Stomach

Stomach Regions

The stomach regions are the cardia, fundus, body, and pylorus.

All have longitudinal gastric folds, or rugae.

Cardia

Fundus

Body

Pylorus

The cardia (See Gross Anatomy) is a transitional zone between the esophagus and the stomach.

[Histology

The cardia as with the pylorus is primarily involved with mucus production and are similar histogically.

[Ghrelin}

The fundus and body regions are identical in microscopic structure [histologic image]and are the sites of gastric glands releasing acidic gastric juice.

The mucosa and submucosa of the empty stomach have large, longitudinally directed folds called rugae, which flatten when the stomach fills with food.

Acid is secreted across the parietal cell canalicular membrane by the H+/K+ ATPase proton pump into the gastric lumen.

The gastrin that is secreted by antral G cells in response to intraluminal dietary peptides acts directly on parietal cells and also stimulates release of histamine from enterochromaffin-like (ECL) cells.

The vagus nerve stimulates postganglionic neurons of the enteric nervous system to release ACh, which acts on parietal and ECL cells.

In the antrum, release of gastrin-releasing peptide (GRP) from postganglionic neurons directly increases gastrin release, whereas release of ACh indirectly increases gastrin secretion by inhibiting release of somatostatin from antral D cells.

The increase in intraluminal H+ concentration causes D cells to release somatostatin and thereby inhibit gastrin release from G cells. CCK, cholecystokinin; R, receptor. (Reproduced, with permission, from Katzung BG, editor: Basic & Clinical Pharmacology,12th ed. McGraw-Hill, 2012: Fig. 62–1.)

Schematic model of physiologic control of hydrogen ion (acid) secretion by the gastric parietal cells, which are stimulated by gastrin (acting on gastrin/CCK-B receptors), acetylcholine (ACh; M3 receptor), and histamine (H2 receptor).

Content 4

The pylorus is the funnel-shaped region that opens into the small intestine.

[Both the cardia and pylorus are primarily involved with mucus production and are similar histogically.

G cell

Control of stomach acid

Details

System Digestive system

Location Stomach and duodenum

Function Gastrin secretion

Identifiers

Latin endocrinocytus G

TH H3.04.02.0.00031

Anatomical terms of microanatomy

[edit on Wikidata]

G Cell

The G cell or gastrin cell, is a type of cell in the stomach and duodenum that secretes gastrin. It works in conjunction with gastric chief cells and parietal cells. G cells are found deep within the pyloric glands of the stomach antrum, and occasionally in the pancreas [1] and duodenum. The vagus nerve innervates the G cells. Gastrin-releasing peptide is released by the post-ganglionic fibers of the vagus nerve onto G cells during parasympathetic stimulation. The peptide hormone bombesin also stimulates gastrin from G cells. Gastrin-releasing peptide, as well as the presence of amino acids in the stomach, stimulates the release of gastrin from the G cells. Gastrin stimulates enterochromaffin-like cells to secrete histamine.[2] Gastrin also targets parietal cells by increasing the amount of histamine and the direct stimulation by gastrin, causing the parietal cells to increase HCl secretion in the stomach.

G cell
Control of stomach acid
Details
System	Digestive system
Location	Stomach and duodenum
Function	Gastrin secretion
Identifiers
Latin	endocrinocytus G
TH	H3.04.02.0.00031
*Anatomical terms of microanatomy* [edit on Wikidata]

Wall of the stomach with rugae.

A low-magnification micrograph of the stomach wall at the fundus shows the relative thickness of the four major layers: the mucosa (M), the submucosa (SM), the muscularis externa (ME), and the serosa (S). Two rugae (folds) cut transversely and consisting of mucosa and submucosa are included. The mucosa is packed with branched tubular glands penetrating the full thickness of the lamina propria so that this sublayer cannot be distinguished at this magnification. The muscularis mucosae (arrows), immediately beneath the basal ends of the gastric glands, is shown. The submucosa is largely loose connective tissue, with blood vessels (V) and lymphatics. (X12; H&E)

The stomach walls consist of an outer mucosa, and inner submucosa, muscularis externa, and serosa.

Mucosa

The gastric mucosa of the stomach consists of the epithelium and the lamina propria(composed of loose connective tissue), with a thin layer of smooth muscle called the muscularis mucosae separating it from the submucosa beneath. The submucosa lies under the mucosa and consists of fibrous connective tissue, separating the mucosa from the next layer. Meissner's plexus is in this layer. The muscularis externa lies beneath the submucosa, and is unique from other organs of the gastrointestinal tract, consisting of three layers:

The inner oblique layer: This layer is responsible for creating the motion that churns and physically breaks down the food. It is the only layer of the three which is not seen in other parts of the digestive system. The antrum has thicker skin cells in its walls and performs more forceful contractions than the fundus.

[The muscularis has three layers.]

The middle circular layer: At this layer, the pylorus is surrounded by a thick circular muscular wall which is normally tonically constricted forming a functional (if not anatomically discrete) pyloric sphincter, which controls the movement of chyme into the duodenum. This layer is concentric to the longitudinal axis of the stomach.
Auerbach's plexus (AKA myenteric plexus) is found between the outer longitundinal and the middle circular layer and is responsible for the innervation of both (causing peristalsis and mixing)
The outer longitudinal layer

The stomach also possesses a serosa, consisting of layers of connective tissue continuous with the peritoneum.

Gastric glands

Different types of cells are found at the different layers of the gastric glands:

Layer of stomach	Name	Secretion	Region of stomach	Staining
Isthmus of gland	Foveolar cells	Mucus gel layer	Fundic, cardiac, pyloric	Clear
Body of gland	Parietal (oxyntic) cells	Gastric acid and intrinsic factor	Fundic only	Acidophilic
Base of gland	Chief (zymogenic) cells	Pepsinogen and gastric lipase	Fundic only	Basophilic
Base of gland	Enteroendocrine (APUD) cells	Hormones gastrin, histamine, endorphins, serotonin, cholecystokinin and somatostatin	Fundic, cardiac, pyloric	–

Parietal or Oxyntic Cells
Chief Cells
Tab 3

Parietal cells are mainly present in the gastric corpus and fundus. Parietal cells are responsible for secretion of hydrochloric acid and also produce intrinsic factor. Parietal cells have large mitochondria with short microvilli and a cytoplasmic canaliculi system in contact with the lumen. The H+/K+-ATPase responsible for acid secretion resides in the apical microvillus membrane.

Acid secretion by gastric epithelial cells is related to the physiologic function of oxyntic cells, which are called parietal cells.

Gastric acid secretion is a process in which multiple central and peripheral factors contribute to the secretion of H+ by parietal cells. Neuronal (acetylcholine, ACh), paracrine (histamine), and endocrine (gastrin) factors all regulate acid secretion.

Physiological and pharmacological regulation of gastric secretion: the basis for therapy of acid-peptic disorders. Shown are the interactions among an enterochromaffin-like (ECL) cell that secretes histamine, a ganglion cell of the enteric nervous system (ENS), a parietal cell that secretes acid, and a superficial epithelial cell that secretes mucus and bicarbonate. Physiological pathways, shown in solid black, may be stimulatory (+) or inhibitory (−). 1 and 3 indicate possible inputs from postganglionic cholinergic fibers; 2 shows neural input from the vagus nerve. Physiological agonists and their respective membrane receptors include acetylcholine (ACh), muscarinic (M), and nicotinic (N) receptors; gastrin, cholecystokinin receptor 2 (CCK2); histamine (HIST), H2 receptor; and prostaglandin E2 (PGE2), EP3 receptor. A red indicates targets of pharmacological antagonism. A light blue dashed arrow indicates a drug action that mimics or enhances a physiological pathway. Shown in red are drugs used to treat acid-peptic disorders. NSAIDs are nonsteroidal anti-inflammatory drugs, which can induce ulcers via inhibition of cyclooxygenase.

Their specific receptors (M3, H2, and CCK2, respectively) are on the basolateral membrane of parietal cells in the body and fundus of the stomach. Some of these receptors are also present on enterochromaffin-like cells (ECL), where they regulate the release of histamine. The H2 receptor is a GPCR that activates the Gs–adenylyl cyclase–cyclic AMP–PKA pathway. ACh and gastrin signal through GPCRs that couple to the Gq–PLC-IP3–Ca2+ pathway in parietal cells. In parietal cells, the cyclic AMP and the Ca2+-dependent pathways activate H+, K+-ATPase (the proton pump), which exchanges hydrogen and potassium ions across the parietal cell membrane. This pump generates the largest ion gradient known in vertebrates, with an intracellular pH of ~7.3 and an intracanalicular pH of ~0.8.

++++++++++++++++++++++++++

HCl production and neutralization in the gastrointestinal tract

This diagram depicts how hydrochloride acid is excreted into the stomach, in exchange for generation of bicarbonate in the blood. The generated bicarbonate is then taken up from blood by the pancreas and excreted into the small intestine with pancreatic secretions, where it neutralizes the HCl that has entered the duodenal lumen from gastric emptying. Any gastric or abomasal outflow obstruction (e.g. gastric dilation volvulus in dogs or left or right displaced abomasum in ruminants) or vomiting of gastric contents in small animals will prevent HCl from entering the duodenum and the stomach-generated bicarbonate in blood will not be neutralized resulting in hypochloremia and metabolic alkalosis (high bicarbonate in blood). Gastric/abomasal excretions can also contain sodium and potassium, resulting in loss of these electrolytes as well (to a far lesser extent than HCl).
1. Stomach: In the gastric parietal cell, hydrogen and bicarbonate are generated from water and carbon dioxide (which freely filters into cells from blood) by carbonic anhydrase. The hydrogen is actively pumped out into the gastric lumen via a hydrogen/potassium ATPase pump at the luminal surface. Chloride also exits into the gastric lumen, with potassium or sodium, and combines with hydrogen forming hydrochloric acid. The chloride is obtained by the parietal cell from blood and exchanges with bicarbonate (generated by carbonic anhydrase) via a basolateral chloride/bicarbonate exchanger (the energy for which is derived from a basolateral sodium/potassium pump). Most of the sodium and potassium are resorbed into the parietal cell. In this way, blood leaving the stomach is “rich” in bicarbonate.
2. Intestine: With a normal functioning stomach, the secreted Hcl enters the duodenum on gastric emptying. Exocrine pancreatic cells take up the bicarbonate from blood leaving the stomach, in exchange for chloride. The bicarbonate is then actively excreted into the pancreatic secretions. Once these enter the duodenal lumen, the bicarbonate neutralizes the hydrogen in hydrochloric acid, forming carbonic acid, then water and carbon dioxide, and the released chloride is resorbed.

In this way bicarbonate is “generated” in stomach blood vessels and “extracted” in pancreatic vessels, resulting in a neutral pH in blood leaving the duodenum. Similarly, chloride is “extracted” from blood in the stomach and “returned” to blood in the duodenum. Inability of the body to neutralize the hydrochloric acid results in retention of bicarbonate in blood (with concurrent loss of chloride) and a metabolic alkalosis. Note, vomiting of duodenal contents (containing pancreatic bicarbonate-rich secretions) will result in a hyperchloremic bicarbonate loss acidosis.

A gastric chief cell (or peptic cell, or gastric zymogenic cell) is a type of cell in the stomach that releases pepsinogen and gastric lipase and is the cell responsible for secretion of chymosin in ruminants.[1] The cell stains basophilic upon H&E staining due to the large proportion of rough endoplasmic reticulum in its cytoplasm. Gastric chief cells are generally located deep in the mucosal layer of the stomach lining.

Chief cells release the zymogen (enzyme precursor) pepsinogen when stimulated by a variety of factors including cholinergicactivity from the vagus nerve and acidic condition in the stomach. Gastrin and secretin may also act as secretagogues.[2]

It works in conjunction with the parietal cell, which releases gastric acid, converting the pepsinogen into pepsin.

TABLE 55-1 Normal Gastrointestinal Motility: Functions at Different Anatomic Levels

Stomach and Small Bowel

Synchronized MMC in fasting

Accommodation, trituration, mixing, transit

Stomach ∼3 h

Small bowel ∼3 h

Ileal reservoir empties boluses

Colon: Irregular Mixing, Fermentation, Absorption, Transit

Ascending, transverse: reservoirs

Descending: conduit

Sigmoid/rectum: volitional reservoir

Abbreviation: MMC, migrating motor complex.

Functions are:

To continue the digestion of carbohydrates initiated by the amylase of saliva,
To add an acidic fluid to the ingested food and mixing its contents into a viscous mass called chyme by the churning activity of the muscularis,
To begin digestion of triglycerides by a secreted lipase
To promote the initial digestion of proteins with the enzyme pepsin.

Parietal cells

Produce intrinsic facter. Intrinsic factor, is a glycoprotein, necessary for the absorption of vitamin B12 (cobalamin) later on in the small intestine.[3] In humans, the gastric intrinsic factor protein is encoded by the GIF gene.[1]. This vitamin is a cofactor required for DNA synthesis; low levels of vitamin B12 can reduce proliferation of erythroblasts, producing pernicious anemia.

Parietal cells can be damaged by autoimmunity.

The stomach has digestive and endocrine functions.

The stomach helps regulate appetite. ¹ (How???)

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