Gastroparesis and disordered eating Flashcards

1
Q

Physiology of the stomach upon eating

A

1) The vagus nerve causes the fundus (top of the stomach) to become flaccid to allow for greater accommodation (more food). This increase in pressure is linked to post-prandial fullness
2) The vagus nerve then causes the fundus to contract and push food to the antrum, where rings of contractions occur (peristalsis)
3) Under vagal stimulation, the corpus then tightens again and pushes food into the antral mill
4) Peristalsis and antral contractions make food into smaller pieces before moving towards the pyloric sphincter

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2
Q

Definition of gastroparesis: symptoms, prevalence, causes

A
  • delays in the progression of food from the stomach into the intestine
  • symptoms: nausea, postprandial fullness, early satiety + vomiting
  • prevalence: 10-30 per 100,000
  • causes: 35.6% idiopathic (unknown cause), 29% diabetes, 13% surgical
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3
Q

Diabetic gastroparesis causes

A
  • myenteric plexus affected
  • atrophy of smooth muscle cells
  • loss of interstitial cells of cajal (mesenchymal cells which are the ‘pacemakers of the gut’ which limits contractile potential)
  • loss of nitric oxide synthase in the enteric nerves
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4
Q

Post-surgery gastroparesis causes

A
  • damage to the vagal nerve
  • constitutively open esophageal sphincter and closed pyloric sphincter
  • causes: nausea + bloating: reduced ability to relax and regain tone
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5
Q

Diagnosis gastroparesis: endoscopy, scintigraphy, wireless pH motility capsule

A
  • endoscopy: upper GI imaging
  • scintigraphy: nuclear medicine study, ingestion of nuclear biomarker with food (at least 30-40% fat containing) with radioactivity measured at fixed intervals. If food not left stomach at 180 minutes then likely to have gastroparesis
  • wireless pH motility capsule: pH falls when in stomach and increases again upon emptying into the intestine
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6
Q

Functional dyspepsia: the 2 types, definitions, what is the difference compared to gastroparesis

A
  • 2 types: post-prandial dyspepsia (nausea, bloating, vomiting after a meal), epigastric pain syndrome (upper abdominal pain and stomach cramps after eating)
  • the difference compared to gastroparesis is that there are similar symptoms but may or may not have dysfunctional emptying (gastroparesis is defined by delayed emptying)
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7
Q

Causes of functional dyspepsia

A
  • hyper-sensitivity reaction to foods in the stomach: gastric distention, duodenal lipid, acid, luminal gas
  • altered cognition upon anticipation of foods: delayed emptying, distributed intragastric distribution, decreased gastric accommodation, increased antral distention
  • may also be due to lifestyle factors such as smoking, alcohol, high fat foods
  • high stress and anxiety may also contribute to symptoms
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8
Q

Bio-psycho-social model for management of functional dyspepsia

A
  • anxiety and stress can lead to dyspepsia symptoms: increased fullness, reduced emptying, impaired accommodation
  • this may lead to disordered eating habits and avoidance of foods which may increase weight loss and perpetuate the problem
  • also common in ED (80% AN patients)
  • therefore also need to manage the anxiety/stress component
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9
Q

3 classifications for gastroparesis

A
  • grade 1: mild, well managed and controlled and no nutrition implications
  • grade 2: moderate symptoms with partial control under pharmacotherapy, needs some dietary adjustments, have some hospital admissions
  • grade 3: severe symptoms, refractory and multiple hospital admissions
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10
Q

Treatment for gastroparesis (6)

A
  • prokinetics e.g. erythromycin (motilline receptor agonist, stimulates migrating motor complex in antrum but can lead to cardiac arrest), metaclopradmine (dopamine D2 receptor antagonism, but can lead to parkinsonian symptoms), domperidone (as with metoclopramide but doesn’t cross blood-brain barrier)
  • anti-emetics
  • weight moniotring
  • psychological interventions
  • dietetic interventions
  • gastric pacemaker: placed in laparoscopic procedure, electrodes placed on stomach and thought to stimulate the vagal nerve
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11
Q

Dietetic approaches to gastroparesis

A
  • avoid fatty foods as this can delay emptying
  • avoid high fibre foods as this can cause bezoars
  • have more liquid/softer consistencies as these are emptied from stomach faster
  • sweetened beverages preferred over water as more kcal
  • eat smaller meals and more frequently (4-5x per day)
  • cook and blenderise (if necessary) fruit and vegetables
  • avoid carbonated drinks, alcohol and smoking
  • always aim for oral feeding, if enteral feeds needed an NJ or jejunostomy is preferable. Jejunostomy may be needed as they are longer-term feed patients
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