GI Motility and Regulation Flashcards
Types of motility in the GI tract
Segmentation (mixing) (predominates)
Peristalsis (propulsive movements)– receptive relaxation occurs due to pressure produced by proximal bolus
-requires myenteric plexus
(stomach– BERs coordinated w/ vagal input leads to peristalsis)
Aboral movement: contraction of circ SM behind, longitudinal musc ahead, circ muscles
–smooth muscle with actin (thin) and myosin as major contractile prot. Complex b/t Ca and calmodulin activates myosin light chain kinase which phosphorylates myosin and allows cross bridge formation. Reverse thru dephosphorylation via myosin light chain phosphatase, inactivation of MLCK
BER and relation to smooth muscle contractile activity
Basic electrical rhythm or “slow waves”
- consist of upstroke depol, partial repolariz, and plateau potential that can last for several secs.
- no external stimulus required (~12/min; spont)
- BER is myogenic (muscle derived)
- each depolariz doesn’t cause contractions. Contrac only occurs when depolarization exceeds a specific membrane potential.
Stomach BER: 3/min
Duodenum BER: 12/min
describe how symp/parasymp systems communicate with intestinal smooth muscle
NE/adrenaline stimulates sympathetic NS; activation of SNS inhibits digestion
Parasympathetic NS (ACh) does opposite: stimulates digestions
Smooth muscle in GI tract
-unitary cell type (single unit)
held together by adherens junctions
communicates electrically via gap junctions
pacemaker cells with spontaneous activity
intriniscally produces BER and muscle tone without tension (myogenic properties)
Tension comes from NTs acting on muscle – role of ANS
Mast cell activity
endocrine
paracrine
neurocrine
Phases of Digestion
cephalic phase: neural control (gastric muscle contracts, body prepares itself for food)
gastric phase: neural early and hormonal
intestinal: mostly hormonal but some neural
swallowing 3 steps
voluntary stage 1: voluntary (oral cavity then bolus pushed by tongue to oropharynx)
pharyngeal stage 2: involuntary (glottis covers trachea; UES relaxes)
esophageal stage 3: involuntary (esophageal peristalsis)
Swallowing becomes a reflex after nasopharynx closed off (pharyngeal phase)
esophagus
transports and adjusts food temp
- has upper and lower esophageal sphincters
- muscular walls transition from skeletal to smooth muscle
- thick muscular walls produce strong peristaltic waves
Peristalsis:
LES relaxes just before bolus arrives
-peristalsis controlled by vagus n. (and myenteric complex)
LES
- gatekeeper b/t esophagus and stomach
- failure to relax due to damage/loss of enteric nerves of LES wall is “achalasia” and can make swallowing difficult
- inapprop LES relaxation can cause acid reflux and damage to the inner lining of the esophagus.
receptive relaxation of stomach and retropulsion
- in synchrony with relaxation of LES
- up to 1.5 L accomodated in stomach without marked increase in intra-gastric pressure
- regulated by vagus n
- contractions start (slow wave)
- push bolus toward antrum, but since pyloric opening is small, most content reflected back toward body of stomach (retropulsion)
- phase 3: contents
Gastrin
-hormone secreted in response to the presence of food in the stomach.
Gastrin also increases peristaltic contraction and decreases pyloric tone.
-the combination of distension and gastrin increase the rate of gastric emptying.
arrival of food in duodenum
- causes distention and irritation by acidity and solutions of high osmolarity
- leads to reflex inhibition of gastric peristalsis and increase in pyloric tone (duodenum controls delivery rate)
- liquification, pH adjustment, release of hormones, and addition of enzymes in response to food entering duodenum
- Key hormones: CCK, Secretin, GIP
- enzymatic digestion occurs in lumen and at enterocyte surface
- absorption of nutrients, water, and ions occurs via cellular/paracellular pathways
- both peristaltic and segmentation motility
arrival of fats in duodenum
- leads to secretion of CCK by enteric endocrine cells
- CCK decreases gastric motility
Rate of gastric emptying
- foods rich in carbs leave stomach in a few hrs
- protein rich foods leave more slowly
- emptying is slowest after meal containing fat
Emesis
-centrally regulated by vomiting center in brain
Steps:
-salivation (HCO3-) and sensation of nausea
-reverse peristalsis from upper small intestine to stomach
-abdominal muscles contract and UES and LES relax
-gastric contents ejected
Intestinal reflexes
-mediated by both ENS and external innervation:
Gastroileal reflex: stomach activity stimulates movement of chyme through the ileocecal sphincter
Gastrocolic reflex: food in stomach stimulates mass movement in colon
Mediated by the enteric nerves:
Localized perstaltic waves and segmentation mixing
Migrating Motor Complex (MMC)
- occurs in the absence of feeding (during fasting); 90-100 mins with 3 phases starting from the stomach and propagating aborally to ileocecal valve.
- “Motilin” hormone intitiates but neural component too
Phase I: quiescence occurs for 40-60 % of the 90 minute duration
Phase II: motility increases but contractions irregular; fails to propel luminal content; Lasts 20-30% of MMC
Phase III: 5-10 mins of intense contractions; from body of stomach to pylorus to duodenum to ileocecal valve
Pylorus fully opens
Ileocecal valve
- normally closed (to prevent reflux of bacteria from colon to ileum)
- opened by distention of end of ileum (local reflex)
- closed by distention of proximal colon (local reflex)
Colon
- reservoir for undigested foodstuff
- main func: reabsorb water, ions
- elimination of waste controlld by two sphincters: internal (involuntary) and external (voluntary) anal sphincters
Types of motility in large intestine/colon
haustration: muscles of the colon wall are contracted intermittently to divide the colon into functional segments known as haustra
mass movements: strong peristaltic waves 1-3x/d; wave of contraction that usually follows a meal and moves content over greater distance than regular peristalsis; colon remains contracted for a while
Overall movement is slow: 5-10cm/hr
rectoanal inhibitory reflex
- filling of the rectum causes relaxation of the internal anal sphincter via release of VIP and NO from intrinsic nerves.
- simultaneously, EAS contracts
evacutation
- defecation
- occurs when EAS is voluntarily relaxed and is enhanced by increased intra-abdominal pressure
