134. GI Motility Flashcards
What are Cajal Cells? How do they create the Staircase phenomenon?
What are migrating motor complexes?
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
Swallowing: what body part acts to control food through the esophagus? How is it stimulated?
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
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?
- 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
- 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 - Mixing/Grinding: depolarization from pacemaker region to antrum = upward contraction (Retropulsion - Propulsion: Grinding)
- Contractions to mix food up/down while pepsin degrades (makes CHYME)
Stomach motility:
- How does the meal content affect stomach emptying?
- How does the intestinal phase of digestion feedback into gastric emptying?
- 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
Small Intestine Motility:
- what is the difference between peristalsis and segmentation? How are they under neural control?
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
How do sphincters act?
What mechanisms of colon motility exist?
LES, Pyloric, Ileocecal sphincters act as ONE-WAY Valves
- 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