Transport 1 - along the alimentary tract Flashcards
Digestive functions of stomach
Accommodation & storage
Mechanical and enzymatic breakdown
Slow delivery of chyme to duodenum
Gastric accomodation
↓ cholinergic activity
VIP/NO promote accommodation
vagovagal reflex will act on mechanoreceptors -> relaxation
Emptying of gastric reservoir: emptying of partially digested food into duodenum
Tonic contraction start at the fundum area -> throw stomach into a force and can last minutes to hours. Contractions from the reservoir and back from the antrum via the pyloric sphincter being tightly regulated will throw the proximal stomach into some propulsive contractions which allows grinding + mixing of this food with enzymes -> mechanical grinding due to antrum muscles therefore digestion occurs
Once receptive accommodation has occurred, the food has to be moved along.
The transport of digested material from the gastric reservoir into the antral pump is caused by two mechanisms: tonic contractions and peristaltic waves in the region of the gastric corpus.
Tonic contractions are caused by pacemaker cells in the proximal stomach, this is then taken over by peristaltic waves in the corpus.
Gastric motility/emptying
Storage: the proximal stomach relaxes to store food at low pressure whilst it is acted upon by acid, enzymes and mechanically
Emptying of partially digested food: this is carefully regulated to ensure adequate acidification/neutralisation, action of enzymes, mechanical breakdown and to avoid swamping of the duodenum.
Disorders: gastric stasis (gastroparesis) -> disorder of motility which leads to constipation
Regulation of gastric motility and emptying
stomach
Distension of stomach to some extent can initiate excitatory reflexes which promote antral pump to switch on + contraction can occur
Distension of the antrum enhances pro-longed relaxation of the reservoir
Either allow food in or pyloric sphincter stays contracted as it can’t accomodate more chyme therefore inhibitory reflex which allows relaxation of the fundus area
Summary
Gastro-gastric reflexes provide balance between the gastric reservoir and antral pump. Distension (enlargement) of the reservoir stimulates antral contractions, distension of the antrum enhances and prolongs relaxation of the reservoir (so has an inhibitory reflex).
Regulation of gastric motility and emptying
small intestine
When dudodenum can accomodate more chyme, contractions of antrum allows descending inhibitory effect causing pyloric relaxation via NO/VIP. The duodenum will notice if lipids + acid present. (if lipids present, CCK will help release bile to emulsify fat. For acid, bi-carbonate is released.) Acidic + fatty chyme have an ascending exciatotry reflex that cause pyloric contractions and increase tone to allow less into duodenum
Summary
Pyloric activity is modulated by antral inhibitory fibres and duodenal excitatory fibres.
So, Contraction of middle antrum elicits the descending inhibitory reflex from antrum causes pyloric relaxation through NO/VIP, while the ascending excitatory reflex causes pyloric contractions and increases tone, this is to prevent food moving back up into the stomach
Reciprocal vagal control of Gastric Motility
During accommodation, there is Ach release to the stomach (which causes contraction) as well as there being the VIP/NO release from NANC nerves (which causes relaxation). However, as it is accommodation when the individual is eating, the VIP/NO nerves override the Ach release.
Once the food is accommodated, we start to see the effects of Ach as the cholinergic fibres increase in activity and the NANC activity decreases.
Gastric emptying
It is dependent upon:
Propulsive force generated by the tonic contractions of proximal stomach
Stomach’s ability to differentiate types of meals ingested and their components
What are the effects of fatty, hypertonic, acidic chyme in the duodenum on gastric emptying?
Force and rate of gastric emptying decline
(hypertonic becasue increased osmlarity may prevent squirting action therefore it slows down)
Gastric emptying - particle size
Liquids pass in spurts
Solids are broken down to 1-2mm sizes
Large indigestible materials remain; cleared by MMC or vomiting
Summary: emptying of different food components into the duodenum
liquid, solids, fatty food, indigestible food
Liquids:
Rapidly disperse, empty without lag time
Rate of emptying is influenced by nutrient content (nutrient-containing liquids retained longer)
Solids:
2 phases (lag time and linear phase); duration of lag time is related to size of particle
Liquid part emptied and solid component is retained in proximal stomach
Trituration of larger particles to smaller ones
(~60min for a typical solid-liquid meal)
Pylorus regulates passage of material
Fatty foods:
Liquefy at body temperature; float on top of liquid layer and empty slowly
Fats are potent inhibitors of gastric motor events and gastric emptying
Indigestible solids
Not emptied in immediate post-prandial period
MMC activity
How is food retained in the stomach?
sieving action of the pylorus
It detects large particles and pushes them back so they can grind
when duodenum can handle, they go through
This process is called trituration
Gastric emptying of a liquid, semi-solid and solid meal _curves
Liquid is very fast
semi-solid has a lag time as size may not fufil 2mm criteria (grinding action + gastric juice)
Solid has an increased lag time
Determinants of the rate of gastric motility
Type of food eaten: carbohydrates>protein>fatty foods>indigestible solids
Osmotic pressure of duodenal contents: hyperosmolar chyme ↓ gastric emptying
Vagal innervation upon over-distension ↓ gastric motility (Ach mediates increased motility)
Hormones (somatostatin, secretin, CCK, GIP): inhibit emptying
Injury to intestinal wall and bacterial infections ↓ motility
(injury can also increase motility and cause diarrohoea)
Pain and fear decrease gastric motility
Big decrease in gastic motility could cause build up of bacteria
Myogenic control of gastric motility
Intrinsic basic electric rhythm (BER) which initiates the contractility
Stomach muscle cells produce electric depolarisations from resting potential from the proximal end of the stomach
Ripples move towards the antrum
Fundus is under vagal excitatory control (which can be inihibited if food in the duodenum)
Slow waves from ICC – regular recurring migrating ripples (3 waves/min) known as BER (a rhythm of depolarisation-repolarisation)
What can alter the BER?
Stretch, ACh, parasympathetic stimulation and GI hormones can alter the GI resting membrane potential and consequently BER of GI smooth muscle.
Factors that decrease BER
Sympathetic system → NA
Effects of NA or adrenaline on the membrane of GI smooth muscle
What else is needed for the slow waves from ICC?
Slow waves alone do not allow action potential generation and contraction to occur (Ca2+-influx is important)
What is the ICC?
The intestinal cells of cajal are specialised pacemaker cells located in the wall of the stomach, small intestine, and large intestine.
Depolarisation and repolarisation of GI smooth muscle
Depolarisation of GI smooth muscle is cased by calcium-sodium entry
Repolarisation of GI smooth muscles is caused by K+ efflux
What is BER and what determines frequency of contractions in GI tract?
The basal or basic electrical rhythm (BER) or electrical control activity (ECA) determines the frequency of the contractions in the gastrointestinal tract
The basal electrical rhythm allows the smooth muscle cell to depolarise and contract rhythmically when exposed to hormonal signals.
The cell membranes of the pacemaker cells undergo a rhythmic depolarisation and repolarisation
This rhythm of depolarization-repolarisation of the cell membrane creates a slow wave known as a BER, and it is transmitted to the smooth muscle cells.
Neurohormonal control of gastric motility
The following mediate a decrease in fundic motor activity Gastrin-releasing peptide (GRP) Cholecystokinin (CCK) Secretin VIP Somatostatin Glucagon Duodenal distension, duodenal acid
Motilin increases fundic contractions
Neurohormonal control of gastric motility
proximal stomach
Proximal stomach
CCK, gastrin, and secretin inhibit contractions of proximal stomach, thereby decrease intragastric pressure and slow gastric emptying of liquids.
Gastric inhibitory polypeptide (GIP), glucagon, VIP may also slow gastric emptying, since they also inhibit proximal gastric contractions
Motilin augments proximal gastric contractions and speeds gastric emptying of liquids.
Neurohormonal control of gastric motility
distal stomach
Distal stomach
Gastrin, CCK, and motilin stimulate the contractions of the distal stomach
Secretin, GIP and VIP inhibit the contraction of the distal stomach
The modulation of distal gastric contractions by these hormones may influence gastric trituration and emptying of solids
CCK and secretin enhanced pyloric contractions, an effect blocked by gastrin
Control of movement through the small intestine
Intestine
CCK, gastrin, and motilin stimulate contractions
Secretin inhibits contractions
CCK and motilin speed small bowel transit
Motilin causes the cyclical bursts of gastroduodenal contractions during fasting
The contractions characteristic of the fed state are caused by gastrin and CCK
Of all these actions, only those of CCK on the proximal stomach, and gastrin on the distal stomach, have been shown to be physiologic so far
VIP and glucagon slow transit/decrease motility
Serotonin and insulin can increase motility
Motility in the intestine
Segmentation (mixing contractions): stationary contraction & relaxation
Peristalsis (propulsive): in stomach (3 waves/min)
Migrating Motor Complex
Mass movements (evacuation)
Motility in the intestine
Segmentation (mixing contractions): stationary contraction & relaxation -> Segmenting contractions primarily churn the food but also propel it towards the anus
Peristalsis (propulsive): in stomach (3 waves/min) -> circular propulsive contractions propagating aborally. Peristaltic (propulsive) contractions spread the food out allowing digestive enzymes to mix with it but primarily push food towards the anus. Peristalsis is global in nature
Migrating Motor Complex Mass movements (evacuation)
Segmentation
Originates in the pacemaker cells (ICC)
Segmentation → divisions and subdivisions of chyme, bringing chyme in contact with intestinal walls (back and forth movement to allow churning + mixing of contractions with secretions from intestinal wall which promote the digestion of fats + proteins)
Segmentation causes the slow migration of chyme towards ileum
Duodenum/jejunum: 10-12 contractions/min
Ileum: 8-9 contractions/min
Differences between segmentation + peristalsis
Peristaltic (propulsive) contractions spread the food out allowing digestive enzymes to mix with it, but primarily push the food towards the anus (global movement)
Segmenting (mixing) contractions primarily churn the food, but also propel it towards the anus - some localisation
Segmentation contraction in the small intestine
Chyme is divided, subdivided, mixed with luminal contents and pushed back and forth
Slow moving contraction, mixing + churning -> over time, mixing contractions occurs therefore going back + forth but overall the movement is going towards ileum
Regulation of peristalsis requires neural reflexes
Peristalsis is a propagating contraction of successive sections of circular smooth muscle preceded by a dilatation
Sensory neurones detect stimulation of the bolus and through cholinergic interneurones will stimulate inhibitory motor neurones to relase VIP/NO to cause relaxation of circular muscle in the receiving segment as well as activating excitatory motor neurones that release Ach/substance P and cause contraction of smooth muscle to propel the bolus forward in the behind segment.
A circuit for the small intestinal peristaltic reflex
• Luminal contents are detected by sensory
neurons
• These send APs to the vagal centre, which send
vago vagal reflexes to the integrating and
program circuits in the ENS
• This produces contractions/relaxations
Migrating motor complex (MMC)
Highly organised motor activity
Cyclically recurring sequence of events
Occurs between meals when the stomach / intestine are “empty”
Only phase III is of interest
Burst of high frequency, large amplitude contractions that migrate along the length of intestine and die out
Interval between phase IIIs is 90-120min
Starts in lower portion of stomach
Functions of MMC
“Intestinal housekeeper”
Indigestible residues moved out of stomach by large contractions and wide opening of the pyloric sphincter during phase III
Removes dead epithelial cells by abrasion
Prevents bacterial overgrowth
Prevents colonic bacteria from entering small intestine
Occurs following digestion and absorption of a meal (empty stomach)
Control of MMC
Not fully known
Smooth muscles cells of stomach can produce “slow waves”
Contractions are coordinated by the enteric nervous system by pacemaker cells (interstitial cells of Cajal)
Initiated by the vagus nerve in upper tract
Some evidence for cyclical secretion of the hormone motilin from stomach & duodenum
Feeding inhibits release of motilin
Motor activity in the small intestine in the fed state
Mixing contractions: segmentation, mixes and stirs contents with enzymes, prevents unstirred layer formation
Peristaltic contractions (slow waves): these move the contents in an oral to anal direction (law of the gut) -local reflex mediated via ENS but can be enhanced or suppressed by extrinsic innervation (i.e. parasympathetic/sympathetic); ↑sympathetic and parasympathetic inhibit and stimulate motility, respectively
Pain and fear ↓ motility
Functions of the Large Intestine
There is intensive mixing and slow movement of waste and indigestible aborally
There are also fermenting chambers on the sides where there is hydrolysis of fibre and indigestible nutrients
The large intestine also produces faeces by the absorption of water
Motility of the large intestine
Segmental or haustral contractions-mix contents/ key role for taenia coli longitudinal muscle
Peristalsis: slow in large intestine in comparison to small intestine; moves contents towards the anus; distension initiates contraction
Mass movement: powerful contraction of mid-transverse colon that sweeps colon contents into rectum (responsible for colonic evacuation).
Features of motility in Large intestine
Intensive missing;
Fermentation;
Slow propagating - slow aboral flow
The Genesis of Diarrhoea and Constipation
Disorders of motility, fluid secretion and absorption and important in the pathogenesis of diarrhoea and constipation.
These occur due to the transit time spent in the gut
Diarrrhoea is frequent (over 3x a day) discharge of liquid faeces
Constipation is difficulty/some constraint in opening/emptying bowels (hard faeces)
Taenia Coli of large intestine
Longitudinal muscle which divide the 2 together
contract which create bulges allow intense mixing + promote fermentation
