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
defn of gastritis. How is this diff than the defn of PUD?
gastritis = infalmmation of mucosa
PUD = inflammation and damage extends thru the muscularis mucosa
common causes of gastritis:
extreme stress (ICU
(less common: chemo, bile reflux, truama, burns, sepsis, shock)
“blood under plastic wrap” on endoscopy indicates
multiple subepi hemorrhages without any breaks in mucosa = assc with alcohol use
numerous petechiae and erosions of on gastric mucosa
acute hemorrhagic gastritis
causes of chronic gastritis
H pylori > autoimmune and bile reflux
chronic gastritis can lead to
atrophy, intestinal metaplasia/dysplasia/neoplasia
WHere is the stomach is chronic gastritis due to H pylori likely to affect? autoimmune?
Bacteria = Antrum
Autoimmune = Body
what type of cells will predominate in chronic active gastritis
neutrophils = ACTIVE!!
chronic gastritis due to (autoimmune or H pylori) commonly displays lymphoid follicles/germinal centers
where will the H pylori organisms be found in chronic gastritis
superficial MUCOUS layer (above the epi)
most important virulence factors for H pylori
CagA protien **degrades p53**
also, T4SS (found in CagPAI)
characteristics of autoimmune chronic gastritis
Abs to parietal cells
pernicious Anemia (Abs to intrinsic factor)
Atrophy*all chronic gastritis cuases atrophy, so maybe only 3 A's?
↑ risk for MALT lymphoma
H pylori chronic gastritis
assc with G cell and partial cell hyperplasia
assc with parietal cell hyperplasia (No G cell)
BOTH: autoimmune chronic gastritis
**loss of parietal cells at the same time since there are Abs made against it
Parietal only: PUD (due to ↑Ach/vagal stim and gastrin)
seen in histo of chronic PUD
necrosis, inflammation, granulation tissue, scar
bigger or smaller ulcers are signs of benignity
deeper or shallow ulcers are signs of benignity
stress ulcers occur with
Brain injury = Cushing ulcer (↑vagal stim → inc Ach and H+ secretion)
**C(r)ush the brain and you may get stress ulcer**
Burns = Curling ulcer (↓plasma volume → sloughing of gastric mucosa)
**burned by a curling iron**