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PBL SEM 4 > digestion and absorption mechanism of nutrient absorption > Flashcards

digestion and absorption mechanism of nutrient absorption Flashcards

1
Q

what is digestion?

A

the breakdown of large molecules into small molecules which can then be absorbed

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2
Q

what are proteins broken down into?

A

amino acids, di and tri peptides

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3
Q

what are brush border enzymes attached to?

A

the luminal membrane of the small intestinal cells

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4
Q

what are polysaccharides broken into?

A

monosaccharides

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5
Q

polysaccharide vs disaccharide breakdown

A

polysaccharides mainly by salivary amylase and pancreatic enzymes

disaccharides mainly by brush border enzymes

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6
Q

what is a triglyceride made of?

A

a back bone of glycerol with 3 fatty acids attached by ester bonds

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7
Q

what are triglycerides broken into?

A

2 free fatty acids and a monoglycerides

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8
Q

what does incomplete digestion result in?

A

malabsorption

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9
Q

what are triglycerides broken down by?

A

gastric lipase (minor), mainly pancreatic lipase, also bile salts

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10
Q

what are the methods of absorption?

A
  • simple diffusion
  • carrier-mediated (amino acids and sugars) — secondary active and facilitated diffusion
  • (receptor-mediated) endocytosis — vit B12 and intrinsic factor (both produced by stomach parietal cells) and cholesterol
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11
Q

what are the different sites of absorption?

A
  1. mouth, oesophagus, stomach — limited diffusion
  2. duodenum and jejunum - MAJOR SITE
  3. ileum
  4. colon
  5. rectum - limited diffusion
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12
Q

what is absorbed in the ileum?

A

vit B12, bile salts and K+ (all in terminal ileum)

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13
Q

what is absorbed in the colon?

A

Na+, some H2O, and short chain fatty acids

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14
Q

describe the sublingual and suppository routes of drug delivery

A
  • avoid 1st pass metabolism by the liver
  • mouth and rectum — the blood at these sites of absorption goes straight to heart instead of liver via portal vein
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15
Q

what is the total SA of the SI?

A

200 m2

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16
Q

what does a decreased SA lead to?

A

malabsorption

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17
Q

what transport proteins are expressed on the apical/brush border membrane for glucose and galactose transport?

A

SGLT1 - mediate Na+ dependent co-transport of glucose and galactose

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18
Q

what generates the sodium gradient for the movement of glucose and galactose into the cell?

A

NaK ATPase on the interstitial membrane

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19
Q

what does the sodium gradient enable in CHO absorption?

A

sodium gradient is used to drive glucose transport into the cell, so it can move in against its conc gradient throguh SGLT1- secondary active transport process

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20
Q

what is secondary active transport? what is an example of primary active transport?

A

against a conc gradient, energy derived from Na+ gradient created by Na+ pump

Na+ pump = primary active transport

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21
Q

what is absorbed along with glucose?

A

sodium

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22
Q

what happens as glucose accumulates in cell?

A

sets up a conc grad — allows glucose to leave the cell via glucose transporters (GLUT2) = facilities diffusion

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23
Q

via what does fructose enter and leave the cell?

A

enters via GLUT5 and leaves via GLUT2

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24
Q

what does GLUT4 have a dependency for?

A

insulin

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25
Q

what does a lack of transporters result in?

A

malabsorption

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26
Q

describe glucose-galactose malabsorption syndrome

A
  • genetic disease
  • SGLT1 (glucose transporter on apical membrane) mutated = no absorption of glucose or galactose
  • severe and potentially fatal diarrhoea in infants (manifests early, lack nutrition and become dehydrated rapidly)
  • treatment = avoid glucose and galactose
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27
Q

how many dietary amino acids are there?

A

20

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28
Q

50% of amino acids are absorbed as di and tri peptides by what?

A

PepT1

other 50% by specific transporters

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29
Q

what happens to peptides in enterocyte?

A

hydrolysed to amino acid (released into blood as aa)

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30
Q

name some amino acid specific transporters. superfamily?

A
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31
Q

PepT1 uses what gradient for transfer of peptides across the membrane?

A

H+ gradient — cotransport

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32
Q

alanine transport?

A

Bo cotransport — alanine and Na+

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33
Q

XAG- transproter?

A
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34
Q

what is Hartnup disease?

A

a rare genetic disease — B0 transporter affected

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35
Q

what is cystinuria?

A

an inherited condition characterized by a buildup of the amino acid, cystine, in the kidneys and bladder. This leads to the formation of cystine crystals and/or stones which may block the urinary tract.

B0 transproter is affected

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36
Q

fat digestion problems leads to deficiencies in which vitamins?

A

K, A and D

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37
Q

what enzyme mainly influences fat digestion?

A

pancreatic lipase

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38
Q

what are the 2 major roles of bile salts?

A
  1. emulsification of large fat droplets to increase the SA for action of lipase
  2. formation of mixed micelles = stabilises products of triglyceride hydrolysis (monoglyceride and fatty acids) while they are ‘translocated’ to apical membrane
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39
Q

what do mixed micelles consist of?

A

monoglcyerides, fatty acids, bile slats, phospholipids and cholesterol

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40
Q

what does a lack of bile result in?

A

steatorrhoea

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41
Q

what is the average dissociation constant of free fatty acids? what does this mean?

A

pKa of 4.9

means that at a pH of 4.9, 50% of the fatty acids will be in the undissociated form (simple diffusion is possible in the undissociated form)

if you go more acidic than 4.9, more than 50% will be in the undissociated form, opposite for above 4.9 (more alkali)

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42
Q

what is the pH of the lining/wall of the SI?

A

pH 6.5 (slight acidity) — therefore few FFAs in the undissociated state

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43
Q

name 2 fatty acid transporters

A

FAT (fatty acid transproter) + CD36

SFCA (short chain fatty acid) transporters in colon

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44
Q

what happens after fatty acids and monoglycerides are absorbed?

A
  • triglycerides resynthesised in endoplasmic reticulum and packaged into chylomicrons
  • chylomicrons then leave by exocytosis
  • chylomicrons transproted in lymphatic system to liver (lacteal)
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45
Q

where is cholesterol absorbed?

A

duodenum

46
Q

what is cholesterol absorption largely dependent on?

A

Niemann-Pick C1-Like 1 (NPC1L1) protein

47
Q

what does NPC1L1 enable?

A

receptor-mediated endocytosis in cholesterol absorption

48
Q

what does ezetimibe do?

A

inhibits cholesterol endocytosis — decreases plasma cholesterol

can be used in combination with statins or when statins aren’t tolerated

49
Q

name 3 short chain fatty acids

A

butyrate, propionate, acetate

50
Q

describe SCFA

A
  • not major component of diet
  • produced by bacterial fermentation of undigested polysaccharides in the colon
51
Q

what are SCFAs absorbed with and via what?

A

with Na+ via the sodium co transproter called the SMCT1

52
Q

what are SCFAs mainly used by the colonocyte for?

A

intracellular metabolism

53
Q

what enhances health of colon epithelium and may help prevent colon cancer?

A

butyrate

54
Q

bacteria that mainly produce _____ are much better for you than ____ and _____

A
  • butyrate
  • proprionate and acetate
55
Q

via what does water move across the wall of the SI?

A

osmotic gradient

56
Q

what is the osmotic gradient mainly created by?

A

the absorption of gradients

57
Q

how many litres of water are absorbed each day?

A

8.4 L

(6.5L in SI whereas only 1.9L in colon)

58
Q

route for H20 absorption in SI?

A
  • via junctional complexes between cells
  • via SGLT1 and aa transporters
  • NOT aquaporin water channels
59
Q

what enters the gut via saliva (mouth)?

A

NaCl

60
Q

what enters the gut via the stomach (gastric secretion)?

A

HCl

61
Q

what enters the gut via pancreatic and bile secretion (duodenum)?

A

HCO3-

62
Q

what enters the gut in the jejunum?

A

NaCL

63
Q

what enters the gut in the ileum?

A

HCO3-

64
Q

what enters the gut in the colon?

A

K+ and HCO3-

65
Q

what transporters are present in the jejnumum and ileum?

A

Na/glucose or Na/amino acid cotransporters

66
Q

what exchanger is present in the duodenum and jejunum?

A

Na-H exchanger

67
Q

what exchangers are present in the ileum and proximal colon?

A

parallel Na-H and Cl-HCO3- exchangers

68
Q

what channel is present in the distal colon?

A

epithelial Na+ channel

69
Q

what are sodium channels in the distal colon regulated by?

A

steroid hormone called aldosterone — increases sodium absorption in the colon

70
Q

what has no active absoprtion in the SI or LI?

A

HCO3-

71
Q

how is K+ absorbed in the ileum?

A

para cellular diffusion

72
Q

K+ in the LI?

A

predominantly secretion

73
Q

concentrations of K+ and HCO3- in faeces?

A

quite HIGH

[K+] = 90 mM
[HCO3-] = 30 mM

74
Q

what does severe/chronic diarrhoea lead to?

A

hypokalaemia and metabolic acidosis

75
Q

what does an increased osmotic load in the colon lead to?

A

increased fluid in faeces — diarrhoea

76
Q

what causes increased osmotic load?

A

incomplete digestion and absorption of food
- lack of enzymes or transporters
- damage to mucosal cells

secretion of ions by gut
- enhanced secretions of NaCl (esp in SI) — oversaturated the capacity to reabsorb fluid

77
Q

describe lack of enzymes or transporters causing diarrhoea

A
  1. congenital (neonate) = ‘watery’
    - glucose-galactose malabsorption (SGLT1)
    - lactase deficiency
  2. disease of pancreas and biliary systems = steatorrhoea — fats passed into LI where it is metabolised by bacteria — flatulence — abdominal pain and foul smelling stool
    - pancreatitis, cystic fibrosis
    - hepatitis, gall stones
78
Q

what autoimmune disease can cause damage to mucosa?

A

coeliac disease and chron’s disease

79
Q

effects of shigella and campylobacter

A

bacteria (shigella and campylobacter) cause destruction of intestinal wall (decreases SA) —> blood in faeces (dysentery)

80
Q

effects of salmonella

A

inflammation —> chronic diarrhoea

81
Q

what are the main causes of diarrhoea in the UK?

A

rotavirus and norovirus

82
Q

describe vibrio cholera, some strains of E. Coli and rotavirus infections

A

secretions of ions by gut

  • toxin produced by bacteria which “hi-jacks” normal cellular processes
  • intestinal cells normally secrete H2O 9togegtehr with mucus and HCO3-) — roughly 1 litre a day
  • in cholera secretion exceeds 20 litres a day
  • toxins may also inhibit sodium absorption BUT not SGLT1 — basis of oral rehydration therapy
83
Q

name the fat vs water soluble vitamins

A

fat soluble = vitamins A/D/E/K
water soluble = B group and C vitamins

84
Q

how are fat soluble vitamins absorbed?

A

facilitated diffusion and/or endocytosis at physiological concentrations

85
Q

what does the absorption of fat soluble vitamins require? clinical significance?

A

optimal fat digestion — means what people with pancreatic and biliary disease have deficiencies in these vitamins (esp vit K which doesnt have large stores in the body)

86
Q

how are water soluble vitamins absorbed? exception?

A

have specific transporters (facilitated and secondary)

exception is B12 — endocytosis — requires intrinsic factor secreted from parietal cells in the stomach which binds to B12 - this complex is then absorbed via endocytosis

87
Q

vitamin C has a specific transporter coupled to what?

A

Na+ entry

88
Q

what 2 routes can Ca++ absorption in the SI occur by?

A

trans cellular and paracellular

89
Q

which route for Ca++ absorption in the SI is regulated by vitamin D?

A

transcellular

90
Q

calcium enters the cell apical membrane by what channel?

A

TRPV6

91
Q

TRPV5 vs V6

A

both for calcium absorption
V5 - kidney
V6 - SI

92
Q

what does Ca++ bind to once in the cell?

A

calbindin

93
Q

why does Ca++ have to bind to something in the cell?

A

high concentrations of calcium in the cell can be bad for the cell

94
Q

functions of calbindin binding

A
  • sequest Ca++ out of cytoplasm
  • enable Ca++ movement from apical to basolateral membrane
95
Q

how is Ca++ removed from the cell at the basolateral membrane?

A

by active transport using PMCA (plasma membrnae Ca++ ATPase)

96
Q

describe PMCA

A

expends ATP to pump out Ca++ in exchange for H+ coming in

97
Q

what regulates calcium absorption?

A

the active form of vitamin D (1,25 - dihydroxy-vitamin D)

98
Q

what does the active form of vitamin D do?

A

binds to intracellular receptors which trigger transcription of mRNA. mRNA transcribed codes for 3 proteins:
• TRPV6 channel
• calbindin protein
• PMCA

each of these proteins are upregulated by vitamin D to increase Ca++ absorption

99
Q

where does iron absorption occur?

A

duodenum

100
Q

what kind of transport process is iron absorption?

A

transcellular (has to cross apical and basolateral membranes)

101
Q

at the apical membrane, via what 2 mechanisms can iron enter the cell?

A
  1. divalent metal transporter (DMT) - transports ferrous/reduced form of iron at the same time as protons — secondary active transport
  2. iron can also be absorbed in the form of heme (we don’t know how this crosses membrane) - heme oxidised once in cell to release iron in the form of ferric iron — then reduced to ferrous iron
102
Q

once oxidised what does the remained of the heme protein go to produce?

A

biliverdin = precursor to bilirubin (excreted in bile)

103
Q

once in the cell, the ferrous irons are potentially toxic so must be bound to what?

A

a protein called mobilferrin

104
Q

what does mobilferrin do?

A

sequesters the iron out of the cytoplasm and facilitates its movement from the apical to basolateral membrane

105
Q

how does iron leave the cell at the basolateral membrane?

A

via facilitated diffusion in a transporter called ferroportin 1 (FP1)

106
Q

what happens to the ferrous iron once released from the cell?

A

reoxidised to ferric irons which can then bind to the plasma transport protein = plasma transferrin

107
Q

the oxidation of ferrous to ferric iron once outside of the cell is mediated by what?

A

hephaestin (located at basolateral membrane)

108
Q

name the hormone that regulates iron absorption

A

hepcidin

109
Q

what produces hepcidin and when?

A
  • produced by liver cells
  • produced when there is plenty of iron in the body
110
Q

what does hepcidin do/result in?

A

binds to ferroportin — results in the internalisation of ferroportin transporters — decreased ferroportin transporters — inhibit exit step in absorption, entry step continues

therefore iron gets stored in enterocytes bound to mobilferrin, but within a day or 2 the enterocytes slough off in the villus tip into the lumen of the intestine — iron lost from the body with faeces

111
Q

what happens if you are deficient in iron?

A
  • reduced hepcidin release
  • more ferroportin in membrane
  • enhances rate of iron absorption

PBL SEM 4 (50 decks)

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