Gastric secretion

Question 1

what 3 mechanisms control gastric acid secretion

Answer 1

neurocrine (vagus/local reflexes)
endocrine (gastrin)
paracrine (histamine)

Question 2

what is the cephalic phase of gastric secretion?

Answer 2

occurs before food enters the stomach, especially while it is being eaten.

Results from the sight, smell, thought, or taste of food;

greater appetite = more intense stimulation.

Question 3

what is the gastric phase mediated by?

Answer 3

vagus nerve and the release of Gastrin

Question 4

How would you inhibit the cephalic phase?

Answer 4

stopping eating as this decreases vagal activity

Question 5

How would you inhibit the gastric phase?

Answer 5

Decreasing the release of gastrin. Gastrin release is inhibited by a low pH ie when HCL in the lumen is too high.

Question 6

What is the intestinal phase and how does it inhibit gastric acid secretion?

Answer 6

The duodenum reacts to the arrival of chyme to by moderating gastric acid activity. It initially enhances gastric secretion, but soon inhibits it.

The ways it inhibits gastric acid secretion is:

If it detects acid in duodenum - enterograstric reflex and secretin release kicks in - decreased gastrin secretion and decreased gastrin stimulation of parietal cells (ie less HCL moving into lumen).

If it detects FA’s/CHO in the duodenum - GIP is released which decreases gastrin secretion and decreases parietal HCL secretion

Question 7

What are enterogastrones?

Answer 7

Hormones released from gland cells in duodenal mucosa.

They are released in response to acid, hypertonic solutions, FA’s or monoglycerides in the duodenum and work together to prevent acid build up here.

They inhibit gastric acid secretion or reduce gastric emptying.

Question 8

Give some examples of enterogastrones? (3)

Answer 8

secretin
cholecystokinin (CCK)
GIP

Question 9

Why are enterogastrones produced/ what is their function?

Answer 9

They are produced in response to acid, hypertonic solutions, fatty acids or monoglycerides in duodenum.

They act collectively to prevent further acid build up in duodenum.

Question 10

what are the 2 ways in which enterogastrones prevent further acid build up in the duodenum?

Answer 10

inhibit gastric acid secretion

reduce gastric emptying (inhibit motility/contract pyloric sphincter)

Question 11

What secretes pepsinogen?

Answer 11

chief cells

Question 12

when are pepsins inactivated?

Answer 12

at a neutral pH

Question 13

what is the role of gastric mucus

Answer 13

Produced by surface epithelial cells and mucus neck cells to carry out cytoprotective role

Protects mucosal surface from mechanical injury

Neutral pH (HCO3) => Protects against gastric acid corrosion and pepsin digestion

Question 14

what is required for vitamin B12 absorption

Answer 14

intrinsic factor produced by parietal cells

Question 15

where is the intrinsic factor/ B12 complex absorbed from

Answer 15

the distal ileum (final section of the small intestine)

Question 16

What do parietal cells secrete?

Answer 16

HCl and intrinsic factor

Question 17

Describe the mechanism that creates an acidic environment in the stomach lumen

Answer 17

CO2 moves from the blood into parietal cell and binds with water within the cytoplasm

This creates H2CO3 which is very unstable and dissociates quickly to make 1 H+ ion and HCO3.

HCO3 is pushed out the cell in exchange for a Cl- which then moves into the stomach lumen through a channel.
H+ ion moves into lumen and K+ comes in 1:1

H+, Cl- are now in the lumen and all that is needed is H20 - this moves into the lumen due to the osmotic gradient that is built up

Question 18

What type of hormone is histamine?

Answer 18

paracrine - released into blood and acts locally

Question 19

Increased vagal activity causes the release of Ach which in turn does what?

Answer 19

stimulates parietal cells to secrete HCl

Question 20

What type of hormone is gastrin?

Answer 20

Endocrine

Question 21

distension of your stomach (food arriving) has what affect on vagal activity etc?

Answer 21

it increases vagal activity which releases Ach - stimulates Parietal cells - releases HCl which works to digest the food

Question 22

A decrease in pH has what effect on Gastrin?

Answer 22

this would mean an increase in HCl which would cause a decrease in gastrin

Question 23

What is the enterogastric reflex?

Answer 23

The enterogastric reflex is stimulated in the stomach by a pH of 1.5.

Upon initiation of the reflex, release of gastrin by G-cells in the antrum is shut off. This in turn inhibits gastric motility and the secretion of gastric acid + the stimulation of parietal cells

Question 24

When fat or carbohydrates enter the duodenum, gastric-inhibitory peptide (GIP) is released- what effect does this have?

Answer 24

decrease in gastrin secretion

decrease in parietal HCl secretion

Question 25

What is pepsinogen?

Answer 25

a substance secreted in the stomach and converted into the enzyme pepsin by gastric acid

pepsinogen prevents cellular digestion - it only works in low pH (stomach) it is inactivated at a neutral pH

Question 26

What is a zymogen

Answer 26

an inactive substance which is converted into an enzyme when activated by another enzyme

ie pepsinogen is the zymogen for pepsin

Question 27

Which cells produce gastric mucus?

Answer 27

Surface mucous cells and mucus neck cells

Question 28

How does mucus play a cyoprotective role?

Answer 28

Protects mucosal surface from mechanical injury

As the layer of mucus is of a neutral pH (HCO3 - pH is 7 at cell surface) it protects against gastric acid corrosion and pepsin digestion

Question 29

What is intrinsic factor?

Answer 29

Only essential (non-compensated) function of stomach

Its secretion is stimulated via all pathways known to stimulate gastric acid secretion: histamine, gastrin, and acetylcholine.

produced by parietal cells and needed for vitamin B12 absorption

Intrinsic factor/B12 complex absorbed from ileum

Question 30

If a patient has a defect in intrinsic factor secretion what can occur?

Answer 30

Pernicious Anaemia (failure of erythrocyte maturation)