Transport Along & Across the GI Tract Flashcards

1
Q

Describe how food is emptied from the stomach into the first part of the intestines

A
  • Contractions of the stomach start early on in the fundus of the stomach because the fundus has pacemaker cells within it which can initiate contraction which then sweeps along the stomach
  • The propulsive contractions travel along the body of the stomach to the antrum of the stomach which has thick muscle that allows the grinding of food to occur
  • Once the particle size is small enough those particles get squirted into the duodenum which becomes distended which slows the motility to control how much is entering the duodenum from the stomach
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2
Q

Describe what prevents the food passing into the duodenum and why it would do this

A
  • Contraction of the pyloric sphincter stops food passing from duodenum into intestines
  • If the particles in the duodenum become too big then the pyloric canal detects this and the food is pushed back into the stomach to be ground more
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3
Q

What 2 things is gastric emptying dependent on?

A
  1. Propulsive force generated by the tonic contractions of proximal stomach
  2. Stomach’s ability to differentiate the types of meals ingested and their composition
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4
Q

Describe what emptying of liquids, semi solids and solids looks like on a graph

A
  • When a liquid is ingested there is no lag time, it is emptied straight out of the stomach in spurts
  • Liquids have no lag time because there is no need to grind the food into smaller components
  • Solids have to be broken down until they are 1-2 mm in size hence a solid meal has a lag time
  • Large indigestible materials will be cleared over time by the migrating motor complex or vomited out
  • Semi solid foods are in between these- there is a shorter lag time as food still needs to be ground into smaller parts but this doesn’t need to be done as much
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5
Q

Describe the determinants of the rate of gastric motility

A
  • Type of food eaten - carbohydrates > protein > fatty foods > indigestible solids (from fastest to slowest to be emptied)
  • The effects of fatty, hypertonic, acidic chyme in the duodenum on gastric emptying is that the force and rate is decreased
  • Osmotic pressure of duodenal contents - hyperosmolar chyme decreases gastric emptying
  • Vagal innervation upon over dissension e.g. duodenum decreases gastric motility
  • Hormones - somatostatin, secretin, CCK - inhibit emptying
  • Injury to intestinal wall and bacterial infections decrease motility
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6
Q

Describe how there is myogenic control of gastric motility

A
  • Elicited by intrinsic basic electric rhythm (BER) from intestinal cells of cajal (ICC)
  • The stomach muscle cells (pacemaker cells) produce electric depolarisations from resting potential
  • 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 - repolarisation creates slow waves from ICC which mediates regular recurring migrating ripples (3 waves / min) known as BER
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7
Q

Describe the neurohormonal control of gastric motility - split this in to what decreases fundic motor activity and what increases it

A

The following mediate a decrease in fundic motor activity -
- Cholecystokinin (CCK) - allows gallbladder to contract to release bile and relaxes fundus to stop more food being pushed into the duodenum
- Secretin - stops fundus contracting to allows HCO3- ions to neutralise acids
- VIP - decreases fundus contraction
- Somatostatin - decreases fundus contraction
- Duodenal distension - signals release of other things like CCK ,duodenal acid
Gastrin releasing peptide

Motilin increases fundic contractions
- Allows the MMC the migrating motor complex (MMC) to begin to work
- This aids in the removal to indigestible materials

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8
Q

What controls the movement of food through the small intestine?

A

Localised distension of the duodenum decreases motility
Hormonal and nervous factors initiate and maintain peristalsis and mixing
Cholecystokinin (CCK), gastrin and motilin increase intestinal activity

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9
Q

Describe the negative feedback mechanisms which contribute to gastric emptying

A
  • Antral over distension - vago vagal reflex - enhances and prolongs relaxation of the reservoir
  • Duodenal over distension and chemical stimulation (components in the food) - vago vagal reflex and hormones e.g. CCK and secretin
  • The pyloric sphincter contracts in response to antral or duodenal rhythm e.g. lipids/fatty acids in the duodenum causes contraction of the pylorus as they need to be emulsified before passing onto the intestines - if the antrum contracts but the duodenum cannot handle more food then the sphincter contracts to prevent overload of duodenum
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10
Q

Describe the reflexes controlling and pyloric contractions and what initiates them

A

If the duodenum is able to hold more food then contraction of the antrum will allow squirting of food into the duodenum - there is a descending inhibitory reflex causing pyloric relaxation to allow food to pass into duodenum

When there is acidic chyme in the duodenum the pyloric sphincter will contract to ensure no more food enters the duodenum - there is an ascending excitatory reflex causing pyloric contractions

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11
Q

What is motility in the small intestine characterised by?

A
  1. Segmentation - stationary contraction and relaxation
  2. Peristalsis of the stomach (3 waves per minute)
  3. Migrating motor complex
  4. Mass movements (evacuation)
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12
Q

State the 3 phases of motor activity in the GI tract

A

Phase 1 - quiescence/quiet period
Phase 2 - irregular propulsive contractions
Phase 3 - burst of uninterrupted phasic contractions

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13
Q

Describe segmentation, its role and how the number of contractions differs throughout the small intestine

A
  • Originates in the pacemaker cells
  • Segmentation - divisions and subdivisions of chyme bringing chyme in contact with the intestinal walls
  • Segmentation causes the slow migration of chyme towards the ileum
  • Duodenum/jejunum - 10-12 contractions/min
  • Distal ileum - 8-9 contractions/min
  • The number of contractions decreases towards the anus
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14
Q

State the 2 layers of smooth muscle in the intestines and whether they are contracted/relaxed behind or in front of a bolus of food

A
  • The smooth muscle consists of an outer layer of longitudinal cells and an inner layer of circular cells
  • Behind a bolus of food the longitudinal muscles are relaxed and the circular muscles are contracted
  • In front of the bolus of food the longitudinal muscles are contracted and the circular muscles are relaxed
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15
Q

Describe what the migrating motor complex (MMC) is, when it occurs and what initiates it

A
  • Initiated by vagus nerve in the upper GI tract - prominent in the lower portion of the stomach
  • Highly organised motor activity
  • Cyclically recurring sequence of events
  • Occurs between meals when the stomach/ intestine are empty
  • Only phase III is of interest
  • There is a burst of high frequency, large amplitude contractions that migrate along the length of the intestine and die out
  • There is an interval between phase IIIs of about 90-120 mins
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16
Q

State the functions of the MMC

A
  • Acts as an intestinal housekeeper
  • The control is unclear but may involve motilin-pacemaker cells (ICC)
17
Q

State the functions of the large intestine

A
  • Bacterial fermentation
  • Absorption of water and ions
  • Elimination of waste
  • Storage of waste and indigestible material

There is intensive mixing and slow movement of waste and indigestible material
It contains fermenting chambers which allow the hydrolysis of fibre and indigestible nutrients
Faeces is formed in the large intestine as well

18
Q

Describe the main points of motility of the large intestine

A

Motility within the large intestine is complex and poorly understood

  1. Segmental or haustral contractions - mix contents/key role for taenia coli longitudinal muscle - contract to produce the bulges in the colon
  2. Peristalsis - slow in large intestine in comparison to small intestine - moves contents towards the anus - dissension initiates contraction
  3. Mass movement - powerful contraction of mid transverse colon that sweeps colon contents into the rectum
19
Q

Describe how diarrhoea and constipation arise and define what each is

A
  • Disorders of motility, fluid secretion and absorption are important in the pathogenesis of diarrhoea and constipation
  • Diarrhoea is frequent (more than 3x a day) discharge of liquid faeces
  • Constipation is difficulty/some constraint in opening and emptying the bowel - hard faeces
20
Q

Describe the anatomy of the wall of the intestines including the functions of the cells

A
  • Villus cells that have villi along the surface
  • Crypt cells which are underneath the villus cells - these are involved in signalling and host defence - regrowth of epithelial cells
  • The villus cells have lots of blood vessels
  • The cells provide a thin, moist surface with a high surface area to allow substances to easily pass into the bloodstream via capillaries
  • These cells also secrete gastric juice with digestive enzymes to allow digestion
  • The surface area of the intestine is greatly increased via epithelial folds, villi and microvilli - internal SA of 200m squared
  • All dietary nutrients water and electrolytes that enter the upper small intestine are absorbed
21
Q

State and describe the 2 ways in which a substance can be transported across the enterocytes

A
  • Transport can occur in 2 ways
  • Transcellular - some molecules can be transported directly through epithelial cells such as glucose
  • Paracellular - molecules can pass through the tight junction between epithelial cells - this is a passive process but is selectively variable and regulated such as Na+, Cl-, H2O transport
22
Q

Describe what happens to carbohydrates before they are absorbed

A
  • Can only be absorbed in the form of monosaccharides
  • Complex CHO is reduced to disaccharides by amylases in the saliva/ secreted from the pancreas
  • Specific brush border enzymes convert disaccharides into monosaccharides e.g. glucose and galactose

Sucrase = sucrose -> glucose + fructose
Glucoamylase = glucose oligomers -> glucose
Lactase = lactose -> glucose + galactose

23
Q

Describe how monosaccharides are absorbed

A
  • Monosaccharides are absorbed by specific transporters at apical and basolateral aspects of enterocytes -
  • There is a sodium potassium pump whereby 3 Na+ ions are pumped out of the enterocytes and 2K+ are pumped into the enterocytes
  • This creates an Na+ ion gradient
  • There is then a sodium -glucose/galactose cotransporter whereby Na+ enters the enterocyte down the concentration gradient and glucose/galactose also enters the enterocyte (via a SGLT 1 transporter)
  • Fructose enters the enterocyte via a GLUT 5 or GLUT 2 transporter
  • Fructose, glucose and galactose then all leave the enterocyte to enter the bloodstream via a GLUT 2 transporter
24
Q

Describe what happens to proteins before they are absorbed

A
  • Polypeptides produced by action of pepsin
  • Polypeptides, di and tri peptides by action of pancreatic proteases
  • Di peptidases in brush border complete digestion to amino acids
25
Q

Describe how amino acids and di/tri peptides are absorbed

A
  • Amino acids -
  • The Na+/K+ ATPase pumps 3Na+ ions out of the enterocyte and 2K+ into it forming a concentration gradient of Na+
  • Na+ then enters the enterocyte down the concentration gradient via a secondary active transporter which cotransporters the amino acid into the enterocyte
  • The amino acid is then able to enter the bloodstream from the enterocyte down a concentration gradient
  • Di and tripeptides -
  • The Na+/K+ ATPase pumps 3Na+ ions out of the enterocyte and 2K+ into it forming a concentration gradient of Na+
  • Na+ then enters the enterocyte down the concentration gradient and H+ ions leave the cell via the same transporter
  • This creates a H+ gradient so H+ ions enter the enterocyte via a different transporter which cotransports di and tripeptides into the enterocyte
  • The peptides are then hydrolysed before the amino acids enter the bloodstream down their concentration gradient
26
Q

Describe how triglycerides are broken down before they are absorbed

A
  • Dietary triglycerides are broken into simpler units to facilitate absorption
  • The mouth contains saliva with lipase which digests a small fraction of the triglycerides
  • Most dietary triglycerides are digested in the small intestine
  1. Emulsification
  2. Micelle formation
  • Gastric lipase breaks down around 10-30% of fats
  • Remainder of the fat is broken down by pancreatic lipase
  • Lipase action requires emulsification by bile salts which dissolve triglycerides in water
  • Pancreatic lipases then bind to the surface of the small emulsion particles and digest them
  • The breakdown and micelle formation occurs in the duodenum and the jejunum while the absorption occurs in the small intestine
27
Q

Why do triglycerides need to dissolve in an aqueous phase to be digested?

A

Because triglycerides are water insoluble they must be dissolved in an aqueous phase before they can be fully digested as lipase is a water soluble enzyme

28
Q

Describe how lipids are absorbed

A
  • Once the triglycerides have been broken down into smaller components by lipases to form micelles they are able to get closer to the lumen of the gut
  • These then fuse with the luminal surface
  • There is then resynthesis of the triglycerides which then when added to apolipoproteins form chylomicrons which transport in the lymph and then into the circulation
  • Short chain fatty acids once fusion has occurred will go directly into the portal vein into circulation
29
Q

How do chylomicrons change lymph?

A

An absorption of a large number of chylomicrons causes lymph draining from the small intestine to appear milky

30
Q

Describe what disorders can lead to fat being excreted in the faeces

A

Disorders such as gallstones, pancreatitis, Crohn’s disease and liver disease can lead to fat malabsorption so fat is found in the faeces