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GI > Physiology of Digestion and absorption > Flashcards

Physiology of Digestion and absorption Flashcards

1
Q

what is the major site for digestion and absoption

A

the small intestine

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2
Q

what are the three parts of the small intetsine

A

duodenum, jejunum, ileum

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3
Q

what does the small intestine recieve

A

chyme from stomach, pancreatic juice from the pancreas, bile from the gall bladder

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4
Q

what does the small intestine move its contents to

A

the large intestine via the ileocaecal valve

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5
Q

what increases the surface area of the small intestine

A

circular folds, villi, microvilli

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6
Q

what peptide hormones does the small intestine secrete

A

gastrin, cholecystokinin (CCK), secretin, motilin, glucagon like insulintropic peptise (GIP a.k.a gastric inhibtory peptide), glucagon like peptide 1 (GLP-1), ghrelin

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7
Q

what do all peptide hormones secreted by the small intestine work on

A

G-protein coupled receptors

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8
Q

what controls the secretions of the small intestine

A

Distension/irritation, gastrin, CCK, secretin, parasympathetic nerve activity (all enhance), sympathetic nerve activity (decreases)

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9
Q

what does intestine juice contain

A

mucus (protection and lubrication- goblet cells)

aqueous salt (for enzymatic digestion)

NO digestive enzymes

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10
Q

what initiates segmentation in the small intestine

A

small intestine pacemaker cells causing the BER which is continuous. At threshold activates segmentation which in the duodenum is primarily due to distension by entering chyme

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11
Q

what is segmentation in the empty ileum triggered by

A

gastrin from the stomach (gastroileal reflex)

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12
Q

why is the movement of chyme slow (3-5 hrs)

A

allows time for absorption

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13
Q

what is the strength of segmentation affect by

A

enhanced by parasympathetic and decreased by sympathetic activity

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14
Q

what is the migrating motor complex (MMC)

A

strong peristaltic contraction passing length of the intestine (stomach to ileocaecal valve)
clears small intestine of debris, mucus and sloughed epithelial cells between meals – ‘housekeeper function’

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15
Q

what is the MMC inhibited by

A

feeding and vagal activity, gastrin and CCK

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16
Q

what trigger the MMC

A

motilin

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17
Q

when does the MMC happen

A

between meals every 90 to 120 min

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18
Q

what are the endocrine secretions of the pancreas

A

insulin and glucagon (secreted to blood)

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19
Q

what is the difference between endocrine and exocrine

A

Endocrine glands release chemical substances directly into the bloodstream or tissues of the body

Exocrine glands release chemical substances through ducts to outside the body or onto another surface within the body

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20
Q

what are the exocrine secretions of the pancreas

A

digestive enzymes, aqueous NaHCO1- solution (secreted to the duodenum collectively as pancreatic juice)

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21
Q

where do pancreatic duct cells drain into

A

the duodenum (1-2 litres of alkaline fluid a day)

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22
Q

what is the role of the alkaline fluid secreted from the pancreatic duct cells

A

neutralises chyme entering the duodenum

  • provides optimum pH for pancreatic enzyme function
  • protects the mucosa from erosion by acid
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23
Q

what do patients with CF have

A

reduced fluid secretion for the pancreatic duct cells

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24
Q

what ability do pancreatic enzymes have

A

to digest food in absence of all other enzymes

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25
Q

give example of pancreatic enzymes secreted within the pancreatic juice

A

inside brackets name for active state- outside inactive
no brackets means active when secreted

(trypsin)ogen
(chymotrypsin)ogen
pro(carboxypeptidase A & B)
pancreatic amylase
pacreatic lipase

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26
Q

where are many pancreatic enzymes activated

A

in the duodenum

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27
Q

what are the three stages of pancreatic secretion

A

cephalic, gastric and intestinal

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28
Q

what is the cephalic stage of pancreatic stimulation mediated by

A

vagal stimulation of mainly acinar cells

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29
Q

what is the gastric stage of pancreatic stimulation mediated by

A

gastric distention evokes a vagovagal reflex resulting in parasympathetic stimulation of acinar and duct cells

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30
Q

what is the secretory pathway for the neutralisation of duodenal lumen

A

acid in duodenal lumen

increased release of secretin from S cells

secretin carried by blood to pancreatic duct cells

increased secretion of aqueous NaHCO3 solution into duodenal lumen

neutralisation

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31
Q

what is the secretory pathway of the digestion of fat and protein in the duodenal lumen

A

fat and protein in duodenal lumen

increased CCK release from I cells

CCK carried in blood to pancreatic acinar cells

increased secretion of digestive enzymes into duodenal lumen

digestion

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32
Q

what are the main constitutes of food

A

carbohydrates (starch, cellulose, glycogen, disaccharides)

lipids (triacylglycerols, phospholipids, cholesterol and cholesterol esters, free fatty acids, lipid vitamins)

proteins

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33
Q

define digestion

A

enzymatic conversion of complex dietary substances to a from that can be absorbed

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34
Q

what are the two types of digestion that occur in the small intestine

A

luminal and membrane digestion

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35
Q

what is luminal digestion mediated by

A

pancreatic enzymes secreted into the duodenum

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36
Q

what is membrane digestion mediated by

A

enzymes situated at the brush border of epithelial cells

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37
Q

describe absorption in digestion

A

the absorbable products of digestion are transferred across both the apical and basolateral membranes of enterocytes (absorptive cells of the intestinal epithelium)

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38
Q

what is assimilation

A

overall process of digestion and absorption

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39
Q

what must all dietary carbohydrate be converted into for absorption

A

monosaccarhides

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40
Q

what is the sequence of carbohydrate digestion (not including enzymes)

A

starch to oligosaccharides to monosaccharides to absorption

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41
Q

what is involved with intraluminal hydrolysis

A

starch converted to oligosaccharides (not absorbed)

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42
Q

what is involved in membrane digestion

A

oligosaccharides and lactose and sucrose from diet are converted into monosaccarhides, (+ glucose and frutose) from diet = absorption

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43
Q

where does membrane digestion happen

A

at brush border

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44
Q

what enzyme facilitates the conversion of starch to oligosaccharides

A

alpha- amylase

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45
Q

what enzyme facilitates the conversion of oligosaccharides to monosaccharides

A

oligosaccharidases (lactase, maltase)

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46
Q

give examples of oligosaccharides

A

maltose, alpha-limit dextrins, maltotriose (lactose and sucrose from diet)

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47
Q

give exmaples of monosaccharides

A

glucose, fructose, galactose

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48
Q

what is the role of amylase

A

is an endo enzyme - breaks down linear internal α-1,4 linkages but not terminal α-1,4 linkages. Hence, no production of glucose

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49
Q

what can alpha amylase not cleave

A

α-1,6 linkages at branch points (in amylopectin) or α-1,4 linkages adjacent to branch points

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50
Q

what are the products made by alpha amylase

A

linear glucose oligomers (maltotriose, maltose) and α-limit dextrins

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51
Q

what are olisacchardiases

A

integral membrane proteins with a catalytic domain that faces the lumen of the GI tract

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52
Q

what is the role of lactase

A

breaks down lactose to glucose and galactose

53
Q

what do all oligosaccharidases do expect lactase

A

cleave the terminal alpha 1,4 linkages of maltose, maltriose and alpha-limit dextrins to yield glucose

54
Q

what is sucrase specifically responsible for

A

hydrolysing sucrose to glucose and fructose

55
Q

what is the only enzyme that can split up branches

A

isomaltase

56
Q

what enzymes hydrolysis is rate limiting is assimilation

A

lactase

57
Q

what causes lactose intolerance

A

the inability to adequately digest lactose- cause by lactase insufficiency

58
Q

what can cause lactase intolerance

A

primary (lack of lactase persistence),
secondary (damage/ infection of small intestine),
congenital (rare autosomal recessive disease)

59
Q

what is lactase persistence

A

Lactase activity is generally lost in mammals following weaning, but human populations exhibit a variable degree of lactase persistence

60
Q

when does hypolactasia (lactase insufficiency) cause disturbance

A

when lactose containing food in comsumed and activity of remaining enzyme is overwhelmed, meaning lactose is delivered to the colon

61
Q

what do the ileum colonic microflora produce when lactose is delivered to the colon

A

short chain fatty acids (can be absorbed), hydrogen, carbon dioxide, methane

62
Q

what are the symptoms cause by by products made when lactose in the colon

A

bloating, abdominal pain, flatulence

63
Q

what does undigested lactose cause

A

acidification of the colon, an increased osmotic load (loose stools and diarrhoea)

64
Q

where does the absorption of the final products of carb digestion occur

A

duodenum and jejunum

65
Q

what are the final products of carb digestion

A

glucose, galactose and fructose

66
Q

how are the final products of carb digestion absorbed

A

two step process involving entry from the enterocytes via the apical and exit basolateral membranes.

Glucose and galactose are absorbed by secondary active transport mediated by SGLT1; fructose by facilitated diffusion mediated by GLUT5.

Exit for all monosaccharides is mediated by facilitated diffusion by GLUT2

67
Q

what forms must proteins be in to be absorbed

A

must be digested to oligopeptides and amino acids for efficient absorption

68
Q

how much on daily energy intake does protein assimilate to

A

10-15%

69
Q

how is protein digested in the stomach

A

HCL begins to denature proteins, pepsin cleaves proteins into peptides

70
Q

describe the pH of pepsin

A

optimum of 1.8 to 3.5, inactivated at alkaline pH

71
Q

is pepsin essential for protein digestion

A

no

72
Q

what type of enzyme is pepsin

A

endopeptidase

73
Q

describe the enzyme active in protein digestion in the duodenum and how they get there

A

five pancreatic proteases are secreted as proenzymes from the exocrine pancreas and converted to active form in the duodenum. They function as either endopeptidases, or exopeptidases

74
Q

what are the 5 pancreatic proteases

A

trypsin, chymotrypsin, elastase, procaroxypeptidase A and B

75
Q

what is the ratio of converted oligopeptides and free amino acid from pacreatic protease protein digestion

A

70% oligopeptides

30% AA

76
Q

where are additional proteases present

A

at the brush border and within the cytoplasm of the enterocyte

77
Q

where are amino acids absorbed

A

at the brush border and basolateral membranes

78
Q

how are di- tri- and tetra- peptides absorbed

A

at bush border

further hydrolysed to amino acids within the enterocyte
Na+-independent systems at the basolateral membrane (facilitated transport) takes into interstitium PepT1

79
Q

when things are absorbed where do they go

A

from lumen, inter enterocyte, out to interstitium

80
Q

what do peptidases at the brush border do

A

further hydrolyse oligopeptides to amino acids

81
Q

how are amino acids absorbed

A

Amino acids are transported across the apical membrane via a variety of amino acid transporters, some of which are Na+-dependent and others Na+-independent

82
Q

how are oligopeptides transported across the apical membrane

A

by the H+/oligopeptide co-transporter, PepT1

83
Q

how are oligopeptides hydrolysed to amino acids within the enterocyte

A

by peptidases

84
Q

how do amino acids exit the enterocyte

A

across the basolateral membrane by several, Na+-independent. transporters

85
Q

what enzymes can proteins be digested by

A

luminal or brush border enzymes (digest protein to peptide and then to amino acid)

86
Q

what is the path of the amino acids

A

apical membrane transporters with the enterocytes, then basolateral membrane transporters take them from enterocyte into the blood (or peptides can go through entracellular hydrolysis and go straight into the blood)

87
Q

what are the luminal proteins

A

gastric and pancreatic proteases

88
Q

who does as endopeptide do

A

breaks down amino acids from anywhere in chain, not just at terminal ends

89
Q

how can the five pancreatic proteases function

A

as endopeptidases and exopeptidases (breakdown terminal ends)

90
Q

why are there so many peptidases

A

as large diversity of peptide bonds, specialised enzymes needed to cleave different types of bonds

91
Q

what are two exopepditases

A

aminopeptidases and carboxypeptidases

92
Q

what is present at the brush border IMPORTANT

A

5 Na+ dependant co transporters that mediates movement against gradient, mediates uptake of neutral amino acids

2 Na+ independent co transporters that mediates uptake of cationic amino acids

93
Q

what are the 5 mechanisms of amino acid transport in the basolateral membrane

A

3 medaite efflux from enterocytes into blood (Na+ independent)
2 mediate influx from blood into enterocyte and are Na+ dependent

94
Q

how are di- tri- and tetra peptides moves across apical membrane IMPORTANT

A

via H+ dependent (c transport with a proton) mechanism PepT1 at brush border- further hydrolised within enterocyte

95
Q

how soluble are lipids in water

A

insoluble or poorly soluble

96
Q

what is the most important part of the GI tract for lipid digestion

A

small intestine

97
Q

what stops droplets of lipids in an emulsion coagulating

A

by the addition of a amphiphillic coat

98
Q

what are the phases of lipid digestion

A

mouth- lingual phase
stomach- gastric phase (gastric lipase)
small intestine- most important, emulsification of bile

99
Q

what type of fatty acid cannot be absorbed by the liver

A

long chain

100
Q

what does pancreatic lipase do

A

hydrolyses TAGs (triacytglycerols) to monoglyceride and free fatty acids

101
Q

what is the main lipid digestive enzyme in in adults

A

pancreatic (TAG) lipases - in duodenum

102
Q

describe the secretion of pancreatic (TAG) lipases

A

secreted from acinar cells of pancreas in response to CCK which also stimulates bile flow

103
Q

what is the role of bile salts

A

secreted in bile, released into duodenum from the gall bladder in response to CCK act as detergents to emulsify large lipid droplets to small droplets- increase the surface area of lipase action

104
Q

what does a failure to secrete bile result in

A

lipid malabsorption- steatorrhoea

secondary vitamin deficiency due to failure to absorb lipid vitamins (A, D, E and K)

105
Q

how are bile salts amphipathic

A

as both hydrophilic (projects from surface of doplet) and hydrophobic (absorbs onto droplet)

106
Q

what is the relationship of bile salts and pancreatic lipase

A

bile salts increase SA for attach by PL but block access to the lipid with the hydophobic core of the small droplets

107
Q

how is the lipid bloackage by bile salts overcome

A

by colipase which binds to bile salts and lipase allowing access to tri and di glycerides

108
Q

what is colipase

A

an amphipathic polypeptide secreted with lipase by the pancreas

109
Q

digestion of triglyceride by pancreatic lipase produces what

A

2-monoglyceride and 2 free fatty acids

110
Q

where are the final products of lipid digestion stored in and released from

A

mixed micelles

111
Q

how do free fatty acids and monoglycerides enter the enterocytes

A

by passive diffusion/ transport proteins

112
Q

where do short chain (<6 carbons) go after entering the enterocyte

A

exit through basolateral membrane and enter the villus capillaries

113
Q

where do long chain fatty acids (>12 carbons) and monoglycerides go after entering the enterocyte

A

are resynthesized to triglycerides in the endoplasmic reticulum and are incorporated into chylomicrons

114
Q

what happens to chylomicrons in the enterocytes

A

leaves via exocytosis into central lacteal-

carried in lymph vessels to systemic circulation via the thoracic duct

115
Q

what happens to chylomicron triglyceride once it is distributed to tissues (particularly muscle ans adipose tissue)

A

metabolised in capillaries by lipoprotein lipase on endothelial cells - fatty acids and glycerol released which bind to albumen and are taken up by tissues

116
Q

what happens to the chylomicron remnant- not metabolised

A

enriched with phospholipids and cholesterol then undergoes endocytosis by hepatocytes- cholesterol released to be stores, secreted in bile, oxidised to bile salts

117
Q

how is cholesterol absorped

A

via NPC1L1 protein

118
Q

what drug prevents cholestrol absorption by NPC1L1 and is used with statins in hypercholesterolaemia

A

ezetimibe

119
Q

what regulates acitve Ca+ absorption

A

calcitriol and parathyroid hormone

120
Q

how is calcium absorped

A

passive (paracellular) in small intestine

active (transcellular) in duodenum and upper jejunum

121
Q

what converts Fe3+ to Fe2+

A

Vit c

122
Q

what is the storage form of iron

A

ferratin

123
Q

what negatively regulates the absorption of iron when levels in body are high

A

hepcidin- released from liver

124
Q

what is needed to absorb vit B12

A

firstly binds to haptocorin, then released and binds to intrinsic factor which makes complex which is absorbed via endocytosis

125
Q

what are the fat soluble vitamins

A

A,D,E and K

126
Q

how are fat soluble vitamins absorbed

A

Incorporated into mixed micelles
Usually passively transported into enterocytes

Incorporated into chylomicrons, or VLDLs
Distributed by intestinal lymphatics

127
Q

what are the water soluble vitamins

A

B (not B12), C, H

128
Q

how are water soluble vitamins absorbed

A

Transport processes in the apical membrane are similar to those described for monosaccharides, amino acids and di- and tri-peptides

GI (64 decks)

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