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Peptic ulcer

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Peptic ulcer Presentation Transcript

  • 1. PEPTIC ULCER SARA SADAF
  • 2. CONTENTS
    • DEFINITION AND DESCRIPTION
    • CLASSIFICATION
    • HISTORY CHART
    • SYMPTOMS
    • CAUSES
    • RISK FACTORS
    • COMPLICATIONS
    • TESTS AND DIAGNOSIS CHART
    • TREATMENT
    • LIFE STYLE AND HOME REMEDIES
    • STUDIES & RECENT RESEARCHES
  • 3.
    • 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.
    • 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).
  • 4.
    • 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.
  • 5.
    • 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 30-50 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.
  • 6.  
  • 7. 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
  • 8. HISTORY CHART
  • 9. Launched a national education campaign to inform health care providers and consumers about the link between H. pylori and ulcers. Centers for Disease Control and Prevention 1997 The Food and Drug Administration approves the first antibiotic for treatment of ulcer disease 1996 National Institutes of Health convened a Consensus Panel that issued guidelines for management of ulcer cancer, taking H. pylori into account 1994 First study showing that eradication of the organism reduces duodenal ulcer recurrence 1987 Helicobacter pylori was rediscovered as a causative factor for ulcers Barry Marshall & Robin Warren (Two Australian scientists) 1982 Treatment of patients for peptic ulcer disease with antibiotics Lykoudis (general practitioner in Greece) 1958 First discovery of human gastric bacteria 1900s WORK NAME OF SCIENTISTS YEAR
  • 10. SYMPTOMS
  • 11. 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)
  • 12. SYMPTOMS Burning pain bloating Nausea water brash Unexplained weight loss hematemesis (vomiting of blood) Appetite changes   Melina vomiting Blood in the stools low blood cell count (anemia) Stomach pain wakes you up at night frequent burping or hiccupping An early sense of fullness with eating
  • 13. CAUSES
  • 14. stretch receptors Medulla oblongata endocrine cells gastrin Circulatory system stomach secretes gastric juice
  • 15.  
  • 16.
    • Helicobacter pylori, a bacteria that is frequently found in the stomach
    • Nonsteroidal anti-inflammatory drugs (NSAIDS) such as ibuprofen
    •   In addition, smoking and certain other genetic and environmental factors (such as medications) may influence the course of peptic ulcer disease.
    • Psychological stress and dietary factors were once thought to be the cause of ulcers, although these factors are no longer thought have a major role.
  • 17. Helicobacter pylori infection
  • 18. Helicobacter pylori infection  
    • H. pylori is a helix-shaped
    • Gram-negative, slow-growing organism
    • about 3 micrometres long with a diameter of about 0.5 micrometres
    • has 4–6 flagella
    • Helicobacter pylori is composed of a single circular chromosome with 1,667,867 base pairs, containing about 1590 coding regions
    • It is microaerophilic; that is, it requires oxygen, but at lower concentration than is found in the atmosphere
    • It contains a hydrogenase which can be used to obtain energy by oxidizing molecular hydrogen (H2) that is produced by intestinal bacteria
  • 19.
    • It produces oxidase , catalase , and urease
    • It is capable of forming biofilms and can convert from spiral to a possibly viable but nonculturable coccoid form, both likely to favor its survival and be factors in the epidemiology of the bacterium.
  • 20. + WATER Hydroxyl ions + Bicarbonate AMMONIUM ION AMMONIA CARBONDIOXIDE UREASE UREA
  • 21. Molecular model of H. pylori urease enzyme
  • 22.
    • 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
  • 23.
    • Regular use of pain relievers. Nonsteroidal anti-inflammatory drugs (NSAIDs) can irritate the lining of stomach and small intestine. These medications, which are available both by prescription and over-the-counter, include aspirin, ibuprofen (Advil, Motrin, others), naproxen (Aleve), ketoprofen and others. Other prescription medications that can also lead to ulcers include medications used to treat osteoporosis called bisphosphonates (Actonel, Fosamax and others).
    • NSAIDs inhibit production of an enzyme ( cyclooxygenase ) that produces prostaglandins . These hormone-like substances help protect stomach lining from chemical and physical injury. Without this protection, stomach acid can erode the lining, causing bleeding and ulcers.
  • 24.
    • Effects of smoking on PUD
      • Increased rate of gastric emptying
      • Diminished pancreatic bicarbonate secretion
      • Decreased duodenal pH
      • Reduced mucosal blood flow
      • Inhibition of mucosal prostaglandins
  • 25. NICOTINE parasympathetic nerve activity in gastrointestinal tract increase stimulation to the enterochromaffin-like cells and G cells increases the amount of histamine and gastrin secreted
  • 26.
    • Gastrinomas (Zollinger Ellison syndrome), rare gastrin-secreting tumors, also cause multiple and difficult to heal ulcers.
    • Excessive alcohol consumption Alcohol can irritate and erode the mucous lining of stomach and increases the amount of stomach acid that's produced. It's uncertain, however, whether this alone can progress into an ulcer or if it just aggravates the symptoms of an existing ulcer.
  • 27.
    • Caffeine
    • Beverages and foods that contain caffeine can stimulate acid secretion in the stomach. This can aggravate an existing ulcer, but the stimulation of stomach acid can't be attributed solely to caffeine.
  • 28. Role of Stress
    • A study of peptic ulcer patients in a Thai hospital showed that chronic stress was strongly associated with an increased risk of peptic ulcer, and a combination of chronic stress and irregular mealtimes was a significant risk factoR.
    • An expert panel convened by the Academy of Behavioral Medicine Research concluded that ulcers are not purely an infectious disease and that psychological factors do play a significant role. Researchers are examining how stress might promote H. pylori infection.
    • For example, Helicobacter pylori thrives in an acidic environment, and stress has been demonstrated to cause the production of excess stomach acid. This was supported by a study on mice showing that both long-term water-immersion-restraint stress and H. pylori infection were independently associated with the development of peptic ulcers.
    • Physical stress, is different. It can increase the risk of developing ulcers, especially in the stomach. Examples of physical stress that can lead to ulcers are that suffered by people with injuries such as severe burns, and people undergoing major surgery.
  • 29.
    • The incidence of duodenal ulcers has dropped significantly during the last 30 years, while the incidence of gastric ulcers has shown a small increase, mainly caused by the widespread use of NSAIDs. The drop in incidence is considered to be a cohort-phenomena independent of the progress in treatment of the disease. The cohort-phenomena is probably explained by improved standards of living which has lowered the incidence of H. pylori infections.
  • 30.
    • Risk Factors for Ulcers
  • 31.
    • 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)
  • 32. COMPLICATIONS
  • 33.
    • Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life-threatening. It occurs when the ulcer erodes one of the blood vessels. Bleeding can occur as slow blood loss that leads to anemia or as severe blood loss that may require hospitalization or a blood transfusion.
    • Perforation (a hole in the wall) often leads to catastrophic consequences. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into the abdominal cavity. Perforation at the anterior surface of the stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intense abdominal pain. Posterior wall perforation leads to pancreatitis; pain in this situation often radiates to the back.
  • 34.  
  • 35.
    • Penetration is when the ulcer continues into adjacent organs such as the liver and pancreas
    • Scar tissue Scarring and swelling due to ulcers causes narrowing in the duodenum and gastric outlet obstruction . Patient often presents with severe vomiting. Peptic ulcers can also produce scar tissue that can obstruct passage of food through the digestive tract, causing you to become full easily, to vomit and to lose weight.
  • 36. WARNING SIGNS blood in your stools losing weight pain doesn't go away With medication vomit blood sudden, severe pain vomit food eaten hours or days before ongoing nausea or repeated vomiting. feel cold or clammy feel unusually weak or dizzy
  • 37.
    • TESTS AND DIAGNOSIS CHART
  • 38. Noninvasive Urea Breath Test (UBT) Blood test Invasive Biopsy Urease Test Histology
  • 39. Culture Stool antigen test Upper gastrointestinal (upper GI) X-ray Other tests Endoscopy
  • 40. TREATMENT
  • 41.
    • GOALS OF TREATMENT
    • 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
  • 42. Antibiotic medications. Doctors use combinations of antibiotics to treat H. pylori because one antibiotic alone isn't always sufficient to kill the organism. Antibiotics prescribed for treatment of H. pylori include amoxicillin (Amoxil), clarithromycin (Biaxin) and metronidazole (Flagyl). Combination drugs that include two antibiotics together with an acid suppressor or cytoprotective agent (Helidac, Prevpac) have been designed specifically for the treatment of H. pylori infection. Acid blockers. Acid blockers — also called histamine (H-2) blockers — reduce the amount of hydrochloric acid released into digestive tract, which relieves ulcer pain and encourages healing. Acid blockers work by keeping histamine from reaching histamine receptors. Histamine is a substance normally present in body. When it reacts with histamine receptors, the receptors signal acid-secreting cells in stomach to release hydrochloric acid. Available by prescription or over-the-counter (OTC), acid blockers include the medications ranitidine (Zantac), famotidine (Pepcid), cimetidine (Tagamet) and nizatidine (Axid). Antacids. An antacid may be taken in addition to an acid blocker or in place of one. Instead of reducing acid secretion, antacids neutralize existing stomach acid and can provide rapid pain relief.
  • 43.
    • Proton pump inhibitors. Another way to reduce stomach acid is to shut down the "pumps" within acid-secreting cells. Proton pump inhibitors reduce acid by blocking the action of these tiny pumps. These drugs include the prescription and over-the-counter medications omeprazole (Prilosec), lansoprazole (Prevacid), rabeprazole (Aciphex) and esomeprazole (Nexium). Doctors frequently prescribe proton pump inhibitors to promote the healing of peptic ulcers. Proton pump inhibitors also appear to inhibit H. pylori.
    • Cytoprotective agents. In some cases, your doctor may prescribe these medications that help protect the tissues that line your stomach and small intestine. They include the prescription medications sucralfate (Carafate) and misoprostol (Cytotec). Another nonprescription cytoprotective agent is bismuth subsalicylate (Pepto-Bismol).
    • Bowel rest : Bed rest and clear fluids with no food at all for a few days. This gives the ulcer a chance to start healing without being irritated. 
    • Nasogastric tube : Placement of a thin, flexible tube through your nose and down into your stomach. This also relieves pressure on the stomach and helps it heal. 
    • Urgent endoscopy or surgery if indicated: Damaged, bleeding blood vessels can usually be repaired with an endoscope. The endoscope has a small heating device on the end that is used to cauterize a small wound.
  • 44.  
  • 45.  
  • 46.  
  • 47. Surgery Vagotomy Antrectomy Pyloroplasty Tying off an  artery Acupuncture Chiropractic Homeopathy Herbs Other modes Of treatment
  • 48. LIFE STYLE AND HOME REMEDIES
  • 49. Don't smoke Limit or avoid alcohol Avoid nonsteroidal anti-inflammatory drugs (NSAIDs) Fruits and Vegetables Less Coffee and Carbonated Beverages Use of Olive Oil Exercise Stress Relief
  • 50. STUDIES & RECENT RESEARCHES
  • 51.
    • . A 2009 Japanese study in Cancer Prevention Research found that eating as little as 70 g (2.5 ounces) of broccoli sprouts daily for two months reduces the number of colonies of H. pylori bacteria in the stomach by 40% in mice and humans. This treatment also seems to help by enhancing the protection of the gastric mucosa against H. pylori , but is relatively ineffective on related gastric cancers. The previous infection returned within two months after broccoli sprouts were removed from the diet, so an ongoing inclusion in the diet is best for continued protection from H. pylori.
    • A 2009 study has found that green tea can prevent inflammation if ingested prior to exposure to Helicobacter infection.
  • 52. Nexium(R) Reduces Peptic Ulcer Incidence in Patients Taking Low Dose Aspirin LOS ANGELES, California, May 23,2008 Results from a new large-scale study, presented at Digestive Disease Week (DDW) , show that taking Nexium(R) (esomeprazole) in addition to low dose aspirin therapy significantly reduces the incidence of gastric and duodenal ulcers in patients at risk. Treatment with Nexium(R) resulted in a 70 per cent reduction in ulcer development Peptic ulcer bacterium alters the body's defense system June 29, 2009 The study shows that a type of cells in the immune system called regulatory T cells down-regulate the body's defence against Helicobacter pylori and thereby enable the bacterium to develop a chronic infection. 'If we could control the regulatory T cells, we could strengthen the immune system and help the body eliminate the bacterium.
  • 53. The Peptidergic Brain-Gut Axis: Influence on Gastric Ulcer Formation  Center for Ulcer Research and Education, West Los Angeles,2006 The existence of a relationship between the brain and the formation of gastric ulcers has been suspected since the last century. The advancement of stereotaxic procedures and the use of electrical lesion or stimulation have allowed localization within the limbic system, hypothalamus and brain stem, of discrete nuclei that influence the formation of gastric ulceration in experimental animals. Recently, further progress in the understanding of how the brain may influence gastric pathogenesis has been made by the demonstration that specific peptides act in the central nervous system to induce or prevent the formation of gastric ulcers and to markedly alter gastric secretary and motor function. Peptides established to have a centrally mediated protective effect are bombesin, calcitonin, corticotropin-releasing factor, neurotensin and opioid peptides .
  • 54. Immunohistochemical study of dopamine in rat gastric June 1993      Recent studies have shown the presence of dopamine (DA) in gastric and duodenal mucosa, and changes in gastric mucosal DA content have been observed in patient with acute ulcers. Immunohistochemical demonstration of the distribution of DA in gastric mucosa under stress was studied by light and electron microscopy. In the control group, DA was present in the gastric gland proper in the gastric corpus and antrum on light microscopy, and on the surface of mucous granules in chief cells, mucous neck cells, and surface epithelium on electron microscopy. In the stress group, DA in gastric mucosa was almost undetectable on light and electron microscopy. Further, in this group serum DA concentration was significantly higher in the portal vein than in the abdominal aorta. Endogenous DA in gastric mucosal cells may affect gastric mucosa differently from exogenous DA, and stress may release endogenous intracellular DA into extracellular spaces.
  • 55. HM Ashraf, *Shahzad Ashraf, *Farrukh Saeed, *Mazhar Mehtab, **Saba Asad
    • To evaluate the efficacy of H pylori eradication in patients with nonulcer dyspepsia, an interventional study was carried out in the Dept of Gastroenterology, MH Rawalpindi from Jan to Feb 2004. Five hundred consecutive patients, who were referred for UGI Endoscopy, were studied. Out of these 500 patients, gastric biopsy was done in 245 patients. The patients in whom gastric biopsy was done, histopathology revealed gastritis in 187 patients and 129 (69%) were found H pylori positive. The subgroup of patients who were H pylori positive was further studied. These patients were given one week’s course of eradication therapy and subsequently followed up. Sixty three percent (n=81) responded to treatment and reported improvement in their symptoms; whereas in thirty seven percent (n=48) of patients the dyspeptic symptoms persisted. In our set up where H pylori infection is pandemic, in the absence of alarm symptoms; all patients with nonulcer dyspepsia below 45 years of age should be considered for H pylori eradication.
  • 56. SHUKRIA THE END