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Flashcards in Transport along and across the GI Tract Deck (33)
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1

What is the emptying of the gastric reservoir caused by?

  • The transport of digesta from the gastric reservour into the antral pump is caused by two mechanims:
    • tonic contraction and peristaltic waves in the region of the gastric corpus.
  • Tonic contractions are contractions that are maintained from minutes to up to hours at a time. They can occur in the stomach and the sphincters of the GIT.

2

Describe storage and gastric emptying (and a disorder relating to it).

  • STORAGE:
    • The proximal stomach relaxes to store food at a low pressure whilst it is acted upon by acid, enzymes and mechnically.
  • EMPTYING:
    • This is carefully regulated to ensure adequate acidification/neutralisation, action of enzymes, mechanical breakdown and to avoid swamping of the duodenum (If the acidic conditions in the duodenum are not neutralised it could lead to the formation of a duodenal ulcer).
  • Disorder: Gastroparesis:
    • ​It is a chronic (long-term) condition in which the stomach cannot empty itself of food in the normal way, causing food to pass through it slowly.

3

What is gastric emptying dependent upon?

Gastric emptying is dependent upon:

  1. The propulsive force generated by the tonic contractions of the proximal stomach.
  2. The stomach's ability to differentiate types of meals ingested and their components (weather it has carbohydrates, proteins, lipids in it).
    • Fatty, hypertonic, acidic chyme in the duodenum decreases the force and rate of gastric emptying.

4

Summarise the emptying of different food components (liquids, solids, fatty foods and indigestable solids).

  1. LIQUIDS:
    • Rapidly disperse, empty without lag time (There is no lag time because the size is small).
    • Rate of emptying is influenced by the nutrient content (nutrient-containing liquids retained longer).
  2. SOLIDS:
    • 2 phases (lag time and linear/emptying phase).
    • Duration of lag time is related to size of particle.
    • Liquids part is emptied and solid component is retained in proximal stomach.
    • If the solid is large it has to be broken down (triturated) to 1-2mm in size in order to pass into the duodenum.
    • The pylorus regulates the passage of materal.
  3. FATTY FOODS:
    • Liquefy at body temperature and float on top of liquid layer and empty slowly.
    • Fats are potent inhibitors of gastric motor events and gastric emptying.
  4. INDIGESTIBLE SOLIDS:
    • They do not empty during the immediate post-prandial period (the period that comprises and follows a meal)
    • They are cleared by vomiting or MMC (migrating motor complex) that allows the cleansing of the stomach.

5

List some determinants of the rate of gastruic motility.

  • Type of food eaten:
    • carbs > proteins > fatty foods > indigestible solids.
  • Osmotic pressure of duodenal contents:
    • hyperosmolar (increase in the osmolar concentration of body fluids) chyme decreases emptying.
  • Vagal innervation upon over-distension decreases gastric motility.
  • Hormones (somatostatin, secretin, CCK, GIP): inhibit emptying.
  • Injury to intestinal wall and bacterial infections decreases motility.

6

Describe the myogenic control of gastric motility.

  • The Intestinal Cells of Cajal (ICC) are specialised pacemaker cells located in the wall of the stomach, small intestine and large intestine.
  • The cell membranes of the pacemaker cells undergo a rhythmic depolarisation and repolarisation.
  • This rhythm of depolarisation-repolarisation of the cell membrane creates a slow wave known as a BER, and it is transmitted to the smooth muscle cells.
  • The intrinsic basal or basic electrical rhythm (BER) or electrical control activity (ECA) determines the frequency of the contractions in the GI tract.
  • Contraction of the smooth muscle can occur when the BER reaches its plateau.
  • The basal electrical rhythm allows the smooth muscle cell to depolarise and contract rhythmically when exposed to hormonal signals.
  • Depolarisation of the GI smooth muscle is caused by calcium-sodium entry.
  • Repolarisation of the GI smooth muscle is caused by K+ efflux (flowing out).

7

List some factors that will mediate a decrease in fundic motor activity.

  • Cholecystokinin (CCK).
  • Secretin.
  • VIP.
  • Somatostatin.
  • Duodenal distention, duodenal acid.
  • Gastrin-releasing peptide (GRP).
  • Motilin, on the other hand, increases fundic contractions.
  • Glucagon also decreases fundic motor activity.

8

How is movement through the small intestine controlled?

  • Hormonal and nervous factors initiate and maintain peristalsis and mixing.
  • Localised distention of the duodenum.
  • Cholecystokinin (CCK), gastrin and motilin increase intestinal motility (colonic motility).
  • Secretin (and insulin) decreases intestinal motility (colonic motility).

9

Describe the feedback control of gastric emptying.

  • Gastric emptying is regulated by negative feedback systems.
  • When you have distension of the fundus that initiates exitatory effects within the antrum, leading to the contraction of the antrum. This contraction will tend to send inhibitory signals (inhibitory signals tend to be prolonged). Examples:-
    • Antral over-distension: Vago-vagal reflex.
    • Duodenal over-distension and chemical stimulation: Vago-vagal reflex and hormones (such as CCK).
  • Note : the pyloric sphincter contracts in response to antral or duodenal rhythm; fatty acids in duodenum cause contraction of pylorus.

10

Describe the regulation of gastric motility and emptying.

  • When the duodenum has no food inside it, then the factors that promote the relaxation of the pyloric sphincter (NO and VIP) are released which allow the pylorus to relax and the middle antrum to contract. This is called the descending inhibitory reflex.
  • If acidic chyme has just been squirted into the duodenum, it will be sensed by the enteric nervous system and it will not allow more acidic chyme to be squirted in. It will cause the pylorus to contract and increases the tone. This is called the ascending excitatory reflex. This prevents the forming of duodenal ulcer.

11

What are the different components of motility in the intestine?

  • Segmentation (mixing contractions): stationary contractions and relaxation (allows greater mixing of chyme with the secretions of the intestines).
  • Peristalsis (propulsive): in the stomach [3 waves/min] (allows the mixing, continued digestion and absorption if nutrients of chyme in the intestines).
  • Migrating motor complex: They are waves of electrical activity that sweep through the intestines in a regular cycle during fasting to cleanse the remaining food out of the intestines.
  • Mass movements (evacuation): Getting rid of undigested material.

12

What are the phases of motor activity?

  • PHASE 1: quiscence / quiet period.
  • PHASE 2: irregular propulsive contractions.
  • PHASE 3: burst of uninterrupted phasic contractions (peristaltic rush) (its the rumbling sounds your stomach makes).

13

Describe segementation and its role in the GI tract.

  • Segmentation originates in the pacemaker cells (ICC)  and tends to be more of a churning action.
  • Segmentation creates divisions and subdivisions of chyme, bringing chyme in contact with intestinal walls.
  • Segmentation causes the slow migration of chyme towards the ileum.
  • The duodenum/jejunum contract 10-12 times per minute, whereas the ileum contracts 8-9 times per minute.

14

Describe peristalsis and its role in the GI tract.

  • On the outer surface of the GI tract there are longitudinal muscles which contract infront of the bolus of food. This shortens the area of the GI tract immediately infront of the bolus of food.
  • On the inner surface of the GI tract there are circular muscles which contract behind the bolus of food. This pushes the food along the GI tract.

15

Explain the circuit for the small intestinal peristaltic reflex.

  • Whatever is in the intestinal lumen (food particles) such as glucose, long chain fatty acids, amino acids these can initiate activity within the gut.
  • If there is fat present (lipids) CCK will be released.
  • This will set in motion reflexs which will allow (in the case of CCK the gall bladder to contract and release bile. 
  • It doesnt have to rely on the higher centres of the brain as some of these processes can occur within the enteric nervous system in the gut lumen.
  • This leads to the activation of specific motor neurones that are responsible for specific contractile pattern.

16

What is the difference between peristalsis and segmentation?

  • Peristaltic (propulsive) contractions spread the food out, allowing digestive enzymes to mix with it, but primarily push the good towards the anus (global movement).
  • Segmenting (mixing) contractions primarily churn the food, but also propel it towards the anus (some localisation).

17

Describe the migrating motor complex (MMC).

  • It is highly organised motor activity, a cyclically recurring sequence of events.
  • It occurs between meals, when the stomach / intestines are 'empty'.
  • It starts in the lower portion of the stomach.
  • Only Phase 3 is of interest.
  • There is a burst of high frequency, large amplitude contractions that migrate along the length of the intestine and die out.
  • The interval between Phase 3s waves is 90 - 120 minutes.

18

What are the functions of the MMC?

  • It is the 'intestinal housekeeper'.
  • Indigestible residues are moved out of the stomach by large contractions and there is the wide opening of the pyloric sphincter during Phase 3.
  • It removes dead epithelial cells by abrasion (scraping away).
  • It prevents bacterial overgrowth.
  • It prevents colonic bacteria from entering the small intestine.
  • It occurs following digestion and absorption of a meal (empty stomach).

19

Describe the control of the MMC.

  • The control of MMC is not fully known.
  • We know that the smooth muscle cells of the stomach can produce 'slow waves'.
  • These contractions are coordinated by the enteric nervous system by pacemaker cells (ICC).
  • This is initiated by the vagus nerve in the upper tract.
  • There is some evidence for cyclical secretion of the hormones motilin from the stomach and duodenum.
  • Feeding inhibits the release of motilin.

ICC is for a complex network of specialised smooth muscle fibres; they lie between smooth muscle layers and can form synaptic connections with GI smooth muscle fibres.

20

Describe the motor activity in the small intestine in the fed state.

  • There are mixing contractions, such as segmentation, which mixes and stirs the contents with enzymes, and prevents an unstirred layer formation.
  • There are peristaltic contractions (slow waves); these mover the contents in an oral to anal directions (law of the gut).
  • It is a local reflex mediated via the ENS, but can be enhacned or suppressed by extrinsic innervation (ie. parasympathetic/sympathetic).
  • Sympathetic and parasympathetic activity inhibit and stimulate the smotility, respectively.
  • Pain and fear decrease motility.

21

Describe storage in the large intestine.

  • Storage occurs in the large intestine, particularly whilst water is absorbed from the contents.
  • Intensive mixing and slow movements of waste and indigestible material occur aborally (away from the mouth).
  • It contains 'fermentation chambers' which allow for the hydrolysis of fibre and indigestible nutrients, leading to faeces formation.

22

Describe the motility of the large intestine.

  1. Segmental or haustral contractions: mix the contents; this is a key role for taenia coli longitudinal muscle (these are a muslce structure that run along the middle of the large colon. Its presence allows the large intestine to have folds or sacculations. Within the sacculations you can have fragmentations occuring there).
  2. Peristalsis: slow in the large intestine in comparison to the small intestine, moves the contents towards the anus; the distention initiates contraction.
  3. Mass movement: powerful contraction of the mid-transverse colon that sweeps the colon contents into the rectum (responsible for colonic evacuation).
  • Features of motility in the large intestine: -
    • Intensive mixing.
    • Fermentation.
    • Slow propagating - slow aboral flow (away from the mouth).
  • The inflammation of the appendices epiploicae (fat filled peritoneum) can cause a lot of pain and can be mistaken for appendicitis.

23

Describe diarrhoea and constipation.

Disorders of motility, fluid secretion and absorption are important in the pathogenesis of diarrhoea and constipation.

  • Diarrhoea is the frequent (> 3 times / day) discharge of liquid faeces.
  • Constipation is the difficulty / some constraint in emptying bowels (hard faeces).

24

Describe the gross and microscopic structure of the small intestine.

  • The small intestine is thin, has a large surface area (an internal surface area of 200 m2) and highly vascularised.
  • The surface area is increased by the presence of epithelial folds, villi and microvilli.
  • The small intestine can also replace itself (it has stem cells within the crypt cells that allow rejuvenation and replacement of dead cells).
  • All dietary nutrients, water and electrolytes that enter the upper small intestine are absorbed.

25

What are the two types of solute transport across the enterocyte.

  1. Transcellular transport :-
    • Transport of solutes by a cell through a cell. E.g., transport of glucose from the intestinal lumen to extracellular fluid by epithelial cells.
  2. Paracellular transport :- 
    • Passage of solutes between cells.

26

Describe carbohydrate (CHO) digestion and absorption.

  • Carbohyrates can only be absorbed in the form of monosaccharides.
  • Complex CHO is reduced disaccharides by amylase.
  • Specific brush border enzymes convert disaccharides to monosaccharides (eg. glucose and galactose).

27

Describe the transport of glucose and galactose across the apical membrane.

  • The basolateral side (blood side) of the enterocyte (gut cell) tends to be transporting Na+ into the blood from the lumen.
  • This creates a Na+ gradient.
  • This driving force of Na+ allows glucose to come in with it.
  • This cotransporter is called the Na+/glucose cotransporter (SGLT1).
  • This same transporter is also good at transporting galactose.
  • If galactose is able to get to the blood first it will inhibit glucose.
  • Once glucose is within the cell there are glucose transporters called Glut-2 that will transport it to the blood.
  • Fructose does not need any transporter, it is passively transported and moves from the cell to the blood via the Glut-5 transporter.

28

Describe protein digestion and absorption.

  • Polypeptides are produced by the action of pepsin.
  • Polypeptides, di- and tri- peptides are produced by the action of the pancreatic proteases.
  • Di-peptidases in the brush border complete their digestion to amino acids.
  • Hydrolytic digestive products such as tripeptides, dipeptides and amino acids can be absorbed intact across the intestinal mucosa and into the blood.

29

Describe amino acid transport.

  • Amino acids are transported on a sodium-coupled carrier system similar to that for glucose.
  • There are seperate carriers for different types of amino acids.
  • Some di- and tri-peptdies are transported on a carrier system using an inwardly directed H+ gradient.

30

Generally, describe the digestion of lipids.

  • Triglycerides(TGs) are the majority (90%) of dietary lipids.
  • These also include phospholipids, cholesterol, fat-soluble vitamins (A,D,E,K).
  • Dietary triglycerides are broken down into simpler units to facilitate absorption.
  • In the mouth, salivary lipase digests a small fraction of the triglycerides.
  • However, most dietary triglycerides are digested in the small intestine.
  • But TGs are water-insoluble; chyme (emulsion of large fat particles in water); lipase is water-soluble.
  • So, triglycerides must be dissolved in the aqueous phase before they can be digested.

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