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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
Q

What 3 substances stimulate parietal acid stimulation?

A
  • ACh (neural)
  • histamine (paracrine)
  • gastrin (endocrine)
26
Q

Describe vagal stimulation of parietal acid secretion.

A

vagus => ACh => muscarinic M3 receptors on parietal cells => increases IP3/Ca2+ => increased H secretion

vagus => ACh => ECL cells => histamine => parietal cells => H secretion

27
Q

What blocks ACh activity?

A

atropine blocks muscarinic receptors from taking up ACh

28
Q

Describe paracrine stimulation of parietal acid secretion.

A
  • ECL cells are stimulated by gastrin or ACh

=> histamine => H2 receptors on parietal cells => increased cAMP => increased H secretion

29
Q

What blocks histamine activity?

A

cimetidine

30
Q

Describe endocrine stimulation of parietal acid secretion.

A
  • 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
Q

Define potentiation.

A

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
Q

Describe secretion during the cephalic and oral phases.

A
  • 30% of HCl secretion

- mechanisms = ACh, histamine, gastrin

33
Q

Describe secretion during the gastric phase, stimulants, and mechanisms.

A
  • 60% of HCl secretion
  • stimulated by distension and peptide presence
    MECHANISMS
  • distension => vagovagal reflex => gastrin
  • AA/peptides => gastrin
  • OH/caffeine => HCl
34
Q

Describe secretion during the intestinal phase.

A
  • 10% HCl secretion

- protein metabolism

35
Q

Describe the negative feedback loop of gastrin secretion

A

when luminal pH directly blocks histamine effects on parietal cells
=> indirectly inhibits histamine and gastrin release

36
Q

Describe digestion in the stomach.

A
  • 20% of protein digestion through pepsin
  • some amylase
  • 10% lipids via lipase
    all nonessential
37
Q

What is the orad?

A

thin-walled, proximal fundus

38
Q

What is the caudad?

A

thick-walled, distal fundus

39
Q

What is receptive relaxation? What controls it?

A
  • distension of the lower esophagus stimulates relaxation of the LES and orad
  • vagovagal reflex
40
Q

Describe the vagovagal reflex.

A

distension of the stomach => CNS => efferents fibers secrete vasoactive intestinal peptide => orad => relaxation

41
Q

Describe motility in the caudad.

A
  • 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
Q

Define retropulsion.

A

During caudad contractions, some chyme is propelled backwards into the stomach for further mixing and digestion

43
Q

Describe the mechanism of control of gastric motility.

A
  • sensory receptors in the gastric mucosa => intramural plexi => vagovagal reflexes => excitatory parasympathetic innervation via ACh and substance P => increased motility
44
Q

What does the vagovagal reflex control?

A

acid secretion, distension, and motility

45
Q

What controls rate of caudad contractions?

A

ICC cells (pacemakers)

46
Q

What controls magnitude of caudad contractions?

A

neural input

47
Q

Describe gastric emptying.

A
  • slow (> 3 hours)
  • liquids easier than solids
  • solids require retropulsion to pass through duodenum
  • isotonic contents empty faster
48
Q

List functions of the gastroduodenal junction.

A
  • filtration of large particles
  • controls gastric emptying rate to assure digestion
  • prevents reflux
49
Q

What is peptic ulcer disease?

A
  • gastric or duodenal ulcers
  • H and pepsin lead to erosion
    causes: increased H secretion or loss of mucosal barrier
50
Q

Describe gastric ulcers.

A
  • 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
Q

Describe duodenal ulcers.

A
  • increased acid secretion overpowers bicarbonate buffer

- more common than gastric

52
Q

What is Zollinger-Ellison Syndrome?

A
  • 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
Q

What is treatment for ZE?

A
  • PPI
  • H2 antagonists
  • surgical removal

FHB Exam 3 (23 decks)

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