Peptic Ulcer.ppt
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• Etiology
Peptic Ulcer
• Pathogenesis • Microbiology • Gross Pathology
• Microscopic features • Clinical features
Introduction • Peptic ulcer disease encompasses gastric, duodenal, and esophageal ulcers.
• They are typically named by their anatomical location, such as gastric or duodenal ulcers. • Increased HCl associated gastritis is the primary cause of PUD.
• Common etiologies of PUD are Helicobacter pylori infection and chronic use of NSAID. • Other controversial etiological factors are - cigarette smoking, psychological stress, caffeine intake, and alcohol ingestion. • Involvement of the gastric muscularis mucosa differentiates PUD from more superficial acid-related disorders such as erosions and gastritis.
Pathogenesis •
Pathogenesis of PUD is multifactorial.
•
Hyperchlorohydric chronic gastritis is the precursor lesion of PUD.
•
It is present in 85 - 100% patients with duodenal ulcer (DU) and in 65% of patients with gastric ulcer (GU).
•
Imbalance between gastric luminal factors (hypersecretion of hydrochloric acid and pepsin) and defensive function of the gastric mucosa results in chronic gastritis.
•
Mucosal defenses include mucus, secretion of bicarbonate, mucosal blood flow, and epithelial cell defense (epithelial regeneration and elaboration of PGs).
•
As acid and pepsin invades some weakened area of mucosal barrier, histamine is released.
•
Histamine stimulates parietal cells to secrete more acid.
•
With continuation of this vicious cycle, erosions occur to form an ulcer.
•
H Pylori infection has been shown to produce chronic gastritis and hyperchlorohydria.
•
More than 70% of patients of PUD show colonization by H pylori.
•
However, only 20% of patients infected by H pylori develop PUD. Possibly host genetic factors and variation in microbial pathogenicity are responsible.
•
Exactly how H Pylori infection results in hyperchlorohydria not understood completely.
•
Duodenal colonization by H pylori produces impaired bicarbonate secretion and this in association with increased gastric acid results in
pyloric metaplasia of duodenum.
Gross Pathology of PU •
In stomach, GU are predominantly found in lesser curvature at margins of body and antrum.
•
DU are usually found in anterior duodenal wall within few cm of pyloric antrum
•
Generally PU are solitary (Multiple ulcers may be seen in ZE syndrome).
•
PU are sharply punched out lesions and are level with the surrounding mucosa (cf malignant ulcer).
•
Base of the ulcer is usually clean (cf - malignant ulcer) and BVs may be seen.
Peptic Ulcer eroding a vessel
Peptic Ulcer
Carcinoma stomach
Peptic ulcer
Histology of Peptic Ulcer Layer of fibrinoid necrosis and neutrophilic exudate
Granulation tissue layer
Layer of fibrinoid necrosis and neutrophilic exudate
Granulation tissue layer
Complications • Bleeding: – Most common complication of PUD – Occurs in up to 15% of patients.
– More common in patients > 60 years of age. – 5 - 10% mortality. – In up to 20% patients no preceding warning symptom.
• Perforation: – Occurs in 6 - 7% patients. – If ulcer tunnels into adjacent organ, it is called penetration. – DU penetrate posteriorly into pancreas: - pancreatitis. – GU penetrate into left hepatic lobe.
• Obstruction: – Usually of gastric outlet. – Temporary obstruction due to inflammation and edema – Fixed obstruction due to scar formation
Peptic Ulcer
• Pathogenesis • Microbiology • Gross Pathology
• Microscopic features • Clinical features
Introduction • Peptic ulcer disease encompasses gastric, duodenal, and esophageal ulcers.
• They are typically named by their anatomical location, such as gastric or duodenal ulcers. • Increased HCl associated gastritis is the primary cause of PUD.
• Common etiologies of PUD are Helicobacter pylori infection and chronic use of NSAID. • Other controversial etiological factors are - cigarette smoking, psychological stress, caffeine intake, and alcohol ingestion. • Involvement of the gastric muscularis mucosa differentiates PUD from more superficial acid-related disorders such as erosions and gastritis.
Pathogenesis •
Pathogenesis of PUD is multifactorial.
•
Hyperchlorohydric chronic gastritis is the precursor lesion of PUD.
•
It is present in 85 - 100% patients with duodenal ulcer (DU) and in 65% of patients with gastric ulcer (GU).
•
Imbalance between gastric luminal factors (hypersecretion of hydrochloric acid and pepsin) and defensive function of the gastric mucosa results in chronic gastritis.
•
Mucosal defenses include mucus, secretion of bicarbonate, mucosal blood flow, and epithelial cell defense (epithelial regeneration and elaboration of PGs).
•
As acid and pepsin invades some weakened area of mucosal barrier, histamine is released.
•
Histamine stimulates parietal cells to secrete more acid.
•
With continuation of this vicious cycle, erosions occur to form an ulcer.
•
H Pylori infection has been shown to produce chronic gastritis and hyperchlorohydria.
•
More than 70% of patients of PUD show colonization by H pylori.
•
However, only 20% of patients infected by H pylori develop PUD. Possibly host genetic factors and variation in microbial pathogenicity are responsible.
•
Exactly how H Pylori infection results in hyperchlorohydria not understood completely.
•
Duodenal colonization by H pylori produces impaired bicarbonate secretion and this in association with increased gastric acid results in
pyloric metaplasia of duodenum.
Gross Pathology of PU •
In stomach, GU are predominantly found in lesser curvature at margins of body and antrum.
•
DU are usually found in anterior duodenal wall within few cm of pyloric antrum
•
Generally PU are solitary (Multiple ulcers may be seen in ZE syndrome).
•
PU are sharply punched out lesions and are level with the surrounding mucosa (cf malignant ulcer).
•
Base of the ulcer is usually clean (cf - malignant ulcer) and BVs may be seen.
Peptic Ulcer eroding a vessel
Peptic Ulcer
Carcinoma stomach
Peptic ulcer
Histology of Peptic Ulcer Layer of fibrinoid necrosis and neutrophilic exudate
Granulation tissue layer
Layer of fibrinoid necrosis and neutrophilic exudate
Granulation tissue layer
Complications • Bleeding: – Most common complication of PUD – Occurs in up to 15% of patients.
– More common in patients > 60 years of age. – 5 - 10% mortality. – In up to 20% patients no preceding warning symptom.
• Perforation: – Occurs in 6 - 7% patients. – If ulcer tunnels into adjacent organ, it is called penetration. – DU penetrate posteriorly into pancreas: - pancreatitis. – GU penetrate into left hepatic lobe.
• Obstruction: – Usually of gastric outlet. – Temporary obstruction due to inflammation and edema – Fixed obstruction due to scar formation
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