Modifiable Risk Factors Non-modifiable Risk Factors

Excessive Stress Heavy Smoking Frequent NSAID Use Helicobacter pylori Poor Oral Hygiene Irregular Eating Pattern Food and Beverages Genetics Advancing Age (50-70 Type O Blood Type
infection y/o)

Decrease gastric renewal
prostaglandin(protective
Atrophy of the gastric
mucosa
Blocks the enzyme COX-1 Microorganism in dental Prolonged period of • Excessive greasy Familial Increased density to
Nicotine decreases Mild
which is involve in the plaque and saliva empty stomach foods intake hyperpepsinogemia type Stomach tends to get colonization of epithelial
Toxin Release Fatty
prostaglandin generation • Heavy alcohol I thinner, weaker and less cells and higher
factor in the mucosal Liver
layer of stomach) drinking efficient. inflammatory response
generation in gastric Inflammatory response Oral cavity as potential No food for the gastric • Frequent to H. Pylori
acid to be neutralize Genetic phenotype
mucosa with neutrophils, reservoir for H. Pylori. consumption of
leading to enhanced
lymphocytes, plasma caffeinated drinks
secretion of pepsin
cells, and macrophages
within the mucosal layer
Increase gastric acid
production

Gastric acid irritates

the gastric mucosa

Decreased Gastric Mucosal Lining Integrity

The cells in the lining of

the stomach or esophagus Erosion of Gastric Mucosal Lining
Chronic
Gastric change to resemble the Inflammation Ability of the mucosal cells to
Metaplasia tissues that line the Acid ingestion is
intestines. altered secrete bicarbonate is Inner layers are susceptible to acidity
Increase gastric compromised
Dysplasia acid Erosion of the ulcer through the Perforation (erosion of the ulcer Partially digested food, bacteria,
Erosions become larger and extend deeper into gastric serosa into adjacent through the gastric serosa into and enzymes from the digestive Peritonitis
the gastric tract lining structures. the peritoneal cavity) tract spill into the belly cavity.
Neoplasia Gastric acid further irritates
the inner gastric layers

Gastric Cancer Erosion proceed into the blood vessels Bleeding into the esophagus Irritation of Somatic Pyloric channel ulcers
innervation (T5-T8)

Bleeding into the stomach Blood passes through GI tract, Blood get oxidized by HCL Hematemesis Epigastric Pain
becomes oxidized by HCL and Visceral sensitization and
but moves back into the (vomiting blood)
digestion gastroduodenal
esophagus
Dyspepsia dysmotility.
Loss of blood for long periods
Melena (black tarry, foul Coffee-ground emesis • Epigastric pain
smelling stool) Food-provoked • Epigastric fullness
Iron stores are depleted. symptoms • Postprandial belching
• Early satiety
• Fatty food intolerance
The normal process of Altered intra-
Changes in the activity of Absorption of the • Nausea
making red blood cells is and extracellular Hyponatremia
the red cell membrane- nitrogenous end products Increase BUN • Occasional vomiting
altered (Erythropoiesis). cation
bound sodium-potassium into the blood.
adenosine triphosphatase homeostasis
There is not enough iron to Hyperkalcemia
make hemoglobin for red Fatigue Electrolyte
blood cells.
imbalances Hyperchloremia
Dizziness and
Low hemoglobin level Lightheadedness

Drowsiness
Low levels of circulating
oxygen Shortness of breath

Pallor

Slow capillary refill