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Peds GI RC > Motility > Flashcards

Motility Flashcards

1
Q

What are 5 benefits of MII studies over pH studies

A

Detects reflux regardless of its pH value (nonacidic reflux) Distinguishes swallows (antegrade flow) from GER (retrograde flow)
Detects accurately the height of the refluxate
Determines whether the refluxate is liquid, gas or mixed
Measures symptoms associated with GER even while on acid suppressants

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2
Q

What are syndromes associated with Hirschsprungs

A

-T21
-Waardenburg-Shah syndrome
-Congenital central hypoventiliation syndrome (PHOX2B gene)
-Multiple endoscrine neoplasia (MEN)2
-Neurofibromatosis
Neuroblastoma
-rarely - Smith Lemi Opitz

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3
Q

What percentage of Hirschsprungs is limited to the rectum/distal sigmoid colon
What % is total colonic aganglionosis

A
  • 85% limited to rectum/distal SC

- 15% total colonic aganglionosis

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4
Q

What gene are associated with Hirschspurngs

A
  • RET
  • GDNF
  • GFRalpha1
  • NRTN
  • ET3
  • PHOX2b
  • SOX10
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5
Q

How high must a rectal suction biopsy be taken?

A

At least 2-3 cm above the dentate line because the very distal portion of the rectum normally lacks ganglion cells

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6
Q

What do you see on a Hirschsprung’s biopsy

A

-aganglinosis
-hypertrophied nerve trunks
increase level of acetylcholinesterases if stained for

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7
Q

What are risk factors of Hirschsprung’s disease associated enterocolitis (HAEC)

A
  • family history of HD
  • T21
  • long segment disease
  • previous episodes of HAEC
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8
Q

What are the 3 components of LES

A
  1. LES (hypertrophy of circular and longitudinal muscles layers of the esophagus)
  2. Crural diaphragm
  3. Sling and clasp muscle fibers

Crural diaphragm and sling/clasp muscle fibers lost in hiatal hernia - which is why they have a lower resting LES pressure

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9
Q

What is the resting pressure of the UES

A
  • between 30-150 mmHg
  • tonically contracted btw swallows
  • relaxation coordinated with pharyngeal contraction to receive the food bolus from hypopharynx
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10
Q

How in the LES innervated

A
  • vagal excitatory (acetylcholine) and inhibitory (NO, vasoactive intestinal peptide) fibers
  • resting pressure 10-45
  • relaxes at initiation of swallow and remains relaxed until peristaltic wave arrives and bolus passes
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11
Q

How is the upper 1/3 of esophagus innervated

A
  • striated muscle

- somatic efferent vagal cholinergic fibers originating from nucleus ambiguus

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12
Q

How is the lower 1/3 of the esophagus innervated

A

-smooth muscle
preganglionic vagus nerve fibers from dorsal motor nucleus that innervate excitatory cholinergic neruons and inhibitory nitronergic neurons of myenteric plexus

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13
Q

What are the differnent types of peristalsis in the Esophagus

A

Primary peristalsis:

  • initiated by swallowing
  • contracts at velocity of 2-4 cm/s
  • duration of 4 sec
  • 35-180 mmHg that propel food towards stomach

Secondary peristalsis:

  • initiated by luminal distension (refluxate and retained food)
  • resembles primary peristalsis

Tertiary peristalsis:
-spontaneous and/or simultaneous low-amplitude nonperistalitc contractions

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14
Q

How does the motility of the proximal stomach differ from the distal stomac

A

Proximal stomach:

  • reservoir with high distensibility
  • accommodates food
  • no basal electrical activity
  • slow tonic contractions

Distal stomach

  • mixing and grinding
  • low distensibility
  • slow waves of depolarization at 3/min
  • intermittent high pressure phasic antral contractions
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15
Q

What occurs in the stomach at the fasting state

A

Antral phase III of MMC:

  • high amplitude (>40 mmHg) rhythmic contractions of 3/min (lasting 3-7 mins) associated with maximum pyloric relaxation
  • allows clearance of undigested food residue

Phase III followed by Phase I:
-antral quiescense

Phase II:
mixture of low and high pressure waves

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16
Q

What occurs in the stomach during the fed state

A

-meal ingestion = proximal stomach relaxation via 2 vagally mediated phas

a) Receptive relaxation: rapid relaxation of proximal stomach - initiated by deglutition
b) Adaptive relaxation or gastric accomodation: maintenance of gastric relaxation through activate gastric wall mechanoreceptors by food bolus

  • slow tonic contractions of the fundus regulate intragastric pressure and aid in transfer of solids into the distal stomach
  • slow wave depolarization at 3/min originate in gastric corpus (pacemaker region) - propagate circumferentially to pylorus moving solid bolus to pylorus
  • intermittent high-pressure phasic antral contractions against a closed pylorus continuously grind and homogenized food particles (retropulsion) down to < 1 mm to allow for passage through pylorus
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17
Q

What are the MMCs that occur in the fasting state in the Small Intestine

A

Phase I: motor quiescence
Phase II: irregular and intermittent contractions varying amp and freq
Phase III: regular rhythmic peristaltic contractions that migrate from distal stomach to ileum with contractions in antrum at 3/min and small intestine 11-12/min (>20 mmHg)
-housekeepr - sweeps intestinal content into ileum

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18
Q

What occurs in the SI in the fed state

A
  • irregular and random bursts of contractions of varying amp - for mixing and absorption
  • w/n 5-10 mins of starting a meal, peaks in 10-20 mins
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19
Q

What are the 2 primary contractions of colonic motility

A
  1. Segmental:
    - short and long duration arrhythmic contractions - mixing of luminal content
  2. Propagated
    - low-amplitude propagated contractions: < 50 mmHg in amplitude
    - high-amplitude propagated contracts (HAPCs): > 60 mmHg, last > 10 sec and propagate over 30 cm of colon
    a) originates in proximal colon and propels content distally to sigmoid colon
    - 4-6x/day - after meals, morning and prior to defecation
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20
Q

Gastrocolic reflux

A
  • segmental contractions - phasic and tonic activity in colon (postprandial increase in motility index > 15%)
  • w/n few minutes of start of meal and may last up to 3 hours
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21
Q

Internal Anal sphcinter

A
  • smooth muscle

- 75-85% of intra-anal pressures

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22
Q

External Anal sphcinter

A
  • striated muscle

- 15-25% of intra-anal pressures

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23
Q

What is RAIR

A

-distention of rectal wall by fecal bolus

RAIR =rectoanal inhibitory reflux

  • reflux relaxation of IAS and transient contraction of EAS
  • independent of the spinal reflux
  • absent when there is lack of inhibitor ganglion cells

-allows rectal content to come into contact with specialized receptors in anal canal - allow differentiation btw gas, liquid or solid (sampling reflux)

Rectum accomodates and IAS recovers as we conciously decided to defecate or not

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24
Q

How does defecation occur

A

Defection desired:

  • Valsalva and forward peristalsis of fecal content
  • widening of anorectal angle
  • IAS relaxation
  • voluntary EAS relaxation

Defection not desired:

  • voluntary contraction of EAS
  • reverse peristalsis and rectal accommodation
  • maintained acute anorectal angle
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25
Q

Functions of ACh

A

-primary stimulant of GI motility
-increase mucosal secretions
-decrease neurotransmitter release
-dilates artery
releases enteric hormones

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26
Q

Neurotransmitters for stimulating motility and inhibitiy motility

A

Stimulating:

  • ACh
  • Serotonin

Inhibiting

  • norepinephrine
  • NO
  • Vasoactive peptide
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27
Q

Role of the Enteric nervous system

A
  • GI motility
  • Gastric, intestinal, pancreatic and biliary secretion
  • local blood flow
  • fluid flux
  • digestion
  • mucosal immunity
  • secretion of GI hormones
  • intestinal epithelial barrier function
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28
Q

Myenteric (Auerbach Plexus)

A
  • located btw longitudinal and circular muscle layers in muscularis externa
  • extends from mid esophagus to internal anal sphicnter
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29
Q

Submucosal (meissner) plexus

A
  • located within dense fibrous connective tissue of the submucosa
  • absent in esophagus, sparse in stomach and well developed SI and LI
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30
Q

Difference between Afferent and efferent

A

Afferent:
-sensory projection to the CNS that communicate signals from GI tract

Efferent:
-projection from CNS to gut that influence motility and secretion

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31
Q

ENS/CNS control of gut

A
  • UES and LES controlled entirely by CNS
  • NES plays role in mid and distal esophageal motility only
  • Gastric motility largely controlled by CNS through vagal projections but ENS also plays a role
  • Small/large bowel primarily by ENS but CNS can modulate rates of motility
  • Defecation is largely regulated by the CNS (lumbosacral spinal cord) but internal anal sphincter function requires an intake ENS
32
Q

What is triple A syndrome (Allgrove syndrome)

A

Achalasia
Alacrima
Addison’s disease

33
Q

Causes of Achalasia

A

-Can be primary or secondary

Secondary:

  • Chagas disease and other infections
  • Genetic disorders
  • Autoimmunity
34
Q

Management for Achalasia

A

1) Pneumatic dilation - tear the LES muscle fibers - successful in 60% - recurrent common
2) Laparoscopic Heller myotomy - longitudinal divison of the LES muscle and proximal stomach and often fundo
3) POEM- peroral endoscopic myotomy

4) Other interventions: botux injection into LES and medications to decrease LES pressure:
- nitrates
- Ca channel blockers
- phosphodiesterase inhibitors

35
Q

Diffuse esophageal spasms

A
  • intermittent dysphagia and chest pain

- esophageal manometry: simultaneous distal esophageal contractions after > 20% of wet swallows

36
Q

Nutcracker esophagus

A
  • intermittent dysphagia and chest pain
  • high amplitude peristaltic contractions
  • associated with increased somatization, anxiety and depression
37
Q

Causes of gastroparesis

A 
Idiopathic (70%)
Drug induced (18%)
Post surgical (12.5%)
Post infectious (5%)
Associated with DM (4%)
38
Q

When does postinfectious gastroparesis occur and how long does it last

A

Can occur days to months after acute infection

-Generally resolves spontaneously after 6-18 months

39
Q

How do you diagnosis gastroparesis

How do you define delayed emptying

A

-4 hour solid-phase gastric emptying study showing delay is the gold standard for dx

Delayed emptying:
> 60% remaining at 2 hours
or
> 10% at 4 hours

40
Q

Management for Gastroparesis

A

a. dietary modifications:
- more frequent, smaller meals
- avoid high fat/fiber food
- avoid carbonated beverages

b. Prokinetics: erythromycin, metaclopramide and domperidone
c. Antiemetics
d. Botox injections
e. Gastric electrical stimulation- improves symptoms w/o improving gastric emptying

41
Q

What is MMIHS

A

-megacystic-microcolon-intestinal hypoperistaslsis syndrome

  • involves GI dysmotiligy
  • urinary tract involvement
  • microcolon
42
Q

What are they different classifications of CIPO

A
  • neuropathic
  • mypothatic
  • mesenchymopathic defect
43
Q

Evaluation for CIPO

A

-x-rays, contrast studies

Manometry:

  • can identify affected segments, assess severity and guide prognosis/management
  • Antroduodenal manometry: abnormal in nearly all CIPO pts and presence of Phase 3 MMC good prognostic factor

-Full thickness bx to look for underlying mechanism

44
Q

What medications can be used in CIPO

A

Prokinetics:
erythromycin
Cisapride/prucalopride
Octreotide

Acetylcholinesterase inhibitors:

  • neostigmine
  • pyridostigmine
45
Q

Major peristaltic disorders of the esophagus

A
  • absent contractility
  • distal esophageal spasm
  • hypercontractile esophagus (jackhammer)
46
Q

EM findings in achalasia (Chicago Classification)

A

Incomplete LES relaxation (to baseline) and increased baseline pressure (IRP) plus:

Type I (classic): 100% failed peristalsis; minimal pressurization within the esophagus

Type II (with esophageal compression): failed peristalsis: panesophageal pressurization with >/20% of swallows

Type III (spastic achalasia): failed peristalsis; preserved fragments of nonpropagating distal peristalsis or premature (spastic) contractions

47
Q

Phases of an Antroduodenamanometry study

A

a) fasting: measure >/3 hours

b) med challenge:
- erythro IV if no small bowel phase 3 MMC seen during fast
- octreotide SC if no phase 3 MMC seen during fasting or during IV erythromycine

c) Postparandial l :
- 1 hour after standardized meal provided

48
Q

Normal findings in ADM study

A
  • presence of phase 3 MMC (indicator of GI neuromuscular integrity) during fasting; IV erytho of SC ocreotide
  • presence of fed response or interruption of fasting pattern after meal
49
Q

Abnormal findings in ADM study

A

CIPO: absence of abnormal propagation of phase 3 MMC

Gastroparesis: postprandial antral hypomotility, decreased amplitude antral contractios (< 20mmHg after meal)

Rumination: presence of R waves or simultaneous contractions associated with regurgitation

Mechanical obstruction: presence of clustered, simultaneous contractions of long duration (>30 mins)

50
Q

Phases of Colonic Manometry

A

a. Fasting: measurement of 1-2 hrs
b. Postprandial: >/1 hr after standardized meal provided (20kcal/kg) > 30% kcal from lipids) given over 30-60 mins
c. Medication challenge: >/1 hr after standard bisacodyl dose (0.25) given via motility catheter lumen

51
Q

Normal findings for Colonic Manometry

A
  • Fasting phase: segmental contractions or presence of HAPCs (amplitude > 60 mmHg propagating > 30 cm of colon)
  • Postparandial: presence of gastrocolic response (increase in colon motility)
  • Postbisacodyl phase: presence of HAPCs and increase in segmental contractions
52
Q

Abnormal study for Colonic Manometry

A
  • abnormal propagation of HAPCs may indicate segmental colonic dysfunction
  • absent HAPCs, motility or postprandial response may indicate severe colonic dysfunction
53
Q

Indications for Anorectal Manometry

A
  • suspected nonrelaxing IAS
  • suspected hirschsprung
  • diagnose pelvic floor dyssynergia
  • candidates for biofeedback therapy (older pts)
  • evaluation of fecal incontienence
  • evaluate imperforated anus after surgical correction
  • evaluate postoperative HD with obstructive symptoms
  • evaluate for spinal problems potentially affecting anorectal function
54
Q

How to perform ARM

A
  • measurement of IAS resting pressure
  • rectal balloon is distended at different volumes to elicit the rectal anal inhibitory reflex (RAIR)
  • if cooperative, pt asked to squeeze and bear down and indicate sensation at different balloon volumes
55
Q

Normal ARM findings

A
  • normal baseline IAS resting pressure and presence of RAIR

- normal squeeze and bear down efforts

56
Q

Abnormal ARM findings

A

Hirschsprung disease: absent RAIR (absent ganglion cells on rectal suction bx)

Nonrelaxing IAS (IAS achalasia): absent RAIR (ganglion cells present on rectal bx)

Anismus/dyssynergia: paradoxical contraction of anal sphincter/puborectalis during attempted defecation

Presence of rectal spams and/or prolonged IAS relaxation with sustained balloon distentions: suggestive of spinal neuropathy

57
Q

How does Dopamine antagonists work

A

Dopamine due to activation of D2 dopamine receptors decreases

  • LES tone
  • gastric
  • impairs antroduodneal coordination

Dopamine antagonists block these inhibitory receptors
= prokinetic effect
= increased LES pressure, rate of gastric emptying and antroduodenal contractions

Metoclopramide and Domperidone

58
Q

Metaclopramide MOA

A
  • D2 receptor antagonist (D2RA)
  • moderate partial 5HT4 receptor agonist = ACh release
  • Weak 5-HT3 antagonist

Site of action:
Anti-emetic = D2RA in chemoreceptor Trigger zone (CTZ)
-prokinetic = limited to esophagus, stomach and duodenum

Common side effects: restlessness, drowsiness, dizziness and dystonic reactions

59
Q

Domperidone MOA

A

-Peripheral D2RA and D3RA

Site of action:

  • Antiemetic activity: D2/D3 in CTZ; poor CNS system penetration
  • Prokinetic = limited to esophagus, stomach and duodenum

Adverse effects:
-headache, somnolence, diarrhea, abdo pain, hyperprolactinemia leading to galactorrhea and lactation and menstrual irregularity

60
Q

How do serotonergic agents work

A

Serotonin (5-H) regulates the initiation of peristaltic reflex on enteric neurons

5-HT4 agonists - release ACh to cause peristalsis

5HT1 receptors control accommodation by increase NO

5HT3 receptors induce nausea and vomiting

61
Q

Cisapride MOA

A
  • Nonselective 5HT4 agonist promotes ACh release from myenteric plexus (longitudinal muscles in GI tract)
  • partial weak 5-HT3 receptor anagonist

Site of action

  • Antiemetic activity: 5HT3 receptor agonist in CTZ
  • Prokinetic activity: increase LES pressure and esophageal motility, increase gastric emptying, improves antroduodenal coordination and decrease colonic transit time

Adverse effects: HA/N/V/AP, rhinitis and diarrhea
-serious AE: prolong QT, ventricular arrhythmias and Torsades

62
Q

Motilin effects

A

Motilin initiates phase III MMC

-motilin receptors present from stomach to TI - highest density in upper gut

63
Q

Erythromycin

A

-macrolide abx mimics motilin effect on smooth muscles and enteric neurons

Site of action:
motilin receptors in gastric antrum and proximal duodneum

Adverse effects:
N/V/D/AP
anorexia, rash
increase transaminiases, jaundice
prolong QT

Uncommon - hepatotoxicity, Erythema multiforme, SJS

64
Q

Cyproheptidine

A

-antagonizes central and peripheral H1 along with 5HT receptors

Site of action

  • Completely antagonizes H1 receptors in the Gi tract, uterus, large blood vessels and bronchial smooth muscle
  • Competes with 5HT at intestinal smooth muscle receptors
  • Antagonism of 5HT on the appetite center of the hypothalamus

Adverse effects:
sedation, anticholinergic effects, appetite stimulation and weight gain

65
Q

How does octreotide work for motility

A

-somatostatin receptor agonist

Site of action:
-prolongs gastric emptying time by resetting MMC (phase III) to fasting level

Adverse effects:
AP/D/N/V ileus, abdo distension, epigastric pain, abdo tenderness, bradycardia, growth retardation, cholelithiasis and gallbladder sludge

66
Q

How does Botox A work

A

-Neurotoxin that prevents ACh release from cholinergic neurons- causing temporary chemical denervation

Works at injection site

AE:
rare when used locally but could cause paralysis of surrounding gastric wall

67
Q

Risk factors for IBS

A
  • chronic stress
  • anxiety
  • depression
  • atopic history
  • history of trauma/abuse
  • acute gastroenteritis
  • intestinal dysbiosis
68
Q

4 subtypes of IBS

A
  • diarrhea predominant (IBS-D)
  • constipation predominant (IBS-C)
  • mixed type (IBS-M)
  • pain predominant (IBS-P)
69
Q

Laxative classes

A
  • Stimulants: senna and bisacodyl
  • Osmotic agents: PEG, Milk of magnesia, Lactulose
  • Emollients: docusate and mineral oil
70
Q

What are the 2 subtypes of Functional Dyspepsia

A

Postprandial distress syndrome:
-postprandial fullness or earily satiation that prevents finishing a regular meal
upper abdominal bloating

Epigastric pain syndrome

  • epigastric pain or burning severe enough to interfere with normal activities
  • pain not generalized or localized to other abdominal or chest regions and not relieved by defecation or passage of flatus
    a. burning quality of the pain but without a restrosternal component
    b. Pain is commonly induced or relieved by a meal but may occur while fasting
71
Q

What is the antroduodenal manometry findings of rumination syndrome

A

-increased pressure in all recording sites known as “r” waves

Also on 24 hour impedance - will have increased activity during waking hours and non during sleep time - different from GERD

72
Q

Comorbid conditions associated with CVS

A
  • Anxiety/depression
  • constipation/IBS
  • POTS
  • fatigue
  • complex regional pain syndrome
  • paroxysmal and daily nausea
  • sleep disorders
73
Q

What is the Sato Variant

A

Variant of CVS:

surge in hyothalamic axis associated with HTN and elevated adrenocorticotropic hormone, ADH, coritsol and catecholamine levels

corticotrophin-release factor (inhibits foregut)

74
Q

Aprepitant MOA

A

-NK 1 antagonist

75
Q

Options for abortive therapy for CVS

A
  • Antimigraine agents: triptans (sumatriptan)
    -Antiemetics: 5HT3 (ondansetron), NK1 antagonist (aprepitant)
    -Analgesia: ketorolac or hydromorphone
    -Sedative: diphenhydramine, lorazepam, chlorpromazine
    Hydration- oral or IV use D10

Peds GI RC (12 decks)

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