Gastric Secretions / Peptic Ulcer Disease Flashcards
describe the anatomy of the cardia
transition zone from squamous to columnar epithelium
protects surface of stomach from corrosive gastric contents + previous reflux shallow gastric pits: surface mucus cells
what kind of cells are found in the fundus and body?
deep gastric pits: contain surface and neck mucus cells, PARIETAL cells, CHIEF cells, endocrine cell (ECL cells, D cells)
main functions of fundus and body
accommodation gastric acid secretion
function of the antrum
mixing, grinding, sieving ingested particles regulation of gastric secretory function via gastrin/somatostatin intermediate gastric pits: surface and neck mucus cells, endocrine cells
surface cell and neck cells: product and function
products: mucus, HCO3-, trefoil peptides
function: lubrication, protection
parietal cells: product and function
product: H+, intrinsic factor
function: protein digestion, binding of cobalamin, protection from bacteria
chief cells: product and function
product: pepsinogen, gastric lipase
function: protein digestion, TG digestion
endocrine cells: product and function
product:
- gastrin from G-cells
- histamine from ECL cells
- somatostatin from D-cells
function: regulation of acid secretion
what type of cell is this? describe some characteristics
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parietal cell: describe resting and stimulated states
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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what stimulates the parietal cell?
acetylcholine
gastrin/CCK - unclear importance
histamine - most important
diagram gastric acid secretion
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describe acid/electrolyte composition of gastric juice in resting and stimulated states
resting: non-parietal, resembles interstital fluid w/ high Na
stimulated: parietal, high H+ content
how does the stomach protect itself from acid?
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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what agents disrupt gastric mucosal barrier?
weak acids (aspirin), alcohols (ethanol), NSAIDs , bile salts
overview of phases of acid secretion stimulation
- name
- stimulus
- % response to a meal
- interdigestive
- cephalic
- gastric
- intestinal
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describe what happens in the cephalic phase
- 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
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describe what happens in the gastric phase
- 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)
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why do ulcer pts have relief of pain after meals, but pain returns 2 hrs later?
H+ buffered by food, but then acid is secreted in response
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describe what happens in the intestinal phase of acid secretion
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)
alkaline tide
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
most likely endoscopy finding in a pt w/ gnawing pain in epigastrium
normal! - 60-90% of the time, pts get ulcer-like symtpoms WITHOUT ulcer = non-ulcre dyspepsia
dx of peptic ulcer disease
upper endoscopy
- can exclude cancer, detect H. pylori
complications of peptic ulcer disease
hemorrhage
perforation or penetration to adjacent organ (pancreatitis)
gastric outlet obstruction
pathogenesis of peptic ulcers
- 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
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- PGE2 important for maintaining mucosa