1. PEPTIC ULCER DISEASE
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2. DEFINITION AND DESCRIPTION
Peptic ulcers are produced by an imbalance between the gastro-duodenal mucosal defense mechanisms and damaging forces of gastric acid and pepsin, combined with superimposed injury from environmental or immunologic agents.
It is a focal or circumscribed defect in the mucosa extending into the submucosa or deeper ,due to acid or pepsin digestion
The mucous membrane lining the digestive tract erodes and causes a gradual breakdown of tissue.  This breakdown causes a gnawing or burning pain in the upper middle part of the belly (abdomen).
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3. EPIDEMIOLOGY
As many as 80% of ulcers are associated with Helicobacter pylori, a spiral-shaped bacterium that lives in the acidic environment of the stomach.
Ulcers can also be caused or worsened by drugs such as aspirin and other NSAIDs.
Although H. pylori infection is usually contracted in childhood, perhaps through food, water, or close contact with an infected individual. usually doesn't cause problems in childhood, if left untreated it can cause gastritis (the irritation and inflammation of the lining of the stomach), peptic ulcer disease, and even stomach cancer later in life.
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4. EPIDEMIOLOGY
Contrary to general belief, more peptic ulcers arise in the duodenum (first part of the small intestine, just after the stomach) than in the stomach.
Duodenal ulcers usually first occur between the ages of years and are twice as common in men as in women.
 Stomach (or gastric) ulcers usually occur in people older than 60 years and are more common in women.
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5. EPIDEMIOLOGY It is one of the most prevalent GI diseases
Commoner in males
Peak age of occurrence for DU is 35years.
Gastric ulcers usually occurs in the older age group (45-65 years)
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6. LOCATIONS
It can occur in any of these locations- lower esophagus, stomach, duodenum, jejunum, meckel’s diverticulum
Mostly occur at/or near mucosa junctions e.g-oesophago-gastric, antra-pyloric;pyloro-duodenal ,gastrojejunostomy sites.
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7. RELEVANT ANATOMY
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8. PATHOGENESIS
Peptic ulcer usually occurs as a result of imbalance between noxious agents and the gastro duodenal defence barrier
These mechanisms prevent and repair injury to the mucosa.It includes the following
Mucus bicarbonate layer-bicarbonate and mucous are produced by surface epithelium of the stomach and duodenum
It neutralizes diffusing H+ ions.
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9. PATHOGENESIS AGGRESSIVE FACTORS. DEFENSIVE FACTORS -Acid
-Pepsin
-Helicobacter pylori
-NSAIDS
DEFENSIVE FACTORS
Prostaglandins
Mucosal blood flow
Mucous gel layer
HCO3
Epithelial junctions
Regeneration of the epithelial layer
Epidermal growth factor
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10. CLASSIFICATION Stomach (called gastric ulcer)
Duodenum (called duodenal ulcer)
Oesophagus (called Oesophageal ulcer)
Types of peptic ulcers:
Type I: Ulcer along the lesser curve of stomach
Type II: Two ulcers present - one gastric, one duodenal
Type III: Prepyloric ulcer
Type IV: Proximal gastroesophageal ulcer
Type V: Anywhere
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11. ETIOLOGICAL FACTORS H. Pylori Infection NSAIDs Smoking & Alcohol
Acid Hypersecretion
Stress
Family History of PUD.

12. ETIOLOGICAL FACTORS 1.HELICOBACTER PYLORI
Most important trigger for development of PUD
Associated with 90% of DU and 75% of GU
Mechanisms of ulcerogenesis includes
Production of toxic products causing local injury-cytotoxins, phospholipase, mucinase, urease, oxidase, catalase
Colonization of the antrum with reduced somatostatin D cells normally produced in the antrum, leading to stimulation of gastrin and acid production
Ammonia from urease activity creates an alkaline environment which has a feedback effect for increased gastrin production
H/pylori induced inflammatory reaction with cellular infiltration and consequent epithelial damage.

13. The bacterium persists in the stomach for decades in most people
The bacterium persists in the stomach for decades in most people. Most individuals infected by H. pylori will never experience clinical symptoms despite having chronic gastritis. Approximately 10-20% of those colonized by H. pylori will ultimately develop gastric and duodenal ulcers. H. pylori infection is also associated with a 1-2% lifetime risk of stomach cancer and a less than 1% risk of gastric MALT lymphoma
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15. ETIOLOGICAL FACTORS 2.NSAIDS
It is the next most important factor in ulcer pathogenesis after H/pylori
Mechanisms of ulcerogenesis include
Inhibition of mucosa prostaglandin synthesis by suppressing COX-1 activity
NSAIDs are weak acids that are able to migrate into surface epithelial cells
NSAIDs decrease the hydrophobicity of gastric mucus which normally repels acid
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16. ETIOLOGY FACTORS This may result from the following www.medrockets.com
3. Increased gastric acid secretion
This may result from the following
Increased vagal stimulation from worry, anxiety, stress, alcohol
Increased parietal cell mass-this may be genetic or acquired (e.g gastrinoma)
Hypercalcemia-stimulates increased gastrin secretion
4.Alcohol
stimulates increased acid production
Leaches out glycolipid under the mucus coat
5.Smoking
increases gastric acid production
decreases gastroduodenal PGH and HCO3 production
increases duodenogastric reflux
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17. ETIOLOGICAL FACTORS 6.Ischemia 7.Enterogastric bile reflux
Reduces the mucosa defence barrier
7.Enterogastric bile reflux
This occurs if the pyloric sphincter is incompetent or following a gastrojejunostomy
Bile acids and pancreatic secretions stimulate gastrin release with increased acid output as well as repair the mocosa barrier allowing acid back diffusion
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18. PATHOLOGY Duodenal ulcer Most involve the first part of the duodenum
May be anterior, posterior, antero-posterior(kissing ulcer), anterosuperior, posterosuperior
Anterior ulcers tend to perforate while posterior ulcers tend to penetrate sometimes into large vessels like the GD artery causing UGI bleeding
Chronic ulcers may heal with fibrosis with extensive cicatrisation leading to gastric outlet obstruction.
They are not usually associated with malignancy
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19. PATHOLOGY Gastric ulcer
Most are found in the lesser curvature especially at the incisura angularis
Tend to be larger than DU
May also be complicated by perforation or penetration
Unlike DU,they tend to be more associated with malignancy,which must be excluded in all cases.
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20. You’re at risk for peptic ulcer disease if you:
Are 50 years old or older.
Diabetes may increase your risk of having H. pylori
Drink alcohol excessively
Smoke cigarettes or use tobacco.
Have a family history of ulcer disease.
You’re at risk for NSAID-induced ulcers if you:
Are age 60 or older (your stomach lining becomes more fragile with age).
Have had past experiences with ulcers and internal bleeding
Take steroid medications, such as prednisone.
Take blood thinners, such as warfarin.
Consume alcohol or use tobacco on a regular basis.
Experience certain side effects after taking NSAIDs, such as upset stomach and heartburn.
Take NSAIDs in amounts higher than recommended
Take NSAIDs for long periods of time
Stress does not cause an ulcer, but may be a contributing factor
Chronic disorders such as liver disease, emphysema, rheumatoid arthritis may increase vulnerability to ulcers
Improper diet, irregular or skipped meals
Type O blood (for duodenal ulcers)
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21. Clinical presentation
Symptoms
Burning abdominal pain
Haematemesis
Melena
Nausea or vomiting
Unexplained weight loss
Anorexia
Abdominal fullness
Symptoms of H. pylori
Abdominal pain
Feeling of Fullness
Indigestion
Feeling very hungry 1 to 3 hours after eating
Mild nausea
Pain Starts 2/3 hours after meals, or in the middle of the night
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22. Pain(most common presentation-90% of cases)
Usually a gnawing or burning pain in the epigastrum,intermittent and may radiate to the back.
Pain may be aggravated by meals as in GU,or aggravated by hunger and relieved by meals or antacids(DU)
Diurnal variation(DU)
Vomiting
More common in cases of gastric outlet obstruction but may occur even in acute PUD exercebation

23. Gastric versus duodenal ulcer — Although there is much overlap, symptoms of a gastric ulcer may be different than those of a duodenal ulcer.
Duodenal ulcer — "Classic" symptoms of a duodenal ulcer include burning, gnawing, aching, or hunger-like pain, primarily in the upper middle region of the abdomen below the breastbone (the epigastric region). Pain may occur or worsen when the stomach is empty, usually two to five hours after a meal. Symptoms may occur at night between 11 PM and 2 AM, when acid secretion tends to be greatest.
Feel better when you eat or drink and then worse 1 or 2 hours later (duodenal ulcer).
Gastric ulcer — Symptoms of a gastric ulcer typically include pain soon after eating. Symptoms are sometimes not relieved by eating or taking antacids.
Feel worse when you eat or drink (gastric ulcer)

24. Gastric ulcer Duodenal Ulcer middle age 50-60 Any age specially 30-40
More in male
Sex
Same
Stress job eg. Manager
Occupation
Epigastric. Can radiate to back
Epigastric , discomfort
Pain
Immediately after eating
2-3 hours after eating & midnight
Onset
Eating
Hunger
Agg.by
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25. Gastric ulcer Duodenal Ulcer Lying down or vomiting Eating Relived by
Few weeks
1-2 months
Duration
Common(to relieve the pain)
Uncommon
Vomiting
Patient is afraid to eat
Good
Appetite
Avoid fried food
Good , eat to relieve the pain
Diet
wt. Loss because patient is afraid to eat.
No wt. loss because patient eats to avoid pain.
Weight
60%
40%
Hematemesis
Melena
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26. Differential diagnosis
Reflux oesophagitis
Cholelithiasis
Pancreatitis
Gastric cancer
Ca transverse colon
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27. INVESTIGATIONS Upper GIT endoscopy Barium meal
In all patients with “Alarming symptoms” endoscopy is required.
Dysphagia.
Weight loss.
Vomiting.
Anorexia.
Hematemesis or Melena.

28. Test for diagnosing H.pylori
Urea breath test :by measuring the amount of co2 in exhaled breath.
Blood test: by identifying H.pylori antibodies by ELISA test.
Stool test :stool sample tested with H.pylori antigen and occult blood
Rapid urea test
Culture
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29. TREATMENT GOALS OF TREATMENT neutralizing the acid
lowering the amount of acid that stomach makes,
neutralizing the acid
protecting the injured area so it can heal
It's also very important to stop smoking and drinking alcohol
Prevent complications (bleeding, perforation, penetration, obstruction)
Minimize recurrences
Reduce financial costs
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30. Treatment
Medical management is the main stay of treatment of uncomplicated peptic ulcer disease.
Life style modification
Neutralization of the acid: antacids e.g magnesium trisilicate, Alumilium hydroxide
Reduction of acid secretion-H2 receptor blockers(cimetidine, ranitidine), proton pump inhibitors(omeprazole, rabeprazole)
H/pylori eradication therapy is currently the main stay of treatment
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31. Life-style modification in PUD
Stop smoking
Limit alcohol intake
Avoid spicy foods
Avoid caffeine containing foods
Good rest and sleep
Exercise
Eat fruits often
Avoid NSAIDS
USE OLIVE OIL
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32. REDUCTION OF GASTRIC ACID SECRETION
Histamine antagonist: Cimetidine, ranitidine
Proton pump inhibitors: omeprazole, pantaprazole
Acetyl choline antagonist: pirenzepine, propantheline
Prostaglandin analogue: misoprostol
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33. Nonsystemic : Magnesium hydroxide , Aluminium hydroxides
Neutralization of gastric acid(antacids) Systemic : Sodium bicarbonate, Sodium citrate
Nonsystemic : Magnesium hydroxide , Aluminium hydroxides
Ulcer protectives : Sucralfate
Anti helicobacter pylori: amoxicillin, clarithromycin etc
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34. Histamine antagonist Cimetidine
.Histamine antagonists inhibit the action of histamine on the acid-producing cells of the stomach and reduce stomach acid
SIDE EFFECTS; it include constipation, diarrhea, fatigue, headache, insomnia, muscle pain, and vomiting. Major side effects include confusion and hallucinations, gynacomastia (enlargement of the breasts); impotence.
USES: it is used in treatment of duodenal ulcer,
Gastric ulcer, stress ulcer, GERD, zollinger ellison syndrome
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35. PROTON PUMP INHIBITORS
Proton pump inhibitors act by irreversibly blocking the hydrogen/potassium adenosine triphosphatase enzyme system of the gastric parietal cells.
The proton pump is the terminal stage in gastric acid secretion
SIDE EFFECTS Stomach pain, Diarrhea,Constipation,Dizziness,Pain,Hives, Itching,seizures
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36. ACETYL CHOLINE ANTAGONIST
PIRENZEPINE
MECHANISM:
It selectively block M1 muscaranic recptors and inhibits gastric secretion.
Because of their relatively poor efficacy, side effects, and risk of blood disorders, they are rarely used today
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37. AGENTS THAT ENHANCE MUCOSAL DEFENSE
Prostaglandin Analogues:
prostaglandins are produced in the gastric
mucosa and appear to serve a protective role by inhibiting acid secretion and promoting mucus
and bicarbonate secretion.
In addition, PGs inhibits gastrin production, increase mucosal blood flow and probably have an ill defined cytoprotective action.
DRUGS: Misoprostol
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38. ULCER PROTECTIVES SUCRALFATE MECHANISM:
Sucralfate is a locally acting substance that in an acidic environment (pH < 4), reacts with hydrochloric acid in the stomach to form a cross-linking, viscous, paste-like material capable of acting as an acid buffer for as long as 6 to 8 hours after a single dose. It also attaches to proteins on the surface of ulcers, such as albumin and fibrinogen, to form stable insoluble complexes. These complexes serve as protective barriers at the ulcer surface, preventing further damage from acid, pepsin, and bile.
USES: It is used in treatment of Gastritis, Stress ulcers
Side effects
The most common side effects seen are constipation. Less commonly reported include flatulence, cephalalgia (headache), xerostomia (dry mouth).
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39. Sodium bicarbonate (antacid)
It is water soluble, acts instantaneously, but duration of action is short. It is a potent neutralizer, pH may raises above 7.
Adverse reactions
It causes systemic alkalosis, gastric distention, rebound acidity and milk-alkali syndrome
Uses
It is restricted to casual treatment of heartburn and to treat acidosis

40. ANTI H.PYLORI DRUGS
Anti microbials that have been found clinically effective against H.pylori are: amoxicillin, clarithromycin, tetracycline and metronidazole.
A combination regimen is preferred, using gastric acid inhibitors and antibiotics. TRIPLE THERAPY
Example:
A proton pump inhibitor or H2 blocker + amoxicillin + clarithromycin or metronidazole
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41. Surgical Treatment
The role of surgery has reduced significantly since the advent of H/pylori eradication therapy
Indicated only in intractable cases and in the management of complications.
Acid reducing procedures include
Truncal vagotomy+drainage
Selective vagotomy+drainage(preservation of the coeliac and hepatic branches)
Highly selective vagotomy-preservation of the nerve of latarjet(no need for drainage)
Vagotomy+antrectomy
Bilroth 1 Partial gastrectomy
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42. Complications Upper gastrointestinal bleeding
Perforation leading to peritonitis
Penetration
Gastric outlet obstruction
Malignization
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43. Thank you
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