GI motility disorders Flashcards

1
Q

What innervates the gut wall?

A

parasympathetic nerves from vagus nerve and pelvic nerve innervate the longitudinal muscle directly (pelvic only) and the myenteric plexus which innervates the circular muscle and submucosal plexus, which innervates the muscularis mucosaa and endocrine/secretory cells in mucosa

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2
Q

List processes that cause motility disorders

A

enteric nervous system problems (neuropathic), diseased GI muscles (myopathic), abnormalities of interstitial cells of Cajal (pacemaker) or central nervous system disorders

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3
Q

How long does it take for a swallowed bolus to reach the stomach

A

5-10 seconds

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4
Q

Components of esophageal function test

A

upper esophageal sphincter relaxation, proximal peristalsis (striated), propagation of swallow along esophageal body, distal peristalsis (smooth muscle), post-deglutitive lower esophageal sphincter relaxation

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5
Q

what does an esophageal function test show in pt with dysphagia and heartburn

A

UES relaxation but no peristalsis or LES relaxation

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6
Q

What is Scleroderma/Progressive Systemic Sclerosis (PSS)

A

Multisystem disorder characterized by: Obliterative small vessel vasculitis and Connective tissue proliferation with fibrosis of multiple organs. 80-90% have GI issues, including smooth muscle atrophy and gut wall fibrosis

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7
Q

Esophageal manifestations of Scleroderma/Progressive Systemic Sclerosis (PSS)

A

Smooth Muscle Atrophy > Weak Peristalsis >Dyspahgia.
Smooth Muscle Atrophy > Weak LES > GERD.
Unrepentant GERD > Esophagitis > StrictureSmooth Muscle Atrophy > Weak Peristalsis >Dyspahgia.
Smooth Muscle Atrophy > Weak LES > GERD.
Unrepentant GERD > Esophagitis > StrictureSmooth Muscle Atrophy > Weak Peristalsis >Dyspahgia.
Smooth Muscle Atrophy > Weak LES > GERD.
Unrepentant GERD > Esophagitis > Stricture

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8
Q

How are esophageal diseases diagnosed

A

esophageal manometry

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9
Q

scleroderma esophageal manometry results

A

UES relaxation but no peristalsis or LES relaxation

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10
Q

describe gastric motility patterns

A

retropulsion and receptive relaxation (gastric emptying)

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11
Q

describe physiology of gastric emptying

A

receptive relaxation occurs by vagally mediated inhibition of body tone. Liquid emptying occurs by tonic pressure gradient and solid emptying occurs by vagally mediated contractions. Residual solids are emptied during non fed state by MMC every 90-120 minutes

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12
Q

What is the gastric pacemaker

A

Interstitial cells of cajal located in proximal body along greater curvature.

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13
Q

Function of fundus/ proximal body and antrum/distal body

A

fundus/proximal body: storage. Antrum/distal body: processing and emptying

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14
Q

Factors contributing to gastric reservoir function

A

receptive relaxation and accommodation(where smooth muscle relaxation is elicitd by mechanical distention of the stomach and gastric mechanoreceptors)

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15
Q

What is functional dyspepsia

A

•Discomfort or pain centered in the upper abdomen. Includes postprandial heaviness, early satiety, epigastric pain or burning. No organic etiologies (such as PUD, atypical GERD, gastric cancer, pacreatico-biliary disorders, food/drug intolerance)

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16
Q

gastric motility in functional dyspepsia

A

40% have impaired gastric accomodation and delayed gastric emptying (caused by gastric dysrhytmias and ineffective antropyloroduodenal contraction patterns)

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17
Q

What is gastroparesis

A

stomach paralysis. Impaired transit of food from the stomach to the duodenum. Mechanical obstruction of the gastric outlet excluded

18
Q

Clinical features of gastroparesis

A

Nausea, Vomiting, Early satiety, Postprandial abdominal distention, Postprandial abdominal pain

19
Q

Causes of gastroparesis

A

idiopathic, post infectious, post-surgical (ie. vagal nerve injury), diabetes, medications (opiates), paraneoplastic, rheumatologic, neurologic, myopathic

20
Q

How is gastroparesis diagnosed

A

gastric empyting study: Abnormal: retention >60% at 2 hr or >10% at 4 hr

21
Q

gastroparesis management

A

Small frequent meals, low fat, low fiber, glucose control in diabetics, prokinetic agents, antiemetics, gastric electric stimulation and/or surgery

22
Q

describe normal motility in small intestine

A

Fed state: primary motility is segmentation, pacemaker cells facilitate 9-12 contractions per minute and total transit time is 3-5 hrs. Fasted state: migrating motor complex facilitates sequential short peristaltic waves from stomach caudally. This sweeps the gut between meals

23
Q

compare neuropathic vs myopathic small bowel motility disorders

A

Neuropathic: Normal amplitude but sustained bursts of uncoordinated phasic contractions. Early return of MMC. Increased frequency of MMC. Myopathic: Decreased amplitude of contractions or complete lack of any motor activity

24
Q

What is Chronic Intestinal Psuedo-Obstruction

A

•Signs and symptoms of mechanical obstruction of the small bowel without a lesion obstructing flow of intestinal contents. Characterized by the presence of dilation of the bowel on imaging. Manifestation of small intestinal dysmotility

25
Q

Complication of Chronic Intestinal Psuedo-Obstruction

A

small intestinal bacterial overgrowth

26
Q

Chronic Intestinal Psuedo-Obstruction symptoms

A

N/V, abdominal pain, distention, constipation, diarrhea, urinary symptoms

27
Q

Etiologies of small intestinal motility disorders

A

neuropathic: Degenerative Neuropathies (eg Parkinon’s) Paraneoplastic Autoimmune (anti-Hu Ab), Chagas Disease: parasite Trypanosoma cruzi, Diabetes associated (neuropathy). Myopathic and neuropathic: scleroderma, amyloidosis, eosinophilic gastroenteritis
neuropathic: Degenerative Neuropathies (eg Parkinon’s) Paraneoplastic Autoimmune (anti-Hu Ab), Chagas Disease: parasite Trypanosoma cruzi, Diabetes associated (neuropathy). Myopathic and neuropathic: scleroderma, amyloidosis, eosinophilic gastroenteritis

28
Q

childhood vs adult CIPO

A

In children: congenital, primary condition, absent MMC predicts need for IV nutrition. 1/3 die in 1st year

29
Q

Types of motor activity in colon

A

Low amplitude tonic and phasic contractions for mixing luminal contents (Haustra). High-amplitude propagated contractions (HAPCs) for propelling

30
Q

How is colon transit tested

A

Sitz marker, scintigraphy or wireless capsule

31
Q

describe scintigraphy

A

Isotope in delayed-release capsule dissolves in alkaline pH of distal ileum. Gamma camera scans in 4,24, and 48 hours to show colonic distribution

32
Q

Describe Sitz marker

A

24 radioopaque markers in a capsule given on Day 1. Plan abd xray on day 5. 5 markers in recto-sigmoid suggests defecatory disorder. >5 markers throughout colon= slow transit

33
Q

innervation of circular smooth muscle and striated muscle of rectum

A

circular smooth muscle: autonomic innervation by pelvic plexus. Striated-volitional muscle (puborectalis muscle) is innervated by pudendal nerve

34
Q

Function of anal manometry

A

provides comprehensive information regarding anal sphincter function at rest and during defecatory maneuvers. Evaluates incontinence: resting and volitional squeeze, cough reflex test, rectal sensation testing

35
Q

What is Hirschsprungs disease

A

Congenital absence of myenteric neurons of the distal colon (Neuropathic Motility Disorder). No reflex inhibition of the IAS following rectal distention (No Recto-anal inhibitory reflex)

36
Q

Hirschsprungs disease anal manometry results

A

megarectum/megacolon on defecography,

37
Q

What is pelvic floor dysfunction

A

•Inability to coordinate the abdominal, rectoanal and pelvic floor muscles during defecation. Results in anismus (high resting anal pressure), incomplete anal relaxation, Paradoxical contraction of the pelvic floor and external anal sphincters (dyssynergia)

38
Q

Pelvic floor dysfunction causes

A

bad toilet habits, Painful defecation, Obstetric or back injury, Brain gut dysfunction

39
Q

How is dyssynergia diagnosed?

A

Abnormal anorectal manometry. Reveals: Paradoxical contraction of the pelvic floor and external anal sphincters

40
Q

Treatment of dyssynergia

A

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