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DEMS unit 1 > Motility Disorders > Flashcards

Motility Disorders Flashcards

1
Q

etiologies of GI motility disorder

A

CNS, neuropathic (enteric nervous system), myopathic, abnormalities in interstitial cells of Cajal

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2
Q

is esophagus skeletal or smooth muscle

A

upper = striated muscle, distal = smooth muscle

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3
Q

voluntary swallowing phase

A

chewing, bring bolus back with tongue, which raises soft palate and closes off nasopharynx

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4
Q

Dysphagia

A

difficulty swallowing/discomfort in swallowing

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5
Q

Achalasia

A

muscles in lower esophagus fail to relax and food can’t get into stomach

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6
Q

Scleroderma

A

multisystem disorder with obliterative small vessel vasculitis and connective tissue proliferation with fibrosis of multiple organs

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7
Q

Main pathologic abnormalities of GI tract in sclertoderma

A

smooth muscle atrophy and gut wall fibrosis

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8
Q

Esophageal manifestations of scleroderma

A

smooth muscle atrophy can cause weak peristalsis –> dysphagia

  • can also cause weak LES –> GERD
  • unrepentant gerd can lead to esophagitis and stricture
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9
Q

is smooth muscle atrophy and gut wall fibrosis myopathic or neuropathic

A

MYOPATHIC

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10
Q

how to diagnose esophageal disease

A

Esophageal manometry (transnasal probe)

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11
Q

Main characteristic of scleroderma patients

A

PERISTALSIS ABSENT due to atrophy of smooth muscle and weak LES

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12
Q

Main characteristic of spastic disorders of esophagus

A

PERISTALSIS PRESERVED!!

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13
Q

symptoms of spastic disorders of esophagus

A

chest pain, dysphagia

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14
Q

postulated pathophys of spastic disorders of esophagus

A

overactive excitatory nerves (neuropathic) or overreacting smooth muscle response (myopathic)

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15
Q

how are inhibitory nerves distributed in esophagus

A

fewer proximal and more as you go distal

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16
Q

Jackhammer esophagus

A

hypercontractile; contractions coordinated but excessive amplitlude

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17
Q

2 main ideas of stomach motility

A

retropulsion and receptive relaxation

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18
Q

Receptive relaxation

A

vagally-mediated inhibition of smooth muscle tone of stomach body–maintain low intragastric pressure

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19
Q

what drives liquid emptying

A

tonic pressure gradient

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20
Q

what drives solid emptying from stomach

A

vagall-mediated contractions and enteric nervous system

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21
Q

how are residual solids emptied

A

migrating motor complex every 90-120 minutes

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22
Q

what causes retropulsion

A

mixing/churning of stomach tries to push food contents along but pyloric sphincter only opens so much/too big of particles get retropulsed back for more digestion

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23
Q

Gastric reservoir function

A

receptive relaxation and accomodation

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24
Q

gastric accommodation

A

stomach likes to keep things low pressure, so smooth muscle relaxation due to mechanical distention (gastric mechanoreception from enteric nervous system); vasovagal response

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25
Q

Function of fundus/proximal body of stomach

A

storage

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26
Q

main function of distal body/antrum

A

processing/emptying

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27
Q

dyspepsia

A

syndromic term

- discomfort or pain centered in upper abdomen usually related to eating

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28
Q

symptoms of dyspepsia

A

postprandial heaviness, early satiety, epigastric pain or burning

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29
Q

organic causes of dyspepsia

A

PUD, atypical GERD, gastric/esophageal cancer, pancreaticobiliary disorders, food/drug (NSAIDs) intolerance

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30
Q

functional dyspepsia

A

when no organic causes found

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31
Q

prevalence of dyspepsia

A

20-25%

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32
Q

alterations in gastric motility in functional dyspepsia

A

40% have impaired gastric accomodation; 45% have imparied gastric emptying (gastroparesis)

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33
Q

Gastroparesis

A

impaired transit of food from stomach to duodenum (excludign mechanical obstruction of gastric outlet)

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34
Q

Clinical manifestations of gastroparesis

A

nausea, vomiting, early satiety, postprandial abdominal distention, postprandial abdominal pain

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35
Q

Major causes of gastroparesis

A

idiopathic-(postinfectious?), Post surgical, diabetic, med related, paraneoplastic syndrome, rheumatologic, neurologic, myopathic (scleroderma)

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36
Q

Diagnose gastrophoresis

A

Gastric emptying study

37
Q

how is a gastric emptying study performed

A

pt eats low fat EggBeaters radiolabeled with 1 mCi Technetium 99; microwaved/served wtih toast, jam, and water

  • take serial lpictures at 0,1,2,3,4 hours and look at percept of emptied food
  • abnormal when retention >60% at 2 hr or >10% at 4 hr
  • Normally almost gone at 4 hours
38
Q

How to manage gastrophoresis

A

small frequent meals, low-fat and low-residue diet, glucose control in diabetes, prokinetic agents, antiemetics, gastric electrical stimulation, surgery (2%)

39
Q

gastroparesis in funcitonal dyspepsia

A

up to 45% FD pts have delayed gastric emptying, potential pacemaker cell dysfunction/ineffective muscle function of distal stomach

  • ineffective antropyloroduodenal contraction patterns
40
Q

Small intestine size

A

21’ long 1” diameter with increased surface area due to villi/microvilli

41
Q

Small intestine motility

A

when fed–primary motility is segmentation (mixing)

  • when fasting– migrating motor complex
42
Q

Segmentation

A

mixing of contents to and fro in different segments of small bowel to increase exposure to mucosa for increasing changes of nutrient absorption; 9-12 contractions per min; total transit 3-5 hrs

43
Q

Migrating Motor complex

A

main motility of SI in fasting state; every 90-120 min have sequential orderly peristaltic wave from stomach to ileocecal valve to sweep gut between meals

44
Q

Main categories of SI motility disorders

A

Neuropathic and Myopathic; some diseases with features of both

45
Q

Neuropathic SI motility disorders

A

normal amplitude but sustained bursts of uncoordinated phasic contractions – not progression down small bowel
- early return of MMC and increased frequency which impairs absorption and can cause diarrhea by overwhelming digestive capacity of colon

46
Q

Myopathic SI motility disorders

A

decreased amplitude of contraction or complete lack of any motor activity

47
Q

Chronic Intestinal Pseudo Obstruction (CIPO)

A

signs/symptoms of small bowel without lesion obstructing flow of intestinal contents
- have dilation without transition of bowel on imaging

48
Q

major manifestation of small intestinal dysmotility

A

Chronic intestinal pseudo obstruction (CIPO)

49
Q

complication of CIPO

A

small intestinal bacterial overgrowth

stasis of contents –> bacterial overgrowth –> fermentation adn malabsorption

50
Q

symptoms of CIPO

A

nausea/vomiting, abd pain, distention, constipation, diarrhea, urinary symptoms

51
Q

Neuropathic etiologies of SI motility disorders

A

degenerative neuropathies(parkinsons), paraneoplastic autoimmune (anti-Hu Ab), Chagas dz, Diabetes associated (neuropathy)

52
Q

Mixed myopathic and neuropathic etiologies of SI motility disorders

A
  • infiltrative conditions (scleroderma, amyloidosis, eosinophilic gastroenteritis)
  • idiopathic
53
Q

CIPO in kids

A

mostly congenital, usually a primary condition (visceral neuropathy/myopathy), absent MMC predicts need for IV nutrition

54
Q

mortality of children with CIPO

A

1/3 infants born die in 1st year of life

55
Q

function of colon

A

transport, store and expel stool after absorbing majority of luminal fluid– try to maintain Intravascular volume

56
Q

Muscle in colon

A

smooth and skeletal; circular smooth (internal anal sphincter)– autonomic innervation by pelvic plexus

57
Q

Internal anal sphincter

A

circular smooth muscle innervated by pelvic plexus

58
Q

External anal sphincter

A

striated skeletal muscle innervated by pudendal nerve

59
Q

puborectalis muscle

A

striated-volitional

60
Q

which muscles to we voluntarily control in rectum

A

EAS and puborectalis

61
Q

types of motor activity in colon

A

Low amplitude tonic and phasic contractions; high amplitude propagated contractions

62
Q

role of low amplitude phasic and tonic contractions in colon

A

mix luminal contents (in Haustra) for increasing luminal fluid absorption

63
Q

role of high amplitude propagated contractions (HAPCs)

A

propelling contents forward

64
Q

what increases colonic motility

A

after a meal (gastrocolonic response) and on awakening

65
Q

Causes of constipation

A

drugs, mechanical block,

  • Metabolic (DM, hypoK, hyperCa, HypoMg, hypothyroid)
  • Myopathy (amyloid, scleroderma)
  • Neurogenic (Parkinson’s spinal cord injury, MS, autonomic nneuropathy, Hirschsprung’s)
  • Other: pregnancy, immobility
  • IBS-C
  • Refractory constipation: (normal transit, slow transit, dyssynergic defecation)
66
Q

colonic transit studies

A

Sitz marker, Scintography, Wireless capsule

67
Q

Sitz marker transit study

A

24 radioopaque makers in capsule given Day 1 – plain abdominal xray on day 5

  • 5 markers scattered throughout colon = slow transit (more myopathic or neuropathic motility disorder of colon)
  • > 5 markers in recto-sigmoid suggests defecatory disorder
68
Q

Scintography

A

Isotope in delayed–release capsule dissolves in alkaline pH of distal ileum
- gamma camera scans in 4, 24, 48 hrs to show colonic distribution

69
Q

disorders of esophageal peristalsis

A

achalasia, scleroderma

70
Q

disorders of LES relaxation

A

Achalasia

71
Q

disorders of LES tonic contraction:

A

scleroderma

72
Q

Disordered gastric receptive relaxation/accomodation

A

functional dyspepsia

73
Q

disorders with impaired gastric emptying

A

gastroparesis, functional dyspepsia

74
Q

disorder of impaired SI peristalsis

A

CIPO (scleroderma)

75
Q

disorders of impaired colonic transit

A

slow transit constipation (scleroderma)

76
Q

disorder of impaired sphincter dysfunciton

A

Hirschsprung’s, Dyssynergic defecation

77
Q

Tests for evaluating GI motility

A
  • Esophageal manometry for achalasia, scleroderma
  • gastric emptying study for gastroparesis
  • Anal manometry for Hirschsprung’s and dyssynergic defecation
78
Q

anal manometry

A
  • similar to esophageal manometry but diff muscles/probe

- evaluate incontinence (resting/volition squeeze, cough reflex, rectal sensation)

79
Q

Eval of constipation

A

anal resting pressure, attempted defecation lying left lateral, simulated defecation , recto-anal inhibitory reflex, rectal sensation

80
Q

in what disease is recto-anal inhibitory reflex absent

A

Hirschsprung’s

81
Q

Hirschsprung’s disease

A
  • congenital absence of myenteric neurons of distal colon (Neuropathic Motility Disorder)
82
Q

normal recto-anal inhibitory reflex

A

distended colon –> relaxation of internal anal sphincter

83
Q

abnormality in Hirschsprungs

A
  • can’t relax internal anal sphincter after distention –> rarely or hard to bypass IAS –> dilated ganglionic segment above segment lacking myenteric neurons
84
Q

role of puborectalis muscle

A
  • part of pelvic floor muscles
  • creates acute angle at rest to help maintain continence
  • strain to defecate –> straighten rectal canal and descend pelvic floor – easier to evacuate rectum– wider anorectal angle
85
Q

Pelvic Floor Dysfunction

A

inability to coordinate abdominal, rectoanal, and pelvic floor muscles during defecation

86
Q

symptoms of pelvic floor dysfunction

A
  • anismus (high anal resting pressure)
  • incomplete anal relaxation
  • paradoxical contraction of pelvic floor and external anal sphincters (dyssyndrgia)
  • rectal hyposensitivity
  • excessive perineal descent
  • rectocoele
87
Q

causes of pelvic floor distention

A

bad toilet habits, painful defecation (trauma to canal where relaxing painful), obstetric or back injury, brain gut dysfunction

88
Q

diagnose dyssynergia

A

abnormal anorectal manometry, reveals paradixical contraction of pelvic floor and EAS

89
Q

Treat pelvic floor dysfunction

A

biofeedback therapy effective

DEMS unit 1 (15 decks)

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