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DIG > SECRETIONS OF THE STOMACH > Flashcards

SECRETIONS OF THE STOMACH Flashcards

1
Q

What are the 4 functions of the stomach?

A
  • Stores food
  • Mixes food with secretions
  • Regulates release of food into the duodenum
  • Secretes gastric juices
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2
Q

What cell types does the antrum, pylorus and duodenum contain?

A
  • G cells
  • D cells
  • No parietal cells
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3
Q

What cell types does the fungus and corpus contain?

A
  • Parietal cells
  • Chief cells
  • ECL and D cells
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4
Q

What mechanism does the parietal cells use to make acid and where is it found?

A
  • ATP driven H-K pump
  • Found in an apical membrane
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5
Q

What is the alkaline tide, explain how it works.

A

Every time a proton is made, the equivalent amount of bicarbonate is made

  • The H-K pump pumps a H+ into the lumen of the stomach
  • The H+ combines with a Cl- ion to form HCl
  • K+ recycled back to the lumen via K+ channels
  • The original H+ is generated from carbonic acid (H2CO3)
  • The remaining HCO3- is transported across the basolateral membrane via the HCO3-/ Cl- exchanger
  • HCO3- ends up in the blood
  • This means every time the stomach pumps a proton into the lumen of the stomach a bicarbonate ion ends up in the blood
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6
Q

What 2 things does the H-K pump require for full activity?

A
  • An alpha subunit for catalytic function
  • A beta subunit which is apical membrane targeting
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7
Q

Where are protons from the H-K pump, pumped into?

A

The lumen of the stomach

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8
Q

How does the pH of the blood change after a meal?

A

pH temporarily increases and becomes more alkaline because parietal cells are stimulated which results in HCO3- being transported into the blood

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9
Q

Write out the equilibrium that exists in relation to carbonic acid

A

H+ + HCO3- <—> H2CO3 <—-> CO2 + H2O

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10
Q

What are the 3 direct triggers of acid release?

A
  • ACh
  • Gastrin
  • Histamine
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11
Q

What stimulates ACh release?

A

Stimulation of the vagus nerve

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12
Q

What drives acid production in the cephalic phase?

A

ACh

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13
Q

Which cells produce histamine and what stimulates them to produce histamine?

A
  • ECL cells produce histamine
  • ACh stimulates ECL cells to produce histamine
  • Gastrin also stimulates ECL cells to produce histamine
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14
Q

What stimulates parietal cells to produce acid?

A

Histamine

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15
Q

What stimulates G cells to produce gastrin?

A
  • GRPs - gastrin releasing peptides
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16
Q

What two things does gastrin stimulate?

A
  • Gastrin stimulates ECL cells to produce histamine
  • Gastrin stimulates parietal cells to produce acid
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17
Q

What inhibits acid release and when is it produced?

A
  • Somatostatin produced by D cells inhibits acid release
  • Somatostatin is produced when the pH of the stomach is too low
  • Somatostatin also inhibits G cells which inhibits gastrin release and therefore parietal cell stimulation
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18
Q

What mechanism does somatostatin use to inhibit acid release?

A

Somatostatin antagonises histamine mediated acid production

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19
Q

Which pathways mediate production of ACh, gastrin and histamine?

A
  • ACh - (PLC/PKC)/ Ca2+ mediated intracellular signalling cascade
  • Histamine - PKA pathway mediated by adenylyl cyclase
  • Gastrin - (PLC/PKC)/ Ca2+ mediated intracellular signalling cascade
20
Q

Which receptors do ACh, histamine and gastrin bind to?

A
  • ACh - M3 receptors which stimulate parietal cells to produce acid
  • Histamine - H2 receptors on parietal cells which triggers acid production
  • Gastrin - binds to gastrin receptors on parietal cells which stimulates acid production
21
Q

What effect does ACh have on D cells?

A

Inhibits somatostatin from inhibiting acid release

22
Q

Describe the negative loop and the positive loop in the antrum of the stomach

A
  • Negative loop - High luminal H+ stimulates D cells to produce somatostatin which inhibits acid release
  • Positive loop - Products of protein digestion stimulates the G cell to produce gastrin, stimulating acid secretion
23
Q

Give 2 examples of other things that inhibit acid production and how

A
  • Secretin - released from duodenal S cells inhibits acid production by inhibiting gastrin release
  • CCK - produced by duodenal I cells. Is part of the same family as gastrin and acts as a competitive antagonist. Directly reduces acid secretion from parietal cells
24
Q

Give 2 pharmacological inhibitors of acid secretion

A
  • Proton pump inhibitors - acts directly on the H-K pumps
  • H2 receptor antagonists - competitive antagonists to histamine which binds to H2 receptors
25
Q

What are the 4 phases of gastrin acid secretion?

A
  • Basal
  • Cephalic
  • Gastrin
  • Intestinal
26
Q

What is the basal phase of gastrin acid secretion?

A
  • Follows a circadian rhythm where acid secretion is low a.m and high p.m
27
Q

What is the cephalic phase and what triggers it?

A
  • This phase is triggered by sights, smell, taste and thought of swallowing of food
  • It is mediated by the vagus nerve which triggers acid secretion
  • It accounts for 30% of acid production
  • This occurs before food is even swallowed
28
Q

How much of gastric secretion is the gastric phase responsible for?

A

50-60% of gastrin secretion

29
Q

What happens in the intestinal phase?

A
  • Partially digested peptides/ AA in the proximal section of the small intestine stimulates acid secretion via G cells which secrete gastrin
  • This accounts for 5% to 10% of total gastrin secretion
30
Q

What are pepsinogens, what are they secreted by and what are the active and inactive forms ?

A
  • Pepsinogens are proteolytic proenzymes
  • They are secreted by chief cells
  • The active form is pepsin (an endopeptidase)
  • The inactive form is pepsinogen
31
Q

What triggers pepsinogen secretion?

A

Acetylecholine

32
Q

What is an endopeptidase?

A

A protease that cleaves proteins in the middle of the molecule. Mostly end up with oligopeptides

33
Q

At what pH are pepsinogens irreversibly inactivated?

A

7.2

34
Q

Where does the mucous barrier sit and how does it protect the stomach?

A
  • Sits on mucosal surface
  • In the mucus there is bicarbonate trapped in there meaning if any acid gets into the mucus layer it can be neutralised
35
Q

What are prostaglandins made from and what two things are they involved in?

A
  • Made from precursors known as arachidonic acid
  • Involved in inflammation as well as maintaining normal physiology
36
Q

Which enzymes produce prostaglandins that are involved in inflammation?

A
  • COX - 2
  • These enzymes are induceable meaning they aren’t produced all of the time
37
Q

Which enzymes produce prostaglandins that are involved in normal physiology?

A
  • COX -1
38
Q

What blocks COX-1 and COX-2 enzymes?

A
  • NSAIDS e.g ibuprofen or aspirin
  • They can inhibit prostaglandins that are involved in gastric mucosal protection
39
Q

What 3 things can H pylori bacteria cause?

A
  • Gastritis
  • Gastric and duodenal ulcers
  • Gastric cancer
40
Q

Give 2 adaptations of H pylori

A
  • Flagella –> Mobility
  • ## Has urease which converts urea to ammonia
41
Q

What 2 things can H pylori infection in the antrum cause?

A
  • Hyper secretion of gastrin from G cells
  • Decreased somatostatin release
  • This leads to hypergastrinemia
42
Q

How is hypochlorhydia caused?

A

H. Pylori infection of the corpus leads to reduced acid secretion and this is linked with gastric ulcers

43
Q

Location of hypochlorhydia and hypergastrinaemia?

A
  • Hypochlorhydia - Antrum
  • Hypergastrinaemia - Corpus
44
Q

Where is IF produced and what does it do?

A
  • Absorption of B12 in the terminal ileum
  • Loss of this leads to Addisons anaemia
45
Q

What is Addisons anaemia?

A

Autoimmune atrophic gastritis where antibodies attack parietal cells

DIG (6 decks)

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