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
s/sx of mech obstruction without lesion imaging --> dilation on bowel major manifestation of small intestinal dysmotility
chronic intestinal pseudo-obstruction (CIPO)
26
major complication of CIPO
stasis --> bacterial overgrowth --> fermentation and malabsorption
27
Symptoms of CIPO
nausea/vomiting, abd pain, distention, constipation, diarrhea, urinary sx
28
etiologies of NEUROPATHIC small intestinal motility disorders
Degenerative neuropathies (eg Parkinson's), Paraneoplastic Autoimmune (anti-Hu Ab), Chagas Disease, Diabetic neuropathy
29
etiologies in mixed myopathic/neuropathic small intestinal motility disorders
infiltrative conditions (scleroderma, amyloidosis, eosinophilic gastroenteritis), idiopathic
30
childhood CIPO
congenital, primary absent MMC --> need IV nutrition
31
function of the colon
transport, store, expel stool after absorbing majority of luminal fluid
32
Two types of colonic motor activity
Haustra = low amplitude tonic/phasic contractions for mixing luminal contents High-amplitude propagated contractions (HAPCs) for propelling
33
When does colonic motility increase?
after meal (gastrocolonic response) and on awakening
34
Major causes of constipation
DM, Myopathy (amyloid, scleroderma), Neurogenic (Hirschprung's), dyssynergic defecation
35
Colonic transit studies
Sitz marker, Scintigraphy, Wireless capsule
36
Scintigraphy
isotope in delayed-release capsule dissolves in distal ileum, gamma camera scans in 4, 24, and 48h to show colonic distribution
37
Sitz marker
24 radioopaque markers in a capsule given on Day 1 --> abd xray on Day 5
38
Normal sitz marker result
less than 5 markers
39
Sitz marker result consistent with defacatory disorder
more than 5 markers in recto-sigmoid
40
Sitz marker result showing slow transit
more than 5 markers scattered throughout colon
41
Area of the rectum/anal canal under voluntary control
puborectalis muscle, external anal sphincter
42
control of internal anal sphincter muscle
autonomic innervation via pelvic plexus
43
control of external anal sphincter muscle
pudendal nerve
44
Purpose of anal manometry
evaluate incontinence and constipation
45
anal monometry findings in Hirschprung's
absent recto-anal inhibitory reflex
46
congenital absence of myenteric neurons of distal colon (neuropathic motility disorder) no recto-anal inhibitory reflex
Hirschprung's disease
47
Pelvic floor musculature changes on defecation
descent of pelvic floor --> straightening anorectal angle relaxed external anal sphincter
48
Conditions of pelvic floor dysfunction
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
Causes of pelvic floor dysfunction
bad toilet habits, painful defecation, obstetric or back injury, brain gut dysfunction
50
diagnosis of dyssenergia
abnormal anorectal manometry --> paradoxical contraction of the pelvic floor and external anal sphincters
51
Treatment of dyssynergia
biofeedback therapy
52
altered esophageal peristalsis
achalasia, scleroderma
53
altered LES relaxation
achalasia
54
altered LES tonic contraction
scleroderma
55
altered gastric receptive relaxation/accommodation
functional dyspepsia
56
altered gastric emptying
gastroparesis, functional dyspepsia
57
altered small bowel peristalsis
CIPO (scleroderma)
58
altered colonic transit
scleroderma --> slow transit constipation
59
sphincter dysfunction
Hirschprung's, dyssynergic defecation