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Gastritis & PUD Flashcards

1
Q

What is gastsritis?

A

inflammation associated with mucosal injury

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2
Q

What is gastropathy?

A

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

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3
Q

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

A

acute-neutrophilic

chronic-lymphocytes, plasma cells, macrophages

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4
Q

Key features of acute helicobacter pylori gastritis?

A

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

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5
Q

Key features of chronic helicobacter pylori gastritis?

A

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

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6
Q

Common histological finding of chronic H. pylori?

A

lymphoid follices

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7
Q

What is helicobacter heilmannii gastritis?

A

uncommon

treated like H pylori

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8
Q

What is metaplasic (chronic) atrophic gastritis? Types?

A

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

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9
Q

What is pseudopyloric metaplasia?

A

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

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10
Q

Waht is intestinal metaplasia?

A

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

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11
Q

What are the main types of intestinal metaplasia?

A

Complete (type I)-fully formed SI epithelium

Incomplete (type II&III)-goblet cells interspersed among gastric-type mucin cells

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12
Q

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

A

Type III

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13
Q

Key features of AMAG?

A 
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
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14
Q

AMAG increases the risk of what malignancies?

A

gastric carcinoid tumors
gastric adenocarcinoma
esophageal squamous cell carcinoma

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15
Q

Key features of EMAG?

A

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

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16
Q

EMAG increases the risk for what type of cancer?

A

intestinal type gastric cancer

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17
Q

What is granulomatous gastritis?

A

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

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18
Q

What is mucosal eosinophilic gastritis?

A

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

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19
Q

What is eosinophilic gastritis muscle layer disease?

A

tickened rigid gut, distal antrum

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20
Q

Waht is subserosal eosinophilic gastritis?

A

ascites, can occur w/ mucosal or muscle layer disease

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21
Q

What are the 3 main causes of lymphocytic gastritis?

A

celiac disease,
H pylori
Varioliform gastritis

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22
Q

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

A

damage to epithelium via agents or hypoxia

abdominal pain, nausea, vomiting, hematemesis

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23
Q

What are the causes and symptoms of chronic chemical gastropathy?

A

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

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24
Q

What is hyperplastic gastropathy (menetrier’s disease)?

A

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

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25
Q

Key features of CMV?

A

herpes
dsDNA
owl’s eye inclusion bodies

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26
Q

What are the symptoms of menetrier’s disease?

A

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

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27
Q

Tx of menetriet’s disease?

A

CMV tx
-cetuximab
Gastrectomy
Octreotide

28
Q

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

A

gastric adenocarcinoma

29
Q

What is Zollinger Ellison syndrome?

A

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

30
Q

What is nonhyperplasic gastropathy? causes?

A

non oxyntic gland cells leading to gastric fold enlargement

infiltrative disease, malignancy (lymphoma, adenocarcinoma, carcinoid)

31
Q

What is peptic ulcer disease?

A

defects in the gastrointestinal mucosa extending through the muscularis mucosa

32
Q

What are the major risk factors for PUD?

A 
H pylori
NSAIDs
steroids
stress
(possibly tylenol at high dose)
smoking
increased acid production
decreased duodenal bicarb secretion
33
Q

What leads to duodenal ulcers in h pylori infection?

A

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

34
Q

What leads to gastric ulcers?

A

proximal to distal antrum

normal to low acid

35
Q

How does dueodenal PUD ulcer present?

A

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

36
Q

How does gastric PUD ulcer present?

A

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

37
Q

What are the general clinical presentations of PUD?

A

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

38
Q

Presentation of penetratin PUD?

A

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

39
Q

Presentation of perforated PUD?

A

severe, diffuse abd pain

40
Q

other complicated presentations of PUD?

A

vomiting
GI bleeding (IDA)
Gastrocolic fistula

41
Q

Tx of PUD?

A

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

42
Q

What symptoms comprise dyspepsia

A

postprandial fullness
early satiety
epigstric pain or burning

43
Q

Definition of functional dyspepsia?

A

dyspepsia+no evidence of structural disease

sx 3 of the last 6 months

44
Q

Types of functional dyspepsia?

A

postprandial distress syndrome

epigastric pain syndrome

45
Q

Why does functinoal dyspepsia occur?

A 
gastric dysmotility
visceral hypersensitivity
h. pylori infection
altered gut microbiome (post infec.)
psychosocial
46
Q

Tx of functional dyspepsia?

A 
antidepressants (tricyclics, trazodone)
metoclopramide (promotility)
buspirone (fundic relaxant)
psychosoc. therapy
antinociceptive agents (carbamazepine, tramadol, pregablin)
47
Q

What enzymes are distinctive for H pylori?

A

catalase, oxidase, urease positive

48
Q

What type of epithelium does H pylori infect?

A

gastric type only

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

49
Q

What is VacA?

A

passive urea transporter that can create a favorable environment for infectivity

50
Q

What are the most commonly associated conditions with H Pylori?

A 
gastric adenocarcinoma
MALT lymphoma
Gastritis
IDA w/o bleeding
Functional dyspepsia (?)
Vit B12 def.
Acid reflux
PUD
51
Q

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

A

corpus predominant

antrum predominant

52
Q

H Pylori assoc corpus-predominant gastritis features

A

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

53
Q

H pyrlori assoc antrum predominant gastritis features

A

associated w/increased gastrin level

improvement with treatment

54
Q

What endoscopic testing is done for H pylori?

A

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

55
Q

What can cause false positives for H pylori?

A 
recent bleeding
PPIs 
Abx
bismuth-containing compounds
H2 antagonists
56
Q

What noninvasive testing is done for Hpylori?

A

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
Q

Tx for H pylori gastritis

A

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

58
Q

How do NSAIDs cause gastroduodenal toxicity?

A

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
Q

What are the 2 main repair mechanisms of gastroduodenal toxicity?

A

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
Q

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

A 
duration of therapy (comp usually first 3 mo)
higher dose
age
history of GI tox w/nsaids
history of PUD
other drugs
61
Q

Are dyspepsia and GI toxicity from NSAIDs related?

A

No

62
Q

How do NSAIDs cause toxicity in stomahc?

A

block cox1 mediated prostaglandin production

interfere w/resitution and proliferation

63
Q

How do NSAIDs cause toxicity in the duodenum?

A

dependent on stomach acid

H2 blockers/PPIs to prevent

64
Q

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

A

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
Q

How does NSAID GI toxicity present?

A

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
Q

Tx for NSAID GI toxicity?

A

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

GI (20 decks)

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