Neurogenic Bowel Flashcards

1
Q

The amount of waste pads used by incontinent (bowel and bladder) persons in the US each day if stacked and each remaining (1/4) inch thick would be:
1. Higher than commercial jetliners fly
2. taller than mount everest
3. 9 million in number or over 43 miles or over 227000ft high

A

All of the above.

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2
Q

Which is one of the best predictors for stroke patients to return home
a. urine incontinence
b. frequency of falls
c. bowel incontinence
d dysphagia

A

bowel incontinence

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3
Q

Definition of neurogenic bowel

A

results from autonomic and somatic denervation, and preduces fecal incontinence, constipation, and difficulty with evacuation

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4
Q

What defines neurogenic bowel?
a. loss of intrinsic enteric nervous system
b. loss of direct somatic sensory or motor control
c. loss of sympathetic innervation
d. loss of sphincter contraction

A

loss of somatic sensory or motor control

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5
Q

Bowel management has been found to be one of the areas of _____ among SCI rehab patients

A

least competence

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6
Q

In a recent study of SCI survivors in sweden, what percentage rated bowel dysfunction as a moderate to severe life-limiting problem?
a. 50%
b. 20%
c. 30%
d. 40%

A

d. 40%

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7
Q

Prevalence of fecal incontinence and fecal impaction ranges from _____ in general population

A

0.3% to 5.0%

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8
Q

Prevalence of difficulty with evacution ranges from _____ among hospitalized or institutionalized elderly

A

10-50%

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9
Q

What percentage of the general population has difficulty with evacuation

A

3-5%

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10
Q

1/3 of persons with SCI report or exhibit worsening of bowel function after _____ post injury. 33% develop ___

A

5 years beyond.

megacolon, suggesting inadequate long-term management

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11
Q

IN 1983 report, _____ estimated spent in USA for care of fecally incontinent institutionalized patients

A

$8 billion/year

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12
Q

Difficulty in bowel evacuation or fecal incontinence
a: affects 90% of SCI persons

A

b

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13
Q

There are 3 different neuron types in the enteric nervous system based on fuction:

A
  1. sensory
  2. interneurons
  3. motor neurons.
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14
Q

There is a highly organized intrinsic innervation in 2 layers in enteric system:

A
  1. submucosal (meissner’s) plexus
  2. Intramuscular myenteric (Auerbach’s) plexus
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15
Q

Meissner’s submucosal and intramuscular myenteric (Auerbach’s plexus) have _____ neurons and ______ glial cells/neuron

A

10-100million neurons
2-3 glial cells/neuron

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16
Q

ENS has its own _____

A

blood-nerve barrier

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17
Q

The enteric nervous system:
a: consists of submucosal and myenteric plexuses
b. contains more neurons than the spinal cord
c. has its own nerve-blood similar to that of the brain
d all of the above

A

d. all

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18
Q

GI neurosensory system: Enteric nervous system sensory neurons:
1. ______ -> chemical (mucosal epithelium), thermal & mechanical (intramuscular arrays or intraganglionic) receptors.

2 ______ -> distributed extensively throughout bowel, relaying chemical, thermal & mechanical information.

  1. Chemical changes creates: (4)_______ that contribute to pain and discomfort
A
  1. Vagal afferent nerve endings
  2. Spinal afferent nerve endings
  3. injury, ischemia, infection, or inflammation
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19
Q

GI neurosensory system: Enteric nervous system sensory neurons:

  1. Spinal nerve endings express receptors for (8)
  2. Mechanoreceptors (derived from 2 ).

3 Vagal afferents are primarily implicated in the ____ response, and spinal afferents are primarily implicated in the _____

A
  1. bradykinin, ATP, adenosine, PG, leukotrienes, histamine, mast cell proteases & 5-HT3.
  2. vagal or spinal afferents
  3. emetic, sensation of nausea
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20
Q

Sensory pathway for bowel:

Enteric Nervous System Relationship to the Spinal Cord and Brain (Extrinsic Innervation)

A

Sensory-
1. vagal afferentsin ENS
2. nodose ganglia of vagus
3. nucleus tractus solitarius & area postrema (brainstem)
4. rostral centers in brain.

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21
Q

Describe parasympathetic system of bowel system

A

Parasympathetic: Vagus- from esophagus to splenic flexure. Pelvic- Nervi erigentes-from S2-S4 to descending colon and rectum

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22
Q

Describe spinal afferents pathway of bowel system:

A

Spinal afferents(splanchnic & pelvic)

  1. DRG (or prevertebral sympathetic ganglia)
  2. dorsal horn (laminae I, II, V, X)
  3. spinal cord & dorsal column nuclei.

Dorsal columngreater role in nociceptive. Superior/inferior mesenteric (T9-T12) and hypogastric (T12-L3)-Sympathetic

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23
Q

Describe somatics system of bowel

A

Somatic afferents of pelvic floor-> pudendal n to sacral region of spinal cord. Pudendal N-Somatic (S2-S4) to EAS

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24
Q

_____ travels along bowel wall from esophagus to internal anal sphincter & forms final common pathway to control bowel wall smooth muscle

A

Enteric nervous system

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25
Q

The inferior splanchnic nerve or nervi erigentes is:
A. the somatic mixed nerve that supplies the pevic floor
B. The parasympathetic nerve that supplies the splenic flexure and descending colon
C The sympathetic nerve that sows colonic peristalsis
D The parasympathetic nerve that modulates small intestine peristalsis to the cecum

A

B The parasympathetic nerve that supplies the splenic flexure and descending colon

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26
Q

GI neuromotor system:
1. pacemaker & allow propagation of electrical slow waves into circular muscle layer
2. ____ have their own electromechanical automaticity, modulated by ENS.
3. Contraction is mediated by
4. ______ impedes contractile activity
5. ______ enhances colonic motility & its loss is associated with DWE, Ogilvie’s pseudoobstructive syndrome.
6. ____ & ____ postganglionic neurons transmit excitatory or inhibitory messages to secretomotor neurons for modulation of water sodium chloride, bicarbonate, and mucus

A
  1. Interstitial cells of Cajal
  2. Smooth muscles of bowel
  3. release of excitatory neurotransmitters by vagal afferents at neuromuscular junctions, ACh & substance P.
  4. Release of NO, ATP, and VIP from inhibitory motor neurons
  5. Parasympathetic activity
  6. ENS & sympathetic
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27
Q

The colon functions to:
A. Store waste until convenient to eliminate it
B. Resorb water from chime
C. Expel slid waste products from dietary intake
D All of the above

A

All

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28
Q

Gastric Motility:
1. _____ has sustained, low-frequency contractions & has tonic pattern.
2. _____ has intermittent, powerful contractions & has phasic pattern. Fundus acts as reservoir
3. ____ is a mixer that generates propulsive waves that accelerate as food is propagated towards pylorus.

A
  1. Upper portion (fundus)
  2. Lower portion (antrum)
  3. Antrum
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29
Q

Intestinal motility:
1. ___ occurs during fasting in stomach & small intestine. Influenced by hormone motilin.

  1. Brainstem sends signals that are transmitted to _____, which convert migrating motor complex motility.
  2. The __________ propel waste through the lumen, particularly in large intestine.
A
  1. Interdigestive migrating motor complex pattern
  2. vagal efferents
  3. “giant migratory contractions” (GMCs)
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30
Q

What physiologic variable correlates best with the frequency of human defecation?
A. Giant Migratory contraction
B Resting peristaltic waves
C Slow electrical colonic potentials
D Electrical spike burst colonic potentials

A

A. Giant Migratory contraction

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31
Q

Motility of Anus, Rectum, and Pelvic Floor:
1. Normal defecation& maintenance of fecal continence entail a highly coordinated mechanism involving
2. Pelvic floor is composed of
3. _______ are skeletal muscles that constantly maintain tone & sustain pelvic organs in place against forces of gravity.

A
  1. levator ani, puborectalis, & EAS & IAS
  2. levator ani, underlying sheets of which form a sling.
  3. Levator ani, puborectalis, & EAS
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32
Q

In the neurally intact state, the early sensory sign of a need for defication comes from:
A. Distension of the cecum
B. Relaxation of internal anal sphincter
C. Stretch of the puborectalis muscle as stool fills the rectum
D External sphincter relaxation

A

C. Stretch of the puborectalis muscle as stool fills the rectum

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33
Q

Physiology of normal defecation - storage:
1. Colon is reservoir for food waste until it is convenient for elimination. Storesas long as ____
2. Reabsorb
- fluids (_____ can be reabsorbed from large & small bowel walls, with typically ____ of H20 loss in feces)
- gases (___% of 7 to 10 L of gases produced by intracolonic fermentation is absorbed).

Normal defecation begins with reflexes triggered by rectosigmoid distention produced by approximately 200 mL of feces.

Secretes mucus for feces lubrication; supports growth of symbiotic bacteria

A
  1. colonic pressure is less than that of anal sphincter mechanism.
  2. up to 30 L/day; 100 mL; 90%
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34
Q

Fecal Elimination:
A is an unnatural event
B Occurs when colonic pressure exceeds that of the anal sphincter
C Requires 1-2 hours in most persons
D Occurs by resorption of gases created by clonic bacteria

A

B Occurs when colonic pressure exceeds that of the anal sphincter

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35
Q
  1. Auerbach and Meissner, as wel as mucosal plexus – which have more ganglia?
  2. Adrenergic fibers are all ____ & arise from _____. Adrenergic fibers are distributed largely to mesenteric, submucous, & mucosal plexus to blood vessels
A
  1. Deep muscular plexus contains a few ganglia, subserosal contains an occasional ganglion, & mucosal plexus shows none.
  2. extrinsic, prevertebral sympathetic ganglia
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36
Q

Physiology of bowel propulsion
1. Coordinated primarily within the ____, with some ____ reflexes but minimal ____ influence.

  1. ____ occurs in which bowel proximal to distending bolus contracts & bowel wall distally relaxes, serving to propel bolus further caudal. Reflex relaxation of __ occurs.
  2. ____ correlates with urge “the call to stool.” Volitional contraction of levator ani to open proximal anal canal & relax EAS & puborectalis muscles.
  3. Increasing ____ assists bolus elimination.For 90% of normal individuals, only contents of rectum are expulsed, whereas 10% will clear entire contents of left side of colon from splenic flexure distally.
A
  1. gut wall, spinal cord, brain
  2. Rectorectal reflex; IAS
  3. Rectoanal inhibitory reflex
  4. intraabdominal pressure (squatting & Valsalva’s maneuver)
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37
Q

Which is a characteristic of the external anal sphincter muscle?
A Autonomic innervation
B Striated muscle
C Continued atonic contraction
D It is smaller than the internal anal sphncter

A

The external anal sphincter is physically larger than the internal sphincter and is a striated muscle whose normal resting state is tonic contraction (only striated muscle with that).

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38
Q

Physiology - propulsion:
1. One can elect to defer defecation by
2. ___ generally tenses in response to small rectal distention via a spinal reflex, although reflexive relaxation occurs in presence of greater distention.
3. Centered in _____ & are augmented & modulated by higher cortical influences.In SCI, EAS reflexes usually persist & allow spontaneous defection.
4. ____ refers to the increased colonic activity (GMCs & mass movements) in first 30 to 60 mins after a meal.

A
  1. volitionally contracting puborectalis muscle & EAS.
  2. EAS
  3. conus medullaris
  4. Gastrocolonic response or Gastrocolic reflex

Chemical control modulates colonic activity
with neurotransmitters and hormones (Bassotti et al.,1995; Sarna, 1991). Local neurogenic control is viathe enteric nervous system, which coordinates all segmentalmotility and some propagated movement (Sarna, 1991). Enteric reflexes do not require extrinsiccolonic innervation (Bayliss and Starling, 1899).When the intestinal wall is stretched or dilated, thenerves in the myenteric plexus cause the musclesabove the dilation to constrict and those below thedilation to relax, propelling the contents caudally.The combined contraction of smooth muscle cells is triggered by electric coupling through gap junctions,which allow myogenic transmission from cell to cell(Christensen, 1991).

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39
Q

Which of the following accurately characterizes the gastricolonic response?
A It is weakest in the morning soon after rising
B It is not affected by atropine
C Peristaltic response is limited to the colon
D It is mediated by hormonal and neural mechanisms

A

D It is mediated by hormonal and neural mechanisms

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40
Q

Physiology of bowel - propulsion:
1. Hormonal effects, from release of peptides from _____ increase contractility of colonic smooth musculature & by reduction in threshold for spinal cord–mediated vesicovesical reflexes
2. ____ is often used therapeutically, in patients with SCI, to enhance bowel evacuation during this 30 to 60 mins postprandial time frame.
3. In neurally intact state, colonic transport takes_____ from the ileocecal valve to the rectum

A
  1. upper GIT (gastrin, motilin, cholecystokinin)
  2. Gastrocolonic response
  3. 12 to 30 hours

Extrinsic reflex pathways from the central nervous system to the intestine and colon both facilitate and inhibit motility. Vagal reflexes increase propulsive peristalsis of the small intestine down through the transverse colon. Sacral parasympathetic reflexesare excitatory and are relayed from the colon tosacral spinal cord segments within the conusmedullaris and back along the pelvic nerve. Spinalcord-mediated reflexes via the pelvic nerve are initiatedfrom enteric circuits in response to colonic dilationand serve to reinforce colonic-initiatedpropulsive activity in defecation (Sarna, 1991). Therectocolic reflex is a pelvic nerve-mediated pathwaythat produces propulsive colonic peristalsis inresponse to chemical or mechanical stimulation ofthe rectum and anal canal. Stimulation of theparasympathetic pelvic splanchnic nerve canincrease motility of the entire colon.Colonic movements can be individual segmentalcontractions, organized groups (colonic migrating ornonmigrating), and special propulsive (giant migratingcontractions, or GMC) (Sarna, 1991) waves ofperistalsis that propel stool over long distances. Inthe neurally intact state, colonic transport takes 12 to30 hours from the ileocecal valve to the rectum
(Menardo et al., 1987).

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41
Q

The external anal sphincter is innervated by:
A L2 and L5 nerve roots
B L5 and S1 nerve roots
C S2 through S4 nerve roots
D Inferior splanchnic nerve

A

C S2 through S4 nerve roots

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42
Q

Physiology of bowel - propulsion:
1. Resting anal canal pressure is determined by: (2)
2. ___ are only striated skeletal muscles whose normal resting state is tonic contraction & these muscles consist mainly of _____ fibers
3. EAS is ______ than IAS has reflex & volitional control
4. EAS is innervated by _____, & puborectalis muscle is innervated by branches from

A
  1. angulation & pressure at anorectal junction by puborectalis sling & smooth muscle IAS tone
  2. EAS & puborectalis muscle; slow-twitch, fatigue-resistant type I\
  3. physically larger
  4. S2 to S4 nerve roots via pudendal nerve; S1 to S5 roots
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43
Q

The act of defecation involve contracting which muscles?
A Levator Ani
B Puborectalis
C External anal sphincter
D All of the above

A

B Puborectalis

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44
Q

Physiology of bowel - continence
1. 2 things in resting state:
2. ____ via lumbar colonic nerves increases IAS tone
3. IAS tone is lowered by

A
  1. Closed IAS and acute angle of anorectal canal by puborectalis sling
  2. Sympathetic (L1-L2)
  3. rectal dilation from stool or digital stimulation

Continence
In the resting state, fecal continence is maintained by a closed IAS and by the acute angle of theanorectal canal produced by the puborectalis sling. Sympathetic (L1-L2) discharges via the lumbar colonic nerve increases IAS tone. IAS tone is inhibited
with rectal dilatation by stool (rectalanal inhibitory reflex) or digital stimulation.

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45
Q

Name stage of normal defecation:

Puborectais, external and internal anal sphincters contracted

A

Holding

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46
Q

Name stage of normal defecation:

Puborectalis and external anal sphincter reax
Levator ani, abdominals and diaphragm contract

A

Initiation

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47
Q

Name the stage of normal defecation

Internal anal and external anal sphincters relax. Rectum contracts

A

Completion

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48
Q

Defecation:
describe sequence of defecation 3)

A
  1. Spontaneous, involuntary advancement of stool stretches rectum & puborectalis
  2. Temporary retain stool by voluntary contraction of EAS
  3. Voluntary relaxation of EAS & puborectalis straightens anorectal for stool passage & augmented by peristalsis & valsalva of abdominal musculature
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49
Q

Compared with the external anal sphincter, the internal anal sphincter is:
1. Larger and maintains 80% of the resting anal canal pressure
2. Smaller and maintains 80% of the resting anal canal pressure
3. Larger and maintains 20% of the resting anal canal pressure
4. Smaller and maintains 20% of the resting anal canal pressure

A
  1. Smaller and maintains 80% of the resting anal canal pressure
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50
Q

Pathophysiology of GI dysfunction:
bowel Dysfunction:
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. Normal colon activity and defecation
  2. Chronic intractable constipation, fecal impaction, reflex defecation with or without incontinence
  3. Chronic constipation, no reflex defecation
  4. Chronic constipation; fecal impaction maximal in the rectum
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51
Q

Pathophysiology of GI dysfunction:
Transit time (cecum to anus)
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. 12-48h
  2. prolonged >72h
  3. Very prolonged unless sacral nerve stimulator used
  4. Prolonged >6 days especially left side of colon
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52
Q

Pathophysiology of GI dysfunction:
Colonic motility at rest
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. GMCs aproximatel 4per 24h
  2. GMCs might be reduced in frequency
  3. Reduced GMCs
  4. Reduced GMCS
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53
Q

Pathophysiology of GI dysfunction:
Colonic motility in response to stimuli
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. GMCs facilitated by defecation, exercise, and food ingestion
  2. Less GMC facilitation by defecation, exercise, or food ingestion
  3. Less GMC facilitation by defecation, exercise, or food ingestion
  4. Less GMC facilitation by defecatin, exercise, or food ingestion
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54
Q

Pathophysiology of GI dysfunction:
Anal Sphincter Pressure Resting tone(mmHg)
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. > 30
  2. > 30
  3. Normal
  4. Reduced
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55
Q

Pathophysiology of GI dysfunction:
Anal Sphincter Pressure volitional squeeze
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. > 30 (up to 1800)
  2. absent
  3. absent
  4. absent
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56
Q

Pathophysiology of GI dysfunction:
Anal Sphincter Pressure (rectal compliance)
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. normal
  2. normal but sigmoid compliance decreased
  3. Normal or increased
  4. rectum dilated; increased distension volume; increased compliance
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57
Q

What triggers normal defecation?
A a thought
B Food in stomach
C Dilatation of the rectosigmoid by 200mL of feces
D Valsalva inhibitory maneuver

A

Normal defecation begins with reflexes triggered by rectosigmoid distension of approximately 200 mL of feces. A rectoreflex occurs in which the bowel proximal to the bolus contracts and the bowel wall distally relaxes, serving to propel the bolus.

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58
Q

Pathophysiology of GI dysfunction:
Rectal balloon distension effect on EAS
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. Causes contraction
  2. Causes contraction
  3. No contraction
  4. No contraction
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59
Q

Pathophysiology of GI dysfunction:
Rectal balloon distension effect on IAS
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. normal recto anal inhibitory reflex
  2. Normal recto anal inhibitory reflex
  3. normal recto anal inhibitory reflex
  4. normal recto anal inhibitory reflex
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60
Q

Pathophysiology of GI dysfunction:
Sensory perception threshold
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. < 20ml volume
  2. none
  3. none
    4 none
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61
Q

Pathophysiology of GI dysfunction:
Stimulation of rectal contraction
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. induced by balloon distension
  2. Giant rectal contractions stimulated readily
  3. rectal contraction stimulation
  4. rectal contraction stmulation
62
Q

Pathophysiology of GI dysfunction:
Vesicoanal reflex
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. P (>50mmHg)
  2. present
  3. absent
  4. absent
63
Q

Pathophysiology of GI dysfunction:
Vasalva protective refex
reflex defecation?
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. Yes
  2. Yes
  3. Impaired
  4. Impaired
64
Q

Pathophysiology of GI dysfunction:
Perianal sensation (cut sensation of touch or pp)
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. Normal
  2. No sensory perception
  3. No sensory perception
  4. Loss of perianal and buttock sensation resulting from injury to sacral nerves
65
Q

Pathophysiology of GI dysfunction:
Anocutaneous reflex (“anal wink”)
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. Present
  2. Present, might be increased
  3. Absent
  4. Absent because of injury to afferent or efferent sacral pathways
66
Q

Pathophysiology of GI dysfunction:
Bulbocavernosus reflex
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. Present
  2. Present; might be increased
  3. Absent
  4. Absent
67
Q

Pathophysiology of GI dysfunction:
Anal Appearance
1. Normal:
2. UMNB:
3. UMNB and posterior rhizotomy:
4. LMNB:

A
  1. normal
  2. normal
  3. normal
  4. flattened, scalloped, because of loss of EAS tone
68
Q

Nausea, Vomiting, and bloating

  1. Neurologic dysfunction that affects _____ at any level of neural axis from brain, spinal cord, afferent nerves, or efferent nerves can lead to spasticity of gastric or intestinal and colonic musculature.
  2. Inhibitory motor neurons allow _____ in an organized, segmental, and abnormal pattern.
  3. When inhibitory motor neurons are inactivated or destroyed by disease, ____ contract continuously and nonsystematically.These contractions are incapable of forward propulsion, causing functional obstruction.
A
  1. inhibitory motor neurons in ENS
  2. propagation of contractile activity
  3. circular muscles
69
Q

Abdominal pain and discomfort:

  1. Release of ___ heighten the sensitivity of the spinal sensory endings
  2. Amplified levels of ___ released at vagal & spinal nerve endings facilitate production of pain
  3. Central sensitization occurs in spinal cord from constant stimulation of ___ in dorsal horn & dorsal column nuclei.
  4. _____ develops with actuation of NMDA receptors from release of glutamate from C fibers.
  5. ___ in gut wall receive nociceptive signals from mechanical irritation.
  6. ____of brain through dorsal horn can promote recognition of ordinary sensory input as innocuous
A
  1. bradykinin, ATP etc
  2. 5-HT3
  3. C fibers
  4. “Wind-up” phenomenon
  5. Mechanoreceptors
  6. Descending facilitative modulation
70
Q

Diarrhea

  1. Diarrhea occurs when there is overstimulation of _____, or overstimulation by _____, or overstimulation by all 3 substances
  2. _____ in gut can be a factor in chronic inflammatory states presenting with diarrhea
A
  1. secretomotor neurons by histamine from inflammatory & immune-mediated cells in the mucosa and submucosa

VIP & serotonin from mucosal enterochromaffin cells

  1. Bacterial overgrowth
71
Q

Defecation dysfunction
1. Constipation: Caused by
2. _____by sympathetic stimulation inhibits the firing of secretomotor neurons by hyperpolarization.

A
  1. Lack of rectal sensation and decreased urge to defecate
  2. Norepinephrine released
72
Q

Fecal Incontinence
Lesionsaffecting the: 5.
Denervation leads to 4

A
  1. lumbar spinal cord, cauda equina, S2–S4 nerves, pudendal nerve, & pelvic floor nerves
  2. impaired perineal and rectoanal sensation, aberrant contraction, loss of tone & weakening of pelvic floor muscles & EAS
73
Q

How does a normal person defer defecation?
A Using the rectoanal inhibitory reflex
B Using the Valsalva Maneuver
C By volitionally relaxing the puborectalis muscle
D By volitionally contracting the EAS

A

One can elect to defer defecation by volitionally contracting the puborectalis and external anal sphincter.

74
Q

Upper Motor Neurogenic Bowel
1. Defined as
2. Sensations mediated by bypassing zone of SCI via _____ , or by _____.
3. Passive filling of rectum leads to increases in the _____, abolished by pudendal block. Colonic motility & stool propulsion are known to be affected by SCI.
4. In chronic SCI levels above L2, ___% had constipation; ___% with paraplegia below T10 & above L2 had constipation

A
  1. Any destructive CNS process above conus, from SCI to dementia, can lead to UMNB pattern of dysfunction.
  2. paraspinal sympathetic chain, vagal parasympathetic afferents
  3. resting sphincter tone (rectal sphincter dyssynergia),
  4. 58, 30
75
Q

What can lead to upper motor neurogenic bowel dysfunction?
A Anterior horn cell disease
B Diabetic peripheral neuropathy
C Dementia
D Poliomyelitis

A

Any destructive central nervous system process above the conus, from spinal cord injury to dementia, can lead to the upper motor neurogenic bowel dysfunction pattern of dysfunction

76
Q

UMN bowel
1. In _______, transit times were significantly prolonged in ascending, transverse & descending colon & rectosigmoid

  1. ____, in which EAS pressure increases in response to increased intraabdominal pressure, is usually intact. UMNB pts have normal or increased anal sphincter tone, intact anocutaneous (or “anal wink”) & bulbocavernosus reflexes, palpable puborectalis muscle sling, and normal anal verge appearance
A
  1. SCI with supraconal lesions
  2. Protective vesicorectal reflex
77
Q

LMN bowel:

  1. Causes? 5
  2. These can impair ____ innervation of anal sphincter, sympathetic & parasympathetic deficits.
  3. If an isolated _____ insult occurs then, colonic transit times are normal and FI predominates.Distal colonic sluggishness -loss of parasympathetic supply. DWE to FI compounds difficulties.
    4 Explain process of actual sequelae of LMN issues:
A
  1. Polyneuropathy, conus medullaris or cauda equina , pelvic surgery, vaginal delivery, or chronic straining during defecation\
  2. somatic
  3. pudendal
  4. Accumulation of large amount of hard stool-> colonic inertia -> overstretch weakened anal mechanism -> gaping, patulous, incompetent anal orifice -> rectal prolapse.

Denervation, atrophy & overstretching of EAS & IAS -> loss of protective IAS tone ->stool soilagefrom abdominal pressures

78
Q

Neurogenic bowel management to maintain continence is more successful in UMN than LMN lesions because:
A. LMN lesions lead to more atrophy of the external and sphincter and puborectalis
B. UMN lesions are more likely to have intact anal reflexes which facilitate triggered bowel evacuation
C UMN spasticity helps maintain the bulk and continence function of the external anal sphincter muscle
D All of the above

A

D all

79
Q

LMN bowel:

  1. Presence of ______ can compromise rectoanal angulation at pelvic floor & contribute to paradoxical liquid incontinence around a low impaction, called theball-valve effect.
  2. Will have ______.If no tone is found initially on inserting examining finger, examiner should wait up to 15 sec to allow IAS reflex relaxation to recover & restore tone.
  3. ____ is absent or decreased (depending on completeness of lesion). Bulbocavernosus reflex is weak if present.
  4. Anal canal is (normal 2.5- to 4.5-cm length) & puborectalis muscle ridge might not be palpable. Rectal prolapse with Valsalva
A
  1. large bolus in rectal vault
    2 Decreased anal tone because of IAS
  2. Anocutaneous reflex
  3. shortened
80
Q

The anal sphincter mechanism includes
A. The EAS, bulbocavernosus muscles, and internal anal sphincter
B The levator ani muscles, IAS, and EAS
C The EAS, the puborectalis muscles, and IAS
D The rectal vault and the external anal sphincter

A

C The EAS, the puborectalis muscles, and IAS

81
Q

LMN bowel:

What does the anal-to-buttock contour typically look like?

Why?

A

Anal-to-buttock contour typically appears flattened & “scalloped” because of atrophy of pudendal-innervated pelvic floor muscles & EAS.

82
Q

GI dysfunction in neurological disorders:

  1. Dysphagia results in: 4
  2. Dysphagia in ~____% of pts with stroke
  3. _____ & _____ play a role in GI ulceration, gastroparesis & ileus
  4. ___ & _____ progressively improve
A
  1. delays gastric emptying & ileus, constipation & FI
  2. 45
  3. Cerebral edema & increased ICP
  4. Dysphagia & ileus
83
Q

Parkinsons disease

Up to ____% Parkinson’s pts had dysphagia, ____% had constipation, and ____% had problems with defecation. Compromise nutrition and cause severe morbidity

A

Parkinson’s & Parkinson’s-plus diseases (multiple system atrophy, progressive supranuclear palsy, corticobasal degeneration) are neurodegenerative diseases

Cerebral cortex, basal ganglia, brainstem, cerebral cortex, cerebellum & spinal cord. Dysautonomia, gastric dysmotility & constipation.

  1. 52.1%, 28.7%, 65%
84
Q

MS and GI disease

  1. Presents as: 5
  2. ____% were reported to have GI problems, with ___% had constipation & ___% FI.
  3. _____ & _____ lesions associated with sympathetic & parasympathetic system impairment
A

Demyelinatingdisease involves brain & spinal cord

  1. Dysphagia, gut dysmotility, FI, diarrhea, or constipation
  2. 68%, 43%, 53%
  3. Supraspinal or spinal
85
Q

SCI: Trauma, masses, infection, hemorrhage, or ischemia involving spinal cord & causing tetraplegia or paraplegia, primarily affects colonic motility & perineal & anorectal sensation & function during acute & chronic phases

  1. Upper GIT- with brain & autonomic modulation of ENS, dysfunctionisprincipallyof ____ than _____
  2. pathway of GI disease:
  3. All levels of injury show loss of _____ over bowel movements, with constipation or FI.
A
  1. motility than secretion or absorption
  2. Upper GI-> tetraplegia-> gastroparesis, impaired gastric emptying, dysphagia, gastric and duodenal ulcerations
  3. voluntary control
86
Q

Almost one-third of SCI survivors experience worsening of bowel problems at what time after their initial injury?
A. within 6 months
B After 1 year
C After 2 years
D After 5 years

A

After 5 years

87
Q
  1. 6 causes of peripheral neuropathy
  2. 4 GI consequences of peripheral neuropathy
  3. Injury to the ____ (3) compromise FI & abnormal defecation
A
  1. Metabolic, viral, traumatic, toxic, metastatic & genetic.
  2. Transit disturbances, diarrhea or constipation; diabetes gastroparesis
  3. pudendal N (from childbirth), S2–S4 nerve root lesions, or cauda equina
88
Q
  1. What drugs might decrease GI motility? 6.
  2. What other things might you ask about your patient’s bowel program? 5
  3. Important to know about a premorbid ____
A
  1. Drugs decrease GI motility such as opiates, anticholinergics, tricyclics, antihistamines, calcium channel blockers & phenothiazines
  2. Description of schedule, initiation method (chemical or mechanical stimulation),facilitative techniques, time requirements & characteristics of stool
  3. Premorbid bowel pattern information such as defecation frequency, typical time of day, associated predefecatory activities, bowel medications & techniques or trigger foods & stool consistency.
89
Q

Impactions are
A. Almost never seen outside hospitals or nursing homes
B More safely treated with oral cathartics than enemas
C To be considered a cause of diarrhea
D Easily resolved and never associated with mortality

A

C

90
Q

History/basic exam for GI dysfunction:

  1. Warning sensations for defecation sense of ___
  2. Ability to prevent stool loss during ____
  3. Excessively large-caliber, hard stool – H/o toilet plugging.
  4. Inspect and Check ____
A
  1. urgency
  2. Valsalva activities such as laughing, sneezing, coughing, or transfers noted.
  3. just FYI
  4. sensation side to side
91
Q

Stool consistencies vary from

A

liquid to pudding, pasty, semisolid, soft-formed, medium-formed, and hard

92
Q

What is the peds choose your poo algorithm

A
  1. rabbit droppings - separate hard lumps (like nuts (hard to pass))
  2. bunch of grapes - sausage shaped but lumpy
  3. corn on the cob - like a sausage but with cracks on its surface
  4. Sausage - like a sausage or snake - smooth and soft
  5. chicken nuggets - soft blobs with clear cut edges (passes easily)
  6. porridge - fluffy pieces with ragged edges, a mushy stool
  7. gravy - water, no solid pieces (entirely liquid)
93
Q

Stool: More ____ is required for the weaker anal sphincter mechanism of the LMNBthan for the UMNB (semiformed to soft)

A

firmness (medium-formed)

94
Q

Bristol stool chart:

A

Type 1 - separate hard lumps, like nuts (hard to pass)
Type 2 - sausage shaped but lumpy
Type 3 - Like a sausage with cracks on its surface
Type 4 - like a sausage or snake, smooth and soft
Type 5 soft blobs with clear-cut edges (passed easily)
Type 6 fluffy pieces with ragged edges, a mushy stool
Type 7 water, no solid pieces, entirely liquid

95
Q

Which set of physical findings is most consistent with an UMN neurogenic bowel?
A. absent anal wink, hypoactive knee jerk, decreased anal tone
B. Spastic lower extremities, up-going toes, positive bulbocavernosus reflex, increased anal tone
C Voluntary abdominal contractions, voluntary anal sphincter relaxation, and normal perineal pinprick perception
D Constipation with palpable impaction, dry stools, and difficulty with evacuation

A

B. Spastic lower extremities, up-going toes, positive bulbocavernosus reflex, increased anal tone

96
Q

GI dysfunction:
Digital rectal exam

  1. Anorectal junction indicated by
  2. Puborectalis along posterior wall, ____ cm from anal verge,_____ can be palpated as ridge that will push finger forward as pt resists defecation.No palpable ridge suggests ____
  3. _______: Perianal cutaneous sharp stimulation results in externally visible anal sphincter reflexive contraction. Mediated by inferior hemorrhoidal branch of the pudendal nerve (S2–S5).
  4. ______: anal sphincter contraction with rapidlytapping or squeezing clitoris or glans penis. Delayed up to a few secs in pathologic.
  5. Integrity of pelvic floor muscles can be examined by ability to
  6. length of anus, where pressure is sensed, is normally
A
  1. loss of pressure
  2. 1.5 to 2.5, puborectalis muscular sling. puborectalis atrophy/dysfunction
  3. Anocutaneous reflex
  4. Bulbocavernosus reflex
  5. contract & relax
  6. 2.5 to 4.5 cm
97
Q

What marks the anorectal junction?
A. on digital exam, the point where pressure decreases
B. as above after 6cm
C as above where the pressure increases
D as above at 1cm

A

A. The length of the anus where pressure is sensed is normally 2.5-4.5 cm. The point where the pressure decreases is the anorectal junction

98
Q

4 types of stimulation for GI tract

A
  1. Mechanical - Intraluminal balloon or bag distention with air
    Intraluminal gas perfusion (e.g., nitrogen/carbon dioxide/oxygen with nonabsorbable marker)
    Fluid loading (e.g., water or nutrient drink test)
  2. Chemical - Oral, intraluminal, and intravenous delivery of macronutrients, specific dietary components, and so forth
  3. Pharmacologic - Oral, intraluminal, intravenous, inhaled, and transcutaneous delivery of drugs, peptides, and so forth
  4. Electrical - Intraluminal bags with recirculated warm or cold water
99
Q

What are specific techniques for invasive measurement of GI tract motility?

A

Manometry
Berostat
Tensostat
Electromyography
Intraluminal or needle sigmoidoscopy/colonoscopy
Intraluminal gas perfusion (transit time)
Intraluminal impdance
(multichannel)

100
Q

What are specific techniques for non-invasive measurements of GI tract motility?

A

Imaging (KUB)
Scintigraphy
Barium radiopaque markers, radiography
Videofluoroscopy
Ultrasonography
MRI (stomach wall motion)
SPECT - stomach volume or accommadation
C-substrate breath tests - stomach
Acetaminophen (plasma) - stomach
Lactulose breath test - SB
Sulfasalazine (plasma) SB
MG
Surface (stomach)

101
Q

What is the normal frequency of defecation in 95% of people
A one per day to one per week
B Two per day to two per week
C three per day to three per week
D four per day to four per week

A

C

102
Q

Management of N/v, bloating and early satiety:

  1. Gastroparesis or a small intestinal or colonic pseudoobstruction- air-fluid levels-
  2. Drugs which ____ must be discontinued or minimized.
  3. Prokinetic agents: 3
  4. For chronic subocclusive states, _____ nutrition is preferred
  5. Meals-
  6. ____ can be helpful to optimize nutrition
A
  1. GI decompression with nasogastric & rectal tubes.
  2. diminish motility,
  3. , metoclopramide and domperidone & erythromycin
  4. enteral
  5. small; frequent; liquid; contain polypeptide and hydrolyzed protein; be low in fat, fiber, and lactose; and contain multivitamins (iron, folate, calcium, vitamins D, K, and B12).
  6. Enterostomies
103
Q

management of diarrhea:

  1. Diarrheain neurologic disease is commonly caused by
  2. ____ is helpful in relieving diarrhea, thus preventing malnutrition
  3. 1-week courses (for a period of 2 to 4 wks) of various abxs, including __(5)__ is recommended
A
  1. bacterial overgrowth
  2. 4 wks of abxs
  3. metronidazole, co-trimoxazole, ciprofloxacin, doxycycline, and amoxicillin-clavulanate,
104
Q
  1. _____is a comprehensive, individualized patient-centered treatment plan focused on preventing incontinence, achieving effective & efficient colonic evacuation & preventing complications of neurogenic bowel dysfunction. Subcomponents diet, fluids, exercise, medications.
  2. _____ is individually developed & prescribed procedure for defecation that is carried out by pt or attendant
A
  1. Abowel program
  2. Bowel care
105
Q

How is constipation defined?
A. One defecation per day or less
B One defecation every other day
C Two or fewer per week
D One per 3-4 weeks

A

Two or fewer bowel movements per week or the requirement for digital evacuation.

106
Q

Restoring normal defecation may not be possible.
1. _____ -predictable scheduled adequate defecations without incontinence at other times

Goals:
2. Regular passage of stool on a ____ basis
3. Bowel evacuation at a consistent
4. Complete emptying of ____with every bowel program
5. Stools that are (3)
6. Completion of bowel program within ___

A
  1. “Social continence”
  2. daily or every-other-day
  3. time of day (AMorPM)
  4. rectal vault
  5. soft, formed & bulky
  6. ½ an hr (at most in 1 hr)
107
Q

What is the difference between a bowel program and bowel care?
A the former is the procedure for defecation
B The former is comprehensive, individualized, and patient-centered
C the latter is diet and fluids
D the latter is centered on preventing incontinence

A

A bowel program is a comprehensive, individualized, patient-centered treatment plan focused on preventing incontinence. A bowel care plan is the individually developed and prescribed procedure for defecation

108
Q

Name the 5 laxitive categories:

A

I. Bulk-forming agents
II. Fecal Softners/Lubricants
III. Hyperosmotic
IV. Stimulant
V. Prokinetic

109
Q

During rehab, the ideal time to plan for defecation and bowel care is when?
A. first time in the morning
B after lunch
C any time that is convenient
D in the evening

A

D

110
Q

Class I: Bulk-forming Laxatives

name 4

A

Psyllium (natural; Metamucil)
Dietary fiber (natural; bran)
Methylcellulose (semisynthetic; Citrucel)
Polycarbophil (synthetic; FiberCon)

111
Q

3 characteristics of Class1 bulk forming laxatives:

A
  1. Nonabsorbable
  2. Hydrophilic
  3. Subject to variable bacterial degradation with gas formation
    - Natural preps = some degradation that can reduce compliance
    - Semisynthetic = less
    - Synthetic agents =none
112
Q

MOA for Class I bulk forming laxatives: 5

A

Mechanism of action:
1. Absorbs & retains water forming bulky gel
2. Increase fecal volume
3. Soften stool
4. Increase the rate of transit
5. Fiber increases stool bulk and plasticity, especially the more physically coarse forms of fiber, which also tend to decrease colonic pressures

113
Q

Possible adverse effects of Class I bulk forming laxatives

A

Possible Adverse Effects:
1. Requires lots of water intact to avoid intestinal obstruction
2. Loss of H20 & electrolytes with powdered preparations (prolonged use only)
3. Possible reduced absorption of drugs/vitamins
4. Should be introduced gradually over 1-2 weeks
5. Action is slow with onset 12-72 hours
6. Weak stimulant

114
Q

Class II fecal softners can be divided into

A

IIA lubricants (oral oil, mineral oil enemas)
IIB surfactant agents (Sodium docusage, doss, colace)

115
Q

Describe two Class IIa fecal softners - lubricant oils

A
  1. Oral oil (liquid paraffin, Mineral oil)
    - Onset of Action: 6 - 8 hours
    - Make the stool slippery, decrease absorption of H20 from stools thereby increase stool mass & softness
    - Not palatable
    - Aspiration may occur leading to lipid pneumonia
    - Long term use may lead to deficiency of fat soluble vitamins
  2. Mineral oil enemas
    - Lubricates the feces & distends the rectum
    - Relieves fecal impaction
116
Q

Describe the MOA for Class IIb fecal softeners (4)

A
  1. Soften stools by causing H20 & fats to penetrate stool, making it more bulky & easier for peristalsis
  2. Minimal laxative effect at usual doses.
  3. Onset of Action: 12 - 72 hours
  4. Safer than mineral oil given orally
117
Q

Class IIb surfactant agents (recal)

A

Rectally

Enemeeze, Theravac mini enema

Used with stimulant laxative given rectally

118
Q

Name 5 Class III hyperosmotic agents

A
  1. Magnesium hydroxide (Milk of Magnesia)
    2 Magnesium citrate (Citroma)
    3 Magnesium sulfate (Epson salt oral/enema)
    4 Sodium phosphate (Fleet Phospo-Soda) oral/enema
    5 Polyethylene glycol (synthetic) alone (MiraLax) or with electrolytes (NuLytely, GoLytely solutions)
119
Q

5 MOA for Class III hyperosmotic bowel agents

A

Mechanism of action:
1. Active constituents are relatively nonabsorbable ions
2 Osmotically draws water into GIT increasing volume & transit rate; works much like bulk fibers but much faster
3 Orally administered, empties entire GI tract.
4 Rectally administered, only evacuates the lower colon.
5 Some saline suppositories/enemas also produce CO2 which exerts pressure in rectum & has a gas-lubricant-like effect

120
Q

for class III hyperosmotic agents:
1. Effects are ___ & ____ dependent
- Oral Phospho-soda produces watery stools cathartic effect in _____
- Small doses of MOM may require _____ for laxative effect

  1. Large doses are ___ & ____
A
  1. dose & preparation
    - only 1-3 hours
    - several days
  2. very rapid & not gentle
121
Q

Adverse effects of class III hyperosmotic agents: 6

A
  1. Electrolyte &/or volume overload from absorption of sodium, magnesium, or phosphorus in pts with renal insufficiency or cardiac dysfunction.
  2. Dehydration
  3. Bloating
    4 Cramping
    5 Gas
    6 Slow acting
122
Q

Class III hyperosmotic agents (sugar)
1. ______ is a Galactose-fructose disaccharide which is metabolized by gut bacteria to poorly absorbed organic acids- lactic, formic, and acetic acid
2. both ____ and ____ pull water into the gut resulting in its laxative effect
3. Acidification of the feces increases _____ excretion and provides symptomatic relief of _____

A
  1. lactulose
  2. disaccharide and organic acids
  3. ammonia; portalsystemicencephalopathy (PSE)
123
Q

Class IV stimulant laxatives can be of the Anthraquinone family: two examples

or _____ group (3 examples)

A

(senna, ex-lax)

Bisacodyl (dulcolax, magic bullet, correctol)

124
Q

Class IV: Stimulant Laxatives
1. dosing expressed in _____
2 Normal oral dose:
3. Laxation in ____ or up to _____
4. Antraquinon family have been shown to damage ______ with chronic use and cause ______

A
  1. sennosides
  2. 12.50mg
  3. 6-12h or up to 24h
  4. Myenteric neurons; atonic “cathartic bowel” syndrome
125
Q

Class IV stimulant laxatives:
Bisacodyl:
1. Normal oral constipation dose:
2. Complete evacuation dose:
3. Laxation in ____ orally and ____ rectally
4. ____ used in children

A
  1. 5-15mg
  2. 30mg
  3. 6-8hr, 15mins-1hr
  4. Glycerin
126
Q

In the management of the neurogenic bowel, bisacodyl (Dulcolax) tablets and suppositories are
(a) colonic stimulants that stimulate and enhance the gastrocolic reflex and thereby induce peristalsis in the colon.
(b) stool softeners that aid in softening the stool by emulsifying fats in the gastrointestinal tract.
(c) colonic stimulants that are primarily effective by being directly absorbed through the mucosa of the small intestine or colon.
(d) contact irritants that act directly on the colonic mucosa to produce peristalsis throughout the colon.

A

(d) Bisacodyl (Dulcolax) tablets and suppositories are contact irritants that act directly on the colonic mucosa, and produce peristalsis throughout the colon. Administered orally, the drug exerts its effect through direct contact on the colon, not through absorption in the small intestine

127
Q

Class IV stimulant laxatives:
1. _____ is a triglyceride from castor beans
2. Releases ____ which reduces net movement of electrolytes & H2O out of small intestine & increases fecal bulk.
3. Increased bulk does what?
4. Trigger fairly violent
5. Effective in as little as

A
  1. Castor oil
  2. an anionic surfactant (ricinoleic acid)
  3. speeds fecal transit.
  4. uterine & abdominal contractions (i.e., cramping)
  5. 2 hrs.
128
Q

Class IV stimulant laxatives:
1. MOA (2)
2. adverse effects (2)

A

Mechanisms of Action:
Increase peristalsis through the GI tract
Some also increase fluid & electrolyte absorption resulting in net intestinal fluid accumulation.

Adverse Effects.
Can cause H2O/electrolyte/nutrient loss
All turn urine pink or red or reddish/brown

129
Q

Which is or are preferred for facilitating defecation in SCI chronically?
A. oral bowel stimulants
B. Hydrogenated glycol-based suppositories
C bisacodyl suppositories
D digital stimulation

A

Suppositories have largely been replaced by mini-enemas. The use of digital stimulation alone is effective for many persons with SCI

130
Q

Name 2 class V prokinetic agents:

A

Metoclopramide
Primary effect is on gastric & small bowel motility not colon

Zelnorm
Selective Partial Agonist of 5HT4 Serotonin Receptors

131
Q

Treatment of opioid induced bowel dysfunction:

  1. Opiate antagonist, _____ selectively antagonizes opioids effects on gut which comes in subcutaneous formulation has shown efficacy.
  2. ____ is another peripherally acting mu opioid receptor antagonist with low systemic bioavailability, action limited to gut & administered orally.

3 A new agent on market, _____, has been shown to be efficacious in treatment of chronic constipation

A
  1. Methylnaltrexone
  2. Alvimopan
  3. Lubiprostone
132
Q

A 25-year-old man with L5 complete paraplegia is admitted to your rehabilitation service 2 weeks after his injury. On admission you note that he is tolerating an oral diet but has not produced a bowel movement for 6 days. At this point, you recommend
(a) oxybutynin (Ditropan) 3 times a day.
(b) a contact irritant suppository with digital stimulation daily.
(c) manual removal of stool from the rectum 1–2 times daily.
(d) nasogastric decompression for a presumed ileus.

A

c) Individuals with lower lumbar and sacral level injuries usually experience areflexic bowel function. The use of suppositories are usually not useful in these individuals, because of the absence of spinal reflex activity. Manual evacuation is often required for an effective bowel program in a lower motor neuron injury. Anticholinergic medications may lead to constipation

133
Q

Rectal stimulants work by:
Two types

A

Work by chemical stimulant of receptors and/or mechanical dilation of rectum

  1. Suppositories
    Work only if they contact mucosa so require pre-insertion removal of any stool in vault
    Should remain in anal canal

P2 Enemas
Fluid will work itself around any stool present
More volume in enema less reflexive the activation

134
Q

Dietary considerations for bowel dysfunction:

  1. SCI, transit time is often ____ vs ____ in normals
  2. Gases & liquids are propelled ____ faster than solids by colon.
  3. Stools that have lost their plasticity might not be kneaded & folded properly by ____ impeding transit time.
  4. Stool softeners, both _____, have been used to maintain a more fluid content
A
  1. 96 hrs Vs 30 hrs
  2. 30 to 100 times
  3. haustra,
  4. docusate & food fiber
135
Q

Dietary considerations for bowel dysfunction

a. Sufficient intake of _____ is imperative when consuming a high-fiber diet.
b. Drinking at least ____ is rec. High-fiber diet with insufficient intake of fluids can promote constipation.
c. _____ drinks can lead to dehydration from diuresis. Diet containing at least 15 g of fiber/day recommended
d. Fiber from (4 sources) can be used SCI do not decrease colonic transit time but enhance the rectoanal inhibitory reflex

A
  1. fluids (preferably water)
  2. 2 to 3 L of fluids/ day
  3. Coffee, tea, and energy
  4. vegetables, fruits, and grains, artificial fiber products such as psyllium
136
Q

The degree of fluidity, or plasticity, of the stool is important because:
A. stool becomes exponentially harder to expel the more solid it is
B Too fluid stool may be impossible for an impaired anal sphincter mechanism to resist, leading to incontinence
C it can be modified by fiber intake
D all of the above

A

all of the above

137
Q

How to manage UMN defacatory dysfunction manually?

How to perform rectal stimulation:

A

UMNB defecatory reflex is intact, so trigger of defecation by digital stimulation, rectal stimulant medications, enemas, or electrical stimulation. Reflex relaxation of IAS strong enough can reflexly relax the EAS rectorectal reflex that helps to eliminate any stool that is present.

Gloved, lubricated finger into rectum & rectal wall by gentle circular movements. 20 secs & repeated Q5-10 mins until bowel rectal vault empty

Used to trigger & sustain reflex defecation 30 mins before intended bowel program rationale, least irritating, easily inserted & retained medication.

Oral bowel stimulants can be used, when digital rectal stimulation & rectal medications are not sufficient to achieve goals of the bowel program, by trial and error based on type, dosage, quantity.

138
Q

How do you manage LMN defecatory dysfunction? 2

A

In LMNB bowel is areflexic & most effective way of completely emptying rectum is through manual disimpaction or use of cleansing enemas(water, soapsuds, mineral oil) that aredone daily or twice a day.

Sphincter & pelvic floor muscle tone is lost, increasing the likelihood of FI.

It isimperative to keep the stools well formed & bulky, and to empty the rectal vault more regularly.

139
Q

Which would indicate a LMN neurogenic bowel dysfunction?
A. decreased anal tone
B bulbocavenosus reflex is hyperactive
C anal canal is lengthened
D rectal prolapse is reduced

A

Decreased anal tone. Excessive rectal prolapse can occur, and the anal canal is shortened.

140
Q

Describe the 7 steps of bowel habituation program and how often to move to next step:

A
  1. Perform bowel cleanout if stool is present in the rectal vault or palpable proximal to the descending colon by multiple enemas or oral cathartic
  2. titrate to soft stool consistency with diet and bulking agents (fiber) and stool softeners (docusate)
  3. Trigger defecation with glycerin supp or by dig stim 20-30 mins after a meal; 10 mins later, have the patient attempt defecation on the toilet, limited to less than 40mins, and relieving skin pressure every 10 mins
  4. If defecation is not initiated, a trial of a bisacodyl supp per rectum is initiated
  5. Dig Stim. Start 20 mins after supp placement and replace every 5 mins
  6. Timed oral meds. Administer (per-colaace), senna, or bisacodyl tabs timed so bowel movement would otherwise result 30 min to 1 hr after anticipated triggered bowel timing.
  7. If defecation occurs in less than 10 minutes after supp insertion, transition to dig stim

Each step is added only after 2 weeks’ consistent trial of the previous step has been ineffective. In thisstepwise approach,obtaining elimination at the desired time is emphasized as the first step, andusually precedes development of complete continence by several weeks

141
Q

Which regimen would be expected to be most successful for the LMN neurogenic bowel dysfunction in a patient with L1 ASIA A SCI?
A. Bowel care with a bisacodyl supp per rectum and transfer to toilet for spontaneous detection
B Tap water enemas in morning and evening in side-lying, followed by transfer to the toilet
C Oral stool softners such as docusate (colace) increase dose until stool is semisolid for eas of evacuation with valsalva maneuver
D diet with fiber to produce formed stool, bowel care twice daily with digital rectal evacuation

A

Diet with fiber to produce formed stool, bowel care twice daily with digital rectal evacuation

142
Q

Name the 8 surgical options for neurogenic bowel

A
  1. Gastric Electrical Stimulation: High-energy electric pulses delivered at a frequency higher than normal slow-wave impulses
  2. Gastrostomies and Enterostomies: parenteral nutrition,venting enterostomy: symptomatic relief ->gaseous distention & bloating
  3. Surgeries for Chronic Intestinal or Colonic Pseudoobstruction: Colonoscopic decompression is successful in 75% to 90% of cases where nasogastric or rectal tubes were ineffective
  4. Cases in which conservative treatment has been unsuccessful, subtotal colectomy with ileorectostomy.
  5. Intestinal transplantation is another option for pts with complete small intestinal failure who cannot receive total parenteral nutrition. Liver transplantation for patients with liver failure
  6. Pelvic Floor Sling: Sacral nerve deficits interfere with action of puborectalis, levator ani & EAS. Transposition of innervated gracilis, adductor longus, gluteus maximus, or free muscle graft palmaris longus to replace puborectalis function & restore anorectal junction angle
  7. Internal Anal Sphincter & Partial External Anal Sphincter Myotomy: Incomplete EAS relaxation during defecation (dyssynergia) results in functional outlet obstruction & DWE
  8. Electroprosthesis: Stimulation of anterior sacral roots by transrectal electric stimulation or via stimulator surgically. S2 ->nonperistaltic, low-pressure colorectal motor activity.S3-> high-pressure peristaltic waves. S4-> increases rectal and anal tone. Electrodefecation by sacral root stimulation in up to 50%
143
Q

How does the external sphincter respond to small rectal distension?
A. it relaxes then tightens
B it tenses
C there is no response
D reflexic relaxation

A

The external sphincter generally tenses in response to small rectal distentions via a spinal reflex, although reflexive relaxation of the external sphincter occurs in the presence of greater distentions.

144
Q

What is an antegrage continence enema?

A

Surgical construction of catheterizable appendicocecostomy stoma mobilized through Rt lower quadrant incision & brought against abdominal wall.Tip of appendix is then amputated & opening into appendix lumen is modified into a catheterizable stoma. stoma can be infused with 200 to 600 mL of H2O to trigger propulsive colonic peristalsis & defecation within 10 to 20 mins

145
Q

Colostomy remains a procedure of last resort for neurogenic bowel in these 4 senarios:

A
  1. When conservative medical measures & training have failed
  2. When intrinsic bowel deficits exist, such as in Hirschsprung’s disease, Chagas’ disease, and “cathartic colon”
  3. When pressure ulcers or other skin lesions occur that cannot be effectively healed because of frequent soiling
  4. When recurrent UT seeding by repetitive bowel impactions occurs
146
Q

compared with difficulty with evacuation and prolonged bowel care times, studies show that patients with colostomies report:
A continued constipation and prolonged elimination
B less total bowel care time and improved quality of life
C increased need for attended to manage colostomy sites
D more frequent stool incontinence because of dislodging of colostomy bag

A

Less total bowel care time and improved quality of life

147
Q
  1. Complications of gastroparesis or intestinal pseudoobstruction: 3
  2. Risk for perforation is increased -> cecal diameters
  3. Mortality rate is approximately (range%) & is determined by age, diameter of cecum, delay of decompression & comorbidities
  4. Significant bowel complicationsrequiring 27% of persons with SCI by 5 yrs or greater beyond their injury
A
  1. chronic malnutrition, dehydration & electrolyte imbalance
  2. > 12cm
  3. 36% to 44%
148
Q

how many patients with SCI have a chronic problem with fecal incontinence
A 34%
B 2%
C 21%
D most

A

Although all patients with complete SCI have episodic fecal incontinence, this is a chronic problem in 2%.

149
Q

Complications of neurogenic bowel:

  1. ____% of SCI report bowel impactions & 20% had chronic bowel impaction & DWE problems
    2 Hemorrhoids are more symptomatic when pts have ______.
  2. _____% pts with SCI have high pressures in anorectal marginal veins
    4 Overstretched, patulous, non-competent sphincter associated with ____
    5 FI is a common cause of ______ because of substantial time, lubrication with lidocaine gel is recommended to decrease additional nociceptive sensory input from richly innervated anal region.
  3. ____ & _____ are common in hyperactive EAS
A
  1. 80%
  2. intact sensation,
  3. 74
  4. rectal prolapse in LMNB
  5. autonomic dysreflexia
  6. Bloating & abdominal distention
150
Q

What percentage of patients with SCI have rectal bleeding from hemorrhoids?
A 0%
B 75%
C 50%
D 25%

A

Hemorrhoids in 74% of patients with SCI. Stool softening was the best preventive

151
Q

1._____ by means of suppositories, digital stimulation, or both, resulted in 83% of compliant pts having less than 1 incontinent stool per mth
2. All patients with complete SCI have episodic FI, is chronic problem for only ___ %
3. ____ can provide a means of achieving socialcontinence
4. Pts who develop _____ are able to venture into public without fear of malodorous embarrassment & unpredictable social disasters that humiliate as well as require substantial cleanup time

A
  1. Myelomeningocele
  2. 2%
  3. Colostomy
  4. social bowel continence
152
Q

Simple bowel habituation training can result in social continence for approximately what percentage of myelomeningocele children who have intact anal reflexes?
A 0%
B 80%
C 40%
D 20%

A

80%