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GI Week 2 > Gastric Secretion Prunuske > Flashcards

Gastric Secretion Prunuske Flashcards

1
Q

How long does food usually hang out in stomach?

A

~4 hours

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2
Q

Main enzyme in stomach?

A

Pepsin

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3
Q

What part of the stomach is important as a secretion reservoir and is important for acid secretion?

A

Fundus and body

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4
Q

What happens in the antrum?

A

Mixing and grinding

*Technical word is…Truition

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5
Q

Where are the oxyntic/parietal glandular mucosa?

A

Body

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6
Q

What cells secrete pepsinogen?

A

Chief cells

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7
Q

What do parietal (oxyntic) cells secrete?

A

HCl
Intrinsic factor
Gastroferrin

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8
Q

Do parietal cells and chief cells get turned over regularly?

A

Nope, they are pretty stable!

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9
Q

What cells secrete gastrin?

Where are they?

A

G cells in the Antrum

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10
Q

What does gastrin do?

A

Activates parietal cells in the fundus/body to secrete acid!

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11
Q

What are the 2 triggers for gastrin release from G cells?

A
  1. Seeing food or stomach distension causes vagal stimulation causing release of Gastrin-releasing peptide (GRP)
  2. Aromatic amino acids in the lumen
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12
Q

What 3 things come in to bind to parietal cells to activate acid secretion?

A

Gastrin
Histamine
Ach

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13
Q

What does Atropine do to gastric acid secretion?

A

Inhibit!

*Its a muscarinic antagonist

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14
Q

Where does Histamine get released?

A

ECL cells

*Another target of gastrin…it binds to them and triggers histamine release!

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15
Q

Where are H+/K+ ATPases found in pareital cells?

A

Tubulo-vesicles

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16
Q

What happens to tubulovesicular cells when the parietal cells are stimulated?

A

They fuse with the canalicular membranes to increase their density at the apical membrane!

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17
Q

What is the consequence of your Na+/K+ ATPase being active on basolateral membrane?

A

Alters electrical membrane potential b/c pumping out 3 Na for every 2 K coming in…going to have low sodium inside these cells.

There are potassium channels on the apical surface

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18
Q

What special enzyme is active in parietal cells to generate H+ and Bicarbonate?

A

Carbonic anhydrase!

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19
Q

“Alkaline tide”

A

Blood in that immediate region is at a higher pH because bicarbonate is being excreted by parietal cells into the bloodstream

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20
Q

What organelle is abundant in parietal cells?

A

Mitochondria!

*Lots of ATP generation needed

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21
Q

What do proton pump inhibitors bind?

A

H+ K+ ATPase

So they directly interfere with H+ ions being pumped into lumen!

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22
Q

Where are D cells?

A

Adjacent to our G cells in the antrum

23
Q

What do D cells release to inhibit G cells?

When are they going to release it?

A

Somatostatin!

If pH is really low and you don’t need active parietal cells! pH

24
Q

Is there more or less somatostatin released when you eat food?

A

Less!

Because as food enters the stomach, the pH rises…therefore more gastrin is needed so less somatostatin is released!

25
Q

What do prostaglandins do in parietal cells?

A

Inhibit cAMP formation

**Fill in why this is important

26
Q

Which hormone is secreted due to increase in H+ in duodenum?

What does this block the secretion of?

A

Secretin

Histamine by ECL cells

27
Q

What is required for B12 absorption?

A

Intrinsic factor

28
Q

In what form is pepsinogen secreted?

A

As a proenzyme

*Doesn’t become active until it gets to gastric lumen

29
Q

What cells start the process of enzymatic digestion of protein and fat?

A

Chief cells

30
Q

What two things are positive regulators of chief cell secretion?

A

ACh

Gastrin

31
Q

What inhibits chief cell secretion?

A

Secretin

32
Q

What is Zollinger-Ellison Syndrome?

A

Gastrinoma!
GASTRIN-secreting tumor in PANCREAS or SMALL INTESTINE

Excess H+ secretion and hyperplasia/hypertrophy of parietal cells

*Most patients develop gastric ulcers

33
Q

What is peptic ulcer disease?

A

Hyperacidity…Deterioration of gastro-mucosal barrier

34
Q

Infection from what organism can cause gastric and duodenal ulcers?

A

Helicobactor pylori

35
Q

What 2 broad things contribute to ulcers?

A

Increase in acidity

Decrease in protective factors

36
Q

How does H Pylori contribute to ulcers?

A

Inhibits somatostain so Gastrin is highly active.

Gastrin binds to parietal and ECL cells to increase acidity!

37
Q

What does Achlorhydria mean?

A

Reduced acid secretion

38
Q

What secretes trefoil factors that can lead to regeneration of epithelial layer?

A

Surface mucous cells!

39
Q

What does Gastroferrin do?

A

Aids in Ferrous (Fe++) iron absorption

40
Q

Where are chief cells?

A

In the body by the parietal cells

41
Q

What is secreted when there is increased H+ ions, fats, and peptides in the duodenum?

What does this do to parietal HCl secretion?

A

Enterogastrones are secreted (CCK, secretin etc.)

They inhibit ECL cell release of Histamine so the Histamine can’t bind parietal cells…therefore there is a decrease in acid secretion

42
Q

When is pepsinogen secreted?

A

In response to ACh and gastrin

43
Q

What inhibits pepsinogen release?

A

Secretin

44
Q

What is meant by the term “autoactivation” in terms of pepsinogen?

A

Once pepsinogen hits the acidic environment of the stomach…it is cleaved into pepsin which is a POTENT PROTEOLYTIC ENZYME!

45
Q

Besides pepsinogen, what else do chief cells secrete?

A

Lipase!

46
Q

Surface epithelial cells secrete mucus and bicarbonate in response to what?

A

PGE2

47
Q

How do NSAIDs lead to gastric irritation?

A

They block the production of PGE2…therefore there is reduced mucus secretion…this contributes to gastric irritation

48
Q

How do catecholamines contribute to stress ulcers?

A

Catecholamines suppress mucosal BICARBONATE secretion…this contributes to gastric irritation and the formation of stress ulcers

49
Q

What are the 4 phases of digestion?

A

Interdigestive
Cephalic
Gastric
Intestinal

50
Q

If peptic ulcer disease is caused by H pylori, what two things are you going to use to tx?

A

Antibiotic

PPI

51
Q

How may H pylori contribute to an increase in acid production?

A

Urease may inhibit somatostatin…this lets Gastrin go wild to act on parietal and ECL cells

52
Q

What 2 ways do NSAIDs contribute to ulcer formation?

A

No prostaglandins!
Normally PGE2 contributes to mucus formation…without it we have less mucus.

Without prostaglandins we have tons of histamine release so there is a ton of acid production.

53
Q

What are foveolar cells?

A

Epithelial cells that secrete mucin.

54
Q

How may H pylori contribute to ulcers?

A

H pylori has urease which makes the environment more basic. This inhibits somatostatin. We, therefore, have no inhibition of gastrin so a crap ton of gastrin is secreted and we get lots of acid production!

GI Week 2 (11 decks)

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