GI V & VI: Gastric Phase Flashcards by Alexis S.

Why does the distal part of the stomach have a thicker wall than the proximal part?

because it is responsible for pushing the bolus forward, so it requires strong contraction

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Regulation of both motor and secretory responses in the stomach are via:

1) Neural: extrinsic and intrinsic
2) Paracrine: histamine is a powerful stimulator of H+ secretion
3) Endocrine: gastrin and somatostatin

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Why is intrinsic factor (IF) significant? What is it secreted by?

It is essential for the absorption of vitamin B12, and it is secreted by the stomach.

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Intrinsic factor is a(n) ______ factor.

essential

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What is the strongest stimulant for gastric H+ secretion?

parasympathetic stimulation via vagus nerve (extrinsic efferent fibers terminate on intrinsic neurons that innervate parietal cells, ECL cells, G cells)

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Which 3 substances stimulate H+ secretion by parietal cells?

acetylcholine (neurocrine)
histamine (paracrine)
gastrin (endocrine)

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What blocks the direct affects of ACh?

atropine, as it is a muscarinic receptor antagonist

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What blocks the direct effects of histamine?

cimetidine, as it is an H2 receptor antagonist

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What is the receptor that ACh, gastrin, and histamine act on, respectively?

ACh: M3 receptor
Gastrin: CCKb receptor
Histamine: H2 receptor

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Which materials have a negative feedback effect on gastric acid secretion?

somatostatin and prostaglandins

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Where does the digestion of lipids begin?

in the oral cavity (10%)

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Where does the digestion of proteins begin?

in the stomach (20%)

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The stomach can be divided into 2 regions based on ______________.

differences in motility

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Is the caudad region of the stomach thick walled or thin walled compared to the orad region? Why?

thick walled because a lot of motility happens there (contractions in caudad region generated by strong muscles mix the food and propel it into the small intestine)

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What are the best ways to treat Zollinger-Ellison syndrome?

inhibitors of H+ secretion, like cimetidine and omeprazole

- surgical removal of tumor

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What is the function of somatostatin?

inhibits gastric secretion and reduces rate of gastric emptying; also suppresses exocrine secretory action of pancreas

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What is the function of histamine?

it is a powerful stimulator of H+ secretion

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Does any carbohydrate digestion take place in the stomach?

No, as there is no amylase present in the stomach.

Describe the functional anatomy of the stomach.

The lining contains columnar epithelium folded into gastric pits. These pits are the openings where the gastric glands empty.

In the pylorus of the stomach, there are _____ pits and _____ glands.

long; short

Are there goblet cells in the stomach? (potential exam question)

No! Instead, goblet cells are the main cells of the small and large intestine.

The fundus and antrum of the stomach contain 6 types of secretory cells:

1) Parietal (oxyntic) cells: secrete HCl and IF
2) Mucous neck cells: secrete mucus
3) Chief (peptic) cells: secrete pepsinogens
4) Enterochromaffin-like (ECL) cells: secrete histamine
5) D cells: secrete somatostatin
6) G cells: secrete gastrin

In the GI tract, does histamine have an endocrine, paracrine, or neural effect?

paracrine

What is the function of gastrin?

it is an HCl secretagogue

What are the major gastric secretions that form gastric juice?

- HCl - Pepsinogen - Bicarb+mucous - IF

Are there serious implications for digestion if the stomach is resected?

No, as most digestion occurs in the duodenum.

In a healthy human, ______ is the only essential component of gastric juice; the other components serve redundant functions.

intrinsic factor (IF)

What does omeprazole target?

It targets the H+/K+ ATPase on the luminal side of gastric parietal cells, thus reducing H+ secretion.

What is the reason for the "alkaline tide" in gastric venous blood after a meal?

HCO3- is absorbed into the blood via the Cl-/HCO3- exchanger of gastric parietal cells. This HCO3- is eventually secreted back into the GI tract by the pancreas, which is how pH is restored.

What forms the mucosal barrier in the stomach?

HCO3- entrapped by viscous mucous coating the stomach (surface epithelial cells of stomach secrete a watery fluid that contains a high conc. of HCO3-; bicarb is then trapped by the mucous)

Carbohydrates compose roughly what percentage of mucous?

80%

Describe "potentiation" of H+ secretion.

The rate of H+ secretion can be regulated by each of the 3 stimulatory substances (gastrin, histamine, ACh) independently, as well as by interactions among the three.

What are the second messengers for the 3 substances that stimulate H+ secretion?

1) ACh: IP3/Ca2+ 2) Histamine: cAMP 3) Gastrin: IP3/Ca2+

Describe the feedforward control happening during the cephalic and oral phase.

-direct stimulation of parietal cells by vagus via ACh -indirect stimulation of G cells by vagus via GRP -indirect stimulation of ECL cells by vagus (via ACh) and gastrin (all of these promote HCl secretion by the parietal cell; this prepares the GI tract for receiving a meal)

When does the majority of HCl secretion happen?

gastric phase (60%); 30% happens during oral and cephalic phases, while 10% happens during intestinal phase

True or false: the gastric component cannot handle an acid load that's too high.

True- this is why somatostatin is released by endocrine cells when gastric luminal pH drops below 3.

What do prostaglandins do?

Inhibit stimulatory effect of histamine, thereby decreasing H+ secretion from parietal cells. (prostaglandins help control the acid load in the stomach)

How does chronic NSAID use affect the gastric compartment?

- NSAIDs reduce the production of prostaglandins - chronic use can block the feedback inhibition pathway for gastric acid secretion - this can led to erosion of the stomach lining, causing ulcers and bleeding

What are the functions of the gastroduodenal junction?

- filtering large size particles of food - emptying gastric content at a rate consistent w/ duodenum's ability to digest chyme - prevention of reflux of bolus into stomach

Are gastric or duodenal ulcers more common?

duodenal

What are gastric vs. duodenal ulcers formed by?

- gastric: primarily a defect in the mucosal barrier | - duodenal: high H+ secretory rates

What is a major causative agent of gastric ulcers?

gram negative bacteria (like H. pylori), which release cytotoxins that destroy the protective mucosal barrier

High gastrin secretion in patients with ZE syndrome produces which 2 direct effects?

1) Increased H+ secretion by parietal cells | 2) Increased parietal cell mass