Peptic Ulcer Disease Flashcards
Peptic Ulcer Disease - characterised by?
–Erosion of GI mucosa resulting from the digestive action of HCl and pepsin
–Any portion of GI tract that comes in contact with gastric secretions is
susceptible to ulcer development including lower esophagus, stomach, &
duodenum
–Includes gastric and duodenal ulcers
Types of pepetic ulcer disease?
Acute
–Superficial erosion
–Minimal inflammation
–Resolves quickly when cause is identified & removed
Chronic
–Muscular wall erosion with formation of fibrous tissue
–Present continuously for many months or intermittently
–4 times more common than acute ulcers
Etiology and Pathophysiology
Develop only in presence of acid environment
Excess of gastric acid not necessary for ulcer development
Person with a gastric ulcer has normal to less than normal gastric acidity
compared with person with a duodenal ulcer
Some acid does seem to be essential for a gastric ulcer to occur
Under specific circumstances the mucosal barrier can be broken and HCL
freely enters the mucosa & injury to tissues occurs
This results in cellular destruction & inflammation
Histamine is released
–Vasodilation, ↑ capillary permeability
–Further secretion of acid and pepsin
Agents known to to destroy the mucosal barrier include:
H. Pylori - causes chronic inflammation making mucosa more vulnerable to
noxious agents
drugs (aspirin, NSAIDs, corticosteroids) – cause abnormal permeability
Gastric Ulcers
Commonly found on lesser curvature in close proximity to antral junction
Less common than duodenal ulcers
Prevalent in women, older adults, persons from lower socioeconomic class
Characterized by a normal to low secretion of gastric acid
Back diffusion of acid is greater (chronic)
The ability of the gastric acid to penetrate the mucosal barrier is more important
than the amount of gastric acid produced
Critical pathologic process is amount of acid able to penetrate mucosal barrier
H. pylori is present in 50% to 70%
H. pylori is thought to be more destructive when noxious agents are used e.g..
drugs or smoking
Drugs can cause acute and chronic gastric ulcers
–Aspirin, corticosteroids, and NSAIDs
–Other known causative factors are:
Chronic alcohol abuse, chronic gastritis
Cigarette smoking is positively linked with gastric ulcers
Ingestion of hot, spicy foods may be a cause but no evidence to support this
Duodenal Ulcers
Occur at any age and in anyone
Incidence is high between ages of 35 to 45 years
Affect more men than women
Account for 80% of all peptic ulcers
Associated with ↑ HCl acid secretion
H. pylori is found in 90-95% of patients
–Direct relationship has not been proven
Diseases with ↑ risk of duodenal ulcers -
COPD, cirrhosis of liver, chronic pancreatitis, hyperparathyroidism, chronic renal
failure
Treatments used for these conditions may promote ulcer development
Psychological Stress Ulcers
Acute ulcers that develop following a major physiologic insult such as trauma or
surgery
A form of erosive gastritis
Gastric mucosa of body of stomach undergoes a period of transient ischaemia
in association with
–Hypotension
–Severe injury
–Extensive burns
–Complicated surgery
Peptic Ulcer Pain
Gastric
Burning or gaseous
Can occur when stomach empty or immediately after food
Located high in epigastrium
Not necessarily relieved by food
Duodenal
Burning or cramp-like
Occurs 2-4 hrs after meals
Located in mid-epigastrium
Usually relieved by food or antacids
Peptic Ulcer Disease
Complications
3 major complications –Hemorrhage –Perforation –Gastric outlet obstruction Initially treated conservatively May require surgery at any time during course of therapy
Hemorrhage
Most common complication of peptic ulcer disease
Develops from erosion of
–Granulation tissue found at base of ulcer during healing
–Ulcer through a major blood vessel
Perforation
Most lethal complication of peptic ulcer
Commonly seen in large penetrating duodenal ulcers that have not healed and
are located on posterior mucosal wall
Perforated gastric ulcers often located on lesser curvature of stomach