Intestines Flashcards

1
Q

Into where does the stomach empty chyme?

A

The duodenum

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2
Q

What happens to chyme in the duodenum?

A

It is conditioned

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3
Q

What features of chyme are modified in conditioning?

A
  • Acidic
  • Hypertonic
  • Partly digested
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4
Q

How is the acidity of chyme modified in conditioning?

A

It is corrected by HCO3-

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5
Q

Where does the HCO3- used to correct the acidic nature of chyme in conditioning come from?

A

Secreted from the pancreas, liver, and duodenal mucosa

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6
Q

When is the HCO3- used to correct the acidity of chyme in conditioning produced?

A

During the production of gastric acid

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7
Q

How is hypertonicity of chyme modified in conditioning?

A

Corrected by the osmotic movement of water into the duodenum across its wall

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8
Q

How is the partly digested nature of chyme modified in conditioning?

A

Digestion is completed by enzymes

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9
Q

Where do the enzymes used to finish digestion of chyme in conditioning come from?

A

The pancreas and duodenal mucosa

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10
Q

Other than enzymes, what is required from the completion of digestion of chyme in conditioning?

A

Bile acids from the liver

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11
Q

What conditions does absorption require?

A

A large surface area, to which the luminal contents of the small intestine needs to be exposed to through gentle agitation for hours

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12
Q

How is the surface area of the small intestine maximised?

A
  • Very long
  • Increased by millions of villi projecting into the lumen
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13
Q

How do epithelial cells (enterocytes) arise?

A

By rapid division in the crypts between the villi, and migration towards the tips

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14
Q

What happens to enterocytes at the tips of the villi?

A

They are shed

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15
Q

What happens to newly formed enterocytes as they migrate to the tip?

A

They mature

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16
Q

What covers the luminal surface of the enterocytes?

A

Microvilli

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17
Q

What is the purpose of the microvilli present on the enterocytes?

A
  • Further increase surface area
  • Form the brush border
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18
Q

What does the brush border form?

A

An ‘unstirred layer’

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19
Q

What happens at the unstirred layer?

A

Nutrients meet and react with enzymes secreted by the enterocytes, completing digestion prior to absorption

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20
Q

Label this diagram

A
  • A - Muscle layers
  • B - Villi
  • C - Hepatic portal vein
  • D - Lumen
  • E - Capillary bed
  • F - Lacteal
  • G - Microvilli
  • H - Villi
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21
Q

What is the function of the large intestines?

A

Absorb water from the indigestible residues of chyme

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22
Q

What do the large intestines do to the indigestible residues of chyme?

A

Convert them into semi-solid stool or faeces

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23
Q

What happens to the faeces formed by the large intestines?

A

It is stored temporarily and allowed to accumulate until defecation occurs

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24
Q

What are teniae coli?

A

The thickened bands of smooth muscle of the large intestines

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25
Q

What do the teniae coli constitute?

A

Most of the longitudinal coat of the large intestines

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26
Q

Where do the teniae coli run?

A

The length of the large intestine

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27
Q

What is the effect of the teniae coli on the part of the wall they are associated with?

A

They shorten it

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28
Q

Why do the teniae coli shorten the part of the wall they are associated with?

A

Because of their tonic contraction

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29
Q

What does the shortening of the wall due to teniae coli form?

A

Haustra

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30
Q

What are haustra?

A

Where the colon becomes sacculated, or ‘baggy’, between the teniae

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31
Q

Label this diagram

A
  • A - Right colic (hepatic) flexure
  • B - Transverse colon
  • C - Superior mesenteric artery
  • D - Haustrum
  • E - Ascending colon
  • F - Ileum
  • G - Ileocecal valve
  • H - Cecum
  • I - Vermiform appendix
  • J - Rectum
  • K - Anal canal
  • L - External anal sphincter
  • M - Sigmoid colon
  • N - Tenia coli
  • O - Cut edge of mesentery
  • P - Descending colon
  • Q - Epiploic appendages
  • R - Transverse mesocolon
  • S - Left colic (splenic) flexure
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32
Q

What are the sections of the small intestine?

A
  • Duodenum
  • Jejenum
  • Ileum
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33
Q

What functions are common between all sections of the small intestine?

A
  • Secrete protease and carbohydrase enzymes to complete digestion
  • Secrete hormones
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34
Q

What hormones are secreted by all sections of the small intestine?

A
  • Secretin
  • Gastrin
  • Cholecystokinin
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35
Q

What are the functions of the duodenum?

A
  • Addition of bile and pancreatic secretions
  • Secretes HCO3- to neutralise chyme
  • Osmotic movement of water into the duodenum, making chyme more hypotonic
  • Absorption
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36
Q

Where in the duodenum are bile and pancreatic secretions added?

A

Ampulla of Vater

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37
Q

What is absorbed in the duodenum?

A

Iron

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38
Q

What are the functions of the jejunum?

A
  • Absorption
  • Uptake of things small enough to soak through the villi
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39
Q

What is absorbed in the jejenum?

A
  • Carbohydrates
  • Amino acids
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40
Q

What substances are small enough to soak through the villi?

A
  • Fatty acids
  • Vitamins
  • Minerals
  • Electrolytes
  • Water
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41
Q

What is the function of the ileum?

A

Absorption

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42
Q

What is absorbed by the ileum?

A
  • Vitamin B12
  • Bile
  • Anything not absorbed by the jejenum
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43
Q

Label this diagram

A
  • A - Duodenum
  • B - Ileocecal junction
  • C - Cecum
  • D - Appendix
  • E - Duodenojejunal junction
  1. Jejunum
  2. Ileum
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44
Q

How long does the large intestine take to finish the digestion of food?

A

About 16 hours

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45
Q

What are the functions of the large intestine?

A
  • Absorption
  • Sends indigestible matter to the rectum
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46
Q

What does the large intestine absorb?

A
  • Water
  • Any remaining absorbable nutrients
  • Vitamins created by colonic bacteria
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47
Q

What vitamins are created by colonic bacteria?

A
  • Vitamin K
  • B12
  • Thiamine
  • Riboflavin
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48
Q

What is the function of the rectum?

A

Stores and compacts faecal matter

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49
Q

In what form are carbohydrates ingested in the small intestime?

A

In the form of amyloses, amylopectins, or dissacharides such as sucrose

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50
Q

What is the structure of amylose?

A

Straight chain with α-1,4 bonds

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51
Q

What is the structure of amylopectin?

A

Branched, with α-1,6 bonds at branches

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52
Q

What do α-amylases act on?

A

α-1,4 bonds

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53
Q

Where are α-amylases secreted?

A
  • In saliva
  • By pancreas
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54
Q

What do α-amylases yield?

A
  • Glucose and maltose from amyloses
  • α-limit dextrins from amylopectins
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55
Q

What completes the breakdown of glucose?

A

Brush border enzymes

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56
Q

What enzymes are found in the brush border?

A
  • Isomaltase
  • Maltase
  • Sucrase
  • Lactase
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57
Q

What does isomaltase do?

A

Breaks down branched molecules at α-1,6 bonds

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58
Q

What does maltase do?

A

Converts maltose to glucose

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59
Q

What does sucrase do?

A

Converts sucrose to glucose and fructose diamer

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60
Q

What does lactase do?

A

Converts lactose to glucose and galactose diamer

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61
Q

Where does the energy from the active absorption of glucose come from?

A

The Na+ gradient set up by Na/K/ATPase in the basolateral membrane

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62
Q

Where does glucose enter the epithelial cell?

A

Across its apical membrane

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63
Q

What transport is required to move glucose across the epithelial apical membrane?

A

Na+/Glucose Symporter, SGLT1

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64
Q

Other than glucose, what does SGLT1 transport?

A

Galactose

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65
Q

Where does glucose leave the epithelial cell into the bloodstream?

A

Across the basolateral membrane

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66
Q

How does glucose leave the epithelial cell across the basolateral membrane?

A

Via facilitated diffusion through the GLUT2 transporter

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67
Q

How does fructose enter the epithelial cell from the lumen?

A

Via facilitated diffusion

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68
Q

What are proteins digested to?

A

Oligopeptides

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69
Q

What is an oligopeptide?

A

Short peptides, 10-20 AA’s long

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70
Q

Where are proteins first digested?

A

In the stomach

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71
Q

What digests proteins in the stomach?

A

Pepsin

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72
Q

What secretes pepsin in the stomach?

A

Chief cells

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73
Q

What enzymes digest proteins in the duodenum?

A

Peptidases

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74
Q

What secretes the peptidases in the duodenum?

A

The pancreas

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75
Q

How do different peptidases vary?

A

They ‘prefer’ breaking different bonds

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76
Q

What peptidases are present in the duodenum?

A
  • Pepsin
  • Trypsin
  • Chymotrypsin
  • Carboxypeptidase
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77
Q

What bonds does pepsin prefer to break?

A

Bonds near aromatic AA side chains

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78
Q

What bonds does trypsin prefer to break?

A

Bonds near basic AA side chains

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79
Q

What bonds does chymotrypsin prefer to break?

A

Bonds near aromatic AA side chains

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80
Q

What bonds does carboxypeptidase prefer to break?

A

C-terminal AA’s with basic side chains

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81
Q

In what form can proteins be absorbed by the small intestine?

A

Both amino acids and small peptides (2/3 AA’s)

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82
Q

How does absorption of proteins by the small intestine differ in neonates?

A

In neonates, the gut is ‘open’, so in addition to amino acids and small proteins, they are able to pick up whole proteins

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83
Q

What is the clinical importance of the ‘open’ gut in neonates?

A

It allows breast milk to confer passive immunity on babies via IgA absorption

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84
Q

What transporter is required for the active uptake of amino acids?

A

Na+/Amino acid co-transporters

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85
Q

How many types of Na+/Amino acid co-transporters are there?

A

At least 5

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86
Q

How do Na+/Amino acid transporters get the energy required for the active uptake of amino acids?

A

Using the Na+ gradient set up by Na/K/ATPase

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87
Q

Give 5 types of Na+/Amino acid co-transporters

A

Those that take up -

  • Small, neutral AA’s
  • Neutral AA’s, basic AA’s, and cysteine
  • Acidic AA’s
  • Imuno-AA’s
  • ß AA’s (mainly taurine)
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88
Q

What facilitates some AA uptake?

A

Passive diffusion

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89
Q

How are dipeptides and tripeptides taken up?

A

By an active mechanism associated with pumping H+ into the lumen, which then returns by co-transport with the peptide

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90
Q

What is the result of fats being relatively insoluble in water?

A

They tend to aggregate into large globules

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91
Q

What is the result of fats tending to aggregate into large globules?

A

It prevents effective action of digestive enzymes

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92
Q

What excerbates the aggregation of fat into large globules?

A

Acid in the stomach

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93
Q

What happens to fats in the duodenum?

A

They are incorporated into micelles

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94
Q

What allows fats to be incorporated into micelles in the duodenum?

A

Bile acids

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95
Q

How big are the micelles formed by fats and bile acids in the duodenum?

A

4-6nm

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96
Q

Describe the structure of the fat micelles formed in the duodenum?

A

Fats in the middle and polar components of bile acids on the outside

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97
Q

What is the function of the fat micelles?

A
  • Generate a high surface area for the action of lipases
  • Carry products into the ‘unstirred layer’
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98
Q

What is the effect of lipases on the fat micelles?

A

They cleave the fatty acids from glycerol

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99
Q

Where is the ‘unstirred layer’ located?

A

Immediately next to the mucosa

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100
Q

What happens to micelles in the unstirred layer?

A

Fatty acids can be released to slowly diffuse into the epithelial cells

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101
Q

What happens to the fatty acids from micelles once inside epithelial cells?

A

They are reconstituted into triacylglycerols and re-expelled as chylomicrons

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102
Q

What are chylomicrons?

A

Structured small particles

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103
Q

What are chylomicrons made up of?

A

Lipids covered in phospholipids

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104
Q

What do chylomicrons do?

A

Facilitate the transport of fat in the lymphatic system from the gut to systemic veins

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105
Q

How is sodium taken up by the small intestine?

A

Via diffusion into the cell, and actively transported across the basolateral membrane by Na-K-ATPase

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106
Q

What is the importance of sodium uptake by the small intestine?

A

It provides the driving force for the majority of absorption

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107
Q

What ion follows the movement of Na+?

A

Chloride

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108
Q

What does the movement of Na+ and Cl-, coupled with all of absorption, give?

A

An osmotic gradient

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109
Q

What does the osmotic gradient in the small intestine do?

A

Leads to the uptake of water

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110
Q

What minerals are taken up by the small intestine?

A
  • Calcium
  • Iron
  • Vitamins
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111
Q

How much calcium is absorbed from the small intestine each day, compared to how much is consumed?

A

700mg/day absorbed out of 6g consumed - >10%

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112
Q

How does Ca2+ enter the epithelial cell?

A

Facilitated diffusion

113
Q

What allows Ca2+ to be taken up into the small intestinal epithelial cell by facilitated diffusion?

A

There is a low intracellular concentration

114
Q

How is Ca2+ pumped out of the basolateral membrane?

A

By Ca2+-ATPase

115
Q

What does both the facilitated diffusion of calcium and transport through the basolateral membrane require?

A

Vitamin D

116
Q

What is the uptake of calcium by the small intestine stimulated by?

A

Parathyroid hormone (PTH)

117
Q

How much iron is consumed per day?

A

20mg

118
Q

What constitutes most of the iron consumed?

A

Haem

119
Q

In what form can iron be absorbed?

A

Only its ferrous form (Fe2+)

120
Q

How is iron made into its ferrous form?

A

Gastric acid solubises iron complexes, making them ferrous

121
Q

What happens to ferrous iron once it has been formed in the stomach?

A

Gastroferrin binds iron and keeps it ferrous

122
Q

What secretes gastroferrin?

A

The stomach

123
Q

What secretes transferrin?

A

Intestinal mucosal cells

124
Q

What does transferrin do?

A

Finds ferrous ions in the lumen

125
Q

What happens once transferrin has found ferrous iron in the lumen?

A

The complex is taken into cells by endocytosis, spplit, and the iron is exported to the blood

126
Q

What happens once the iron split from transferrin is exported to the blood?

A

It binds again to transferrin

127
Q

How are water-soluble vitamins absorbed in the small intestine?

A

Via passive diffusion

128
Q

What vitamins are water soluble?

A
  • Vitamin C
  • B vitamins
129
Q

What is vitamin B12 absorbed with?

A

A co-factor

130
Q

Where is vitamin B12 absorbed?

A

In the terminal ileum only

131
Q

When does the intrinsic factor bind to vitamin B12?

A

In the stomach

132
Q

What is the purpose of the intrinsic factor binding to vitamin B12?

A

To keep in soluble

133
Q

What secretes the intrinsic factor that binds to vitamin B12?

A

The stomach mucosa

134
Q

What occurs with vitamin B12 deficiency?

A

Pernicious anaemia

135
Q

What causes pernicious anaemia?

A

Damage to the stomach, preventing it from secreting the intrinsic factor, or when the terminal ileum has been damaged or removed

136
Q

When may the terminal ileum be damaged?

A

Crohn’s

137
Q

How is the uptake of Na+ related to the uptake of water?

A

It generates an osmotic gradient, which water follows

138
Q

What does glucose uptake do?

A
  • Stimulates Na+ uptake
  • Generates its own osmotic gradient
139
Q

What will stimulate maximum water uptake?

A

A mixture of glucose and NaCl

140
Q

What is the mixture of glucose and NaCl known as?

A

Oral rehydration fluid

141
Q

What must happen to the intestinal contents for effective absorption?

A

It must move very slowly (transit time in hours), whilst being gently agitated

142
Q

How is the slow movement and agitation of intestinal contents achieved?

A

By a pattern of motility called segmenting

143
Q

Are segmenting and perilstalsis the same thing?

A

No, they are very different

144
Q

How is the small intestine divided?

A

Into sections

145
Q

What does each section of the small intestine have?

A

A pacemaker

146
Q

How does the frequency of the pacemaker change through the small intestine?

A

It gets less from the duodenum to the terminal ileum (12 times a minute to 8)

147
Q

What is the decrease in pacemaker frequency phenomenom known as?

A

The intestinal gradient

148
Q

What does each pacemaker drive?

A

A small section of intestine

149
Q

What does the pacemaker driving of the section of small intestine cause?

A

Intermitted contraction of the smooth muscle along its length

150
Q

What is the result of the intermittent smooth muscle contraction caused by the pacemaker?

A

It seperates the intestine into segments where the muscle is not contracted

151
Q

What happens to the intestinal contents at each segment?

A

It is effectively mixed by movement from the portions that do contract

152
Q

What happens after a few seconds of contraction of a segment?

A

The contractions relax, and the next pacemaker fires to make different areas contract

153
Q

What is the purpose of segmenting?

A

Mixes the contents of the intestine

Segmenting itself does not proper contents

154
Q

What does the intestinal gradient result in?

In terms of movement

A

There is a net movement, albeit slow, in a caudal direction

155
Q

What is the large intestine naturally divided into?

A

Segments known as Haustra

156
Q

How are Haustra formed?

A

The circular muscles are more complete than the longitudinal, which have been reduced to taenia coli

157
Q

Describe the structure of taenia coli

A
  • Thick circular muscle
  • Thin longitudinal muscle
  • Only 3 layers
158
Q

What is the effect of contraction of hte smooth muscle in the walls of the Haustra?

A

It shuffles the contents back and forth

159
Q

What happens as the intestinal contents is being shuffled back and forth by the Haustra?

A

There is slow absorption of the remaining water and salts, forming faeces

160
Q

Where does the intestinal contents progress too from the Haustra?

A

The sigmoid colon

161
Q

How is Haustral shuffling controlled?

A

Segmenting like control

162
Q

What happens in mass movement of the colon?

A

Once or twice a day, there is a perilstaltic propelling pattern from the transverse through to the descending colon

163
Q

What is the result of mass movement?

A

It forces faeces rapidly into the rectum

164
Q

What happens when faeces is forced into the rectum?

A

It induces the urge to defecate

165
Q

Why does faeces being forced into the rectum induce the urge to defecate?

A

Because the rectum is normally empty

166
Q

What is mass movement often triggered by?

A

The gastro-colic reflex, triggered by eating

167
Q

Does mass movement occur at certain times of the day?

A

Often does, because people ‘like to be regular’

168
Q

How many anal sphincters are there?

A

Two, internal and external

169
Q

What kind of muscle is present in the internal anal sphincters?

A

Smooth

170
Q

What control is the internal anal sphincter under?

A

Parasympathetic

171
Q

What happens to the internal anal sphincter when it recieves parasymphathetic stimulation?

A

It relaxes

172
Q

What kind of muscle is present in the external anal sphincter?

A

Voluntary striated muscle

173
Q

What control is the external anal sphincter under?

A

Voluntary (normally)

174
Q

What happens once both anal sphincrers are relaxed?

A

Intra-abdominal pressure is increased, forcing expiration

175
Q

What is the result of the increase in intra-abdominal pressure caused by the relaxation of the internal and external anal sphincters?

A

There is an expulsion of faeces

176
Q

When is the voluntary control of the external sphincter overriden?

A

If rectal pressure becomes too high

177
Q

What are the types of inflammatory bowel disease?

A
  • Ulcerative colitis
  • Crohn’s disease
  • Diversion Colitis
  • Diverticular colitis
  • Radiation
  • Drugs
  • Infections
  • Ischaemic colitis
178
Q

What is ulcerative colitis?

A

An inflammatory disorder

179
Q

Where does ulcerative colitis affect?

A

The rectum, and extends proximally in continuity to affect a variable extent of the colon

180
Q

What is meant by UC extending in continuity?

A

There are no breaks in the inflammation

181
Q

Where is there a high incidence of UC?

A
  • US, UK and northen Europe
  • Young adults
    • More commonly in females
182
Q

What is the mucosa of UC patients dominated by?

A

Th2 (T-helper) cells

183
Q

What do Th2 cells produce?

A
  • Transforming Growth Factor (TGF)
  • IL-5
184
Q

How does ulcerative colitis present?

A
  • Rectal bleeding
  • Diarrheoa
  • Abdominal pain
185
Q

Where does extensive colitis affect?

A

Entire colon and rectum

186
Q

What is extensive colitis also known as?

A

Pancolitis or total colitis

187
Q

What is affected in distal colitis?

A
  • Rectum
  • Sigmod colon
  • Descending colon
188
Q

What is affected in proctitis?

A

Rectum only

189
Q

What is Crohn’s disease?

A

A condition of chronic inflammation

190
Q

Where does Crohn’s Disease affect?

A

Potentially any location of the GI tract from mouth to anus

191
Q

When does CD have the highest incidence?

A

Two peaks-

  • 15-30 years
  • 60 years
192
Q

What is the mucosa of CD patients dominated by?

A

Th1 (T-helper) cells

193
Q

What do Th1 cells produce?

A
  • Interferon Gamma (IFN-γ)
  • IL2
194
Q

What does the presentation of CD depend on?

A

The diseases location

195
Q

What is the presentation of CD with upper GI involvement?

A
  • Nausea and vomiting
  • Dyspepsia
  • Small bowel obstruction
  • Anorexia
  • Weight loss
  • Loose stools
196
Q

What is the presentation of CD when its a colonic disease?

A
  • Diarrhoea
  • Passage of obvious blood
197
Q

What may occur when there is termianal ileum involvement in CD?

A

Anaemia

198
Q

Why may terminal ileum involvement in CD cause anaemia?

A

Because of poor absorption of vitamin B12

199
Q

What causes inflammatory bowel disease?

A
  • May have genetic predisposition
  • Environmental factors
200
Q

What genes may give genetic predisposition to inflammatory bowel disease?

A
  • IBD1
  • NOD2/CARD15
201
Q

By how much does having one copy of a risk allele increase the risk of Crohns?

A

2-4x

202
Q

By how much does having two copies of a risk allele increase the risk of Crohn’s?

A

20-40x

203
Q

What environmental factors may increase the risk of inflammatory bowel disease?

A
  • NSAIDs
  • Early appendectomy
  • Smoking
204
Q

Why does NSAIDs increase the risk of IBD?

A

May be the altered intestinal barrier

205
Q

What is an early appendectomy linked to?

A

Increased UC incidence

206
Q

What is the effect of smoking on the risk of IBD?

A
  • Protects against UC
  • Increases risk of CD
207
Q

What are the triggers for inflammatory bowel disease?

A
  • Antibiotics
  • Diet
  • Acute infections
  • NSAIDs
  • Smoking
  • Stress
208
Q

How deep is the inflammation in UC?

A

Mucosal

209
Q

How deep is the inflammation in CD?

A

Transmural

210
Q

What is the difference in the pattern of disease between UC and CD?

A

In UC it is continuous. In CD, it may skip area

211
Q

What is the location of UC?

A

Colorectum

212
Q

What is the location of CD?

A

Mouth to anus

213
Q

Is there rectal involvement in UC?

A

Usually

214
Q

Is there rectal involvement in CD?

A

Can be, but less common than in UC

215
Q

What kind of ileal disease is sometimes present with UC?

A

Backwash ileitis

216
Q

What % of UC patients also have backwash ileitis?

A

15-20%

217
Q

Does Crohn’s disease present with ileal disease?

A

Yes, it is common

218
Q

Does UC cause fistulas?

A

Rarely

219
Q

Does CD cause fistulas?

A

Commonly

220
Q

Does UC cause perianal disease?

A

Rarely

221
Q

Does CD cause perianal disease?

A

Commonly

222
Q

Does UC cause granulomas?

A

Unlikely

223
Q

Does CD cause granulomas?

A

Yes, in 50-60% of patients

224
Q

Does UC cause overt bleeding?

A

It is unusual

225
Q

Does CD cause overt bleeding?

A

It is less common

226
Q

Does UC cause malnutrition?

A

It is unlikely

227
Q

Does CD cause malnutrition?

A

It is more common

228
Q

What cancer risk does UC confer?

A

Colorectal cancer

229
Q

What cancer risk does CD confer?

A

Colorectal cancer or small bowel cancer, depending on location

230
Q

What will be seen on a radiograph in UC?

A

Collar button ulcers

231
Q

What will be seen on a radiograph in CD?

A

String sign of Kantor

232
Q

What methods are commonly used for investigating inflammatory bowel disease?

A
  • Colonoscopy
  • Stool analysis
  • Barium radiographs
  • CT scan
  • Capsule endoscopy
  • Plain X-ray
233
Q

How is a colonoscopy used to investigate IBD?

A
  • Biopsies of involved mucosa
  • Ulceration
234
Q

What will be looked for in stool analysis?

A
  • Parasites
  • Clostridium difficile toxin
235
Q

How is a stool analysis conducted?

A

Using a culture

236
Q

When will a plain X-ray be used to investigate IBD?

A

If bowel obstruction or perforation suspected

237
Q

What is this image showing?

A

Crohn’s disease

238
Q

What macroscopic changes will be seen in CD?

A
  • Involved bowel usually thickened, often narrowed
  • Deep ulcers and fissures in mucosa may produce cobblestone apperance
  • Fistulae and abscesses may be seen
239
Q

What does the presence of fistulae and abscesses in CD reflect?

A

Penetrating disease

240
Q

What macroscopic changes will be seen with UC?

A
  • Mucosa looks reddened, inflamed and bleeds easily
  • In severe disease, there is extensive ulceration with the adjacent mucosa appearing as inflammatory (pseudo) polyps
241
Q

What microscopic changes will be seen with CD?

A
  • Inflammation through all layers of the bowel (transmural)
  • Increase in chronic inflammatory cells
  • Lymphoid hyperplasia
  • Granulomas
242
Q

Why can you see granulomas microscopically with CD?

A

TH1 response

243
Q

What microscopic changes will be seen with UC?

A
  • Superficial inflamamtion
  • Chronic inflammatory cells infiltrate in the lamina propria
  • Crypt abscesses
  • Goblet cell depletion
244
Q

How can differentation be made between UC and CD?

A
  • Clinical data
  • Radiological data
  • Histological differences in rectal and colonic mucosa
245
Q

How are samples of rectal and colonic mucosa obtained?

A

By biopsy

246
Q

When may it not be possible to distinguish between UC and CD?

A

If the biopsies are obtained in the acute phase

247
Q

What are patients considered to have when their disease cannot be distinguished between CD and UC?

A

Colitis of Undetermined Type and aEtiology (CUTE)

248
Q

What may be of value when determining between CD and UC?

A

Serological testing for anti-neutrophil cytoplasmic antibodies (ANCA) in UC, and anti-Saccharomyces cervisiae antibodies (ASCA) in CD

249
Q

What may be required to make an exact diagnosis sometimes?

A

Examination of a surgical colectomy specimen

250
Q

When is a colonscopy performed with CD?

A

If colonic involvement is suspected

251
Q

What will be seen on a colonscopy with CD?

A

Mild, patchy surface ulceration to cobblestoning

252
Q

When is an upper GI endoscopy required with CD?

A

To exclude oesophageal and gastroduodenal disease in patients with relevant symptoms

253
Q

When is small bowel imaging mandatory?

A

In patients with suspected Crohn’s

254
Q

How is small bowel imaging conducted?

A
  • Barium follow through
  • CT scan with oral contrast
  • Small bowel ultrasound
  • MRI
255
Q

What will be seen in small bowel imaging in a patient with CD?

A
  • Asymmetrical alteration in the mucosal pattern with deep ulceration, and areas of narrowing or structuring
  • String sign of Kantor
256
Q

When is a perianal MRI or endoanal ultrasound used in patients with CD?

A

To evaluate perianal disease

257
Q

When is a capsule endoscopy used in Crohn’s disease patients?

A

When they have a normal radiological examination

258
Q

What is the ‘gold standard’ investigation for the diagnosis of UC?

A

Colonscopy with biopsy

259
Q

What is a colonscopy used for in UC?

A

To assess the disease activity and extent

260
Q

Why is a plain abdominal X-ray used in UC?

A

To exclude colonic dilation

261
Q

Why are other imaging techniques rarely used in UC?

A

As endoscopy is preferred

262
Q

What is often seen on imaging with UC patients?

A

Collar Button Ulcers

263
Q

What are Collar Button Ulcers?

A

Ulcer through the bowel mucosa to the muscle, then up and down in a ‘T’ shape

264
Q

What treatment options are available for CD?

A
  • Induction of remission
  • Maintenance of remission
  • Treatment of perianal disease
  • Surgical management
265
Q

How is remission induced in CD patients?

A
  • Oral or IV glucocorticosteroids
  • Enteral nutrition
  • Anti-TNF antibodies
266
Q

What is the name of the anti-TNF antibodies given in CD?

A

Infliximab

267
Q

How is remission maintained in CD?

A
  • Methotrexate
  • Azathioprine
  • Anti-TNF antibodies
268
Q

How is perianal disease treated?

A
  • Ciprofloxacin and Metrronidazole
  • Azathioprine
  • Anti-TNF antibodies
269
Q

How do anti-TNF antibodies treat CD?

A

They bind to membrane bound TNF-α and induce immune cell apoptosis

270
Q

When is surgical management required for CD?

A
  • Failure of therapy with acute or chronic symptoms
  • Complications
  • Failure to grow in children, despite children
271
Q
A
272
Q

What complications of CD may necessitate surgical management?

A
  • Dilation
  • Obstruction
  • Perforation
  • Abscesses
273
Q

What surgical management may be performed in patients with CD?

A
  • Colectomy
  • Ileorectal anastomosis
274
Q

What is used to treat distal UC (proctitis)?

A

Topical or suppository corticosteroids

275
Q

What is used to treat left sided UC?

A

Topical corticosteroid enema

276
Q

What is used to treat extensive UC?

A
  • Oral corticosteroids
  • Infliximab
277
Q

When is surgical management required in patients with UC?

A
  • Patients with complications
  • Patients with corticosteroids dependence
278
Q

What is the favoured surgical management in patients with acute UC?

A

Subtotal colectomy with end ileostomy and preservation of the rectum