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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
Q

How is acid secretion inhibited during the intestinal phase?

A
  • 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.
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26
Q

What is the effect of increased sympathetic discharge?

What is the effect of decreased parasympathetic discharge?

A

Increased sympathetic discharge is inhibitory.
Decreased parasympathetic discharge is stimulatory.

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27
Q

List some HCl secretion stimulants or factors that increase HCl secretion.

A
  • histamine
  • acetylcholine
  • gastrin
  • NSAIDs
  • H. Pylori
  • hyperparathyroidism
  • stress
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28
Q

[HCl] can reach 150 mM. What does this depend on?

A
  • rate of secretion
  • amount of buffering
  • gastric motility
  • rate of gastric emptying
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29
Q

In what ways is HCl essential for life?

A
  • defence
  • protein digestion: activates pepsinogen to pepsin
  • stimulates flow of bile and pancreatic juice
30
Q

What is the result of low [HCl]?

A
  • Failure of protein digestion
  • Achlorhydria - reduced gastric acid secretion
31
Q

What stimulates the secretion of pepsinogen?

A
  • 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
Q

What inactivates pepsin secretion?

A
  • Entry of food in the small intestine
  • HCO3- and peptides neutralise the H+
33
Q

What is the point of pepsin secretion?

A

Initiates the digestion of proteins by degrading food proteins into peptides

34
Q

What are some symptoms of HCl deficiency?

A
  • presence of undigested food in the stool
  • white spots on fingernails
  • drowsiness after meals
  • increased chances of H. Pylori infection
35
Q

What would be the treatment of HCl deficiency?

A
  • bitter herbs may stimulate HCl secretion
  • lemon juice and vinegar stimulate HCl secretion
  • Vit B1 stimulates HCl secretion
36
Q

How do NSAIDs (e.g. aspirin) play a role in gastric acid secretion disorders? PART 1

A
  • 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
Q

How do NSAIDs (e.g. aspirin) play a role in gastric acid secretion disorders? PART 2

A
  • 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
Q

Describe the mechanism of peptic (gastric or duodenal) ulcer formation.

A
  • Breakage of the mucosal barrier causes an imbalance between protective and damaging factors.
  • Exposes tissues to the effects of HCl and pepsin.
39
Q

List some factors predisposing to peptic ulceration.

A
  • H. Pylori
  • smoking
  • genetic factors
  • stress
  • NSAIDs
40
Q

List some factors that prevent the infection of the gastric mucosa.

A
  • HCl, pepsin
  • mucus production
  • peristalsis and fluid movement
  • IgA secretion at mucosal surfaces
  • Peyer’s Patches
41
Q

List some protective factors that prevent the autodigestion of the stomach.

A
  • 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
Q

Describe H. Pylori.

A
  • Gram-negative, spiral-shaped aerobic bacterium.
  • Penetrates the gastric mucosa (survives the harsh conditions of the stomach).
  • Pathogenic, with many virulence factors.
43
Q

List some virulence factors of H. Pylori. PART 1

A
  • motility: flagella, moves close to the epithelium
  • produces urease (which converts urea to ammonia, which buffers gastric acid and produces CO2)
44
Q

List some virulence factors of H. Pylori. PART 2

A
  • 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
Q

Describe the mechanism of H. Pylori causing mucosal damage. PART 1

A
  • 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
Q

Describe the mechanism of H. Pylori causing mucosal damage. PART 2

A
  • 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
Q

Where/ under which circumstances are peptic ulcers more common? PART 1

A
  • 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
Q

Where/ under which circumstances are peptic ulcers more common? PART 2

A
  • 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
Q

What is Meckel’s diverticulum?

A

Abnormal pouch in the intestine that’s present from birth

50
Q

A suspected ulcer must be investigated.
What diagnostic tests can are done?

A
  • endoscopy
  • histological examination and staining of an EGD biopsy
51
Q

How would you test for the presence of H. Pylori?

A
  • stool antigen test
  • evaluate urease activity (with a marked carbon urea tablet)
  • urea breath test
52
Q

List some symptoms of a peptic ulcer.

A
  • nausea
  • dyspepsia (indigestion)
  • epigastric pain
  • chest discomfort
  • weight loss
  • anaemia
53
Q

Describe chronic peptic ulcers.

A
  • 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
Q

Describe acute peptic ulcers.

A
  • 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
Q

What are some complications of peptic ulcers?

A
  • 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
Q

What are the contents of gastric juice?

A

→ Cations : Na+, K+, Mg2+, H+
→Anions : Cl-, HPO42+, SO42-
→Pepsinogen
→Lipase
→Intrinsic factor

57
Q

How does H. Pylori break down mucus?

A

→Makes mucinases - hydrolyse mucus

58
Q

What are the functions of HCl and pepsin?

A

→Kill aerobic microorganisms
→Decrease infection of gastric mucosa

59
Q

What are factors predisposing to peptic ulcers?

A

→Gastric and duodenal infection with H.pylori

60
Q

What are the outcomes of acute peptic ulcer?

A

→severe bleeding
→healing without scarring
→chronic peptic ulcer

61
Q

What does secretin release?

A

HCO3-

62
Q

What do enterogastrones release and what is the result of this?

A

→CCK
→secretin
→GLP-1
→ GIP
→these have inhibitory effects on ECL, G and Parietal cells

63
Q

What does the intestinal phase do?

A

→ Balances the secretory activity of the stomach and digestive capacities of the small intestine

64
Q

What kind of feedback do meals elicit?

A

→feedback inhibitory and stimulatory signals

65
Q

What do neuronal inputs promote?

A

→ ACh-mediated acid secretion
→stimulation of acid called GRP (gastrin-releasing peptide)

66
Q

Why should people who have acid secretion problems not eat a lot of protein?

A

Causes acid hypersecretion

67
Q

What is HCl secretion regulated by?

A

→neuronal pathways and duodenal hormones

68
Q

What happens if you don’t release lipase?

A

→ Steatorrhea

69
Q

Why is histamine not considered exocrine?

A

Wide-ranging effects in the body

70
Q

What does the pylorus provide for the chyme?

A

→ An exit route for the chyme to pass through into the duodenum

71
Q

What are the walls of the tubular glands lined with?

A

→ Parietal cells
→ HCl and intrinsic factor

SGUL - Physiology 1 (68 decks)

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