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    Peptic Ulcer Disease

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    Pradip Bk
    Peptic ulcer disease is defined as mucosal ulceration in the acid-bearing regions of the gastrointestinal tract, most commonly the stomach and duodenum. It is classified based on location and can be caused by H. pylori infection, NSAIDs, stress, smoking, and other factors. Clinical features include abdominal pain, nausea, vomiting, and bleeding. Treatment involves eradicating H. pylori with triple therapy antibiotics, reducing acid with PPIs or H2 blockers, and managing complications surgically if needed.

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    Peptic Ulcer Disease

    Uploaded by

    Pradip Bk
    17 views19 pages
    Peptic ulcer disease is defined as mucosal ulceration in the acid-bearing regions of the gastrointestinal tract, most commonly the stomach and duodenum. It is classified based on location and can be caused by H. pylori infection, NSAIDs, stress, smoking, and other factors. Clinical features include abdominal pain, nausea, vomiting, and bleeding. Treatment involves eradicating H. pylori with triple therapy antibiotics, reducing acid with PPIs or H2 blockers, and managing complications surgically if needed.

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    Peptic ulcer disease is defined as mucosal ulceration in the acid-bearing regions of the gastrointestinal tract, most commonly the stomach and duodenum. It is classified based on location and can be caused by H. pylori infection, NSAIDs, stress, smoking, and other factors. Clinical features include abdominal pain, nausea, vomiting, and bleeding. Treatment involves eradicating H. pylori with triple therapy antibiotics, reducing acid with PPIs or H2 blockers, and managing complications surgically if needed.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    17 views19 pages

    Peptic Ulcer Disease

    Uploaded by

    Pradip Bk
    Peptic ulcer disease is defined as mucosal ulceration in the acid-bearing regions of the gastrointestinal tract, most commonly the stomach and duodenum. It is classified based on location and can be caused by H. pylori infection, NSAIDs, stress, smoking, and other factors. Clinical features include abdominal pain, nausea, vomiting, and bleeding. Treatment involves eradicating H. pylori with triple therapy antibiotics, reducing acid with PPIs or H2 blockers, and managing complications surgically if needed.

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    Peptic ulcer disease

    Define Peptic ulcer disease PUD). Describe etiological classification,


    pathophysiology, clinical features, pharmacological treatment guidelines
    and non-pharmacological management of PUD.
    Defination

     The term peptic ulcer applies to mucosal ulceration near the acid bearing
    regions of the gastrointestinal tract. Most ulcers occur in the stomach or
    proximal duodenum but they may also occur in the esophagus (due to acid
    reflux), in jejunum and rarely in relation to ectopic gastric mucosa.
    Types of peptic ulcer

    Peptic ulcers classified based on region or location of illness-


    1. Stomach (called gastric ulcer)
    2. Duodenum (called duodenal ulcer)
    3. Esophagus (called Esophageal ulcer)
    4. Meckel's Diverticulum (called Meckel's Diverticulum ulcer)
    Etiology

    1. Helicobacter pylori
    2. NSAIDS
    3. Stress
    4. Ingestion of food like tea, coffee, beverages, spicy food
    5. Gender: more common in male
    6. Smoker
    7. Genetic factor: family history of peptic ulcer
    8. Age: Elderly
    9. Blood group type "O'
    Pathophysiology

    1. Life Style: Smoking, acidic drink, junk foods, high alcohol consumption →
    Increase the aggressive factors (pepsin, HCI)
    2. H. pylori infection: H. pylori bacteria commonly live in mucous layer that
    covers and protects the tissue. it can cause inflammation and produce ulcer.
    It can be spread by close contacts. It may cause increase in gastrin and
    pepsinogen levels.
    H. Pylori (Gram -ve Bac)→ produce heat shock proteins→ Cytokines, Histamines,
    certain enzymes Phospholipase, urease, protease in acidic media urease converts
    urea into Ammonia and CO2→ Ammonia can damage the mucosal lining → Ulcer
    Cont......

     Chronic Stress may worsen the ulcer


    Stress increase energy consumption (glycolysis)→that occurs due to Cortisol
    hormone→ inhibit the PLA2→ inhibit prostaglandin → increase acid secretion
    and inhibit mucous and bicarbonatesecretion ULCER
     Zollinger Ellison Syndrome (ZES)
    Tumor of goblet cell→ increase gastrin activity → Increase Acid secretion→
    ULCER
    *Other medications: SSRIs (Fluoxetine). Steroids, Antibiotics, etc
     NSAIDS:
    Aspirin and other NSAIDS cause gastric and duodeum damage through inhibition
    of cox1,which is important for the formation of protective prostaglandins
    Clinical features

    1. Abdominal pain
    2. Nausea and vomiting
    3. Malena (blood in stool)
    4. Water brash
    5. Acid reflux
    6. Anorexia
    7. Loss of weight
    8. Heart burn
    Diagnosis

    1. Radiological Diagnosis: Barium x-ray or upper GI series is a widely used for


    diagnosis. Barium x-ray is difficult to analysis and less sensitive and accurate.
    2. Laboratory test:
     Noninvasive urea breath test
     Patient with refractory or recurrent peptic ulcer may have underlying H.
    pylori infection, histopathology investigation may req.
     Serologic test for detecting H. pylori (levels of IgG and IgA ELISA test)
     Stool antigen test for non-invasive detecting the presence of H. pylori.
    3. Endoscopic diagnosis
    Complications

     Gastrointestinal Bleeding
     Stricture obstruction
     Perforation
     Gastric carcinoma
     Chronic Anaemia
    Treatment of Peptic Ulcer Disease

     AIM OF TREATMENT:
     Relieve symptoms
     Heal the ulcer
     Prevent complications-
     Prevent recurrences
    Non-pharmacological Treatment of
    Peptic ulcer
     Avoid spicy food
     Avoid Alcohol
     Avoid Smoking
     Avoid heavy meals
     Encourage small frequent low caloric meals
     Avoid ulcerating drugs e.g. NSAIDs, corticosteroids
    Pharmacological

     For non- H. pyroli ulcer


    1.Pharmacological:
     Drugs that inhibit gastric acid secretion
    (a) Proton-Pump Inhibitors (PPIs):
     Omeprazole-20mg OD
     esomeprazole- 20-40 mg OD
     lansoprazole-30 mg OD
     Pantoprazole-40mg OD
     Rabeprazole- 20 mg OD
    Cont...

    (b) H-receptor antagonists (Hy-blockers):


     Cimetidine-400mg bd or 800mg hs
     Ranitidine-150mg bd or 300mg hs
     Famotidine – 20mg bd or 40 mg hs,
     Nizatidine -150 mg bd or 300mg hs
    (c) Antimuscarinic agents (anticholinergic agents): Pirenzepine(50mg bd),
    telenzepine
    (d) Prostaglandin analogues: Misoprostol 200 mg qid
    Cont..

    2. Ulcer protectives:
     Sucralfate
     colloidal bismuth subcitrate (CBS)
    3. Drugs that neutralize gastric acid (antacids)
    (a) Nonsystemic antacids: Magnesium hydroxide, magnesium trisilicate, aluminium hydroxide,
    calcium carbonate.
    (b) (b) Systemic antacids: Sodium bicarbonate, sodium citrate.
    Eradication of H.pyroli

    Triple Therapy

     The BEST among all the Triple therapy regimen is


     Omeprazole/Lansoprazole - 20/30 mg bd
    +
     Clarithromycin- 500 mg bd
    +
     Amoxycillin /Metronidazole-1gm/500 mg bd
     Given for 14 days followed by P.P.I for 4-6 weeks
     Short regimens for 7 days
    Triple Therapy-cont

     Some other Triple Therapy Regimens are


    a) Bismuth subsalicylate - 2 tab qid
    Metronidazole250 mg qid
    Tetracycline- 500 mg qid
    Duration: For 7-14 days
    b) Bismuth subsalicylate - 2 tab qid
    Metronidazole250 mg qid
    Amoxycilin- 500 mg qid
    Duration: For 7-14 days
    Quadruple Therapy
     Given when Triple Therapy fails
     Omeprazole/Lansoprazole20/30 mg bd
     Bismuth subsalycilate 2 tabs qid
     Metronidazole250 mg qid
     Tetracycline 500 mg qid
     Duration: Given for 7 days
    Surgery

     Surgery is done for people who do not respond to medication, or who develop
    complications:

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