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Physiology 1 > 28) Transport along the GI tract > Flashcards

28) Transport along the GI tract Flashcards

1
Q

What is GI emptying dependent on?

A
  • Propulsive force generated by tonic contractions of proximal stomach. The Fundus (top of the stomach) is under vagal excitatory control leading to tonic contractions which can last from mins to hours
  • The stomach’s ability to differentiate the types of meals ingested and their composition as it has its own little brain that will allow it to respond appropriately
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2
Q

What is lag time/phase?

A
  • The time/phase in which the food is grinded so that emptying can occur
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3
Q

How big is the lag time in liquid emptying?

A
  • Liquids have no lag time and there is no need to grind liquids in the stomach
  • Their emptying phase starts instantly
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4
Q

How are substances cleared from the stomach?

A
  • Liquid pass in spurts
  • Solids are broken down into smaller pieces. Larger food molecules take longer to be cleared than smaller molecules
  • Large indigestible materials can remain in the stomach and can be cleared by migrating motor complex or vomiting
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5
Q

How does type of food eaten determine rate of gastric motility?

A
  • The amount of time that food spends in the stomach varies from one food type to another
  • From fastest to slowest (carbohydrates>proteins>fatty acids>indigestible solids)
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6
Q

How does osmotic pressure determine rate of gastric motility?

A
  • Osmotic pressure of the duodenum is altered if the foods contain hyperosmolar chyme
  • The presence of this chyme causes a decreased gastric emptying
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7
Q

How do chymes in the duodenum determine rate of gastric motility?

A
  • If the food is fatty or hypertonic there is a lot of large particles in it
  • This decreases force and rate of gastric emptying causing us to be full for longer
  • If the food is acidic it needs to be neutralised first and so cannot move along.
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8
Q

How does innervation determine rate of gastric motility?

A
  • Vagal innervation can cause over-distension in the duodenum leading to decreased gastric motility.
  • Distension often means there is a lot of food particles present.
  • This means it cannot pass on the food material until it is handled appropriately
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9
Q

How do hormones determine rate of gastric motility?

A
  • Some hormones such as somatostatin, secretin, CCK inhibit emptying
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10
Q

How does injury and infection determine rate of gastric motility?

A
  • Injury to intestinal wall and bacterial infection can decrease motility
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11
Q

How is gastric motility myogenically controlled?

A
  • It is elicited by intrinsic Basic Electric Rhythm (BER) which is the reoccurring migrating ripples which travels the length of the stomach
  • They are elicited by intestinal cells of the cajal which are pacemaker cells in the stomach muscles that produce depolarisation
  • BER allows smooth muscles to depolarise and contract rhythmically when exposed to hormonal signals
  • BER moves ripples towards the antrum causing it to contract
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12
Q

What hormones decrease gastric motility?

A
  • Cholecystokinin (CCK): When CCK is released into the gall bladder, to release bile, it also sends messages to the fundus to prevent any food entering the duodenum by preventing contraction
  • Secretin
  • VIP
  • Somatostatin
  • Duodenal distension, duodenal acid
    (These factors decrease gastric motility by decreasing fundic motor activity)
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13
Q

What hormone increases gastric motility?

A
  • Motilin. It does this by increasing fundic contraction
  • Motilin enables the migrating motor complex (MMC) to work to allow contraction which moves indigestible material along the GI tract
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14
Q

How is gastric emptying controlled by a feedback system?

A
  • Gastric emptying is regulated by negative feedback systems/
  • Antral over-distension (vago-vagal reflex): When distension occurs it has an inhibitory effect on the fundus causing no contractions to occur.
  • Duodenal over-distension and chemical stimulation: This chemical stimulation occurs through the components of the food which will initiate a vago-vagal reflex and will also cause hormones (CCK and secretin) to be released
  • The pyloric sphincter can contract or relax in response to antral or duodenal rhythm. Lipids and fatty acids in duodenum can also cause contraction in pylorus
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15
Q

How is movement in the small intestine controlled?

A
  • There is a localised distension of the duodenum which decreases motility
  • Hormonal and nervous factors initiate peristalsis and mixing (called segmentation)
  • Cholecystokinin (CCK), gastrin and motilin increase intestinal motility
  • Secretin decreases activity
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16
Q

How is motility in the small intestines characterised?

A
  • Segmentation (mixing contractions): stationary contractions and relaxation to churn the food (moving backwards and forwards)
  • Peristalsis (propulsive): In the stomach
  • Migrating Motor Complex (MMC)
  • Mass movement (evacuation)
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17
Q

What are the phases of motor activity in the alimentary tract?

A
  • Phase 1: quiescence/ quiet period
  • Phase 2: irregular propulsive contractions
  • Phase 3: burst of uninterrupted phasic contractions (peristaltic rush)
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18
Q

How does segmentation occur in the stomach?

A
  • It originates in the ICC pacemaker cells which causes divisions and subdivisions of the chyme which brings the chyme in contact with intestinal wall
  • Segmentation allows the slow migration of chyme towards the ileum
  • As we move towards the anus we get fewer and fewer contrations in the intestines
19
Q

How is peristalsis regulated?

A
  • Peristalsis is regulated through neural reflexes

- These neural reflexes cause successive sections of circular smooth muscles to contract or relax

20
Q

What is the mechanism of peristalsis?

A
  • Receptors can detect food contents in the lumen along with distension
  • These receptors (once activated) stimulate sensory neurones which stimulate the vagal centre to trigger a vago-vagal reflex
  • This allows for the stimulation of interneurons in the enteric nervous system (through the communication of integrating and programming circuits)
  • Together they stimulate motor neurones which leads to the contractile pattern
  • Relaxation and secretion can also occur during this process
21
Q

What is the Migrating Motor Complex (MMC)?

A
  • It is the intestinal housekeeper which is controlled by motilin and pacemaker cells.
  • It has a highly organised motor activity which involves a cyclically reoccurring sequence of events
  • It occurs between meals when the stomach/intestines are empty of food but may still contain indigestible material
  • It is initiated by the vagus nerve of the upper GI tract but is prominent in the lower part of the stomach
  • It is commonly associated with Phase 3 contractions with intervals between each phase 3
  • It has bursts of high frequency, large amplitude contractions that migrate along the length of the intestines
22
Q

What are the parts and functions of the large intestines?

A
  • Ascending colon: Absorption of water and ions
  • Transverse colon: (Bacterial fermentation) Contains fermenting chambers which allow for the hydrolysis of fibre and indigestible nutrients
  • Descending colon: Storage of waste and indigestible material
23
Q

How does motility occur in the large intestines?

A
  • Segmental contractions mix contents through intensive mixing and slow movement of the bolus
  • Peristalsis which moves contents towards the anus through contraction (initiated by distension). It occurs at a slower rate than it does in the smaller intestines
  • Mass movement through powerful contractions of mid-transverse colon that sweeps colon contents into the rectum (responsible for colonic evacuation)
24
Q

What is constipation?

A
  • Difficulty in emptying bowel (hard faeces)
25
Q

What is diarrhoea?

A
  • Frequent discharge of liquid faeces
26
Q

How does diarrhoea and constipation occur?

A
  • Disorders of motility, fluid secretion and absorption can lead to diarrhoea and constipation
27
Q

What a villus cells?

A
  • Finger like projections that stick out of the wall of the small intestines.
  • They are highly vascularised (rich blood supply) that carry out absorption of dietary nutrients and secretion of gastric juices
  • They have large surface areas
28
Q

What are crypt cells?

A
  • Cells that lie underneath the villus cells and are involved in signalling and host defence
  • They have stem cells which allow for the regrowth of the epithelial cells
29
Q

What is an enterocyte?

A
  • A functional unit of the epithelial cell (i.e. they come together to make up the epithelial lining of the small intestines)
  • They consist of a villus cell and a crypt cell
30
Q

What are the different types of transports across the enterocyte?

A
  • Transcellular: Transport from one side of the lumen through the cell and to the other side where blood vessels are found. E.g. Glucose transport
  • Paracellular: Passive or selective movement of ions through tight junctions (found between two enterocytes) and is regulated. E.g. Na+ transport
31
Q

How does carbohydrate digestion occur?

A
  • Carbohydrates can only be absorbed as monosaccharides
  • Complex carbohydrates are reduced to disaccharides by amylase
  • Specific brush border enzymes convert disaccharides to monosaccharides (e.g. glucose to galactose)
32
Q

How does carbohydrates absorption occur?

A
  • Monosaccharides are absorbed by transporters at apical sites and basolateral sites of the enterocytes
  • From here they travel into the blood stream via GLUT 2 transporters
  • Fructose are able to diffuse into the enterocyte directly via the GLUT 5 or GLUT 2 transporters
  • Glucose and Galactose pass through the SGLT 1 transporter with Na+.
  • This process is initiated by exchange of Na+ (out of the cell) and K+ (into the cell) via the sodium-potassium pump.
  • There is a reduction in the concentration of Na+ in enterocytes which creates a concentration gradient between the lumen and the enterocyte
33
Q

How do monosaccharides enter the blood stream?

A
  • When the monosaccharides are inside the enterocytes they are transported out of the cell by GLUT 2 transporters into the blood vessels
34
Q

How does protein digestion occur?

A
  • Proteins are broken down into polypeptides by pepsin (activated from pepsinogen using HCl)
  • Polypeptides, tripeptides and dipeptides are broken down by pancreatic proteases to smaller units such as dipeptides and amino acids
  • Dipeptidases in brush border complete digestion of dipeptidases (which are remaining) to amino acids
35
Q

How does protein absorption occur?

A
  • Amino acids are absorbed into the enterocytes via Na+ transporters
  • Dipeptides and tripeptides to enter the enterocyte through an inward proton current (movement of H+ into the enterocyte)
  • Protons enter the enterocyte via a transporter and brings the dipeptides and tripeptides in with it
  • Once in the enterocyte hydrolysis of these molecules occurs (via cytoplasmic peptidases) forming amino acids
  • These amino acids are then transported into the blood
36
Q

How do amino acids enter the blood stream?

A
  • Amino acids within the enterocytes enter the blood stream via transporters
37
Q

How does lipid digestion occur?

A
  • Triglycerides (which form majority of lipids) are broken down into simpler units to facilitate absorption and starts with lipase found in the saliva
  • Gastric juices break down a small amount of fats in the stomach as it is very inefficient
  • The remainder (and majority) of the fat is digested by pancreatic lipases in the small intestines
  • Lipase requires the emulsification of triglycerides by bile salts for them to be digested fully
  • This is because triglycerides are water insoluble so forms chyme (an emulsion of large food particles, like fat, in water) whereas lipase are soluble
  • Pancreatic lipase binds to the surface of the small emulsion particles and digests them
38
Q

What is the role of bile salts?

A
  • They emulsify fats by breaking down larger fat globules into smaller globules
  • This increases the surface area where lipase can act so allows for a faster and more efficient digestion of lipids
  • They are constantly being recycled
39
Q

How do lipids enter the enterocytes?

A
  • Bile causes miscells (spherical lipid molecules) to form on which lipases act on
  • Since miscells are smaller they are able to get closer to the epithelial of the gut allowing them to fuse with the epithelial gut surface
  • In doing so they release short-chain free fatty acids and monoglycerides that can combine with each other and glucose to reform chylomicrons
40
Q

How do lipids enter circulation?

A
  • The lipids are found as chylomicrons in the enterocyte which are transported into the lymph and then into blood circulation
  • Some short chain fatty acids can also end up in circulation through the portal vein
41
Q

How are bile salts recycled?

A
  • When the micelle fuses with the epithelial cells the bile is unable to pass through
  • They are released by the micelles into the lumen where they diffuse into the ileum
  • Here some of them are excreted while others are recycled
42
Q

Why can lymph draining from the small intestine appear white?

A
  • Absorption of large amounts of chylomicrons causes the lymph drainage of the small intestine to appear milky
43
Q

What does disorder of fat digestion/ absorption cause?

A
  • Gallstones
  • Pancreatitis
  • Crohn’s disease
  • Liver disease
  • Malabsorption of fat causing steatorrhea
44
Q

What is steatorrhea?

A
  • Excess fat in faeces (also called fat-diarrhoea)

Physiology 1 (64 decks)

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