19. Gastric Secretions

Question 1

Roughly how much fluid does the intesting have to reabsorb/day?

Describe what the contents of saliva do.

How much saliva do we secrete/day?

Answer 1

6.5L/day

Amylase (breaks down polysaccharides), Lysozyme (lyses bacterial cell walls), Bicarbonate (neurtalises food and bacterial acids), Growth factors (stimulate epithelial proliferation to protect oesophageal epithelium), Transcobalamin II (binds and chaperones B₁₂ or else broken down by gastric acid)

1-2L

Question 2

List the 5 main gastric luminal secretions and what they do.

Answer 2

1) Mucus: from mucous cells, cover lumenal surface and glands (mucous neck cells), secrete bicarbonate-rich mucus that coats and lubricates gastric surface and protects epithelium

2) Acid: HCl from parietal cells, activates pepsinogen, inactivates ingested microorganisms

3) Proteases: pepsinogen (inactive zymogen) from chief cells, acivated by low pH -> pepsin (digests proteins). Chymosin (renin) coagulates milk protein (in infants) from cheif cells too

4) Lipase: triglyceride digestion

5) Intrinsic factor: glycoprotein from parietal cells, takes vit B₁₂ away from transcobalamin II and binds it for absorption

Question 3

Label A-E

Answer 3

A: gastric pit

B: mucus cell

C: parietal cell (produce acid)

D: chief cell (produce pepsinogen)

E: G cell (secretes gastrin - hormonal regulation of other cells)

Question 4

Explain how gastric acid secretion works.

Are the transporters always in the cell membranes?

Answer 4

Parietal cell. Energy expensive process.

1) Plasma CO₂ -> into parietal cell + H₂O = carbonic acid -> seperates into H⁺ and HCO₃^-.
2) H⁺ pumped out of cell into lumen in exchange for K⁺. (NB. this proton pump is the target of lots of drugs e.g. PPIs like omeprazole). HCO₃^{<strong>-</strong>} exported back out into plasma in exchange for Cl^- transported in.
3) K⁺ diffuses back out of cell into lumen and Cl^- diffuses out into lumen too. H⁺ combines with Cl^- = HCl

No - recruited to membrane when needed via external stimuli.

Question 5

What 2 mechanisms allow gastric acid secretion with no detriment to the host?

Answer 5

1) Canaliculi: acid secreted into the canaliculi (channels) in parietal cell = isolated from rest of cell. Canaliculi join up and acid eventually passes out into lumen

2) Mucous layers: organised like thousands of overlapping leaflets - acid can burst out of mucous ‘flap’ but can’t get back.

Question 6

Describe the feedback control of acid secretion.

Answer 6

1) Nervous system: vagus nerve synapses in enteric NS and the postganglionic release ACh onto M3 receptors of parietal cells, ECL-cells and D cells.

2) Other receptors: H2 receptor on parietal cell responds to histamine from ECL-cell. SSR receptor on parietal cell responds to somatostatin from D cell = inhibitory!

3) CCKB/CCK2 receptors respond to gastrin - excitatory.

4) Receptors to AAs produce gastrin from G cells -> into circulation -> works on receptors
5) Enteric neurone releases gastrin releasing peptide (GRP) which releases gastrin

Question 7

Describe the neural control of gastric secretion.

Answer 7

3 phases: cephalic phase (conditioned reflex if think/see/smell food), gastric phase (gastric distension), intertinal phase (acid in small intestine)

Cerebral cortex -> medullary nuclei -> secretion (parasympathetic). Gastric distension = +ve fb via vagus to medullary nuclei. Acid in small intestine = -ve fb via spinal cord to secretion and to medullary nuclei (sympathetic). Secretin, GIP and vagus nerve all -ve fb.

Question 8

What is the most likely cause of peptic ulcer disease?

Why does it cause this?

What are some other less common causes of peptic ulcer disease?

How would you diagose PUD?

How would you treat PUD?

Answer 8

Helicobacter pylori. If have it up to 2-% risk factor for developing peptic ulcer. >50% of world pop infected!

Thrives in acid environment and uses urea metbolism to produce NH₃ = alkaine stimulus that neutralises area around it so can live in hostile conditions. Migrates and destroys host tissue, damaging it’s ability to produce mucus -> inflmmation, bleeding and sometimes perforation. Ulcers occur more in duodenum than stomach.

Stress, smoking, alcohol, NSAIDs

Urea breath test/biopsy/foecal sample

Combination therapy: 2 antibiotics (amoxycillin + clarithromycin) and a PPI (omeprazole = reduce stomach acid secretion)

Question 9

Give an example of a H2 receptor blocker.

What is GORD?

List 3 things that can cause GORD.

What is the treatment (give 2 examples)?

Answer 9

Ranitidine

Retrograde flow of gastric contents into oesophagus = reflux, and GORD develops when reflux causes troublesome symptoms/complications. NOT EXCESSIVE HCl SECRETION!

Excessive reflux of normal gastric juice (TLOSR), weakened oesophageal epithelium (e.g. by previous reflux/genetic conditions), hypersensitivity of oesophageal pain sensing nerves

All mitigated by PPIs (e.g. omeprazole, lansoprazole)