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DIG > Secretions of the Stomach > Flashcards

Secretions of the Stomach Flashcards

1
Q

List 4 functions of the stomach.

A

1 - Stores food.

2 - Mixes food with secretions.

3 - Regulates the release of food into the duodenum.

4 - Secretes gastric juices.

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2
Q

List the 7 layers of the stomach in order from inside out.

A

1 - Mucosa (containing gastric glands).

2 - Muscularis mucosa.

3 - Submucosa.

4 - Oblique muscle.

5 - Circular muscle.

6 - Longitudinal muscle.

7 - Peritoneum.

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3
Q

List 6 cell types found within gastric glands.

A

1 - Mucous neck cell.

2 - Parietal cell.

3 - Enterochromaffin-like cell.

4 - Chief cell.

5 - D cell.

6 - G cell.

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4
Q

What do mucous neck cells secrete?

A

Mucus and bicarbonate.

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5
Q

What do parietal cells secrete?

A

Acid and intrinsic factor.

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6
Q

What do enterochromaffin-like cells secrete?

A

Histamine.

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7
Q

What do chief cells secrete?

A

Pepsinogen and lipase.

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8
Q

What do D cells secrete?

A

Somatostatin.

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9
Q

What do G cells secrete?

A

Gastrin.

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10
Q

Which cells are predominantly found in the body of the stomach?

A

Parietal and chief cells.

*Although also some ECL and D cells.

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11
Q

Which cells are found in the antrum and pylorus of the stomach?

A

G and D cells (no parietal cells).

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12
Q

How does H+ enter the parietal cell?

A

Via the H-K exchanger.

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13
Q

What is the importance of carbonic anhydrase in parietal cell stimulation?

A
  • Forms HCO3- and H+ form H2CO3.
  • HCO3- exits across the basolateral membrane via the Cl-HCO3 exchanger.
  • Cl- needed to form HCl (in the lumen).
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14
Q

Where does H2CO3 in parietal cells come from?

A

H2O and CO2 diffuse into the cell to form H2CO3.

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15
Q

How does stimulation of the vagus nerve lead to parietal cell stimulation?

A
  • The vagus nerve either stimulates the parietal cell directly (releases ACh onto M3 receptors) or stimulates an ECL cell.
  • The stimulated ECL releases histamine.
  • Histamine binds to H2 receptors on parietal cells to trigger acid secretion.
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16
Q

What binds to CCKb receptors?

A

Gastrin.

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17
Q

Where are CCKb receptors found?

What does activation of CCKb receptors lead to in each of these cells?

A

On parietal cells (stimulates acid secretion) and ECL cells (stimulates histamine release which in turn stimulates acid secretion).

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18
Q

How do secretagogues impact on the H-K pump?

A
  • All secretagogues trigger one of the Gi, Gs or Gq pathways.
  • The Gi and Gs pathways lead to PKA activation.
  • The Gq pathway leads to PKC activation and Ca2+ release.
  • Ca2+, PKA and PKC activate H-K pumps.
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19
Q

What happens to K+ once in the parietal cell?

A

It is recycled back into the lumen through the K+ pumps.

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20
Q

Which pathway is triggered by gastrin binding to CCKb receptors on parietal cells?

A

The Gq pathway.

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21
Q

Which pathway is triggered by ACh binding to M3 receptors on parietal cells?

A

The Gq pathway.

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22
Q

What binds to M3 receptors?

A

ACh.

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23
Q

Which pathway is triggered by histamine binding to H2 receptors on parietal cells?

A

The Gs pathway.

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24
Q

Which pathway is inhibited by somatostatin binding to somatostatin receptors on parietal cells?

How does it inhibit the pathway?

A
  • The Gi pathway.

- Inhibits adenylyl cyclase.

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25
Q

Which pathway is inhibited by prostaglandins binding to prostaglandin receptors on parietal cells?

A

The Gi pathway.

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26
Q

List 3 secretagogues that stimulate the secretion of acid from parietal cells.

A

1 - Gastrin.

2 - ACh.

3 - Histamine.

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27
Q

Summarise the production and secretion of HCl from parietal cells.

A
  • H2O and CO2 diffuse into the cell.
  • H2O + CO2 -> H2CO3
  • By carbonic anhydrase, H2CO3 -> H+ + HCO3-.
  • HCO3- is exchanged for Cl-.
  • H+ is extruded from the parietal cell by the H/K exchanger.
  • Cl- is extruded from the parietal cell by Cl- pumps.
28
Q

Where are somatostatin-producing D cells found?

How are they stimulated in each of these locations?

How do the hormones travel to their target cells?

A
  • In the corpus (paracrine) and in the antrum (endocrine).
  • Corpus: Triggered by neural and hormonal mechanisms.
  • Antrum: Triggered by a low intra-luminal pH.
29
Q

List 2 ways in which somatostatin can inhibit histamine secretion from ECL cells.

A

1 - Somatostatin released by D cells of the corpus can directly inhibit the release of histamine from ECL cells in the corpus.

2 - Somatostatin released by D cells of the antrum can inhibit the release of gastrin from G cells in the antrum

  • Remember gastrin stimulates ECL cells to secrete histamine.
30
Q

What stimulates acetylcholine release by the vagus nerve?

A

Distension of the stomach.

31
Q

What are the target cells for ACh?

A

1 - Parietal cells (increase acid secretion).

2 - ECL cells (increase histamine secretion).

3 - D cells (decrease somatostatin secretion).

32
Q

What is the negative feedback mechanism for acid secretion?

A
  • Increased acid secretion decreases luminal pH.

- A low luminal pH in the antrum stimulates D cells to release somatostatin.

33
Q

What is the positive feedback mechanism for acid secretion?

A

Products of protein digestion stimulate G cells to secrete gastrin.

34
Q

List 7 inhibitors of acid secretion other than somatostatin and prostaglandin.

A

1 - CCK.

2 - VIP.

3 - GIP.

4 - Neurotensin.

5 - Peptide YY.

6 - Secretin.

35
Q

Which cells secrete secretin?

A

Duodenal S cells.

36
Q

What stimulates the secretion of secretin from S cells?

A

The presence of fat and acid in the duodenum.

37
Q

List 2 ways in which secretin inhibits acid secretion.

A

1 - Inhibits antral gastrin release.

2 - Stimulates somatostatin release.

38
Q

Which cells secrete CCK?

A

Duodenal and jejunal I cells.

39
Q

What stimulates the secretion of CCK?

A

The presence of fat in the duodenum or jejunum.

40
Q

How does secretin inhibit acid production?

A

Acts directly on parietal cells to reduce acid secretion.

41
Q

How does omezaprole reduce acid secretion?

A

Inhibits the parietal cell’s proton pump (H/K exchanger).

42
Q

How do cimetidine and ranitidine reduce acid secretion?

A

Act as competitive antagonists for the H2 receptor on parietal cells.

43
Q

What are the phases of gastric acid secretion?

A

1 - Basal.

2 - Cephalic.

3 - Gastric.

4 - Intestinal.

44
Q

Describe the basal phase of gastric acid secretion.

A
  • Follows a circadian rhythm (low in the morning high at night).
  • Secretion is a function of the number of cells.
45
Q

Describe the cephalic phase of gastric acid secretion.

A
  • Smell, sight, taste, thought and swallowing of food initiates the cephalic phase.
  • Accounts for 30% total secretion.
46
Q

Describe the gastric phase of gastric acid secretion.

A
  • Distension of the stomach and digestion of protein stimulates G cells (gastrin) and ECL cells (histamine).
  • Accounts for 50-60% total gastric secretion.
47
Q

Describe the intestinal phase of gastric acid secretion.

A
  • Partially digested peptides in the proximal small intestine stimulates acid secretion by stimulation of duodenal G cells.
48
Q

What are pepsinogens?

A

Proteolytic proenzymes.

49
Q

Which cell secretes pepsinogens?

A

Chief cells.

50
Q

What is the major trigger for pepsinogen secretion?

A

Acetylcholine.

51
Q

At which pH does conversion of pepsinogen to pepsin start to occur?

When is conversion most active?

A

Begins at pH 5.

Most active <3.

52
Q

Which molecule converts pepsinogen to pepsin?

53
Q

At which pH is pepsinogen irreversibly inactivated?

54
Q

Why is pepsinogen secretion interlinked with acid secretion?

A
  • Both are triggered by ACh.

- The peptides resulting from pepsin activity stimulate gastrin secretion from G cells, increasing acid secretion.

55
Q

How is the stomach mucosa protected from the environment?

A

A mucus layer traps local HCO3-, maintaining a pH of ~7.

56
Q

Why are prostaglandins important in protecting the stomach mucosa?

A
  • Prostaglandins help maintain the mucosal diffusion barrier.
  • Prostaglandins also inhibit acid secretion, stimulate HCO3- secretion and stimulate mucus secretion.
57
Q

How do NSAIDs (nonsteroidal anti-inflammatory drugs) work?

A
  • NSAIDs inhibit prostaglandin synthesis by blocking the conversion of arachidonic acid to prostaglandins.
  • Enzymes COX-1 and COX-2 are inhibited by NSAIDs.
58
Q

List 2 common side effects of NSAIDs.

A

1 - Gastric ulceration.

2 - Dyspepsia (indigestion)d

59
Q

What is Helicobacter pylori?

A
  • A gram negative bacterium.
  • Colonises the stomach of 40% of humans.
  • The leading cause of peptic ulceration.
60
Q

How does Helicobacter pylori cause peptic ulceration?

A

By stimulating acid production and causing barrier damage.

61
Q

List 3 conditions that can be caused by Helicobacter pylori.

A

1 - Gastritis.

2 - Gastric + duodenal ulceration.

3 - Gastric cancer.

62
Q

How does Helicobacter pylori inflict damage on the GI tract?

A
  • Produces urease.
  • Urease converts urea into NH4+ and HCO3-.
  • HCO3- neutralises the stomach acid.
63
Q

How would Helicobacter pyrlori affect the antrum?

How would the effects differ in the body of the stomach?

A
  • G cells hypersecrete gastrin.
  • D cells hyposecrete somatostatin.
  • Results in hypergastrinaemia in the antrum.
  • In the corpus, Hp infection would cause hypochlorhydria.
64
Q

Which cells produce intrinsic factor?

A

Parietal cells.

65
Q

What is the function of intrinsic factor?

A

It is necessary for the absorption of vitamin B12 in the terminal ileum.

66
Q

What is pernicious / Addison’s anaemia?

A
  • An autoimmune atrophic gastritis in which auto-antibodies are directed against parietal cells.
  • Since parietal cells produce intrinsic factor, this leads to a reduction in vitamin B12 absorption.
  • Results in megaloblastic anaemia as vitamin B12 is needed for the production of RBC precursors.

DIG (20 decks)

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