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HOM > Digestion > Flashcards

Digestion Flashcards

1
Q

What are the layers in the gut wall?

A

mucosa raised into villi > lamina propria > muscularis mucosae > submucosa (and submucosal plexus) > circular muscularis externa > myenteric plexus > longitudinal muscularis externa > serosa

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2
Q

What is the enteric nervous sytem?

A

Myenteric and submucosal plexus

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3
Q

What does the submucosal plexus control?

A

Secretion

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4
Q

What does the myenteric plexus control?

A

Motility

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5
Q

What kind of nervous input is important in the proximal gut? What about further down?

A

ANS in proximal gut, hormonal and intrinsic ENS control further down

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6
Q

What are some neurocrine transmitters in the GI tract?

A

ACh, NO, VIP, NA

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7
Q

What are some paracrine transmitters in the GI tract?

A

Histamine, Somatostatin

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8
Q

What is stimulated in the gut by sympathetic supply?

A

Sphincters

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9
Q

What transmitters are used in sympathetic supply to the gut?

A

Cholinergic synapse at ganglion in sympathetic chain or abdominal cavity, then NA synapse in plexi

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10
Q

What carries parasympathetic supply to the gut?

A

Vagus and pelvix nerves

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11
Q

What neurotransmitters are used in sympathetic supply to the gut?

A

Both synapses cholinergic

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12
Q

How are sphincters relaxed by the parasympathetic supply?

A

Inhibitory postganglionic fibres which release transmitters like VIP

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13
Q

Which cells produce secretin and in response to what?

A

S cells in response to acid

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14
Q

What are the effects of secretin?

A

Stimulates pancreatic growth, bicarb and water secretion, inhibits gastric acid secretion and motility, promotes sphincter contraction (pyloric)

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15
Q

What does ACh do in the gut?

A

Excites smooth muscle and secretion

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16
Q

What do NO and VIP do in the gut?

A

Relax smooth muscle

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17
Q

What does NA do in the gut?

A

Inhibitory but promotes sphincter and vascular smooth muscle contraction

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18
Q

What is xerostomia?

A

No saliva

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19
Q

How do hormones help gastric bypass effectiveness?

A

Hormones peak at different times - increased PYY, GLK-1 which decrease appetite

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20
Q

Which ions does aldosterone affect?

A

Promotes ion exchange, Na+ reabsorbed, K+ secreted

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21
Q

Which extra glands do dogs have?

A

Zygomatic

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22
Q

Which species don’t have salivary amylase?

A

Cats, dogs and horses

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23
Q

What are the different types of saliva?

A

Serous, mucous or both

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24
Q

What are the glycoproteins in saliva called?

A

Mucins

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25
Q

What are some ways saliva helps with defence?

A

Lysozymes, lactoferrin removes iron which bacteria need, IgA, proline-rich protein binds to tannin

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26
Q

Which cells produce primary salivary secretion and where do they secrete it into?

A

Acinar cells into acinus

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27
Q

What two kinds of ducts modify saliva?

A

Intercalated and striated

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28
Q

How is saliva modified?

A

Cl- swapped for HCO3-, Na+ swapped for K+, but reabsorption exceeds secretion

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29
Q

Which cells contract around the acinus?

A

Myoepithelial

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30
Q

Is saliva hypotonic or hypertonic?

A

Hypotonic

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31
Q

How does parasympathetic stimulation affect saliva?

A

Vasodilation, myoepithelial contraction, increased secretory volume

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32
Q

How does sympathetic stimulation affect saliva?

A

Myoepithelial contraction and increased enzyme contraction

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33
Q

Which cells release gastrin?

A

From G cells of gastric antrum and duodenum

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34
Q

What is gastrin released in response to?

A

Nervous stimulation and presence of peptides and amino acids

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35
Q

What does gastrin stimulate?

A

Gastric acid secretion from parietal cells and promotes growth of oxyntic mucosa

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36
Q

Which cells release cholecystokinin?

A

I cells in duodenum and jejunum

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37
Q

What is CCK released in response to?

A

Long-chain free fatty acids and monoglycerides

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38
Q

What does CCK stimulate?

A

Gall bladder contraction, pancreatic stimulation and growth

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39
Q

What does CCK inhibit?

A

Gastric emptying and appetite

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40
Q

What are the incretins?

A

GIP (glucose dependent insulinotropic polypeptide) and GLP-1 (glucagon-like peptide 1)

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41
Q

Where are the incretins released from?

A

Upper small intestine (GIP) and jejunum to rectum (GLP-1)

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42
Q

What do the incretins do?

A

Augment insulin release from pancreas following a meal

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43
Q

What can GLP-1 agonists be used to treat?

A

Type II diabetes

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44
Q

Where is motilin released from?

A

M cells in upper small intestine

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45
Q

What happens to motilin release during fasting?

A

Cyclically

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46
Q

What controls motilin release?

A

Neural control

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47
Q

What does motilin do?

A

Initiates MMC

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48
Q

Where is ghrelin released from?

A

Endocrine cells of stomach

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49
Q

What is ghrelin released in response to?

A

Fasting

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50
Q

What does ghrelin do?

A

Works on hypothalamus to stimulate appetite and promotes growth hormone release from pituitary gland

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51
Q

What can peristalsis be initiated by?

A

CNS (in the oesophagus), slow waves (in the antrum and small intestine) or the ENS (peristaltic reflex, mass movements)

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52
Q

What drives segmental contractions?

A

Slow waves initiated by ICCs

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53
Q

What does parasympathetic and sympathetic stimulation do to segmentation?

A

Parasympathetic is excitatory, sympathetic is inhibitory

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54
Q

How does peristaltic release work?

A

Stretch means mucosal enterochromaffin cells release paracrine serotonin > ENS sensory neurones > myenteric plexus

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55
Q

What do neurones on anal side release for relaxation?

A

NO with or without ATP

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56
Q

What do neurones on oral side release for contraction?

A

ACh

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57
Q

What creates the basal electrical rhythm?

A

Interstitial cells of Cajal

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58
Q

What causes the smooth muscle to contract in the basal electrical rhythm?

A

Depolarisation causes VG Ca2+ channel to open, reaches contraction threshold, smooth muscle will contract

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59
Q

How do you EXCITE the basal electrical rhythm?

A

Use ACh to open cation channels to help depolarisation

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60
Q

How do you INHIBIT the basal electrical rhythm?

A

Use NA to open hyperpolarising K+ channels

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61
Q

What are the three kinds of sensory neurones in the gut?

A

IPANs, IFANs and sensory fibres with cell body in dorsal root ganglia going gut > spinal cord for stomach reflexes, pain and defecation

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62
Q

What do IPANs do?

A

Intrinsic primary afferent neurone, sensory, entirely within ENS, afferent part of local reflexes inc. peristalsis, mixing, secretion

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63
Q

What is a vagovagal reflex?

A

Where both afferent and efferent neurones are carried by the vagus

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64
Q

Which nerves carry pain signals?

A

Sympathetic

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65
Q

What is referred pain?

A

Other neurones synapse onto same CNS fibres as gut ones so feels like pain is coming from somewhere else

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66
Q

Where are the sensory afferent fibres from the gut carried?

A

Vagus

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67
Q

How does the ileal brake work?

A

Too much fat/nutrients in ileum means not enough absorption and moving too quickly - PYY? GLP-1? IFANS?

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68
Q

What is an IFAN?

A

Intestinofugal afferent neurone - cell body in gut, neurone which leaves for long distance reflexes from proximal > distal gut (shortcut instead of going through thousands of ENS neurones), goes proximal gut > IFAN > prevertebral ganglion > postganglionic sympathetic fibre

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69
Q

What is the gastro-colic reflex?

A

Stomach stretch causes colon to move faster - gastrin/CCK?

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70
Q

What is swallowing initiated by?

A

Touch receptors in pharynx

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71
Q

How does swallowing work?

A

Bolus to back of mouth, soft palate upwards to block nasal cavity, palatopharyngeal folds limit bolus size, larynx upwards to epiglottis to close it, vocal cords pull together to narrow glottis, respiratory centre of medulla inhibited, upper oesophageal sphincter relaxes, constrictor muscles of pharynx contract sequentially

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72
Q

What is it called when the respiratory centre of the medulla is inhibite?

A

Deglutition apnoea

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73
Q

What is the chemoreceptor trigger zone?

A

Area postrema

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74
Q

What muscle makes up the upper oesophageal sphincter? What does it do?

A

Cricopharygeus muscle prevents air swallowing

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75
Q

What happens if bolus fails to go all the way down the oesophagus?

A

Secondary wave initiated by persistent distension

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76
Q

What is the process of vomiting?

A

Increased salivation, reverse peristalsis, close glottis, breathe in, diaphragm and abdominal muscles contract, LOS relaxes

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77
Q

Why is there increased salivation during vomiting?

A

Alkaline to protect teeth

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78
Q

What can vomiting cause?

A

Metabolic alkalosis, hypovolaemia, hypokalaemia

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79
Q

What is the lower oesophageal sphincter controlled by?

A

Inhibitory and excitory ENS fibres

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80
Q

When does the lower oesophageal sphincter relax?

A

Relaxes before food arrives during feedforward vagovagal reflex

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81
Q

Which transmitter promotes relaxation of the LOS?

A

NO

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82
Q

What is megaoesophagus caused by?

A

If ENS neurones are damaged and nothing causes LOS to open so food builds up

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83
Q

What is receptive relaxation?

A

A vagovagal reflex causing fundus and body to relax in response to stretch so more food can be accomodated with little pressure increase

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84
Q

What is nutrient sampling?

A

Some food drains into duodenum so there’s nutrient sampling followed by feedback

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85
Q

What does retropulsion in the stomach do?

A

Breaks in large particles

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86
Q

What lacks ICCs?

A

Pyloric sphincter

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87
Q

What does the MMC do?

A

Contractions sweeping food from pylorus > duodenum > terminal ileum

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88
Q

What do cardiac glands produce? Why?

A

Mucus to prevent acid reaching oesophagus

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89
Q

What do pyloric glands secrete?

A

Mucus and gastrin into the blood

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90
Q

What do oxyntic glands produce?

A

HCl, pepsinogens, intrinsic factor and mucus

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91
Q

What converts prochymosin > chymosin?

A

Acidity

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92
Q

What does chymosin do? Why?

A

Turns soluble caseinogen into insoluble casein so milk can stay in stomach long enough to be acted on by pepsins

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93
Q

What promotes pepsinogen release?

A

Vagal ACh and cholinergic reflex in response to acidity

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94
Q

Where is intrinsic factor produced in dogs and cats?

A

Pancreas

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95
Q

How to parietal cells have such a high secretion rate?

A

Vesicles and tubules fuse with luminal membrane and luminal membrane is very large

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96
Q

What does B12 bind to? Why?

A

Haptocorrin to protect from stomach acidity

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97
Q

Where is haptocorrin secreted?

A

Saliva and stomach

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98
Q

Where does B12 bind to intrinsic factor?

A

Small intestine

99
Q

Where is B12 taken up?

A

Ileum epithelium by receptor-mediated endocytosis

100
Q

What does gastric acid do?

A

Delays gastric emptying, improves Ca2+, Fe and B12 absorption, activates pepsinogen, destroys microbes

101
Q

What happens to gastric acid after a meal?

A

Na+ decreases, H+ increases but costs energy and may cause ulcers

102
Q

Which hormones promote acid secretion?

A

Gastrin, histamine, ACh

103
Q

Which hormones inhibit acid secretion?

A

Secretin, somatostatin and prostaglandins

104
Q

How is gastric acid produced?

A

CO2 > HCO3- > exchanged for Cl- which goes into stomach and HCO3- goes into the ECF

105
Q

What is the alkaline tide?

A

During acid production, bicarbonate added to plasma and CO2 removed causing alkaline tide

106
Q

Which three substances control acid secretion?

A

Gastrin, histamine acetylcholine

107
Q

What promotes gastrin release?

A

Local stretch receptors via ACh, vagal stimulation via GRP, proteins, amino acids, and Ca2+ in stomach lumen

108
Q

What is Zollinger-Ellison syndrome?

A

Gastrin-secreting tumour

109
Q

What is the strongest agonist of acid secretion?

A

Histamine

110
Q

Which cells release histamine?

A

Enterochromaffin-like cells within gastric glands

111
Q

What does ACh promote release of?

A

Acid, histamine and gastrin

112
Q

What does ACh inhibit release of?

A

Somatostatin

113
Q

Which three substances inhibit acid release?

A

Somatostatin, secretin, prostaglandins

114
Q

How does somatostatin inhibit acid release?

A

Effects on ECL and parietal cells

115
Q

How does secretin inhibit acid secretion?

A

Indirectly by stimulating vagal afferent fibres

116
Q

How does secretin affect gastrin release?

A

Reduces

117
Q

What do prostaglandins promote production of?

A

Bicarb and mucus

118
Q

What happens during the cephalic phase of disgestion?

A

Feedforward ACh release, acid secretion increases but no pH change because negative feedback through somatostatin and neural reflexes

119
Q

What happens in the gastric phase of digestion

A

pH rises, large rise in secretions (gastrin and acid)

120
Q

Why does the pH rise during the gastric phase of digestion?

A

Protons buffered by proteins in food

121
Q

What happens in the intestinal phase of

A

Duodenal stretch triggers stomach acid secretion, products of protein digestion cause gastrin release, then enteric reflexes and secretin decrease acid production

122
Q

How are gastric ulcers treated?

A

Drugs suppressing acid secretion like H2 receptor antagonists and K+/H+ proton pump inhibitors

123
Q

How does aspirin cause more acid secretion?

A

Reduced prostaglandins = more acid secretion

124
Q

How does helicobacter pylori protect itself from acid?

A

Secretes urease to make ammonia from urea to protect from acid

125
Q

What promotes relaxation of the pyloric sphincter?

A

Inhibitory postganglionic vagal fibres which release NO

126
Q

How are ketamine and alcohol absorbed?

A

Lipid soluble so absorbed across stomach wall

127
Q

How is aspirin absorbed?

A

Weak acid, protonated then diffuses across stomach epithelium

128
Q

How is gastric smooth muscle contraction increased in the fed state?

A

ACh and gastrin increase plateau duration and amplitude of plateau

129
Q

How do neuronal and hormonal reflexes slow stomach emptying?

A

Inhibit motility or tighten sphincter

130
Q

What happens in coeliac disease?

A

Microvilli are destroyed

131
Q

What are the larger folds of the intestine called?

A

Folds of Kerckring

132
Q

What are the Crypts of Lieberkuhn?

A

Between villi, secrete fluid, contain stem cells

133
Q

What do pancreatic secretory trypsins inhibitors do?

A

Found in trypsin granules, protects acinar cells against innappropriate trypsin activation

134
Q

What does the gastroileal reflex do?

A

Opens ileocaecal valve, motility enhanced if stomach full

135
Q

What does the colonoileal reflex do?

A

Closes ileocaecal valve, inhibits movement through sphincter if colon full

136
Q

What are Na+ and K+ like in pancreatic juice?

A

Always high

137
Q

What happens to pancreatic juice after a meal?

A

HCO3- increases to neutralise acid and Cl- decreases

138
Q

What happens in the cephalic phase of pancreatic secretion?

A

Feedforward vagal ACh

139
Q

What happens in the gastric phase of pancreatic secretion?

A

Vagovagal and local reflexes

140
Q

What happens in the intestinal phase of pancreatic secretion?

A

Lots of secretin in response to low pH stimulating HCO3- and water secretion, CCK release triggering vagovagal reflexes, enzyme secretion and potentiates secretin

141
Q

What increases Ca2+ in pancreatic cells?

A

ACh and CCK

142
Q

What increases cAMP in pancreatic cells?

A

Secretin and VIP

143
Q

Which luminal chloride channels does cAMP open?

A

Cystic fibrosis transmembrane conductance regulator (GFTR)

144
Q

What happens to GFTR in cystic fibrosis?

A

Defective so water doesn’t follow gradient so mucus too sticky

145
Q

What does cholera toxin do?

A

Increases cAMP in gut epithelium, permanently activated G protein, CFTR open too much, too much chloride and water secreted, causes hypovolaemia and shock and diarrhoea

146
Q

Glucose + fructose = ?

A

Galactose

147
Q

Which bonds can’t amylases break?

A

1-6 or the 1-4 either size

148
Q

What converts oligosaccharides to glucose?

A

Glucoamylases

149
Q

What converts alpha-limit dextrins and to glucose?

A

Alpha-dextrinase

150
Q

Which transporter for glucose and galactose?

A

SGLT-1

151
Q

Which transporter for fructose?

A

GLUT5

152
Q

Which transporter takes glucose and galactose and fructose to ECF?

A

GLUT2

153
Q

What are the primary bile acids?

A

Cholic and chenodeoxycholic acids

154
Q

WHat are the secondary bile acids?

A

Deoxycholic and lithocholic acids

155
Q

Which enzyme catalyses trypsinogen to trypsin?

A

Enteropeptidase

156
Q

What does trypsin catalyse?

A

Its own activation, chymotrypsin, elastins and carboxypeptidases

157
Q

What are the three functions of bile acid?

A

Fat absorption, waste removal, protection

158
Q

How is bile used for waste removal?

A

Cholesterol, bilirubin, heavy metals

159
Q

How is bile used for protection?

A

IgA, tocopherol (antioxidant) and mucus

160
Q

How is bile used for fat absorption?

A

Bile acids (surfactant) and phospholipids

161
Q

What is bile acid conjugated with?

A

Glycine or taurine for solubility, found as Na+ salt

162
Q

What is the cholerectic effect?

A

Recycled bile acids stimulate more bile acid secretion but inhibit new bile acid synthesis

163
Q

What happens to most bile acid?

A

Some lost in faeces, most taken up and returned to liver by hepatic portal vein bound to albumin and then resecreted

164
Q

How are bile salts absorbed by the brush border?

A

Form emulsion droplets, attacked by pancreatic lipase and colipase, form mixed micelle with free fatty acids, cholesterol, phospholipids and monoglycerides, then absorbed by brush border

165
Q

How does bilirubin travel in blood?

A

Bound to albumin

166
Q

What is bilirubin conjugated with before being excreted in the bile?

A

Glucaronic acid

167
Q

What’s needed in rehydration salts so SGLT can work?

A

Water, salt and glucose

168
Q

What are the two ways of taking up chloride?

A

Paracellularly or exchanging for bicarb

169
Q

How does haem > urobilinogen?

A

Haem > biliverdin > bilirubin > urobilinogen

170
Q

What converts bilirubin > urobilinogen?

A

Bacteria

171
Q

How are urobilin and sercobilin excreted?

A

Stercobilin in faeces, urobilin in urine

172
Q

How does urobilinogen > stercobilib?

A

Oxidised

173
Q

How does urobilinogen > urobilin?

A

Reabsorbed and oxidised

174
Q

What happens if bile duct is blocked?

A

Faeces lose colour and become fatty, also jaundice because of yellow bilirubin

175
Q

What happens once calcium enters the duodenum?

A

Enters down electrochemical gradient, calbindin ferries it to basolateral membrane then it’s extruded into ECF

176
Q

What upregulates expression of proteins needed for calcium absorption?

A

D3

177
Q

What other uptake is needed if high Ca2+ intake?

A

Paracellular

178
Q

When is hepcidin produced?

A

In response to inflammatory mediators

179
Q

What does hepcidin do?

A

Reduces gut iron uptake, less circulating iron

180
Q

What does B12 travel bound to?

A

Transcobalamin II

181
Q

What converts Fe3+ > Fe2+?

A

Fe reductase

182
Q

What transporter lets Fe2+ into the cell?

A

Fe2+/H+ cotransporter DMT1

183
Q

How is Fe2+ transported out of the cell?

A

Ferroportin

184
Q

How does Fe2+ travel in blood?

A

Via transferrin

185
Q

What happens if hepcidin is present?

A

Fe is trapped in cell bound to ferritin (removes ferroportin)

186
Q

How is hepcidin lost?

A

When epithelial cells are shed

187
Q

What prolongs the duration of slow waves in the colon?

A

ACh

188
Q

In what kind of muscle in the colon are action potentials not needed for contraction?

A

Circular muscle

189
Q

What promotes segmental contractions in the colon?

A

Vagal parasympathetic activity

190
Q

What inhibits colon motility?

A

Sympathetic stimulation

191
Q

What coordinates mass movements?

A

ENS

192
Q

What promotes mass movements?

A

Gastrocolic and duodenocolic reflexes

193
Q

What kind of muscle is the internal anal sphincter?

A

Smooth muscle

194
Q

What modulates myogenic tone of the internal anal sphincter?

A

ANS

195
Q

What relaxes the internal anal sphincter?

A

NO and VIP

196
Q

What contracts the internal anal sphincter?

A

ACh

197
Q

What kind of muscle is the external anal sphincter?

A

Striated muscle

198
Q

What controls the external anal sphincter?

A

Somatic motor control (pudendal nerves)

199
Q

When does tone increase in the external anal sphincter?

A

During rise in intrabdominal pressure

200
Q

What happens following a mass movement from the sigmoid colon?

A

Internal sphincter relaxes, sensory nerves in rectum cause parasmpathetic pelvic nerves to produce highly propulsive movements, external sphincter voluntarily relaxed, relaxing pelvic floor straightens ano-rectal angle, Valsalva manoevre

201
Q

Why is there more bacteria in the hindgut?

A

Less bile

202
Q

What happens in Hirschsprung’s disease?

A

ENS ganglion cells are lacking in descending colon and internal anal sphincter, no reflex relaxation of rectum and IAS, colon dilates and perforates

203
Q

What is raffinose?

A

Indigestible carbohydrate

204
Q

What do opioid receptors in the GI tract do?

A

Stimulated by B endorphins, promote decreased propulsion, decreased secretion and increased sphincter tone

205
Q

What is a Helminth?

A

Roundworm, fluke, tapeworm

206
Q

How does breath hydrogen test for lactose intolerance work?

A

Undigested lactose in colon causes colonic bacteria to produce H2 gas, some gets into blood and alveolar gas

207
Q

WHich are the main anaerobic species in the gut?

A

Bacteroides, Bifidobacterium, Eubacterium

208
Q

Which way do arterial and venous blood go in the villus?

A

Arterial blood goes up villus, venous blood goes down villus

209
Q

Why is there functional hyperaemia after a meal?

A

Parasympathetic stimulation only increases flow locally

210
Q

What reduces splanchnic circulation?

A

Sympathetic vasoconstriction

211
Q

What empties the central lacteals?

A

Smooth muscle contraction of lamina propria followed by interstitial pressure increase

212
Q

What prevents backflow in the lacteals?

A

Valves

213
Q

How does liver interconvert amino acids, pyruvate and Krebs intermediates?

A

Uses transamination

214
Q

What is a “conditionally essential” amino acid?

A

An amino acid that can’t be produced fast enough

215
Q

What can the liver store?

A

A, D, E, K, B12, and Fe

216
Q

What does conjugation with glucaronic acid in the liver do?

A

Makes lipid-soluble compounds water-soluble

217
Q

What do fat digestion products and cholesterol bind to?

A

Fatty-acid binding proteins (FABPs) in epithelial cells of the small intestine

218
Q

What is in a chylomicron?

A

Triglycerides, apolipoproteins, phospholipids, cholesterol

219
Q

Where do chylomicrons go from the gut epithelium?

A

Exported from golgi and released by exocytosis to central lacteal of villi

220
Q

Where is lipoprotein lipase found?

A

Bound to capillary walls in muscle, fat and lactating mammary gland

221
Q

What does lipoprotein lipase do?

A

Catalyse hydrolysis of triglyerides within chylomicrons

222
Q

Where do fatty acids go from the chylomicrons?

A

Transported across endothelium, diffuses into cells where they are resynthesized into triglycerides

223
Q

What takes up chylomicron remnants and glycerol?

A

Liver

224
Q

What secretes very low-density lipoproteins and why?

A

Liver when fasting to export triglycerides and hepatic cholesterol to tissues

225
Q

Where do high-density lipoproteins go?

A

Take cholesterol from tissues > liver

226
Q

What breaks down insulin?

A

Kidney and liver

227
Q

What promotes anticipatory insulin release?

A

Parasympathetic stimulation of B cells via vagal ACh

228
Q

What potentiates insulin release in response to oral glucose?

A

Incretins and certain amino acids

229
Q

What allows glucose to rise during exercise?

A

Insulin inhibition by sympathetic stimulation of alpha2 receptors

230
Q

What is the incretin effect?

A

Oral glucose causes large insulin increase

231
Q

How do you get hyperglycaemia during type 2 diabetes?

A

B cells can fail and die as they can’t sustain extra production

232
Q

What is the risk in type 1 diabetes?

A

Unrestrained triglyceride brakdown and high rate of ketone body production = ketoacidosis

233
Q

How does insulin affect ketone bodies and K+?

A

Decrease

234
Q

How does insulin affect muscle?

A

GLUT4 to cell surface, glucose oxidation and storage as glycogen, fat oxidation and uptake inhibited, stimulates amino acid uptake (anabolic effect)

235
Q

How does insulin affect adipose tissue?

A

GLUT4 promotes uptake, conversion to fatty acids stimulated, promotes fatty acid uptake from chylomicrons, inhibits lipase, reduces FFAs

236
Q

How does insulin affect the liver?

A

Promotes glucose oxidation, glycogen synthesis and triglyceride synthesis, inhibits fat oxidation, AA uptake, gluconeogenesis, glycogenolysis and hepatic glucose output

237
Q

What is the standing gradient model?

A

Solute gradient is set up by pumps and channels, water follows by tight junctions, hydrostatic pressure increases and water is forced out of cleft to be taken up by capillaries

238
Q

Where is sodium absorption highest?

A

Small intestine

239
Q

What is the sodium transporter with monosaccharides?

A

SGLT1

240
Q

Which sodium channel is used in the colon?

A

ENaC

241
Q

Where is bicarbonate absorbed?

A

Jejunum

242
Q

How is potassium absorbed?

A

Paracellular uptake by small intestine and net secretion in the colon via apical potassium channels

243
Q

What is the gastrin receptor?

A

CCKB

HOM (7 decks)

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