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GI- Week 2 > Prunuske: Gastric Secretion > Flashcards

Prunuske: Gastric Secretion Flashcards

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1
Q

Bezoar

A

ball of foreign material trapped in the stomach (hair ball)

get it out w/ the MMC

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2
Q

emesis

A

vomiting, forcible ejection of stomach contents through the mouth

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3
Q

dyspepsia

A

indigestion, pain in upper abdomen after eating

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4
Q

gastroparesis

A

delayed emptpying

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5
Q

migrating motor complex

A

clears undigested material from GI track

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6
Q

regurgitation

A

flow of material that has not reach stomach back up esophagus

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7
Q

rugae

A

stomach folds which expand as stomach fills, help to facilitate relaxation

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8
Q

scintigraphy

A

using a dual- radiolabeled solid and nutrient liquid meal to measure gastric emptying

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9
Q

trituration

A

grinding of food into small molecules

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10
Q

What is the mucosa called that lines the stomach?

A

oxyntic/parietal glandular mucosa

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11
Q

What do superficial epithelial cells, parietal (oxyntic) and chief cells all secrete?

A

Superficial epithelial cells= mucus and bicarbonate

Parietal= HCl, IF

Chief= pepsinogne

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12
Q

What activates parietal cells in the fundus/corpus to secrete acid?

A

Gastrin secreted from G cells in the ANTRUM

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13
Q

What is Gastrin and what type of receptors does it bind to?

A

Polypeptide w/ variable length and sequence

Binds CCK1 receptors

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14
Q

What triggers Gastrin release from G cells in the antrum?

A
  1. Seeing food/stomach distension–> vagal stimulation–> gastrin releasing peptide
  2. Aromatic AA in the lumen
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15
Q

Would you expect atropine to inhibit gastrin release?

A

No because atropine binds to muscarinic receptors.

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16
Q

What are the MAJOR stimulates that cause gastric acid secretion from parietal cells in the corpus?

A

Gastrin
Histamine
ACh

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17
Q

How does ACh release lead G cells to release gastrin?

A

Vagal fibers/enteric neural excitatory fibers>
bind MR on parietal cells>
activates ECL cells release of histamine>
activates enteric neurons to release GRP>
stimulates G cells to secrete Gastrin

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18
Q

How does Gastrin lead to the release of histamine?

A 
G cells>
release gastrin>
binds to parietal cells>
activates ECL cells>
releases histamine
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19
Q

How does Histamine activate parietal cells?

A

ECL cells>
release histamine>
cAMP dependent pathway>
activates parietal cells

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20
Q

What happens to tubulovesicular membranes and canalicular membranes when parietal cells are stimulated and how does this lead to a more acidic environment?

A

These membranes FUSE and increase the density of H, K, ATPase molecules at the apical membrane which are eventually used to pump protons into the lumen and make the environment more acidic

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21
Q

How are protons generated and exported out of parietal cells?

A

Via CA II in the CYTOSOL

H, K ATPase pumps them into the lumen

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22
Q

Why do parietal cells contain a large number of mitochondria?

A

Need a lot of ATP to power the H K ATPase

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23
Q

How does parietal cell stimulation cause an alkaline tide?

A

While H are exported to the lumen on the basolateral side:

Bicarb ions are exported OUT into the blood stream by VESICULAR FUSION and Cl/bicarb exchanger…this is referred to as the alkaline tide

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24
Q

Where do PPIs act?

A

On the H, K ATPase on the luminal side of parietal cells.

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25
What happens to the Cl that is pumped into the parietal cell via the Cl/bicarb exchanger end up?
Moves down the EC gradient when the luminal channel opens and water follows
26
What pump in the parietal cell is essential for maintaining gradients that allows the proton pump to work?
Na/K ATPase on the BASOLATERAL membrane
27
How does the electrical potential that exists across the mucosa differ in the parietal cell at rest and during activation?
rest -70 mv DECREASED during activation to -30mV
28
What inhibits gastrin release?
When the pH is less than 3, somatostatin is secreted from D cells in the antrum,, so during the gastric phase, the rise in pH leads to a DECREASE in somatostatin secretion
29
How does somatostatin inhibit gastric acid secretion?
When pH is less than three.... 1. prevents G cells release of gastrin 2. inhibits the formation of cAMP via G dependent signaling pathways in parietal cells 3. Prevents ECL cell secretion of histamine
30
What affect do prostaglandins have on cAMP formation?
inhibit cAMP
31
How does feedback from the duodenum lead to the inhibition of gastric acid secretion?
Nervous reflex form the duodenum BLOCKS ACh activation of parietal cells. Enterogastrones like secretin block secretion of histamine by ECL cells.
32
What are the phases of gastric secretion?
interdigestive cephalic gastric intestinal
33
interdigestive phase
Low acid secretion, D cells secrete somatostatin to maintain low levels of Gastrin
34
cephalic phase
dorsal vagal complex integrates input from higher centers (seeing and tasting food) to activate Vagus nerves. GRP activates gastrin release and Ach activates ECL and parietal cells.
35
gastric phase
distension of the stomach activates vagal afferents and the enteric nervous system. Amino acids activate gastrin secretion and food raises pH decreasing somatostatin secretion.
36
intestinal phase
introduction of the gastric contents into the small intestine activates duodenal G cell secretion of gastrin. Activation of secretin and other enterogastrones and neural reflex decreases secretion.
37
What is required for B12 absorption in the ileum?
Intrinsic factor (a glycoprotein secreted by parietal cells)
38
Do PPIs affect IF?
PPIs do nOT inhibit the secretion of IF but may decrase protein digestion
39
What decreases B12 absorption?
autoimmune destruction of parietal cells or bypass surgery
40
Decreased B12 absorption leads to...
megaloblastic anemia | neurologic deficiencies
41
What leads to the secretion of pepsinogen?
Ach/gastrin> | stimulate secretion of pepsinogen by CHIEF CELLS
42
What inhibits pepsinogen secretion?
secretin
43
Once pepsinogen enters the stomach, what happens to it?
Pepsinogen (inactive proenzyme protease) is ACTIVATED by the ACIDIC environment to PEPSIN which is a proteolytic enzyme
44
What is pepsin?
an endopeptidase that activates pepsiniogen by autolysis
45
How do chief cells lead to FA release?
They also secrete gastric lipase
46
How is the mucus gel layer/diffusion barrier created and what does it do?
PGE2 causes surface epithelial cells to secrete mucus and bicarbonate. This increases the pH at the surface to 7 while the luminal pH remains around 2. H ions and pepsin that then cross the diffusion barrier are neutralized by bicarbonate.
47
How does taking NSAIDs lead to gastric irriation?
NSAIDS BLOCK PGE2, so your surface epithelial cells won't secrete as much mucous and bicarb, so you don't have that protective buffer and are more prone to gastric irritation.
48
What else causes gastric irritation can lead to stress ulcers?
catecholamines (also suppress bicarb secretion)
49
If the stomach epithelium does get damaged, what is used for restitution and regeneration?
Trefoil factors | Growth factors
50
What is Zollinger Ellison syndrome (Gastrinoma)?
Gastrin secreting tumor in the pancreas or intestine that leads to EXCESS H secretion and eventual hyperplasia and hypertrophy of parietal cells
51
What causes peptic ulcer disease?
Hyperacidity | Deterioration of the gastro-mucosal barrier
52
What can lead to gastric and duodenal ulcers?
1. H. pylori infection 2. Poor secretion of mucus and bicarb by the surface epithelium 3. stress 4. irritation by alcohol, acid, digestive enzymes, bile
53
How do you treat gastric and duodenal ulcers?
Stop NSAID and tx w/ antibiotics and PPI
54
What is the pathophysiology of peptic ulcers?
Gastrin levels often increased in gastric ulcers since somatostatin inhibition of gastrin during the fasting state is not activated (may be related to urease activity of H. pylori) Increased gastrin can cause acid hypersecretion, pepsin secretion, hyperplasia of ECL and Parietal cells and stomach contractions. Subset of individuals with hypochlorhydria is related to gastritis and destruction of the gastric epithelial cells (parietal cells) Inflammatory response to H. pylori or loss of protective factors due to NSAID inhibition of PG synthesis further contributes to ulcer formation. Infection and high acidity can spread to duodenum resulting in decreased bicarbonate and duodenal ulcers (damaging cells in small intestine so can’t neutralize acidic chyme as well)
55
What is achlorhydria and what causes it?
Reduced acid secretion Caused by aging, gastric resection, genetic factors, auto-immune attack of the H+/K+ ATPase, taking proton pump inhibitor, infection– atrophic gastritis Bacterial overgrowth, diarrhea, pneumonia Hip fractures and iron deficient anemia- decreased Ca++ and iron absorption Decrease in pepsin activation doesn’t seem to cause problems (no increase in nitrogen excretion)
56
Hydrochloric acid
parietal cell Hydrolysis; sterilization of meal
57
IF
Parietal cell B12 absorption
58
Pepsinogen
chief cell protein digestion
59
Mucus, bicarbonate
surface mucous cells Gastroprotection
60
Trefoil factors
surface mucous cells gastroprotection
61
Histamine
ECL Regulates gastric secretion
62
Gastrin
G cells Regulates gastric secretion
63
Gastrin releasing peptide
nerves Regulates gastric secretions
64
ACh
Nerves Regulates gastric secretions
65
Somatostatin
D cells Regulates gastric secretions

GI- Week 2 (11 decks)

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