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SGUL - Physiology 1 > Regulation and Disorders of Gastric Secretion > Flashcards

Regulation and Disorders of Gastric Secretion Flashcards

1
Q

Describe the stomach anatomically.

A
  • Made up of a fundus, body, antrum, and pylorus
  • Cardiac area is where the contents of the oesophagus enter the stomach
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2
Q

What does the fundus secrete?

A
  • Pepsinogen and mucus
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3
Q

What do the cardiac and pyloric areas secrete?

A
  • Mucus
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4
Q

What does the body of the stomach contain?

A
  • Chief cells (pepsinogen-secreting)
  • Parietal cells (intrinsic factor-secreting)
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5
Q

What does the antrum secrete?

A
  • Mucus, pepsinogen and gastrin
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6
Q

How is gastric acid made in the stomach lumen? PART 1

A
  • HCO3- is exchanged for Cl- in the blood
  • This decreases the acidity of the venous blood from the stomach
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7
Q

How is gastric acid made in the stomach lumen? PART 2

A
  • Excess Cl- diffuses into the stomach through chloride channels
  • H+ is pumped into the stomach lumen (K+/H+ ATPase pumps H+ out of the stomach lumen).
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8
Q

How is gastric acid made in the stomach lumen? PART 3

A
  • Net effect of PART 1 and 2 is net flow of H+ and Cl- out of the parietal cells and into the stomach lumen.
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9
Q

List some gastric secretions.

A
  • Mucus
  • Rennin
  • Lipase
  • Intrinsic Factor
  • HCl
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10
Q

Describe mucus

A
  • Alkaline
  • Forms a water-insoluble gel on epithelial surfaces, protecting against H+ secretion
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11
Q

Describe rennin

A
  • Curdles milk into casein clots
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12
Q

Describe lipase

A
  • Hydrolyses triglycerides into fatty acids and glycerol
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13
Q

Describe Intrinsic Factor

A
  • Aids in Vitamin B12 absorption
  • Prevents pernicious anaemia
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14
Q

Describe HCl

A
  • Kills bacteria
  • Acid denaturation of digested food
  • Activates pepsinogen (for protein digestion)
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15
Q

What is the direct way in which we can control HCl secretion?

A
  • ACh, gastrin and histamine stimulate the parietal cell directly
  • Triggers secretion of H+ into the lumen.
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16
Q

What is the indirect way in which H+ secretion can be controlled?

A
  • ACh and gastrin also stimulate the ECL cells, resulting in histamine secretion.
  • Histamine then acts on the parietal cell.
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17
Q

What are the three phases of digestion?

A

Cephalic
Gastric
Intestinal

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18
Q

Describe acid secretion regulation during the cephalic phase.

A
  • Smell, sight, taste, chewing, etc. stimulate ACh release.
  • ACh stimulates histamine release from ECL cells.
  • ACh also acts directly on the parietal cells, stimulating HCl secretion.
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19
Q

Acid secretion decreases as the acidity of the lumen increase.
Explain how.

A
  • HCl-stimulating somatostatin-releasing cells (D cells).
  • Somatostatin inhibits ECL and G-cells to curtail the hypersecretion of acid.
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20
Q

Describe acid secretion regulation during the gastric phase. PART 1

A
  • Increased distention of the stomach increases peptide concentration
  • Increases the acidity of the stomach.
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21
Q

Describe acid secretion regulation during the gastric phase. PART 2

A
  • Combination of H+ and proteins decreases the [H+].
  • By acting as a buffer, the proteins remove the inhibitory powers of HCl on gastric secretion.
  • Increases gastrin-mediated acid secretion.
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22
Q

Describe acid secretion regulation during the intestinal phase.

A
  • High acidity of the duodenal contents inhibits acid secretion
  • Increased acidity would inhibit the activity of digestive enzymes, bicarbonate and bile salts
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23
Q

What inhibits acid secretion during the intestinal phase?

A
  • Distention of the duodenum
  • Hypertonic solution (indicating that the food has already been digested)
  • Amino acids, fatty acids, and monosaccharides
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24
Q

What does inhibition of acid secretion in the small intestine depend on?

A
  • Composition and volume of chyme
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25
How is acid secretion inhibited during the intestinal phase?
- Short (within the ENS) neuronal reflexes - Long (vagal) neuronal reflexes - from brain to gut - Hormones (enterogastrones) inhibit acid secretion by the parietal cells or gastrin secretion by the G cells, which is inhibited by somatostatin.
26
What is the effect of increased sympathetic discharge? What is the effect of decreased parasympathetic discharge?
Increased sympathetic discharge is inhibitory. Decreased parasympathetic discharge is stimulatory.
27
List some HCl secretion stimulants or factors that increase HCl secretion.
- histamine - acetylcholine - gastrin - NSAIDs - H. Pylori - hyperparathyroidism - stress
28
[HCl] can reach 150 mM. What does this depend on?
- rate of secretion - amount of buffering - gastric motility - rate of gastric emptying
29
In what ways is HCl essential for life?
- defence - protein digestion: activates pepsinogen to pepsin - stimulates flow of bile and pancreatic juice
30
What is the result of low [HCl]?
- Failure of protein digestion - Achlorhydria - reduced gastric acid secretion
31
What stimulates the secretion of pepsinogen?
- Pepsin is secreted by chief cells in the form of pepsinogen. - Activated if [H+] is high - shape of the enzyme is altered by the high acidity which exposes its active site (allows conversion to occur)
32
What inactivates pepsin secretion?
- Entry of food in the small intestine - HCO3- and peptides neutralise the H+
33
What is the point of pepsin secretion?
Initiates the digestion of proteins by degrading food proteins into peptides
34
What are some symptoms of HCl deficiency?
- presence of undigested food in the stool - white spots on fingernails - drowsiness after meals - increased chances of H. Pylori infection
35
What would be the treatment of HCl deficiency?
- bitter herbs may stimulate HCl secretion - lemon juice and vinegar stimulate HCl secretion - Vit B1 stimulates HCl secretion
36
How do NSAIDs (e.g. aspirin) play a role in gastric acid secretion disorders? PART 1
- Impair the barrier properties of the mucosa by suppressing gastric prostaglandin synthesis. - Decrease gastric mucosal blood flow and inhibit platelet aggregation - Interfere with the repair of superficial injury.
37
How do NSAIDs (e.g. aspirin) play a role in gastric acid secretion disorders? PART 2
- Presence of acid in the stomach promotes NSAID-mediated gastric disorders. - Impairs the restitution (healing) process. - Inactivates FGF (fibroblast growth factor), which interferes with the haemostasis process.
38
Describe the mechanism of peptic (gastric or duodenal) ulcer formation.
- Breakage of the mucosal barrier causes an imbalance between protective and damaging factors. - Exposes tissues to the effects of HCl and pepsin.
39
List some factors predisposing to peptic ulceration.
- H. Pylori - smoking - genetic factors - stress - NSAIDs
40
List some factors that prevent the infection of the gastric mucosa.
- HCl, pepsin - mucus production - peristalsis and fluid movement - IgA secretion at mucosal surfaces - Peyer’s Patches
41
List some protective factors that prevent the autodigestion of the stomach.
- secretion of alkaline mucus and HCO3- - presence of tight junctions between epithelial cells lining the stomach and fibrin coat - replacement of damaged cells within the gastric pits - prostaglandins (E and I): inhibit acid secretion and enhance blood flow
42
Describe H. Pylori.
- Gram-negative, spiral-shaped aerobic bacterium. - Penetrates the gastric mucosa (survives the harsh conditions of the stomach). - Pathogenic, with many virulence factors.
43
List some virulence factors of H. Pylori. PART 1
- motility: flagella, moves close to the epithelium - produces urease (which converts urea to ammonia, which buffers gastric acid and produces CO2)
44
List some virulence factors of H. Pylori. PART 2
- cytotoxin-associated antigen (CagA): inserts pathogenicity islands and confers ulcer-forming potential; causes apoptosis of cells and affects tight junctions - vacuolating toxin A (VacA): alters the trafficking of intracellular proteins in gastric cells
45
Describe the mechanism of H. Pylori causing mucosal damage. PART 1
- H. Pylori passes the mucosa, and attaches to the epithelium using some of the virulence factors. - Releases urease to convert urea to ammonia, which neutralises any acid in the area, and stops it from being secreted.
46
Describe the mechanism of H. Pylori causing mucosal damage. PART 2
- Therefore, any bacteria can come and survive in the area. - Epithelium starts bleeding and being inflamed due to the HCl, pepsin and toxin exposure.
47
Where/ under which circumstances are peptic ulcers more common? PART 1
- duodenal cap (first part of the duodenum - exposed to a lot of acidic chyme) - the stomach (junction of the antrum and the body) - in the distal oesophagus - Barrett’s oesophagus
48
Where/ under which circumstances are peptic ulcers more common? PART 2
- in Meckel’s diverticulum (as the cells are thinner there) - after a gastroenterostomy (as we affect how long before acidic products go without being neutralised)
49
What is Meckel's diverticulum?
Abnormal pouch in the intestine that’s present from birth
50
A suspected ulcer must be investigated. What diagnostic tests can are done?
- endoscopy - histological examination and staining of an EGD biopsy
51
How would you test for the presence of H. Pylori?
- stool antigen test - evaluate urease activity (with a marked carbon urea tablet) - urea breath test
52
List some symptoms of a peptic ulcer.
- nausea - dyspepsia (indigestion) - epigastric pain - chest discomfort - weight loss - anaemia
53
Describe chronic peptic ulcers.
- Occurs in the upper GIT (pepsin and HCl) - Asymptomatic in >80% of people - More common in people over 50 - Inflammation plays a key role in the disease process
54
Describe acute peptic ulcers.
- Develops from areas of corrosive gastritis (oesophagus, stomach, proximal duodenum) and severe stress or shock (burns or trauma) - Acute hypoxia of the surface epithelium (i.e., ischaemia of the gastric mucosa) is also a cause
55
What are some complications of peptic ulcers?
- haemorrhage (GI bleeding) - perforation (peritonitis) - leakage of luminal contents - narrowing of the pyloric canal (causing acquired pyloric stenosis in the stomach or oesophageal strictures)
56
What are the contents of gastric juice?
→ Cations : Na+, K+, Mg2+, H+ →Anions : Cl-, HPO42+, SO42- →Pepsinogen →Lipase →Intrinsic factor
57
How does H. Pylori break down mucus?
→Makes mucinases - hydrolyse mucus
58
What are the functions of HCl and pepsin?
→Kill aerobic microorganisms →Decrease infection of gastric mucosa
59
What are factors predisposing to peptic ulcers?
→Gastric and duodenal infection with H.pylori
60
What are the outcomes of acute peptic ulcer?
→severe bleeding →healing without scarring →chronic peptic ulcer
61
What does secretin release?
HCO3-
62
What do enterogastrones release and what is the result of this?
→CCK →secretin →GLP-1 → GIP →these have inhibitory effects on ECL, G and Parietal cells
63
What does the intestinal phase do?
→ Balances the secretory activity of the stomach and digestive capacities of the small intestine
64
What kind of feedback do meals elicit?
→feedback inhibitory and stimulatory signals
65
What do neuronal inputs promote?
→ ACh-mediated acid secretion →stimulation of acid called GRP (gastrin-releasing peptide)
66
Why should people who have acid secretion problems not eat a lot of protein?
Causes acid hypersecretion
67
What is HCl secretion regulated by?
→neuronal pathways and duodenal hormones
68
What happens if you don’t release lipase?
→ Steatorrhea
69
Why is histamine not considered exocrine?
Wide-ranging effects in the body
70
What does the pylorus provide for the chyme?
→ An exit route for the chyme to pass through into the duodenum
71
What are the walls of the tubular glands lined with?
→ Parietal cells → HCl and intrinsic factor

SGUL - Physiology 1 (68 decks)

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