Secretions of the Stomach Flashcards

1
Q

What are the 4 main functions of the stomach?

A

Stores food
Mixes food with secretions
Regulates release of food into duodenum
Secretes gastric juices

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2
Q

Describe the anatomy of the stomach

A
Oesophagus
Cardia
Fundus
Corpus
Antrum
Pylorus
Duodenum
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3
Q

What are the 6 cell types in the stomach? What do they secrete?

A
Mucous Neck cells - mucous, bicarbonate
Parietal cell - IF and acid
ECL cell - histamine
G cell - gastrin
D cell - somatostatin
Chief cell - pepsinogen and lipase
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4
Q

Describe the difference in terms of cells present between the corpus and antrum of the stomach.

A

Corpus - parietal cells and chief cells (ECL and D cells)

Antrum - D cells, G cells

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5
Q

What is the H-K made up of and what are their separate functions?

A

Requires both for full activity
alpha subunit - catalytic function
beta subunit - apaical membrane targeting

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6
Q

Which enzyme is involved in generation of H+ ions. What is the equation?

A

carbonic anhydrase

H2CO3 –> H2O + CO2

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7
Q

How does the HCO3 leave the parietal cell? What phenomenon does this lead to?

A

exits across the basolateral membrane via the Cl-HCO3 exchanger, Alkaline tide!

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8
Q

What is involved in the direct and indirect stimulation of acid secretion?

A

Direct - ACh, gastrin, histamine

Indirect - ACh, gastrin –> histamine

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9
Q

By what receptor and following pathway do each of the following affect the H-K pump:

  • acetylcholine
  • gastrin
  • histamine
A
  • M3 receptor, Gq protein –> PKC –> Ca2+
  • CCKb receptor, Gq protein –> PKC –> Ca2+
  • H2 receptor, Gs protein –> adenylyl cyclase –> cAMP –> PKA
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10
Q

What kind of hormone is somatostatin?
Which cells is it released from? Where are these? What triggers release from these areas?
What is its affect on parietal cells?

A
  • protein hormone
  • D cells in corpus (neural and hormonal mechanisms)
  • D cells in antrum (low intra-luminal pH)
  • inhibits adenylyl cyclase so antagonising the stimulatory effect of histamine
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11
Q

Describe indirect regulation of histamine by somatostatin in the corpus and antrum

A

Corpus - somatostatin inhibits the release of histamine from ECL cells
Antrum - somatostatin inhibits release of gastrin from G cells

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12
Q

What triggers acid secretion in the corpus?

A

Distention of the stomach causes ACh release by the vagus nerve

  • direct effect on parietal cells
  • direct effect on ECL cells –> histamine
  • stimulation of D cells -/-> inhibits somatostatin release
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13
Q

What triggers acid secretion in the antrum?

A

G and D cells are subject to vagal stimulation

  • G cells, gastrin release
  • D cells, inhibits release of somatostatin
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14
Q

What are the 2 consequences of the antral luminal environment?

A

high luminal H+ stimulates the D cells to release somatostatin (-ve regulatory loop)
Products of protein digestion stimulates the G cells to release gastrin, stimulating acid secretion (+ve loop)

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15
Q
Name 8 things that inhibit acid secretion:
s
C
V
G
n
p
p
s
A
somatostatin
CCK 
VIP
GIP
neurotensin
peptide YY
prostaglandins
secretin
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16
Q

What is the main pharmacological inhibitors of acid secretion?
What is a common drug used?

A

Proton pump inhibitors –> Omeprazole

17
Q

What drugs used to be used to reduce acid secretion?
Why are they less effective?
What were side effects?

A

H2 receptor antagonists
Inferior to PPI as only target one trigger of secretion
Peristalsis and Gastric emptying (may require pyloroplasty)

18
Q

What are the 4 phases of gastric acid secretion?

Describe each

A
  1. Basal - circadian rhythm (high at night)
  2. Cephalic - smell, sight, taste –> vagus nerve, ACh only
  3. Gastric - stomach distention, Ach release, also presence of protein in stomach leads to gastrin release
  4. Intestinal – inhibitory phase, HCl in duodenum leads to secretin, somatostatin and CCK release. Somatostatin inhibits effect of histamine,
19
Q
  1. What are pepsinogens?
  2. What is the major trigger for pepsinogen release?
  3. What is it converted to and what triggers this?
A
  1. Proteolytic proenzymes secreted by chief cells
  2. Acetylcholine
  3. low pH converts pepsin
20
Q

How do prostaglandins protect the gastric mucosa?

A

stimulate HCO3- release to maintain pH of 7
inhibit acid secretion
stimulate mucous secretion

21
Q

Describe the mechanism of action of NSAID’s and their subsequent side effects?

A

COX 1 - platelet aggregation, gastric mucosa, kidney
COX 2 - inflammation
non selective so inhibit both pathways –> gastritis, peptic ulcers, dyspepsia
COX 2 seletive inhibitors removed from the market due to increased risk of heart attack

22
Q

What is H. pylori?
What does it cause?
What is it classed as?

A

Helicobacter pylori - gram-negative microaerophilic bacterium
colonises the stomach of 40% of humans
Causes acid production and barrier damage –>
- gastritis
- gastric and duodenal ulcers
- gastric cancer
Class 1 carcinogen

23
Q

What is the mechanism of action for damage caused by H.pylori?

A

Urease produced by HP converts urea into ammonium ions which is toxic to the mucosa.

24
Q

What effects does H.pylori have in the antrum and corpus?

A

Corpus
- reduced acid secretion and hypochlorhydria –> gastric ulcers
Antrum
- hypergastrinaemia and decreased somatostatin release –> increase acid procuction –> duodenal ulcers

25
Q

What is the treatment for H.pylori?

A

Triple therapy

  • amoxicillin
  • clarithromycin
  • proton pump inhibitor e.g. omeprazole
26
Q

Explain the relationship between intrinsic factor and pernicious anaemia.

A

IF produced by parietal cells
Necessaru for absorption of vitamin B12 in the terminal ileum
Loss of this axis results in pernicious anaemia –> megaloblastic anaemia
Pernicious anaemia is an autoimmune atrophic gastritis, in which auto-antibodies are directed against parietal cells and results in their destruction