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Phys pharm > Gastrointestinal system > Flashcards

Gastrointestinal system Flashcards

1
Q

What are the 6 main structures of the GI wall?

A
  • Mucosal layer
  • Submucosal layer
  • Circular muscle layer
  • Longitudinal muscle layer
  • Serosa
  • 2 plexuses
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2
Q

What are the 2 main plexuses of the GI tract?

A
  • Submucosal plexus

- Myenteric plexus

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3
Q

Where is the submucosal plexus located?

A

Between the submucosa and the circular muscle layer

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4
Q

Where is the myenteric plexus located?

A

Between the circular and longitudinal muscle layers

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5
Q

What are the 3 elements of the mucosal layer?

A
  • Epithelial cells
  • Lamina propria
  • Muscularis mucosae
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6
Q

What is the lamina propria?

A

Thin layer of connective tissue in the mucosa also consisting of blood and lymph vessels

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7
Q

What is the muscularis mucosae?

A

Layer of smooth muscle cells

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8
Q

What are the 4 elements of the submucosal layer?

A
  • Collagen
  • Elastin
  • Glands
  • Blood vessels
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9
Q

What is the function of elastin?

A

Expansion and recoil

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10
Q

What is the difference between between the longitudinal and circular muscle layers?

A

Longitudinal layer is thinner and less densely innervated than the circular muscle layer

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11
Q

What is the serosa?

A

Outer lining of the GI tract, sometimes has a mesothelium to reduce friction

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12
Q

What does contraction of circular muscle cause?

A

Smaller diameter of GI tract

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13
Q

What does contraction of longitudinal muscle cause?

A

Smaller segment lengths

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14
Q

What is the ENS? (3)

A
  • Enteric Nervous System
  • Collection of nerve plexuses surrounding the GI tract
  • Division of the autonomic nervous system (ANS) therefore involuntary
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15
Q

What is the biliary system?

A

Liver and gall bladder (bile)

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16
Q

What is the extrinsic control of the GI tract?

A

Parasympathetic and sympathetic innervation

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17
Q

Which 2 parasympathetic nerves are involved in GI neural control?

A
  • Vagus nerve

- Pelvic nerve

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18
Q

What is the intrinsic control of the GI tract?

A
  • The ENS itself, primarily via ganglia within the submucosal and myenteric plexuses
  • The ENS can direct all function of the GI tract without extrinsic innervation
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19
Q

How does the parasympathetic nervous system innervate the GI tract?

A

Parasympathetic ganglia relay information from PNS to smooth muscle, endocrine and secretory cells

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20
Q

What kind of neurones are parasympathetic postganglionic neurones?

A

Cholinergic or peptidergic

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21
Q

What do cholinergic neurones release?

A

Acetylcholine

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22
Q

What do peptidergic neurones release?

A

Peptides e.g. substance P or VIP

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23
Q

How does the sympathetic nervous system innervate the GI tract?

A

Afferent and efferent nerve fibres are mixed so information is relayed between the GI tract and the CNS which is coordinated by the plexuses

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24
Q

What kind of neurones are sympathetic postganglionic neurones?

A

Adrinergic

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25
Q

What do adrinergic neurones release?

A

Norepinephrine

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26
Q

What are the 3 classes of GI signalling peptides?

A
  • Hormones
  • Paracrines
  • Neurocrines
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27
Q

How do GI hormones act?

A

Released from GI endocrine cells and can travel to the liver via portal circulation and then re-enter systemic circulation in order to reach their target cell

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28
Q

What is an example of a GI hormone?

A

GIP (Gastric Inhibitory Polypeptide)

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29
Q

How do paracrines act?

A

Released from GI endocrine cells and act locally

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30
Q

What is an example of a GI paracrine?

A

Somatostatin

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31
Q

What does somatostatin do?

A

Inhibits the secretion of all GI hormones

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32
Q

How do neurocrines act?

A

Released from neurones following an action potential

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33
Q

What are some examples of neurocrines? (4)

A
  • Nitric oxide
  • GRP (Gastrin Releasing Peptide)
  • Neuropeptide Y
  • Substance P
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34
Q

What makes up the majority of the contractile tissue?

A

Unitary smooth muscle

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35
Q

What makes smooth muscle unitary?

A

Cells are electrically coupled via gap junctions which leads to coordinated contraction since APs can spread from cell to cell

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36
Q

What are the 2 types of contraction in the GI tract?

A
  • Phasic

- Tonic

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37
Q

What is phasic contraction?

A
  • Periodic contraction and relaxations (3-12 per min)

- Stomach has 3 contractions per minute (slowest)

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38
Q

What is tonic contraction?

A

Constant level of contraction (tone)

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39
Q

What are slow waves?

A

Periodic depolarisations and repolarisations which are subthreshold so don’t cause an AP or contraction of the muscle

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40
Q

How does depolarisation occur in slow waves?

A

Influx of Ca2+

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41
Q

How does repolarisation occur in slow waves?

A

Efflux of K+

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42
Q

What is the purpose of slow waves?

A
  • Cause weak tonic contractions

- Phasic contractions occur at the depolarisation peaks (action potentials)

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43
Q

What is the GI pacemaker?

A

ICC (Interstitial Cells of Cajal)

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44
Q

What are the 6 sphincters in the GI tract?

A
  • Upper Oesophageal Sphincter
  • Lower Oesophageal Sphincter
  • Pyloric sphincter
  • Sphincter of Oddi
  • Ileocecal sphincter
  • Internal and external anal sphincters
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45
Q

What does the upper oesophageal sphincter separate?

A

Pharynx and oesophagus

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46
Q

What does the lower oesophageal sphincter separate?

A

Oesophagus and stomach

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47
Q

What does the pyloric sphincter separate

A

Stomach and duodenum

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48
Q

What does the sphincter of Oddi separate?

A

Stops fluid transit from the pancreas and gall bladder

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49
Q

What does the Ileocecal sphincter separate?

A

Ileum (SI) and cecum (LI)

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50
Q

What is mastication?

A

Chewing

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51
Q

What is a bolus?

A

Ball-like mixture of food and saliva which forms in the mouth while chewing

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52
Q

How many salivary glands are there?

A

3

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53
Q

Which nerves innervate mastication muscles?

A

Mandibular nerve of Cranial Nerve 5

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54
Q

Is chewing voluntary?

A

It is an involuntary reflex but can be overridden

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55
Q

What are the 3 phases of swallowing?

A
  • Oral
  • Pharyngeal
  • Oesophageal
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56
Q

What happens during the oral phase of swallowing?

A
  • Bolus transferred into the oropharynx by the tongue

- Somatosensory receptors in this area signal to the medulla to activate the pharyngeal phase

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57
Q

What happens during the pharyngeal phase of swallowing?

A
  • Soft pallet pulled upwards
  • Larynx opening covered by the epiglottis
  • Upper oesophageal sphincter relaxes to open
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58
Q

What is the epiglottis?

A

Flap of tissue which covers the windpipe when eating to prevent food particles going into the lungs

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59
Q

What happens during the oesophageal phase of swallowing?

A

Swallowing reflex:

  • Upper oesophageal sphincter closes
  • Primary peristaltic wave of contraction pushes food down
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60
Q

What lines the oesophagus?

A
  • Squamous epithelia

- Top layer is naturally sloughed off by food action

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61
Q

What happens if food gets stuck in the oesophagus?

A
  • Continued distention triggers secondary peristaltic wave (by ENS)
  • Wave starts at the point of distention
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62
Q

What causes the lower oesophageal sphincter to open?

A

Release of VIP neurotransmitter from the vagus nerve

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63
Q

Which number cranial nerve is the vagus nerve?

A

Cranial nerve 10

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64
Q

What 3 sections can the stomach be split into?

A
  • Fundus
  • Body
  • Antrum
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65
Q

What is the fundus of the stomach?

A

Upper part

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66
Q

What is the body of the stomach?

A

Middle/main part

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67
Q

What is the antrum of the stomach?

A

Lower part near the small intestine

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68
Q

What 2 regions can the stomach be split into?

A

Orad and Caudad regions

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69
Q

What is the Orad region of the stomach?

A

Top region (thin walled)

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70
Q

What is the Caudad region of the stomach?

A

Bottom region (thicker walled with 3 muscular layers)

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71
Q

What are the 3 phases to motility in the stomach?

A
  • Relaxation in the Orad to receive food
  • Contraction of 3 muscular layers in the Caudad to mix food with gastric juice forming chyme
  • Gastric emptying
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72
Q

What is chyme?

A

Food digested in the stomach (bolus is food in the mouth)

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73
Q

What is gastric juice made of?

A
  • HCl
  • Pepsinogen
  • Gastric Intrinsic factor (GIF)
  • Mucus
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74
Q

What controls secretion of gastric juice from mucosal glands?

A

Autonomic nervous system

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75
Q

What happens during gastric emptying?

A

Chyme leaves slowly through the pyloric sphincter into small intestine

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76
Q

What happens during relaxation in the Orad?

A
  • Relaxation causes a decrease in pressure so food comes in

- Lower oesophageal sphincter closes to prevent backflow

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77
Q

What volume of food can the stomach accept in a relaxed state?

A

1.5 litres

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78
Q

Why is gastric emptying slow?

A

To allow for:

  • Neutralisation of stomach acid before entering the SI
  • Time for digestion and absorption further on
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79
Q

What is the purpose of HCl in the gastric juice?

A
  • Kill pathogens

- Optimum pH for digestive enzymes

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80
Q

What is the purpose of intrinsic factor in the gastric juice?

A

Important protein for the absorption of B12

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81
Q

What is the purpose of pepsinogen in the gastric juice?

A

Pepsinogen is cleaved into pepsin which activates other digestive enzymes

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82
Q

What is the purpose of mucus in the gastric juice?

A
  • Protects the stomach lining

- Lubricates the chyme

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83
Q

How does neuronal and hormonal input affect contraction of the stomach?

A
  • Frequency of contractions don’t change

- Force of waves increase/decrease

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84
Q

What are the 3 sections of the small intestine?

A
  • Duodenum
  • Jejunum
  • Ileum
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85
Q

What is the duodenum?

A

First section of the small intestine

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86
Q

What is the jejunum?

A

Middle part of the small intestine

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87
Q

What is the ileum?

A

The last part of the small intestine

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88
Q

What happens in the small intestine?

A
  • Digestion and absorption of nutrients

- Chyme is mixed with pancreatic secretions and bile

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89
Q

What are the 3 ways in which the surface area of the small intestine is increased?

A
  • Plicae
  • Villi
  • Microvilli
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90
Q

What are plicae?

A

Muscular folds

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91
Q

What occurs in the ileum?

A

Absorption of B12 and bile acids which haven’t already been absorbed

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92
Q

What volume of exocrine pancreatic secretion enters the duodenum per day?

A

1 litre

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93
Q

What does pancreatic secretion contain?

A
  • HCO3- (bicarbonate ions)

- Digestive enzymes

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94
Q

Which cells of the pancreas secrete HCO3-? (2)

A
  • Centroacinar cells

- Ductal cells

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95
Q

Which cells of the pancreas secrete digestive enzymes?

A

Acinar cells

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96
Q

What is the endocrine function of the pancreas?

A

Secretion of insulin and glucagon

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97
Q

What is the purpose of HCO3- in the pancreatic secretion?

A

Neutralise H+ being delivered from the stomach

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98
Q

Which branch of the nervous system stimulates pancreatic secretion?

A

Parasympathetic (rest and digest)

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99
Q

Which branch of the nervous system inhibits pancreatic secretion?

A

Sympathetic (fight or flight)

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100
Q

What are the 3 secretion phases of the pancreas?

A
  • Cephalic
  • Gastric
  • Intestinal
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101
Q

What triggers the cephalic phase of pancreatic secretion?

A

Smell, taste and act of eating food

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102
Q

What triggers the gastric phase of pancreatic secretion?

A
  • Distention of the stomach

- Vagus nerve

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103
Q

What triggers the intestinal phase of pancreatic secretion?

A

Chyme entering the small intestine stimulates enteroendocrine cells which release hormones to stimulate the pancreas

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104
Q

How much of the pancreatic secretion is the intestinal phase of secretion responsible for?

A

80%

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105
Q

Which cells secret bile?

A

Hepatocytes in the liver

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106
Q

What is in bile? (4)

A
  • Bile salts
  • Pigments
  • Bilirubin
  • Cholesterol
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107
Q

How is bile concentrated in the gall bladder?

A

Epithelial cells absorb water and ions

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108
Q

What do bile salts do?

A

Amphipathic molecules which emulsify fat and form lipids into micelles so they can be absorbed

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109
Q

What is CCK?

A
  • Cholecystokinin

- Digestive hormone

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110
Q

What does CCK do?

A
  • Secreted from the small intestine when chyme enters
  • Causes the gall bladder to contract
  • Causes the sphincter of Oddi to relax so bile can enter the duodenum
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111
Q

Which cells secrete CCK?

A

I cells in the duodenum

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112
Q

What happens to bile acids after digestion?

A

Recirculated to the liver via enterohepatic circulation

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113
Q

What proportion of bile acids are recycled?

A

95%

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114
Q

What are the 2 types of contraction in the small intestine?

A
  • Peristaltic contractions

- Segmentation contractions

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115
Q

What do peristaltic contractions in the small intestine do?

A

Propel the chyme (waves)

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116
Q

What do segmentation contractions in the small intestine do?

A

Split and expose chyme to secretions through coordinated actions of circular and longitudinal muscle layers

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117
Q

What is released as part of the peristaltic reflex in the small intestine?

A

Enterochromaffin cells release serotonin

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118
Q

What happens to material which hasn’t been absorbed by the end of the small intestine?

A

Passes through the Ileocaecal sphincter into the caecum of the large intestine

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119
Q

What are the 3 primary functions of the large intestine?

A
  • Absorbs water and electrolytes
  • Makes and absorbs vitamins K and B
  • Forms and propels faeces for excretion
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120
Q

What does aldosterone do in the large intestine?

A

Hormone which increases Na+ absorption

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121
Q

What is the role of bacteria in the large intestine?

A
  • Make vitamins

- Ferment indigestible food

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122
Q

What are the sections of the large intestine?

A
  • Caecum
  • Ascending colon
  • Transverse colon
  • Descending colon
  • Sigmoid colon
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123
Q

What kinds of cells are in the large intestine?

A
  • Surface columnar epithelial cells

- Crypts

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124
Q

What is the function of surface columnar epithelial cells?

A

Absorption

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125
Q

What is the function of crypts?

A

Secretion e.g. mucus

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126
Q

What are the Taenia Coli?

A

3 bands of longitudinal muscle which run along the length of the large intestine

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127
Q

What is the function of the Taenia Coli?

A
  • Propel faecal matter

- Form Haustra

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128
Q

What are Haustra?

A

Pouches which form in the large intestine which form due to the Taenia Coli being shorter than the length of the LI, causing rouching

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129
Q

What are the 2 kinds of motility in the large intestine?

A
  • Segmented contraction

- Mass movement

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130
Q

What is segmented contraction in the large intestine?

A
  • Occurs in caecum and proximal colon

- Mixes the contents in the haustra

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131
Q

What is mass movement in the large intestine?

A
  • Moving the contents from one segment of the large intestine to another
  • Gastrocolic reflex
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132
Q

How many mass movements occur in the large intestine per day?

A

1-3

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133
Q

What is in saliva? (4)

A
  • Alpha amylase
  • Lingual lipase
  • Kallikrein
  • Mucus
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134
Q

What does salivary amylase target? (2)

A
  • Amylose

- Amylopectin

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135
Q

Why is pancreatic amylase needed?

A

Salivary amylase is deactivated in the acidic conditions of the stomach

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136
Q

What does lingual lipase do?

A

Breaks down triglycerides to diglycerides and fatty acids

137
Q

Why is there a higher proportion of lingual lipase is infants?

A

Needed for digestion of breastmilk

138
Q

Does lingual lipase continue into the stomach?

A

Yes

139
Q

What is kallikrein?

A

Enzyme which converts kininogen to bradykinin

140
Q

What is the purpose of mucus in saliva?

A

Lubricate the food

141
Q

What is secreted in the oesophagus? (2)

A
  • Mucus

- HCO3-

142
Q

Where do secretions come from in the oesophagus?

A

Submucosal glands

143
Q

What is the function of HCO3- in the oesophagus?

A

Protect the lining against acid reflux from the stomach

144
Q

What is secreted in the stomach? (4)

A
  • HCl
  • Pepsinogen
  • Intrinsic factor
  • Mucus
145
Q

What is secreted in the small intestine? (3)

A
  • Mucus
  • HCO3-
  • Receives pancreatic secretions and bile
146
Q

What is secreted in the large intestine? (1)

A

Mucus

147
Q

How much fluid is secreted per day?

A

8.5 litres

148
Q

Where do secretions in the stomach come from?

A

Mucosal layer

149
Q

What cells are present in the oxyntic glands? (5)

A
  • Enterochromaffin-like cells
  • Epithelial cells
  • Mucus neck cells
  • Parietal cells
  • Chief cells
150
Q

What do enterochromaffin-like cells do? (2)

A
  • Regulate parietal cells

- Secrete histamine

151
Q

What do epithelial cells in the oxyntic gland secrete?

A

HCO3-

152
Q

Where are oxyntic glands located?

A

Body of the stomach (main part)

153
Q

What is the opening of the oxyntic gland called?

A

Gastric pit

154
Q

What do mucus neck cells in the oxyntic gland secrete?

A

Mucus

155
Q

What is pepsinogen cleaved into?

A

The protease enzyme pepsin

156
Q

What do parietal cells in the oxyntic gland secrete? (2)

A
  • HCl

- Intrinsic factor

157
Q

What do chief cells in the oxyntic gland secrete?

A

Pepsinogen

158
Q

What glands are present in the body of the stomach?

A

Oxyntic glands

159
Q

What glands are present in the antrum of the stomach?

A

Pyloric glands

160
Q

Where in the stomach are pyloric glands located?

A

Antrum

161
Q

What cells are present in the pyloric glands? (4)

A
  • G cells
  • D cells
  • Mucus neck cells
  • Epithelial cells
162
Q

How do pyloric glands differ from oxyntic glands?

A

Very similar but no parietal cells and deeper pits

163
Q

What do G cells in the pyloric glands secrete?

A

Gastrin

164
Q

What does gastrin do?

A
  • Hormone which enters the circulation rather than the lumen of the stomach
  • Stimulates the secretion of gastric acid by parietal cells
165
Q

What do D cells in the pyloric glands secrete?

A

Somatostatin

166
Q

What is the function of somatostatin?

A

Suppresses hormone release from the GI tract

167
Q

What is the pH of the stomach?

A
  • 1-2

- Allows for conversion of pepsinogen to pepsin

168
Q

What proteins are present in the apical membrane of the parietal cells? (2)

A
  • H+/K+ ATPase

- Cl- channel

169
Q

What proteins are present in the basolateral membrane of the parietal cells? (2)

A
  • Na+/K+ ATPase

- HCO3-/Cl- exchanger

170
Q

How is carbonic acid formed in intracellular fluid?

A

CO2 from metabolism combines with H2O

171
Q

Which enzyme catalyses the formation of carbonic acid?

A

Carbonic anhydrase

172
Q

What does carbonic acid dissociate into?

A

H+ and HCO3-

173
Q

What is the formula for carbonic acid?

A

H2CO3

174
Q

How is HCl secreted from parietal cells?

A
  • H+ ions from carbonic acid enter the lumen of the stomach via the H+/K+ ATPase on the apical membrane
  • Cl- follows via the Cl- channel on the apical membrane
175
Q

What is absorbed into the blood via the basolateral membrane of the parietal cells?

A
  • HCO3-

- Na+

176
Q

What is the alkaline tide?

A

Temporary high pH of gastric venous blood after a meal due to secretion of HCO3- into the blood from parietal cells

177
Q

What enters parietal cells via the apical membrane?

A

K+

178
Q

What enters parietal cells from the blood via the basolateral membrane?

A
  • K+

- Cl-

179
Q

What happens to the HCO3- which is absorbed from parietal cells into the blood?

A

Later secreted back into the GI tract via the pancreas

180
Q

What is the resulting net movement of molecules in parietal cells?

A
  • Secretion of HCl into lumen

- Absorption of HCO3- into blood

181
Q

What is a secretagogue?

A

Substance that stimulates secretion

182
Q

How does histamine release affect HCl secretion?

A

Stimulates HCl secretion

183
Q

What kind of hormone is histamine?

A

Paracrine hormone

184
Q

Which receptor on parietal cells does histamine bind to?

A

H2

185
Q

Which G protein is the H2 receptor coupled to?

A

Gs (stimulatory)

186
Q

How does histamine upregulate HCl secretion?

A
  • Histamine binds to H2 receptors which activates Gs coupled protein
  • Upregulates production of cAMP
  • Activates protein kinase A
  • Leads to secretion of HCl
187
Q

Where is acetylcholine released from?

A

Vagus nerve

188
Q

Which receptor on parietal cells does acetylcholine bind to?

A

M3

189
Q

Which G protein is the M3 receptor coupled to?

A

Gq

190
Q

What are the second messengers involved in acetylcholine signalling to parietal cells?

A

IP3 and Ca2+

191
Q

How does acetylcholine release affect HCl secretion?

A

Stimulates HCl secretion

192
Q

How does acetylcholine indirectly stimulate HCl secretion?

A

Stimulates enterochromaffin-like cells to secrete histamine

193
Q

Where is gastrin released from?

A

G cells in the antrum of the stomach

194
Q

Which receptor does gastrin bind to?

A

CCKb receptors

195
Q

Which signalling pathway does gastrin act by?

A

Same pathway as acetylcholine

196
Q

How does gastrin release affect HCl secretion?

A

Stimulates HCl secretion

197
Q

How does gastrin indirectly stimulate HCl secretion?

A

Stimulates enterochromaffin-like cells to secrete histamine

198
Q

Which molecules stimulate HCl secretion from parietal cells? (3)

A
  • Histamine
  • Acetylcholine
  • Gastrin
199
Q

Which molecules/conditions inhibit HCl secretion from parietal cells? (3)

A
  • Low pH
  • Somatostatin
  • Prostaglandins
200
Q

How does low pH inhibit HCl secretion?

A

Inhibits gastrin secretion from G cells

201
Q

Where is somatostatin secreted from?

A

D cells

202
Q

Which G protein is the somatostatin receptor coupled to?

A

Gi (inhibitory)

203
Q

How does somatostatin affect HCl secretion?

A

Inhibits HCl secretion

204
Q

Which pathway does somatostatin act via?

A

Same as histamine but has an inhibitory effect of cAMP instead of a stimulatory effect

205
Q

How do prostaglandins inhibit HCl secretion?

A

Same pathway as somatostatin

206
Q

Which cells absorb fluids in the small intestine?

A

Villus cells

207
Q

Where do the enzymes in the small intestine come from?

A
  • Embedded in the brush border

- From the accessory organs

208
Q

Where do secretions in the intestines come from?

A

Epithelial cells in the Crypts of Lieberkuhn

209
Q

What do the intestines secrete?

A
  • Intestinal fluid

- Electrolytes

210
Q

What is the purpose of intestinal secretions?

A

To protect against bacteria/toxins in the lumen

211
Q

How do epithelial cells in the intestines protect against harmful substances in the lumen?

A
  • Polar- have apical and basolateral membranes separated by tight junctions
  • Tight junctions determine whether transport can be trans/paracellular
212
Q

What proteins are present in the apical membrane of epithelial cells in the crypts of the intestines?

A

Cl- channels

213
Q

What proteins are present in the basolateral membrane of epithelial cells in the crypts of the intestines? (2)

A
  • Na+/K+/2Cl- transporter

- Na+/K+ ATPase

214
Q

Which direction does Cl- travel across epithelial cells of crypts in the intestines?

A

From blood to lumen through basolateral Na+/K+/2Cl- transporters and apical Cl- channels

215
Q

How are apical Cl- channels in epithelial cells of crypts controlled?

A
  • Hormones/neurotransmitters bind to receptors on the basolateral membrane
  • Activates adenylyl cyclase which makes cAMP from ATP
  • cAMP causes opening of Cl- channels
216
Q

Which hormones/neurotransmitters control Cl- in intestinal epithelial cells?

A
  • Acetylcholine

- Vasoactive Intestinal Peptide (VIP)

217
Q

Which enzyme catalyses formation of cAMP from ATP?

A

Adenylyl cyclase

218
Q

What happens when apical Cl- channels in epithelial cells of crypts are opened?

A
  • Cl- enters the lumen of the intestines

- Na+ and H2O follow via paracellular transport

219
Q

How does cholera toxin cause diarrhoea?

A
  • Overstimulates adenylyl cyclase in intestinal epithelial cells
  • Cl- channels open and too much Cl- is secreted which is followed by Na+ and H2O
  • The secretions are too much for the villus cells to absorb
220
Q

What proteins are present in the apical membrane of villi epithelial cells in the jejunum?

A
  • Na+/sugar or amino acid co-transporter

- Na+/H+ exchanger

221
Q

What proteins are present in the basolateral membrane of villi epithelial cells in the jejunum?

A
  • Na+/K+ ATPase
  • Sugar and amino acid transport proteins
  • HCO3- transport protein
222
Q

What proteins are present in the apical membrane of villi epithelial cells in the ileum?

A
  • Na+/sugar or amino acid co-transporter
  • Na+/H+ exchanger
  • HCO3-/Cl- exchanger
223
Q

What proteins are present in the basolateral membrane of villi epithelial cells in the ileum?

A
  • Na+/K+ ATPase
  • Sugar and amino acid transport proteins
  • Cl- channels
224
Q

What is the net absorption in the ileum?

A

NaCl

225
Q

What is the net absorption in the jejunum?

A

NaHCO3

226
Q

How is bicarbonate formed intracellularly?

A
  • CO2 and H2O from metabolism form carbonic acid (H2CO3) via carbonic anhydrase enzyme
  • Carbonic acid dissociates into H+ and HCO3-
227
Q

What does the pancreas secrete?

A
  • Enzymes

- Bicarbonate ions (HCO3-)

228
Q

Which pancreatic enzymes are released in active forms? (2)

A

Pancreatic lipase and amylase

229
Q

Which pancreatic enzyme is released in its inactive form?

A

Pancreatic protease

Cleaved, pepsinogen to pepsin

230
Q

Which receptors does CCK act on?

A

Receptors on acinar cells in the pancreas

231
Q

What protein is present in the apical membrane of the ductal cells in the pancreas?

A

Cl-/HCO3- exchanger

HCO3 secreted into pancreatic juice

232
Q

What proteins are present in the basolateral membrane of the ductal cells in the pancreas?

A
  • Na+/K+ ATPase

- Na+/H+ exchanger

233
Q

What causes acidification of pancreatic venous blood?

A

Absorption of H+ into the blood via Na+/H+ exchanger on the basolateral membrane of ductal cells
(H+ from dissociation of carbonic acid)

234
Q

What proteins are present in the apical membrane of epithelial cells in the colon?

A
  • Na+ channel (in)

- K+ channel (out)

235
Q

What proteins are present in the basolateral membrane of epithelial cells in the colon?

A
  • Na+/K+ ATPase

- K+ channel

236
Q

What does aldosterone do in the colon?

A

Induces synthesis of Na+ channels in the apical membrane of epithelial cells in the colon which causes an increase in Na+ absorption and K+ secretion

237
Q

In which sections of the small intestine are digestion products absorbed?

A

Jejunum and ileum

238
Q

What carbohydrases are present in the GI tract? (6)

A
  • Alpha amylase
  • Alpha dextrinase
  • Maltase
  • Sucrase
  • Trehelase
  • Lactase
239
Q

Where are the products of carbohydrase digestion absorbed?

A

Into villus blood in the small intestine

240
Q

What proteases are present in the GI tract? (5)

A
  • Pepsin
  • Trypsin
  • Chymotrypsin
  • Elastase
  • Carboxypeptidases
241
Q

Where are the products of protease digestion absorbed?

A

Into villus blood in the small intestine

242
Q

Where are the products of lipase and bile salt digestion absorbed?

A

Into the lacteals within villi

243
Q

What are lacteals?

A

Lymphatic vessels inside the villi of the small intestine which absorb digested fats.

244
Q

What are the 3 end products of carbohydrate digestion?

A
  • Glucose
  • Galactose
  • Fructose
245
Q

What does SGLT1 mean?

A

Sodium Glucose Transporter

246
Q

How are glucose and galactose absorbed into epithelial villus cells?

A
  • Enter via SGLT1 with Na+ across the apical membrane against an electrochemical gradient
  • Na+ travels from a high to low concentration from the lumen into the cell and brings glucose/galactose with it
  • Basolateral Na+/K+ ATPase sets up driving force for Na+ entry
247
Q

How is fructose absorbed into epithelial villus cells?

A

Facilitated diffusion through GLUT5 on the apical membrane

248
Q

How do glucose, galactose and fructose enter the blood once inside the intestinal epithelial cells?

A

Facilitated diffusion through GLUT2

249
Q

What are the 3 end products of protein digestion?

A
  • Amino acids
  • Dipeptides
  • Tripeptides
250
Q

Where does most protein digestion take place?

A

Stomach

251
Q

How are amino acids absorbed into epithelial villus cells?

A

Sodium/amino transporter on the apical membrane

252
Q

How do amino acids enter the blood once inside intestinal epithelial cells?

A

Facilitated diffusion

253
Q

How are dipeptides and tripeptides absorbed into epithelial villus cells?

A
  • H+ dependent co-transport across the apical membrane

- Low intracellular H+ set up by Na+/H+ exchanger on apical membrane

254
Q

How do dipeptides and tripeptides enter the blood once inside intestinal epithelial cells?

A
  • Hydrolysed into amino acids by peptidases

- Absorbed same way as amino acids

255
Q

Where does lipid hydrolysis occur?

A

Duodenum and jejunum

256
Q

What are the end products of lipid digestion which are solubilised in micelles?

A
  • Cholesterol
  • Lysophospholipids
  • Monoglycerides
  • Fatty acids
257
Q

Which end product of lipid digestion is water soluble?

A

Glycerol

258
Q

What lipases are present in the GI tract? (4)

A
  • Pancreatic lipase
  • Colipase
  • Milk lipase
  • Other esterases
    (Aided by bile salts)
259
Q

What is an enterocyte?

A

A cell of the intestinal lining

260
Q

How are products of lipid digestion absorbed?

A
  • Micelle exterior is lined with amphipathic bile salts so can enter enterocyte across the luminal cell membrane
  • Products are modified and absorbed into lacteal in the form of chylomicrons
261
Q

How do fatty acids leave micelles?

A
  • Alkaline gel mucus layer protecting cell lining, acidic layer underneath caused by Na+/H+ exchanger
  • Fatty acids become protonated in the acidic layer and leave the micelle
262
Q

Which 3 ways can fatty acids enter enterocytes?

A
  • Simple diffusion
  • Incorporated into enterocyte membrane
  • Carrier-mediated transport
263
Q

Which 3 carrier proteins can fatty acids use to enter enterocytes via carrier-mediated transport?

A
  • FAT
  • FABP
  • FATP
264
Q

What does FAT stand for?

A

Fatty Acid Translocase

265
Q

What does FABP stand for?

A

Fatty Acid Binding Protein?

266
Q

What does FATP stand for?

A

Fatty Acid Transport Protein

267
Q

Where are bile salts absorbed?

A
  • Distal ileum

- 95% recycled because body couldn’t cope with demand for making new bile salts if they were lost in faeces

268
Q

What happens to products of lipid digestion once inside enteroctyes?

A
  • Converted back into triglycerides, phospholipids, esters, cholesterol in the SER
  • Associate with apolipoproteins from RER and form chylomicrons
  • Chylomicrons packaged into secretory vesicles at the Golgi and leave via exocytosis across basolateral membrane
269
Q

How do chylomicrons enter the blood stream?

A
  • Too large to go straight into capillaries
  • Enter the lacteal, lymphatic circulation carries chylomicrons to the thoracic duct where lymph fluid is emptied into the bloodstream
270
Q

How is glycerol absorbed?

A

Enters the bloodstream straight away

271
Q

How much of the pancreas is endocrine tissue?

A

1-2%

272
Q

What is the pancreatic endocrine tissue called?

A

Islets of Langerhans

Embedded within exocrine tissue

273
Q

What are the 3 main secretory cells of the Islets of Langerhans?

A
  • Alpha cells (α)
  • Beta cells (β)
  • Delta cells (δ)
274
Q

What proportion of the Islets of Langerhans is beta cells?

A

65% (main cells)

275
Q

What proportion of the Islets of Langerhans is alpha cells?

A

20%

276
Q

What proportion of the Islets of Langerhans is delta cells?

A

10%

277
Q

What are the 3 other endocrine cells scattered in the Islets of Langerhans?

A
  • F cells
  • Epsilon (ε) cells
  • Enterochromaffin cells
278
Q

How richly perfused with blood are the Islets of Langerhans?

A

5x the cardiovascular system

279
Q

What do beta cells produce? (4)

A
  • Insulin
  • Proinsulin
  • C-peptide
  • Amylin (IAPP)
280
Q

What do alpha cells produce?

A

Glucagon

281
Q

What is proinsulin?

A

Pre-cursor for insulin

282
Q

How is insulin formed from proinsulin?

A

Proinsulin is cleaved into C-peptide and insulin

283
Q

What is the function of amylin? (3)

A

Co-secreted with insulin after a meal to:

  • Locally prevent glucagon release
  • Slow gastric emptying to prevent spikes in blood glucose
  • Promotes satiety
284
Q

What do delta cells produce?

A

Somatostatin

285
Q

What is the function of somatostatin?

A

Regulates production of other hormones

286
Q

What do F cells produce?

A

Pancreatic polypeptide

287
Q

What is the function of pancreatic polypeptide?

A

Suppresses exocrine pancreatic secretion

288
Q

What do ε cells produce?

A

Ghrelin protein

289
Q

What is the function of Ghrelin protein?

A

Stimulates hunger

290
Q

What do enterochromaffin cells produce?

A

Substance P

291
Q

What are fenestrated capillaries?

A

‘Leaky’ capillaries with pores

292
Q

What are the features of the blood supply of the Islets of Langerhans?

A
  • Fenestrated capillaries
  • Venous blood of one cell type bathes others around it so signalling molecules can have paracrine and endocrine function
293
Q

How do alpha and beta cells in the Islets of Langerhans communicate?

A

Gap junctions

294
Q

How do delta and beta cells in the Islets of Langerhans communicate?

A

Delta cells send out dendrite-like processes to beta cells

295
Q

Which 3 types of neurons are the Islets of Langerhans innervated by?

A
  • Adrenergic
  • Cholinergic
  • Peptidergic
296
Q

How is insulin secretion regulated by blood glucose?

A
  • High blood glucose detected by receptors on beta cells stimulates insulin synthesis and secretion
  • Low blood glucose inhibits synthesis and secretion
297
Q

Which receptors on beta cells increase insulin secretion when stimulated by the sympathetic nervous system?

A

Beta adrenergic receptor stimulation

298
Q

Which receptors on beta cells inhibit insulin secretion when stimulated by the sympathetic nervous system?

A

Alpha adrenergic receptor stimulation

299
Q

What neurotransmitter does the vagus nerve release?

A

Acetylcholine

300
Q

Which branch of the nervous system is the vagus nerve part of?

A

Parasympathetic

301
Q

How does parasympathetic innervation of the beta cells affect insulin secretion?

A

Release of ACh from the vagus nerve increases insulin secretion

302
Q

Which 3 humoral factors have an effect on insulin secretion?

A
  • GIP
  • Amylin
  • Somatostatin
303
Q

What is does GIP stand for?

A

Glucose-dependent insulinotropic peptide

304
Q

What is does GIP stand for?

A

Glucose-dependent Insulinotropic Peptide

305
Q

What is the function of GIP?

A
  • Released by the small intestine in response to a meal

- Causes insulin release

306
Q

What is the most potent activator of insulin secretion by beta cells?

A

Glucose

307
Q

How does glucose affect insulin secretion from beta cells?

A
  • Glucose enters beta cell via GLUT2 channel by facilitated diffusion
  • Glucose metabolised with glucokinase to form ATP
  • Closes ATP dependent K+ channels
  • Induces depolarisation
  • Depolarisation opens voltage gated Ca2+ channels
  • Increase in intracellular Ca2+ causes exocytosis of vesicles containing insulin
308
Q

How do ACh and CCK affect insulin secretion in beta cells?

A
  • Bind to Gq coupled protein receptors
  • Activates intracellular intermediate PKC (Protein Kinase C)
  • Causes exocytosis of vesicles containing insulin
309
Q

How do beta adrenergic agonists affect insulin secretion in beta cells?

A
  • Bind to beta adrenergic receptors (Gs protein coupled receptors)
  • Causes conversion of ATP to cAMP via adenylyl cyclase
  • Activates PKA (Protein Kinase A) which causes exocytosis of vesicles containing insulin
310
Q

How do somatostatin and alpha adrenergic agonists affect insulin secretion in beta cells?

A
  • Bind to Gi coupled protein receptors
  • Down regulates adenylyl cyclase
  • Down regulates formation of cAMP
  • No secretion of insulin
311
Q

How does glucagon affect insulin secretion in beta cells?

A
  • Bind to beta adrenergic receptors (Gs protein coupled receptors)
  • Causes conversion of ATP to cAMP via adenylyl cyclase
  • Activates PKA (Protein Kinase A) which causes exocytosis of vesicles containing insulin
312
Q

What is the structure of the insulin receptor?

A
  • Heterotetramer
  • 2 extracellular alpha chains
  • 2 membrane-spanning beta chains
  • Intracellular tyrosin kinase domain
  • Intracellular phosphorylation sites
313
Q

What does activation of the insulin receptor cause?

A
  • Insulin binds to activate
  • Autophosphorylates to downregulate the receptor itself
  • Phosphorylates other substrates to cause various downstream effects
314
Q

What substances can the insulin receptor phosphorylate to cause downstream effects? (4)

A
  • PKC
  • Phosphatases
  • Phospholipases
  • G proteins
315
Q

What downstream signalling effects can insulin cause by binding to insulin receptors? (4)

A
  • Cell growth
  • Cell proliferation
  • Gene expression
  • Synthesis of glycogen, lipids, proteins
316
Q

How does insulin trigger glucose uptake in target cells?

A
  • Insulin binds to insulin receptors
  • Triggers signal transduction cascade
  • Causes exocytosis of vesicles containing GLUT4 channels
  • Channels embed in the membrane which increases glucose uptake into the cell
317
Q

What are the 5 functions of insulin?

A
  • Increases uptake of glucose by muscle and fat cells
  • Promotes glycogenesis in liver and muscle cells
  • Excess glucose is converted to fat (lipogenesis)
  • Inhibits glycogenolysis
  • Inhibits gluconeogenesis (reducing blood glucose)
318
Q

What is glycogenesis?

A

Conversion of glucose to glycogen

319
Q

What is lipogenesis?

A

Conversion of glucose to fat

320
Q

Which enzymes does insulin upregulate transcription of to promote glycogenesis in the liver?

A
  • Glucokinase
  • Hexokinase
  • Glycogen synthase
321
Q

What is glycogenolysis?

A

Breakdown of glycogen to glucose

322
Q

What is gluconeogenesis?

A

Production of glucose from non-carbohydrates

323
Q

What are the 4 major effects of insulin on hepatocytes?

A
  • Promotes glycogenesis by upregulating glucokinase
  • Promotes glucose metabolism
  • Promotes lipogenesis
  • Promotes protein synthesis
324
Q

What are the 4 major effects of insulin on muscle cells?

A
  • Promotes glucose uptake by embedding GLUT4 in the membranes
  • Promotes glycogenesis by upregulating hexokinase
  • Promotes glucose metabolism
  • Promotes protein synthesis
325
Q

What are the 4 major effects of insulin on adipocytes?

A
  • Upregulates expression of GLUT4 in the membrane
  • Glucose converted into fatty acids and stored as triglycerides
  • Inhibits breakdown of lipids
  • Increases synthesis of lipoprotein lipase which frees fatty acids for triglyceride synthesis
326
Q

What is the effect of insulin on Na+/K+ ATPase?

A

Promotes K+ uptake into cells by increasing activity of Na+/K+ ATPase

327
Q

What is the effect of insulin of the hypothalamic satiety centre?

A

Causes feeling of being full

328
Q

What is Diabetes Mellitus?

A
  • High blood sugar over prolonged periods

- Type 1 or 2

329
Q

What is Type 1 Diabetes Mellitus?

A
  • ‘Insulin dependent’
  • Autoimmune destruction of pancreatic Islets of Langerhans (alpha and beta cells)
  • No insulin or glucagon produced
330
Q

What is Type 2 Diabetes Mellitus?

A
  • ‘Non-insulin dependent’
  • Low insulin production
  • Peripheral insulin resistance
  • Linked to obesity
331
Q

What are the effects of Type 1 Diabetes Mellitus? (7)

A
  • Hyperglycaemia
  • Increased blood fatty acid and ketoacid concentration
  • Increased blood amino acid concentration
  • Osmotic diuresis
  • Polyuria
  • Hypotension
  • Hyperkalaemia due to K+ moving out of cells
332
Q

What are the symptoms of Type 1 Diabetes Mellitus? (7)

A
  • Increased thirst and urination
  • Hunger
  • Weight loss
  • Fatigue
  • Irritability
  • Fruity smelling breath (DKA)
  • Blurred vision
333
Q

What is the treatment for Type 1 Diabetes Mellitus?

A

Insulin replacement therapy

334
Q

What are the effects of Type 2 Diabetes Mellitus? (2)

A
  • Downregulation of insulin receptors in target tissues causing insulin resistance
  • Elevated blood glucose even at normal insulin levels
335
Q

What are the symptoms of Type 2 Diabetes Mellitus? (7)

A
  • Thirst
  • Hunger
  • Frequent urination
  • Weight loss
  • Fatigue
  • Blurred vision
  • Headaches
336
Q

What are the treatment options for Type 2 Diabetes Mellitus?

A
  • Sulphonylurea drugs which stimulate insulin secretion
  • Biguanide drugs which upregulate receptors on target tissues
  • Calorie restriction
337
Q

What is an example of a sulphonylurea drug for Type 2 Diabetes treatment?

A

Tolbutamide

338
Q

What is an example of a biguanide drug for Type 2 Diabetes treatment?

A

Metformin

Phys pharm (11 decks)

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