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MAMS Physio > Gastric Secretions > Flashcards

Gastric Secretions Flashcards

1
Q

What does chyme consist of?

A
  • Protein
  • polysaccharide fragments
  • Fat droplets
  • ions, H2O
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2
Q

Which part of the stomach is responsible for mixing and grinding stomach contents and why?

A

The Antrum, because it contains a thicker layer of smooth muscle

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3
Q

Cells near the opening of gastric glands secrete what?

A

Mucus and HCO3-

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4
Q

Parietal cells secrete what?

A

Acid (HCl) and Intrinsic Factor

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5
Q

Which cells secrete Pepsinogen?

A

Chief cells

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6
Q

Which cells secrete Gastrin?

A

G cells

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7
Q

Gastrin has what effect on parietal cells?

A

Increases the secretion of acid

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8
Q

Where are G cells located?

A

In the Antrum

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9
Q

Which cells secrete Histamine?

A

Enteroendocrine cells

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10
Q

Which cells secrete Somatostatin?

A

D cells

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11
Q

How much HCl is secreted per day?

A

2L

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12
Q

What is the concentration of H+ in the lumen, and how does it compare to the blood?

A

> 150mM

1-3 million x of blood

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13
Q

Carbonic Anhydrase equations

A

H2O+CO2 -> H2CO3 -> HCO3- + H+

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14
Q

Which cell produces H+?

A

Parietal cells

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15
Q

How does H+ get into the lumen from parietal cells?

A

H+/K+ ATPase

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16
Q

When HCO3- is transported into the capillaries, what is it exchanged for?

A

Cl-

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17
Q

Which three hormones stimulate insertion of Na+/K+ ATPase into the membrane?

A

Gastrin, Histamine and Ach

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18
Q

How do Gastrin, Histamine and Ach influence each other?

A

Histamine stimulates secretion of Gastrin and Ach and vice versa

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19
Q

The cephalic phase is mediated by which nervous pathways?

A

Parasympathetic neurons carried in the vagus nerves
- activate neurons in the plexi, which affect secretory and contractile activity

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20
Q

Parasympathetic stimulation in the cephalic phase to the stomach causes

A

1) Ach release from neural plexus
2) Gastrin release from G cells
3) Histamine release from ECL cells

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21
Q

Effect of distention, increase in amino acids/peptides on acid secretion in gastric phase

A

Increases the release of acid

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22
Q

Effect of H+ in lumen

A

Directly inhibits Gastrin secretion, stimulates release of Somatostatin from D cells

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23
Q

Effect of Somatostatin on release of Gastrin and Histamine

A

Inhibitory effect

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24
Q

Effect of acid entering small intestine

A

Inhibits gastric acid secretion

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25
Q

What converts pepsinogen into pepsin

A

Exposure to low pH in the lumen

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26
Q

What happens to Pepsin in the small intestine?

A

Inactivated by HCO3- secreted by the small intestine and pancreas

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27
Q

What causes the release of Pepsin

A

Parallels acid secretion, inout to chief cells
- parasympathetic input to enteric NS during cephalic
- gastric phase stimuli during gastric phase

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28
Q

Is Pepsin essential for protein digestion

A

No, but it accelerates it and accounts for 20% of protein digestion

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29
Q

Which enzyme is important in the digestion of collagen?

30
Q

What factors prevent the stomach from self-digestion?

A

1) Mucus
2) Tight Junctions
3) Damaged cells

31
Q

Where can ulcers occur and most often?

A

Stomach, Esophagus, Duodenum (10x more than stomach)

32
Q

Major factor in ulcer formation?

A

Helicobacter Pylori

33
Q

What does Cimetidine do?

A

H2 receptor (Histamine) antagonist

34
Q

What do Omeprazole/Lansoprazole do?

A

Inhibit H+/K+ ATPase in parietal cells

35
Q

What happens to the K+ in parietal cells?

A

Leaks back out into the lumen via leak channels

36
Q

What opposes the alkaline tide?

A

Pancreatic endocrine secretion of H+ and exocrine secretion of HCO3-

37
Q

What does Intrinsic Factor do?

A

Allows for absorption of Vitamin B12

38
Q

Mechanism of Vit B12 absorption

A

1) B12 is initially bounds to R-protein (Haptocorrin) in the stomach
2) R protein degraded by pancreatic proteases in proximal intestine
3) B12 binds IF
4) B12 absorbed by enterocytes in distal ileum via endocytosis
5) IF digested by lysozymes, B12 bound to Transcobalamin in bloodstream

39
Q

What is pernicious anemia

A

Production of antibodies to IF or parietal cells

40
Q

No B12, No…

41
Q

Which pH causes autoactivation of Pepsin?

42
Q

How is Pepsin cleaved from Pepsinogen?

A

High acidity causes unwinding and cleavage of the N-terminal domain which is blocking its own active site

43
Q

Can Pepsin activate other Pepsinogen?

44
Q

When is Pepsin inactivated?

A

At pH 7 in the small intestine

45
Q

Effect of mucus on diffusion rate of H+

A

Reduces the rate to 25%

46
Q

What does the mucus layer do to HCO3-?

47
Q

Relation of phospholipids to mucus

A

Phosphlipid layer on the mucus

48
Q

What causes the release of Prostaglandin E2

A

Any sort of irritation

49
Q

What is the effect of Prostaglandin E2 release?

A

Increases blood flow which is alkaline, and that transports the H+ away
Increase mucus production, decreases HCl production

50
Q

What’s Restitution?

A

If the gastric mucosal barrier is compromised, the cells change form simple columnar to squamous and make tight junctions
- complete after one hour
- stem cells replenish afterwards

51
Q

Gastric phase stimuli cause Enteroendocrine cells to do what?

A

Secret Histamine (paracrine) which binds to the H-2 receptors on parietal cells to increase acid secretion

52
Q

Significance of Histamine to Parietal cells

A

Histamine is the most potent agonist of parietal cells

53
Q

Gastric phase stimuli affect G cells how?

A

They secrete Gastrin (hormone), which enters the bloodstream and binds to CCK2 receptors on Parietal and EEC cells, promoting their secretion to increase acid

54
Q

Gastrin acts on which receptors and cells?

A

CCK2 receptors on Parietal and EEC cells

55
Q

What happens if there is too much acid in the stomach?

A

It will directly inhibit Gastrin secretion from G cells, and promote the secretion of Somatostatin from D cells, which inhibits Parietal, G and EEC cells

56
Q

Effect of Vagus nerve on gastric acid secretion

A

Release of Ach and GRP which promote secretions from G cells

57
Q

What happens to gastric secretions during the cephalic phase?

A

Vagal tone is increased, which stimulates G-cells
- if pH goes under 3, inhibited by D cells
- low stimulation of EEC and Parietal cells

58
Q

What happens to gastric secretions during the gastric phase?

A

Distention activates local nerves
- Food buffers acid, deinhibiting G cells, which is a potent agonist of ECE cells
- ECE produces Histamine, which increases effect of CCK-2 and Ach receptors on parietal cells

59
Q

If acid overwhelms the buffering capacity of food, what happens?

A

The D-cell is activated, releasing Somatostatin which shuts everything down

60
Q

Effect of Pepsin on Gastric secretions?

A

Breaks down proteins, creating more of a buffering effect. The peptides and amino acids also act on G cell receptors, which increases the release of Gastrin

61
Q

Do D-cells have receptors for Secretin?

62
Q

Which cell produces secretin, and what stimulates it?

A

S cell, pH < 4.5

63
Q

Which cell produces CCK, and what activates it?

A

I cell, activated by peptides and free FAs

64
Q

Which cell produces Gastric Inhibitory Peptide, and what activates it?

A

K cell, triggered by glucose and free FAs

65
Q

Which cell release peptide YY, what triggers it, and where is it found?

A

L cell, responds to glucose and free FAs, found in the Ileal region

66
Q

What factors trigger the D cell to release Somatostatin, and where are they found?

A

GIP, CCK, Secretin, found near EEC and Parietal cells

67
Q

What effect does CCK have on EEC and Parietal cells?

A

Displaces Gastrin at the CCK2 receptor
- has the same affinity, but is a weak agonist

68
Q

Why do the CCK receptors on D cells not react to Gastrin?

A

CCK has 1000x greater affinity

69
Q

What does Peptide YY do?

A

Directly inhibits EEC cells

70
Q

What are the intestinal inhibitory hormones of acid secretion

A

Secreting, GIP, YY, CCK

MAMS Physio (4 decks)

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