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SI Flashcards

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1
Q

When does chyme move into the stomach

A

0-3 hrs after entering the stomach

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2
Q

How long does it take for chyme to move through the SI (6m)

A

1-6 hours

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3
Q

Role of

  1. Duodenum
  2. Jejunum
  3. Ileum

in absorption

A
  1. Digestion and a small amount of absorption
  2. Digestion and absorption
  3. Absorption
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4
Q

Conduction rate of the SI

A

1 cm/min

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5
Q

What is the conduction rate of the SI influenced by

A
  • Enteric nervous system
  • Hormones
  • Gastrin (increase)
  • Cholecystokinin (increase)
  • Secretin (increase)
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6
Q

Relationship between structure and SA of the SI

A
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7
Q

Actual SA of the SI

A

120-140 m2

> 95% of nutrients are absorbed

Increasing food intake, limited capacity - reserve capacity (when we over-eat)

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8
Q

Structure of SI

A

ENS regulates digestion, motility and absorption

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9
Q

Gut layer organisation

A

Gut wall has a layered organisation, with the absorptive cells lining the lumen and neural muscular components below

Blood and lymph vasculature is abundant to transport absorbed nutrients

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10
Q

Function of villi

A

By projecting into the lumen, the villi increase the SA for absorption of nutrients

Microvilli (brush border) fringe the villi to further increase SA

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11
Q

What does lymph carry

A

Fat and fat-soluble vitamins

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12
Q

Structure of SI

A
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13
Q

What is the epithelial mucosa composed of

A

Absorptive cells

Secretory cells - enzymes, hormones, fluid (follows secretion of solutes), mucus (for protection)

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14
Q

What do the exocrine cells in the pancreas do

A

Play a central role in the production of digestive enzymes

(beta cells - islets of langerhans - secrete insulin into circulation)

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15
Q

Where are digestive secretions from the liver and pancreas delivered into

A

Into the duodenum through the SPHINCTER OF ODDI

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16
Q
  1. Acini secrete…
  2. What stimulates acini
A
  1. Enzymes
  2. CCK and ACh
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17
Q
  1. Ducts secrete…
  2. What are the ducts stimulated by
A
  1. Bicarbonate
  2. Secretin
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18
Q

What does CCK do

A

Makes gallbladder contract

CCK mediates gastric emptying rate in response to fat

Reduces appetite and induces nausea

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19
Q

What protects the pancreas from autodigestion

A

Kazal inhibitor secreted from pancreas to protect it

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20
Q

Bicarbonate secretion in pancreas or intestine

A

(Position of transporters is reversed in the stomach)

  • BASOLATERAL - Na+ will be used to export H+ out of the cell into circulation
  • H+ came from carbonic anhydrase that broke down from CO2 and H2O
  • Bicarbonate is exchanged for chloride on the luminal side of pancreas - Cl- can flow back in
  • Chloride is circulating across
  • NET EFFECT: Bicarbonate into lumen - sodium goes between cells and leaks into lumen, dragging water by osmotic load
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21
Q

What does the stomach have (in relation to HCO3- secretion)

A

Stomach has defensive mucus layer filled with continuous secretion of bicarbonate, so the mucus layer in the stomach protects the gastric wall from being attacked by acid

We must neutralise acidic chyme to prevent intestinal ulcers

Also neutral pH for enzymes to act

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22
Q

What is secreted from the pancreas

How is it secreted

A
  • NaHCO3- solution
  • Cl-/HCO3- antiport co-transporter on apical membrane
  • HCO3- enters pancreatic duct
  • Na+ secreted through cell junctions
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23
Q

How else is NaHCO3 secreted, apart from the pancreas

A

By liver (bile)

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24
Q

Response of an increase in acid from the stomach

A
  • Sensors in duodenum
  • Secretin conc will rise
  • Stimulate pancreas to release bicarbonate, bicarbonate will flow into SI, neutralise acid and reduce the stimulus on secreting cells
  • -ve feedback loop controls HCO3-
  • Sensor picks up pH of SI
  • Acid is neutralised, SI protected
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25
Q

Where are secretin’s receptors

A

Found in the pancreas, which responds with additional bicarbonate delivery

Gastric motility and secretion are inhibited

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26
Q

TRYPSIN, CHYMOTRYPSIN, ELASTASE

  1. Substrate
  2. Action
A
  1. Protein
  2. Breaks peptide bonds in proteins to form peptide fragments

5-10 AAs long

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27
Q

CARBOXYPEPTIDASE

  1. Substrate
  2. Action
A
  1. Proteins
  2. Splits off terminal AA from carboxyl end of protein
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28
Q

LIPASE

  1. Substrate
  2. Action
A
  1. Fats
  2. Splits off 2 FAs from TAGs, forming free FAs and monoglycerides

Secretion of lingual lipase in saliva is MINOR - mostly lipases from pancreas split FAs from TAGs

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29
Q

AMYLASE

  1. Substrate
  2. Action
A
  1. Polysaccharides
  2. Splits polysaccharides into glucose and maltose
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30
Q

RIBONUCLEASE, DEOXYRIBONUCLEASE

  1. Substrate
  2. Action
A
  1. Nucleic acids
  2. Splits nucleic acids into free mononucleotides

Digestive enzymes isn’t just about breakdown of building blocks into smaller ones - causing amnesia in food - loses its original aim/design and become completely inert building blocks

Coronavirus will have RNA in it - injected into cells and our mechanisms will express the proteins of the coronavirus rather than our own RNA, which is important because it will break down external RNA

Ribonucleases are important, not just to bring energy into the cell or generate BBs, but protect us too

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31
Q

Examples of carbohydrates in foods

A
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32
Q

What is the importance of glucose homeostasis

i.e. [Glu]plasma

A

Major fuel for brain function

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33
Q

Food energy sources

A
  • Fat
  • Protein
  • CHOs
  • Alcohol
  • Water
  • Vitamins
  • Minerals
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34
Q

Rule of 2

A
  • Survive 2 mins without O2
  • Survive 2 days without water
  • 2 months without food
  • 2 years without vitamins and minerals
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35
Q

How much CHO do we use a day

How much of this does our brain use

A

250g

125g

CHO intake does not change much over the years

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36
Q

Glucose usage in muscle and adipose tissue

A
  • Major end target for glucose is muscle - largest mass of tissue in the body
  • Adipose tissue can take some glucose in
  • Adipose tissue and muscle are INSULIN DEPENDENT (some glucose uptake in muscle is INdependent)
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37
Q

Glucose uptake in brain

A

Insulin INDEPENDENT

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38
Q

When might we lose glucose from plasma into urine

A

If plasma conc is high as glucose will not be absorbed quickly enough in the PCT

39
Q

What is normal plasma glucose conc

A

Plasma glucose conc is 5mM (which in 3L of plasma is 6g of glucose and yet we’ll push 250g across a small compartment - turnover rate will change dramatically) fasting and doesn’t rise above 10 mM in healthy

40
Q

Schematic representing glucose absorption

A
41
Q

CHO digestion

A

Oligosaccharides (4-10 monosaccharides)

42
Q

Examples of CHOs

A
43
Q

What is starch

A

The way plants store CHOs

44
Q

What is glycogen

A

The way animals store CHOs

45
Q

Digestion of CHOs

A

Digestion in lumen of starches into shorter and shorter bonds until we have disaccharides floating the lumen

Finally digested on brush border membrane by disaccharidases (e.g. sucrose -> glucose and fructose in the presence of sucrase)

46
Q

Lactase deficiency

A

Inability to digest lactose, ends up in LI, bacteria in LI feast and produce gas and toxins

47
Q

CHO absorption

A
  • Na+ gradient couples sugar absorption into cell
  • 2 sodium ions in, 1 glucose in also
  • Chloride is meant to be transported both through the cell and between cells
  • Net effect - sodium glucose absorption, ends up in blood stream, dragging water by osmotic load
48
Q

Challenges in CHO absorption

A

Glucose, galactose and fructose are all polar molecules

SGLT1 imports sodium and glucose

Glucose will go through the GLUT 2 transporter which facilitates diffusion on the basolateral side of the membrane, into the bloodstream

49
Q

What was SGLT1 predicted to be

A

A transmembrane protein

50
Q

What does this graph show

A

SGLT1 does not account for all the absorption of glucose

At 50 mM it peaks and there’s no further increase in its rate of glucose absorption

GLUT2 into apical membrane that is responsible for the high concentrations

51
Q

Conc of glucose in experiments

A
  • 1 M conc of glucose has 180g of glucose in 1 L of water
  • Over the years, experiments have used 100 - 800 mM of glucose
  • Conc have gone down to 50-300 mM
  • No more than 100 mM in SI
  • Proximal SI - 100-150 mM is reasonable
  • Distal SI (jejunum and ileum) - conc drop - 1-2 mM
  • LI - 0.5 mM or less
  • Conc in plasma - 7-10 mM (in rats)
  • Secrete more into stomach to dilute content
  • Keep experimental data relevant to humans - testing at 800 mM is not relevant
52
Q

How are most CHOs in the diet consumed

A

As disaccharides or polysaccharides

53
Q

Name the major disaccharides and polysaccharides

A

DISACCHARIDES:

  • Sucrose
  • Lactose
  • Maltose

POLYSACCHARIDES:

  • Starch
  • Glycogen
  • Cellulose (only in LI as we do not have the enzymes to break the glucose glucose bonds in cellulose, so bacteria in LI is used to digest some of these fibres)
54
Q

CHO absorption

A
  • Brush border enzymes are attached to the luminal surface of enterocytes
  • Disaccharides -> monosaccharides
  • Fructose
  • Glucose
  • Galactose
  • SGLT1 will transport either glucose or galactose against a conc gradient
  • Na+ gradient generated
  • Glucose is being absorbed - for glycogen, make proteins out of it, oxidise and get ATP
55
Q

Another function of CHO absorption

A

Any bacteria still in chyme are exposed to a low glucose conc

  • glucose is produced directly next to glucose transporters
  • brush border membrane area that generates glucose and quickly absorbs it, keeping conc of glucose in the lumen low
  • also a feature of protecting the body from bacterial infection as bacteria also like glucose - enters glycolysis, generates energy for any cell very quickly so we keep conc of glucose in lumen low by having disaccharides on the brush border enzyme and not floating around inside lumen
56
Q

What is different about the digestion of protein

A

Site of the end of digestion is NOT in the lumen

57
Q

What is this structure

What do the sulfur bonds provide

A

Insulin

S bonds provide stability

58
Q

What would be the effect if I expressed insulin in an artificial solution and drank it - would plasma glucose change

A
  • Plasma glucose would not change as insulin is a protein - it will be digested in the stomach by pepsin and then trypsin in the SI - AAs will then be absorbed
  • In order to act as insulin it must retain its structure - injected into venous system
59
Q

What would happen if digestive enzymes were synthesised in their active form

A

They would digest the very cells that make them

HENCE inactive precursors (e.g. trypsinogen) become activated (trypsin)

60
Q

How does trypsinogen become trypsin

A
  • Enterokinase is stuck onto the brush border - luminal side
  • Cleave some Aas off trypsinogen and turn it into trypsin
  • ** in the stomach pepsin was activated by pepsinogen and acid
61
Q

Where are CCK’s receptors located

A
  • In the pancreas, which responds with additional enzyme delivery (activates through 2nd messenger)
  • In the gallbladder, which contracts to deliver more bile
  • In the sphincter of Oddi, which relaxes to facilitate delivery of the enzymes and bile salts
62
Q

What is the major stimulus for the release of CCK

A

FAs and AAs are sensed in the duodenum

63
Q

-ve feedback loop of CCK secretion

A

Digestion and absorption of FAs reduces the signal and at the end of the meal we will end this digestion phase and SI will be empty

64
Q

Pancreatic enzymes (PROTEASES) involved in digestion of proteins

A

Trypsin, chymotrypsin

  • Digest proteins to peptides
  • Trypsin activates other proteases, peptidases
  • Trypsin inhibitor secreted by pancreas to block action - KAZAL FACTOR adheres to trypsin and prevents it from being active
65
Q

Pancreatic enzymes (CARBOXYPOLYPEPTIDASES) involved in digestion of proteins

A
  • Digest polypeptides to small peptides and AAs
  • Carboxy-terminal AA
66
Q

Brush border proteases

A

ENTEROKINASE

Activates trypsin

67
Q

Brush border peptidases

A

AMINOPOLYPEPTIDASES

  • Digest polypeptides to small peptides and AAs
  • Amino-terminal

FUNCTION

  1. Digestion for purpose of absorption
  2. Helps to keep bacteria under control
68
Q

How are free AAs, mono, di and tri-peptides absorbed *UNUSUAL*

A
  • Absorbed into epithelium by active transport/facilitated diffusion, mainly in crypts (Na+ co-transport mechanism similar to glucose - SGLT1)
  • Digested inside the enterocytes - site where digestion ends is inside the enterocyte (epithelial cell)
69
Q

What do cytoplasmic peptidases do

A

Digest peptides to AAs

70
Q

How are some small peptides carried across the epithelium

A

By transcytosis

71
Q

Antigens involved in protein absorption

A
  • Development of food allergies and intolerances (e.g. gluten, coeliac disease)
  • Autism, schizophrenia, Parkinson’s disease
  • Prion disease
  • Potential for development of indigestible peptide drugs (e.g. peptide hormone replacement therapy)
72
Q

Protein digestion overview

A
  • Proteins are broken down to peptide fragments in the stomach by pepsin, and in the SI by trypsin and chymotrypsin, the major proteases secreted by the pancreas
  • These fragments are further digested to free AAs by carboxypeptidase from the pancreas and aminopeptidase, located on the luminal membranes of the SI epithelial cells
  • The free AAs then enter the epithelial cells by secondary active transport coupled to Na+
  • Short chains of 2 or 3 AAs are also absorbed by a secondary active transport coupled to the H+ gradient
73
Q

Movement of peptides across lumen, intestinal epithelial cell and IS fluid

A

AAs leave by faciliated diffusion and get carried away through the portal vein into the liver

74
Q

Why does lipid digestion take longer than other nutrients

A
  • Takes longer than all the other nutrients
  • Lipids are not soluble in water
  • Most of our proteins are water soluble material
  • Lipid environment requires emulsification
  • Full of fat, but lots of it not available for digestion or absorption
  • Must access fat before we can digest it - long delay
75
Q

What is essential for emulsification

A

Bile salts

76
Q

CCK and lipid digestion

A
  • Bile salts are secreted by the liver, stored in gallbladder
  • in response to CCK gallbladder will contract and release bile salts into duodenum because CCK also relaxes the sphincter of Oddi
77
Q

What is bile secreted by

A

Hepatocytes

78
Q

Contents of bile

A
  • Cholesterol
  • Bile salts - cholesterol and AAs
  • Lecithin (phospholipid)
  • Bile pigments - bilirubin, biliverdin
  • Water
  • NaHCO3
79
Q

Max capacity of the gallbladder

A

60 ml

80
Q

How can bile be concentrated

A

By absorption of fluid and electrolytes by epithelium of gallbladder

81
Q

Trigger of the release of bile

A

CCK

ACh

Sphincter of Oddi relaxes

82
Q

What are gall stones

A

Crystals of cholesterol

High fat diet and inflammation of mucosa

83
Q

Function of bile - DIGESTION

A

EMULSIFICATION

  • Bile salts and lecithin
  • Mechanical processes break up fat droplets
  • Lipases digests fats in the presence of colipase - a cofactor needed for lipase to penetrate bile salts
84
Q

Function of bile - ABSORPTION

A

MICELLE FORMATION

  • Complexes with a sterol nucleus that ferrys fats through the brush border to allow absorption into epithelial cells
  • Bile salts reabsorbed in ileum - 94%
  • Re-secreted
85
Q

Structure of bile salt

A

Non-polar surface helps to emulsify fats

Polar surface promotes water solubility

86
Q

MOA of bile salts

A
  • Biphasic molecule - bile salts can attach to fat molecules with its fat soluble side and attach to water with its polar side
  • => EMULSIFY FAT
  • Emulsify is the bringing together of fat and water in very close approximation
  • Making a very well mixed solution of fat
  • We’re really increasing the surface area
  • Imagine a football full of marbles - Skin is suitable to aqueous environment, but when marbles are allowed out SA increases massively (emulsification)
  • SA:vol ratio is INCREASED - making it accessible to our water soluble enzymes
  • Phospholipids can help - every cell membrane is composed of phospholipids - they too have a polar end and a fat soluble end
  • Importance of CHEWING - breaking up cell membranes - maybe the function is to facilitate emulsification of fat - so fat can be sensed in the duodenum
  • +VE FEEDBACK LOOP - release of phospholipids will facilitate emulsification - facilitate digestion in SI
87
Q

What happens once the fat globule has been broken down into smaller pieces

A
  • Lipases from pancreatic origin will digest the emulsified fat
  • TAGs = 95%
  • LCFAs - 16 or 18 Cs
  • Lipases cleave off/hydrolyse the FAs off the TAG and take position 1 and 3 off
  • Molecules must migrate across the mucus layer
  • Cannot readily diffuse across the mucus layer - form micelles, spheres with water soluble component of the molecule facing out and fat soluble component inside
  • These micelles will migrate across the brush border membrane and end up adjacent to the epithelial cell
  • Diffusion does NOT happen - fat is an energy dense nutrient
  • Diffusion suggests that when conc of FAs is low in the lumen, FAs can just diffuse back out - extremely unlikely that we’d just lose this nutrient after we used so much energy to acquire and digest food
88
Q

Overview of fat digestion

A
  • NOT DIFFUSION but at least 3 classes of specified transporters that transport Fas into the cell
  • End of digestion by pancreatic lipases and absorption of Fs is TRANSPORTER mediated
  • Inside the cell we re-synthesise TAG and re-package them
  • Enzymes inside enterocytes that will take Fas and monoacylglycerols and form a TAG again
  • ER will package those cells - CHYLOMICRON, which has an apolipoprotein (specialised protein in enterocytes that allows binding of lipids, together with some cholesterol)
  • Chylomicron has a water-soluble outside, lipid soluble core - way to transport fats in the bloodstream - we can’t have free FAs in the bloodstream as they’ll just float to the top and damage the brain
  • We must have similar density molecules and chylomicrons serve that function
  • In systemic circulation chylomicrons will be re-circulated so they can feed tissues or else stored in adipocytes
89
Q

Structures in this image

A
  • Microvilli at the top
  • Middle cell - nucleus - chromatin (DNA) around the rim
  • Secreted on basolateral side - rate-limiting step for absorption of lipids is the ability of cell to export chylomicrons into the left
90
Q

How are the fat soluble vitamins absorbed

A
  • Like other lipids
  • Move freely with lipid phase
  • Taken up by diffusion
91
Q

How are water-soluble vitamins absorbed

A

By diffusion or mediated transport, except for VITAMIN B12, which must first bind to a transport protein known as intrinsic factor (secreted by the stomach)

92
Q

Summary of liver functions

A
93
Q

Water homeostasis

A
  • Secrete into lumen and then reabsorb in the lumen
  • Water secretion make up 6L a day
  • We reabsorb about 7 L daily
  • Much greater absorptive capacity than we’d imagine
  • 1L drinking
  • 0.5L from food
  • Reabsorbed in SI by osmosis
  • Osmotic drag - across epithelium into IS fluid and then plasma
  • What moves through? 1.5L of water, some fibre that wasn’t digested or absorbed, some cells shed from villi
  • Low energy density moves to LI

GIT physiology (11 decks)

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