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GI/Nutrition > 04b: Gastric secretion > Flashcards

04b: Gastric secretion Flashcards

1
Q

Aside from storing/mixing food, stomach secretes (X) for bacteriostasis/digestion and (Y) for (Z) absorption.

A 
X = acid/pepsins
Y = intrinsic factor (IF)
Z = vitamin B12
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2
Q

List the cell types producing gastric juice.

A
  1. Parietal
  2. Chief
  3. Mucus (neck) cells
  4. Epithelial cells
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3
Q

Gastric mucosa contains cells, (X), with endocrine secretion. Also cells, (Y), with paracrine secretion.

A 
X = G cells
Y = EEC and D cells
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4
Q

Which endocrine/paracrine cells are found in cardiac region of stomach?

A

None

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5
Q

Which endocrine/paracrine cells are found in fundus/corpus region of stomach?

A

D cells and EECs (paracrine)

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6
Q

Which endocrine/paracrine cells are found in pyloric region of stomach?

A

D cells (paracrine) and G cells (endocrine)

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7
Q

Gastric (X) cell distinguished by large mito content and infolding of (basal/apical) membrane. What do the intracellular vesicles contain?

A

X = parietal
Apical
H-K ATPases

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8
Q

H-K ATPases in (luminal/basal) membrane (X) gastric cells allow (co-transport/exchange) of the ions (into/out of ) cell.

A

Luminal;
X = parietal
Exchange
1 H out for 1 K in

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9
Q

Parietal cells: (H/K) is replenished in (cell/lumen) via (X) (channel/transporter) on (luminal/basal) membrane.

A

K; lumen
X = K channel
Luminal

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10
Q

Parietal cell: (secretion/absorption) of (X) across luminal border as counter-ion for K is essential.

A

Secretion;

X = Cl

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11
Q

Parietal cell: thanks to (X) movement, the luminal membrane is (repolarized/depolarized) and K moves (uphill/downhill) via (ATPase/channel).

A

X = Cl (moving out of cell)
Depolarized
Downhill; channel (out of cell)

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12
Q

Parietal cell: where did the H+ even come from?

A

Dissociation of H2CO3 (via carbonic anhydrase)

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13
Q

Parietal cell: for every H moving into (lumen/cell), one HCO3 moves into (X). This is responsible for (Y) phenomenon seen in venous blood.

A

Lumen;
X = ISF
Y = alkaline tide (high HCO3 and pH)

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14
Q

T/F: Vit B12 (cobalamin) is only available from dietary sources.

A

True

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15
Q

Ingested vitamin B12 dissociates from dietary (X) and is bound by (Y).

A 
X = proteins
Y = R-proteins (glycoproteins)
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16
Q

Aside from R-proteins, (X) can also bind (Y) in the stomach. Its affinity is (higher/lower).

A

X = Intrinsic Factor (IF)
Y = Vitamin B12
Lower

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17
Q

T/F: R protein is resistant to stomach acid/pepsin and pancreatic proteases.

A

False - not pancreatic proteases

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18
Q

In (X) part of GI tract, Vit B12 is freed from its bonds to (Y) and thus binds to IF.

A 
X = small intestine
Y = R-protein
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19
Q

T/F: Intrinsic Factor (IF) is resistant to stomach acid/pepsin and pancreatic proteases.

A

True

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20
Q

When B12 passes to ileum, it is (free/bound) and absorbed via (X) mechanism. Afterwards, it’s exocytosed into (Y), bound to (Z).

A

Bound (IF-B12 complex)
X = receptor-mediated endocytosis
Y = plasma
Z = transcobalamin

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21
Q

Where is IF (degraded/recycled)? Be specific.

A

Degraded;

Lysosomes following endocytosis of IF-B12 complex in ileum

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22
Q

A lack of IF leads to (X) disease, in which:

A

X = pernicious anemia

RBCs fail to mature normally

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23
Q

Below pH (X), pepsinogens activated to pepsins via (Y) mechanism.

A 
X = 4.0 (optimal is 1.8-3.5)
Y = cleavage of acid-sensitive peptide bonds
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24
Q

Pepsins have broad specificity, but prefer cleaving (X) bonds involving (Y) structures.

A 
X = peptide
Y = aromatic AAs, Met, Leu
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25
Q

T/F: Pepsins can be irreversibly inactivated.

A

True - at neutral/alkaline pH

26
Q

(X) cells in stomach produce mucus along with (Y), forming protective, (acidic/alkaline) barrier.

A

X = neck and epithelial
Y = HCO3
Alkaline

27
Q

Gastric mucosal barrier: (X) prevent intercellular passage of H+ from lumen to underlying tissue.

A

X = tight junctions between mucosal cells

28
Q

Gastric mucosal barrier: Prostaglandin (PGE2) is released in response to (X). What are its effects?

A

X = mucosal damage

  1. Decrease acid secretion
  2. Increase mucus production
  3. Dilates arterioles
29
Q

List the three phases of gastric secretion.

A
  1. Cephalic
  2. Gastric
  3. Intestinal
30
Q

Stimuli for (X) phase of gastric secretion include sight/smell, chewing, swallowing of food. Activation of secretion is mediated entirely by (Y).

A 
X = cephalic
Y = vagus nerve
31
Q

Cephalic phase of secretion: aside from the gastric secretory cells, (X) stimulation also influences which cell types?

A

X = vagal

  1. EEC
  2. G-cell
  3. D-cell
32
Q

G-cell (secretes/absorbs) (X). D-cell (secretes/absorbs) (Y).

A

Secretes;
X = Gastrin
Secretes;
Y = Somatostatin

33
Q

Cephalic phase of secretion: EEC cell is stimulated by (X) to release (Y).

A 
X = cholinergic stimulation;
Y = histamine
34
Q

Cephalic phase of secretion: histamine has (direct/indirect) impact which (increases/decreases) acid secretion. Elaborate a bit.

A

Direct (on parietal cells) and indirect (by potentiating action of ACh and gastrin)

Increases

35
Q

Cimetidine is a drug that (increases/decreases) acid secretion by:

A 
Decreases;
Blocks histamine (H2) receptor on parietal cells
36
Q

Gastrin-releasing Peptide (GRP) is released by (X) in (Y) part of stomach. What’s their function?

A 
X = peptidergic neurons
Y = pyloric antrum

Activate G-cells (to secrete gastrin)

37
Q

T/F: Full range of physiologic actions of gastrin hormones resides in the four middle AA residues.

A

False - four terminal AA residues

38
Q

Gastrin has (direct/indirect) effect of (stimulating/inhibiting) acid secretion. List these effect(s) and star the most effective.

A

Stimulating;

Direct: stimulates parietal cells
Indirect: stimulates His secretion from EEC

39
Q

T/F: His is the most potent agonist for parietal cell.

40
Q

In the stomach, gastrin’s actions are mediated by (X) receptor.

41
Q

(X) release from G-cells is inhibited when pH is less than (Y).

A 
X = gastrin
Y = 3
42
Q

Acid in (X) part of stomach (stimulates/inhibits) D-cell secretion of (Y). What does this do?

A

X = antrum
Stimulates;
Y = somatostatin

Blocks G-cell secretion of gastrin

43
Q

Somatostatin secretion from D-cells stimulated (directly/indirectly) via which mechanisms?

A

Direct: H in gastric juice
Indirect: H sampled by sensory fibers that release CGRP

44
Q

Calcitonin Gene related peptide (CGRP) is released from (X) in response to (Y). What’s CGRP effect?

A 
X = sensory fibers
Y = H sampling (acidic environment)

Stimulates D-cell release of somatostatin

45
Q

Plasma levels of gastrin are typically (higher/lower/same) during cephalic phase when there’s no food in stomach, compared to when food is ingested.

A

Lower (no food means luminal pH low, so somatostatin secreted to inhibit gastrin secretion)

46
Q

Gastrin and ACh mediate their effects on parietal cells via which mechanism?

A

Signaling cascade that raises intracell Ca

47
Q

His mediates its effect on parietal cells via which mechanism?

A

Activates AC, increases cAMP, increases vesicle trafficking (H-K ATPases)

48
Q

Most acid secretion during course of meal occurs during (X) phase. List the mechanisms that mediate this.

A

X = gastric

  1. Distension reflex
  2. Chemical stimulation
49
Q

Distension reflexes play role in (X) phase of secretion. Along with intramural reflexes, long reflex arcs are mediated by (Y) (afferents/efferents).

A 
X = gastric
Y = vagal

Afferents and efferents (vago-vagal reflex)

50
Q

Distension reflexes during gastric phase cause secretion of which hormone(s)?

A
  1. Gastrin

2. His

51
Q

Chemical stimulation mechanism in gastric secretion phase: (X) bathe (Y) region of stomach. What key effect does this have?

A 
X = peptides and AAs
Y = pyloric antrum

Raise serum gastrin levels (via direct G-cell stimulation)

52
Q

Introduction of (X) into duodenum inhibits acid secretion. Is this also true in vagally denervated gastric pouches?

A

X = fat, acid, or hypertonic solutions

Yes; under hormonal control

53
Q

Enterogastrones are (X) responsible for (Y).

A 
X = hormones
Y = inhibition of acid secretion when duodenum sees acid/fat/hypertonic solution
54
Q

List the enterogastrones and respective cell source.

A
  1. Secretin (S-cells)
  2. Cholecystokinin (CCK; I-cells)
  3. Gastric Inhibitory Peptide (GIP; K-cells)
55
Q

S-cells in (X) tissue releases (Y) in response to:

A 
X = duodenal mucosa
Y = Secretin

pH (of chyme) less than 4.5

56
Q

Secretin is likely to (stimulate/inhibit) acid secretion via which mechanism?

A

Inhibit;

Stimulates Somatostatin secretion from D-cells

57
Q

I-cells in (X) tissue releases (Y) in response to:

A 
X = duodenal mucosa
Y = CCK

FA, peptides, and AA in duodenum

58
Q

(X) hormone has same terminal sequence as gastrin, thus binding to (Y) with (higher/lower/same) affinity. Does it have the same effect as gastrin?

A

X = CCK
Y = CCK-2 receptor (in stomach)
Same

No - weak agonist that competes with gastrin

59
Q

T/F: CCK and gastrin bind CCK-2 receptor with same affinity, but gastrin is stronger agonist.

60
Q

K-cells in (X) tissue releases (Y) in response to:

A 
X = duodenal mucosa
Y = GIP

FAs and CHO

61
Q

T/F: GIP likely has the greatest effect, of the enterogastrones, on inhibition of acid secretion.

A

False - minor effect in humans

62
Q

GIP affects acid secretion by (stimulating/inhibiting) (X) release. But, its more important role is to (promote/inhibit) (Y).

A

Inhibiting;
X = H and gastrin
Promote;
Y = insulin secretion from pancreas

GI/Nutrition (17 decks)

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