04b: Gastric secretion Flashcards by Nuna H

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

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

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List the cell types producing gastric juice.

Parietal
Chief
Mucus (neck) cells
Epithelial cells

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

X = G cells
Y = EEC and D cells

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

None

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

D cells and EECs (paracrine)

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

D cells (paracrine) and G cells (endocrine)

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

X = parietal
Apical
H-K ATPases

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

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

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

K; lumen
X = K channel
Luminal

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

Secretion;

X = Cl

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

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

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

Dissociation of H2CO3 (via carbonic anhydrase)

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

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

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

True

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

X = proteins
Y = R-proteins (glycoproteins)

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

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

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

False - not pancreatic proteases

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

X = small intestine
Y = R-protein

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

True

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

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

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

Degraded;

Lysosomes following endocytosis of IF-B12 complex in ileum

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

X = pernicious anemia

RBCs fail to mature normally

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

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

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

X = peptide
Y = aromatic AAs, Met, Leu

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T/F: Pepsins can be irreversibly inactivated.

True - at neutral/alkaline pH

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

X = neck and epithelial Y = HCO3 Alkaline

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

X = tight junctions between mucosal cells

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

X = mucosal damage 1. Decrease acid secretion 2. Increase mucus production 3. Dilates arterioles

List the three phases of gastric secretion.

1. Cephalic 2. Gastric 3. Intestinal

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

``` X = cephalic Y = vagus nerve ```

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

X = vagal 1. EEC 2. G-cell 3. D-cell

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

Secretes; X = Gastrin Secretes; Y = Somatostatin

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

``` X = cholinergic stimulation; Y = histamine ```

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

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

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

``` Decreases; Blocks histamine (H2) receptor on parietal cells ```

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

``` X = peptidergic neurons Y = pyloric antrum ``` Activate G-cells (to secrete gastrin)

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

False - four terminal AA residues

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

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

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

True

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

X = CCK-2

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

``` X = gastrin Y = 3 ```

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

X = antrum Stimulates; Y = somatostatin Blocks G-cell secretion of gastrin

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

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

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

``` X = sensory fibers Y = H sampling (acidic environment) ``` Stimulates D-cell release of somatostatin

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.

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

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

Signaling cascade that raises intracell Ca

His mediates its effect on parietal cells via which mechanism?

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

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

X = gastric 1. Distension reflex 2. Chemical stimulation

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

``` X = gastric Y = vagal ``` Afferents and efferents (vago-vagal reflex)

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

1. Gastrin | 2. His

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

``` X = peptides and AAs Y = pyloric antrum ``` Raise serum gastrin levels (via direct G-cell stimulation)

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

X = fat, acid, or hypertonic solutions Yes; under hormonal control

Enterogastrones are (X) responsible for (Y).

``` X = hormones Y = inhibition of acid secretion when duodenum sees acid/fat/hypertonic solution ```

List the enterogastrones and respective cell source.

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

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

``` X = duodenal mucosa Y = Secretin ``` pH (of chyme) less than 4.5

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

Inhibit; Stimulates Somatostatin secretion from D-cells

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

``` X = duodenal mucosa Y = CCK ``` FA, peptides, and AA in duodenum

(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?

X = CCK Y = CCK-2 receptor (in stomach) Same No - weak agonist that competes with gastrin

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

True

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

``` X = duodenal mucosa Y = GIP ``` FAs and CHO

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

False - minor effect in humans

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

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