • 3 layers

*inner and outer longitudinal

*intermediate circular

  • Randomly oriented smooth muscle which provides ability to maintain continuous tension at diff. muscle lengths

*an extracellular matrix (ECM) surrounds the muscle and acts as scaffold

*ECM is constantly remodeled containing collagen (type 1 and 3), elastic fibers, adhesive proteins, glycans and glycoproteins

*strain from neurologic injury may result in stiffening of the matrix, increasing type 3 collagen and leading to reduced detrusor capacity which ultimately contributes to neurogenic voiding dysfunction

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7
Q

Bladder storage physiology

A
  • Requires stimulation of the sympathetic nervous system via adrenergic receptors
  • Primary subtype alpha1 is responsible for contraction to the bladder outlet to prevent incontinence
  • Smooth muscle relaxation of detrusor mediated by beta3 receptors
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8
Q

Bladder emptying physiology

A
  • Facilitated by parasympathetic stimulation of muscarinic receptors
  • M3 is primarily responsible for detrusor contraction
  • Medications bind to M2 and M3 recetpros to reduce detrusor contractility
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9
Q

Alpha -1a adrenergic receptors locations

A
  • Smooth muscle of prostate
  • Bladder neck
  • Ureter
  • Seminal vesicles
  • Vas deferens
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10
Q

Alpha-1b adrenergic receptors locations

A
  • Blood vessels
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11
Q

Alpha-1d adrenergic receptors locations

A
  • Nasal passages
  • Bladder
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12
Q

Alpha blockers 1st generation

A
  • Terazosin, doxazosin, alfuzosin
  • Non-selective alpha blockers
  • Equal long term efficacy to 2nd gen agents
  • Traditionally used by primary care physicians in dual therapy to treat concominant hypertension
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13
Q

Alpha blockers 2nd generation

A
  • Tamsulosin, silodosin
  • High affinity for alpha-1A receptors
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14
Q

Alpha blockers side effects

A
  • Dizziness
  • Fatigued
  • Nasal congestion
  • Orthostatic hypotension
  • Syncope
  • Retrograde ejaculation
  • Intraoperative floppy eye syndrome
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15
Q

Antimuscarinic drugs

A
  • Oxybutinin
  • Tolteridone
  • Trospium
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16
Q

Antimuscarinic drugs pharmacology

A
  • Used antagonize miuscarinic receptors in the bladder
  • Used for over active bladder (OAB)
  • Off label use for bladder spasm
17
Q

Antimuscarinics side effects

A
  • Urinary retention
  • Dry mouth
  • Constipation
  • Altered mental status
18
Q

Beta3- adrenoreceptor agonists

A
  • Mirabegron
19
Q

Beta3-adrenoreceptor agonist pharmacology

A
  • Stimulates beta3-adrenoreceptors in detrusor muscle to facilitate storage
  • Used for OAB and lower urinary tract symptoms (LUTS) related to BPH
20
Q

Beta3- adrenoreceptor agonist side effects

A
  • Elevated BP
  • Retention

*UTI

  • Tachycardia
  • Dry mouth
21
Q

Normal bladder voiding mechanism relies on

A
  • External sphincter relaxation
  • Detrusor muscle contraction
22
Q

Key CNS structure in micturition

A
  • Periqueductal grey (PAG)

*midbrain area known for its role in nociception and emotional responses

  • Pontine micturition center (PMC)

*aka Barringtons nucleus: located in dorsomedial pontine tegmentum

  • Onufrowicz’s nucleus

*small motor neuron group in ventral horn of sacral spinal cord (S2-4)

23
Q

Basic voiding mechanics

A
  • Distention of the bladder sends signals to periaqueductal grey and pontine micturition center (PMC)
  • PMC communicates w/ periaqueductal grey
  • PMC inhibits spinal guarding (sympathetic and somatic outflow to urethra)
  • Synergic micturition via long descending pontinespinal pathway
  • Acetylcholine binds to M2 and M3 receptors in detrusor
  • Sympathetic/somatic inhibit voding

*voluntary relaxation of sphincter inhibits this system

24
Q

Supraspinal vesicovesical reflex

A
  • Brain is responsible for inhibtion of voiding at all times
  • Bladder fills up sends a signal to the spine up to the pontine micturition center (PMC), cross talk b/w the PMC and the periaqueductal grey results in a signal that comes down thru the spine thru Onuf’s nucleus to the bladder and you get voiding
  • Parasympathetic goes up and sympathetic goes down and you can pee
25
Q

Neurogenic bladder presentation

A
  • Incontinence
  • Urinary retention
  • Urinary tract infection
  • Urolithiasis
  • Hydronephrosis
  • Renal failure
26
Q

Neurologic lesion in suprapontine region

A
  • Detrusor overactivity
27
Q

Neurologic lesion in infrapontine - suprasacral region

A
  • Detrusor overactivity
  • Detrusor sphincter dyssynergia (DSD)
28
Q

Neurologic lesion in infrasacral region

A
  • Acontractility
29
Q

Detrusor overactivity

A
  • Occurs in lesions above the sacral spinal cord
  • Implies the detrusor is not receiving appropriate cerebral inhibtion
  • Involuntary detrusor contractions
  • May be spontaneous or provoked
  • Diagnosed on urodynamics
30
Q

Detrusor overactivity treatment

A
  • Antimuscarincis/Mirabegron
  • Botox
31
Q

Detrusor sphincter dyssynergia

A
  • Secondary to lesions below the PMC but above sacral spine
  • Normal voiding requires synchronous detrusor contraction and external sphincter relaxation
  • External urethral sphincter contracts instead of relaxing
  • Diagnosed during voiding phase of urodynamics

*EMG recording

32
Q

Detrusor sphincter dyssynergia (DSD) treatment

A
  • Botox
  • Catheterization
  • Sphincterotomy
33
Q

Acontractility

A
  • Occurs secondary to infrasacral lesions
  • Appropriate function of muscle in the body requires nervous input
  • Any lesion in the sacral spine that compromises the nerves innervating the bladder can cause acontractility
  • Acontractility = no contraction
  • No sensation of fullness, will leak once capacity has been reached
  • Treatment invovles chronic decompression
34
Q

Autonomic dysreflexia

A
  • Autonomic dysreflexia manifests as rapidly escalating hypertension, diaphoresis, and bradycardia
  • Unregulated sympathetic nervous system stimulation
  • Occurs predominantly in spinal lesions above lvl T6
  • Triggered by noxious stimuli below lvl of lesion:

*urinary retention, UTIs, constipation, fecal impaction, and decubitus ulcers

35
Q

Autonmoic dysreflexia treatment

A
  • Drain the bladder
  • Remove tight clothing or straps
  • Assess for constipation or fecal impaction
  • Place the pt on a monitor

*HR and BP at least every 5min

  • If persistently hypertensive

*nitroglycerine (sublingual or paste)

*captopril sublingual

RGU Exam 3 (19 decks)

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