umms.GI03.acid peptic ds

1. cardia
2. fundus
3. body
4. antrum
5. pylorus

Fundus and body make acid
Antrum has g cells that make gastrin
There are pits and glands everywhere

2 endocrine cells:
1. P cells: everywhere, make acid
2. G cells: in antrum, make gastrin

1. Peptic Ulcer Ds
2. Esophageal reflux

Oxyntic Gland: pit covered by mucus glands

Surface mucosal cell: make mucus layer
Parietal cell: complex, make gastric acid
Neck cells: make acidic glycoprotein
Stem cells: make all other cells
Chief cells: make intrinsic factor

Chronic mucosal defect with frequent recurrances

acid is secreted into the lumen of the gland from the parietal cells and is sprayed into stomach yielding acid tracts through the thick mucus

There is no strong link between acid and ulcers

There is very strong link between ulcers and H pylori:
92% of Duodenal ulcers and 65% of gastric ulcers
Other causes are cancers, nsaids and –for DU ulcers- zollinger Ellison
Eradicating the bacteria --> remission of the ulcers

a cancer syndrome where the pancreas makes increased gastrin --> increases the amt of acid made

Transmission = fecal oral

Adheres to the mucus layer

Hp increases with age
Inverse relation ship to SES (suboptimal sanitary conditions, crowded living)

1. Hp dows not invade but lives in the mucus layer.
2. It produces menay factors (NH3, LPS, urease and toxin) that allow it to live there
3. Urease takes Urea ‡ ammonia and CO2 Ë are more basic and buffer acid (allow bact to live)
4. This induces inflammatory cell
5. inflammation upregulates gastrin
6. gastrin --> increased parietal cell acid production by overwealming somatostatin from D cells

1. changes the cell balance : increases g cell pop and decreases d cell pop
2. up regulates gastrin --> upregulate acid production
3. injects CapA and peptidoglycan in to the cells which activates proinflam genes (IL-1)

Gastric cancers (but this req many cofactors):
Adenocarcinoma of body and antrum
Gastric lymphoma

classically gastric burning pain that increases with not eating and decreases with eating

May also present as complication such as : bleeding, perforation or obstruction

Idiopathic dyspepsia
GERD
Pregnancy
Medications
Delayed emptying
Biliary/Pancreatic ds
Mesentaric ischemia
IBD: gastroduodenal crohns
Muscular skeletal problem

CBC,
chemistries,
gastrin level (rarely increase except w ZE),
acid secretory study

radiographic eval
endoscopy

Double contrast barium meal (detect 80-90%) but low sens for scaring


-->Useful for infiltrating ds and extrinsic compression

Noninvasive:
1) serology: cannot detect active ds just the exposure to Hp
2) Stool antigen:
3) Carbon labeled urea breath test: great as a follow up
-->pt ingest radiolabeled urea and if there’s urease there will be radiolabeled CO2 made which is measureable on exhaled breath

Invasive:
1) Rapid urease assay: take tissue bx and test for urease
2)Histology: pathologist can directly see bug
3)Culture: hard and not specific

1. Acid inhibitory / Neutralizing agents
• H2 receptor antagonists = block parietal cell H2 R
• Proton pump inhibitors = very potent and successful
• Antacids
• Anticholinergics: block on parietal cell
• Prostaglandins: inhib acid but have high side effects.

(first two are std of care)

2. Cryoprotective agents: both are a little dated and the bold have replaced them
• Sucralfate
• Prostaglandins

No tx: feel bad (non-ulcer dyspepsia) or asx or any ds with no Hp
Tx: any ulcer

Drug combo to prevent resistance and reach the bacteria in its mucus coat

2 antibiotics (or more)
PPI or ranitidine/bismuth citrate

Metallic taste (metronidazole): 30%
n/v
oropharynx/vaginal infect
diarrhea
rash
malaise dyspepsia
psudomembranous colitis

GI bleed
Scarring -> outlet obstruction
Perforation
Malignancy

Controversial pts:
Those with a high risk of gastric cancer
Sx without ulcer
Long term antisecretory tx (PPI) --> parietal cell atrophy