Motility Disorders of the GI Tract Flashcards

1
Q

What causes motility disorders?

A

ENS: missing, immature, damaged by infection, influenced by chemical substances; =Neuropathic

Diseased GI muscles: genetic defect (muscular dystrophy) or acquired (progressive systemic sclerosis) =Myopathic

Abnormalities of interstitial cells of Cajal– pacemaker

CNS disorders

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2
Q

Achalasia

A

seen as absence of esophageal peristalsis and no LES relaxation

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3
Q

Scleroderma/Progressive Systemic Sclerosis (PSS)

A

Multisystem disorder:

  • obliterative small vessel vasculitis
  • Connective tiss proliferation w/ fibrosis of multiple organs

GI manifestations in 80-90%
GI abnormalities: smooth muscle atrophy and gut wall fibrosis (thus a myopathic process)

Esophageal manifestations:
smooth muscle atrophy–>weak peristalsis–>dysphagia
SM atrophy–>weak LES–>GERD
Unrepentant GERD–>Esophagitis–>stricture

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4
Q

How do you dx esophageal disease?

A

esophageal manometry

seen with Scleroderm/PSS

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5
Q

Spastic Disorders of the esophagus

A
  • conditions of uncertain etiology
  • peristalsis PRESERVED
  • Sx: chest pain, dysphagia
  • poss pathophys: overactivity of excitatory nerves or overreactivity of smooth muscle response
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6
Q

physiology of gastric emptying

A
  • receptive relaxation (vagally mediated inhibition of body tone)
  • liquid emptying by tonic pressure gradient
  • solid emtying by vagally mediated contractions
  • residual solids emptied during non-fed state MMC every 90-120 mins
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7
Q

Gastric Motility

A

Gastric pacemaker:

  • interstitial cell of Cajal?
  • proximal body along greater curvature

Fundus and proximal body:
storage

Distal body and antrum
-processing and emptying

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8
Q

Receptive relaxation

A

swallowing induced vagal response

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9
Q

accomodation

A
  • smooth muscle relaxation elicited by mechanical distention of the stomach (Gastric mechanoreceptors)
  • vasovagal response
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10
Q

Dyspepsia

A
  • discomfort or pain centered in the upper abdomen usually related to eating
  • postprandial heaviness, early satiety, epigastric pain or burning

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

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11
Q

Functional dyspepsia

A

dyspepsia without organic etiologies

-40% w/ FD will have impaired gastric accommodation

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12
Q

Gastroparesis

A

“stomach paralysis”

  • impaired transit of food from the stomach to the duodenum
  • Mechanical obstruction of the gastric outlet excluded
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13
Q

Clinical Manifestations of gastroparesis

A

n/v, early satiety, postprandial abdominal distention or pain

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14
Q

Major causes of gastroparesis

A

idiopathic (?post infectious)
post surgical (vagal nerve injury): gastric, esophageal, thoracic surgical procedures (lung transplant)
Diabetic
Meds (opiates)
Others: paraneoplastic, rheumatologic, neurologic, myopathic (Scleroderma)

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15
Q

Dx of gastroparasis

A

-Gastric emptying study
gastric scintigraphy
Low fat EggBeaters w/ radiolabel
abnormal: retention >60% at 2 hr or >10% at 4 hr

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16
Q

Management of gastroparesis

A

Lifestyle/dietary: small and infrequent meals, low fat and low residue diet, glucose control in diabetics

Meds:
Prokinetic agents, antiemetics

Gastric electric stimulation

Surgery ~2%

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17
Q

Small Intestine motility fed vs fasted

A

-in fed state: primary motility is segmentation
-9-12 contractions/min (pacemaker cells)
-transit time 3-5 hrs
-Fasted state: Migrating motor complex: sequential orderly short peristaltic waves
stomach–>caudally
sweep gut b/t meals

18
Q

Small bowel motility disorders

A

Neuropathic:

  • normal amplitude, but sustained bursts of uncoordinated phasic contractions
  • early return and increased freq of MMC (can be bad because decrease absorption and can overwhelm the colon)

Myopathic:
decreased amp of contractions or lack of any motor activity

some diseases show both

19
Q

Chronic Intestinal Pseudo-Obstruction (CIPO)

A
  • signs/sx of mech obstruction of SI w/o lesion obstructing flow
  • dilation of the bowel on imaging
  • major manifestation of SI dysmotility
  • SI bacterial overgrowth =complication of CIPO: stasis–> bacterial overgrowth–>fermentation and malabsorption

Sx: n/v, abd pain, distention, constipation, diarrhea, urinary sx

20
Q

What might you see in myopathic forms of CIPO?

A

hypoactive motility

21
Q

Etiology of Small Intestinal Motility Disorders (and CIPO)

A

Neuropathic:

  • degenerative neuropathies (eg Parkinson’s)
  • Paraneoplastic Autoimmune (anti-Hu ab)
  • Diabetes associated (neuropathy)
  • Chagas Disease: parasite Trypanosoma cruzi

Mixed myopathic and neuropathic:

  • infiltrative conditions: **Scleroderma, amyloidosis, eosinophilic gastroenteritis
  • idiopathic
22
Q

CIPO in kids

A
  • mostly congenital
  • mostly primary condition (visceral neuropathy/myopathy)
  • absent MMC predicts need for IV nutrition
  • one third of infants born die in 1st year of life
23
Q

Two types of motor activity in Colon

A
  • low amp tonic and phasic contractions for mixing luminal contents (Haustra)
  • high amp propagated contractions (HAPCs) for propelling
24
Q

Causes of constipation

A

drugs
mechanical
metabolic: *DM, hyopK, hyperCa, hypoMg, hypothyroid
Myopathy: amyloid, scleroderma
Neurogenic: Parkinson’s, spinal cord injury, MS, autonomic neuropathy, Hirschsprung’s
Other: preg, immob
IBS-C
Normal transit, slow transit, dyssynergic defecation

25
Q

Colonic Transit studies

A
Sitz marker (get XR day 5; >5 markers in recto-sigmoid= defecatory disorder; >5 throughout colon =slow transit)
Scintigraphy (dissolves in alkaline distal ileum, scans 4, 24, 48 hrs show colonic distrib)
wireless capsule
26
Q

Evaluation of incontinence

A

-anal manometry

resting and volitional squeeze, cough reflex test, rectal sensation testing

27
Q

Eval of constip

A

-anal manometry
anal resting pressure, attempted defectation lying left lateral, simulated defecation w/ 50cc balloon, rectoanal inhibitory reflex (absent in Hirschsprung’s), rectal sensation testing

28
Q

Hirschsprung’s 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)
29
Q

internal and external anal sphincter muscle, puborectalis muscle

A

IAS: circular smooth; autonomic innervation: pelvic plexus

EAS: striated volitional
innervation: pudendal nerve

Puborectalis muscle: striated–volitional
(helps form anorectal angle; w/ contraction and descent of pelvic floor–>decreased angle)

30
Q

Pelvic floor dysfunction

A
  • inability to coordinate the abdominal, rectoanal, and pelvic floor muscles during defecation
  • anismus (high anal resting pressure)
  • incomplete anal relaxation
  • paradoxical contraction of pelvic floor and EAS (*dyssynergia)
  • rectal hyposensitivity
  • excessive perineal descent
  • rectocoele

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

31
Q

Dx of Dyssynergia

A

-abnormal anorectal manometry
-reveals: paradoxical contraction of pelvic floor and EAS
Tx: biofeedback therapy is effective

32
Q

Alteration of esophageal peristalsis

A

achalasia

scleroderma

33
Q

Alteration of LES relaxation

A

achalasia

34
Q

Alteration of LES tonic contraction

A

scleroderma

35
Q

Alteration of gastric receptive relaxation/accomodation

A

functional dyspepsia

36
Q

Alteration of gastric emptying

A

gastroparesis, functional dyspepsia

37
Q

Alteration of small bowel motility (peristalsis)

A

CIPO (scleroderma)

altered SI motility w/ underlying neuropathic cause: DM, primary pediatric visceral neuropathy

w/ underlying myopathic:
scleroderma, amyloidosis, primary pediatric visceral myopathy

38
Q

Alteration of colonic tranist

A

slow transit constipation (scleroderma)

39
Q

Alteration of sphincter function

A

Hirschsprung’s

Dyssynergic defecation

40
Q

Esophageal manometry can dx

A

achalasia

scleroderma

41
Q

Gastric emptying study (gastric scintigraphy) can dx

A

gastroparesis

42
Q

Anal manometry can dx

A

Hirschsprung’s

Dyssynergic defecation