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PEPTIC ULCER
-By Aashi Srivastava (Roll No.-2)
B.pharm,2nd semester
College of Pharmacy,JSSATE Noida
. The stomach is a ‘gland with cavity’, extending from its junction with lower end of
the esophagus (cardia) to its junction with the duodenum (pylorus).
It consists of 4 anatomical regions-
CARDIA
FUNDUS
BODY
PYLORUS
It constitutes of 4 layers namely the – Serosa, Muscularis,Submucosa and Mucosa
Histology of Stomach
Terminology of Peptic Ulcer
Peptic ulcers are the areas of degeneration and necrosis(death of cells of the
organ or tissue) of gastrointestinal mucosa exposed to acid-peptic secretions.
Although they can affect any level of the alimentary tract,they occur most
commonly in either the duodenum or the stomach.
They are generally chronic in nature.
Acute ulcer arises due to psychological stress.
Types of Ulcers
 Gastric ulcer- occurring in the stomach
 Duodenal ulcer-occurring in the first part of the
small intestine
● Usual age -25-50 years
● Mucosal digestion due to
hyperacidity
● No vomiting
● More in males
● Pain from a duodenal
ulcer often occurs when
the stomach is empty,
several hours after
eating, and may improve
after eating
● Happens after 6th decade
● Mucosal digestion due to
serum gastrin levels
● Vomiting common
● More in females
● Pain from a gastric ulcer
often occurs when food is
still in the stomach,
shortly after eating.
Distinguishing features between the two ulcers
Duodenal ulcer Gastric ulcer
Etiology of Peptic ulcer
1. The immediate cause of peptic ulcer disease is disturbance in normal protective
mucosal ‘barrier’ by acid pepsin, resulting in digestion of mucosa.
2. Besides, 10-20% patients of gastric ulcer may have coexistent duodenal ulcer
as well.
3. Thus, the etiology of peptic ulcers possibly may not be explained on the basis of
a single factor but is multi factorial.
Multiple Factors responsible for Ulcer
1. Helicobacter pylori gastritis- About 15-20% cases infected with H.
pylori in the antrum develop duodenal ulcer in their life time while gastric
colonization by H. pylori never develops ulceration and remain asymptomatic.
2. NSAIDs induced mucosal injury-Non-steroidal anti inflammatory
drugs cause gastric and duodenal mucosal injury (Drugs include ibuprofen,
Advil etc.)
3.Dietary factors-Nutritional deficiencies have been regarded as etiologic
factors in peptic ulcers e.g. occurrence of gastric ulcer.
4. Miscellaneous- Alcoholic cirrhosis, pancreatitis, hyperparathyroidism etc.
PATHOPHYSIOLOGY
● Helicobacter pylori (H. pylori) is highly adapted to the gastric environment
where it lives within or beneath the gastric mucous. The bacterium generally
does not invade gastro duodenal tissue. Instead, it renders the underlying
mucosa more vulnerable to acid peptic damage by disrupting the mucous
layer, liberating enzymes and toxins, and adhering to the gastric epithelium. In
addition, the host immune response to H. pylori incites an inflammatory
reaction which further perpetuates tissue injury.
● Tissue injury induced by H. pylori depends upon bacterial attachment and the
subsequent release of enzymes and other microbial products that can cause
cellular damage.
● Helicobacter pylori exclusively colonizes gastric type epithelium, where it lives
within or beneath the gastric mucus layer.
1. H.pylori induced ulcer
●
Also releases urease and protease
Urease releases ammonia and CO2
which itself destroys the mucosal lining
and causes neutralization of gastric
Ammonia causes infection of mucosal
lining and releases inflammatory
Leucocyte adhesion and inflammatory
reaction starts
Damage of mucosal wall leading to
ulcer
Inflammatory mediators include IL-1,IL-
2,TNF
2. Drug induced ulcer
● NSAIDs can cause damage to the
gastro duodenal mucosa via several
mechanisms, including the topical
irritant effect on the epithelium,
impairment of the mucosa,
suppression of gastric prostaglandin
synthesis, reduction of gastric
mucosal blood flow and interference
with the repair of superficial injury
● Prostaglandins regulate blood flow
and are responsible for inflammation.
Drugs like NSAIDs (non
selectively inhibit cox1 and
cox2 in body
Arachidonic acid cannot
effectively produce
prostaglandins
Leads to ischemia and increase
in HCL secretion leading to ulcer
3. ZES(Zollinger-Ellison Syndrome)
Tumor of goblet
cell occurs
Abnormal
increase in mucus
secretion
Increased
secretion of
gastric juice
Mucosal lining
damage
● “No gastric acid, no peptic ulcer” is
a misconception. Excessive gastric
acid secretion is only one factor in
the pathogenesis of peptic ulcer
disease. Decreased mucosal
defense against gastric acid is
another cause. The integrity of the
upper gastrointestinal tract is
dependent upon the balance
between “hostile” factors such as
gastric acid, H. pylori, NSAIDs and
pepsin, and “protective” factors
such as prostaglandins, mucus,
bicarbonate, and blood flow to
mucosa affecting gastrointestinal
mucosa
Diagnosis
● Laboratory tests for H. pylori. -The doctor may
recommend tests to determine whether the bacterium H.
pylori is present in our body. He or she may look for H.
pylori using a blood, stool or breath test(Urea breath test).
● Endoscopy- Doctor may use a scope to examine the upper
digestive system (endoscopy). During endoscopy, a hollow
tube equipped with a lens (endoscope) is passed down the
throat and into the esophagus, stomach and small intestine.
Using the endoscope, ulcers are detected
.
● Biopsy-If the doctor detects an ulcer, a small tissue sample
(biopsy) may be removed for examination in a lab. A biopsy
can also identify whether H. pylori is in our stomach lining
or not.
● Barium swallow- You drink a thick white liquid (barium)
that coats your upper gastrointestinal tract and helps your
doctor see your stomach and small intestine on X-rays.
Complications
● OBSTRUCTION-Development of fibrous scar at or near the
pylorus results in pyloric stenosis. Healed duodenal ulcers
cause duodenal stenosis.
● HAEMORRHAGE-Chronic blood loss may result in iron
deficiency anemia. A penetrating chronic ulcer may erode a
major artery (e.g. left gastric, gastro duodenal or splenic
artery) and cause a massive and severe haematemesis
and sometimes death.
● PERFORATION- A perforated peptic ulcer is an acute
abdominal emergency. Perforation occurs more commonly
in chronic duodenal ulcers than chronic gastric ulcers which
leads to peritonitis and can involve liver or pancreas.
Symptoms
1. Epigastric pain
2. Dyspepsia
3. Bloating, Distension and fatty food
intolerance
4. Heartburn
5. Chest Discomfort
6. Haematemesis due to GIT bleeding
7. Loss of weight is a common finding in
gastric ulcer patients.
To reduce your risk of developing a peptic
ulcer:
‱Avoid tobacco smoking
‱Avoid alcohol.
‱Use caution with aspirin and/or NSAIDs.
‱Don’t ignore your ulcer symptoms.
‱Protect yourself from infections by
washing. hands regularly and consuming
foods that have been cooked thoroughly.
Precautions
1. If tests show that you have an H. pylori infection, your doctor will prescribe a
combination of medication. The medications include antibiotics to help kill
infections and proton pump inhibitors(PPIs).
2. Proton pump inhibitors are-
o Reduce acid levels and allow ulcer to heal
o Omeprazole
o Lansoprazole
3. Antibiotics used are – Tetracycline, Amoxicillin and clarithromycin etc.
4. If one doesn’t have an H. pylori infection, they may be recommended a
prescription or over-the-counter PPI (such as Prilosec or Prevacid) for up to
eight weeks to reduce stomach acid and help the ulcer heal.
Treatment
5. The doctor may also prescribe sucralfate (Carafate) which will
coat one’s stomach and reduce symptoms of peptic ulcers.
6. Acid blockers like famotidine (Pepcid) can also reduce
stomach acid and ulcer pain.
7. Surgery might be done if the complications increase.
CREDITS: This presentation template was created
by Slidesgo, including icons by Flaticon,
infographics & images by Freepik
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Peptic ulcer modified 2

  • 1. PEPTIC ULCER -By Aashi Srivastava (Roll No.-2) B.pharm,2nd semester College of Pharmacy,JSSATE Noida
  • 2. . The stomach is a ‘gland with cavity’, extending from its junction with lower end of the esophagus (cardia) to its junction with the duodenum (pylorus). It consists of 4 anatomical regions- CARDIA FUNDUS BODY PYLORUS It constitutes of 4 layers namely the – Serosa, Muscularis,Submucosa and Mucosa Histology of Stomach
  • 3. Terminology of Peptic Ulcer Peptic ulcers are the areas of degeneration and necrosis(death of cells of the organ or tissue) of gastrointestinal mucosa exposed to acid-peptic secretions. Although they can affect any level of the alimentary tract,they occur most commonly in either the duodenum or the stomach. They are generally chronic in nature. Acute ulcer arises due to psychological stress.
  • 4. Types of Ulcers  Gastric ulcer- occurring in the stomach  Duodenal ulcer-occurring in the first part of the small intestine
  • 5. ● Usual age -25-50 years ● Mucosal digestion due to hyperacidity ● No vomiting ● More in males ● Pain from a duodenal ulcer often occurs when the stomach is empty, several hours after eating, and may improve after eating ● Happens after 6th decade ● Mucosal digestion due to serum gastrin levels ● Vomiting common ● More in females ● Pain from a gastric ulcer often occurs when food is still in the stomach, shortly after eating. Distinguishing features between the two ulcers Duodenal ulcer Gastric ulcer
  • 6. Etiology of Peptic ulcer 1. The immediate cause of peptic ulcer disease is disturbance in normal protective mucosal ‘barrier’ by acid pepsin, resulting in digestion of mucosa. 2. Besides, 10-20% patients of gastric ulcer may have coexistent duodenal ulcer as well. 3. Thus, the etiology of peptic ulcers possibly may not be explained on the basis of a single factor but is multi factorial.
  • 7. Multiple Factors responsible for Ulcer 1. Helicobacter pylori gastritis- About 15-20% cases infected with H. pylori in the antrum develop duodenal ulcer in their life time while gastric colonization by H. pylori never develops ulceration and remain asymptomatic. 2. NSAIDs induced mucosal injury-Non-steroidal anti inflammatory drugs cause gastric and duodenal mucosal injury (Drugs include ibuprofen, Advil etc.) 3.Dietary factors-Nutritional deficiencies have been regarded as etiologic factors in peptic ulcers e.g. occurrence of gastric ulcer. 4. Miscellaneous- Alcoholic cirrhosis, pancreatitis, hyperparathyroidism etc.
  • 8. PATHOPHYSIOLOGY ● Helicobacter pylori (H. pylori) is highly adapted to the gastric environment where it lives within or beneath the gastric mucous. The bacterium generally does not invade gastro duodenal tissue. Instead, it renders the underlying mucosa more vulnerable to acid peptic damage by disrupting the mucous layer, liberating enzymes and toxins, and adhering to the gastric epithelium. In addition, the host immune response to H. pylori incites an inflammatory reaction which further perpetuates tissue injury. ● Tissue injury induced by H. pylori depends upon bacterial attachment and the subsequent release of enzymes and other microbial products that can cause cellular damage. ● Helicobacter pylori exclusively colonizes gastric type epithelium, where it lives within or beneath the gastric mucus layer.
  • 9. 1. H.pylori induced ulcer ● Also releases urease and protease Urease releases ammonia and CO2 which itself destroys the mucosal lining and causes neutralization of gastric Ammonia causes infection of mucosal lining and releases inflammatory Leucocyte adhesion and inflammatory reaction starts Damage of mucosal wall leading to ulcer Inflammatory mediators include IL-1,IL- 2,TNF
  • 10. 2. Drug induced ulcer ● NSAIDs can cause damage to the gastro duodenal mucosa via several mechanisms, including the topical irritant effect on the epithelium, impairment of the mucosa, suppression of gastric prostaglandin synthesis, reduction of gastric mucosal blood flow and interference with the repair of superficial injury ● Prostaglandins regulate blood flow and are responsible for inflammation. Drugs like NSAIDs (non selectively inhibit cox1 and cox2 in body Arachidonic acid cannot effectively produce prostaglandins Leads to ischemia and increase in HCL secretion leading to ulcer
  • 11. 3. ZES(Zollinger-Ellison Syndrome) Tumor of goblet cell occurs Abnormal increase in mucus secretion Increased secretion of gastric juice Mucosal lining damage
  • 12. ● “No gastric acid, no peptic ulcer” is a misconception. Excessive gastric acid secretion is only one factor in the pathogenesis of peptic ulcer disease. Decreased mucosal defense against gastric acid is another cause. The integrity of the upper gastrointestinal tract is dependent upon the balance between “hostile” factors such as gastric acid, H. pylori, NSAIDs and pepsin, and “protective” factors such as prostaglandins, mucus, bicarbonate, and blood flow to mucosa affecting gastrointestinal mucosa
  • 13. Diagnosis ● Laboratory tests for H. pylori. -The doctor may recommend tests to determine whether the bacterium H. pylori is present in our body. He or she may look for H. pylori using a blood, stool or breath test(Urea breath test). ● Endoscopy- Doctor may use a scope to examine the upper digestive system (endoscopy). During endoscopy, a hollow tube equipped with a lens (endoscope) is passed down the throat and into the esophagus, stomach and small intestine. Using the endoscope, ulcers are detected . ● Biopsy-If the doctor detects an ulcer, a small tissue sample (biopsy) may be removed for examination in a lab. A biopsy can also identify whether H. pylori is in our stomach lining or not. ● Barium swallow- You drink a thick white liquid (barium) that coats your upper gastrointestinal tract and helps your doctor see your stomach and small intestine on X-rays.
  • 14. Complications ● OBSTRUCTION-Development of fibrous scar at or near the pylorus results in pyloric stenosis. Healed duodenal ulcers cause duodenal stenosis. ● HAEMORRHAGE-Chronic blood loss may result in iron deficiency anemia. A penetrating chronic ulcer may erode a major artery (e.g. left gastric, gastro duodenal or splenic artery) and cause a massive and severe haematemesis and sometimes death. ● PERFORATION- A perforated peptic ulcer is an acute abdominal emergency. Perforation occurs more commonly in chronic duodenal ulcers than chronic gastric ulcers which leads to peritonitis and can involve liver or pancreas.
  • 15. Symptoms 1. Epigastric pain 2. Dyspepsia 3. Bloating, Distension and fatty food intolerance 4. Heartburn 5. Chest Discomfort 6. Haematemesis due to GIT bleeding 7. Loss of weight is a common finding in gastric ulcer patients.
  • 16. To reduce your risk of developing a peptic ulcer: ‱Avoid tobacco smoking ‱Avoid alcohol. ‱Use caution with aspirin and/or NSAIDs. ‱Don’t ignore your ulcer symptoms. ‱Protect yourself from infections by washing. hands regularly and consuming foods that have been cooked thoroughly. Precautions
  • 17. 1. If tests show that you have an H. pylori infection, your doctor will prescribe a combination of medication. The medications include antibiotics to help kill infections and proton pump inhibitors(PPIs). 2. Proton pump inhibitors are- o Reduce acid levels and allow ulcer to heal o Omeprazole o Lansoprazole 3. Antibiotics used are – Tetracycline, Amoxicillin and clarithromycin etc. 4. If one doesn’t have an H. pylori infection, they may be recommended a prescription or over-the-counter PPI (such as Prilosec or Prevacid) for up to eight weeks to reduce stomach acid and help the ulcer heal. Treatment
  • 18. 5. The doctor may also prescribe sucralfate (Carafate) which will coat one’s stomach and reduce symptoms of peptic ulcers. 6. Acid blockers like famotidine (Pepcid) can also reduce stomach acid and ulcer pain. 7. Surgery might be done if the complications increase.
  • 19. CREDITS: This presentation template was created by Slidesgo, including icons by Flaticon, infographics & images by Freepik Thanks

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