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GI Week 2 > Gastric Secretions > Flashcards

Gastric Secretions Flashcards

1
Q

What are the functions of the stomach?

A
  1. highly acidic environment to protect against organisms
  2. reservoir for a large amount of food
  3. fragment bolus into chyme
  4. protein digestion through acid hydrolysis and pepsin cleavage
  5. controls rate of chyme entrance to small intestine
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2
Q

What’s scintigraphy?

A

using a radio-labeled solid and nutrient liquid meal to measure gastric emptying

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3
Q

What is trituration?

A

grinding of food into small molecules

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4
Q

What do parietal cells secrete?

A

HCl and Intrinsic factor

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5
Q

What is intrinstic factor for?

A

it binds to vitamin B12 (cobalamine or extrinsic factor) to allow absoprtion

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6
Q

What cells secrete gastrin and where are they located?

A

G cells in the antrum of the stomach

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7
Q

What is the purpuse of gastrin?

A

it activates parietal cells in the fundus/corpus to secrete acid

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8
Q

Describe the structure of gastrin.

A

it’s a polypeptide with variable length and sequence

Preporgrastrin is broken down to progastrin, which can then be spliced to either Big, Little or Mini gastrin. Big and Little are the ones that bind to CCK2 receptors to activate parietal cells

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9
Q

What are the triggers for gastrin release form the G cells?

A
  1. seeing food causing vagal stimulation leadig to release of gastrin releasing peptide
  2. stomach distension causing vagal stimulating and GRP release
  3. arotmatic amino acids in the lumen activating the G cell directly
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10
Q

Would you expect atropine to inhibit gastrin release?

A

No - the ACh binds to a nicotinic receptor on the GRP nerve, not a muscarinic receptor (which is what atropine blocks)

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11
Q

What are the three molecules that will activate acid secretion from parietal cells?

A

gastrin
histamine
ACh

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12
Q

Which two moleucles will activate acid secretion from parietal cells via Ca2+ dependent pathway and which does it thorugh a cAMP-dependent pathway?

A

ACh and Gastrin via Ca2+

Histamine via cAMP

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13
Q

What are the three ways that ACh will trigger gastric acid secretion?

A
  1. directly binds muscarinic receptors on parietal cells
  2. activates ECL cells to release histamine, which binds parietal cells
  3. activates enteric neurons to release GRP which stimualtes G cells to releas gastrin, which triggers parietal cells
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14
Q

What are the two ways gastrin will trigger gastric acid secretions?

A
  1. binds directly to and activates parietal cells

2. activates ACL release of histamine

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15
Q

How does histamine stimualte gastric acid secretion?

A

binds directly to parietal cells and activates them

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16
Q

Describe how the parietal cell secretes acid when activated.

A

in the inactive state: the H/K ATPases are on tubulovesicular membrane and thus don’t do anything

when the parietal cell is activated, the H/K ATPases migrate to the canalicular membranes and fuse - after which H+ is secreted and K is absorbed in exchange

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17
Q

How are those protons generated in the cytosol in the first place?

A

via carbonice anhydrase II reactions

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18
Q

If the proton pump requires ATP, what structure is highly prevalent in the parietal cells?

A

mitochondria

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19
Q

How do parietal cells trigger an “alkaline tide” in the blood when they are secreting acid?

A

bicarbonate ions are exported frm the basolateral side by vesicular fusion or the Cl/Bicarb exchanger to enter the blood

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20
Q

How do PPIs stop all this?

A

they directly inhibit the H/K ATPase

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21
Q

How does Cl get to the luminal side?

A

it’s exchanged for bicarb and then just passively moves down it’s electrical gradient

22
Q

What on the basolateral membrane is essential for maintaining gradients that allow the H/K ATPase to work?

A

the Na/K ATPase

23
Q

What’s the electrical potential across the gastric mucos at rest? During activity?

A

at rest = -70 mV

actiity = -30 mV

24
Q

What molecule is hte main inhibitor of gastrin release (and thus acid release)? From what cells?

A

Somatostatin from D cells in the antrum

25
Q

What’s the trigger for somatostatin release?

A

acidity = released when pH is less than 3

26
Q

Why does somatostatin secretion decrease during the gastric phase of eating?

A

food in the stomach raises the pH so it’s not as acidic, thus turning off the D cell secretion of somatostatin

27
Q

What are the three ways somatostatin blocks acid secretion?

A
  1. inhibits G cell release of gastrin directly
  2. inhibits formation of cAMP via a Gi-dependent signaling pathway in parietal cells
  3. inhibits ECL cell secretion of histamine
28
Q

What molecules will also inhibit cAMP formation, thus decreasing acid secretion?

A

prostaglandins

29
Q

How does feedback from the duodenum decrease acid secretion?

A
  1. nervous reflex blocks ACh activation of parietal cells

2. Enterogastrones like secreting block secretion of histamine by ECL cells

30
Q

What are the phases of gastric secretion?

A

interdigestive phase
cephalic phase
gastric phase
intestinal phase

31
Q

Describe what’s happening with acid secretion, somatostatin and gastrin levels dueing the interdigestive phase?

A

D cells secrete somatostatin to maintain low levels of gastrin
thus acid levels are kept low

32
Q

What happens to acid, gastrin and somatostatin during the cephalic phase?

A

dorsal vagal complex integrates input from higher centers (seeing and tasting food) to activate Vagus nerves. GRP activates gastrin release and Ach activates ECL and parietal cells.

somatostatin isn’t affected because just seeing food is not a trigger for the D cells

33
Q

What happens to acid, gastri and somatostatin levels during the gastric phase?

A

distension of the stomach activates vagal afferents and the enteric nervous system. Amino acids activate gastrin secretion and food raises pH decreasing somatostatin secretion.

34
Q

What happens to acid, gastrin, and somatostatin during the intestineal phase?

A

introduction of the gastric contents into the small intestine activates duodenal G cell secretion of gastrin. Activation of secretin and other enterogastrones and neural reflex decreases secretion.

still food in the stomach, so low somatostatin

35
Q

Why is the fact that intrinsic factor is a glycoprotein important?

A

it means it can resist protease degradation

36
Q

True or false: PPIs also inhibit the secretion of intrinsic factor, so megaloblastic anemia is a side effect.

A

False - it blocks acid secretion from the parietal cells, but intrinsic factor secretion is via a completely different mechanism and is thus unaffected

37
Q

What cells secrete pepsinogen?

A

cheif chief cells

38
Q

What will trigger pepsinogen release?

A

ACh and gatrin

39
Q

What will inhibit pepsinogen release?

A

secretin

40
Q

What does pepsinogen require to become active pepsin?

A

just an acidic environment

after that, pepsin can activate more pepsinogen

41
Q

What else do chief cells secrete?

A

gastric lipase for digestion of fatty acids

42
Q

Surface eptihelial cells will secrete mucus and bicarb in response to what?

A

PGE2

43
Q

so how do NSAIDs cause stomach irritation?

A

they block PGE2, so you lose the activation of mucus and bicarb secretion. this means you lose their protection against the acid and the epithlium gets irritated

44
Q

How can catecholamiens contribute to ulcers?

A

they suppress mucosal bicarb secretion, contributing to gastric irritation

45
Q

What two major molecules are involved in the repairing of dirupted gatric epithelium?

A

trefoil factors and growth factors

46
Q

What is Zolllinger-Ellison Syndrome?

A

It’s when a patient has a gastrinoma of the pancreas or itnestine which constantly secretes gastrin leading to an overproduction of acid in the stomach

47
Q

Why are gastrin levels usually increased in gastric ulcers?

A

the urease activity of H pylori keeps the pH abnormally high, so you don’t get release of somatostatin. this removes the inhibition on gastrin release, so you get more gastrin and thus higher acid production, pepsin secretion and hyperplasia of ECL and parietal sells - also stomach contractions

48
Q

What’s achlorhydria?

A

reduced acid secretion in the stomach - caused by aging, gastric resection, genetic factors, auto-immune, PPIs, infection

49
Q

What are the symptoms of achlorhydria?

A

bacterial overgrowth with diarrhea and increased risk of aspiration peumonia

also hip fracturesdue to decreased Ca++ absorptoin and iron deficient anemia due to decreased iron absoprtion

50
Q

True or false: The decrease in pepsin activation in achorhydria doesn’t seem to cause problems. Why?

A

True - because you still have proteases from the pancreas

GI Week 2 (11 decks)

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