Gastric Physiology 1

Question 1

What is the function of a mucous cell?

Answer 1

Secretes mucus

Question 2

What is the function of a parietal cell?

Answer 2

Secretes HCl and intrinsic factor.

Question 3

What is the function of a chief cell?

Answer 3

Secretes pepsinogen

Question 4

What is a G cell? What is its function?

Answer 4

G cells are enteroendocrine cells that secrete gastrin.

Question 5

What is gastric acid?

Answer 5

Hydrochloric acid

Question 6

How much gastric acid is secreted each day?

Answer 6

Approx. 2l

Question 7

How is H2CO3 formed in parietal cells?

Answer 7

CO2 and H2O react together, catalysed by carbonic anhydrase.

Question 8

What happens to H2CO3 in parietal cells?

Answer 8

Spontaneously dissociates into HCO3- and H+

Question 9

How are HCO3- and Cl- related (gastric acid secretion)?

Answer 9

HCO3- is transported into the capillary, while Cl- is transported into the parietal cell in exchange. This happens via an anion exchanger.

Question 10

How is H+ secreted from parietal cells?

Answer 10

H+ is exchanged for K+ via an ATPase pump.

Question 11

How is Cl- secreted from parietal cells?

Answer 11

Via a chloride channel.

Question 12

How does HCl form in the stomach lumen?

Answer 12

H+ and Cl- react to form HCl.

Question 13

What 3 things increase gastric acid production?

Answer 13

• ACh
• gastrin
• histamine

Question 14

How is ACh released during the cephalic phase of digestion?

Answer 14

Released from the vagus nerve when food is seen or chewed.

Question 15

How is ACh released during the gastric phase of digestion?

Answer 15

Stomach distention detected by intrinsic nerves.

Question 16

How does ACh increase acid production?

Answer 16

Directly stimulates parietal cells = increased vesicular fusion.

Question 17

How are G cells stimulated to produce gastrin?

Answer 17

• vagus nerve
• gastrin-related peptide
• peptides in stomach lumen

Question 18

How does gastrin stimulate parietal cells?

Answer 18

G cells secrete gastrin into the blood. Gastrin travels to parietal cells and binds to CCK receptors, leading to elevated calcium levels. This leads to increased vesicular fusion.

Question 19

How do enterochromaffin-like cells increase gastric acid production?

Answer 19

They secrete histamine which binds to H2 receptors on parietal cells. This leads to increased cAMP production, leading to increased vesicular fusion.

Question 20

What causes ECL cells to release histamine?

Answer 20

Stimulation by ACh and gastrin.

Question 21

Apart from stimulating gastrin secretion, how do peptides in the stomach lumen stimulate acid production?

Answer 21

Peptides act as a buffer and mop up H+ ions, so pH rises. This leads to decreased secretion of somatostatin. Somatostatin inhibits parietal cell activity, so decreased secretion results in more parietal cell activity.

Question 22

How is gastric acid production decreased (gastric phase)?

Answer 22

When pH in stomach lumen is low:

• gastrin secretion is directly inhibited
• histamine release inhibited indirectly, via gastrin inhibition
• somatostatin release stimulated, inhibiting parietal cell activity

Question 23

What stimulates gastric acid production decrease (intestinal phase)?

Answer 23

Duodenal distention
Low luminal pH
Hypertonic luminal contents
Presence of amino acids and fatty acids

Question 24

How is gastric acid production decreased (intestinal phase)?

Answer 24

Release of enterogastrones triggered: secretin and CCK (cholecystokinin).

Secretin and CCK inhibit gastrin release and promote somatostatin release.

ACh release reduced by stimulation of neural pathways.

Question 25

What is a peptic ulcer?

Answer 25

A breach in the surface of the gastric mucosa.

Question 26

What causes gastric ulcers?

Answer 26

- Helicobacter pylori infection - NSAIDS - Chemical irritants (alcohol, bile salts, etc) - Gastrinoma (tumour of G cells)

Question 27

How do peptic ulcers arise?

Answer 27

- increased mucosal attack | - reduced mucosal defence

Question 28

How might there be an increased mucosal attack?

Answer 28

Inflammatory response.

Question 29

How might mucosal defences be reduced?

Answer 29

- washing away of mucus | - damaging of cell connections

Question 30

What defences does the gastric mucosa have?

Answer 30

- alkaline mucus - tight junctions between epithelial cells - damaged cells are replaced - feedback loops to control the environmental conditions

Question 31

Which stains can be used to see Helicobacter pylori?

Answer 31

H&E, Giemsa, immunohistochemistry

Question 32

Where does Helicobacter pylori live in the body?

Answer 32

In the gastric mucus.

Question 33

What does Helicobacter pylori secrete?

Answer 33

- urease - proteases - phospholipases (from cell membrane) - vacuolating cytotoxin A

Question 34

How do the secretions of Helicobacter pylori damage the gastric epithelium?

Answer 34

- urease splits urea into ammonia and CO2 - ammonia forms ammonium by joining with H+ - ammonium, proteases, phospholipases and vacuolating cytotoxin A cause direct damage to the gastric epithelium.

Question 35

What happens when the gastric epithelium is damaged?

Answer 35

Inflammatory response (acute or chronic) results in reduced mucosal defence.

Question 36

What are NSAIDs?

Answer 36

Non-steroidal anti-inflammatory drugs = painkillers that reduce inflammation.

Question 37

How do NSAIDs cause peptic ulcers?

Answer 37

- NSAIDs inhibit cyclo-oxygenase 1, which is needed for prostaglandin synthesis - prostaglandins stimulate mucus secretion - therefore reduced synthesis of prostaglandins results in reduced mucosal defence

Question 38

How do bile salts cause peptic ulcers?

Answer 38

Duodeno-gastric reflux causes bile to be regurgitated into the stomach. The bile strips away the mucus layer, resulting in reduced mucosal defence.

Question 39

How are peptic ulcers caused by Helicobacter pylori treated?

Answer 39

Triple therapy: 1 proton pump inhibitor and 2 antibiotics. | Proton pump inhibitor means that the environment becomes too alkaline for the bacteria.

Question 40

How are peptic ulcers caused by NSAIDs treated?

Answer 40

Misoprostol is a prostaglandin analogue (drug with similar structure to a prostaglandin). Therefore it rebuilds mucosal defences. Also use a proton pump inhibitor or H2 receptor antagonist to reduce acid secretion.

Question 41

Give 3 examples of proton pump inhibitors.

Answer 41

- omeprazole - lansoprazole - esomeprazole

Question 42

Give an example of a H2 receptor antagonist.

Answer 42

Ranitidine