Gastric Secretions / Peptic Ulcer Disease Flashcards

1
Q

describe the anatomy of the cardia

A

transition zone from squamous to columnar epithelium

protects surface of stomach from corrosive gastric contents + previous reflux shallow gastric pits: surface mucus cells

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2
Q

what kind of cells are found in the fundus and body?

A

deep gastric pits: contain surface and neck mucus cells, PARIETAL cells, CHIEF cells, endocrine cell (ECL cells, D cells)

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3
Q

main functions of fundus and body

A

accommodation gastric acid secretion

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4
Q

function of the antrum

A

mixing, grinding, sieving ingested particles regulation of gastric secretory function via gastrin/somatostatin intermediate gastric pits: surface and neck mucus cells, endocrine cells

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5
Q

surface cell and neck cells: product and function

A

products: mucus, HCO3-, trefoil peptides
function: lubrication, protection

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6
Q

parietal cells: product and function

A

product: H+, intrinsic factor
function: protein digestion, binding of cobalamin, protection from bacteria

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7
Q

chief cells: product and function

A

product: pepsinogen, gastric lipase
function: protein digestion, TG digestion

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8
Q

endocrine cells: product and function

A

product:

  • gastrin from G-cells
  • histamine from ECL cells
  • somatostatin from D-cells

function: regulation of acid secretion

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9
Q

what type of cell is this? describe some characteristics

A
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10
Q

parietal cell: describe resting and stimulated states

A

resting:

  • gastric acid pump is present in tubulovesicles but inactive

stimulation by ACh, Gastrin, Histamine

  • gastric acid pump in tubulovesicles is incorporated into the canaliculus and becomes active
  • action: exchanges H for K, creates HCl to be released into lumen
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11
Q

what stimulates the parietal cell?

A

acetylcholine

gastrin/CCK - unclear importance

histamine - most important

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12
Q

diagram gastric acid secretion

A
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13
Q

describe acid/electrolyte composition of gastric juice in resting and stimulated states

A

resting: non-parietal, resembles interstital fluid w/ high Na
stimulated: parietal, high H+ content

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14
Q

how does the stomach protect itself from acid?

A

mucus: glycoproteins w/ disulfide bridges –> mucus gel

made through physical stimualtion and ACh stim by mucus neck cells and mucus surface cells

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15
Q

what agents disrupt gastric mucosal barrier?

A

weak acids (aspirin), alcohols (ethanol), NSAIDs , bile salts

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16
Q

overview of phases of acid secretion stimulation

  • name
  • stimulus
  • % response to a meal
A
  1. interdigestive
  2. cephalic
  3. gastric
  4. intestinal
17
Q

describe what happens in the cephalic phase

A
  • sight, smell and taste of food –> excites central vagus efferents
  • Ach released to enteric nervous system –> stimulates…
    • parietal cells
    • chief cells (a little) - pepsinogen
    • ECL to produce histamine –> local action
    • G cells
  • vagal efferents tim G cells in neuroendocrine fashion via GRP - STRONG effect
18
Q

describe what happens in the gastric phase

A
  • food causes increase in pH –> increased gastrin release
  • AA and proteins stimulate G-cells to release gastrin
  • fundal distension –> increase in parietal cell secretion of acid (vagally mediated)
19
Q

why do ulcer pts have relief of pain after meals, but pain returns 2 hrs later?

A

H+ buffered by food, but then acid is secreted in response

20
Q

describe what happens in the intestinal phase of acid secretion

A

not well understood

  • stimulatory factors: AAs in small intestine stim release of gastrin
  • inhibitory factors: chyme in upper intestine inhibits gastric acid secretion (maybe via secretin, GIP)
21
Q

alkaline tide

A

for each H+ secreted into the stomach lumen, HCO3- is secreted into the blood

  • HCO3- is used by surface mucus cells to maintain mucus layer and protect enterocytes
22
Q

most likely endoscopy finding in a pt w/ gnawing pain in epigastrium

A

normal! - 60-90% of the time, pts get ulcer-like symtpoms WITHOUT ulcer = non-ulcre dyspepsia

23
Q

dx of peptic ulcer disease

A

upper endoscopy

  • can exclude cancer, detect H. pylori
24
Q

complications of peptic ulcer disease

A

hemorrhage

perforation or penetration to adjacent organ (pancreatitis)

gastric outlet obstruction

25
Q

pathogenesis of peptic ulcers

A
  • H. pylori –> chronic superficial gastritis in antrum + intestinalized gastric mucosa + acid hypersecretion (somatostatin suppression —> less inhibition of gastrin release)
  • compromised mucosal defense: NSAIDS or H. pyloria –> diffuse superficial antral gastritis
    • PGE2 important for maintaining mucosa
      *