1. Dianaʼs Diarrhea
Physiology at a Glance: GI Tract Overview & Stomach
1. Name the 6 structural layers of any given cross-section of the GI tract from lumen
outwards and give a brief description of each1
2. What are the three saliva secreting glands?2
3. Which two main nerves control the involuntary part of the swallowing mechanism
in conjunction with the ‘swallowing centre’ in medulla and pons?3
4. What parts of the stomach are (i) at the end of the oesophagus, (ii) at the very to
of the stomach where air collects (iii) the bottom of the stomach leading to the
pyloric sphincter (iv) the bottom of the stomach body
5. Which nerves innervate peristalsis in the pyloric sphincter and upper small
intestine?4
6. What volumes can the stomach vary between when it is empty and full?5
7. What enzyme group breaks down proteins in the stomach?6
8. What type of cells produce HCl in the stomach?
9. What maintains the right pH balance in the stomach with regards to secretion of
HCl?7
1 1. Mucosal Layer (Epithelium), 2. Lamina Propria (connective tissue containing blood & lymph, 3.
Muscularis Mucosa (thin layer of SM for making folds and ridges), 4. Submucosa (connective tissue
containing more blood and lymph and innervated by the submucosal plexus) 5. Muscularis externa (thick
circular layer of muscle covered by a less thick longitudinal layer, 6. Serosa (outermost layer made up of
squamous mesothelial cells.
2 Parotid, Submandibular and Sublingual glands
3 9th cranial (glossopharyngeal) and 10th cranial (vagus) nerves
4 Vagus and enteric nerve plexuses
5 Varies between 50ml (empty) and 4L (full)
6Proteins broken into smaller polypeptides (only partially digested) by pepsins in stomach, these are
produced in inactive form as pepsinogens by chief cells in gastric mucosa (activated by HCl)
7 Exchange of intracellular H+ for extracellular K+ using H+/K+ ATPase

2. 10.What stops gastric epithelial cells from digesting themselves, and what mechanism
comes into action when there is an increased level of HCl in the stomach?8
11. What happens during the cephalic stage of gastric secretion? 9
12.What happens during the gastric stage of gastric secretion?10
13.What is the name of the sludge produced by the gastric stage?11
14.What factors contribute to an increased rate of stomach emptying? 12
Physiology at a Glance - Small Intestines
15.What happens during the intestinal stage of gastric secretion?13
16.What two things are released when fat is detected in the duodenum?14
17.Other than the alkaline mucus in the small intestine, what two substances
secreted by the liver and pancreas neutralize the contents?15
18.What is the average epithelial cell turnover in the small intestine?16
19.What is the main mechanism for absorbtion of water and ions from the intestinal
lumen? 17
8Epithelial cells are coated in an alkaline mucosa which neutralizes the acid before it causes damage to the
cells, when the acid level gets too high then prostaglandins are released which cause increased mucosal
secretion and HCO3- levels
9 Pre stomach, smell/sight/taste and chewing stimulate the release of Ach and gastrin which stimulates the
release of histamine causing parietal cells to produce more acid
10In the stomach, food chemicals and stretch mechanoreceptors stimulate the release of the same
chemicals as the cephalic phase, plus mucus and pepsinogen. Vagal stimulation also releases gastrin via
gastrin releasing peptide. A lower pH once food has left the stomach finally inhibits gastrin secretion.
11 Chyme - which leaves the stomach and enters the duodenum
12Increased volume in the pyloric antrum (pre-pyloric sphincter), increase in pH of chyme. (whereas
distention of duodenum, presence of fats and decrease in pH of chyme inhibit stomach emptying
13 Food contents of duodenum stimulate gastric secretion by G cells, secretin released in response to acid
stimulation which inhibits gastrin secretion
14 Gastric inhibitory peptide (GIP) and cholecystokinin (CCK) which both inhibit gastrin and acid release and
stimulate the release of pepsinogen from chief cells
15 Bile secreted by the liver and bicarbonate secreted by the pancreas
16 6 days, due to the harsh environment
17 Na+/K+ ATPase generate an osmotic gradient where cellular Na+ is low, therefore Na+ moves from lumen
into cell. It also means K+ levels are high in the cell.

3. 20.How does K+ move out of the cells in the intestinal wall?18
21.Which two proteases break down polysaccharides in the small intestine?19
22.What are the products of this reaction broken down into and by what enzymes?
20
23.How is Ca2+ absorbed from the lumen?21
24.How is Fe2+ absorbed from the lumen? 22
25.Which pancreatic enzyme breaks down fats into monoglycerides and fatty acids?23
26.What are responsible for emulsifying fat droplets in the intestine?24
27.How are fats absorbed into the epithelial membrane? 25
28.Which vitamins follow the fat pathway for absorbtion and which follow the water
pathway?26
Physiology at a Glance: The Liver, Pancreas and Gallbladder
29.What is secreted into the duodenum in addition to bile at the junction with the
common bile duct? 27
30. What stimulates the release of pancreatic juice into the duodenum?28
18 Using a Cl-/K+ coupled mechanism
19 trypsin and chymotrypsin
20 Carboxylpeptidase and aminopeptidase break peptides down into single amino acids
21Single Ca2+ molecules are able to free flow into cellular wall as intracellular Ca2+ conc. is low, these are
then transported out of the epithelial cells by Ca2+ ATPase
22Fe3+ cannot be reabsorbed. Fe2+ makes a soluble compound with ascarbate which can be absorbed via
carrier proteins across epithelium
23 lipase
24 Bile salts, cholic acid and chenodeoxycholic acid
25 They form soluble micelles (hydrophilic outer layer, hydrophobic inner region)
26 B12 follows water pathway, Vitamins A, D, E and K follow the fat pathway
27Pancreatic juice, consisting of enzymes secreted by acinar cells (amylase, lipase, ribonuclease,
deoxyribonuclease)
28 Release of CCK (cholesystokinin) by duodenum in response to presence of fats and protein

4. 31. What function does pancreatic juice have other than enzyme based digestion of
fats, proteins and carbohydrates?29
32. What is the weight of a typical liver?30
33. What is the difference between endocrine and exocrine?31
34. What are the main functions of the liver? 32
35. What is a liver lobule?33
36. What do hepatocytes do? 34
37. What ultimately happens to the bile salts secreted into the duodenum?35
38. Other than storage of bile, what function does the gallbladder have? 36
Physiology at a Glance - Large Intestine
39.Label features A-I on the diagram37
40. Approximately how much chyme enters the colon through
the ileocaecal sphincter 38
41.Which nerves/plexuses innervate sympathetic and
29It contains H20 and HCO3- so is important in neutralizing acidic chyme. The intestines need to have a
neutral environment to foster digestive bacteria needed for breakdown of food into absorbable products.
30 At 1kg in most adults, the liver is the largest organ in the body.
31 Endocrine refers to hormones that are used internally, exocrine refers to the production of something used
in an external environment
32Metabolism and storage of metabolic fuels (e.g. glycogen), Exocrine function: production of bile and
alkaline digestive fluids for storage in gallbladder, detoxification of noxious substances.
33Hexagonal structures of which there are tens of thousands in the liver, each consists of a central vein
surrounded by columnar hepatocytes between which are canaliculi that drain into the bile duct. Portal triads
corner each liver lobule which consist of an artery, vein and bile duct branches).
34 Hepatocytes secrete hepatic bile (bile salts, bile pigments, cholesterol, mucus) Liver produces 500mL-1L
bile per day.
35 5% end up in faeces, 95% are reabsorbed in some form via active transport in distal ileum
36 Concentration of bile by reabsorbtion of Na+, H20, HCO3- and Cl- out of bile.
37A = caecum, B = ascending colon, C = transverse colon, D = descending colon, E = sigmoid colon, F =
Rectum, G = caecal mesentery, H = transverse mesentery, I = sigmoid mesocolon, J = superior mesenteric
artery/plexus, K = inferior mesenteric artery/plexus
38 Approximately 1.5L of chyme per day, after the colon around 150ml of faeces is left of which 50ml is solid

5. parasympathetic nerves in the colon?39
42. What are the main functions of the duodenum?40
43. What leads to ‘mass movement’ in the colon? 41
44. What are the main actions in the ‘defecation reflex’? 42
45. Why is reabsorbtion in the colon driven by Na+/K+ ATPase? 43
46. What are contained in the ‘crypts’ of the colon?44
47. What is the role of ‘tight junctions’ between epithelial cells in the colon?45
48. Why are there so many bacteria in the colon as opposed to the upper GI tract,
where food is more rich in nutrients, and what are the roles of these bacteria?46
Scenario Introduction
1. According to site of origin, pathogenesis and stool type, name eight classifications
of diarrhoea47
2. What are the duration of symptoms for acute, persistent and chronic diarrhoea? 48
39Sympathetic nerves innervated by superior mesenteric plexus, parasympathetic by pelvic nerves
branching from sacral nerves. Some nervous stimulation from vagus nerve.
40Storage of chyme/faeces, reabsorbtion of water and electrolytes. Chyme usually remains in the colon for
around 20 hours, the longest time spent anywhere in the GI tract.
41 Distention of the stomach after the consumption a large meal.
42 1/ Contraction of rectum, 2/ contraction of external sphincter, relaxation of internal sphincter, 3/reflex
relaxation of external sphincter, can be inhibited voluntarily (striated muscle) inducing ʻreverse peristalsisʼ
43Because the chyme is isotonic at the start of the colon so reabsorbtion requires an active mechanism
working against the concentration gradient.
44 Columnar, absorbtion focussed epithelial cells and mucus secreting goblet cells
45Allow diffusion of H20 out of lumen because Na+/K+ ATPase has pumped out sodium and created a
hypertonic environment adjacent to the lumen which draws water out, K+ diffuses out into chyme.
46The hostile acid environment has been neutralised by pancreatic juice and mucus, so enveloped bacteria
can survive. Bacteria in the colon are responsible for breakdown of bilirubin into non-pigmented bilirubin.
Role in vitamin synthesis, breakdown of primary bile salts into secondary bile salts
47Origin: Small intestine or large intestine, Pathogenesis: Infectious, functional (no obvious cause),
inflammatory (allergic response), Stool type: Osmotic (watery), secretory or fatty (steathorrea)
48 Acute = 2 weeks, persistent = 2-4 weeks, chronic = over 4 weeks

6. 3. What symptoms are typical of malabsorbtion? 49
4. What is the commonest cause of malabsorbtion? 50
5. What are the symptoms of chronic pancreatitis?51
The Intestines
1. Define foregut, midgut and hind gut 52
2. What membranous structure is stretched between the liver/gallbladder and
stomach? 53
3. What membranous structure is stretched from just below the stomach across the
intestines? 54
4. What are the right and left spaces superficial to the colon? 55
5. What are the divisions of the intestine? 56
6. Which artery supplies the midgut?57
7. Which artery supplies the hindgut?58
8. What is the suspensory ligament of the duodenum?59
49Steathorrea, diarrhoea, nutritional deficiency (weight loss, anaemia, oedema (albumin deficiency), muscle
weakness (Ca2+ deficiency), sensory loss (B12 deficiency)), general malaise, low bone mass
50 coeliac disease, immunological reaction to gluten in diet
51Relentless abdominal pain, diarrhoea or steatorrhoea, anorexia/weight loss, polyuria, inflammation and
fibrosis lead to slow destruction of the pancreas
52 Foregut: ends after entry of common bile duct into duodenum, Midgut: ends 2/3rds of the way along the
transverse colon, Hindgut: Ends halfway down the anal canal.
53 Lesser omentum
54 Greater omentum
55 Right and left paracolic gutters
56 Small Intestine (6m) (3-6 hours): Duodenum (5%), Jejunum (roughly 40%) and Ileum (roughly 60%). Large
Intestine (20 hours): Caecum, ascending colon, transverse colon, descending colon, sigmoid colon, rectum.
57 Superior mesenteric artery
58 Inferior mesenteric artery
59 Ligament of Treitz

7. 9. What is the most significant difference in the structure of the epithelium between
the small and large intestines?60
10.What are the name of the anatomical folds in the membrane of the duodenum?61
11.Which surface abdominal region does most of the duodenum lie within? 62
12.Which organ does the duodenum encircle on three out of four sides?63
13.What is the name of the opening into the duodenum where pancreatic juice and
bile are secreted from the pancreas and gallbladder?64
14.What is the name of the feature between (13) and the hepatopancreatic ampulla?
65
15.What is the main difference between the epithelium of the ileum and duodenum66
16.In which surface abdominal regions are the jejunum and ileum located? 67
17.Which part of the small intestine contains Peyer’s patches?68
18.What are vasa recta?69
19.What are the three main structural components of the large intestine which are
not found in the small intestine?70
20.What is the difference between appendages and diverticula? 71
60 Small intestine contains villi whereas large intestine does not
61 Plicae circularis
62 The umbilical (central) region
63 Pancreas
64 Major and minor duodenal papillae
65 Sphincter of Oddi
66 The Ileum lacks the plicae circularis of the duodenum
67 Jejunum mostly located in umbilical region, Ileum located in hypogastric/pubic and right inguinal regions
68 Lymph nodules involved in fat absorbtion, found uniquely in ileum
69 Arcades off the mesenteric arteries which run straight to the gut wall
70Haustra (sac like divisions), Epiploic/Omental appendages (fatty tags on surface), Teniae coli (strips of
longitudinal muscle which contract to produce the haustra)
71
Appendages are normal fatty pouches in the serosa whereas diverticula are pathological pouches of the
whole gut wall and may signify the presence of a blockage or cancer.

8. 21.Which organ does the corner of the ascending and transverse colon turn just
below (at the right colic flexure)?72
22.Which part of the large intestine is the appendix attached to?73
23.Which part of the pelvis does the caecum sit within?74
24.What and where (surface location) is McBurney’s point?75
25.Which parts of the the large intestine and small intestine are retroperitoneal and
which are intraperitoneal? 76
26.What are the names for the anastemoses of blood vessels that supply the
ascending and descending colon?77
27.Which parts of the colon are mobile
within the peritoneum and which are not?78
28.Where does the superior mesenteric
artery arise from?79
29.Where does the inferior mesenteric
artery arise from?80
30.Label arteries A-H on the diagram81
72 The right lobe of the liver
73 The caecum
74 The right iliac fossa
75The tip of the appendix, it lies 2/3rds of the way down a line drawn from the umbilicus to the anterior
superior iliac spine. It is the point of maximum pain in appendicitis.
76 Retroperitoneal: Rectum, ascending and descending portions of the colon, duodenum. Intraperitoneal:
transverse colon, sigmoid colon, caecum, jejunum and ileum.
77 Right colonic or hepatic flexure and left colonic or splenic flexure
78Transverse and sigmoid colon are mobile because they have mesenteries and are within the peritoneum
whereas the descending colon is not because it has no mesentery and is retroperitoneal. The transverse
colon has a mesentery however it is retroperitoneal.
79 The abdominal aorta around L1
80 The abdominal aorta around L3
81
A= Ileocaecal artery, B = right colic artery, C=middle colic artery, D=superior mesenteric artery, E= inferior
mesenteric artery, F=left colic artery, G= sigmoid artery, H=superior rectal artery

9. General Histological Organisation and Development of the Gut
1.How does the embryological formation of the
gut begin?82
2.What is the importance of the yolk sac? 83
3.What do the head fold and tail fold become and
what happens to the the divided halves of the
‘midgut/yolk sac’?84
4. What is the vitelline duct?85
5. What embryological feature do the umbilical artery, vein and bladder emerge
from?86
6. The foregut, midgut and hindgut are supplied by which arteries? 87
7. What is the foregut?88
8. What is differential growth?89
9. What is the process of ‘recanalisation’ in relation to formation of the oesophagus?
90
10.What causes the greater curvature of the stomach in terms of development?91
82 During week 3 of development, the flat trilaminar embryonic disc folds under cranially, caudally and
laterally, incorporating part of the yolk sac.
83Nutritional function before the placenta develops, start of blood development, posterior part of the yolk sac
will become the gut.
84 The lateral folds make up the abdominal wall, the space enclosed becomes the peritoneal cavity and the
bit left out of the abdominal wall becomes the umbilical cord.
85Diverticulum which connects the dorsal part of the yolk sac with the remnant of the yolk sac at the front, it
eventually dissapear
86 Allantois
87 Foregut - coeliac artery, Midgut - superior mesenteric artery, Hindgut - Inferior mesenteric artery
88 Mouth all the way down to duodenum, includes liver and pancreas and biliary apparatus
89
Ventral and dorsal mesogastrium are spaces in the embryo which become mesentery when the ventral
mesogastrium is lost (differentially)
90The oesophagus forms as a tube which is initially filled with cells in some areas, recanalisation refers to
apoptosis of these cells to open the tube up and make the oesophagus
91Posterior half of the stomach ʻtubeʼ grows faster than the anterior part (differential growth) and then the
whole structure ʻrotatesʼ to the stomachʼs final position.

10. 11.Which mesogastrium is lost when the liver forms? 92
12.What does the hepatic diverticulum give rise to?93
13.What pathological effect could result from an ‘annular pancreas’? 94
14.What is physiological umbilical herniation?95
15.What is Meckel’s diverticulum? 96
Digestion and Absorbtion of Nutrients
1. How do long chain fatty enter the blood circulation from the GI tract?97
2. Describe the variation in cells in a small intestine villus epithelium?98
3. Which pumps and ion channels in the intestinal lumen epithelium are involved in
sugar absorbtion? 99
4. Which pancreatic enzymes aid duodenal breakdown of proteins? 100
5. Which pumps and transporters take peptides from the lumen to the circulation?
101
92 Posterior mesogastrium disappears and leaves lesser sac as space below the liver
93 Liver and gallbladder and hepatic vessels
94An annular pancreas is development of the pancreas at an abnormal angle which can cause constriction of
the duodenum
95Normal part of development around 6 weeks where liver expands with rapid growth and fills the peritoneal
cavity, pushing the gut down the umbilicus and rotating it as this happens. By week 10 the rest of the embryo
has grown allowing the gut back in and rotating it again, this giver rise to the rotations in the fully formed gut
96A usually asymptomatic deformity. A bulge in the small intestine which is all that remains of the vestigal
duct or yolk sac. Can become inflamed and mimic appendicitis symptoms. Can lead to fistula in umbilicus.
97 First absorbed into lymph by lacteals in the small intestine then enter bloodstream via thoracic duct
98Goblet cells throughout, absorptive cells in upper 2/3, stem cells in ʻcryptʼ region for continual epithelial
renewal
99Basolateral Na/K ATPase create osmotic gradient which makes Na+ diffuse into the cell, bringing with it
glucose and galactose (products of carbohydrate breakdown). Single ion basolateral channels remove these.
100 Carboxypeptidases, trypsin, chymotrypsin
101Similar to glucose absorbtion, a concentration gradient is created by Na+/K+ ATPase which brings amino
acids, Na+ and H+ ions from the limen to the epithelial cells

11. 6. What does the basolateral side of the epithelium do differently depending on
concentration gradient?102
7. What are used to carry vitamins A and E from the intestine to the liver? 103
8. How are vitamins B and C absorbed? 104
Salt and Water Balance 1 & 2
1. What are the average volumes for secretion of: saliva, gastric fluid, bile, pancreatic
juice, intestinal fluid per day?105
2. How much fluid is absorbed by the small intestine per day? 106
3. Where are the Na/K ATPase pumps on the lumen epithelial cells?107
4. What causes absorbtion of water from the intestinal lumen into the submucosa?
108
5. Why does glucose accumulate in epithelial cells without going back into lumen? 109
6. How much of the glucose in the chyme is reabsorbed in the small intestine?110
7. Which molecule in a glucose co-transporter attaches to the pump first and
therefore drives absorbtion of the other? 111
8. What is the normal blood glucose and normal concentration of glucose in the gut
lumen without having recently eaten? 112
102 Can allow for transport of sodium and glucose either in or out of the cell depending on the gradient
103 Transported in chylomicrons (fat droplets) in the lymph, which are used to transport fat around the body
104Similar to sugars and peptides, vitamin C and B are transported in Na+ co-transporters according to
sodium gradient created by Na/K ATPase across the lumen epithelium
105 Saliva - 1.5L/day, gastric - 2L/day, 500ml/day, pancreatic secretion 1.5L/day, intestinal 1.5L/day
106 8L/day
107 Across the basal and lateral sides of the cell (i.e. all 3 sides but not the lumen)
108Na+ is pumped out of the lumen by Na/K ATPase creating osmotic potential in the submucosa around the
epithelial cells into which water diffuses across apical and basal membranes. The pressure builds up and
forces fluid further into the submucosal fluid and ultimately the circulation.
109 Glucose transport is driven by sodium movement in Na+/Glucose co-transporters,
110 100%, none gets into the colon
111
Sodium attaches first and is released last from the transporter, pushing glucose out. It is driven by an
osmotic gradient from the lumen to the submucosa
112 5mmol in the blood and 0.5mmol in the lumen

12. 9. What happens in glucose glalactose malabsorbtion?113
10.What is the difference between GLUT1 and GLUT5? 114
11.Which transport protein in particular is responsible for transporting glucose
across the basolateral membrane into the submucosa?115
12.What is the effect of sweeteners like saccharin and sucrulose on the lumen
epithelium?116
13.Which peptide found in the crypts of the lumen epithelium is responsible for the
up-regulation of GLUT2 and though to cause obesity? 117
14.What may lead to excessive uptake of fructose? 118
15.How is glucose-galactose malabsorbtion diagnosed?119
16.What two things are required for normal intestinal uptake of sugars?120
17.What is coeliac disease? 121
18.Which substance blocks the sodium channels in the colon?122
113SGLT1 transport protein (the Sodium/Glucose co-transporter) fails to transport glucose from the lumen to
the epithelial cell.
114
GLUT1 found in the red blood cells and does not transport fructose, whereas GLUT5 is found in the gut
and can transport many different sugars including fructose
115 GLUT2, glucose uniport
116 Up-regulation of transport proteins such as GLUT2 mean more glucose is absorbed
117 Glucagon-like-peptide 1 (GLP 1)
118
Fructose is absorbed by GLUT2 channels, GLP 1 is responsible for up-regulation of glut 2, so having
more GLP1 = you will absorb more fructose
119 Hydrogen breath test is the most simple way of determining carbohydrate breakdown. If carbs are broken
down in the colon, hydrogen is produced, which does not happen if they are broken down in the small
intestine. Carbs only reach the colon if there is some problem absorbing them in the small intestine. The
levels of H2 in the patientʼs breath are measured after a glucose meal and again after a fructose meal. In the
case of fructose, they will not have hugely raised H2 because fructose can be absorbed by GLUT2, but after
glucose the H2 levels will rise because glucose absorbtion relies on SGLT1.
120 Presence of SGLT1 channel and an Na+ gradient across the apical membrane
121An autoimmune disorder caused by a hypersensitivity to wheat (gluten). The inflammatory reaction
attacks the intestinal submucosa leading to ʻsloughingʼ (shedding dead matter) of the epithelial cells so
therefore the intestine cannot function properly because its villi and crypts have been destroyed.
122 Amiloride (K+ sparing diuretic which blocks sodium uniporter Enac)

13. 19.Other than EnaC, how is Na+ reabsorbed in the colon? 123
20.Given the answer to (19), how does pH compare between the two sides of the
epithelium?124
21.What serves to balance out the pH change caused by (19)?125
22.What is the process of ‘double exchange’?126
23.What are the ratios of liquid:solid of chyme entering the colon and faeces leaving
it? 127
24.How do crypts suck in faeces to dehydrate it?128
25.What does aldosterone stimulate in colonic epithelial cells?129
26.Which molecules act as second messengers to activate the following channels
Cl-, Cl-/HCO3-, Na+/H+, Na+/K+ATPase?130
27.How is chloride transported against its electrochemical gradient into epithelial
cells across the basolateral membrane before it can be secreted?131
28.What causes apical chloride channels to open? 132
123Na+/H+ antiporters, driven by ʻelectroneutral exchangeʼ (swapping one charged substance for another of
the same charge)
124
Because of the Na+ gradient, Na+ moved into the epithelium and H+ is driven out into the lumen,
meaning the lumen is more acidic and the epithelium more alkaline
125 Cl-/HCO3- anti-porters absorb Cl- from the lumen and pump HCO3- into the lumen which acts as a buffer
for the excess H+
126The process which is created by the export of H+ and HCO3- into the lumen, creating carbonic acid,
which dissociates into water in the presence of carbonic anhydrase, leading to more water in the lumenal
fluid. The presence of more water in the lumen heightens the osmotic gradient between the lumen and
epithelium meaning more water gets reabsorbed from the lumen into the epithelium.
127 When chyme enters the colon it is 20:1 liquid:solid, when it leaves as faeces it it 2:1 (roughly 50g-100g of
solid per day)
128Crypts create an osmotic pressure across their walls which draws water into the crypt space and
reabsorbs it. So there is an osmotic gradient coupled with large suction force.
129Aldosterone (higher in a low salt diet, lower in high salt diet) stimulates autocoid (protein messenger)
secretion from myofibroblasts (smooth muscle), which causes epithelial cell proliferation and adhesion.
Aldosterone also increases the rate of sodium absorbtion, as in the kidney.
130 Cl- channels are activated by cAMP, the rest are activated by Ca2+
131Transported into the cells by a co-transporter which takes Na+, Cl- and K+ into the cell, the positive
charge of the Na+ and K+ (which are both going down gradients) carries negative Cl- against its gradient.
132 stimulation by cAMP or Ca2+

14. 29.How is Na+ secreted into the lumen? 133
30.What happens to the CFTR channel in Cystic Fibrosis?134
31.Which channels secrete H+ into the interstitial fluid from epithelial cells in the
pancreas and liver? 135
32.Which channel secretes HCO3- into the lumen from epithelial cells in the
pancreas and liver? 136
33.How are proteins secreted by the pancreas or salivary glands? 137
34.What stimulates enzyme secretion from the pancreas?138
35.Why (chemically) is trypsinogen an inactive enzyme when it is released? 139
36.Why is squatting a more effective posture for defecation than sitting? 140
37.What are the three main categories of laxative?141
38.Which type of laxative would you not use to clear out the colon for an
endoscopy?142
133 Through tight junctions between epithelial cells
134 It is blocked, so whilst CF can lead to respiratory failure it does protect against cholera symptoms
135 Na+/H+ exchangers, and H+/K+ATPase exhangers
136HCO3-/Cl- exchanger, so a failure in CFTR and so reduced lumenal Cl- can cause a failure in alkaline
secretion too
137Vesicles containing protein are formed in the Golgi body (protein packaging organelle) then exocytosis
through plasma membrane.
138 Cholecystokinin (CCK) and vagal nerve activity
139 Trypsinogen is a pancreatic enzyme but is in its inactive form because it has been so densely packed in
to vesicles to cross the membrane. For it to be activated it must be hydrated in the lumen, having left the
vesicles and expanded, then converted by an enzyme into its active form trypsin.
140When sitting, the angle of the anal canal is sharp against the rectum. When squatting, the angle is more
obtuse (straighter) which allows pressure from the abdominal muscles and diaphragm to be directly (linearly)
transmitted through the anus.
141 1/ bulk forming (bran, methyl cellulose) 2/ Stimulant (castor oil), 3/ Osmotic laxatives (lactulose)
142Bulk laxatives, because they fill up the colon with indigestible ʻbulkʼ which aids flow but will not clear the
colon of material

15. 39.What is the mechanism of lactulose in relieving constipation?143
40.How does mineral oil/paraffin work as a laxative?144
41.What are loperamide and diphenoxylate? 145
GI System at a Glance
1. What is the most common way for a diverticulum to form in the colon wall? 146
2. Which 3 structural features of the duodenum contribute to increased surface
area?147
3. Where are the preferred uptake sites for: Iron, folic acid, bile salts & vitamin B12,
water and electrolytes148
4. Where does most of the liquid in the small intestine come from? 149
5. What substance in the digestive system inhibits amylase (starch to sugar enzyme)
and activates pepsinogen (pepsin enzyme, protein digestion)?150
6. What is an enterocyte?151
7. What is intrinsic factor? 152
8. Which vitamin can be synthesised in the intestine by commensal bacteria? 153
143Lactulose is an osmotic laxative, osmotic laxatives work by stimulating the myenteric plexus to increase
peristalsis, reduce absorbtion of salt and water to increase faeces volume, may inhibit the Na+ pump and
increase prostaglandins and cAMP, adding to this effect.
144 Paraffin oil droplets block the crypt lumens and prevent them from sucking fluid out of the faeces
145 Opioid anti-motility agents, used to treat diarrhea
146 Penetrating artery though the muscularis mucosa created space for diverticulum to form outside of
circular layer of smooth muscle, pushes artery out of the way.
147 Villi, microvilli and plicae circulares
148 Iron (duodenum), folic acid (jejunum), bile salts & vitamin B12 (ileum), water and electrolytes (colon)
149Most of the liquid in the intestinal lumen does NOT come from food but is secreted by digestive exocrine
glands. It is subsequently reabsorbed by the colon to maintain fluid balance.
150 Stomach acid, this initiates protein digestion. Only sugar/carb digestion begins in the mouth.
151 An simple columnar epithelial cell found in the small intestine and colon
152A glycoprotein produced by the stomach which binds vitamin B12 and protects it from breakdown in the
proximal intestine. In the terminal ileum, vitamin B is released and absorbed
153 Vitamin K

16. 9. What and where is CFTR in the intestinal lumen? 154
10.How does HCO3- come to be in the intestinal lumen?155
11.What might stimulate secretion of water into the lumen?156
12.What receptors does serotonin act on to increase or decrease secretion? 157
13.What do opioids do? 158
14.What does cholera toxin A do? 159
15.How does heat-stable enterotoxin E-coli cause diarrhoea?160
154CFTR stands for cystic fibrosis transmembrane regulator, this is a Cl- channel present only on the apical
side of the membrane, it is regulated by cAMP. (other chloride channels are regulated by cGMP)
155It is secreted by the pancreas and goblet cells but also through an apical HCO3-/Cl- exchanger and
produced from water and Co2 by the presence of carbonic anhydrase in the lumen.
156Enteric hormones, cytokines, bacterial and viral toxins, prostaglandins, vasoactive peptide (VIP).
(Misoprosol, a prostaglandin, is used therapeutically to counteract ulcerogenic effects of some other drugs
(e.g. NSAIDs).
157 5HT3 (stimulate vomiting, depolarize plasma membrane) or 5HT4 (increase cellular levels of cAMP)
158 Inhibit intestinal secretion and may promote reabsorbtion by reducing intestinal mobility
159Irreversibly activates adenyl cyclase, generating excess cAMP which stimulates mass secretion of Cl-
through CFTRs, followed by K+ and Na+ because of the electrochemical gradient created, followed by H20
because of the osmotic gradient created. Result is watery diarrhoea.
160Stimulates cell surface receptors that have guanyl cyclase activity and produces excess cGMP which
stimulates cl- secretion, the rest of the mechanism is the same as cholera (14)