Acid production and regulation Flashcards

1
Q

4 main types of cells in stomach

A

Mucous cells, parietal cells (HCl and intrinsic factor), chief cells and enterendocrine cells (hormones, G cells secrete gastrin)

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2
Q

Approx __ litres of acid produced per day

A

2

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3
Q

Hydrogen pump is…

A

energy requiring, as H+ pumped against gradient

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4
Q

Gastric acid secretion mechanism

A

H2O + CO2 –> H2CO3), catalysed by carbonic anhydrase. Spontaneously dissociates into a H+ and HCO3–.

The H+ is transported into stomach lumen via the H+– K+ ATPase ion pump, uses ATP to exchange K+ with H+.

HCO3– transported out of cell into blood via a transporter protein called anion exchanger in exchange for Cl–. This chloride ion is then transported into the stomach lumen via a chloride channel.

This results in both hydrogen and chloride ions being present within the stomach lumen. Their opposing charges leads to them associating with each other to form hydrochloric acid (HCl).

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5
Q

Gastric phase (2) of regulating gastric acid secretion

A

Gastric distension, presence of peptides and amino acids

Gastrin released
Acts directly on parietal cells.

Triggers release of hormone histamine.
Acts directly on parietal cells.
Increased acid production.

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6
Q

Proteins as regulator of acid production

A
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7
Q

Effect of pH

A

Low luminal pH directly inhibits gastrin secretion, indirectly inhibits histamine release. Stimulates somatastatin (turns parietal cells off, inhibits acid production)

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8
Q

Duodenum in regulation

A

duodenal distension, senses chyme is hypertonic, low pH and presence of amino acids and fatty acids so triggers release of enterogastrones.

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9
Q

2 Enterogastrones

A

Secretin - inhibits gastrin release, promotes somatostatin release

Cholecystokinin (CKK)

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10
Q

Cephalic phase (1) of acid production regulation

A

Parasympathetic nervous system
sight, smell, taste and chewing
Acetylcholine release
ACh acts directly on parietal cells
ACh triggers release of gastrin and histamine
Increased acid production.

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11
Q

What are paracrine factors

A

Cells signal to each other, acts on neighbouring cells eg. histamine and somatostatin.

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12
Q

What is a peptic ulcer?

A

An ulcer is a breach in a mucosal surface. (epithelium stripped away due to gastric acid)

Caused by:
helicobacter pylori infection
Drugs (NSAIDS - ibuprofen, aspirin)
Chemical irritants (alcohol, bile salts)
Gastrinoma (tumour, too much acid made and not regulated)

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13
Q

How does gastric mucosa defend against attacks leading to ulcers?

A

Alkaline mucus,
tight junctions between epithelial cells,
replacement of damaged cells,
feedback loops to prevent too much acid being produced (negative feedback loop).

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14
Q

How does helicobacter pylori work

A

Lives in gastric mucus. Secretes urease, splitting urea into CO2 and ammonia.
Ammonia + H+ –> ammonium

Damages gastric epithelium along with proteases, phospholipases and toxin known as vacuolating cytotoxin A.

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15
Q

How do NSAIDs attack epithelium?

A

Non-steroidal anti-inflammatory drugs
Inhibit cyclo-oxygenase 1 which is needed for prostaglandin synthesis which stimulates mucus secretion.

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16
Q

How do Bile salts attack epithelium?

A

Duodeno-gastric reflux
Strips away mucus layer

17
Q

Treating helicobacter pylori

A

Proton pump inhibitor
antibiotics

18
Q

What do omeprazole, lansoprazole and esomeprazole do?

A

Turn off hydrogen pump

19
Q

What does ranitidine (Zantac) do?

A

Histamine blocker

20
Q

Where is pepsinogen made

A

By chief cells, is a zymogen (inactive form)

21
Q

Secretion of pepsinogen is parallel to

A

HCl secretion

22
Q

Pepsin production is __ feedback loop

A

A positive feedback loop.

Pepsin catalyses reaction of pepsinogen to pepsin. Rapidly cascades to make lots of pepsin.

23
Q

Why is pepsinogen made not pepsin from beginning?

A

Pepsin would break down the chief cells themselves as made from protein! (would be autodigestion)

24
Q

Conversion of pepsinogen to pepsin is dependent on what

A

pH
Most efficient when pH < 2.

Irreversible inactivation in small intestine by HCO3-.

25
Q

Can you survive without pepsin?

A

Yes - it is not essential. Only accelerates protein digestion.
You can even live without a stomach.

26
Q

Receptive relaxation

A

Mediated by vagus nerve (parasympathetic nervous system acting on enteric nerve plexuses)
Triggered by sight/smell/chewing and presence of food.

27
Q

Peristalsis of stomach

A

Waves begin in gastric body, weak contraction.
More powerful contraction in gastric antrum. Pylorus closes as peristaltic waves reaches it (mixes).

28
Q

Pacemaker cells of stomach

A

Interstitial cells of Cajal.
In muscularis propria, undergo slow depolarisation-repolarisation cycles. 3 per minute.
Depolarisation waves transmitted through gap junctions to adjacent smooth muscle cells.

29
Q

Factors effecting strength of peristaltic contractions

A

Excitatory neurotransmitters and hormones (gastrin) further depolarise membranes.

Reduced peristaltic contraction by:
increase duodenal luminal fat, osmolarity, sympathetic NS action or decreased duodenal luminal pH, parasympathetic NS action.