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FHB Exam 3 > GI: Gastric Phase > Flashcards

GI: Gastric Phase Flashcards

1
Q

List the functions of the stomach.

A
  • storage of a meal
  • acid secretion for pepsinogen conversion and killing microorganisms
  • IF secretion for B12 absorption
  • secretion of mucus and HCO3 (gastric mucosal barrier)
  • secretion of water for lubrication of bolus and suspension of nutrients
  • mixing
  • emptying
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2
Q

List the neural, paracrine, and endocrine regulations of the stomach.

A
  • neural = ENS and ANS
  • paracrine = histamine => H+
  • endocrine = gastrin and somatostatin
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3
Q

What are the parts of the stomach?

A
  • cardia (and LES)
  • Fundus (body)
  • Antrum (and pylorus)
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4
Q

Describe the luminal secretions and motility of the cardia.

A
  • secretions = mucus and bicarb

- motility = prevents reflux, receptive relaxation, belching

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5
Q

Describe the luminal secretions and motility of the fundus.

A
  • secretions = mucus, bicarb, acid, IF, pepsinogens, lipase

- motility = tonic contractions during emptying

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6
Q

Describe the luminal secretions and motility of the antrum.

A
  • secretions = mucus and HCO3

- motility = mixing, grinding, filtering, grinding

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7
Q

Describe the columnar cells of the gastric epithelial lining.

A

gastric glands secrete into the gastric pits of the columnar cells

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8
Q

What do parietal cells secrete?

A
  • HCl

- IF

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9
Q

Describe the function of parietal HCl secretion.

A
  • kills microorganisms
  • activates pepsinogens to pepsin
  • provides the low pH required for active pepsin, which initiates 20% of protein digestion in the stomach
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10
Q

Describe the function of parietal IF secretion

A
  • binds to B12
  • allows absorption in small intestine
  • only essential secretion in healthy individuals
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11
Q

What do mucus neck cells secrete?

A

mucus to protect mucosa

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12
Q

What do chief or peptic cells secrete?

A

pepsinogens - zymogen form of pepsin, enzyme involved in gastric protein digestion.
- pepsin requires acidic environment

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13
Q

What do ECL cells secrete? What is its purpose?

A
  • histamine, which stimulates paracrine secretion of HCl from parietal cells
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14
Q

What do D cells secrete? What is its purpose?

A

somatostatin - inhibits parietal HCl secretion

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15
Q

What do G cells secrete? What is its purpose?

A

gastrin - HCl secretagogue

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16
Q

Describe an activated parietal cell.

A
  • tubulovesicular membranes fuse with secretory canaliculi to increase H/K antiporters which dump H into the lumen
  • Carbonic anhydrase generates all the H
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17
Q

Describe the transport mechanisms of parietal cells.

A

APICAL MEMBRANE

  • H/K ATPase = secretes H, absorbs K
  • Cl channel passively secretes Cl

BASOLATERAL MEMBRANE
- Cl/HCO3 exchanger - absorption of HCO3 in venous blood

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18
Q

What does omeprazole do?

A

blocks the H/K ATPase pump => inhibits H+ secretion

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19
Q

What are the effects of cAMP and intracellular Ca2+?

A

increased conductance of K => secretion of H

increased conductance of Cl

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20
Q

Define the alkaline tide.

A

Due to the HCO3- reabsorption on the basolateral membrane, there is high concentration of bicarb in the blood after a meal => high pH => alkaline tide in venous blood

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21
Q

Describe the secretion of HCO3.

A

epithelial cells secrete fluid that has a NaCl concentration similar to plasma, but a K, HCO3 concentration higher than plasma. HCO3 becomes trapped in the mucus providing a normal pH on the epithelial cells.

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22
Q

Describe the gastric mucosal barrier.

A

barrier = mucus + HCO3

keeps pH normal at the cells even though lumen has a low pH

23
Q

Describe the structure of mucin and the result of pepsins.

A
  • mucin is a tetramer with disulfide links in the middle

- pepsins break the disulfide links => proteolytic fragments => loss of gel => damage to cell

24
Q

What is the strongest acid secretion stimulant?

A

parasympathetic vagal stimulation

25
What 3 substances stimulate parietal acid stimulation?
- ACh (neural) - histamine (paracrine) - gastrin (endocrine)
26
Describe vagal stimulation of parietal acid secretion.
vagus => ACh => muscarinic M3 receptors on parietal cells => increases IP3/Ca2+ => increased H secretion vagus => ACh => ECL cells => histamine => parietal cells => H secretion
27
What blocks ACh activity?
atropine blocks muscarinic receptors from taking up ACh
28
Describe paracrine stimulation of parietal acid secretion.
- ECL cells are stimulated by gastrin or ACh | => histamine => H2 receptors on parietal cells => increased cAMP => increased H secretion
29
What blocks histamine activity?
cimetidine
30
Describe endocrine stimulation of parietal acid secretion.
- G cells are stimulated by gastrin-releasing peptide (GRP) => gastrin in the circulation => gastrin acts on ECLs and on parietal cells => binds to CCK-B receptors on parietal cells => increased IP3/Ca2+ => H secretion
31
Define potentiation.
potentiation is the summation of regulation of H secretion through ACh/histamine/gastrin probably through a variety of receptors and 2ndary messenger systems. This means that if one of these mechanisms isn't working, there are still 2 others that affect acid secretion
32
Describe secretion during the cephalic and oral phases.
- 30% of HCl secretion | - mechanisms = ACh, histamine, gastrin
33
Describe secretion during the gastric phase, stimulants, and mechanisms.
- 60% of HCl secretion - stimulated by distension and peptide presence MECHANISMS - distension => vagovagal reflex => gastrin - AA/peptides => gastrin - OH/caffeine => HCl
34
Describe secretion during the intestinal phase.
- 10% HCl secretion | - protein metabolism
35
Describe the negative feedback loop of gastrin secretion
when luminal pH directly blocks histamine effects on parietal cells => indirectly inhibits histamine and gastrin release
36
Describe digestion in the stomach.
- 20% of protein digestion through pepsin - some amylase - 10% lipids via lipase all nonessential
37
What is the orad?
thin-walled, proximal fundus
38
What is the caudad?
thick-walled, distal fundus
39
What is receptive relaxation? What controls it?
- distension of the lower esophagus stimulates relaxation of the LES and orad - vagovagal reflex
40
Describe the vagovagal reflex.
distension of the stomach => CNS => efferents fibers secrete vasoactive intestinal peptide => orad => relaxation
41
Describe motility in the caudad.
- main function = mixing, filtering, emptying - contractions begin mid-body and get stronger as they get closer to the pylorus - mixing - propels chyme small enough into the duodenum - retropulsion
42
Define retropulsion.
During caudad contractions, some chyme is propelled backwards into the stomach for further mixing and digestion
43
Describe the mechanism of control of gastric motility.
- sensory receptors in the gastric mucosa => intramural plexi => vagovagal reflexes => excitatory parasympathetic innervation via ACh and substance P => increased motility
44
What does the vagovagal reflex control?
acid secretion, distension, and motility
45
What controls rate of caudad contractions?
ICC cells (pacemakers)
46
What controls magnitude of caudad contractions?
neural input
47
Describe gastric emptying.
- slow (> 3 hours) - liquids easier than solids - solids require retropulsion to pass through duodenum - isotonic contents empty faster
48
List functions of the gastroduodenal junction.
- filtration of large particles - controls gastric emptying rate to assure digestion - prevents reflux
49
What is peptic ulcer disease?
- gastric or duodenal ulcers - H and pepsin lead to erosion causes: increased H secretion or loss of mucosal barrier
50
Describe gastric ulcers.
- defective mucosal barrier allows H and pepsin to digest the mucosa - mostly due to H. Pylori bacteria that releases cytotoxins to destroy barrier - pts. exhibit low H secretions and high gastrin levels due to loss of negative feedback
51
Describe duodenal ulcers.
- increased acid secretion overpowers bicarbonate buffer | - more common than gastric
52
What is Zollinger-Ellison Syndrome?
- due to gastrinoma tumor in pancreas => high gastrin production => increased H secretion => increased parietal cell mass ==> duodenal ulcers, steatorrhea (fat in stool due to inactivation of pancreatic lipases in duodenum)
53
What is treatment for ZE?
- PPI - H2 antagonists - surgical removal

FHB Exam 3 (23 decks)

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