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SMP - GI > Lectures 12 & 13 - Digestion & Absorption > Flashcards

Lectures 12 & 13 - Digestion & Absorption Flashcards

1
Q

What is found in between the villi of the small intestine?

A

Crypts of Luberkuhn

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2
Q

What 4 digestive enzymes act on polypeptides?

A
  1. Gastric pepsins
  2. Pancreatic proteases
  3. Intestinal mucosal polypeptides
  4. Enterocyte cytoplasm peptidases (di and tripeptides only)
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3
Q

What are the 7 digestive enzymes secreted by the intestinal mucosa in the brush border membrane?

A
  1. Enterokinase
  2. Peptidases
  3. Maltase
  4. Isomaltase
  5. Lactase
  6. Sucrase
  7. Cystoplasm peptidases
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4
Q

What 2 digestive enzymes act on proteins? Products?

A
  1. Gastric pepsins
  2. Pancreatic proteases

Products: smaller peptide chains

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5
Q

Products of lipases?

A

Diglycerides, monoglycerides and FAs

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6
Q

Products of salivary and pancreatic amylases?

A

alpha-limit dextrins, maltotriose, and maltose

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7
Q

What is the activator of amylases?

A

Cl-

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8
Q

Products of enterocyte cytoplasm peptidases?

A

AAs

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9
Q

Products of brush border peptidases?

A

AAs, di and tripeptides

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10
Q

Forms of carbs ingested? Majority?

A
  1. Starch***
  2. Disaccharides***
  3. Fibers = cellulose
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11
Q

Does the small intestine have both villi and microvilli? Difference? Which make up the brush border?

A

YUP

Villi sit on folds and ***microvilli sit on the villi

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12
Q

What is the central lacteal covered by in the villi?

A

Capillary net

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13
Q

Where are the small intestinal villi located exactly?

A

From the major papilla in the duodenum through the ileum, although they are less dense in the distal areas

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14
Q

2 types of brush border enzymes?

A
  1. Proteases

2. Saccharidases

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15
Q

What are starches?

A

Polymers of glucose attached via alpha glycosidic bonds

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16
Q

What is sucrose?

A

Fructose + glucose

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17
Q

What is lactose?

A

Galactose + glucose

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18
Q

What is maltose?

A

Glucose + glucose

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19
Q

What is cellulose?

A

Polymers of glucose attached via beta glycosidic bonds

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20
Q

Do humans have cellulase?

A

NOPE

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21
Q

Can disaccharides be absorbed by the enterocytes?

A

NOPE

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22
Q

Describe the breakdown of starch.

A
  1. In the mouth digestion by salivary alpha-amylase into maltose oligosaccharides (and some isomaltose oligosaccharides)
  2. Majority of digestion occurs in the small intestines by pancreatic alpha amylase producing small glucose polymers (alpha-limit dextrins, maltotriose, maltose, sucrose, lactose)
  3. Final digestion done by brush border enzymes
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23
Q

In how much time are all polysaccharides digested in the small intestine?

A

Within 10-20 min (by the time the chyme reaches the upper jejunum)

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24
Q

What can maltase and isomaltase digest? Products?

A

Maltose and 3-9 glucose polymers

Products: glucose, maltose, and oligosaccharides

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25
Q

Other name for isomaltase?

A

Alpha-limit dextrinase

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26
Q

What 2 enzymes are actually synthesized as a single polypetide chain? How/where are they cleaved?

A

Sucrase and isomaltase

At the brush border, proteases cleave the protein into the two enzymes.

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27
Q

What are the effects of membrane disaccharidase deficiency? Example?

A

Increase in lumenal osmolarity, lumenal lactic acid, diarrhea, gas formation

Example: lactose intolerance

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28
Q

Other name for maltase?

A

Glucoamylase

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29
Q

What happens to undigested cellulose?

A

These remain in intestines and since carbohydrates are strong osmotic agents (they carry a lot of water) => avoids complete dehydration of the feces and constipation

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30
Q

Why is there water in our feces under normal circumstances?

A

Osmotic effect of:

  1. Fibers
  2. Bile
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31
Q

What are maltose oligosaccharides?

A

Polymers of 3-9 glucose

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32
Q

Specific gastric starch digestion?

A

NONE

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33
Q

How does the activity of the salivary alpha-amylase and lingual lipase change once the food enters the stomach?

A

Decrease with decrease in pH until pH of 5 (no activity at this point)

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34
Q

Limits of the brush border?

A

Late duodenum to jejunum

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35
Q

Do we end up with more glucose, fructose, or galactose in the small intestine?

A

More glucose

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36
Q

Can the pancreatic enzymes and brush border enzymes work at a low pH?

A

NOPE

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37
Q

What are alpha-limit dextrins?

A

Isomaltose

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38
Q

Describe how glucose is transported from the intestinal lumen to the cytoplasm of the enterocytes. How does it work? What other monosaccharide does it transport?

A

Glucose-sodium transporter (SGLT1): sodium-dependent secondary active transport by using Na+/K+ ATPase on the basolateral side of cell

Also carries galactose

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39
Q

What happens to all monosaccharides once they enter the enterocyte cytoplasm?

A

They will leave the basolateral membranes by facilitated transport through GLUT2 transporters and then diffuse from the interstitial space to the capillaries and into the portal circulation

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40
Q

What factors influence transport by the SGLT1?

A

The Na+/K+ ATP ase pump, NS specific monosaccharide structure (allose, not gulose)

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41
Q

What factors influence transport by the SGLT1?

A

The Na+/K+ ATPase pump, NS specific monosaccharide structure (allose, not gulose)

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42
Q

Describe how fructose is transported from the intestinal lumen to the cytoplasm of the enterocytes. How does it work?

A

Specific GLUT5 carrier proteins via facilitated transport

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43
Q

What is the principle behind oral rehydration therapy?

A

Rapid reabsorption of glucose facilitates Na+ absorption (SGLT1 transporter) and hence Cl- and H2O transport

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44
Q

Are GLUT 5 transport insulin dependent?

A

NOPE

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45
Q

Why is it dangerous to rely on FA beta oxidation for energy?

A

Ketone bodies production

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46
Q

What are Olestra and Sucralose? Risks?

A

Dietary supplements:

  • Olestra: fat supplement that is a sucrose polyester not digestible nor absorbed (0 caloric content), but can cause digestive problems like gas, increased motility, and reduced absorption because the carb part of it is great food for colonic bacteria and because it’s an osmotic agent => cramps, diarrhea, and flatulence
  • Sucralose: sugar supplement that is a chlorinated sugar compound (chlorocarbon) that for the most part is not digested nor absorbed => same types of issues as Olestra because of the sugar moiety (BUT we usually do not eat as big amounts as with Olestra)
47
Q

What do unabsorbable gases cause in the intestines?

A

Gases that cannot be absorbed (H2 or methane) => distend the intestines => mechanoreceptors activated => smooth muscle contractions => cramps

48
Q

Describe the breakdown of proteins.

A
  1. In the stomach HCl digests proteins and activates pepsinogens to pepsins, which aid specific protein digestion into oligopeptides (4-10 AAs)
  2. In the small intestine, pancreatic proteases are secreted as zymogens into the duodenum where they are activated by enterokinase and proteins are digested into smaller oligopeptides
  3. At the brush border, specific proteases break down the oligopeptides into di- and tri-peptides and AAs, which can be absorbed into the enterocytes
  4. In the enterocyte, cytoplasmic peptidases break any di- and tri-peptides into AAs => therefore, the final products are AAs
49
Q

Describe how digested proteins are transported from the intestinal lumen to the cytoplasm of the enterocytes. How does it work?

A
  1. Di- and tri-peptides enter cell by a specific peptide transport protein by facilitated transport
  2. AAs enter cells by a variery of mechanisms
50
Q

What happens to AAs once they enter the enterocyte cytoplasm?

A

Leave the enterocyte via facilitated transport

51
Q

Can di/tripeptides get out of the enterocytes, into the blood?

A

NOPE

52
Q

Can di/tripeptides get out of the enterocytes, into the blood?

A

NOPE

53
Q

Are AA transporters into enterocytes Na+ dependent?

A

Some yes, some no

54
Q

Describe the breakdown of lipids.

A
  1. In the mouth lingual lipase cleaves TAGs to FAs and diglycerides
  2. In the stomach gastric lipase cleaves TAGs to FAs and diglycerides
  3. In the small intestine pancreatic lipase cleaves TAGs to FAs and monoglycerides; cholesterol esterase cleaves cholesterol esters into cholesterol and water soluble acid and also cleaves ester-type substances like fat-soluble vitamins D & E; phospholipase A2 cleaves phospholipids (like lecithin) into lysolecithin
  4. Micelle brings lipids to the enterocytes and releases them so that they can diffuse into the enterocytes
55
Q

Can cholesterol esters enter the enterocytes?

A

NOPE

56
Q

How is pancreatic lipase different from lingual and gastric lipases? Describe how it works. What is this critical for?

A

It requires a co-lipase to work: it is secreted in active form, but is inactive in the presence of bile salts and acids because the bile binds to the surface of TAG oil drops to form an emulsion (by the time lipids get to the intestine, a lot of bile has been secreted) => co-lipase secreted from the pancreas is activated in the duodenum by trypsin => colipase binds to bile salts by the oil drops => one lipase molecule forms a complex with one co-lipase molecule => this process “opens a door” for the pancreatic lipase to access the lipids and is critical to the formation of micelles

57
Q

What lipase accounts for the majority of lipid digestion?

A

Pancreatic lipase (70-80%)

58
Q

3 necessary elements for micelle formation in small intestine?

A
  1. Bile salts
  2. Pancreatic lipase
  3. Pancreatic co-lipase
59
Q

What is the rate limiting step for lipid absorption?

A

Passage of lipids past the unstirred layer of water

60
Q

Once past the unstirred layer of water, describe how lipids are transported from the intestinal lumen to the cytoplasm of the enterocytes. What kind of lipids can do this?

A

By simple diffusion

FAs, monoglycerides, cholesterol, lysolecithin, fat-soluble vitamins (ADEK)

61
Q

What happens to the lipids once they have entered the enterocytes?

A

They are re-esterified with FFAs in the SER to form TAGs, cholesterol esters, and phospholipids, packaged into chylomicrons, and then they exocytose into the lacteal

62
Q

Why is there fat in stool under normal conditions?

A

From colonic bacteria and desquamated intestinal cells

63
Q

What is steatorrhea? What is this sometimes associated with? Characteristics of stool?

A

Fat in stool from malabsorption or bile salt insufficiency

If the steatorrhea is caused by ineffective bile => bile salts are not appropriately reabsorbed and this also has an osmotic effect => diarrhea

Feces: bulky and difficult to flush, have a pale and oily appearance and can be especially foul-smelling

64
Q

Reaction of lipases on lipids?

A

Hydrolysis

65
Q

Effect of very fatty meal on digestion? How many times would the bile cycle in this case?

A

Slows gastric emptying

Up to 6 times

66
Q

What allows the chylomicrons to exocytose from the enterocytes?

A

Beta-lipoprotein coat

67
Q

Where is beta-lipoprotein synthesized?

A

In cells of the small intestine and the liver

68
Q

What is betalipoproteinemia? Explain it.

A

Lack of beta-lipoprotein => massive lipid accumulation in the ER of the enterocytes

69
Q

Can the liver synthesize phospholipids de novo if we do not absorb enough in our diet?

A

YUP

70
Q

Where does water absorption primarily occur in the SI? How much?

A

Jejunum and ileum

0.5 L

71
Q

Where does extra water absorption occur if we drink more than 2 L of water a day?

A

Colon in haustra

72
Q

Mechanism of water absorption by intestine?

A

Osmosis

73
Q

How is Na+ absorbed by the intestine? Where does this occur?

A

Na+/K+ ATPase on the basolateral side of the enterocytes sets up a concentration gradient (3 Na+ for 2 K+) => this makes the interstitial fluid hypertonic and positively charged, so water and anions (like Cl-) follow to preserve electroneutrality.

Then there are 3 different lumenal transporters:

  1. In the jejunum and colon, enterocytes produce carbonic anhydrase, and Na+ is absorbed and H+ ions enter the lumen through an Na+/H+ antiporter
  2. In the small intestine there is specific Na+ co-transport with AAs and monosaccharides (glc, gal)
74
Q

Describe Cl-/HCO3- exchange in the intestine. Where does this occur?

A

Cl-/HCO3-exchanger in ileum and proximal colon: lots of bicarbonate is secreted into the ileum and colon to neutralize the H+ products secreted by bacteria

75
Q

Describe K+ absorption by the intestine.

A
  • Passively absorbed in jejunum and ileum: concentration gradient increases as water is absorbed–has to have high concentration in the lumen to move, since intracellular K+ is high!
  • Primarily secreted in the colon, but can be absorbed if lumenal concentration is high (over 25mM)
76
Q

How does aldosterone affect K+ secretion in colon?

A

Increases secretions in colon in exchange for Na+

77
Q

Describe iron absorption by the intestine. In what form is iron absorbed?

A

Ferrous (Fe2+) forms are less likely to form insoluble salt forms, and thus, is more easily absorbed than ferric (Fe3+) forms, so ferric forms can be produced from ferrous forms by ferrireductase on the lumenal membrane

Free iron is toxic to the cells, so to get into the enterocyte (from duodenum and jejunum), iron needs a carrier protein (DMT1) to cross the membrane and enter cell => brush border membrane receptors bind the complex and it enters the cell (probably by endocytosis) => iron is stored bound to intracellular ferritin, or released at the basolateral membrane (through hephestin/IREG1 complex) and bound to plasma transferrin => iron taken up by liver or bone marrow and the transferrin is resecreted into lumen

78
Q

What 2 factors will favor the ferrous form of iron in the intestine?

A
  1. Low pH, so acidic pH of the stomach and duodenum helps iron absorption by producing the ferrous form
  2. Vitamin C (and other reducing agents) also produce the ferrous form
79
Q

What does DMT1 stand for?

A

Divalent metal transporter 1

80
Q

What does IREG1 stand for?

A

Iron-regulated transporter 1

81
Q

How is heme iron absorbed by the intestine?

A

Well absorbed by facilitated transport => inside the enterocyte iron is split from heme by xanthine oxidase => can be stored or bound to transferrin

82
Q

What people need extra iron?

A
  1. Women
  2. Pregnant women
  3. Children
83
Q

What is absorption of iron determined by?

A

NEED! Amount needed to replenish stores

84
Q

How much iron is ingested a day? How much of it is absorbed?

A

Iron ingested = ~20 mg, ~1 mg absorbed

85
Q

Where do men and women usually lose iron?

A

Iron stored in enterocytes in ferritin pools is lost when they slough off every 3 to 4 days

86
Q

Describe calcium absorption by the intestine. Where does this occur?

A

Jejunum is the major site of absorption

Calcium enters the enterocyte bound to CaBP (to maintain very low intracellular free calcium levels) => can then be utilized by organelles in cytoplasm or stored bound to cytosolic CaBP => exits basolateral side in exchange for sodium by Na+/Ca++ antiporter or by the Ca++-ATPase

87
Q

What regulates calcium absorption by the intestine? What is the goal?

A
  1. Bile salts facilitate calcium absorption
  2. Acidic environment facilitates absorption
  3. Vitamin D increases CaBP binding sites on the luminal membrane and basolateral Ca++-ATPase so will double the uptake of calcium into the enterocyte
  4. PTH increases membrane calcium-binding protein (CaBP)

=> ALL OF THESE ARE AIMED TO REGULATE PLASMA LEVELS IN RESPONSE TO CHANGES

88
Q

What is the major site of plasma Ca++ regulation? Kidneys or intestines?

A

Intestinal absorption is major site of regulation

89
Q

How are vitamins absorbed by the intestine?

A
  1. Fat-soluble vitamins are incorporated into micelles and diffuse into the enterocytes
  2. Water-soluble like niacin, thiamine, folic acid, and vitamin C are absorbed by secondary active transport with Na+
  3. Pyridoxine by diffusion
  4. Riboflavin by facilitated transport
  5. B12 (cobalamin): B12/intrinsic factor complexes dimerize and are absorbed in the terminal ileum by binding to a receptor => B12 enters the cell as a dimer and probably is stored in the mitochondria until it exits the basolateral side before being attached to TC2
90
Q

How is phosphate absorbed by the intestine? What is this similar to? What is this regulated by?

A

Na+-Pi cotransporter, just like in the kidney!

  • The intestines will readily absorb Pi, except if there is a surplus of calcium, which can form insoluble Ca++-Pi compounds
  • Absorption enhanced by increased plasma Vitamin D3 or PTH (indirectly)
91
Q

How is magnesium absorbed by the intestine? Where does this occur? What are high absorption rates due to?

A

Passive diffusion through entire small intestine

Higher rates proximally due to acidic environment

92
Q

What is VB12 bound to in the blood?

A

Transcobalamin II

93
Q

List the gases found at different parts of the GIT.

A
  1. Stomach: O2, N2
  2. Duodenum: CO2
  3. Ileum and colon: CO2, H2, CH3, H2S, NH3
94
Q

What are the 2 main electrolytes in feces?

A
  1. K+

2. HCO3-

95
Q

What are gases in the intestines formed by?

A

Bacterial digestion of starches/sugars/fiber is the main source of gas that will be expelled as flatus

96
Q

% feces weight that is water?

A

75%

97
Q

% feces weight that is solid bacteria?

A

30%

98
Q

% feces weight that is solid inorganic material (calcium and phosphates)?

A

15%

99
Q

% feces weight that is solid fat and fat derivatives?

A

5%

100
Q

% feces weight that is solid desquamated mucosal cells, mucus, small amounts of digestive enzymes?

A

Trace amounts

101
Q

Does Ca++ need to be bound in blood? What % of it is bound?

A

NOPE

40%

102
Q

What can diarrhea be caused by?

A
  1. Viral or bacterial infections
  2. Antibiotics
  3. Irritation of the intestines (e.g. spicy, garlicky foods)
  4. Inflammation (e.g. IBD)
  5. Osmotic agents (e.g. undigested carbs, bile, and laxatives)
103
Q

When you think diarrhea, think…

A

INCREASED MOTILITY => REDUCED ABSORPTION

104
Q

Where do most gut bacteria live?

A

Ileum and colon

105
Q

What are “good” bacteria in the gut biota? Example?

A

Good bacteria, including Bifidobacteria, can process plant polysaccharides making products including vitamins (K and Biotin) which can diffuse through the intestinal lining into blood.

They are considered “protective” because they help maintain GIT and systemic immunity and are some of the probiotics we hear about.

106
Q

Can we repopulate intestinal flora with yogurt?

A

Mixed evidence

107
Q

What has been implicated in initiation of colon cancer that is related to gut bacteria?

A

Bacteroides (not E. coli!) can cause infection if abscesses occur and have been implicated in initiation of colon cancer and possibly colitis

108
Q

Can gut bacteria become resistant to antibiotics?

A

YES

109
Q

Is E. Coli present in the intestine? Is it harmful?

A

Not much is normally present in intestines and it is not harmful- except some strains that can be present in contaminated food, and then it can cause big problems in the small intestine.

110
Q

What has been show to repopulate gut bacteria? Explain.

A

Fecal transplants especially in people with C. Diff

111
Q

% feces weight that is solid cellulose and other indigestible fibers?

A

Depends on diet

112
Q

Purpose of bile emulsifying the TAGs?

A

Break them down into smaller droplets so that the pancreatic lipase can access them = increase in surface area

113
Q

Are sucrose and lactose digested before entering the SI?

A

NOPE

SMP - GI (21 decks)

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