Flashcards in Peptic Diseases and Gastritis (Jackson/Nichols) Deck (48)
gastric cells that make HCl
gastric cells that make pepsinogen
gastric cells that make bicarbinate rich mucos
gastric cells that make gastrin
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:
What chronic diseases is PUD assc with? how is it prevented in these conditions (i.e. what is the prophylactic treatment?)
symptoms of PUD
abd pain (nocturnal or with food)
**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?
1. inhibit somatostatin secretion → gastrin → ↑H+ secretion
2. inhibits duodenal HCO3- secretion → duodenal contents become abnormally acidic → mucosa eroded
3. ↑ gastrin has trophic effect on parietal cells →↑H
4. increased inflammatory cells and cytokines
top 2 causes of PUD
H pylori and NSAIDs
How does H pylori elicit an inflammatory response
secretes LPS and peptides that will cross gastric epithelium and are then chemotactic for neutrophils and monocytes in the lamina propria → monocytes secrete TNF< IL-1, O2-, Prostaglandins
how does NSAID use leas to PUD
▪︎ ↓glutathione → ↑ROS
pareital cell hyperplasia occurs as a result of
↑ vagal stimulation and gastrin
how is the diagnosis of PUD made
UGI barium X ray
upper endoscopy **also allows for biopsy
What are the complications of PUD?
bleeding → hematemesis, melana, anemi
penetration into adj organs (pancreas, liver, colon)
obstruction (due to edema or fibrosis)
perforated duodenal ulcers are assc with
ZES, NSAIDs, cocaine
Acute PUD → obstruction due to ____.
Chronic PUD → obstruction due to _____.
Acute PUD → obstruction due to edema.
Chronic PUD → obstruction due to fibrosis.
Obstruction causes pt to _____ several hours after they eat
Treatment of PUP
H2 blockers or PPIs
can you assume a pt with a + serological test for H pyloru has an active H pylori infection
no, they may have cleared it but they still have Abs made to it