Gastric Motility Flashcards

1
Q

What are important components of gastric motility?

A

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

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2
Q

Describe mixing process in post-prandial phase

A

Food processing: mixing wave (contractions) and retropulsion

Food emptying via pyloric pump

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3
Q

Describe the emptying process in post-prandial phase: Liquids vs. Solids

A

Liquid: antroduodenal pressure gradient. Dependent on liquid volume

Solids: broken down into chyme then emptying contractions of pyloric pump

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4
Q

Rules of gastric emptying rate: volume, consistency and content

A

Large volume>smaller
Liquids>semiliquids>solids
Starch>protein>fat

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5
Q

How does duodenum regulate gastric emptying?

What activates duodenal feedback? (4)

A

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

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6
Q

What are the three feedback loops in the enterogastric nervous reflexes?

A

Inhibitor vagal efferent nerve
Enteric nerves connecting duodenum and stomach
Inhibitory sympathetic nerve fibers

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7
Q

Which hormones are involved in duodenal feedback? (4)

A

CCK, SS, DA, secretin

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8
Q

Describe the contraction pattern during the fasting phase

A

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

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9
Q

What are the major causes of gastroparesis?

A
Idiopathic (1 in 3)
Post-surgical
Diabetic
Medication related (i.e narcotic)
Others: paraneoplastic, rheumatologic, neurologic, myopathic
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10
Q

How common is diabetic gastropathy? In which type is it most prevalent

A

Observed in 50% of long-standing type I DM

Also occurs in Type II DM

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11
Q

What are the consequences of diabetic gastropathy? (4)

A

Delayed emptying of solids but rapid emptying of liquids
Bezoar formation
Poor blood sugar control– tendency to hypoglycemia
Malnutrition/weight loss

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12
Q

What are the clinical manifestations of gastroparesis?

A
Nausea 
Vomiting
Early satiety
Postprandial abdominal distention
Postprandial abdominal pain
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13
Q

How is gastroparesis diagnosed?

A

Gastric emptying study: scintigraphy, radiolabeled eggbeaters with toast, jam and water

If retention>60% at 2hr or >10% at 4hr then you got it

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14
Q

Other diagnostic tests for gastric emptying (2)

A

Breath test involving labeled spirulina

SmartPill

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15
Q

How is gastroparesis managed? (4)

A

Lifestyle/dietary measures: small/frequent meals, low fat diet, glucose control in DM
Medications: prokinetic agents and antiemetics
Gastric electric stimulation
Surgery (2%)

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16
Q

What are common prokinetic agents (3)

A

Metocloprimaide (DA antagonist)
Domperidone (DA antagonist)
Erytromycin (Motilin agonist)

17
Q

What are AE of common pro kinetics?

A

Metocloprimaide: prolactin, arrhythmia, extrapyramidal symptoms
Domperidone: prolactin, arrhythmia
Erythromycin: cramping, nausea, vomiting

18
Q

What are indications for enteral nutrition?

A
Surgical jejunostomy
Severe weight loss
Repeated admissions for IVF/IV meds
Inability to absorb meds due to vomiting
Need for gastric decompressions
19
Q

What is dumping syndrome? When is it seen?

A

Rapid gastric emptying of hypertonic liquids

Seen in gastrojejunostomy patients

20
Q

Compare the clinical presentation of early dumping vs. late dumpying

A

Early dumping: nausea, flushing, syncope due release of vasoactive factors
Late dumping: hypoglycemia due to release of insulin

21
Q

What is criteria for non-ulcer dyspepsia or functional dyspepsia?

A

Postprandial distress (early satiety, fullness from normal meal) or epigastric pain without structural disease

22
Q

Describe motility observed in patients with non-ulcer dyspepsia

A

45% have delayed gastric emptying
Poor gastric compliance
Gastric dysrhythmias
Ineffective contraction patterns

23
Q

How is NUD managed?

A

Meds: antisecretory therapy, prokinetics, gastric compliance enhancers, visceral perception blockers
Psychological approaches