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GI Lectures > Gastric Physiology 1: Parietal cells and peptic ulcers > Flashcards

Gastric Physiology 1: Parietal cells and peptic ulcers Flashcards

1
Q

What are the functions of the stomach?

A
  • Store and mix food
  • Dissolve and continue digestion
  • Regulate emptying into duodenum
  • Kill microbes
  • Secrete proteases
  • Secrete intrinsic factor
  • Activate proteases
  • Lubrication
  • Mucosal protection
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2
Q

What does intrinsic factor do?

A

Helps absorb Vitamin B12

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3
Q

What does mucosal protection do?

A

Stops stomach digesting itself

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4
Q

What are four key cell types in the stomach lining?

A
  • Mucous cells
  • Parietal cells
  • Chief cells
  • Enteroendocrine cells
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5
Q

What do Parietal cells secrete?

A
  • Secrete HCl
  • Secrete intrinsic factor
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6
Q

What do chief cells secrete?

A

Secrete proteases

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7
Q

What do enteroendocrine cells secrete?

A

Hormones, they are a type of epithelial cells

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8
Q

What acid is gastric acid secretion?

A

Hydrochloric acid
(secrete approx 2 litres/day)

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9
Q

What ion is pumped out in gastric acid secretion?

A

H+ is pumped out at a very high concentration against a concentration gradients so it is very energy dependent

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10
Q

What is HCl secretion regulated by?

A
  • Neural (via vagus nerve)
  • Hormones
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11
Q

What ions are pumped out of the parietal cell and into the stomach lumen?

A

K+, Cl-, H+

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12
Q

What ions are pumped from the stomach lumen into the parietal cell?

A

K+

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13
Q

Which ions don’t require any energy to be pumped (e.g. passive diffusion)?

A
  • K+ going into parietal cell
  • Cl- being pumped out of cell
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14
Q

Where are the H+ ions that are being pumped out of cell coming from?

A
  • From cellular respiration
  • From the formation of H2CO3 from CO2 and H20
  • H2CO3 then broken down into HCO3 and H+ ions
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15
Q

What ions are pumped into parietal cell from capillary and vice versa?

A
  • HCO3- pumped out of cell and into capillary
  • Cl- pumped into parietal cell from capillary
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16
Q

What is the cephalic phase of gastric acid secretion?

A

It is turning it on phase and part of regulation

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17
Q

What activates the cephalic phase?

A
  • Parasympathetic nervous system
  • Sight, smell, taste of food and chewing
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18
Q

What does the release of acetylcholine do during the cephalic phase?

A
  • It is a neurotransmitter (through the vagus nerve to the stomach)
  • Acts directly on parietal cells
  • Triggers the release of gastrin and histamine (which turns parietal cells on)
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19
Q

What does the release of acetylcholine do during the cephalic phase?

A
  • It is a neurotransmitter (through the vagus nerve to the stomach)
  • Acts directly on parietal cells
  • Triggers the release of gastrin and histamine (which turns parietal cells on
20
Q

What is the net effect from the release of acetylcholine in the cephalic phase?

A

Increased acid production (HCl)

21
Q

What stimulates the turning on during the gastric phase?

A
  • Gastric distension (stretching)
  • Presence of peptides and amino acids
22
Q

What is released during the gastric phase?

A

Gastrin (hormone)

23
Q

What does the release of gastrin do in the gastric phase?

A
  • Acts directly on parietal cells
  • Triggers the release of histamine (which acts directly on parietal cells)
  • The net effect is an increase in acid production
24
Q

What does histamine do?

A
  • Acts directly on parietal cells
  • Mediates the effects of gastrin and acetylcholine
25
Q

What does having protein in the stomach do?

A

Direct stimulus for gastrin release

26
Q

What do proteins in the lumen do?

A
  • Acts as a buffer, mopping up H+ ions, causing pH to rise (which further increases HCl production)
  • Decreases the secretion of somatostatin (turns parietal cells off) so a decrease in this means more parietal cell activity
27
Q

What stimulates the turning off of gastric secretion in the gastric phase?

A
  • Low luminal pH (high H+ ions)
28
Q

What happens in order to turn off gastric acid secretion in the gastric phase?

A

Having a low luminal pH…
- Directly inhibits gastrin secretion
- Indirectly inhibits histamine release (via gastrin)
- Stimulates somatostatin release which inhibits parietal cell activity

29
Q

What are the stimuli in the duodenum that turns off gastric acid secretion?

A
  • Duodenal distension (stretching)
  • Low luminal pH
  • Hypertonic luminal contents (large number of ions)
  • Presence of amino acids and fatty acids
    Duodenum senses these and sends message to stomach to turn off via hormone (enterogastrones)
30
Q

What does the release of enterogastrones do?

A
  • Secretin released (inhibits gastrin release, promotes somatostatin release)
  • Cholecystokinin (CCK)
  • Short and long neural pathways, reducing the Acetylcholine release (because the duodenum is innervated by vagus nerve)
31
Q

Conclusion: What affects the gastric acid secretion?

A
  • 1 parasympathetic neurotransmitter (ACh +)
  • 1 hormone (gastrin +)
  • 2 paracrine factors (histamine +, somatostatin -)
  • 2 Key enterogastrones (secretin -, CCK-)
    + turns stomach on
  • turns stomach off
32
Q

What is autocrine factor?

A

Acts on own cell surface

33
Q

What is a paracrine factor?

A

Cells talk to neighbouring cells

34
Q

What does a hormone do?

A

Acts of other cells at a distant sites

35
Q

What is the definition of an ulcer?

A

It is a breach in a mucosal surface
So a peptic ulcer is one caused by gastric enzymes

36
Q

What bacteria causes peptic ulcers?

A

Helicobacter Pylori infection

37
Q

What else can cause peptic ulcers?

A
  • Drugs (NSAIDS e.g. aspirin, ibuprofen)
  • Chemical irritants (alcohol, bile salts)
  • Gastrinoma (tumours of enteroendocrine cells that produce gastrin)
38
Q

What can cause an ulcer in terms of mucosal attack/defence?

A
  • Normal defences sufficient to resist attack means no ulcer
  • Increased mucosal attack creates an ulcer
  • Reduced mucosal defence creates an ulcer
39
Q

How does the gastric mucosa defend itself?

A
  • Alkaline mucus (So can resist acid attack)
  • Tight junctions between epithelial cells (prevents liquid getting into tissues)
  • Replacement of damaged cells (so epithelial stays in tact)
  • Feedback loops prevent overproduction of gastric acid
40
Q

Where does helicobacter pylori live?

A

In gastric mucus

41
Q

How does helicobacter pylori cause a reduced mucosal defence?

A
  • Secretes urease, splitting urea into CO2 and ammonia
  • Ammonia reacts with H+ ions and forms ammonium which is toxic to gastric epithelium
  • Ammonium secretes proteases, phospholipases which damage gastric epithelium
  • This causes an inflammatory response
  • Reducing mucosal defence
42
Q

How do NSAIDs cause peptic ulcers?

A
  • Non-steroidal anti-inflammatory drugs
  • Mucus secretion is stimulated by prostaglandins
  • Cyclo-oxygenase 1 needed for prostaglandin synthesis (important in inflammatory process)
  • NSAIDs inhibit cyclo-oxygenase 1
  • Reduced mucosal defence
  • So increased risk of peptic ulcers
43
Q

How do bile salts create peptic ulcers?

A
  • Duodeno-gastric reflux (throwing up bile)
  • Regurgitated bile strips away mucus layer
  • Reduced mucosal defence
44
Q

How to treat peptic ulcer disease?

A
  • proton pump inhibitor
  • antibiotics (e.g. amoxicillin)
45
Q

How to treat a peptic ulcer caused by NSAIDs?

A
  • Prostaglandin analogues - misoprostol (stimulates gastric mucus production)
  • Reduce acid secretion
  • Could also use proton inhibitor
46
Q

What are some proton pump inhibitors?

A

Omeprazole, Lansoprazole, Esomeprazole

47
Q

What are some H2 (Histamine) receptor antagonists?

A

Cimetidine, Ranitidine

GI Lectures (14 decks)

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