Motility of the GI tract Flashcards
Functions of organs
Oesophagus: transport
Stomach: storage, secretion, mixing, digestion
Small intestine: secretion, mixing, majority of digestion, absorption
Large intestine: limited absorption (water/ions), faeces formation, gut microbiota
Digestion depends on coordinated motility
Motility is governed by involuntary contraction of smooth muscle with pacemaker interstitial cells of Cajal (ICC)
Except upper oesophagus and external anal sphincter (striated skeletal muscle/voluntary)
Smooth muscle is a single unit - gap junctions allow electrical coupling and contraction as a functional syncytium
Smooth muscle organised into connected bundles of outer longitudinal and inner circular smooth muscle in muscularis layer
Motility occurs autonomously with external regulation
The intrinsic enteric NS controls CI motility and secretion independently
2 interconnected plexuses in gut wall - myenteric plexus, submucosal plexus
Extrinsic autonomic sympathetic and parasympathetic innervation allows central modification
Intrinsic Enteric Nervous System (ENS) and Extrinsic Autonomic Nervous System (ANS)
ENS: reflex contraction in response to local stimuli (stretch, nutrients, irritation, hormones); myenteric plexus (Auerbach’s) in muscularis layer; submucosal plexus (Meissner’s) in submucosal layer - secretion and local blood flow
ANS: ANS modifies basal activity of ENS - parasympathetic innervation: excitatory to motility and secretion (via Vagus and pelvic splanchnic nerves); sympathetic innervation - inhibitory to motility and secretion (via thoracolumbar innervation)
GI motility is affected by hormonal secretions
Hormones are secreted by entero-endocrine cells in the epithelial layer of the GI mucosa, and enter portal blood circulation
Cholecystokinin CCK is secreted into I cells of small intestine when there is protein, fat or acid here. It stimulates pancreatic secretions, gallbladder contraction and prevents gastric emptying.
Motilin, stimulated by fat, acid and nerve, is secreted into M cells of duodenum and jejunum, and stimulates gastric/intestinal motility
What mechanisms cause contraction
Smooth muscle cells have fluctuating negative electrical potential difference, resulting in 2 types of electrical activity
Slow waver: cyclic oscillations of membrane potential spontaneously initiated by pacemaker ICCs; provide a basic electrical rhythm (3-12 mins)
Spike potentials: generated once threshold is reached resulting in Ca2+ influx and smooth muscle contraction (causes contraction by further depolarisation to threshold levels)
Depolarisation stimulated by stretch, hormones, excitatory neurotransmitter acetylcholine release from ENS motor neurones or P/S
Inhibition by hyperpolarisation caused by inhibitory ENS, sympathetic NT noradrenaline or hormones (secretin)
2 types of contraction
Segmentation for mixing: bursts of circular muscle contraction and relaxation; back and forth pendular movements also occur
Peristalsis for propulsion: Local distension triggers contraction behind bolus and relaxation in front; wave of contraction; requires functional myenteric plexus; law of the intestines - movement aborally
ENS innervation dysfunction
Hirschsprung’s Disease: a rare congenital absence of myenteric plexus, usually involving a portion of the distal colon; the pathological aganglionic secretion of colon lacks peristalsis and undergoes continuous spasm, leading to functional obstruction and severe constipation
3 stages of swallowing (deglutition) - 1) oral phase; 2) pharyngeal phase; 3) oesophageal phase
1) under voluntary control; tongue pushes up against hard palate and contracts to force lubricated bolus into pharynx; bolus enters oropharynx initiating 2 through stimulation of sensory receptors.
2) (involuntary) Swallows centre in medulla oblongata and pons (reflex); motor efferents in trigeminal glossopharyngeal and vagal nerves cause series of muscle contractions moving bolus through oropharynx and into oesophagus
3) primary peristalsis moves bolus downwards; circular muscle contracts bolus, longitudinal muscle contracts in front to shorten fibres and push wall outward; mucus lubricates and reduces friction; relaxation of lower oesophageal sphincter (LOS) occurs; secondary peristalsis stimulated by stretch; coordination is via intrinsic myenteric and extrinsic vagal innervation
Oesophageal motility dysfunction
Achalasia: LOS fails to relax causing food to remain in oesophagus; may be caused due to vagal or myenteric defect; distension, inflammation, infection and ulceration
Gastro-oesophageal reflux: LOS tone lost leading to flow of acidic gastric contents into oesophagus; inflammation/ulceration; may be linked to hiatus hernia, where portion of stomach protrudes through diaphragm into thorax, causing gastric reflux
Stomach’s 3 primary motor functions - storage mixing emptying
Storage: Vasovagal reflex mediates receptive relaxation reducing muscle tone and allowing reservoir function
Mixing: Fragmentation of food and mixing with secreted gastric juice for digestion; slow peristaltic waves initiated in body of stomach, moving stomach contents towards pyloric antrum; food is forced back further for mixing and digestion - this process occurs in cycles to produce chyme
Emptying: Highly regulated with primary inhibitory feedback signals from s intestine; more powerful peristaltic contractions build to force chyme into duodenum
Regulation of emptying: excitatory - ENS/ANS neuronal stimulation and hormones (motilin); inhibitory - ANS regulation, duodenal enterogastric reflexes and hormones (CCK, secretin)
Gastric Motility Dysfunction
Dumping Syndrome: rapid emptying of gastric contents into small intestine; occurs following ingestion of large meal after gastrectomy; nausea, pallor, sweating, cramps, vertigo, fainting; may be caused by hypertonic duodenal contents causing rapid entrance of fluid.
Gastroparesis: stomach fails to empty; prevents proper digestion; causes bloating and nausea; may be caused by gastric cancer or peptic ulcers; occasionally observed through impaired vagal stimulation to stomach in severely diabetic patients who develop autonomic neuropathy
Small Intestine
Motility patterns allow the majority of digestion and absorption of nutrients over 3-5 hours here; larger SA provided by circular folds, villi and brush border microvilli on epithelial cell apical surface
Two types of motility: mixing and circulation for max exposure to absorptive epithelium & propulsion of chyme aborally
Motility in Small Intestine
Motility controlled by intrinsic motor patterns modified by hormonal and ANS neural stimuli
Segmentation for mixing: stretch receptors trigger myenteric stimulation of muscle contraction, no net movement
Propulsive peristalsis: stretch and hormones (excitation = gastrin, CCK, insulin, motilin, serotonin; inhibition = secretin and glucagon)
Propulsive Peristaltic Reflexes and Disruption to Peristalsis
PPRs: gastroenteric reflex -gastric distention activated myenteric plexus to promote SI peristalsis; Gastroileal reflex - gastric distention promotes peristalsis in the ileum to force chyme through ileocaecal valve into caecum
Migrating motor complex (MMC): series of peristaltic contractions between meals every 90 mins sweeps contents into colon; intrinsic enteric control (motilin); absence can lead to bacterial overgrowth.
Disruption: peristaltic rush - mucosal irritation, ENS and ANS rapid sweeps into colon; paralytic ileus - loss of peristalsis following mechanical trauma; vomiting - reverse peristalsis
