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GI > PHYS: Gastric Secretion > Flashcards

PHYS: Gastric Secretion Flashcards

1
Q

List the 5 secretory products of the stomach and their functions.

A 
Hydrogen ion
Pepsinogens
Mucus
Intrinsic Factor
Water
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2
Q

What are the 3 major functions of the hydrogen ion in the stomach?

A

1) Kills bacteria (most important)
2) Activates conversion of pepsinogen to pepsin
3) Digests protein

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3
Q

What is the function of pepsinogen in the stomach?

A

Pepsin digests protein by cleaving interior peptide bonds

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4
Q

What are the 2 roles of mucus in the stomach?

A

1) Lubricates food

2) Protects lining of stomach (part of the gastric mucosal barrier)

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5
Q

What is the ONLY reason the stomach is necessary for life?

A

it is the source of intrinsic factor

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6
Q

What is the function of intrinsic factor?

A

Necessary for absorption of Vitamin B12

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7
Q

If you remove Vitamin B12 from the diet, how long would it take to develop pernicious anemia?

A

4-5 years (tons of storage)

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8
Q

What is the function of water in the stomach?

A

dissolves and dilutes ingested material

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9
Q

What is the location/cell type that secretes H+?

A

parietal cells in the body

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10
Q

What is the location/cell type that secretes pepsinogen?

A

chief cells in the body

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11
Q

What is the location/cell type that secretes gastrin?

A

G cells in the antrum

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12
Q

What is the location/cell type that secretes intrinsic factor?

A

parietal cells in the body

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13
Q

What is the location/cell type that secretes mucous?

A

mucous cells in the antrum

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14
Q

What is the major cell type in oxytinic gland mucosa?

A

80-85% parietal cells

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15
Q

What is the major cell type in the pyloric gland mucosa?

A

G cells (NO parietal cells)

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16
Q

What cell type is located “deepest” in gastric oxytinic glands?

A

chief cells

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17
Q

What type of cells are located superficial to chief cells in gastric oxytinic glands?

A

parietal cells

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18
Q

At what concentration of acid can parietal cells achieve?

A

150-160 meq/L (millions fold higher than blood concentration)

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19
Q

What type of cells are located superficial to parietal cells in the gastric oxytinic glands?

A

mucous neck cells

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20
Q

What stimulates mucous neck cells? What do these release?

A

vagus nerve (to secrete a watery mucous

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21
Q

What is another role of mucous neck cells?

A

act as stemcells

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22
Q

What is located at the surface of the gastric oxytinic gland (duct)?

A

surface epithelial cells (folveolar cells) that secrete a mucous

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23
Q

What is the role of carbonic anhydrase in gastric acid production?

A

Anhydrase converts H2O and CO2 into H2CO3 which dissociates into H+ and bicarbonate.

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24
Q

Can you completely inhibit gastric acid production by blocking carbonic anhydrase?

A

no (but you can slow down acid production)

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25
Q

How does this H+ produced by carbonic anhydrase get secreted into the gastric lumen?

A

H+/K+ ATPase (primary active transporter that moves ions against their concentration gradient)

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26
Q

What drug inhibits the H+/K+ ATPase in the stomach?

A

PPIs (prazoles)

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27
Q

How does HCO3- get secreted into the blood?

A

HCO3- is absorbed into the venous blood via a Cl-/HCO3- exchanger

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28
Q

What is the word for a high blood pH after a meal?

A

alkaline tide

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29
Q

What happens to the Cl- that is pumped into cells by the Cl-/HCO3- exchanger?

A

enter lumen via apical membrane passive conductance channels (down their concentration gradient)

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30
Q

Why is the passive flow of Cl- into the lumen important for acid secretion?

A

Cl- secretion accounts for most of the potential difference across the oxytinic gland mucosa (allows H+ to be secreted down its electrochemical gradient!)

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31
Q

What is responsible for neutralizing gastric acid that comes into contact with the epithelium?

A

gastric mucosal barrier

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32
Q

What substance is responsible for destruction of peptides in the gastric mucosal barrier and possible gastric ulcers?

A

ethanol

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33
Q

What substance is responsible for separation of charges across the gastric mucosa and cellular damage?

A

aspirin

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34
Q

How does aspirin decrease the potential difference across the mucosa (separate charges)?

A

aspirin is a weak acid that becomes unionized in stomach (lipid soluble) and crosses into the gastric mucosal cells where it breaks back down and releases H+ into cells

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35
Q

How does acid not destroy parietal cells?

A

acid is always maintained within tubulovesicles within parietal cells (so it never gets into the cytoplasm)

36
Q

How does acid move from parietal cell tubulovesicles into the gastric lumen?

A

canaliculus within cells will create a channel between the lumen and the tubulointersitial cell (snake-like)

37
Q

What is ion characteristics of gastric secretion at high secretory rates?

A

As secretory rate increases, the concentration of H+ ions in the secretion increases and the concentration of sodium decreases.

38
Q

True or false: gastric secretion is hyperosmotic to plasma at all secretory rates.

A

FALSE: gastric juice is essentially iso-osmotic to plasma at all secretory rates

39
Q

What theory divides gastric secretions into non-oxyntic secretion (produced continually at low rates) and oxyntic secretion (acid produced from parietal cells)?

A

two component hypothesis

40
Q

According to the two component hypothesis, what happens when the stomach is stimulated?

A

The stimulated stomach causes increased oxyntic secretion that “overwhelms” the non-oxyntic.

41
Q

What are the three major stimulators of gastric acid secretion?

A

Ach
Gastrin
Histamine

42
Q

What type of chemical is Ach?

A

neurocrine (released from interneurons)

43
Q

What is the target of Ach on parietal cells?

A

M3 receptors

44
Q

What happens when Ach activates M3 receptors?

A

Ach activates PLC which liberates DAG and IP3 from PIP2. IP3 releases Ca2+ from intracellular stores and this Ca2+ and DAG activate protein kinases that cause the H+ secretion from parietal cells

45
Q

What blocks M3 receptors on parietal cells?

A

atropine

46
Q

Other than stimulating gastric acid secretion, what is the role of Ach in the stomach?

A

stimulates ECL cells to release histamine (which also increases H+ secretion)

47
Q

What type of chemical is gastrin?

A

endocrine (released from G cells into the blood)

48
Q

What is the target of gastrin on the parietal cell?

A

CCKb receptors

49
Q

What does the binding of gastrin to CCKb cause?

A

Gastrin binding to CCKB acts in the same way as Ach on M3 receptors (via IP3/Ca2+ second messenger system).

50
Q

Other than stimulating gastric acid secretion, what is the role of gastrin in the stomach?

A

stimulates ECL cells to release histamine (which also increases H+ secretion)

51
Q

What type of chemical is histamine?

A

paracrine (released from ECLs in the gastric mucosa and diffuse to parietal cells)

52
Q

What is the target of histamine on parietal cells?

A

H2 receptors

53
Q

What happens when H2 binds to H2 receptors?

A

Histamine binds to the Gs receptor→ stimulates adenylyl cyclase to increase production of cAMP→ activates PKA→ leads to secretion of H+ by parietal cells

54
Q

What can block H2 receptors on parietal cells?

A

cimetidine

55
Q

What is the word for Ach and Gastrin being able to stimulate ECL cells to release histamine?

A

potentiation (two stimuli can produce a combined response that is greater than the sum of individual responses)

56
Q

Basal acid secretion is usually correlated with what?

A

gastrin secretion

57
Q

When is basal acid secretion independent of serum gastrin?

A

fasting human (acid peak at night that is NOT related to gastrin)

58
Q

True or false: you secrete more gastric acid when you like a food than when you don’t like it.

A

TRUE

59
Q

List the 3 phases of gastric acid secretion. (and their percentage contribution to HCl secretion)

A
  • Cephalic phase (30%)
  • Gastric phase (60%)
  • Intestinal phase (10%)
60
Q

What are the stimuli for the cephalic phase of gastric HCl secretion?

A

smelling, tasting, chewing, swallowing and conditioned reflexes in anticipitation of food.

61
Q

What are the two ways that stimuli promote gastric HCl secretion in the cephalic phase?

A
  • Direct stimulation of parietal cell by vagus nerves (via Ach)
  • Indirect stimulation of parietal cells by gastrin (vagus release GRP at G cells and stimulate the gastrin secretion→ blood)
62
Q

What are the stimuli for the gastric phase of gastric HCl secretion?

A
  • distention of stomach

- presence of breakdown products (amino acids and small peptides)

63
Q

How can distention of the stomach lead to gastric HCl secretion?

A
  • vagovagal reflex

- direct Ach release

64
Q

List the 4 physiological mechanisms involved in the gastric phase to release HCl.

A
  • Direct stimulation of parietal cell by vagus nerves (via Ach)
  • Indirect stimulation of parietal cells by gastrin
  • Distention of antrum→ local reflex (Ach) that stimulates gastrin release
  • AAs and peptides directly stimulate G cells to release gastrin
65
Q

What chemical can prevent the release of gastrin REGARDLESS of the stimuli?

A

somatostatin

66
Q

What stimulates the release of somatostatin?

A

pH of <3

67
Q

What inhibits release of somatostatin?

A

vagus nerve

68
Q

What is the “direct pathway” for somatostatin action?

A

acts through Gi to inhibit AC and lower cAMP

69
Q

What is the “indirect pathway” for somatostatin action?

A

inhibits histamine and gastrin release from cells

70
Q

What mediates the intestinal phase of gastric acid secretion?

A

products of protein digestion

71
Q

Where is somatostatin released from?

A

Oxytinic gland area and antrum

72
Q

In what part of the GI system is Secretin released?

A

duodenum

73
Q

What is the stimulus for secretin release?

A

acid

74
Q

What is the role of secretin?

A

inhibits gastrin release and directly inhibits acid secretion

75
Q

What other stimuli at the duodenum (other than secretin) leads to the inhibition of gastric acid secretion?

A

Hyperosmotic solutions (via unidentified enterogasterone)

76
Q

What substance is released from the duodenum and jejunum in response to fatty foods that inhibit gastrin release and directly inhibits acid secretion?

A

GIP

77
Q

Before a meal, what is the condition of the stomach?

A

very acidic (but a low rate of secretion due to somatostatin release)

78
Q

After a meal, what is the condition of the stomach?

A

pH increases (food acts like buffer)

79
Q

At what point in a meal will gastric acid secretion really increase?

A

only after both the pH and volume have increased

80
Q

What is the major stimulus for pepsinogen secreiton?

A

vagal stimulation

81
Q

Under what conditions would H+ trigger pepsinogen release?

A

ONLY WHEN the gastric contents is lowered by H+ secreiton so that pepsinogen can properly be converted to pepsin

82
Q

What other entity can stimulate pepsinogen release?

A

secretin

83
Q

Where does H pylori live in the stomach?

A

antrum

84
Q

What does H pylori do in the stomach?

A

produces damaging cytokines and urease (converts urea to ammonia which is a strong base that takes up H+ in the stomach to make ammonium)

85
Q

What is the consequence of ammonia and ammonium production by H pylori?

A
  • local reduction in pH (allows bacterial survi val)

- damage of gastric mucosa

86
Q

What is the cause of gastric ulcers in an H pylori infeciton: too much acid or too little protection?

A

Too little protection (ammonium damages the gastric mucosal barrier and acid that is released may back diffuse through the damage and actually lead to less acid production)

87
Q

What is the cause of duodenal ulcers in an H pylori infeciton: too much acid or too little protection?

A

Ammonium releases gastrin (and inhibits somatostatin from inhibiting gastrin). This leads to increased acid secretion, increased numbers of parietal cells, and damage to the duodenum (which does not have a protective mucosa in the first place) due to the excessive acid.

GI (21 decks)

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