L11+14 - Stomach physiology

Question 1

What are the components of the stomach? (anatomy)

Answer 1

1. Lower oesophageal sphincter:
   - between oesophagus and stomach
   - prevents acid reflux
2. Fundus:
   - uppermost portion of stomach
3. Body:
   - middle + main part of stomach
   - secretes mucus, pepsinogen, HCl
4. Antrum:
   - lower part of stomach
   - thicker layer of smooth muscle
   - secretes mucus, pepsinogen, gastrin
   - mixing + grinding of stomach contents - chyme
5. Pyloric sphincter:
   - ring of contractile smooth muscle between antrum + duodenum
   - opens + closes to control gastric emptying

Question 2

What are the main functions of the stomach?

Answer 2

• Mixing of chyme with gastric secretions - segmentation contractions via circular muscles (mostly in antrum)
• Temporary storage of food
• Mechanical digestion by peristalsis + segmentation
• Chemical digestion of proteins (little/no absorption)
• Regulation of passage of chyme into small intestine via pyloric sphincter
• Secretion of intrinsic factor for absorption of vitamin B12

Question 3

How is gastric motility achieved?

Answer 3

1. Receptive relaxation:
   - Smooth muscle relaxes at arrival of food
   - Mediated by parasympathetic nerves which stimulated myenteric plexus — NO + serotonin released for relaxation
2. Peristalsis:
   - Wave-like contractions by longitudinal smooth muscles
   - More powerful waves in antrum — allows mixing of chyme + closes pyloric sphincter

Question 4

What are the secretory cells in the gastric glands of the stomach? What do they secrete?

Answer 4

GASTRIC JUICES:
1. Zymogenic (chief) cells
-> secrete pepsinogen (inactive form of enzyme pepsin)

2. Parietal cells
   -> secrete HCl - acidic pH for pepsinogen converted to pepsin
   -> secrete intrinsic factor
3. Goblet cells
   -> secret mucus - mixing purposes

HORMONES:
1. D cells
-> secrete somatostatin

2. Enterochromaffin (ECL) mast-like cells
   -> secrete histamine
3. G cells
   -> secrete gastrin

Question 5

How is the stomach acid produced?

Answer 5

• CO2 diffuses into parietal cells => source of H+ ions
• Proton pump in membrane of parietal cells - pumps out H+ ions into lumen of stomach
• pumps K+ into cell to maintain electro-balance
• HCO3- (product from CO2) moved across parietal cell into blood capillary
• Cl- ions move through parietal cell from capillary - moved into lumen of stomach to maintain electroneutrality in parietal cell
• HCl formed in lumen of stomach

Question 6

What stimulates the increase of acid secretion?

Answer 6

3 chemical messenger:

1. GASTRIN - gastric hormone
2. ACETYLCHOLINE - neurotransmitter
3. HISTAMINE - paracrine hormone

Question 7

What stimulates the inhibition of acid secretion?

Answer 7

NEURONAL INPUT:

• Enterogastric reflex:
• caused by partially-digested protein, presence of fat + lower pH
• mediated by medulla oblongata via afferent nerves
• leads to ↓parasympathetic stimulation — ↓acid secretion

HORMONAL INPUT:

• Hormones => secretin + cholecystokinin (CCK) +gastric inhibitory peptide (GIP)
• secreted by enterocytes in small intestine
• Somatostatin - paracrine agent
• released in response to ↑ HCl

Question 8

What are the 3 phases of gastric secretion? (phases of GI control)

Answer 8

1. CEPHALIC PHASE
   - ↑ secretions
2. GASTRIC PHASE
   - ↑ secretions
3. INTESTINAL PHASE
   - ↓ secretions

Question 9

What happens during the Cephalic phase?

Answer 9

• Stimuli - sight, taste, smell, thought of food, ↓ blood glucose – sensory nerves in brain
• Stimuli stimulates medulla oblongata
• Medulla oblongata sends signal via vagus nerve to parasympathetic nerves to ENS where plexuses activated
  Response: -> ↑HCl + ↑pepsin
• Inhibitory action in cephalic phase – via sympathetic nerves
  -> due to stress, fear, etc.
  -> to effector cells (parietal cells) – ↓HCl + ↓pepsin

Question 10

What happens during the Gastric phase?

Answer 10

• Stimuli: distension of stomach, partially digested proteins, lower pH — stretch receptors in muscularis
• Stretch receptors send signal to medulla oblongata via afferent fibres – producing vagus/parasympathetic reflex (long reflex)
• Efferent fibres - signal from medulla oblongata to ENS (submucosal plexus) – response: ↑HCl + ↑pepsin in parietal cells
• Responses to stimuli also mediated by short neural reflexes - straight to ENS (without CNS input)

Responses:
- G cells secrete gastrin (presence of partially digested proteins)
- Gastrin binds to parietal cell to stimulate proton pump - ↑HCl
- Gastrin binds to chief cell to allow secretion of pepsinogen - ↑pepsin

• Inhibitory action:
• sympathetic pathways
• somatostatin from D cells (response to very low pH)

Question 11

Neuronal input in Cephalic and Gastric phases

Answer 11

ACETYLCHOLINE (neurotransmitter) from parasympathetic pathways help increase HCl + pepsin secretions:

Binds to:

• D cells in antrum
  => inhibits secretion of somatostatin hormone
• G cells in antrum
  => stimulates secretion of gastrin hormone
• Parietal cells
  => stimulates Ca++ levels to increase - stimulates proton pump
• Chief cells
  => stimulates Ca++ levels - increase secretion of pepsinogen
• ECL cells
  => stimulates secretion of histamine – ↑HCl + ↑pepsin

Question 12

What happens during the intestinal phase? (hormonal inhibition)

Answer 12

• Stimuli: distension in duodenum, partially digested proteins, presence of fat, low pH in duodenum
• Ultimate effect => inhibition of gastric acid secretion (HCl+pepsin)

How? :

• Stimulation of S cells in duodenum to secrete secretin
• Secretin:
  -> inhibits G cell to secrete gastrin - ↓HCl
  -> stimulates bile production in liver - emulsifies fatty acids
  -> endocrine duct cells in pancreas - HCO3- secreted to neutralise H+ in duodenum
• Stimulation of enterocytes in duodenum to secrete CCK hormone
• CCK:
  -> inhibits proton pump in parietal cells - ↓HCl
  -> stimulates bile - emulsify fat
  -> stimulates gall bladder to contract - concentrated bile in duodenum
  -> stimulates acinar cells in pancreas to secrete enzymes to break down food molecules
• Stimulation of K cells in duodenum to secrete GIP hormone
• GIP:
  -> inhibits proton pump in parietal cells - ↓HCl

Question 13

What happens during the Intestinal phase? (neuronal inhibition)

Answer 13

• Stimuli: distension in duodenum, partially digested proteins, presence of fat, low pH in duodenum
• Ultimate effect => inhibition of gastric acid secretion (HCl+pepsin)

How? :

• Acetylcholine from vagus nerve - inhibited
• Chemoreceptors in duodenum send impulses via afferent fibres of vagus nerve to medulla oblongata
• Leading to inhibition of parasympathetic pathway - ↓HCl
• Stimulation of sympathetic pathways - allows contraction of pyloric sphincter to prevent chyme entering duodenum

Question 14

Why does the stomach not digest itself?

Answer 14

• Stomach is lined with mucosal barrier
• Mucosal barrier:
  -> top layer - gel layer
  -> bottom layer - high conc. HCO3- (neutralisation of H+)
• Gel layer:
  -> prevents H+ to penetrate thick mucus layer
  -> acts like chemical barrier
• Breakdown of mucosal barrier causes stomach ulcers!
• Prostaglandins – ↑mucosal thickness + ↑HCO3- production

Question 15

Factors influencing gastric emptying

Answer 15

• Presence of fat in duodenum (causes ↓HCl)
• Meal size
• Composition of food (high fat meals cause ↓HCl)
• Posture
• Volume
• Temperature
• Pregnancy
• Conditions - migrants, gastric ulcers, etc.
• Other factors - drugs, alcohol, anticholinergics, etc

Question 16

What are the main causes of gastric ulcers?

Answer 16

What?
- Erosion of mucosal barrier in stomach (+ lower oesophagus + duodenum), leading to inflammation + damage to underlying tissues

Causes:

• Helicobacter Pylori - bacterial infection
• Excessive NSAIDs use – inhibits prostaglandin secretion which inhibits gastric emptying
• Other factors:
  -> smoking, caffeine, alcohol, stress, etc.