Gastritis + PUD + Gastric CA Flashcards
What are some normal damaging forces and some normal defensive forces of the stomach?
Damaging:
Gastric Acidity
Peptic Enzymes
DEFENSIVE: Surface Mucous secretion Bicarb Secretion Mucosal blood flow apical surface membrane transport epithelial regenerative capacity elaboration of prostaglandins
What causes acute gastritis. Explain. Describe various risk factors. What is the pathological result?
A C U T E G A S T R I T I S
A. Acidic damag e to the stomac h mucos a
B . Due to imbalanc e between mucosal defenses and acidic environment
1 . Defenses include muci n layer produced by foveolar cells, bicarbonate secretion b y surface epithelium, and normal blood supply (provides nutrients and picks up
leaked acid).
C. Risk factors
1 . Severe burn (Curling ulcer) — Hypovolemia leads to decreased blood supply.
2. NSAID s (decreased PGE. )
3 . Heavy alcohol consumptio n
4. Chemotherap y
5 . Increased intracranial pressure (Cushing ulcer)—Increased stimulatio n of vagus
nerve leads to increased acid production.
6. Shock—Multiple (stress) ulcers may be seen in 1CU patients.
D. Acid damag e results in superficial inflammation, erosion (loss of superficial epithelium), or ulcer (loss of mucosal layer)
What is chronic gastritis? What are 2 categories of Chronic Gastritis?
A. Chroni c Inflammatio n of stomach mucosa
B . Divided into two types based on underlying etiology: chronic autoimmune gastritis
and chronic H pylori gastritis
What causes chronic autoimmune gastritis? Where is the damage? What is the pathogenesis? Clinical/physiological features? How is the diagnosis made? Microscopic features?
Chronic autoimmune gastritis is due to autoimmun e destructio n of gastric parietal cells, which are located in the stomach body and fundus .
1 . Associated with antibodies against parietal cells and/o r intrinsic factor; useful for diagnosis, but pathogenesis is mediated by T cells (type IV hypersensitivity)
2, Clinical features
i. Atrophy of mucos a with intestinal metaplasia (Fig. 10.11)
ii. Achlorhydria with increased gastrin levels and antral G-cell hyperplasia
iii. Megaloblastic (pernicious) anemia due to lack of intrinsic factor (vit. b12 defiency)
iv. Increased risk tor gastric adenocarcinoma (intestinal type)
MICROSCOPIC
Loss of parietal cells
Loss of glands (atrophy)
Intestinal metaplasia,
pseudopyloric metaplasia,
and endocrine cell
hyperplasia
Describe the pathogenesis of chronic h. pylori gastritis? Where is it located? Microscopic pathology? How common is it? How does it present? What is the treatment? How effective is it? How do you know if its working?
Antrum
Spiral-shaped H. pylori are highlighted in this
Warthin-Starrysilver stain
Intraepithelial and lamina propria neutrophils
Lymphoid aggregates with germinal centers
subepithelial plasma cells within the superficial
lamina propria
Chroni c H pylori gastritis is due to H pylori-induced acute and chronic inflammation; mos t c o m m o n form of gastritis (90%)
1 . H pylori ureases and proteases along with inflammatio n weaken mucosal
defenses; a n t r u m is the most commo n site (Fig. 10.12),
2. Presents with epigastric abdominal pain; increased risk for ulceration (peptic
ulcer disease), gastric adenocarcinoma (intestinal type), and MALT lymphoma
3 . Treatment involves triple therapy (PPI, clarithromycin, amoxicyllin).
i. Resolves gastritis/ulcer and reverses intestinal metaplasia
ii. Negative urea breath test and lack of stool antigen confirm eradication of H pylori.
What are two hypertrophic gastropathies?
Menetrier?s Disease
Zollinger-Ellison syndrome
Describe Menetriers disease.
Hypoproteinemia due to protein-losing enteropathy
Diffuse hyperplasia of the foveolar
epithelium of the body and fundus
Caused by excessive
secretion of
transforming growth
factor a (TGF-a)
Glandular atrophy is typical
Describe Zollinger Ellison Syndrome.
Caused by gastrinoma in the
small bowel or pancreas
Presented with duodenal ulcers
or chronic diarrhea
Doubling of oxyntic mucosal
thickness due to fivefold
increase in the number of
parietal cells
What is a gastric CA? What are the 2 subclassifications? How does it present? To which lymph nodes does it spread? What does it metastasize? What are two pathogeneses and which subclassification are they associated with?
A. Malignant proliferation of surface epithelial cells (adenocarcinoma)
B. Subclassilied into intestinal and diffuse types
o The loss of E-cadherin (encoded by CDH1 gene) function seems to be a key step in the development of diffuse gastric cancer
o Mutation in β-catenin (a protein binds to both E-cadherin and APC), microsatellite instability and hypermethylation of several genes are involved in sporadic intestinal-type gastric cancer.
E. Gastric carcinoma presents late with weight loss, abdominal pain, anemia, and early satiety; rarely presents as acanthosis nigricans or Leser-Trelat sign
F. Spread to lymph nodes can involve the left supraclavicular node (Virchow node).
G. Distant metastasis most commonl y involves liver; other sites include:
I. Periumbilical region (Sister Mary Joseph nodule); seen with intestinal type
2.Bilateral ovaries (Krukenberg tumor) ; seen with diffuse type
Describe Diffuse type gastric CA both grossly and microscopically. What is it not associated with?
D. Diffus e typ e is characterized by signet ring cells that diffusely inliltrate the gastric wall (Fig. 10.14B); desmoplasia results in thickening of stomach wall (linitis plasties, Fig, 10.I4A).
1 , Not associated with H pylori, intestinal metaplasia, or nitrosamine s
Signet-ring cells: large cytoplasmic mucin vacuoles and peripherally displaced, crescent-shaped nuclei.?
LINITIS PLASTICA
markedly thickened gastric wall and partially lost rugal folds
What is the more common gastric CA type? How does it present? Where is it most commonly? What are the risk factors?
C. Intestinal typ e (more common) presents as a large, irregular ulcer with heaped up
margins; most commonl y involves the lesser curvature of the a n t r u m (similar to
gastric ulcer)
1 . Risk factors include intestinal metaplasia (e.g., due to H pylori and autoimmune gastritis), nitrosamines in smoked foods (Japan), and blood typ e A.
What are some examples of neoplastic gastric polyps? Non-neoplastic?
Neoplastic
Adenoma
Non-neoplastic
Hyperplastic polyp ? Is there any dysplasia Elongated dilated foveolae
Fundic gland polyp
Sporadic vs FAP
Dilated oxyntic glands
What is a MALToma?
MALToma (Mucosal associated lymphoid
tissue lymphoma). Associated with H. Pylori chronic gastritis.
What is a peptic ulcer? Where does it occur? What is most common? What are peptic ulcers? What are the symptoms? compare and contrast duodenal and gastric ulcers. What are some alarm symptoms?
A. Solitary mucosal ulcer involving proximal duodenum (90%) or distal stomach (10%)
Defects or breaks in the mucousa with depth and have
extended through muscularis mucousa
Epigastric pain ? ?dull, aching, hunger like,
empty?
Duodenal ulcer-relieved with ingestion of
milk, food, antacids, recurs 2-4 hours later or
at night
Gastric ulcers-eating makes symptoms worse
Alarm symptoms: acute change in pain, overt
GI bleeding, anemia, weight loss, vomiting,
early satiety
What is a duodenal ulcer most likely due to? What else might it be due to? How does it present? What is seen on biopsy? What are the complications?
B. Duodenal ulcer is almost always due to H pylori (> 95%); rarely, may be due to ZE syndrome
! , Presents with epigastric pain that improves with meals
2. Diagnostic endoscopic biopsy shows ulcer with hypertrophy of Brunne r glands .
3 . May rupture leading to bleeding fro m the gastroduodenal artery (posterior) or acute pancreatitis (posterior ulcer)
