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PHYS: Gastric Secretion Flashcards

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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
How does this H+ produced by carbonic anhydrase get secreted into the gastric lumen?
H+/K+ ATPase (primary active transporter that moves ions against their concentration gradient)
26
What drug inhibits the H+/K+ ATPase in the stomach?
PPIs (prazoles)
27
How does HCO3- get secreted into the blood?
HCO3- is absorbed into the venous blood via a Cl-/HCO3- exchanger
28
What is the word for a high blood pH after a meal?
alkaline tide
29
What happens to the Cl- that is pumped into cells by the Cl-/HCO3- exchanger?
enter lumen via apical membrane passive conductance channels (down their concentration gradient)
30
Why is the passive flow of Cl- into the lumen important for acid secretion?
Cl- secretion accounts for most of the potential difference across the oxytinic gland mucosa (allows H+ to be secreted down its electrochemical gradient!)
31
What is responsible for neutralizing gastric acid that comes into contact with the epithelium?
gastric mucosal barrier
32
What substance is responsible for destruction of peptides in the gastric mucosal barrier and possible gastric ulcers?
ethanol
33
What substance is responsible for separation of charges across the gastric mucosa and cellular damage?
aspirin
34
How does aspirin decrease the potential difference across the mucosa (separate charges)?
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
35
How does acid not destroy parietal cells?
acid is always maintained within tubulovesicles within parietal cells (so it never gets into the cytoplasm)
36
How does acid move from parietal cell tubulovesicles into the gastric lumen?
canaliculus within cells will create a channel between the lumen and the tubulointersitial cell (snake-like)
37
What is ion characteristics of gastric secretion at high secretory rates?
As secretory rate increases, the concentration of H+ ions in the secretion increases and the concentration of sodium decreases.
38
True or false: gastric secretion is hyperosmotic to plasma at all secretory rates.
FALSE: gastric juice is essentially iso-osmotic to plasma at all secretory rates
39
What theory divides gastric secretions into non-oxyntic secretion (produced continually at low rates) and oxyntic secretion (acid produced from parietal cells)?
two component hypothesis
40
According to the two component hypothesis, what happens when the stomach is stimulated?
The stimulated stomach causes increased oxyntic secretion that “overwhelms” the non-oxyntic.
41
What are the three major stimulators of gastric acid secretion?
Ach Gastrin Histamine
42
What type of chemical is Ach?
neurocrine (released from interneurons)
43
What is the target of Ach on parietal cells?
M3 receptors
44
What happens when Ach activates M3 receptors?
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
What blocks M3 receptors on parietal cells?
atropine
46
Other than stimulating gastric acid secretion, what is the role of Ach in the stomach?
stimulates ECL cells to release histamine (which also increases H+ secretion)
47
What type of chemical is gastrin?
endocrine (released from G cells into the blood)
48
What is the target of gastrin on the parietal cell?
CCKb receptors
49
What does the binding of gastrin to CCKb cause?
Gastrin binding to CCKB acts in the same way as Ach on M3 receptors (via IP3/Ca2+ second messenger system).
50
Other than stimulating gastric acid secretion, what is the role of gastrin in the stomach?
stimulates ECL cells to release histamine (which also increases H+ secretion)
51
What type of chemical is histamine?
paracrine (released from ECLs in the gastric mucosa and diffuse to parietal cells)
52
What is the target of histamine on parietal cells?
H2 receptors
53
What happens when H2 binds to H2 receptors?
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
What can block H2 receptors on parietal cells?
cimetidine
55
What is the word for Ach and Gastrin being able to stimulate ECL cells to release histamine?
potentiation (two stimuli can produce a combined response that is greater than the sum of individual responses)
56
Basal acid secretion is usually correlated with what?
gastrin secretion
57
When is basal acid secretion independent of serum gastrin?
fasting human (acid peak at night that is NOT related to gastrin)
58
True or false: you secrete more gastric acid when you like a food than when you don't like it.
TRUE
59
List the 3 phases of gastric acid secretion. (and their percentage contribution to HCl secretion)
- Cephalic phase (30%) - Gastric phase (60%) - Intestinal phase (10%)
60
What are the stimuli for the cephalic phase of gastric HCl secretion?
smelling, tasting, chewing, swallowing and conditioned reflexes in anticipitation of food.
61
What are the two ways that stimuli promote gastric HCl secretion in the cephalic phase?
* 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
What are the stimuli for the gastric phase of gastric HCl secretion?
- distention of stomach | - presence of breakdown products (amino acids and small peptides)
63
How can distention of the stomach lead to gastric HCl secretion?
- vagovagal reflex | - direct Ach release
64
List the 4 physiological mechanisms involved in the gastric phase to release HCl.
* 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
What chemical can prevent the release of gastrin REGARDLESS of the stimuli?
somatostatin
66
What stimulates the release of somatostatin?
pH of <3
67
What inhibits release of somatostatin?
vagus nerve
68
What is the "direct pathway" for somatostatin action?
acts through Gi to inhibit AC and lower cAMP
69
What is the "indirect pathway" for somatostatin action?
inhibits histamine and gastrin release from cells
70
What mediates the intestinal phase of gastric acid secretion?
products of protein digestion
71
Where is somatostatin released from?
Oxytinic gland area and antrum
72
In what part of the GI system is Secretin released?
duodenum
73
What is the stimulus for secretin release?
acid
74
What is the role of secretin?
inhibits gastrin release and directly inhibits acid secretion
75
What other stimuli at the duodenum (other than secretin) leads to the inhibition of gastric acid secretion?
Hyperosmotic solutions (via unidentified enterogasterone)
76
What substance is released from the duodenum and jejunum in response to fatty foods that inhibit gastrin release and directly inhibits acid secretion?
GIP
77
Before a meal, what is the condition of the stomach?
very acidic (but a low rate of secretion due to somatostatin release)
78
After a meal, what is the condition of the stomach?
pH increases (food acts like buffer)
79
At what point in a meal will gastric acid secretion really increase?
only after both the pH and volume have increased
80
What is the major stimulus for pepsinogen secreiton?
vagal stimulation
81
Under what conditions would H+ trigger pepsinogen release?
ONLY WHEN the gastric contents is lowered by H+ secreiton so that pepsinogen can properly be converted to pepsin
82
What other entity can stimulate pepsinogen release?
secretin
83
Where does H pylori live in the stomach?
antrum
84
What does H pylori do in the stomach?
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
What is the consequence of ammonia and ammonium production by H pylori?
- local reduction in pH (allows bacterial survi val) | - damage of gastric mucosa
86
What is the cause of gastric ulcers in an H pylori infeciton: too much acid or too little protection?
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
What is the cause of duodenal ulcers in an H pylori infeciton: too much acid or too little protection?
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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