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PEPTIC ULCER DISEASE- A BRIEF INSIGHT

This presentation provides a detailed view of peptic ulcer disease, including its definition, epidemiology, etiology, pathophysiology, clinical presentation, diagnosis, and management. Happy reading!

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PEPTIC ULCER DISEASE- A BRIEF INSIGHT

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  1. PEPTIC ULCER DISEASE- A BRIEF INSIGHT BY: VISHNU.R.NAIR, 4TH YEAR PHARM.D, NATIONAL COLLEGE OF PHARMACY, KERALA UNIVERSITY OF HEALTH SCIENCES, KERALA STATE.

  2. WELCOME TO A DETAILED VIEW ON PEPTIC ULCER DISEASE!!! HAPPY READING!!   

  3. INDEX/ CONTENTS OF THIS PPT : • GENERAL ACKNOWLEDGEMENT • DEFINTION OF PUD • EPIDEMIOLOGY OF PUD • ETIOLOGY/ CAUSES OF PUD • PATHOPHYSIOLOGY OF PUD • CLINICAL PRESENTATION OF PUD • DIAGNOSIS OF PUD • MANAGEMENT OF PUD

  4.  GENERAL ACKNOWLEDGEMENT : DEDICATED TO THE ALMIGHTY, MY PARENTS, RELATIVES,TEACHERS, FRIENDS, WELL-WISHERS, PEERS, LOVED ONES, AND TO ALL MY READERS…………… THANKS FOR READING………………. I AM PRIVILEDGED AND FORTUNATE TO WORK ON A SELFLESS NOTE FOR THE RELEASE OF THIS PPT……… LOVE YA ALL!! @RXVICHU-ALWZ4UH!

  5.  DEFINITION OF PUD  : • “DISEASE, in which there is DISCONTINUITY in the entire thickness of GASTRIC/ DUODENAL MUCOSA, that persists, as a result of ACID& PEPSIN in GASTRIC JUICE”………………….

  6.  TYPES OF PUD  : • ACUTE PUD : • Caused by STRESS ULCERS (Physiological/ psychological) 2. CHRONIC PUD : - Classified into GASTRIC and DUODENAL ulcers………….

  7.  EPIDEMIOLOGY  : • Around 4.5 million people in US are affected annually • Hospitalization rate for PUD is 30 patients per 1,00,000 cases • Of those infected with H. pylori , lifetime prevalence is approximately 20% • Increasing rates in older women is observed • Although the rate of simple gastric ulcer has reduced, the incidence of COMPLICATED GASTRIC ULCER and HOSPITALIZATION has remained stable, partly due to CONCOMITANT USE OF ASPIRIN in ageing populations……………………

  8.  ETIOLOGY OF PUD  : • HELICOBACTER PYLORI INFECTION • DRUGS: • NSAIDs • (NSAIDs + anticoagulant) combination • Oral steroids • Chemotherapeutic agents (5-Fluorouracil, Methotrexate, Cyclophosphamide) 3. ALCOHOL CONSUMPTION

  9. CONTINUED……………………………………… 4. SEVERE PHYSIOLOGIC STRESS : Observed in conditions, like: • Burns b. CNS trauma c. Surgery d. Sepsis e. Cushing ulcers (associated with increased gastric output in the stomach/ duodenum) f. Multiple traumatic injuries 5. HYPERSECRETORY STATES: Observed in conditions, like: • Gastrinoma (Zollinger- Ellison Syndrome) b. Cystic fibrosis c. Multiple Endocrine Neoplasia Type-I (MEN-I)

  10. CONTINUED…………………………………… d. Antral ‘G’ cell hyperplasia e. Hyperparathyroidism f. Basophilic leukemias g. Short Bowel Syndrome 6. GENETICS : • People, who do not secrete ABO ANTIGENS in their SALIVA/ GASTRIC JUICES  are at higher risk of getting the disease • FAMILIAL HYPERPEPSINOGENEMIA TYPE I (Rare genetic phenotype, associated with increased pepsin secretion) 7. RADIATION THERAPY : - Radiation  causes mucosal damage  causes duodenal ulcers  PUD occurs

  11. CONTINUED……………………………………… 8. SECONDARY DISEASE CONDITIONS: Includes: • Hepatic cirrhosis b. COPD c. Henoch- Schonlein gastritisd. Autoimmunity e. Crohn’s disease f. Graft vs host disease g. Emphysematous gastritis h. Gastropathy (Bile, uremic) 9. OTHER INFECTIONS: Includes: • CMV b. HSV c. HIV d. Helicobacter heilmannii e. EBV f. C.albicans g. Histoplasma

  12. CONTINUED………………………………….. 10. DRUG ABUSE: • Crack cocaine  causes localized vasoconstriction  decreases blood flow  leads to mucosal damage 11. OTHER REASONS: Include: • Stress e. Previous history of PUD • Depression f. Anemia……………………………. • Smoking • Social deprivation

  13.  PATHOPHYSIOLOGY OF PUD  : • NORMAL GASTRIC PHYSIOLOGY: Gastric physiology is controlled by 2 factors: • AGGRESSIVE/ PROGRESSIVE FACTORS: • Neuronal impulses, initiated by sight, smell, taste  causes release of ACETYLCHOLINE  ACh stimulates ANTRAL G CELLS to secrete GASTRIN  Proton pump (K+ H+- ATPase enzyme system) is activated  release of H+ ions • PEPSINOGEN is also released along with ACh, which in the presence of HCl , secretes PEPSIN 2. DEFENSIVE FACTORS: • Include PROSTAGLANDIN(E) and SOMATOSTATIN • Located on parietal cells

  14. CONTINUED………………………………………. • Maintain mucosal blood flow • Stimulate production of MUCUS and BICARBONATES • Reduce gastric acid secretion • MUCUS: ‘Viscous gel, that protects against the corrosive effect of acid’ • Mucosal blood flows through arterioles and capillaries  transport oxygen and substrates to mucosa  removes acid, that can be damaging to the epithelium……

  15. CONTINUED…………………………………….. 2. H. PYLORI INDUCED PUD: • Microaerophilic bacterium • Found primarily in stomach • Bacteria  produces large amounts of UREASE  hydrolyzes UREA present in gastric juice to AMMONIA and CARBON DIOXIDE • Local buffering action produced by ammonia  creates a NEUTRAL MICROENVIRONMENT within and surrounding the bacterium  protects it from lethal effects of the acid…………….

  16. CONTINUED……………………………………….. • Actions exerted by H.Pylori include: • DIRECT MUCOSAL DAMAGE, BY PRODUCING VIRULENCE FACTORS AND ENZYMES: • Virulence factors include: • Vacuolating cytotoxins b. Cytotoxin associated gene protein c. Growth inhibitory factors • Enzymes include : • Urease b. Protease c. Lipase • ALTERATION IN HOST IMMUNE SYSTEM: • Directly: By Cell-mediated immunity (CMI) • Indirectly : By activated neutrophils and macrophages

  17. CONTINUED………………………………………. c. ALTERATION IN GASTRIC ACID SECRETION: • H.Pylori  inhibits ANTRAL D CELLS  Decreased production of SOMATOSTATIN  Withdrawal of inhibitory effect of SOMATOSTATIN on GASTRIN  Increased GASTRIN PRODUCTION…………………….. 3. NSAIDs INDUCED PUD: • NSAIDs  block COX pathway  Prostaglandin synthesis is inhibited  withdrawal of protective effect of Prostaglandins on mucosa  increased secretion of gastrin  increased production of HCl in stomach • Inhibition of COX pathway  causes activation of LOX pathway  activation of LEUKOTRIENES  Stimulation of NEUTROPHIL ADHERENCE  Mucosal damage occurs……………………….

  18. CONTINUED………………………………………. 4. STRESS ULCERS: • Several physiological stress (Trauma, injury, burns, surgery )  induces SUPERFICIAL MUCOSAL EROSIONS / GI ULCERS • Causes of ulcers include: • Decreased prostaglandin production • Decreased cell renewal • Decreased mucosal blood flow…………………………….

  19.  CLINICAL PRESENTATION OF PUD :

  20. CONTINUED………………………………… OTHER SYMPTOMS: • HEMATOCHEZIA (Rare) • MALAENA (Dark, tarry stools, due to intense GI bleeding) • Abdominal cramps • Dyspepsia (Bloating, belching, fatty food intolerance) • Upper GI pain • Hematemesis • Progressive dysphagia • Heartburns………………………………………………

  21.  DIAGNOSIS OF PUD  : • H. PYLORI TESTING: • Invasive / endoscopic tests for H.Pylori include: • Rapid urease test (Endoscopic diagnostic test of choice) • Histopathology • Culture testing • Presence of bacteria in gastric mucosal biopsy specimen is confirmed by detecting the presence of UREASE • Fecal antigen test is done to confirm the presence of H.Pylori, by checking its presence in stools • 3 H.Pylori kits (CLO-test, HP-fast, Pyloritek)  are used for bacteria testing

  22. CONTINUED……………………………………….. • Each kit  consists of combination of UREA SUBSTRATE and PH- SENSITIVE INDICATOR • Place 1/ more gastric biopsy specimen in the kit  if bacteria is present  bacteria will convert urea into ammonia using enzyme urease  produces change in PH  Detected by colour change • UREA BREATH TEST: • Detects H.Pylori infection, by testing for enzymatic activity of bacterial urease • In presence of UREASE produced by bacteria  labelled Carbon dioxide is produced (using heavy isotope, C-13/ C-14)  Absorbed into bloodstream  diffused into lungs  exhaled • HISTOPATHOLOGY: • Applicable in cases, in which rapid urease test turns out to be negative, and there is strong suspicion of H.Pylori infection……… - Antibodies to H.Pylori (IgG) can be measured via whole blood, serum, or plasma…….

  23. CONTINUED…………………………………. 2. ENDOSCOPY: ENDOSCOPY is warranted for the following conditions: • Suspected PUD • To distinguish between GASTRIC and DUODENAL ULCERS • To distinguish between BENIGN ULCERS and MALIGNANT LESIONS • To establish H.Pylori infection by suitable detection 3. RADIOGRAPHY: • CHEST RADIOGRAPH is done to detect GASTRIC PERFORATION 4. ANGIOGRAPHY: - Warranted in patients with massive GI bleeding, in whom ENDOSCOPY can’t be performed

  24. CONTINUED……………………………………………..CONTINUED…………………………………………….. 5. SERUM GASTRIN LEVEL : • Fasting serum gastrin level is obtained in some cases, to detect ZES, associated with : • Patients, with multiple ulcers • Strong family history of PUD • PUD, not associated with H.Pylori/ NSAIDs • PUD, associated with diarrhea and weight loss 6. SECRETIN STIMULATION TEST: • Required, if ZES diagnosis can’t be made on basis of serum gastric level alone • Helps distinguish ZES from other conditions, with a high serum gastrin level (Eg: Use of anti-secretory therapy with a PPI, renal failure/ gastric outlet obstruction……………

  25. CONTINUED……………………………………….. 7. BIOPSY : • Offers 70% accuracy in diagnosing GASTRIC CANCER 8. HISTOLOGICAL FINDINGS: • Depends on DISEASE CHRONICITY • Surface is covered with SLOUGH and INFLAMMATORY DEBRIS • Beneath this NEUTROPHILIC INFILTRATION  ACTIVE GRANULATION , with MONONUCLEAR LEUKOCYTIC INFILTRATION and FIBRINOID NECROSIS may be seen • In CHRONIC SUPERFICIAL GASTRITIS  LYMPHOCYTES, MONOCYTES and PLASMA CELLS often infiltrate mucosa and submucosa

  26. CONTINUED…………………………………………….CONTINUED……………………………………………. 9. EMERGENCY DEPARTMENT (ED) WORKUP DIAGNOSIS: • ED workup varies based on presentation • Includes: • CBC : To evaluate ACUTE/ CHRONIC BLOOD LOSS • ELECTROLYTES, BUN, SERUM CREATININE: For critical- appearing patients, who require fluid- resuscitation • Activated prothrombin time, PT, INR : For patients, with active bleeding, under ANTICOAGULANT therapy • AMYLASE, LIPASE and LIVER TRANSAMINASE LEVELS: To rule out common causes of EPIGASTRIC PAIN………………………………………..

  27.  MANAGEMENT OF PUD  : INCLUDES: • GOALS OF THERAPY • PHARMACOTHERAPY • NON-PHARMACOTHERAPY/ PATIENT COUNSELLING TIPS+ HOME REMEDIES FOR PUD

  28. 1. GOALS OF THERAPY: • To alleviate from pain • To relieve ulcers as soon as possible • Prevention of complications (bleeding, perforation) • Prevention of relapse • To focus on medication adherence, food restrictions , and home remedies • To improve QOL(Quality of Life)……………………………….

  29. 2. PHARMACOTHERAPY OF PUD: DIVIDED INTO 4 THERAPIES: • THERAPY, INVOLVING REDUCTION OF GASTRIC ACID SECRETION • ANTACID THERAPY • ULCER PROTECTIVE/ CYTOPROTECTIVE THERAPY • ANTI H-PYLORI THERAPY………..

  30. CONTINUED…………………………………… • THERAPY, INVOLVING REDUCTION OF GASTRIC ACID SECRETION: Drugs include: • H2- ANTIHISTAMINES • ANTICHOLINERGICS • PROSTAGLANDIN ANALOGUES • PROTON PUMP INHIBITORS (PPIs)

  31. H2- ANTIHISTAMINES: • MOA: Drugs  competitively inhibit HISTAMINE at H2- RECEPTOR of GASTRIC PARIETAL CELLS  Causes reduction in gastric acid secretion, gastric volume and Hydrogen ion concentrations • ADRs: a. Headache b. Dizziness c. Decreased libido, gynecomastia and impotence (for high doses of CIMETIDINE) • DRUG INTERACTIONS: • CIMETIDINE  inhibits metabolism of THEOPHYLLINE, CARBAMAZEPINE, METRONIDAZOLE, PHENYTOIN, WARFARIN  increases their toxicities • CIMETIDINE + ANTACIDS  Decreased absorption of former • DOSES: • Cimetidine (CIMETIDINE) : 400 mg BD/ 800 mg at bed time • Ranitidine (RANTAC) : 150 mg BD/ 300 mg at bed time • Famotidine (FAMTAC) : 40 mg at bed time, or 20 mg BD

  32. d. Roxatidine (ROTANE) : 75 mg BD/ 150 mg at bed time e. Nizatidine (AXID) : 150 mg BD/ 300 mg at bed time…………………… II. ANTICHOLINERGICS: • Drugs  reduce volume of gastric juice, without raising it PH(In the absence of food presence in stomach) • Associated with intolerable anticholinergic ADRs • Due to comparatively less efficacy and more ADRs  anticholinergics are usually replaced by H2- BLOCKERS and PPIs, for choice of therapies • Drugs include: • ATROPINE • PROPANTHELINE • OXYPHENONIUM • PIRENZEPINE………………………………………………………………………..

  33. III. PROSTAGLANDIN(PG) ANALOGUES : • PG analogues have the following actions: • Stimulate mucus production • Increase blood flow throughout GIT lining • Form coating to protect ulcerated tissue • Drug includes MISOPROSTOL • MISOPROSTOL  enters body  de-esterified to MISOPROSTOL ACID  This compound is responsible for activity mainly used in NSAID-induced PUD • ADRs: • Diarrhea b. Abdominal cramps c. Poor patient acceptability d. Uterine bleeding • CONTRAINDICATION: Pregnancy abortion can occur • DRUG INTERACTION: Drug + DICLOFENAC  Increased abdominal pain, diarrhea - DOSE : MISOPROSTOL (MISOPROST) : 200 microgram QID…………………………………………..

  34. IV. PROTON- PUMP INHIBITORS (PPIs): MOA: • Drug  blocks GASTRIC H+-K+ ATPase ENZYME SYSTEM IN PARIETAL CELLS  Decreased exchange of H+ and K+ occurs  decreased gastric acid secretion occurs ADRs: • Nausea b. Loose stools c. Dizziness d. Arthralgia e. Atrophic gastritis (On prolonged OMEPRAZOLE THERAPY) DRUG INTERACTION: • OMEPRAZOLE + CLOPIDOGREL  Inhibition of CYP2C19 by OMEPRAZOLE  Decreased efficacy of CLOPIDOGREL DOSES: • OMEPRAZOLE (OMIZAC) : 20 mg capsule • ESOMEPRAZOLE ( IZRA) : 20-40 mg OD

  35. c. LANSOPRAZOLE (LANPRO) : 15-30 mg OD d. PANTOPRAZOLE (PANTOCID) : 40 mg OD e. S- PANTOPRAZOLE (PANPURE; Twice potent that pantoprazole) : 20 mg tablet f. RABEPRAZOLE ( RABLET) : For ZES: 60 mg/day g. DEXRABEPRAZOLE (DEXPURE, dextro-enantiomer of rabeprazole) : 10-20 mg/day…………………………………………………..

  36. B. ANTACID THERAPY: INCLUDES: • SYSTEMIC ANTACIDS • NON-SYSTEMIC ANTACIDS

  37. SYSTEMIC ANTACIDS: • SODIUM BICARBONATE : • Short duration of action • Potent neutralizer (raises PH> 7) • ADRs: • Alkalosis • CO2 production in stomach  discomfort, belching and risk of ulcer perforation • Drug Causes increased sodium levels  may worsen edema and CHF • Mainly used to treat HEARTBURNS • SODIUM CITRATE  : • Properties, similar to sodium bicarbonate • No carbon dioxide produced, contrary to NaHCO3………………………….

  38. II. NON- SYSTEMIC ANTACIDS: • Insoluble, basic compounds • Poorly absorbed • Drugs  reach in stomach to form corresponding CHLORIDE SALT  CHLORIDE SALT reacts with intestinal bicarbonates  prevents non-absorption of HCO3-  Prevents acid-base disturbances • Drugs include: • MAGNESIUM HYDROXIDE  : • Aqueous suspension is known as “MILK OF MAGNESIA” • Low alkalinity • ADR: Rebound acidity(mild) • DOSE: MILK OF MAGNESIA (0.4 g/ 5 ml. suspension)

  39. MAGNESIUM TRISILICATE : • Low solubility and reactivity • Possesses laxative property • Avoid in people with compromised RENAL FUNCTION • ALUMINIUM HYDROXIDE GEL : • Weak, slowly reacting antacid • Aluminum ion relaxes smooth muscle  delays gastric emptying • ADRs: • Constipation • If used in patient with RENAL FAILURE  decreased AL3+ excretion occurs  encephalopathy, osteoporosis can occur • Drug  binds to phosphate in intestine  prevents is absorption  used for PHOSPHATE STONES and HYPERPHOSPHATEMIA (Due to its HYPOPHOSPHATEMIA effect) - DOSE: ALUDROX : 0.84 g tablet……………………….

  40. MAGALDRATE : • Hydrated complex of hydroxyl magnesium aluminate  reacts with acid rapidly  released ALUMINUM HYDROXIDE  Shows its action slowly • Sustained neutralizing action • CALCIUM CARBONATE  : • Rapidly acting acid neutralizer • ADRs: • Distention • Acid rebound • Constipation • MILK-ALKALI SYNDROME (rare now)

  41. ANTACID COMBINATIONS  : • DIGENE : Dried AL(OH)3 gel (300 mg) + Mg.Al.Silicate (50 mg) + Mg(OH)2 [25 mg] • GELUSIL : Dried Al (OH)3 gel (250 mg) + Mg.trisilicate (500 mg) • MUCAINE : [ Al(OH)3 {290 mg} + Mg(OH)2 {98 mg} + Oxethazaine {10 mg}] / 5 ml. suspension. • ANTACID DRUG INTERACTION  : - Antacids  decrease gastric PH and form complexes  decrease absorption of TETRACYCLINES, IRON SALTS, FLUOROQUINOLONES, H2- BLOCKERS, etc…………………

  42. C. ULCER PROTECTIVE/ CYTOPROTECTIVE THERAPY: INCLUDES: • SUCRALFATE • COLLOIDAL BISMUTH SUBCITRATE(CBS)

  43. SUCRALFATE: • Basic aluminum salt of OCTA-SULFATED SUCROSE • Drug  binds with positive charged proteins in exudates  forms viscous adhesive substance  protects GI lining against PEPSIN, GASTRIC ACID, BILE SALTS, etc • Drug  also initiates production of EPITHELIAL GROWTH FACTOR and PROSTAGLANDINS • Delays gastric emptying and heals GI ulcers • Avoid in renal failure patients • ADRs: • Dry mouth b. Hypophosphatemia c. Constipation • DOSE: ULCERFATE( 1 g, in empty stomach, 1 hr. before each of three meals, and at bed time; for 4-8 weeks) • DRUG INTERACTION: ANTACIDS + SUCRALFATE  Decreased efficacy of latter…..

  44. II. COLLOIDAL BISMUTH SUBCITRATE(CBS): • Water- soluble • Actions include: • Increased gastric mucosal PGE2, mucus and HCO3- production • Precipitation of mucus glycoproteins and coating of ulcer base • Detachment and direct inhibition of H.Pylori • Avoid concomitant use of milk and antacids • Treats non-ulcer dyspepsia and gastritis caused by H.Pylori • ADRs: • Headache b. Dizziness c. Dark tongue and stools • DOSE: TRYMO: 120 mg (half an hour before each of three meals , and at bed time for 4-8 weeks……

  45. D. ANTI-H.PYLORI THERAPY: Includes: • AMOXICILLIN • CLARITHROMYCIN • TETRACYCLINE • METRONIDAZOLE/ TINIDAZOLE

  46. AMOXICILLIN (AMOXIL): • Used as combination therapy • Treats duodenal/ gastric ulcers associated with H.Pylori • Drug  interferes with synthesis of cell wall mucopeptides during active multiplication of bacteria  bactericidal activity occurs • Administer as PPT based TRIPLE THERAPY • DOSE: (1 g AMOXICILLIN + 20 mg OMEPRAZOLE/ 30 mg LANSOPRAZOLE + 500 mg CLARITHROMYCIN) II. CLARITHROMYCIN (BIAXIN): • Semisynthetic macrolide • Drug  binds to ‘P’ site of 50S ribosomal subunit of microbe  stimulates dissociation of peptidyl t-RNA from ribosomes  prevents protein synthesis • ADR : Reversible ototoxicity, GI irritations • DOSE: Same as the regimen prescribed for AMOXICILLIN combo therapy…………………

  47. III. TETRACYCLINE (SUMYCIN): • PROTEIN SYNTHESIS INHIBITOR • Treats duodenal/ gastric ulcer • Used in combination therapy • ADR: Photo toxicity, bone growth suppression • DOSE: Mainly as QUADRUPLE THERAPY, like: • CBS (120 mg QID) + TETRACYLINE (500 mg QID) + METRONIDAZOLE ( 400 mg TDS) + OMEPRAZOLE (20 mg BD) OR • H2 receptor antagonist (BD) + METRONIDAZOLE (250 mg) + BISMUTH SUBSALICYLATE (525 mg) + TETRACYCLINE (1500 mg QID)

  48. IV. METRONIDAZOLE (FLAGYL): • Used as combination therapy • Treats duodenal/ gastric ulcers • Drug  binds to DNA of microbe  inhibits protein synthesis  causes cell death • ADR: a. CNS disturbances b. GI irritations • DOSE :{ AMOXICILLIN (750 mg) + OMEPRAZOLE(20 mg) / LANSOPRAZOLE (30 mg) + METRONIDAZOLE (400 mg)} ANTI H-PYLORI KITS: • HELIBACT : OMEPRAZOLE (20 mg, 2 capsules) + AMOXICILLIN (750 mg, 2 tabs) + TINIDAZOLE (500 mg, 2 tabs) • LANPRO AC : LANSOPRAZOLE (30 mg, 2 capsules) + CLARITHROMYCIN (250 mg , 2 tabs ) + AMOXICILLIN (750 mg, 2 tabs)…………………………..

  49. 3. NON- PHARMACOTHERAPY/ PATIENT COUNSELLING TIPS+ HOME REMEDIES FOR PUD: • SMOKING CESSATION • TRY NON- PRESCRIPTION MEDICATIONS, THAT REDUCE STOMACH ACID(MAKE SURE THAT YOU TELL YOUR DOCTOR ABOUT ANY MEDICATIONS THAT YOU ARE TAKING) • MAKE CHANGES TO YOUR DIET (EAT SMALLER, MORE FREQUENT MEALS) • MODERATE TO NO ALCOHOL CONSUMPTION • AVOID FRIED, SPICY AND OILY FOODS, UNTIL ULCER HEALS

  50. 6. VITAMIN E: • According to DOCTORS at KIEV MEDICAL INSTITUTE  300 mg of VITAMIN E DAILY  treats PUD ulcers • Also increases protein repair in intestinal linings 7. BANANAS: • BANANAS( dried, unripe)  contain SITOINDOSIDES  Increase mucus in GIT  Provides strong protective coating to help treat and prevent ulcers • Bananas  contain water- soluble polysaccharides  help in ulcer treatment • Banana powders are most effective • Peel bananas  cut them into thin slices  put them under sun, over/ food dehydrator  dry them slowly  when dry, grind them into fine powder  mix 2 tbsp. of powder with 1 tbsp. of honey  take this mixture thrice a day

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