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Flashcards in Gastritis & PUD Deck (66):
1

What is gastsritis?

inflammation associated with mucosal injury

2

What is gastropathy?

epithelial cell damage and regeneration with minimal to no associated inflammation from irritants

3

What immune cell to you expect to see in acute and chronic gastritis respectively?

acute-neutrophilic
chronic-lymphocytes, plasma cells, macrophages

4

Key features of acute helicobacter pylori gastritis?

epigastric pain, nausea, vmoiting, NO fever
acute inflamatory changes
antrum
usually goes to chronic

5

Key features of chronic helicobacter pylori gastritis?

antrum and body
early-increased gastrin, decreased somatostatin-->increased acid sec
late-fall in acid secretion w/loss of G cells facilitates proximal migration

6

Common histological finding of chronic H. pylori?

lymphoid follices

7

What is helicobacter heilmannii gastritis?

uncommon
treated like H pylori

8

What is metaplasic (chronic) atrophic gastritis? Types?

mucosal thinning, gland loss, change in epithelial cell types
autoimmune and environmental types

9

What is pseudopyloric metaplasia?

replacement of parietal and chief cells in oxyntic glands by mucus secreting cells found in the antrum

10

Waht is intestinal metaplasia?

replacement of suface, foveolar and glandular epithelium in oxyntic or antral mucosa by intestinal epithelium (goblet cells)

11

What are the main types of intestinal metaplasia?

Complete (type I)-fully formed SI epithelium
Incomplete (type II&III)-goblet cells interspersed among gastric-type mucin cells

12

Which type of intestinal metaplasia is associated with an increased risk of gastric adenocarcinoma?

Type III

13

Key features of AMAG?

inherited, associated w/immune response in the oxyntic mucosa against the parietal cells AND IF
more common in women
risk of pern. an. (vit B12 deficiency)
assoc. w/other autoimmune
body and fundus

14

AMAG increases the risk of what malignancies?

gastric carcinoid tumors
gastric adenocarcinoma
esophageal squamous cell carcinoma

15

Key features of EMAG?

environemental exposure to nitroso compouds or H. pylori
NO achloriydia, serum gastrin NOT elevated, NO abs against parietal cells/IF, NO pern. an.
increased risk of gastric ulcer

16

EMAG increases the risk for what type of cancer?

intestinal type gastric cancer

17

What is granulomatous gastritis?

organized aggregate of histiocytic, lymphocytic and plasma infiltrate
rare
can be infectious, non infectious or idiopathic
can be non caseating, caseating or necrotizing

18

What is mucosal eosinophilic gastritis?

distral antrum, nonspecific symptoms
nodularity on EGD
30s, assoc w/allergies, tx w/prednisone

19

What is eosinophilic gastritis muscle layer disease?

tickened rigid gut, distal antrum

20

Waht is subserosal eosinophilic gastritis?

ascites, can occur w/ mucosal or muscle layer disease

21

What are the 3 main causes of lymphocytic gastritis?

celiac disease,
H pylori
Varioliform gastritis

22

What are the causes and symptoms of acute hemorrhagic erosive gastropathy?

damage to epithelium via agents or hypoxia
abdominal pain, nausea, vomiting, hematemesis

23

What are the causes and symptoms of chronic chemical gastropathy?

long-term exposure to substances that injure the gastric mucosa
foveolar hyperplasia, edema, inc sm muscle in lamina propria, vascular dilation and congestion

24

What is hyperplastic gastropathy (menetrier's disease)?

enlarged gastric folds/hyperplasia of gastric epithelial cells
caused by overproducition of TGFa which leads to proliferation of epithelials cells
CMV may cause in kids

25

Key features of CMV?

herpes
dsDNA
owl's eye inclusion bodies

26

What are the symptoms of menetrier's disease?

abdominal pain, protein losing enteropathy, wt loss, nausea, vomiting

27

Tx of menetriet's disease?

CMV tx
-cetuximab
Gastrectomy
Octreotide

28

What malignancy does menetrier's disease increase the risk of?

gastric adenocarcinoma

29

What is Zollinger Ellison syndrome?

gastric acid hypersecretion due to hyperplasia of parietal cell
increase in histamine-secreting enterochromaffin-like cells
body and fundus

30

What is nonhyperplasic gastropathy? causes?

non oxyntic gland cells leading to gastric fold enlargement
infiltrative disease, malignancy (lymphoma, adenocarcinoma, carcinoid)

31

What is peptic ulcer disease?

defects in the gastrointestinal mucosa extending through the muscularis mucosa

32

What are the major risk factors for PUD?

H pylori
NSAIDs
steroids
stress
(possibly tylenol at high dose)
smoking
increased acid production
decreased duodenal bicarb secretion

33

What leads to duodenal ulcers in h pylori infection?

increased gastric acid secretion
gastric metaplasia
immune response
downregularion of mucosal defense mechanisms

34

What leads to gastric ulcers?

proximal to distal antrum
normal to low acid

35

How does dueodenal PUD ulcer present?

dyspepsia
burning or hunger-like epigastric pain 2-5hr after meals or at night
relief w/food, antacids or antisecretory meds

36

How does gastric PUD ulcer present?

dyspepsia
burning or hunger like epigastric pain
less freq relief w/food/antacids
pain soon after meals

37

What are the general clinical presentations of PUD?

dyspepsia (food provoked or relflux-like)
silent
w/constipation or IBS sx

38

Presentation of penetratin PUD?

localized intense pain that radiates to the back, not relieved with food or antacids

39

Presentation of perforated PUD?

severe, diffuse abd pain

40

other complicated presentations of PUD?

vomiting
GI bleeding (IDA)
Gastrocolic fistula

41

Tx of PUD?

acid suppression--helps stabilize blood clots
PPIs
somatostatin/octreotide (decreased blood flow, inhibit gastric acid sec.)
endoscopic
angiography w/transarterial embolization
surgery

42

What symptoms comprise dyspepsia

postprandial fullness
early satiety
epigstric pain or burning

43

Definition of functional dyspepsia?

dyspepsia+no evidence of structural disease
sx 3 of the last 6 months

44

Types of functional dyspepsia?

postprandial distress syndrome
epigastric pain syndrome

45

Why does functinoal dyspepsia occur?

gastric dysmotility
visceral hypersensitivity
h. pylori infection
altered gut microbiome (post infec.)
psychosocial

46

Tx of functional dyspepsia?

antidepressants (tricyclics, trazodone)
metoclopramide (promotility)
buspirone (fundic relaxant)
psychosoc. therapy
antinociceptive agents (carbamazepine, tramadol, pregablin)

47

What enzymes are distinctive for H pylori?

catalase, oxidase, urease positive

48

What type of epithelium does H pylori infect?

gastric type only
s noninvasive, but stimulates an imflamm resonse (IL-8 activates PMNs, recruits other cell types)

49

What is VacA?

passive urea transporter that can create a favorable environment for infectivity

50

What are the most commonly associated conditions with H Pylori?

gastric adenocarcinoma
MALT lymphoma
Gastritis
IDA w/o bleeding
Functional dyspepsia (?)
Vit B12 def.
Acid reflux
PUD

51

H pyrlori associated Acid reflux causes what two types of gastritis?

corpus predominant
antrum predominant

52

H Pylori assoc corpus-predominant gastritis features

decreased acid secretion due to local inflammation and increased cytokines, mild worsening with treatment

53

H pyrlori assoc antrum predominant gastritis features

associated w/increased gastrin level
improvement with treatment

54

What endoscopic testing is done for H pylori?

urease testing
histology +/- special stains
brush cytology
bacterial culture

55

What can cause false positives for H pylori?

recent bleeding
PPIs
Abx
bismuth-containing compounds
H2 antagonists

56

What noninvasive testing is done for Hpylori?

Urea breath test (for initial dx and confirmation of eradication)
IgG serology (only way to prove complete cure)
Stool Antigen
13C-urea blood test

57

Tx for H pylori gastritis

Abx (2-3)
Acid suppression w/PPIs
10-14 day regiment

58

How do NSAIDs cause gastroduodenal toxicity?

inhibits constitutively active COX1, which makes prostaglandins--have cytoprotective effects (ie/ mucin, bicarb and phospholipid secretion)
blocks cytoprotective effects of nitric oxide through NO synthase

59

What are the 2 main repair mechanisms of gastroduodenal toxicity?

restitution-rapid migration of new epithelial cells from progenitor cells
proliferation-less rapid regeneration of new epithelial cells from progenitor cells
(prostaglandins and NO important in both)

60

What are risk factors for development of PUD w/NSAID use?

duration of therapy (comp usually first 3 mo)
higher dose
age
history of GI tox w/nsaids
history of PUD
other drugs

61

Are dyspepsia and GI toxicity from NSAIDs related?

No

62

How do NSAIDs cause toxicity in stomahc?

block cox1 mediated prostaglandin production
interfere w/resitution and proliferation

63

How do NSAIDs cause toxicity in the duodenum?

dependent on stomach acid
(H2 blockers/PPIs to prevent)

64

How do NSAIDs cause toxicity in the small intestine and colon?

high local concentration necessary
localized injury->inflammation and ulceration->fibrosis and stricture
via inhibition of prostaglandins, alterations of blood flow and increased SI permeability

65

How does NSAID GI toxicity present?

stomach/duodenum: edema, erythema, subepithelial hemorrhage, erosions, ulcers
distal SI and colon-IDA, bleeding, hypoalbuminemia, malabsorption, bow obstruction form strictures, diarrhea, acute abdomen from perforation
diaphragm (benign)
ulcers

66

Tx for NSAID GI toxicity?

stomach/duodenum: stop nsaid, start PPI, asses H pylori status, treat if positive
distal small intestine/colon: stop nsaid, dilation of strictures, surgery