Gastric Motility Flashcards
What are important components of gastric motility?
Gastric pacemaker: ICC located in proximal body along greater curvature.
Gastric slow waves: internal rhythm at 3 per minute with contraction threshold and a maximum contraction frequency
Describe mixing process in post-prandial phase
Food processing: mixing wave (contractions) and retropulsion
Food emptying via pyloric pump
Describe the emptying process in post-prandial phase: Liquids vs. Solids
Liquid: antroduodenal pressure gradient. Dependent on liquid volume
Solids: broken down into chyme then emptying contractions of pyloric pump
Rules of gastric emptying rate: volume, consistency and content
Large volume>smaller
Liquids>semiliquids>solids
Starch>protein>fat
How does duodenum regulate gastric emptying?
What activates duodenal feedback? (4)
Inhibits pyloric pump via neuronal and hormonal feedback.
It is activated by too much gastric acid, high protein or fat, excessive chyme volume, hypertonic fluids
What are the three feedback loops in the enterogastric nervous reflexes?
Inhibitor vagal efferent nerve
Enteric nerves connecting duodenum and stomach
Inhibitory sympathetic nerve fibers
Which hormones are involved in duodenal feedback? (4)
CCK, SS, DA, secretin
Describe the contraction pattern during the fasting phase
Full migrating motor complex (MMC) is 84-112minutes
Long phase I: no contractions
Shorter phase II: few irregular contractions
Brief phase III (5-10min): intense contractions– house keeping function and motilin
What are the major causes of gastroparesis?
Idiopathic (1 in 3) Post-surgical Diabetic Medication related (i.e narcotic) Others: paraneoplastic, rheumatologic, neurologic, myopathic
How common is diabetic gastropathy? In which type is it most prevalent
Observed in 50% of long-standing type I DM
Also occurs in Type II DM
What are the consequences of diabetic gastropathy? (4)
Delayed emptying of solids but rapid emptying of liquids
Bezoar formation
Poor blood sugar control– tendency to hypoglycemia
Malnutrition/weight loss
What are the clinical manifestations of gastroparesis?
Nausea Vomiting Early satiety Postprandial abdominal distention Postprandial abdominal pain
How is gastroparesis diagnosed?
Gastric emptying study: scintigraphy, radiolabeled eggbeaters with toast, jam and water
If retention>60% at 2hr or >10% at 4hr then you got it
Other diagnostic tests for gastric emptying (2)
Breath test involving labeled spirulina
SmartPill
How is gastroparesis managed? (4)
Lifestyle/dietary measures: small/frequent meals, low fat diet, glucose control in DM
Medications: prokinetic agents and antiemetics
Gastric electric stimulation
Surgery (2%)
What are common prokinetic agents (3)
Metocloprimaide (DA antagonist)
Domperidone (DA antagonist)
Erytromycin (Motilin agonist)
What are AE of common pro kinetics?
Metocloprimaide: prolactin, arrhythmia, extrapyramidal symptoms
Domperidone: prolactin, arrhythmia
Erythromycin: cramping, nausea, vomiting
What are indications for enteral nutrition?
Surgical jejunostomy Severe weight loss Repeated admissions for IVF/IV meds Inability to absorb meds due to vomiting Need for gastric decompressions
What is dumping syndrome? When is it seen?
Rapid gastric emptying of hypertonic liquids
Seen in gastrojejunostomy patients
Compare the clinical presentation of early dumping vs. late dumpying
Early dumping: nausea, flushing, syncope due release of vasoactive factors
Late dumping: hypoglycemia due to release of insulin
What is criteria for non-ulcer dyspepsia or functional dyspepsia?
Postprandial distress (early satiety, fullness from normal meal) or epigastric pain without structural disease
Describe motility observed in patients with non-ulcer dyspepsia
45% have delayed gastric emptying
Poor gastric compliance
Gastric dysrhythmias
Ineffective contraction patterns
How is NUD managed?
Meds: antisecretory therapy, prokinetics, gastric compliance enhancers, visceral perception blockers
Psychological approaches
