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Emma GI > Gastritis, Peptic Ulcer Disease, Gastric Neoplasia > Flashcards

Gastritis, Peptic Ulcer Disease, Gastric Neoplasia Flashcards

1
Q

UGI bleed potential causes

A

esophagus

  • severe esophagitis
  • Mallory-Weiss tear
  • esophageal varices

stomach

  • peptic ulcer disease (gastric ulcer)
  • AV malformation
  • gastric varices
  • malignancy

duodenum

  • peptic ulcer disease (duodenal ulcer)
  • AV malformation
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2
Q

atrophic gastritis = risk factor for

A
  • gastric intestinal metaplasia/dysplasia

- gastric cancer (adenocarcinoma)

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3
Q

How do NSAIDs promote acute gastritis?

A

block prostaglandins, inc H+, promote mucus/bicarb prod

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4
Q

causes of chronic gastritis

A

H. pylori

  • non-atrophic
  • atrophic

AI gastritis

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5
Q

H. pylori

A

microaerophilic, gram neg, spiral shape, multiple polar flagella

most protein products allow survival, colonization, virulence

UREASE

fecal-oral transmission

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6
Q

H. pylori infects which boundaries of the stomach

A

entire stomach (acute, 85% of chronic)

isolated antrum (15% of chronic, mostly CagA strains, ulcer disease assoc.)

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7
Q

Which type of H. pylori infection leads to inc gastric pH?

A

chronic atrophic gastritis

via damage to parietal cell and urease effects (urea –> NH3 +CO2)

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8
Q

Which type of H. pylori infection leads to dec gastric pH?

A

chronic non-atrophic gastritis

more duodenal and gastric ulcer disease

colonization of astral G cells

  • hyperplasia of G cells
  • inc gastrin –> inc acid
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9
Q

NSAIDs –> ulcers, major MOA

A

toxicity to GI mucosa due to COX 1** inhibition (RLS) in prostaglandin synthesis

(prostaglandins usu enhance mucosal BF, so if blocked, mucosa vulnerable)

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10
Q

H. pylori testing

A

non-invasive

  • serology
  • stool antigen
  • urea breath test

invasive
-biopsy

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11
Q

+ urea breath test will show

A

CO2 in exhaled breath

suggests H. pylori infec

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12
Q

AI gastritis

A

inflamm @ body/fundus

Abs against parietal cells, IF, and block proton pump

–>B12 deficiency, megaloblastic anemia (inc MCV), hypOchlorhydria or achlorhydria

dx: serum parietal cell Abs

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13
Q

AI gastritis low/no acid levels lead to high ___ which is a risk factor for which 2 pathologies?

A

low/no acid –> inc gastrin

risk factor for

  • type 1 gastric neuroendocrine tumors (carcinoid) via xs ECL stim
  • intestinal metaplasia (precursor to gastric adenocarcinoma)
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14
Q

punched out pathology

A

peptic ulcer

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15
Q

NSAIDs –> ulcers, minor MOA

A

topical effect

  • nonselective NSAIDs are weak acids, un-ionized in stomach, lipid soluble
  • diffuse across gastric epithelial cell
  • in cell - ionize in neutral pH
  • high intracellular [NSAID] –> toxic
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16
Q

peptic ulcer sx

A 
epigastric pain (gnawing)
N/V
poss improve w/ oral intake
poss bleeding (hematemesis "coffee ground")
17
Q

NSAID induced ulcers may cause no sx except ____

A

bleeding

18
Q

ulcer obstruction usually occurs at

A

pylorus

19
Q

tx of gastric and peptic ulcer disease

A

tx H. pylori
H2 receptor antagonists
PPIs
NSAID prophylaxis (misoprostal)

20
Q

Zollinger-Ellison syndrome

A
  • massive amounts of acid secretion
  • neuroendocrine tumor secretes gastrin
  • tumor arises in gastrinoma triangle, most from pancreas
  • ulcers in somach, duodenum (outside of bulb), jejunum
  • severe reflux esophagitis possible
  • can be metastatic

dx: clinical history, gastrin level, CTscan or octreotide scan

21
Q

gastrinoma triangle

A

defined by duodenal walls, bile ducts, pancreas

22
Q

octreotide

A

somatostatin

splanchnic vasoconstrictor

inhibits gastrin, VIP, insulin, others

23
Q

which gastric polyp has a high risk of malignancy?

A

adenomatous polyps

most comm in antrum

24
Q

common location of fundus gland polyps

A

fundus and gastric body

25
Q

common location of hyperplastic polyps

A

anywhere in stomach, most comm in antrum

26
Q

which gastric neoplasia develop in setting of high gastrin levels?

A

fundic gland polyps

27
Q

gastric adenocarcinoma, intestinal type

A
  • declining incidence
  • east Asia (china, Japan)
  • M>F, mean 70 y/o
  • usu asympotomatic until advanced
  • risk fx: H. pylori, chronic atrophic gastritis, intestinal metaplasia/dysplasia, adenomatous gastric polyps, cigarette smoking
28
Q

gastric adenocarcinoma, diffuse type

A
  • linitis plastica, broad region of thickened gastric wall
  • signet ring cells, nuclei pushed to periphery
  • cells=iniltrative, poorly differentiated, and discohesive

Emma GI (18 decks)

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