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FHB Block 3 > Gastric Phase > Flashcards

Gastric Phase Flashcards

1
Q

What is the reason for H+ secretion in the stomach?

A

Killing microorganisms and conversion of pepsinogen to pepsin

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2
Q

What is the role of intrinsic factor?

A

intrinsic factor is essential for the absorption of vitamin B12 (which is essential for RBC formation)

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3
Q

What is the motor activity of the stomach for?

A

Mixing secretions of H+ and pepsin with the bolus of food

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4
Q

What is the effect of histamine release from ECL like cells

A

Histamine binds to nearby parietal cells and stimulates secretion of HCl

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5
Q

What is the general role of gastrin?

A

Gastrin is the “go” hormone- stimulates gastric acid secretion in the stomach and duodenum

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6
Q

What is the general role of somatostatin?

A

Somatostatin is the “stop” hormone- inhibits gastric secretion in the stomach, duodenum and pancreas

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7
Q

What two enzymes are released by the cells of the stomach?

A

Pepsinogens and lipase are both released from the fundus of the stomach

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8
Q

Where does mixing/grinding of the bolus of food occur in the stomach?

A

The antrum/pyloris.

The upper part, the fundus/body, is primarily a food reservoir/place where enzymes are secreted.

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9
Q

Where do gastric gland empty?

A

Into the gastric pits

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10
Q

What do chief cells secrete?

A

Pepsinogen

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11
Q

Under what environment are pepsins active?

A

acidic

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12
Q

What is secreted by enterochromaffin-like cells?

A

Histamine (a paracrine hormone)- it is the most powerful stimulator of HCl secretion (through the stimulation of parietal cells)

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13
Q

What is secreted by D cells?

A

Somatostatin- a powerful endocrine inhibitor of HCl secretion

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14
Q

What is secreted by G cells?

A

gastrin- an HCl secretagogue (indirect stimulation of parietal cells through ECL cells)

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15
Q

In healthy humans, what is the only essential component of gastric juice?

A

Intrinsic factors. All of the others are redundant

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16
Q

Where do the protons secreted by parietal cells come from?

A

CO2 and H2O –> H+ + HCO3-

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17
Q

How are protons secreted from parietal cells?

A

H+/K+ ATPase. It is an active process that transports both H+ and K+ across their chemical gradient

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18
Q

What drug blocks the H+/K+-ATPase?

A

Omeprazole (Prilosec)

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19
Q

How is Cl- secreted from parietal cells?

A

Facilitated diffusion through Cl- channels

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20
Q

What is the alkaline tide?

A

When H+ + HCO3- is made, protons are pumped out of hte parietal cells and are secreted into the gastric juice. HCO3- is transported out of hte basolateral membrane through a Cl- HCO3- antiporter. This results in alkaline tide, or a high pH of the blood following a meal.

The HCO3- is eventually secreted back into the GI tract by the pancreas (into the duodenum)

21
Q

What is the net results of ion movements through the parietal cells?

A

Secretion of HCl and absorption of HCO3-

22
Q

Why is it necessary to constantly secrete mucus?

A

Proteases (such as pepsin) digest the mucus tetramer into single units which cannot form a mucus barrier. Therefore the mucus neck cells must constantly secrete mucus to replenish the barrier.

23
Q

What is the single strongest stimulation for gastric H+ secretion?

A

Parasympathetic stimulation via the vagus nerve

24
Q

Name three substances that stimulate H+ secretion by parietal cells

A

Acetylcholine (neurocrine), Histamine (paracrine) and Gastrin (endocrine)

25
Q

How does ACh released from the vagus nerve stimulate H+ secretion from the gastric mucosa?

A

ACh binds to M3 muscarinic receptors and stimulates H+ secretion through the Ca2+/IP3 secondary pathway

26
Q

What receptors does Atropine block?

A

Muscarinic

27
Q

How does histamine stimulate H+ secretion?

A

Histamine, released from ECL cells binds to H2 receptors on nearby cells (paracrine) and stimulates H+ secretion through the cAMP secondary messenger pathway

28
Q

What receptors does cimetidine block?

A

H2 receptors- therefore blocks the effects of histamine

29
Q

How does Gastrin stimulate gastric H+ secretion?

A

Secreted by G-cells, gastrin binds to cholecystokinin B (CCKB) receptors on both parietal cells and ECL cells to stimulate H+ secretion.

The second messengers are cAMP, IP3 and Ca2+

30
Q

What is potentiation?

A

The rate of H+ secretion can be regulated by each of the three substances (ACh, Histamine and gastrin) as well as by each three independently.

31
Q

What is ultimate step in the stimulation of gastric H+ that allows for an increase in H+ secretion?

A

Increase in H+/K+ ATPase on the apical membrane of the gastric epithelial cells

32
Q

What drug most effectively decreases H+ secretion and why?

A

Omeprazole- it stops H+ secretion from H+/K+-ATPases, the final common step in the H+ secretion pathways

33
Q

How does distention of the stomach stimulate gastrin release?

A

Vagovagal reflex: sensory information goes into the brain and comes back to stimulate H+ secretion

34
Q

When/why is somatostatin released?

A

SS is released when the pH of the lumen is below 3 by D cells. SS inhibits the release of further H+ into the gastric lumen

35
Q

How does somatostatin decrease H+ release?

A

Indirectly via inhibition of histamine and gastrin release

Directly via binding to parietal cell receptors/blocking the stimulatory effects of histamine

36
Q

What is the role of prostaglandin?

A

Prostaglandin inhibits the stimulatory effects of histamine

37
Q

Why might aspirin cause GI ulcers?

A

Aspirin inhibits prostaglandin and somatostatin. Inhibition of the inhibitors leads to over secretion of H+ into the stomach

38
Q

What is the most important role of the stomach?

A

Gastric motility- mixing of the bolus of food with gastric juices and the propulsion of food through the pylorus into the duodenum.

39
Q

What is receptive relaxation?

A

Distention of the lower esophagus by food causes relaxation of the LES and relaxation of the orad stomach.

Distention upstream by food leads to relaxation downstream to make way for the food.

40
Q

What regulates receptive relaxation?

A

Vagovagal reflex

41
Q

What neurotransmitter released from postganglionic peptidergic vagal fibers cause the relaxation of the LES and orad stomach?

A

VIP

42
Q

What is retropulsion?

A

Retropulsion is the propulsion of chyme back from the pylorus into the caudad region of the stomach. This leads to further mixing and break-down.

43
Q

What regulates the rate and magnitude of contractions in the lower stomach?

A

Parasympathetic innervation increases the magnitude of contractions

The rate of contractions is set by the gastric pacemaker

44
Q

What is the main limiting factor for gastric emptying time?

A

Size- liquid empties much faster than food.

Solids must be reduced to a particle size

45
Q

What causes gastric vs duodenal ulcers?

A

Gastric: breakdown of the HCO3-/mucus barrier

Duodenal: increased H+ secretion

Peptic ulcer= gastric or duodenal ulcer

46
Q

What is a major causative agent of gastric ulcers?

A

Gram negative bacteria H. Pylori. - releases cagA cytotoxins that destroy the protective barrier and cells underneath

47
Q

What is Zollinger-Ellison syndrome?

A

Gastrinomas- tumor, usually located in the pancreas- that secretes high levels of gastrin.

Increased gastrin leads to increased H+ from parietal cells and increased parietal cells mass.

48
Q

Why does Zollinger-Ellison sydrome lead to steatorrhea?

A

Low duodenal pH inactivates pancreatic lipase and so fatty acids are not properly broken down.

FHB Block 3 (26 decks)

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