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GI > Transport 1 - along the alimentary tract > Flashcards

Transport 1 - along the alimentary tract Flashcards

1
Q

Digestive functions of stomach

A

Accommodation & storage
Mechanical and enzymatic breakdown
Slow delivery of chyme to duodenum

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2
Q

Gastric accomodation

A

↓ cholinergic activity
VIP/NO promote accommodation
vagovagal reflex will act on mechanoreceptors -> relaxation

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3
Q

Emptying of gastric reservoir: emptying of partially digested food into duodenum

A

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.

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4
Q

Gastric motility/emptying

A

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

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5
Q

Regulation of gastric motility and emptying

stomach

A

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).

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6
Q

Regulation of gastric motility and emptying

small intestine

A

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

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7
Q

Reciprocal vagal control of Gastric Motility

A

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.

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8
Q

Gastric emptying

A

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

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9
Q

What are the effects of fatty, hypertonic, acidic chyme in the duodenum on gastric emptying?

A

Force and rate of gastric emptying decline

(hypertonic becasue increased osmlarity may prevent squirting action therefore it slows down)

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10
Q

Gastric emptying - particle size

A

Liquids pass in spurts
Solids are broken down to 1-2mm sizes
Large indigestible materials remain; cleared by MMC or vomiting

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11
Q

Summary: emptying of different food components into the duodenum

liquid, solids, fatty food, indigestible food

A

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

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12
Q

How is food retained in the stomach?

A

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

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13
Q

Gastric emptying of a liquid, semi-solid and solid meal _curves

A

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

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14
Q

Determinants of the rate of gastric motility

A

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

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15
Q

Myogenic control of gastric motility

A

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)

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16
Q

What can alter the BER?

A

Stretch, ACh, parasympathetic stimulation and GI hormones can alter the GI resting membrane potential and consequently BER of GI smooth muscle.

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17
Q

Factors that decrease BER

A

Sympathetic system → NA

Effects of NA or adrenaline on the membrane of GI smooth muscle

18
Q

What else is needed for the slow waves from ICC?

A

Slow waves alone do not allow action potential generation and contraction to occur (Ca2+-influx is important)

19
Q

What is the ICC?

A

The intestinal cells of cajal are specialised pacemaker cells located in the wall of the stomach, small intestine, and large intestine.

20
Q

Depolarisation and repolarisation of GI smooth muscle

A

Depolarisation of GI smooth muscle is cased by calcium-sodium entry
Repolarisation of GI smooth muscles is caused by K+ efflux

21
Q

What is BER and what determines frequency of contractions in GI tract?

A

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.

22
Q

Neurohormonal control of gastric motility

A 
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

23
Q

Neurohormonal control of gastric motility

proximal stomach

A

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.

24
Q

Neurohormonal control of gastric motility

distal stomach

A

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

25
Q

Control of movement through the small intestine

A

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

26
Q

Motility in the intestine

A

Segmentation (mixing contractions): stationary contraction & relaxation
Peristalsis (propulsive): in stomach (3 waves/min)
Migrating Motor Complex
Mass movements (evacuation)

27
Q

Motility in the intestine

A

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)
28
Q

Segmentation

A

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

29
Q

Differences between segmentation + peristalsis

A

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

30
Q

Segmentation contraction in the small intestine

A

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

31
Q

Regulation of peristalsis requires neural reflexes

A

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.

32
Q

A circuit for the small intestinal peristaltic reflex

A

• 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

33
Q

Migrating motor complex (MMC)

A

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

34
Q

Functions of MMC

A

“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)

35
Q

Control of MMC

A

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

36
Q

Motor activity in the small intestine in the fed state

A

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

37
Q

Functions of the Large Intestine

A

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

38
Q

Motility of the large intestine

A

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).

39
Q

Features of motility in Large intestine

A

Intensive missing;
Fermentation;
Slow propagating - slow aboral flow

40
Q

The Genesis of Diarrhoea and Constipation

A

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)

41
Q

Taenia Coli of large intestine

A

Longitudinal muscle which divide the 2 together

contract which create bulges allow intense mixing + promote fermentation

GI (19 decks)

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