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Physiology 1 : GI > Regulation and disorders of gastric secretion > Flashcards

Regulation and disorders of gastric secretion Flashcards

1
Q

What are the contents of gastric juice (fasting)?

A 
→ Cations : Na+, K+, Mg2+, H+
→Anions : Cl-, HPO42+, SO42-
→Pepsinogen
→Lipase
→Mucus
→Intrinsic factor
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2
Q

How much does gastric juice add (volume) to intestinal contents?

A

→ 2.5L

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3
Q

What do the fundus and body secrete?

A

→ Mucus
→HCl
→Pepsinogen

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4
Q

What does the antrum secrete?

A

→less HCl secretion but more gastrin secretion

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5
Q

What kind of cells does the body have?

A

→ numerous epithelial cells with numerous tubular glands

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6
Q

What are the walls of the tubular glands lined with?

A

→ Parietal cells

→ HCl and intrinsic factor

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7
Q

What does the pylorus provide for the chyme?

A

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

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8
Q

What are the exocrine secretions of the stomach?

A

→mucus
→acid,
→pepsinogen

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9
Q

Why don’t you want histamine to be exocrine?

A

→ It has wide ranging effects in the body

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10
Q

What do ECL cells secrete?

A

→ Paracrine agents such as histamine

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11
Q

How is gastric acid made in the stomach?

A

→CO2 diffuses into the cell
→It forms carbonic acid via carbonic anhydrase
→Carbonic acid dissociates into bicarbonate and H+
→HCO3- is transported out and Cl- is transported in to maintain charge
→The H+ can form water and flux into the lumen
→It can be exchanged for K+ by an ATPase
→H+ and Cl- form HCl in the lumen

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12
Q

What is the pH of gastric juice?

A

→ pH 7.4 -7.7

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13
Q

What are the properties of mucus and what does it form?

A

→ thick
→ sticky
→ forms water insoluble gel on epithelial surface

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14
Q

What does mucus do?

A

→ Protects against H+

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15
Q

What does rennin do?

A

→ Curdles milk into casein clot

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16
Q

What does lipase break down and what are the products?

A

→ triglycerides

→ into fatty acids and glycerol

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17
Q

What happens if you don’t release lipase?

A

→ Steatorrhea

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18
Q

What is intrinsic factor for?

A

→ Absorption of B12

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19
Q

What converts pepsinogen to pepsin?

A

→ High acidity

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20
Q

What do parietal cells secrete?

A

→ Acid

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21
Q

What do non parietal cells secrete?

A

→ Juice similar to plasma

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22
Q

When does HCl secretion increase?

A

→ HCl secretion increases

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23
Q

What are the three phases of secretion?

A

→Cephalic phase
→Gastric phase
→Intestinal Phase

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24
Q

What is HCl secretion regulated by?

A

→neuronal pathways and duodenal hormones

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25
Q

What is the direct pathway?

A

→act on parietal cells and increase acid secretion

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26
Q

What is the indirect pathway?

A

→ Influence the secretion of gastrin and histamine increases acid secretion

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27
Q

What kind of a secretion is gastrin?

A

→ A hormonal secretion

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28
Q

What starts the cephalic phase?

A

→ Sight
→ Smell
→ taste
→ chewing

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29
Q

What happens during the cephalic phase?

A

→there is ACh release
→Increases the parasympathetic preganglionic neuron activity.
→This stimulates the enteric neurons
→ACh binds to receptors on the parietal cells and stimulates them
→Stimulates release of gastrin from G cells
→Gastrin binds to ECL cells
→ECL cells secrete histamine
→This causes secretion

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30
Q

What happens if there is hypersecretion of acid?

A

→D cells are stimulated
→secrete somatostatin which has inhibitory effects on ECL cells and parietal cells.
→Acid secretion is reduced.

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31
Q

What happens in the gastric phase?

A

→Distention of the stomach occurs
→Increased acidity
→When the food has peptides in it the food acts as a buffer
→They will stop HCL stimulating D cells
→The inhibition of acid secretion is removed

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32
Q

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

A

→it causes acid hypersecretion

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33
Q

What do proteins do to luminal acidity?

A

→ Proteins act as buffers in the gastric lumen so HCl secretion increases

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34
Q

What do neuronal inputs promote?

A

→ACh mediated acid secretion

→stimulation of acid called GRP (gastrin releasing peptide)

35
Q

What kind of feedback do meals elicit?

A

→feedback inhibitory and stimulatory signals

36
Q

What does the intestinal phase do?

A

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

37
Q

What reflexely inhibits acid secretion?

A

→High acidity of duodenal contents

38
Q

What does increased acidity inhibit?

A

→inhibits the activity of digestive enzymes, bicarbonate and bile salts

39
Q

What inhibits acid secretion?

A 
→Distension of the duodenum
→ hypertonic solution
→amino acids
→ fatty acids
→monosaccharides
40
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
41
Q

What does secretin release?

A

→ Bicarbonate

42
Q

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

A

→Composition of chyme
→Volume of chyme
→Distension of the duodenum

43
Q

What do short and long neuronal reflexes and hormones (enterogastrones e.g CCK, secretin, GIP) inhibit ?

A

→Acid secretion by the parietal cells
→Gastric secretion by G cells
→This is inhibited by somatostatin (stomach, intestine, delta cells of pancreas, hypothalamus, brainstem and hippocampus)

44
Q

Where do long neurones go?

A

→Long neurons - brain to gut

45
Q

Where do short neurones go?

A

→Short neurons - within gut

46
Q

What negatively regulates HCl secretion?

A

→ PGE2

47
Q

How do prostaglandins work?

A

→ promotes bicarbonate secretion
→ mucus secretion
→ negatively regulate the hyperacidity of parietal cells.

48
Q

How can acid secretion become elevated?

A 
→ Histamine
→ ACh 
→ Gastrin
→ Caffeine
→ Alcohol
→ NSAIDs
→ Nicotine
→ Helicobacter pylori 
→ Zollinger-Ellison syndrome 
→ Hyperparathyroidism (8-30%)
49
Q

What are the 6 things that the concentration of HCl depends on?

A 
→Rate of secretion
→Amount of buffering provided by resting juice
→Composition of ingested food
→Gastric motility 
→Rate of gastric emptying 
→Amount of diffusion back into mucosa
50
Q

What is HCl essential for?

A

→Defence
→Protein digestion : activates pepsinogen to pepsin
→Stimulates flow of bile and pancreatic juice

51
Q

What does lack of HCl cause?

A

→Lack of HCl causes failure of protein digestion (achlorydia or hypochlorydia)
→ production of gastric acid in the stomach is absent or low

52
Q

What stimulates the secretion of pepsinogen?

A

→Inputs to chief cells from nerve plexus

53
Q

How is pepsinogen inactivated?

A

→Inactivated upon entry of food in the small intestine (HCO3-, peptides neutralize the H+)

54
Q

How is pepsinogen activated?

A

→shape is altered high acidity which exposes its active site

55
Q

What else do parietal cells secrete apart from acid?

A

→ Intrinsic factor

56
Q

What is the point of pepsin secretion?

A

→Initiates digestion of proteins - degrades food proteins into peptides
→Pepsin is not required for food digestion

57
Q

What do NSAIDs cause?

A

→ acidic and cause topical irritation of the gut

58
Q

How do NSAIDs cause irritation?

A

→Impair the barrier properties of the mucosa
→Suppress gastric prostaglandin synthesis
→Decrease gastric mucosal blood flow
→Interfere with repair of superficial injury
→Inhibit platelet aggregation - takes away thromboxane A2

59
Q

Why can you get bloody feces if you take NSAIDs?

A

→Inactivates FGF which interferes with haemostasis

60
Q

What happens if there is a malformation of the GIT?

A

→decreased nutrient status

61
Q

What are the sites affected by peptic ulcers?

A

→oesophagus
→ stomach
→duodenum

62
Q

What is peptic ulcer caused by?

A

→Imbalance between protective and damaging factors of GIT

→Exposure of the tissues to the erosive effects of HCl, bile acids and pepsin

63
Q

What are the symptoms of a peptic ulcer?

A 
→Nausea 
→Dyspepsia 
→Anorexia
→Vomiting blood 
→Black, tarry stools 
→Anaemia 
→Epigastric pain
64
Q

Where are peptic ulcers common?

A

→Duodenal cap : first part of the duodenal cap
→Stomach - Junction of antrum and body
→Distal oesophagus - Barrett’s oesophagus

65
Q

What is presence of H. Pylori a risk factor for?

A

→ Gastric cancer

66
Q

What is the usual outcome of a peptic ulcer?

A

→ complete healing and replacement of tissues and some scarring

67
Q

Where does chronic peptic ulcer occur?

A

→Occurs in upper GIT

68
Q

What age group are chronic peptic ulcers common in?

A

→ over 50

69
Q

Where does acute peptic ulcer happen?

A

→areas of corrosive gastritis (oesophagus, stomach, proximal duodenum)

70
Q

What are the outcomes of acute peptic ulcer?

A

→severe bleeding
→healing without scarring
→chronic peptic ulcer

71
Q

What are factors predisposing to peptic ulcers?

A

→Gastric and duodenal infection with H.pylori

72
Q

What are factors that prevent infection of the gastric mucosa?

A 
→Mucus production
→Peristalsis and fluid movement 
→Seamless epithelium with tight junctions 
→Fast cell turnover 
→IgA secretion at mucosal surfaces 
→Peyer’s patches - protection
73
Q

What are factors that prevent autodigestion of the stomach?

A

→Secretion of Alkaline mucus and HCO3-
→Protein content of food
→Presence of tight junctions between epithelial cells lining stomach and fibrin coat
→Replacement of damaged cells within the gastric pits
→Prostaglandins (E and I) inhibit acid secretion and enhance blood flow

74
Q

What are the functions of HCl and pepsin?

A

→Kill aerobic microorganisms

→Decrease infection of gastric mucosa

75
Q

What kind of bacterium is H. Pylori?

A

→ spiral shaped aerobic bacterium

76
Q

How do H. Pylori get inside the stomach?

A

→Penetrates gastric mucosa

→Flagella enables ‘corkscrew’ motility towards gut epithelium

77
Q

What does H. Pylori produce?

A

→Produces urease

→converts urea to ammonia which buffers gastric acid and produces CO2

78
Q

What does H. Pylori insert?

A

→inserts pathogenicity islands and confers ulcer forming potential

79
Q

What does VaCa do?

A

→Vacuolating toxin A (VaCA) alters the trafficking of intracellular proteins in gastric cells

80
Q

How does H. Pylori break down mucus?

A

→Makes mucinases which breaks down mucus

81
Q

What are diagnostic tests for a suspected peptic ulcer?

A

→Endoscopy

→Histological examination and staining of EGD biopsy

82
Q

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

A

→Stool antigen test
→Evaluate urease activity
→Urea breath test

83
Q

What are complications of peptic ulcer?

A

→Haemorrhage (GI bleeding)

→Perforation (peritonitis) and penetration (liver and pancreas may be affected), leakage of luminal contents

→Narrowing of pyloric canal ( stricture causing acquired pyloric stenosis in stomach or oesophageal stricture)

Physiology 1 : GI (15 decks)

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