Peptic Diseases and Gastritis (Jackson/Nichols) Flashcards
gastric cells that make HCl
parietal
gastric cells that make pepsinogen
chief
gastric cells that make bicarbinate rich mucos
mucous cells
gastric cells that make gastrin
g cells
what intracellular processes drigger H/K ATPase activity
↑ Ca (thru IP3) and ↑ cAMP (thru AC)
exert a negative feedback on acid secretion in partial cells?
distention, low pH, somatostatin, and prostaglandins inhibit parietal cell H+ secretion
CCK and secretin inhibit action of gastrin
what is the cephalic phase of acid secretion
Taste, smell, and chewing food stimulates acetylcholine release via the vagal nerve → partial cells secrete HCl (30% of total secretion)
What is the gastric phase of acid secretion?
Chemical effects of food and distension of stomach causes:
- release of gastrin by the G cells (indirect stim of parietal cells)
- release of Ach from vagal N to directly act on parietal cells
how does gastric acid secretion in pts with DUODENAL ulcers compare to secretion in normal patients? GASTRIC ulcers?
Duodenal: ↑H+ (2x nml) and ↑gastrin
Gastric: ↓H+ and ↑gastrin (H+ leaks out due to damage to the mucosa and gastin ↑ to compensate)
what prevents auto digestion?
mucos-bicarb layer in stomach
how does duodenal bicarb secretion in pts with DUODENAL ulcers compare to secretion in normal patients
↓ basal [bicarb] and ↓ acid stimulated secretion of bicarb
definition of PUD
defect in GI mucose extending THROUGH THE MUSCULARIS MUCOSA
Risk factors for PUD
PUD HANGS around with H pyloir:
H pylori ASA NSAIDs Genetics Smoking
What chronic diseases is PUD assc with? how is it prevented in these conditions (i.e. what is the prophylactic treatment?)
Stress
Transplanted organs
Cirrhosis
COPD
prophylactic PPIs
symptoms of PUD
abd pain (nocturnal or with food)
nausea
anorexia
**may be asympomatic and present with complication = bleeding or perforation
morphology of H pylori
gram - spiral shaped with 4-6 flagella
pts infected with h pylori will have ↑ or ↓ response to gastrin/acid production. why?
↑ due to ↓somatostatin release
Since H pylori colonize gastric mucosa, how do they cause a duodenal ulcer?
- inhibit somatostatin secretion → gastrin → ↑H+ secretion
- inhibits duodenal HCO3- secretion → duodenal contents become abnormally acidic → mucosa eroded
- ↑ gastrin has trophic effect on parietal cells →↑H
- increased inflammatory cells and cytokines
top 2 causes of PUD
H pylori and NSAIDs