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30 Cards in this Set

  • Front
  • Back
Peptic ulcer:
What is it?
Complications?
Break in mucosa greater than 5mm, with depth to sub-mucosa

Complications:
Bleeding
Perforation
Stenosis (narrowing)
Malignancy (can present as ulcer)
Causes of duodenal ulcers.
Mostly H pylori, some due to NSAIDs (10%)
Causes of gastric ulcers.
Mostly H pylori, A LOT more due to NSAIDs (30%), some due to cancers (10%)
Parietal cells are found in the ____ of the stomach.

Where in the gland are they located?

What do they secrete?
Parietal cells found in CORPUS

Parietal cells located near apex of gland

secrete HCl and IF
Chief cells are found in the ____ of the stomach

Where in the gland are they located?

What do they secrete?
Chief cells located in corpus of stomach

Located near basal aspect of gland

Secrete pepsinogen
Surface mucus cells:
Apical/Basal
Secretions
Apical

Secrete mucus and HCO3- (protect stomach from being digested by HCl)
Neuroendocrine cells:
Subtypes, their location and secretions
Apical/basal
All neuroendocrine cells are basal (but not as basal as chief cells) in gland

G Cells: Gastrin, in antrum

D Cells: Somatostain, everywhere

ECL (enterochromaffin-like) cells: histamine; corpus
Parietal Cells:
What structural changes occur when going from resting to active form?
Tubulovesicles-->Canaliculi to increase surface area for HCl to release from
What stimulates parietal cells to secrete acids?
1) vagal nerve stimuln (think, smell, see food) Ach

2) H2-receptor receives histamine from ECL cell (ECL cells release histamine in response to vagal stimulation as well)
Cephalic vs Gastric Phase of Gastric Secretion
Cephalic: think, see, smell food (cholinergic, vagus)

Gastric phase: eat food; amines and distention-->secrete gastrin from G cells-->acid release
Events of intestinal phase of gastric secretion.
Fat in duodenum stimulates multiple GI peptides (SOMATOSTATIN)-->inhibits gastrin and acid secretion
Pre-epithelial defenses of stomach
Mucus
Bicarb
Epithelial defenses of stomach
Apical barrier of tight jns to prevent H+ back diffusion

Restitution/replication: should stomach lining be injured, neighboring cells will flatten out and adjacent cells divide to fill in gap (regulated by EGF, TGFalpha, trefoil peptides)
Subepithelial defenses of stomach
Blood flow (lack of blood flow will result in ulcers!)
Why do NSAIDs result in peptic ulcers?
NSAIDs inhibit production of prostaglandins. Prostaglandins are essential to gastroduodenal defense mechanisms (pre-epith, epith, and subepith!)

More specifically:
Direct injury
Indirect injury via COX-inhibition and anti-platelet effects
Duodenal ulcers:
Pathophys
Inc'd basal acid output
Inc'd peak (digestive) acid output
Inc'd meal-stimulated acid output

Lose negative feedback (somatostatin secretion)
Key difference between duodenal and gastric ulcers.
Gastric ulcers have normal or low acid secretion.

Duodenal ulcers have elevated acid secretion.
H. pylori:
Gram -/+
Virulence factors
Gram (-)

Virulence factors:
VacA (vacuolating cyotoxin)

cag pathogenicity genes--inserts into gastric epithelial cells causing release of pro-inflammatory cytokines
H. pylori:
Risk factors
Age of transmission
Method of transmission
Inc'd age, poverty, overcrowding, foreign-born (developing countries)

Transmission during childhood

Transmission: oro-fecal
H. pylori infection:
Patient effects
100% get chronic superficial gastritis
Of these pts:
10% develop peptic ulcer dz
20% atrophic gastritic-->1-2% carcinoma
<1%-->lymphoma

so, 70% remain with chronic superficial gastritis (ASYX)
H. pylori:
Pathophysiology
Effects on gastric physiology
Direct cell damage
Degrades mucus
Induces immune response in gastric mucosa

f/x on gastric physio:
Dec'd somatostatin, inc'd gastrin
SNPs affecting inflammatory response to H. pylori.

Associated outcome with SNPs.
High IL-1beta and TNF-alpha-->gastric cancer

Normal/Low IL-1beta & TNF-alpha-->duodenal ulcer
Rapid urease test
H pylori test
H. pylori:
Dx
Stool antigen
Urea breath test--pt swallows radio-labeled urea, if have h. pylori, urea will be split into CO2 and can be measured (will be radioactive)

Don't do serology (Ab's): it's lame.
NSAID:
Examples
Sites of ulcerations
What other damage can they cause to these areas?
ASA, ibuprofen, naprosyn

Sites of ulceration: Stomach > duodenum >> intestine

Can also cause erosions, petechiae, hemorrhages, occult bleeding (manifests as anemia); OFTEN ASYX
NSAID injury risk factors.
Old people that take many drugs
Gastrinoma:
What is it?
Associated diseases
Presentation
Tumor that secretes gastrin

Assocd w/MEN I (parathy, panc, pit)

Up to 50% mets at presentation!

Presentation: SEVERE ulceration, +/- diarrhea
Zollinger-Ellison Syndrome:
What is it?
Gastrinoma!
Stress-induced ulcers:
Pathophys
Common in pts in ICU

Head is being shunted to brain, results in chronic ischemia of stomach-->ulceration
Acid inhibition treatment:
DU vs GU
DU: 1qd x 4 weeks
GU: 1 qd x 8 weeks