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GI- Week 2 > Prunuske: Gastric Secretion > Flashcards

Prunuske: Gastric Secretion Flashcards

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
Q

What happens to the Cl that is pumped into the parietal cell via the Cl/bicarb exchanger end up?

A

Moves down the EC gradient when the luminal channel opens and water follows

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26
Q

What pump in the parietal cell is essential for maintaining gradients that allows the proton pump to work?

A

Na/K ATPase on the BASOLATERAL membrane

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27
Q

How does the electrical potential that exists across the mucosa differ in the parietal cell at rest and during activation?

A

rest -70 mv

DECREASED during activation to -30mV

28
Q

What inhibits gastrin release?

A

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
Q

How does somatostatin inhibit gastric acid secretion?

A

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
Q

What affect do prostaglandins have on cAMP formation?

A

inhibit cAMP

31
Q

How does feedback from the duodenum lead to the inhibition of gastric acid secretion?

A

Nervous reflex form the duodenum BLOCKS ACh activation of parietal cells.

Enterogastrones like secretin block secretion of histamine by ECL cells.

32
Q

What are the phases of gastric secretion?

A

interdigestive
cephalic
gastric
intestinal

33
Q

interdigestive phase

A

Low acid secretion, D cells secrete somatostatin to maintain low levels of Gastrin

34
Q

cephalic phase

A

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
Q

gastric phase

A

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
Q

intestinal phase

A

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
Q

What is required for B12 absorption in the ileum?

A

Intrinsic factor (a glycoprotein secreted by parietal cells)

38
Q

Do PPIs affect IF?

A

PPIs do nOT inhibit the secretion of IF but may decrase protein digestion

39
Q

What decreases B12 absorption?

A

autoimmune destruction of parietal cells or bypass surgery

40
Q

Decreased B12 absorption leads to…

A

megaloblastic anemia

neurologic deficiencies

41
Q

What leads to the secretion of pepsinogen?

A

Ach/gastrin>

stimulate secretion of pepsinogen by CHIEF CELLS

42
Q

What inhibits pepsinogen secretion?

A

secretin

43
Q

Once pepsinogen enters the stomach, what happens to it?

A

Pepsinogen (inactive proenzyme protease) is ACTIVATED by the ACIDIC environment to PEPSIN which is a proteolytic enzyme

44
Q

What is pepsin?

A

an endopeptidase that activates pepsiniogen by autolysis

45
Q

How do chief cells lead to FA release?

A

They also secrete gastric lipase

46
Q

How is the mucus gel layer/diffusion barrier created and what does it do?

A

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
Q

How does taking NSAIDs lead to gastric irriation?

A

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
Q

What else causes gastric irritation can lead to stress ulcers?

A

catecholamines (also suppress bicarb secretion)

49
Q

If the stomach epithelium does get damaged, what is used for restitution and regeneration?

A

Trefoil factors

Growth factors

50
Q

What is Zollinger Ellison syndrome (Gastrinoma)?

A

Gastrin secreting tumor in the pancreas or intestine that leads to EXCESS H secretion and eventual hyperplasia and hypertrophy of parietal cells

51
Q

What causes peptic ulcer disease?

A

Hyperacidity

Deterioration of the gastro-mucosal barrier

52
Q

What can lead to gastric and duodenal ulcers?

A
  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
Q

How do you treat gastric and duodenal ulcers?

A

Stop NSAID and tx w/ antibiotics and PPI

54
Q

What is the pathophysiology of peptic ulcers?

A

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
Q

What is achlorhydria and what causes it?

A

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
Q

Hydrochloric acid

A

parietal cell

Hydrolysis; sterilization of meal

57
Q

IF

A

Parietal cell

B12 absorption

58
Q

Pepsinogen

A

chief cell

protein digestion

59
Q

Mucus, bicarbonate

A

surface mucous cells

Gastroprotection

60
Q

Trefoil factors

A

surface mucous cells

gastroprotection

61
Q

Histamine

A

ECL

Regulates gastric secretion

62
Q

Gastrin

A

G cells

Regulates gastric secretion

63
Q

Gastrin releasing peptide

A

nerves

Regulates gastric secretions

64
Q

ACh

A

Nerves

Regulates gastric secretions

65
Q

Somatostatin

A

D cells

Regulates gastric secretions

GI- Week 2 (11 decks)

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