L4: secretions of the stomach Flashcards

1
Q

Functions of the stomach

A
  • stores food - compliant
  • kills bacteria with acid
  • liquefies food
  • mixes chyme with gastric secretions
  • kneading of food particles to less than 1mm
  • regulates chyme release into duodenum
  • produces intrinsic factor
  • very little digestion (proteins) and absorption (alcohol, aspirin) takes place in the stomach
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2
Q

Microscopic view of the stomach

A

Has many indents which are gastric pits which contain cells that secrete mucous, hydrochloric acid and enzymes into the stomach.

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3
Q

What cells make up the gastric pits and what substances do they secrete?

A

Mucous neck cells - mucous and bicarbonate
Parietal cells - gastric acid (HCl) and intrinsic factor
Enterochromaffin-like (ECL) cell - histamine
Chief cells - pepsin and gastric lipase
D cells - somatostatin
G cells - gastrin

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4
Q

What secretes mucous and what is the function?

A

Goblet (surface and mucous neck cells)

They neutralise acid at the lining of the stomach to prevent damage to the stomach wall

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5
Q

What secretes gastric acid and what is it’s function?

A

Parietal cells
Mechanical digestion - denatures proteins
Chemical digestion - pepsinogen into pepsin which denatures and digests proteins
Converts poorly absorbed ferric iron (Fe3+) into absorbable ferrous iron (Fe2+)
Causes iron deficiency anaemia without acid

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6
Q

What secretes pepsinogen and what is it’s function?

A

Chief (zymogen) cells

Starts protein digestion in the stomach

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7
Q

What secretes histamine and what is it’s function?

A

Entereochromaffin-like cells

Stimulates acid secretion from parietal cells

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8
Q

What secretes gastrin and what is it’s function?

A

G - cells
Stimulates acid secretion from parietal cells
Stimulates ECL. Ells to release histamine

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9
Q

What secretes somatostatin and what is it’s function?

A

D-cells

Inhibits acid secretion from parietal cells

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10
Q

What secretes intrinsic factor and what is it’s function?

A

Parietal cells
Aids absorption of vitamin B12 from the ileum - vitB12 is essential for RBC maturation
So causes pernicious anemia without the intrinsic factor

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11
Q

How is acid secreted?

A

HCl production is is stimulated by gastrin, ACh and histamine
Stimulates parietal cells to secrete HCl
Increases hydrogen potassium ATPases and chloride channels on parietal cells
Energetically expensive process

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12
Q

How are stimulators signals delivered to the parietal cell to induce HCl secretion?

A

Paracrine - histamine released from a neighbouring gastric ECL cell
Endocrine - gastrin released from stomach G cells into the blood, where it comes back to the stomach and stimulates the parietal cell
Neurocrine - ACh release from neurones of the vagus nerve to act on parietal cell

Synergistic response

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13
Q

What are the receptors on the parietal cells?

A

Histamine H₂ receptor
Gastrin receptor CCK’B
ACh M3 receptor (muscarinic 3)

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14
Q

What is the most potent acid secretor?

A

Histamine, but when all 3 stimulator present, maximum secretion occurs

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15
Q

Resting parietal cell properties

A

Full of mitochondria as acid production uses lots of energy
Has lots of tubulovesicles containing proton pumps which can come together to increase the parietal cell surface area when acid needs to be secreted.

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16
Q

Stimulated parietal cell properties

A

Histamine, gastric and ACh will signal tubulovesicles to come together to produce canaliculi which increase the cell surface area ready for acid secretion and insert proton pumps on the surface

17
Q

How does HCl get to the stomach lumen?

A
  • when eating, parietal cells are stimulated with gastrin, histamine and ACh
  • the tubulovesicles put many proton pumps/hydrogen potassium ATPases on the stomach lumen side of the parietal cell
  • carbon dioxide from the blood will enter the parietal cell and bind with water forming carbonic acid using carbonic anhydrase which dissociates to bicarbonate and a proton
  • the proton gets pumped out into the stomach lumen, using energy
  • the bicarbonate moves out into the blood (causing alkaline tide) and chloride moves through the parietal cell and out to the stomach lumen
18
Q

Why does the alkaline tide occur?

A

Effluent of lots of bicarbonate ions from the parietal cells into the blood after eating a meal disturbs the plasma buffer system.
The bicarbonate ions would react with the circulating protons, increasing plasma pH, detected by a temporary rise in pH = alkaline tide

19
Q

Why does acid secretion need to be controlled?

A

Acid should only be secreted when food is in the stomach. If the stomach is empty, acid secretion should not occur as it could irritate the stomach lining.

20
Q

What is the cephalic phase of acid secretion?

A

An entirely neural phase in which the thought, sight, smell or approach of food leads to ACh release from the vagus nerve. Chewing or swallowing can do this too. Produces a small amount of acid.

21
Q

What is the gastric acid phase of acid secretion?

A

Once food is in the stomach, it can distend it. This is detected by mechanoreceptors that lead to ACh release. Also, the products of protein digestion (peptides and amino acids) in the stomach are detected by chemoreceptors that can lead to gastrin release. Largest phase and lasts the longest, hours.

22
Q

What is the intestinal phase of acid secretion?

A

Primarily an acid inhibitory phase. Once food enters the duodenum, HCl secretion needs to be turned off. Presence of HCl in the duodenum leads to somatostatin, secretion and CCK (cholecystokinin) release, which all inhibit acid secretion from parietal cells.
Secretion also stimulates bicarbonate release from the pancreas, which neutralises acid entering the duodenum.
CCK is also stimulated by lipids entering the duodenum. CCK can also stimulate digestive enzyme and bile release from pancreas and gallbladder respectively.

23
Q

Where are secretin and CCK released from?

A

Secretin is released from duodenal S-cells
CCK is released by duodenal I-cells
Both endocrine release

24
Q

What stops the efflux of acid into the oesophagus and unnecessary leakage of acid into the duodenum?

A

Lower Oesophageal sphincter (LOS) stops the efflux of acid into the oesophagus
Pyloric sphincter stops leakage of acid into duodenum

25
Q

What is Barrett’s Oesophagus?

A

Pre-cancerous condition bought about by persistent acid reflux

26
Q

What are duodenal ulcers?

A

Erosions on the first part of the small intestine due to acid

27
Q

Peptic ulcer treatments (anti-acids)

A

H₂-receptor antagonists block the action of histamine receptor, e.g. cimetidine, ranitidine
Proton-pump inhibitors block ATP driven hydrogen and potassium ion exchange. More effective than hydrogen receptor antagonists. E.g. omeprazole, lansoprazole

28
Q

How can reflux disease affect the mouth?

A

Reflux disease causes tooth decay
Dentist is often the first to notice it
Patient may not be aware - asymptomatic reflux
If acid attacks the teeth aggressively: high sensitivity rate, lots of cavities, lose vertical dimension
Could wear mouth guard at night
Bulimia has similar effects

29
Q

Helicobacter pylori

A
  • bacterium strongly associated with peptic ulcer disease (PUD)
  • linked with gastric cancer
  • rate of re-infection after antibiotics is high
  • route of transmission unclear, oral-oral?
  • may survive on dental plaque
  • dentists may be at greater risk of infection and may aid transmission