Secretions of the Stomach Flashcards

1
Q

Functions of the stomach?

A
  • store food
  • mixes food with secretions
  • regulates release of food into duodenum
  • secretes gastic juices
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2
Q

Moving from the duodenum to the oesophagus, what are the sections of the stomach?

A
  • pylorus
  • antrum
  • corpus (next to cardia which joins to the oesophagus)
  • fundus
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3
Q

What are the cell types of the stomach and what do they secrete?

A
  • mucous neck cell (mucous and bicarbonate)
  • parietal cell (acid and IF)
  • ECL cell (histamine)
  • chief cell (somatostatin)
  • G cell (gastrin)
  • D cell (somastatin)
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4
Q

What are the layers of the stomach?

A
  • peritoneum
  • longitudinal muscle
  • circular muscle
  • oblique muscle
  • submucosa
  • muscularis mucosa
  • mucosa (containing gastric glands)
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5
Q

What types of cell does the antrum consist of?

A
  • G cells

- D cells

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6
Q

What cells does the corpus consist of?

A
  • mainly parietal and chief
  • some ECL and D
  • mainly acid producing cells
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7
Q

What is acid secretion mediated by?

A

-parietal H-K pump

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8
Q

What are the two subunits of the H-K pump and what do they do?

A
  • α for catalytic function

- beta for which is apical membrane targeting and is needed for full activity

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9
Q

How are H+ ions produced in the parietal cells and how do they enter the lumen?

A
  • carbonic anhydrase catalyses (the forward and backward reaction) converting CO2 and H2O into carbonic acid and then into HCO3- (bicarbonate) and H+
  • The H+ is exchanged by the H-K pump for K+ which enters the parietal cell
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10
Q

What happens to the bicarbonate produced?

A

-exits across the basolaterla membrane via the Cl-HCO3 exchanger

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11
Q

What is the alkaline tide?

A

increasing PH in the blood due to bicarbonate entering it

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12
Q

What are the 3 triggers that make the parietal cells produce acid?

A
  • Ach
  • histamine
  • gastrin
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13
Q

What are the direct causes of acid release?

A
  • Ach
  • gastrin
  • histamine
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14
Q

What is the indirect cause of acid release?

A

-Ach and gastrin mediated histamine release by ECL cells

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15
Q

Where does Ach come from?

A

vagus nerve

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16
Q

Why does gastrin bind to?

A

CCK(small B) receptor

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17
Q

What does histamine bind to?

A

H2 histamine receptor

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18
Q

Where does histamine come from?

A

ECL cells

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19
Q

Where is gastrin produced?

A

G cells

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20
Q

What stimulates the ECL cells to produce histamine?

A

Gastrin and Ach

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21
Q

What trigger has the biggest contribution to acid production and why?

A

histamine because gastrin and Ach can act on the ECL cells to produce more histamine

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22
Q

How do the secretagogues impact on the H-K pump?

A
  • histamine does to through a cAMP and PKA pathway

- gastrin and Ach do it through a PKC pathway

23
Q

What does somatostatin inhibit?

A

acid production by antagonising histamine mediated acid production

24
Q

In what ways can soma statin be produced?

A
  • D cells in the corpus triggered by neural and hormonal mechanisms
  • D cells on the antrum of the stomach triggered by low intra-luminal PH
25
Q

How is histamine indirectly regulated by somastatin?

A
  • somatostatin released by D cells of corpus can inhibit release of histamine from ECL cells
  • somatostatin released by D cells can inhibit the release of gastrin from G cells in the antrum
26
Q

What happens in the corpus during distension of the stomach?

A

-Ach please by vagus nerve
Ach acts:
-direct stimulation of parietal cell to induce acid release
-direct stimulation of ECL cells enhancing histamine release
-stimulation of D cells in corpus culminates in inhibition of somatostatin release
-all trigger acid secretion

27
Q

What happens in the antrum when G and D cells are stimulated by the vagus nerve?

A
  • vagal stimukation of G cells promotes gastrin release which causes direct and indirect release of acid
  • vagal stimulation of D cells inhibits the release of somatostatin
28
Q

What happens when there is a high luminal H+ conc in the antrum?

A

-stimulates D cells to release somatostatin

29
Q

What do products of protein digestion stimulate?

A

G cells to release gastrin stimulating acid secretion

30
Q

What are the inhibitors of acid secretion?

A
  • somatostain
  • CCK
  • VIP
  • GIP
  • neurotensin
  • peptide YY
  • prostaglandins
  • secretin
31
Q

How does secretin work?

A
  • released by duodenal S cells and is stimulated by fat and acid in the duodenum
  • inhibits acid secretion by: inhibiting astral gastrin release and by causing release of somatostatin
32
Q

How does CCK work?

A
  • produced by I cells of duodenum and jejunum in response to fat
  • directly reduced parietal cell acid secretion
33
Q

What are the pharmacological inhibitors of acid secretion?

A
  • proton pump inhibitors

- H2 receptor antagonists (competitive antagonists of histamine at the parietal cell H2 receptor)

34
Q

What are the 4 phases of gastric acid secretion?

A
  • basal
  • cephalic
  • gastric
  • intestinal
35
Q

What is the basal phase?

A
  • follows a circadian rhythm (low acid in am, high acid pm)

- acid secretion is a direction function of the number of parietal cells

36
Q

What is the cephalic phase?

A

-smell, sight, taste, thought and swallowing initiate it which is mediated by vagus nerve (triggering acid secretion)

37
Q

Which phase causes the most acid release

A

-gastric (50-60%)

then cephalic

38
Q

What is the gastric phase?

A

acid release when the food is in the stomach

39
Q

What is the intestinal phase?

A

partially digested peptides in the proximal portion of small intestine stimulates acid secretion mainly by stimulation of G cells to secrete gastrin

40
Q

What are pepsinogens?

A

proteolytic proenzymes secreted by chief cells

41
Q

What is the main trigger for pepsinogen secretion?

A

Ach

42
Q

When is pepsinogen active?

A

spontaneously active at PH5

Most active at below a PH of 3

43
Q

What is pepsin?

A

an endopeptidase that initiates protein digestion (auto-activates pepsinogen)

44
Q

How does the stomach protect itself?

A
  • mucous layer which traps HCO3- to maintain a PH of around 7
  • prostaglandins maintain the mucosal diffusion barrier (inhibit acid secretion and stimulating HCO3- and mucus secretion)
45
Q

What are prostaglandins made from?

A

arachidonic acid

46
Q

What type of enzyme is COX1 and what does it produce?

A

-constitutive enzyme (always present) creates prostaglandins which are involved in platelet aggregation, gastric mucosa and kidney

47
Q

What type of enzyme is COX2 and what does it produce?

A
  • inducible enzyme

- produces prostaglandins that induce inflammation

48
Q

What is helicobacter pylori and what do they do?

A

-gram-neg bacterium
-cause acid production and barrier damage
(peptic ulceration)

49
Q

What diseases can helicobacter pylori cause?

A
  • gastritis
  • gastric and duodenal ulcers
  • gastric cancer
50
Q

How does helicobacter pylori survive in the stomach?

A
  • produces urease
  • urease converts urea into ammonia, CO2 and H2O and then into ammonium and bicarbonate
  • bicarbonate neutralises stomach acid
51
Q

What does Hp infection in the antrum cause?

A
  • G cells to hyper secrete gastrin
  • decrease D cell somatostatin release
  • leading to hypergastrinaemia and duodenal ulcers
52
Q

What does Hp infection in the corpus lead to?

A
  • reduced acid secretion
  • hypochlorhydria (loss of stomach acid secretion)
  • association with gastric ulcers
53
Q

Why is intrinsic factor important and where is it made?

A

important in absorption of vit B12
important in red blood cells
-parietal cells

54
Q

How is megaloblastic anaemia caused?

A
  • red cells are mature but larger than normal
  • parietal cells are destroyed in pernicious anaemia so no intrinsic factor us produced
  • B12 not absorbed