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Physiology 1 > 32) Regulation and disorders of gastric secretion > Flashcards

32) Regulation and disorders of gastric secretion Flashcards

1
Q

What is the function of the Fundus?

A
  • Allows accomodation to occur
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2
Q

What is the function of the body?

A
  • Secretion of mucus, pepsinogen and HCl
  • It has numerous epithelial cells which contain a number of tubular glands
  • The walls of the glands are lined with parietal cells that secrete HCl and intrinsic factors
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3
Q

What is the function of the antrum?

A
  • Secrets gastrin which mediates HCl secretion
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4
Q

What are the contents of the gastric juice?

A
  • Cations: Na+, K+, Mg2+ and H+
  • Anions: Cl-, HPO42-. SO42-
  • Pepsinogen
  • Lipase
  • Mucus
  • Intrinsic factors
    (pH is around 1-3)
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5
Q

How is gastric acid made in the stomach?

A
  • CO2 and H2O diffuses into the epithelial cells of the stomach where they form H2CO3 (carbonic acid) via the enzyme carbonic anhydrase
  • It acid can then dissociate to form HCO3- (bicarbonate) and H+
  • The bicarbonate ions are transported out of the cell into the blood via secondary active transport which (in return) brings Cl- into the cell (as a result the blood side is a bit more alkaline)
  • The Cl- is released into the stomach lumen via chloride channels
  • A K+/H+ ATPase pump pumps H+ into the stomach lumen and pumps K+ into the epithelial cells
  • THe H+ and Cl- (in the lumen) come together to form HCl which is the gastric juice
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6
Q

What do ECL cells do?

A
  • They release histamine
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7
Q

Why is some of the gastric juice described as resting juice?

A
  • It is not acidic as non-parietal cells secrete HCO3- which increases the pH making it more alkaline
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8
Q

How does mucus affect pH?

A
  • Mucus is alkaline and thick
  • It forms a water-insoluble gel n the epithelial surface which increases HCO3- secretion and protects against H+ secretion
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9
Q

What is renin?

A
  • Renin is an enzyme that is quite important in the digestion of milk at birth
  • Over time renin is replaced by pepsinogen
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10
Q

What is lipase?

A
  • Lipase is an enzyme that digests fats
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11
Q

What is the purpose of intrinsic factor?

A
  • Absorbtion of Vitamin B12
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12
Q

What is the role of gastric acid?

A
  • Kills bacteria
  • Digestion/denaturation of food
  • Acidic pH activates pepsinogen to pepsin for protein digestion
  • Promotes action of gastric lipase and secretion of pancreatic HCO3-
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13
Q

What are the three phases of gastric juice secretion?

A
  • Cephalic phase: At the start (e.g. when we smell or see food and when we are chewing)
  • Gastric phase: In the stomach
  • Intestinal phase: The duodenum
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14
Q

What regulates HCl secretion?

A
  • Neuronal pathways and duodenum hormones
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15
Q

How is HCl secretion regulated?

A
  • Direct pathways: By acting directly on parietal cells to increase acid secretion
  • Indirect pathway: By influencing the secretion of gastrin and histamine which increases acid secretion
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16
Q

How does regulation in the cephalic phase occur?

A
  • ACh stimulates histamine release from the ECL cells
  • ACh acts directly on parietal cells to cause HCl to be released
  • Gastrin stimulates histamine release from ECL cells
  • Gastrin acts directly on parietal cells to promote HCl secretion
17
Q

How does regulation occur at the gastric phase?

A
  • Distension of the stomach causes neuronal reflexes to mouth a vagovagal reflex. There will be an increase in peptide concentration and also an increase in acid secretion
18
Q

How does acid secretion decrease as acidity in the lumen increases?

A
  • Gastrin interacts with ECL cells and cause them to release histamine.
  • This histamine interacts with parietal cells to release HCl.
  • However as more HCl is produced it promotes the somatostatin releasing cell causing them to release more somatostatin
  • This somatostatin interacts with G-cells (to stop them from producing Gastrin), ECL cells (to prevent them from releasing histamine) and parietal cells (to stop them from producing further HCl)
19
Q

How will meals containing proteins regulate gastric secretion?

A
  • A meal containing proteins elicits feedback inhibitory and stimulatory signals which ultimately increases acid secretion via stimulation of gastrin secretion
20
Q

How does regulation occur at the intestinal phase?

A
  • Balances out secretory activity of stomach with absorptive capacities of the small intestines
  • Increased acidity inhibits activity of digestive enzymes, bicarbonate and bile salts
  • High acidity of duodenal contents inhibit acid secretion
  • Distension of the duodenum, hypertonic solution, fatty acids, amino acids, monosaccharides all inhibit acid secretion
  • Thus inhibition of acid secretion in the small intestine depends on composition of chyme, volume of chyme and distension of chyme
21
Q

Why does stimuli in the small intestines decrease acid secretion?

A
  • Intestinal phase stimuli causes a neural reflex that inhibit enteric neurones and so ACh is not produced and cannot work on parietal cells. Hence HCl is not secreted.
  • Intestinal phase stimuli can also release CCK and secretin which have inhibitory mechanisms on G-cells, ECL cells and parietal cells and so in general HCl secretion is decreased.
22
Q

What stimulates the secretion of pepsinogen?

A
  • Inputs from nerve plexus to chief cells which secrete the pepsinogen. Vagal innervation causes pepsinogen secretion
  • There are parallels between gastric acid secretion and pepsinogen secretion
  • This means that stimulators and inhibitors of acid secretion during the cephalic and intestinal phase exert the same effect on pepsinogen secretion
  • Secretion is activated if [H+] is too high
  • It is inactivated by the entry of food into the small intestines
23
Q

Why is pepsin not released in its active form by the chief cells?

A
  • If pepsin were to be released by the chief cells it would proceed to digest the stomach
24
Q

What is the function of pepsin?

A
  • Initiates the breakdown of proteins into peptides

In protein digestion pepsin is not the only enzyme we rely on

25
Q

How does prostaglandin affect the body?

A
  • It inhibits parietal cells causing a decrease in acid secretion
  • It stimulates mucus secreting cells causing more mucus to be secreted
  • It causes vasodilation
26
Q

What are the effects of NSAIDS on prostaglandins?

A
  • NSAIDS inhibit prostaglandins.

- As a result acid secretion increases, vasodilation decreases and mucus production also decreases

27
Q

What are the protective factors that prevent autodigestion of the stomach by HCl and pepsin?

A
  • Mucus layer protects the gastric mucosa from low pH
  • Secretion of alkaline mucus and bicarbonate (HCO3-)
  • Somatostatin inhibits gastrin release and provides a negative feedback control of HCl release
  • Protein buffers
  • Epithelial cells can remove excess H+ via membrane transport systems and tight junctions prevent the diffusion of H+ back
  • Prostaglandins inhibit acid secretion and enhance blood flow
  • Blood flow removes excess acid that has diffused across the epithelial layer into the blood
  • Prostaglandins maintain the mucosal integrity and repair through growth factors
  • Replacement of gastric cells within gastric pits
28
Q

What are the factors responsible for gastric secretions?

A
  • Histamine, ACh, gastrin
  • Food
  • NSAIDS
  • Zollinger-Ellison syndrome
  • Hyperparathyroidism
  • Stress
  • Bile acids
  • Genetics
  • Helicoacter pylori
29
Q

What are symptoms of a peptic (stomach) ulcer?

A
  • Anaemia
  • Black, tarry stool
  • Nausea
  • Dyspepsia (indigestion)
  • Anorexia
  • Vomiting (blood)
  • Epigastric pain
  • Chest discomfort
  • Weight loss
30
Q

How do NSAIDS play a role in gastric secretion disorders?

A
  • NSAIDS are acidic that cause irritation of the gut
  • They impair the barrier property of the mucosa and supress gastric prostaglandin synthesis
  • This decreaes gastric mucosal blood flow and so intereferes iwth the repair of superficial injury
  • It also inhibits platelet aggregation
31
Q

How are ulcers formed?

A
  • There is a breakage of the mucosal barrier as there is too much acid being secreted
  • There is an imbalance between protection and damaging factors of the GI tract
  • Exposure of the tissue to the erosive effects of the gastric acids and pepsin leads to ulcers
32
Q

What are common areas in the alimentary tract where peptic ulcers can occur?

A
  • Distal oesophagus
  • The stomach: Junction of the antrum and body
  • Duodenal cap: First part of the duodenum
  • Meckel’s diverticulum: Bulge in the small intestine
  • Weight loss surgery
33
Q

What are acute peptic ulcers?

A
  • Less common ulcers that develop from areas of corrosive gastritis, severe stress and shock
  • Acute hypoxia of surface epithelium is also associated with acute peptic ulcers
34
Q

What is H. Pylori?

A
  • A gram negative spiral shaped aerobic bacterium
  • It penetrates gastric mucosa and is able to survive harsh conditions in the stomach (i.e. pH of 1-3)
  • They are highly pathogenic with many virulence factors
  • It has flagella that enables it to have a “corkscrew” mechanism that provides it motility allowing it to move towards the gut epithelium
  • They cause peptic ulcer in the digestive tract
35
Q

What are the virulence factors of H. pylori?

A
  • They produce urease which converts urea to ammonia which buffers gastric acid and produces CO2
  • Cytotoxin-associated antigen which inserts the pathogenicity islands and confers ulcer-forming potential
  • Vacuolating toxin A alters the trafficking of intracellular proteins in gastric cells
36
Q

What diagnostic test can be used on someone suspected with peptic ulcer?

A
  • Endoscopy

- Histological examination and staining of an EDG biopsy

37
Q

How can we test for the presence of H. pylori?

A
  • Stool antigen test
  • Evaluate urease activity
  • Urea breath test
38
Q

What are the complications commonly associate with a peptic ulcer?

A
  • Haemorrhage (GI bleeding)
  • Perforation and penetration causing leakage of luminal contents
  • Narrowing of pyloric canal or oesophageal stricture

Physiology 1 (64 decks)

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