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GI motility disorders Flashcards

1
Q

Causes of motility disorders

A

ENS (missing, immature, damaged by infection, influenced by chemical substances) = neuropathic

Diseased GI muscles

Abnormalities of interstitial cells of Cajal (pacemakers)

CNS disorders

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2
Q

myopathic causes of motility disorders

A

genetic (muscular dystrophy) or acquired (progressive systemic sclerosis

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3
Q

Time course of swallowing

A

10 seconds for UES –> peristalsis –> LES relaxation

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4
Q

Patients with dysphagia and heartburn, unresponsive to H-pump inhibitors

A

Achalasia type 1 (absence of peristalsis, no LES relaxation)

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5
Q

multisystem disorder characterized by obliterative small vessel vasculitis, fibrosis of multiple organs

GI sx in 80-90% (smooth muscle atrophy, gut wall fibrosis)

A

Scleroderma/Progressive systemic sclerosis (PSS)

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6
Q

Effects of Scleroderma/PSS smooth muscle atrophy and gut wall fibrosis

A

smooth muscle atrophy –> weak peristalsis and LES –> dysphagia and GERD

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7
Q

Effects of unrelenting GERD

A

esophagitis –> stricture

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8
Q

peristalsis preserved, chest pain and dysphagia, due to possible overreactivity of excitatory nerves or overreactivity of sm muscle response

A

spastic disorders of the esophagus (eg: Jackhammer esophagus)

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9
Q

High concentration of cholinergic (excitatory) nerves in the esophagus

A

Body of esophagus –> peristalsis

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10
Q

High concentration of noncholinergic (inhibitory) nerves in the esophagus

A

near the LES –> relaxation

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11
Q

Physiology of gastric emptying

A

vagus –> inhibition of body tone

tonic pressure gradient –> liquid emptying

Vagally-mediated contractions –> solid emptying

Migrating motor complex –> emptying of residual solids during fasting state every 90-120 min

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12
Q

Location of interstitial cells of cajal

A

proximal body along greater curvature

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13
Q

discomfort or pain centered in the upper abdomen, usually related to eating

A

Dyspepsia

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14
Q

Organic causes of dyspepsia

A

PUD, atypical GERD, gastric/esophageal cancer, pancreatico-biliary disorders, food/drug (NSAIDs) intolerance

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15
Q

dyspepsia with no organic etiologies, impaired gastric accommodation

A

functional dyspepsia

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16
Q

dyspepsia prevalence

A

20-25%

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17
Q

clinical manifestations of gastroparesis

A

nausea, vomiting, early satiety (impaired gastric accommodation), postprandial abdominal distention, postprandial abdominal pain

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18
Q

impaired transit of food from the stomach to the duodenum

excluded mechanical obstruction of the gastric outlet

A

gastroparesis

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19
Q

major causes of gastroparesis

A

idiopathic, post-surgical (vagal nerve injury), diabetic, opiates, scleroderma, rheum, paraneoplastic

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20
Q

diagnosis of gastroparesis

A

gastric emptying study (labeled egg beaters with toast, jam, water)

abnormal: retention > 60% at 2h or > 10% at 4h

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21
Q

gastroparesis management

A

small, frequent meals; prokinetic/antiemetic meds; gastric electric stimulation; surgery

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22
Q

Types of small bowel motility disorders

A

neuropathic, myopathic, mixed

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23
Q

normal amplitude, but sustained bursts of uncoordinated phasic contractions

early return and increased frequency of MMC

A

neuropathic small bowel motility disorders

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24
Q

decreased amplitude of contractions or complete lack of any motor activity

A

myopathic small bowel motility disorders

25
Q

s/sx of mech obstruction without lesion

imaging –> dilation on bowel

major manifestation of small intestinal dysmotility

A

chronic intestinal pseudo-obstruction (CIPO)

26
Q

major complication of CIPO

A

stasis –> bacterial overgrowth –> fermentation and malabsorption

27
Q

Symptoms of CIPO

A

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

28
Q

etiologies of NEUROPATHIC small intestinal motility disorders

A

Degenerative neuropathies (eg Parkinson’s), Paraneoplastic Autoimmune (anti-Hu Ab), Chagas Disease, Diabetic neuropathy

29
Q

etiologies in mixed myopathic/neuropathic small intestinal motility disorders

A

infiltrative conditions (scleroderma, amyloidosis, eosinophilic gastroenteritis), idiopathic

30
Q

childhood CIPO

A

congenital, primary

absent MMC –> need IV nutrition

31
Q

function of the colon

A

transport, store, expel stool after absorbing majority of luminal fluid

32
Q

Two types of colonic motor activity

A

Haustra = low amplitude tonic/phasic contractions for mixing luminal contents

High-amplitude propagated contractions (HAPCs) for propelling

33
Q

When does colonic motility increase?

A

after meal (gastrocolonic response) and on awakening

34
Q

Major causes of constipation

A

DM, Myopathy (amyloid, scleroderma), Neurogenic (Hirschprung’s), dyssynergic defecation

35
Q

Colonic transit studies

A

Sitz marker, Scintigraphy, Wireless capsule

36
Q

Scintigraphy

A

isotope in delayed-release capsule dissolves in distal ileum, gamma camera scans in 4, 24, and 48h to show colonic distribution

37
Q

Sitz marker

A

24 radioopaque markers in a capsule given on Day 1 –> abd xray on Day 5

38
Q

Normal sitz marker result

A

less than 5 markers

39
Q

Sitz marker result consistent with defacatory disorder

A

more than 5 markers in recto-sigmoid

40
Q

Sitz marker result showing slow transit

A

more than 5 markers scattered throughout colon

41
Q

Area of the rectum/anal canal under voluntary control

A

puborectalis muscle, external anal sphincter

42
Q

control of internal anal sphincter muscle

A

autonomic innervation via pelvic plexus

43
Q

control of external anal sphincter muscle

A

pudendal nerve

44
Q

Purpose of anal manometry

A

evaluate incontinence and constipation

45
Q

anal monometry findings in Hirschprung’s

A

absent recto-anal inhibitory reflex

46
Q

congenital absence of myenteric neurons of distal colon (neuropathic motility disorder)

no recto-anal inhibitory reflex

A

Hirschprung’s disease

47
Q

Pelvic floor musculature changes on defecation

A

descent of pelvic floor –> straightening anorectal angle

relaxed external anal sphincter

48
Q

Conditions of pelvic floor dysfunction

A

anismus (high anal resting pressure), incomplete anal relaxation, paradoxical contraction of the pelvic floor and external anal sphincters (dyssynergia), rectal hyposensitivity, excessive perineal descent, rectocele

49
Q

Causes of pelvic floor dysfunction

A

bad toilet habits, painful defecation, obstetric or back injury, brain gut dysfunction

50
Q

diagnosis of dyssenergia

A

abnormal anorectal manometry –> paradoxical contraction of the pelvic floor and external anal sphincters

51
Q

Treatment of dyssynergia

A

biofeedback therapy

52
Q

altered esophageal peristalsis

A

achalasia, scleroderma

53
Q

altered LES relaxation

A

achalasia

54
Q

altered LES tonic contraction

A

scleroderma

55
Q

altered gastric receptive relaxation/accommodation

A

functional dyspepsia

56
Q

altered gastric emptying

A

gastroparesis, functional dyspepsia

57
Q

altered small bowel peristalsis

A

CIPO (scleroderma)

58
Q

altered colonic transit

A

scleroderma –> slow transit constipation

59
Q

sphincter dysfunction

A

Hirschprung’s, dyssynergic defecation

GI (19 decks)

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