134. GI Motility Flashcards

1
Q

What are Cajal Cells? How do they create the Staircase phenomenon?

What are migrating motor complexes?

A

Cajal: slow wave pacemakers in GI smooth muscle, oscillating resting membrane potential determines rhythm of GI contraction (slow undulating subthreshold Vm change), need additional stim for activation
Staircase phenomenon: slow wave freq decreases as you move distally thru GI tract

MMC: in duodenum/jejunum: delay of cajal activity (staircase) causes slow wave activity to sweep thru entire intestine length - slow waves have RATE OF PROPAGATION - help move bolus and clean out gut b/w meals

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2
Q

Swallowing: what body part acts to control food through the esophagus? How is it stimulated?

A

Lower Esophageal Sphincter: ICM/OLM
ICM: normally contracted - relaxed by NO when stim by Vagus Nerve (ACh)
Parasymp stim is BOTH excitatory and inhibitory: excite and inhibit neurons to relax and contract smooth muscle

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3
Q

Stomach Motility

  • Where is the pacemaker zone?
  • When does the stomach have highest motility?
  • How do pacemaker cells here operate?
  • what are the 2 functions of stomach? What is the mechanism of these functions?
A
  • Pacemaker zone: corpus/oxyntic zone
  • Highest motility when most acid/pepsinogen secreted
  • Slow waves determine freq of contraction and rate of propagation - NOT strength of contraction - require ACh to cause acid secretion and stim gut smooth muscle
  1. Storage: relax proximal stomach w/o raising intragastric pressure
    - mechanism: continue swallow reflex (relax LES and proximal stomach together); stretch in proximal stomach = relaxation of proximal stomach and depolarization of distal stomach = initiate slow wave contractions
    - Extrinsic Control: vago-vagal loop: sensory to brainstem - motor vagal to inhibitory fibers - NO/VIP - stomach relaxation
    - Intrinsic Control: ENS causes receptive relaxation w/o vagus nerve
  2. Mixing/Grinding: depolarization from pacemaker region to antrum = upward contraction (Retropulsion - Propulsion: Grinding)
    - Contractions to mix food up/down while pepsin degrades (makes CHYME)
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4
Q

Stomach motility:

  • How does the meal content affect stomach emptying?
  • How does the intestinal phase of digestion feedback into gastric emptying?
A
  • solid meal > protein solution > glucose solution (fastest); fatty meal > acid meal > salty meal (fastest)
  • High stomach acid in duodenum = secretin release from S Cells = hyperpolarizes stomach pacemakers (decrease slow wave freq and stomach emptying), decrease stomach acid production, increase bicarb secretion from pancreas
  • High fats in duodenum = CCK release = decrease stomach emptying, decrease stomach acid secretion (net inhibitory effect b/c less agonism than gastrin), increase exocrine pancrease enzyme secretion, decrease satiety
  • Hypertonicity in duodenum = decrease gastric emptying
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5
Q

Small Intestine Motility:

- what is the difference between peristalsis and segmentation? How are they under neural control?

A

Peristalsis: rhythmic activity based on slow wave freq, contractions generated by ENS (CM contracts behind bolus, LM contracts at bolus)
trigger - food bolus stretch (STRONG)
circuitry of ENS well mapped - drug targets (5HT agonists stimulate GI motility/peristalsis)
ENS control: NO/VIP = relaxation; ACh = contraction

Segmentation: reciprocal contractions/relaxations in CM - reverse in order to mix food and enzymes, move chyme against brush border, based on slow wave freq, requires ENS
trigger - distention (weak)
Circuitry of ENS well mapped - opiate ingestion locks gut in segmentation

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6
Q

How do sphincters act?

What mechanisms of colon motility exist?

A

LES, Pyloric, Ileocecal sphincters act as ONE-WAY Valves

  1. Haustral Contractions: segmentation in colon - shuttle fecal material back and forth (reverse peristalsis/contractions) to form hard stool
    - presence of fecal matter in rectum stimulates urgency/defecation
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