GI Physiology of the Stomach Flashcards

1
Q

Which cells secrete H+ and Cl- to make HCl?

A

The parietal cells

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2
Q

What is the process of HCl production?

A

1) hydrolysis of C02+H2o->H2CO3
2) H2CO3 dissociates to HCO3 and H+
3) Bicarb is pumped into surrounding capillaries and Cl- is pumped back in to maintain charge ballence.
4) H+/K+ antiporter, H+ into stomach lumen. Cl- is pumped out into the stomach lumen.
5) Cl-+ H+ -> HCl

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3
Q

What is the first step in turning on the production of gastric acid?

A

Cephalic phase, at the sight, smell or chewing of food. ACh is released which stimulated parietal cells to increase HCl production and also stimulates Histamine and gastrin secretion which stimulates parietal cells.

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4
Q

What is the second step in turning on the production of gastric acid?

A

Gastric phase, due to gastric distension. Gastrin release stimulates parietal cells and also stimulates histamine production further stimulating parietal cells.

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5
Q

What is the first stage of turning off the production of gastric acid?

A

Gastric phase, due to low pH. Low pH inhibits gastrin and histamine but stimulates somatostatin which inhibits parietal cells.

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6
Q

What is the second stage of turning off the production of gastric acid?

A

Intestinal phase, due to dueodenal distention +low pH. Causes release of enterogastrones such as secretin which inhibits gastrin and stimulates somatostatin, and CCK.

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7
Q

What stimulates gastric acid secretion?

A

Gastrin, ACh, Histamine, high pH.

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8
Q

What inhibits gastric acid secretion?

A

Somatostatin- (stimulated by secretin)

Low pH

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9
Q

How do enterogastrones affect gastric acid secretion?

A

Secretin and CCK inhibit gastric acid secretion by stimulating somatostatin release.

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10
Q

What hormone affects gastric acid secretion?

A

Gastrin activates secretion.

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11
Q

What neurotransmitter affects gastric acid secretion?

A

ACh stimulates secretion.

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12
Q

What paracrine factor affects gastric acid seretion?

A

Histamine stimulates secretion and inhibits somatostatin.

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13
Q

What is the role of protien in the stomach?

A

Protien acts as a buffer mopping up H+ ions increasing the pH this causes a decrease in somatostatin secretion and therefore decrease pH in a cycle.

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14
Q

Which cells make proteases in the stomach?

A

Chief cells.

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15
Q

What do chief cells manufacture?

A

Pepsinogens (inactive zymogen form of pepsin)

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16
Q

How is pepsinogen converted to pepsin?

A

By the low pH in the lumen of the stomach.

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17
Q

How does pepsin affect pepsinogen?

A

Positive feedback loop. Pepsin stimulates pepsinogen conversion.

18
Q

Why do chief cells secrete pepsinogens not pepsins?

A

To avoid having the protiens in the cell broken down.

19
Q

What regulates pepsin secretion?

A

Runs in parallel with HCl secretion. Is mediated by ACh.

20
Q

What is the role of pepsins?

A

They break down collagen in proteins allowing a larger surface area for digestion.

21
Q

How does the mucosa of the stomach protect itself from gastric acid?

A

It is lined with an alkaline mucos-bicarbonate layer.

22
Q

What are the major causes of peptic ulcers?

A

NSAIDS, Helicobacter pylori, Bile salts.

23
Q

How do NSAIDs cause peptic ulcers?

A

Alkaline mucos layer is screted by prostaglandins. COX-1 makes prostaglandins.
NSAIDs inhibit COX-1 decreasing mucosal defense.

24
Q

What is a peptic ulcer?

A

A breach in the mucosal defense causing the stomach to digest itself.

25
Q

Which layer of the stomach contains the gastric pits?

A

The mucosal layer

26
Q

How many types of cells are there the gastric pits?

A
  1. Surface mucous cells, Mucous neck cells, Parietal cells, Chief cells and G cells.
27
Q

What do surface mucous cells secrete?

A

Secrete alkaline mucous for protecting the lining of the stomach.

28
Q

What do mucous neck cells secrete?

A

Acidic fluid containing mucin

29
Q

What do parietal cells secrete?

A

HCl and Intrinsic Factor.

30
Q

What do chief cells secrete?

A

Pepsinogen and gastric lipase.

31
Q

What do G cells produce?

A

Enteroendocrine cells (hormone secreting cells of the gut) secrete Gastrin.

32
Q

What initiates the process of causing gastric emptying to slow?

A

Distention in the duodenum+ increased H+, fat and amino acid concentration in the duodenum.
This causes the release of enterogastrons and stimulates neural receptors.

33
Q

How do increased enterogastrones affect stomach emptying?

A

They decrease the rate directly.

34
Q

How does stimulation of neural receptors in the duodenum influence rate of gastric emptying?

A

Short neural reflexes directly decrease stomach emptying.
Long neural reflexes are sent to the CNS causing increased sympathetic and parasympathetic activity deceasing stomach emptying.

35
Q

What are the two types of gastric motility?

A

Receptive relaxation and peristalsis.

36
Q

What is receptive relaxation?

A

Relaxation of the muscles of the stomach to increase the volume available for food.

37
Q

Which nerve is involved in receptive relaxation?

A

The vagus.

38
Q

Where does receptive relaxation occur?

A

Body and fundus.

39
Q

What is peristalsis?

A

Waves of contraction beginning in the body. Pylorus remains closed to allowing churning.

40
Q

What controls the rhythm of gastric motility?

A

Pace maker cells that have gap junctions that allow for the propagation of impulses to adjacent cells.

41
Q

What increases contraction in the stomach?

A

Gastrin and gastric distention.

42
Q

What decreases contraction in the stomach?

A

Duodenal distention and increased sympathetic activity.