motility of the GI tract Flashcards
1
Q
what is the role of the GI tract?
A
to extract chemical energy, vitamins, minerals and water from ingested products
2
Q
what is the basic four layer structure of the GI tract? 4
A
- mucosa (epithelium, lamina propria, muscularis mucosae)
- submucosa ( artery, vein, submucosal nerve plexus)
- muscularis externa (circular muscle, myenteric nerve plexus, longitudinal muscle)
- serosa
3
Q
what are the functions of the:
oesophagus 1
stomach 4
small intestine 4
large intestine 3
A
Oesophagus:
- Transport
Stomach:
- Storage
- Secretion
- Mixing
- Digestion
Small intestine:
- Secretion
- Mixing
- Majority of digestion
- Absorption
Large intestine:
- Limited absorption
- Faeces formation
- Gut microbiota
4
Q
what is motility governed by? 4
A
- 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 is organised into connected bundles of outer longitudinal and inner circular smooth muscle in the muscularis layer
5
Q
how does motility occur? 4
A
- autonomously with external regulation
- the intrinsic nervous system (ENS) controls GI motility and secretion independently
- there are 2 interconnected plexuses in the gut wall, myenteric plexus and submucosal plexus
- extrinsic autonomic sympathetic and parasympathetic innervation allows central modification
6
Q
what is the intrinsic enteric nervous system? 3
A
- reflex contraction in response to local stimuli (stretch, nutrients, irritation, hormones)
- myenteric plexus (Auerbach’s) in muscularis layer for motility
- submucosal plexus (Meissner’s) in submucosal layer for secretion and local blood flow
7
Q
what is the extrinsic autonomic nervous system (ANS)? 3
A
- ANS modifies basal activity of the ENS
- parasympathetic innervation= excitatory to motility and secretion (via vagus and pelvic splanchnic nerves)
- sympathetic innervation= inhibitory to motility and secretion (via thoraco-lumbar innervation)
8
Q
how can hormonal secretion affect GI motility?
name 2 hormones?
A
- endocrine hormones are secreted by the entero-endocrine cells in the epithelial layer of the GI mucosa and enter the portal blood circulation
- cholecystokinin (CCK)
- motilin
9
Q
cholecystokinin (CCK)
- stimulus for secretion 3
- site of secretion
- actions 3
A
- protein
- fat
- acid
-I cells of the small intestine
- stimulates pancreatic secretions
- gallbladder contraction and growth of exocrine pancreas
- inhibits gastric emptying
10
Q
motilin
- stimulus for secretion 3
- site of secretion
- actions 2
A
- fat
- acid
- nerve
-M cells of the duodenum and jejunum
- stimulate gastric motility
- stimulates intestinal motility
11
Q
what mechanisms can cause contraction in the GI tract? 4
A
- Like all excitable cells, smooth muscle cells have a fluctuating negative electrical potential difference across the membrane
- Results in two types of electrical activity:
- Slow waves= cyclical oscillations of membrane potential spontaneously initiated by pacemaker ICCs
- Spike potentials= generated once threshold is reached resulting in Ca2+ influx and smooth muscle contraction
12
Q
describe the stimulation of smooth muscle contraction in the GI tract? 4
A
- Slow waves provide a basic electrical rhythm
- Spike potential causes contraction by further depolarisation to threshold levels
- Depolarisation stimulated by stretch, hormones, excitatory neurotransmitter acetylcholine release from the ENS excitatory motor neurons or P/S
- Inhibition by hyperpolarisation caused by inhibitory ENS, sympathetic NT norepinephrine or hormones
13
Q
what are the two types of contraction that occur in the GI tract?
A
- segmentation for mixing
- peristalsis for propulsion
14
Q
describe segmentation for mixing? 2
A
- bursts of circular muscle contraction and relaxation
- back and forth pendular movements also occur
15
Q
describe peristalsis for propulsion? 4
A
- Local distention triggers contraction behind bolus and relaxation in front
- Wave of contraction
- Requires functional myenteric plexus
- Law of intestines= movement aborally
16
Q
describe an end innervation dysfunction? 3
A
- Hirschsprung’s disease:
- A rare congenital absence of the myenteric plexus, usually involving a portion of the distal colon
- The pathological aganglionic section of colon lacks peristalsis and undergoes continuous spasm, leading to functional obstruction and sever constipation
17
Q
what are the three stages of swallowing? 3
A
- oral
- pharyngeal
- oesophageal
18
Q
describe the oral stage of swallowing? 4
A
- Under voluntary control
- Tongue pushes up against hard palate and contracts to force lubricated bolus into the pharynx
- The pharynx consists of the oropharynx, nasopharynx and laryngopharynx
- Bolus enters the oropharynx initiating the pharyngeal stage through stimulation of sensory receptors
19
Q
describe the pharyngeal phase of swallowing? 7
A
- Swallowing centre in the medulla oblongata and pons in the brain stem (reflex)
- Motor efferents in trigeminal, glossopharyngeal and vagal nerves cause series of muscle contractions moving bolus through oropharynx into laryngopharynx and into oesophagus
- Soft palate elevates over posterior nares to close nasal pharynx
- Epiglottis closes larynx
- Respiration is inhibited
- Upper oesophageal sphincter relaxes
- Pharyngeal muscle contraction propels bolus into oesophagus
20
Q
describe the oesophageal phase of swallowing? 6
A
- Primary peristalsis moves bolus downwards
- Circular muscle contracts behind bolus, longitudinal muscle contracts in front to shorten fibres and push wall outward
- Mucus lubricates and reduces friction
- Relaxation of lower oesophagus and lower oesophageal sphincter (LOW) occurs
- Secondary peristalsis stimulated by stretch
- Coordination is via intrinsic myenteric and extrinsic vagal innervation
21
Q
name some oesophageal motility dysfunctions? 2
A
- achalasia
- gastro-oesophageal reflux
22
Q
describe achalasia? 3
A
- LOS fails to relax causing food to remain in the oesophagus
- Cause may be vagal or myenteric defect
- Distension, inflammation, infection, ulceration
23
Q
describe gastro-oesophageal reflux? 3
A
- 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
24
Q
what are the 3 primary motor functions of the stomach?
A
- Storage= the vasovagal reflex mediates receptive relaxation reducing muscle tone and allowing reservoir function
- Mixing= fragmentation of food and mixing with secreted gastric juice for digestion
- Emptying contents into the duodenum at a controlled rate
25
Q
how does the mixing stage of the stomach happen? 3
A
- slow peristaltic wave are initiated in the body of the stomach moving stomach contents towards the pyloric antrum
- food is forced back for further mixing and digestion
- this process of propulsion and retropropulsion occurs in cycles to produce chyme
26
Q
describe the emptying stage of the stomach? 2
describe the regulation of this? 2
A
- highly regulated with primary inhibitory feedback signals from the small intestine
- more powerful peristaltic contractions build to force chyme into the duodenum
- excitatory= ENS/ANS neuronal stimulation and hormones (motilin)
- inhibitory= ANS regulation, duodenal enterogastric reflexes and hormones (CCK, secretin)
27
Q
how can we slow gastric emptying? 2
why do we do this?
A
- ANS/ENS reduction
- hormonal reduction
- to slow the presence of chyme in the duodenum and give enough time for digestion to occur
28
Q
name 2 gastric motility dysfunctions?
A
- dumping syndrome
- gastroparesis
29
Q
describe dumping syndrome? 4
A
- Rapid emptying of gastric contents into the small intestine
- Occurs following ingestion of a large meal after gastrectomy
- Characterised by nausea, pallor, sweating, cramps, vertigo and sometimes fainting within minutes
- May be cause by hypertonic duodenal contents causing rapid entrance of fluid
30
Q
describe gastroparesis? 5
A
- Stomach fails to empty
- Prevents proper digestion
- Causes bloating and nausea
- May be cause by gastric cancer or peptic ulcers
- Occasionally observed through impaired vagal stimulation to the stomach in severely diabetic patients who develop autonomic neuropathy
31
Q
describe motility in the small intestine? 3
A
- Motility patterns allow the majority of digestion and absorption of nutrients here over 3-5 hours
- Large surface area for absorption provided by circular folds (plicae circulares), villi projections of the mucosa and ‘brush border’ microvilli on the epithelial cell apical surface
- Two types of motility= mixing and circulation for maximum exposure to absorptive epithelium, propulsion of chyme aborally
32
Q
how is motility in the small intestine controlled? 4
A
- 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, hormones= excitation= gastrin, CCK, insulin, motilin, serotonin, inhibition=secretin and glucagon
33
Q
describe propulsive peristaltic reflexes? 6
A
- Gastroenteric reflex= gastric distention activates myenteric plexus to promote SI peristalsis
- Gastroileal reflex= gastric distention promotes peristalsis in the ileum to force chyme through ileocaecal valve into the caecum
- Migrating motor complex (MMC):
- Series of peristaltic contractions, between meals, every 90 mins sweeps contents into colon
- Intrinsic enteric control, hormone motilin
- Absence can lead to bacterial overgrowth
34
Q
describe disruption to peristalsis in the small intestine? 3
A
- Peristaltic rusk= mucosal irritation, ENS and ANS neural reflexes rapidly sweep contents of SI into colon
- Paralytic ileus= loss of peristalsis following mechanical trauma
- Vomiting= reverse peristalsis initiated in distal small intestine to expel intestinal and gastric contents
35
Q
describe motility in the small intestine? 3
A
- Motility is more sluggish to allow optimal absorption of water and electrolytes (proximal), formation and storage of faeces (distal)
- commensal microbiome aids, digestion, synthesises B and K vitamins
- Longitudinal muscle in muscularis thickened to form three bands, taniae coli, which tonically contract to form haustral bulges
36
Q
how is motility in the small intestine controlled? 5
A
- Via mixing and propulsion under intrinsic enteric control modified by neural and hormonal stimuli
- Mixing contractions via haustral churning
- Peristalsis:
- Mass movements occur 2-3x a day= forceful peristaltic contractions force contents into sigmoid colon and rectum
- Gastro-colic and duodeno-colic reflexes= mass movements occur after meals on stretching via ANS
37
Q
describe the defecation reflex? 5
A
- Initiate’s defecation to expel faeces containing residues of digestion, bacteria, bile pigment, mucosal debris
- Mass movements push faecal matter into normally empty rectum
- Stretch receptors in are stimulated and activate the ENS and parasympathetic ANS
- Involuntary contraction of longitudinal muscle in the rectum opens the internal anal sphincter
- the constricted external anal sphincter is voluntarily relaxed to allow defecation
