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GI & Liver > Gastric Physiology 1 > Flashcards

Gastric Physiology 1 Flashcards

1
Q

What is the function of a mucous cell?

A

Secretes mucus

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2
Q

What is the function of a parietal cell?

A

Secretes HCl and intrinsic factor.

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3
Q

What is the function of a chief cell?

A

Secretes pepsinogen

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4
Q

What is a G cell? What is its function?

A

G cells are enteroendocrine cells that secrete gastrin.

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5
Q

What is gastric acid?

A

Hydrochloric acid

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6
Q

How much gastric acid is secreted each day?

A

Approx. 2l

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7
Q

How is H2CO3 formed in parietal cells?

A

CO2 and H2O react together, catalysed by carbonic anhydrase.

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8
Q

What happens to H2CO3 in parietal cells?

A

Spontaneously dissociates into HCO3- and H+

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9
Q

How are HCO3- and Cl- related (gastric acid secretion)?

A

HCO3- is transported into the capillary, while Cl- is transported into the parietal cell in exchange. This happens via an anion exchanger.

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10
Q

How is H+ secreted from parietal cells?

A

H+ is exchanged for K+ via an ATPase pump.

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11
Q

How is Cl- secreted from parietal cells?

A

Via a chloride channel.

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12
Q

How does HCl form in the stomach lumen?

A

H+ and Cl- react to form HCl.

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13
Q

What 3 things increase gastric acid production?

A
  • ACh
  • gastrin
  • histamine
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14
Q

How is ACh released during the cephalic phase of digestion?

A

Released from the vagus nerve when food is seen or chewed.

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15
Q

How is ACh released during the gastric phase of digestion?

A

Stomach distention detected by intrinsic nerves.

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16
Q

How does ACh increase acid production?

A

Directly stimulates parietal cells = increased vesicular fusion.

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17
Q

How are G cells stimulated to produce gastrin?

A
  • vagus nerve
  • gastrin-related peptide
  • peptides in stomach lumen
18
Q

How does gastrin stimulate parietal cells?

A

G cells secrete gastrin into the blood. Gastrin travels to parietal cells and binds to CCK receptors, leading to elevated calcium levels. This leads to increased vesicular fusion.

19
Q

How do enterochromaffin-like cells increase gastric acid production?

A

They secrete histamine which binds to H2 receptors on parietal cells. This leads to increased cAMP production, leading to increased vesicular fusion.

20
Q

What causes ECL cells to release histamine?

A

Stimulation by ACh and gastrin.

21
Q

Apart from stimulating gastrin secretion, how do peptides in the stomach lumen stimulate acid production?

A

Peptides act as a buffer and mop up H+ ions, so pH rises. This leads to decreased secretion of somatostatin. Somatostatin inhibits parietal cell activity, so decreased secretion results in more parietal cell activity.

22
Q

How is gastric acid production decreased (gastric phase)?

A

When pH in stomach lumen is low:

  • gastrin secretion is directly inhibited
  • histamine release inhibited indirectly, via gastrin inhibition
  • somatostatin release stimulated, inhibiting parietal cell activity
23
Q

What stimulates gastric acid production decrease (intestinal phase)?

A

Duodenal distention
Low luminal pH
Hypertonic luminal contents
Presence of amino acids and fatty acids

24
Q

How is gastric acid production decreased (intestinal phase)?

A

Release of enterogastrones triggered: secretin and CCK (cholecystokinin).

Secretin and CCK inhibit gastrin release and promote somatostatin release.

ACh release reduced by stimulation of neural pathways.

25
Q

What is a peptic ulcer?

A

A breach in the surface of the gastric mucosa.

26
Q

What causes gastric ulcers?

A
  • Helicobacter pylori infection
  • NSAIDS
  • Chemical irritants (alcohol, bile salts, etc)
  • Gastrinoma (tumour of G cells)
27
Q

How do peptic ulcers arise?

A
  • increased mucosal attack

- reduced mucosal defence

28
Q

How might there be an increased mucosal attack?

A

Inflammatory response.

29
Q

How might mucosal defences be reduced?

A
  • washing away of mucus

- damaging of cell connections

30
Q

What defences does the gastric mucosa have?

A
  • alkaline mucus
  • tight junctions between epithelial cells
  • damaged cells are replaced
  • feedback loops to control the environmental conditions
31
Q

Which stains can be used to see Helicobacter pylori?

A

H&E, Giemsa, immunohistochemistry

32
Q

Where does Helicobacter pylori live in the body?

A

In the gastric mucus.

33
Q

What does Helicobacter pylori secrete?

A
  • urease
  • proteases
  • phospholipases (from cell membrane)
  • vacuolating cytotoxin A
34
Q

How do the secretions of Helicobacter pylori damage the gastric epithelium?

A
  • urease splits urea into ammonia and CO2
  • ammonia forms ammonium by joining with H+
  • ammonium, proteases, phospholipases and vacuolating cytotoxin A cause direct damage to the gastric epithelium.
35
Q

What happens when the gastric epithelium is damaged?

A

Inflammatory response (acute or chronic) results in reduced mucosal defence.

36
Q

What are NSAIDs?

A

Non-steroidal anti-inflammatory drugs = painkillers that reduce inflammation.

37
Q

How do NSAIDs cause peptic ulcers?

A
  • NSAIDs inhibit cyclo-oxygenase 1, which is needed for prostaglandin synthesis
  • prostaglandins stimulate mucus secretion
  • therefore reduced synthesis of prostaglandins results in reduced mucosal defence
38
Q

How do bile salts cause peptic ulcers?

A

Duodeno-gastric reflux causes bile to be regurgitated into the stomach. The bile strips away the mucus layer, resulting in reduced mucosal defence.

39
Q

How are peptic ulcers caused by Helicobacter pylori treated?

A

Triple therapy: 1 proton pump inhibitor and 2 antibiotics.

Proton pump inhibitor means that the environment becomes too alkaline for the bacteria.

40
Q

How are peptic ulcers caused by NSAIDs treated?

A

Misoprostol is a prostaglandin analogue (drug with similar structure to a prostaglandin). Therefore it rebuilds mucosal defences.

Also use a proton pump inhibitor or H2 receptor antagonist to reduce acid secretion.

41
Q

Give 3 examples of proton pump inhibitors.

A
  • omeprazole
  • lansoprazole
  • esomeprazole
42
Q

Give an example of a H2 receptor antagonist.

A

Ranitidine

GI & Liver (3 decks)

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