Path-Gastritis

Question 1

name the 5 sections of the stomach from top to bottom

Answer 1

cardia, fundus, body, antrum, pyloris

Question 2

rugae of the stomach contain which layers of stomach tissue?

Answer 2

mucosa and submucosa

Question 3

what type of epithelium is in the stomach?

Answer 3

simple columnar epithelium with gastric pits and glands

Question 4

gastric pits are also known as?

Answer 4

foveola (together = foveolar compartment)

Question 5

which portion of the gatric mucosa varies depending on the region of the stomach?

Answer 5

gastric glands (the foveola is the same throughout)

Question 6

gastric glands of the fundus and body contain?

Answer 6

parietal cells (acid, IF) and chief cells (pepsinogen)

Question 7

gastric glands of the cardia, antrum, and pyloris contain?

Answer 7

mucous cells and G cells (gastrin)

Question 8

parietal cells are (higher/lower) than chief cells and appear (pink/blue)

Answer 8

higher; pink (chief cells are purple/blue)

Question 9

short pits are found in the ____, while long pits are found in the _____

Answer 9

cardia, antrum

Question 10

G cells are only found in the _____

Answer 10

antrum

Question 11

h pylori is a gram ____ rod found in the _____ only

Answer 11

negative; layer of mucus adherent to gastric foveolar cells ONLY (not intestinal)

Question 12

h pylori is located where ____ levels are highest

Answer 12

urea

Question 13

how has h pylori adapted to the acidic environment of the stomach?

Answer 13

it synthesizes urease, which degrades urea into ammonia causing local pH to rise

Question 14

pathogenesis of h pylori

Answer 14

proteases degrade mucus barrier (lose protection) + produce ammonia, cytotoxins which directly injure epithelium

Question 15

what 4 natural histories are possible as a result of epithelial injury from h pylori?

Answer 15

acute gastritis, chronic gastritis, gastric lymphoma/adenoCA, peptic ulcer dz

Question 16

how to detect h pylori infection (histo)

Answer 16

silver stain (black dots on yellow background)

Question 17

definition/pathogenesis of acute gastritis

Answer 17

direct/indirect injury -> acute inflammation of mucosa with neutrophils +/- necrosis (erosion) +/- hemorrhage if deep enough

Question 18

name 4 etiologies of acute gatritis

Answer 18

drugs (NSAIDs, EtOH, Chemo), infection (h pylori), complication of other dz (uremia), mucosal hypoxia=”stress” (shock, trauma, burns, surgery)

Question 19

name 3 etiologies of chronic gastritis

Answer 19

1. h pylori, 2. autoimmune, 2. diet

Question 20

pathogenesis of chronic gastritis

Answer 20

lymphocytes, plasma cells, macrophages = immune response = epithelial necrosis +/- atrophy of glands (eventually mucosa) +/- cancerous changes (metaplasia?)

Question 21

gross pathology of chronic gastritis

Answer 21

thin, atrophic gatric wall lacking rugae

Question 22

if metaplasia occurs in chronic gastritis, what are gastric cells converted to?

Answer 22

intestinal cells with both columnar absorptive cells and goblet cells

Question 23

autoimmune chronic gastritis has what inheritance pattern, and attacks what cells?

Answer 23

AD; parietal cells

Question 24

autoimmune chronic gastritis results in what other condition?

Answer 24

pernicious anemia due to decreased intrinsic factor

Question 25

in peptic ulcer dz, where are ulcers most commonly found (two locations)?

Answer 25

duodenum (proximal), stomach (lesser curvature of antrum, pre-pylorus)

Question 26

name 3 causes of PUD

Answer 26

H pylori, NSAIDs, gastrinoma (Zollinger-Ellison)

Question 27

describe the gross pathology of a peptic ulcer

Answer 27

“punched out” or “cookie cutter” excavation with perpendicular sides and flat surface

Question 28

four characteristic histopathologic zones of a peptic ulcer

Answer 28

fibropurulent exudate, necrotic tissue, granulation tissue, fibrotic tissue/scar

Question 29

name 3 complications of a peptic ulcer

Answer 29

hemorrhage (common), perforation (usually in duodenum), obstruction (gastric outlet)

Question 30

what occurs upon perforation of a peptic ulcer?

Answer 30

peritonitis

Question 31

what is the most common location of a gastrinoma?

Answer 31

pancreas

Question 32

pathogenesis of Zollinger-Ellison syndrome

Answer 32

gastrinoma leads to increased gastrin secretion, causing parietal cell hyperplasia and increased gastric HCl secretion, which causes severe peptic ulceration (uncomon cause of ulcers)