Gastrointestinal Secretions Flashcards

1
Q

How much water leaves the gut in 24 hours?

A

~150ml

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2
Q

Where is water absorbed in the gut?

A

Small intestine

Large intestine

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3
Q

What is the cephalic phase of digestion? (3)

A

Thinking about food/presence of food in mouth promotes salivary and gastric secretions

Chewing breaks food down into smaller particles

Amylase in saliva initiates starch digestion

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4
Q

What controls the cephalic phase of digestion?

A

CNS

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5
Q

What is the gastric phase of digestion? (3)

A

Stomach secretes in response to presence of food in stomach

Gastric motility for further mechanical breakdown

Protein digestion starts

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6
Q

What controls the gastric phase of digestion?

A

CNS

ENS

Hormones

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7
Q

What is the intestinal phase of digestion? (3)

A

Food entering small intestine gradually causes release of hormones that inhibit gastric secretion and motility

Hormones provoke release of biliary and pancreatic secretions into duodenum

Digestion and absorption

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8
Q

What controls the intestinal phase of digestion?

A

Mostly ENS (some CNS)

Hormones

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9
Q

Which cells in salivary glands produce saliva?

A

Acinar cells

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10
Q

Describe the process by which the primary salivary secretion is produced. (6)

A

BL Na/K-ATPase moves Na out of cell

BL NKCC2 allows 2Cl to enter cell; Cl also enters in exchange for HCO3

BL K channel

Cl leaves cell via luminal channels

Negative charge in lumen attracts Na paracellularly

Water follows by osmosis and aquaporins

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11
Q

What is the tonicity of the primary salivary secretion in relation to plasma?

A

Isotonic

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12
Q

When is the primary salivary secretion modified?

A

As it passes along the duct

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13
Q

How is the primary salivary secretion modified?

A

Some Na and Cl reabsorbed (tight junctions prevent paracellular movement back) which also results in water reabsorption

K and HCO3 added

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14
Q

Describe the secretion produced after the primary salivary secretion has been modified.

A

HCO3 rich, hypotonic secretion

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15
Q

How does high flow rate affect the tonicity of saliva (compared to plasma) and why?

A

Modification is less effective

Less hypotonic

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16
Q

What are the other components of saliva (other than Na, Cl, water, K, HCO3)?

A

Calcium and phosphate

Large molecule components (mucins, lysozyme, amylase)

IgA

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17
Q

How are large molecule components transported into saliva?

A

Produced by acinar cells and released by exocytosis

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18
Q

What cells produce the IgA in saliva?

A

Nearby plasma cells of salivary gland

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19
Q

What are the functions of saliva? (4)

A

Lubrication

Amylase initiates starch digestion

Antimicrobial activities

pH and ions protect teeth from demineralisation

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20
Q

What is the relative amount of amylase and mucus in saliva produced by the parotid gland?

A

Amylase > mucus

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21
Q

What is the relative amount of amylase and mucus in saliva produced by the submandibular gland?

A

Amylase < mucus

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22
Q

What is the relative amount of amylase and mucus in saliva produced by the sublingual gland?

A

Mucus and no amylase

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23
Q

Which salivary gland has the highest flow rate during basal conditions?

A

Submandibular

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24
Q

Which salivary gland has the highest flow rate during stimulation (eg. by eating)?

A

Parotid

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25
How does ANS control generally affect saliva?
Parasympathetic - increase formation of fluid and electrolyte components Sympathetic - increase release of large molecule components
26
Describe the glands in the oesophagus.
Widespread minor glands which only produce mucus
27
What do gastric chief/peptic cells produce?
Pepsinogen
28
What do gastric parietal cells produce?
HCl and intrinsic factor
29
What is another name for a gastric parietal cell?
Oxyntic cell
30
What do the gastric enterocytes produce?
Mucus
31
What are the main gastric secretions? (6)
Pepsinogen HCl Intrinsic factor Mucus Gastric lipase Water
32
What does intrinsic factor bind?
Vitamin B12/cobalamin
33
Describe the mechanism of gastric acid secretion. (4)
Main drive is H/K-ATPase Carbonic acid dissociates into HCO3 (into blood exchanged for Cl) and H+ (into lumen via ATPase) K and Cl balance maintained by luminal channels Water follows net ion movement into lumen
34
How much more acidic is the stomach lumen than the blood?
3 times
35
How does gastric acid secretion increase in response to stimulation?
Resting = proton pumps confined to intracellular tubulovesicles Stimulated = tubulovesicles rearrange and fuse with canaliculi (continuous with luminal membrane)
36
Describe how stomach distension/presence of food in mouth affects gastric acid secretion.
Triggers CNS/ENS = ACh released which acts on: - M3 receptors on parietal cells - Activates enterochromaffin-like cells = histamine = H2 receptors on parietal cells Protein and amino acids in stomach cause gastrin release from G cells which travel via blood to bind CCKB receptors on parietal cells Increased gastric acid secretion
37
What is the effect of ACh on D cells?
Binds muscarinic receptor to release somatostatin
38
What negative feedback system prevents oversecretion of stomach acid in response to ACh?
ACh binds muscarinic receptors on D cells to release somatostatin SST: - Inhibits ECL cells - Inhibit G cells - Directly inhibit parietal cells
39
Which endocrine factors affect the stomach and where are they released from? (5)
Gastrin from pyloric antrum Cholecystokinin from duodenal wall Secretin from duodenal wall GIP from small intestine GLP-1 from ileum/colon
40
What is another name for cholecystokinin?
Pancreozymin
41
How does gastrin affect the stomach?
Induces gastric secretions Increases motility
42
What affects the release of gastrin (non-hormonal)?
Stimulated by proteins, coffee, alcohol... Inibited by low gastric pH
43
How does cholecystokinin affect the stomach?
Depresses gastric motility and secretion
44
What stimulates the release of cholecystokinin from the duodenal wall?
Fats
45
How does secretin affect the stomach?
Inhibits gastric secretion
46
What stimulates the release of secretin from the duodenal wall?
Acid
47
How do GIP and GLP-1 affect the stomach?
Inhibit gastric motility and secretion
48
What stimulates the release of GIP and GLP-1?
Fat and chyme in lumen
49
What is secreted to achieve efficient absorption in the small intestine? (4)
Mucus (goblet cells) Isotonic saline (crypt cells) Alkaline mucus (Brunner's glands) Digestive enzymes and HCO3 rich fluid (surface enterocytes)
50
Where are the digestive enzymes produced by small intestine enterocytes found?
Embedded in the glycocalyx of their brush border
51
The relaxation of which sphincter allows secretions to enter the duodenum?
Sphincter of Oddi
52
What are the two main components of pancreatic exocrine secretions and what produces them?
Alkaline, HCO3-rich fluid by pancreatic duct cells Digestive enzymes by acinar cells
53
Why are pancreatic secretions alkaline?
To neutralise acidic chyme entering from stomach
54
How are the digestive enzymes of pancreatic secretions stored before exocytosis?
Intracellularly as inactive precursor forms in zymogen granules
55
What hormones affect pancreatic exocrine secretion and where are they released from?
Cholecystokinin Secretin Both from duodenal wall
56
How does cholecystokinin affect the pancreas?
Induces release of enzyme-rich secretions
57
How does secretin affect the pancreas?
Induces release of HCO3-rich secretions
58
Describe the mechanism of alkaline fluid secretion by pancreatic duct cells. (6)
Driven by BL Na/K-ATPase BL Na and HCO3 move into cell in exchange for H CO2 from blood => carbonic acid in cells (carbonic anhydrase) => HCO3 + H HCO3 into lumen via anion exchanger (Cl into cell) Cl leaks into lumen Negative charge in lumen attracts Na paracellularly and water by osmosis
59
What disorder can affect the alkaline fluid secretion of pancreatic duct cells and why?
Cystic fibrosis Defect in Cl channels (CTFR-type)
60
What does the primary biliary secretion consist of? (4)
Solutes extracted from blood by hepatocytes Bile salt/acids Bile pigments Cholesterol and lecithin
61
When is the primary biliary secretion modified?
As it passes along bile duct
62
How is the primary biliary secretion modified?
Water and HCO3 added (similar to pancreatic alkaline secretion)
63
What stimulates the modification of the primary biliary secretion?
Secretin
64
What causes the gall bladder to contract and the sphincter of Oddi to relax?
Cholecystokinin
65
What does GIP do?
Stimulates insulin release (feed-forward)
66
What does GLP-1 do?
Stimulates insulin release (feed-forward) Inhibits glucagon release Promotes satiety
67
Which hormones promote satiety?
Cholecystokinin GLP-1
68
What is ghrelin and what inhibits its release?
Hunger hormone (promotes appetite) Food digestion
69
What ions are secreted in the colon?
K+ HCO3-
70
Describe the secretory/reabsorptive process in the colon. (4)
Na/K-ATPase drives process Luminal Na channel allows Na to enter cell; Na enters in exchange for H More Na is absorbed than Cl = negative charge in lumen driving K paracellularly into lumen Water follows sodium paracellularly and via aquaporins for reabsorption
71
What can inadequate production of saliva lead to? (4)
Dry mouth Difficulty swallowing Enamel damage Reduced microbiological protection
72
What can gastric atrophy lead to?
Lack of intrinsic factor Pernicious anaemia
73
What can gastritis lead to?
Gastric (and duodenal) ulcers
74
What can excess gastric acid production lead to? (3)
Duodenal ulcers Malabsorption Diarrhoea
75
What can pancreatitis lead to?
Inadequate enzyme production so malabsorption
76
How does cystic fibrosis affect digestion?
Decreased Cl conductance so decreased formation of pancreatic alkaline fluid Decreased delivery of enzymes to duodenum so less digestion
77
What can insufficient biliary secretions lead to?
(Fat) malabsorption