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Gastric secretion 2
1. Gastric secretions -2
Dr. Sai Sailesh Kumar G
Associate Professor
Department of Physiology
RDGMC
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2. Learning objectives
List the different types of gastric glands and
indicate their secretions
List the composition and functions of gastric juice
Outline the steps involved in the formation of
gastric acid
Describe the regulation of gastric acid secretion
List different phases of gastric acid secretion and
factors influencing them
Outline the basis of various forms of treatment for
acid peptic disease DR Sai Sailesh Kumar G 2
3. Phases of Gastric secretion
Gastric secretion occurs in three phases
1. Cephalic phase
2. Gastric phase
3. Intestinal phase
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4. Cephalic Phases
Occurs even before food enters stomach
Especially while it is being eaten
It results from sight, smell, thought or taste of
food
Greater the appetite, more intense is stimulation
This phase of secretion normally accounts for
about 30% of gastric secretion associated with
eating a meal
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5. Regulation of Cephalic Phases
Neurogenic signals that cause the cephalic
phase originates in
1. Cerebral cortex
2. Appetite centers of amygdala
3. hypothalamus
Signals transmitted through dorsal motor
nucleus of vagus
Then through vagus nerve to stomach
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8. Sham feeding
In classic “sham” feeding studies performed on
dogs equipped with an oesophageal stoma and a
gastric fistula, Pavlov demonstrated that food
was a prompt and powerful stimulant of gastric
secretion.
This stimulation occurred despite the fact that
the ingested food entered the dog's mouth and
pharynx and exited through the stoma, never
actually reaching the stomach
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9. Gastric Phases
Occurs once food enters stomach
Causes secretion of gastric juice during several
hours while food remains in the stomach
This phase of secretion normally accounts for
about 60% of gastric secretion associated with
eating a meal
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10. Regulation of Gastric Phases
This phase is regulated by
1. Long vago vagal reflex from stomach to brain
and back to stomach
2. Local enteric reflexes
3. Gastrin- histamine mechanism
Signals transmitted through dorsal motor
nucleus of vagus
Then through vagus nerve to stomach
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11. Intestinal Phases
Occurs when food enters upper portion of small
intestine
Particularly in the duodenum
Small amounts of gastric juice secreted
This phase of secretion normally accounts for
about 10% of gastric secretion associated with
eating a meal
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12. Regulation of intestinal Phases
This phase is regulated by
1. Nervous mechanisms
2. Hormonal mechanisms – probably partly
because of small amounts of gastrin released
by duodenal mucosa
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13. inhibition of gastric secretion
Intestinal chyme slightly stimulates the gastric secretion
during the early intestinal phase
It paradoxically inhibits gastric acid secretion at other
times
This inhibition results from
1. Presence of food in the small intestine initiates a
reverse entero gastric reflex
2. Transmitted through myentric nervous system,
sympathetic and vagus nerves that inhibits gastric
secretion
3. Secretin, gastric inhibitory peptide, vasoactive
intestinal poly peptide and somatostatin
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14. Why inhibition?
The inhibitory factors inhibits gastric secretion
and motility
To slow passage of chyme from stomach to
intestine
Which is already filled or already over active
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15. Gastric secretion during inter
digestive period
Inter digestive period – when little or no
digestion occurring anywhere in the gut
Stomach secretes few milliliters of gastric juice
each hour
Non oxyntic type of secretion
Mainly mucus little pepsinogen and no acid
Emotional factors may increase the secretion to
50 ml or more
May leads to peptic ulcer
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16. Secretion and activation of
pepsinogen
Several types of pepsinogen secreted
Basic function is same for all types
Pepsinogen has no digestive activity
When it comes in contact with HCL, it become
activated and become pepsin
Pepsin is a active proteolytic enzyme in highly
acidic medium
HCL is necessary for its action
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17. Regulation of pepsinogen
secretion
Acetyl choline – released from vagus or from
gastric enteric nervous plexus
Acid in the stomach
Acid may not directly stimulate peptic cells
Acid elicit local reflexes that stimulates peptic
cells
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18. Secretion of intrinsic factor
Essential for absorption of vitamin B12 in ileum
Secreted by parietal cells
When parietal cells destroyed
Occurs in person with chronic gastritis
Achlorhydria – lack of acid secretion
Perniciuos anemia – lack of RBC maturation
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19. GIT hormones
GIT is considered as one of the largest endocrine
glands
Around 30 peptide hormone genes are found
Some important hormones
1. Gastrin
2. Secretin
3. Cholecystokinin
4. Gastric inhibitory peptide
5. Motillin
6. Peptide YY
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20. Gastrin
Secreted by: G cells in the antrum of stomach
and duodenum
Primary stimulus: stretch, peptides and amino
acids, vagus
Functions
1. Increases gastric HCL
2. Increase in gastric mixing
3. Increase in lower GIT motility
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21. Secretin
Secreted by: S cells of duodenum
Primary stimulus: Acidic chyme
Functions
1. Increases pancreatic buffer secretion
2. Increase in biliary and small intestine buffer
secretion
3. Decrease in gastric motility
4. Decrease in gastric HCL
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22. CCK
Secreted by: I cells of duodenum and jejunum
Primary stimulus: Small peptides, amino acids and
fats
Functions
1. Increases pancreatic enzyme secretion
2. Increase in pancreatic and biliary buffer secretion
3. Contraction of gall bladder
4. Relaxation of sphincter of oddi
5. Decrease gastric emptying
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23. Gastric inhibitory peptide
Secreted by: Duodenum and jejunum
Primary stimulus: Fatty acids, amino acids and
glucose
Functions
1. Decreases gastric HCL secretion
2. Increase in pancreatic insulin secretion
3. Decrease gastric emptying
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24. Peptic ulcer
Excoriated area of stomach or intestinal mucosa
Primary cause:
1. Digestive action of gastric juice
2. Or upper small intestine secretion
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26. Basic cause
Imbalance between the rate of secretion of
gastric juice and degree of protection offered by
1. Gastroduodenal mucosal barrier
2. Neutralization of gastric acid by duodenal
juices
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27. Specific causes
Helicobacter pylori infection
1. Break down of Gastroduodenal mucosal barrier
2. Stimulation of gastric acid secretion
3. About 75% of cases are due to this bacterial
infection
4. This infection last life time unless eradicated by
anti bacterial therapy
5. This bacteria can penetrate the gastric mucosal
barrier
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28. Other causes
Smoking – increases nervous stimulation of
stomach secretory glands
Consumption of alcohol – breakdown mucosal
barrier
Consuming asprin and other NSAIDs –
breakdown of mucosal barrier
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29. Treatment
1. Use of antibiotics along with other agents to kill
infectious bacteria
2. Administration of gastric suppresant drugs
Ranitidine – antihistaminic agent – blocks stimulatory
effect of histamine on gastric glands (histamine 2
receptors)
Omeprazole – proton pump inhibitors
1. Neutralize the gastric acids with antacids
2. Use of bismuth products that enhances mucosal barrier
3. Quitting smoking, alcohol consumption
4. Stress management
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