Transport along and across alimentary tract Flashcards
What is the sieving effect
sieving effect: viscous and solid matter are retained in the stomach
What are two main phases of gastric motility
1) Accommodation- to relax the stomach so it can receive food without increasing internal pressure
It does this by:
-There is a reduction in excitatory vagal input (less ACh) to the smooth muscle.
Inhibitory pathways (VIP/NO) are activated, causing relaxation of the stomach wall.
This is mediated by the vagal efferents acting via the myenteric plexus, using
VIP (vasoactive intestinal peptide) and NO (nitric oxide) as neurotransmitters.
2) Emptying- to contract the stomach and push food towards the duodenum.
It does this by:
Increased excitatory vagal input (more ACh) to the antrum, triggering contractions.
Inhibitory input (VIP/NO) is reduced in the proximal stomach, allowing contraction to occur.
What are all the neural components of accommodation and emptying
Pre-ganglionic vagal efferents: These are the initial signals from the brainstem (via the vagus nerve).
Myenteric plexus: Network of neurons in the stomach wall that coordinate local responses.
Post-ganglionic neurons: Located in the stomach wall, they release neurotransmitters like:
ACh (Acetylcholine): Excitatory → causes contraction.
VIP/NO: Inhibitory → causes relaxation.
What is gastric emptying dependent on?
Gastric emptying is dependent on:
1) propulsive force generated by the tonic contractions of the proximal stomach
2) stomach’s ability to differentiate the types of meals ingested and their composition
Explain gastric emptying of a liquid, semi solid and solid meal
-liquids pass through in spurts
-solids are broken down to 1-2mm sizes
-large indigestible materials remain; cleared by MMC or vomiting
What are different determinants of the rate of gastric motility
-type of food eaten: carbohydrate > protein > fatty food > indigestible food
-osmotic pressure of duodenal contents: hyperosmolar chyme causes decreased gastric emptying
-vagal innervation upon over-distension—-> decreased gastric motility
-hormones (CCK, samotastatin etc)—-> inhibit emptying
-injury to intestinal wall and bacterial infections —-> decrease motility
Explain myogenic control of gastric motility
-elicited by intrinsic basic electric rhythm (BER) from intestinal cells of cajal (ICC)
-pacemaker cells produce electric depolarisations
-BER allows the smooth muscle cell to depolarise and contract rhythmically when exposed to hormonal signals
-BER moves ripples towards the antrum
The rhythm of depolarisation-depolarisation creates the slow waves from ICC-mediate regular recurring migrating ripples known as BER
What mediates a decrease in fundic motor activity
the following mediate a decrease in fundic motor activity:
-cholecystokinin (CCK)
-secretin
-VIP
-somatostatin
-duodenal distension
What is the control of movement through the small intestine
-localised distension of the duodenum decreases motility
-hormonal and nervous factors initiate and maintains peristalsis and mixing
-cholecystokinin (CCK), gastrin and motility increase intestinal motility
-secretin deceases the activity
Explain how gastric emptying is regulated by negative feedback systems
Gastric emptying is regulated by negative feedback systems e.g.:
-astral over distension (vago-vagal reflex)
-duodenal over distension and chemical stimulation: vago-vagal reflex and hormones
-pyloric sphincter contracts in response to antral or duodenal rhythm; lipids/fatty acids in duodenum cause contraction of pylorus.
Explain how there is a regulation of gastric motility and emptying
Gastro-gastric reflexes provide balance between gastric reservoir and antral pump.
Distension of reservoir stimulates antral contractions. Distension of the antrum enhances and prolongs relaxation of the reservoir
Explain how regulation is elicited from the middle antrum and small intestine
-ascending excitatory reflex causing pyloric contractions and increasing tone
What is motility in the small intestine characterised by?
-segmentation: stationary contraction and relaxation
-peristalsis: in stomach
-migrating motor complex (MMC)
-mass movements (evacuation)
what are the phases of motor activity in the alimentary tract
Phase 1: quiescence/quiet period
Phase 2: irregular propulsive contractions
Phase 3: burst of uninterrupted phase contractions (peristaltic rush)
Explain segmentation in the small intestine
-originates in the pacemaker cells
-segmentation—-> divisions and subdivisions of the chyme—> bringing chyme in contact with intestinal walls
-segmentation causes the slow migration of chyme towards ileum
-duodenum/jejunum: 10-12 contractions per minute
-distal ileum: 8-9 contractions per minute
How do intrinsic senses in the gut co-ordinate contraction and relaxation
- Distension (stimulus):
The presence of a bolus stretches the intestinal wall.
This activates sensory neurons in the enteric nervous system.
2. Behind the Bolus – Contraction:
Sensory neurons activate:
Cholinergic interneurons → activate excitatory motor neurons
These release:
Substance P (SP)
Acetylcholine (ACh)
→ These neurotransmitters stimulate contraction of circular muscle behind the bolus.
3. Ahead of the Bolus – Relaxation:
Sensory neurons also activate:
Cholinergic interneurons → activate inhibitory motor neurons
These release:
VIP (vasoactive intestinal peptide)
NO (nitric oxide)
→ These cause relaxation of circular muscle ahead of the bolus.
How does NO cause smooth muscle relaxation
NO is synthesized from L-arginine by NO synthase (NOS) in endothelial cells.
NO diffuses into smooth muscle cells.
Inside smooth muscle:
NO activates guanylyl cyclase (GC)
GC converts GTP → cGMP
cGMP induces muscle relaxation
PDE5 (phosphodiesterase type 5) breaks down cGMP → turning off the signal.
How is peristalsis produced
Peristalsis is produced by coordinated contraction and relaxation of muscle coats
Explain the circuit for small intestinal peristaltic reflex
Stimuli in the Intestinal Lumen
Nutrients like:
Glucose (osmolality)
Long-chain fatty acids
Amino acids
These bind to specific receptors on the intestinal mucosa, leading to the release of peptides like CCK (cholecystokinin).
- Sensory Neurons (in Intestinal Wall)
These receptors activate sensory neurons in the enteric nervous system (ENS).
Sensory neurons detect chemical and mechanical signals (e.g., presence of nutrients or distension).
3. Integration in the Enteric Nervous System
Inside the ENS (red box), sensory inputs are processed by:
Interneurons:
Integrating circuits → process spatial/temporal info
Program circuits → determine the type of motor response
These circuits then activate motoneurons.
4. Motoneurons
These neurons control muscle contractions.
Based on the sensory input and processing, specific motor patterns are generated → e.g., peristaltic waves.
5. Contractile Patterns
The end result is a coordinated contraction pattern:
Contraction behind the bolus
Relaxation in front
Propelling content forward
Describe characteristics of the migrating motor complex (MMC)
-highly organised motor activity
-cyclically recurring sequence of events
-occurs between meals when the stomach/intestine are ‘empty’
-initiated by vagus nerve in the upper GIT; prominent in lower portion of stomach
-only phase 3 is occuring
-burst of high frequencies—> large amplitude contractions
-interval between phase 3’s is 90-120 minutes
What is the function and control of MMC
Function- ‘intestinal housekeeper’—> cleans up any left over substances left in the intestines.
Control- unclear, but may involve motilin, pacemaker cells
Explain characteristics of the large intestine
-motility in the large intestine is complex and misunderstood
-intensive mixing and slow movement of waste and indigestible material aborally.
-contains ‘fermenting chambers’- allows hydrolysis of fibres and indigestible nutrients
-faeces formation
Explain the motility of the large intestine
1) segmental or austral contractions mixes contains and is a key role for taenia coli longitudinal muscle
Features of motility in the large intestine:
-intensive mixing
-slow propagating—> slow aboral flow
How is peristalsis and mass movement in the large intestine
Peristalsis: slow in large intestine in comparison to small intestine; moves contents towards the anus
Mass movement: powerful contraction of mid transverse colon that sweeps colon contents into rectum
