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Flashcards in Gastric Secretion - Prunuske Deck (17)
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1
Q

Fundal part of stomach is important for:

A

Reservoir for food and acid secretion

2
Q

Antrum deals with that physical mechanism for processing food?

A

Mixing and grinding

3
Q

Which of the following: body, antrum, or cardiac would you expect to have longest glands?

A

Body

4
Q

In cardiac, body, and pyloric sections of stomach, what is the % of glands and main type of cell found?

A

Cardiac 50% gland- lots of mucous cells
Body 70% gland- lots of parietal, chief cells
Pyloric 40% gland- mucous cells and enteroendocrine

5
Q

What does Gastrin stimulate? Where are Gastrin secreting cells located?

A

Hormone gastrin is secreted from G cells in the antrum, which:
Activates parietal cells in the fundus/corpus to secrete acid
Activates ECL cells release of histamine

6
Q

Name two triggers for Gastrin release:

A

Triggers for Gastrin release from G cells in the antrum

  1. Seeing food or stomach distension causes vagal stimulation causing release of Gastrin-releasing peptide
  2. Aromatic amino acids in the lumen
7
Q

Gastrin, histamine (H2), and ACh activate what?

A

Gastrin, histamine (H2), and ACh activate acid secretion of parietal cells via cAMP or Ca++ dependent pathways

8
Q

Would you expect atropine to stimulate or

inhibit gastric acid secretion?

A

Inhibit

9
Q

What type of cells release histamine?

A

ECLs

10
Q

You eat some food. What happens to somatostatin secretion?

What is somatostatin activated by?

A

Somatostatin is secreted from D cells in the antrum when pH

11
Q

Three actions of Somatostatin when pH

A

Somatostatin when pH

12
Q

Name the stage:

Low acid secretion, D cells secrete somatostatin to maintain low levels of Gastrin

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 gastric secretion.

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.

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

A

Interdigestive Phase: Low acid secretion, D cells secrete somatostatin to maintain low levels of Gastrin

Cephalic Phase – 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.

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

Intestinal Phase – 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 gastric secretion.

13
Q

(T/F) Protein-pump inhibitor drugs act on parietal cells but do not inhibit secretion of intrinsic factor.

A

True

14
Q

Chief Cell secrete what?

A

Pepsinogen and gastric lipase

15
Q

Where are gastrinomas usually found?

A

Zollinger-Ellison Syndrome (gastrinoma):

Usually caused by a Gastrin-secreting tumor in the pancreas or small intestine

16
Q

What are some causes of gastric and duodenal ulcers?

A

Infection – Helicobactor pylori
Poor secretion of mucus, bicarbonate by the surface epithelium
Stress (may contribute but doesn’t cause)
Irritation by alcohol, acid, digestive enzymes, bile
Treat with antibiotics and proton pump inhibitor. Stop NSAID

17
Q

What often happens to Gastrin and Somatostatin levels in gastric ulcers?

A

Gastrin levels often increased in gastric ulcers since somatostatin inhibition of gastrin during the fasting state is not activated (may be related to urease activity of H. pylori)