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MISS. KALYANI R. SAUDAGAR
Anatomy
■ Appears in week 5.
■ • A pliable, saccular organ.
■ • Located in the LUQ and epigastrium.
■ • Separated from the GI tract (2 locations).
Gross Anatomy
■ Proximal= Cardia (attaches to esophagus) attaches at the LES.
■ • Fundus= most superior portion, receives food.
■ • Body= largest portion, contains parietal, chief and ECL cells.
■ • Distal= antrum, contains the G cells.
Anatomy
■ The stomach is almost entirely covered with peritoneum.
■ • The peritoneum forms the outer gastric serosa.
■ • Beneath the serosa is the muscularis propria.
■ • The MP is made up of 3 layers of
■ smooth muscle.
■ • The middle layer is the circular muscle and is the only “complete” layer of muscle
■
■ As you progress distally the middle layer of muscle begins to thicken and form the __________?
Which functions as a true sphincter.
■ • This and the GE junction form the gastric “borders” and are the two “fixed” points of the
stomach.
■ • The outer muscle layer (longitudinal) is contiguous with the outer layer of the esophagus.
■ Within the layers of the MP, there is a rich plexus of autonomic nerves and ganglia
called_______________.
■ • The submucosa lies between the MP and the mucosa. It is a collagen rich layer of connective
tissue and is the weakest/strongest layer of the gastric wall.
■ • The submucosa also contains the rich blood vessel network and the lypmhatics as well as
Meissner’s plexus.
■ The mucosa consists of 3 layers:
• Surface epithelium (columnar).
• Lamina propria
• Connective tissue layer that supports the surface epithelium.
■ • Muscularis mucosae (probably the reason for rugal folds).
•The MM is the boundary for invasive/noninvasive gastric cancer.
Anatomy/Morphology
Anatomy/Morphology
Cell Types
■ Parietal:
• Location: Body
• Function: secrete acid and intrinsic factor
■ • Mucus:
• Location: Body, Antrum
• Function: mucus production
■ • Chief:
• Location: Body
 • Function: produce Pepsin
 Surface epithelium:
• Location: Diffuse
• Function: produce mucus, bicarb, prostaglandins(?)
■ • ECL:
• Location: Body
• Function: Histamine production
■ • G cells:
• Location: Antrum
• Function: Gastrin production
■ D cells:
• Location: Body, Antrum
• Function: produce Somatostatin
■ • Gastric mucosal interneurons:
• Location: Body, Antrum
• Function: produce Gastrin-releasing peptide
■ • Entric Neurons:
• Location: Diffuse
• Function: CGRP, others production
Vascular Supply
■ R&L gastrics
■ • R&L gastroepiploics
■ • Short gastrics
■ • Inferior phrenics
■ • Gastroduodenal
■ • Venous drainage:
■ • R&L gastric veins drain to the portal, R gastroepiploic drains to the SMV, L ge drains to the
splenic
Nerve supply
Gastric Physiology
■ Principle Function:
• Storage:
•Receptive relaxation
• Start digestion:
•Separates meal into fat/protein/carbohydrates
■ Regulation of Function
• The stomach is under both neural and hormonal control.
Gastric Hormones
■ Gastric Hormones:
• Chemical messengers that regulate intestinal and pancreatic function.
■ • The “gut” is the largest endocrine organ in the body.
■ • The messengers can act as:
• Endocrine: distant target
• Paracrine: close target
• Autocrine: self target
• Neurocrine: neurotransmitter or stimulator.
■ Gastric Hormones:
• Synthesized as inactive precursors
• Converted to active form by post-translational modification
• #1 stimulus for release is: FOOD
• Composition of food dictates timing and specific hormone release.
■ Gastric Hormones:
• Inhibition:
•Removal of stimulus
• Negative feed-back loops
•Inhibitory peptides, ie. Somatostatin
Gastrin
• Somatostatin
• Gastrin-releasing peptide (GRP)
• Histamine
Gastrin
■ Synthesis: G-cells in the antrum
• Release:
• AA, protein, vagal tone, antral distention, GRP, pH > 3.0, ETOH, Histamine.
• Inhibition:
• pH < 3.0, somatostatin, secretin, CCK, VIP, GIP, glucagon.
• Target cells:
• Parietal and Chief cells
Action(s):
• Stimulates acid secretion
• Direct action on parietal cells
• Potentiating interaction with histamine
• Possible: releasing of histamine
• Increases release of lytes & water from stomach, pancreas, liver and Brunner’s glands
• Stimulates motility in stomach, intestine, and gall bladder
• Inhibits contraction of pylorus and sphincter of Oddi.
■ • Stimulates GI mucosal growth.
Somatostatin
■ Tetradecapeptide
■ • Synthesis:
• CNS, antrum, fundus, sm. bowel, colon, and D-cells in pancreas.
• Release:
• Antral acidification
• Fats, protein, acid in duodenum
• Pancreatic: glucose, amino acids, CCK
• Inhibition:
• Release of acetyl-choline from vagal nerve fibers
Action(s):
• The “master off switch”
• Inhibits the release of most GI hormones
• Inhibits pancreatic and GI secretion(s)
• Inhibits intestinal motility.
• Clinical:
• Octreotide- decrease fistula output
• Treatment of esophageal variceal bleed
• Can ameliorate symptoms of endocrine tumors
GRP
■ Mammalian equivalent of Bombesin
• Synthesis:
• Gastric antrum, small bowel mucosa
• Release: vagal stimulation
Action(s):
• The “master on switch”
• Stimulates the release of all GI hormones (? Secretin).
• Stimulates GI secretion
• Stimulates GI motility
• * most important: stimulates gastric acid secretion and release of antral gastrin
• Stimulates bowel and pancreatic mucosal growth and stimulates various GI and pancreatic
CA’s
Histamine
■ Stimulates parietal cells
• Found in the acidic granules of ECL cells and resident Mast cells.
• Release is stimulated by:
• Gastrin, acetyl-choline, epinephrine
• Inhibited by Somatostatin.
• ? A necessary intermediary of acid production.
Acid Secretion
■ Two forms:
• Basal Acid Secretion
• Stimulated Acid Secretion
Stimulated Acid Secretion
• Three Phases:
• Cephalic phase
• Gastric phase
• Intestinal Phase
• These phases occur concurrently NOT consecutively.
Cephalic Phase
■ Originates with the sight, smell, thought or taste of food.
■ • Stimulates the cortex and hypothalamus.
■ • Signals cause Vagus to release Ach, Ach causes increase in parietal cell acid production.
■ • Accounts for 20-30% of acid production.
Gastric Phase
■ Begins when food enters the gastric lumen (gastric distention).
■ • Digestion products stimulate the G cells, they release gastrin, parietal cells release acid.
■ • Distention alone can increase acid production.
■ • Accounts for 60-70% of acid production.
■ • Phase lasts until the stomach is empty.
Intestinal Phase
■ Poorly understood.
■ • (?) initiated by chyme entering the small bowel.
■ • Accounts for ~10% of acid production.
Other functions
■ Gastric acid suppression
■ • Mucosal protection
■ • B12 absorption

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Stomach

  • 1. MISS. KALYANI R. SAUDAGAR
  • 2. Anatomy ■ Appears in week 5. ■ • A pliable, saccular organ. ■ • Located in the LUQ and epigastrium. ■ • Separated from the GI tract (2 locations).
  • 3. Gross Anatomy ■ Proximal= Cardia (attaches to esophagus) attaches at the LES. ■ • Fundus= most superior portion, receives food. ■ • Body= largest portion, contains parietal, chief and ECL cells. ■ • Distal= antrum, contains the G cells.
  • 5. ■ The stomach is almost entirely covered with peritoneum. ■ • The peritoneum forms the outer gastric serosa. ■ • Beneath the serosa is the muscularis propria. ■ • The MP is made up of 3 layers of ■ smooth muscle. ■ • The middle layer is the circular muscle and is the only “complete” layer of muscle ■ ■ As you progress distally the middle layer of muscle begins to thicken and form the __________? Which functions as a true sphincter. ■ • This and the GE junction form the gastric “borders” and are the two “fixed” points of the stomach. ■ • The outer muscle layer (longitudinal) is contiguous with the outer layer of the esophagus.
  • 6. ■ Within the layers of the MP, there is a rich plexus of autonomic nerves and ganglia called_______________. ■ • The submucosa lies between the MP and the mucosa. It is a collagen rich layer of connective tissue and is the weakest/strongest layer of the gastric wall. ■ • The submucosa also contains the rich blood vessel network and the lypmhatics as well as Meissner’s plexus. ■ The mucosa consists of 3 layers: • Surface epithelium (columnar). • Lamina propria • Connective tissue layer that supports the surface epithelium. ■ • Muscularis mucosae (probably the reason for rugal folds). •The MM is the boundary for invasive/noninvasive gastric cancer.
  • 9. Cell Types ■ Parietal: • Location: Body • Function: secrete acid and intrinsic factor ■ • Mucus: • Location: Body, Antrum • Function: mucus production ■ • Chief: • Location: Body  • Function: produce Pepsin  Surface epithelium: • Location: Diffuse • Function: produce mucus, bicarb, prostaglandins(?) ■ • ECL: • Location: Body • Function: Histamine production
  • 10. ■ • G cells: • Location: Antrum • Function: Gastrin production ■ D cells: • Location: Body, Antrum • Function: produce Somatostatin ■ • Gastric mucosal interneurons: • Location: Body, Antrum • Function: produce Gastrin-releasing peptide ■ • Entric Neurons: • Location: Diffuse • Function: CGRP, others production
  • 11. Vascular Supply ■ R&L gastrics ■ • R&L gastroepiploics ■ • Short gastrics ■ • Inferior phrenics ■ • Gastroduodenal ■ • Venous drainage: ■ • R&L gastric veins drain to the portal, R gastroepiploic drains to the SMV, L ge drains to the splenic
  • 13. Gastric Physiology ■ Principle Function: • Storage: •Receptive relaxation • Start digestion: •Separates meal into fat/protein/carbohydrates ■ Regulation of Function • The stomach is under both neural and hormonal control.
  • 14. Gastric Hormones ■ Gastric Hormones: • Chemical messengers that regulate intestinal and pancreatic function. ■ • The “gut” is the largest endocrine organ in the body. ■ • The messengers can act as: • Endocrine: distant target • Paracrine: close target • Autocrine: self target • Neurocrine: neurotransmitter or stimulator. ■ Gastric Hormones: • Synthesized as inactive precursors • Converted to active form by post-translational modification • #1 stimulus for release is: FOOD • Composition of food dictates timing and specific hormone release.
  • 15. ■ Gastric Hormones: • Inhibition: •Removal of stimulus • Negative feed-back loops •Inhibitory peptides, ie. Somatostatin Gastrin • Somatostatin • Gastrin-releasing peptide (GRP) • Histamine
  • 16. Gastrin ■ Synthesis: G-cells in the antrum • Release: • AA, protein, vagal tone, antral distention, GRP, pH > 3.0, ETOH, Histamine. • Inhibition: • pH < 3.0, somatostatin, secretin, CCK, VIP, GIP, glucagon. • Target cells: • Parietal and Chief cells Action(s): • Stimulates acid secretion • Direct action on parietal cells • Potentiating interaction with histamine • Possible: releasing of histamine • Increases release of lytes & water from stomach, pancreas, liver and Brunner’s glands • Stimulates motility in stomach, intestine, and gall bladder • Inhibits contraction of pylorus and sphincter of Oddi. ■ • Stimulates GI mucosal growth.
  • 17. Somatostatin ■ Tetradecapeptide ■ • Synthesis: • CNS, antrum, fundus, sm. bowel, colon, and D-cells in pancreas. • Release: • Antral acidification • Fats, protein, acid in duodenum • Pancreatic: glucose, amino acids, CCK • Inhibition: • Release of acetyl-choline from vagal nerve fibers Action(s): • The “master off switch” • Inhibits the release of most GI hormones • Inhibits pancreatic and GI secretion(s) • Inhibits intestinal motility. • Clinical: • Octreotide- decrease fistula output • Treatment of esophageal variceal bleed • Can ameliorate symptoms of endocrine tumors
  • 18. GRP ■ Mammalian equivalent of Bombesin • Synthesis: • Gastric antrum, small bowel mucosa • Release: vagal stimulation Action(s): • The “master on switch” • Stimulates the release of all GI hormones (? Secretin). • Stimulates GI secretion • Stimulates GI motility • * most important: stimulates gastric acid secretion and release of antral gastrin • Stimulates bowel and pancreatic mucosal growth and stimulates various GI and pancreatic CA’s
  • 19. Histamine ■ Stimulates parietal cells • Found in the acidic granules of ECL cells and resident Mast cells. • Release is stimulated by: • Gastrin, acetyl-choline, epinephrine • Inhibited by Somatostatin. • ? A necessary intermediary of acid production.
  • 20. Acid Secretion ■ Two forms: • Basal Acid Secretion • Stimulated Acid Secretion Stimulated Acid Secretion • Three Phases: • Cephalic phase • Gastric phase • Intestinal Phase • These phases occur concurrently NOT consecutively.
  • 21. Cephalic Phase ■ Originates with the sight, smell, thought or taste of food. ■ • Stimulates the cortex and hypothalamus. ■ • Signals cause Vagus to release Ach, Ach causes increase in parietal cell acid production. ■ • Accounts for 20-30% of acid production.
  • 22. Gastric Phase ■ Begins when food enters the gastric lumen (gastric distention). ■ • Digestion products stimulate the G cells, they release gastrin, parietal cells release acid. ■ • Distention alone can increase acid production. ■ • Accounts for 60-70% of acid production. ■ • Phase lasts until the stomach is empty.
  • 23. Intestinal Phase ■ Poorly understood. ■ • (?) initiated by chyme entering the small bowel. ■ • Accounts for ~10% of acid production.
  • 24. Other functions ■ Gastric acid suppression ■ • Mucosal protection ■ • B12 absorption