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Embryology, Anatomy & Physiology of Stomach

Embryologic Development of the Stomach

Key Points

  1. Origin and Formation
    • The stomach arises from the embryonic endoderm.
    • It forms a portion of the foregut along with the esophagus, the first portion of the duodenum, liver, bile ducts, and pancreas.
    • During the fourth week of gestation, the foregut is oriented as a craniocaudal tube, with the primitive stomach and first portion of the duodenum forming the caudal end.
  2. Mesogastrium and Suspensory Structures
    • The ventral and dorsal mesogastrium attach to the stomach anteriorly and posteriorly, suspending it in the peritoneal cavity.
    • The greater and lesser curvatures of the stomach are formed due to the faster growth rate of the dorsal portion of the gastric wall compared to the ventral portion.
  3. Foregut Rotation (Weeks 7-8)
    • Around weeks 7 and 8, the foregut rotates 90 degrees clockwise on its long axis.
    • This rotation positions the ventral mesogastrium to the right of the stomach and the dorsal mesogastrium to the left.
  4. Development of the Omenta
    • Ventral Mesogastrium: Forms the lesser omentum, which includes the gastrohepatic and hepatoduodenal ligaments, and contains the liver.
    • Dorsal Mesogastrium: Develops into the greater omentum, which includes the gastrophrenic, gastrosplenic, and gastrocolic ligaments, and contains the spleen.
  5. Positioning of Vagal Nerve Trunks
    • The rotation positions the left vagal nerve trunk anterior to the stomach and the right vagal nerve trunk posterior to it (LARP: Left Anterior, Right Posterior).
  6. Descent of the Stomach
    • The stomach descends as cephalad structures grow and is eventually located between the T10 and L3 vertebral levels in the adult.

Multiple Choice Question (MCQ)

Answer: c. Left vagal trunk is anterior to the stomach

Explanation:

  • The rotation of the foregut positions the left vagal nerve trunk anterior to the stomach and the right vagal nerve trunk posterior to it. This is summarized by the mnemonic LARP: Left Anterior, Right Posterior. The ventral mesogastrium forms the lesser omentum, and the dorsal mesogastrium forms the greater omentum.

Summary Table

Developmental Origin Final Position/Function
Stomach Embryonic endoderm (foregut) Between T10 and L3 in the adult
Ventral Mesogastrium Foregut mesentery Forms lesser omentum
Dorsal Mesogastrium Foregut mesentery Forms greater omentum
Left Vagal Nerve Trunk Positioned anterior to stomach
Right Vagal Nerve Trunk Positioned posterior to stomach

Gross Anatomy and Anatomic Relationships of the Stomach

Key Points

  1. Location and Borders
    • The stomach is a dilated cylindrical J-shaped organ.
    • Located in the epigastric and left hypochondrial region at the level of the first lumbar vertebra (L1).
    • Anterior Borders: Left hemidiaphragm, left lobe of the liver, part of the right lobe of the liver, parietal portion of the anterior abdominal wall.
    • Posterior Borders: Pancreas (neck, body, and tail), left kidney, adrenal gland.
    • Posterolateral Border: Spleen.
    • Inferior Border: Transverse colon.
    • Attached at the gastroesophageal junction superiorly and retroperitoneal duodenum inferiorly.
  2. Ligamentous Attachments
    • Gastrophrenic: Diaphragm.
    • Hepatogastric (lesser omentum): Liver.
    • Gastrosplenic (gastrolienal): Spleen.
    • Gastrocolic (greater omentum): Transverse colon.
  3. Anatomic Regions
    • Cardiac Portion: Just inferior to the abdominal portion of the esophagus and gastroesophageal junction.
    • Fundus: Superior and to the left, forming a cardiac notch with the distal esophagus.
    • Body (Corpus): Extends and curves inferiorly, forming the lesser and greater curvatures.
    • Gastric Antrum: Region from the angular notch to the pyloric canal.
    • Pyloric Canal: Leads to the pyloric sphincter, which empties into the first portion of the duodenum.

  4. Muscularis Externa

    • Composed of three layers:

      • Outermost Longitudinal Layer: Concentrated proximally at the gastroesophageal junction and along the curvatures.
      • Middle Circular Layer: Covers the stomach completely, contiguous with the lower esophageal sphincter and thickened at the pylorus.
      • Innermost Oblique Layer: Blended with the circular layer at the collar of Helvetius, covering the anterior and posterior gastric walls incompletely.

      **in Hellers myotomy we only cut the clasp fibres but not the sling fibres because sling fibres help in maintenance of LES during contraction.**

      in Hellers myotomy we only cut the clasp fibres but not the sling fibres because sling fibres help in maintenance of LES during contraction.

  5. Additional Layers

    • Submucosa: Strength layer of the gastric wall (MCQ).
    • Muscularis Mucosae: Below the submucosa.
    • Mucosa: Contains the lamina propria, blood vessels, and mucosal epithelium.
    • Rugae: Irregular folds on the inner surface to increase surface area and allow expansion.

Multiple Choice Question (MCQ)

Answer: a. Muscularis externa is composed of outer longitudinal and inner circular layer.

Explanation:

  • The muscularis externa of the stomach wall comprises three layers: the outermost longitudinal layer, the middle circular layer, and the innermost oblique layer. Therefore, statement (a) is false as it does not account for the oblique layer.

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Vascular, Lymphatic, and Neural Supply to the Stomach

Key Points

  1. Vascular Supply

    • Arterial Supply:
      • Celiac Trunk: Primary source.
      • Left Gastric Artery: Branches from the celiac trunk, courses along the lesser curvature, and anastomoses with the right gastric artery (branch of the common hepatic artery).
      • Gastroduodenal Artery: Branches from the common hepatic artery, supplies the greater curvature via the right gastroepiploic artery.
      • Left Gastroepiploic Artery: Branches from the splenic artery, supplies the proximal greater curvature, and anastomoses with the right gastroepiploic artery.
      • Short Gastric Arteries: Branch from the splenic hilum, supplying the fundus and proximal body.

    • Venous Drainage:

      • Lesser Curvature: Drained by left and right gastric veins into the portal vein.
      • Greater Curvature: Drained by the right gastroepiploic vein (into the superior mesenteric vein) and the left gastroepiploic vein (into the splenic vein).
      • Short Gastric Veins: Drain into the splenic vein.
      • Portal Vein Formation: Splenic vein joins the superior mesenteric vein.

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  2. Lymphatic Drainage

    • Cardia and Proximal Lesser Curvature: Drain to superior gastric lymph nodes near the left gastric artery.
    • Distal Lesser Curvature: Drains into the suprapyloric lymph nodes.
    • Fundus and Proximal Greater Curvature: Drained by pancreaticosplenic nodes near the splenic hilum.
    • Distal Greater Curvature, Antrum, and Pylorus: Drain to the subpyloric lymph nodes.
    • Ultimate Drainage: Celiac axis nodal basin, then to the cisterna chyli nodes and into the thoracic duct.

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  3. Neural Supply

    • Parasympathetic Innervation:
      • Originates in the dorsal motor nucleus.
      • Travels via left and right vagus nerves (anterior and posterior to the esophagus, respectively).
      • Synapses at the myenteric (Auerbach) plexus and submucosal (Meissner) plexus.
    • Sympathetic Innervation:
      • Presynaptic fibers travel in the sympathetic chain alongside the eighth to tenth thoracic vertebrae.
      • Synapse in the splanchnic (celiac) ganglia.
      • Terminate in the gastric neuronal plexuses.
    • Enteric Nervous System (ENS):
      • Functions autonomously.
      • Afferent fibers travel via vagus nerve, synapsing in the nucleus of the solitary tract.

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Microscopic Anatomy

Key Points

  1. Gastric Mucosa
    • Characterized by simple columnar epithelium (SCE) uniformly lining the stomach.
    • Surface mucous cells (SMs) form gastric pits (GPs) leading to long, branched, tubular glands, giving a leafy appearance termed gastric foveolae.
    • Each gland has distinct regions: gastric pit, isthmus, neck, and base.
  2. Glandular Regions and Cell Types
    • Cardiac Glands: Located in the cardia.
      • Composed of mucous cells, a few scattered parietal cells, undifferentiated cells in the neck, and a majority of endocrine cells at the base.
      • Function: Producing mucus.
    • Oxyntic Glands: Located in the fundus and body.
      • Surface epithelial cells.
      • Mucous cells in the GPs, isthmus, and neck.
      • Parietal cells secrete hydrochloric acid (HCl) and intrinsic factor, heavily concentrated in the neck.
      • Basal chief (zymogenic) cells secrete pepsinogen.
      • Enterochromaffin-like (ECL) cells produce histamine, stimulating parietal cell acid production.
    • Antral Glands: Located in the pyloric portion.
      • Lack acid-producing cells.
      • Higher proportion of gastrin-secreting G cells.
      • Functions of the Gastric Antrum
        • Does not secrete acid: Unlike the body and fundus, the antrum lacks acid-producing cells.
        • Contains gastrin-secreting G cells: These cells stimulate acid production in the body and fundus.
        • Lymphatic Drainage: Drains towards Station 5 (suprapyloric nodes) and Station 6 (subpyloric nodes).
        • Anatomical Extent: Extends from the incisura angularis to a point along the inferior line to the distal greater curvature.
    • Chief Cells: Located primarily in the body of the stomach.
    • D Cells: Found in the fundus and body, secrete somatostatin.
    • G Cells: Found in the antrum, secrete gastrin.
    • A/X Cells: Located in the body, secrete ghrelin.
  3. Oxyntic Glands Functions
    • Parietal cells: Secrete HCl and intrinsic factor.
    • Chief cells: Secrete pepsinogen.
    • ECL cells: Produce histamine.

**Mucous Neck Cells [ not surface cells] are the stem cells (pluripotent) which can evolve into any kind of gastric cells.**

Mucous Neck Cells [ not surface cells] are the stem cells (pluripotent) which can evolve into any kind of gastric cells.

Multiple Choice Question (MCQ)

Answer: a and d

Explanation:

  • Oxyntic glands are located in the fundus and body of the stomach (answer a).
  • Enterochromaffin-like (ECL) cells in oxyntic glands secrete histamine, a powerful stimulus for acid production by parietal cells (answer d).
  • Parietal cells are not located at the surface of the glands; they are heavily concentrated in the neck.
  • Chief cells secrete pepsinogen, not intrinsic factor.

Summary Table

Gland Type Location Main Cell Types Functions
Cardiac Cardia Mucous cells, few parietal cells Produce mucus
Oxyntic Fundus and body Surface epithelial, mucous, parietal, chief, ECL cells Acid production (HCl), intrinsic factor, pepsinogen, histamine
Antral Pyloric portion Gastrin-secreting G cells Secrete gastrin, no acid production

Multiple Choice Questions (MCQ)

Explanation:

  • The gastric antrum does not secrete acid; it lacks acid-producing parietal cells. Instead, it contains G cells that secrete gastrin.

Answer: c. A/X cells - gastric body

Explanation:

  • A/X cells (also known as ghrelin-secreting cells) are located in the body of the stomach within the oxyntic glands.

Summary Table

Cell Type Primary Anatomic Location Function
Chief Cells Gastric body Secrete pepsinogen
D Cells Gastric fundus and body Secrete somatostatin
A/X Cells Gastric body Secrete ghrelin
G Cells Gastric antrum Secrete gastrin
Parietal Cells Gastric body Secrete HCl and intrinsic factor
Mucin-secreting Gastric cardia Produce mucus

Mucosal Protective Factors in the Stomach

Key Points

  1. Blood Flow
    • Function: Buffering effect minimizes the effect of luminal acid. Delivery of nutrients allows rapid turnover of epithelium.
    • Source: Systemic circulation.
  2. Bicarbonate Mucus
    • Function: Acid buffering, creates an "unstirred layer" as a physical barrier between luminal contents and epithelium. Concentrates bicarbonate creating an alkaline layer.
    • Source: Epithelial cells, surface, and gland mucous cells.
  3. Prostaglandins (PGE₂, PGI₂)
    • Function: Increase mucosal blood flow and reduce acid production locally.
    • Source: COX-1 and COX-2 expressing epithelial cells.
  4. Neuropeptides (Bombesin)
    • Function: Increase prostaglandin production (induces expression of COX-2).
    • Source: Nonadrenergic, noncholinergic efferent neurons.

Multiple Choice Question (MCQ)

Which of the following are gastric mucosal protective barriers except?

a. Trefoil factor

b. PGE₂, PGI₂

c. Bombesin

d. None of the above

Answer: d. None of the above

Explanation:

  • Trefoil factor, prostaglandins (PGE₂, PGI₂), and neuropeptides like bombesin all contribute to the protective mechanisms of the gastric mucosa. Trefoil factors are involved in epithelial restitution and repair, prostaglandins increase mucosal blood flow and bicarbonate production, and bombesin stimulates prostaglandin production.

Summary Table

Protective Factor Function Source
Blood Flow Buffers effect of luminal acid, delivers nutrients for rapid epithelial turnover Systemic circulation
Bicarbonate Mucus Acid buffering, creates a physical barrier between luminal contents and epithelium Epithelial cells, surface, and gland mucous cells
Prostaglandins Increase mucosal blood flow, reduce acid production locally COX-1 and COX-2 expressing epithelial cells
Neuropeptides Increase prostaglandin production (induces expression of COX-2) Nonadrenergic, noncholinergic efferent neurons
Trefoil Factor Epithelial restitution and repair Gastric mucosa

Physiology of Stomach

Mechanisms of Acid Production in the Stomach

Key Points

  1. Stimulation and Regulation of Acid Secretion
    • G Cells: Secrete gastrin, which stimulates acid production by binding to CCK-B receptors on parietal cells and ECL cells.
    • D Cells: Secrete somatostatin in response to antral acidification, inhibiting acid production.
    • ECL Cells: Secrete histamine, which stimulates acid production by increasing cAMP levels in parietal cells.
    • Parietal Cells: Produce hydrochloric acid (HCl) through the action of H+/K+ ATPase.
  2. Key Pathways and Receptors
    • Histamine: Binds to H2 receptors on parietal cells, stimulating adenylate cyclase, increasing cAMP, and activating protein kinases that enhance acid secretion.
    • Acetylcholine (Ach): Binds to M3 receptors on parietal cells and ECL cells, activating phospholipase C (PLC), leading to the release of intracellular calcium and further stimulating acid production.
    • Gastrin: Binds to CCK-B receptors, stimulating PLC and increasing intracellular calcium, which promotes acid secretion.
  3. Regulatory Mechanisms
    • Somatostatin: Inhibits acid production by acting on D cells and ECL cells, reducing histamine release and direct inhibition on parietal cells.
    • Secretin and CCK: Generally inhibit gastric acid secretion and are involved in the regulation of pancreatic enzyme secretion and bile flow.

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Figures Explanation

  • Figure 56.8: Illustrates the intracellular events in parietal cells during acid production, showing the roles of histamine, acetylcholine, and gastrin in stimulating H+/K+ ATPase activity.
  • Figure 56.9: Depicts the central role of ECL cells in regulating acid secretion, including the interactions between G cells, D cells, and vagal stimulation.

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Multiple Choice Question (MCQ)

Answer: a. Antral acidification stimulates D cells to secrete somatostatin.

Explanation:

  • Antral acidification: Stimulates D cells to secrete somatostatin, which inhibits further acid production.
  • Secretin and CCK: Generally inhibit gastric acid secretion, contrary to option (b). These hormones play a significant role in regulating pancreatic enzyme secretion and bile flow.
  • Histamine: Stimulates acid production by binding to H2 receptors and increasing cAMP levels, not intracellular Ca²⁺ concentration.
  • Acetylcholine (Ach): Stimulates acid secretion by increasing intracellular Ca²⁺ concentration through M3 receptor activation, not cAMP production.

Summary Table

Pathway Receptor Mechanism Effect
Histamine H2 receptor Increases cAMP Stimulates acid production
Acetylcholine (Ach) M3 receptor Increases intracellular Ca²⁺ Stimulates acid production
Gastrin CCK-B receptor Increases intracellular Ca²⁺ Stimulates acid production
Somatostatin Somatostatin receptor Decreases histamine and acid production By cAMP Inhibits acid production
Secretin and CCK Various receptors Generally inhibit gastric acid secretion Inhibits acid production (primarily)

Vitamin B12 is initially bound to haptocorrin (R factor)after which exposure to higher pH and proteolytic enzymes of the duodenum dissociates haptocorrin-B12 complex and allows for intrinsic factor binding

Gastric Motility

Migratory Motor Complex (MMC) in the Stomach

Key Points

  1. MMC Function and Phases
    • Function: MMC is responsible for moving indigestible items in its lumen further along the digestive tract during the fasting state.
    • Phases:
      • Phase I: Motor quiescence, little to no contractile activity.
      • Phase II: Irregular contractions, increasing in intensity and frequency.
      • Phase III: Strong, regular propulsive contractions that propagate distally.
    • Duration: The entire MMC cycle occurs every 90-120 minutes, with phase III contractions lasting about 5-10 minutes.
  2. Feeding vs. Fasting State
    • Fasting State: MMC operates to clear the stomach and small intestine of residual undigested material.
    • Feeding State: MMC is suppressed; stomach transitions to a different motility pattern to aid digestion and emptying of ingested food.
  3. Hormonal Regulation
    • Motilin: Primary hormone regulating MMC. It peaks during phase III contractions and stimulates strong peristaltic waves.
  4. Adaptive and Receptive Relaxation
    • Adaptive Relaxation: Mediated by stretch receptors through a local reflex arc, not abolished by vagotomy.
    • Receptive Relaxation: Mediated by food and cholinergic vagal efferent fibers, abolished by vagotomy.
  5. Post Feeding State
    • Emptying of Solids and Liquids:
      • Liquids empty faster than solids.
      • Intragastric pressure and gastric distension regulate the emptying of liquids.
      • Antral propulsive contractions regulate the emptying of solids.
    • Postoperative Ileus: Mediated by vagal efferent fibers and CGRP (calcitonin gene-related peptide).

Multiple Choice Questions (MCQs)

1. Which of the following statements is false regarding MMC in the stomach?

a. Process by which stomach empties its content during feeding state.

b. Duration is about 5-10 minutes.

c. Most are phase III contractions.

d. Adaptive relaxation is abolished during vagotomy.

Answer: a and d

Explanation:

  • a. MMC operates during the fasting state, not the feeding state.
  • d. Adaptive relaxation is not abolished by vagotomy; it is mediated by stretch receptors through a local reflex arc.

2. MMC is regulated by which hormone?

a. Ghrelin

b. Bombesin

c. Motilin

d. Gastrin

Answer: c. Motilin

Explanation:

  • Motilin is the primary hormone regulating the MMC, with peak levels corresponding to the initiation of phase III contractions.

Summary Table

Aspect Details
MMC Phases Phase I (quiescence), Phase II (irregular contractions), Phase III (strong propulsive contractions)
Duration 90-120 minutes cycle, with phase III lasting 5-10 minutes
State of Operation Fasting state (disappears during feeding)
Hormonal Regulation Motilin
Adaptive Relaxation Mediated by local reflex arc, not abolished by vagotomy
Receptive Relaxation Abolished by vagotomy
Post Feeding State Differential emptying of solids and liquids, antral contractions for solids

Gastric Varices

Key Points on Gastric Varices

  1. Development and Causes
    • Gastric varices develop due to increased flow in short and posterior gastric veins.
    • They are more often associated with portal hypertension than splenic vein thrombosis.
    • Isolated gastric varices are typically due to splenic vein thrombosis rather than portal hypertension.
  2. Management
    • Isolated gastric varices due to splenic vein thrombosis are best managed with splenectomy.
    • Endoscopic banding is not the preferred treatment for isolated gastric varices.

Multiple Choice Question (MCQ)

Answer: a and d

Explanation:

  • a. Gastric varices develop due to increased flow in the short and posterior gastric veins.
  • d. Gastric varices are more commonly associated with portal hypertension than splenic vein thrombosis.

Phases of Gastric Acid Secretion

  1. Cephalic Phase
    • Triggered by the sight, smell, taste, and thought of food.
    • Mediated by vagal stimulation.
    • Contributes about 30% of total acid secretion.
  2. Gastric Phase
    • Triggered by the presence of food in the stomach.
    • Stimulated by luminal amino acids, peptides, and gastric distension.
    • G cells secrete gastrin, which significantly increases acid secretion.
    • This phase accounts for the maximum gastric acid secretion, contributing about 60%.
  3. Intestinal Phase
    • Triggered by the presence of chyme in the small intestine.
    • Contributes to a smaller portion of total acid secretion.
    • Helps to maintain a normal basal level of acid secretion.

Multiple Choice Question (MCQ)

Answer: b. Gastric phase

Explanation:

  • The gastric phase has the maximum gastric acid secretion due to stimulation by luminal amino acids, peptides, and gastric distension, leading to significant gastrin release from G cells.

Summary Table

Aspect Details
Gastric Varices Development Increased flow in short and posterior gastric veins
Common Cause Portal hypertension
Isolated Varices Cause Splenic vein thrombosis
Management of Isolated Varices Splenectomy
Maximum Acid Secretion Phase Gastric phase
Cephalic Phase Vagal stimulation, 30% of acid secretion
Gastric Phase Luminal amino acids, peptides, gastric distension, 60% of acid secretion
Intestinal Phase Normal basal level of acid secretion