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Gastric Cancer - Coggle Diagram
Gastric Cancer
Risk Factors
Environmental
H.pylori (Helicobactor pylori) infection
dietary factors
high content salted food
foods contain high nitrates
alcohol consumption & cigarette smoking
occupational exposure
mining, farming
refining, fishing
asbestos, timber, rubber
Non-environmental
family history
blood type group A
pernicious anemia
Genetic
Familial contributes 10 to 15%
genomic instability
chromosomal instability- gain or loss of whole chromosome during seggregation, DNA damage
microsatellite instability- errors in DNA replication
genetic defect of CDH1 gene found in chromosome 16
Pathophysiology & Etiology
Multifactorial causes, but H.pylori accounts 80% of gastric cancer
Atrophic and intestinal metaplasia are linked to development of gastric cancer
Duodenal reflux contains caustic bile salts that destroy mucosal barrier
Insufficient acid secretion creates alkaline environment and allows bacteria to multiply and acts on nitrates, which damages DNA of mucosal cell
High salty food induces hypergastrinemia & endogenous mutations which promotes epithelial cell proliferation and leads to parietal cell loss and gastric cancer progression
Smoking and alcohol decrease production of prostaglandins that maintain gastric mucosal integrity
H. pylori induces chronic gastritis
H.pylori contains a virulent factor of cytotoxin-associated gene A (cagA)
During inflammatory process, cagA factor releases into gastric epithelial cells where it undergoes tyrosine phosphorylation by SRC family kinases
The phosphorylated cagA then binds and activates SHP2, a phosphatase that transmits positive signals for cell growth and motility
As a result, it activates growth factor receptors, releases of proinflammatory cytokines, and tumor promotors, which increases in proliferation of damaged cells, inhibits apoptosis and promotes invasion angiogenesis
Infection H. pylori
causes gastric mucosal damage by secreting different enzyme products (urease, protease, phospolipase and acetaldehyde)
disrupts gastric functions by urease-mediated myosin II activation
leads to oxidative DNA damage through production of reactive oxygen and nitrogen species and suppresses the host antioxidant defense mechanisms
Causative Factors
H.pylori infection
Severe gastritis
Clinical Manifestations
Early stages
asymptomatic
loss appetite
malaise
weight loss
heartburn
Later stages
upper abdominal pain
nausea, vomiting
irregular bowel habits
anemia due to bleeding
Diagnostic Tests
blood tests
upper endoscopy
upper GI series
CT scan
Biopsy
Prevention
Dietary modification
Reduce intake of salt & salted food
Avoid food contain high nitrate level
Reduce intake of red meat
Increase intake of fruits & vegeables
Screening & eradication of H. pylori infection
Treatments
Chemotherapy
Radiation
Surgery