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Gastrointestinal > Gastric secretion > Flashcards

Gastric secretion Flashcards

1
Q

What is the range of volume that the stomach can hold?

A

50-1000ml.

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2
Q

What allows the stomach to digest proteins?

A

Pepsin and HCl.

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3
Q

What is the end product of stomach digestion?

A

Semi-liquid chyme.

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4
Q

Where is gastric juice secreted from and how much does it secrete?

A

Gastric glands in the gastric mucosa. Approx 2 litres a day.

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5
Q

What is retropulsion?

A

When gastric contents rebound from the close pylorus.

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6
Q

What is the direction of movement of peristaltic contraction in the stomach?

A

Towards the pylorus.

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7
Q

What determines whether chyme will go through the pyloric sphincter?

A

The strength of the antral wave.

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8
Q

What is the strength of the antral wave governed by?

A

Gastric factors and duodenal factors.

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9
Q

What are the gastric factors that determine the antral wave strength?

A

The volume of chyme in the stomach (by distension) and the consistency of chyme (thick liquid chyme will leave).

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10
Q

How does distension increase motility?

A

Due to stretch of smooth muscles, stimulation of instrinsic nerve plexuses, increased vagus nerve activity and gastrin release.

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11
Q

Describe the neuronal response that allows the duodenum to delay stomach emptying.

A

The enterogastric reflex: decreases antal activity by signals from intrinsic nerve plexuses and the ANS.

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12
Q

Describe the hormonal response that allows the duodenum to delay stomach emptying.

A

Release of enterogastrones (e.g. secretin and cholescystokinin CKK) from duodenum inhibits stomach contraction.

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13
Q

What stimuli within the duodenum drive the neuronal and hormonal responses that delay gastric emptying?

A

Fat, acid, hypertonicity, distension.

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14
Q

Why do large amounts of fat delay gastric emptying?

A

Time is required to digest and absorb it in the duodenum.

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15
Q

Why does acid in the duodenum cause delay in gastric emptying?

A

Time is required for neutralisation of gastric acid by bicarbonate secreted from the pancreas - important for optimal function of pancreatic digestive enzymes.

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16
Q

Why is it important that hypertonicity in the duodenum delays gastric emptying?

A

Products of carbohydrate and protein digestion are osmotically active and draw water into the small intestine which could reduce plasma volume and cause circulatory disturbances (dumping syndrome).

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17
Q

What are the 2 types of gastric gland and where are they located?

A

Pyloric gland area (PGA) in the antrum, oxyntic mucosa (OM) in the fundus and body.

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18
Q

What type of cells are found in the PGA and what do they secrete?

A

D cells (somatostatin), G cells (gastrin).

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19
Q

What type of cells are found in the OM and what do they secrete?

A

Chief cell (pepsinogen), enterochromaffin-like cell (histamine), parietal cell (hydrochloric acid, intrinsic factor, gastroferrin).

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20
Q

What is the function of hydrochloric acid in the stomach?

A

Activates pepsinogen to pepsin, denatures protein, kills most (not all) micro-organisms ingested with food.

21
Q

What is meant by pepsin being autocatalytic?

A

Pepsin once formed activates pepsinogen.

22
Q

What are the functions of intrinsic factor and gastroferrin?

A

Intrinsic factor: binds vitamin B12. Gastroferrin: Binds Fe2+. Facilitates subsequent absorption.

23
Q

What is the function of histamine in the stomach?

A

Stimulates HCl secretion.

24
Q

What are the functions of gastrin and somatostatin?

A

Gastrin: stimulates HCl secretion.
Somatostatin: inhibits HCl secretion.

25
Q

How is carbonic acid produced in the stomach cell?

A

CO2 and H2O react with carbonic anhydrase as the catalyst.

26
Q

What is the function of the bicarbonate produced from the carbonic acid?

A

It moves out of the cell by an antiporter that pumps Cl- into the cell. The Cl- moves through a channel into the gastric pit to combine with hydrogen to form HCl.

27
Q

How is hydrogen pumped into the lumen of the gastric pit?

A

Through the H+/K+ATPase (K+ is pumped into cell).

28
Q

What transporter is used to keep the intracellular and extracellular sodium and potassium concentrations normal?

A

Na+/K+ATPase.

29
Q

What are the 3 important secretagogues that induce acid secretion from the parietal cell?

A

ACh, gastrin and histamine.

30
Q

What type of G protein does histamine activate when it binds to H2 receptors on the parietal cell?

A

Gs.

31
Q

What type of G protein does somatostatin activate when it binds to H2 receptors on the parietal cell?

A

Gi.

32
Q

What pathway do gastrin and ACh activate which causes secretion of H+?

A

PLC-IP3.

33
Q

What pathway do histamine, somatostatin and prostaglandins affect to cause or inhibit secretion of H+?

A

cAMP-PKA. Somatostatin and prostaglandins cause inhibition of adenylyl cyclase which decreases concentration of cAMP.

34
Q

What happens to the proton pumps when the parietal cell is stimulated to secrete acid?

A

They traffic to the apical membrane taking residence in extended microvilli.

35
Q

What are the 3 phases of gastric secretion? Describe them.

A

Cephalic - before food reaches stomach, preparing stomach to receive food (CNS and vagus).
Gastric - when food is in stomach (both physical and chemical mechanisms).
Intestinal - after food has left stomach (weak stimulation of gastric secretion via neuronal and hormonal mechanisms).

36
Q

What cells are inhibited during the cephalic phase and by what substance?

A

D cells (so they don’t secrete somatostatin), ACh.

37
Q

Which of gastrin and histamine works in a paracrine and an endocrine way?

A

Gastrin - endocrine.

Histamine - paracrine.

38
Q

What stimulates G cells in the gastric phase?

A

Distension (mechanoreceptors) and protein digestion products (amino acids).

39
Q

What happens when the antral pH falls when food exits the stomach?

A

Somatostatin release from D cells recommences, decreasing gastrin secretion.

40
Q

What enzyme do NSAIDs block?

A

Cyclo-oxygenase (COX).

41
Q

What effect do locally produced prostaglandins (PGE2, PGI2) have in the stomach?

A

They reduce acid secretion, increase mucus and bicarbonate secretion, increase mucosal blood flow.

42
Q

What 2 things protect the mucosa from attack by HCl and pepsin?

A

The hydrophobic monolayer and the mucus gel layer.

43
Q

Why do NSAIDs cause peptic ulcers?

A

They reduce prostaglandin formation by inhibition of COX 1 which means more acid is secreted.

44
Q

What can gastric damage due to NSAIDs be prevented by and what is the adverse effects of this?

A

Stable PGE1 analogue (misoprostolol). Inhibits basal and food stimulated gastric acid formation, maintains (or increases) secretion of mucus and bicarbonate.

45
Q

When do proton pump inhibitors change from prodrugs to drugs?

A

In a strongly acidic environment i.e. the canaliculus.

46
Q

What is unusual about the length of action of a PPI?

A

It greatly exceeds plasma half-life (most PPIs is 1-1.5hours, duration 10-14 hours).

47
Q

Give 2 examples of mucosal strengtheners.

A

Sucralfate (complex of aluminium hydroxide and sulphated sucrose), bismuth chealate.

48
Q

What is the mechanism of action of mucosal strengtheners?

A

Binds to the ulcer base and forms complex gels with mucus - provides a mucosal barrier. Increases mucosal blood flow, mucus, bicarbonate and prostaglandin production.

49
Q

What other effect does bismuth chealate have?

A

It is toxic towards H pylori.

Gastrointestinal (26 decks)

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