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GI > Session 4: Introduction to the Stomach > Flashcards

Session 4: Introduction to the Stomach Flashcards

1
Q

What are the four divisions of the stomach?

A

Cardia

Fundus

Body

Antrum

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2
Q

Stomach can also be divided into to gross regions. Which?

A

Orad (fundus and upper body)

Caudad (lower body and antrum)

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3
Q

How is the stomach regulated during feeding?

A

Endocrine, paracrine and neural control.

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4
Q

How do the two divisions of the stomach differ?

A

Orad is bigger and its wall is thinner.

As we approach the caudad the stomach becomes more narrow and the wall is thicker.

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5
Q

How many muscle layers does the stomach have?

Which are they?

A

3

Outer Longitudinal

Middle Circular

Inner Oblique

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6
Q

Innervation by the stomach muscles

A

Extrinsic innervation from autonomic nervous system.

Intrinsic innervation from the myenteric and submucosal plexuses.

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7
Q

Explain the three components of gastric motility.

A

Relaxation of the orad region to receive the food bolus from the oesophagus

Contractions that reduce the size of the bolus and mix it with gastric secretions.

Gastric emptying that propels the chyme into the small intestine.

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8
Q

Explain the neuromuscular control of the orad region.

A

Receptive relaxation in response to mechanoreceptors detecting distention. This is called the vagovagal reflex where an impulse is sent to the CNS via sensory neurons.

CNS then send impulse to smooth muscle wall of the orad to contract.

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9
Q

Explain the muscular action of the caudad region.

A

Mixing and digestion in the stomach of the food bolus.

Breaks the food bolus into smaller constiutent and mix it with gastric secretions.

The muscular contraction is in form of a wave starting at the beginning of the caudad region (middle of body) and go distally with increased strength as they approach the pylorus.

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10
Q

Explain retropulsion in the stomach.

A

Too large pieces are not immediately injected into duodenum as the waves of contraction also narrows the pylorus. This means that too large chunks are being propelled back into the stomach for further mixing until the content is small enough to pass.

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11
Q

What is the frequency of contraction waves of the caudad stomach?

A

3-5 waves a minute

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12
Q

Explain hormones route from secretion to target cell in the stomach.

A

Peptides are released from endocrine cells into portal circulation. It passes through the liver and enter the systemic circulation. They will eventually end up pretty close to where they were to begin with.

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13
Q

Explain the paracrine function of the stomach.

A

Peptides released by glands and act in the local environment of the stomach diffusing short distances.

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14
Q

Explain the neurocrine function of the stomach.

A

Peptides released by neurones in the GI tract.

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15
Q

State the main gastrointestinal hormones.

A

Gastrin Cholecystokinin Secretin Gastric inhibitory peptide (GIP) Motilin

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16
Q

What increases the frequency of AP and force of contraction of the caudad region?

What decreases it?

(Neuronal/endocrine/paracrine)

A

Increase -> Parasympathetic, gastrin and motilin

Decrease -> Sympathetic + secretin + GIP

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17
Q

Basic functions of the stomach

A

Short term storage

Mechanical breakdown of food

Starting of digestion

Protect against pathogens

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18
Q

Explain the blood supply of the stomach.

A

The celiac trunk divides in the common hepatic artery, splenic artery and left gastric artery.

Common hepatic will give off a branch called the gastroduodenal artery which will in its turn give off a branch called the right gastroepiploic artery.

The common hepatic will then give off another branch called the right gastric artery.

The splenic artery will gove off a branch called the gastroepiploic artery.

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19
Q

What allows stretching of the stomach?

A

The stomach has folds called rugae which can be distended.

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20
Q

What epithelial cells can be found in the stomach?

A

Mucous cells

Parietal cells

Chief cells

G cells

(Simple columnar epithelium)

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21
Q

What is the main gland found in the body of the stomach?

A

Oxyntic glands

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22
Q

What cells can be found in the oxyntic glands?

A

Parietal cells and chief cells.

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23
Q

What is the main gland found in the antrum of the stomach?

A

Pyloric glands

24
Q

What cells can be found in the pyloric glands?

A

G cells and mucous neck cells

25
Q

What does the gastric juice mainly consist of?

A

HCl

Pepsinogen

Intrinsic factor

Mucus

26
Q

Production pepsinogen and its action.

A

By chief cells.

Its purpose is to convert into its active form called pepsin which is a protease that will start to digest protein in the food bolus.

27
Q

Production of HCl and its purpose.

A

Produced by parietal cells.

Its action is to lower the pH of the stomach in order to make pepsinogen turn into pepsin.

28
Q

Production of intrinsic factor and its purpose.

A

Produced by parietal cells.

Absorption of vitamin B12 in ileum.

This is the only essential component of the gastric juice.

29
Q

Production and purpose of mucus.

A

Produced by mucous neck cells of the pyloric glands.

The mucus protects the gastric mucosa from the acidic environment of the stomach. Offers lubrication as well.

30
Q

What else does mucous neck cells produce?

A

HCO3- and pepsinogen.

31
Q

Which channels can be found on the apical membranes of the parietal cells of the stomach?

A

H+/K+-ATPase and Cl- channels.

32
Q

Explain where parietal cells get their H+ which they secrete into the stomach.

A

CO2 reacts with water to produce H2CO3 by the help of carbonic anhydrase.

This then dissociates into H+ and HCO3-.

H+ is then transported via H+/K+-ATPase to the lumen of the stomach.

33
Q

What channels can be found on the basolateral membrane of the parietal cells?

A

Na+/K+-ATPase and Cl-/HCO3- exchangers.

The HCO3- is therefore secreted into general circulation leaving the venous blood of the stomach slightly alkaline. This HCO3- will be picked up later on in digestion.

34
Q

Clinical significance of the H+/K+-ATPase of the parietal cells.

A

Protonpump inhibitors (PPI) will inhibit it to lower the acidity of the stomach.

An example is omeprazole to treat stomach ulcers.

35
Q

State three substances that stimulates HCl secretion.

A

Histamine

ACh

Gastrin

36
Q

Where is histamine produced?

Explain its action.

A

By ECL cells.

It’s a paracrine secretion binding to H2 receptors on nearby parietal cells. The second messenger is cAMP and this will further down the line stimulate secretion of H+ by parietal cells.

37
Q

What is the clinical significance of the H2 receptors?

A

Drugs like cimetidine block the H2 receptors and block their action of histamine.

38
Q

Explain the vagal stimulation of HCl secretion.

A

It is a dual stimulation.

Direct stimulation by ACh acting on muscarinic M3 receptors on the parietal cells to stimulate H+ secretion.

Indirect stimulation by vagus nerves also innervating G cells. GRP (neurotransmitter) stimulates release of gastrin into circulation to stimulate parietal cells.

39
Q

Explain the significance of M3 receptors on parietal cells.

A

Atropine blocks the action of ACh here.

40
Q

Explain why atropine doesn’t block the complete vagal stimulation.

A

Because of the indirect stimulation being via GRP neurotransmitter. Atropine doesn’t block GRP and not gastrin either.

41
Q

Where is gastrin produced? What is its purpose?

A

Produced by G cells found in the antrum in pyloric glands.

They reach the parietal cells via endocrine mechanism. The gastrin binds to CCKb receptors which got the same affinity to gastrin as cholecystokinin.

Gastrin stimulates H+ secretion.

42
Q

Explain potentiation regarding HCl stimulation.

A

The ability of two stimuli to produce a combined response that is greater than the sum of the individual responses.

Histamine potentiates the actions of ACh and gastrin.

ACh also potentiates the actions of histamine and gastrin.

Gastrin can also bind to ECL cells in order to stimulate the secretion of histamine potentiating it.

43
Q

What is the clinical consequence of potentiation?

A

That H2 receptors like cimetidine meant to block histamine have a greater effect than expected.

Same goes for atropine meant to block ACh.

44
Q

What inhibits HCl secretion?

A

Decreased pH

Somatostatin

Prostaglandin

45
Q

Why isn’t HCl secretion inhibited while the gastric content is in the stomach?

A

Because the food acts like a buffer for H+. This means that when the food leaves the environment will become increasingly acidic and shut off.

46
Q

What is somatostatin secreted by?

Explain how it inhibits H+ secretion.

A

Secreted by D cells.

Directly by binding to parietal cells coupled to adenylyl cyclase via a Gi protein to work as an antagonist.

Indirectly by inhibiting both histamine release from ECL cells and gastrin release from G cells.

47
Q

Explain prostaglandins inhibition on HCl secretion.

A

Antagonise histamine stimulatory action on H+ secretion by activating Gi inhibiting adenylyl cyclase.

48
Q

State the phases of digestion.

A

Cephalic

Gastric

Intestinal

49
Q

Explain the cephalic phase and its stimulation.

A

30% of total HCl secreted.

Stimulated by smelling, tasting and conditioned reflexes for food.

Stimulated by vagus nerve directly.

Indirect vagal stimulation by increasing gastrin secretion via GRP neurotransmitter.

50
Q

Explain the gastric phase and its stimulation.

A

60% of total HCl secreted.

Stimulated by distention of stomach, proteins, amino acids and small peptides.

Vagal stimulation in response to distention stimulating parietal cells (directly) and G cells (indirectly) via vagus nerves.

Amino acids and small peptides act on G cells to stimulate gastrin release.

51
Q

Explain the intestinal phase.

A

10% of HCl secretion.

Chyme initially stimulates gastrin secretion.

52
Q

Effect of chyme after the initial stimulation.

A

Chyme stimulates CCK and secretin to suppress secretion.

Presence of lipis activate enterogastric reflex to reduce vagal stimulation as well.

53
Q

In basic terms; what is needed for a peptic ulcer to be created?

A

Loss of protective mucous barrier.

Excessive H+ and pepsin secretion

or a combination of the two.

In other words an imbalance in the protective factors vs. the damaging factors.

54
Q

State the protective factors of the stomach.

A

Mucus

HCO3- trapped in the mucus. Any H+ that would pierce the mucus will be neutralised by the HCO3-.

Prostaglandin E2 maintaining the mucosal barrier and stimulating HCO3- secretion.

Mucosal blood flow getting rid of acid.

Growth factors (turnover of epithelial cells)

55
Q

Damaging factors of the stomach.

A

H+

Pepsin

Helicobacter pylori infection

NSAIDs

Stress (physiological)

Smoking

Alcohol consumption

56
Q

Briefly explain how alcohol causes damage.

A

Dissolves the mucus layer

57
Q
A

GI (30 decks)

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