STOMACH Flashcards by Lauren Nguyen

Major functions of the stomach

Temporal storage for food
Absorption of water-soluble and lipid-soluble substances
- E.g. alcohol, some drugs
Preparation of the “chyme” (semi-fluid material produced by gastric digestion of food) for digestion in the small intestine

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Digestion in the stomach

Physical - muscles contract and relax
Chemical - pepsin breaks down proteins
- Requires acidic medium

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Name the major cells of the gastric (oxyntic) gland and what they secrete

Surface mucous cells - mucus (more alkaline & viscous), HCO₃^-, water
Mucus neck cells - soluble mucus, HCO₃^-, water
Parietal (oxyntic) cells: HCl & intrinsic factor
Chief (zymogen) cells - pepsinogen
D cell - somatostatin
Enterochromaffin-like (ECL) cells: histamine
G cell - gastrin

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What cells are found in teh basal region of gastric glands?

Chief (zymogen) cells

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What cells are found in the antrum?

D cells

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What cells are found in the pyloric region?

G cells

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Functions of HCl & intrinsic factor from parietal cells

HCl -
- Denatures proteins
- Breaks up cell membranes
- Activates pepsinogen
- Antibacterial
- Solubilizes calcium salts
IF - absorption of vitamin B12 in ileum for production of mature RBCs

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Pepsin

Endopeptidase auto-catalytically activated from chief cells’ inactive pepsinogen

refers to all enzymes activated at a pH below 3 by HCl

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Somatostatin from D cells

inhibits acid secretion & gastrin release

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Histamine from ECL ells

Stimulates acid secretion

Increases local blood flow

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Gastrin from G cells

Secreted into the blood (not stomach lumen) to stimulate gastric juice secretion & gastrin/intestinal motility

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Function of gastric acid

Digestion of proteins via acid & proteolytic enzyme production
Absorption, esp vitamin B12
Protects mucosa from bacteria & autodigestion from its own acid & proteolytic enzymes

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Gastric lipase

Homologous to lingual lipase

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Loss of intrinsic factor causes

achlorhydria & pernicious anemia

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Gastric juice:

mucous
pepsin
gastric lipase
intrinsic factorHCl
Other electrolytes: ___, __, and ___

HCO₃- from mucous cells

K+ for H,K-ATPase

Na+ from mucous cells

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How do [HCl], [K+], and [Na+] change as the rate gastric juice secretion increases?

HCl increases sharply (food acts a buffer)

K increases a bit

Na+ falls

As the stomach empties, what happens to the rate of H+ secretion?

It increases

What makes the parietal cell distinct?

Intracellular canliculi

Abundance of mitochodnria

Extensive smooth ER (tubulovesicular membranes)

Resting state of parietal cell vs Stimulated for acid secretion

Resting state: tubulovesicles w H/K-ATPase are underneath the plasma membrane on the apical side.

Stimulation: tubulovesicle membranes fuse into the canalicular membrane to increase the apical membrane’s surface area

–> increases the # of H/KATPase, K+ and Cl- channels into the plasma membrane
–> increases O₂ consumption to support acid secretion

Name the transporters in the parietal cell on the apical vs the basoalteral membrane

Apical:
- H,K-ATPase
- K+ channel
- Cl- channel
Basolateral:
- Na,K-ATPase
- K+ channel
- Cl-/HCO₃^- exchanger

Secreted H+ from the parietal cell are derived mostly from ___

During active HCl secretion, the blood coming from the stomach contains a lot of ___.

H+ secretion is derived mostly from the dissociation of water & the carbonic anhydrase rxn

The blood coming from the stomach contains a lot of HCO₃^- (alkaline tide)b

Name the parietal cell receptors for gastrin, Ach, and histamine (secretagogues) and hwo they mediate their effects

Gastrin: gastrin-cholecystokinin (CCK-B)

Ach: muscarinic receptor, M3

HIstamine: H2 receptor

CCK-B & M3 increase intracellular Ca2+ –> HCl secretion

H2 increases intracellular cAMP –> HCl secretion

Potentiation effect

The effect of any 2 stimulants is greater than the effect of either stimulant alone.

The effect of gastrin, Ach, and histamine will result in an increase in cAMP & Ca2+ –> greatly enhances H/K-ATPase –> more acid secretion

Describe parietal cell activation

Stomach distension stimulates mechanoreceptors
Activates parietal directly thru
1. Short local reflexes
2. Long vago-vagal reflexes (traveling on vagus n)

**Direct** vs **Indirect** action of secretagogues

* Direct*:* Ach, gastrin, and histamine bind **directly** to their respective receptors on the parietal cell --\>stimulate & potentiate gastric acid secretion * Ach from vagus n (CN10) * Gastrin from D cells * Histamine from ECL cells * Indirect: ACH & gastrin stimulate histamine release from ECL cells & mast cells (histaminocytes) in the lamina propria

Cimetidine & Ranitidine

H2 recepto rblockers The block H2 receptors on parietal cells, thus also blocking Ach & gastrin indirect stimulation

Phases of gastric acid secreiton

1. **Basal** (inter-digestive period) 2. **Cephalic** 3. **Gastric** 4. **Intestinal**

**Cephalic phase (shortest)**

Initiated by thought, sight, smell, and taste of food; also influenced by emotion * **Neuro influence**: parasympathetic vagus n releases Ach to stimulate acid secretion by * stimulating parietal cells, G cells, and ECL cells * stimulating chief cells for pepsinogen * **Endocrine mechanism**: Vagal stimulation also causes gastrin release, which acts like Ach

**Gastric** phase (longest)

Triggered by presence of food in stomach due to distension & chemical nature * **Neuro**: stomach distension stimualtes mechanoreceptors --\> parasympathetic secretion of Ach * **Endocrine**: Amino acids & peptides activate G cells --\> Gastrin --\> acid secretion & histamine reslease * Gastrin falls when * stomach pH falls between 2-3 * somatostatin is released from D cells

**Intestinal phase**

Triggered by chyme in the duodenum --\> eneterogastric relfelx * Acid in duodenum --\> **s****ecretin:** inhibits G cells & the parietal response to gastrin * Fatty acids in duodenum --\> **gastric inhibitory peptide (GIP)** and **cholecystokinin (CCK)** inhibits acid secretion and suppress gastrin release

Gastritis & peptic ulcers are ____ caused by \_\_\_

Both are **inflammation of gastric mucosa** cauased by bacterial infection of the mucosa (e.g. h pylori) that stimulates gastric secretion

H Pylori

* Survives acid bc it produces **urease** (hydrolyzes urea to produce ammonia, which neutralizes gastric acid) * Adheres to epithelial cells and stimulates **adhesins, ammonia, proteases,** and **immune response** * Induces G-cells to secrete **gastrin** --\> HCl from parietal cells * However, its augmentation occurs at a moderate rate

What factors predispose to ulcers?

* **Smoking** - increased nervous stimulation of stomach secretory glands * **Alcohol** - breaks down mucosal barrier * **Aspirin & NSAIDs** - breaks down mucosal barrier

How to differentiate between **H pylori infection** and **Zollinger-Ellison Syndrome (ZES)**

**In ZES, there's an abnormally high gastric acid secretion rate associated w duodenal ulcers and tumors** - whereas, gastric ulcers do not produce excessive gastric secretion.

Zollinger-Ellison syndrome

Gastrinomas secrete very high amts of gastrin unregulated --\> extremely high rates of gastric acid secretion * Usually comes w **gastric and duodenal ulcers** * Gastrinomas are typically located in the **pancreas** * **Tx**: * Proton pump inhibitor * H2R blocker * Surgical removal of gastrinoma