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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
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

GI (20 decks)

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