2 - Gastric Acid And Enzymes

Front 1

How is the tone of the esophageal sphincter controlled? How is the tone of the pyloric sphincter controlled?

Back 1

*An inhibitory branch of the vagus nerve
*enteroendocrine hormones, specifically CCK

Front 2

Where are chief cells found? What do they secrete?

Back 2

They are found at the bottom of both pyloric and oxyntic glands and secrete pepsinogen and gastric lipase.

Front 3

What are the functions of HCl in the GI system? (There are three)

Back 3

*antibacterial
*denatures macromolecules
*catalyzes pepsinogen to pepsin

Front 4

What is the function of intrinsic factor? What condition results from its deficiency?

Back 4

It is required for the absorption of vitamin B-12. Deficiency results in pernicious anemia.

Front 5

What role is ghrelin thought to play?

Back 5

It is thought to play a role in satiety and hunger.

Front 6

Describe the feedback that regulates secretion of H+ in the stomach during the interdigestive phase?

Back 6

*stimulates the release of somatostain which inhibits the release of gastrin and H+
*directly inhibits the release of H+ and gastrin

Front 7

Vagus nerve endings release ACh during the cephalic phase...what are the functions of ACh during this phase?

Back 7

*stimulates the release of pepsinogin from chief cells
*stimulates the release of H+ and intrinsic factor from parietal cells

Front 8

Besides releasing ACh, what action does the vagus have in the stomach during the cephalic phase?

Back 8

It stimulates the enteric nervous system to release GRP which causes the release of gastrin from enteroendocrine cells.

Front 9

Other than vagal action, how is the enteric nervous system stimulated during the gastric phase?

Back 9

*amino acids and peptides activate chemoreceptors
*food bulk activates stretch receptors

Front 10

What are the actions of gastrin during the gastric phase?

Back 10

*stimulates parietal cells
*stimulates the release of histamine

Front 11

What factors stimulate parietal cells to release H+?

Back 11

*ACh from vagal nerve endings (weak)
*gastrin (weak)
*histamine (strong)

Front 12

What is the first thing to enter the duodenum from the stomach? What is the last thing?

Back 12

Amino acids enter first and fats enter last.

Front 13

What breaks down carbohydrates in the stomach?

Back 13

Nothing - these molecules are broken down some by salivary enzymes but are not further digested until they reach the duodenum.

Front 14

The release of what hormone is stimulated when food moves into the duodenum in the early intestinal phase?

Back 14

CCK (there is continued release of gastrin, but this hormone is already in circulation).

Front 15

What are the actions of CCK during the early and late intestinal phases?

Back 15

*stimulates contraction of the pyloric sphincter
*weakly stimulates the release of somatostatin in the stomach
*stimulates relaxation of sphincter of Oddi
*stimulates contraction of gall bladder
*stimulates release of pancreatic enzymes

Front 16

What are the actions of secretin, "nature's antacid"?

Back 16

*directly inhibits the release of H+ from parietal cells
*stimulates the release of HCO3- from the pancreas

Front 17

Name three factors that inhibit the release of H+ from parietal glands.

Back 17

1.H+
2.Somatostatin
3.Secretin

Front 18

How is H+ moved across the apical membrane of parietal cells?

Back 18

H+/K+ ATPase moves it against its gradient into the lumen.

Front 19

What happens to HCO3- after it is produced in the cytoplasm of parietal cells?

Back 19

It is transported across the basolateral membrane by a HCO3-/Cl- antiporter, thus creating the alkaline tide in the blood.

Front 20

Describe the movement of Cl- across the apical and basolateral membranes of the parietal cells.

Back 20

It is transported across the basolateral membrane into the cell by a Na+/Cl- symporter and a HCO3-/Cl- ATPase; across the apical membrane into the lumen by a K+/Cl- symporter.

Front 21

How does histamine stimulate the release of H+ from parietal cells?

Back 21

1.Binds receptor and activates adenylate cyclase
2.[cAMP] increases
3.cAMP and Ca++ stimulate the fusion of vesicles carrying H+/K+ ATPases with the plasma membrane
4.This results in more transporters present on the apical membrane and thus increases the secretion of H+

Front 22

Which cells make the mucus coat of the stomach?

Back 22

Goblet cells and neck cells secrete mucus.

Front 23

How does H+ secreted by the parietal cells pass through the mucus coat to reach the lumen of the gastric gland?

Back 23

By a process known as viscous fingering wherein the H+ forms small channels through the mucus. This is possible because mucus becomes very viscous at its interface with H+, thus creating a wall for the channel.

Front 24

T/F:
The plasma membrane of parietal cells is very resistant to acid.

Back 24

True and false! The apical membrane is very acid resistant, but the basolateral membrane is not particularly.

Front 25

What is the basic defect in any kind of gastric ulcer?

Back 25

The mucus coat is breached which allows acid and gastric enzymes to come into contact with the epithelia.

Front 26

What is wrong in Zollinger-Ellison disease?

Back 26

There is a gastrin-secreting tumor which stimulates overproduction of H+ by the parietal cells.

Front 27

How is Zollinger-Ellison disease diagnosed?

Back 27

1.Take a baseline measure of serum gastrin.
2.Administer exogenous secretin.
3.Take another measure of serum gastrin.
In normal persons, secretin inhibits the release of gastrin. In patients with the disease it stimulates the release of gastrin.

Front 28

How is H. pylori able to survive in the acidic environment of the stomach?

Back 28

The bacteria has a urease that catalyzes urea into CO2 and ammonia which creates a local alkaline environment for the bug.

Front 29

How can H. pylori be diagnosed?

Back 29

Either by antral biopsy or by urease breath test. However, positive results should be taken with care as H. pylori is very often carried asymptomatically.

Front 30

How are compounds such as NSAIDs or aspirin thought to cause gastric ulcers?

Back 30

The mechanism is unclear but is thought to involve the inhibition of prostaglandins.

Front 31

What role do stress, alcohol, and caffeine play with ulcers?

Back 31

They may exacerbate an ulcer but they are never the cause.

Front 32

Why isn't the release of gastrin targeted for treatment of ulcers?

Back 32

Because gastrin has strong structural similarity to CCK, and this compound would be reduced as well.

Front 33

How do H2 blockers work?

Back 33

The block the binding site of histamine on the parietal cell.

Front 34

What risk is associated with the use of H+/K+ ATPase inhibitors?

Back 34

Along with a reduction in gastric acidity, they will cause a dramatic increase in the release of gastrin which has powerful mitogenic effects and may be carcinogenic.